Sports Injuries - Mechanisms, Prevention and Treatment 2nd Ed - F. Fu, D. Stone Lippincott 1994) WW

Sports Injuries: Mechanisms, Prevention, Treatment 2nd edition (December 1994): by Freddie H.
Fu (Editor), David
A., M.D. Stone (Editor) By Lippincott, Williams & Wilkins
By OkDoKeY
Sports Injuries: Mechanisms, Prevention, Treatment
CONTENTS
Editors
Dedication
Contributing Authors
Preface
Acknowledgments
SECTION 1: EVALUATION, TRAINING, AND SPECIAL CONCERNS
1 Customizing the Preparticipation Evaluation

Dan M. Somogyi and Ian Shrier
2 Conditioning and Training

Paul A. Borsa and Scott M. Lephart
3 The Athletic Trainer

Robert O. Blanc, Kevin M. Conley, Stacey C. Inglis, Karl A. Salesi, and Jennifer B. White
4 Environmental Factors in Athletic Performance

Timothy A. Barker, H. Andrew Motz, and Wayne K. Gersoff
5 Biomechanics of Ligaments in Sports Medicine

Savio L.-Y. Woo, Mark A. Knaub, and Maria Apreleva
6 Rehabilitation
David J. Pezzullo and James J. Irrgang
7 Medical Problems
Thomas H. Trojian
8 Cardiovascular Evaluation of the Athlete

James D. Mills
9 Ergogenic Drug Use in Sports

Richard T. Ferro
10 Special Concerns of the Pediatric Athlete

Morey S. Moreland
11 The Aging Athlete

Robert E. Leach
12 Special Concerns of the Female Athlete

Mary Lloyd Ireland and Susan M. Ott
13 Disabled Athlete
Henry H. P. Ho
SECTION 2: SPORT-SPECIFIC INJURIES
14 Baseball Injuries
Russell S. Petrie, John J. Klimkeweicz, and Christopher D. Harner
15 Basketball
Delmas J. Bolin and Craig Bennett
16 Bicycling
Matthew J. Morelli and David A. Stone
17 Boxing
Lyndon B. Gross
18 Competitive Diving
Richard L. Carter
19 Cricket
Thomas Crisp, John B. King, and Answorth A. Allen
20 Dance
David A. Stone, Ruth Kamenski, Julia (Chuan-Hsiu Liu) Shaw, Kathleen M. J. Nachazel, Stephen F. Conti, and Freddie H. Fu
21 Emergency Medical Care at Sports Events

Ronald Roth and Vincent Verdile
22 Equestrian Sports
David M. Jenkinson and Sarah W. Jenkinson
23 Fencing
Julie M. Knowles, Rebecca Jaffe, and Marlene Adrian
24 Football
Robert O. Blanc and Deryk G. Jones
25 Golf
Peter J. Carek
26 Gymnastics
Patrick E. Greis, Jeffery R. Weiss, and Robert T. Burks
27 Ice Hockey
Jeffrey Minkoff, Steven Stecker, Gerard P. Varlotta, and Barry G. Simonson
28 Skating: Figure, Speed, Long-Distance, and In-Line

David L. Muller and Per A. F. H. Renstrom
29 Judo and Karate

Joseph F. Fetto
30 Canoeing and Kayaking

David M. Jenkinson and Sarah W. Jenkinson
31 Lacrosse
Leslie S. Matthews, Richard Y. Hinton, and Nancy Burke
32 Nordic and Alpine Skiing

Gloria M. Beim
33 Power Lifting, Weight Lifting, and Bodybuilding

Thomas C. Namey and Peter J. Carek
34 Racquet Sports
Marc R. Safran
35 Rugby
Mark Ferguson and Clive Noble
36 Running
David N. M. Caborn, Thomas D. Armsey II, Larry Grollman, John A. Nyland, and Joseph A. Brosky, Jr.
37 Scuba Diving
Kevin O'Toole
38 Soccer
John H. Lohnes, William E. Garrett, Jr., and Raymond R. Monto
39 Surfing
Ronald A. Navarro
40 Swimming
Peter J. Fowler
41 Track and Field

Jerome V. Ciullo and Jeremy R. Ciullo
42 Triathlon
Mary L. O'Toole, Thomas K. Miller, and W. Douglas B. Hiller
43 Volleyball
Kathleen A. Swanik and Stacey C. Inglis
44 Water Skiing
Robert L. Waltrip and Noelle Grace
45 Wrestling
Mark C. Mysnyk
SECTION 3: MANAGEMENT AND TREATMENT OF SYSTEMIC AND REGIONAL INJURIES
46 Soft Tissue Athletic Injury

Wayne B. Leadbetter
47 Dermatology
Arlene S. Rogachefsky, Wilma F. Bergfeld, and James S. Taylor
48 Sports Neurology
Steven Goldstein, Lawrence R. Wechsler, and Neil A. Busis
49 Head Injuries
Donald W. Marion
50 Treatment of Sports Eye Injuries

Robert G. Devenyi, Robert C. Pashby, and Thomas J. Pashby
51 Cervical Spine and Spinal Cord Injuries

Robert G. Watkins and Robert G. Watkins IV
52 Lumbar Spine Injuries in Athletes

Robert G. Watkins and Lytton A. Williams
53 Shoulder Injuries
John J. Perry and Laurence D. Higgins
54 Elbow Injuries
Marc R. Safran and James P. Bradley
55 Hand and Wrist Injuries

James R. Williams and Matthew M. Tomaino
56 Knee Injuries
Mark B. Silbey and Freddie H. Fu
57 Foot and Ankle Injuries

John C. Linz, Stephen F. Conti, and David A. Stone
58 Abdominal Injuries
Russell D. Dumire and Andrew B. Peitzman
59 Chest Injuries
Claire Chase and Stephen Z. Turney
60 The Emotionally Intelligent Sports Medicine Practitioner

P. Kevin Elko and Robert O. Blanc
Editors
FREDDIE H. FU, M.D.

David Silver Professor and Chairman
Department of Orthopaedic Surgery
University of Pittsburgh
Pittsburgh, Pennsylvania
DAVID A. STONE, M.D.

Assistant Professor
Department of Orthopaedic Surgery
University of Pittsburgh
To my wife, Hilda; our son, Gordon; our daughter, Joyce; and to my parents.
F.H.F.
To my wife, Debra Bruckman; our sons, Bradley and Todd; my parents,
Joseph and Rosalind Stone; and to my mentor, William F. Fishbaugh, M.D.
D.A.S.
PREFACE
This second edition of Sports Injuries: Mechanisms • Prevention • Treatment provides the latest advances in sports
medicine and, with the rise in popularity of some new sports, includes important information for the sports medicine
specialist. We have added new chapters to each section of the book and have updated all of the original chapters.
Coverage of a particular sport includes discussions on conditioning, and when possible, on sport-specific treatment
options. Our goal to present comprehensive material without repetition made the editing process a challenge, but we
believe we have accomplished this to a greater degree than in our first edition.
We want to present a solid foundation for the fledgling sports physician while providing a solid reference tool. As the
treatment and evidence-based options become more clearly defined, we hope this text will be regarded as one that
provides a comprehensive look of the sports literature at the start of the twenty-first century.
ACKNOWLEDGMENTS
So many people contributed to this project, it is difficult to know whom to thank first. We are, above all, indebted to our
authors and their families. Ms. Dorothy Roman has again handled correspondence, and coordinated the filing and
transfer of documents in her highly efficient way. The staff at Lippincott Williams & Wilkins have been supportive and
patient, and have provided excellent technical support; and our thanks go in particular, to Lisa Consoli and James Merritt.
This project would not have succeeded without them.
1 Customizing the Preparticipation Evaluation
CUSTOMIZING THE PREPARTICIPATION EVALUATION

DAN M. SOMOGYI
IAN SHRIER
General Concepts
Purpose of the Preparticipation Evaluation
Cost-Effectiveness
Format
Timing and Frequency
Who Should Conduct the Examination?
Components of the Evaluation
History
Physical Examination
Laboratory Investigations
Hemoglobin and Ferritin
Urinalysis
Electrocardiography and Echocardiography
Cholesterol Screening
Clearance/Disqualification Issues
Conclusions
Appendix A. Overview of All Studies that Specifically Evaluated the Entire Preparticipation Physical Examination (PPE)
Appendix B. Medical Conditions and Sports Participation
Chapter References
It is appropriate to begin a text devoted to sports injuries with a discussion of the preparticipation evaluation (PPE)
because the goal of the PPE fulfills one of the basic tenets in medicine: to detect problems before they occur. To achieve
this goal, the PPE uses screening and targeted case finding to diagnose conditions that predispose to injury, reinjury, or
illness.
Despite the large amount of literature regarding the epidemiology of sports injuries ( 1), there are few data that
specifically evaluate risk factors and prevention issues of the PPE. As a result, it is impossible to discuss the
effectiveness of the PPE in terms of specificity, sensitivity, and positive or negative predictive values. An excellent review
of specific items that are often incorporated in the PPE has been endorsed by five major medical societies in the United
States (2). In addition, a number of reviews have focused on the PPE according to age group ( 3,4,5,6 and 7), sex (8), or
sport (9,10). Rather than repeat this information, we have chosen a conceptual approach. Our experience has shown that
different institutions and team physicians have different objectives they wish to accomplish with a PPE. This means that
any standardized approach to the PPE, as has been promoted by some authors ( 2,11), cannot be appropriate for all
situations. Rather, there should be a standardized approach to deciding which specific parts of the PPE to include in
order to achieve the institution's or team physician's objectives. Therefore, we first review the various objectives of the
PPE. Next, we summarize the key points of the history, physical examination, and laboratory tests so as to give readers
an easy “user's guide” to creating a PPE that best fulfills their individual needs. We have focused this discussion on the
young athlete. PPEs for elderly persons who are beginning an exercise program or for disabled athletes should focus on
the medical problems that are prevalent in those populations.
GENERAL CONCEPTS
Purpose of the Preparticipation Evaluation
Five major American medical societies have published a Consensus Statement indicating that the overall goal of the PPE
is to allow athletes to participate in sports in the safest manner possible. In addition, they categorized individual
objectives according to priority of importance ( 2). We have included their analysis and also categorized the individual
objectives as relating to primary or to secondary prevention. Table 1.1 lists the objectives according to screening type
and gives the corresponding priority stated in the Consensus Statement.
TABLE 1.1. OBJECTIVES OF THE PREPARTICIPATION EVALUATION ORGANIZED BY TYPE OF PREVENTION

CATEGORY
In addition to both screening and meeting medicolegal and insurance requirements, there are a number of additional
objectives that can be achieved by the PPE. These can be grouped into objectives for elite and for nonelite athletic
subjects (Table 1.2).
TABLE 1.2. ADDITIONAL OBJECTIVES OF THE PREPARTICIPATION EVALUATIONa
Despite this long list, many clinicians focus almost exclusively on whether athletic participation places the athlete at an
unacceptable risk for serious injury or illness ( 2). Even though athletes are rarely excluded from sports participation
(0.3% to 1.3%) (Appendix A; 12,13,14,15,16 and 17), a well-conducted PPE can often lead to the diagnosis of correctable
conditions that would otherwise increase the risk of mild to moderate injury if not properly treated (e.g., poorly
rehabilitated ankle sprains with residual weakness and poor proprioception) ( 18). This can have a large impact on
athletic participation during the season as well as on the general health care of the active population. For instance, Bijur
et al. (19) estimated that 4.3 million injuries to children aged 5 to 17 years and 978,000 serious injuries occur annually
involving sports and recreation. At the high school level, approximately 22% to 39% of sports participants are injured
every year (20,21 and 22); an estimated 1.5 million injuries occurred in the United States for basketball, football,
gymnastics, soccer, volleyball, and wrestling in 1991 (cited in reference 19). During the period 1996–1997, some 6
million high school students participated in organized sports, with an injury rate ranging from 3.4 (baseball) to 9.6 (spring
football) per 1,000 athlete exposures (cited in reference 4).
In addition to injury and illness detection, some PPE proponents plead that a more holistic approach is needed ( 23,24
and 25). This approach stems from studies suggesting that the PPE represents the only contact with a health care
provider for 23% to 90% of the adolescent population ( 12,16,25). As a result, many authors have tried to broaden the
objectives of the PPE to include other forms of health maintenance, addressing issues that affect the adolescent's health
such as sexuality, school performance, and use of tobacco, drugs, and alcohol ( 26). As an example, the American
Medical Association Report of the Board of Trustees (22) states that the health professional should question young
athletes regarding their use of anabolic-androgenic steroids or other ergogenic aids.
Although these are laudable goals, we believe that there is a danger of the PPEs becoming too all-encompassing. There
is usually limited time available for this examination, and introducing too many issues may dilute the effectiveness of
achieving the most important objectives (15,27). In fact, elite athletes have expressed concerns that personal questions
about sexual activity, eating disorders, smoking, and other issues should not be asked ( 28) and that the PPEs are “not
targeted enough on past athletic injuries” ( 29). In addition, it may be inappropriate to assume the care of athletes if their
primary care physician already appropriately treats them. Consequently, we advise explaining the focused and limited
nature of the PPE to both parents and athletes. If the PPE truly represents the athlete's only health evaluation, it is up to
physicians or other health professionals to modify their approach.
Cost-Effectiveness
The overall cost-effectiveness of the PPE has been questioned. Risser et al. ( 16) analyzed the costs of performing the
PPE on 763 adolescent athletes. His data demonstrated that the evaluations were not cost-effective because of their low
yield of significant abnormalities. Despite this lack of “scientific” cost-effectiveness, many parents and coaches still
believe that the potential loss of productivity of the athlete outweighs the significant financial costs generated from
screening. This is particularly true in the high-visibility sports and in upper-level athletic programs. In addition, there has
been a push to find the “needle in the haystack” when the needle is a lethal disease that may kill the athlete on the
playing field ( 30). Although there is no right or wrong answer to this question, the cost of the PPE can be decreased by
using a format that is specifically designed to meet the needs of the team or institution. The following section describes
the advantages and disadvantages of the various proposed PPE formats.
Format
The chosen format for the PPE depends on the individual physician's or institution's objectives ( Table 1.1 and Table 1.2).
The four most common options are (a) a private physician, (b) a single-physician “assembly line,” (c) a multistation
approach, and (d) a computerized questionnaire followed by a single-physician or multistation physical examination. The
private physician is the athlete's personal physician, who probably has known the athlete for a long time. The
assembly-line physician may or may not be the team's physician. This format is set up in a large room with a semiprivate
area, sometimes a locker room, to facilitate the evaluations. The athletes line up to be evaluated sequentially, and few
support staff are needed. The multistation format usually takes place in a similar setting but there are multiple stations,
each focused on one evaluation (e.g., Vital Signs, Vision, Flexibility); significant support in addition to the physician is
required. The information from each of the stations is collated before the athlete is seen at a final “clearance” station.
Finally, a newer method uses a computerized, web-based history form that incorporates the information into a database
(31), which is then printed for the physician to use during the physical examination.
Each of these approaches has its own advantages and disadvantages ( Table 1.3 and Table 1.4). A complete discussion
is beyond the scope of this chapter, and the reader is referred to the Consensus Statement on PPE ( 2). Briefly, whereas
the private personal physician may have the benefit of a long-standing physician-patient relationship to help in the
decision-making process, he or she may not be familiar with each of the sport-specific health concerns of the athlete. In
addition, this physician may not be the health care provider during the actual playing season. Still, the long-standing
relationship and trust between patient and physician may be an important factor in obtaining more truthful responses to
psychosocial and sensitive questions.
TABLE 1.3. ADVANTAGES AND DISADVANTAGES OF THE VARIOUS FORMATS USEDa FOR THE
PREPARTICIPATION EVALUATION
TABLE 1.4. ABILITY OF PREPARTICIPATION EVALUATION FORMATS TO ACHIEVE DESIRED OBJECTIVESa
If a sports medicine clinician is used, there remain two choices for the format. Either one physician sees all athletes as
they pass through the office (i.e., assembly line), or athletes rotate through multiple stations with each station staffed by a
different person. DuRant et al. ( 32) compared single versus multiple examiners in a station-based format for 922 PPEs.
They found that the station-based examination uncovered a greater number of abnormal findings in the spines, hip,
knees, thighs, and ankles compared with the single-examiner model. Furthermore, 6.4% of athletes were prescribed
additional evaluation or conditioning in the station-based examination, compared with 2.4% in the single-examiner group
(p=0.05). Because the private physicians detected far fewer abnormalities, the authors concluded that the station-based
method is preferable. On the other hand, it is unclear how “significant” these additional abnormalities were. For instance,
it is possible that treatment for some of these injuries would not alter, or would minimally alter, athletic performance or
injury risk. Furthermore, the multistation design may limit the rapport between physician and patient. In summary, the
most appropriate format depends on the objectives of the particular PPE. The legends for Table 1.3 and Table 1.4 should
help the reader understand how the information can be put together to decide the optimal format for each individual
institution.
Timing and Frequency
Most experts now agree that a full evaluation is necessary only before the start of a new athletic program (e.g., high
school, college), with a brief interim evaluation performed before each subsequent year ( 33,34). During these interim
evaluations, the athlete may fill out the complete questionnaire or just a simple update form. Apart from the fact that long
questionnaires often yield inaccurate information ( 35), athletes who have to redo a questionnaire several years in a row
may have problems with recall of events that occurred in the more distant past (e.g., high school injuries). Therefore, we
believe that the use of an update form is the most appropriate method. In addition, a “problem list” (description of injury or
illness, date started, date resolved) should accompany each athlete's chart. Another advantage is that the problem sheet
can facilitate transfer of information among medical team members when the athlete moves between institutions (e.g.,
high school to college) or when the team physician or trainer changes. Furthermore, if full PPEs are limited to new
athletes, then more time can be allocated for each examination and there may be less likelihood of missing an important
finding.
There are no studies that specifically evaluate the most appropriate time to conduct the evaluation. To allow enough time
for identification, workup, and treatment of both medical and orthopedic injuries, scheduling the PPE at 6 weeks before
the start of preseason practice has been recommended ( 2). However, for some multisport athletes and in sports for which
the athlete trains and competes at different times of the year, 6 weeks before the start of the school year would actually
be midseason. Furthermore, in a practical sense, such timing would mean scheduling the football PPE in the middle of
the summer, when university athletes are not in the school vicinity ( 36). Therefore, the PPE may need to be conducted at
the end of the previous school year. Realizing that injuries may occur in the summer, rookies would still be examined at
the beginning of the school year, and veterans would be responsible to notify the physicians of any change in health
status once school begins.
Timing of the PPE may also depend on other components of a complete performance evaluation. For instance, many
universities conduct fitness testing (e.g., maximal oxygen consumption, strength, flexibility) at the beginning of the school
year and have their PPEs done at the same time as part of a multistation design. In this case, it would not be possible to
conduct the PPE 6 weeks before the start of the season. These PPEs may still be effective in determining
contraindications to participation, but they would not be effective in diagnosing injuries in time to complete an effective
rehabilitation program before the start of the season. This reemphasizes that the best format for the PPE depends on the
particular objectives of the PPE being done.
Who Should Conduct the Examination?
There is no ideal provider or group of providers to perform the PPE. These vary with the setting, the level of sports
participation, and the objectives of the PPE. To adequately assess the way in which an athlete's health will be affected by
the chosen sport requires an understanding of injury risks, illness risks, predominant motions, psychological stress, and
the environment in which the sport will be played. A single examiner needs to be proficient in the entire scope of the
evaluation, whereas a station-based examiner only needs proficiency in performing the specific duties assigned. This
may be the reason the station-based examination has been able to detect more abnormalities in the PPE ( 32). The
greater experience and more specific areas of expertise of the station-based examiners certainly improves the
effectiveness of the examination, but many institutions must weigh these benefits against the cost of the process. For
example, if there is a limited budget, the athletes may be better served by using the funds to improve rehabilitation
services rather than using them for a multistation PPE. However, as a minimum, the American Heart Association (AHA)
recommends (11,37) that the cardiovascular examiner be “a health care worker with the requisite training, medical skills,
and background to reliably obtain a detailed cardiovascular history, perform a physical examination, and recognize heart
disease.”
COMPONENTS OF THE EVALUATION
History
A history alone can identify most of the athletes requiring further evaluation for possible exclusion from sports ( 12,13).
However, of greater importance is the effectiveness of the history section of the PPE in identifying abnormalities that
predispose the athlete to injury or illness. For this question there are few data. Effectiveness is maximized if the following
three components are considered: language limitations, completion of the history by the athlete and parent together, and
review of the questionnaire with the athlete before the examination.
Most authors (2,25,38) agree that the primary aspects of the history are the inquiries into a few key components,
including previous musculoskeletal injury, sudden cardiac death (SCD) in family members, previous concussions,
exercise-induced respiratory symptoms, the female athlete triad, missing organs, and an allergy history. We believe that
these are key components because they screen for absolute and relative contraindications to play. For a complete list of
absolute and relative contraindications see Appendix B. The history may vary with regard to the broader issues that may
affect the adolescent athlete, such as immunizations or psychological components and counseling ( 2).
What is the best method for history taking? Although the essential history information may be collected by
self-administered questionnaire in a timely fashion, this has the disadvantage of decreasing the physician-patient
interaction. The need for efficiency must be weighed against the benefits of face-to-face interaction. Many forms have
been presented and endorsed by various authors and societies ( 2,33,38).
The length of the questionnaire is important. If it is too short, the necessary information will not be obtained. However, if it
is too long, the patient may adopt a strategy that completes the task in the shortest possible time ( 35). For PPE-type
questionnaires, patients may simply answer Yes (or No) to every question ( 35). In follow-up questionnaires, they may
choose to accept the status quo ( 35). It is therefore important that every question should “count.” As an exercise, Table
1.5 includes a column that explicitly states which objective of the PPE each question is designed to answer. Some
questions help to answer more than one objective. Using a table such as this may help the reader choose which
questions are most appropriate for the specified purposes of the PPE.
TABLE 1.5. OBJECTIVES FULFILLED BY PREPARTICIPATION EVALUATION HISTORY QUESTIONS, DIVIDED BY

ORGAN SYSTEMa
A questionnaire for veteran athletes should be modified so that only recent changes are noted. For example, it might ask,
“Since your last examination, have you experienced....” Another alternative exists when computer resources are
available. In this case, all the data can be entered into a computer, and the previous year's answers can be presented to
the athlete (either on a printed form or through a computer network or website) so that the athlete can mark any changes
directly on the form. A pilot project is currently underway at Stanford University ( 31).
The entire questionnaire of the PPE should be an area of active research. There are currently no PPE questionnaires
that have been tested for psychometric properties such as reliability or validity. Evaluation of these properties could also
help determine which questions are redundant and which need to be repeated in a different manner to ensure accurate
detection of injury or illness ( 39). Although this is not an easy undertaking, such research would greatly improve the
quality and effectiveness of PPE questionnaires.
The proposed components of the PPE physical examination are listed in Table 1.6. Just as “every question counts,” we
believe that the time and cost of the physical examinations can be minimized if the procedures are focused toward the
individual institution's particular objectives. Therefore, we developed a grid for the physical examination similar to the one
for the questions to be posed in the history. This table should help the reader choose which aspects of the physical
examination to include, and which to exclude, depending on the particular objectives of the PPE. Two of the specific
systems deserve in-depth discussion.
TABLE 1.6. OBJECTIVES FULFILLED BY EACH PHYSICAL EXAMINATION MANEUVER, DIVIDED BY ORGAN
SYSTEMa
Musculoskeletal Examination
The basic musculoskeletal screening examination has been described by Stone and Blanc ( 40) and incorporates a
number of maneuvers designed to demonstrate the full, painless range of motion of all joints. The orthopedic component
of the PPE should pay specific attention to problems that may predispose the athlete to injury. However, there are
conflicting data regarding the ability of the musculoskeletal examination to predict athletic injuries. Meeuwisse and
Fowler (41) investigated the relation between preseason findings and subsequent injuries in an analysis of 712
intercollegiate athletes and found that the preseason examination did not help in the prediction of sports injuries. In a
prospective analysis, Lysens et al. ( 42) found that athletes in high-intensity sports who had loose ligaments and good
flexibility were more prone to injuries. However, among endurance athletes muscle tightness was a risk factor for injury.
More research is needed in this area to clearly determine what the musculoskeletal part of the PPE can actually predict.
Because most injuries are reinjuries, a past history of injury and the completeness of the rehabilitation are probably the
best predictors of musculoskeletal injuries. In 1977 Garrick ( 43) developed the 12-step orthopedic screening examination
(i.e., physical examination only). By examining for asymmetry in muscle bulk, strength, or range of motion, these
maneuvers detect recent injuries or incompletely healed and rehabilitated injuries. Gomez et al. ( 44) prospectively
compared three approaches: the 12-step screening physical evaluation alone, the history alone, and the combination of a
history and an orthopedic physical evaluation together. The screening physical examination alone had a sensitivity of
50.8% and a specificity of 97.5%, with a 40.9% positive predictive value and a 98.3% negative predictive value. However,
the history alone had a sensitivity of 91.6% (other statistics not obtainable from article). Because of the low sensitivity of
the orthopedic screening examination, the authors suggested some improvements, such as adding tests for dynamic
strength, balance, and stability (e.g., hop test). Table 1.7 summarizes a musculoskeletal examination (2,43,44).
TABLE 1.7. MUSCULOSKELETAL SCREENING EXAMINATION
One of the strong beliefs in sport medicine is that poor biomechanics predisposes to injury. However, to date, little
epidemiologic research exists to support this hypothesis ( 45). Because the theory appears logical and the analyses thus
far have generally been univariate, more large-scale studies with multivariate analyses are required before the concept
should be abandoned. That being said, Table 1.8 lists the biomechanical factors that are commonly thought to
predispose toward injury.
TABLE 1.8. POTENTIAL BIOMECHANICAL FACTORS CONTRIBUTING TO INJURY
Specific sports are often associated with specific injuries. Therefore, we have included a sport-specific injury table ( Table
1.9) to guide the examiner when performing the PPE. For example, biomechanical factors are likely to be important in
long-distance runners. A closer examination of Table 1.9 may also provide help for improving sport-specific
questionnaires. Another example would be a question on previous dislocations of the upper extremity asked of athletes in
Judo. For a more complete discussion of sport-specific injuries, see Caine et al. ( 1).
TABLE 1.9. SPORTSPECIFIC MUSCULOSKELETAL INJURIESa
Cardiovascular Examination
The cardiovascular system requires special attention because in this area the PPE screens for both relatively common
illnesses and rare, life-threatening illnesses. Table 1.10 lists the essential components for the screening physical
examination. If the history suggests certain cardiorespiratory pathology, then a more detailed physical examination of
associated areas is suggested. Note that the standard format for both the assembly-line and the multistation PPE could
be improved if the cardiovascular examination were performed in a quiet room.
TABLE 1.10. OUTLINE FOR THE CARDIAC HISTORY AND PHYSICAL EXAMINATION IN PREPARTICIPATION
SCREENING
Blood pressure limits for hypertension are age dependent ( 46). Although Magnes et al. (47) reported that high blood
pressure represented 38% of all abnormal findings in the PPE for adolescents, the diagnosis of hypertension requires a
measurement of high blood pressure on three separate occasions ( 48). That study did not report whether a pediatric cuff
was used for those children with small arms (age range was 11 to 19 years). Also, it was limited by the use of a
multistation design without a description of which stations subjects performed prior to the the blood pressure
measurement. For example, did students perform a 20-m dash or do pull-ups or the bent arm hang immediately before
their blood pressure was measured?
Because height remains a large advantage in many sports, all clinicians should examine for the signs associated with
Marfan syndrome (49,50) (Table 1.11).
TABLE 1.11. DIAGNOSTIC CRITERIA FOR MARFAN SYNDROMEa
Finally, although it is much less common in Europe ( 51), hypertrophic cardiomyopathy (HCM) is the major cause of SCD
in young athletes in the United States ( 52). Table 1.12 lists the common symptoms and physical findings associated with
this life-threatening condition ( 49).
TABLE 1.12. SYMPTOMS AND SIGNS OF HYPERTROPHIC CARDIOMYOPATHY COMPARED WITH ATHLETE'S
HEARTa
LABORATORY INVESTIGATIONS
Laboratory screening tests are usually done on diseases with high prevalence. Otherwise, even a very sensitive and
specific test will yield many false-positive results. An example of this is screening for sudden cardiac death (SCD) in the
athlete. Of the 4 million high school athletes, it is estimated that between 15 and 25 per year will suffer SCD ( 30). Epstein
and Maron (53) estimated that 200,000 athletes younger than 30 years of age would need to be screened to identify
1,000 individuals with potential underlying congenital heart disease. Of these, 10 athletes would have a condition that
could cause SCD, and 1 of these would actually die from it. Therefore, even if a screening test were 100% sensitive and
99.5% specific, 200,000 individuals would have to be screened to save 1 life. This may indeed be appropriate. However,
1,000 of these individuals would undergo additional invasive testing, which also has risks that cannot be ignored. The
population-attributable risk of morbidity or mortality if no testing is done must be balanced against the risk if testing is
done. Furthermore, another factor should probably be added to the equation: in the example cited, 1,000 individuals
would be temporarily prohibited from competitive athletics, and 10 might be permanently prohibited. We believe that
whatever decision is eventually taken, this type of information is essential towards making an informed decision.
Hemoglobin and Ferritin
Many studies have shown that endurance performance is affected by anemia ( 54). Screening for anemia would therefore
seem logical. However, interpretation of results of the usual tests for anemia in an athlete can be difficult and misleading.
For instance, the associated increase in plasma volume in endurance athletes leads to an artificially low concentration of
hemoglobin even though there is no true anemia. This has been called pseudoanemia ( 54), and it is believed to be
beneficial because it allows for increased sweating and improved temperature regulation.
In addition to the hemoglobin test being nonspecific for true anemia, it does not allow prevention of the anemia before it
occurs (i.e., primary prevention). The first two stages of anemia occur when there is not enough iron in the body (tested
by low ferritin levels) even though the hemoglobin levels remain normal. However, in a review of the literature, Garza et
al. (54) found that low ferritin levels did not predict who would develop true anemia ( 54) and that supplemental iron in
individuals with low ferritin levels did not lead to improved performance.
In summary, hemoglobin and ferritin levels can be used to screen for anemia, but low values should be interpreted
carefully. If a trial of 8 weeks of iron supplementation in suspected cases does not lead to an increase in hemoglobin
levels, the iron supplementation can be stopped without concern.
Urinalysis
Several studies have shown that screening urinalysis reveals a high number of athletes with asymptomatic proteinuria
who do not have evidence of renal or metabolic abnormality on further testing. For this reason, a urinalysis should
probably not be part of a screening examination in athletes. However, this may change with the development of a
leukocyte esterase test, which is being promoted as a cost-effective screening method for Chlamydia (55). Currently
there are only isolated case reports of this form of screening, and it has not been adequately tested to be recommended
as part of the PPE at this time.
Electrocardiography and Echocardiography
Sudden death of a young individual is a major tragedy, particularly when it occurs in an apparently healthy athlete. Such
a death produces an enormous emotional impact on society that leads to pressure on the medical community to devise
ways to detect and prevent future occurrences. The goal of the cardiac component of the PPE is to identify any cardiac
lesions that may result in significant morbidity to the athlete or SCD related to exercise. How to achieve this goal
effectively is a source of great controversy and debate.
What are the most sensitive, specific, practical, and cost-effective screening tools available to the practitioner? Based on
a review of the literature and expert opinion, the AHA recommended that a health care worker with the appropriate
training to detect the important clues of disease from a history and physical examination should perform the screening
(11). The specific components of the history and physical examination that should be included in the PPE are listed in
Table 1.10 (49). The panel recommended this screening process as the most practical strategy for screening large
groups of athletes. Initially the group recommended examinations every 2 years. However, because of practical
considerations, this was later modified in an addendum statement ( 37) to one detailed examination before the start of an
athletic program and an interim history before every subsequent season. Additional tests such as electrocardiography
(ECG), echocardiography, and exercise testing have not been recommended by the AHA for mass screening, essentially
because of cost and practicality considerations, but should be used when the history and physical examination suggest
an abnormality (11,37).
There are limitations to these recommendations. For instance, a retrospective study of 115 patients who died of SCD
suggested that only 3% had abnormalities detected or suspected on the basis of a history and physical evaluation, and in
only 1 athlete (0.9%) was the abnormality correctly identified ( 56). Therefore, it is understandable that the public remains
very concerned about SCD and applies pressure to continue some form of laboratory screening despite the low
prevalence of disease.
ECG and echocardiography are commonly proposed screening measures. ECG has been proposed as a screening tool
to diagnose conduction abnormalities, arrhythmias, hypertrophy, and HCM. A limitation of ECG in the screening of
athletes is the variety of abnormalities seen. In a study in which 501 college athletes underwent ECG screening in
conjunction with a history and physical examination ( 57), ECG abnormalities were found in 14% of subjects. However,
Foote and Michaud reviewed the literature and found reports of sinus arrhythmia in 13% to 69% of athletes,
atrioventricular block in 10% to 33%, ventricular hypertrophy in more than 50%, and T-wave inversions in up to 30% ( 58).
These common ECG findings may be considered as variations associated with “athlete's heart” ( 59,60). Because it is
virtually impossible to distinguish these normal variations from true pathology, the use of a simple screening tool such as
ECG would lead to invasive testing in a large percentage of healthy individuals.
Despite these problems, Fuller et al. ( 61) prospectively added ECG to the PPE of 5,615 high school athletes. They
concluded that ECG is a practical and specific tool that can be incorporated into the PPE. However, their outcome
measure was defined as the need for further testing. They did not give any evidence that ECG screening helped to detect
a person who required treatment or one who was eventually considered too sick to participate in sports. Therefore, we
believe that there remain insufficient data to support the addition of ECG to every PPE at the current time, but more
research is needed to definitively answer the question.
Echocardiography is useful to diagnose HCM. This test is sensitive for detecting HCM and in the absence of other
diseases associated with hypertrophy can be used to differentiate athlete's heart from HCM. Several authors have used
various limited echocardiographic studies in large series of PPEs ( 62,63 and 64) that together evaluated more than 5,000
athletes. No definitive cases of HCM were identified, although a number of other abnormalities were found. If one decides
to use echocardiography, one should be aware of the high cost. Weidenbener et al. ( 62) and Lewis et al. (64) reported a
very low cost of $20 per person; however, both technicians and physicians had volunteered their time for the study. The
procedure would obviously be much more expensive if it was done on a regular basis and not funded by research grants.
Finally, it should be pointed out that even though many of these young patients with HCM die during exercise, this does
not prove that sports participation increases their overall chance of dying. Similarly, the risk of myocardial infarction and
death is higher during exercise for the general population, but regular exercise decreases the risk of mortality outside
exercise periods and therefore overall mortality is reduced ( 65). In fact there is a wide variation in the phenotype of HCM.
Some patients with HCM live long and healthy lives ( 66), and there have been reports of athletes with HCM competing at
elite levels ( 67), albeit against the advice of their physician. Current tests are unable to distinguish which patients with
HCM will develop problems and which will not. Much more research is needed in this area.
In summary, laboratory tests for screening for cardiovascular disease in the young athletic population do not appear to be
cost-effective (i.e., where the dollar is the bottom line). However, cost-benefit analyses (where quality of life is included)
have yet to be made. These analyses may yield different results depending on the individual's perception of danger or
anxiety level, because perceived danger or anxiety would decrease quality of life.
Cholesterol Screening
Although screening for cholesterol is traditionally recommended only for men 35 to 65 years of age and women age 45 to
65 (68), some research has been done in screening of adolescents. Cholesterol was tested in a station-based PPE on
former high school students and found to be abnormal in 15.4% of boys and 13.6% of girls ( 69). Although these results
suggest that cholesterol screening may be an important component of the annual adolescent physical examination, it is
probably excessive for a focused PPE. If the PPE represents the only annual health evaluation of the athlete, then the
physician may decide to expand the objectives of the PPE and include this screening test.
CLEARANCE/DISQUALIFICATION ISSUES
Appendix B presents the guidelines developed in 1994 by the American Academy of Pediatrics, the most current source
regarding which conditions should disqualify athletes from sports ( 38). This information, together with the 26th Bethesda
Guidelines (70) and the Consensus Statement on PPE physical examinations (2), should allow the examiner to determine
whether the athlete is cleared, requires specific investigations or treatment, or is not cleared. Each problem should be
addressed specifically and may require consultation with a specialist, team trainer, family physician, or other
professionals. The follow-up plan may vary based on the format used (see Table 1.3 and Table 1.4) and will most likely
lead to decreases in morbidity and, possibly, mortality.
CONCLUSIONS
The PPE physical examination has been less than optimal in many settings in the past ( 63,71). One proposed solution is
to fully standardize the examination process to avoid the inconsistencies that occur with different levels of experience.
Whereas this approach may improve the quality of the PPE in many institutions, it cannot address the particular needs
and concerns of specific institutions or team physicians. This chapter was designed to give readers an easy-to-use
method of tailoring the PPE to fit their own needs. It should be recognized that the goal of any PPE is to detect injuries or
illnesses that may preclude safe participation in sports. Even in the completely healthy individual, other interventions
(e.g., proper strength training, use of prophylactic bracing) may be used to minimize the risk of injury in sports. These are
discussed in subsequent chapters.
APPENDIX A. OVERVIEW OF ALL STUDIES THAT SPECIFICALLY EVALUATED THE ENTIRE

PREPARTICIPATION PHYSICAL EXAMINATION (PPE)
Author N Athlete Methods Results

(Reference) Level
Goldberg et 701 High Station 80% identified by history, no details given

al. (12) school Included urine dip, body 13.6% required more followup
composition, flexibility, 1.3% denied clearance
strength 40 referred for proteinuria but all normal with further
78% used PPE as only testing
assessment
Linder et al. 1,268 High Station 5% required more followup
(13) school Male students only 0.2% denied clearance
Incorporated American Greater abnormalities found the second year
Medical Association (AMA)
evaluation form (ortho/med
only, no evaluation for health
maintenance or health habits)
Consisted of two 1-year
cohorts
Tennant et al. 2,719 High Assembly line Significant decrease in diagnosis from year to year
(14) school Male students only 8% required more followup
4-year study 1.2% denied clearance
Included only physical
examination and not history
Thompson et 2,670 High Station–4 9.6% required more followup
al. (15) school Mostly male students 1.2% denied clearance (67% musculoskeletal, 15%
Used AMA form cardiovascular)
Check vital signs, urinalysis,
history, and physical
examinations
Risser et al. 2,114 High Station 3.1% required more followup
(16) school Assessed athlete-parent 0.3% denied clearance
differences in completion of 39% of athletes agreed with parents
form 88% reported PPE only form of health care
Assessed cost analysis Each significant disqualifying factor cost $3,636.50
(unfavorable costeffectiveness)
Author N Athlete Methods Results

(Reference) Level
DuRant et al. 1,259 High Station–8 African-Americans had higher rates of biomechanical
(17) school abnormalities but fewer incidence of injuries
Girls had fewer problems than boys
3 boys and 1 girl not allowed to participate in
interscholastic sports
Magnes et al. 1,054 High Station Hypertension and visual abnormality the greatest
(47) school reasons for referral
Rifat et al. 2,574 High Physician Logistic regression showed a 78.6% positive predictive
(82) school Analysed items associated value and 90.4% negative predictive value for denying
with denial participation if the following variables are included:
dizziness with exercise, asthma history, body mass
index, systolic blood pressure, visual acuity, heart
murmur, musculoskeletal examination
Smith & 2,739 High Station 11.9% required more follow-up
Laskowski school 1.9% not allowed to play
(83) 80% of clinically significant cardiac abnormalities
detected by history
DuRant et al. 922 High Physician or station–8 Private physician detected more injuries on history but
(32) school fewer injuries on physical examination
APPENDIX B. MEDICAL CONDITIONS AND SPORTS PARTICIPATION
Condition May
Participate?
Atlantoaxial instability (instability of the joint between cervical vertebrae 1 and 2) Qualified Yes
Explanation: Athlete needs evaluation to assess risk of spinal cord injury during sports participation.
Bleeding disorder Qualified Yes
Explanation: Athlete needs evaluation.
Cardiovascular diseases
Carditis (inflammation of the heart) No
Explanation: Carditis may result in sudden death with exertion.
Hypertension (high blood pressure) Qualified Yes
Explanation: Those with significant essential (unexplained) hypertension should avoid weight and power
lifting, body building, and strength training. Those with secondary hypertension (hypertension caused by a
previously identified disease), or severe essential hypertension, need evaluation. Reference 4 defines
significant and severe hypertension.
Congenital heart disease (structural heart defects present at birth) Qualified Yes
Explanation: Those with mild forms may participate fully; those with moderate or severe forms, or who have
undergone surgery, need evaluation. Reference 3 defines mild, moderate, and severe disease for the
common cardiac lesions.
Dysrhythmia (irregular heart rhythm) Qualified Yes
Explanation: Athlete needs evaluation because some types require therapy or make certain sports
dangerous, or both (3).
Mitral valve prolapse (abnormal heart valve) Qualified Yes
Explanation: Those with symptoms (chest pain, symptoms of possible dysrhythmia) or evidence of mitral
regurgitation (leaking) on physical examination need evaluation. All others may participate fully ( 3).
Heart murmur
Explanation: If the murmur is innocent (does not indicate heart disease), full participation is permitted. Qualified Yes
Otherwise the athlete needs evaluation (see congenital heart disease and mitral valve prolapse above).
Cerebral palsy
Explanation: Athlete needs evaluation. Qualified Yes
Diabetes mellitus Yes
Explanation: All sports can be played with proper attention to diet hydration, and insulin therapy. Particular
attention is needed for activities that last 30 minutes or more.
Condition May
Participate?
Diarrhea Qualified No
Explanation: Unless disease is mild, no participation is permitted, because diarrhea may increase the risk of
dehydration and heat illness. See “ Fever” below.
Eating disorders
Anorexia nervosa, Bulimia nervosa Qualified Yes
Explanation: These patients need both medical and psychiatric assessment before participation.
Eyes (functionally)
One-eyed athlete Qualified Yes
Loss of an eye, Detached retina, Previous eye surgery or serious eye injury
Explanation: A functionally one-eyed athlete has a best corrected visual acuity of <20/40 in the worse eye.
These athletes would suffer significant disability if the better eye was seriously injured as would those with
loss of an eye. Some athletes who have previously undergone eye surgery or had a serious eye injury may
have an increased risk of injury because of weakened eye tissue. Availability of eye guards approved by
the American Society for Testing Materials (ASTM) and other protective equipment may allow participation
in most sports, but this must be judged on an individual basis ( 9,10).
Fever No
Explanation: Fever can increase cardiopulmonary effort, reduce maximum exercise capacity, make heat
illness more likely, and increase orthostatic hypotension during exercise. Fever may rarely accompany
myocarditis or other infections that may make exercise dangerous.
Heat illness (history of) Qualified Yes
Explanation: Because of the increased likelihood of recurrence, the athlete needs individual assessment to
determine the presence of predisposing conditions and to arrange a prevention strategy.
HIV infection Yes
Explanation: Because of the apparent minimal risk to others, all sports may be played that the state of
health allows. In all athletes, skin lesions should be properly covered, and athletic personnel should use
universal precautions when handling blood or body fluids with visible blood ( 6).
Kidney (absence of one) Qualified Yes
Explanation: Athlete needs individual assessment for contact/collision and limited contact sports.
Liver (enlarged) Qualified Yes
Explanation: If the liver is acutely enlarged, participation should be avoided because of risk of rupture. If the
liver is chronically enlarged, individual assessment is needed before collision/contact or limited contact
sports are played.
Malignancy Qualified Yes
Explanation: Athlete needs individual assessment.
Musculoskeletal disorders Qualified Yes
Neurologic
Serious head or spine trauma, severe or repeated concussions, craniotomy (history of) Qualified Yes
Explanation: Athlete needs individual assessment for collision/contact or limited contact sports, and also for
noncontact sports if there are deficits in judgment or cognition. Recent research supports a conservative
approach to management of concussion ( 5,11)
Condition May
Participate?
Convulsive disorder (well controlled) Qualified Yes
Explanation: Risk of convulsion during participation is minimal.
Convulsive disorder (poorly controlled) Yes
Explanation: Athlete needs individual assessment for collision/contact or limited contact sports. Avoid the
following noncontact sports: archery, riflery, swimming, weight or power lifting, strength training, or sports
involving heights. In these sports, occurrence of a convulsion may be a risk to self or others.
Obesity Qualified Yes
Explanation: Because of the risk of heat illness, obese persons need careful acclimatization and hydration.
Organ transplant recipient Qualified Yes
Ovary: absence of one Yes
Explanation: Risk of severe injury to the remaining ovary is minimal.
Respiratory
Pulmonary compromise including cystic fibrosis Qualified Yes
Explanation: Athlete needs individual assessment, but generally all sports may be played if oxygenation
remains satisfactory during a graded exercise test. Patients with cystic fibrosis need acclimatization and
good hydration to reduce the risk of heat illness.
Asthma Yes
Explanation: With proper medication and education, only athletes with the most severe asthma will have to
modify their participation.
Acute upper respiratory infection Qualified Yes
Explanation: Upper respiratory obstruction may affect pulmonary function. Athlete needs individual
assessment for all but mild disease. See “Fever” above.
Sickle cell disease Qualified Yes
Explanation: Athlete needs individual assessment. In general, if status of the illness permits, all but high
exertion, collision/contact sports may be played. Overheating, dehydration, and chilling must be avoided.
Condition May
Participate?
Sickle cell trait Yes
Explanation: It is unlikely that individuals with sickle cell trait (AS) have an increased risk of sudden death
or other medical problems during athletic participation except under the most extreme conditions of heat,
humidity, and possibly increased altitude ( 12). These individuals, like all athletes, should be carefully
conditioned, acclimatized, and hydrated to reduce any possible risk.
Skin: boils, herpes simplex, impetigo, scabies, molluscum contagiosum Qualified Yes
Explanation: While the patient is contagious, participation in gymnastics with mats, martial arts, wrestling,
or other collision/contact or limited contact sports is not allowed. Herpes simplex virus probably is not
transmitted via mats.
Spleen (enlarged) Qualified Yes
Explanation: Patients with acutely enlarged spleens should avoid all sports because of risk of rupture.
Those with chronically enlarged spleens need individual assessment before playing collision/contact or
limited contact sports.
Testicle absent or undescended Yes
Explanation: Certain sports may require a protective cup
This table is designed to be understood by medical and nonmedical personnel. In the “Examination” section below, “needs
evaluation” means a physician with appropriate knowledge and experience should assess the safety of a given sport for an
athlete with the listed medical condition. Unless otherwise noted, this is because of the variability of the severity of the
disease and/or of the risk of injury among the specific sports in Table 1.9.
From Medical conditions affecting sports participation. Pediatrics 1994;94:757–760, with permission.
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2 Conditioning and Training
CONDITIONING AND TRAINING

PAUL A. BORSA
SCOTT M. LEPHART
Conditioning of the Athlete

Performance Characteristics
Body Composition
Strength Training
Anaerobic Conditioning
Aerobic Conditioning
Year-Round Strengthening and Conditioning Program
Periodization
Phases
Summary
Physiologic Effects of Training
Central Adaptations
Peripheral Adaptations
Neuroendocrine Adaptations
Implications for Exercise Training
Effects of Warming Up and Down
Warming Up
Warming Down
Stretching as an Adjunct
Pain Associated with Exercise
Acute Pain
Exercise-Induced Muscle Damage
Summary
Chapter References
Exercise training and conditioning have become integral components of competitive athletic participation. Athletes,
coaches, and athletic trainers concerned with enhancing athletic performance and minimizing the risk of athletic-related
injury have developed the various elements of conditioning into scientifically based principles that focus on physiologic
and metabolic adaptations that enhance efficiency and function of the human organism. Many sciences within the sports
medicine discipline have contributed to the methodologic development of athletic conditioning in an effort to enable
optimal physiologic function resulting in peak performance characteristics for the athlete.
Training and conditioning involve a systematic modeling of the physiologic elements of the human organism that result
from induced stress and use of the respective metabolic systems. The adaptations that occur after systematic
conditioning include somatomorphic alterations, muscular strength and endurance, soft tissue proliferation and enhanced
plasticity, central and peripheral cardiorespiratory efficiency, and the ability of all metabolic systems to withstand greater
amounts of stress without fatigue or failure ( 1).
This chapter focuses on the elements of athletic performance that adapt to training and conditioning, including
identification of those characteristics that are desirable for optimal athletic performance, the means by which these
characteristics can be quantified, modes that induce physiologic and metabolic adaptations, and methodologic
approaches to implement efficient and effective training and conditioning of the athlete.
CONDITIONING OF THE ATHLETE
Performance Characteristics
Although the requirements of each sport vary according to the specific skills necessary to perform the activity, there are
general underlying functional components that are common to all athletic performance. Strength, endurance, speed, and
coordination are elements that lay the foundation of all sports activity ( 1). Regardless of the activity, whether it be cyclic
or acyclic, these four characteristics are the limiting factors in the ultimate performance. Although the relative importance
of those components is a function of the particular sport, conditioning programs must ultimately address them all in an
effort to enhance the athlete's performance and decrease the risk of injury.
Seldom does a sport demand any of these four functional components exclusively, and often the demand requires
combinations of the components (1). For instance, many sports require both strength and speed, which is characterized
as power. Other sports require strength to be exerted over extended periods of time, which is characterized as muscular
endurance. Other activities demand the combination of speed and coordination that is characterized as agility. Finally, all
performance characteristics necessitate mobility and muscular flexibility for ambulation. The ultimate success in
optimizing a particular athlete's conditioning for a particular sport depends on implementing the appropriate exercises to
enhance the aforementioned components needed for the sport.
Strength
Muscular strength is the tension generated within muscle groups against a fixed resistance and angular velocity in one
maximal effort (2,3). Athletes require muscular strength to compete at high levels of exercise intensity. Strength derives
from the combination of the structure of the muscle and neurologic stimulation that enables the muscle's functional unit to
contract (1). Maximal strength development, therefore, is a combination of morphologic alteration, known as hypertrophy,
and neurologic adaptations that result in enhanced neural stimulation.
When a combination of force and speed of muscle contraction are necessary for performance, ultimate muscular power is
desirable. Muscular power enhancement depends on the force and acceleration of the contraction. Therefore, power
training necessitates neuromuscular adaptations that increase the speed and force at which the muscular contraction
takes place.
Endurance
For athletes whose performance demands sustained levels of strength, a key element of conditioning is the enhancement
of muscular endurance. Muscular endurance involves both strength and the ability to delay the onset of fatigue.
Endurance in the general sense refers to an athlete's capacity to perform work over an extended period. The endurance
capacity of an athlete is a function of the oxidative pathways, which are both centrally and peripherally mediated. Many
factors affect aerobic endurance, including cardiorespiratory capacity and efficiency (transport), metabolic substrate
availability, and cellular metabolic activity (use) ( 1). Also important is the power output (workload) in terms of skeletal
muscle function. Therefore, conditioning responses for endurance athletes involves both mechanical (power output) and
metabolic (substrate transport and utilization) adaptations. Because endurance activities usually induce fatigue, physical
conditioning goals are to delay the onset of fatigue and to allow the athlete to work at high levels of intensity before
fatigue is reached. These adaptations can be achieved only if the training sessions are intense enough to produce
fatigue.
Speed
One of the most important characteristics for successful athletic performance is speed. Speed is defined as the capacity
to move quickly and refers to locomotion (1). An athlete's speed is mediated predominantly by neuromuscular factors that
include contractile capacities (power) and mechanical characteristics (gait and technique). Physiologically, speed
adaptations are induced when selective neuromuscular units are enhanced through increased metabolic substrate
availability and speed of muscular contractions (i.e., increased frequency and force of muscular contractions).
Coordination
Coordination is generally defined as harmonious action, as seen in muscles. This particular component of performance
requires input from the other three components (strength, speed, and endurance) to allow the athlete to function at peak
performance levels. The central nervous system (CNS) is the most basic system that mediates coordinated motion. The
peripheral afferent and efferent branches of the CNS regulate coordinated motion by inhibiting or activating specific
muscle groups, which produces movement patterns. Through repetition from physical training, the neuromuscular system
is conditioned to provide the requisite movement patterns, or engrams, for developing the strength, speed, endurance,
and agility that are necessary for athletic performance.
The general and specific movement patterns acquired with training are programmed centrally in the brain. The motor
cortex and cerebellum play important roles in the acquisition of sophisticated movement patterns. The motor cortex is the
learning center that programs the specific pattern, and the cerebellum is responsible for the precision and accuracy of
that particular movement (1).
Coordination has been classified by Bompa ( 1) as general or specific, depending on the degree of complexity. General
coordination encompasses normal body movements such as walking and climbing stairs. Specific coordination refers to
the technical movements required for a specific sport. For instance, the tennis serve and the basketball jump shot require
specific movement patterns developed and fine-tuned through repetition. Sport-specific coordination may not carry over
to general coordination; for example, someone adept at wrestling may be grossly uncoordinated at basketball. On the
other hand, general coordination has been attributed to athletes who are very skilled at their sport; for example, Michael
Jordan possesses both general and specific coordination.
Typed Activity
Athletic performance and exercise training is made up of various types of activities. These activities may be
systematically broken down and categorized as cyclic, acyclic, or cyclic and acyclic combined (semicyclic). Cyclic
movements are continuous activities that require identical movement patterns done repetitively. Distance running and
cycling are sports that require cyclic movements. Athletes in these particular sports may show a coordinated gait pattern,
yet they are not necessarily agile. Sprinters and jumping athletes are performing acyclic or cyclic and acyclic combined
activities, and their sports may or may not require agility. Sports that require agility are acyclic or semicyclic in nature,
mainly because these particular activities use common movement patterns done in repetition or in discontinuous cycles.
Agility movements include activities that require constant directional changes such as forward and backward running,
lateral movement, acceleration and deceleration, and diagonal cutting ( Fig. 2.1) (1). Basketball, wrestling, gymnastics,
and soccer are cyclic and acyclic combined sports that require high levels of agility. Because it is difficult to classify a
sport as strictly acyclic, both acyclic and combined sports are referred to as semicyclic. Both cyclic and semicyclic
activities require strength, speed, and endurance, but in varying degrees. The distance runner typically uses cyclic
movement coordinated over long durations, whereas the athlete in an acyclic sport requires greater levels of strength and
speed to perform at near-maximal intensities.
FIGURE 2.1. Agility is a performance characteristic that is important for activities requiring lateral mobility, acceleration
and deceleration, and diagonal cutting.
The five characteristics of athlete performance are interrelated by the regulatory effects of the CNS. Coordinated
movement, whether simple or complex, cyclic or semicyclic, requires varying amounts of strength, speed, and endurance.
These three components of performance are discussed throughout the remainder of this chapter in regard to
measurements, training, adaptation, and injury.
Body Composition
Morphometric structure and body composition are closely related to athletic performance ( 4,5,6,7 and 8) and to
susceptibility to injury during physical activity ( 9). As the athlete strives to maximize performance, he or she also must
consider the ratio of lean body tissue to fat tissue.
The assessment of body composition involves measurement and evaluation of the rudimentary structural components of
the human body. Body composition is subdivided into body fat content (percent body fat [%BF]) and lean body mass
(LBM). Body fat is the adipose tissue deposited throughout the whole body and is classified as essential or nonessential.
Essential fat is necessary for normal physiologic functioning. Essential fat is found in nerve myelination, blood lipids, and
glandular hormones. Nonessential fat is the excess deposition of adipose tissue around the viscera, skeletal muscles,
and subcutaneous fat layer. LBM is the nonessential fat-free tissue that constitutes the remaining tissue of the body. This
includes skeletal and smooth muscle (protein), bone (mineral), essential fat, and the volume of water within the various
compartments of the body. The normal subdivision of lean tissues is total body water 73%, protein 19%, mineral 3%, and
essential fat 5% (10).
Assessment techniques have been developed for estimating %BF and LBM. Direct measurement of body composition
was initially performed through chemical analysis of dissected human cadavers; the tissue was differentiated into fat and
fat-free portions for comparison (11). As a result of these direct methods, and more recent indirect methods such as the
classic hydrostatic weighing studies done by Behnke at the U.S. Naval Academy, body density (BD) estimates for the
“reference man and woman” were established (11,12). Other examples of indirect methods to predict %BF and LBM
include skinfold thickness and circumferential measurements.
Measurement of Body Composition
Hydrostatic Weighing
Hydrostatic weighing (underwater densitometry) is a method of estimating body composition by volumetrically measuring
BD (Fig. 2.2) (13,14). Volumetric measurements of a body submerged in water can be calculated through the application
of Archimedes' principle, which states that the mass of an object is equal to its displacement volume when submerged in
water (15). Specific gravity is a variable related to and often mentioned along with density. Specific gravity (SG) can be
calculated by dividing the dry mass (M d) of an individual by the loss of mass in water (M w).
FIGURE 2.2. Hydrostatic weighing (underwater densitometry) measures body density by employing Archimedes'
principle.
The effect of water temperature on the buoyancy of the body when submerged is what separates specific gravity from
BD. To account for water temperature, correction factors were incorporated into the prediction equations.
or
where Md is the dry mass or body weight in air, M w is the wet mass or body weight in water, RLV is the residual lung
volume, and D w is the density of water (correction factor). The ideal temperature for hydrostatic weighing is
approximately 39.2°F (4°C), which is relatively uncomfortable for humans to withstand. Therefore, a correction factor (D w)
is incorporated in the BD equation as a means of statistically controlling for water temperature variation.
Residual lung volume is the amount of air trapped in the lungs after a maximal exhalation; it can be measured directly, or
indirectly by less reliable alternative methods. Because residual lung volume is least affected by water temperature, it is
used most often with hydrostatic weighing and also is accountable as a potential source of error. Unaccountable sources
of error are trapped air within the intestinal tract, hair, and excess clothing worn during assessment ( 10,16).
Once the BD has been calculated, %BF and LBM are estimated through the use of a prediction equation. Siri ( 17) and
Brozek et al. (18) developed standard equations for calculating %BF by incorporating the BD value into an equation that
uses constants derived from BD estimates of fat and fat-free tissue:
After %BF is determined, LBM is calculated from the mass of fat (M f) and total body mass (TBM):
Investigations have identified other random sources of measurement error. For example, cadaveric analysis has shown
LBM to be inconsistent compared with the reference man and woman as earlier described by Behnke ( 12). Other sources
of random variation are age, gender, bone mineral content, and total body water. Although these sources of error exist,
hydrostatic weighing is still considered to be the most reliable estimate of body composition ( 9,10,20).
Skinfold Thickness
The %BF may be predicted from measurement of the subcutaneous layer of adipose tissue at various anatomic sites on
the body. The rationale for this method is based on the relationship between subcutaneous fat and whole-body fat.
Measurements are made with the use of calipers that measure the thickness of skin and subcutaneous fat ( Fig. 2.3). The
technique used for skinfold measurement permits the separation of skin and subcutaneous fat from the underlying
muscle tissue.
FIGURE 2.3. Skinfolds, indicators of subcutaneous fat, are measured with calipers.
Skinfold measurements provide reliable data concerning body fat distribution ( 21,22,23 and 24). Various sites throughout
the body that are believed to provide the most accurate predictions for overall body fat content have been selected
experimentally for caliper readings ( 21). The seven most popular sites are the subscapular, triceps, axilla, chest,
abdomen, suprailium, and midthigh skinfolds ( 21).
All measurements are taken on the right side of the body while the subject is standing. The mean of two or three trials is
recorded for each site. The measurement should be performed by an experienced technician who is capable of
duplicating measures on a consistent basis. Several gender-specific regression equations for the prediction of %BF have
been developed ( 12,21,22,23,24 and 25). Once BD has been estimated, the score is entered into the Brozek or Siri
equation to compute %BF (17,18).
Circumferential Measurements
Another method of estimating body fat is by measuring girth at specific anatomic sites on the body that are known to be
target areas of fat deposition ( Fig. 2.4) (26). This is a relatively quick, accurate, and inexpensive method to assess %BF
and LBM. Often circumferential measurements are used to estimate %BF in obese individuals because it is difficult to
perform accurate skinfold and underwater assessments. This method also can be used to quickly identify patterns of fat
distribution on the body for comparison after weight loss. Body fat conversion tables estimate the %BF from the sum of
the girth measures. Popular sites of measurement include the abdomen, buttocks, right thigh, right upper arm, right
forearm, and right calf. The equations and tables are age and gender specific ( 15,27).
FIGURE 2.4. Circumferential (girth) measurements are also used to estimate body fat.
Some methods combine skinfold and girth measurements to estimate body composition (10,12,21). Potential sources of
error are inherent with the skinfold and girth methods. The intramuscular hydration level, as well as the texture and
pliability of the skin and underlying fat layer, can affect measurements and lead to error. To ensure valid measurements,
the measurement instrument should be routinely calibrated.
Alternative Methods of Assessing Body Composition
The various methods of assessing body composition discussed thus far are all calculated through external or surface
anthropometric measurements. These methods are relatively simple, inexpensive, and reliable. Some alternative
methods exist that are not generally used because of added expense and inconvenience to the patient. However, they
are generally more accurate because they use internal images for estimating body composition. Magnetic resonance
imaging, computed tomography, radiography, and ultrasound assessments of body composition use pictorial imaging
techniques that delineate the tissues to measure the percentages of bone, muscle, and fat ( 10,15). Bioelectrical
impedance and potassium (K + ) emission methods require electrochemical means of assessing BD. BD may then be
converted to %BF and LBM through the use of Siri's or Brozek's equation ( 10).
Strength Training
Physiology of Strength Training
As early as the ancient Olympic games, muscular strength was acknowledged as an integral component of most athletic
events. In general terms, strength is simply the force that can be generated when a muscle is contracting. Today's athlete
is constantly striving to enhance muscular strength and, ultimately, sport performance. Strength development is a
function of muscle growth, which has been shown to be 8 to 12 times greater in the athlete who engages in strength
training than in the athlete who conditions by practicing only sport-specific activities ( 1). Therefore, strength training has
become a specialized element in most competitive athletics.
The maximum force a muscle can generate is determined by the cross-sectional area of the muscle and the complex
integration of the biochemical composition and neural input to that muscle. In addition, most strength characteristics are
required for activities that involve limb motion, so that the limb biomechanics affects muscular contraction.
Muscular power is a component of strength and has become an important goal of strength-training programs. The
strength of a muscle depends on the joint range of motion (ROM) in which the muscle acts. The rotary action of a muscle
about a joint axis that produces force is referred to as torque. Muscular power is created by the torque generated and the
speed of a muscular contraction. This dynamic action is essential to sports that require accelerated rates of force
generation. This concept of strength-speed or power has become an important issue in strength-training programs.
Substantial attention is being directed toward the acquisition of strength-speed or “explosive” power. Research has
shown a strong relationship between the generation of peak power and intramuscular concentrations of fast-twitch fibers
(28). This implies that an athlete possessing inherent strength is more able to develop muscular power if he or she is
endowed with a high concentration of fast-twitch (type II) muscle fibers.
Another component of strength training is the acquisition of muscular endurance, which is defined as the capacity of a
muscle group to perform repeated contractions against a resistance. Depending on their sport, athletes need varying
degrees of endurance training for those muscles that require force generation over protracted periods. Muscle fiber type
has been found to play an important role in activities that require muscular endurance ( 29,30). For instance, athletes who
perform cyclic activities over prolonged periods, such as distance runners and swimmers, use mainly the type I and IIa
fibers. Athletes who perform acyclic activities at high intensities for short bursts, such as baseball pitchers and tennis and
volleyball players, use type IIa and IIb fibers.
Athletes train for muscular endurance in various ways. Some athletes use circuit resistance training (CRT), and others
use high-repetition progressive resistance exercise (PRE) or speed-specific isokinetic exercise to reduce the fatigability
of muscles. By reducing fatigability, the muscles increase their capacity to metabolize lactic acid ( 30). Muscular
endurance exercise induces aerobic and anaerobic metabolic system adaptations within the muscle, with the ultimate
goal of maintaining forceful contractions (anaerobic power) over prolonged periods of time (aerobic power). Training also
is sport specific, and some athletes require endurance-type activities. For instance, a baseball pitcher or swimmer may
train the shoulder girdle muscles for endurance. Little research has been done to document the most efficient means of
acquiring muscular endurance, although many experts use their own programs with varying degrees of success.
Adaptations to Strength Training
As the result of a strength-training program, certain morphologic and neural adaptations occur. Morphologically, the
primary alteration that occurs is muscle hypertrophy or enlargement. For years there was considerable debate about
whether hypertrophy (enlargement of muscle fibers) or hyperplasia (increased number of muscle fibers) was responsible
for the increase in muscle size. Contemporary research has concluded that hyperplasia occurs only during the
developmental stages of growth and maturation, and beyond adolescence most muscle growth is a function of
hypertrophy (28). Hypertrophic changes occur from a number of mechanisms, primarily related to increased muscle
protein synthesis, which results in the anabolic process of muscle growth.
From a practical perspective, strength development needs to occur functionally to enhance selected performance
characteristics. It is, therefore, necessary to discuss functional strength that creates movement. The extent to which force
is generated by a muscle through a ROM is closely linked with neurally mediated activities. The neural components
include intramuscular innervation and intermuscular coordination of the movement. Maximal muscular contraction is
limited by the number of motor units that are activated. In addition to the hypertrophic changes that occur within the
muscle fiber to enable greater force-generating capacity, an increase in motor unit activation occurs as a function of
strength training. The combination of morphologic and neurologic adaptations results in a greater force-generating
capacity per area of the muscle unit.
For strength gains to be functional, there needs to be enhanced capacity for movement through a ROM. These
adaptations are closely linked to the coordinated activity of the agonist, antagonist, and synergistic muscle groups that
are neurally mediated. The activity of all of these muscle groups results in a coordinated movement which, as a result of
intramuscular adaptations, results in greater potential for force to be generated through the desired motion.
For strength adaptations to occur within muscle tissue, the overload principle must be applied to the specific
strength-training program. The overload principle is defined as the process of overloading a muscle or muscle group with
a resistance that exceeds a threshold, or level of intensity, at which adaptive changes occur within the muscle fiber. The
mechanical and metabolic changes enable the muscle fiber to increase its force-generating capability ( 15,28). The
specific adaptations to imposed demands principle (SAID principle) is often equated with the overload principle, because
both require training above threshold levels to systematically prompt the neuromuscular system to function more
efficiently. The SAID principle applies to any training program and is specific to the demands of an athlete's sport.
Strength developed functionally through sport-specific training involves activity that produces greater force with more
precision. This involves neural intramuscular and intermuscular mediation. The overload principle is more general to the
muscular system; through the application of the SAID principle more functional strength is developed for sport-specific
purposes. For example, a baseball pitcher requires overall upper- and lower-body strength; but, specific to the position of
pitcher, the player requires sport-specific strength training of the shoulder girdle, hip, and thigh to maintain the muscular
power and endurance needed for pitching.
Along with overload, any training or conditioning program must follow an agenda for incorporating intensity and volume
(frequency and duration) and mode of exercise. These factors are the stimuli that dictate systematic progress in
functional performance, and they are manipulated according to the seasonal phase of training (see later discussion).
Muscular strength, power, and endurance are developed through various modes of training. The training modes are
specific to the type of force-generating capabilities within the exercising muscle. The four major modes of training
discussed here are isometric, isotonic, isokinetic, and plyometric.
Modes of Strength Training
Isometric
Isometric contraction is classified as static, because the length of the muscle does not change in response to the
generation of force within the muscle against an externally applied resistive force. Isometric training gained popularity in
the late 1960s as a means of supplementation to other forms of resistance training. Early experimentation indicated that
muscular strength increased after isometric training programs ( 31,32), although these adaptations were limited to the joint
angle exercised. Strengthening and conditioning experts have used isometrics in an attempt to release “sticking points”
that develop at specific angles within the ROM ( 15). These adaptations have limitations relative to athletic performance;
therefore, isometric exercise is most often limited to the early states of orthopedic rehabilitation when angular motion of
anatomic joints is contraindicated ( 2). As a therapeutic modality, isometric exercise permits maximum tension generation
within the muscle. This may retard disuse atrophy while also maintaining the normal neuromuscular firing patterns of the
muscle groups. Functionally, isometric exercise rehabilitation and training is usually performed at various angles
throughout the ROM of a particular joint, if not contraindicated. The static contraction is held for 5 to 10 seconds with a
specified protocol of sets and repetitions. This permits the muscle to generate force at various lengths and has been
found to result in strength gains throughout the range exercised ( 33).
Isotonic
Isotonic training involves exercise at a fixed resistance with variable angular velocity occurring throughout the ROM. This
type of exercise is different from isometric exercise in that the force generated within the muscle overcomes the external
counterresistance, causing the muscle fibers to change their length. As a result, angular motion occurs in a specified
range against a fixed resistance. PRE training is a popular mode of isotonic resistance training. In orthopedic
rehabilitation, low to moderate PREs are performed using rubberized tubing (Theraband or Sport Cord), free weights, or
modified equipment machines such as the Nautilus or Universal systems ( Fig. 2.5).
FIGURE 2.5. Strength training via the progressive resistance exercise (PRE) method has various modes. A: Isotonic
mode (dumbbells). B: Multiaxial cable resistance.
When exercising isotonically, the muscle changes length as a result of cross-bridge formation along the sarcomere.
Muscular contractions occur concentrically (shortening) or eccentrically (lengthening). Both concentric and eccentric
contractions have been shown to result in the development of muscular strength ( 34). Eccentric or negative contractions
occur while the muscle is lengthening. Eccentric contractions generate greater tension within the muscle at faster angular
velocities than concentric contractions do ( 33). Concentric or positive contractions occur while the muscle shortens and
have been shown to increase tension at slower angular velocities ( 33). Concentric contractions are equated with
acceleration-type movements, such as the wind-up in baseball, while eccentrics are equated with deceleration-type
movements such as the follow-through in the baseball throw. Dudley et al. ( 35) reported that a combination of concentric
and eccentric contractions in resistance exercises produces the greatest gains in strength ( 34). Also, hypertrophy has
been shown to occur in both type I and type II muscle fibers ( 34).
From a training perspective, concentric exercise expends more muscle energy and eccentric contractions impart greater
damage to the muscle fiber. Therefore, eccentrics appear to be more economical, but concentrics appear to be safer. To
minimize muscle damage and maximize energy, a slow progression in intensity and volume with a combination of both
types of contractions should be prescribed to achieve safe and effective gains in muscular strength.
Isokinetic
Isokinetic training is speed-specified exercise with accommodating resistance throughout the ROM. Isokinetic exercise
permits the athlete to train at fast, intermediate, or slow angular velocities, with a counterresistive force matching the
force exerted by the athlete. Isokinetic testing devices have the advantage of quantifying muscular force generated at
preset speeds. In addition, isokinetics permit the measurement of muscular power and resistance to fatigue (endurance).
Contemporary isokinetic devices are equipped with training programs for both concentric and eccentric exercise. Most
commercially available isokinetic devices are interfaced with a computer that is able to store large quantities of
information. Available devices are equipped for multijoint testing and exercise protocols. Much research has been
devoted to isokinetic exercise, but little conclusive evidence has been forthcoming in regard to its purported benefits as a
testing or training device ( 33). Isokinetic exercise has been used as a measurement tool to compare muscular strength
and power and as a strength-training modality. Furthermore, isokinetic exercise has been recommended for use during
the late stages of orthopedic rehabilitation because of its proposed functional benefits, although researchers have shown
that isokinetic scores do not correlate well with functional performance ( 36). The implementation of isokinetic devices for
functional training has been questioned. Researchers now suggest that differences in the “kinetic chain” of force
distribution represent a major failure of isokinetic training, particularly in the lower extremities. Isokinetics are classified
as “open kinetic chain” activities, and most functional skills are performed under the “closed kinetic chain,” thus
accounting for the weak relationship between isokinetic parameters and functional performance ( 36).
Strength-Training Programs
In recent years the athlete's focus on strength development has escalated. Today's athletes devote extensive time to
weight-training programs designed to develop functional strength specific to their sport. The basis for these programs
evolved from the PRE experiments of DeLorme and Watkins ( 37). PRE programs follow the overload principle, which
requires a systematic progression of resistance. This principle combined with a set training protocol of intensity, duration,
and frequency induces the specific muscle fiber adaptations discussed earlier ( 30). The following are some of the popular
PRE programs used for strength development.
Progressive Resistance Exercise
DeLorme's PRE program is based on exercise that is performed at a percentage of the maximal amount of resistance
(weight), in sets of 10 repetitions ( 2,37). The progression occurs both within each session and between successive
sessions as the athlete develops greater strength over the course of the program ( Table 2.1). This form of strength
training focuses mainly on isotonics. The training apparatus for PRE includes free weights, resistive tubing, circuit
devices, and cable-pulley systems.
TABLE 2.1. DELORME'S PROGRAM
DeLorme's method of resistance training has been modified for purposes of orthopedic rehabilitation. Sanders' modified
PRE program uses a formula based on a percentage of the individual's body weight to predict the starting weight ( Table
2.2) (2). Knight developed the daily adjusted progressive resistance exercise (DAPRE) programs, which allow for
individual variations in progression ( Table 2.3) (2). Berger further modified the DAPRE method by altering the number of
repetitions from 10 to between 6 and 8 for each of the three sets ( Table 2.4) (2,31).
TABLE 2.2. SANDERS' MODIFIED PROGRAM
TABLE 2.3. KNIGHT'S DAILY ADJUSTED PROGRESSIVE RESISTANCE EXERCISE PROGRAM

TABLE 2.4. BERGER'S PROGRAM
Most clinicians and strength-training experts advise alternating PRE programs with moderate- to high-intensity resistance
training to permit at least 48 hours of recovery between PRE workouts. The recovery intervals permit muscle fiber repair
and regeneration that not only acts as a prophylaxis against injury but also facilitates the necessary metabolic pathway
adaptations that increase muscular strength.
Circuit Resistance Training
CRT is used mainly by endurance athletes who are interested in gaining muscular strength and endurance. CRT involves
protracted periods of repeated muscle contractions followed by short periods of recovery between resistance machines.
Athletes begin training at a resistance level that is estimated to be 40% to 50% of their one-repetition maximum (1 RM).
The 1 RM is a method of measuring absolute strength, using a one-repetition lift at maximal intensity. The process can
be applied to all exercises (e.g., squat, military press).
The circuits are arranged before the actual training sessions; they consist of 10 to 14 machines that exercise the major
muscle groups of the body. The athlete begins the circuit by repeatedly lifting the set resistance for a specified period (30
seconds) or specified number of repetitions (20 to 30), followed by a brief recovery period (10 to 30 seconds). The
athlete moves to the next resistance machine in the circuit and continues the procedure until the entire circuit is
completed. Theoretically, exercising the muscle at high repetitions with moderate resistance and limited recovery time
enables the athlete to maintain a heart rate (HR) that is sufficient for endurance adaptations to occur. CRT is a
contemporary idea that has not been extensively studied scientifically, although initial findings are encouraging ( 15).
Plyometric Training
Plyometrics is a relatively new method of training that is gaining popularity among athletes that require explosive
muscular power for performance. Plyometrics use the athlete's body mass as well as the force of gravity for resistance.
The plyometric technique is performed by having the athlete repeatedly jump from and land on surfaces of different
heights. Plyometric training employs the ballistic properties of skeletal muscle, resulting in the development of muscular
strength for explosive power. The underlying premise of plyometrics is to train the muscle fibers to maximize their
inherent elastic properties via the stretch-recoil response modulated by the myotactic reflex. ( 38). The myotactic reflex, or
the muscle stretch reflex, occurs whenever a muscle is placed on stretch. The sudden implosive elongation of the muscle
stimulates the muscle spindle, which in turn acts as a sensory relay to the CNS. Once the CNS has identified the
intensity of the signal, a neural response indicated by the efferent pathways stimulates the muscle fibers to contract
explosively. This activity is called a reflex because of the instantaneous response of the muscle. With training,
adaptations occur within fast-twitch fibers that maximize not only the sensitivity of the stretch but, more importantly, the
speed and number of motor units recruited for the resultant muscle contraction. The rapid change from stretch to recoil
involves two types of muscle contractions. First, the muscle is elongated and loaded eccentrically. This decelerates the
muscle in preparation for the recoil. The recoil involves the concentric contraction, which accelerates the explosive
movement. This process also is known as the amortization phase. This coupling action has been found to take place
within hundredths of a second, thus classifying the plyometric mechanism as a reflex.
A plyometric training program consists of explosive jumps and bounds on one or both legs in a vertical or horizontal
direction. Various heights of jumping and landing are used in progression. Athletes should begin plyometric training at
low intensity, working up to more intense levels. Plyometrics may begin as general training and progress to a more
functional or sport-specific activity. The progression from straight ahead to lateral and diagonal patterns of jumping is an
example of a functional program for the athlete who requires high levels of agility. More vertical training applies to those
athletes who seek vertical displacement, such as long jumpers, ice skaters, and volleyball and basketball players.
Plyometrics also are performed for upper-body activities that require explosive muscle action. Shot-putters, gymnasts,
and wrestlers may benefit from plyometric training as a means of gaining explosive power from the shoulder girdle ( Fig.
2.6).
FIGURE 2.6. Plyometric training involves repetitious jumping from and landing on surfaces of various heights.
In summary, plyometric training uses the athlete's body mass and the force of gravity for resistance as the athlete
repeatedly performs bounding (jumping) maneuvers. The major muscle groups that are usually exercised are the
musculature surrounding the knee and hip joints. More recent techniques have been developed for the shoulder girdle,
using external resistance such as medicine balls rather than body mass and gravity. The risk of orthopedic injury is high
due to repetitive eccentric loading of the musculotendinous units. Therefore, proper warmup techniques are indicated to
increase the flexibility of muscle and connective tissue surrounding the involved joints.
Isokinetic Training
Isokinetic training is useful for speed-specific strength training. Fast- and slow-speed training have been studied with
respect to gains in absolute strength and other parameters of muscle performance. Perrin et al. ( 39) revealed the benefits
of isokinetic training on muscular strength and power, demonstrating that 7 weeks of fast-speed training (270 degrees per
second) is adequate for increases in peak torque, torque acceleration energy (TAE), and average power at variable
speeds (60, 180, and 270 degrees per second). Pipes and Wilmore ( 33) and Thomee et al. (40), in related studies, also
revealed strength gains from fast-speed isokinetic training. It is suggested that the gains result from adaptations within
the fast-twitch (type II) fibers caused by increases in cross-sectional area, metabolic function, and recruitment patterns.
These reported strength gains also were found to carry over to slower speeds ( 33,39,40). In conclusion, fast-speed
isokinetic exercise has been reported to increase muscular strength as well as power. Therefore, athletes who require
muscular power may benefit from isokinetic resistance training at high angular velocities.
Increases in muscular strength and power are not beneficial unless they carry over to functional performance. Therefore,
one must question the value of isokinetic strength gains for the purpose of performance enhancement. Investigations
have revealed low correlations between isokinetic strength or power and functional performance ( 36). The lack of kinetic
chain specificity is speculated to be responsible for the weak relationship.
Measurement of Muscular Strength, Power, and Endurance
Quantitative assessment of an athlete's strength is essential for determining baseline levels and progress during training.
Objective strength data can be used to compare individuals, identify strength gains during training, or provide evidence
that one protocol is more effective than another. Because little is known about the mechanism of strength gains, more
research is necessary to identify which strength programs currently in use are the most beneficial ( 33,41). Muscular
strength may be measured in three different modes: isometrically, isotonically, and isokinetically.
Isometric
Isometric (static) strength assessments measure the maximal tension produced by one or more muscles or muscle
groups independent of changes in muscle length ( 2,15). Static measures can be obtained with the use of cable
tensiometry or dynamometry, or both. Cable tensiometry has the potential to measure the static strength of specific
muscles or groups of muscles at various joint angles. The cable is attached to a dynamometer that records the tension or
force produced during an isometric contraction ( Fig. 2.7). This method is effective for making strength measurements
when joint motion is contraindicated. Furthermore, static measures are easily obtained clinically and are easily
reproducible for bilateral or reciprocal muscle group comparisons. The dynamometer alone also can measure static
strength. The dynamometer differs from the cable technique in that compressive rather than tensile forces are measured.
Typically, grip strength is measured with a dynamometer ( Fig. 2.8).
FIGURE 2.7. Cable tensiometry measures static strength of muscle groups through distraction forces. A cable is attached
to a dynamometer.
FIGURE 2.8. Static strength also can be measured with compressive forces on a handheld dynamometer.
Isotonic
Isotonic (dynamic) strength measurements are assessed with the use of a constant weight at variable angular velocities
through a full ROM of a joint. Isotonic assessments include measurement of the maximum weight moved through 1 RM
(31,42). This classic procedure usually is performed with barbell or dumbbell devices to provide a reference weight
before planning a strength-training program. The most common 1 RM test is the bench press. This method effectively
establishes a submaximal starting weight as a percentage of the 1 RM. The 1 RM isotonic strength assessment also is an
efficient means of evaluating the strength levels of large groups of athletes ( 12,42).
Isokinetic
Isokinetic assessment has become the standard for all muscle strength evaluation. With the innovation of computer
technology, the assessment of muscular strength, power, and endurance can be quantified by interfacing dynamometers
with digital microprocessor computers. Isokinetic assessments measure strength at preset angular velocities. Strength is
measured as torque, a component of force and velocity. Isokinetic devices are speed controlled with accommodating
resistance to maintain preset angular velocities. The velocity spectrum typically ranges from 0 (isometric) to 300 degrees
per second with contemporary isokinetic devices. The isokinetic devices provide rapid and accurate data relative to
muscular strength, power, and endurance. These data permit the clinician to make rapid bilateral and reciprocal muscle
group comparisons across a spectrum of test velocities ( Fig. 2.9 and Fig. 2.10).
FIGURE 2.9. Isokinetic strength is quantitatively measured by a dynamometer interfaced with a computer.
FIGURE 2.10. The computer printout from a Cybex II isokinetic testing device (Lumex Inc., Ronkonkoma, NY) indicates
strength and power output variables associated with knee extension (quadriceps, a) and knee flexion (hamstrings, b).
The vertical axis, or amplitude, represents peak torque, and the horizontal axis represents the total time (c) of the muscle
contraction. The shaded area represents the total work output (torque times duration of muscle contraction), and average
power is computed by dividing the total work output by the duration of contraction.
Isokinetic testing devices also can measure power and endurance at various angular velocities (low-high) and at
accommodating resistances. Most joints of the body can be isolated for testing. The Cybex II dynamometer (Lumex Inc.,
Ronkonkoma, NY) is a popular device that is used at many sports medicine clinics and universities. The main isokinetic
parameters for measuring strength, power, and endurance are peak torque, TAE, average power, total work, and
endurance. Isokinetic testing is an easy and reliable method to establish preseason strength measures or strength
progressions with rehabilitation programs.
Anaerobic Conditioning
Anaerobic conditioning is important for athletes who require near-maximal, quick bursts of muscular power, such as
sprinters, rowers, and soccer and lacrosse players. Anaerobic conditioning results in the enhanced efficiency of
anaerobic energy during exercise. This type of conditioning uses high-energy anaerobic pathways (adenosine
triphosphate-creatine phosphate [ATP-CP]) and glycolysis for generating the energy necessary to power skeletal muscle
contractions.
Exercise that requires near-maximal effort for up to 2 to 3 minutes is generated mainly by the ATP-CP and glycolytic
energy systems. The two energy systems are anaerobic in nature, because molecular oxygen is not assisting in the
formation of the high-energy phosphates (ATP-CP). The ATP-CP system supplies the immediate source of fuel for
approximately the first 10 seconds of exercise or until the intracellular supply of ATP-CP is exhausted. After depletion of
ATP-CP from the exercising cells, a quick shift to glycolysis occurs to continue the yield of ATP-CP. The glycolytic or
short-term energy system uses the breakdown of glycogen to resynthesize the high-energy phosphates.
Immediate and Short-Term Exercise
Immediate (0 to 10 seconds)
High-intensity, short-duration activity is performed using predominantly fast-twitch, glycolytic muscle fibers (type IIb).
These fibers are densely concentrated and consist of high-energy phosphate molecules, which generate most of the
muscle contractions associated with activities that are explosive in nature.
Examples of activities that should be incorporated into a program that trains the immediate energy pathways include
sport-specific and general-conditioning drills to enhance agility, sprint training (50, 100, 200, and 400 m), and
plyometrics. Interval training also induces metabolic adaptations within the type II fibers, resulting in increased use of
ATP-CP for energy.
Short-Term (10 to 180 seconds)
Activities using the short-term energy pathway generally last from 10 to 180 seconds and are powered by fast-twitch,
glycolytic and intermediate, fast oxidative glycolytic muscle fibers (types IIa and IIb). Training to enhance glycolysis
results in production of ATP-CP. Once the immediate ATP-CP sources are exhausted, the short-term pathway breaks
down glycogen to produce fresh supplies of ATP-CP. Exercise of high intensity (more than 60% of maximum), and
medium duration (30 to 120 seconds) conditions this system to function more efficiently. The power output of this
short-term, high-intensity system (75% to 90% of maximal oxygen consumption [V O2max]) is referred to as an athlete's
anaerobic capacity, because of the reliance on anaerobic metabolism for this type of activity ( 43).
Examples of short-term energy system training include interval training of distances ranging from 100 to 800 m, with short
periods of recovery (30 to 60 seconds). Resistance training with high repetitions and low to moderate weight requires
anaerobic pathways to provide muscular endurance and fatigue resistance during exercise. Isokinetic training also uses
this energy system for muscular contractions at a variety of speeds.
Anaerobic Conditioning Programs
Sprint Training
Athletes who compete in sports that are acyclic and use the immediate energy pathway benefit from exercises that
require explosive power or sprinting. A variety of exercises have been found to be effective for enhancing reaction time,
speed of contractility, and explosive power. Speed athletes run interval sprints or, more recently, sprint against
resistance. Many professional and intercollegiate football programs now have their speed athletes sprint with
parachute-like devices for increased resistance. Other methods of resistance sprinting include having the athlete run
against resistive tubing or run in water. These methods follow the overload principle for specific adaptation enhancing the
force and speed (acceleration) of contraction.
Athletes such as jumpers (high, long, and triple jump) and throwers (shot put, discus, hammer, and javelin) typically use
plyometrics as a means to increase contractile strength or power. Isokinetic training at fast speeds also may enhance
contractility, but the carryover to functional activities has not been proved scientifically.
Interval Training
Interval training is cyclic and incorporates high-intensity exercise for short (50 to 800 m) or moderate (1 mile) distances
or durations (10 seconds to 6 minutes). This form of training is more beneficial during the preseason. The frequency of
interval training is usually two to four times per week, with active recovery in between sessions. Modes of interval training
vary according to the specific demands of the sport. Some examples are running on a track, pedaling a stationary or
nonstationary bicycle ergometer, and swimming. The anaerobic pathways are trained in combination with the aerobic
pathway, although the anaerobic system receives the greatest benefits. Interval training is an efficient means of
conditioning the body to function anaerobically. Athletes receive mechanical benefits from interval training; movements
become more efficient or economical. This energy-sparing benefit is significant for athletes who compete against time.
Isokinetic Training
New isokinetic equipment has been developed by Lumex that provides isokinetic resistance during exercise. Lumex has
designed a stationary bike and an upper-body ergometer that provide accommodating resistance at various workloads.
Athletes use these devices to enhance their anaerobic power output.
Measurement of Anaerobic Power
Most of the immediate and short-term power output tests assess the athlete's ability to perform a maximal-intensity
activity, using either time or distance as the indicator of power output. Each measurement must be specific to the energy
system that is being tested. For example, tests of immediate power last approximately 1 to 10 seconds, and tests for
short-term power last from approximately 30 seconds to 3 minutes. When these systems are measured in human
performance laboratories, they are recorded as units of power output or work. Power is generally expressed in standard
units (foot-pounds [ft-lb]) or in metric units (kilogram-meters [kg-m] per minute or per second), horsepower (hp), Newton
meters (N-m), or watts (W).
Immediate Tests
The most popular modes of measuring immediate power output use high-intensity explosive tests such as jumping,
sprinting, stationary bicycling, and isokinetics.
Vertical Jump
The vertical jump assesses an athlete's explosive power. The test is designed to isolate the musculature about the hip
and thigh. The goal is to measure the displacement of the body vertically against the force of gravity. It is an easy test to
conduct and can be used for large groups of athletes. The test is most applicable to volleyball, basketball, track and field,
and other sports that rely heavily on the immediate energy system. The test is normalized to individual body weight with
the use of the Lewis nomogram (3).
The 40- or 50-Yard Dash
The 40- or 50-yard dash is a popular test for horizontal sprint speed. It is a test of acceleration more than of speed, with
typical times ranging from 4 to 6 seconds. Many sports, such as football, use the 40-yard dash as a criterion measure for
assessing speed. Sprint speed is highly related to tests of anaerobic power ( 44), and therefore it may be used as a test of
explosive power because of the short duration of the test.
Torque Acceleration Energy
Isokinetic testing devices have the capability of measuring specific parameters of power output. The Cybex II measures
TAE, which is a gauge of the explosiveness of a muscle contraction and thus an assessment of work per unit time, which
defines power. TAE is defined as the total work produced in the first one-eighth of a muscular contraction. TAE has been
found to correlate strongly with other tests of anaerobic power ( 45).
Margaria-Kalamen Step Test
The Margaria-Kalamen step test was originally designed by Margaria et al. ( 46) and later modified by Kalamen ( 44). The
test requires stair climbing at maximal speed and combines horizontal and vertical components, or vectorial
displacements, against time. The subject starts 6 m from the stairs, and timing plates are situated on the third and ninth
steps (to start and stop the timer, respectively). The subject climbs the stairs at maximal speed, making contact with the
timing plates, which record time in milliseconds. The time measure is incorporated into an equation used to calculate
power output. The test has proved valid and is readily used as a test of power ( 44,45 and 46).
Interrelationships of Tests
Lephart et al. (45) found strong correlations among results for TAE, the vertical jump, and the Margaria-Kalamen step
test. Furthermore, Kalamen (44) found strong relationships between the Margaria-Kalamen step test and sprint speed.
This suggests that these tests for immediate power may be used as valid indicators of anaerobic power under explosive
conditions.
Short-Term Tests
100-, 200-, 400-, and 800-m Runs
These runs range in time from 10 seconds to 2 to 3 minutes. The tests are valuable for assessing the anaerobic capacity
of athletes who participate in sports that require extended periods of anaerobic power output, such as middle-distance
track, soccer, and basketball.
Bicycle Ergometer
The bicycle ergometer measures anaerobic power or capacity indirectly by measuring specific variables associated with
power. The test protocols consist of pedaling a stationary bicycle ergometer at a preset resistance with near-maximal
levels of intensity for a specified period ( Fig. 2.11). The wheel circumference in meters (Circ), the athlete's body weight,
and the number of repetitions (Reps) are recorded and incorporated into an equation that uses distance (Reps times
Circ) and resistance (in haptograms [hg]) to calculate power output in kilogram-meters per time unit (seconds or minutes):
FIGURE 2.11. A stationary bicycle ergometer is a popular mode for measuring power output.
The most popular bicycle ergometer tests are the Gillum-Katch, Margaria-Kalamen, and Wingate tests for anaerobic
power output (43,44,45,46,47 and 48).
Average Power, Total Work, and Endurance Ratio
Isokinetic testing devices also can assess anaerobic capacity by measuring torque production over the time it takes to
perform muscle contractions at a constant angular velocity. Total work is the sum total of power produced over the time of
contractions. Average power is the total work produced divided by the time it takes for the entire set of contractions.
Clinicians may assess muscular endurance through the 50% decrement test. This index of muscular endurance is simply
the number of repetitions at a preset speed (e.g., 180 or 240 degrees per second) performed by the athlete before failing
to produce 50% of the peak torque ( 49). Another method used for assessing muscular endurance is the endurance ratio,
which is calculated by dividing the work performed during the first five contractions by the work performed during the last
five contractions when a preset number of repetitions (e.g., 25) are performed at a preset speed (e.g., 240 degrees per
second).
Individual Differences
Several parameters may significantly affect individual scores in performance testing. Factors such as age, sex,
motivational level, body weight and composition, and levels of skill and training create differences in scores, resulting in
potential errors when compared with the normative data.
Long-Term Exercise
Acquiring an aerobic base has often been suggested as a prerequisite to training. The term aerobic implies that oxygen
is used to generate power for endurance exercise, whereas base describes a subthreshold level of aerobic power.
Oxygen consumption, VO 2, is the volume of oxygen used in the process of cellular respiration. Aerobic conditioning
involves submaximal endurance training for mainly cyclic activities with durations exceeding 3 minutes. Although an
aerobic base is beneficial, it is important not to ignore the other metabolic systems associated with athletic performance.
Dynamic exercise does not use one system exclusively but draws from both aerobic and anaerobic systems when
necessary. For example, marathon runners principally use molecular oxygen (aerobic pathways) as their means of
regenerating ATP-CP. But because marathoners run at high intensities (75% to 80% or more of V O2max), they also use
anaerobic pathways for the generation of muscular power. In addition, runners apply strategies that require short bursts
of energy at particular points during the race to overtake an opponent. These bursts require energy supplied from the
anaerobic (immediate and short-term) systems.
Unlike anaerobic conditioning, aerobic conditioning uses molecular oxygen to synthesize ATP-CP for energy. Aerobic
metabolism oxidizes available substrates (glucose, free fatty acids, and amino acids) to form ATP. This consistent supply
of ATP is sufficient to maintain low to moderate submaximal endurance exercise for prolonged periods. Therefore, to train
this system, athletes must exercise for long durations (3 minutes to 1 hour or longer) at low to moderate intensities (up to
60% of maximum). This training predominantly uses slow-twitch oxidative (type I) fibers, which have high concentrations
of oxidative enzymes and organelles. The fast-twitch oxidative glycolytic, or intermediate, muscle fibers (type IIa) also are
used, in smaller supply, to maintain aerobic power. Through training, the metabolic demands on these fibers increase,
producing adaptations in the athlete's oxidative capability.
Examples of aerobic or endurance-type activities induce distance training for running, cycling, rowing, stair climbing,
cross-country skiing, and aerobics.
Aerobic Conditioning Program
Over-Distance Training
Over-distance training is performed purely for endurance benefits. Athletes who require an aerobic base or need
endurance adaptations for long-distance events use over-distance, or long-slow distance, training. The athlete runs for
protracted distances (more than 5 miles) for long durations (more than 30 minutes) at low to moderate intensity (40% to
70% of VO 2max). This submaximal exercise produces peripheral adaptations commensurate with this type of activity. For
example, the slow-twitch muscle fibers increase oxygen consumption capacity by increasing mitochondrial and enzymatic
efficiency. Lactic acid turnover also is enhanced. This form of training is beneficial during the preseason for athletes who
need to acquire an aerobic base or endurance for their sport.
Steady-Rate or Tempo Training
Steady-rate training has become popular among endurance athletes and is used as an adjunct to long-slow distance and
interval training. Steady rate implies that oxygen consumption is constant and proportional to the submaximal work load.
The volume (frequency and duration) and intensity vary according to personal preference and period of training. Tempo
training may be implemented for sports that require aerobic power over an extended time period. Sports that may benefit
include track (distance events), basketball, soccer, wrestling, lacrosse, and swimming.
Combined Program
Fartlek Training
Fartlek is a Swedish term meaning “speed play.” This type of training consists of continuous aerobic exercise with
interval periods of anaerobic bursts. Distance runners use this type of training to simulate competitive running. Long-slow
distance running is combined with short periods of speed running. The intensities and durations are flexible with each
athlete, so protocols vary according to personal preference. Overall, this form of training lacks sophistication and is not
scientifically recommended; but if it is done properly, all three systems can be trained simultaneously.
Hill Training
Hill training produces metabolic adaptations for power. The format consists of high-intensity running for specified
distances. The hills vary in grade and length, so the athlete must titrate parameters such as repetition of climbs and
recovery between climbs.
These types of training styles are not sport specific and may be formatted to apply to any sport. The training format
should match the demands of the specific sport and also should be incorporated during the proper phase of training.
Measurement of Aerobic Power
Maximal and Peak Oxygen Consumption
The most popular method of directly measuring aerobic power is the V O2max/peak test, which is a volumetric measure of
oxygen consumption taken when the muscles are at near-maximal effort. The V O 2max value is the highest volume of
oxygen consumption, whereas V O2peak is the peak level relative to the mode of testing. The subject is tested on a
motor-driven treadmill or stationary bicycle ergometer; a gas analyzer attached to the mouth analyzes the gas exchange
ratio (i.e., the ratio of carbon dioxide to oxygen). The exercise apparatus is interfaced with a computer, which calculates
and prints the variables associated with this form of exercise. A graded, continuous-exercise test protocol is used to
reach maximum intensity levels by increasing the intensity in increments of time. Intensity is increased by increasing the
speed and grade of the treadmill or the resistance and revolutions per minute of the bicycle ergometer, until the subject
reaches the point of exhaustion, at which time the test is terminated. V O2max values are recorded by volume (mL), mass
(kg), and time (minutes) (Fig. 2.12).
FIGURE 2.12. A computer printout from a graded exercise treadmill test quantifies variables associated with oxygen
consumption during maximal or peak exercise. Volume is indicated in liters per minute. Vo 2, oxygen consumption
(milliliters per kilogram per minute); CO 2, ventilation; RER, respiratory exchange ratio; HR, heart rate; RR, respiratory
rate. The variables are measured as a function of time.
Other Predictors of Maximal Oxygen Consumption
Several other tests may be used to predict or estimate V O2max through the use of a normative or predictor scale ( 50,51).
The mode of testing varies, but all tests require submaximal efforts for a specified time. The tests are easily administered
but is not always valid. These tests include endurance runs, step tests, and bicycle ergometer tests.
Endurance Runs. The Cooper 12-minute run/walk measures the distance the athlete covers during 12 minutes. The
distance is the criterion measurement, which is used to estimate V O2max.
Maximal Heart Rate. Maximal HR rate tests require running or pedaling for a specified distance or time, while HR is
assessed as the criterion measurement. Maximal HR values are then compared with prediction tables to estimate V O2max.
Step Tests. The Howard and Queens step tests use cadence stepping for a known height and time. The recovery HR is
measured, recorded, and then incorporated into a prediction equation to estimate V O 2max.
Bicycle Ergometer Tests. The Young Men's Christian Association (YMCA) test requires pedaling at a preset number of
revolutions per minute for a specified time period. Interval HR measures are taken and compared with a normative data
table to estimate the V O2max.
Isokinetic Tests.
The muscular endurance index (described earlier) may be used as a test of local muscular endurance.
Relationships among Tests of Maximal Oxygen Consumption
Relationships among measurements of V O2max and submaximal tests to estimate VO 2max have been established, with
measurement errors varying between 10% and 20%. Cooper found a strong correlation in U.S. Air Force personnel
between V O2max and the distance covered during a 12-minute run/walk ( r = .90) (52). Some investigators have been
unsuccessful in reproducing strong relationships among the tests, while others have found a linear relationship between
HR and oxygen consumption at submaximal exercise (52).
The limitations of estimates made from submaximal tests are implicit in the design of each particular test. Furthermore,
VO 2max has not been found to predict athletic performance strongly, although these tests do provide an avenue for the
purpose of screening and classifying large numbers of athletes in terms of aerobic fitness.
YEAR-ROUND STRENGTHENING AND CONDITIONING PROGRAM
The ever-increasing demand for excellence in athletic performance has prompted sports scientists and coaches to
develop comprehensive 12-month strengthening and conditioning programs for their athletes. The premise for a
year-round program is to develop and maintain various general and sport-specific performance parameters throughout
the year. Most advocates of year-round programs break down or cycle their program to attain peak performance levels at
a preplanned time during the competitive season. This is known as periodization. For example, Olympic athletes train
year round with the ultimate goal of peaking exactly when the Olympics begin. For the program to be successful, the
athlete must abide by the principles of overload, specificity, and recovery. The volume, intensity, and mode of exercise
must be varied systematically and in a sophisticated manner to obtain maximal benefits. This section outlines a 12-month
strengthening and conditioning program to demonstrate the benefit of a systematic format of training to achieve peak
performance.
Periodization
The design and implementation of a periodized training program was introduced in the 1950s by Russian sports
scientists (15). Their objective was to break down athletes' training into component parts that incorporated both short-
and long-range goals. For most athletes, especially at the amateur, professional, and intercollegiate levels, the year is
broken down into preseason, precompetition, in-season competition, and postseason recovery periods.
The preseason objective is to attain a foundation or base level of fitness, whereas the goal in the precompetition phase is
to work on technical skills in preparation for competition. The in-season phase of the program is dedicated to improving
skills and technique while obtaining peak performance. “Peaking” is manifested from the combined increases of
technique, strength, and conditioning. The postseason phase of the program is dedicated to recovery, followed by the
beginning of light training in preparation of the impending preseason training.
When designing a year-round program, one must abide by certain parameters to achieve outcome goals. These
parameters include volume (frequency times duration), intensity, and mode of training. If these parameters are not strictly
monitored, unwanted setbacks such as overtraining, premature performance peaking, or chronic fatigue may result. The
year-round program incorporates both a strengthening and a conditioning phase, and both are integral to the athlete's
overall performance.
Strengthening Program
Each sport has its specific requisites for muscular strength, although common objectives for strength acquisition apply to
all sports. Strength training results in enhanced generation of muscular force by increasing the morphologic and
neurologic components of muscle contraction. Strength training uses resistance exercise and produces gains by
employing the overload principle for specific muscles or muscle groups. The measurable gains in strength are a direct
result of the overload principle in action. When the muscle is overloaded, the external force of resistance is significantly
greater than the internal force of the muscle contraction; the result is hypertrophic changes that occur within the muscle
fiber and that adapt to the external resistive forces. The overload force also results in enhanced recruitment of available
motor units within the surrounding muscle tissue ( 15,28). The combination of increased recruitment and hypertrophy
permits greater force generation during muscle contractions. The strength phase has three important components that
must be addressed to have a progressive and injury-free program: flexibility, sport-specific strength, and muscular
endurance. The strength-training programs discussed earlier may be used by the athlete according to phase of training,
personal preference, sport specificity, or accessibility for the athlete.
In addition to the development of muscle strength for the whole body, athletes must streamline their training to match
their particular sport. This includes training the specific muscle groups that generate force for the techniques that are
required for the athlete's performance. The SAID principle works in conjunction with the overload principle and involves
sport-specific training, which induces adaptations that improve athletic performance ( 15,28). This component is usually
addressed during the preseason and in-season training periods.
Flexibility training has been shown to improve joint ROM and to prevent exercise-induced muscle injury ( 2,3). Therefore,
flexibility training is used as an adjunct to other types of training and conditioning. Flexibility exercises are classified as
active, passive, or active assistive and are performed through “static” or ballistic stretching methods. Active stretching is
performed solely by the athlete, whereas passive and active assistive exercises require a partner. Static stretching is
preferred before warmup. The slow, progressive process of static stretching permits the muscle to lengthen efficiently
without the risk of injury. Ballistic stretching uses fast, bouncing-type movements that require the muscle to respond
quickly to the imposed changes in length. Ballistic stretching is performed after warmup and requires care because of the
high risk of muscle injury ( 2,3). Flexibility training is addressed later in this chapter.
Conditioning Program
The way an athlete uses the three energy systems depends on his or her specific sport. Most sports combine speed with
endurance for optimal levels of athletic performance. Soccer players need explosive power and speed for breakaway
moves but also require an aerobic base to have enough energy to last through the match. When a conditioning protocol
is developed, both the anaerobic and the aerobic aspects of the sport must be addressed. For instance, to train the
immediate and short-term energy systems effectively, an athlete must train at near-maximal intensities for periods of 1 to
10 seconds for explosive power and for 30 to 180 seconds to increase anaerobic capacity. The transition from
predominantly anaerobic to aerobic exercise requires a shift from glycolytic to oxidative pathways. This shift in
metabolism requires protracted exercise at moderate to high intensity (70% to 85% of V O2max) for 2 to 3 minutes. The
frequency of training intensity varies according to the season, but high-intensity training is normally alternated with low-
to moderate-intensity training.
Concomitant with conditioning of the metabolic pathways, the agility requisites also must be addressed. Agility drills for
sports that demand balance, coordination, and lateral mobility condition the neuromuscular system for those types of
activities.
Phases
As noted previously, the 12-month program is divided into four phases: preseason training, precompetition, in-season
competition, and postseason recovery. The overall objectives of the program are to develop during the preseason,
streamline during precompetition, maintain and peak during the in-season, and recover during the postseason. The
principal components of athletic performance are strength development, anaerobic and aerobic conditioning, and skill
acquisition. Each component is trained and used differently during each phase, according to the specific demands of the
athlete's sport.
Preseason Training
Preseason training usually takes place during the 3 months before precompetition training. It is the foundation from which
the athlete develops his or her fitness base. Strengthening and conditioning are combined within this phase to prepare
the athlete for precompetition, when training volume tapers and skill refinement takes precedence. Preseason training
also may include active rehabilitation of acute and chronic injuries, as well as the identification and correction of any
preexisting weaknesses in technique or musculoskeletal imbalances. The training consists of high-volume, moderate- to
high-intensity exercise with gradual, progressive increases. Strength training involves low-repetition, high-resistance
work, and conditioning consists of anaerobic and aerobic endurance activities.
Precompetition Phase
Precompetition usually begins 1 month before the in-season competition phase. The objective here is to prepare the
athlete for competition. During this phase, the athlete tapers off from high-volume preseason training and concentrates
on sport-specific skills. For example, wrestlers use this period to refine their moves both on their feet (takedowns) and on
the mat (top and bottom). Precompetition workouts are shorter and are performed at moderate to high intensity levels.
The emphasis is on competition simulation. Strengthening and conditioning work continues, but the volume and intensity
are not as great.
In-Season Competition Phase
The in-season competition phase includes peaking in terms of strength, power, conditioning, and technique. During the
in-season phase of the program, general preseason strengthening and conditioning exercises are streamlined and
fine-tuned for sport-specific activities that relate to technique, speed of movement, and timing. The volume of practice
time is often reduced to levels that sustain the strength and conditioning that were established during the preseason. The
intensity of the practice sessions is usually increased dramatically to mimic competition. By reducing the volume, the
athlete maintains conditioning and strength to meet the demands of the particular sport. The in-season phase lasts 3 to 4
months.
Postseason Recovery Phase

Immediately after the competitive season, most athletes rest 2 to 3 weeks to recover mentally, physically, and emotionally
from the stress of competition. The athlete may wish to concentrate on other aspects of life (e.g., coursework, family,
friends, hobbies). The next 3 to 4 months are used for active rest and recovery: the athlete engages in activities other
than his or her sport. This practice is known as cross-training, and it can be an effective means for the athlete to stay
active, fit, and injury-free without feeling burned out. This period also may be used for rehabilitation of any injuries
incurred during the competitive season. Postseason recovery is important for long-term progress.
Summary
In summary, each program must follow the principles associated with exercise training. Overload, specificity, and timing
are the crucial ingredients for the progressive increase in skill acquisition, strength, power, endurance, and recovery.
Each program must take advantage of the overload and SAID principles to develop the requisite balance of strength and
condition for a particular sport. In addition, the proper prescription of volume, intensity, and mode must be applied during
the annual cycle of training. This produces a systematic progression in the performance parameters necessary to carry
the athlete to proper peaks in training. The postseason recovery phase is a necessary component that permits mental,
physical, and emotional rest to prepare the athlete for the next season.
PHYSIOLOGIC EFFECTS OF TRAINING
Exercise training produces many biophysical adaptations that enable the athlete to meet the increased physiologic
demands of strenuous exercise. Cardiovascular, respiratory, and neuroendocrine adaptations occur as a result of
endurance training and are centrally and peripherally manifested. These adaptations provide the smooth transition from
rest to exercise during endurance training.
Endurance training has shown to increase V O 2max (29). Much debate has centered on the relative contributions of the
central and peripheral nervous systems to the increase in oxygen consumption. Holloszy and Coyle ( 29) stated that the
great capacity of the cardiovascular system to deliver oxygen to the exercising muscles is the primary factor responsible
for increases in oxygen consumption. Other researchers have suggested that oxidative respiration is the primary
rate-limiting factor during strenuous exercise ( 30). Oxidative respiration, or the arteriovenous oxygen difference, is equal
to the arterial oxygen concentration (Ca O 2) minus the venous oxygen concentration (Cv O2). The oxygen consumption
equation is
where Q is the cardiac output (HR times stroke volume).
Central Adaptations
As a result of exercise training, the cardiovascular system becomes more efficient in (a) transporting nutrients (oxygen,
glucose, and hormones) to the exercising muscles, (b) extracting the nutrients from the blood, (c) removing metabolic
wastes from the muscles, and (d) maintaining thermoregulation. With the onset of exercise, the cardiovascular system
responds by increasing Q, which is the volume of blood pumped from the heart per beat. This increase is the result of
increases in both HR and stroke volume.
Cardiac Output
Q has been shown to increase by 6 L per minute for every 1 L per minute increase in V O 2 during strenuous exercise
involving large muscle masses (53). The relationship between Q and Z has been found to be consistent with all types of
exercise (28,54) and is regulated by the CNS. The V O 2 is suggested to be the best noninvasive measurement of overall
cardiovascular function ( 28,53,54).
Stroke Volume and Heart Rate
Stroke volume has been found to increase in proportion to the intensity of exercise until approximately 25% to 50% of
VO 2max, when a plateau effect occurs ( 28,53). Further increases in Q are a result of increased HR, which also has been
found to increase in direct proportion to exercise intensity. From a research standpoint, HR is the most consistent factor
involved with increases in Q and V O2 during exercise, and stroke volume is considered the rate-limiting factor for
determining individual differences in V O2max (28).
The VO 2 and cardiovascular function depend on the relative amount of muscle mass used during exercise. For instance,
exercises that use large muscle masses (e.g., cross-country skiing, cycling, running) induce greater cardiovascular and
VO 2 adaptations than exercises that use small or localized muscle masses (e.g., weight lifting). Also, the volume
(frequency and duration) of training determine cardiovascular function and V O2.
Blood Pressure and Flow
As Q increases steadily, blood pressure rises to maintain adequate blood flow to the active tissues. Blood pressure is the
product of Q times the total peripheral resistance. During exercise, Q increases the volume of blood pumped from the
heart, while total peripheral resistance decreases blood flow to the inactive tissues and increases blood flow to the
exercising muscles. The CNS regulates blood pressure and blood flow at levels appropriate for the amount of muscle
mass used or oxygen consumed during exercise (54). Increased areas of blood flow include the brain, heart (coronary
circulation), lungs (pulmonary circulation), and skeletal muscles. Blood flow at rest (5 L per minute) can increase fivefold
(up to 25 L per minute) with exercise at near-maximal work loads ( 28). This adaptation maximizes blood flow to the
exercising muscles and minimizes blood flow to inactive tissue ( 55). The ultimate adaptation is greater use of oxygen for
peak levels of performance.
Ventilation
An often overlooked yet critical central adaptation to exercise is ventilation. Once venous blood returns to the heart, it is
pumped into the pulmonary circulation for gas exchange. During exercise, minute ventilation is increased linearly with Q;
this response is commonly known as the ventilation-perfusion ratio ( / ). Chemoreceptors located in peripheral blood
vessels returning deoxygenated blood to the heart are stimulated by high concentrations of carbon dioxide. This
stimulation causes the lungs to hyperventilate so as to expel the carbon dioxide in exchange for oxygen. This adaptation
is known as the perfusion percentage of blood gases ( 28). After oxygenation, the blood returns to the heart for transport
and use at the periphery. The energy cost of hyperventilation on the intercostal muscles is compensated through the
increase in blood flow, as discussed previously.
Peripheral Adaptations
During exercise, blood flow to the peripheral vessels (arteries, capillaries, and veins) and active muscles increases. As a
result of training, the working muscles become more efficient in extracting oxygen and returning carbon dioxide to the
blood to meet the elevated metabolic demands of exercise. This process subserves oxidative respiration and is known
physiologically as the arteriovenous oxygen difference.
Arteriovenous Oxygen Difference and Oxygen Consumption
A linear increase in the arteriovenous oxygen difference has been shown to occur with increases in exercise intensity
(30,56). Oxygen consumption (VO2) by the active tissues increases until near-maximal levels of exercise intensity are
reached, at which time a much-debated plateau in V O 2 has been shown to occur, indicating an oxidative peak. Any
further increases in power output after the plateau are suggested to be from anaerobic mechanisms ( 30). The muscle
tissue uses oxygen for oxidative metabolism, and as a result of this increase in V O2 the metabolic demand of exercise is
met, allowing the athlete to train at higher levels of intensity.
Hematologic Adaptations
Hematologic adaptations to aerobic exercise training result in an increase in plasma volume. This adaptation allows for
facilitated nutrient and oxygen transportation and also compensates for the loss of total body water as a result of sweat
loss (thermoregulation). The hemoconcentration of hemoglobin does not change, although it may become diluted as a
result of the increase in plasma volume. When the intensity of exercise increases, a shift in the oxygen dissociation curve
(Bohr effect) occurs to facilitate gas exchange at the tissue level. This effect works in conjunction with the arteriovenous
oxygen difference. When exercise is performed at intensities near V O2max, the CNS mediates hematologic responses
through vasodilatory and constrictive mechanisms to satisfy the metabolic needs of the exercising muscles. At the
cellular level, the muscle tissue is able to metabolize lactic acid more efficiently, which enhances the efficiency of the
exercising muscles.
Thermoregulation
The mechanisms involved in evaporative cooling have been found to increase in efficiency as a result of training ( 57).
The temperature of venous blood becomes elevated through conduction of heat produced from exercise. The blood is
then shunted to the subcutaneous tissue layers, where it is expelled to the environment. When sweat glands (apocrine
and eccrine) are activated, the epidermal surface pores open, allowing heat to escape as a result of the evaporation of
sweat. The cooled venous blood is then recirculated to the heart.
Fiber Type
Skeletal muscle contractions are generated by the muscle fibers concentrated within the tissue. Metabolic adaptations
occur with exercise training and are specific to fiber type and format of training (endurance versus speed). Each athlete's
fiber type ratio is genetically determined and does not change as a function of training. Research has indicated that
metabolic capacity, in some instances, adapts to the specific type of training (SAID principle), but the adaptations are
fiber specific (15,28). Furthermore, some exercise scientists suggest that an athlete's performance capacity may be
predicted by the use of biomechanical profiles done from muscle biopsies ( 28). It has been observed that speed athletes
are genetically endowed with a higher percentage of fast glycolytic (white) fibers, whereas predominantly endurance
athletes have been found to possess a higher percentage of slow oxidative (red) fibers. Speed athletes who combine
speed and endurance training develop the intermediate fast oxidative glycolytic fibers ( 15,28,58). This adaptation has
been seen with elite track athletes who initially compete at middle distances (800 and 1,500 m) and later become
competitive marathoners as a result of combining speed and endurance training.
Neuroendocrine Adaptations
Neural
The role of the CNS during exercise is important in regard to regulating metabolic function. Sympathetic and
parasympathetic stimulation of the CNS elicits specific cardiovascular changes in response to exercise. The adrenal
glands release epinephrine and norepinephrine, and along with acetylcholine these hormones regulate the rate, force,
and contraction speed of the heart ( 59). Peripherally, during exercise these hormones induce vasoconstriction of the
vessels that supply inactive tissue and vasodilation of the vessels that supply active tissue, thus increasing transport of
oxygenated blood for use in the tissues and heated venous blood to the cutaneous regions for evaporative cooling.
Endocrine
The effects of exercise on muscle tissue also result in a need for increased transport of fuel substrates into the muscle
cell. Insulin, secreted by specialized cells located in the pancreas, facilitates substrate transport across cell membranes,
and if the level of substrates in the blood drops below a certain threshold, the pancreas releases glucagon to maintain
blood glucose levels. Thyroid and growth hormones are secondary hormones that also help to regulate fuel substrates at
the cellular level, as well as growth and repair of muscle tissue.
The hormones renin and angiotensin are released by the kidney as a defense mechanism against rapid fluctuations of
plasma volume and blood pressure. These adapted responses maintain or increase plasma volume and indirectly
mediate blood pressure and blood flow, primarily through vasoconstriction of renal arteries, which redirects the blood
back into general circulation. A secondary response of angiotensin is stimulation of the adrenal glands to release
aldosterone, which increases salt and water retention at the kidney and in cutaneous regions during evaporative cooling.
This also indirectly maintains plasma volume.
Implications for Exercise Training
As noted earlier, athletic performance and exercise training involve activities that are cyclic, acyclic, or cyclic and acyclic
combined (semicyclic). Appropriate exercise training results in refined athletic performance that is sport specific. Sports
that are cyclic involve technical skills or movement patterns that are repeated continuously for extended periods. Cycling,
crew, gymnastics, swimming, and track and field are sports that may be classified as cyclic. Sports that are acyclic in
nature involve nonrepetitive activities or spontaneous movement. Soccer, basketball, lacrosse, tennis, baseball,
volleyball, and wrestling are sports that may be categorized as acyclic, although not exclusively. Most sports involve
combinations of both cyclic and acyclic activities. These semicyclic sports integrate both repetitious and spontaneous
activities. The sports mentioned as acyclic are classified as such because athletes perform by responding to external
stimuli (i.e., spontaneous movement). External stimuli may be defined as anything in the immediate environment that
changes in response to the activity, such as an opponent, a moving ball, or the field of play.
To train athletes to compete at optimal performance levels, sport-specific methods of training should be used to match
the requirements of the sport. For example, each sport requires some degree of muscular strength, power, and
endurance to overcome the form of external resistance that is inherent to the sport. Wrestlers must overcome the
resistance provided by their opponents, and athletes whose sports require jumping (e.g., high jump, long jump,
basketball, volleyball) must overcome the weight of their bodies and the force of gravity to propel themselves horizontally
and vertically. Sports that involve throwing activities (baseball, volleyball, tennis, soccer, and shot put) require the athlete
to propel an object horizontally and vertically, taking into consideration the weight of the object and the force of gravity.
Most athletes also need muscular endurance to resist fatigue and to maintain maximal strength and power levels for long
periods.
Each sport uses specific metabolic pathways to provide the necessary central and peripheral adaptations for maximal
and submaximal exercises. Athletic performance requires input from both anaerobic and aerobic pathways, and the
relative contributions of each pathway depends on the type of activity performed, its intensity, and its volume as well as
the overall level of fitness and motivation of the athlete. Exercise that is strenuous or near maximal in intensity demands
the recruitment of both type I and type II muscle fibers. During immediate anaerobic exercise, a higher percentage of type
IIb fibers are recruited, whereas short-term anaerobic and long-term aerobic exercise use type I and IIa fibers.
Compositionally, the muscle fibers vary according to capillary, mitochondrial, and enzyme density as well as
cross-sectional area. Through endurance training, the fast oxidative glycolytic (IIa) fibers become more oxidative ( 30).
For example, a speed athlete who develops a high percentage of fast oxidative glycolytic fibers has the potential to
become more efficient at longer distances (e.g., marathon) as a result of the aerobic adaptations within the muscle fiber.
Biomechanically, the speed of contraction does not change significantly, but the oxidative capacity of the muscle fiber
has the ability to adapt. These adaptations also have been shown to be specific for the muscle groups trained in a
particular sport. For example, runners and cyclists have demonstrated increases in type IIa fibers in the lower body,
whereas swimmers have demonstrated the same adaptation in the upper body (29,30). Interval training has been
suggested by exercise scientists to be the best method for training both metabolic systems (aerobic and anaerobic) to
adapt to strenuous exercise.
These adaptations benefit athletes that compete in both cyclic and semicyclic sports, but semicyclic training does not
produce the same adaptations as cyclic training. Semicyclic sports are usually discontinuous and do not function under
the same metabolic conditions as cyclic sports. Furthermore, sports are aerobic. Sprinting is classified as a cyclic sport,
yet it functions under strictly anaerobic conditions.
Several acyclic or semicyclic sports require agility as well as other sport-specific technical skills. This component of
athletic performance must be developed as part of the overall strengthening and conditioning program. General and
sport-specific drills have been designed to enhance and refine agility and technique. Agility drills are general movement
patterns that carry over to the demands of acyclic and semicyclic sports. These drills involve combinations of lateral,
diagonal, and backward movements and include changing direction, stopping and starting, practicing carioca, and doing
cutting maneuvers. Technique drills are more sport specific. The serve in tennis is an example of a technical skill that
must be developed to optimal performance. In addition, athletic trainers recommend agility and sport-specific technical
drills during the late stages of many rehabilitation programs.
In sum, each sport is classified according to the specific types of activity (cyclic, acyclic, or semicyclic) used during
performance. Each sport has specific requirements for muscular strength, power, and endurance as well as metabolic
power and technical skills. To condition and train athletes effectively for a particular sport, sport-specific exercise training
programs need to be designed to match the performance demands of that activity. Athletes who adhere to their training
programs should benefit in terms of overall performance.
EFFECTS OF WARMING UP AND DOWN
No training or conditioning program is complete without protection against injury. Proper warmup before exercise and a
warmdown after exercise have been found to reduce the incidence and severity of overuse-type injuries and
exercise-induced muscle damage (60,61,62 and 63).
Warming Up
The physiologic demands placed on the muscle fiber during strenuous exercise are often excessive, causing injury to the
musculotendinous unit ( 60,61,62 and 63). Therefore, an active warmup should include low-intensity exercise such as light
jogging or pedaling on a stationary bike for short periods (5 minutes), followed by muscular stretching to increase tissue
temperature and extensibility of the exercising muscles. The increase in tissue temperature results mainly from the heat
produced during exercise, while the increase in tissue extensibility lubricates the exercising muscles and supplies them
with oxygenated blood (64,65). In addition, the warmup initiates increased cardiorespiratory function.
Warming Down
After intense exercise it is beneficial to bring the temperature of the muscle tissue down gradually. The warmdown
permits the exercising muscles to return gradually to their preexercise condition and also may help reduce the
occurrence of exercise-induced muscle injury. Stretching after warming down also is advocated to maintain flexibility
levels and guard against postexercise muscle spasms ( 38).
Stretching as an Adjunct
A stretching program used as an adjunct to the warmup and warmdown increases the flexibility of the soft tissues about a
joint (60,61,62,63,64 and 65). Flexibility has long been used as a component of rehabilitation and also has been found to
enhance athletic performance and prevent the occurrence of musculotendinous injury ( 61,64). Stretching should involve
the major articulations and muscle groups for the upper and lower body. Repeated episodes of stretching of the soft
tissue structures about the major articulations increases their ROM. This is the result of mechanical adaptations within
the musculotendinous unit that increase the soft tissue extensibility ( 60,61,62,63,64 and 65).
There are various stretching techniques for increasing and maintaining flexibility. The techniques most often used by
athletes, coaches, and athletic trainers are presented in the following sections.
Techniques for Stretching
Static Stretching
Static stretching uses the progressive relaxation effects of soft tissue in response to a slow, continuous stretch. This
method involves stretching a muscle group or groups to a position of mild discomfort, then holding that position for a brief
period (10 to 30 seconds) ( 2,63). This process should be repeated several times; the amount of stretch is increased in
small increments with each repetition. Static stretching has been found to be an effective and safe means of increasing
tissue extensibility (63). An advantage to this method of stretching is that it may be performed with or without a partner.
Ballistic Stretching
Ballistic stretching is the oldest and most often misused technique for stretching. This method uses the stretch-relax
reflex of muscle tissue (2) that occurs at very rapid speeds. The stretching technique involves repetitive bouncing
motions, resulting in increased tissue extensibility. The bouncing motion causes the rapid, repetitive stretch of a muscle
group. For example, the athlete wishes to stretch the hamstrings would flex the trunk forward, which in turn would stretch
the hamstrings. If the muscles are not properly warmed up or prestretched by other means, the sudden forces generated
by the bouncing action of ballistic stretching may exceed the extensibility of the musculotendinous unit, inducing tissue
damage (2).
Ballistic stretching does have applications to athletic performance when training for strength, speed, or power. Athletes
who use plyometric training impose similar demands on the musculotendinous units, but at higher intensities. Therefore,
ballistic stretching may be an effective precursor or warmup for plyometric training.
Proprioceptive Neuromuscular Facilitation
Proprioceptive neuromuscular facilitation (PNF) is a neurophysiologic phenomenon that was initially used as a
rehabilitative modality; it is now used universally as a means of muscle stretching. PNF requires a partner to assist
actively in the stretching process. The stretch-relax reflex is a neurophysiologic mechanism used to stretch specific
muscle groups. This reflex is inhibited by alternating the contract-relax phases of specific antagonist and agonist muscle
groups. The contract-relax phases function to inhibit muscle resistance to stretch autogenically and reciprocally and thus
to allow for greater levels of tissue extensibility ( 2,66,67) (Fig. 2.13).
FIGURE 2.13. Proprioceptive neuromuscular facilitation (PNF) is a popular method of increasing muscle flexibility. A
disadvantage of this method is that a partner is needed for active assistance.
PNF methods are theoretically sound, yet their efficacy has not been proven scientifically. Personal testimonies and
anecdotal evidence from trainers, coaches, and athletes provide support for this method of stretching.
Precautions
All three stretching techniques have been found to increase flexibility, but their use requires some precautions. Most
athletic trainers recommend warming up before stretching, especially for ballistic stretching. This technique should be
implemented only when an athlete is thoroughly warmed up, because of the risk of injury. Static stretching is the most
widely recommended method because it is safe, effective, and easy to perform. PNF, on the other hand, has been
suggested to be the most effective in producing increases in flexibility ( 65,68), but it requires a partner, as well as some
practical experience, because of its elaborate protocol.
In addition, significant relationships have been shown between muscular strength and flexibility, and some experts
suggest that strength training combined with a flexibility program may greatly enhance athletic performance ( Fig. 2.14).
FIGURE 2.14. Any strength-training program should include flexibility training to increase strength throughout the entire
range of motion (ROM) and to prevent injury.
PAIN ASSOCIATED WITH EXERCISE
Pain associated with exercise is experienced by most athletes during their training. This pain may occur acutely during
exercise or after exercise, depending on the physical condition of the athlete and the type and intensity of exercise.
Exercise-induced pain is produced mechanically from damage to the contractile elements within the muscle fiber, or
metabolically from the accumulation of noxious chemicals within the muscle cell, or both. This section discusses the
major concepts, mechanisms, and management procedures involved with exercise-induced pain.
Acute Pain
Concept and Mechanisms
Functionally, the initial sign of acute pain during strenuous exercise is muscular fatigue ( 69), which is thought to be
induced both mechanically and metabolically. The symptoms of acute pain are often described as a “burning” or
unpleasant sensation felt within the muscle during strenuous exercise ( 70). The metabolic component associated with
acute pain is thought to be caused by the accumulation of metabolites such as lactic acid and noxious chemicals at the
cellular level ( 28,71,72). Some researchers suggest that mechanical damage or microtrauma to the contractile elements
within the muscle fiber causes the initial sensations of acute pain ( 69,71).
Management
The best treatment for pain associated with exercise is preparation. An athlete who is well conditioned and physically
trained is able to withstand the painful effects of strenuous exercise better than the untrained individual ( 73,74 and 75). A
proper warmup and stretching program also may lessen the effects of acute pain during exercise ( 65). In addition,
warming down followed by cryotherapy after exercise may decrease the associated effects of pain and muscle spasm
commonly seen during the inflammatory response ( 38).
Exercise-Induced Muscle Damage
Concept and Mechanisms
Exercise-induced muscle damage occurs during strenuous and prolonged exercise and manifests long after exercise.
The initial mechanism is thought to be mechanically induced through structural damage to the contractile elements of the
muscle fiber (69,76,77,78 and 79). High-intensity or prolonged exercise in which eccentric muscle contractions are used
is thought to cause structural damage or microtrauma with metabolically induced secondary damage ( 76,77,78,79 and
80). The pain and stiffness of exercise-induced muscle damage is seen clinically as loss of contractile force and pain with
attempted movement. The symptoms experienced 24 to 72 hours after exercise are clinically referred to as delayed-onset
muscle soreness (DOMS). This form of retroactive pain may occur as a result of microtrauma to the fibers and the
subsequent reparative phases of healing ( 76,77,78,79 and 80).
Management
Proper conditioning and training before strenuous exercise helps lessen the incidence and severity of exercise-induced
muscle damage. A warmdown and stretching after exercise have been suggested as effective safeguards against DOMS
(38). Once DOMS is present, early treatment (up to 24 hours after exercise) with rest and cryotherapy often lessens the
intensity of the pain. Late treatment (24 to 72 hours after exercise) should focus on restoring the extensibility of muscle
tissue. Warm whirlpool treatments followed by low-intensity static stretching facilitate recovery from DOMS.
SUMMARY
1. Although the specific requirements of each sport vary according to the skills necessary to perform the activity, there
are general underlying functional characteristics that are common to all performance. Muscular strength, power,
speed, endurance, and agility are elements that lay the foundation of all sports activity.
2. Sports are classified according to their degree of continuity. Cyclic sports are continuous and vary little in regard to
technique. Acyclic and semicyclic sports are discontinuous and require a variety of movement patterns.
3. An athlete's body composition has been shown to be closely related to athletic performance and susceptibility to
injury. Therefore, athletes should consider their ratio of lean body tissue to fat tissue.
4. The assessment of body composition involves the measurement of BD and the estimation of %BF and LBM.
Hydrostatic weighing and skinfold thickness and circumferential measurements are methods used to estimate body
composition.
5. Muscular strength is an integral component of athletic performance. Strength development is a function of muscular
growth and adaptation. Muscular power is an extension of strength, combining strength and speed of muscular
contraction. Muscular endurance is the ability of muscles to resist fatigue during work output.
6. Skeletal muscle is composed of fibers that are adaptable to exercise training. Hyperplasia and hypertrophy are
specific adaptations that occur with strength training. Strength development needs to occur functionally, thus
enhancing selected performance characteristics.
7. Muscular strength, power, and endurance are developed via various modes of training. The modes are specific to
the type of force-generating capabilities within the exercising muscle. The four principal modes of strength training
are isometric, isotonic, isokinetic, and plyometric. Specific strength-training programs using these modes have been
designed to develop functional strength specific to particular sports. PRE, CRT, and plyometric training are some
popular programs designed to develop functional strength.
8. Assessment of muscular strength, power, and endurance, using quantitative measurements, is essential for
determining baseline data and progress of training. These factors can be objectively measured by isometric,
isotonic, and isokinetic techniques.
9. Exercise that requires near-maximal effort for up to 2 to 3 minutes is generated mainly by anaerobic pathways.
Anaerobic power is divided into immediate and short-term power, depending on the duration of exercise. Immediate
power uses high-energy phosphates, whereas short-term power uses glycogen to resynthesize the high-energy
phosphates. The measurement of anaerobic power assesses the athlete's ability to perform maximal-intensity
exercise, and each measurement must be specific to the energy system used.
10. Aerobic conditioning involves submaximal endurance exercise for periods exceeding 3 minutes. Aerobic
conditioning enhances aerobic power, which uses oxygen to resynthesize the high-energy phosphates needed
during exercise. The most popular method of assessing aerobic power is graded exercise testing, which measure
oxygen consumption during intense exercise.
11. The ever-increasing demand for excellence in athletic performance has prompted sports scientists and coaches to
develop comprehensive 12-month strengthening and conditioning programs for their athletes. Most advocates of
the year-round program implement some form of periodization to attain peak performance levels at a preplanned
time during the competitive season. The 12-month program is broken down into four phases: preseason,
precompetition, in-season, and postseason.
12. For the year-round strengthening and conditioning program to be successful, the athlete must abide by the
principles of overload, SAID, timing, and recovery. These principles are applied progressively to develop the
requisite balance of muscular strength, power, endurance, and skill needed for a particular sport. In addition, the
prescription of volume, intensity, and mode of exercise must be applied during the annual phases of training. This
prescription produces a systematic progression in the performance parameters necessary to carry the athlete to
proper peaks in training. If these parameters are not strictly adhered to, unwanted setbacks such as overtraining,
chronic fatigue, injury, and premature performance peaking may result.
13. Exercise training produces many biophysical adaptations that enable the athlete to meet the increased physiologic
demands of strenuous exercise. These central and peripheral adaptations provide a smooth transition from rest to
exercise during endurance training.
14. Proper warmup before exercise and a warmdown after exercise have been found to reduce the incidence and
severity of overuse-type injuries and exercise-induced muscle damage. A stretching program used as an adjunct to
the warmup and warmdown increases the flexibility of the soft tissues about a joint. Flexibility has long been used
as a component of rehabilitation and also has been found to enhance athletic performance and prevent the
occurrence of musculotendinous injury. Static, ballistic, and proprioceptive neuromuscular facilitation are the
stretching techniques most often used by athletes, coaches, and trainers.
15. Pain associated with exercise is experienced by most athletes during training. This pain may occur acutely during
or after exercise, depending on the physical condition of the athlete and the type and intensity of exercise.
Exercise-induced pain is produced mechanically from damage to the contractile elements within the muscle fiber, or
metabolically from the accumulation of noxious chemicals, or both. The best treatment for exercise-induced pain is
rest, warm whirlpool therapy, light stretching, and cryotherapy.
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3 The Athletic Trainer
THE ATHLETIC TRAINER

ROBERT O. BLANC
KEVIN M. CONLEY
STACEY C. INGLIS
KARL A. SALESI
JENNIFER B. WHITE
Athletic Training
Education Programs
Certification
Employment
Prevention of Athletic Injuries
Reduction of Risk Factors
Preparticipation Examination
Physical Conditioning and Training
Protective Equipment and Devices
Nutrition
Environmental Risks
Emergency Management of Athletic Injuries
Emergency Plan
Patient Primary and Secondary Assessment
Respiratory Injuries
Internal Injuries
Musculoskeletal Injuries
Evaluation of Athletic Injury and Illness
Clinical Evaluation Process
On-Field Evaluation
Rehabilitation of Athletic Injuries
Stage One: Acute Care
Stage Two: Subacute Care (Physical Conditioning)
Stage Three: Chronic Care (Return to Competition)
Chapter References
ATHLETIC TRAINING
Sports medicine is a multidisciplinary field that focuses on providing health care to the physically active. The one
profession that exclusively provides sports medicine services is athletic training. The athletic trainer is the primary health
care provider for the athlete; he or she makes use of various other professionals to make up the sports medicine team
when such professional expertise is required. The athletic trainer's role encompasses the athletic health care gamut from
prevention of injuries to safely returning the athlete to activity after injury. For these reasons, it is the athletic trainer who
is the focal professional of this multidisciplinary field.
The profession of athletic training has evolved from its early days of simply providing basic first aid and emergency
management into its present-day sophistication and has now been acknowledged by the American Medical Association
as an allied health profession. The National Athletic Trainers Association (NATA) was formed in 1950 for the purpose of
establishing and disseminating a knowledge base regarding injury prevention and management ( 1). Today the NATA has
more than 10,000 certified members practicing athletic training throughout the world.
Education Programs
Education programs were established in 1969 when the NATA approved its first curriculum. The original athletic training
education programs were designed to provide the student with a basic science foundation in human anatomy and
physiology and an extensive clinical education in athletic training settings. In 1982, educational programs underwent
significant changes following the release of the landmark “Role Delineation Study” conducted by the NATA, which
established the roles and responsibilities of the certified athletic trainer by surveying its members ( 2). As a result of this
study, areas of emphasis were identified and academic programs restructured their curricula accordingly. Table 3.1
illustrates the subject matter requirements of current accredited athletic training educational programs.
TABLE 3.1. SUBJECT MATTER REQUIREMENTS OF ACCREDITED ATHLETIC TRAINING EDUCATION

PROGRAMS
Today, the academic curricula are structured to provide instruction in six major task areas, which were established by the
Joint Review Committee–Athletic Training after the most recent Role Delineation Study ( 3). Each of the task areas is
weighed in terms of its relative importance, criticality, and frequency of exposure to the practicing athletic trainer ( Table
3.2). Within each task area, competencies have been established in the cognitive, psychomotor, and affective domains.
These competencies provide the framework for the presentation of subject matter within the athletic training education
programs.
TABLE 3.2. MAJOR TASK AREAS IN ATHLETIC TRAINING
The six major task areas and their respective competencies are taught in both classroom and clinical settings. Education
programs can be either major academic degree programs (accredited education programs) or interdisciplinary degree
programs (internship programs) in which the student completes specific course requirements. The clinical component of
the athletic training education program requires the student to accumulate 800 to 1,500 hours of athletic training
experience under the supervision of a certified athletic trainer. Those students enrolled in a NATA-approved education
program must accrue a minimum of 800 hours, and internship students must accrue a minimum of 1,500 hours. Effective
January 1, 2004, all education programs must conform to guidelines consistent with those of the approved curricula to
satisfy the requirements of the Commission on Accreditation of Allied Health Education Programs.
Certification
On completion of the designated education program, the prospective athletic trainer is eligible to sit for the certification
examination administered by the NATA Board of Certification. After successful completion of the examination, the
candidate receives the credential of Athletic Trainer, Certified (ATC). The certification examination reflects the
responsibilities of the athletic trainer as identified by the Role Delineation Study and, therefore, reflects the educational
preparation. The examination evaluates the athletic trainer's proficiency in all three of the domains within each task area
in both written and practical formats.
Employment
The athletic trainer enjoys a wide array of employment opportunities. Entry-level athletic training positions exist in high
schools, colleges and universities, professional sports organizations, and private health care facilities. Today, many high
school athletic training positions are available because of the exposure of the athletic training profession coupled with
the institutions' awareness of liability regarding improper management of sports-related injuries. Athletic training positions
vary within the high schools from providing athletic training services for the school district to a dual role as teacher and
athletic trainer. In addition, some school districts contract athletic training services through local sports medicine clinics
that employ athletic trainers.
College and university athletic training positions vary from providing athletic training services to an entire athletic
department (usually in smaller colleges) to providing services to a specific team or group of teams, along with the support
of an athletic training staff. The athletic training staff at a larger university may include 6 to 10 full-time certified athletic
trainers and an array of both undergraduate and graduate student athletic trainers. Furthermore, some athletic training
staff members may serve as academicians and scholars in those programs offering athletic training curricula at both the
undergraduate and graduate level.
Athletic training positions in professional sports are limited and extremely competitive because there are relatively few
teams at this elite level. Employment usually begins at the lower levels within organizations, and promotion occurs
internally. For example, Major League baseball trainers often spend a number of seasons working with Minor League ball
clubs and are promoted to the Major League only when head athletic trainers retire or resign. Most professional football
teams employ two or often three full-time athletic trainers, and initial employment is often a function of association with
members of management.
The final primary area of employment for certified athletic trainers is in the private and corporate setting. Private sports
medicine clinics have offered excellent opportunities for athletic trainers. The athletic trainer's responsibilities vary
tremendously within the clinical setting, including assisting physicians and physical therapists who provide
athletic-related health care to recreational athletes and providing high school athletic training services that are contracted
by the clinic.
The remainder of this chapter focuses on the athletic trainer's role and responsibility in the health care of physically
active individuals. Specifically, the chapter focuses on the athletic trainer's contributions in the areas of prevention,
emergency management, evaluation, and rehabilitation of athletic injuries.
PREVENTION OF ATHLETIC INJURIES
Prevention of athletic injuries and illnesses is a crucial portion of the athletic trainer's duties. By using strategies such as
preparticipation physical examinations and screenings; conditioning programs; proper fitting, design, and maintenance of
protective equipment; proper fitting and application of special pads and tapings; nutrition; and knowledge of
environmental risks, athletic trainers can help to reduce risk factors and prevent injuries.
Reduction of Risk Factors
Injuries are inherent to sport. Athletic trainers have illustrated problematic areas through research, and sports medicine
personnel (4,5,6,7 and 8) have initiated changes as the result of epidemiologic studies. These efforts have centered on
injury frequency, sport-specific injuries, and the mechanisms that result in these injuries. Studies have focused primarily
on neck, knee, and ankle injuries; heat illnesses; catastrophic injuries; and injury rates in contact sports.
A 3-year study by the NATA in 1995–1997 focused on high school athletic injuries ( 5). The study concluded that 55.5% of
all reported injuries occurred during practice, when most schools do not have a qualified on-site health care professional
available. This study supported NATA's claim of the need for improved programs of early injury recognition and
management and the need for preventive care for high school athletes. NATA is promoting the need for athletic trainers
to cover practices as well as games in high schools across the country. A certified athletic trainer who is present at
practices can give prompt care to any injury and initiate rehabilitation programs as necessary. The athletic trainer also
can inform the coaching staff of any unsafe drills or playing conditions that have resulted in injuries that could have been
prevented.
The rates of head and cervical spine fatalities have dramatically reduced during the past two decades ( 9). Studies of
hockey and football have resulted in several key preventive measures credited with aiding the reduction of injury rates
(10). Rule changes for the 1976 football season that eliminated the head as a primary and initial contact area for blocking
and tackling were significant ( 4,10). The National Operating Committee on Standards for Athletic Equipment (NOCSAE)
helmet standard adopted in 1978 by colleges and in 1980 by high schools significantly improved helmet equipment safety
(9,10 and 11). Emphasis and education on safer techniques of blocking and tackling and improved medical care have
also been key areas contributing to the decline in direct fatalities ( 10). Continued research in injury prevention,
management, and return to participation standards are crucial to continue this decline.
There has been a great deal of discussion regarding the incidence of knee injuries that occur in men and in women. A
significantly increased (two to four times greater) risk of noncontact injury to the anterior cruciate ligament (ACL) has
been noted in female soccer and basketball athletes, high school athletes, and Olympians when compared with male
athletes in the same sports (12,13 and 14). The rate of incidence, cost of health care, and severity of injury have led to a
focus on ACL injury in female athletes as a priority in research networks and medical communities. To establish
prevention methods, it is necessary to examine the risk factors. Many intrinsic and extrinsic factors, including ligamentous
laxity (13,15,16 and 17), lower-extremity muscular strength considerations ( 15,16,17 and 18), neuromuscular control or
proprioception (15,19,20), hormonal influence (15,20), intercondylar notch width ( 15,21), and biomechanics of player
techniques, have been investigated ( 15,21,22 and 23). Debate continues on how best to prevent the high rate of ACL
tears in female athletes.
Epidemiologic studies continue to provide valuable data on the number and mechanisms of injury and factors pertaining
to the incidence of injury. Previous studies have led to important rule changes and improvements in equipment that have
significantly affected the rates of injuries. Analysis into the next decade will reveal the impact of these preventive
measures and current research efforts on the number of fatalities and serious injuries.
Preparticipation Examination
The preparticipation examination is a vital element of any sports medicine program. The athletic trainer and team
physician should be involved in the planning, design, and implementation of the preparticipation examination of their
athletes. This ensures that the design of the physical examination will allow an evaluation of the health status of the
athlete and whether the athlete can meet the demands of the sport safely.
The physical examination is a preventive tool used by the sports medicine staff to determine whether an athlete is at risk
for injury or has preexisting injuries. In addition, the examination may help to determine the athlete's general health and
any disqualifying conditions. Detection of problem areas and general health weaknesses before an injury or illness
occurs gives the athletic trainer and the athlete the opportunity to make corrections.
The preparticipation examination is a screening tool designed to assess the overall health status of the athlete,
concentrating primarily on the musculoskeletal and cardiovascular systems ( 24). Before the physical examination, the
athletic trainer should have each prospective athlete complete a detailed medical history. This should focus on prior
cardiovascular complications, family history of early cardiovascular death, and any other significant medial problems
such as asthma, allergies, diabetes, surgeries, and mental illness. The physical examination can be divided into several
stations so as to use available sports medicine staff and provide a detailed examination in a short period of time. Height
and weight, blood pressure and pulse, urinalysis, and eye examinations can be performed by student athletic trainers or
certified athletic trainers. Physical examination of the ear, nose, and throat; lymph nodes; and heart, lungs, and abdomen
and the orthopedic examination can be performed by team physicians with the aid of internists, otolaryngologists,
cardiologists, and orthopedists.
In addition to the normal body systems and musculoskeletal assessment, some preparticipation examinations include
laboratory tests and electrocardiographic (ECG) studies. These tests are expensive; they may not be done on a regular
basis but rather as a screening tool for those individuals who have risk factors discovered during the history or physical
examination. ECG screening has increased as a result of the increase in sudden death from unknown heart conditions in
athletes. Many of these conditions still go undetected, although the ECG along with a complete medical history and
physical evaluation assists the sports medicine staff in detecting athletes who are susceptible to heart conditions before
they occur.
Physical Conditioning and Training
Athletic trainers and coaches recognize that improper conditioning is one of the principal causes of sports injuries ( 25).
Poor flexibility, muscular imbalance, and inadequate muscular and cardiovascular endurance are major causes of injuries
to athletes. An athlete who maintains proper muscular balance and strength, cardiovascular conditioning, and flexibility is
less likely to sustain an injury than an athlete who does not maintain good levels of conditioning year round. An
appropriately organized training program works the soft and bony tissues of the body. Over time, stress and stretch
positively affects these structures, increasing their blood supply, density, width, and strength ( 25).
It is important to design conditioning and training programs that adapt to the four phases of the sport: in-season,
postseason, off-season, and preseason. Postseason programs must focus on physical restoration of the athlete's body,
particularly if the athlete sustained any injury during the course of the season. This period should be used for any needed
rehabilitation. If no rehabilitation is necessary, this phase should include low-intensity work and rest.
The off-season workout is a combination of cardiovascular fitness, strength, and endurance exercises. The athlete may
want to participate in alternative sports that require physical exertion. The activity level should maintain the athlete's
general muscular and cardiovascular fitness. The workouts, however, should be less strenuous than during the season,
gradually increasing in intensity so that the athlete is in good physical condition at the start of the preseason phase.
The need for maintaining general physical conditioning in the off-season cannot be overstressed by the athletic trainer. If
a high level of fitness is maintained in the off-season, the preseason will be much more productive and the athlete will be
less susceptible to injury ( 25). During the season, the competition schedule may not include enough strenuous activity to
maintain preseason fitness levels. Athletes should undergo structured maintenance programs throughout the competitive
season. This allows them to keep their level of cardiovascular fitness and maintain strength and flexibility throughout the
entire season, reducing the risk of injury as the season progresses.
The athletic trainer must stress the importance of a well-rounded fitness program to both coaches and athletes. To
benefit the athlete, the program must include the aspects of cardiovascular fitness, muscular strength and endurance,
and flexibility. The athlete who maintains preseason levels throughout the season and a conditioning base during the
off-season will be less prone to injury than the athlete who does not work out during the off-season.
Protective Equipment and Devices
The main function of protective equipment is to prevent injury and to protect those injuries already sustained. The extent
of equipment used is dictated by the sport (i.e., collision versus noncontact) or by the severity of the pathology sustained.
When choosing equipment or protective devices, one should opt for a reliable manufacturer that offers quality at a price
that is within budget restraints ( 26). Competition within the market has resulted in the lightest, least inhibitive equipment
designs allowable under safety standards.
The NOCSAE is the organization responsible for setting most of the standards for certification and reconditioning of
athletic equipment ( 25). The committee is known primarily for its rules governing the safety of athletic helmets used in
contact sports such as football, ice hockey, and lacrosse.
Although most colleges hire a separate employee to deal with all aspects of ordering and fitting equipment, it is
imperative that athletic trainers and coaches at least be aware of general guidelines for proper fit and upkeep of any
equipment. This is particularly important in the high school setting, where there must be daily inspection to ensure that no
device is damaged or altered. From a liability aspect, there are several procedures that must be followed. First, assembly
of equipment should always be done according to the manufacturer's instructions, and there should be no alterations to
suit an alternative purpose. Second, equipment should be used for the purpose of its design. Equipment should be
maintained according to guidelines and should be examined routinely for defects. Finally, athletes should be warned of
the risks involved (equipment does not prevent 100% of all injuries) ( 25).
From a practical aspect, any devices used should be analyzed as to effectiveness and comfort in both practice and game
situations. The design factors for any protective device include (a) type of force, (b) impact area of the body, (c) allowable
range of motion (ROM) limitations, (d) size and weight restrictions, and (e) the energy absorption properties of the
material used (25,26).
Design and Implementation of Protective Devices
In the event of an injury that does not have specific equipment designed for its protection, it is the athletic trainer's
responsibility to design and construct a suitable device. Materials and resources may be limited depending on budget
restraints and availability. It is therefore important for the athletic trainer to be as creative and resourceful as possible to
create an appropriate protection for the athlete. Usually customized protection may be categorized as made of soft or of
nonyielding materials (25).
Soft Materials
These materials include but are not limited to tape, foam, felt, and gauze padding. Tape is one of the primary means of
support applied in the training room. As one of the psychomotor competencies required in the preparation of athletic
trainers, this protective measure is used in conjunction with a regimented rehabilitation program after an injury.
Supportive taping is typically used for additional bracing of an injury that is in the remodeling phase of healing and needs
additional support for return to activity.
Customized padding is another means of protection that is prevalent in the training room. When designing a pad, the
athletic trainer must first determine what is allowable under the rules and regulations for that particular sport. A material
must be chosen that is accommodating with the area and function of the body part. It is also imperative that the padding
be secured properly to avoid slippage that may lead to negation of function.
Nonyielding Materials
These hard materials may be used to make splints or protective shells. Thermomoldable plastics have become
widespread throughout the sports medicine community (25). These materials may be custom-fit to a body part by heating
them to create a pliable medium that can be molded to a desired shape. Once that shape is reached, the material is
wrapped in place to allow cooling, which results maintenance of a hardened state. Casting materials such as fiberglass
may also be used to provide a protective shell or splint for an injury ( Fig. 3.1).
FIGURE 3.1. Materials for protective equipment (clockwise from upper left): adhesive foam, Hexelite (Smith–Nephew,
Germantown, WI), Orthoplast (Johnson & Johnson, New Brunswick, NJ), and felt.
Bracing and Orthotics
Most braces used on athletes are prescribed by a physician after a ligamentous injury. Typically, commercial braces are
incorporated into the functional return of an athlete after surgery ( Fig. 3.2). An athlete who opts for nonsurgical treatment
of a damaged ligament may be advised to wear a functional brace for an indefinite period during activity ( 25).
FIGURE 3.2. Postsurgical functional knee brace.
Orthotics have become a widespread tool used by athletic trainers, particularly in the prevention of certain overuse
injuries of the lower leg and foot. For the most part, orthotics designed and constructed in the training room are made of
soft materials such as foam or felt and are used for temporary support. After it is determined that there is a biomechanical
problem that may possibly be corrected by orthotics, the athlete should be referred to a podiatrist or specialist in order to
have a more durable, customized orthotic manufactured.
Nutrition
In many settings where budget restraints do not allow availability of a dietitian, the athletic trainer must act as a
nutritional consultant to the athletes. In most cases this involves education of both athletes and coaches regarding food
myths, fad diets, supplements, and overall healthy eating for today's athletes. With increasing competition in the
supplementation market, it is important to stay current on trends that may not be in the best interest of the athlete. Young
athletes in competition for a starting spot may be inclined to sacrifice their health to get ahead. It is the responsibility of
the coaches and trainers to be aware of any use supplements by their team members, no matter what the substance. Any
athlete who is taking both medication and supplements should be monitored for possible harmful interactions.
The athletic trainer is often the person responsible for precompetition meals and possibly for meal planning throughout
the season. A pregame meal should be eaten 3 to 4 hours before the start of competition and should include easily
digestible foods and fluids. For wrestlers, who need to meet a weight requirement, the meal may be eaten after the
designated weigh-in time. A meal high in carbohydrates helps to provide adequate glycogen stores for competition. Fatty,
fried foods should be avoided, as should meals high in protein, to minimize any gastrointestinal problems.
Eating Disorders
Eating disorders have become prevalent primarily in sports in which judging is based on appearance (e.g., gymnastics,
figure skating, diving) or a low body fat content is desired (e.g., wrestling, distance running). Anorexia nervosa and
bulimia nervosa are the two disorders most commonly seen in the athletic population. These disorders involve
psychological issues as well as physical ones, and the athletic trainer must be able to identify athletes at risk for these
problems so that preventive measures may be taken.
Some identifying factors for a person with anorexia are (a) unreasonable fear of obesity, (b) distorted body image, (c)
weight loss of at least 25% of original body weight, and (d) refusal to maintain weight within the normal range for height
and weight. Identifying factors for bulimia include (a) recurring episodes of binge eating followed by purging, (b) weight
fluctuations of more than 10 pounds, and (c) depression after binge eating.
The stigmas associated with counseling often make athletes hesitant to pursue professional help on their own. The
athletic trainer must be prepared to work with the athlete to gain access to a specialist in eating disorders with whom the
athlete feels comfortable. The athletic trainer should act as a liaison between the counselor and the coaching staff to
maintain lines of communication and to protect the privacy of the athlete.
Environmental Risks
Athletic trainers must often respond to injuries produced by the environments in which athletes participate ( 27). The
major environmental areas of concern are heat (hyperthermia) and cold (hypothermia).
Hyperthermia
Heat illnesses are preventable, yet cases of heat exhaustion and death from heat stress continue to occur ( 28). Heat
illnesses and injuries are a major concern to the athletic trainer, who must inform the coaching staff about this
environmental risk. Heat must be taken into account when planning practices and scheduling games. The sling
psychrometer is used to determine the wet-bulb-globe temperature index. The athletic trainer and coach must clearly
understand when environmental heat and humidity are at dangerous levels and restrict activity accordingly ( 25,26,27 and
28). Heat illnesses include heat cramps, heat exhaustion, and heat stroke ( Table 3.3). The athletic trainer should be
aware of the signs and symptoms of the heat illnesses and be able to make a differential diagnosis.
TABLE 3.3. HEAT ILLNESSES
Athletes in fall sports, primarily football, cross-country, soccer, field hockey, and volleyball, are most susceptible to heat
illness, because practices and games are held late in the summer when the heat and humidity are high. Football is most
often associated with heat illnesses. The protective equipment worn by football players decreases the athletes' ability to
dissipate heat, and the added weight of the equipment increases heat production ( 28). Wrestlers also are extremely
susceptible to heat illnesses as a result of self-imposed fluid and dietary restrictions.
Normal body temperature is maintained through a balance of heat production and heat loss ( 25,27). If this system is not
in balance, the athlete is susceptible to heat illness. Heat is eliminated from the body through convection, conduction,
evaporation, and radiation. Most of these methods of heat loss rely on the environmental temperature's being lower than
body temperature. If the external temperature is higher than body temperature, the primary source of heat loss is
evaporation of sweat, assuming that the ambient humidity is low enough to accept the moisture ( 27).
Since 1974 there has been a dramatic reduction in heat stroke deaths. Heat stroke and heat exhaustion are prevented by
control of various factors in the conditioning program of the athlete ( 10). First, the athlete must slowly acclimatize to the
new (warm) environment. The athletic trainer should monitor the athletes' workouts, especially those of athletes who are
obese, heavily muscled, or poorly conditioned. Initial practices for those sports that require protective equipment (e.g.,
football, field hockey, soccer) should be conducted in T-shirts and shorts for several days to allow for acclimatization and
conditioning.
Second, the athletic trainer should identify those athletes who may be susceptible to heat illnesses—that is, those who
obese, heavily muscled, or out of shape. One preventive measure is to weigh athletes before and after all practice
sessions. Any athlete who has sustained a 3% to 5% weight loss per practice session that is not negated by the next
session should be kept out of practice ( 25,27,28 and 29).
Third, environmental conditions can be monitored using a sling psychrometer or the local weather service. Practice times
must be adjusted according to the heat and humidity. Finally, an unlimited supply of fluids should be available to the
athletes at practice. Frequent water breaks should be scheduled throughout the practice session. The athletes should be
encouraged to drink plenty of fluids before, during, and after practice.
Hypothermia
The athletic trainer must take precautions in cold weather as well as hot. Decreasing temperature and wind can cause
hypothermia, frostbite, or peripheral problems ( 28). The athletic trainer must help coaches and athletes recognize the
signs and symptoms of cold disorders and inform them of the proper course of treatment. Common signs and symptoms
of hypothermia include uncontrollable shivering, decreased coordination, decreased level of consciousness (LOC),
sleeplessness, and apathy ( 25,26,27 and 28).
Sports susceptible to hypothermia are those that do not require heavy protective clothing and yet continue into the cooler
seasons. Consequently, weather becomes a pertinent factor, particularly for athletes who are sweating and exhausted,
and thereby predisposed to injury ( 25).
Prevention during cold-weather practices and games should include the following: (a) instructing the athletes how to
dress for cold-weather practices; (b) instructing the athletes to bring spare gloves and socks; (c) making sure the athletes
warm up properly; and (d) requiring proper fluid hydration.
EMERGENCY MANAGEMENT OF ATHLETIC INJURIES
Rarely is an injury sustained during athletic participation considered to be an emergency. An emergency is defined as “an
unforeseen combination of circumstances and the resulting state that calls for immediate action” ( 30). Because of the
infrequency of such events, sports medicine personnel must be prepared for these situations. The athletic trainer is
responsible for preparation and effective implementation of the emergency management of athletic injuries.
Emergency Plan
The most critical element in reacting to an emergency is time. A sport-specific management plan may eliminate costly
mistakes or delays. A well-organized emergency plan may lessen the severity of injury and possibly save a life. Many
variables must be addressed when developing an emergency plan, including the following:
1. Location of telephones (and accessibility during practice times), with numbers clearly listed
2. Proper communication of information
a. Caller identifies self
b. Exact location (special directions if needed)
c. Exact nature of injury
d. Call-back telephone number
3. Special entrances needed (including maps of all fields, buildings, and courses)
4. Defined roles of available personnel
a. Athletic trainer
b. Coach and assistants
c. Student athletic trainers
d. Administrators
e. Local emergency medical service (EMS)
5. Medical helicopter landing zones, if appropriate
On completion of this plan, the athletic trainer should review the procedures with coaches, administrators, team
physicians, and local emergency service providers. A well-designed emergency plan requires the cooperation of all
personnel involved, and the plan must be practical.
Patient Primary and Secondary Assessment
The priorities when assessing athletic injuries are similar to those for any injuries. The primary assessment includes
evaluation of airway, breathing, and circulation (ABC). If an injury to the spinal cord is suspected, stabilization of the
head and neck must be obtained before the assessment continues. If the athlete is conscious, a thorough history must be
obtained before the physical assessment is done. The information from the history is especially important in
emergencies.
Airway
Unless cervical spine injury is suspected, the airway should be opened with a head tilt–chin lift method. In an athlete with
a suspected cervical spine injury, the modified jaw thrust technique should be used.
The availability of an automated external defibrillator should also be examined. Such a defibrillator contains
microcomputers that accurately identify cardiac arrhythmias such as ventricular fibrillation (V-Fib) ( 31). Survival of
patients who experience V-Fib can be remarkably high if defibrillation is administered within the first few minutes after
onset. “For each minute V-Fib persists, the likelihood of successful resuscitation decreases by approximately 10%” ( 31).
Breathing
Looking, listening, and feeling for air exchange from the mouth and nose should be used to assess breathing. If breathing
is not present, the attending personnel should begin mouth-to-mask resuscitation.
Circulation
Palpation of the carotid artery in the neck is performed to assess circulation. If no pulse is found, cardiopulmonary
resuscitation (CPR) must be initiated. Significant bleeding must be controlled, if present.
Secondary Assessment
If findings of the primary survey are unimpressive, assessment should continue with a very thorough secondary survey.
The secondary assessment includes a head-to-toe examination.
An integral portion on the secondary survey is monitoring of vital signs. These include LOC, pulse, blood pressure, skin
temperature and color, respiration, and papillary reaction. LOC, especially important for determining the effectiveness of
brain tissue perfusion, is evaluated by conversing with the athlete and noting the appropriateness of the responses. The
assessment must determine whether the athlete is conscious, alert, and oriented as to person, place, time, and purpose.
While evaluating LOC, it is important to note the injured athlete's behavior in general. Restlessness and anxiety are early
signs of hypoxemia or internal bleeding ( 25). These signs can easily be overlooked.
Respiratory Injuries
The respiratory system is composed of the nasopharynx, oropharynx, laryngopharynx, trachea, and lungs ( 30). If this
system is disrupted at any level for a period of time the result can be catastrophic.
Disruption of the respiratory system is rare in athletics, but it does occur. Problems most often observed at sporting
events include obstruction by a foreign object, trauma to the neck and larynx, closed head injuries accompanied by
diminished LOC, and angioedema and anaphylaxis ( 30). Any irregularities in breathing pattern or cessation of respiration
must be identified and corrected immediately. Cardinal signs of respiratory difficulty include nasal flaring, tracheal
tugging, intercostal muscle retraction, use of diaphragm and neck muscles, and especially cyanosis ( 30).
Once the mechanism of the distress is identified, a decision can be made about the proper steps to correct the difficulty.
Adjunctive equipment should be available and should be divided into basic and advanced life support.
Basic equipment for management of respiratory injuries includes a pocket mask, oropharyngeal airways, nasopharyngeal
airways, a bag-valve-mask system (Fig. 3.3), and a suction unit. This equipment is easy to use; however, frequent
practice with each piece is important to ensure familiarity in an emergency.
FIGURE 3.3. Airway equipment: bivalve mask, pocket mask, nasopharyngeal airway, and oral airway.
If technicians with advanced airway skills are available, the following equipment should be included: laryngoscope with
blades, a variety of endotracheal tube sizes, stylets, and Magill forceps. In addition, a prepackaged cricothyrotomy kit
should be available in case a surgical airway is needed.
In the event of airway obstruction, the athletic trainer should follow the guidelines of the American Heart Association or
the American Red Cross for management of foreign body obstruction. If acceptable results are not obtained, extraction by
direct laryngoscopy should be attempted.
Airway obstruction from a head injury is usually caused by blockage of the airway by the athlete's tongue. This can be
corrected with the use of basic airway control techniques such as the head tilt–chin lift maneuver.
As with any outdoor activity, an athlete may be a victim of an insect bite, and anaphylaxis is a distinct possibility.
Epinephrine 1:1000 should be readily available. A dose of 0.3 to 0.5 mL for an adult or 0.01 mL per kg for a child should
be administered by subcutaneous injection by the team physician ( 25).
Internal Injuries
Internal injuries are most often the result of blunt force trauma. In the athletic setting, the forces needed to produce
internal injury are most often inflicted by a projectile (e.g., hockey puck, baseball). Any injury to the abdomen should raise
the suspicion of internal injury. Blunt trauma to the abdomen is especially deceptive, because it can cause devastating
injury with few external signs (32).
Athletes sustaining abdominal trauma should be closely monitored for 24 to 48 hours. If the athlete presents with
abdominal pain, nausea, vomiting, rigidity, or discoloration around the umbilicus, a further examination should be
performed. An athlete with complaints of pain radiating into the left shoulder (Kehr sign) may have sustained a ruptured
spleen, which necessitates immediate medical attention.
Any athlete with suspected internal injury should be treated for shock. Shock treatment includes ensuring an adequate
airway, administering supplemental oxygen when warranted, placing the patient in a supine position, and transporting the
patient to an appropriate medical facility ( 30).
Musculoskeletal injuries are by far the most common injuries seen by sports medicine specialists. Although these injuries
are rarely life threatening, improper management can exacerbate the initial injury.
The most common signs of a musculoskeletal injury are swelling, ecchymosis, deformity, point tenderness, crepitus,
guarding, and an open wound with bone ends exposed. If a fracture or dislocation is suspected, the injured region should
be immobilized. Before immobilization, the examiner should perform a neurovascular assessment, including distal pulses,
sensation, and movement. If distal pulses are not present, immediate reduction or transport is required.
Splinting may be accomplished with any commercially available device. Rigid splints usually consist of a padded board
covered in vinyl and are held in place with cravats or an elastic bandage. Pneumatic splints are most often used for wrist,
forearm, ankle, and lower leg fractures. These splints are inflated to compress and stabilize the fracture site. Traction
splints are commonly used for femur fractures, and in-line traction is used to override muscular contraction.
A spine board is used in case of suspected spinal cord injury. If the athlete is prone, he or she should be rolled as a unit
to a supine position. The log roll method is most effective; four or five people are needed to assist ( Fig. 3.4). One person
should immobilize the head and control the immobilization process. First a rigid cervical collar is applied, and the long
board is placed next to the athlete. The assistants roll the athlete while maintaining in-line axial alignments. The spine
board is then slid under the athlete as far as possible, and the athlete is placed in a supine position on the board. Either
a commercially available device or sandbags must be used to immobilize the head. Immobilization of the body is
accomplished by placing straps over the thorax, hips, and legs.
FIGURE 3.4. Use of a spine board. The athlete is rolled to a supine position onto the spine board while axial alignment is
maintained.
Some variations are necessary when using the spine board with an injured football player. Before the athlete is moved,
the face mask should be removed by cutting the plastic clips that attach the mask to the helmet ( Fig. 3.5). If the player is
wearing both shoulder pads and a helmet, he or she should be immobilized with them in place. If just the helmet is worn,
it must be removed to prevent flexion of the neck when lying supine. Only persons familiar with the proper removal of a
football helmet should perform this procedure, which requires two people. One person stabilizes the athlete's head by
holding the helmet in axial alignment throughout the removal process. The second person cuts the clips to remove the
face mask, cuts the chin strap, and very carefully removes the two jaw pads by using a tongue depressor or similar object
to pry open the snaps. The second person should then place one hand on the occiput, reaching as far into the helmet as
possible, and the other hand on the mandible. On the second person's command, the first person tilts the helmet slightly
forward and slides it off the player's head ( Fig. 3.6). The first person then retakes control of the athlete's head and places
it in a neutral position. A rigid cervical collar is then applied, and the athlete is immobilized as described previously.
FIGURE 3.5. Face mask removal. The face mask can be cut away while stabilization of the head and neck is maintained.
FIGURE 3.6. Helmet removal. The helmet may be removed by tilting it slightly forward.
EVALUATION OF ATHLETIC INJURY AND ILLNESS
Clinical Evaluation Process
Successful treatment and rehabilitation of athletic injuries and illnesses is inherently dependent on a comprehensive and
systematic evaluation of the athlete's condition. Often signs and symptoms of a particular lesion may lead the clinician to
any of several possible assessments. This differential diagnosis process hinges on the individual's knowledge and skill in
carrying out the appropriate procedures for arriving at the correct diagnosis. Several models exist that attempt to
sequentially define the evaluation process. Regardless of the model used, its components should meet two criteria: (a)
each step of the model must be justified, and (b) the model must be reproducible and followed at all times for purposes of
documenting changes in the athlete's condition during subsequent reassessments ( 33). The ultimate goal of the
evaluation process is to ensure that all possible scenarios have been addressed, giving rise to a plan that best suits the
needs of each individual athlete.
For the purposes of this text, a five-step evaluation process will be described. Variations in the amount of pain the athlete
is experiencing and the venue in which the examination is taking place may dictate that subtle modifications be made in
carrying out these procedures. Nonetheless, it is incumbent on the clinician to ensure that a thorough assessment of
subjective and objective information is performed in order to arrive at a proper diagnosis.
History
Initially a complete, detailed medical history of the injured athlete should be gathered and recorded. This portion of the
evaluation process is often the most important, because it aids the clinician in focusing on the most clinically relevant
information for identifying the type and extent of injury as well as any predisposing factors or conditions that may have
led to the current complaint. A thorough history takes into account the athlete's demographic information (i.e., age,
gender, sport, level of competition) along with the primary complaint, mechanism of injury, characteristics of the
symptoms, disability resulting from the injury, related medical history, and previous treatments or surgeries ( 34). In some
cases, information regarding the social and family history of the athlete may prove pertinent. Lifestyle habit patterns
including sleep patterns, stress, workload and recreational pursuits should also be noted ( 34). Clearly, the physical
examination is of utmost importance. However, the athlete's psychological state of mind must not be discounted, because
individuals react to injury differently with regard to perception of pain, anxiety, and desire to return to activity.
Of particular concern during the recording of the history is the ability of the clinician to keep an open mind concerning the
relative significance of the subjective information being gathered. Pain, for example, is one component of the pathologic
process that can arise from several origins. The quality of pain may shed some light on the organ system source
responsible for creating the signs and symptoms (35). The clinician should take steps to isolate and localize the pain as
accurately as possible. The presence of referred pain indicates that the root of the pathology is at a source other than the
site of trauma, and it is generally diffuse in nature. The ability of the athlete to describe a specific location for the pain
better enables the clinician to narrow down the structures involved ( 33,35). In addition, the athlete should be provided the
opportunity to describe the functional activities that exacerbate as well as those that alleviate the symptoms. Once the
history has been gathered, the more objective portion of the evaluation can be performed; the remainder of the
evaluation stands to substantiate or disprove what was initially found in the history.
Observation
During the evaluation, observation is used to visually assess the status of the injured athlete. This portion of the
examination begins immediately, allowing for a candid inspection of normal and abnormal movement patterns.
Observation should initially consider the athlete's LOC, body language, level of anxiety, and ability or willingness to
move. A cursory assessment of body alignment and the presence of any antalgic or compensatory changes in posture or
gait should be noted. Care should be taken to observe the athlete from head to toe and to avoid any premature
conclusions that may result in a failure to recognize the severity of the injury. Next, in the case of an injured extremity, the
observation may be narrowed to a bilateral comparison of the involved and uninvolved sides, taking into account obvious
deformities, signs of swelling, ecchymosis, infection, muscle tone, and dermatologic variations such as skin color, texture,
and presence of skin markings. The importance of the past history as it relates to the contralateral extremity is apparent
here, because previous injury to the uninvolved side may affect the findings of any bilateral comparison. In addition,
dominance of one side should be considered, because it may create subtle variations in posture and appearance,
especially in an athletic population.
Observation should continue throughout the entire examination. As the evaluation process unfolds, the injured athlete's
level of apprehension may decline, allowing for a more accurate representation of the injury state and determination of
the most appropriate course of action.
Palpation
This “hands on” component of the evaluation process can be thought of as a continuation of the observation; the clinician
is now able to feel what may previously have gone unnoticed. As with every part of the examination, the sequence in
which the palpation is conducted is important to avoid subtle variations and to identify all structures that may be involved.
Typically the palpation begins at a point on the periphery, away from the site of pain, and gradually moves closer to the
most painful area. This enables the clinician to define the borders of the injury and consider all structures contained
within those borders that may be involved. There are several factors that should be considered when conducting the
palpation, each of which may lend itself to better isolation of the pathology. These include point tenderness, crepitus,
deformity, swelling, tissue temperature, and sensation. The presence or detection of any of these factors is critical in
determining the most appropriate course of action.
Range of Motion
Appreciation of the functional abilities of an injured segment involves measurement of the active, passive, and resistive
ranges of motion of the affected joints. Significant limitations in motion often dictate that assessments be repeated for
joints proximal and distal to the injury site. Findings here may prove to be important when determining the need for and
degree of immobilization. ROM measurements should include all motions that occur about a joint and should be
compared both to established reference ranges and to the contralateral side. The examiner may choose to simply rely on
subjective assessment or to incorporate the use of a goniometer for a more precise measurement.
Initially, active ROM is measured to determine the possible presence of injury to the contractile units. Here, the athlete is
given the opportunity to demonstrate the amount of movement at a given joint. This assessment also provides a
benchmark for the clinician to use when gauging the amount of motion that may be available as the examination
progresses to the assessment of passive ROM.
Passive ROM is accomplished by the clinician with the athlete in a relaxed posture. This technique is used to identify
injury to noncontractile tissues and relies on the detection of an “endpoint” or “end feel.” Common normal end feels
include bone-to-bone (elbow extension), soft tissue approximation (knee flexion), and tissue stretch (extension of the
metacarpophalangeal joint). Abnormal end feels, on the other hand, include muscle spasm, springy block (meniscal tear),
empty (no movement due to pain), and capsular.
Knowledge of appropriate and inappropriate end feels for each joint is useful in determining the scope of subsequent
special tests as the evaluation continues.
Finally, resistive ROM is evaluated to determine the strength of the muscles that cross a particular joint. This can be
accomplished by movement through the ROM or, more commonly, by isometric contractions at various points throughout
the ROM (Fig. 3.7), referred to as a break test. At the midrange of motion, the break test places minimal stress on inert
tissue and allows for maximal recruitment of muscle fibers by mechanical advantage. As resistance is applied, the
clinician must limit the amount of accessory motion through proper use of stabilization, effectively eliminating input from
adjacent joints. Table 3.4 illustrates one of several subjective strength scales that have been developed to assist the
clinician in quantifying the strength of a muscle or muscle group.
FIGURE 3.7. Manual muscle testing. A: Knee extension. B: Elbow flexion.
TABLE 3.4. RESISTIVE RANGE OF MOTION (ROM) AND MANUAL MUSCLE TESTS—GRADING SCALE
Special Tests
This category of the evaluation encompasses several components designed to specifically identify the particular site
and/or extent of the pathology. Such testing often includes ligamentous and capsular stress testing to quantify joint laxity
and instability and tests to elicit compromise of cartilaginous and meniscal structures. In cases of traumatic injuries
involving moderate to severe tissue damage, protective spasm or muscle guarding frequently masks the extent of injury,
preventing the clinician from accurately assessing joint laxity. In these situations, it is critical to perform the tests and
assess joint instability at the beginning of the evaluation, in a timely fashion, to ensure an accurate impression.
A complete neurologic examination is often indicated to assess the integrity of the central and peripheral nervous
systems. Motor and sensory functions of both nerve roots and peripheral nerves are evaluated to identify the exact site or
level of the lesion. Myotomes, dermatomes, and corresponding reflexes should be compared bilaterally for any
asymmetry or deficits, which would suggest possible spinal cord or nerve root pathology ( Fig. 3.8). Examples of specific
neurologic tests include the Tinel sign, which is elicited by percussion over a superficial peripheral nerve, creating an
abnormally increased sensation or hyperesthesia along its corresponding distribution ( 35). This may indicate a peripheral
nerve irritation, entrapment, or dysfunction. The Babinski reflex may be tested by running a semisharp object along the
plantar aspect of the foot. If the great toe flexes and there is a concurrent splaying of the lateral four toes, a positive test
is noted, indicating an upper motor neuron lesion ( 35,36).
FIGURE 3.8. Reflex testing. A: Biceps tendon reflex. B: Patellar tendon reflex.
Further diagnostic tests may be necessary to confirm suspicions produced in the evaluation. Radiography, magnetic
resonance imaging, bone scans, computed tomographic scans, blood analyses, and other tests can be useful to clarify
subjective findings and document the extent of injury ( 37).
On completion of all parts of the clinical evaluation, the examiner studies the relation between the history and the
objective and subjective signs and symptoms to determine the etiology and pathology. Once an impression is formed,
medical referral and/or subsequent management and treatment may be determined.
On-Field Evaluation
The components of an injury evaluation in which the athletic trainer is summoned to the playing field are consistent with
those of the clinical evaluation but are considered only after an emergent or catastrophic situation has been ruled out. A
primary survey must first be conducted to determine the ABC status; the presence of head, neck, or spinal cord
pathology; and the presence of gross fractures or joint dislocations. After this initial assessment, the athletic trainer may
proceed through the same steps as in the clinical evaluation, making note of the chief complaint and the most appropriate
means of transporting the athlete off the playing field.
Efficient communication during the on-field evaluation is essential to managing the scene for the purposes of calming the
injured athlete as well as timely disposition. Ideally, two responders participate in the on-field evaluation, one performing
the actual examination and the other communicating with the athlete and other personnel as needed. If only one athletic
trainer is available, an organized plan must be in place, one that identifies what steps are to be followed and which
personnel are to carry out those steps. Coaching staff, administrators, and athletes alike should be aware of and well
versed in such a plan should the need to enact it arise.
REHABILITATION OF ATHLETIC INJURIES
It is important to distinguish between athletic rehabilitation and clinical or orthopedic rehabilitation. The intricacies of
athletic rehabilitation are often overlooked by practitioners of orthopedic rehabilitation, who believe there is no difference
between the two. The distinguishing elements include the following: (a) immediate acute care; (b) treatment on a more
frequent basis; (c) psychological preparedness; and (d) functional return of the individual to high-level athletic activity.
When a weekend warrior sustains an ankle sprain, he or she applies heat or ice at home or goes to the hospital for an
x-ray examination. This negligence of appropriate care can result in painful inflammation. An athlete under the care of a
certified athletic trainer, on the other hand, is immediately examined and treated with modalities designed to limit the
effect of pain associated with inflammation. The athlete may eventually require an x-ray study, but only after following
thorough instructions regarding the use of ice or heat; ambulation with crutches; and use of compression bandages,
braces, and splints. The immediate care rendered by the athletic trainer minimizes early stages of injury and enables the
athlete to progress more rapidly through all aspects of rehabilitation.
The athletic trainer's relationship with an athlete can greatly enhance the rehabilitation of injuries. The injured athlete
typically progresses through four psychological phases: denial, anger, depression, and acceptance ( 27). These phases
differ in intensity and sequence, and, depending on the athlete and severity of the injury, some phases may be omitted.
Athletic trainers and athletes often have a mutual respect and trust, which is essential for developing a positive goal and
plan for the athlete's well-being and eventual return to competition. The trainer's sensitivity to the psychological aspects
of an athlete's injury often accelerates the process of rehabilitation because of the positive focus the athlete is able to
employ.
The rehabilitation program of an injured athlete can be divided into three stages: (a) acute care, or control of the
inflammatory response; (b) subacute care, or physical reconditioning; and (c) chronic care, or return to activity. Each
stage within the rehabilitation process should be clearly defined for the athlete, keeping in mind the athlete's design to
return to full competitive participation. If the injury process requires a long rehabilitation time, several sets of goals may
be needed within each stage of the process to motivate the athlete to return to full competitive activity.
Stage One: Acute Care
Acute care is a particular area of expertise of the athletic trainer. Appropriate acute care can prevent or minimize the
effects of initial trauma, including hemorrhage and edema. Athletic trainers provide on-site care of injuries, using typical
acute care measures—such as protection, rest, ice, compression, and elevation (PRICE)—that minimize the effects of
the initial inflammatory response.
After an injury, protective devices can be used effectively and efficiently to assist in the healing process. These devices
enable the athlete to rest the injured area adequately; when they are coupled with the use of other modalities, pain and
swelling of an injured area also are decreased ( Fig. 3.9). The acute stage of rehabilitation focuses on minimizing initial
hemorrhage and edema and slowing down the tissue metabolic rate through PRICE, which diminishes histamine release,
thereby decreasing the inflammatory response. The athletic trainer is skilled in controlling and assessing the
inflammatory phase of the injury. The use of PRICE and other modalities is determined by the inflammatory response to
injury and treatment. Athletic trainers are well versed in recognizing the signs of the inflammatory processes and in
determining the appropriate modalities to allow rapid progression through the rehabilitation plan.
FIGURE 3.9. Ice and elevation are used to minimize swelling.
When treating the athlete during the acute stage of the rehabilitation program, the athletic trainer must be aware of the
healing process. This process consists of a series of phases that overlap one another: the inflammatory, fibroplastic, and
maturation phases. The goal of the trainer in this process is to avoid problems that may exacerbate the inflammatory
process, which would delay healing. The ultimate product of proper acute-care management is a strong, functional scar
that will permit full return to competitive activity.
The early stage of rehabilitation involves minimizing the effects of inflammation and enhancing repair of the pathologic
tissue while also maintaining the athlete's overall conditioning. Deconditioning can result in exacerbation of the athlete's
current injury. The athletic trainer draws on his or her background in exercise physiology to design an activity program
that will prevent the athlete's deconditioning and will not exacerbate the symptoms of the injury. Such activities include
alternative conditioning modalities such as cycling and pool therapy to prevent deconditioning and weight training to
prevent general musculature atrophy of the noninvolved and noninjured sites. These alternative modalities enable the
athlete to maintain aerobic capacity and overall strength, resulting in the efficient return to activity on healing of the
injury.
Stage Two: Subacute Care (Physical Conditioning)
Stage two of rehabilitation begins when pain and swelling are controlled and the athlete does not require continued
immobilization. The athlete may be placed in a removable splint or required to use an assistive device ( Fig. 3.2) The
primary goal of the athletic trainer in stage two of the rehabilitation program is to restore ROM, strength, and endurance
to the affected site. The progression is based on the physician's prescribed therapy as well as the athletic trainer's
assessment of the status of the injury. It includes subjective and objective variables such as the athlete's pain and
limitation in ROM, observable swelling, and strength deficits. In stage two of the rehabilitation program, the athletic
trainer develops an individualized therapy plan for each athlete.
Restoring full ROM to an injured limb is of paramount importance to the rehabilitation process. ROM is typically
measured against and compared with the normal contralateral limb. Occasionally, athletes such as javelin throwers and
pitchers do not have normal symmetric motion, although most athletes have equal ROM bilaterally. ROM can easily be
assessed with the use of a goniometer, which identifies any deficits in ROM and provides information about attainable
ROM goals. Functional ROM can be reestablished with a combination of passive, active assistive, and active exercises
that facilitate normal motion and enhance strength in the injured limb.
Passive ROM exercises are those exercises that are performed by the athletic trainer through manual movements of the
athlete's limb. Active assistive ROM exercises are performed by the athlete with the assistance of the athletic trainer; the
goal is to reach the terminal limits of the motion ( Fig. 3.10). Active ROM exercises allow the athlete to perform within his
or her full pain-free ROM. Passive, active assistive, and active exercises are used to regain the full ROM. When
prescribing these exercises, the clinician must keep in mind the athlete's pain and any changes in inflammation that may
be caused by any of these activities.
FIGURE 3.10. Active assistive range of motion (ROM). Assistance is provided by the clinician to increase ROM during
the subacute healing phase.
Alternative therapeutic modalities should be continued during stage two rehabilitation, because they play an important
role in facilitating progression. Modalities of choice include moist heat packs and warm whirlpool treatments, which
increase blood flow to the effected area and help facilitate ROM. In addition, once the tissues have been warmed,
therapeutic massage can be used to release scar tissue and adhesions that could prevent normal ROM. Occasionally,
cold modalities can be used before activity in an attempt to minimize pain and enable the athlete to exercise within his or
her ROM comfortably. After the therapeutic exercise, cold whirlpools and ice packs help minimize or prevent secondary
swelling or effusion resulting from the activities.
A variety of equipment devices are available to assist the athletic trainer with increasing the athlete's ROM. These
devices include the continuous passive motion machine that is used postoperatively and splints that can provide static
stretch to areas where ROM has been diminished because of adhesions. Isokinetic machines also are capable of
providing static stretch to an extremity by isometrically setting the joint at various points throughout the ROM.
As the athlete progresses through stage two and regains ROM, the strengthening process should be initiated. In the early
portion of the rehabilitation program, strengthening exercises can be performed daily; as strength increases to
approximately 25% of that of the noninjured muscle group, the frequency should be decreased to alternate days to
facilitate cellular adjustments in the muscle tissue ( 27). This allows for superior strength gains while minimizing the
effects of inflammation caused by excessive frequency and intensity of exercise. Strength gains can be achieved through
modes of strengthening, including isometrics, isotonics, and isokinetics. Isometric exercises are employed during the
early stages of strengthening and can be used when ROM needs to be limited. Isometrics help prevent significant disuse
atrophy in an immobilized athlete. Isotonic exercises are performed through a ROM with a fixed resistance. Isotonic
exercise may be incorporated to an athlete's rehabilitation program whenever resistive exercise will not exacerbate the
healing process.
Many programs are available to help an athlete increase strength. Examples of these progressive resistive strengthening
programs are the DeLorme program (39), the Oxford technique (40), and Knight's daily adjusted progressive resistance
exercise (DAPRE) program (41). Progressive resistive exercises are initiated once the athlete has completed a program
of active exercise without signs of increased inflammation secondary to the exercise. If inflammation does appear, the
exercise program should be curtailed until the inflammatory process is controlled.
The use of isokinetic devices in the rehabilitative process provides an advantage by allowing resistance to accommodate
to pain and fatigue as the athlete exercises through the full ROM. Closed kinetic chain exercises are advocated by many
orthopedic surgeons, resulting in less reliance on isokinetic devices for lower- and upper-extremity injuries. Certainly,
isokinetic exercises will continue to have a role in the rehabilitative process, but their continued use as the sole criterion
for return to play has been eliminated from the athletic trainer's program ( 42).
Proprioceptive and coordination exercises in stage two of rehabilitation are extremely important. After a
non–weight-bearing period, coordination and balance are compromised as a result of decreases in neurophysiologic
stimuli (Fig. 3.11). Promoting balance and coordination during the early stages of rehabilitation is important to help the
athlete regain not only full use of the limbs but also the self-confidence to perform.
FIGURE 3.11. Proprioception training using a biomechanical ankle platform system (BAPS) board.
Furthermore, it is important that the athlete appreciate the link between rehabilitation and participation. Therefore,
functional activities that are sport specific should be implemented to ensure that the athlete remains motivated. Examples
include pool exercises and the use of rubber tubing resistance activities that mimic or reproduce the motions involved in
the desired sport ( 43). These sport-specific activities enhance the athlete's motivation while inducing adaptations specific
to the functional requirements of the particular sport.
The goals that an individual establishes in stage two of the rehabilitation program can easily be documented to provide a
motivational tool for the athlete. Achievement of full ROM, near-normal strength levels, and near-normal levels of power
and endurance, as well as increases in balance and coordination and maintenance of cardiovascular endurance, provide
the athlete with increased motivation.
Stage Three: Chronic Care (Return to Competition)
Return to competition is often the most difficult decision for both the athletic trainer and athlete. The decision must be
based on a thorough assessment of the athlete's physical status to ensure that the risk of reinjury has been minimized.
Often the decision to return an athlete to competition is based on the athletic trainer's understanding of the mechanical
demands of the sport and the athlete's ability to perform without the risk of injury. Obviously, if the athlete is unable to
perform the basic mechanical movements of his or her sport, the likelihood of reinjury or injury to another area increases.
It is the trainer's responsibility to ensure that the athlete's physical abilities are appropriate for the activity and that they
are consistent with repeated use, thus lowering the likelihood of reinjury and preventing any injuries to other joints or
musculoskeletal soft tissue caused by compensation for the injured region.
Another important, yet often neglected, component of returning the athlete to competition is the proprioceptive
mechanisms, training of kinesthetic awareness, and balance. The rehabilitation program at this point can be isolated to
ensure that the athlete is able to perform certain activities that are functional within his or her sport without causing any
abnormal mechanics at competitive speed. Activities such as jogging straight ahead, doing carioca, running figure-eights
and zigzags, running and cutting at 45-degree angles, and performing specific agility drills should be employed to ensure
that the athlete is able to engage in all activities at full speed and without pain.
On return of the athlete to competition, consideration should be given to use of a splint, brace, or protective strapping to
assist maintenance and provide additional stability. It is important for the athlete to understand that braces, taping, and
splints do not replace the rehabilitation program but help in performance.
The return of normal strength, power, and endurance during the final phase of rehabilitation provides not only the athlete
with the aforementioned functional requirements but also assists the athlete with the psychological component of
rehabilitation and provides confidence to return to competition without fear of reinjury. Information about preinjury
strength, aerobic fitness, and power provides objective goals for the athlete.
Return to activity should be gradual and should be considered by the athletic trainer, the athlete, and the coach. Gradual
return can be obtained in small-group activities such as one-on-one in basketball and performing full-court drills. Such
practice enhances the athlete's confidence in his or her ability to perform. Once the athlete meets the requirements for
the sport, the length of practice sessions can increase. Practice duration can vary from 25% to full practice, depending on
the nature of the injury and any residual effects (e.g., swelling, pain) that may occur after activity.
Before return to competition, the athlete must have regained full mechanical ability, balance, coordination, and general
fitness. The athletic trainer must decide, along with the physician, whether taping or bracing will facilitate the athlete's
activity without compromising performance. The decision to return to play is made by the physician, athletic trainer,
athlete, and coach and is based on the athlete's ability to fulfill all requirements demanded by the sport.
Athletic rehabilitation is made up of three stages. These stages often overlap, and each can last from 3 days to 6 months.
Because of this variation in recovery time, the athletic trainer's role is critical with respect to return to play. Often the
motivated athlete wants to return prematurely; however, the athletic trainer must make that decision, taking into
consideration the initial care and the progress of the rehabilitation. Thus the athletic trainer plays an important role in
deciding when to return the athlete to his or her sport at a competitive level.
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4 Environmental Factors in Athletic Performance
ENVIRONMENTAL FACTORS IN ATHLETIC PERFORMANCE

TIMOTHY A. BARKER
H. ANDREW MOTZ
WAYNE K. GERSOFF
Effects of Heat on the Athlete

Thermoregulation
Heat Injury
Predisposing Factors
Effects of Cold on the Athlete
Cold Weather Physiology
Specific Cold Injuries
Effects of Altitude on the Athlete
Physiologic Considerations
Acclimatization
Altitude Disorders
Training and Performance
Chapter References
The environment in which we live contributes greatly to our lifestyles. The role of environment is even more pronounced
when its impact on exercise and athletic participation are considered. Although there are many components of the
environment that can potentially affect ability to exercise, only three are considered in this chapter: cold, heat, and
altitude. Each of these environmental factors is reviewed in terms of its effect on athletic performance.
EFFECTS OF HEAT ON THE ATHLETE
Thermoregulation
Hyperthermia
The main center for thermoregulation in the human body is the hypothalamus. This structure is a group of specialized
nerve cells that serve to protect the body from the buildup or loss of heat. These cells are stimulated in two ways:
directly, by sensing change in the temperature of the blood perfusing them, and indirectly, through special
thermoreceptors in the skin. Once these cells are stimulated, there are five mechanisms to facilitate the loss of heat:
radiation, conduction, convection, evaporation, and respiration ( 1,2).
Radiation
Heat is exchanged between all objects through electromagnetic waves. Through these waves, heat is transferred from
warm objects to cooler ones. When the ambient temperature is lower than body temperature, heat is released from the
body to objects in the environment. This exchange does not require molecular contact. However, if the objects in the
environment are warmer than body temperature, no net heat loss from the body occurs. This explains why
thermoregulation is more efficient in the shade than in direct sunlight. The sun warms objects through radiation, and the
objects in the environment are cooler when shaded. If they are cooler than body temperature, heat can be released.
Generally, 50% of body heat is released through radiation. This avenue is lost when the ambient temperature exceeds
body temperature.
Conduction
Conduction involves the direct transfer of heat from one object to another and requires molecular interaction. One of the
first responses to increases in body temperature is vasodilation. This enables the body to transfer most of the core heat
to the surface rapidly. The heat can be transferred from the surface molecules on the skin directly to clothing or air
molecules. Again, this transfer depends on the environmental objects' being cooler than body temperature. This
phenomenon explains the cooling benefit of a wet shirt or wet towel.
Convection
Convection refers to the motion of fluids (gases or liquids) and their ability to carry molecules of higher temperature away
from the body and replace them with cooler molecules. It is codependent on conduction for actual heat loss. The air or
water molecules immediately adjacent to the skin are warmed by conduction. The convective currents then move these
molecules away and replace them with other molecules that can be heated. If these convective currents are not present,
the warmed molecules of air or water remain adjacent to the warm body and actually provide a layer of insulation that
impedes further heat loss. Together, conduction and convection account for 15% of heat loss.
Evaporation
Although heat loss through evaporation accounts for only 30% of heat loss in normal situations, it is the principal
physiologic defense mechanism against hyperthermia, because it does not depend on the ambient temperature to have
an effect. As body temperature increases, the hypothalamus stimulates the cholinergic sympathetic fibers, which in turn
stimulate the 3 million sweat glands in the human body. This stimulus causes the release of a hypotonic saline solution,
which is then vaporized on the skin surface. For 1 g of saline solution vaporized, approximately 0.6 kcal of heat are
removed. Because this occurs on the skin surface, it is the skin that is cooled. This in turn, by convection and conduction,
cools the blood that supplies it. At high ambient temperatures, radiation, conduction, and convection all serve to increase
body temperature, because the objects around the body are equally as hot or hotter. In this situation, only evaporation
cools the body.
Studies have shown that the rate of sweating is directly proportional to the ambient temperature. The major limitation to
this method of heat loss is humidity. Humidity refers to the amount of moisture in the air. For a given temperature, the air
can only hold so much water. As this limit is reached, the relative humidity increases. As the vapor pressure in the air
begins to approach that on the skin, less and less sweat evaporates. Sweating, by itself, is not enough to release heat; in
fact, if sweat rolls off or is wiped off, its ability to release heat is lost.
Respiration
Respiration is not truly a different avenue of heat loss. It is actually a composite of the other four methods, although the
heat loss does not occur on the skin surface. As cool air is inspired, heat is exchanged through radiation, conduction,
and convection. In addition, vaporization occurs from the mucous membranes of lungs, and they are thus cooled. It does
appear that respiratory rate increases may be triggered by increases in core temperature ( 3). This accounts for less than
5% of normal heat loss.
Heat Injury
Although the body has developed means to lose heat, it is still overcome at times and heat injury can occur. There are
three heat exposure syndromes that represent different levels of injury.
Heat Cramps
To ensure proper functioning of all muscles, a delicate balance of electrolytes and water must be maintained. During
exercise in the heat, this balance can be altered by the loss of both electrolytes and water through perspiration ( 4). When
this occurs, the involved muscles may spasm. Although any muscle can be affected, the most common is the calf muscle.
These spasms are unrelated to the fibrillations of overexerted muscles or the spasms of injured (pulled) muscles.
As with all heat injuries, the best treatment is prevention. Proper ingestion of fluids—both in the days and hours
preceding exercise and in the normal diet—is necessary to avoid cramps. Once cramps have occurred, the proper
treatment is rest, passive stretching, and rehydration.
Heat Exhaustion
Heat exhaustion (also known as heat prostration or heat syncope) is a manifestation of an inadequate cardiovascular
response to heat stress. During heat stress, blood is directed to the skin so that heat can be released. During exercise in
the heat, the muscles also require more blood flow. These increased demands on blood volume require that blood be
shunted from other bodily systems. In physically fit, well-acclimatized individuals, the cardiovascular system is able to
compensate for this dual stress. However, in persons who are unfit or unacclimatized, the stress is too much and central
blood volume is insufficient to maintain cardiac output. The symptoms are, therefore, primarily those of shock: weak,
rapid pulse; low blood pressure; dizziness or postural syncope; headache; pallor; nausea and/or vomiting; loss of
appetite; urge to defecate; and general weakness. Body temperature usually is not elevated.
Treatment consists of having the victim lie down in a cool environment and administering hypotonic fluid replacement; in
some cases, the fluids should be replaced intravenously. Athletes with heart disease and those who have recently had
bouts of vomiting or diarrhea are more susceptible than other athletes.
Heat Stroke
Heat stroke represents a true medical emergency. The mortality rate is 20% to 75% if cooling is not effective. The cause
of death is damage to the cells of the central nervous system, and survivors may have persistent symptoms of nerve
damage. Heat stroke may develop either as a sequela to heat exhaustion or suddenly, without warning. Heat stroke
represents a failure in the temperature-regulating system. It occurs most commonly in conditions of high ambient
temperature and high humidity, but it can occur in the absence of both. Under conditions of heat stress, the body cannot
respond indefinitely. When dehydration occurs, sweat production stops. In high ambient temperatures, this is usually the
last of the defense mechanisms and so the body temperature begins to climb. This is further aggravated by the increase
in metabolic rate that accompanies increases in core temperature. The increased metabolic demands especially affect
the central nervous system, and cell damage occurs when these demands are not met. Symptoms of heat stroke include
mental status changes, emotional lability, and unsteady gait. The pulse is usually strong initially, respiration is rapid, and
the body temperature is high. The skin is warm and dry. The athlete lapses into unconsciousness and, as further cell
damage occurs, the pulse weakens and blood pressure drops.
Immediate treatment involves taking any steps available to lower body temperature; alcohol rubs, ice packs, and wet
sheets with fans are acceptable temporary measures, but whole-body immersion in a tub with iced water is best.
Although cooling should be the priority, treatment for shock also may be necessary ( 5). Acetaminophen and aspirin are
not helpful, because their antipyretic effects depend on intact heat-regulating mechanisms. It is important to note that oral
and tympanic membrane measurements of body temperature do not provide an accurate indication of core temperature in
athletes after exercise. Rectal temperatures are much more accurate and should be used for both diagnosis and
subsequent monitoring of treatment (6,7).
Predisposing Factors
Although all athletes are susceptible to any of the heat illness syndromes, there are several factors that can place certain
athletes at risk. These factors and various popular misconceptions about heat illness are addressed in the following
sections.
Dehydration
From the previous discussion it is clear that dehydration is by far the most important factor in heat illness ( 4). The body's
defense system is completely dependent on proper hydration. Many of the adverse effects of heat illness are not seen in
hyperthermic conditions if the body is well hydrated ( 8). Three deaths occurred among collegiate wrestlers in 1997, and
weight-loss methods that promoted dehydration were implicated in each case. Thirst is a notoriously poor indicator of
dehydration because it is a delayed response. Encourage athletes to drink regularly even if they are not thirsty. Water
still appears to be the best source during activities, but compliance is better with some of the flavored drinks. They may
need to be diluted to avoid carbohydrate loading. Training methods that encourage dehydration should not be allowed.
Drugs
The most important class of drugs implicated in heat illness is the diuretics. When they are used by prescription (e.g., for
hypertension, edema), the body usually makes adjustments over time in the cardiovascular system to decrease this risk.
However, athletes who are required to make weight, especially wrestlers, abuse diuretics. Short-term use just before an
event does not allow compensation and puts the athlete at risk for thermal and cardiovascular breakdown ( 9). In addition,
diuretics are known to interfere with neuromuscular function through an unknown mechanism that seems to be
independent of fluid and electrolyte concentrations ( 10). These athletes also abuse cathartics and laxatives. In addition
to dehydration, such drugs are associated with potassium loss, which causes muscle weakness.
Creatine is a very popular supplement among professional and amateur athletes. It appears to enhance exercise
capacity and to result in greater gains toward lean body mass. The weight gain associated with creatine use is probably
caused by increased muscle water. Therefore, there is a theoretic risk of dehydration while using this supplement, and
one of the side effects is muscle cramping ( 11).
Amphetamines can increase the metabolic rate, and therefore temperature generation; fever is a known side effect. This
can certainly complicate hyperthermia even without the cardiac side effects of amphetamines ( 11).
Antihistamines are generally dehydrating and can worsen this condition even when used appropriately.
Although not technically a drug, salt tablets are often abused by athletes. Most Americans get adequate salt intake from
their diets. Although athletes may lose salt through sweating, in most instances only small increases in dietary salt are
needed to replace this loss. Salt tablets are known to cause abdominal cramping and the gastric electrolyte load. If not
accompanied by adequate fluid intake, the excess salt draws fluid out of the cells, exacerbating dehydration.
Acclimatization
Acclimatization involves neural, hormonal, and cardiovascular changes in response to repeated heat stress. Heat illness
frequently occurs at the start of athletic training, before the body has had a chance to adapt to heat stress. This effect is
independent of general condition, because it is known to occur in individuals who are not changing their workouts, just
their environment. The bulk of the acclimatization process is complete within the first week of exposure and results in
increased exercise capacity and decreased discomfort ( 12). The body adapts by becoming better able to shunt blood to
the periphery with less cardiovascular compromise. There also is a lower threshold for sweating, so that the
heat-regulating system is turned on sooner, preventing increases in core temperature. Thus sweating soon after initiation
of exercise is not an indication of being out of shape but of being acclimatized ( 13,14 and 15).
Obesity
Fatal heat stroke is known to occur more than three times as frequently in obese individuals, compared with thinner
persons. The increased metabolic requirement needed simply to move the heavier load stresses the heat-regulatory
system. In addition, body fat serves as insulation that prevents conduction of heat to the skin surface.
Gender
Although men do sweat more and at lower core temperature, they do not possess better heat-regulating capabilities than
women. If controlled for level of conditioning and acclimatization, women are able to tolerate heat as well as men. This
indicates that women probably have better adapted circulatory responses for the release of heat ( 13,16,17).
Age
Although there is a delayed onset of sweating associated with advancing age, there is controversy as to whether this
affects heat-regulating capabilities. Studies comparing young and middle-aged marathon runners showed no difference
in ability to regulate temperature. The increased incidence of cardiac disease with age is probably the most likely
explanation for any difference in heat tolerance.
Clothing
The choice of clothing can have the most pronounced effect on the body's ability to regulate heat for a variety of reasons.
As discussed earlier, sweating works to control heat only if evaporation occurs. Dry clothing of any type absorbs the
sweat from the skin before it has a chance to evaporate; evaporation occurs only when the clothing is soaked. Many
athletes like to change their shirts when they become soaked with sweat, but this only inhibits the body's ability to
regulate heat. The best choice is clothes that are light-colored (to reflect radiant energy from the sun), are loosely fitting
(to enhance convection), are made of a highly absorbent material; the clothing should be left in place throughout the
exercise. The use of sweat suits, especially in warm climates, is dangerous and of no benefit. They are usually made of
synthetic, nonabsorbent material. The relative humidity between the suit and the skin rises quickly, regardless of the
humidity in the environment, because the moisture is not allowed to escape. Evaporation is retarded, convection and
conduction are prevented, and the body's increased temperature becomes difficult to regulate. Because there is no
documented advantage to the use of sweat suits in conditioning, athletes should be discouraged from wearing them. The
National Collegiate Athletic Association has recommended that their use by wrestlers be prohibited. Football uniforms
interfere with heat regulation in a similar way; they also increase the metabolic load because of the increased weight the
athlete must carry (18,19).
Heat injury syndromes are common and potentially life-threatening. They also are totally preventable. Athletes should be
made aware of these entities and instructed in simple methods of prevention: avoid dehydration before exercise, properly
rehydrate during and after exercise, condition, acclimatize, and wear proper clothing. Through these simple measures,
heat injuries can be avoided.
EFFECTS OF COLD ON THE ATHLETE
Cold temperature is one of the most common athletic environmental hazards. Indeed, cold can play an important role in
any outdoor sport. Although cold-related problems are usually associated with winter sports such as skiing, skating,
mountaineering, and snowshoeing, other sports also introduce risk, including running, cycling, swimming, and hiking.
Cold Weather Physiology
The human body represents a remarkable temperature-controlled machine. It has the ability to maintain a relatively
constant body temperature in varying types of environments. Unfortunately, the human body has evolved in such a way
that makes efficient acclimatization to cold very difficult. However, there are several mechanisms that not only generate
but also conserve body heat. The generation of body heat can be divided into four categories of mechanisms: basal heat
production, muscular thermoregulatory heat, high-intensity exercise-induced heat, and mild- to moderate-intensity
exercise-induced heat.
Basal heat production is associated with the heat that is produced by the normal metabolic processes of the body.
Although this is sufficient to maintain the body under various resting conditions, it is relatively ineffective in generating
body heat during exposure to cold environments.
Muscular thermoregulatory heat is the heat that is produced by the mechanisms of shivering. Along with the
commencement of shivering, there also is an alteration in the circulatory flow to provide more heat to the internal organs.
Therefore, the blood circulation in the toes, fingers, and facial structures is affected first. In the event that cooling
progresses further, the core body temperature will be lowered. Moderate exercise during exposure to cold, wet, windy
conditions does not result in hypothermia until fatigue, associated with exhaustion of shivering, occurs. Although
shivering may increase heat production to three to five times the basal level, it also has the negative effect of using large
amounts of energy, which is reserved in the body. The actual act of shivering also can reduce coordination and useful
movements that may be needed to perform tasks that help conserve body heat ( 1,20).
High-intensity exercise-induced heat is simply the heat that is produced by the body during various activities, such as
walking or running, in which there is increased muscular activity. Although this type of heat production can generate up to
10 times the basal heat, it can be maintained only for several minutes, because it rapidly exhausts the energy stored
within the body (1).
Mild- to moderate-intensity exercise-induced heat is provided by the same mechanisms as other exercise-induced heat.
However, because of the lower rate and intensity of exercise, this form of heat production is only approximately five times
greater than the basal level. Because it uses less of the body's stored energy, it can be maintained for longer periods
than high-intensity exercise-induced heat can ( 1,20).
In addition to mechanisms for generating body heat, the body also has developed mechanisms for conserving body heat.
These include superficial forms of constriction, body insulation, and, although not totally developed by the body itself,
exposure to external heat sources (1). When the body is exposed to a cold environment, blood flow is shunted away from
the surface area of the body to the core. Blood is moved away from areas where it can easily lose heat to the cooler
environment and is brought to areas that greatly depend on optimal temperatures for their function. The body also
insulates itself to conserve heat, most commonly by layering subcutaneous fat in the body. In addition, the application of
external heat sources, such as proper clothing or exposure to external sources of heat such as fire, sun, and hot food,
also provide insulation against heat loss. As mentioned earlier, the body also has several mechanisms of transferring
heat. These are important to the processes involved in maintaining the steady state not only against hot environments
but also against cold environments ( 1).
When discussing the various physiologic factors in cold weather and cold environments, the body may be considered as
consisting of a core and a shell. The core consists of internal structures such as the brain, heart, lungs, and abdominal
organs. The shell refers to the skin, muscles, and extremities. When the shell temperature decreases and the core
temperature is maintained, the result is local injuries to the shell. However, if both the shell temperature and the core
temperature decrease, systemic problems will develop ( 1).
Cold environments also have an effect on the potential performance capabilities of the individual. Cold environments
reduce exercise efficiency. This is probably related to the fact that in the cold environment muscle function is decreased
and nerve conduction may be slowed. In addition, if it gets cold enough, the first body defense mechanism to be
implemented is shivering, which also inhibits performance ( 20,21 and 22).
Various factors predispose individuals to the development of problems in a cold environment. These include inadequate
insulation of the body, restricted peripheral circulation (Raynaud's disease or diabetes), fatigue, poor nutrition, the use of
alcohol, the use of tobacco, age, and the body's ability to shunt the blood ( 1,23,24).
Specific Cold Injuries
Cold injuries can be classified as being either local or systemic. Local cold injuries result when the shell temperature (i.e.,
that of the skin and peripheral tissues) is exposed to freezing temperatures but the core body temperature is maintained.
If the cold induces a drop in the core temperature as well as the peripheral temperature, more systemic manifestations,
such as hypothermia, can be produced. In this section the local cold injuries—frostnip, chilblains, and frostbite foot—are
discussed along with the systemic injury of hypothermia.
Frostnip
Frostnip is a slow-developing condition that results in blanching or whiteness of the skin. It is usually associated with
reversible formation of ice crystals on the skin's surface. Frostnip usually develops slowly and painlessly and usually
affects the tips of the ears, nose, cheeks, chin, fingertips, and toes. This condition frequently is not first recognized by the
victim but rather by a companion. Frostnip often is confused with frostbite. It is often seen in conditions of high wind,
extreme cold, or both (1).
Most commonly, no permanent tissue damage is realized from frostnip. It is important to treat this condition appropriately
to prevent tissue damage. The treatment that is recommended for frostnip is to provide warming of the affected tissue by
the firm, steady contact of a warm hand, by blowing hot breath on the affected tissue, or by holding the injured body part
in either the axilla or the groin area. It is extremely important not to rub the skin with snow. This old folklore treatment can
actually result in more damage to the tissue. As the tissue gradually warms and thaws out, the color returns and the
victim may experience tingling in that body part. The skin may continue to be red for several days after the tissue has
warmed, and there may even be some flaking of the skin. As in all types of cold injuries, it is best to try to prevent their
onset. There is no guaranteed prevention for frostnip, except to allow for adequate protection of exposed body parts and
to recognize environmental risks.
Chilblains
Chilblains and trench or immersion foot are commonly grouped together. Trench foot usually refers to the lower extremity
and chilblains to either the hands or the feet. The etiology of this condition is repeated exposure of bare skin to cold
water or the presence of wet extremities for prolonged periods at a temperature near freezing. Initially, this condition
damages the capillaries of the skin. With further progression of the injury, necrosis or gangrene of the skin, underlying
muscles, nerves, and other associated soft tissues occurs. This injury results in swollen, cold, pale, numb skin and
progresses to mottled skin with a pale or grayish blue tint. The usual initial symptom is tingling or burning. The extremity
also may feel cold and numb (1,11).
On rewarming of the affected body part, there is a typical sequence of events. The skin may become red, swollen, and
hot. Areas of increased burning and itchy sensations may develop. The skin may blister or develop localized gangrene,
or both. Recurrence of this injury tends to happen in the same area of the body. Other victims may have permanent
hypersensitivity to cold and paresthesias in the affected skin. This is probably related to some degree of permanent injury
to the peripheral vascular and nervous system in that body part. The treatment of chilblains includes cleaning, drying,
and careful rewarming of the limb. The rewarming should take place in an appropriate environment where there will not
be reexposure to the cold. There is no effective treatment once permanent skin injury has been established. Therefore,
all treatment should be geared to prevent initial occurrence and to protect the area once rewarming has occurred ( 1).
Frostbite
Frostbite represents the worst of the local cold-related injuries. It is caused by the actual freezing of the soft tissue. The
danger of frostbite must be considered very strongly whenever there is exposure to extreme cold. It is also important to
be aware of the effects of windchill, direct contact with frozen objects, and hypoxia from high altitudes. It is believed that
intranasal cocaine use can increase the risk of nasal frostbite by contributing to vasoconstriction. The areas of the body
that are commonly involved in frostbite injury are the fingertips, earlobes, tip of the nose, toes, and any exposed areas of
skin. Frostbite can be classified into various stages based on the degree of injury. First-degree frostbite is associated
with local pain or discomfort with numbness, erythema, and swelling of the affected area. Second-degree frostbite
displays all of the previously mentioned symptoms along with the development of a serous superficial blistering.
Third-degree frostbite brings on the development of deep, hemoserous blistering. Fourth-degree frostbite involves the
deep soft tissues including bone and can result in mummification of the tissues and the need for amputation ( 22,23).
Initially, the victim experiencing frostbite develops itching or prickling sensations and then swelling and redness of the
affected body part. With progression, the skin on the frostbitten area may appear white, often with a yellowish to bluish
tint that gives it the appearance of wax ( 1,11).
The treatment of frostbite is divided into prehospital care, immediate care (thawing), and postthaw care ( 23). Generally,
treatment should be directed toward preventing further injury to the tissue and deterring the necrosis of any damaged
tissue. Although it may appear to be a justifiable treatment, rubbing or massaging of frostbitten tissues is strongly
contraindicated because it may lead to further damage ( 2). The accepted therapy for frostbite is rapid rewarming. In this
regard, a whirlpool is ideal. It is recommended that the water temperature be 40° to 42°C (104° to 108°F) ( 1,2,24,26). The
use of dry heat, such as from a campfire, car exhaust, or radiator, is contraindicated for several reasons. This type of
rewarming is slow, and the heat is often not equally distributed. In addition, because of numbness, there is a chance for
the skin to become burned from this type of heat. It is strongly recommended not to thaw the frostbitten parts while still in
the field unless there is a mechanism available to keep them thawed. If the frostbitten part is thawed and then allowed to
refreeze, the risk of more extensive damage is higher. Depending on the extent of the frostbite and the penetration into
deeper tissues, thawing can take from 30 to 45 minutes. On rewarming of the frostbitten body part, the victim will
experience pain proportional to the degree of frostbite injury. An analgesic my be required to help deal with the pain. The
victim should be told that this pain is not a dangerous sign but rather part of the natural process of rewarming ( 1,2,11).
Once the body part has been rewarmed and blood flow returns, the injured tissue may appear mottled, blue, or purple.
There may also be swelling, resulting in large blisters or gangrenous areas several days after treatment. These blisters
eventually form blackened, necrotic areas of tissue that are easily separated from the normal skin. The new skin is
usually of poorer quality than the original and is very sensitive to cold ( 1,2,11,24).
Management of frostbite injuries after thawing should be of a protective nature. The skin should be protected with soft,
sterile bandages and topical or systemic antibiotics used judiciously. Blisters should be left intact when possible, but
debridement may be required after the patient arrives at a health care facility. The inflammatory cascade can be inhibited
by ibuprofen and aloe vera cream, which are potent inhibitors of prostaglandin and thromboxane. Tetanus toxoid should
be administered to all patients. The involved skin should be protected from prolonged contact. This can be done by
elevating the limb or designing a protective cradle around the limb to prevent any pressure. Range of motion exercises
are important to prevent stiffness of the involved joints and loss of function ( 24). Anyone who has experienced a frostbite
injury should be examined in a medical facility, and those with injuries greater than first degree should be observed in a
hospital. It is difficult to access viability accurately from the initial gross appearance of the damaged part. Such injuries
must be observed over time, especially when the possibility of amputation is being considered. Amputation should be
delayed as long as possible—sometimes weeks to months—to demonstrate which tissues are truly necrotic and which
are salvageable (1,2,23,24). Numerous adjuvant therapies for frostbite have been used with mixed results and have been
reviewed (23).
Ultimately, the best way to treat frostbite is prevention. Preparation for the environment is the most important method to
prevent frostbite injury. This requires awareness of not only the actual temperature but also the windchill factor.
Prevention includes adequate and properly fitted clothing as well as protection of exposed body parts (e.g., hands, feet,
nose, ears). It is also important to keep clothing dry to avert subsequent chilling from moist clothing next to the body. If a
body part feels as though it is getting cold, the individual should move it continually, being careful not to keep it in one
position for a long time. For example, if the face is beginning to feel cold, use the facial muscles to generate some heat in
that area while searching for definitive shelter from the elements. Adequate nutrition and hydration status are essential,
as is the avoidance of alcohol and cigarette smoking. Lastly, remember that when out in a harsh environment, it is
imperative for people to observe each others' faces and any other exposed skin for possible signs of frostbite injury
(1,23).
Hypothermia
Unlike the previously discussed injuries, hypothermia is a systemic injury. Hypothermia occurs when the body's core
temperature drops to less than 35°C (95°F). Hypothermia causes 500 to 700 deaths per year in the United States. It can
occur at almost any altitude and in any temperature that is lower than body core temperature. Several types of individuals
have been identified with an increased risk for hypothermia, including accident and trauma victims, the very young and
the very old, people with chronic metabolic disease, people with acute or chronic alcoholism and/or acute intoxication or
drug overdose, and those who are mentally impaired ( 1,24).
Hypothermia has been classified as mild, moderate, or severe and within these classes as acute, subacute, or chronic.
Mild hypothermia is diagnosed when the rectal core temperature (RCT) is less than 37°C (98.6°F) but greater than 35°C.
Moderate hypothermia occurs when the RCT is less than 35°C but greater than 32°C (90°F). Severe hypothermia occurs
when the RCT drops to below 32°C.
Hypothermia represents a true medical emergency. It is important to recognize the condition as soon as possible. Once it
is recognized, action should be taken to prevent further loss of body heat and to rewarm the individual safely and quickly.
Because the development of cardiac ventricular fibrillation is a distinct possibility, it is imperative that care be taken in
treating victims in the field, in transporting them, and also in rewarming them. Hypothermia must be suspected whenever
an individual is found in a cold environment with an altered mental status. It also must be strongly considered if there is a
history of trauma or cold water immersion. Any person with hypothermia and altered mental status should not be given
the opportunity to make important decisions, because judgment will certainly be impaired. To assess the degree of
hypothermia, a low-temperature thermometer—one that is calibrated below 34.5°C (94°F)—is needed. Both oral and
axillary temperatures are relatively unreliable in this regard, and rectal temperatures must be taken ( 1,26).
Victims of hypothermia are very sensitive metabolically, especially in their cardiovascular system. Therefore, they must
be handled very carefully and any unnecessary agitation must be avoided. As in any emergency, it is important to
maintain an airway for respiration. Rewarming should be carefully done. Various possible sources of heat for rewarming
may be considered, but the victim should not engage in vigorous exercise and should not be rubbed, massaged, or
immersed. If cardiopulmonary arrest occurs, cardiopulmonary resuscitation (CPR) should be initiated and continued until
the victim is revived or death is pronounced. CPR should never be stopped because the patient appears to be clinically
dead. This appearance is common in people who are hypothermic, and often the patient recovers. It is imperative that
anyone who has experienced cardiopulmonary arrest be transported to a medical facility as quickly as possible ( 1,26).
Specific Levels of Hypothermia
The individual experiencing mild hypothermia (RCT, 35° to 37°C) usually has a sensation of cold fingers and toes and
may develop chills and shivering. On a physiologic level, victims have an increased pulse rate and an increased
respiratory rate. They also may experience slight incoordination and a urinary urgency. Mild hypothermia is the most
common of all stages of hypothermia; it needs to be recognized because of the possibility of an increase in severity.
Individuals experiencing mild hypothermia should be placed in a shelter that will protect them from environmental factors.
Any wet clothing should be replaced with dry clothing. Some type of external heat source should be developed, such as a
fire. Efforts also should be made to avoid heat loss from the victim's body. When traveling or competing in groups, it is
important that the earliest signs of hypothermia be recognized and that all teammates participate in the treatment of the
victim.
Moderate hypothermia involves increased fatigue and loss of the shivering mechanism. There also is an increase in
muscular uncoordination. Victims have the potential to develop an altered mental state and also are not good historians
or reporters of their state. In addition, they experience numbing of the fingers and toes with actual functional loss. It is
important to recognize the development of moderate hypothermia. It must be suspected in any individual who
demonstrates decreased signs of shivering, slow reactions, or any other altered state of mental capacity. It should be
treated immediately. The victim should be warmed and protected from the environment. If there is alteration of the mental
state, the victim should not be given fluids or foods by mouth. If anything is given by mouth and the patient is not fully
awake, there is a risk of aspiration. Attention should be directed toward rewarming of the body core before the extremities
(1).
Severe hypothermia results in a complete loss of shivering, marked confusion, inappropriate behavior, and visual
disturbances. There also may be changing levels of consciousness. As the core body temperature continues to drop, and
especially if the RCT goes below 29.5°C (85°F), muscle rigor may develop. At the physiologic level, the victim's blood
pressure, pulse, and respiratory rate are depressed. Pulmonary edema may develop. Such an individual is in severe
danger of developing cardiac arrhythmias. If there is any sign of cardiorespiratory compromise, the victim needs to be
very closely monitored. The hypothermia (low body core temperature) may be somewhat protective, because the victim
may not require a high pulse or respiratory rate to support life. Indeed, if CPR is initiated before it is needed, an
arrhythmia may develop because of the fragile state of the cardiac muscle. The individual with severe hypothermia must
be monitored very closely and transported safely to a medical facility as quickly as possible ( 1,26).
Prevention
The prevention of hypothermia is of the utmost importance. Hypothermia can affect anyone who is exposed to a cold
environment, including competitive outdoor athletes, spectators, and recreational athletes. The human body cannot
acclimatize well to the cold environment. There is some degree of adjustment, but it varies greatly with physical condition,
overall health, nutrition, and age ( 25). Because hypothermia can represent a life-threatening situation, appropriate
measures should be undertaken to prevent its development. Some ways to prepare for outdoor exposure and prevent
hypothermia include appropriate preparation for the worst conditions, appropriate food supplements for the duration of
the outdoor exposure, appropriate fluid intake to avoid dehydration, appropriate clothing that may be placed in layers,
clothing that is windproof and well insulated and allows for water to evaporate, avoidance of becoming wet, avoidance of
alcoholic beverages, recognition of high-risk situations and individuals at risk, and use of common sense ( 1).
Nature provides a wonderful arena for athletic activities at all levels. However, outdoor environments can be dangerous.
It is important to be prepared to recognize any of the dangers that can cause injury. Those people who choose to
recreate or compete in potentially dangerously cold environments also need to know how to prepare themselves for this
participation and how to prevent both local and systemic injuries.
EFFECTS OF ALTITUDE ON THE ATHLETE
Athletic performance at increased altitudes first became important during the 1968 Olympic Games in Mexico City.
Exercise physiologists and athletes were concerned about the effect that an altitude of 2,237 m would have on
performance capabilities. Before that time, this was a concern only of mountaineers and other individuals who were doing
labor at altitude. It was known from the experience of mountaineers that certain types of tasks are difficult to perform at
higher altitudes, and the principal question was which events would be affected. Since 1968, there has been a continuing
growth of research into the effects of increased altitude on athletic performance. However, there are still many
unanswered questions, and there are many theories that are yet to be supported by well-organized research. This
section delves into the areas of physiologic considerations, acclimatization, the general altitude disorders, and the effects
of training and performance at altitude.
Physiologic Considerations
As altitude increases, there is a reduced availability of oxygen for the body to use. For example, at sea level the partial
pressure of oxygen is 159 mm Hg, but at 2,438 m it is only 118 mm Hg. The body experiences a restriction of the oxygen
delivery system that is believed be directly related to the decrease in total oxygen pressure and inversely related to
altitude.
The alteration in the availability of oxygen has direct effects on the pulmonary system that also lead to changes in the
acid-base balance in the body. At altitude there is an increase in the rate of pulmonary ventilation both at rest and during
exercising (27). The increased ventilatory rate is actually a compensatory mechanism. Because there is less oxygen
available with each breath, the individual must breathe more rapidly to obtain the necessary amount of oxygen in the
lung. This results in hyperventilation, which is similar to that seen at sea level. As a result of hyperventilation, carbon
dioxide is forced out of the alveoli and its concentration rises in the blood. The increased carbon dioxide delivery to the
blood raises the pH of the blood (respiratory alkalosis). The kidneys immediately compensate by removing excess
bicarbonate in an effort to normalize the pH of the blood. This leads to excretion of base and a decrease in the alkaline
reserve (11).
The effects of altitude on the cardiovascular system can be divided into immediate effects and long-term effects. The
immediate effects are an increase in submaximal heart rate and cardiac output. At altitude, stroke volume remains the
same or decreases slightly along with the maximal heart rate and cardiac output ( 28).
The long-term effects of altitude on the cardiovascular system include an increase in the submaximal heart rate and a
decrease in the stroke volume, maximal heart rate, and maximal cardiac output. The submaximal cardiac output also falls
to rates lower than those seen at sea level ( 28).
The hematopoietic system also is affected by exposure to altitude. A loss in plasma volume occurs on arrival at a high
altitude, but this is believed to be a transient response. There is also an increase in the number of red blood cells
circulating throughout the body. This is demonstrated by not only an increased hematocrit but also by increases in
hemoglobin and in the total red blood cell count. These latter changes allow the body to increase its oxygen-carrying
capacity within a fixed volume of blood ( 23,24,25,26,27,28,29 and 30).
At the local cellular level, research has indicated that there is an increase in the capillarization of the skeletal muscle.
This is associated with an increase in the red blood cell content of the organic phosphate 2,3-diphosphoglycerate, an
increase in the number of mitochondria within the cell, and an increase in the number of aerobic enzymes ( 11,29).
Acclimatization
Acclimatization can be defined as the adaptive responses that the body undertakes to improve its tolerance to altitude
hypoxia. For the individual involved in athletic competition at altitude, acclimatization requires not only physiologic but
psychological components. At a physiologic level, the athlete's body needs to respond with an increase in red blood cell
production and concentration and eventually an increase in total blood volume. The monitoring of red blood cell
concentration can be misleading, however, because immediate responses to altitude include hydration and loss of
plasma volume. The athlete's body also must adjust acutely by increasing pulmonary ventilation, which helps regain a
normal alveolar and arterial partial pressure of oxygen ( 27,31).
On a psychological level, the athlete must adjust to what has been termed competitive acclimatization. This simply means
that the athlete learns how to compete at high altitude. This encompasses both the physiologic adaptations and the idea
of actually being able to compete at altitude. Experience allows the athlete to determine the best strategies for his or her
own training and competition within a specific sport ( 11).
There is a great deal of variation among authorities regarding how long it takes to become totally acclimatized to altitude.
It is generally agreed that long-term acclimatization and total physiologic adaptation requires 6 to 8 weeks. A lot of the
short-term adaptations that can take place greatly depend on the specific altitude. For example, it is generally accepted
that exposure to altitudes up to 2,300 m may require up to 2 weeks for the body to become fairly acclimatized ( 29). It
would then require approximately 1 week more for each 610-m increase in altitude up to 4,572 m. Again, these are
general guidelines and do not refer to fully acclimatized physiologic adaptations.
For the athlete who will be soon competing at altitude, it is recommended that intense training start as soon as possible
after exposure to altitude and the period of acclimatization. Once the athlete is acclimatized, it is predicted that the
effects will last from 2 to 3 weeks after returning to sea level ( 29). Training at altitude for performance at sea level is
discussed later.
Altitude Disorders
No one, not even the highly trained athlete, is immune from illnesses that can develop secondary to rapid exposure to
high altitudes. The actual severity and onset of symptoms vary among individuals and with the specific altitude. The
symptoms that develop from altitude exposure are believed to be directly proportional to not only repeated descent but
also to the duration and degree of exertion. Furthermore, symptoms are inversely proportional to the amount of
acclimatization and physical conditioning ( 33,34). In general, the initial signs and symptoms felt by the individual who is
exposed to increased elevations are the result of hypoxia. This is a direct result of the physiologic response described
earlier. It should be noted that the symptoms of altitude exposure can be present even at elevations as low as 1,615 m.
The disorders that are most commonly associated with acute altitude exposure are acute mountain sickness (AMS),
high-altitude pulmonary edema (HAPE), and high-altitude cerebral edema (HACE).
Acute Mountain Sickness
AMS represents the mildest form of altitude disorder and can actually occur at almost any increased altitude. Most people
who go to a high altitude from sea level experience this type of disorder. Most commonly, there is a time lag of 6 to 96
hours between arrival at altitude and the onset of symptoms. The more common symptoms associated with AMS are
headaches, difficulty sleeping, dyspnea on exertion, loss of appetite, fatigue, lightheadedness, weakness, and sometimes
confusion and edema (11,35). If these symptoms are recognized and care is taken to keep the body well hydrated and
not overexerted, the individual can experience resolution after 72 hours ( 36). Many people experience AMS when
traveling, for example, from Texas to the mountains of Colorado to go skiing ( 35).
High-Altitude Pulmonary Edema
HAPE, a more severe disorder that can occur with exposure to higher altitudes, represents a noncardiac form of
pulmonary edema (37). HAPE occurs more commonly in children than in adults ( 35,36). Although symptoms vary in
severity, this is a dramatic form of altitude illness. The more common symptoms associated with HAPE are shortness of
breath, increased respiratory rate, irritating cough, and sometimes hemoptysis ( 36). In addition, the diagnosis is strongly
suspected when rales can be heard on auscultation of the chest ( 35,36).
Any athlete or individual suspected of having HAPE must be returned to a lower altitude as quickly and as safely as
possible and must be given oxygen when possible ( 36). If immediate descent is not possible, prudent use of nifedipine
may help by decreasing oxygen demands, but this treatment is controversial ( 31,37). Other medications that have been
used with varying success include furosemide, morphine, and nitroglycerine ( 37). Because HAPE is often seen with
reascent to a higher altitude, any individual who experiences HAPE must be thoroughly reevaluated before being allowed
to return to an increased altitude ( 11,31,38).
High-Altitude Cerebral Edema
Although it is uncommon, HACE is the most dangerous and serious form of altitude sickness. HACE has been reported at
altitudes as low as 2,438 m, but it is usually considered rare below 3,658 m. The relation between the development of
HAPE and HACE remains uncertain. Individuals who are developing HACE present initially, like all those with altitude
disorders, with the signs and symptoms of AMS (33). However, the individual with HACE experiences increasing severity
of headaches, often followed by confusion, forgetfulness, emotional instability, ataxia, hallucinations, motor weakness,
and reflex changes. This entity may progress to coma and death ( 36). Increased cerebral pressure and swelling of the
brain results in bradycardia on initial evaluation and leads to impaired judgment and coordination. As further swelling of
the brain—especially the cerebellum—occurs, various ocular signs such as blurring of vision, papilledema, and retinal
and vitreous hemorrhage may develop (36). As with HAPE, victims of HACE must be moved to a lower altitude as quickly
and safely as possible ( 36).
Other Concerns
At higher altitudes, the ambient temperature is low and exposure to ultraviolet light is high. Although these are not
considered to be direct altitude disorders, the individual who is competing or training under these conditions must
remember not only to protect the skin with appropriate sun block but also to protect the eyes, so as not to damage the
cornea and retina ( 11, 39).
Preparation and Prevention of Illness
Although there are no specific guarantees for the prevention of any type of altitude disorder, several guidelines have
been suggested for individuals who are planning to compete or recreate at increased altitudes. One of the keys to
minimizing the chance of developing AMS for the athlete is to compete within 24 hours after arrival at the altitude
destination. For example, if a team arrives in Boulder or Denver the night before competition, few athletes have difficulty
with the altitude. If this timing is not possible, they should try to allow at least 2 weeks for training at altitude. This allows
the fundamental physiologic adaptations to occur so that the athlete is able to compete effectively. Preparation for
athletic activities at high altitude should begin months before exposure and should include the development of a high
level of cardiovascular fitness. Although this may not be of concern to the highly trained athlete, it is important for the
recreational athlete.
Because of the acute loss of plasma volume and insensible water loss at altitude, it is necessary to drink lots of water or
a fluid-replacement drink. Studies have shown that high-carbohydrate meals should be eaten at high altitudes, because
they are easily digested, providing a high-energy source ( 11). Alcoholic beverages should be avoided because they
contribute to dehydration of the body.
Mountaineers have recognized that the use of acetazolamide, a carbonic anhydrase inhibitor, lessens the effects of
altitude (40). However, acetazolamide has several side effects, including tingling of the ears and mouth, and it should not
be taken by persons who have any history of cardiac illness. Acetazolamide also is considered to be a diuretic, and, as
such, it is banned from use by competitors in the Olympics and in many other international events.
Training and Performance
When training for events at altitude, the athlete must consider several factors. It is important, of course, to understand the
physiologic effects of altitude; however, the athlete must also be aware of the effects that altitude has on performance. In
general, events or competitions that require strength and flexibility are not affected by altitude. Events that involve skill
can be either negatively or positively affected by altitude exposure, depending on whether the activity involves a
high-endurance or a high-speed component ( 11). Many athletes whose events involve speed through the air, such as
sprinting or cycling, achieve better results at altitude because they are moving through a less dense atmosphere.
Swimmers do not experience this phenomenon, because water at altitude is the same density as it is at sea level. Athletic
events that require endurance are adversely affected by altitude because of the lower blood oxygen concentration and
the reduced atmospheric oxygen content. Therefore, altitude does not adversely affect anaerobic events, but the
decreased oxygen pressure does have a negative effect on aerobic activities. However, performance in endurance
events that do not involve running (e.g., bicycling, speed skating, Nordic skiing) may be improved, because the positive
aspects of decreased air resistance become more important than the negative effects of decreased oxygen availability
(29).
When training for events at altitude, the athlete must take appropriate measures to prevent altitude sickness. In addition,
the training program should be designed to counterbalance the negative effects of altitude on endurance. A prime
consideration is the amount of time that is available for training. If the athlete has less than 1 week available for
acclimatization, it is probably best to arrive at the event site just before competition. The ideal situation is to have several
weeks at altitude before the competition, which would allow time for acclimatization.
There has been much discussion and research concerning the benefits of training at altitude for an athletic event that will
occur at sea level ( 29). Much of the information, however, appears anecdotal and contradictory. Research does suggest
that altitude-trained athletes have the capability to perform better at sea level than equally trained athletes who train only
at sea level (30). The concept of “living high—training low” has been offered as an even better training regimen: the
cardiac and hematopoietic advantages still occur from living at higher altitude, while the dense air at lower altitudes
creates more resistance and thus a training advantage ( 29,30). An important consideration in altitude training for
sea-level events is the amount of time needed for training before the return to sea level. The athlete should probably train
at least 2 weeks at altitude to prepare for a sea-level event ( 29,30). It is important also to consider the effects of going
from a cooler and dryer atmosphere at altitude to a warmer and possibly humid environment at sea level. After the return
to sea level, the effects of training at altitude are usually lost within 2 or 3 weeks ( 26). In all cases, it should be
remembered that altitude training alone is not a substitute for hard work and appropriate levels of training.
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5 Biomechanics of Ligaments in Sports Medicine
BIOMECHANICS OF LIGAMENTS IN SPORTS MEDICINE

SAVIO L.-Y. WOO
MARK A. KNAUB
MARIA APRELEVA
Structure of Ligaments
Biomechanics of Ligaments of the Knee
Medial Collateral Ligament
Anterior Cruciate Ligament
Posterior Cruciate Ligament
Biomechanics of Ligaments of the Shoulder
Acromioclavicular Joint
Glenohumeral Joint
Biomechanics of Ligaments of the Ankle
Lateral Ankle Ligaments
Acknowledgments
Chapter References
The motion of the appendicular skeleton is powered by the muscles that cross the various synovial joints. In turn, these
joints are stabilized and guided by ligaments—bands of tough connective tissue that traverse the joints and help to limit
excessive displacements between the bones. Once thought of as inert, static structures designed solely to maintain
proper skeletal alignment, ligaments are now known to have many functions. Ligaments are subjected to a relatively low
level of forces during repetitive activities of daily living. However, during running, throwing, or jumping the loads can be
high, and loss of biomechanical integrity of the ligament may result. The high loads carried by the ligaments during
strenuous activity can cause acute ruptures or tears of the midsubstance of the ligament or an avulsion injury at the
insertion site.
Intense laboratory study has shown that ligaments, as well as tendons, exhibit complex and nonlinear load-elongation
behavior under uniaxial tensile loads. A more complete understanding of their biomechanical function can provide insight
into the mechanisms that cause ligament injury. Treatment of ligament injuries by immobilization and by controlled motion
has also been studied in the laboratory. These factors can have significant effects on outcome as well as on the design
of treatment and rehabilitation programs for patients with ligamentous injuries.
The goal of this chapter is to provide the reader with a basic understanding of the biomechanical properties of ligaments
and how ligaments contribute to the motions of various synovial joints of the body, specifically the knee, shoulder, and
ankle. The structure of ligaments and the basic concepts of biomechanics are described by using the medial collateral
ligament (MCL) of the knee as an example. The effects of age, stage of skeletal maturation, immobilization, and exercise
on the biomechanical properties of the MCL are covered. Major ligaments associated with the three synovial joints (i.e.,
knee, shoulder, and ankle) are presented in separate sections. In each section, a brief review of the anatomy is
presented, followed by a description of the tensile properties and functions of the ligaments. Afterward, injuries of
ligaments and current treatment options are described, together with biomechanical methods available to evaluate their
outcome. The information presented in this chapter is a useful reference for clinicians who diagnose, treat, and
rehabilitate patients with ligamentous injuries of the knee, shoulder, or ankle.
STRUCTURE OF LIGAMENTS
A ligament consists of a complex arrangement of extracellular matrix with randomly interspersed cellular elements. These
cells, called fibrocytes, are randomly embedded throughout the matrix and are responsible for extracellular matrix
production. The fibrocytes are also responsible for biologic adaptation to the mechanical environment, remodeling, and
healing of injured ligaments ( 1,2). The extracellular matrix is predominantly a network of fibrillar collagen structures
arranged parallel to the long axis of the ligament. The collagen network has an architectural hierarchy similar to that of
the tendon—beginning with tropocollagen as the basic molecular component, and systematically arranged into a
hierarchic structure of microfibrils, subfibrils, fibrils, and fibers ( Fig. 5.1) (3). This well organized, collagenous network is
responsible for the stiffness and strength of the ligament. Type I collagen is the major component of all ligament fibers;
collagen types III, V, VI, X, and XII exist in small amounts (1,4,5). Small amounts of glycoproteins (e.g., fibronectin) and
proteoglycans also exist as part of the extracellular matrix. The proteoglycans are hydrophilic and consequently play an
important role in the interaction with the collagen fibers to yield viscoelastic properties of the ligament. Elastin, a fibrillar
protein, present in small amounts, usually accounts for less than 1 of the dry weight, and contributes to the mechanical
properties of ligaments.
FIGURE 5.1. Ligament architectural hierarchy. (Adapted from Kastelic J, Galeski A, Baer E. The multicomposite structure
of a rat tail tendon. Connect Tissue Res 1978;6:11–23, with permission.)
The insertion of a ligament into bone represents a transition that is quite complex. Insertion sites are of particular
importance because an abrupt transition from soft to hard tissues can create large, localized stress concentrations under
applied tensile loads. Therefore, the transitional zones must be formed to minimize stress concentration. Two distinct
ligament insertion sites, referred to as direct and indirect, have been identified ( 6). Direct insertions are those in which
the fibers of the ligament insert directly into the bone. Morphologically, they can be divided into four distinct zones:
ligament fibers, uncalcified fibrocartilage, calcified fibrocartilage, and bone. An example of a direct insertion is the
femoral insertion of the MCL of the knee. Indirect insertions, such as the tibial insertion of the MCL, are those in which
the superficial fibers blend with the periosteum and the deep fibers insert obliquely into the bone with little or no
transitional zone. Indirect insertions can be found where ligaments cross the epiphyseal plate. During skeletal
maturation, remodeling of the interface of the deep fibers takes place regularly, as evidenced by the osteoclastic
activities, while the attachment of the superficial fibers to the periosteum is lengthened to allow for bone growth at the
epiphysis.
In most ligaments, a thin layer of tissue called “epiligament” covers the ligament ( 7). This layer is abundant in cells and
blood vessels and may be a major source of cells needed for remodeling and healing responses. Compared with other
connective tissues such as bone and skin, ligaments are poorly vascularized ( 7). Free nerve endings have been
discovered in ligaments ( 8). Activation of these nerve fibers, by an increase in ligament tension, leads to appropriate
muscular function so that the joint functions properly to prevent possible injury. From this finding, it is thought that
ligaments play an important role in proprioception.
BIOMECHANICS OF LIGAMENTS OF THE KNEE
The medial collateral (or tibial collateral) ligament of the knee is an extraarticular structure that attaches the tibia to the
femur (Fig. 5.2). It is an ideal ligament to study in the laboratory because of its accessibility, relatively uniform
cross-sectional area, and reasonable length-to-width ratio. Most importantly, it is able to heal after rupture. However,
what has been learned about ligaments from study of the MCL may not be completely applicable to other ligaments. In
the relaxed or unloaded state, the fibrillar components of the MCL are arranged in an undulating path (described as the
“crimp”) between origin and insertion.
FIGURE 5.2. Anterior view of a right knee joint. (Adapted from McGinty JB. Athletic training and sports medicine. Park
Ridge, IL: American Association of Orthopaedic Surgeons, 1991, with permission.)
Anatomy and Function of the Medial Collateral Ligament
The MCL originates from the medial epicondyle of the femur and inserts onto the anterolateral portion of the tibia, just
deep to the insertion of the pes anserinus tendons. The MCL can be divided into superficial and deep layers. The
superficial portion of the MCL is a distinct extracapsular structure that is considered to be in layer II of the supporting
structures of the medial side of the knee. The anterior fibers of the superficial portion of the MCL provide the primary
restraint to valgus knee stress and appear to become taut with knee flexion of 70 to 105 degrees. The deep MCL is
actually a thickening of the joint capsule and is referred to by some as the middle capsular ligament. Along with the joint
capsule itself, it is a component of layer III and contributes very little to the stability of the knee joint. The MCL and its
associated medial structures also act as secondary restraints, resisting anteroposterior translation.
Tensile Properties of Medial Collateral Ligament
One of the primary functions of ligaments is to resist tensile loads, thereby guiding joints through their physiologic range
of motion. It is common practice to measure the biomechanical properties of ligaments by uniaxial tensile tests. Because
of the limited length of the MCL, these tests should be done with the bones, or using the femur-MCL-tibia complex
(FMTC). Typically, a nonlinear, concave load-elongation curve that represents the structural properties of FMTC is
obtained (Fig. 5.3). Structural properties of ligaments are represented by parameters such as stiffness, ultimate load,
ultimate deformation, and energy absorbed to failure, which are defined as follows:
FIGURE 5.3. Load-elongation curve obtained from a test of a femur–medial collateral ligament–tibia complex (FMTC).
Stiffness (N per mm): The relationship between load and elongation measured as the slope of the linear portion of
the load-elongation curve.
Ultimate Load or Load at Failure (N): The highest load observed just before failure of the tissue during a tensile
test. In the literature, this parameter is sometimes erroneously referred to as “tensile strength.”
Ultimate Elongation (mm): The maximum length a tissue can be stretched from its initial unloaded length until
failure.
Energy Absorbed at Failure (N-mm): The entire area under the load-elongation curve.
This load-elongation curve results from the contributions of the substance of the ligament and the bony insertions. Two
regions of this curve must be distinguished. Initially, there is nonlinear region, referred to as the “toe” region. When
subjected to tensile loads, the MCL, like most soft tissues, exhibits a nonlinear load-elongation curve as well as a
time-dependent response. This nonlinear response is thought to be the result of progressive straightening and stretching
of an increasing number of fibers, in a process called recruitment ( 9). With increasing tensile load, increased stiffness is
seen, and eventually a “linear” region is reached where the slope of the curve is constant. Under these loads, ligaments
are stiff and can help to limit excessive displacement between the two bones. In this way the ligaments maintain joint
position and alignment when large muscle forces act on the joint.
From the same test, the quality of the MCL substance (i.e., its mechanical properties), as represented by a stress-strain
curve, can also be determined. The stress (s) in a ligament is defined as the load per unit of cross-sectional area of the
ligament substance. Accurate measurement of the cross-sectional area is very important and ensures that the tensile
stress values are correct. A laser micrometer system has been used to determine the cross-sectional area as well as the
shape of the midsubstance of the ligament ( 10). Strain (e), is defined as the change in length divided by the original
length. In addition, for the stress-strain curves to be valid in a uniaxial tensile test, the ligament must have a uniform
cross-section along its length and an adequate length-to-width ratio.
Similar in shape to the load-elongation curve, a nonlinear stress-strain curve for an MCL is shown in Figure 5.4.
Mechanical properties of the ligament are represented by parameters such as the modulus, tensile strength, ultimate
strain, and strain energy density, which can be obtained from the stress-strain curve and are defined as follows:
FIGURE 5.4. Stress-strain curve of ligament midsubstance obtained from a test of a femur–medial collateral
ligament–tibia complex (FMTC).
Modulus (N per mm2): The relationship between stress and strain measured as the slope of the linear portion of the
stress-strain curve.
Ultimate Tensile Stress, or Tensile Strength (N per mm 2): The maximum stress observed on the stress-strain curve
before failure of the tissue.
Ultimate Strain (%, mm per mm): The strain at failure of the ligament substance.
Strain Energy Density (MPa). The area under the stress-strain curve.
Ligaments also exhibit complex time- and history-dependent, viscoelastic behavior resulting from the interactions of
collagen, proteoglycan molecules, and water with the surrounding elastin and other ground substance ( 11,12). Therefore,
the paths of the load-elongation curve for the ligament during loading and unloading are different, forming what is known
as a hysteresis loop. The area enclosed by the hysteresis loop represents the internal energy loss between loading and
unloading (Fig. 5.5). Other important viscoelastic characteristics are stress relaxation, a decline in stress over time under
constant elongation ( Fig. 5.6), and creep, an increase in length over time under a constant load ( Fig. 5.7). Ligament
behavior depends on the previous loading history and the time during which the load is applied.
FIGURE 5.5. Hysteresis during cyclic loading of a knee ligament.
FIGURE 5.6. Schematic representation of stress-relaxation (decreasing stress over time under a constant elongation).
FIGURE 5.7. Schematic representation of creep (increasing deformation over time under a constant load).
During walking or jogging, ligaments experience repeated cyclic stretching ( 13). Elastic materials would normally
experience fatigue failure under these loading conditions—that is, application of repetitive loading would cause failure at
a much lower value than that required to cause failure from a single application of load. As a ligament undergoes many
cycles of loading and unloading in vivo, its cyclic relaxation behavior results in continuously decreasing stress ( Fig. 5.8).
This helps to protect the ligament from fatigue failure.
FIGURE 5.8. Schematic representation of cyclic creep in a medial collateral ligament of the knee.
Biologic Factors
There is profound variation in the properties of ligaments reported in the literature. Many biologic factors and
experimental procedures have been identified for these discrepancies. Specifically, biologic factors such as species,
skeletal maturation, age, biochemistry, immobilization, and exercise are well known. The following section discusses
some of these factors using the MCL of the knee as example.
For skeletally immature rabbits, failure of the FMTC during tensile testing occurred at the tibial insertion site, suggesting
that the tibial insertion site is the weakest link. On the other hand, in mature animals failures consistently occurred at the
ligament midsubstance (14). Furthermore, structural properties of the rabbit MCL showed a dramatic increase between 6
and 12 months of age, after which the differences between the age groups diminished up to age 4 years ( 15). Similar
trends were seen in mechanical properties of the MCL substance.
Other experiments have shown that immobilization of joints leads to significant decreases in ligament tensile properties
and to stiffening of the joints (16). Laros et al. found that immobilization of the canine FMTC for up to 12 weeks reduced
the ultimate load-to-body-weight ratio by approximately 27% compared with controls ( 17). Immobilization also led to bone
resorption and disruption of ligament fibers at the MCL tibial insertion site. In rabbits and rats, stiffness and ultimate load
of the FMTC were reduced by 25% to 33% after 4 to 9 weeks of immobilization ( 18,19). The reduction of structural
properties appeared to result from changes at the insertion sites, as well as in the ligament substance, because there
was a marked disruption of the deep fibers inserting into bone. Osteoclastic activity resulted in subperiosteal bone
resorption for the tibial insertion but little change to the femoral insertion. This resorption correlates with an increasing
occurrence of failure by tibial avulsion for the FMTC from immobilized knees.
Remobilization can reverse the deleterious effects of immobilization on the structural properties of the FMTC, but much
longer time periods are required. Experimentally, 18 weeks of remobilization were necessary to reverse the detrimental
effects of 6 weeks of immobilization on the structural properties of canine MCLs ( 17). Studies from our research center on
the effects of a 9-week immobilization period revealed that, histologically, the tibial insertion of the rabbit MCL was not
reestablished until after 52 weeks of remobilization ( 20). These data imply that, clinically, after a period of immobilization,
caution must be exercised for an extended period to limit the risk of subsequent injury.
Exercise can enhance the structural properties of ligaments (e.g., stiffness, ultimate load) by about 10% to 20% ( 21).
Tipton et al. demonstrated a 10% increase in both FMTC ultimate load and the ratio of ultimate load to body weight and a
20% increase in the energy absorbed at failure in rats that had undergone 10 weeks of treadmill training ( 22). Figure 5.9
represents our view on tissue homeostasis, that is, the effects of immobilization and exercise and their relation to mass
and tissue properties of ligaments. Immobilization significantly compromises both the structural properties of the
bone-ligament-bone complex and the mechanical properties of the ligament, with weakening being more pronounced at
the insertion sites. The mechanical properties of the ligament substance return to control levels after a relatively short
period of remobilization, but the insertions require a much longer period of recovery to regain their previous stiffness and
strength. Therefore, the complex remains weak, and avulsion injuries are more likely during this interval. The gains in
these properties resulting from exercise or increased stress are not markedly large; only moderate improvements of the
properties are seen. Therefore, a nonlinear relationship exists between the stress and strain duration and mechanical
properties of a ligament (Fig. 5.9).
FIGURE 5.9. Schematic diagram illustrating ligament homeostasis secondary to stress and motion. (From Woo S L-Y,
Chan SS, Yamaji T. Biomechanics of knee ligament healing, repair and reconstruction. J Biomech 1997;30:431–439, with
permission.)
Injury, Healing Response, and Treatment Options
Fetto and others reported that the MCL is the most frequently injured ligament of the knee and accounts for 55% of all
acute knee injuries (23,24). Most isolated MCL injuries occur during sports activities such as football, soccer, baseball,
and skiing.
The term healing refers to tissue repair after injury. The potential for healing varies greatly and depends mainly on the
blood supply and the metabolic rate of the involved tissue. Although skin and bone, with some limitations, heal relatively
quickly and predictably, ligaments are believed to have slow and limited healing potential ( 1). Ideal healing would lead to
complete restoration of the original tissue with identical morphologic and functional characteristics, but ligaments have
been shown to heal with qualities that are inferior to those of the original tissue. The healing of ligaments follows a
predictable pattern, which occurs in three specific phases ( 7).
Hemorrhage or Inflammatory Phase. This phase is characterized by formation of a blood clot within the damaged
region and the invasion of polymorphonuclear cells and monocytes/macrophages. The monocytes remove debris
and attract granulation tissue–producing reparative cells.
Proliferative Phase. In this phase, new blood vessels are formed while fibroblasts are recruited from the local
environment or circulation to produce new matrix material (mainly collagen).
Remodeling Phase. This phase starts within weeks after the injury and can last up to several years. It is
characterized by a progressive maturation of collagen fibers, which align in a longitudinal orientation in response to
loads applied to the ligament.
Investigators have documented that injuries of the MCL can heal with resulting structural properties of the FMTC equal to
or almost equal to those of the normal ligament, thus providing the needed function for the involved joint ( 25,26 and 27).
Other ligaments, such as the cruciate ligaments of the knee, heal with diminished strength or do not heal at all, often
resulting in increased joint laxity. In isolated ruptures of the MCL, the ligament healed macroscopically without any
surgical intervention within 6 weeks ( 26,28). Compared with the preinjury state, the cross-sectional area of the healed
ligament was larger at 6 to 12 weeks and slowly continued to increase with time to reach structural properties of the
normal ligament (29). Even though the structural properties of the FMTC may return to almost normal values, the
mechanical properties of the healing MCL always remain inferior when compared with normal tissue ( Fig. 5.10). This
occurs because the healing tissues increase in mass to compensate for inferior quality. In some studies, the
cross-sectional area of the healed MCL was up to 2.5 times larger than that of controls after 52 weeks ( 30). When severe
joint laxity is associated with the ligament injury, such as in a combined injury to the MCL and anterior cruciate ligament
(ACL) of the knee, the quality of the healed tissue (i.e., its mechanical properties) is even worse and the increase in
cross-sectional area is even more pronounced ( 31,32).
FIGURE 5.10. Healed medial collateral ligament (MCL) exhibits inferior mechanical properties when compared with the
intact state. A: Load-elongation curve for MCL. B: Stress-strain curve for femur-MCL-tibia complex.
Histologically, healed MCL tissue differs from normal in three regards. First, the collagen fibers are more disorganized,
with more random pattern and more defects between them, and the number of larger-diameter collagen fibrils is reduced
(33,34). Second, the cell density and vascularity of the tissue are also increased, suggesting that metabolic rates are
higher than normal (35). It takes time for the vascularity of the ligament to diminish and even longer for the fibers to orient
in the direction of applied physiologic stresses. Finally, there are no fibrils with large diameters, and it takes up to 2 years
before a small population is observed. This lack of large-diameter collagen fibrils in the healing MCL is important
because greater stiffness and strength of the tissue are associated with the larger-diameter fibrils ( 36).
Biochemical analysis of healing MCLs revealed that although the collagen content of the tissue returns to nearly normal
within 12 to 14 weeks, collagen cross-links remain at less than 50% of normal MCL up to 1 year after injury ( 26,29,37).
Further, the amount of type I collagen is reduced in favor of minor collagen types, and the size of the proteoglycan
molecules is increased ( 35).
Clinical protocols for MCL injuries have evolved from the aggressive surgical treatment of most MCL tears to the current
emphasis on nonoperative treatment for most of these injuries. This change has been a result of studies in experimental
animals. Nevertheless, laboratory studies continue to evolve, because there are three major variables that affect the
healing response of ligaments: nonrepair versus surgical repair, immobilization versus early motion, and biologic
manipulations such as the use of growth factors.
Using the MCLs of dogs and rabbits as a model, the effects of surgical repair of ligaments was compared with those of
conservative treatment. A long-term study failed to demonstrate a benefit from suture repair compared with conservative
treatment (25,26). The MCL had macroscopically healed after 12 weeks; varus-valgus knee laxity was slightly increased
initially and returned to normal after 1 year. Structural properties of the FMTC, such as stiffness and ultimate load, were
slightly diminished even at 1 year. Mechanical properties of the healed MCL remained at about 50% of normal, indicating
that the tissue quality remained below normal ( 26). Further, in a more severe injury model (in which both MCL and ACL
were injured), surgical repair of the MCL improved structural properties in the early phase ( 31,38) but the long-term
results did not show clinical benefit from initial repair of the MCL ( 38).
Although immobilization has often been used in combination with ligament repair to protect the tissue from damage
during the early stages of healing, its deleterious side effects, including increased joint stiffness, proliferation of fibrofatty
connective tissue, and synovial adhesions, are well known ( 16,20). Studies in our research center as well as others have
revealed that ligaments regain a higher strength after rupture when treated with passive motion instead of immobilization
(39,40). Clinical studies also suggest that well-controlled protocols including early mobilization and more aggressive
rehabilitation are effective in restoring joint motion without compromising stability ( 41,42).
Because restoration of normal tissue quality in ligament healing has yet to be accomplished under usual circumstances,
several biologic approaches to enhance the quality of the healing tissue have been investigated, including cell
manipulations by cytokines. Cell migration and proliferation, as well as protein and collagen synthesis, are essential
characteristics of the tissue's healing response. Endogenous growth factors that are released by inflammatory cells can
act as mediators of the healing response. Growth factors such as epidermal growth factor (EGF), platelet-derived growth
factor (PDGF), and transforming growth factor-b1 (TGF-b1) have been evaluated both in vitro and in vivo as to their effect
of ligament healing with variable results ( 43,44 and 45). We found that EGF and PDGF increase fibroblast proliferation in
vitro, whereas TGF-b1 increases protein synthesis ( 46,47). When these growth factors were combined and tested in an in
vivo model, the structural properties of the healing rabbit FMTC and the mechanical properties of the healing MCL
appeared to be enhanced (48). Longer-term studies are ongoing.
Advances in the fields of molecular and cell biology have led to the development of novel techniques for the delivery and
production of both cells and growth factor proteins at sites of ligament injury. Biodegradable scaffolds that act to deliver
both cellular elements (fibrocytes, mesenchymal stem cells) and humoral elements (growth factor proteins) to injured soft
tissues are being developed and evaluated. Genetic manipulation of cells via ex vivo and in vivo gene transfer
techniques is also being investigated. Issues such as cell viability and regulation of growth factor protein gene
expression remain problematic and are the focus of intense laboratory study.
Anatomy and Function of the Anterior Cruciate Ligament
The ACL of the knee is an intraarticular, extrasynovial structure that crosses the knee joint from the medial aspect of the
lateral femoral condyle to the anterior aspect of the middle portion of the tibial plateau ( Fig. 5.2). The enveloping synovial
membrane is thought to protect the ligament substance from the harsh environment created by the synovial fluid. The
fascicular structure of the ACL allows for separation of the ligament into two “bands” ( 49). These have been described by
many investigators as the anteromedial (AM) and posterolateral (PL) bundles, referencing the anatomic positions of the
fascicular attachments of the tibial insertion ( 50,51,52 and 53). Several investigators have reported a functional difference
between the bundles, noting that the AM bundle is taut in flexion while the PL bundle is taut in extension. The
morphology and geometry of the tibial and femoral insertion sites of the ACL have also been studied. The insertions of
the ACL have been described as morphologically similar to the femoral insertion of the MCL, passing through four zones
before inserting directly into bone ( 54). Studies investigating the details of the femoral and tibial insertion sites revealed
that both are relatively planar, with the femoral insertion being more semicircular and the tibial insertion more oval
(53,55,56). However, the cross-sectional area of either insertion was 3.5 times greater than that of the midsubstance of
the ACL.
Tensile Properties of the Anterior Cruciate Ligament
The structural properties of femur-ACL-tibia complexes (FATCs) have been characterized by several investigators
(57,58,59 and 60). To assess the effects of specimen orientation with respect to specimen age on the structural
properties of the human FATC, Woo et al. performed tensile testing with paired specimens in which the tensile load was
applied along the axis of the ACL with preservation of the normal anatomic angles of ACL insertion (anatomic orientation)
in one knee, while the tensile load in the other knee was applied along the long axis of the tibia (tibial orientation) ( 60).
Young specimens (age 22 to 35 years) tested in the anatomic orientation were found to have higher stiffness (mean ±
SD, 242 ± 28 N per mm) than those tested in the tibial orientation (218 ± 27 N per mm). The ultimate load of the young
specimens in anatomic orientation was 2,160 ± 157 N, significantly greater than that of the specimens with tibial
orientation (1,602 ± 167 N). There was also a significant decrease in stiffness and ultimate load as donor age increased,
regardless of specimen orientation. Testing of the FATC along the anatomic axis of the ACL, maintaining the anatomic
insertion angles, allows a greater portion of the fibers of the ACL to be loaded equally during tensile testing. This is
substantiated by the higher values of ultimate load and linear stiffness for specimens tested in the anatomic orientation.
To determine the mechanical properties of the human ACL, early investigators tested the ligament by removing the
specimen from its bony attachments. This approach induced premature specimen failure at the ligament-clamp interface
due to the destructive forces generated by the clamps. For this reason, most investigators began using FATCs, in which
the insertions remain intact; this provided smooth load transmission from bone to ligament. Uniform application of force to
all of the fibers of the intact ACL is extremely difficult because of the complex arrangement of fibers within the ligament
substance. Therefore, some investigators have divided the ligament into bundles and tested them individually ( 61,62).
Separating the ligament into smaller bundles allows for a more parallel orientation of the fibers in the individual units and
a more uniform orientation of the fibers inserting into bone. In this manner, the tensile stress across the fibers is more
evenly distributed, increasing the reliability of the measurements of mechanical properties. Newton et al. separated the
AM and PL bundles of the ACL with a common tibial bone block and individual femoral bone blocks, and then performed
tensile testing on the AM bundle only ( 62). They found that the modulus of the AM bundle was 420 ± 70 MPa. Butler et al.
tested individual units from human FATCs and found that the average modulus of all units was 278 MPa and the ultimate
tensile strength was 35 MPa (61). The same group later reported nonuniform properties among bundles within the ACL.
The AM and PL bundles exhibited larger modulus, ultimate stress, and strain energy density values than the posterior
bundle of the ACL did, with no significant differences found between the two anterior bundles ( 63).
Function of the Anterior Cruciate Ligament
A complete understanding of the contribution of the ACL to normal knee function is needed to appreciate the function of
the ACL, the mechanisms involved in its injury, and the basis for ACL reconstruction. It is generally accepted that the
ACL resists anterior translation of the tibia with respect to the femur. The ACL also helps to limit hyperextension ( 53,64).
With the knee fully extended, the ACL contributes to the rotational stability of the knee, resisting both internal and
external rotation of the tibia. As the knee is brought into flexion, it resists internal rotation only ( 53,64,65 and 66). The
ACL also controls valgus rotation of the tibia, even more so than the MCL, when five degrees of freedom (DOF) motion of
the tibia are measured (29). Piziali et al. found that the ACL also plays a minor role in resisting medial displacement of
the tibia (66).
Early studies on the function of the ACL applied constant forces to the tibia and measured anterior translation of the tibia
with respect to the femur before and after sectioning of the ACL ( 67,68,69,70 and 71). More recently, quantitative
assessment of the force carried by the ACL in response to applied loads has gained significant attention ( 72,73,74 and
75). Approaches developed to examine the forces in the ligament include direct methods, which require contact with the
ligament (e.g., the use of buckle transducers and implantable transducers), and noncontact methods that use strain
gauges placed near the ligament insertion site, kinematic linkage systems, in-line external force transducers, or load cells
implanted in the subchondral bone at the ligament insertion sites ( 72,73 and 74,76,77,78,79,80,81 and 82).
We have employed a robotic/universal force moment sensor (UFS) testing system that consists of a six-DOF robotic
manipulator with a UFS mounted to the end effector of the robot ( 83,84 and 85). This testing system enables accurate
determination of multiple-DOF knee kinematics as well as direct measurement of the in situ force in a ligament without
physical contact with the ligament. In addition, no significant dissection of the joint is necessary. The robotic manipulator
is a position (or displacement) control device that records and reproduces positions in three-dimensional space ( 85). In
combination with the UFS, which records three forces and three moments, the robotic/UFS testing system is also capable
of operating under a force (or load) control mode—that is, the testing system can apply a force or moment with specified
direction and magnitude.
To investigate the kinematics of intact and ACL-deficient knees and the in situ force in the intact ACL in response to
externally applied loads, the end effector of the robot applies an external load to the intact knee at a chosen flexion angle
while the position of the intact knee in space is recorded. The ACL is then transected and the robotic manipulator, in
position control mode, reproduces the previously recorded position of the intact knee while the UFS records the force. By
the principle of superposition, the vector difference in forces measured by the UFS before and after removal of the ACL
represents the in situ force of the ACL (84,85 and 86). With this approach, the in situ force in multiple ligaments, under
multiple loading conditions, can be studied in the same specimen, thus minimizing interspecimen variations. The changes
in kinematics of the ACL-deficient knee can then be measured by applying the same external load to the specimen. In
this respect, the robotic/UFS testing system mimics clinical examination maneuvers, such as the Lachman and pivot-shift
tests, that rely on the detection of abnormal kinematics in response to external loads to make the diagnosis of ACL
deficiency.
Studies at our research center have examined the in situ forces in human ACLs as well as the force distribution between
the AM and PL bundles of the ligament in response to applied anterior tibial load as a function of knee flexion ( 87). In the
intact knee, anterior tibial translation in response to a 110-N anterior tibial load was greatest at 60 degrees of knee
flexion and least at full extension. The magnitude of in situ force in the ACL was at a minimum at 90 degrees of flexion
(71 ± 30 N) and greatest at 15 degrees of flexion (111 ± 15 N). The in situ force in the AM bundle of the ACL in response
to an anterior tibial load did not change significantly with respect to knee flexion angle, but that in the PL bundle followed
the trend of the whole ACL and increased as the knee neared full extension. In fact, with the knee flexion angle at less
than 30 degrees, the in situ force in the PL bundle was greater than that in the AM bundle. The results imply that each
bundle of the ACL plays a separate but equally important role in the complex function of the ACL. Specifically, the PL
bundle of the ACL probably plays an important role in knee stability when the knee is in less than 30 degrees of flexion.
Therefore, restoration of normal knee function with ACL reconstruction may necessitate attention to the contribution of
both bundles of the ligament.
An advantage of the robotic/UFS testing system is its ability to apply multiple external loads, mimicking clinical
examinations that are used to diagnose injuries of the ACL. In one study, the clinical pivot shift test was simulated using a
combined internal tibial torque and valgus torque. In the ACL-deficient knee, there were significant increases in anterior
tibial translation of 103%, 61%, and 32%, when compared with the intact knee, at full extension, 15 degrees, and 30
degrees of flexion, respectively ( 88). These results suggest that the ACL functions to restrain anterior tibial loads as well
as internal tibial torques, especially when the knee is in near-full extension.
Another factor to consider when performing functional tests is the application of muscle loads and their effect on the knee
kinematics and in situ forces in the ACL. The robotics/UFS testing system was used to evaluate the effect of quadriceps
and hamstring muscle loads on the kinematics and in situ force in the ACL (89). It was determined that the addition of an
antagonist hamstring load (80 N) to a quadriceps load (200 N) significantly reduced both the anterior tibial translation
and the internal tibial rotation. Specifically, between 15 and 60 degrees of knee flexion, both movements were
significantly reduced. Accordingly, these muscle loads also reduced the in situ force of the ACL between those angles.
This work suggests that rehabilitation of the hamstring musculature may play an important role in maximizing outcome
after ACL reconstruction.
Injuries and Treatment Options
The incidence of acute ACL tears is estimated at 1 in 3,000 in the general population of the United States ( 90), while that
in certain populations, such as competitive football, skiing, and soccer athletes, is even higher ( 91,92,93 and 94). It has
been reported that 70% of all acute ACL injuries are sports related, involving both recreational and competitive athletes
(95,96). Athletes who injure the ACL often experience knee instability that prevents continued participation in sports.
Those who are fortunate enough to return to sporting activities often do not return to their previous level of participation.
Earlier reports detailed the natural sequelae of ACL injury, the clinical outcome of nonsurgical treatment, and the benefits
of various reconstructive techniques ( 97,98). Despite the good results of conservative, nonsurgical management of
ACL-deficient knees documented by some authors, most have reported that chronic ACL deficiency results in significant
knee instability, secondary damage to other knee structures (e.g., menisci, articular cartilage, collateral ligaments), and
the possibility of early onset of degenerative joint disease ( 99,100,101,102,103,104,105,106 and 107). Surgery to restore
the function of the intact ACL is recommended in most patients in an attempt to avoid these potential long-term
complications.
Biomechanics of Anterior Cruciate Ligament Reconstruction
ACL reconstruction is a complex issue that requires an understanding of many biomechanical factors. A graft with
biomechanical properties similar to those of the native ACL is but one piece of the puzzle. Other issues, such as graft
fixation and restoration of normal knee kinematics and in situ forces in the graft, are likely to be as important for good
long-term results after ACL reconstruction surgery.
Graft Selection
Evaluation of the biomechanical properties of graft materials by tensile testing has been a subject of intense laboratory
research. Table 5.1 summarizes structural properties, specifically stiffness and ultimate load, for the normal ACL, the
bone–patellar tendon–bone (BPTB) grafts, and various hamstring graft constructs as reported in selected literature
(60,108,109 and 110). Careful examination of the data reveals that there are differences in specimen type and testing
methods that have profound effects on the results. Currently, most surgeons choose either BPTB or hamstring grafts for
primary ACL reconstruction. An advantage of the BPTB construct is the presence of bone blocks on each end of the
graft. This allows for earlier bone-to-bone healing within the bone tunnel and contributes to initial stability of the graft
(111). The bone blocks of the BPTB constructs also contribute to its superior stiffness and strength. The ultimate load of
a 10-mm BPTB graft is equivalent to that of the normal ACL ( 60). Proponents of hamstring tendon grafts believe that
donor site morbidity associated with the use of autogenous BPTB grafts is reduced. The stiffness and ultimate load of
double-loop hamstring grafts are, in recent studies, greater than those of BPTB grafts. Nevertheless, problems
associated with tendon fixation in the bone tunnel and relatively slow bone-tendon healing in the tunnel are potential
concerns (112,113,114 and 115). Multiple-loop hamstring grafts generally have larger cross-sectional areas and,
therefore, fill the bone tunnel more completely. This increases the surface area in which bone-tunnel healing can take
place and possibly enhances the healing process. Use of grafts with multiple strands also allows for tensioning of each
strand of the graft at a different flexion angle in an attempt to accurately reproduce the AM and PL bundles of the intact
ACL.
TABLE 5.1. STIFFNESS AND ULTIMATE LOAD VALUES FOR THE NORMAL ANTERIOR CRUCIATE LIGAMENT
(ACL) AND VARIOUS ACL REPLACEMENT GRAFTS
Graft selection for ACL reconstruction surgery remains a highly debated issue. Clinicians must take into account all of the
biomechanical data available as well as the potential complications of each type of graft. Ultimately, well-designed,
randomized, prospective studies comparing BPTB grafts and double-strand hamstring grafts are needed to assess which
type has more favorable long-term results.
Graft Fixation
It has been postulated that the graft-fixation construct should be stiff enough to resist the tensile forces that the graft will
encounter, so that the relative motion between the graft and the bone tunnel is minimized to facilitate graft-tunnel healing.
Uniaxial tensile tests and cyclic loading experiments have been used to investigate the stiffness, ultimate load, and
viscoelastic behavior of graft-fixation constructs. Motion of the graft within the tunnel may also have a significant effect on
the healing potential for various fixation constructs.
Investigators have studied the initial stiffness and ultimate load of various ACL replacement grafts and graft-fixation
constructs. Graft materials investigated include the central third of the BPTB, single-strand gracilis or semitendinosus,
double-strand gracilis or semitendinosus, triple-strand hamstring grafts, and quadruple-strand hamstring grafts. These
graft materials were fixed with devices such as cancellous screws, metal and biodegradable interference screws,
suture-button and suture-post constructs, staples, press-fit technique, and soft tissue washers. Table 5.2 provides a
summary of the data available for stiffness and ultimate load of BPTB grafts fixed with various devices. Kurosaka et al.
compared BPTB grafts fixed with a 6.5-mm cancellous screw to similar grafts fixed with a 9.0-mm interference screw in
young cadaveric knees (116). The stiffness (57.9 ± 3.9 N per mm) and ultimate load (475.8 ± 110.9 N) for the 9.0-mm
interference screw were significantly higher than for the 6.5-mm cancellous screw (36.2 ± 2.9 N per mm and 208.0 ± 27.5
N, respectively) (116). Advances in biomaterials research have resulted in the production of interference screws made of
biodegradable materials. Potential advantages to these screws are that their use will produce less distortion on
postoperative magnetic resonance imaging scans and may eliminate the need for hardware removal once the graft is
healed within the tunnel. Several investigators have compared the stiffness and ultimate load of BPTB grafts fixed with
titanium versus biodegradable interference screws ( 117,118). In general, the stiffness and ultimate load of BPTB grafts
fixed with biodegradable screws are similar to those of grafts fixed with titanium screws, but the data depend on the
thread height of the screws (118). From this finding it was suggested that the design of the screw may be more important
than the material from which it is made.
TABLE 5.2. STIFFNESS AND ULTIMATE LOAD OF BONE–PATELLAR TENDON–BONE GRAFTS FIXED WITH
VARIOUS FIXATION DEVICES
Fixation of soft tissue replacement grafts that lack bone blocks, such as semitendinosus, gracilis, quadriceps, and
Achilles tendon grafts, have presented a challenge with respect to adequate stiffness and ultimate load of the
graft-fixation construct. Available data on the ultimate load and stiffness of various hamstring grafts and soft tissue
fixation methods are summarized in Table 5.3. Fixation of a double-loop semitendinosus-gracilis graft with soft tissue
washers provided relatively high stiffness (29 ± 7 N per mm) and ultimate load (821 ± 219 N) ( 119).
TABLE 5.3. STIFFNESS AND ULTIMATE LOAD OF HAMSTRING GRAFTS SECURED WITH VARIOUS FIXATION
TECHNIQUES IN HUMAN SPECIMENS
The use of interference screws for fixation of hamstring grafts has also been considered. Concerns for this method
include a decrease in stiffness and strength of fixation, a decrease in bone-tendon contact area for healing, and the
potential for damaging the graft. Several groups have compared the initial stiffness and ultimate load of various
hamstring grafts fixed with titanium versus biodegradable interference screws ( 118,121,122 and 123). In general, there
were no significant differences in ultimate load. Additional comparisons showed that the stiffness and ultimate load of soft
tissue grafts were less than those of BPTB grafts fixed with the same interference screw. Simonian et al. compared
placement of the interference screw centrally (i.e., in the middle of the loops of double-loop semitendinosus-gracilis
grafts) to eccentric placement of the screw and found no difference in ultimate load (245 ± 61 and 265 ± 48 N,
respectively) ( 123). Nevertheless, central placement of the screw increases the bone-tendon contact area, which may
enhance bone-to-tendon healing.
The viscoelastic behavior of graft fixation constructs plays a role in the healing of the graft within the bone tunnel. In our
research center, cyclic loading of a double-loop semitendinous and gracilis hamstring graft fixed with a titanium
button–polyester tape device was performed to examine the motion between the graft and the osseous tunnel ( 124).
Significant graft tunnel motion, ranging from 0.7 to 3.3 mm, occurred during a loading range of 50 to 300 N. This motion,
occurring at the proximal fixation site (button-polyester tape), represented approximately 90% of the total elongation of
the graft-fixation construct. Therefore, this technique for hamstring fixation results in a large amount of motion of the graft
within the tunnel and could potentially interfere with bone-tendon healing within the tunnel.
Current methods of both BPTB and soft tissue graft fixation do not adequately reproduce the stiffness and ultimate load
of the intact ACL. A graft fixation construct that is too stiff may limit full range of motion in the ACL-reconstructed knee,
whereas inadequate stiffness of the graft fixation construct may fail to stabilize the knee, leading to compromised results.
Inability to reproduce the ultimate load of the intact ACL may lead to catastrophic loss of fixation if the reconstructed knee
is subjected to a traumatic event before graft-tunnel healing is complete. Few studies report the behavior of graft-fixation
constructs subjected to cyclic loading. Further work in this area will allow for an understanding of how grafts and
graft-fixation constructs behave when subjected to the repetitive, low-intensity loads encountered during rehabilitation.
Functional Testing of Anterior Cruciate Ligament Reconstructions
The robotic/UFS testing system can be used to obtain the kinematics of the ACL-reconstructed knee and the in situ force
in the ACL replacement graft. Kinematics of the intact knee and the in situ force in the intact ACL are determined as
described previously. Briefly, an ACL-reconstructed knee is tested on the robotic/UFS testing system in response to
external loads, and the kinematics of the ACL-reconstructed knee are recorded. The graft is released, and the robotic
manipulator reproduces the previously recorded motions of ACL-reconstructed knee. The vector difference of the forces
recorded by the UFS before and after release of the replacement graft represents the in situ force in the ACL
replacement graft. The kinematics of the ACL-reconstructed knee in response to external loads are also measured and
can be compared with those of the intact knee.
Using this method, the variables of the ACL reconstruction can be evaluated under applied loads. The effects of distal,
central, and proximal (anatomic) tibial tunnel fixation were evaluated in the porcine model by the robotic/UFS testing
system (125). In this study, the site of graft fixation in the tibial tunnel was found to have a significant effect on the
kinematics of the ACL-reconstructed knee. Proximal (anatomic) fixation produced the most stable reconstructed knee.
Increases in anterior tibial translation and internal tibial rotation were noted as the tibial fixation was moved distally. In
situ forces in the replacement graft were highest when proximal fixation was employed. Therefore, proximal graft fixation
in the tibial tunnel may be the best choice, because the results were closer to those of the intact knee.
The biomechanical relationships of the intact and reconstructed ACL and the medial meniscus have been defined with
the use of the robotic/UFS testing system. Deficiency of the ACL results in increased in situ forces in the medial meniscus
when the knee is subjected to an anterior tibial load ( 126). This may help explain the high incidence of medial meniscus
tears in chronic ACL-deficient knees. In addition, absence of the medial meniscus in an ACL-reconstructed knee results
in an increase in the in situ forces encountered by the ACL replacement graft ( 127). The increased forces encountered by
the ACL replacement graft in the medial meniscus–deficient ACL-reconstructed knee may account for the increased
incidence of graft failure in meniscus-deficient knees. The effects of medial meniscus transplantation on knee kinematics
and in situ forces in the intact ACL and in ACL replacement grafts are currently being evaluated. The robotic/UFS testing
system is also being used to directly compare BPTB and double-loop hamstring grafts in human cadaveric knees. A
reconstruction using each type of graft will be performed in the same specimen, allowing for direct comparison of the two
graft types. The kinematics and in situ forces in the replacement grafts in response to both an anterior tibial load and a
simulated pivot-shift test will be compared. The results of this study will contribute further information to the ongoing
debate concerning graft choice for primary ACL reconstruction.
Anatomy and Function of the Posterior Cruciate Ligament
The posterior cruciate ligament (PCL) of the knee originates from the lateral surface of the medial femoral condyle and
inserts on the posterior aspect of the tibial plateau ( Fig. 5.2). Like the ACL, the PCL is an intraarticular but extrasynovial
structure. The PCL is oriented almost vertically when the knee is extended and becomes more horizontal as the knee is
flexed. Based on anatomy, the PCL has been divided into two “bundles,” anterolateral (AL) and posteromedial (PM), each
with distinct insertions onto the tibia ( 128). The nomenclature used refers to the anatomic location from femoral origin to
tibial insertion ( 53). These bundles have been shown to possess unique anatomic and biomechanical properties, as well
as specific geometry at the bony insertions. Functionally, the AL and PM bundles have different patterns of tension,
depending on the angle of knee flexion. The AL bundle shows increasing tension with increasing knee flexion, while
tension in the PM bundle decreases ( 128). The anterior and posterior meniscofemoral ligaments (MFL), known
respectively as the ligaments of Humphrey and Weisburg, originate from the lateral meniscus and insert anteriorly and
posteriorly to the PCL on the medial femoral condyle; they are also considered to be part of the PCL complex. The
presence of these ligaments is variable, with some knees having one, both, or none. The importance of the MFLs has not
been well characterized, but their reasonably high stiffness and strength properties suggest that they aid in stabilization
of the lateral meniscus (129).
In our research center, the geometry of the PCL, including the shape and size of the ligament and its insertion sites, was
studied in detail ( 55,128,130). The AL bundle was found to be two times larger in cross-sectional area than the PM
bundle (128,131). The mean total cross-sectional area of the MFLs was approximately 22% of the entire PCL. The
femoral and tibial insertion sites of the PCL were complex and were three times larger than the midsubstance of the PCL.
The femoral insertion was typically shaped like a half-moon, whereas the tibial insertion was rectangular in configuration
(130).
Anatomically, the posterolateral structures of the knee (PLS) are not components of the PCL, but functionally they have
been shown to interact with the PCL to provide posterior knee stability and resistance to external tibial rotations
(132,133,134 and 135). There are two major components of the PLS: the lateral collateral ligament and the popliteus
complex, which includes the popliteus muscle-tendon unit, the popliteofibular ligament, and various popliteotibial and
popliteomeniscal fascicles ( 136,137,138 and 139).
Tensile Properties of the Posterior Cruciate Ligament
The tensile properties of the human PCL have been investigated by several authors ( 57,130,131,140). When the
femur-PCL-tibia complex (FPTC) from cadaveric knees was tested with the knee at 45 degrees, the linear stiffness was
204 ± 49 N per mm and the ultimate load was 1,627 ± 491 N (140). In our research center, the structural properties of the
AL and PM bundles of the PCL and the meniscofemoral ligaments were measured (130). The AL and PM bundles were
separated with their respective femoral bone-blocks and potted in polymethyl methacrylate; the tibia and lateral meniscus
were left intact so that the tensile loads could be applied along the anatomic axis of the PCL. The cross-sectional areas
of the three components were measured with a laser micrometer (10). The average cross-sectional area of the
midsubstance of the AL bundle was found to be two times that of the PM bundle. Uniaxial tensile tests revealed that the
stiffness of the AL bundle was 120 ± 37 N per mm, which was significantly higher than that of the PM bundle (57 ± 22 N
per mm) or the MFL (49 ± 18 N per mm). The ultimate load for the AL bundle was 1,120 ± 362 N, that of the PM bundle
was 419 ± 128 N, and that of the MFL was 297 ± 141 N. Because of its superior stiffness and ultimate strength, it is
believed that the AL bundle should be the focus of reconstructive procedures ( 130).
Functional Testing of the Posterior Cruciate Ligament
To gain data on force or tension in the PCL when external loads are applied to the knee, a number of methods have been
developed, both direct (e.g., buckle transducers, pressure probes) and indirect ( 73,76,80,141). However, there are
limitations of direct methods. Contact with the ligament is required, and forces can be measured only in the segment of
the ligament in which the transducers are placed. Other investigators have used indirect methods to measure forces in
knee ligaments. For example, the lengths of various segments of the ligament are measured and the force in the ligament
is then calculated from the load-elongation curve ( 82,142). However, the in situ forces in the ligament may not be
repeated as the ligament is being tensile tested. More recently, Markolf et al. developed a method to determine the in situ
forces in the PCL by rigidly fixing a load cell to the subchondral bone at the femoral insertion of the PCL ( 74,81,143).
We have used the robotic/UFS testing system to evaluate the in situ forces in the PCL. During passive flexion-extension
of the knee, these forces ranged from 6 ± 5 N at 30 degrees of flexion to 15 ± 3 N at 90 degrees. Also, the distribution of
the in situ forces between the AL and PM bundles in response to a 110-N posterior tibial load were determined in nine
cadaveric knees (144). Under these conditions, the in situ force in the PCL increased with knee flexion, ranging from 36
N at 0 degrees to 112 N at 90 degrees of flexion. No significant differences between the bundles could be determined.
These findings are consistent with those of other investigators ( 141). Further, in response to an 80-N isolated hamstring
load, the in situ force in the PCL increased with knee flexion, from 12 ± 5 N at 0 degrees to 80 ± 20 N at 90 degrees of
flexion (145). With the addition of a 200-N quadriceps load, these forces decreased significantly, by 23 to 31 N at 30 to
90 degrees of knee flexion. These results suggest the importance of quadriceps rehabilitation during the postoperative
period after PCL reconstruction. Strengthening of the quadriceps may decrease the in situ forces that the newly
reconstructed PCL graft encounters.
The effects of a popliteus muscle load on knee kinematics and in situ forces in the PCL also were investigated ( 146).
Under a 110-N posterior tibial load, the addition of a 44-N popliteus load significantly reduced the in situ force in the PCL
by 36% at 30 degrees of knee flexion. The popliteus muscle load also significantly reduced posterior tibial translation of
the PCL-deficient knee by 1 to 3 mm.
In addition to the information on structural properties of the FPTC, determination of its in situ forces provides data on
knee joint kinematics and contributes to a better understanding of the functional role of this ligament. Traditionally,
cutting studies are used to examine the contributions of the PCL and other soft tissue structures to knee stability
(67,132,133,135,147). In these studies, external loads are applied to the tibia while motion of the tibia with respect to the
femur is allowed. The difference in kinematics between the intact and the PCL-deficient knee represents the contribution
of the PCL. These cutting studies have demonstrated that the primary function of the PCL is to restrain posterior tibial
translation ( 67,132,133,135,147). In our research center, the PCL has been shown to work in conjunction with the PLS of
the knee to provide knee stability ( 132,133,134 and 135). In response to a 100-N posterior tibial load, sectioning of the
PLS resulted in small increases in posterior tibial translation, compared with sectioning of the PCL. However, combined
sectioning of the PCL and PLS resulted in posterior tibial translation up to three times that of the PCL alone. Further, the
PLS and PCL work together to restrain external and varus rotations. In response to a varus moment of 21 Nm or an
external tibial moment of 5 Nm, small increases in rotations occurred after sectioning of the PCL alone. Significantly
larger increases in both rotations were observed with combined deficiency of the PCL and PLS ( 132,133).
Studies which evaluate the effect of knee flexion angle on function of the PCL have revealed that the PCL provides more
restraint to posterior tibial translation, varus rotation, and external rotation when the knee is at higher flexion angles. The
PLS, on the other hand, contribute to restraining posterior translation, varus rotation, and external rotation when the knee
is in near-full extension ( 133). These findings are consistent with the observation that, in response to posterior tibial
loads, the PCL is more taut with the knee in flexion but the PLS is more taut with the knee near extension ( 53,148,149).
Studies have also found that PLS deficiency results in significant increases in external tibial rotation and posterior tibial
translation in response to an external tibial moment or a posterior tibial load, respectively ( 81,134). Further, the in situ
forces in the PCL were up to six times higher in PLS-deficient knees compared with the intact knees for each loading
condition. These results suggest that there is a biomechanical interdependence between the PCL and PLS and that they
function together to limit posterior tibial translation and external tibial rotation in response to externally applied loads.
In the general population, PCL injuries account for 3% to 23% of all knee ligament injuries ( 150,151,152,153 and 154).
Among a population of trauma patients this number may be as high as 40% ( 155). In the past, isolated injuries to the PCL
have been considered relatively benign and have traditionally been treated nonoperatively ( 156,157,158 and 159).
However, in some studies, patients have developed increased instability and degenerative changes over time ( 158,159
and 160). Meanwhile, surgical management of isolated PCL injuries has not enjoyed the success of ACL reconstruction,
with a high number of patients experiencing residual knee instability ( 151,161,162,163,164 and 165). Clinical outcomes of
PCL reconstruction remain inconsistent, and the long-term prognosis of surgically treated PCL injuries remains
unsatisfactory (166). More than 60% of PCL injuries involve other soft tissue structures of the knee, most frequently the
PLS (155,167). Nonoperative treatment of these injures has universally failed, and surgical management without
addressing the PLS injury has also yielded poor results ( 164,165 and 166,168).
We have evaluated the effect of PLS deficiency on PCL reconstruction using the robotic/UFS testing system. In a
combined PCL/PLS injury, PLS deficiency resulted an increase in posterior tibial translation after PCL reconstruction.
External tibial rotation increased up to 14 degrees, while varus rotation increased up to 7 degrees. In situ forces in the
PCL graft also increased significantly (by 22% to 150%) for all loading conditions ( 169). These results also suggest that
the PLS should be addressed surgically at the time of PCL reconstruction.
Biomechanics of Posterior Cruciate Ligament Reconstruction
Surgical variables for PCL reconstruction involve highly controversial issues: (a) choice of which bundle to reconstruct
when a single bundle graft is used; (b) onlay technique versus tunnel fixation of the tibial portion of the graft; (c)
placement of the tibial and femoral tunnels; (d) position of the tibia relative to the femur at the time of graft fixation; and
(e) the possible use of double-bundle PCL reconstruction techniques. Because of its superior stiffness and strength, the
AL bundle of the PCL has been the focus of reconstructive procedures ( 130). Because the AL bundle exhibits increasing
tension with knee flexion, tensioning and fixation of the graft are performed with the knee in flexion to avoid graft
impingement, which could occur with the knee in extension. Theoretically, large in situ forces in the graft could result in
either graft failure or decreased range of motion.
The optimal knee flexion angle and position of the tibia in the anterior-posterior direction at the time of graft fixation are
other important factors affecting PCL reconstruction. Some authors have advocated fixation of the graft with the knee in
flexion, and others have suggested full extension or lower-knee flexion angles ( 170,171). The application of an anterior
tibial load to reduce posterior sag before graft fixation has also been advocated by some ( 170). In our research center,
the effect of knee flexion angle and applied anterior tibial load at the time of graft fixation on the knee kinematics and in
situ forces in a single-bundle PCL reconstructed knee were evaluated ( 172). Fixation of the graft with the knee at full
extension overconstrained the knee and resulted in higher in situ forces than those found in the intact PCL in response to
a 134-N posterior tibial load. Fixation of the graft with the knee in flexion with a 134-N anterior tibial load applied at the
time of graft fixation closely reproduced the intact knee kinematics and the in situ force in the intact PCL.
A number of studies have focused on the effects of tunnel placement within the insertion site of the PCL. Although the
tension in the PM bundle does not change significantly as the knee is moved through its range of motion, the AL fibers
represent the bulk of the PCL ( 128,173,174). Some authors have advocated placement of the tunnel in the location of the
PM bundle, but it has been shown that this graft placement is ineffective in restoring normal joint laxity ( 170,175,176 and
177). More recent studies suggest that anterior location of the femoral tunnel (in the anatomic location of the AL bundle
insertion) more closely restores intact knee biomechanics when compared with isometric graft placements ( 170,173,177).
Variations in tibial tunnel position were found to have less effect on graft behavior than variations in the femoral tunnel
placement (174,178).
A double-bundle PCL reconstruction technique has received much attention because it tends to mimic the complex
functional anatomy of the PCL (179,180,181 and 182). Use of Achilles tendon or BPTB for the AL bundle and hamstring
tendons for the PM bundle restored the kinematics of the PCL-reconstructed knee, in response to a 134-N posterior tibial
load, to the level of the intact knee. The in situ force in the double-bundle PCL graft was not significantly different from
that in the intact PCL between full extension and 30 degrees of knee flexion. At greater knee flexion angles (60 to 120
degrees), the in situ force in the graft was significantly less than in the intact PCL ( 183). These results suggest that the
double-bundle reconstruction may have an advantage over a single-bundle reconstruction.
BIOMECHANICS OF LIGAMENTS OF THE SHOULDER
The shoulder has the greatest range of motion of all joints in the body, and this motion is distributed between three
diarthrodial joints—the glenohumeral (GH), the acromioclavicular (AC), and the sternoclavicular joints—and the
scapulothoracic joint. In this section, the anatomy and function of these joints and their surrounding ligaments are
addressed. Specific injuries, their treatment options, and the biomechanical basis for treatments of injuries to the GH and
AC joints are also discussed.
Anatomy and Function of Acromioclavicular Ligaments
The AC joint is the articulation between the distal end of the clavicle and the acromion process of the scapula ( Fig. 5.11).
The capsule of the AC joint surrounds this diarthrodial joint, which is incompletely divided by an articular disk. The AC
joint capsule has distinct thickenings that are referred to as the superior, inferior, anterior, and posterior AC ligaments
(184). Anteroposterior stability of the AC joint is thought to be rendered by the AC ligaments, while vertical stability is
attributed to the coracoclavicular (CC) ligaments ( 184,185,186 and 187). The CC ligaments are strong ligaments whose
fibers run from the anteroinferior surface of the clavicle to the base of the coracoid process of the scapula. They consist
of two components: the conoid ligament and the larger, longer, and stronger trapezoid ligament.
FIGURE 5.11. Normal anatomy of the acromioclavicular joint. (From Matsen RA, Rockwood CA. The shoulder.
Philadelphia: WB Saunders, 1998, with permission.)
We examined the in situ forces in ligaments of the AC joint using the robotics/UFS testing system mentioned previously
(188). The results of this study suggested that the trapezoid and conoid ligaments play a major role in limiting excessive
AC joint translations in both the superior and posterior directions. The directions of the in situ force in the trapezoid and
conoid ligaments were different. Therefore, they should not be treated as single ligament during reconstruction
procedures, even though they carry similar magnitudes of force during most modes of loading. Comparison of the data
obtained in this study to previous one-DOF experiments reveals a significant difference in the magnitude of the force in
each structure (185,187). This suggests that kinematic constraints placed on the AC joint during loading are important
and the role of individual ligaments is affected by coupled motions that occur during loading.
The effect of AC joint capsule disruption on AC joint kinematics and the resultant in situ forces in the CC ligaments were
also investigated ( 189). Disruption of the AC capsule resulted in increases in anterior (6.4 mm) and posterior (3.6 mm)
translation when a 70-N anterior or posterior force was applied through the distal clavicle. Capsule transection did not
significantly affect superior translation. Under applied anterior loading, the in situ force in the conoid and trapezoid
ligaments increased significantly with transection of the AC capsule. Posterior loading of the clavicle in the deficient state
of the AC capsule resulted in a significant increase in the in situ force of the trapezoid ligament only. These results
suggest that disruption of the AC capsule alone causes abnormal AC joint kinematics.
Injury and Treatment Options
The most common cause of AC joint injury is a direct force produced when the patient falls onto the point of the shoulder
with the arm at the side in an adducted position. The force is directed inferiorly and medially to the acromion, which can
result in mild, moderate, or severe injury to the AC ligaments, injury to the sternoclavicular joint, or fractures of the shaft
of the clavicle (184). A fall on the adducted arm can also create an indirect superior force that is transmitted through the
humeral head to the acromion process of the scapula. If the force is large enough, it may result in a fracture of the
acromion, rupture of the AC ligaments, or even a superior dislocation of the GH joint.
Injuries to the AC joint can be classified according to the degree of injury to the AC and CC ligaments ( Fig. 5.12)
(190,191). The majority of AC joint injuries are type I, II, or III injuries and do not require surgery ( 184). Although optimum
treatment of type III injuries, in which both the AC and CC ligaments are disrupted, remains controversial, in most
patients excellent functional results can be obtained with nonoperative management ( 192). Some speculate that younger,
more active patients with more severe injuries may benefit from operative stabilization. Types IV, V, and VI AC joint
injuries are often treated surgically by open reduction of the AC joint itself and reconstruction of the CC ligaments.
Options for reconstruction include augmentation with suture bands, synthetic loop augmentation through drill holes in the
base of the coracoid and through the clavicle, CC fixation with transfer of the coracoacromial ligament, use of an AC
hook plate, and AC reconstruction with clavicular corticotomy ( 184).
FIGURE 5.12. Types of acromioclavicular joint injuries. Types I through III are the most common. (Adapted from Matsen
RA, and Rockwood CA. The shoulder. Philadelphia: WB Saunders, 1998, with permission.)
Glenohumeral Joint
Anatomy and Function of Glenohumeral Ligaments
The GH joint is formed by the articulation of the large, spherical humeral head with the smaller glenoid surface of the
scapula. The GH capsuloligamentous complex consists of anterior and posterior components. The anterior component
comprises the anterior band of the inferior glenohumeral ligament (AB-IGHL), the superior glenohumeral ligament
(SGHL), and the middle glenohumeral ligament (MGHL). The posterior band of the IGHL (PB-IGHL) and the rest of the
posterior capsule form the posterior portion of the GH capsuloligamentous complex. The GH ligaments are composed of
discrete collagenous bands within an interwoven collagen mesh that forms the joint capsule ( Fig. 5.13) (193). The GH
capsule is similar in composition to other joint capsules in the body and contains types I, II, and III collagen. Because of
the orientation of the ligaments, portions of the capsule reciprocally tighten and loosen as the GH joint rotates. The
SGHL and the coracohumeral ligament (CHL) are usually described together because their anatomic courses are
parallel. These ligaments form the region of the GH capsule referred to as the “rotator interval,” which constitutes the
triangular space between the anterior border of the supraspinatus tendon and the superior border of the subscapularis
tendon (193,194 and 195).
FIGURE 5.13. The anterior band of the inferior glenohumeral ligament (AB-IGHL), the posterior band of the IGHL
(PB-IGHL), the superior glenohumeral ligament (SGHL), and the middle glenohumeral ligament (MGHL) are discrete
collagenous bands within the joint capsule. (From Warner JP. The gross anatomy of the joint surfaces, ligaments, labrum,
and capsule. In: Matsen FA, Fu FH, Hawkins RJ, eds. The shoulder: a balance of mobility and stability. Park Ridge, IL:
American Academy of Orthopaedic Surgeons, 1994; 21, with permission.)
Through most ranges of motion, the GH ligaments and capsule are relatively lax, acting mainly as checkreins to limit
extreme rotations or translations of the joint surfaces in relation to one another ( 194,196,197). However, the primary
stabilizer of the GH joint is the concavity-compression effect. This observation is consistent with the fact that the capsule,
ligaments, and glenoid labrum are structurally less robust than ligaments of the knee and therefore less likely to
withstand large forces during joint motions ( 195,198). The stabilizing effect of the GH ligaments and joint capsule has
been assessed by measuring their elongation during various joint motions with the use of experimental techniques such
as radiography, mercury and Hall effect strain gauges, electromagnetic tracking devices, metallic beads, and
computational models (199,200,201,202,203 and 204). Turkel et al. found that the SGHL was important in preventing
inferior subluxation of the GH joint at 0 degrees of abduction ( 202). Many authors have suggested that the CHL plays a
major role in inferior stability of the GH joint ( 199,201,203). O'Connell and associates found that the MGHL works
together with the CHL to restrain external rotation and serves as a secondary restraint to both inferior and anterior
instability ( 200,201 and 202,205). The IGHL has been reported to function as a primary stabilizer for anterior instability in
a fashion analogous to a hammock supporting the humeral head in the glenoid during abduction and rotation of the GH
joint (202,203,206).
Forces in the GH ligaments and joint capsule have also been measured with the use of buckle transducers and
differential variable reluctance transducers ( 207). We evaluated the in situ force distribution in the GH capsule during
anterior-posterior loading using the robotics/UFS testing system ( 208). The results showed that the GH capsule carries
no load when the humeral head is centered on the glenoid; however, once an anterior or posterior load is applied to the
joint, the capsuloligamentous structures carry force (SGHL-CHL at 0 degrees of abduction, 26 ± 16 N; AB-IGHL at 90
degrees of abduction, 30 ± 21 N).
Tensile Properties of the Glenohumeral Ligaments
A summary of the structural and mechanical properties from selected literature can be found in Table 5.4 and Table 5.5.
Previous studies in our research center have documented the tensile properties of the CHL and SGHL ( 195). The CHL
was found to have twice the stiffness of the SGHL and three times the ability to withstand tensile loads. The CHL also
absorbed six times the amount of energy to failure but only elongated 1.5 times as much as the SGHL during tensile
testing. The values obtained for stiffness and ultimate load of the CHL were 150% of those reported for the
coracoacromial ligament (209).
TABLE 5.4. MECHANICAL PROPERTIES OF THE LIGAMENTS AND CAPSULE OF THE SHOULDER FROM
SELECTED LITERATURE
TABLE 5.5. STRUCTURAL PROPERTIES OF BONE-LIGAMENT-BONE COMPLEXES: SGHL, CHL, AND THE CA
LIGAMENT
The modulus of the anterior band of the human IGHL complex was reported to be greater than the modulus of the
posterior band (198). The tensile strength of the anterior and posterior bands and the axillary pouch ranged from 5.9 ±
1.7 to 8.4 ± 2.2 MPa. The strain at failure was found to be greatest for the axillary pouch and least for the posterior band.
It was hypothesized that these results reflect the variability in the functional roles of the different portions of the IGHL
complex.
The anatomic, structural, and mechanical properties of four different sites (anterior, posterior, superior, and inferior) of
the GH joint capsule were examined by Itoi et al. (210). They found the thickness of the posterior capsule (1.0 ± 0.4 mm)
to be less than that of the anterior (1.8 ± 0.3 mm), superior (1.6 ± 0.4 mm), or inferior (1.5 ± 0.3 mm) section. The
posterior capsule exhibited the greatest ultimate stress and modulus, and the superior section had the least strength. No
significant differences in ultimate load could be demonstrated. The authors postulated that the greater ultimate stress for
the posterior capsule explained the low incidence of posterior shoulder dislocations.
When the stiffness of the human ACL was compared with that of the SGHL and CHL, significant differences were found.
The SGHL and CHL had approximately 10% the stiffness of the ACL (211). Ultimate load also differed significantly, with
values for the SGHL and the CHL only 5% and 15% of the ACL value, respectively. The modulus of the human IGHL
complex was only 10% of the modulus measured in rabbit MCL, and the tensile strength was only 15%. These
differences suggest that the soft tissues at the shoulder do not function in the same capacity as those at the knee joint.
Injury and Treatment Options
Athletes who participate in overhead sports such as throwing, swimming, tennis, volleyball, and weightlifting subject their
shoulders to repetitive stresses when the arm is in extreme positions of motion. Repetitive overuse of the shoulder may
cause cumulative injury to the capsule, GH ligaments, and glenoid labrum, resulting in GH instability or the inability to
maintain the humeral head centered in the glenoid fossa. Clinical cases of instability can be characterized according to
the circumstances under which they occur, the degree of instability, and the direction of instability. Instability may arise
from an episode in which an injury occurs to the bone, rotator cuff, labrum, capsule, or a combination of these structures.
Anterior Dislocation
Anterior GH dislocation accounts for almost 85% of all shoulder dislocations ( 212). The usual mechanism of injury is a
combination of shoulder abduction, extension, and external rotation that challenges the anterior capsule and ligaments,
the glenoid rim, and the rotator cuff. The humeral head is displaced anteriorly with respect to the glenoid and translates
inferiorly to the coracoid process. A common feature of traumatic anterior dislocations is avulsion of the anterior-inferior
GH ligaments and capsule from the glenoid rim (Bankart lesion). This avulsion injury often does not heal and contributes
to recurrent traumatic instability.
Although clinical studies have shown a direct relation between traumatic anterior shoulder instability and a capsulolabral
injury, electromyographic and histologic studies suggest a more complicated lesion ( 213,214 and 215). In biomechanical
studies, a Bankart lesion did not significantly affect GH joint stability during various loading conditions and arm positions
(216,217 and 218). Using the dynamic shoulder testing apparatus in our research center, we found that GH translations
during active abduction and external rotation were minimally affected by disruption of the anterior-inferior capsulolabral
complex (219). Simulated rotator cuff muscles maintained “ball and socket” kinematics during these motions, with small
translations of the humeral head occurring in all three directions.
Posterior Dislocation
Posterior dislocations may leave the humeral head in a subacromial (behind the glenoid and beneath the acromion),
subglenoid (behind and beneath the glenoid), or subspinous (medial to acromion and beneath the spine of the scapula)
location. The subacromial dislocation is the most common one. The incidence of posterior dislocations is estimated to be
2% of all shoulder dislocations, but the diagnosis is frequently missed ( 220). Posterior dislocation may result from axial
loading of the adducted, internally rotated arm or from violent muscle contractions or convulsive seizures. Fractures of
the posterior glenoid rim and the proximal humerus are common in traumatic posterior dislocations of the shoulder.
Inferior Dislocation
Inferior dislocation may be produced by a hyperabduction force that causes abutment of the neck of the humerus against
the acromion process, which levers the humeral head out inferiorly. The humerus is locked, with the humeral head below
the glenoid fossa and the humeral shaft pointing overhead. Severe soft tissue injury occurs with this dislocation, including
avulsion of the supraspinatus, pectoralis major, or teres minor muscles.
Treatment Options
The optimal method to surgically stabilize the joint and reestablish the delicate balance between mobility and stability
after a capsulolabral injury continues to be a controversial topic in sports medicine. Surgical stabilization of the GH joint
is considered if instability repeatedly compromises shoulder comfort or function despite a reasonable trial of rotator cuff
and scapular stabilizer strengthening and coordination exercises. The procedures for anterior instability include
tightening and realigning of the subscapularis tendon and reinforcement of the anterior capsule (Putti-Platt operation),
reattachment of the capsule and glenoid labrum to the glenoid rim (Bankart repair), capsulorrhaphy, augmentation of the
bony anterior glenoid rim, and transfer of the tip of the coracoid process with its muscle attachments (Bristow procedure)
(212,221).
Surgical intervention for recurrent posterior dislocation of the shoulder also remains controversial because of the high
rates of failure after such surgical procedures as posterior staple capsulorrhaphy or anterior capsular shift ( 222,223).
Biomechanical Testing of Surgical Reconstructions
Several studies have evaluated the biomechanics after surgical repair of lesions in the capsule, ligaments, and labrum.
Janevic et al. measured humeral head translations, contact areas, and contact force magnitude at the extremes of motion
after correction of anterior GH instability ( 217). They found that the translations and contact after repair did not duplicate
the normal joint mechanics. Klein et al. compared two repair techniques after a simulated Bankart lesion in cadaveric
specimens using a shoulder testing apparatus ( 224). They measured strain in the IGHL, torsional resistance as an
indication of instability of the joint, and load to failure in order to compare traditional and suture anchor repair techniques.
The results showed that repair of the defect restores strain and rigidity to control conditions with traditional techniques,
providing greater load-to-failure values.
Speer et al. evaluated the effect of superior and medial anterior capsular shift strategies on multidirectional GH motion
induced by repetitive loading after a simulated Bankart lesion ( 218). They found the two shift procedures to be equivalent
in decreasing anterior GH translation. However, for posterior and inferior translations at 45-degree elevation, the superior
shift decreased translations more than the medial shift did.
Although the function of the capsuloligamentous complex in the normal joint is becoming more clear, it is evident that the
biomechanics of current instability repair procedures remain poorly understood.
BIOMECHANICS OF LIGAMENTS OF THE ANKLE
Lateral Ankle Ligaments
Anatomy and Function of the Lateral Ankle Ligaments
Ankle sprains are among the most common sports-related injuries of the musculoskeletal system ( 225,226). They account
for approximately 40% of all athletic injuries. In an epidemiologic study, the overall incidence of ankle sprains in the
general population was found to be 7 per 1,000 person-years ( 227). The vast majority of these injuries are sprains of the
lateral ligaments that result from inversion of the plantar-flexed foot.
The major ligamentous structures on the lateral side of the ankle include the three fasciculi of the lateral collateral
ligament: the anterior talofibular ligament (ATFL), the posterior talofibular ligament (PTFL), and the calcaneofibular
ligament (CFL). The ankle capsule is also present laterally but contributes little to the stability of joint. The ATFL and
PTFL are thickenings of the capsule itself, whereas the CFL is a discrete extracapsular structure. A cadaveric study
performed by Burks et al. revealed that the ATFL averages 7.2 mm in width and inserts into the talus 18 mm proximal to
the subtalar joint and just distal to its superior articular surface ( Fig. 5.14) (228). It originates 10 mm from the tip of the
lateral malleolus. The CFL originates adjacent to the origin of the ATFL, approximately 8 mm proximal to the tip of the
fibula, and courses in a posteroinferior direction at an average angle of 133 degrees from the axis of the fibula when the
ankle is in a plantigrade position. The CFL inserts onto the calcaneus approximately 13 mm distal to the subtalar joint.
The PTFL originates on the posteromedial aspect of the distal fibula and passes posteriorly to the talus. It is rarely
disrupted with inversion injuries.
FIGURE 5.14. Schematic drawing of the normal anatomic relationships of the anterior talofibular ligament (ATFL), the
calcaneofibular ligament (CFL), and the bony architecture of the ankle.
The motion about the ankle arises from the articulation of four bones; tibia, fibula, talus, and calcaneus. The position of
the ankle and motion about the ankle joint are defined geometrically by three axes ( 229). The normal range of motion at
the tibiotalar joint is from approximately 20 degrees of dorsiflexion to 50 degrees of plantiflexion. The bony architecture of
the talar dome within the ankle mortise contributes significantly to the stability of the ankle. The shape of the talar dome
within the ankle mortise allows for more motion when the ankle is plantarflexed, rendering it less stable. During an
inversion injury to the ankle, the anterolateral joint capsule is disrupted initially, followed by the ATFL and CFL
sequentially, depending on the magnitude of the injury. Because the CFL spans both ankle and subtalar joints, injury to
this ligament results in increased subtalar motion as well as ankle instability.
Tensile Properties of the Lateral Ankle Ligaments
The ligaments of the ankle have received little attention in the literature compared with those of the knee and shoulder.
Uniaxial tensile tests of the human ATFL, CFL, and PTFL with their bony complexes revealed that the PTFL was the most
stiff (163 ± 56 N per mm), followed by the ATFL (142 ± 79 N per mm) and the CFL (127 ± 43 N per mm) ( 230). The values
for ultimate load to failure were approximately 418, 139, and 346 N, respectively ( Table 5.4) (230,231). It was concluded
that the ankle joint has the least amount of ligamentous support anteriorly. This is consistent with the finding that the
ATFL is the most frequently injured ligament of the ankle during inversion ankle sprains ( 229).
Functional Testing of the Lateral Ligaments of the Ankle
The function of the lateral ligaments of the ankle have been investigated with the use of radiographic techniques to
measure changes in ankle stability after experimentally induced ligament injuries ( 232,233). Others have measured talar
displacement and rotation after selective sectioning of the ATFL, CFL, PTFL, and combinations of these ligaments
(234,235,236,237 and 238). However, these studies have reported conflicting results.
Strains of the ATFL and CFL during physiologic motion of the ankle were measured using Hall effect strain transducers in
cadaveric ankles ( 239). In the neutral position, neither the ATFL nor the CFL was strained. In 10 degrees of dorsiflexion
the CFL was strained, approximately 1%, and the ATFL was relaxed. In 30 degrees of ankle plantiflexion the ATFL was
strained, approximately 2%, and the CFL was relaxed. The addition of supination and internal rotation/supination did not
significantly change the strain in the ATFL. The strain in the CFL increased significantly when the ankle was placed in
supination and external rotation. These results suggest that the lateral ankle ligaments work synergistically: when one is
strained the other is relaxed, and vice versa, throughout the range of plantar-dorsiflexion tested. Most published literature
supports this concept of lateral ankle stability. The ATFL plays a primary role when the ankle is in plantiflexion, and the
CFL is important in stabilization when the ankle is dorsiflexed. Strain in the ATFL, CFL, PTFL, anterior tibiofibular, and
posterior tibiofibular ligaments were also measured with the use of mercury-filled Silastic strain gauges ( 240). Strain in
the ATFL increased as the ankle was moved from dorsiflexion to plantiflexion. Inversion and internal rotation moments
increased ligament strain, especially when the ankle was in plantiflexion. Strain in the CFL was generally small at all
positions of plantar-dorsiflexion. Strain values decreased as the ankle was moved from 20 degrees of dorsiflexion to 20
degrees of plantiflexion, with a slight increase as the ankle was moved to 30 degrees of plantiflexion. Inversion or
external rotation increased while eversion or internal rotation decreased strain in the ligament throughout the entire
range of plantar-dorsiflexion. The results emphasize the importance of the ATFL in limiting internal rotation and
inversion, especially when the ankle is plantarflexed. The relatively low strain in the CFL supports the concept that it
does not play an independent role in ankle stability but is important in limiting inversion when the ankle is held in
dorsiflexion. In the clinical setting when the ATFL is disrupted, the CFL may become even more important for restraining
talar inversion.
Although the anterior drawer test is a common clinical examination maneuver used to evaluate the status of the ATFL,
there is controversy about its usefulness in the evaluation of the integrity of the ATFL ( 229,238,241,242,243 and 244). It
has been suggested that the anterior drawer test should be performed with the ankle between 10 and 20 degrees of
plantiflexion and that an excessive magnitude of force may not be necessary to diagnose a disruption of the ATFL ( 245).
The forces in the ATFL and CFL and the ankle kinematics during simulated anterior drawer and talar tilt tests were
measured with the use of buckle transducers and an instrumented spatial linkage ( 246). In the intact ankle, the largest
forces in the ATFL were recorded with the ankle in plantiflexion, whereas the largest forces in the CFL were observed in
dorsiflexion. An isolated injury to the ATFL did not significantly change the kinematics of the ankle or the force in the CFL
in response to the two simulated clinical examinations. However, when both of the ligaments were disrupted, a significant
increase in both anterior translation, up to 7 to 9 mm, and internal rotation, up to 6 to 9 degrees was observed in
response to simulated anterior drawer testing. Simulation of a talar tilt test in the ATFL/CFL deficient ankle could result in
significant increases of up to 10 degrees of supination. These results suggest that the largest laxity increase after an
isolated ATFL injury would be observed when testing the ankle in plantiflexion. With the addition of a CFL injury, testing
the ankle in dorsiflexion may be more appropriate.
The majority of lateral ligament sprains of the ankle can be managed nonoperatively with good results. Early controlled
motion with the use of a functional brace, which allows limited plantar-dorsiflexion while preventing inversion, has been
demonstrated to be advantageous compared with casting or surgical repair ( 247). However, up to 20% of patients do
experience symptoms of functional instability, such as recurrent inversion sprains, pain, or difficulty walking on uneven
ground (248,249,250,251 and 252). Symptoms may be controlled in some patients with a rehabilitation program aimed at
improving proprioception and strengthening of the lower leg muscles. ( 253) Bracing is also effective in improving
functional symptoms of instability.
Surgical reconstruction is reserved for patients who continue to suffer multiple recurrent inversion injuries despite
adequate rehabilitation and bracing. Operative techniques can be divided into four general categories: (a) repair of the
attenuated ligaments without augmentation (Bröstrom procedure) ( 248); (b) procedures that prevent inversion of the foot,
such as tenodesis of the base of the fifth metatarsal to the lateral malleolus using the peroneus brevis tendon (Evans
procedure) (254); (c) procedures that prevent inversion of the foot through reconstruction of the ATFL, such as directing
the peroneus brevis tendon through bone tunnels in the distal fibula and talus to replace the ATFL (Watson-Jones
procedure) (255); and (d) procedures that reconstruct both the ATFL and CFL, such as using half of the peroneus brevis
tendon or a free fascia lata graft to replace the injured ATFL and CFL (Chrisman-Snook procedure). The Bahr procedure,
in which the peroneus brevis tendon is routed through the calcaneus, fibula, and talus to anatomically reconstruct the
ATFL and CFL has also been described ( Fig. 5.15) (256,257).
FIGURE 5.15. Schematic drawings of various lateral ligament reconstructive procedures described in the literature. A:
Brostrom direct repair. B: Evans reconstruction. C: Watson-Jones reconstruction. D: Chrisman-Snook reconstruction. E:
Bahr “anatomic” reconstruction.
Biomechanical Testing of Lateral Ankle Ligament Reconstructions
A successful reconstruction of the lateral ankle ligaments should fulfill three criteria. First, the placement of the grafts
should approximate the normal ligament anatomy. Second, the graft material used should have tensile properties similar
to those of the intact ligaments. Finally, the replacement grafts should have in situ forces and force distribution similar to
those of the intact ligaments when the ankle is subjected to externally applied loads.
A summary of the biomechanical properties of commonly used autografts for lateral ligament reconstruction is shown in
Table 5.6 (231). The ultimate loads for the peroneus brevis (258.2 N) and split peroneus brevis (258.8 N) tendons are
significantly greater than that of the ATFL (231 N) but not significantly different from the CFL (307 N). The ultimate load
for the fourth toe extensor tendon (130.1 N) is significantly less than that of the CFL but not significantly different from the
ATFL.
TABLE 5.6. CROSS–SECTIONAL AREA, ULTIMATE LOAD, AND LINEAR STIFFNESS OF THE LATERAL ANKLE
LIGAMENTS AND COMMONLY USED RECONSTRUCTION GRAFTS
Several of the reconstructive procedures have been evaluated to assess their effect on joint motion when the ankles are
subjected to externally applied loads ( 256,257,258 and 259). In cadaveric ankles, the Chrisman-Snook and Evans
procedures allowed more motion than intact ankles but significantly restricted subtalar motion; the Watson-Jones
reconstruction controlled anterior talar translation and internal rotation but was less effective in controlling talar tilt and
also restricted subtalar motion. A new, more “anatomic” reconstruction was proposed; it returned internal rotation,
anterior talar translation, and talar tilt to near-normal levels but did not restrict subtalar motion ( 256). Hollis et al. also
used cadaveric ankles and subjected them to anterior-posterior loads and supination-pronation moments. In the
ATFL/CFL-deficient state, all three reconstructions increased stability during supination-pronation loading.
Anterior-posterior translation was stabilized by the Evans and Chrisman-Snook procedures, but the Watson-Jones
reconstruction had little effect. Subtalar motion was restricted by all three reconstructions, most notably with the
Chrisman-Snook technique (258). Anterior drawer and talar tilt tests were performed on cadaveric ankles with a clinically
used testing jig. The Bröstrom, Watson-Jones, and Chrisman-Snook procedures reduced talar tilt and anterior translation
when compared with the combined ATFL/CFL-deficient state ( 259).
Under simulated anterior drawer and talar tilt testing, the forces in the intact ATFL and CFL and their replacement grafts
were measured with the use of buckle transducers and were found to change with ankle joint motion with the Bröstrom
repair, the Watson-Jones reconstruction, and the new “anatomic” reconstruction technique ( 257). All three procedures
reduced the ankle joint laxity that is observed after sectioning of the ATFL and CFL. The Watson-Jones technique
restricted joint motion, as reported previously ( 256,258). Analysis of the forces in the ligaments and grafts during anterior
drawer and talar tilt testing revealed that, unlike the Watson-Jones technique, the forces and force patterns observed in
the Bröstrom and “anatomic” techniques resembled those observed in the intact ankle.
High clinical success rates, with 85% to 100% good to excellent results, have been reported for ankle ligament
reconstructions, both augmented and nonaugmented, anatomic and nonanatomic ( 260,261,262 and 263). Large,
prospective, randomized clinical studies are necessary to determine whether the “anatomic” reconstruction techniques
offer significant long-term benefits, in terms of functional stability and progression to ankle osteoarthritis, when compared
with the “nonanatomic” procedures.
ACKNOWLEDGMENTS
We acknowledge the assistance of Richard Debski, PhD; Tracy Vogrin, MS; Jennifer Zeminski, BS; and Sven Scheffler
and the financial support of the Musculoskeletal Research Center and NIH Grant #AR39683.
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6 Rehabilitation
REHABILITATION
DAVID J. PEZZULLO
JAMES J. IRRGANG
Therapeutic Use of Cold and Heat

Cold Therapy
Heat Therapy
Forms of Therapeutic Exercise
Active Dynamic Exercise
Passive Exercise
Principles for Improvement of Range of Motion
Range of Motion Exercises
Stretching
Joint Mobilization
Principles for Improvement of Muscle Performance
Strength
Endurance
Precautions, Fatigue, and Muscle Soreness
Isometric Exercises
Exercise Programs
Principles for Improvement of Proprioception
Summary
Chapter References
Rehabilitation involves any procedure designed to maximize function after injury or illness. In sports medicine it includes
procedures designed to restore athletes to their previous level of function within the shortest period of time.
Rehabilitation begins immediately after the injury and progresses through the acute and subacute phases of injury or
surgery, culminating in return to sport. For an athlete, it must also include a period of reconditioning to ensure optimal
levels of fitness, including flexibility, strength, and endurance, which are necessary to achieve optimum performance and
to minimize the risk of reinjury. Rehabilitation includes the application of therapeutic exercise and physical agents.
Physical agents include various forms of heat, cold, electricity, and massage that are used to relieve pain and swelling
and to aid in the healing process. Therapeutic exercise includes a variety of movements designed to restore function to
the greatest possible degree in the shortest period of time and to attain high levels of physical conditioning.
Rehabilitation requires that athletic trainers and physical therapists have basic knowledge of the effects of exercise and
physical agents. The purpose, indications, contraindications, and precautions of these procedures must be known.
Athletic trainers and physical therapists must be able to relate the effects of the physical agents and therapeutic exercise
to the rehabilitation goals for the athlete. Establishment of appropriate goals during rehabilitation depends on the ability
to assess the extent of injury and the functional status of the injured athlete. An understanding of pathology and the
healing process is also necessary to ensure appropriate rehabilitation. Anatomy, kinesiology, and biomechanics must
also be considered when developing the rehabilitation program.
The ultimate goal of rehabilitation after athletic injury is to restore symptom-free movement and function, allowing
individuals to return to their previous level of activity in the shortest time possible. Specific goals in the rehabilitation
program depend on the phase of rehabilitation. They include limiting inflammation, decreasing pain and swelling,
improving mobility and flexibility, improving muscle strength and endurance, improving cardiovascular endurance, and
promoting coordination. Rehabilitation procedures must be designed to meet these goals. The injured athlete must
progress through the rehabilitation program as successive goals are accomplished.
Immobility and decreased activity adversely affect many tissues. Decreased stresses on bone due to prolonged
immobilization, relief of weight bearing, or decreased muscle activity result in decreased deposition of bone while
resorption remains unchanged, resulting in an overall decrease in bone mass.
Articular cartilage depends on synovial fluid for maintenance of its nutrition. Intermittent compression of joint surfaces
enhances the exchange of synovial fluid within the articular cartilage. Prolonged immobilization adversely affects nutrition
of articular cartilage and may result in adherence of the synovial membrane to the margins of the articular cartilage,
preventing movement of synovial fluid into the underlying articular cartilage. The result of this synovial fluid deprivation is
known as obliterative degeneration of articular cartilage ( 1). Continuous pressure of joint surfaces for a period as short as
8 days deprives the articular cartilage of nutrition by movement of synovial fluid and can result in the development of a
compression sore, also termed compression necrosis of the articular cartilage ( 1).
Prolonged immobilization of a joint also results in synovial adhesions that can limit motion. It can also decrease stiffness
and strength of ligaments and joint capsules. Immobilization of the knee in rhesus monkeys resulted in a significant
decrease in maximum load to failure, even after 12 months of reconditioning ( 2).
The response of muscle to decreased use is atrophy. Type I fibers atrophy faster than type IIa or IIb fibers ( 3).
Immobilization also results in decreased oxidative capacity of the muscle fiber.
In the growing child, intermittent compression of the epiphyseal plate is necessary for growth of long bones.
Immobilization and inactivity decrease normal intermittent pressures on the growth plate, with a potential effect on
growth.
Living tissues respond and adapt to the stresses placed on them. The effects of increased stress on the body result in
changes that are essentially opposite to those imposed by decreased use. Wolff's law states that bone adapts to the
stresses placed on it. Stresses from weight bearing and muscular contraction result in increased bone mass. Soft tissue
structures respond in a similar manner. Wallis and Logan ( 4) coined the phrase “specific adaptations to imposed
demands” and gave it the acronym SAID. The SAID principle implies that tissues adapt to altered patterns of use.
Increased use results in specific adaptations of structure or function or both that enable those tissues to withstand the
stresses imposed on them. This is an important concept in rehabilitation. It implies that the degree of functional capacity
achieved depends on the intensity, duration, and frequency of exercise. To achieve the highest levels of structure and
function, it is necessary to progressively increase the load applied to the tissues. During rehabilitation, tissues within the
body must be stressed in a positive, progressive, and appropriately planned manner, with the ultimate goal of
improvement of overall function to meet the demands of the individual's sport.
Rehabilitation of the injured athlete is a problem-solving process that can be depicted as a feedback loop. It includes
assessment of the athlete and leads to development of needs, goals, and a plan of care. As the athlete progresses, the
plan of care must be modified to allow for continued progress. This requires frequent reassessment. The ability to
accurately evaluate and identify rehabilitation goals is critical to this process. The reader is referred to individual chapters
for reviews of the physical examination of specific joints.
THERAPEUTIC USE OF COLD AND HEAT
Cold Therapy
Cold modalities are used to decrease pain and promote healing ( 5,6). Cold application is frequently used as the initial
treatment of acute injuries or inflammatory conditions. The application of cold decreases skin and subcutaneous tissue
temperature. The decrease in tissue temperature causes vasoconstriction of small blood vessels, which results in
decreased blood flow ( 5). This, in turn, results in reduction of intramuscular and intraarticular temperature. The
decreased temperature of the muscle and joint can last for several hours after cold application, but the amount of
temperature reduction is less significant than the skin and subcutaneous tissue cooling ( 5,7).
Ice applied in the acute stage can decrease histologic evidence of the inflammatory process in injured tissues ( 6). Cold
decreases the metabolic activity of the injured tissue, which limits further damage from hypoxia ( 8). Cold application
inhibits histamine release and neutrophil and collagenase activity when it is used during the acute inflammatory process
(5).
Cold applied during the acute stage has been shown to increase swelling of the injured limb ( 5,6,9). The increase in
swelling is caused by an increase in the permeability of the superficial lymph vessels. It is recommended to combine
compression and elevation with the application of cold during the acute stage to control swelling ( 5).
Cold application also has an effect on nerve conduction velocity. The cooling of nerves slows the signal conduction
velocity and results in pain reduction for the injured athlete. Pain reduction through cooling is most effective when tissue
temperature is reduced by 10° to 15°C, but the duration of pain relief is highly variable ( 5). The reduction in nerve
conduction velocity also decreases muscle spasticity by decreasing muscle spindle activity ( 5). This can help reduce
muscle spasms during the acute phase of healing.
When cold is applied to the injured area, the athlete typically reports a feeling of cold followed by a sense of burning,
then aching, and finally numbness of the area ( 10). Cold application should be avoided in athletes with Raynaud's
disease or cold-induced allergy. Caution should be taken with prolonged application of cold and with cold applied directly
over superficial nerves. Although they are rare, some cases of nerve palsy after application of cold have been reported in
the literature (11).
Cold can be applied in many forms, including ice packs, frozen gel packs, cold whirlpool, and commercial products that
circulate cold water through a bladder secured to the injured area ( 10). In all of these cases ice should be applied for 15
to 30 minutes. Ice massage is another common form of cold application that can be performed by freezing water in a
paper cup with a tongue depressor as a handle. The ice is rubbed over the painful or spasming area for 7 to 10 minutes
or until the athlete reports analgesia. A cold whirlpool allows the patient to exercise in a cold medium. The cold reduces
pain, allowing for less restricted active range of motion (ROM). Ideal water temperature for a cold whirlpool is 13° to 18°C
(10); lower temperatures are not well tolerated.
Heat Therapy
The application of heat increase the tissue temperature of the skin and subcutaneous tissue. The increase in
temperature occurs rapidly and steadily with the initial application of heat ( 12). The increased temperature causes
vasodilation of the blood vessels in the heated area. The flow of blood slows the rate of heating by dissipating the
applied heat. The skin in the area of localized heating turns red as sign of increased blood flow through the cutaneous
vessels.
Vasodilation also increases the delivery of oxygen and nutrients and the removal of waste products ( 13). Vasodilation is a
normal response to heating and is controlled by axon or local spinal reflexes, release of a chemical mediator, or
stimulation of the anterior hypothalamus ( 13).
Studies have shown that intraarticular and intramuscular temperatures decrease or are unaffected by the application of
superficial heat (14,15). It was theorized that blood flow is shunted away from deeper tissues to the skin to help dissipate
the increase in temperature. Blood flow through the muscle is more dependent on active exercise than on application of
heat modalities (15). There is a ninefold increase in blood flow through muscle after 1 minute of exercise, compared with
resting blood flow ( 15). After an acute injury, heat application can increase pain and promote further tissue trauma.
Application of heat increases tissue metabolism, creating a greater demand for oxygen and nutrients. This increase in
metabolism can cause secondary tissue damage due to hypoxia. Heat application during the acute phase of injury can
also promote further release of histamine and prostaglandins. These chemical mediators increase pain and cause
vasodilation through an increase in capillary membrane permeability ( 13). The vasodilation of the blood vessels
increases tissue hemorrhaging, which causes increased pressure on the free nerve endings. For these reasons, heat
application should be avoided during the acute inflammatory phase of injury.
During the subacute phase of injury, the increase in blood flow may help neutralize noxious stimuli and increase the
removal of cellular debris and waste. The application of heat can reduce pain, soreness, and stiffness in the later phases
of the inflammatory process. This occurs because heat application increases the threshold for pain perception of free
nerve endings and peripheral nerves ( 16). Heat also enhances the plasticity of connective tissue, allowing for permanent
deformation to be more easily achieved. Greater elongation is achieved when heat is applied during the stretching
process and the stretching force is maintained during cooling of the tissue.
Heat application should be avoided in athletes with an acute injury or active hemorrhaging of tissues. Athletes with an
elevated core body temperature due to infection or malignancy should avoid application of superficial heat. Heat applied
to a febrile athlete could cause further elevation of the core body temperature, resulting in increased stress on the
cardiorespiratory system. Heat applied to an athlete with a malignancy could cause an increased rate of cell growth and
possible metastasis. Caution should be taken when applying heat to ischemic or insensitive areas because of the
increased risk of superficial burns.
Ultrasound is a heating modality that penetrates to a deeper level than superficial heating modalities such as
Hydrocollators and whirlpools do. Superficial heating modalities increase the temperature of the skin and subcutaneous
tissues by penetrating 1 to 5 mm; heating produced from ultrasound can penetrate to a depth of 5 cm. Ultrasound
produces minimal temperature increase of the skin, subcutaneous tissue, and fat but vigorous heating in deeper tissues.
The thermoreceptors in skin do not detect the increased temperature produced by ultrasound. This explains why the
athlete has a minimal sensation of heat during the application of ultrasound.
Ultrasound energy is more readily absorbed in tissues that have a high protein content. The tissues that are selectively
heated by ultrasound are nerve, muscle, tendon, ligament, and joint capsule. Ultrasound can increase tissue temperature
to 40° to 45°C when applied for 5 to 10 minutes at 1.0 to 2.0 W per cm 2. Application of ultrasound requires an acoustic
medium (gel) and continuous movement of the sound head to avoid burning the deeper tissue.
Nonthermal effects of ultrasound are a result of formation of oscillating cavities of gas. This fluid movement in the area of
cavitation, also called acoustical microstreaming, increases membrane permeability. The increased movement of
metabolites and ions across cell membranes can enhance collagen formation, improve orientation of collagen fibers, and
improve elasticity of scars ( 17).
FORMS OF THERAPEUTIC EXERCISE
Therapeutic exercise is defined as those movements designed to restore the greatest possible degree of function in the
shortest period of time and to attain high levels of physical fitness. A therapeutic exercise program must consider the
nature and severity of the illness or injury, the purpose of the exercise, sequencing, and progression of the exercise, as
well as contraindications and precautions. In addition, the intensity, frequency, and duration of exercise must be
appropriate for the stage of inflammation, healing, and conditioning.
Therapeutic exercise can be categorized into static or dynamic exercise ( Fig. 6.1). Static exercise includes isometric
exercises in which no observable movement occurs. The length of the muscle appears to be constant; however, there is
shortening at the sarcomere level. Isometric contractions occur when the torque produced by muscle tension is equal to
the external resistance. Dynamic exercise may be either active or passive.
FIGURE 6.1. Scheme describing the categorization of therapeutic exercise as it pertains to treatment of the
musculoskeletal system.
Active Dynamic Exercise
Active dynamic exercise results from voluntary contraction of muscles. Free active exercise occurs when muscles
produce movement without the application of additional external resistance. Free active exercise includes ROM exercise
and stretching. Active ROM exercise includes those movements within the unrestricted available ROM that are produced
by voluntary contraction of the individual's muscles. Active stretching exercises are those in which the athlete uses
voluntary effort to move beyond the restricted ROM. ROM exercises are performed to maintain motion, whereas
stretching exercises are designed to increase motion. Active resistive exercises are those exercises in which the
individual uses voluntary muscle contraction to move against an applied resistance. They include isotonic and isokinetic
exercises.
Isotonic exercises, by definition, should result in constant tension within the muscle through the range of shortening ( 18).
However, this condition rarely occurs, and the term isotonic exercise has come to imply movement against a fixed
external resistance. Motion against a fixed external resistance results in variable muscle tension due to the
length-tension relationship of the muscle fiber itself and the changing mechanical advantage that the line of muscle
action has on the skeletal system. Speed is not controlled during isotonic exercise.
Isokinetic exercise involves movement at a constant speed. External resistance is variable and accommodating.
Resistance during isokinetic exercise is proportional to the effort put forth by the athlete.
Variable resistance machines have been developed in an attempt to provide variable resistance that matches the torque
curves produced by a particular muscle or muscle group. In variable resistance exercises, the resistance is not
accommodating and the speed is not controlled.
Isotonic, isokinetic, and variable resistance exercises can be performed concentrically or eccentrically. Concentric
contraction implies that the muscle shortens as it contracts, whereas eccentric contraction implies lengthening as the
muscle contracts. Concentric contractions are necessary to accelerate the body, and eccentric contractions are
necessary for deceleration. The force-velocity relationship is different for each type of contraction. During a concentric
contraction, the force created by the muscle decreases as the speed of contraction increases. During an eccentric
contraction, however, the force created by the muscle increases as the speed of lengthening increases. This is believed
to result from facilitation of the stretch reflex and stretching of the connective tissue component within the
musculotendinous unit, both of which give rise to increased muscle tension with increased speed of lengthening.
Concentric contractions occur when the internal force created by the muscle is greater than external resistance.
Conversely, eccentric contractions occur when external resistance overcomes internal resistance created by the muscle.
Eccentric exercise is associated with increased muscle soreness and increased injury.
Passive Exercise
Passive exercise occurs without voluntary muscular effort on the part of the athlete. Passive movement is the result of
forces external to the body. Passive exercise can be either physiologic or accessory.
Physiologic passive exercise implies angular displacement of the bone. These are movements that the patient could
perform under voluntary muscular control. Passive physiologic motion can be performed either as ROM or as stretching
exercises. Passive physiologic ROM is motion that occurs within the unrestricted ROM. Passive stretching movements
are those movements beyond the restricted range; they are performed in an attempt to increase motion.
Accessory motions are those that the individual is not capable of producing by voluntary muscle action. Accessory motion
includes motions of the joint surfaces that are necessary for normal physiologic movement of the joint, such as
distraction, compression, rolling, gliding, and spins of the joint surfaces. Passive accessory motion is performed to
increase joint play, which is necessary for normal physiologic motion. Joint mobilization is passive accessory motion that
is performed at slow speeds. Mobilization can be performed with the use of oscillatory or sustained movements to
decrease pain and increase joint mobility. Manipulations are passive movements performed with a quick low-amplitude
thrust at the end of the available ROM. Manipulation is used to regain the final degrees of motion.
Both physiologic and accessory passive exercise can be graded in terms of the total amount of motion available at the
joint (18). The normal ROM for a joint is the amount of motion that is normal or expected for a particular joint. However,
the available ROM may be less than the normal ROM for a particular joint. The total available ROM is equal to motion in
the unrestricted range and motion beyond the motion barrier that is achieved with overpressure. Grade I motion is a
small-amplitude movement at the beginning of the ROM. Grade II motion is a large-amplitude movement performed within
the available ROM but not up to the motion barrier. Grade III passive motion is a large-amplitude movement performed
up to and beyond the motion barrier. Grade IV passive motion is a small-amplitude movement performed at and beyond
the motion barrier. Grade V movements are those high-velocity, small-amplitude movements performed beyond the
motion barrier (Fig. 6.2).
FIGURE 6.2. Grading system for passive motion. A: Normal range of motion (ROM) for a given joint. B: ROM available
for a joint with restricted motion. The motion barrier represents resistance to motion engaged near the end of the motion.
Motion beyond the motion barrier is achieved with overpressure. C: Grade I motion—small-amplitude movement at the
beginning of the range. D: Grade II motion—large-amplitude motion within the available range but not up to the motion
barrier. E: Grade III motion—large-amplitude movement up to and beyond the motion barrier. F: Grade IV
motion—small-amplitude motion at and beyond the motion barrier. G: Grade V motion—high-velocity, small-amplitude
motion performed beyond the motion barrier.
Grade I and II movements constitute ROM exercises and are used to maintain motion during the acute and early
subacute phases, when excessive motion may be detrimental to healing. Grade III and IV movements are stretching
exercises used during the subacute and chronic stages of recovery to increase motion. Grade V motions include
manipulations and are designed to increase motion; they are discussed in a later section.
PRINCIPLES FOR IMPROVEMENT OF RANGE OF MOTION
The ROM available at a particular joint is determined by the configuration of the joint surfaces and the surrounding soft
tissue structures (e.g., capsule, ligament, muscle, tendon, fascia, skin). The ROM available at a particular joint is termed
joint range (19). Joint range is measured in degrees with a goniometer. Muscle range is related to the functional
excursion produced by muscles that cross the joint (19). The functional excursion of a muscle is the distance that it is
capable of lengthening and shortening. For a one-joint muscle, the functional excursion is directly influenced by the joint
that the muscle crosses. A one-joint muscle is expected to shorten and lengthen sufficiently to permit full active ROM at
the joint that it crosses. The functional excursion of multijoint muscles exceeds the joint range of any one of the joints that
it crosses. Multijoint muscles, however, cannot lengthen or shorten sufficiently to simultaneously permit the extreme ROM
at all of the joints that it crosses. For example, the hamstrings cannot lengthen sufficiently to permit simultaneous full hip
flexion and full knee extension. In this position, the hamstrings are said to be passively insufficient. In the passive,
insufficient position, further motion is limited by tension in the musculotendinous unit. Similarly, the hamstrings cannot
shorten sufficiently to permit simultaneous full active knee flexion and hip extension. In this position, the hamstrings are
said to be actively insufficient. In the active insufficient position, the muscle fibers cannot shorten any further and are
ineffective in generating additional tension.
To increase motion, the properties of the tissues that limit the motion must be considered. Traditionally, these tissues are
divided into noncontractile and contractile tissues. Noncontractile tissues include ligaments, tendons, capsule, fascia,
connective tissue components of muscle, and skin. The material strength of a tissue is its ability to resist load or stress.
Stress is defined as force per unit of cross-sectional area; it can be tensile, compressive, or shearing. Strain is defined as
the deformation that occurs in response to stress. It is typically expressed as a percentage of elongation (i.e., change in
length divided by original length). The mechanical properties of a tissue are often plotted in a stress-strain curve (Fig.
6.3), which relates strain as a function of stress for a given tissue. The toe region occurs at the beginning of the
stress-strain curve. This is the region in which little force is required to elongate the tissue. It probably represents
straightening of the wavy pattern of connective tissue fibers. The elastic range consists of that area of the stress-strain
curve in which the tissue returns to its original size and shape when the stress is removed. The upper end of the elastic
range is termed the elastic limit. This is the point beyond which the tissue will not return to its original size or shape when
the stress is removed. The plastic range of the stress-strain curve represents the range beyond the elastic limit that
results in permanent elongation when the stress is removed. The upper end of the plastic range is associated with failure
of the tissue. Sequential failure of collagen fibers in tendon occurs at 4% to 8% strain. Failure of the tissue occurs
beyond 8% to 10% strain of the collagen fibers ( 20). This corresponds to 20% to 40% strain of the entire tendon ( 21).
FIGURE 6.3. Typical stress-strain curve for connective tissue. The toe region is the region in which little stress is
required to lengthen the tissue; it probably represents straightening of the wavy pattern of collagen fibers. The elastic
region is that portion of the curve in which the tissue returns to its original length when the stress is removed. The plastic
region is that portion of the curve that results in permanent elongation when the stress is removed. (Modified from Kisner
C, Colby LA. Therapeutic exercise: foundations and techniques, 2nd ed. Philadelphia: FA Davis, 1990, with permission.)
Connective tissue is viscoelastic—that is, it exhibits properties of viscosity and elasticity. Elasticity refers to a tissue's
ability to return to its original length when stress is removed. Viscosity refers to a tissue's ability to resist elongation.
Because of the viscoelastic nature of connective tissue, it exhibits properties of creep, relaxation, and stiffness. Creep is
the elongation of tissue that results from constant loading ( Fig. 6.4). Creep can be increased by increasing tissue
temperature (22). Relaxation is the progressive decrease in internal stress over time that occurs as a result of
lengthening to a constant strain. Stiffness is the ability of the tissue to resist elongation; it is indicated by the slope of the
stress-strain curve shown in Figure 6.3. Because connective tissue is viscoelastic, stiffness depends on the rate of
loading: increased rate of loading is associated with greater stiffness.
FIGURE 6.4. Graphic representation of the phenomenon of creep. Tissue undergoes gradual elongation over time when
subjected to constant stress.
The mechanical characteristics of connective tissue should be considered when attempts are made to increase ROM.
Lengthening of connective tissue requires plastic deformation that results in gradual rearrangement of the connective
tissue. Adequate time must be provided for remodeling to prevent fatigue or rupture of the tissue, or both. Plastic
deformation of connective tissue can be maximized by using the principles of creep, relaxation, and stiffness. To
maximize permanent lengthening, low-magnitude forces should be applied for prolonged periods. This process can be
facilitated by the use of heating modalities and by maintaining the lengthened position during the period of cooling ( 22).
The mechanical characteristics of contractile tissue must also be considered when attempting to increase ROM. It should
be remembered that muscle consists of both contractile and noncontractile components ( 23). The noncontractile
components include the series elastic and parallel elastic components. The series elastic component includes the
connective tissue that connects the muscle fiber to bone, while the parallel elastic component consists of the connective
tissue that surrounds each muscle fiber. Lengthening of the musculotendinous unit lengthens both the series and the
parallel elastic component, producing a sharp rise in tension. Continued lengthening of the musculotendinous unit
causes mechanical disruption of the cross-bridges, as the actin and myosin filaments slide apart and an abrupt
lengthening of sarcomere occurs. This is termed sarcomere give (24). Sarcomeres are elastic: when short-term stretch is
removed, they return to their original length. This implies that short-term stretching is not effective in increasing the
length of the contractile components of a muscle.
Plastic deformation of contractile tissue can be achieved with prolonged immobilization. Prolonged immobilization in the
lengthened position results in the addition of sarcomeres and permanent lengthening of the contractile tissues. This
occurs to maintain the greatest functional overlap of the actin and myosin filaments. Prolonged immobilization in the
shortened position results in a decreased number of sarcomeres ( 25,26).
The neurophysiologic properties of contractile tissue must also be considered when attempting to increase ROM limited
by musculotendinous structures. The muscle spindle is a sensory organ that is sensitive to muscle lengthening. Sudden
stretching of the muscle results in lengthening of the muscle spindle and initiation of the monosynaptic stretch reflex.
Consequently, sudden or ballistic stretching of musculotendinous units may cause the muscle to contract while it is being
lengthened, resulting in increased soreness.
Another sensory organ, the Golgi tendon organ, is found in the musculotendinous junction and is sensitive to tension
caused by passive stretching or active contraction of the musculotendinous unit. Excessive musculotendinous tension
causes the Golgi tendon organ to discharge, inhibiting contraction. Stretching techniques such as contract-relax use the
Golgi tendon organ to inhibit the muscle contraction, allowing it to lengthen.
Reciprocal inhibition occurs when an antagonist muscle is inhibited as the corresponding agonist muscle contracts. This
principle can also be incorporated into stretching techniques, such as contract-relax-contract and agonist contraction.
Range of Motion Exercises
ROM exercises are exercises that are performed within the unrestricted ROM in order to maintain joint mobility. They can
be passive, active assistive, or active. Passive ROM exercises are movements that are produced by an external force
without voluntary muscular effort on the part of the athlete. The external force may be applied by an athletic trainer or
therapist, another part of the athlete's own body, a machine, or gravity. Passive ROM is indicated when the athlete is not
able to move the body segment voluntarily or when voluntary muscle activity would be detrimental to the healing process.
This technique can be used to limit the adverse effects of immobility and to demonstrate motion when teaching other
forms of exercise. In addition, passive ROM techniques may be applied before stretching. Passive ROM does not prevent
muscle atrophy and does not affect muscle strength or endurance. Nor does it improve circulation to the same extent as
voluntary, active use of the muscles. True passive movement may be difficult to obtain when muscles are innervated.
Active ROM exercises are exercises within the unrestricted ROM that are produced by active voluntary muscle
contraction. Active assistive exercises combine active voluntary contraction with an outside force to complete motion
within the unrestricted range. Both active and active assistive ROM exercises are used when the athlete is able to
actively contract the muscles to move the segment and there are no contraindications for active voluntary muscle
contraction. Active and active assistive ROM exercises can be used for the following purposes:
1. To limit the adverse effects of immobility and maintain contractility of muscles
2. To provide sensory feedback
3. To provide a stimulus for maintaining integrity of bone
4. To increase circulation
5. To improve coordination and motor skills necessary for functional activities
6. To improve strength of very weak muscles
Sustained exercises involving large muscle groups can be used to improve cardiorespiratory function. However, active
assistive and active exercises cannot be used to strengthen or maintain strength of muscles that are already strong.
Furthermore, active exercises develop skill and coordination only in the movement patterns used.
ROM exercises are contraindicated when motion is disruptive to the healing process. It is important to recognize signs of
excessive exercise if ROM exercises are performed acutely after injury. These signs include increased pain, swelling,
warmth, redness, and loss of motion that persists for longer than 1 to 2 hours after completion of the exercise. ROM
exercises should not replace stretching exercises when the treatment goal is to increase ROM.
ROM exercises may be performed in anatomic planes or in combined patterns incorporating movement in several planes
simultaneously. ROM exercises also can be performed using sport-specific functional patterns. They should be
performed within the pain-free ROM. Motion beyond the available ROM should not be forced. Usually, 5 to 10 repetitions
several times per day is adequate to limit the adverse effects of immobility. The athlete's response to ROM exercises
should be closely monitored and documented. Treatment must be modified as the athlete progresses.
Stretching
Stretching exercises are designed to increase ROM and lengthen pathologically shortened soft tissue structures.
Stretching may be performed actively or passively. During passive stretching, the stretch is produced by external forces
applied to the body. In active stretching, the stretching force is created by active voluntary contraction of the athlete's
muscles. Active stretching allows for incorporation of the neurophysiologic principles of stretching.
Flexibility is defined as the ability of the muscle to relax and yield to a stretching force ( 19). Flexibility exercises are used
to increase length of the musculotendinous unit. The term flexibility exercise is often used synonymously with stretching
exercise.
A contracture is a shortening of a muscle or other tissues that cross a joint that results in loss of motion. Contractures are
defined by identifying the muscle group that limits the ROM. For example, a lack of full knee extension would be termed a
knee flexion contracture, and a lack of full knee flexion would be termed a knee extension contracture. A myostatic
contracture refers to an adaptive shortening of the musculotendinous unit that results in loss of motion. Tightness is a
nonspecific term used to describe mild shortness of the musculotendinous unit that does not result in loss of joint motion.
Tightness is common in multijoint muscles such as the hamstrings, rectus femoris, and gastrocnemius. Tightness can be
improved by self-stretching or flexibility exercises.
During passive stretching exercises, the stretching force is produced externally to the body. The external force can be
applied manually or mechanically. Manual passive stretching exercises are usually of short duration, lasting 15 to 30
seconds per repetition. The stretch can be applied statically or ballistically. A slow static stretch is less likely to elicit a
stretch reflex response. Ballistic stretching refers to a high-intensity, short-duration stretch that results in rapid
lengthening of the muscle, which, in turn, stimulates the muscle spindle and facilitates a stretch reflex. The
musculotendinous unit is susceptible to microtrauma with ballistic stretching. Ballistic stretching may be beneficial
immediately before engaging in exercise, but should be performed only after a warmup that includes slow static
stretching.
Passive mechanical stretching is performed by applying a low (5 to 10 lb) external load to the shortened tissues for a
prolonged period (15 to 30 minutes). Passive mechanical stretching may be performed with the use of ankle weights ( Fig.
6.5) or other mechanical equipment. Prolonged mechanical stretch may result in greater permanent lengthening of
contractile and noncontractile tissues.
FIGURE 6.5. Passive mechanical stretching can be performed with the use of ankle weights or other similar equipment.
In the prone position, an ankle weight applied to the distal leg can be used to increase knee extension. A low load is
applied for a prolonged period. Heat may be applied simultaneously to maximize plastic deformation.
Neurophysiologic principles can be incorporated to relax muscles before elongation. This allows the contractile
component to be lengthened more easily. These techniques may be used to stretch tight contractile structures, such as
those associated with muscle spasm, more comfortably; however, they do not generally result in a permanent increase in
length. Examples of neurophysiologic stretching techniques include contract-relax and contract-relax-contract.
Contract-relax stretching techniques involve isometric contraction of the tight muscle followed by lengthening of the
muscle. The prestretch contraction of the short muscle results in autogenic inhibition stimulation of the Golgi tendon
organ. A contract-relax stretching technique to stretch the hamstrings, for example, would incorporate contraction of the
hamstring by simultaneous hip extension and knee flexion, followed by passive lengthening of the hamstrings after the
contraction has been completed.
Contract-relax-contract stretching techniques incorporate an isometric contraction of the tight muscle, followed by
relaxation and contraction of the antagonistic muscle while the tight muscle is lengthened. Contract-relax-contract
stretching techniques combine autogenic inhibition with the principle of reciprocal inhibition. A contract-relax-contract
technique to lengthen the hamstrings would incorporate contraction of the hamstring by simultaneous hip extension and
knee flexion, followed by relaxation of the hamstring muscle and contraction of the quadriceps and hip flexors while the
hamstring is lengthened.
The athlete should be taught self-stretching techniques that incorporate use of the athlete's body weight with active
inhibition to stretch the tight muscle. These techniques should be performed after the passive stretching and active
inhibition techniques already described. The athlete also should be instructed to perform self-stretching exercises several
times daily to make continued gains in ROM.
Stretching exercises are indicated when the athlete demonstrates limited ROM in the subacute or chronic phase of
healing. It is necessary to regain the full ROM required for athletic activity to avoid interference with sports-related skills.
Stretching exercises also can be used to correct muscle imbalances that result when a muscle group is tight and its
opposing muscle group is weak. Generally, the tight muscle group should be stretched before strengthening exercises
are performed to improve the strength of the opposite muscle group. Stretching exercises may also be indicated before
activity as a warmup and after activity as a cool down. Proper warmup and cool down minimize the risk of
musculotendinous injuries associated with physical activity and sports. Stretching exercises should avoid forcing the joint
beyond the normal ROM required for athletic activity. In carrying out these exercises, care should be taken to avoid
creating a hypermobile joint. Stretching exercises should not be performed in the acute stages of healing. Stretching
during this period may jeopardize the healing tissue and aggravate inflammation. During this time, ROM exercises rather
than stretching exercises should be used. Stretching exercises should not cause a persistent increase in pain that lasts
longer than 1 to 2 hours. Caution must be used when stretching across the fracture site of a newly united fracture.
Stretching exercises should not be used in an attempt to increase motion that is limited by a bony block.
Before stretching, a local application of heat or engagement in active exercise to elevate body temperature may be
beneficial because it increases soft tissue extensibility. Massage and biofeedback may be employed to promote
relaxation and decrease muscle spasm, making it easier to stretch tight muscles. If mobility of a joint surface is limited,
mobilization techniques should be used before stretching exercises.
Joint Mobilization
In order to understand the principles of joint mobilization, which is used to restore normal movement of the joint surfaces,
it is necessary to understand arthrokinematics and osteokinematics. Arthrokinematics refers to movements of the joint
surfaces that are necessary for normal physiologic movement of the joint through a full ROM. Movements of the joint
surfaces include distraction, compression, rolling, gliding, and spinning. Osteokinematics refers to the angular
displacement of the bone during physiologic motion ( 27).
The shapes of the joint surfaces determine the amount and type of motion available at a joint. An ovoid joint is one in
which one joint surface is convex and the other is concave. A sellar-shaped joint is one in which a surface is convex in
one direction and concave in the opposite direction. The other surface is reciprocally shaped. ( Fig. 6.6). The mechanical
axis of the joint is a line perpendicular to the center of the joint surface ( Fig. 6.7).
FIGURE 6.6. A: Ovoid joint—one surface is convex and the other surface is concave. B: Sellar joint—one surface is
convex in one direction and concave in the opposite direction. The other joint surface is reciprocally shaped. (Modified
from Kisner C, Colby LA. Therapeutic exercise: foundations and techniques, 2nd ed. Philadelphia: FA Davis, 1990, with
permission.)
FIGURE 6.7. The mechanical axis is a line perpendicular to the center of the joint surface.
Angular movement of a bone about its axis of rotation is termed a swing. Rolling occurs when new points on one joint
surface meet new points on an opposing joint surfaces, much like a tire rolling along a road ( Fig. 6.8A). Rolling of the joint
surface always occurs in the same direction as the swing of the bone. The joint surfaces are compressed on the side to
which the bone is rolling and separated on the opposite side. This may traumatize articular surfaces when gliding of joint
surfaces is limited.
FIGURE 6.8. A: Representation of rolling. New points on one surface contact the new points on the opposing surface. B:
Representation of gliding. New points on one surface contact the same point on the opposing surface. (Modified from
Kisner C, Colby LA. Therapeutic exercise: foundations and techniques, 2nd ed. Philadelphia: FA Davis, 1990, with
permission.)
Rolling does not occur in isolation during the normal movement of a joint. Rolling is accompanied by sliding of the joint
surfaces to prevent the convex joint surface from rolling off the concave surface. Sliding of joint surfaces involves contact
of the same point on one surface with new points on the opposing surface, much like a locked tire sliding over a road
(Fig. 6.8B). The direction of the gliding depends on the shape of the articular surface. Convex joint surfaces glide in a
direction opposite to the swing of the bone, while concave joint surfaces glide in the same direction as the swing of the
bone. Normal joint motion combines both rolling and gliding of the joint surfaces. Joint mobilization techniques are
designed to restore the normal gliding of joint surfaces that is necessary for physiologic motion.
Joint mobilization techniques can be used to increase joint play in hypomobile joints. Restoration of normal joint play is
necessary to restore full physiologic motion. Joint mobilization increases the extensibility of tight capsules and ligaments
that limit mobility of the joint surfaces.
Joint mobilization can also be used to reduce pain and spasm. Small-amplitude, oscillatory joint mobilization stimulates
joint mechanoreceptors and can inhibit the perception of pain. Joint mobilization techniques may also reduce pain by
stimulating movement of synovial fluid and preventing fluidostasis.
Joint mobilization is contraindicated in hypermobile joints. These same techniques are also contraindicated during the
period of active inflammation. During this period, joint mobilization aggravates inflammation. Joint mobilization is also
contraindicated in the presence of a large joint effusion in which the capsule is already stretched because of distention of
the joint. Use of mobilization techniques after fracture of a bone should be delayed until there is radiographic evidence of
union.
Proper application of joint mobilization techniques requires grading of the forces that are used. The Maitland or
Australian system uses oscillatory techniques ( 28). Techniques are graded I through IV. Grade I oscillations are
small-amplitude movements at the beginning of the available ROM. Grade II oscillations are large-amplitude motions
performed within the available range but not up to the motion barrier. Grade III oscillations are large-amplitude motions
performed up to and beyond the motion barrier. Grade IV oscillatory movements are small movements performed at and
beyond the motion barrier. In the Australian system, grade I and II oscillatory motions are used to stimulate
mechanoreceptors so as to decrease pain. Grade III and IV oscillatory movements are used to stretch tight structures in
order to increase joint mobility and ROM.
The Kaltenborn or Norwegian system uses sustained mobilization techniques ( 29). This system has three grades of
motion. Grade I, also called piccolo motion, separates the joint surfaces just enough to equalize intraarticular and
atmospheric pressure and is typically used to decrease pain. Grade II, or slack technique, removes the slack from the
capsule and surrounding ligaments and can be used as a trial treatment to increase ROM. Grade III, or stretch technique,
uses sufficient force to stretch joint structures to improve mobility.
In general, the oscillatory motions of the Australian system are used to decrease pain and the sustained movements in
the Kaltenborn system are used to improve joint mobility and ROM.
Proper application of joint mobilization techniques requires a thorough examination of the involved joint to determine the
tissues limiting motion as well as the stage of pathology. The mobilizing force should be correlated with the sequence of
pain in relation to resistance to motion. Pain occurring before resistance to motion is reached indicates an acute
condition. Mobilization for acute conditions should consist of grade I and II oscillating techniques to decrease pain and
maintain joint play. Pain synchronous with resistance to motion indicates a subacute condition. A trial of gentle stretching
should be used for subacute conditions. Grade III oscillatory or grade II (slack) mobilization techniques are appropriate
for subacute conditions. Pain engaged after resistance to motion has been encountered is indicative of a chronic
condition. Vigorous stretching is indicated for chronic conditions. Joint mobilization techniques for chronic conditions
include grade III and IV oscillatory or grade III (stretch) sustained techniques.
Joint mobilization techniques should be used only when mobility testing reveals decreased joint play. Hypermobile joints
should not be mobilized. In general, mobilization techniques are used when passive ROM is limited in a capsular pattern
with a capsular or firm end feel. Joint mobilization techniques may be used when passive ROM is limited in a
noncapsular pattern if joint play is limited in the direction of the restricted motion.
For joint mobilization procedures, the athlete should be positioned to promote relaxation and stabilization of the part to be
mobilized. Initially mobilization should be performed with the joint in the position in which the capsule has the greatest
amount of laxity (usually in the middle of the available ROM). As ROM improves, joint mobilization techniques can be
performed in the restricted position. Forces should be applied as close to the opposing joint surfaces as possible. The
area of contact with the hand should be as large as possible to improve patient comfort. The force of the mobilization
technique should be graded according to the stage of the condition and the intended goals of treatment as described
previously.
The direction of movement is dictated by the direction of the restricted motion and the shape of the joint surface. The
treatment plane is a plane perpendicular to a line from the axis of rotation to the center of the concave articulating
surface (Fig. 6.9). When joint surfaces are distracted, the force should be applied perpendicular to the treatment plane.
When gliding of joint surfaces is performed, the forces should be applied parallel to the treatment plane, using the
following rule: concave joint surfaces should be glided in the direction of the limited swing of the bone, and convex
surfaces should be glided in the direction opposite the limited swing of the bone. When joint mobilization techniques are
performed, angular motion of the bone should be minimized. Angular motion during gliding of joint surfaces may result in
compression of the joint surfaces, which could damage the articular surface.
FIGURE 6.9. The treatment plane (T.P.) is a line perpendicular to the line drawn from the axis of rotation for the joint to
the center of the concave joint surface. Forces to distract the joint are applied perpendicular to the treatment plane.
Forces to glide the joint are applied parallel to the treatment plane. (Modified from Kisner C, Colby LA. Therapeutic
exercise: foundations and techniques, 2nd ed. Philadelphia: FA Davis, 1990, with permission.)
When oscillatory joint mobilization techniques are performed, they should be done at a rate of 1 to 2 cycles per second
for 1 to 2 minutes. When sustained joint mobilization techniques are performed, they should be sustained for 5 to 15
seconds and repeated 10 times. Joint mobility and ROM should be assessed at the completion of joint mobilization. The
athlete also should perform ROM and stretching exercises as a follow-up treatment to joint mobilization. The athlete
should be warned that it is common to experience some increase in soreness; however, this should subside within
several hours.
PRINCIPLES FOR IMPROVEMENT OF MUSCLE PERFORMANCE
Rehabilitation of athletes must also address muscle performance, including strength, power, and endurance. Strength is
defined as the maximal force that a muscle can generate at a specified velocity. Force is a linear measure that changes
the state of rest or motion of matter. When applied to the musculoskeletal system, muscle force causes rotation of a joint
about its axis. Force is measured in newtons (N). Torque is the effectiveness of the force to produce rotation about an
axis; it is the product of force times the perpendicular distance from the line of action of the force to the axis of rotation.
Torque is measured in newton-meters (N-m). Work is force expressed through a distance with no limitation on time.
Mathematically, work is force times distance. It is expressed in joules (J). Power is the rate of doing work per unit of time.
It is expressed as force times distance over time, or as force times velocity. It is expressed in watts (W). Power is not
force at high contractile velocities. Maximum power occurs at intermediate contractile velocities for concentric
contractions. Endurance is the ability of the muscle or muscle group to perform work over time. It can be measured as the
time during which a person is able to maintain a particular level of isometric force or power involving a combination of
concentric and eccentric contractions.
Strength
The strength of normal muscle is influenced by several factors. The amount of force that a muscle can generate is related
to its cross-sectional size. Length of the muscle also influences force generation. According to the length-tension
relationship, muscle can generate maximal force at its resting length. This is the position at which there is a maximum
number of cross-bridges between the actin and myosin filaments. As the muscle shortens, there is greater overlap of the
actin-myosin filaments, resulting in a decreased number of cross-bridges. As a result, the force that a muscle can
generate in a shortened position is decreased. The contractile force generated by a muscle also decreases as the
muscle is lengthened beyond its resting position. However, there is increased force because of passive lengthening of
the connective tissue. Therefore, the total force produced by the musculotendinous unit (including both contractile and
noncontractile forces) increases as the muscle lengthens ( Fig. 6.10).
FIGURE 6.10. Relationship of contractile and noncontractile tension to total tension of a muscle. Contractile tension is
greatest at the resting length of the muscle. As the muscle is shortened or lengthened, contractile tension decreases.
Noncontractile tension increases as the muscle is lengthened. The total tension produced by a muscle is the sum of
contractile and noncontractile tension.
The number of motor units recruited also influences the level of force generated. The level of force increases as the
number of motor units recruited increases. According to Henneml's size principle, small motorneurons are recruited
before large motorneurons. Small motorneurons innervate slow-twitch (type I) muscle fibers. These fibers produce low
levels of force and are resistant to fatigue. Large motorneurons innervate fast-twitch (type II) muscle fibers. Fast-twitch
muscle fibers produce high levels of force, but they fatigue rapidly. Because small motorneurons are recruited before
large motorneurons, activities involving low levels of muscle tension are accomplished primarily by slow-twitch muscle
fibers. As force requirements increase, progressively more fast-twitch fibers are recruited.
The speed and type of muscle contraction also influence the amount of force that a muscle can generate. For concentric
contractions, force decreases as speed increases; for eccentric contractions, force increases as speed increases up to
some maximal value. A maximal eccentric contraction produces greater force than a maximal isometric contraction, and a
maximal isometric contraction produces greater force than concentric contraction.
Motivation also influences the amount of force generated by a muscle. The individual must be willing and motivated to put
forth maximum effort in order to generate maximum forces.
Strength-training exercises are designed to increase the maximum force that a muscle can generate. Traditionally,
strength training involves heavy-resistance, low-repetition exercise. The definition of heavy resistance varies among
individuals and from muscle group to muscle group. In general, heavy resistance is considered to mean the amount of
weight that can be lifted for 6 to 12 repetitions before fatigue develops. Strength-training exercises using heavy
resistance are typically performed for 6 to 12 repetitions.
Response to strength training includes hypertrophy of muscle fibers. The increase in cross-sectional area of muscle
fibers is related to increased contractile protein and the number of fibrils within the muscle fiber, as well as an increased
density of the capillary bed surrounding individual muscle fibers. Hypertrophy also may be related to an increase in the
connective tissue component of muscle. Heavy-resistance training appears to selectively hypertrophy fast-twitch (type II)
muscle fibers.
Hyperplasia is an increase in the number of muscle fibers that results from longitudinal splitting of muscle fibers.
Hyperplasia has been observed in laboratory animals exposed to heavy resistance exercise ( 30,31 and 32); however,
hyperplasia in humans is controversial. In response to strength training, individuals are able to recruit an increased
number of motor units. Improved recruitment and synchronization of motor units results in greater generation of muscle
force. This may explain increases in strength that occur early in the training program in the absence of hypertrophy.
Biochemical changes associated with strengthening are small and inconsistent.
Endurance
Endurance training makes use of low- to moderate-resistance, high-repetition exercises. Endurance training results in
peripheral and central adaptations that improve an individual's ability to sustain work.
The peripheral adaptations are localized to the muscle or muscles involved in the endurance-training exercises. The
peripheral responses generally result in an improved oxidative capacity of the muscle fiber. This is caused by an
increased concentration of myoglobin within the muscle fibers. Increased myoglobin concentration aids in the delivery of
oxygen from the cell membrane to mitochondria. A muscle fiber's ability to oxidize carbohydrates and fats is improved.
This is caused by an increase in the size, number, and membrane surface area of mitochondria, as well as an increase in
the concentration and activity of oxidative enzymes. The intramuscular stores of adenosine triphosphate and creatine
phosphate are increased. There appears to be selective hypertrophy of slow-twitch (type I) muscle fibers; however, this
may be modified by the intensity of the endurance exercise. High-intensity endurance training (greater than 90%) results
in improved endurance capabilities in type II fibers ( 33,34). Anaerobic glycolysis is not appreciably affected by endurance
training.
Cardiovascular responses to endurance training occur if the training stimulus is sufficient. These responses include
increased cardiac output, which is related to increased stroke volume. Resting heart rate and heart rate at a given work
load decrease in response to endurance training.
Precautions, Fatigue, and Muscle Soreness
Contraindications to resistive exercise include active inflammation and pain. Use of resistive exercise in the presence of
active inflammation can lead to further tissue trauma and aggravate pain and swelling. Resistive exercises should be
eliminated or reduced if they produce an increase in pain that persists more than a few hours after exercise.
Several precautions should be observed when performing resistive exercises. These include avoidance of a Valsalva
maneuver, which may cause a transient but marked increase in blood pressure that places abnormal stress on the
cardiovascular system. Athletes should be warned directly to avoid use of the Valsalva maneuver; they also should be
instructed to exhale while performing resistance exercises—particularly during isometric and heavy-resistance exercises.
Prolonged resistive exercises result in local muscular fatigue and total body fatigue. Local muscular fatigue is a
diminished response of a muscle to sustained work. The fatigue may be caused by disturbances in the contractile
mechanism of the muscle, including decreased energy stores, insufficient oxygen, and lactic acid accumulation. Local
muscular fatigue also may result from inhibitory influences from the central nervous system, pain, and discomfort. Total
body fatigue occurs in response to prolonged resistance exercises and may result from decreased blood glucose or
depletion of muscle and/or liver glycogen. No biologic marker of overtraining exists. Adequate time must be included in
the training program for recovery from vigorous exercise in order to avoid fatigue. Recovery is associated with removal of
lactic acid and replenishment of energy and oxygen stores. Light exercise may facilitate recovery, and recovery after
each exercise session is required in order to improve performance. This requirement has implications for
rehabilitation—particularly in the later stages, when the intensity of exercise is increased and more time for recovery is
required from session to session.
The athlete must be observed carefully when performing resistance exercises to detect substitute motions, in which
alternative motions or muscles complete the motion when the prime movers are weak or fatigued. Use of substitute
motion allows muscle weakness to persist. Substitute motions can be avoided by using appropriate amounts of
resistance and instructing the athletes to perform the exercise precisely.
Resistance exercises also may result in the development of muscle soreness. Immediate muscle soreness occurs during
or directly after strenuous exercise. It may be related to muscle injury, ischemia, or the buildup of metabolites.
Immediate-onset muscle soreness usually subsides quickly after exercise with rest.
By contrast, delayed-onset muscle soreness develops 24 to 48 hours after vigorous exercise. Numerous causes have
been postulated, none satisfactory. Accumulation of lactic acid in the muscle was one of the postulated causes; however,
lactic acid is cleared approximately 1 hour after exercise. The reflex pain—spasm theory, as proposed by DeVries ( 35),
held that ischemia produces pain, which in turn produces a reflex muscle spasm. A positive feedback loop develops as
spasm creates further pain and ischemia. The original evidence for this theory included increased electromyographic
(EMG) activity from muscles with delayed muscle soreness; however, this evidence has not been duplicated by others.
Currently, the most plausible explanation for delayed-onset muscle soreness is microscopic tearing of muscle or
connective tissue or both during vigorous exercise. Disruption of tissue results in inflammation and pain. This theory is
supported by the observation that delayed-onset muscle soreness is more common after eccentric exercise. Microtearing
of muscle and connective tissue may be more pronounced as the muscle lengthens against resistance.
Prevention of delayed-onset muscle soreness includes appropriate periods of warmup and cooldown before and after the
resistance exercise. In addition, delayed-onset muscle soreness may be prevented by a gradual progression of the
resistive exercise program and by avoidance of the eccentric component of exercise.
Isometric Exercises
Isometric exercises are one form of resistive exercise in which the muscle contracts without an appreciable change in the
length of the muscle (i.e., no visible joint motion). Because isometrics occur in the absence of joint motion, they can be
used when motion is contraindicated. They are also easy to perform and require little equipment. However, isometric
exercises develop strength only at the joint position at which the exercise is performed; they must be performed at
increments of 15 to 30 degrees to develop strength throughout the full ROM. Isometric exercises do not significantly
improve endurance.
When performing isometric exercises, the athlete should be instructed to contract the muscle maximally, holding it for 5 to
10 seconds to allow time for development of peak tension. The isometric exercises should be performed at multiple
angles to improve strength throughout the ROM. Submaximal isometrics can also be used to maintain mobility between
muscle fibers during the healing phase.
Isotonic exercises make use of movement against a constant external resistance. They can be performed manually or
mechanically to improve strength, power, and endurance. In order to make continued improvements in muscle function,
the overload principle must be applied, and the muscle must be progressively loaded by increasing resistance or
repetitions or both.
When designing an isotonic exercise program, specificity of the exercise must be considered. This means that the
exercise program must be designed to strengthen the muscle or muscle groups used during specific functional activities.
The speed of the exercise should match the speed of the functional movement. The resistive exercise program should
also reproduce the type of contraction required during function. Isometric exercises should be used to develop muscles
that stabilize the body or body segment. Concentric exercises should be used to develop muscles that are responsible for
acceleration of the body, and eccentric exercises to develop those that are responsible for deceleration. Specificity of the
exercise program should also consider the intensity of force required by the muscles during activity. The exercises
should be performed through the entire ROM in which strength is required. When possible, functional exercise patterns
should be used to develop strength. This implies the use of closed-chain activities for the lower extremity and open-chain
activities for the upper extremity. During closed-chain activities, the distal aspect of the extremity is fixed and motion
occurs simultaneously at all joints that comprise the kinetic chain. During open-chain activities, the distal extent of the
extremity is free to move. In order for exercises to be specific, the variables must match the requirements and demands
placed on the athlete during functional activities.
When developing an isotonic exercise program, several variables must be considered, including load, repetitions, sets,
and frequency. Load is the amount of resistance used during the exercise. To improve strength, the load must be
progressively increased. Repetitions are the number of times an exercise is performed in a given bout. The number of
repetitions must be progressively increased to improve endurance. Sets are the number of bouts of repetitions that are
performed. There are many combinations of sets and repetitions that can be used to improve strength, endurance, or
both. Frequency is the number of times the exercises are performed per day or per week. Early in rehabilitation, isotonic
exercises are usually submaximal and can be performed several times daily. As rehabilitation progresses to
reconditioning, the isotonic exercising should become more vigorous, but they should be performed less frequently to
allow adequate time for recovery and prevention of fatigue. Most heavy-resistance exercise programs designed to
improve strength are done every other day. Six weeks may be required before increased strength is seen.
Exercise Programs
The intensity of exercise depends on the stage of inflammation and healing as well as the goals of the exercise program.
Generally, submaximal exercises are used to increase muscle endurance. They are emphasized during the early stages
of rehabilitation to protect healing tissues and to avoid pain and further aggravation of the injury. Maximal exercises are
used in the later stages of rehabilitation, when the goal is to recondition the athlete to improve strength and power.
Several specific exercise regimes to improve strength have been proposed. DeLorme and Watkins ( 36) proposed a
technique of progressive resistance exercises (PREs) that begins by establishing a 10-repetition maximum (RM) weight.
This is defined as the amount of weight that can be lifted precisely 10 times, and it is usually established by trial and
error. In the scheme proposed by DeLorme, 3 sets of 10 repetitions are performed. The first set is against one half of the
10-RM weight, the second is against three quarters of the 10-RM weight, and the third is against the full 10-RM weight. A
new 10-RM weight is determined each week. The method proposed by DeLorme builds in a gradual warmup.
The Oxford technique ( 37) is the opposite of the Delorme method. The first set is performed against the full 10-RM
weight, and the third set is performed against one half of the 10-RM weight. This method attempts to accommodate for
the effects of fatigue; however, warmup is required before beginning.
Knight (38) proposed a program of daily adjustable progressive resistive exercises (DAPRE). This program attempts to
objectively determine when and by how much to increase resistance. Knight originally proposed using a 6-RM weight,
which is the amount of resistance that can be lifted precisely 6 times. Four sets of exercise are performed. The first set of
10 repetitions is performed with one half of the 6-RM weight. The second set of 6 repetitions is performed with three
quarters of the 6-RM weight. The third set consists of as many repetitions as possible at the full 6-RM weight. The
number of repetitions performed during the third set is used to determine the resistance for the fourth set. If more than 6
repetitions are performed during the third set, then the weight for the fourth set is increased. If less than six repetitions
are performed for the third set, then the weight for the fourth set is decreased. The number of repetitions performed
during the fourth set determines the amount of weight used for the next session.
The methods proposed by DeLorme, Oxford, and Knight make use of heavy-resistance, low-repetition exercise in an
attempt to increase strength. It should be noted that heavy-resistance exercise may be inappropriate for the early stages
of healing. Heavy resistance may not be tolerated by the joint and the healing structures during this time. For this reason,
exercises using submaximal resistance for a greater number of repetitions (e.g., 30 to 50) may be performed during this
period. Use of heavy-resistance exercises is delayed until the athlete enters the reconditioning phase of rehabilitation.
As noted earlier, isotonic exercises can be performed mechanically or manually. Mechanical resistance exercises have
several advantages. The amount of resistance and the number of repetitions performed can quantify the patient's
baseline level of muscle performance and progression. In addition, the athlete can see his or her progress when
performing mechanical resistance exercise. This visible progress provides motivation. Resistance applied during
mechanical resistance exercises is not limited by the strength of the athletic trainer or therapist. A variety of equipment
can be used to provide mechanical resistance.
During manual resistance exercises, resistance is applied by the therapist or athletic trainer. Manual resistance exercise
can make use of dynamic or static muscular contractions and can be performed in the cardinal planes or in more
functional diagonal patterns. Proprioceptive neuromuscular facilitation is a technique of manual resistance exercise that
emphasizes movement in diagonal patterns.
The popularity of isokinetic exercise has increased over the last 20 years. During isokinetic exercise, the speed of
exercise is controlled by a dynamometer. Most isokinetic dynamometers allow concentric and eccentric exercise ranging
from 0 to 450 degrees per second. During isokinetic exercise, the resistance is accommodating and proportional to the
effort put forth by the athlete. Research indicates that there may be some carryover of training from one speed to
another. However, to ensure improvement in muscle performance across the spectrum of speeds, isokinetic training
should be performed at a variety of contractile velocities ( 39). Ideally, the speed of exercise selected for isokinetic
training should be comparable to the speed of movement required by function. However, the angular velocity during
function typically exceeds the speed of movement permitted by the isokinetic dynamometer. Caution must be used when
performing isokinetic exercise to ensure that further inflammation or injury does not occur. Inappropriate use of isokinetic
exercise can be detrimental. During the earlier phases of rehabilitation, isokinetic exercise should be submaximal.
Maximal isokinetic exercise should be reserved for the final stages of rehabilitation. Isokinetic testing has been used to
measure muscle performance and to determine when an athlete is ready to return to full activity. However, there is little
scientific validation for the use of isokinetic testing to predict athletic function.
PRINCIPLES FOR IMPROVEMENT OF PROPRIOCEPTION
The central nervous system receives sensory input from multiple sources and processes this information to help regulate
musculoskeletal control. Information on the perception of joint movement, body posture, and position is delivered to the
central nervous system through the somatosensory system, the vestibular system, and the visual system. Pain, pressure,
touch, and movement of the musculoskeletal system are sensory stimuli detected by the somatosensory system. The
vestibular system receives sensory stimuli from the vestibular apparatus of the inner ear and uses this information for
conscious and unconscious awareness and control of body position and posture. The visual system provides sensory
stimuli regarding body position and orientation in space ( 40).
Proprioception has been described as the part of the somatosensory system that includes sensation of joint motion and
position, as well as muscle length and tension ( 41). Proprioception is mediated by sensory receptors that are located in
the skin, musculotendinous units, ligaments, bones, and joint capsules ( 42). These sensory receptors transduce
mechanical deformation to a neural signal that modulates conscious and unconscious responses. It has been
hypothesized that proprioception is important for providing smooth, coordinated movement and for protection and
dynamic stabilization of joints. There also has been interest in the role that proprioception plays in the prevention and
progression of injuries.
Mechanoreceptors have been identified in the ankle ( 43), knee (44,45,46,47 and 48), and shoulder (49,50). These
receptors have been identified in the joint capsules, ligaments, menisci, labrum, and fat pads. Four types of joint
mechanoreceptors have been described ( 43). Type I mechanoreceptors are Ruffini-like receptors that respond at rest
and during movement to convey the direction, velocity, and amplitude of movement. They have a low threshold for
excitation, and they adapt slowly. Type II mechanoreceptors are pacinian-like receptors that have a low threshold for
excitation and adapt rapidly. They are responsible for signaling acceleration and deceleration of the joint. Type III
mechanoreceptors are similar to the Golgi tendon organs that lie in the musculotendinous unit. They have a high
threshold for excitation and are nonadapting. They respond at the extremes of motion and may be responsible for
mediating protective reflex arcs. Type IV mechanoreceptors are free nerve endings that convey pain.
Joint proprioception is also dependent on sensory information from skeletal muscle. Specialized mechanoreceptors found
within the skeletal muscle respond to changes in muscle length and are integrated with joint sensibility information from
the joint receptors. The neural contribution from joint and muscle receptors provides information regarding joint position,
motion, and acceleration (51).
It has been proposed that joint mechanoreceptors mediate protective reflexes. Solomonow et al. ( 52) described an
anterior cruciate ligament (ACL) hamstring arc in anesthetized cats. High loading of the ACL resulted in increased EMG
activity in the hamstrings and electrical silence in the quadriceps. The increase in hamstring EMG activity was not
evident when light to moderate loads were applied to the ACL. It was proposed that this ACL-hamstring reflex arc serves
to protect the ACL during conditions of high load. However, it is unknown whether this reflex arc can protect the joint from
injury if high loads are applied rapidly. Under rapid loading conditions, the ligament may be loaded and ruptured before
sufficient muscle tension can be generated to protect the ligament. It is likely that similar reflex arcs exist in other joints.
Other proprioceptive reflexes originating from the joint capsule or musculotendinous unit probably exist. This was
demonstrated by Solomonow et al. (52), who reported increased hamstring EMG activity in a patient with an
ACL-deficient knee during maximal slow-speed isokinetic testing of the quadriceps. The increased hamstring EMG
activity occurred simultaneously with anterior subluxation of the tibia at approximately 40 degrees of knee flexion and
was associated with a sharp decrease in quadriceps torque and EMG activity. Because the ACL was ruptured, reflex
contraction of the hamstrings could not have been mediated by receptors originating in the ACL. It was proposed that this
reflex contraction is mediated by receptors in the joint capsule or in the hamstring muscles, or both. It is likely that similar
reflex arcs exist in other areas of the body.
Several clinical studies have evaluated proprioception in terms of the threshold to detection of passive motion and
reproduction of joint position. Barrack et al. ( 53) demonstrated deficits in the threshold to detection of passive motion in
subjects with a unilateral ACL-deficient knee. Lephart et al. ( 54) studied threshold to detection of passive motion in
patients who had undergone ACL reconstruction. Testing was performed at 15 and 45 degrees of flexion. Three trials
were performed moving into flexion-extension. The results indicated that threshold to detection of passive motion was
less sensitive in the reconstructed knee compared with the noninvolved knee. Threshold to detection of passive motion
was more sensitive both in the reconstructed knee and in the normal knee at 15 degrees of flexion compared with 45
degrees of flexion. The enhanced sensitivity to passive motion near full extension may be a result of increased stress on
the ligament that makes it more sensitive to detection of motion. Kinesthetic deficits in the shoulder after anterior
glenohumeral dislocation were demonstrated by Smith and Brunolli ( 55). They found deficits in angular reproduction,
threshold to detection of motion, and end-range reproduction of joint angle in the shoulder that had been dislocated.
Injury to a joint may result in abnormal sensory feedback and altered neuromuscular control; the latter may account for
recurrent injury. Proprioceptive training after injury should attempt to maximize use of sensory information mediated by
the joint structures and musculotendinous unit to dynamically protect the area. Proprioceptive training requires repetition
to develop motor control of abnormal motion. Initially, control of abnormal motion requires conscious effort. Conscious
performance of the rehabilitation activities incorporates the higher brain centers and allows the athlete to facilitate
maximum sensory input (41). Through repetition of training, motor control of abnormal motion may become automatic and
occur subconsciously. This requires learning how to recruit muscles with the proper force, timing, and sequencing to
protect the area. However, the extent to which an individual can develop neuromuscular control of abnormal joint motion
to dynamically stabilize a joint is currently unknown. Further research is required to determine the effectiveness of
proprioceptive training to dynamically protect an injured area.
Initial proprioceptive activities are designed to enhance conscious awareness of joint position. This can be developed by
asking the injured athlete to match and rematch the position of the joint with eyes closed. Proprioceptive neuromuscular
facilitation techniques can also be used to enhance proprioception. Specifically, rhythmic stabilization can be used to
enhance joint stability. This should initially be performed with the joint in the resting position. As the patient improves,
dynamic stabilization can be performed at the extremes of motion. Likewise, the amplitude and velocity of the
perturbances applied during rhythmic stabilization can be increased. The application of force to produce rapid changes in
joint position promotes unconscious dynamic muscular stabilization. This reflex joint stabilization addresses the spinal
level of motor control ( 41).
Rehabilitation exercises that challenge balance and maintenance of posture develop motor control at the brainstem level
(41). Initially, these are performed on a firm surface with contribution from the visual system. With improvement in their
sense of balance, athletes can progress to balancing on unstable surfaces such as a foam mat, minitrampoline, or
balance board. The visual system input can be withdrawn by having the athlete close the eyes while performing the
balance activities. The balance activities performed by the athlete should be specific tasks required for return to his or
her sport.
Return to athletic activity must include a transference of proprioceptive training to athletic activity. This can be
accomplished by slow, deliberate rehearsal of the particular activity to ensure that proper mechanics are being used.
Visual feedback can be given with the use of mirrors or videotape. EMG biofeedback can be used to ensure that muscles
are being recruited with the proper force, timing, and sequencing to protect the area.
A variety of sport-specific activities should be used to develop motor control of abnormal joint motion. To develop motor
control, activities are usually progressed from slow to fast speed, from low to high force, and from controlled to
uncontrolled activities. Emphasis should be on establishing proper movement patterns to dynamically protect the area.
General progression of activities to enhance proprioception and dynamic stability of the lower extremity moves from
walking to jogging, running, sprinting, acceleration and deceleration, jumping and cutting, pivoting, and twisting. The
athlete's sport should determine the specific activities for the upper extremity. The return to throwing for throwing athletes
has been described by Papas et al. ( 56) and Blackburn et al. (57). Return to throwing should progress from mirror
throwing, to a short-toss program, and finally to a long-toss program. Velocity should be increased gradually as tolerated.
The functional progression for return to activity must provide the athlete with adequate time to ensure a safe return to
sport with minimal risk for reinjury.
SUMMARY
The basic principles of rehabilitation for an injured athlete have been presented. These principles can be applied to
rehabilitate the common musculoskeletal injuries that occur in athletics. Development of a rehabilitation program is a
problem-solving process. It requires a thorough evaluation of the athlete in order to develop goals and a plan of care.
The basic principles of rehabilitation reviewed in this chapter can be applied to accomplish specific rehabilitation goals.
Finally, the athlete must be monitored continuously to ensure optimal progression through the rehabilitation program.
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7 Medical Problems
MEDICAL PROBLEMS
THOMAS H. TROJIAN
Anemia in the Athlete

Sports Anemia
Hemolytic Anemia (Exertion Hemolysis)
Blood Loss
True Anemia
Respiratory Problems
Exercise-Induced Asthma
Exercise-Induced Anaphylaxis
Laryngeal Spasm
Renal Problems
Proteinuria
Hematuria
Acute Renal Failure
Single Kidney
Hypertension
Blood Pressure
Treatment
Gynecologic Problems
Effects of the Menstrual Cycle on Exercise
Effects of Exercise on the Menstrual Cycle
Female Athlete Triad
Infectious Diseases
Mononucleosis
Common Cold
Traveler's Diarrhea
Human Immunodeficiency Virus Infection
Gastrointestinal Problems
Gastrointestinal Transit Time
Gastroesophageal Reflux
Gastrointestinal Bleeding
Liver Disease: Hepatitis
Diabetes
Definition
Exercise Response
Screening
Exercise Complications
When to Exercise
Treatment
Internet Resources
Muscle Problems
Delayed-Onset Muscle Soreness
Exertional Rhabdomyolysis
Overtraining
Chronic Fatigue in Athletes
Infection
Drugs
Electrolytes
Chronic Fatigue Summary
Chapter References
Medical problems affect athletes throughout their careers. Medical illnesses limit an athlete's peak performance. Often in
sports medicine, orthopedic injuries are the main focus, yet medical problems more often affect athletes. Many participate
while ill. Whether it is Michael Jordan playing in the National Basketball Association finals with a flulike illness or Jerome
Bettis with exercise-induced asthma (EIA), medical problems regularly influence the achievements of athletes.
ANEMIA IN THE ATHLETE
Anemia is a potential problem for every athlete. It is defined as a decrease in the hemoglobin (Hb) concentration or a
decrease in the number of red blood cells (RBCs). As in the general population, iron deficiency anemia is the most
common type, although there are many other causes of anemia in athletes. The sports medicine physician needs to be
aware of the various forms of anemia in order to differentiate them and treat appropriately.
The causes of anemia can be divided into four main categories: (a) dilutional anemia, as seen in pregnancy and sports
anemia; (b) excess destruction, as seen in congenital conditions such as spherocytosis and in athletes with footstrike
anemia; (c) blood loss from the gastrointestinal (GI) or genitourinary (GU) system; and (d) decreased production from
either too little iron to make Hb or inadequate precursors. All four areas are discussed here.
Sports Anemia
The term sports anemia was coined by Yoshimura (1). It is actually not a true anemia but a false anemia caused by
plasma expansion from exercise. The RBC mass is not decreased, as it is in true anemia but increased ( 2). The
decreased Hb values found are probably caused by the repeated relative hemoconcentration from dehydration during
training and then the subsequent overshoot from the plasma volume expansion. These overshoots cause a dilutional
anemia.
This pseudoanemia does not appear to be pathologic but rather an adaptive response to endurance training ( 3).
Therefore, supplementation with iron or other vitamins is not necessary. Though normalization of the Hb would be seen 5
days after cessation of exercise, no alteration in training is needed. Sports anemia should be considered a diagnosis of
exclusion, because other anemias are as common and do require treatment.
Hemolytic Anemia (Exertion Hemolysis)
This hemolytic anemia has forms including march hemoglobinuria and runner's footstrike anemia. Footstrike hemolysis is
probably the most recognizable cause of exertion hemolysis. It occurs because of the rupture of RBCs in the heel due to
heavy impact. Falsetti et al. ( 4) described foot impact and excess hemolysis as a cause of hematuria. Miller et al. ( 5)
noted that running uphill, which has less heelstrike than does running downhill, resulted in less hematuria. Falsetti's
group (4) noted a decrease in hematuria with running in soft-soled running shoes.
Exertion hemolysis is also seen in non-footstrike sports such as distance swimming. Intense exercise causes production
of factors that destroys RBCs (6). It has been demonstrated that during severe exercise there is an increased destruction
of erythrocytes caused by liberation of lysolecithin from the spleen ( 7). This would explain the RBC destruction in
nonimpact sports. For athletes, non-footstrike hemolysis could be an adaptive measure to reuse proteins for muscle
growth, which has been reported in rats ( 8).
Exertion hemolysis should be a diagnosis of exclusion. A blood smear examination reveals a normochromic and
normocytic anemia. There may be an elevated reticulocyte index in response to the destruction of RBCs. The mean
corpuscular volume is elevated as older, smaller RBCs are cleared. Haptoglobin levels are low because the protein is
used to bind to the excess free Hb that results from RBC destruction ( 4,9,10).
Treatment consists of cushioning of the heel and running with decreased impact, “light on your feet.” In the nonimpact
athlete, proper hydration and monitoring for possible blood loss from the GI or GU system is the best option. The anemia
is usually mild and resolves after cessation of activity.
Blood Loss
GI or GU bleeding caused by exercise most often occurs in endurance athletes ( 7a,11). Documented anemia has
occurred both from the GI and GU system (7a,12). Most often, exercise-related bleeding from GI or GU sources does not
cause anemia. Usually these are small occult bleeds associated with long races or trauma. They are self-limited in
nature.
In the GI system, most often the blood loss is secondary to use of nonsteroidal antiinflammatory drugs (NSAIDs) ( 11).
Recent use of NSAIDs and anemia in an athlete should prompt discontinuation of the NSAID and treatment with a
histamine 2 (H2) blocker or metoclopramide. Besides bleeding, NSAIDs have been noted to cause aplastic anemia and
varying degrees of bone marrow suppression. In endurance athletes, GI bleeds can be caused by intestinal ischemia
(13). Fecal occult blood samples are useful if there is a clinical suspicion of GI bleeding (see later discussion).
Hematuria can occur in athletes with strenuous exercise. There are many causes of hematuria. The benign causes are
intensity related. A careful exercise history is needed to document the amount of exercise. Exercise-induced hematuria
should not be considered without a strenuous level of exercise. Cessation of exercise for 48 to 72 hours resolves the
hematuria if it is exercise related.
Hematuria seldom causes anemia and is not frequently considered in the differential diagnosis of anemia in the athlete
(14). However, when recurrent and untreated, as may happen in endurance athletes, it can cause anemia, and it still
needs to be considered a diagnosis of exclusion when an athlete is evaluated.
True Anemia
Iron Deficiency
Iron deficiency anemia is the most common anemia in the athletic population, as it is among nonathletes. The true
prevalence of the disease is controversial ( 2). The rate is as high as 20% in menstruating women and 6% in
postmenopausal women; in men it is 4% (2). The studies from which these figures are drawn looked at serum ferritin
levels, which overestimate iron deficiency by 50%. Most studies of athletes, especially endurance athletes, have found
them to be at risk for iron deficiency; however, these were uncontrolled studies. More recent investigations have not
shown a difference in prevalence of the disease between athletes and nonathletes ( 3).
Iron deficiency anemia is characterized by a microcytic, hypochromatic anemia. The cause of the deficiency is either
insufficient iron intake or iron loss from bleeding. Typical iron-poor diets of adolescents or weight-restricting athletes can
cause insufficient intake. In women, heavy menstrual bleeding is often a cause of iron loss. In amenorrheic female
athletes, diet should be suspected as the cause and screening for eating disorders should be performed. In male
athletes, iron deficiency is usually caused by GI blood loss instead of poor intake. A thorough evaluation is needed,
because the source may be a colon cancer. A thorough GI evaluation is needed when the athlete is male and older than
30 years of age or female with amenorrhea and a normal diet. Weight-restricting male athletes should be screened for
eating disorders.
The diagnostic features of iron deficiency anemia are a microcytic anemia with a low mean corpuscular volume and low
ferritin levels ( Table 7.1). Once an anemia develops, the total body iron stores are depleted and a large amount of iron
needs to be replaced. Replacement of iron stores takes at least 6 months of 200 to 300 mg elemental iron per day. This
is equal to 325 mg of ferrous sulfate three times per day, although ferrous gluconate or lactate can be used. Iron is best
taken between meals. Vitamin C (e.g., orange juice) enhances the GI uptake of iron. If GI symptoms occur, the dosing
can be decreased to twice daily or administered with meals. When the iron is taken with meals, the absorption is
decreased by 50%.
TABLE 7.1. LABORATORY VALUES IN IRON DEFICIENCY ANEMIA
Sickle Cell Trait
Sickle cell anemia is an autosomal recessive trait that is caused by the change of a glutamic acid for a valine at position
6 on the Hb beta chain. The RBCs with sickle Hb (Hb S) have a protective effect against malaria, which is common in
tropical regions, but at low oxygen tensions the cells can form a sickle shape and occlude the capillaries, causing
ischemia. Sickle cell disease results in a chronic anemia of Hb S in the range of 6 to 7 g per dL. Sickle cell trait, the
heterozygous form, is called Hb AS. Most people with Hb AS have 60% normal Hb (Hb A) and 40% Hb S. For the most
part they are asymptomatic.
In the general population, the incidence of sickle cell trait is about 8% among African-Americans and 1 in 10,000 among
Caucasians. Athletes with Hb AS participate in sports regularly, and surveys of professional athletes reveal rates similar
to those in the general public. Therefore, sickle cell trait does not appear to inhibit athletic performance.
Certain situations may trigger sickling episodes in athletes with Hb AS. These include severe dehydration, altitude higher
than 10,000 feet, and severe heat. Concern was raised by reported deaths among U.S. Army recruits with Hb AS; the
increased rate was postulated to be caused by an increased susceptibility to exertion rhabdomyolysis in untrained
recruits with Hb AS from exertion heat illness ( 15). Most clinicians believe that athletes with sickle cell trait are not at
increased risk (15). Currently, caution is warranted for athletes with Hb AS at severe altitudes or with dehydration (e.g.,
hot environment, after illness).
Athletes with sickle cell trait may present with hematuria. It is usually benign and is often recurrent. It occurs mostly in
men and most often from the left kidney. The cause is unknown, but it is thought to be a vasoocclusive phenomenon.
Treatment is conservative, with hydration and urine alkalization. Urine alkalization can be accomplished by giving sodium
bicarbonate, 10 mg per kg, before a training session. Recurrent episodes are treated with epsilon-aminocaproic acid or
desmopressin.
RESPIRATORY PROBLEMS
Exercise-Induced Asthma
Symptoms
EIA is the transient airflow obstruction that occurs after 5 to 15 minutes of exercise. There is a spontaneous slow return
to baseline lung function. It is a common ailment seen in approximately 10% of the athletic population who have no
history of asthma, 80% to 90% of asthma patients, and 40% to 50% of those with allergic rhinitis. At the Summer Olympic
Games in 1984, the U.S. Olympic Committee reported that 11.2% of U.S. Olympians had EIA ( 16). Seventeen percent of
winter U.S. Olympic athletes had a diagnosis of EIA, and 3% were not using any medication ( 18). Overall, 12% to 15% of
all athletes have EIA ( 18). It is even more common in winter sports; for example, 35% of figure skaters have EIA ( 19). The
condition is found in the recreational as well as the elite athlete, with a higher prevalence in winter sports.
The athlete often presents with coughing, chest tightness, and/or wheezing during or after exercise. The absence of a
postexercise cough has a very high negative predictive value. Dyspnea out of proportion to level of activity is a common
symptom of EIA that can be confused with lack of fitness. Athletes with a history of asthma often believe that they are just
out of shape.
The exact pathophysiology of EIA is uncertain. It is generally accepted that it is closely related to the warming and
humidification of large volumes of breathed air ( 20). Two main mechanisms have been proposed, the respiratory heat
exchange theory (20) and the water loss theory ( 21). The two theories are not mutually exclusive. The respiratory heat
exchange theory states that there is a transfer of heat and humidity from the tracheobronchial tree in order to condition
the air during the increased respiration of exercise. After the bout of exercise, the bronchial vessels rewarm the bronchial
tree; this occurs by swelling of the capillaries and causes bronchial narrowing. The cooling-rewarming cycle is enhanced
by conditions that have low humidity and cold temperatures (e.g., figure skating). The water loss theory was described by
Anderson in 1982 (21). When an athlete exercises, the respiratory rate increases up to 18 times normal. The increased
respiratory rate causes mucosal surface water to evaporate and therefore increases pulmonary mucosal osmolarity. The
increased osmolarity causes release of mediators and bronchoconstriction.
Diagnosis
Diagnosis is often made clinically by a thorough history. There is a need to differentiate between the athlete with EIA and
the asthmatic athlete. Treatment is different for the asthmatic athlete, who needs daily medication not just preexercise
medication. When the history suggests EIA, most physicians try a therapeutic trial of a b 2-agonist. If the history is not
obvious or the trial was not successful, then the diagnosis is made by exercise testing of the athlete at 80% of maximal
oxygen consumption (V O2max) for 8 minutes. Measurements are made of peak expiratory flow rate (PEFR) and of the
1-second forced expiratory volume (FEV 1) at rest and after 1, 3, 5, 10, and 15 minutes of exercise. A decrease of 10% in
FEV1 or 15% in PEFR is suggestive of EIA. Field testing with an 8-minute run, with pretesting and posttesting of PEFR
and FEV1 looking for a drop after exercise and then a return with b-agonist treatment, is probably the most specific
method (22). FEV1 is the best diagnostic measure ( 23), but PEFR meters are readily available and less expensive, so
they are used most often by clinicians. PEFR can be appropriately used to monitor athletes with EIA and asthma.
Methacholine challenge can be used to diagnose EIA if there is a negative exercise challenge test and a significant
clinical history. The test is done by having the athlete inhale varying amounts of methacholine and measuring the airway
response. If there is a decrease in FEV 1 of more than 20%, a diagnosis of asthma is given (24). The test is very sensitive
but lacks specificity.
Published criteria for EIA specify minimum reductions in PEFR and/or FEV 1 after exercise ranging from 10% to 25%. The
lack of precise definition of the disease results in the large variation in reported prevalence rates. There is a need for set
standards in EIA to determine the true prevalence and diagnostic methods.
Treatment
Treatment should be aimed at the triggers of exercise-induced bronchospasm (EIB). Various nonpharmacologic
treatments can be tried. A 5-minute high-intensity warmup can induce a “refractory period” to symptoms in 40% to 80% of
athletes (25,26). Nose breathing maintains moist aeration of lungs. Wearing an inhalation facemask (e.g., all purpose
mask [3M, St. Paul, MN]) while running outside in cold weather and during high-pollen times diminishes triggers. These
treatments alone seldom alleviate all symptoms, but they are helpful.
Medical treatment is the normal standard of care (Table 7.2). Treatment before exercise with short-acting medication is
usually sufficient. A b 2-agonist, such as albuterol, is used 15 minutes before exercise. At the doses indicated in Table
7.2, the side effects are minimal, although athletes can develop mild tremors, tachycardia, and palpitations. If the
b2-agonist does not control symptoms, then the next agent to add is cromolyn or nedocromil. They are thought to be mast
cell degranulation inhibitors, and they prevent increased bronchoreactivity to triggers such as exercise. Cromolyn is
prescribed at 4 to 10 puffs and nedocromil at 2 to 4 puffs before exercise ( 27). These drugs are effective in 70% of
athletes with EIB and work synergistically with b 2-agonists. If EIB is not controlled with these two agents alone, consider
an alternative diagnosis such as asthma with exercise exacerbation.
TABLE 7.2. MEDICATIONS PRESCRIBED FOR EXERCISE-INDUCED ASTHMA
Not all wheezing is EIA, and knowledge of the differential diagnosis is needed. Vocal cord dysfunction, gastroesophageal
reflux disease, pneumonia, foreign body aspiration, and chronic obstructive pulmonary disease are all possible imitators
of EIA. When EIA treatment is not working, then consideration of another diagnosis or concurrent disorder is needed.
Long-acting b2-agonists (e.g., salmeterol) are useful if the athlete is participating in an extended daily event such as a
wrestling or volleyball tournament ( 28) or has difficulty taking medication during school. Salmeterol is not to be used as
“rescue” medication. All athletes with EIA and asthma need to carry a metered-dose inhaler (MDI) containing a
short-acting b2-agonist. Salmeterol used twice daily loses its effectiveness for EIB after 9 hours ( 29), so appropriate
dosing is needed.
Inhaled corticosteroids are occasionally needed on a daily basis for the prevention of EIB. These agents do not work as
preexercise treatments. The use of steroids is best in athletes with underlying chronic asthma. Monitoring of PEFR
should be performed to maintain maximal treatment.
Leukotriene inhibitors are oral medications that show promise in EIB ( 30). They include montelukast (Singulair),
zafirlukast (Accolate), and zileuton (Zyflo). They are dosed the same as for asthma prevention. Leukotrienes should not
be used for acute attacks.
The usefulness of vitamin C in the treatment of EIA cannot be predicted. It may produce a protective effect on airway
hyperreactivity in EIA (31). A positive response was seen in 45% of athletes taking 2 g of vitamin C before exercise.
Eighty percent of athletes who respond to vitamin C treatment continued to have benefit by taking 500 mg per day for the
2 weeks studied.
Inhaled heparin and inhaled furosemide have been used experimentally for the treatment of EIA and have shown
beneficial effect ( 32,33). Neither is used clinically at the current time.
Exercise-Induced Anaphylaxis
Exercise-induced urticaria and exercise-induced anaphylaxis (EIAna) represent a continuum of exercise-related

reactions. EIAna was first described by Maulitz et al. in 1979 ( 34). Exercise-induced urticaria and cholinergic urticaria
(CU) produce hives in athletes; it is important that these two conditions be differentiated, because they carry different
risks for anaphylaxis. CU is associated with small (less than 5 mm), punctate lesions that can coalesce. Exercise-induced
urticaria are larger lesions (more than 1 cm). With exercise-induced urticaria, there is frequent progression to
angioedema and anaphylaxis. Urticaria is nonpitting edema of the superficial dermis, and angioedema is swelling of the
deeper layers of the skin and subcutaneous tissues. Although urticaria is histamine mediated, angioedema is not. The
differentiation is important, because antihistamines will not prevent the progression to laryngeal edema. Sheffer and
Austen (35) described three forms of EIAna: CU, classic EIAna, and variant EIAna ( Table 7.3).
TABLE 7.3. DIFFERENTIATION OF TYPES OF EXERCISE-INDUCED URTICARIA
The experiences of almost 200 athletes with classic EIAna were described by Wade et al. ( 36). Symptoms usually were
precipitated by moderate to hard exercise, warm or humid environments, and most frequently while running. Attacks
typically occurred after approximately 5 minutes of activity, and eating increased the likelihood of attacks. Pruritus was
seen early in an episode in 92% of the athletes. Occasionally, persons with EIAna describe an “sense of impending
doom.” The number of attacks in this study varied widely, but the average was twice a week ( 36).
In CU, the athlete presents with pruritus, urticaria, warmth, and wheezing. CU is often very mild and nondebilitating. It
occurs frequently in people who have a personal or family history of atopy ( 35) and is associated with a rise in
whole-blood histamine levels and an increase in circulating basophils ( 37,38). Sweat activates an irritating chemical on
the skin that can induce pruritus. One attack can lead to a relatively refractory period of 24 hours.
A workup is best begun by taking a careful and thorough history. Usually, the medical evaluation is normal. Two tests that
are available for CU are the passive heat challenge and the methacholine stimulation test. Passive heat challenge can
be done in two ways. One is the use of a heating blanket wrapped around the athlete to raise the core body temperature
by 0.5° to 1.5°C. The other is immersion of an extremity in a container of hot water (40° to 42° C). Urticaria will develop in
patients with CU. The methacholine stimulation test is done by an intradermal injection of acetyl methacholine chloride.
Small urticaria will form in those with CU. Both tests are highly specific for CU but not extremely sensitive. A negative test
does not exclude CU as the diagnosis but a positive test essentially confirms it.
Symptoms can be reduced by taking antihistamines before exercise (39). Start at a low dose to diminish the sedative
effects of the antihistamines. Sedation will decrease, and a full 4- to 6-week trial should be allowed before moving to
another antihistamine. Cimetidine, an H 2 blocker, can be helpful in prevention. Exercising with repeated short, intense
bursts can decrease the likelihood of symptoms ( 40). Avoidance of exercise during pollen season is important. Any
triggering agents such as aspirin or certain foods ( Table 7.4) (41) should be avoided. Exercise should be postponed a
minimum of 4 hours after eating and avoided before breakfast. Taking cromoglycate by inhalation can be helpful ( 42).
TABLE 7.4. FOODS AND DRUGS THAT TRIGGER URTICARIA (EXERCISE-INDUCED COPRECIPITATORS)
An acute attack in which there is either significant swelling of the respiratory tract or face or hypotension should be
treated with an intramuscular injection of epinephrine. However, giving epinephrine without also giving a corticosteroid
often does not stop the reaction. Hypotension can be treated with intravenous dopamine diluted in 500 mL of 5% glucose
solution (D5W) fluids.
Laryngeal Spasm
Athletes with laryngeal spasm present with a tightening in the throat and often have stridor. The athlete's laryngeal
spasm produces a sense of not being able to breathe, which is very anxiety provoking. It can make a runner stop racing.
It is often mistaken for asthma or EIA and treated with asthma medications, which produce no relief ( 43). The
b-adrenergic agents (e.g., albuterol) sometimes even worsen symptoms.
Laryngeal spasm can occur in any type of athlete but is seen most notably in cross-country runners. There is an anxiety
component to the disorder. Athletes present with tightness in the throat, voice changes, a “choking” feeling, wheezing,
dysphonia, dyspnea, and even noncardiac chest pain ( 44). Most athletes with vocal cord dysfunction are highly
competitive, “type A” personalities who are driven to perfection.
The diagnosis is best made by direct laryngoscopy during an episode of spasm. This definitive test may not be readily
available. A less sensitive test is the inspiratory phase of pulmonary function testing, which shows a blunted and variable
curve compared with the normal elliptical pattern. The altered curve is caused by the volume of air that can be moved
across the laryngeal spasm.
Treatment consists mainly of relaxation and biofeedback techniques. Speech therapy is employed to relax the vocal
cords. Asthma is present in vocal cord dysfunction in up to 50% of the cases, so EIA treatment may be necessary as well
(45).
RENAL PROBLEMS
Many renal diseases go undetected and often are of a benign nature. Yet, common occurrences such as hematuria may
bring an athlete to the physician quickly. The athlete with a renal disorder needs monitoring to ensure that a benign
course does occur.
Proteinuria
Proteinuria is a seen in healthy athletes after exercise. Postexercise proteinuria (PEP) is exertion related. There is a
close relation to the lactate level ( r = .87) (46). Fitness and hydration are inversely related to PEP ( 47). Age and gender
do not alter the occurrence of PEP ( 48,49 and 50). The cause of PEP is not certain. The renin-angiotensin system and
renal prostaglandins have been implicated. Angiotensin II inhibitors decrease PEP ( 51), and indomethacin increases it
(52).
The diagnosis of PEP is made by the finding of an increase in urine protein after exercise. The exercise should be
intense, because lactic acid levels need to be elevated. Values are typically 2+ to 3+ on a urine dipstick. The increased
levels should return to normal after 24 to 48 hours. A good history is needed to ensure that the proteinuria is related to
exercise. If the condition does not resolve, other forms of benign proteinuria need to be considered (e.g., benign
positional proteinuria in adolescents). Further evaluation is needed by a physician who is knowledgeable in the multiple
causes of proteinuria. If proteinuria is caused by PEP, it carries a benign prognosis with no long-term affects ( 53).
Hematuria
Hematuria can be a sign of serious illness. Most athletes have a benign cause, but a thorough evaluation is needed.
Urine dipstick testing is positive for heme with other causes as well as hematuria, so microscopy should be done to look
for RBCs. Furthermore, not all red urine is hematuria. A history is needed to help differentiate the causes of
heme-positive urine. Microhematuria is very common among athletes, with reported rates between 20% and 80% ( 54,55).
Many causes have been noted for hematuria, and it appears to be related to both intensity and duration ( 56).
The kidney is not the only source of blood in the urine. Blacklock described hematuria arising from the bladder in
10,000-m runners (57). As the contusions resolved, so did the hematuria. It is hypothesized that emptying of the bladder
before running may promote these lesions ( 58).
Acute Renal Failure
Renal failure in athletes occurs when multiple factors compound each other. The renal blood flow has to reach a critical
point where it is too low and causes renal ischemia and renal failure. The causes of exercise-induced acute renal failure
(EIARF) are dehydration, nephrotoxic agents, and prostaglandin inhibitors. Nephrotoxic agents are produced from
muscle breakdown (e.g., myoglobin from rhabdomyolysis) or from RBC lysis and Hb, as in sickle cell. Dehydration can
cause a significant reduction in renal blood flow to the point of EIARF. NSAIDs and other prostaglandin inhibitors prevent
the protective dilation of the afferent vessels that occurs during exercise, thereby decreasing renal blood flow and
glomerular filtration rate, making EIARF more probable.
Prevention is the best treatment for EIARF. The athlete's environment needs to be monitored and a safe training wet bulb
temperature maintained. Fluids should be available, and athletes should be encouraged to drink the fluids. Athletes
should be cautioned about the use of NSAIDs before strenuous exercise. After exercise, they should continue to drink
fluids to produce urine flow within 1 to 2 hours. These measures will help prevent EIARF.
The athlete with acute renal failure usually does well with careful monitoring and intravenous fluids. If the oliguria persists
despite fluid resuscitation, then further evaluation for life-threatening renal failure is needed. Izumi et al. described the
use of ultrasound Doppler technique to detect EIARF ( 59). Furosemide, mannitol, and dialysis are occasionally needed.
Insulin-like growth factor I (IGF-1) has been safely used in persons at risk for acute renal failure and in patients with
end-stage chronic renal failure to increase the glomerular filtration rate ( 60). Research to determine the role of IGF-I as a
therapeutic agent for EIARF has not been done.
Single Kidney
The issue of solitary kidney and athletic participation is controversial. The loss of an organ is a very rare event in sports,
and the loss of a kidney is extremely rare. A survey of the members of the American Medical Society of Sports Medicine
found that a majority (54.1%) would allow athletes with a single kidney to participate in contact and collision sports ( 61).
The percentage was less (41.6%) when it came to allowing their own child to participate. When making a decision, the
type of single kidney matters: a horseshoe kidney has a better prognosis in injury because of the dual blood supply.
Positioning of the kidney in the body needs to be examined to fully elicit the dangers of playing a sport. If the physician is
recommending participation in a contact or collision sport, there should be a complete discussion of the dangers of
participation and guidance in the choice of activities.
HYPERTENSION
Blood Pressure
Hypertension (HTN) is the most common cardiovascular condition in athletes and in the general population ( 62). Seldom
are symptoms present to warn the athlete of the disease, making early detection and the start of treatment to prevent
end-organ disease difficult. Therefore, screening at the preparticipation evaluation is recommended. Athletes with HTN
can participate with few restrictions.
HTN is defined as systolic blood pressure (SBP) equal to or greater than 140 mm Hg or diastolic blood pressure (DBP)
equal to or greater than 90. With Joint National Committee VI, there are now redefined categories for risk stratification.
The main change is the condensing of the last two groups into one group labeled stage 3 ( Table 7.5) (63). In children
and adolescents the values for HTN are determined by age- and height-adjusted norms ( 64). Abnormal blood pressure
(BP) is defined as a level two standard deviations above the normal value. To classify an athlete as hypertensive, at least
two elevated readings on two separate occasions are needed. The BP is taken with the athlete seated for 5 minutes,
back supported, cuff at heart level, arm rested, and silent. The cuff width must be two thirds ( 62) to three quarters ( 64) of
the length of the upper arm. The bladder should be of adequate length to encircle 80% to 100% of the arm. Use of a cuff
of appropriate size is important for an accurate reading.
TABLE 7.5. STAGES OF HYPERTENSION
HTN is divided into two types: essential and secondary. Essential HTN is the most common cause of HTN (90% of
cases). Secondary HTN causes are pheochromocytoma, Cushing syndrome, renovascular HTN, aldosteronism, and
coarctation of the aorta. It is important to consider secondary causes of HTN.
Exercise has differing effect on the cardiovascular system depending on HTN status. In the normotensive athlete, the
increased cardiac output is balanced by a lower total peripheral resistance (TPR) during exercise. The potential
hypertensive does not get the full lowering of vascular resistance and develops higher than expected BP for the same
activity (65). As resting HTN increases, the exercise response continues to change. Athletes with stage 1 HTN have a
normal cardiac output but increased TPR at rest. The TPR does not compensate, and the BP goes up. Athletes with
stage 2 or 3 HTN do not have the appropriate rise in cardiac output during exercise and also have an increased TPR.
Those with stage 3 may even show signs of diastolic dysfunction.
Regular exercisers, both moderate (66) and strenuous (67), have lower SBPs and DBPs than sedentary people. After
starting a moderate exercise program, hypertensive adults and children ( 68) experience a reduction in BP. An analysis of
exercise programs for HTN did not show added benefit for increased exercise intensity beyond 70% V O2max or increased
frequency beyond three sessions per week ( 66). Even in severe HTN, exercise with medication was shown to lower BP
more than medication alone (69). Therefore, even hypertensive patients taking medication should exercise to lower BP.
Athletes who have high BP but no target organ damage should be allowed to compete in aerobic sports ( 62). However,
there is inadequate information to show whether the extraordinary rise in BP that accompanies strength training and
strength competition can harm athletes. The BP rise that is induced by lifting of heavy weights is exaggerated in people
who have HTN (70). However, regular strength training can reduce the degree of rise in BP ( 71).
Weight lifting by persons with HTN has been a controversial issue. During isometric exercise the SBP can rise to as
much as two times the resting levels. SBPs higher than 400 mm Hg have been recorded ( 70,72,73). The Valsalva
maneuver causes an increase in thoracic pressure when straining against a near-maximal load. This rise in thoracic
pressure is thought to cause the increase in BP ( 73). McCartney (70) pointed out that some of these effects may be
beneficial to the athlete during lifting to maintain counterpressures. While lifting less than 80% to 85% of his or her
one-repetition maximum, the nonfatigued athlete seldom uses the Valsalva maneuver ( 70); at higher intensities, it
becomes almost obligatory. These high BPs are of concern. Studies have shown that repetitive static exercise, unlike
dynamic exercise, produces concentric hypertrophy of the left ventricle. During isometric activity, the left ventricular filling
pattern is the same as in hypertensives, unlike the filling pattern seen in endurance runners ( 74). In addition, there have
been case reports of subarachnoid hemorrhage in weight lifters caused by the increased SBP ( 75). These facts make
weight lifting appear to be maladaptive for athletes with HTN.
Forms of weight lifting have been shown to be beneficial in lowering BP. High-repetition, low-weight training can produce
a lowering of the BP (71). Significantly lower BPs were seen when lifts are performed with an open glottis, as opposed to
the Valsalva maneuver. The mean BP was 198/175 mm Hg with open glottis and 311/284 with Valsalva ( 73). It is
recommended that athletes with stage 3 HTN should not do isometric activities until their BP is lowered. Weight lifters
should not use the Valsalva maneuver during lifts; instead, they should maintain an open glottis by slowly exhaling while
lifting (64,76).
After a thorough history to rule out secondary causes, a complete physical examination is performed. On initial
presentation of an athlete with HTN, an electrocardiogram should be obtained to look for left ventricular hypertrophy. If it
is positive, further testing (e.g., echocardiogram) is indicated. Repeat BP measurements, including both upper extremities
and one lower extremity, should be done. Screening blood work is advised to look for other end-organ damage and
concurrent diseases. Sudden onset of stage 3 HTN should prompt investigation for a secondary cause of HTN.
Laboratory values for blood urea nitrogen, creatinine, sodium, potassium, fasting glucose, and a lipid panel should be
obtained.
Treatment
Nonpharmacologic treatments for HTN should include exercise. In addition, weight reduction ( 63), avoidance of
excessive alcohol consumption, a low-sodium diet ( 77), and calcium supplementation (78) may be helpful (Table 7.6). A
good drug history is important, because some medications and certain illicit drugs have been shown to increase BP—for
example, estrogen in oral contraceptive pills ( 79), anabolic steroids (80), growth hormones, and cocaine. The athlete with
HTN gives the sports medicine physician an additional opportunity to talk about use of illicit and banned drugs.
TABLE 7.6. NONPHARMACOLOGIC TREATMENTS FOR HYPERTENSION
Nonetheless, many people who exercise regularly still need to take medications to control their HTN ( Table 7.7). There
are many different classes of hypertensive agents; the main categories are discussed here. b-Blockers and diuretics are
reviewed in one group and angiotensin-converting enzyme (ACE) inhibitors and calcium-channel blockers in another.
TABLE 7.7. WHEN TO START MEDICATION IN HYPERTENSION
b-Blockers, Diuretics, and Other Agents
b-Blockers and diuretics have proved effective in the treatment of patients with HTN ( 63). Both have their limitations in
athletes and are restricted in use by the IOC and other governing bodies. b-Blockers, especially nonselective agents,
decrease the heart rate response to exercise, increase perceived exertion, and can cause worsening of bronchospasm
(81). Nonselective b-blockers increase susceptibility to hyperthermia; all patients who are taking b-blockers should be
cautioned about that complication during exercise, particularly in hot weather ( 81). Although b-blockers are beneficial,
nonselective b-blockers should be avoided in athletes.
b1-Selective blockers are beneficial in patients with very high SBP during exercise and in those with coronary artery
disease (81). Because b-blockers slow the heart rate and increase perceived exertion, most exercisers who take
b-blockers should have special counseling regarding their exercise prescriptions based on exercise tests done while they
are on medication (82). Labetalol, a combination a- and b-blocker, has been shown to be beneficial and does not have
the same side effect panel as b-blockers during exercise. The major side effect is orthostatic hypotension, which can be
diminished with bedtime dosing. The decrease in cardiac index seen initially with labetalol returns to baseline after 1 to 5
years of use (83). A combination a- and b-blocker could be useful in athletes.
Diuretics are an inexpensive and commonly used medication in HTN, but for the athlete they are laden with danger.
Diuretics work by reducing plasma volume and decreasing sodium. They also can cause hypokalemia and
hypomagnesemia, increasing susceptibility for arrhythmias. Diuretics can worsen dehydration and are dangerous in
endurance athletes. For athletes who exercise in a hot, humid environment, such as a training camp for football, diuretics
are not a good choice. In addition, patients taking diuretics should not use NSAIDs before exercise because of the
increased chance of acute renal failure during strenuous exercise. Athletes who have a readily available source of fluids
and are in a cool environment may use diuretics.
a1-Antagonists (i.e., prazosin and terazosin) are effective in athletes. However, orthostatic hypotension may be an
unacceptable side effect when the drug is first initiated. The medication needs to be started at very low doses at bedtime
and advanced slowly. It is effective in all groups of patients.
Angiotensin-Converting Enzyme Inhibitors and Calcium-Channel Blockers
ACE inhibitors and calcium-channel blockers are the usual first-line medications for athletes with HTN because of their
low side-effect panel and their lack of effect on maximal aerobic capacity. The medications can be very expensive. Most
of the drugs in this group can be administered once daily, a notable exception being the inexpensive captopril, which is
usually given three times per day. Calcium-channel blockers should be prescribed once or twice daily as the long-acting
preparations.
Nicardipine decreases TPR and leaves BP and heart rate response to exercise unchanged ( 84). This is beneficial to
athletes with HTN, because TPR increases with exercise. Not all calcium-channel blockers work this way. Verapamil and
diltiazem both have effects on athletic performance and are not recommended. The dihydropyridines function by lowering
TPR and are recommended.
ACE inhibitors work by blocking the formation of angiotensin II. No deleterious effects were shown with the use of ACE
inhibitors in endurance athletes with mild HTN ( 85). These drugs are well tolerated, with the main side effect being
chronic dry cough. They are not to be used in athletes who have renal artery stenosis or who are pregnant. Monitoring of
creatinine and potassium levels is recommended before and during treatment.
Angiotensin II receptor antagonists prevent the binding of angiotensin II to the receptor and venoconstriction. These
drugs and ACE inhibitors do not impair the overall response to static or dynamic activities. They have effects and side
effects similar to those of the ACE inhibitors, but the dry cough is not found as often. Like ACE inhibitors, they have less
efficacy in African-Americans (generally a low-renin group) and should not be used in pregnant patients ( 63).
GYNECOLOGIC PROBLEMS
Effects of the Menstrual Cycle on Exercise
Many people think that all active female athletes are amenorrheic, but in fact most have a normal or near-normal cycle
(86). Other athletes regulate their cycles with oral contraceptive pills or progesterone injections. The potential effects of
the menstrual cycle on performance may be important when choosing an oral contraceptive or planning competitions. In
a “normal” cycle, the length from start of menstruation to start of menstruation in the next cycle is 28 days, but it can vary
from 23 to 35 days. Normal menstruation lasts 3 to 5 days. The cycle is divided into a follicular phase and a luteal phase,
each lasting 13 to 15 days. Ovulation occurs at the end of the follicular phase. The follicular phase is more variable and
is the major determinant of cycle length (87).
Many studies on the effect of the menstrual cycle on athletic performance have been reported. Most studies did not
include accurate measurement of cycle phase by hormonal testing. The overwhelming majority of the studies have shown
no significant difference in performance in any phase of the cycle ( 86,88,89,90,91 and 92). A blunted respiratory drive has
been seen during luteal phase. Yet, when studies looked at V O2max during luteal phase, varying results were seen ( 93).
Although many athletes have personally noted a decrease in performance during portions of the menstrual cycle, most
often this is secondary to premenstrual syndrome. No study has definitively documented a change in performance during
menstrual cycle.
Effects of Exercise on the Menstrual Cycle
Luteal Phase Dysfunction
The active athlete may develop luteal phase dysfunction in which the luteal phase is shortened, resulting in shorter
menstrual cycles. The syndrome may be subclinical, and athletes can have a normal cycle length. Luteal phase
dysfunction results either from a lack of the normal surge in luteinizing hormone (LH) and anovulation with no
progesterone increase or from occurrence of ovulation with an inadequate development of the corpus luteum, which
produces little progesterone. The long-term effects of the shorter luteal phase are not certain. It is usually reversible with
a decrease in training. The main complication is the lack of ovulation and inadequate corpus luteum: conception is not
possible. Adjustment in training can correct this problem ( 94).
Amenorrhea
Female athletes may be amenorrheic for many months before informing a doctor or trainer ( 95). Amenorrhea is often
viewed as a sign of a hard-working athlete. Because normal cycles return after training is decreased, why should an
athlete be concerned?
Both Drinkwater et al. (96) and Cann et al. (97) noted that bone mineral density in amenorrheic athletes was significantly
lower than in eumenorrheic athletes. Worse, Drinkwater's group ( 98) found that bone mineral density was not regained
after the return to normal cycles. The loss of bone density could be permanent and irreversible, making these women
more susceptible to premature osteoporosis, with its health consequences and associated disabilities. In addition to
decreased bone mineral density, stress fractures are more common in amenorrheic athletes.
Amenorrhea needs to be defined by a standard definition so the incidence and prevalence can be determined. Primary
amenorrhea is the absence of menstruation by the age of 16 years, or by 14 years along with the absence of secondary
sexual characteristics. Secondary amenorrhea is the loss of menstruation for three or more consecutive cycles in a
woman who has experienced menarche (86). The rate of amenorrhea varies by group examined. Up to 5% of
nonpregnant women in the general population and as many as 8.5% of the adolescent girls are amenorrheic. In athletes,
40% to 50% of elite runners and ballet dancers have amenorrhea. In the athletic population, the rate is 10% to 20% of
vigorously exercising women ( 99).
Control of the normal female menstrual cycle lies in the hypothalamic-pituitary-ovarian axis. The pulsatile secretion of
gonadotropin-releasing hormone by the hypothalamus stimulates the production of LH and follicle-stimulating hormone
(FSH) by the anterior pituitary. These hormones, in turn, stimulate ovulation and are under the feedback control of
estradiol and progesterone. Gonadotropin-releasing hormone is influenced by stress and weight loss through
endogenous opioids, corticotropin-releasing factor, and leptin. Alteration in any of these hormones can cause cessation
of menstruation in an athlete ( 100).
Secondary amenorrhea is common in athletes. The most important cause, after pregnancy, is hypothalamic amenorrhea.
Exercise-associated amenorrhea is a form of hypothalamic amenorrhea. Other causes of disruption of the
hypothalamic-pituitary-ovarian axis must be excluded. Other causes of secondary amenorrhea are prolactinoma, thyroid
disease, premature ovarian failure, and polycystic ovarian disease.
The diagnosis of exercise-associated amenorrhea is generally a diagnosis of exclusion ( 94). After a thorough history
including dietary and social history, the athlete should have a physical examination that includes a pelvic examination
and pregnancy test (even if the patient is certain she could not be pregnant). The other laboratory tests recommended
are thyroid-stimulating hormone (TSH), prolactin, and FSH. If the athlete is not pregnant, then a progestin challenge
(medroxyprogesterone acetate, 10 mg orally for 5 days; or progesterone-in-oil, 100 to 200 mg intramuscularly once)
should be done. Bleeding will occur within 10 days if there is enough estrogen present to produce a thickened
endometrium. Normal laboratory findings (FSH and LH may be low or normal in hypothalamic amenorrhea) and a
negative progestin challenge should be followed by an estrogen-progestin challenge. The second challenge should
cause resumption of menstrual bleeding in hypothalamic amenorrhea (including exercise-associated amenorrhea).
Once the diagnosis of exercise-associated amenorrhea is made, appropriate treatment should be started. An energy
(caloric) deficiency is often seen, and nutrition counseling is essential. The athlete needs to take in sufficient calories and
protein to meet energy demands. Supplementing with calcium (1,500 mg per day) should be done. A decrease in training
may not be possible for a competitive athlete. Continued exercise-associated amenorrhea is dangerous, and it is
important for bone health to supplement estrogen. Hergenroeder et al. ( 101) showed that high-dose estrogen, like oral
contraceptive pills, significantly improves bone mineral density in athletes with hypothalamic amenorrhea. Eating
disorders can be found with amenorrhea, and screening is important. A mental health professional can help with
counseling of athletes who have an eating disorder.
In 1993, the American College of Sports Medicine published a consensus conference report entitled, “The Female
Athlete Triad” (95). It described the syndrome of disordered eating, amenorrhea, and osteoporosis in the athletic female.
The diagnosis is often difficult to make and is easily missed for a number of reasons. The athlete may have disordered
eating that is not adequate to fit the exact criteria for bulimia or anorexia listed in Diagnostic and Statistical Manual of
Mental Disorders, 4th edition. It is common for athletes to restrict calories in sports such as swimming, figure skating,
gymnastics, and cross-country running. In these and other sports it is often thought that being lighter and thinner is
essential to success. Amenorrhea is common in athletes and is often considered a sign of hard training. Often, many
months pass before it is noted that the athlete is amenorrheic. Osteoporosis is an insidious illness that frequently does
not reveal itself until a fracture occurs. Premature osteoporosis may not be reversible. Many of these ill athletes go
undetected by the medical community.
Physicians and trainers must be aware of the psychological and physical symptoms of disordered eating. If an athlete
shows herself to be excessively concerned with her weight or dieting, or if she is especially self-deprecating, further
investigation into dietary habits should be done. The athlete can present with fatigue due to the self-imposed energy
balance deficit. External factors (e.g., coaches, family) can be the driving force for these athletes. They may restrict their
diets to please others. In my experience, most athletes with “female athlete triad” are very nice and pleasant to be
around; they are “overpleasers.”
Eating disorders will remain a hidden problem unless addressed. The preparticipation physical evaluation is a good
screening vehicle (99) (Table 7.8). Care should be taken not to confront the athlete initially. Nonthreatening ways to
inquire about eating include discussing with the athlete her “ideal” weight and how she would respond if tomorrow she
awoke 5 pounds heavier. A simple 24-hour dietary recall can also give insight into the patient's regular nutritional habits
and attitudes toward food. Special attention should be made when she reports the fat and caloric content of everything
she eats. The classic physical findings associated with eating disorders (marked thinness, orthostasis, fine lanugo hair,
carotenemia, parotid swelling, erosion of the tooth enamel) can also be noted but most often are not seen.
TABLE 7.8. PREPARTICIPATION EVALUATION SCREENING QUESTIONS—FEMALE ATHLETE TRIAD
Prevention is the key. When education is done at the beginning of each season and a support system is in place,
athletes will be identified by teammates and help can be obtained early in the process. Each school should have a Triad
Coalition to help distribute educational materials and treat athletes.
The management of the athlete with the female athlete triad is best accomplished in a multidisciplinary fashion ( 95). The
treatment team should consist of physician, nutritionist, and mental health professional. Outside the medical team, the
inclusion of family members is important. Developing their support and the athlete's trust is essential for successful
treatment of the illness. On the medical team, the physician should be responsible for coordinating the athlete's care and
is the one with the ultimate responsibility for returning the athlete to participation. A nutritionist is vital in providing
guidance to the athlete both in nutritional education and in moral support. It is also common to involve the services of a
mental health professional for those athletes with subclinical or frank eating disorders.
The primary goals of treatment are to control and manage the athlete's disordered eating, to restore the normal hormonal
milieu, and to monitor and treat other medical complications of their disordered eating ( 100). Ideally, the athlete should
decrease activity by 10% to 20% and increase weight by 2% to 3%. If this is achieved, menses may resume. However,
circumstances may not permit a competitive athlete to decrease her activity by 10% to 20%, and an athlete with an eating
disorder is likely to be extremely resistant to gaining weight. Because of the potential of bone loss, restoration of
eumenorrhea should not be delayed and medication may be needed.
Medical evaluation should include a complete physical examination, including a pelvic examination. The evaluation
should focus on other possible reasons for disordered eating, such as metabolic disease, infection, cancer, and
inflammatory bowel disease. Laboratory evaluation should include a urinalysis, complete blood count, sedimentation rate,
chemistry panel including calcium and magnesium, liver and kidney tests, and laboratory tests for amenorrhea. An
electrocardiogram is recommended to evaluate for effects of electrolyte abnormalities. Dual-energy x-ray absorptiometry
(DEXA) scans are often done to evaluate bone density. The result obtained by DEXA should be considered a reference
point unless a previous test is available for comparison. Competition should be withheld if electrolyte or
electrocardiographic abnormalities and/or continued weight loss occurs.
Treatment
The role of hormone replacement has been well documented. As with postmenopausal women, estrogen
supplementation has been shown to have beneficial effects on bone mineral density in amenorrheic athletes. In contrast
to postmenopausal women, standard low-dose estrogen supplementation may be inadequate to stimulate bone
formation. The literature shows mixed benefits with the use of typical postmenopausal estrogen doses (estradiol, 0.625
mg once per day). The use of estrogen in the form of oral contraceptive pills was documented by Hergenroeder et al. to
significantly improve bone mineral density in athletes with hypothalamic amenorrhea ( 101). Because significant bone loss
may occur within 6 months after onset of hypoestrogenic amenorrhea, prompt evaluation and treatment is essential to
prevent loss of bone mineral density in the amenorrheic athlete.
Calcium supplementation (1,500 mg per day) should be implemented in all athletes with the female athlete triad. The
daily caloric intake of female athletes routinely falls short of their daily energy expenditure, and athletes should be
counseled to take in adequate calories to match energy expenditure. A nutritionist can help determine the appropriate
amount. Inadequate protein intake also predisposes to hypothalamic amenorrhea. Athletes often self-impose special
diets that limit protein intake. Therefore, nutritional counseling should also address adequate protein supplies in the diet.
Both increased calcium and corrected protein intake are insufficient without restoration of estrogen levels.
The athlete may have substantial concerns regarding starting birth control pills. Common side effects of oral
contraceptive pills include weight gain, change in serum lipids, and breast tenderness. Some preparations have been
shown to decrease acne. There currently are no recommendations as to when oral contraceptive pills should be
discontinued. Clinical judgment is needed in making this decision. If menses do not resume within 3 months after
discontinuance of oral contraceptive pills, they should be restarted.
The female athlete triad is a problem that can be addressed and treated. With the eventual true equality of women's
sports, more athletes with these problems will be seen. These athletes should be identified and treated like those with
any other athletic problem. The potential of female athlete triad must not eliminate women from participation in athletics.
INFECTIOUS DISEASES
Mononucleosis
Length of Illness and Symptoms
Infectious mononucleosis (mono) is common among adolescents. It is caused by the Epstein-Barr virus (EBV). The
annual infection rate among college students is 3% ( 102). By the third decade of life, 90% of people have antibodies to
EBV. It occurs earlier in life in lower socioeconomic groups, whereas people from suburban communities are more likely
to acquire mono during college.
EBV infection manifests initially as fatigue, malaise, anorexia, and headache. After 3 to 5 days moderate fever, sweats,
sore throat, and lymphadenitis of cervical nodes (especially of the posterior chain) develop. In one third of cases,
posterior palate petechiae are present, which is highly suggestive but not diagnostic of mono. Most athletes are unable to
compete and initially are bedridden. Roberts reported cases of athletes with poor performance as their only complaint
(103).
The incubation period for the disease is 30 to 50 days, with transmission via saliva either directly or aerosolized. It is not
a highly contagious disease, and roommates of infected individuals are at no greater risk than the general population
(104,105). Isolation of the athlete is unlikely to be helpful.
The mono spot test is the standard test for detecting infectious mononucleosis. Its sensitivity is 90% by the third week. A
standard blood smear reveals atypical lymphocytes of varying amounts; the presence of more than 20% atypical
lymphocytes is pathognomonic for mononucleosis. Testing for antibodies to EBV can be helpful to detect subtle cases or
to document prolonged cases. The antibodies are present in 85% of those infected by the first week and in 100% at 3
weeks. True recurrence of mono is very rare. The mono spot test will be positive for almost 1 year after infection and
sometimes longer. Diseases such as cytomegalovirus infection, early human immunodeficiency virus (HIV) infection, and
toxoplasmosis produce similar illnesses with posterior cervical lymph node enlargement. The disease can appear similar
to streptococcal pharyngitis, and 5% to 30% of patients with mono have concurrent infection with a group A b-hemolytic
streptococcus. There are important differences in treatment, so mono spot testing should be done if clinical suspicion is
present.
Treatment for mono is supportive. Many different treatments (e.g., ciprofloxacin, steroids, cimetidine) have been tried to
shorten symptoms without success when compared with placebo. Complications can occur with mono, and the most
common is airway obstruction that responds well to oral prednisone. Rarer complications include hepatitis, hemolytic
anemia, thrombocytopenia, and Guillain-Barré syndrome. These disorders may also respond to corticosteroids. Hydration
and pain management are the mainstays of treatment. Viscous lidocaine or NSAIDs can be helpful for sore throat. Bed
rest is needed only if the athlete requests it.
Splenic Rupture
Fatigue is usually the limiting factor for the return of an athlete with mono. Most people with active mono do not have the
energy to participate. The major concern is the complication of splenic enlargement. The spleen becomes enlarged in
more than 50% of patients with mono. Splenic rupture occurs in 0.06% of cases ( 106) and occurs between day 4 and day
21 (107). Maki and Reich reviewed cases of splenic rupture and noted that in all cases the spleen was two to three times
the normal size (108). After 4 weeks, splenic rupture is rare. Physical examination is not reliable at ruling out
splenomegaly, with a sensitivity of 72% and a specificity 97% for palpation and percussion ( 109). If no enlargement of the
spleen is detected, no imaging is needed unless the physician is thinking of returning the athlete earlier to competition.
Ultrasonography is the test of choice to rule out an enlarged spleen (13 cm or larger).
Return to Play
Splenic rupture is the main criterion determining return to play; it rarely occurs after 4 weeks and always involves an
enlarged spleen. For contact sports, the return sequence is noncontact play at 3 weeks when there is no palpable spleen
and contact activity at 4 weeks (109). If the spleen is palpable, then an ultrasound study should be done. Return should
be delayed until resolution. In noncontact sports, return to play is limited for 3 weeks. Physicians should image the
spleen before 3 weeks if the athlete is feeling better and wants permission for nonisometric exercise and progressive
return. Return should be to 50% activity initially and then advanced carefully.
Common Cold
The common cold or upper respiratory illness (URI) is caused by a myriad of viruses ( Table 7.9) that produce symptoms
of rhinorrhea, mild sore throat, nasal congestion, and cervical lymphadenopathy. The common cold can cause many
problems for the competing athlete (110). URI has been identified as the cause of more acute disability among athletes
than all other diseases combined ( 111). Up to 20% of athletes with URI missed a practice or game due to their cold ( 112).
The duration of most illnesses is 2 days to 2 weeks, with a short incubation period. Sometimes systemic symptoms are
seen, such as myalgia, malaise, frontal headache, fever, relative tachycardia, and arthralgias, that can be signs of a
more severe illness.
TABLE 7.9. SEASON OF THE VIRUSES
Does Exercise Cause Colds?
It is common for many athletes and coaches to note an increase in colds when workouts become strenuous. Nieman
suggested that the relationship between exercise and URI can be modeled as a “J” curve ( 113). Mild-intensity exercise
provides little immunologic benefit, moderate intensity gives the most benefit, and worsening status is seen with severe
exercise. Studies have helped confirm this model ( 114). In a cohort of runners, the incidence rate was 1.2 colds per
person per year, which is less than the normal adult rate ( 115). Furthermore, as running miles increased, so did the rate
of URI. Severe exercise has been shown to increase the rate of URI after a marathon ( 115). Reduced URI symptoms are
seen in studies involving moderate exercise training, compared with controls ( 116). In addition, a significant elevation in
natural killer cell activity is seen with moderate exercise training ( 117).
Severe exercise bouts have been shown to produce a decrease in immune-mediated cell lines ( 114). Because of this, the
“open window” theory was developed. The “open window” of altered immunity allows for infections to take hold while
immune function is impaired. The immune system impairment may last 3 to 72 hours after a bout of severe exercise
(113). The reason for the alteration in immune response is not certain ( 118). There are many documented decreases in
the immune system with strenuous exercise. Decreased salivary immunoglobulin A (the initial defense against entrance
of infectious agents) was noted by Tomasi et al. in cross-country skiers performing strenuous exercise ( 119). Robertson
et al. noted changes in the immune system and an increase in cortisol after maximal cycling ( 118). A study on URIs and
psychological stress, seen with elite athletes and high-level competition, showed an increased association ( 120). The
strain of strenuous exercise and psychological stress of competition may combine to play a part in the increase in URI
among elite athletes.
Effects of Upper Respiratory Illness on Exercise
The effects of a URI on performance have been shown in multiple systems. Decreased strength was noted with URI
(121), as well as increased airway hyperreactivity in cold, dry air ( 122). Yet, no change was seen in physiologic
responses to pulmonary function testing during submaximal and maximal exercise (123). Most studies showed a
decrease in athletic performance during illness and recovery after illness ( 124).
Athletes not only have decreased performance with URI; they may incur muscle damage ( 125) and risk sudden death.
Coxsackie virus and influenza B virus have been the cause of death in athletes who performed strenuous exercise too
soon after a URI (126). Care must be used in allowing an athlete back to practice and competition after a URI. Among the
many recommendations that have been made, the author finds the “Neck Check” the most useful guide.
The “Neck Check,” as described by Eichner ( 127) uses the neck as the focus for symptoms. If symptoms are “below the
neck,” such as fever, myalgia, hacking or productive cough, vomiting, or diarrhea, then it is best for the athlete not to train
because the gains from exercise will be offset by the loss in muscle and the potential for cardiomyopathy. Symptoms that
are “above the neck,” such as congestion, rhinorrhea, sneezing, or sore throat with no constitutional symptoms, mean an
athlete can try to train moderately. If symptoms worsen, training should stop.
Weidner et al. used a noncardiopathic rhinovirus strain and showed that moderate exercise training during a
rhinovirus-caused URI does not alter the severity and duration of the illness ( 125). They recommended that athletes
should monitor symptoms and training schedules and should rest during a URI ( 111). Return to play should be guided by
the “Neck Check,” with full activity not expected for the same length of time as the illness. Moderate exercise can be done
without systemic symptoms.
Upper Respiratory Illness and the Athlete
As a physician it is useful to know that many athletes initially report their colds to the athletic trainer or coach; when they
do seek help from the doctor or nurse initially, they tend to do so a full day later (average, 3.6 days after onset) ( 112).
Trainers need to be made aware of the risks of exercise during illness. A plan for allowing or withholding athletes from
participation must be set up beforehand.
Differentiating viral URIs from bacterial infections can be difficult. Inappropriate use of antibiotics may worsen an athlete's
condition by initiating side effects without treating the viral illness. Most colds respond to supportive care ( 128).
Antibiotics should be used sparingly.
There are many proposed treatments for colds, with limited data supporting relief with any versus placebo. Studies of
colds prevention have demonstrated some benefit from supplementation with vitamin C. In one study, a pooled rate
reduction ratio of common cold infections was 0.50 (95% confidence interval, 0.35% to 0.69%) with vitamin C ( 129).
Glutamine has had mixed results, and no study has shown benefit clinically ( 113). Use of herbal remedies such as
echinacea and goldenrod is common. Echinacea may decrease the number of illnesses per year by 10% to 20% ( 130). A
review done for the Cochrane Review reported a decrease in the number of colds ( 130a). Echinacea is an
over-the-counter preparation and is not under the control of the U.S. Food and Drug Administration, so the buyer should
beware. Goldenrod can cause severe allergies and has not been shown effective versus placebo.
Treatment of colds is mainly supportive with rest, hydration, and symptomatic treatment. Ipratropium bromide nasal spray
may be used to reduce nasal secretions. Decongestants decrease nasal and sinus congestion. Saline nasal spray also
may have decongestant properties. None of these medications has been shown to reduce the length of illness ( 131). Zinc
lozenges reduce the length of illness if taken within the first 24 hours after onset of symptoms ( 132). The limiting factors
for use of zinc are dosing (every 2 hours) and nausea (25%). A review of studies with echinacea in the acute setting
showed a decrease in illness length of 1 to 2 days ( 133).
Traveler's Diarrhea
With many different World Championships, it is common for athletes to travel to distant locations for competitions. In
developing countries, traveler's diarrhea with 2 weeks' stay had an incidence of 20% to 50% ( 134). It can also occur with
travel to industrialized nations. Many athletes are in danger of developing traveler's diarrhea, and its effects can be
detrimental.
Traveler's diarrhea is usually a self-limited illness. It is defined as three or more unformed stools in 24 hours in a person
traveling to another country. It resolves in 3 to 5 days in 90% of cases but can last longer than a week. In 20% of
patients, the illness is severe enough to cause them to be bedridden, with only 10% to 20% developing fever or bloody
stools (dysentery).
Bacteria are the cause of 80% of cases. The most common isolates from travelers have been enterotoxigenic Escherichia
coli and Shigella species. Campylobacter species, salmonellae, vibrios, Aeromonas, and Plesiomonas are other bacterial
causes. Giardia lamblia is the most common protozoan agent, but it can be difficult to isolate. Cryptosporidia and
cyclospora are unusual causes, and Entamoeba histolytica is rare. Viruses, notably Norwalk virus and rotavirus, also
cause traveler's diarrhea ( 135).
The best treatment is prevention. “Boil it, cook it, peel it, or forget it” is an important phrase in the prevention of traveler's
diarrhea. Water should be boiled or filtered to remove pathologic organisms. Boiled drinks such as coffee and tea should
be safe if served hot. Iodine (0.2 mL of tincture of iodine) or chlorine (0.1 mL of 5% chlorine bleach) added to 1 L of
nonturbid water and left for 30 minutes will purify the water. Ice should be considered frozen packages of
diarrhea-causing organisms. Adding ice to drinks is dangerous. Brushing the teeth with nonpurified water is often
overlooked by travelers and is a common source of infection. Meats should be cooked thoroughly, and dairy products
must be pasteurized. Raw meats and fish products should be avoided. Fruits should be washed and then peeled. Fruit
that cannot be peeled should not be eaten. Leafy greens cannot be cleaned and in some countries are grown in fertilizer
made from human feces. The pathogens are not removed by washing, so it is best to avoid salads.
Preventive medications for traveler's diarrhea are not appropriate for all travelers ( Table 7.10). The medications used for
preventive measures are fluoroquinolones, trimethoprim-sulfamethoxazole (TMP-SMX, Bactrim), and bismuth
subsalicylate (135). Bismuth subsalicylate is an effective treatment. It works by antagonizing the action of a heat-labile
enterotoxin produced by Vibrio species and some E. coli. Bismuth subsalicylate usage is limited by dosing (two tablets
four times daily) and by the common findings of black tongue and stool. Ciprofloxacin and norfloxacin are
fluoroquinolones; they can be administered once daily. As with other antibiotics, resistance has started to develop. These
drugs cannot be used in adolescents or pregnant women because of open growth plates. They also can cause
pseudomembranous colitis. Resistance has developed to TMP-SMX and doxycycline, both previously in wide use.
TMP-SMX is still used when fluoroquinolones cannot be used. The development of resistance is inevitable with
prophylactic antibiotics, and care should be used when choosing to use antibiotic prophylaxis.
TABLE 7.10. WHEN TO USE PROPHYLACTIC ANTIBIOTICS FOR TRAVELER'S DIARRHEA
Avoiding unsafe products is difficult. The reported percentages of travelers who use ice cubes in their drinks (95%); eat
salads (90%); consume dairy products and tap water (80%); and eat ice cream, hamburgers, and incompletely cooked
chicken, lobster, or shrimp (55%) are high. Fewer than 3% reported following recommendations and avoiding all
potentially contaminated food and beverage items ( 136,137). The level of prevention will be higher among athletes if the
risks involved are emphasized.
Dehydration is the main problem that causes symptoms and weakness in travelers. Oral rehydration is very important.
World Health Organization oral rehydration packets are commercially available. A safe water supply, rather than local
water, should be used to rehydrate them. Antibiotic treatment for traveler's diarrhea should be reserved for moderate to
severe illness (e.g., dysentery). When antibiotic treatment is started, the fluoroquinolones are the treatment of choice.
They are given twice daily for 1 to 3 days. Single dosing has been shown effective for ciprofloxacin (Cipro) at 750 mg.
The use of single dosing is discouraged, because the likelihood of resistance increases. Resistance with any antibiotic is
bound to develop, so there is a need for other types of treatment. Oral vaccines for enterotoxigenic E. coli (available
outside the United States) and rotavirus are on the horizon and show much promise ( 138,139). It is yet to be determined
who should receive such vaccines and when.
Antidiarrheal agents can be helpful in the treatment of traveler's diarrhea. They should not be used if fever or bloody
stool is present until definitive treatment is started. Loperamide (Imodium A-D) can be used to decrease the frequency of
bowel movements and is well tolerated. Bismuth salicylate can be used as prophylactic medication ( 140) for up to 3
weeks, and it can be used at the time of symptoms. Dosing is every 2 hours. In high doses, bismuth salicylate can cause
tinnitus, and it should be avoided with aspirin use.
Traveler's diarrhea is a common disease that, because of dehydration, can be very detrimental to a traveling group of
athletes. The level of competition and necessity of the trip are important factors in determining the need for prophylaxis.
The available vaccines may be essential for traveling athletes. The use of bismuth salicylate is highly recommended.
Prevention is a key part of counseling of the athlete. Once symptoms start, hydration is the most important concern.
Because bacterial infection is very common, antibiotic treatment is usually helpful.
Human Immunodeficiency Virus Infection
The incidence of HIV infection in the adolescent population continues to increase. Between the ages of 18 and 59 years,
the rate of HIV infection in the United States is estimated to be 0.78% (95% confidence interval, 0.77% to 1.04%) in men
and 0.16% (0.15% to 0.2%) in women (141). One in 200 college students is HIV positive. HIV rates among collegiate
athletes should take risk-taking behaviors into account. Collegiate female athletes participate in fewer HIV risk-taking
behaviors (142). Collegiate male athletes and especially those in contact sports have been shown to participate in more
risk-taking behaviors compared with nonathletes ( 143). Some athletes who participate in sports are HIV positive. Athletes
who are infected are unlikely initially to know their status.
HIV is transmitted via bodily fluids. Different bodily fluids contain different amounts of HIV and therefore carry varying
risks of infection ( Table 7.11). The normal transmission route is via sexual contact or sharing of intravenous needles.
Before the advent of routine testing, contaminated blood products and allograft tissue were documented sources of
infection in athletes. Health care workers are at risk from percutaneous needlesticks when working with HIV-positive
patients.
TABLE 7.11. BODILY FLUID RISKS FOR HUMAN IMMUNODEFICIENCY VIRUS (HIV)
The risk of transmission of HIV during athletic competition is extremely small; the likelihood of transmission of hepatitis B
infection is much greater (144). There has been one documented case of transmission of hepatitis B virus in sports. Most
estimates of probability of HIV transmission have been calculated for football. Brown et al. estimated a theoretic risk of 1
in 85 million game contacts (145). By comparison, the risk of male-female transmission during sexual contact is 1 in 300
to 1 in 2,000 (chance of seropositive male or female and transmission) ( 146). The chance of acquiring infection from
another player during sports is extremely low. The only reported case of suspected transmission during sports was
among soccer players in Italy in 1990. However, the sexual history and other risk factors for this case were not well
documented (147). The risk is probably lower in other sports, where blood exposure is even less likely than in football.
Health care providers need to be cautious when taking care of athletes with open sores or bleeding; universal
precautions (144) should be used. A pocket mask or similar ventilator should be available for use during cardiopulmonary
resuscitation. Proper disposal units for sharp instruments are needed. Washing of hands after caring for patients, even
with proper gloving, is expected. Towels and other equipment should be cleaned in an HIV-disinfecting detergent.
Players must avoid sharing shaving razors.
Routine testing of athletes for HIV is not recommended (148,149). Athletes can be tested if they wish because of high-risk
behaviors (e.g., unprotected sex, receipt blood products before 1985, intravenous drug and steroid use). The
combination of the enzyme-linked immunosorbent assay (ELISA) and the Western blot test has a false-positive rate of
less than 0.001%. The false-negative rate depends on time of testing after contraction of disease, because the test is for
antibodies to the virus, which take a minimum of 6 weeks to develop. The best course of action is to counsel athletes on
the risks of contracting HIV and avoidance of those risks.
Exercise can be helpful in the care of HIV-infected athletes. An individualized exercise prescription should be designed
for each patient. It will vary depending on the status of the illness and the preference of the athlete. Studies have shown
no increase in viral load with exercise for up to 12 weeks ( 150). Regular exercise has been shown to have many benefits
for HIV-infected athletes, though helper T-cell counts and other immune measures are not enhanced significantly ( 151).
Randomized trials of 12 weeks of exercise showed significant benefit for HIV-positive patients at both moderate and
strenuous levels (152). HIV-positive athletes with the acquired immunodeficiency syndrome (AIDS) who want to continue
strenuous training need to use caution; they should be individually monitored, because their immune-compromised state
may worsen with strenuous exercise. With proper care, there is no current rationale to restrict HIV-infected athletes from
competition.
GASTROINTESTINAL PROBLEMS
GI symptoms are common in the general population, and they also are seen often in the athletic population. Among
endurance athletes, 30% to 50% may have one or more GI symptoms (153). GI complaints in the athlete are
multifactorial. Sometimes, it is difficult to differentiate which symptoms are caused by exercise and which by normal life.
The most common symptoms are heartburn, loss of appetite, urge to defecate, abdominal cramps, and diarrhea. When
running, the most common cause to stop is the urge to defecate. Many symptoms can be eliminated with planning and
some with medication.
The presence of GI symptoms varies with running experience and with length of run ( 154). Runners with less experience
report more symptoms. The GI tract does not adapt to increased exercise training. However, sufficient training leads to
less of a decrease in GI blood flow at submaximal exercise and a decrease of GI symptoms ( 153). GI bleeding is more
common in extended aerobic exercise. Intensity of exercise has many effects on the GI tract.
Gastrointestinal Transit Time
The speed of clearance of the GI tract is affected by exercise. The phrase “speeding the slow and slowing the fast” ( 155)
helps describe the effects of exercise. In the upper GI tract, exercise increases transit time (slows it down), while in the
lower GI tract it decreases transit time (speeds it up). Gastric emptying is influenced by both intensity of exercise and
hydration state. Rehrer et al. showed significant effects of dehydration and intensity, these two effects being additive in
delaying gastric emptying ( 156). The correlation of dehydration with GI symptoms is supported by the fact that in one
study 80% of marathoners who lost 4% of their body weight had GI problems ( 157). Exercise of up to 70% VO2max causes
an acceleration in gastric emptying ( 158,159). This effect is not influenced by level of training ( 160,161 and 162). When
the intensity is increased to more than 70% V O 2max, gastric emptying decreases and symptoms of reflux increase (158).
Moderate exercise before food intake does not interfere with whole-gut transit time ( 163).
Gastroesophageal Reflux
Exercise can induce gastroesophageal reflux ( 164), especially in runners who are symptomatic at rest ( 163). How this
occurs is not certain, because conflicting reports have shown no change or a decrease in the lower esophageal pressure.
The symptoms may be caused by a sensitive esophageus and decreased lower esophageal pressure. A diagnosis of
exercise-induced gastroesophageal reflux disease can be confirmed by means of ambulatory pH monitoring ( 165).
Symptoms should be correlated with the periods of low pH. Studies on noncardiac pain have shown similar rates of low
pH among asymptomatic versus symptomatic patients on pH monitoring. Bernstein testing is an acid challenge test that
has a higher sensitivity and specificity than pH monitoring. Treatment consists of change in diet, time between eating and
exercise, and nature of exercise. If nonpharmacologic treatments fail, an H 2 blocker may be tried. H2 blockers are
effective at preventing the gastroesophageal reflux associated with running. Proton-pump inhibitors prevent acid
production better than H 2 blockers do, but they have not been studied during exercise.
Runner's Trots
Diarrhea is common after running. The cause is multifactorial. The diminished blood supply to the intestine during
exercise decreases uptake of intestinal fluids. There is an increase in intestinal motility and therefore a decrease in
transit time. This produces a softer, watery stool. Dietary factors play role as well. Runners often eat a diet rich in fiber,
which enhances soft stools. Although the diagnosis is common, it is important that it be confirmed by a history and
physical examination ( 166).
GI diseases are often overlooked in athletes. The exercise-induced symptoms should occur only during or immediately
after exercise. Decreasing intensity of exercise should alleviate symptoms. Signs or symptoms of an infectious process
should be absent.
In the history, look for medications that cause diarrhea (e.g., antibiotics, laxatives, magnesium-containing antacids) and
any concurrent medical illness (e.g., inflammatory bowel disease, diabetes, wheat or milk intolerance, irritable bowel
disease). Do not overlook nutritional supplements, which may include dairy or fiber. The physical examination should be
unrevealing in the case of runner's diarrhea; any finding should prompt further workup.
Treatment of runner's diarrhea consists of proper hydration with a safe water supply and avoidance of intestinal motility
agents such as caffeine and cathartics. A change to a nutritional liquid, low-dietary fiber, low-lactose meal before the day
of a race to decrease intestinal contents may help. If this does not solve the problem, then a weak antispasmodic such as
loperamide can be used (167). Avoidance of anticholinergics (e.g., scopolamine) is important, because they can diminish
sweating and predispose to heat illness.
Gastrointestinal Bleeding
Frank GI bleeding most often brings the worried athlete into consult the physician. The bleeding can be classified as
either acute or chronic and either occult or frank. Bleeding in athletes that is caused by exercise appears to be related to
the work intensity. The prevalence of guaiac-positive stools varies from 7% to 80% in runners ( 168), depending on the
length of the race. Ultramarathons have had the largest percentages.
The cause for GI bleeding has been reported as ischemic. The antrum of the stomach is the most common site, but the
colon has also been documented ( 169). Ischemia is plausible because of blood flow to the intestines is reduced by 80%
during maximal exercise (164). The blood flow is reduced by only 30% to 40% at 70% V O2max, and bleeding is not
common at that level of activity (169). Gastric blood flow increases with eating. It has been postulated that liquid meals
taken during a run may minimize the gastric blood flow reduction and decrease ischemia.
Many theories involving jarring microtrauma, such as “cecal slap syndrome” ( 170), have been postulated. There has
been no documented proof, but the theory is logical because running, which results in more GI vibrations than cycling or
swimming, has more GI bleeding (171). NSAID use is common among athletes and can cause ulceration and GI bleeding
(172). Not all studies have shown a correlation between NSAID use and guaiac-positive stools ( 169). Many factors can
cause GI bleeding.
GI bleeding, like all GI complaints, requires a thorough history and physical examination. Any frank bleeding should
prompt an appropriate GI workup for irritable bowel disease, colon cancer, and other nonexercise-related causes.
Irritable bowel diseases such as Crohn's disease (prevalence of 20 to 40 per 100,000 persons) and ulcerative colitis (70
to 150 per 100,000) have a peak incidence at 15 to 35 years of age, when most athletes participate in sports ( 173). Many
athletes with nonexercise-related GI disease have their first occurrence during or around exercise.
Treatment for exercise-induced GI bleeding depends on the location and severity. It begins with a reduction in the
intensity of workouts, followed by a gradual return to the previous level of training after resolution of symptoms. Most
often rest and hydration suffice. However, H 2 blockers can be of help to treat gastritis. The use of an H 2 blocker was
shown to decrease bleeding occurring after an ultramarathon ( 172). The use of an acid suppressor may be considered in
an athlete with bleeding after exercise and a negative workup.
Liver Disease: Hepatitis
Hepatitis is an inflammation of the liver that can be caused by a number of etiologic agents, including alcohol, viruses,
biliary obstruction, toxins, and drugs. Viral hepatitis is caused by five ( 5) known subtypes, known as hepatitis A through
E. The transmission and infectivity for each type is different.
Pseudohepatitis
A rise in the level of the liver enzymes is found in endurance athletes ( 174). During vigorous exercise, muscles can be
damaged, releasing intracellular enzymes into the blood. Liver cells also release lesser amounts of their enzymes ( 175).
The harder and more sustained the exercise, the greater the rise in serum enzymes ( 176). If a marked elevation in serum
enzymes is found, a significant amount of muscle damage has occurred. This should be an indication that the athlete
should rest, hydrate, and restore glycogen reserves.
In virtually all cases of exercise-elevated enzymes, the levels return to normal within 3 days after cessation of exercise. If
the physician is concerned and the athlete with elevated liver enzymes is unable to stop exercising, then liver-specific
enzymes can be measured. Lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) are found in both
myocytes and hepatocytes. Serum g-glutamic transpeptidase (GGT) is found only in hepatocytes and is seen in acute
hepatic injury such as binge alcohol drinking. Alanine aminotransferase (ALT) is another hepatic-specific marker.
Creatine kinase (CK) is found in muscle but not in liver cells. For example, markedly increased concentrations of LDH,
CK, and AST associated with normal or slightly elevated ALT and GGT should lead to a diagnosis of athletic
pseudohepatitis. In that case, the only treatment is rest, hydration, and a carbohydrate-rich diet.
Hepatitis A
Hepatitis A is transmitted via the fecal-oral route. It is not killed by baking, and bread has been a source of infection.
Incubation is 2 to 7 weeks before the onset of symptoms. The most common symptoms are fatigue, fever and chills,
nausea and vomiting, anorexia, and abdominal pain. Jaundice occurs in adults but rarely in children. It is very infectious,
and isolation of patients is essential to prevent spread. Hepatitis A is never life threatening, and no carrier state is found.
The diagnosis is mostly clinical but the diagnosis can be made by finding anti–hepatitis A virus immunoglobulin M.
Monitoring of ALT levels during the illness determines severity. Treatment is supportive. Products such as
acetaminophen and other liver-cleared medications should be adjusted or avoided. Return to sport is allowed after the
ALT level nears normal and symptoms resolve. Prevention is possible with the intramuscular vaccine, Havrix. It is an
inactivated hepatitis A virus vaccine. It is not recommended for the general population but is appropriate for athletes
entering high-risk areas and for local epidemics.
Hepatitis B
Hepatitis B is transmitted by blood products and bodily fluids. The most common mode of transmission is sexual contact
and intravenous drug use. Hepatitis B–positive blood is very contagious, with 100 million infectious particles per milliliter
of blood (177). Universal precautions are essential. The rate of new cases is 1 in 800 persons annually, and 1 in 250
people are carriers. The rates will decrease now with universal immunization for children.
Even though the disease is very contagious, there is only one case of hepatitis B virus (HBV) transmission in sports. The
case occurred in Japan between two high school Sumo wrestlers ( 178). The estimated transmission rate is 1 in 850,000
games (179). This estimate is probably high because it is based on the rates of transmission from accidental
needlesticks, not the lower mucocutaneous exposure rate, which is a more likely mode of transmission. Athletes with
HBV chronic infection should be allowed to participate in sports but need to be aware that caution is needed when
bleeding occurs.
Infection incubation is 1 to 5 months but usually in the 4-month range. HBV infection normally resolves with symptoms
similar to those of hepatitis A. Most infected people, young or old, develop jaundice. Carriers occur more often among
younger children (25% to 50%) than among adults (5% to 10%). The mortality rate is 1.4% from fulminant hepatitis and
liver failure. HBV chronic carrier states are hard to treat. Interferon-a has been used with varying success. Liver enzymes
should be monitored to watch for liver failure. Liver transplantation is not contraindicated in HBV infection.
Hepatitis B surface antigen (HBsAg) is the marker for active virus in the blood. Detection of HBsAg means the person is
infectious. The inner shell of this double-shell virus is the core. HBV core antigen is the reason the body produces
anti–hepatitis B immunoglobulin M; it and HBsAg are seen in acute disease. Antibody to the surface antigen confers
immunity.
On exposure to HBV, hepatitis B immune globulin can be given with 75% success ( 180). The HBV vaccine should be
started at the same time. Once symptoms occur, treatment is supportive. Monitoring of liver function and proper hydration
are important. Most care is outpatient based unless complications such as fulminant hepatitis or severe vomiting occur.
An HBV vaccine has been available since the late 1970s. The original vaccine was made from pooled blood samples, but
for more than a decade the vaccine has been a recombinant HBsAg vaccine made in yeast. The new vaccine carries no
risk of transmission of other diseases, as the pooled-sample vaccine did. HBV vaccine is given in a series of three
intramuscular injections at 0, 1, and 4 months. Most infants are now receiving the immunization, but long-term immunity
has not been documented past 15 years. High school and college athletes should be encouraged to get the vaccine.
Specific guidelines for return to play after acute illness need to be individualized. Severe exercise may worsen the
immune response and make the illness worse if return is too soon. Reduced training is recommended for a period of time
equal to that of the acute illness.
Hepatitis C
Hepatitis C is acquired via parenteral transmission. It is transmitted by blood exposure, with a small but definite chance of
transmission through sexual contact (181). Most new cases are caused by intravenous drug use, but receipt of blood
products needs to be considered, because most people are asymptomatic for long periods. The length of incubation is
estimated to range from 1 to 12 months and usually is 2 to 3 months. The overwhelming majority of affected persons are
asymptomatic or have mild symptoms. In 1% of chronic cases, liver failure or liver cancer occurs. It is the leading cause
of liver transplantation.
Patients with history of blood transfusion or intravenous drug use with epigastric or right upper quadrant pain should be
screened for hepatitis C. Anti–hepatitis C is the screening test for infection. It detects the antibodies made against the
virus but does not determine acute versus chronic disease. The amount of virus can be measured by an expensive test
looking for viral load. Treatment for the 75% of patients who go on to chronic disease is mixed in its success rate.
Interferon-a and ribavirin daily for 6 to 12 months is the treatment of choice. Interferon-a is given intramuscularly, which
can be a problem in intravenous drug users. Exclusive use of new needles does not increase the rate of drug use ( 182)
but can prevent transmission via needle sharing. There is currently no vaccine for hepatitis C virus.
Hepatitis D
The delta virus is an RNA virus that must have hepatitis B present to infect people. It uses the HBsAg to replicate. It
worsens hepatitis B by making the chronic state twice as likely; mortality approaches 30%. If an athlete with hepatitis B
infection suddenly gets worse, hepatitis D coinfection should be suspected.
Hepatitis E
Hepatitis E is transmitted via the fecal-oral route. It is seldom seen in modernized countries. Transmission is noted when
people travel to southeast Asia. Treatment is similar to that for hepatitis A, but no vaccine or immunoglobulin is available.
Onset of illness occurs 3 to 6 weeks after exposure. It is very dangerous to a pregnant woman, with an usually high
mortality rate. Unlike hepatitis A, mortality does occur at the rate of 1% to 2%. Proper hygiene and avoidance of
contaminated food and water is essential.
DIABETES
Definition
Type 1 diabetes mellitus (DM), also known as insulin-dependent diabetes mellitus (IDDM), is an autoimmune disorder
caused by the failure of the pancreatic beta cells to produce insulin. Often the destruction of the beta cells occurs over a
number of months. It is a multigene disorder with an unknown environmental trigger that causes the body to produce
antibodies to the beta cells. Eventually, the cells are destroyed and insulin production ceases. Because of this lack of
endogenous insulin production, an exogenous insulin source is necessary at all times to maintain euglycemia. Without
exogenous insulin, a triad of hyperglycemia, ketosis, and acidemia called diabetic ketoacidosis occurs.
IDDM is found in 0.2% of children younger than 18 years of age. Athletes with IDDM do compete in all levels of sports
and in all ranges of activity, from recreational athletics to professional football and even the Hawaiian Iron Man Triathlon.
IDDM typically begins during childhood (before 20 years of age) but can begin in adulthood (10% of cases). Patients with
type 1 DM are typically normal to thin in appearance.
Patients with type 2 diabetes mellitus, also called non–insulin-dependent diabetes mellitus (NIDDM), are able to produce
insulin to varying degrees but have a relative insensitivity to insulin at the cell receptor. It is a common disease, with up
to 5% of the adult population being affected. The majority of diabetics have type 2 DM (85% to 90%). Eighty per cent of
affected persons are obese. There is an insulin resistance theory called the “deadly quartet” that explains the common
findings of type 2 DM, HTN, obesity, and lipidemia.
Exercise Response
The benefit of exercise for glucose control has been shown in type 2 DM ( 183), with the added benefit of normalization of
all components of the “deadly quartet.” No convincing data have shown a similar benefit of exercise on glucose control in
patients with IDDM. Where the benefits for IDDM are seen is in the reduction of the atherosclerosis risk factors of HTN
and hypercholesterolemia. Regardless of the type of diabetes, exercise is an important part of treatment.
As a person exercises, there is an increased demand for glucose in the muscles. Normally, there is a decrease in insulin
and an increase in glucagon that together promote the early increase in hepatic glycogenolysis and gluconeogenesis
during exercise. In type 1 DM, this normal variation in insulin and glucagon production during exercise is not possible.
There is no decrease in insulin and hepatic glucose production is not stimulated, increasing the risk of hypoglycemia.
Monitoring of blood glucose before exercise is needed, and knowledge of the intensity and duration of the exercise is
essential to prevent hypoglycemic episodes in patients with IDDM.
A second issue for diabetics occurs when blood glucose is very high (more than 250 mg per dL). There is a true or
relative lack of available insulin. The exercising muscles are not able to obtain the needed glucose, because of the
insulin-deficient state. During exercise with hyperglycemia, an actual increase in blood glucose is seen because of
counterregulatory hormones and gluconeogenesis production by the liver. There is a normal release of glucagon,
cortisol, and catecholamines with exercise, which causes an increase in blood glucose by stimulation of liver glucose
production. Exercise should not be undertaken during hyperglycemia.
Screening
A physical examination of the diabetic athlete who wants to participate in sports is needed before initiation of activity. The
physician should pay special attention to the complications of DM: cardiovascular disease, nephropathy, renal failure,
peripheral arterial disease, retinopathy, and neuropathy (autonomic and peripheral). Limitation on activity is warranted if
complications from DM are present. Screening for heart disease is recommended in diabetics because of the high
incidence of “silent” myocardial infarction ( Table 7.12). The physician should use clinical judgment regarding stress
testing if the patient intends to exercise at no more than 60% of V o2max. Peripheral neuropathy should preclude a diabetic
from running; instead, activities such as swimming, bicycling, lifting, and stationary rowing can be done. Athletes with
retinopathy should avoid anaerobic dynamic exercises that involve straining, Valsalva maneuvers, or jarring ( 184). When
nephropathy becomes severe (microalbuminuria more than 20 mg per minute; albumin excretion or proteinuria more than
200 mg per minute), high-intensity exercise should be avoided. Patients with autonomic neuropathy (resisting
tachycardia, orthostasis) will have trouble exercising. Hypotension or HTN after exercise can occur. Sudden death and
silent myocardial infarction have been attributed to autonomic neuropathy. Screening for coronary heart disease is a
must. Supervised exercise is recommended.
TABLE 7.12. WHEN TO PERFORM EXERCISE TOLERANCE TEST FOR DIABETICS
Exercise Complications
Hypoglycemia is a regular concern during exercise. Consider one patient's description of an exercise-induced
hypoglycemic event: “Anyone who has diabetes has had episodes of hypoglycemia. It's scary. After playing a lot of tennis
one day, and having taken the medication before I played, I became disoriented, dizzy, frightened, almost in a drunken
state” (185). It is important for athletes to recognize when they are hypoglycemic and how to prevent these episodes.
Exercise can be performed safely by diabetic athletes.
Hyperglycemia can occur during exercise. Athletes who started with a certain glycemic level and then exercised find their
level to be much higher afterward. This occurs because of the release of catecholamines during exercise and the
stimulation of hepatic gluconeogenesis. Athletes need to monitor their glucose and delay exercise when levels are high
(Table 7.13). Also, if glucose levels increase from start to finish of exercise, then less of an adjustment in insulin or
medication is needed.
TABLE 7.13. FOOD INTAKE BEFORE EXERCISE FOR DIABETICS
It is important that athletes exercise with a partner who can treat hypoglycemia. A glucagon emergency kit and a
MedicAlert bracelet should be recommended for each diabetic athlete. The athlete also needs a glucose source; many
commercially available tablets are on the market. A small squeeze tube of cake frosting works well and also can be given
per rectum to an obtunded DM athlete.
When to Exercise
Exercise should be timed so that the activity levels of insulin are past their peak. The diminishing insulin levels will
simulate an exercise insulin response closer to normal. The following is a list of selected insulins with peak activity time
after injection: Lispro, 1 hour; Regular, 2 to 3 hours; NPH and Lente, 6 to 9 hours; Ultralente, 18 to 24 hours ( Table 7.14).
TABLE 7.14. INSULIN ONSET, PEAK, AND DURATION
Adjusting of insulin needs to be done on an individual basis. Any guideline or recommendation should be considered a
starting point. Each individual athlete with diabetes should keep a log of blood glucose levels before and after exercise,
diet, medications (when taken and what), and exercise (amount and intensity). In type 1 DM, there is intersession
reliability in the decrease of blood glucose for the same exercise, allowing these athletes to plan for the training session
(186). Athletes with type 2 DM are less likely to develop hypoglycemia, unless they are taking sulfonylureas. See Table
7.13 for guidelines.
For exercise that lasts longer than 1 hour, a 20% to 50% reduction in insulin is needed on the day of exercise. Monitoring
of glucose every 30 to 45 minutes is needed, and ingestion of carbohydrates is essential. Dehydration should be
avoided, and ample fluid replacement is important ( Table 7.15).
TABLE 7.15. PREVENTING COMPLICATIONS DURING EXERCISE
Treatment
Type 1 Diabetes Mellitus
Type 1 DM is an insulin-dependent disease. Currently, the treatment consists of subcutaneous insulin injections.
Occasionally an insulin pump, which uses a subcutaneous catheter, is used to continuously infuse insulin. It is
associated with more hypoglycemic episodes, but it can be turned off during exercise, making insulin adjustments easy.
Each athlete must carefully evaluate his or her insulin needs during and after exercise, because hypoglycemia may be
seen during and for many hours after exercise.
Athletes who are using subcutaneous insulin should rotate the site of their injection. The extremities should not be used
for injection before exercise, because the rate of uptake is increased if insulin is injected in an exercising limb ( 187).
Dose reduction before exercise must be made on an individual basis.
During the initial treatment period, a “honeymoon effect” is noted. The amount of insulin needed will be reduced or even
eliminated. This soon fades, and the insulin-dependent state returns. This is important to know, because young athletes
have a difficult time accepting this chronic disease and when the insulin requirement decreases they may believe that
they won't have the disease forever. Continuous monitoring is needed throughout this period.
Type 2 Diabetes Mellitus
Exercise has been shown to help promote euglycemia at rest in patients with type 2 DM ( 188). The muscles become
more efficient at uptake of insulin; this is a result of both increased insulin sensitivity and an increase in glucose transport
molecules (e.g., GLUT 4, hexokinase). These benefits decrease the chronic effects of diabetes.
Type 2 DM can be characterized by three defects: a relative decrease in insulin production to glycemic level, a receptor
insensitivity, and an excess of hepatic gluconeogenesis. Treatment is targeted at any of these three sites—that is,
pancreatic insulin production, hepatic glucose production, or the cell receptor. Knowledge about the various medications
is needed to understand their possible effects during exercise.
The use of sulfonylureas, repaglinides, or exogenous insulin is intended to increase circulating levels of insulin.
Exogenous insulin should be adjusted before exercise, as discussed previously. Exercise is best performed after the
insulin activity has peaked and the effect is starting to diminish. Individual adjustments are needed for each athlete.
Sulfonylureas cause hypoglycemia because of the continuous stimulation of pancreatic beta cells. Care needs to be
employed in tightly controlled diabetics who are using sulfonylureas. A reduction in dose is needed on exercise days.
Some of the pills cannot be cut in half, so two prescriptions or smaller-dose pills should be considered. Repaglinide, a
benzoic acid derivative, is similar to sulfonylureas in function. It is taken before each meal and should be withheld before
exercise.
Decreasing gluconeogenesis is the second method of treating type 2 DM. Metformin works by two methods: inhibiting the
hepatic production of glucose and potentiating insulin action at the peripheral tissue. During exercise, the liver produces
glucose in order to prevent hypoglycemia. Metformin inhibits this action. Care is needed when exercising while taking
metformin, although at present no guidelines for its use have been developed. It is recommended that the dose before
exercise should be withheld and that monitoring of blood glucose before, during, and after exercise should be required
until it is clear that no complications will occur.
Drugs of the thiazolidinedione class are being designed to increase insulin receptors of the cells. There are reports of
thiazolidinediones and liver damage. The newer preparations have fewer reported liver effects. Thiazolidinedione does
not cause hypoglycemia when used alone. No studies have examined thiazolidinediones and exercise. It is
recommended that normal guidelines be followed when thiazolidinediones are used alone, but when they are used with
other agents more care is needed because the hypoglycemic risk is increased.
A final group of type 2 DM medications, called a-glucosidase inhibitors, are used to delay the peak postprandial serum
glucose concentration and thereby control type 2 DM complications. No study has demonstrated a significant decrease in
the diabetic complication rate with this class of drugs. The medication has an extraordinary complication rate of
flatulence, diarrhea, and abdominal cramping. It is not recommended in the treatment of athletic patients. Athletes using
a-glucosidase inhibitors should withhold the dose before and after exercise.
Internet Resources
The American Diabetes Association's site on the internet is a good resource. It has an exercise section
(http://www.diabetes.org/exercise/) featuring frequently asked questions, monthly profiles of diabetic athletes, and articles
on exercise and diabetes. The telephone number is (800) 342-2383.
The website of the International Diabetic Athletes Association ( http://www.diabetes-exercise.org) offers information that
includes a quarterly newsletter and information on regional chapters and association events. The telephone number is
(800) 898-4322.
MUSCLE PROBLEMS
Delayed-Onset Muscle Soreness
Training for competitive sports requires repeated stresses and recoveries. Muscle soreness either occurs during activity
(acute soreness surrounding activity, known as “the burn”) or is delayed in onset. Delayed-onset muscle soreness
(DOMS) starts 8 to 24 hours after exercise, reaches a maximal intensity at 1 to 3 days, and then gradually subsides in 5
to 7 days. This delayed soreness serves as the best available guide to maximize training and avoiding injury.
DOMS is thought to be caused by two mechanisms: mechanical damage to the muscle fibers with disruption of Z lines
(189) or metabolic release of cytosolic enzymes into the blood ( 190). The more muscle damage that occurs, the more
soreness is present. Increased environmental temperature and eccentric contractions (e.g., running downhill, squats) are
factors that increase soreness ( 191). The muscle volume is increased by edema (189). The muscles are firm and tender
and cannot contract with their maximum force (192). Continued exercise and pressure increases soreness.
Though the muscles are swollen, inflammation is not apparently the cause, as evidenced by the lack of granulocytosis
(189). Athletes may be tempted to treat such soreness with NSAIDs (193). However, NSAIDs do not hasten healing and
may mask symptoms and increase susceptibility to injury ( 194). Modalities such as ultrasound ( 195,196); transcutaneous
electrical nerve stimulation ( 196,197); cryotherapy (196,198); postactivity stretching ( 199); massage (200); and
homeopathic medicine (201) have been studied to speed recovery from DOMS and to prevent symptoms. None has
demonstrated relief compared with placebo treatments. A small study of vitamin C showed decreased symptoms in 25%
to 40% of subjects (202). Prevention is the best method to prevent DOMS.
Exertional Rhabdomyolysis
Extreme exercise can produce significant muscle damage, often resulting in rhabdomyolysis and myoglobinuria. It is most
probable in untrained athletes with predisposing risk factors for dehydration such as drug use (e.g., alcohol, diuretics),
concomitant illness, or a hot environment. Athletes can present with symptoms in a single muscle group (biceps, triceps)
after an overstrenuous lifting session. The athlete presents with muscle weakness, tenderness, and swelling which can
develop rapidly. Typical laboratory findings include a markedly elevated CK (up to 10 to 40 times normal) and an
elevated creatinine. Urinalysis can show a dark brown urine with casts and myoglobin. Hb may or may not be present
(see previous discussion). Acute renal failure can develop secondary to direct tubular injury from the myoglobin.
Hydration is very important for recovery. If myoglobinuria is present, admission to an inpatient unit for vigorous hydration
and alkalinization of the urine with bicarbonate to maintain renal function are indicated. Administration of mannitol to
encourage diuresis may be necessary.
Overtraining
Elite athletes train for many hours in a day. This productive stress on the body increases muscle mass and
neuromuscular dexterity, thereby enhancing athletic performance. In a well thought-out training plan, there is overload
training (tailored to the athlete's abilities), then adequate recovery, then repeat overloading. This normal cycle of stress
followed by recovery is important to successful development. When the training stress increases and the recovery time is
insufficient, overreaching occurs. As the stress continues, an overtraining or “staleness” develops. Finally a chronic
fatigue occurs (203). This may not be evident on a day-to-day basis because the athlete is trying to reach the limits of
self-performance and is pushing the boundary of overreaching.
Overreaching is defined as a period of high-intensity training that leads to decreased maximal performance ( 203). It is
characterized by muscle fatigue, which is thought to be caused by insufficient replacement of muscle glycogen. Recovery
time is short (2 days to 2 weeks). It is often a part of training meant to stimulate physiologic adaptation. Studies have had
mixed results with carbohydrate supplementation to treat this problem ( 204).
Overtraining is detrimental. Flynn et al. ( 205) found a 3% to 6% decrement in performance during highest training periods
(overreaching periods). Keeping in mind that the difference in time between first and 10th place for the 1998 Tour de
France was 0.3% and the difference between the gold medal and no medal (fourth place) in the 100-m freestyle at the
1996 Olympic Games was 0.8%, a small decrease in an athlete's performance can be devastating. Therefore, it is
important to be able to detect overtraining and correct it.
Overtraining is the gradual worsening of overreaching. It is seldom caused by training alone; instead, it is the total
amount of stress experienced by an athlete ( 206). Many theories are proposed to explain the cause of overtraining.
Israel, in 1958, described two forms of overtraining: parasympathetic (Addison) and sympathetic (Basedow) ( 207).
The parasympathetic form is characterized by a high fatigue rating, apathy, and altered mood states. It was called
Addison-type because it resembled the clinical pattern of morbus Addison (adrenal insufficiency) ( 207). Findings support
a reduced adrenal responsiveness of corticotropin (ACTH) and an increase in ACTH without increased cortisol levels. In
overreaching, the decreased responsiveness can still be compensated by an increase in ACTH; this ability is lost in
overtraining. With overtraining, other hormones from the pituitary (e.g., growth hormone, TSH) are also decreased ( 207).
It has been proposed that this is caused by a defect in the hypothalamic region or a feedback problem.
The sympathetic form of overtraining is characterized by hyperexcitability, restlessness, and performance incompetence
(207). It is not nearly as common a problem as the parasympathetic form. It has a clinical pattern similar as morbus
Basedow (thyroid hyperfunction). Decreased exercise-associated TSH levels are seen, although these data need
confirmation (207). The overriding theory is that TSH reduction is caused by long-term increased sympathetic nervous
system activity.
The difficulty for researchers is threefold: there is no an appropriate model for overtraining; athletes cannot be subjected
to the debilitating effects of overtraining and resulting injury for research purposes; and when cases of overtraining are
found, pretraining laboratory values are seldom available for comparison. For all of these reasons, it is not possible to
definitively test for early stages of overtraining and allow for recovery. Recovery time can be several weeks to months,
effectively eliminating an elite athlete's season. Therefore, the prevention of overtraining is important.
Many hypotheses exist to explain the cause of overtraining, none of which has been proven. They include imbalance of
branched-chain amino acids, decreased glycogen, neuroendocrine dysfunction, and glutamine deficit. Supplementation
with carbohydrates, branched-chain amino acids, or glutamine has not delayed fatigue in athletes studied.
Catecholamine alterations are seen with overtraining. An increased resting plasma norepinephrine concentration and a
submaximal norepinephrine response are seen, indicating a decreased sensitivity of the target organs and a loss of
training adaptation ( 207). Whether the neuroendocrine changes are a cause or an effect is unknown.
Clinical symptoms of overtraining are muscle fatigue and soreness (overreaching). The athlete has mood disturbances,
emotional instability, premature fatigue, an increased resting heart rate, an increased number of colds, and decreased
motivation (203,208). It can happen in any elite-level sport but is most common among endurance athletes and swimmers
(206).
Many entities, both correctable and dangerous, can mimic overtraining. These should be ruled out before a diagnosis of
overtraining is made. The list includes mono (in which fatigue and overtraining symptoms may be the only sign [103]),
other viral illness, anemia, hypothyroidism, subclinical myocarditis, psychological illness, and drug-induced symptoms. A
careful history that includes when symptoms started, training schedule, recent illnesses, sick contacts, and medications is
needed. The physical examination is usually noncontributory. Laboratory results that can be helpful are the erythrocyte
sedimentation rate, ferritin level, complete blood count, TSH, mono spot test, and electrolytes. Other laboratory studies
may be needed as clinical suspicion guides the physician. Basal heart rate monitoring (overtraining increases the heart
rate) and a symptom diary are important guides to treatment. If pretraining values are available for comparison, an
increased rate of perceived exertion for a given lactate level is useful to indicate a diagnosis of overtraining. A decrease
in salivary immunoglobulin A is seen and is correlated with increased URIs ( 118). The Profile Of Mood States (POMS)
tool is used to test the athletes for alterations in psychopathologic parameters. It is used to monitor athletes for the
psychological changes of overtraining.
Treatment of overtraining consists of rest with cross-training activities and monitoring of basal heart rate, POMS scores,
and symptom chart. Recovery for overtraining is long—weeks to months. It is important to prevent overtraining so as not
to have to stop the athlete's training. A pattern of 4+2+1 is recommended: the athlete trains hard for 4 days, then has 2
days of “easy” training and 1 day of rest ( 209). This sequence allows the athlete to maximize training and recovery.
CHRONIC FATIGUE IN ATHLETES
At some time in their lives, most athletes complain of a drop in performance, a tired feeling, and generalized muscle pain
and weakness. Muscle glycogen depletion and dehydration are the most likely causes. Most respond to a short stoppage
in training for 2 to 3 days and supplementation with extra fluids and carbohydrates, as discussed in the previous section.
Chronic fatigue can develop if overtraining is not diagnosed early. Some athletes do not recover for months or even
years (210). Other complaints often include muscle ache and headaches, amenorrhea, depression, inability to
concentrate or stay awake, loss of libido, insomnia, constipation or diarrhea, enlarged lymph nodes, and frequent colds
and injuries.
An evaluation should include a thorough search for a cause. More than 60% of chronic fatigue cases have no known
cause (211). Depression and infections are the most common known causes. Fatigue is usually a presenting symptom of
depression. Depression affects up to 25% of people who complain of chronic fatigue ( 212). Depression can be situational
or chemical. Situational depression may not require medication and often can be treated with environmental changes and
psychotherapy. Chemical depression is usually treated with medication.
The remaining patients (approximately 15%) will have as a cause either infection, drugs, or an electrolyte abnormality.
Tests should be scheduled appropriately to fit the history of the patient. A thorough history and physical examination are
needed. Multiple visits are often needed. Depression should be addressed in the history, because it is more common
than the other identifiable causes.
Infection
Any infection can induce fatigue. Young, healthy athletes can have chronic sexually transmitted diseases. If indicated,
order chlamydia, gonorrhea, and herpes cultures of the cervix or urethra and consider judicial use of bacterial cultures of
urine, nose, throat, vagina, or semen. Occasionally fatigue may be caused by cytomegalovirus infection, hepatitis,
toxoplasmosis, HIV infection, or other agents that cause mononucleosis-like syndromes.
Drugs
Frequent ingestion of alcohol can impair glycolysis and cause early muscle fatigue ( 213). All potassium-wasting diuretics
can cause hypokalemia and hypomagnesemia. The lipid-lowering drugs (lovastatin, gemfibrozil, niacin, and the
clofibrates) can cause muscle fatigue and pain ( 214). The asthma drug salbutamol can cause muscle pain. Other causes
include glucocorticoids, large doses of vitamin E, and cytotoxic drugs.
Electrolytes
Abnormalities in mineral metabolism are rare causes of chronic fatigue in athletes. Healthy athletes do not develop
potassium, sodium, or calcium deficiencies. Potassium is found in all foods. Low blood levels of potassium are caused by
vomiting, diarrhea, excessive licorice intake, glucocorticoids, and diuretics. If bulimia is suspected, the physician should
start the process of counseling and order a 24-hour urine specimen for potassium analysis. Vomiting causes a metabolic
alkalosis, which forces the kidneys to conserve hydrogen ions and lose potassium.
Sodium abnormalities are unusual causes of fatigue in healthy athletes. The average American takes in more than 4,000
mg of sodium each day, although an individual needs only about 200 mg at rest and a maximum of 3,000 mg when
exercising extensively in hot weather. Even if the athlete is heat acclimatized, does not add salt to food or cooking, and
does not use especially salty-tasting food, he or she will still take in approximately 300 mg sodium each day ( 215).
High blood sodium levels are caused by dehydration, exogenous glucocorticoids, renal disease, and adrenal
hyperfunction. Low blood levels usually are caused by polydipsia, dehydration, GI disturbances such as recurrent
vomiting and diarrhea, diuretics, renal disease, glucocorticoid deficiency, hypothyroidism, or severe salt restriction.
An increased calcium level calls for a search for parathyroid or kidney disease, other hormonal disorders, tumors, and
sarcoidosis. It also can be caused by drugs, such as massive doses of vitamin A or D, thiazides, lithium, estrogen, and
antiestrogens. Low calcium levels are caused by parathyroid and kidney disorders, a deficiency of vitamin D, pancreatitis,
hypophosphatemia, hypomagnesemia, administration of calcitonin, or toxic doses of fluoride.
Chronic Fatigue Summary
If indicated, tests can be ordered for hormonal abnormalities, tumors, primary muscle or neurologic diseases, or immune
diseases. Seldom are these tests needed. The difficulty of chronic fatigue is that the cause is usually idiopathic. The
recovery may be prolonged with a wide range, depending on length of symptoms. Exercise needs to be stopped and then
resumed in a very slow progression, over months. Many plateaus in training should be expected, because symptoms may
return if exercise is reintroduced too soon. All athletes need an evaluation from a mental health standpoint. A sports
psychologist can aid the return to play and help the athlete cope with the down time. Support and understanding are
needed when taking care of these athletes, because players, coaches, and physicians can become very frustrated. Early
prevention is the key to success.
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8 Cardiovascular Evaluation of the Athlete
CARDIOVASCULAR EVALUATION OF THE ATHLETE

JAMES D. MILLS
Historical Perspective
Physiologic Adaptations of the Athlete's Heart
Exercise Physiology
Morphologic Adaptations
Electrophysiologic Findings
Pathologic Causes of Cardiac Complications with Exercise
Cardiac Complications in the Young Athlete
Cardiac Complications in the Adult Athlete
Preparticipation Evaluation of the Athlete
Future Direction
Chapter References
The athlete's heart encompasses a broad range of physiologic adaptations. Prompting the physiologic changes in
athletes are the increased demands of exercise. The cardiac variations that occur with exercise include ventricular
hypertrophy, chamber dilation, and alterations in electrical conduction. Fortunately, pathologic conditions of the heart in
young men and women are rare and sudden cardiac death is even rarer. The leading causes of exercise-related
cardiovascular complications include congenital defects in the young and atherosclerotic coronary artery disease (CAD)
in adults. Differentiating physiologic adaptations from the diseased heart is of obvious importance and is the focus of this
chapter.
HISTORICAL PERSPECTIVE
The original description of the “athlete's heart” is attributed to the 19th-century scientist Henschen ( 1). At the time, many
believed that the cardiovascular findings in athletes were the result of pathologic changes that occurred as a result of
exertion. Through observations made on cross-country skiers, Henschen concluded, “Skiing causes an enlargement of
the heart, and . . . this enlarged heart can perform more work than the normal heart. There is therefore, a physiologic
enlargement of the heart due to athletic activity: the athlete's heart” ( 2). Henschen's hypothesis that cardiac enlargement
in athletes was a normal, beneficial response to exercise was debated throughout the early 20th century. We now know
his theory is correct.
In 1935, Kirch presented anatomic data on 35 athletes and concluded that cardiac hypertrophy was the result of physical
exercise and could regress with deconditioning ( 1). Further work by Linzbach ( 3) emphasized that the number of the
cardiac muscle fibers remains constant in physiologic hypertrophy. He concluded that the relationship between
capillaries and the number of fibers remains constant, even when the critical heart weight is exceeded ( 1). The
contributions of these early investigators broaden our understanding of the physiologic changes that occur in the
cardiovascular system of athletes.
Recognizing normal adaptations and differentiating them from abnormal findings is the impetus behind each
preparticipation evaluation. Although physical activity usually decreases the risk of cardiovascular disease, there remains
a small but definable risk with exercise ( 4,5). This risk is underscored by untimely deaths of nationally known athletes.
The importance of accurate diagnosis of cardiovascular abnormalities to prevent untoward complications of exercise
cannot be overemphasized. Three principles can be applied to the prevention of sudden cardiac death in athletes:
1. Atherosclerotic CAD is the predominant cause of sudden death in athletes during exercise in adults ( 5,6).
2. The dimensions of an athlete's heart, adjusted for body size, rarely exceed the upper limits of normal ( 6,7,8 and 9).
3. Cardiac symptoms and strikingly abnormal physical findings, even in healthy athletes, require a prompt evaluation
by a cardiovascular expert ( 6,10).
These principles are paramount when assessing an athlete for participation in sports activities and form the basis for the
historical and physical evaluation.
PHYSIOLOGIC ADAPTATIONS OF THE ATHLETE'S HEART
Exercise Physiology
There exists a broad range of ability among “athletes,” as seen by comparing the weekend bowler to the ultraendurance
runner. Varying combinations of strength, agility, endurance, and dexterity define the individual athlete. Athletic training
is divided into two broad categories: endurance (aerobic, dynamic) and strength (static) training ( 11,12). Sports activities
can be classified based on the degree to which each activity falls into these categories. For example, golfing is
considered to be a low-dynamic, low-static sport, while rowing is high dynamic, high static ( 13). Physiologic adaptations
of the heart are largely determined by the degree of aerobic and static activity pursued by the athlete.
The heart is considered an obligate aerobic organ; it requires an adequate amount of oxygen delivery for optimal
performance. Oxygen extraction in the coronary circulation at rest is nearly maximal. Hence, increases in oxygen delivery
to the heart must be accompanied by increases in coronary blood flow through a direct, linear relationship. Myocardial
oxygen demand during exertion is determined by three components: heart rate, myocardial contractility, and
intraventricular wall tension. Wall tension is proportional to intraventricular pressure (i.e., left ventricular end-diastolic
pressure) and radius (intraventricular blood volume). Increased physical activity requires increased oxygen delivery
(supply) to the heart and body; this is largely determined by stroke volume (SV) and heart rate (HR), the product of which
is cardiac output (CO) (6):
In addition, autoregulatory changes in arteriolar diameter and intramyocardial blood volume also play a role ( 14). With
high-intensity dynamic exercise, cardiac output rises through an increase in intraventricular end-diastolic volume and a
corresponding decrease in the end-systolic volume, as described by the Frank-Starling mechanism ( 13). The resultant
increase in coronary blood flow and oxygen delivery is regulated by changes in cardiac output and by increases in the
coronary vasodilator reserve. The vasodilator reserve is the difference between resting and peak coronary blood flow; it
can increase fourfold to fivefold during exercise ( 14).
Systemic oxygen delivery varies with changes in cardiac output and in systemic demands. The product of cardiac output
and systemic arteriovenous oxygen difference determines the consumption of oxygen. Mathematically, this relationship is
expressed by the Fick equation:
where VO 2 is oxygen consumption in milliliters per minute; HR is heart rate in beats per minute; SV is stroke volume in
milliliters per beat, and (Ca O2–CvO2) is the arteriovenous oxygen difference, or the oxygen extraction across the capillary
bed, in milliliters of oxygen per deciliter of blood.
Maximal oxygen consumption (VO2max) is defined as the highest rate of oxygen delivery and extraction that can be
achieved at a maximal level of exertion. Importantly, V O 2max varies with type of training, lean body mass, age, gender, and
genetic characteristics. When V O 2max is exceeded, the anaerobic threshold is surpassed and metabolic acidosis through
the formation of lactic acid ensues. This transformation of metabolic energy production is less efficient than the
aerobically fueled glycolytic pathway and heralds the onset of exertional fatigue.
The most important determinant of the cardiovascular response to exercise is the type of exertion performed ( 15). Table
8.1 shows the hemodynamic response to exercise in the dynamic and static athlete. Although response varies widely, the
greatest increase in cardiac output and oxygen consumption is seen in endurance athletes. Moreover, the increases
observed in cardiovascular hemodynamic parameters return to baseline with detraining.
TABLE 8.1. EXAMPLES OF THE HEMODYNAMIC RESPONSE TO AEROBIC AND STATIC TRAINING AS
COMPARED TO THE EXERCISING SEDENTARY MAN (16)
The physiologic concepts just described are the basis for the risk stratification of individuals through diagnostic stress
testing. Formal evaluation of the physiologic response to exercise includes documentation of changes in heart rate and
blood pressure, estimated oxygen consumption, and functional capacity as well as monitoring of the electrocardiographic
(ECG) response. In addition, diagnostic imaging modalities such as echocardiography and nuclear tomography allow the
clinician to improve the predictive value of the stress test for detecting hemodynamically significant atherosclerotic CAD.
Routine cardiovascular testing to prevent untoward exercise-related events has limited utility because of the rarity of
such events, the poor cost-benefit ratio of testing, and the suboptimal predictive value of stress testing in predicting
clinical events during exercise. Nevertheless, atherosclerotic CAD is the overwhelming cause of sudden death during
exercise in adults (4). Furthermore, survivors of exercise-related myocardial infarction and cardiac arrest are often found
to have coronary thrombosis and unstable atherosclerotic coronary plaques on diagnostic coronary angiography ( 18,19).
Although pathology of this kind is rare in athletes younger than 30 years of age, the consequences of atherosclerosis
must be respected in all adults.
The use of routine stress testing to screen for CAD in exercising adults is controversial. In one study, 916 Indiana State
Troopers underwent baseline exercise stress testing with repeat testing performed at intervals of 1 to 5 years for a total
followup of more than 12 years (20). Only 61 (6.6%) of the Troopers had a positive stress test at baseline or over the
course of the study. One third of the Troopers with abnormal test results developed clinical symptoms, and there was one
sudden death. Of the 833 Troopers who had “normal” stress tests, 44 developed symptoms of CAD, 25 had myocardial
infarctions, and 7 had sudden cardiac death. The results of this study emphasize the well-established notion that the
majority of coronary occlusions occur at the sites of unstable atherosclerotic plaque that are not hemodynamically
significant. Consequently, stress testing may not identify many individuals at risk for an ischemic event ( 21).
Morphologic Adaptations
As described earlier, physiologic adaptations to the heart in response to exercise often involve changes in the
morphology and function of the left ventricle. The contrasting patterns of cardiac enlargement with aerobic and static
training are related to changes in pressure and volume within the heart as well as the body's need for increased oxygen
delivery. Physiologic (as opposed to pathologic) hypertrophy of the myocardium can be explained by the Law of LaPlace,
which states that there is a direct relationship between wall tension and the product of pressure (P) and intraventricular
radius (r). Conversely, there exists an indirect relationship between wall tension (T) and wall thickness (h):
This relationship maintains normalized wall tension per cross-sectional area and is conserved throughout a wide range of
normal circumstances (22,23).
Endurance exercise requires an increase in cardiac output and, hence, stroke volume. This dynamic training may result
in ventricular dilation through an increase in left ventricular end-diastolic volume. The increased intraventricular radius is
offset by a small increase in wall thickness, maintaining a constant relationship to systolic pressure ( 22). It is this
ventricular dilation that Henschen originally described in his cohort of cross-country skiers ( 2). Left ventricular
end-diastolic diameter may increase to as much as 7.0 cm, as has been described in some cyclists ( 24). Ventricular
hypertrophy seen in athletes who perform static exercise is a physiologic response to the rise in systemic blood pressure
caused by resistance during skeletal muscle contraction. Importantly, strength-trained athletes usually develop symmetric
hypertrophy with myocardial wall thickness that rarely exceeds 1.6 cm, even in the most elite athletes.
The increase in cardiac dimensions seen with athletic training occurs without evidence of systolic or diastolic dysfunction.
Several echocardiographic studies of primarily endurance athletes suggest that on average there is a 10% increase in
left ventricular end-diastolic diameter, a 15% to 20% increase in left ventricular wall thickness, and up to a 45% increase
in calculated left ventricular mass ( 6,22,25). When training is aborted, myocardial thickness and chamber size often
returns to normal. Olympic rowers have been shown to have a 15% to 33% decrease in septal thickness after 6 to 34
weeks of detraining ( 26). Although ventricular dilation in endurance athletes can be out of proportion to body size, the
increase in myocardial thickness seen in strength-trained athletes such as weight lifters is not observed when cardiac
size is normalized for skeletal muscle mass ( 24). The effect of detraining on the heart may be used as a diagnostic tool to
differentiate adaptation due to exercise from the changes seen in pathologic conditions such as hypertrophic
cardiomyopathy (HCM) (27).
Electrophysiologic Findings
The most common cardiac rhythm in athletes is sinus bradycardia, which occurs in more than 50% of endurance athletes
(22,28). Bradycardia and other electrophysiologic findings in athletes are attributed to increases in vagal tone.
Downregulation of b-adrenergic receptors, a decrease in sympathetic tone, and an intrinsic mechanism may also
contribute (22,29). As many as one third of endurance athletes also have evidence of atrioventricular block within the
atrioventricular node, including first-degree atrioventricular block and Mobitz type I or “Wenkebach” second-degree
block. These rhythms occur more often in athletes than in the general population ( 28). The prevalence of first-degree
atrioventricular block varies between 10% and 33%. High-grade atrioventricular block is rare in athletes but has been
seen with ECG recording during sleep ( 28,30). As with myocardial hypertrophy, bradyarrhythmias often resolve with
detraining.
In addition to bradycardia, the ECG of the athlete may show other unique findings. Increased voltage suggestive of
hypertrophy is a common finding but may be caused by a thin body habitus. Using the Sokolow-Lyon criteria for left
ventricular enlargement, as many as 85% of Olympic endurance athletes meet the diagnostic criteria for left ventricular
hypertrophy (22,28). ST-segment abnormalities including ST elevation, as well as inverted or peaked T waves, may also
be seen (22,28). The changes are typically benign and often resolve with exertion. These ST and T-wave changes are
probably secondary to nonhomogenous repolarization of the ventricles ( 28). Incomplete right bundle branch block, a
vertical or “juvenile” axis, and signs of right ventricular enlargement may also be seen. Figure 8.1 shows an ECG
recording of a highly trained 28-year-old endurance athlete.
FIGURE 8.1. Electrocardiogram from a 28 year-old endurance athlete. Sinus bradycardia, sinus pauses, and junctional
escape beats (arrows) are present. Also note a vertical or “juvenile” axis, incomplete right bundle branch block, increased
precordial voltage, and repolarization abnormality. (From Fahranbach MC, Thompson PD. The preparticipation sports
examination: cardiovascular considerations for screening. Cardiol Clin 1992;10:319–333, with permission.)
PATHOLOGIC CAUSES OF CARDIAC COMPLICATIONS WITH EXERCISE
When discussing the causes of cardiac complications during exercise, it is important to emphasize from the outset that
the most common cause of morbidity and mortality including sudden cardiac death in athletes is atherosclerotic CAD.
Ischemic heart disease is rare in the young athlete. Therefore, this discussion is divided according to the most frequent
causes of cardiac complications in athletes younger and older than 30 years of age.
Cardiac Complications in the Young Athlete
The annual estimated nontraumatic death rate within 1 hour of sports participation among high school and collegiate
athletes in the United States is 1 per 133,000 men and 1 per 769,000 women per year. Congenital cardiac abnormalities
are the main cause of exercise-related cardiac death in young subjects. The National Center for Catastrophic Sports
Injury Research examined the causes of nontraumatic sports-related deaths in high school and college. They
documented 160 deaths over a period of one decade, 100 of which were attributable to cardiac causes. Definite or
probable HCM accounted for 56% of cardiac deaths, followed by coronary artery anomalies (13%), myocarditis (7%),
aortic stenosis (6%), and dilated cardiomyopathy (6%). Less common causes included aortic rupture/Marfan syndrome,
atherosclerotic CAD, preexcitation abnormalities such as the Wolff-Parkinson-White syndrome, the long-QT syndrome,
and vasculitis. Nontraumatic sudden cardiac death in young athletes is twice as frequent as traumatic sports-related
death (28,31). Death from blunt injury to the heart, or commotio cordis, reportedly is caused by a ventricular arrhythmia
induced at the time of impact ( 32). Other causes of death from blunt trauma to the chest include valvular rupture,
coronary artery rupture, cardiac chamber rupture and injury to the great vessels ( 33). Table 8.2 lists the possible causes
of sudden cardiac death in young athletes.
TABLE 8.2. POSSIBLE CAUSES OF EXERCISE-RELATED SUDDEN CARDIAC DEATH IN YOUNG ATHLETES
HCM is the leading cause of sudden cardiac death in young athletes in the United States and accounts for over one-third
of these deaths (34). Patients with HCM often die prematurely due to ventricular arrhythmia or progressive congestive
heart failure with cavitary enlargement and impaired myocardial function. This genetically mediated disease, first
described by Teare in 1958 ( 35), now includes a broad range of genotypic and phenotypic expression including
mutations that may occur on the genes that encode myosin, myosin-binding protein C, troponin T, and tropomyosin
genes. Mutations to the sarcomere genes cause hypertrophy, myocyte disarray, arrhythmias, and chronic heart disease
(36,37 and 38).
Identifying patients who are at risk is of obvious importance. Risk factors for HCM and sudden cardiac death include but
are not limited to a “malignant” family history, the occurrence of syncope, an aborted episode of sudden death, and
asymptomatic, nonsustained ventricular tachycardia ( 36). Hemodynamic left ventricular outflow tract obstruction, if
severe, also may be associated with an increased incidence of sudden death. Treatment of patients who are at greatest
risk as defined by these risk factors may include pharmacologic therapy, the implantation of a defibrillator/pacemaker, or
both (36,39). Without question, athletes with the unequivocal diagnosis of HCM should not participate in competitive
sports and should promptly be evaluated and monitored by a cardiovascular expert ( 40).
Isolated congenital coronary artery anomalies are found in approximately 1% of all patients undergoing coronary
angiography and in 0.3% of autopsies ( 41). Types of anomalies include abnormal origin and course ( Fig. 8.2),
hypoplastic arteries, intramyocardial coronary arteries, and ostial ridges. Taylor et al. retrospectively reviewed the
records of 242 patients with isolated coronary artery anomalies for information on the mode of death ( 42). Fifty-nine
percent of the patients died suddenly, and almost half of these deaths occurred during exercise. The majority of sudden
deaths and exercise-related deaths were caused by an anomalous origin of the left main coronary artery from either the
right coronary sinus or the pulmonary trunk. Moreover, younger patients were more likely than older patients to die
suddenly (62% versus 12%, p = 0.00001) (42). Patients in whom anomalous coronary arteries are detected should be
excluded from all participation in competitive sports. Surgical treatment is indicated. Participation after a successful
surgical correction may be considered at the discretion of the clinician ( 43).
FIGURE 8.2. Anomalous left main coronary artery arising from the main pulmonary artery. (Courtesy of W. Jay
Nicholson, M.D.)
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is defined clinically by abnormalities of conduction,

repolarization and depolarization, ventricular arrhythmias, family history, and structural abnormalities of the right ventricle
(44). In addition to fatty and fibrofatty infiltration of the ventricular myocardium, inflammatory changes are also present.
Arrhythmias that characterize ARVC include ventricular premature systoles, ventricular tachycardia, and ventricular
fibrillation. ARVC is rare in the United States, but it is the most common cause of sudden cardiac death among athletes in
northern Italy. An autosomal dominant condition, ARVC is often associated with ECG findings such as T-wave inversion
and can be identified with echocardiography and radiologic techniques such as magnetic resonance imaging.
Marfan syndrome is another autosomal dominant disorder that causes abnormalities in the transcription and translation of
genes encoding proteins such as fibrillin. These proteins are essential for adequate connective tissue strength, and
abnormalities in their production result in cardiovascular, musculoskeletal, and ocular anomalies. Typical phenotypic
findings in the patient with Marfan syndrome include pectus excavatum, arachnodactyly, high arched palate, lens
dislocation, myopia, mitral valve prolapse, and aortic root dilatation. An ascending aortic aneurysm caused by cystic
medial necrosis predisposes to sudden cardiac death ( 45). Aortic diameters larger than 50 mm may require surgical
correction (Fig. 8.3). Athletes with a family history of Marfan syndrome or premature sudden death without evidence of
aortic root dilation may participate in low- and moderate-intensity competitive sports. Echocardiographic assessment of
the ascending aorta should be repeated every 6 months. Athletes with Marfan syndrome should not participate in sports
in which there is a risk of bodily collision. Those patients with documented aortic root dilation should refrain from
competitive sports (43).
FIGURE 8.3. Preoperative (left) and postoperative (right) views of a 13-year-old patient with Marfan syndrome and severe
dilatation of the ascending aorta. The preoperative diameter of the aorta was 6.2 cm. An aortic homograft was used for
surgical correction. (Courtesy of Duke E. Cameron, M.D.)
Other cardiovascular abnormalities in young athletes are exceedingly rare. Idiopathic dilated cardiomyopathy is usually
caused by viral infection and is associated with left ventricular cavitary dilation and systolic dysfunction. An end-diastolic
diameter of 58 mm or more is generally regarded as pathologic. The absence of systolic dysfunction, however, is more
predictive of a physiologic rather than pathologic process. Acute myocarditis may be caused by an infectious organism
such as the coxsackie B virus (approximately 50% of cases), or it may be a consequence of drug abuse ( 9). Of the
remaining causes of sudden death in young athletes, the incidence of death is exceedingly low.
Cardiac Complications in the Adult Athlete
Although any of the congenital and acquired causes of sudden cardiac death listed for young athletes can also occur in
adults, the most common cause of complications in this group is obstructive CAD. Exercise-related cardiac arrests among
previously healthy adults in the United States have been estimated to cause 5.4 deaths per 100,000 individuals, or 1
death for every 18,000 men, each year ( 46). A study on death during jogging in Rhode Island found a similar incidence of
1 in 15,000 (47). Moreover, the incidence of myocardial infarction, cardiac arrest, and sudden cardiac death increases
transiently during vigorous physical activity ( 47,48). The rate of myocardial infarction may be twofold to sixfold higher
during vigorous exercise than during other activities ( 49). Acute atherosclerotic plaque rupture with resultant coronary
thrombosis is the mechanism that is present in a majority of adult patients with sudden cardiac death. Prevention of these
events is of obvious importance, not only in athletes but also as a general public health issue.
There are no data available that directly compare the presence of CAD with the risk from participation in sports ( 48).
What has been recommended, through the 26th Bethesda Conference on eligibility for competition in athletes with
cardiovascular abnormalities, includes risk stratification based on two levels of risk. The category of mildly increased risk
includes those athletes with CAD diagnosed by noninvasive or invasive testing whose ejection fraction is at least 50%,
whose exercise tolerance is normal for their age, whose exercise testing fails to reveal ischemia or complex arrhythmias
and whose coronary arteries lack a hemodynamically significant stenosis ( 48). Those athletes at substantially increased
risk include individuals whose ejection fraction is less than 50%, who have evidence of stress-induced myocardial
ischemia or complex ventricular arrhythmia, or who have a significant coronary stenosis. The latter group warrants further
investigation and close follow-up. This higher-risk group should generally be restricted to low-intensity competitive sports
with frequent reevaluation. Patients with a recent myocardial infarction should cease activity until recovery is deemed
complete (48). Full details regarding athletic participation in individuals with cardiovascular abnormalities may be found in
the guidelines published by the 26th Bethesda Conference of the American College of Cardiology ( 48).
PREPARTICIPATION EVALUATION OF THE ATHLETE
Despite the widespread use of preparticipation examinations of athletes, there are no well-defined strategies. Although
these evaluations are mandatory in some states, they are not universal ( 6). There are several pitfalls and problems
associated with the routine screening of athletes. First, strategies designed to limit the number of exercise-related events
are inherently limited by the rarity of such events, the poor predictive value of many available tests, and the cost-benefit
ratio of testing, which is invariably high in this population ( 17). At least five echocardiographic studies involving more
than 5,000 young athletes failed to detect a single case of definite HCM ( 6). This result is not surprising given the low
incidence of HCM in the general population (less than 0.2%). Similarly, ECG abnormalities are common in athletes,
decreasing the sensitivity and usefulness of this common test.
Athletes should undergo a routine history and physical examination before sports participation. This should be repeated
every 2 years. It is preferable that the examiner be someone familiar with the athlete and the family, to enhance the
ability to obtain an accurate family history. The history should focus on the presence of recent symptoms or problems
with exertion. To expedite the evaluation, one should avoid asking whether the athlete has “ever” had specific problems.
In many cases, complaints of exercise intolerance and collapse during competition are related to the physical and
psychosocial demands being placed on the athlete rather than a true cardiac anomaly. Nevertheless, all complaints must
be considered thoughtfully and new symptoms with exertion—such as unexplained exercise intolerance, syncope, and
chest discomfort—warrant further investigation ( 6). Adults require detailed questioning regarding symptoms associated
with ischemic heart disease, including chest and arm discomfort, shortness of breath, and lightheadedness. Many adults
approach their physician after having cardiac symptoms but disguise these symptoms as a motivation to embark on a
new exercise program. Motives for exercise, therefore, should be thoroughly reviewed ( 6). Caregivers should inform their
adult patients of the nature of prodromal cardiac symptoms, including the variable nature of angina pectoris ( Table 8.3).
TABLE 8.3. THE PREPARTICIPATION EVALUATION: SUGGESTED INCLUSIONS (6)
The physical examination should be performed in a quiet environment to enhance auscultation of the heart. An
examination focused on excluding the causes of sudden cardiac death should then be undertaken. Specifically, one
should exclude the physical sequelae of HCM, aortic valvular stenosis, Marfan syndrome, and dilated cardiomyopathy.
Vital signs should be documented and blood pressure recorded with the use of an appropriately sized cuff. Cardiac
auscultation should be performed with the subject sitting or standing, or both, because this lessens intraventricular
volume and, consequently, the frequency of innocent “flow” murmurs. The incidence of innocent murmurs may be as high
as 30% to 50% in young athletes (22). Innocent murmurs can be differentiated from the murmur caused by HCM by
having the subject perform maneuvers that change left ventricular end-diastolic volume. For example, during phase 2 of
the Valsalva maneuver, left ventricular volume decreases, thereby increasing the degree of outflow tract obstruction in
HCM and enhancing the ejection murmur. Conversely, the intensity of an innocent murmur decreases during a Valsalva
maneuver. Attention should be focused on listening for extra heart sounds such as S 3 and S4 gallops, opening snaps,
clicks, and rubs (27). The apical impulse should be well demarcated; a bounding impulse may suggest hypertrophy, and
a diffuse impulse suggests ventricular dilation.
The sequelae of Marfan syndrome have already been listed. Height, arm length, and finger length should be
documented, and the examination should exclude myopia, high arched palate, pectus excavatum or carinatum,
cutaneous striae, lax joints, and a murmur of aortic insufficiency. The murmur of congenital aortic stenosis is loud and
radiates to the carotids. The carotid upstroke should be delayed ( 6).
Additional screening in asymptomatic, young athletes is not recommended. Both ECG and echocardiography have a low
sensitivity for identifying significant cardiac disease. Similar problems exist with the use of routine exercise testing as a
screening tool. The American College of Sports Medicine recommends the routine use of exercise stress testing to
screen men older than 40 years of age and women older than 50; individuals with more than one coronary disease risk
factor and those with known coronary disease are advised to undergo stress testing before initiating a vigorous exercise
program (17). The American Heart Association refers to routine exercise testing as part of a preexercise evaluation as
“frequently used, but controversial” ( 50). Nevertheless, exercise testing in asymptomatic adults is a poor predictor of
major cardiac events such as myocardial infarction and sudden cardiac death. As discussed previously, the majority of
coronary occlusions at the time of acute myocardial infarction occur at a site of non–flow-limiting, non–hemodynamically
significant stenosis. These coronary lesions may not be detected with exercise testing. Consequently, it may be
concluded that routine exercise testing is not justified to identify asymptomatic individuals at risk for major cardiac events
during exercise. If cardiovascular abnormalities are discovered, however, a prompt evaluation and referral to a
cardiovascular specialist is appropriate.
Finally, it is recommended that coaches and athletic personnel be encouraged if not required to learn skills in
cardiopulmonary resuscitation and to update them annually. Such efforts may help to prevent additional exercise-related
cardiac deaths.
FUTURE DIRECTION
Many advances in the detection and treatment of heart disease are on the horizon ( 51). Standardization of the
preparticipation evaluation with national implementation should be pursued. The immediate future includes the
widespread use and delivery of cardiopulmonary resuscitation, including the early application of counterdefibrillatory
energy when appropriate. Long-term goals involve improvement of early detection and screening for heart disease. With
the completion of the human genome project, additional insight will be gained with regard to the genetic basis of disease
and may ultimately lead to effective treatment through gene therapy.
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9 Ergogenic Drug Use in Sports
ERGOGENIC DRUG USE IN SPORTS

RICHARD T. FERRO
Stimulants
Amphetamines
Caffeine
Sympathomimetics
Anabolic Agents
Clenbuterol
Peptide and Glycoprotein Hormones and Analogues
Human Growth Hormone
Human Chorionic Gonadotropin
Erythropoietin and Blood Doping
Dehydroepiandrosterone
Dihydroxyacetone Pyruvate
Creatine Monohydrate
Conclusions
Chapter References
The use of ergogenic substances to enhance athletic performance is not a modern phenomenon, although it has in
recent decades reached pandemic proportions. Ever since the ancient Olympic Games, athletes have used a variety of
substances in their quest for enhancement of athletic performance. These practices ranged from the ingestion of
mushrooms, which contained muscarine, to the consumption of bread laced with opium ( 1,2). By the 1800s, the extensive
use of ergogenic substances such as caffeine, nitroglycerin, amphetamines, strychnine, and ephedrine was being
reported, making it obvious that a win-at-any-price attitude had been well established among athletics long before the
modern “professionalization” of sports ( 1,2 and 3).
With the end of the Cold War, the use of drugs to enhance athletic performance could no longer be perceived as simply
the result of scientists working behind the scenes to further the political agendas of their governments. Instead, the use of
ergogenic aids has become a byproduct of a new era of lucrative athletic competition, in which self-proclaimed drug
gurus help athletes circumvent established drug testing procedures to gain a performance advantage ( 3,4). Accordingly,
the knowledge and use of effective ergogenic aids by athletes at all levels appears to be more pervasive than ever
before.
An in-depth discussion of the history and prevalence of ergogenic drug use in sports, is beyond the brief scope of this
chapter. Instead, this chapter explores the use of ergogenic aids in our society and their mechanisms of action, possible
benefits, and associated risks. The many moral and ethical concerns surrounding ergogenic drug use in sports are not
presented or disputed here because, ultimately, those are issues that can be understood only within the context of the
generation, society, and political and religious environments from which a situation evolves. This chapter reviews
categories of pharmacologic agents that are being used to enhance athletic performance and discusses relevant
examples in each class. The drug classification system established by the International Olympic Committee (IOC) ( Table
9.1) is used as a framework within which to examine these ergogenic substances. Although some of these substances
can also fall under the classification of recreational or therapeutic drugs, this chapter focuses specifically on those
agents that are used to enhance sport performance.
TABLE 9.1. BANNED SUBSTANCESa
Generic Name Example IOC USOC NCAA NBAMLB

Stimulants x x x
Amfepramone Apisate x x
Tenuate x x
Tepanil x x
Amfetaminil AN1 (Germany) x x
Amineptine Survector (Europe) x x
Amiphenazole Dapti x x x
Daptizole x x x
Amphisol x x x
Amphetamine Delcobese x x x
Obetrol x x x
Benzedrine x x x
Bambuterol x
Bemegride Megimide x x x
Benzphetamine Didrex x x x
Bromantin Bromantin x x x
Caffeine no >12 no > no > 15
µg/mL 12 µg/mL
µg/mL
Carphedon x x
Cathine (no >5 (g/mL for IOC) (Norpseudoephedrine) x x
Adiposetten N (Germany) x x
Chlorphentermine Pre Sate x x x
Lucofen x x x
Clobenzorex Dinintel (France) x x
Clorprenaline Vortel x x
Asthone (Japan) x x
Cocaine MethylBenzoylecgonine x x x x x
Cropropamide Component of Micoren x x x
Crothetamide Component of Micoren x x x
Desoxyephedrine Vicks Inhaler x x
Diethylpropion x
Diethylpropion HCl Tenuate x x x
Tepanil x x x
Dimetamfetamine Amphetamine x x
Dimethylamphetamine x x
Doxapram x
Ephedrine (no >5 (g/mL for IOC) Tedral x x x
Bronkotabs x x x
Rynatuss x x x
Primatene x x x
Etafedrine Mercodal x x
Decapryn x x
Nethaprin x x
Ethamivan Emivan x x x
Vandid x x x
Ethylamphetamine x x
Etilamfetamine Apetinil (Netherlands) x x
Fencamfamine Envitrol x x x
Altimine x x x
Phencamine x x x
Fenetylline Captagon (Germany) x x
Fenproporex Antiobes Retard (Spain) x x
Appetizugler (Germany) x x
Formoterol x
Furfenorex Frugal (Argentina) x x
Frugalan (Spain) x x
Isoetharine HCl Bronkosol x x
Bronkometer x x
Numotac x x
Dilabron x x
Isoproterenol Isuprel x x
Norisodrine x x
MetihalerI-SO x x
Meclofenoxale Lucidril x x x
Brenal x x x
Mefenorex Doracil (Argentina) x x
Pondinil (Switzerland) x x
Rondimen (Germany) x x
Mesocarbe Mesocarb x x
Mesocarbi x x
Sydnocarb (Europe) x x
Metaproterenol Alupent x x
Metaprel x x
Methamphetamine Desoxyn x x x x
MetAmpi x x x x
Methoxyphenamine Orthoxicol Cough Syrup x x
Methylephedrine Tzbraine x x
(no >5 (g/mL for IOC) Methep (Germany, Great x x
Britain)
Methylphenidate x
Methylphenidate HCl Ritalin x x
Morazone Rosimon-Neu (Germany) x x
Nikethamide Coramine x x x
Pemoline Cylert x x x
Deltamine x x x
Stimul x x x
Pentetrazol/Pentylenetetrazol Leptazol x x x
Phendimetrazine Phenzine x x x
Bontril x x x
Plegine x x x
Phenmetrazine Preludin x x x
Phentermine x
Phentermine HCl ApidexP x x
Fastin x x
Ionamin x x
Picrotoxine Cocculin x x x
Pipradol Meratran x x x
Constituent of Alertonic x x x
Prolintane Villescon x x x
Promotil x x x
Katovit x x x
Propylhexedrine Benzedrex Inhaler x x
Pyrovalerone Centroton x x
Thymergix x x
Reproterol x
Selegiline Eldepryl x x
Plurimen (Spain) x x
Deprenyl x x
Strychnine Movellan (Germany) x x x
And Related Substances x x x
Over-the-counter medications containing prohibited x x
substances
Desoxyephedrine Vicks Inhaler x x
Pseudoephedrine Actifed x x
(no >10 (g/mL for IOC) Ambeny-lD x x
Anamine x x
Afrin Tablets x x
Afrinol x x
CoTylenol x x
Deconamine x x
Dimacol x x
Emprazil-A x x
Fedahist x x
Fedrazil x x
Histalet x x
Isoclor x x
Lo Tussin x x
Nasalspan x x
Novafed x x
Nucofed x x
Poly-Histine x x
Pseudo-Bid x x
Pseudo-Hist x x
Rhinosym x x
Ryna x x
Sudafed x x
Triprolidine x x
Tussend x x
Chlorafed x x
Chlor-TrimetonDC x x
Disphoral x x
Drixoral x x
Polaramine Expectorant x x
Rondec x x
Phenylpropanolamine ARM x x
(no >10 (g/mL for IOC) Allerest x x
Alka-Seltzer Plus x x
Contac x x
Dexatrim x x
Dietac x x
4-Way Formula 44 x x
Naldecon x x
Novahistine x x
Arnex x x
Sine-Aid x x
Sine-Off x x
Sinutab x x
Triaminic x x
Triaminicin x x
Sucrets Cold x x
Decongestant and related
products
Propylhexedrine Benzedrex Inhaler x x
Ephedrine Bronkaid x x x
Collyrium with Ephedrine x x x
Pazo Suppository x x x
Wyanoids Suppository x x x
Vatronol Nose Drops x x x
Herbal Teas and x x x
medicines containing Ma
Huang
Ma Huang (herbal ephedrine) Action Caps x x x
Bishop's Tea x x x
Breathe Easy Herbal x x x
Decongestant Tea
Brigham Tea x x x
Chi Powder x x x
Energy Rise x x x
Ephedra x x x
Excel x x x
Free Herbal “Energy x x x
Tablets”
Joint Fir x x x
Mexican Tea x x x
Miner's Tea x x x
Mormon Tea x x x
Popotillo x x x
Quick Shot Vitamin B 12 x x x
Squaw Tea x x x
Super Charge x x x
Teamster's Tea x x x
Narcotics x x
Alphaprodine Nisentil x x
Anileridine Leritine x x
Apodol x x
Buprenorphine Buprenex x x
Dextromoramide Palflum x x
Jetrium x x
D-Moramid x x
Dimorlin x x
Diamorphine Heroin x x x x x
Dipipanone Pipadone x x
Diconal x x
Wellconal x x
Ethoheptazine Panalgin (Italy) x x
Levorphanol LevoDromoran x x
Methadone HCl Dolophine x x
Amidon x x
Morphine (no >1 (g/mL for IOC) Cyclimorph 10 x x x x
Duromorph x x x x
MST-Continus x x x x
Nalbuphine Nubain x x
Pentazocine Talwin x x
Pethidine Demerol x x
Centralgin x x
Dolantin x x
Dolosal x x
Pethold x x
Phenazocine Narphen x x
Meperidine Demerol x x
Mepergan x x
And Related Compounds x x
Hydrocodone Hycodan x x
Tussionex x x
Vicodin x x
Opiates x
Oxycodone Percodan x x
Tylox x x
Oxymorphone Numorphan x x
Hydromorphone Dilaudid x x
Tincture opium Paragoric x x x x
Anabolic agents x x x
Androstenedione Androsten x x x
Bolasterone Vebonol x x x
Boldenone Equipoise x x x
Clostebol Steranobol x x x
Dehydrochlormethyl testosterone Turinabol x x x
Dehydroepiandrosterone (DHEA) x x x
Dihydrotestosterone Stanolone x x x
Dromostanolone x x x
Fluoxymesterone Android F x x x
Halotestin x x x
OraTestryl x x x
Ultradren x x x
Gestrinone x x x
Mesterolone Androviron x x x
Proviron x x x
Metandienone Danabol x x x
Dianabol x x x
Metenolone Primobolan x x x
Primonabol-Depot x x x
Methandrostenolone Dianabol x x x
Methyltestosterone Android x x x
Estratest x x x
Metandren x x x
Virilon x x x
Oreton Methyl x x x
Testred x x x
Nandrolone Durabolin x x x
Deca-Durabolin x x x
Kabolin x x x
Nandrobolic x x x
Norethandrolone Nilevar x x x
Oxandrololone Anavar x x x
Oxymesterone x x x
Oxymetholone Anadrol x x x
Anapolon 50 x x x
Adroyd x x x
Stanozolol Winstrol x x x
Stromba x x x
Testosterone Malogen x x x
Malogex x x x
Delatestryl x x x
And Related Compounds x x x
Danazol x x x
Danocrine x x x
Dehydroepiandrosterone (DHEA) x x x
Zeranol x x x
Clenbuterol x x x
Growth hormone x x x
Human chorionic gonadotrophin x x x
Beta-2-agonists (only inhaling of these is allowed) x x with
restrictions
Salbutamol Albuterol x x
Ventolin Inhaler x x
Proventil Inhaler x x
Salmeterol Serevent x x
Terbutaline Brethaire x x
Salbutamol/Ipratropium Combivent x x
Diuretics x x x
Acetazolamide Diamox x x x
AKZOL x x x
Dazamide x x x
Amiloride Midamor x x
Bendroflumethiazide Naturetin x x x
Benzthiazide Aquatag x x x
Exna x x x
Hyrex x x x
Marazide x x x
Proaqua x x x
Bumetanide Bumex x x x
Canrenone Aldadiene x x
Aldactone (Germany) x x
Phanurane (France) x x
Soldactone (Switzerland) x x
Chlormerodrin Orimercur (Spain) x x
Chlorothiazide x
Chlortalidone Hygroton x x x
Hylidone x x x
Thalitone x x x
Diclofenamide Daranide x x
Oratrol x x
Fenamide x x
Ethacrynic acid Edecrin x x x
Flumethiazide x
Furosemide Lasix x x x
Hydrochlorothiazide Esidrix x x x
HydroDiuril x x x
Oretic x x x
Thiuretic x x x
Mannitol (intravenous administration only) Osmitol x x
Mersalyl Salyrgan x x
Methylclothiazide x
Metolazone x
Polythiazide x
Quinethazone x
Spironolactone Alatone x x x
Aldactone x x x
Torsemide Demadex x x
Triamterene Dyrenium x x x
Dyazide x x x
Trichlomethiazide x
And Related Substances x x x
Peptide and glycoprotein hormones and analogues x x
Chorionic gonadotrophin (hCG) x x x
Corticotrophin (ACTH) x x x
Growth hormone (hGH, somatotrophin) x x x
Erythropoietin (EPO) x x x
All the respective releasing factors of the x x x
above-mentioned substances
Blood doping x x x
Intravenous administration of blood, red blood cells, or x x x
related red blood products including EPO
Pharmacologic chemical, and physical manipulation x x x
Substances and methods that alter integrity and validity of x x x
urine samples used in testing: catheterization, urine
substitution and/or tampering, inhibition of renal excretion
(e.g., by Probenecid and related compounds, Bromantin),
and epitestosterone (no >200 ng/mL for IOC)
administration
Substances subject to certain restrictions x x
Alcohol x x for rifle
Marijuana x x x x x
Local anesthetics x x
Corticosteroids x x
b-blockers x x for rifle
Street drugs x
Mescaline x
Psilocybin x
Diethylamide (LSD) x
THC (tetrahydrocannabinol) x x x x x
Phencyclidine (PCP) x x
Controlled substances (U.S.) x
Dihydromorphine x
Methaqualone x
Tilidine x
Fenethylline (fenethylline hydrochloride) x
Acetylmethadol x
IOC, International Olympic Committee; MLB, Major League Baseball; NBA, National Basketball Association; NCAA,
National Collegiate Athletic Association; USOC, United States Olympic Committee.
aBecause of the changes in drug testing policy that continuously occur, this table cannot be considered comprehensive.
Please consult with the organizations included in this table for their most up-to-date list of banned substances.
The use of ergogenic aids or “doping,” as defined by the IOC, is “the administration to, or the use by, a competing athlete
of any substance foreign to the body or any physiologic substance taken in abnormal quantity or by an abnormal route of
entry into the body, with the sole intention of increasing in an artificial and unfair manner his performance in competition”
(5).
STIMULANTS
This category of prohibited substances encompasses a variety of central nervous system (CNS) stimulants including
amphetamines, caffeine, clenbuterol, cocaine, and the sympathomimetics, ephedrine and pseudoephedrine. Stimulants
have been used by athletes for centuries to reduce fatigue, enhance aggression and competitiveness, suppress appetite,
decrease sensitivity to pain, and increase alertness, response time, and strength ( 6,7 and 8). Many of these banned
drugs are available without a prescription. Whether they were purposefully or inadvertently used, studies have revealed
that, in drug tests, half of athletes' positive results for stimulants were caused by over-the-counter (OTC) drugs ( 9).
Furthermore, despite the emphasis that the media has placed on steroid use among athletes, the prevalence of
amphetamine use by college athletes was found to be about twice that of anabolic steroids ( 10,11).
Amphetamines
Stimulants were some of the first drugs studied and used as ergogenic aids in the modern era of athletics ( 12).
Amphetamines were originally developed in 1920, and their vasoconstrictive properties allowed them to be used initially
for the treatment of nasal congestion ( 7).Their emergence as an ergogenic aid occurred during World War II, when
German soldiers used amphetamines to delay fatigue and enhance their alertness while on patrol duty ( 13).
Amphetamines are structurally similar to endogenous catecholamines such as epinephrine, and they are believed to
enhance the release of neurotransmitters, especially norepinephrine ( 8).Therefore, much of their ergogenic effect is
believed to result from stimulation of the sympathetic nervous system. Peak plasma concentration is achieved very
rapidly after intravenous administration of amphetamines, and the maximum concentration after oral ingestion usually
occurs within 2 hours (14). Although the question of whether amphetamines truly enhance athletic performance is
debated in the literature, the available studies and anecdotal reports strongly suggest that amphetamines are truly
efficacious for their purported uses, especially in sports in which speed, power, and endurance are essential ( 12,13,15,16
and 17,18). Available research reveals that the ergogenic effects are partially obtained through prolonging the time to
exhaustion, increasing tolerance to strenuous exercise, blunting pain perception and symptoms of fatigue, and increasing
aggression, which may increase the potential for injury in contact sports ( 19).
Many potential adverse side effects of the use of amphetamines are related to their effects on the CNS. Neurologic
symptoms and behavioral effects include restlessness, insomnia, anxiety, tremor, confusion, agitation, irritability,
paranoia, hallucinations, increased aggressiveness, and a potential for psychological addiction ( 12,17). Cardiovascular
complications include a lower threshold for arrhythmias, provocation of angina, hypertension, headaches, tachycardia,
and palpitations. Adverse gastrointestinal side effects include abdominal pain, decreased appetite, and vomiting.
Thermoregulatory disturbances may be caused by the decrease in the ability to sense the body's limitations; this may
lead to an increased incidence of, or predisposition to, heat illness, including heat stroke ( 7,12,20). Furthermore, an
abrupt cessation of amphetamine use can result in chronic fatigue, lethargy, and depression ( 6,21). There are case
reports in which excessive doses led to convulsions, coma, strokes, and death, and long-term exposure to amphetamines
has resulted in dyskinesias, compulsive behavior, and paranoid delusional states ( 7,8,12,13,19,22).
It was not until the death of Danish cyclist Kurt Enemar Jensen at the 1960 Summer Olympic Games in Rome that a
considerable international antidoping movement was initiated ( 23). Many people were stunned by the fact that Jensen
and two of his fellow teammates became ill after ingesting amphetamine and Roniacol (a cough syrup) for performance
enhancement. Jensen ultimately died, and his two teammates were admitted to an Italian hospital in critical condition. In
another incident, Tommy Simpson, a notable British cyclist, died during the 13th day of the Tour de France in 1967. At
the time of his death, a vial of amphetamines was found in his possession ( 24). The following year, amphetamine abuse
was believed to play a major role in the death of yet another cyclist, Yves Mottin, as well as a soccer player, Jean-Louis
Quadri (24). These incidents helped generate considerable antidoping sentiment and began a cascade of significant
worldwide antidoping legislation. From that point forward, a gradual evolution in collective thinking also began. Drug use
for performance enhancement was no longer considered just a matter of personal choice. Instead, it became an unethical
act that clearly carried significant health risks and that directly induced others to use ergogenic substances in order to
compete equitably (25,26).
Caffeine
Caffeine is undoubtedly the most widely consumed stimulant in the world, in part because of its widespread social use
and availability to people of all ages. It is present in many different types of beverages, including numerous cola drinks,
hot chocolate, and tea (6,27). It may also be the most widely abused drug in sports, because it is routinely consumed by
a majority of sports competitors (28). Caffeine is a methylxanthine derivative related to theophylline and theobromine that
occurs naturally in many species of plants and is found in coca, coffee beans, and tea leaves. It is also found in many
prescription and nonprescription medications such as analgesics, weight-loss drugs, and cold preparations ( 27).
Approximately 80% of the adult population in the United States drink coffee or tea on a daily basis. Furthermore, coffee
accounts for 90% of the caffeine consumed in the United States, where an average of approximately 210 mg of caffeine
per person per day is consumed ( 29).
After ingestion, caffeine reaches peak blood levels in approximately 30 to 60 minutes ( 8). It acts as a potent CNS
stimulant, increasing arousal or level of consciousness, reducing fatigue, and decreasing motor reaction time when
concentrations of 85 to 200 mg are consumed (7). Most believe that the ergogenic dose is between 250 and 350 mg ( 8).
The IOC and the U.S. National Collegiate Athletic Association (NCAA) have placed limits on caffeine ingestion, and at
present it is treated as a controlled substance. Certain amounts of caffeine are tolerated because of its presence in
commonly ingested beverages, but greatly excessive amounts constitute grounds for disqualification ( 30). The maximum
acceptable urine concentration established by the IOC is 12 µg per mL, whereas the NCAA limit is 15 µg per mL. To
reach these levels, most athletes would have to drink six to eight cups of coffee in one sitting (approximately 600 to 800
mg of caffeine), 2 to 3 hours before testing. Because the ergogenic effects of caffeine are gained well below these
accepted limits, some question the motives of these organizations and raise ethical issues regarding its ergogenic use
(28). Furthermore, some argue that caffeine should be added to the banned substance list, which would require athletes
to abstain from caffeine ingestion for 48 to 72 hours before competition.
Over the years, there has been much conflicting data in the literature concerning the in vivo reproducibility of caffeine's
ergogenic effects. Although some have questioned the true ergogenic value of caffeine, athletes and coaches have
believed in and used caffeine as an ergogenic aid for years. Only relatively recently has the true ergogenic value of
caffeine, especially in regard to short-term, high-intensity exercise (STHIX)—that is, exercise lasting less than 5 minutes
at greater than 100% maximal aerobic power (V O2max)—been significantly borne out in published research. What the
evidence has more clearly supported is the notion that caffeine is ergogenic during prolonged, moderate-intensity
exercise (i.e., longer than 30 minutes at 75% to 80% of V O2max). For example, in one study, the run time to exhaustion at
85% of VO 2max in elite runners increased by 44% after the ingestion of an acceptable, under-the-limit dose of caffeine
(31).
Information concerning STHIX has often been dismissed, even when positive results were shown. The early in vivo
studies on humans found little evidence for a performance-enhancing effect on STHIX. On the other hand, early animal in
vitro and in situ studies revealed that caffeine could increase muscle force production through CNS stimulation,
enhanced neuromuscular transmission, and/or enhanced muscle fiber contractility ( 32). The cellular mechanisms
hypothesized to account for these changes included a direct effect of caffeine on calcium exchange by the sarcoplasmic
reticulum, inhibition of phosphodiesterase, and adenosine receptor antagonism ( 28). More recently, a number of
well-controlled studies have indicated that caffeine can improve performance during STHIX and repeated bouts of
STHIX. One such study examined the effects of ingestion of 6 mg per kg of caffeine on performance in repeated bouts of
cycling at 100% of VO 2max (33). The cycle time to exhaustion was significantly improved with caffeine use, and the
epinephrine and lactate (muscle and blood) levels were increased. However, muscle glycogen stores did not vary
between placebo and caffeine groups. The authors concluded that improvement in STHIX was not associated with
glycogen sparing and may have been caused by elevated epinephrine concentrations that increased muscle
glycogenolysis at this intensity, thereby increasing anaerobic energy provision. Ultimately, although both adrenaline and
lactate (muscle and blood) levels were elevated after caffeine ingestion and STHIX, the significance of these elevations
is unclear. Additionally, caffeine also appears to influence electrolyte handling and substrate use, which may also further
affect anaerobic performance (32).
There are three major theories that explain the ergogenic effects of caffeine. The first is that caffeine has a direct effect
on the CNS, which alters perception of effort and/or affects the propagation of neural signals somewhere between the
brain and the neuromuscular junction (28). It thereby decreases fatigue and improves the level of consciousness.
Secondly, caffeine is also believed to increase muscle force production through direct CNS stimulation, enhanced
neuromuscular transmission, and enhanced muscle fiber contractility by increasing permeability of the sarcoplasmic
reticulum to calcium, thereby increasing the amount of intracellular calcium available for muscular contraction ( 13).
Thirdly, caffeine has the ability to increase circulating levels of free fatty acids (FFA) by increasing lipolysis. Oxidation of
fatty acids then provides the initial energy source, leaving glycogen available for later use ( 34). Caffeine thereby reduces
an individual's dependence on muscle glycogen as a fuel source during prolonged exercise and improves exercise
endurance (12). Ultimately, caffeine increases the production of plasma catecholamines, including epinephrine, which is
undoubtedly linked to many of its purported effects. Resultant effects therefore include increased psychological arousal,
an increased cardiac output, enhanced muscle contractility, and an increased mobilization and utilization of FFA during
exercise (30).
The possible adverse side effects of caffeine include anxiety, irritability, restlessness, inability to focus, tremor,
headaches, insomnia, diuresis leading to fluid imbalances, gastrointestinal disturbances, hypertension, cholesterol
abnormalities, tachycardia, and hyperesthesia ( 8,12,13). Caffeine can be lethal at doses of 3 to 10 g, causing delirium,
seizures, tachycardia, and/or ventricular dysrhythmias ( 7,28).
Although tolerance to the performance-enhancing effects of caffeine has not been extensively studied, it appears that the
derived ergogenic benefits may be significantly hampered in habitual consumers of caffeine ( 35). Therefore, it has been
suggested that athletes who wish to obtain the maximal ergogenic effect of caffeine should abstain from caffeine use in
the 4 days preceding their competition so as to avoid a tolerance phenomenon ( 34). Additionally, the ingestion of caffeine
should take place 3 to 4 hours before an endurance exercise, to obtain peak plasma concentrations of FFA, rather than 1
hour or less before an event. If ingested an hour or less before competition, only the peak plasma concentration of
caffeine is reached (36,37). However, some speculate that using caffeine 1 hour before competition also provides an
effective ergogenic mechanism, especially in shorter-length races, because in these instances it not only increases the
level of epinephrine but also increases psychological stimulation ( 30).
Finally, studies have shown that doses of up to 9 mg of caffeine per kilogram of body weight produce peak plasma
concentrations, with urine concentrations generally below the 12 µg per mL IOC limit ( 38). The optimal dose for
performance enhancement appears to be between 3 and 6 mg per kg (28). At this level, side effects appear to be
minimized and urine concentrations do not approach illegal limits. Many studies have been done on the appropriate
ergogenic levels even before the American cycling team used caffeine suppositories for performance enhancement in the
1984 Olympic Games (39). Not surprisingly, given the research available at that time, none of the American cyclists
tested positive for caffeine. In fact, only a few athletes with illegal caffeine levels have been detected in Olympic
competition. Those athletes included an Australian pentathlete in 1988, two German swimmers in 1992, and Italian
cyclists in 1992 and 1994 ( 28).
Sympathomimetics
The class of drugs known as sympathomimetic amines are CNS stimulants and include ephedrine, pseudoephedrine,
phenylpropanolamine, and norpseudoephedrine. The prototypic sympathomimetics, phenylpropanolamine and
ephedrine, are found in many OTC common cold remedies. Phenylpropanolamine is a common ingredient in diet pills,
and ephedrine has been used extensively in the treatment of asthma, hay fever, sinusitis, allergic rhinitis, urticaria, and
other allergic disorders ( 13). These drugs, also known as amphetamine look-alikes, were often combined with caffeine in
the early 1970s. Athletes have reported using ephedrine, not only for its stimulant-like effects, but also for its
thermogenic, fat-burning properties ( 4). Apparently, ephedrine also stimulates the thyroid gland to transform the weaker
thyroxine (T 4) hormone into the more potent triiodothyronine (T 3), and when it is combined with caffeine and aspirin the
thermogenic effect can be greatly enhanced. Ephedrine has also been used as a training aid, because it tends to have
amphetamine-like effects. Athletes report a significant boost of energy that increases the quality of their workouts ( 40).
One of the more notable cases of sympathomimetic use occurred at the 1972 Olympic Games when Rick DeMont, an
American swimmer with asthma, was disqualified for taking medication containing ephedrine ( 41).
These stimulants can have significant side effects, especially in larger doses. They include increased heart rate,
palpitations, elevated blood pressure, anxiety, insomnia, headaches, anorexia, hallucinations, psychosis, and possible
addiction (4,13,40). These drugs remain on the prohibited list despite the fact that research has not conclusively shown
an ergogenic effect, even with large doses of ephedrine ( 6,41,42). Although some of these compounds (e.g.,
phenylpropanolamine) have legitimate medical uses at doses not shown to have ergogenic effects, sympathomimetics
are prohibited instead of being treated as controlled substances (e.g., caffeine) for which certain therapeutic or
nonergogenic levels are tolerated.
ANABOLIC AGENTS
Although there have been many discussions about the ethical and legal aspects of the use of anabolic androgenic
steroids (AAS), their use remains prevalent in the athletic community. Survey results among Americans ranging from
junior high school students to middle-aged and older members of health clubs indicate that AAS use is found in
approximately 2% of students between the ages of 10 and 14 years, 5% to 12% of male high school students, and 2% to
20% of college athletes ( 43,44 and 45). Estimates of AAS use in elite athletes (e.g., Olympians, professional football
linemen) range from 44% to 99% (46). The 1993 Drug Abuse National Household Survey found that there were at least 1
million current or former AAS users in the United States (others estimate more than 3 million), that men had higher levels
of AAS use during their lifetime than women did (0.9% and 0.1%, respectively), that the median age at first AAS use was
18 years, and, most alarmingly, that the median age of initiation for the 12- to 17-year-old group was 15 years ( 47).
Furthermore, AAS use was highly correlated with self-reported aggressive behavior and crimes against property. Among
those age 12 to 34 years, steroid use was associated with the use of alcohol as well as illicit drugs ( 47).
In another study, it was reported that 75% of all AAS users began taking steroids before their 17th birthday, which means
that the majority of AAS use begins before high school ends ( 45). It was reported to the NCAA that more than 50% of
college athletes who admitted to AAS usage began in high school ( 10). Buckley et al. conducted the first nationwide
study of AAS use at the high school level in 1987 ( 45). AAS use was found in 6.6% of male high school students. Of this
group, approximately 40% reported having done five or more cycles, 38% had initiated use before 16 years of age, 44%
used more than one steroid at a time, and 38% used injectable AAS. No difference was found in rates between urban and
rural areas, but there was a significant difference by size of enrollment (i.e., the larger the high school, the higher the rate
of reported AAS use). In another study, this time of middle school students in Massachusetts (N = 965), 2.7% reported
using steroids (48).
In 1985 Anderson and McKeag surveyed 2,039 NCAA Athletes at 11 colleges and universities regarding AAS use within
the past 12 months (10). The greatest use was found among football players at 9%. Among male track and field athletes,
tennis players, and basketball players, 4% from each group reported using AAS. Three percent of male baseball players
reported using AAS. The only women's sport in which AAS were used was swimming, in 1% of the athletes. In 1991 the
survey was replicated ( 11). Again, 2,039 male and female athletes were surveyed from 11 colleges and universities,
including 7 of the original participating schools. Overall, AAS use had increased only slightly over the preceding 4 years.
However, this time the incidence of reported AAS use was 10% among football players, 4% for track and field athletes,
and 2% each for baseball, basketball, and tennis. Furthermore, the use of AAS had increased in women's sports: 1% of
women participating in track and field, basketball, and swimming admitted to AAS use. Among those athletes admitting to
AAS use, 25% began using before college, 25% initiated use during the first year of college, and 50% began after the
first year of college.
Why has the use of AAS become so prevalent among athletes? Yesalis' 1987 study ( 4) identified several reasons why
athletes use steroids: 47.1% said they did so to improve athletic performance, 26.7% to improve their appearance, and
10.7% to treat athletic injuries ( 45). Overall, AAS do help athletes achieve size and strength gains when they are used
concurrently with a proper diet and training regimen ( 49). However, studies have shown that long-term AAS use may
have detrimental consequences ( 49,50).
AAS are synthetic hormones, analogues of testosterone, that athletes use in supraphysiologic doses to give them the
effects of high levels of testosterone. Like testosterone, these hormones are synthesized from the parent compound,
cholesterol. Various modifications made to the cholesterol compound yield AAS with differing properties. AAS as a group
have a common structure based on the steroid nucleus, which consists of three six-membered carbon rings and one
five-member carbon ring. The naturally occurring steroids include male and female sex hormones (androgens and
estrogens), the adrenal cortex hormones (corticosteroids), progesterone, bile salts, and sterols (cholesterol).
Natural testosterone is not effective when taken orally because of rapid first-pass liver metabolism. Similarly, natural
testosterone taken by injection undergoes a relatively rapid breakdown in the liver. In an attempt to develop a more
purely anabolic steroid, AAS were molecularly altered to resist this metabolic breakdown. The efficacy of orally
administered AAS is greatly improved by alkylation at the 17 position (C-17 a-alkylation). This change decreases the
first-pass metabolism by the liver and thereby increases the AAS potency, though it also significantly increases the level
of hepatotoxicity. The efficacy of parenteral or injectable AAS is enhanced by esterification of the 17-hydroxyl group. This
modification yields a more lipid-soluble compound with extended activity. Parenteral AAS are suspended in oil or water.
Suspension of AAS in oil for injection helps the compounds remain in the body for weeks or months. For example,
testosterone cypionate (Depo-Testosterone) is detectable for at least 6 to 12 months. Oil-based AAS can also be
administered transdermally. Water-based AAS such as stanozolol (Winstrol) are detectable for 5 to 12 months.
In men, testosterone acts in two ways: anabolically, by stimulating nitrogen retention and muscle growth, and
androgenically, by promoting the development of secondary sexual characteristics. Endogenous testosterone plays a role
in determining male sex characteristics in utero, brings about facial hair and a deepening of the voice during puberty,
regulates the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH), increases protein synthesis,
increases aggression, and increases sex drive. Testosterone is produced primarily by the Leydig cells of the testes and
to some extent by the adrenals (usually less than 10% in men). The majority of daily testosterone production comes from
the peripheral metabolism of prehormones ( 51,52). Serum testosterone levels are regulated by a negative feedback loop
in response to low testosterone levels. In this loop, the hypothalamus releases gonadotropin-releasing hormone, which
stimulates the pituitary to release gonadotrophins that act on testosterone-producing sites (testes and adrenals in men,
ovaries and adrenals in women). FSH then downregulates the number of LH receptors.
The effects that compel athletes to take AAS stem from their anabolic nature. The term anabolic refers to promoting the
process of assimilation of nutritive matter and its conversion into living substance as well as promoting tissue growth by
increasing the metabolic processes involved in protein synthesis. The anabolic effects that are sought after by athletes
include increased protein synthesis; decreased release of cortisol and corticotropin (ACTH), which inhibits catabolic
effects on skeletal muscle; promotion of a positive nitrogen balance that increases muscle mass; increased strength or
force of muscle contraction (which may be a permanent increase), if weight training is paired with a high-protein diet (2.2
g per kg per day); inhibition of protein catabolism, which may hasten recovery from injury; and stimulation of
erythropoiesis, which increases endurance because of the increase in red blood cell (RBC) mass. AAS use may also
allow faster recovery time from repetitive, high-intensity workouts; enhance performance by increasing aggressiveness;
and produce euphoria, thereby decreasing the sense of fatigue during training ( 49,50,53). Therefore, AAS can contribute
to increases in lean body weight, strength, and endurance, if coupled with a proper diet and high-intensity exercise
(54,55,56 and 57). Furthermore, the strength-building effects of AAS are greater in athletes who have trained before AAS
use than in those who have not trained ( 55). Two additional mechanisms theorized to result in the anabolic effects of AAS
include (a) increased messenger RNA and intracellular calcium concentration through the cyclic adenosine
monophosphate pathway and (b) increased acetylcholine release at the neuromuscular junction in the brain, which
increases monoamine levels, in turn increasing aggression and energy ( 51,58).
For athletes, the less desirable effects of AAS stem from their androgenic properties. Androgenic refers to masculinizing
(i.e., stimulating the development of male sex hormones and male secondary sexual characteristics). Androgenic effects
include increased body and facial hair, deepening of the voice, increased sex drive, increased aggressiveness, male
pattern baldness, and acne. Ultimately, AAS bind to androgen receptors, stimulate production of RNA, and are
anticatabolic because they improve the utilization of protein and inhibit the catabolic effect of glucocorticoids ( 49).
Athletes use AAS according to different regimens. One regimen involves stacking, or simultaneously using an average of
five different AAS in both oral and injectable forms in cycles lasting 6 to 12 weeks. Stacking is done because AAS users
believe it will activate and saturate multiple steroid receptor sites, decrease the amount of each AAS that is required,
decrease associated side effects, and provide synergistic benefits. Cycling is done to avoid developing a tolerance to
AAS, to avoid detection, to decrease the incidence of harmful side effects associated with long-term AAS use, and to
allow the body to return to normal function between cycles. This last rationale for cycling is logical, given that
endogenous testosterone levels, sperm production, and the entire hypothalamic-pituitary-gonadal axis are affected by
AAS use; off-cycling allows these processes to return to normal. A drug regimen that involves stacking increasingly larger
dosages of AAS is commonly referred to as “stacking the pyramid.” There are numerous AAS regimens, and they are
becoming increasingly more complex.
AAS users employ dosages that may range from 40 to 100 times what is medically prescribed ( 53). The daily dose and
route of AAS usage depends on the cycle and stacking method used. AAS in dosages ranging from 50 to more than 200
mg per day are not unusual. The oral AAS preparations with shorter half-lives are typically taken up to three times daily.
Parenteral injections vary anywhere from daily to weekly. AAS are taken along with other kinds of drugs that prevent or
counteract their androgenic effects and extend their anabolic effects. Human chorionic gonadotrophin (hCG) is taken to
counteract testicular atrophy; diuretics are taken to block water retention, create the “ripped” look, and circumvent
detection; tamoxifen and other antiestrogens are taken to block gynecomastia caused by aromatization of the androgens;
and antiacne medications are taken to resolve the acne that develops in some AAS users ( 53). Endocrinologists and
steroid users reportedly have experimented with the use of prednisone to retard the loss of muscle mass that is usually
seen after AAS are discontinued ( 59). This is counterintuitive because cortisol is catabolic, but the catabolic link may
have more to do with endogenous ACTH. Not all of the combinations of AAS and other drugs are safe, and some can be
deadly. The riskiest use of AAS involves taking multiple substances at one time while engaging in other self-destructive
behaviors (53).
To avoid detection, athletes adjust their regimens according to the current knowledge of drug testing and discontinue use
within a “safe” time period, make steroid alterations, or use masking techniques, or both. Experienced users are
knowledgeable about detection methods and event testing and can generally beat the system. Annual use patterns vary
with the sport and the likelihood of being tested. Bodybuilders typically cycle on and off several times per year for several
years, in a very systematic fashion oriented to competition dates. The typical 12-week cycle includes a pyramid with at
least three or four different AAS. The athlete then begins taking other drugs that stop the rebound physiologic
bottoming-out, prolong the anabolic effects and positive nitrogen balance, and maintain muscle and strength increases
gained during the cycle.
Gains produced with AAS use are not made without significant risks. In one study, male mice were exposed for 6 months
to four different types of AAS in levels that corresponded to those taken by humans ( 60). Mice were given doses of AAS
at 20 times the normal level for mice, 5 times the normal level, or no AAS (controls). One year after the end of the AAS
exposure, 52% of the high-dose group had died, compared with only 35% of the low-dose group and 12% of the controls.
AAS use leads to many cardiovascular side effects, including hypertension, in susceptible individuals ( 61). AAS may
cause concentric left ventricular hypertrophy with decreasing ventricular compliance without affecting cardiac function
(62,63). AAS use also has led to an increased incidence of myocardial infarction and arterial thrombosis by stimulating
thrombus formation and accelerating atherosclerosis. This appears to be caused by the suppression of prostacyclin
production in arterial smooth muscle cells ( 64,65). AAS also appear to negatively affect lipid profiles. AAS increase the
level of low-density lipoproteins (LDL) and decrease high-density lipoproteins (HDL), although these effects are
reversible after discontinuation of AAS.
Sachtleben et al. (1997) studied the effects of AAS use on serum lipoprotein and apolipoprotein levels ( 57). They
described a well-documented relationship between increased concentrations of serum lipids and both an increased
incidence of coronary artery disease and an increased risk of myocardial infarction. They also showed that
cardiovascular risk is intensely altered by AAS use through negative changes in the ratio of cholesterol to HDL (from 4.8
mg per dL user-off to 6.8 mg per dL user-on). Furthermore, they not only detected significant alterations in serum lipid
values but also observed that the alterations were maintained even after AAS use was stopped for at least 8 weeks. They
concluded that AAS users appear to be at risk for the development of early atherosclerosis ( 57).
However, not all studies have shown significant effects on lipid levels. In a 1996 study of 18 competitive bodybuilders (10
AAS users, 8 nonuser controls), Cohen et al. found that the level of serum lipoprotein(a) actually decreased and total
cholesterol and triglyceride levels remained the same in AAS users ( 66). This occurred despite the higher dietary intake
of cholesterol in the steroid group and the high doses taken of potent AAS such as Anadrol, Deca-Durabolin, Winstrol,
Dianabol, Sostenon 250, Primobolan, and Anavar. In fact, since lipoprotein(a) levels of more than 30 mg per dL translate
into a twofold greater chance of coronary artery disease, AAS users were found to have an advantage: only 30% of AAS
users exhibited levels greater than 30 mg per dL, compared with 88% of the “clean” subjects.
Other studies have shown more detrimental sequelae to AAS use (49,60,62,63,67,68). Because there are testosterone
receptors in most tissues of the human body, AAS exert effects on almost every system. In the liver AAS, especially oral
agents, cause elevated liver enzymes such as aspartate and alanine aminotransferase, bilirubin (cholestatic jaundice),
and alkaline phosphatase, as well as an increased risk of liver tumors such as benign hepatocellular adenoma, peliosis
hepatitis (which is seen in patients who take AAS for chronic medical conditions and does not usually occur in athletes),
and hepatocellular carcinoma (of which there have been several reported cases among athletes, especially those taking
AAS for long periods) (46,69). Other reported side effects are an increase in libido, irritability, headaches, nausea,
muscle spasm resulting in chest pain, nervousness, increased hunger, kidney tumors, hyperinsulinemia, and diabetes
secondary to impaired glucose tolerance ( 70).
Other potential side effects of AAS use include an increased incidence of tendon rupture and ligament strains. The most
frequently reported AAS-related musculotendinous injuries are in the quadriceps femoris and the triceps brachii ( 46).
There are two theories to explain these injuries. AAS use may lead to a decrease in connective tissue strength that
causes tendon and ligament failure. However, most believe that the sudden relative increase in muscle strength and size
obtained by AAS use is actually responsible for the connective tissue failure ( 71).
AAS use also has a pronounced effect on the immune system. Studies have shown that humoral immunity may be
impaired; levels of immunoglobulin G (IgG), IgM, and IgA may be decreased; and killer T-cell function may be altered
(72). However, there does not appear to be any clinical correlation with these changes and therefore their significance is
unknown. There have also been anecdotal reports of leukemia, lymphoma, and melanoma among young athletes ( 73).
Additionally, there has been one reported case of AIDS due to the sharing of needles ( 74).
Men who use AAS experience many side effects. AAS use leads to decreases in FSH, LH, natural testosterone, and
spermatogenesis; testicular atrophy, which usually reverses within 2 to 16 months after discontinuation; scrotal pain,
difficulty urinating (prostatic hypertrophy), and dysuria; paradoxic feminizing side effects (e.g., gynecomastia, elevated
vocal pitch) caused by peripheral conversion of steroids to estradiol; and adenocarcinoma of the prostate ( 54,75,76). This
last effect poses a serious potential risk in men, because the prostate is a very specific target tissue for androgens and
prostate cancer is androgen sensitive. However, more recent studies did not confirm evidence that AAS use altered the
risk of prostate cancer (77).
The effects of prolonged AAS use on the female physiology are most poignantly detailed in an article that delves into the
former German Democratic Republic's experimentation with AAS ( 50). In girls and women, the physiologic adaptations
gained from using AAS and increasing muscle strength do not return to their pre-AAS levels after the steroids are
withdrawn (50). In fact, women experience side effects similar to those experienced by men, including decreased FSH,
LH and natural estrogen levels; breast tissue atrophy; muscle tightness; body weight increases; muscle cramps; irregular
menstruation including amenorrhea; acne; alteration of libido and fertility; edema; diarrhea; constipation; functional and
structural liver damage; hepatocellular tumors, which tend to be larger and more malignant than spontaneous adenomas;
peliosis hepatitis; and water retention in muscle ( 50,55). Irreversible changes include deepening of the voice through
laryngeal hypertrophy, arrest of body growth in adolescents, clitoromegaly, squaring of the jaw, hirsutism, and male
pattern baldness.
The studies on the prevalence of AAS use in high school are particularly worrisome because of the effects exerted by
these drugs on the developing adolescent. Premature epiphyseal closure is a permanent side effect ( 54). As has been
mentioned, AAS effect the pituitary gland and testes, greatly reducing endogenous testosterone and suppressing
spermatogenesis in male users. Although discontinuation of AAS by mature men results in an eventual return to normal
hormonal activity, this has not been established for immature boys or for female users ( 78).
Some believe that the most significant “acute” effects of AAS are psychological. A 1988 Pope and Katz retrospective
study revealed that 22% of AAS users interviewed displayed manic or depressive symptomatology while taking the drugs;
another 12% had transiently become psychotic, 3% to 9% became manic or hypomanic, and 7% suffered from major
depression. The depression usually occurred 6 weeks after withdrawal from AAS, during which time some athletes felt
that they were shrinking, getting weaker, and could not work out as intensely as they could while taking AAS. Overall,
12% to 15% became addicted to AAS (67). Some studies suggest that up to 40% of AAS users will suffer from affective
disorders and up to 40% will become addicted ( 79). AAS use increases aggression and hostility and has resulted in
homicides and suicides (49,80,81 and 82). Others believe that many AAS users have significant personality disorders and
psychiatric problems, and psychoactive drugs may put them over the edge ( 82).
Despite the considerable evidence showing the adverse effects of AAS use, Street et al. (1996) concluded that the risk of
permanent serious health complications is low with the use of injectable steroids at “moderate” dosages of 200 to 300 mg
per week for 6 to 12 weeks per year (46). However, they did warn that the use of oral 17-alkylated AAS is associated with
the greatest health risks.
Clenbuterol
After more stringent drug testing for AAS was developed, clenbuterol became a more popular ergogenic aid. In 1996,
United States hammer thrower, Jud Logan, and shot-putter, Bonnie Dasse, were disqualified for clenbuterol use at the
Barcelona Summer Olympics. It has been estimated that up to one third of elite athletes have used clenbuterol as an
ergogenic aid (83).
Clenbuterol is a b 2-agonist that is prescribed in Mexico and Europe as a bronchodilator ( 84). In the United States, it has
not been approved by the Food and Drug Administration for human or even animal use ( 83). Compared with the
b2-agonists that are marketed in the United States, clenbuterol has a longer half-life and greater potency ( 85). Although
there have been no published studies on the effects of clenbuterol in humans, the purported benefits of clenbuterol use
are drawn from animal studies and animal husbandry in other countries, where it is used as a repartitioning and potent
anabolic agent (83,84 and 85). Repartitioning agents manipulate growth and body composition, enhancing deposition of
body protein and decreasing fat ( 85). Clenbuterol's ergogenic effects are purported to be (a) an increase in lean muscle
mass through the direct promotion of lipolysis and the retardation of adipose tissue deposition and (b) an increase in the
rate of muscle protein deposition (83,84). In rats, clenbuterol causes hypertrophy of skeletal and cardiac muscle but not
hyperplasia ( 83,85). Muscle growth is postulated to be related to the ratio of protein synthesis to protein degradation ( 83).
Clenbuterol suppresses both synthesis and degradation, but it seems to have a greater effect on degradation, with the
net result being increased synthesis ( 83). Clenbuterol also increases heat production in the mitochondria of muscle and
possibly brown fat, thereby increasing energy expenditure ( 85). From studies on rats, it has been determined that the
growth-promoting effect lasts for a limited time and appears to level off with prolonged treatment ( 83). It has been
speculated that this may result from downregulation of receptor numbers and receptor responsiveness ( 27,83).
Athletes who use clenbuterol prefer capsules or tablets rather than the inhalant form, which is also available. Athletes
usually take twice the dosage recommended for the treatment of bronchospasm, or 0.04 to 0.06 mg twice daily. Dosage
follows a 3-week on/off cycle (83). During the on-cycle, clenbuterol is taken for 2 days and discontinued for 2 days, in
order to avoid any diminishing effects ( 83). Despite such precautions, there is a rapid attenuation of clenbuterol's
effectiveness after a few weeks of use (27). Because niacin improves muscle blood flow, it is often taken concurrently
with clenbuterol to hasten distribution ( 83). When AAS are discontinued before a competition, clenbuterol is used to slow
down the loss of muscle mass and to promote lipolysis of subcutaneous fat (known as “stripping”), thereby improving
muscle definition ( 83).
Side effects that have been reported with clenbuterol use include muscle tremor, palpitations, muscle cramps, transient
tachycardia, anxiety, headaches, peripheral vasodilation, anorexia, insomnia, and adrenergic tremor ( 20). Another side
effect, myocardial hypertrophy, has been reported in animal studies; if it were to occur in humans, could lead to outlet
obstruction and ultimately to sudden death ( 83). Other potentially life-threatening side effects include hyperthermia,
myocardial infarction, stroke, and dysrhythmia ( 27).
Incidents of clenbuterol food poisoning have been reported to result from the consumption of animals treated with
clenbuterol (86). In one incident in Italy, meat samples contained clenbuterol at 4.5 mg per kg. People who ate 10 to 20 g
of meat ingested therapeutic dosages of clenbuterol, and the amount of meat found in a normal meal (100 g) resulted in
the ingestion of five times the therapeutic dose ( 86). Effects caused by this consumption included those mentioned
previously as well as gastrointestinal disturbances, vertigo, myalgia-arthralgia, cephalalgia, weakness, and confusion.
The average duration of symptoms was 48 hours (86).
PEPTIDE AND GLYCOPROTEIN HORMONES AND ANALOGUES
As a class, these drugs are banned because of the chemical interactions and effects they have on the production of
endogenous forms of testosterone and similar compounds.
Human Growth Hormone
Human growth hormone (hGH) consists of a single-chain polypeptide of 191 amino acids stabilized by two disulfide
bonds (7,87). The molecular mass is 22,000 Da. The half-life of hGH in plasma ranges from 17 to 45 minutes, and it is
metabolized in the liver ( 88). hGH is synthesized by anterior pituitary somatotropes and is secreted in a pulsatile manner
by the adenohypophysis found in the pituitary gland ( 27,87,89). Growth hormone–releasing hormone (GHRH) and
somatotropin release–inhibiting hormone, which are produced by the hypothalamus, regulate the release of hGH ( 53).
hGH release is also affected by a variety of factors including exercise, diet, drugs, nutrition, stress, sleep,
cardiorespiratory fitness, and feedback mechanisms ( 7,27,53,89). The mean production of hGH is 500 to 875 µg per day
(87). The secretion of hGH increases in response to exercise, hypoglycemia, and, most of all, sleep—with the largest
amount secreted at about 60 to 90 minutes after onset ( 27,53). Endogenous l-arginine, l -lysine, and ornithine also
stimulate the production of hGH (53). Short bouts of intense exercise, such as a 400-yard dash, tend to increase hGH
secretion dramatically, although levels peak and subside gradually ( 87,89,90). In general, the amount of hGH that is
released by exercise is directly related to the intensity of the exercise ( 53). Glucose loading and obesity blunt the release
of hGH during exercise (7). Suppression of hGH is further caused by increased blood levels of hGH, increased blood
levels of insulin-like growth factor I (IGF-I), hyperglycemia, and hypothermia ( 53).
The consumption of recombinant growth hormone (rGH) has become easier to achieve, mainly because biotechnologic
advances have increased availability and safe supplies of the drug ( 87,90). Athletes take one of two available forms of
rGH that are structurally related to hGH and also consist of a single amino acid chain, although one form has 192 amino
acids instead of 191 (90). The range of medically prescribed dosages of rGH varies between 0.06 and 0.1 mg per kg
three times weekly, depending on whether the 191- or 192-amino-acid rGH is used ( 7,27). There have been reports that
athletes using up to 20 times the medically prescribed dosage, from 4 units three times per week to as much as 10 units
per day for many weeks (89,90). rGH is taken by intramuscular injection in 6- to 12-week cycles and is coadministered
with AAS (53). Athletes also attempt to stimulate endogenous hGH secretion by taking clonidine, levodopa, and
vasopressin, which may do so, by acting directly on the pituitary gland or by acting indirectly through the stimulation of
GHRH (88,91). Arginine, ornithine, l -lysine, and tryptophan are also used in an attempt to stimulate endogenous hGH
release.
The desired anabolic properties of rGH are identical to those that result from the effects of endogenous hGH on the
human body. hGH primarily serves to foster growth through stimulation of the secretion of somatomedins by the liver and
other organs, which in turn regulate the activities of other hormones ( 27,89). Along with the somatomedin IGF-I, hGH
facilitates growth of muscle, bone, and cartilage; increases protein deposition; facilitates all aspects of cellular amino acid
uptake; facilitates cell protein synthesis and simultaneously reduces protein catabolism; inhibits glucose uptake in
muscle; and decreases protein metabolism by lipolysis ( 27,53). Administration of rGH results in increased FFA, increased
hepatic lipid stores, and decreased peripheral fat stores, with the ultimate result being decreased body fat and increased
lean body mass (27). All of this is achieved without the risk of detection, because there are currently no IOC-approved
urine tests for the detection of doping with rGH ( 27,90).
However, some of the ergogenic benefits of rGH use, although popularly touted, are in practice limited in scope.
Whereas it has been shown that rGH use increases the size and strength of muscles in hGH-deficient individuals, its
impact on nondeficient users is less dramatic ( 92). In fact, research has shown that increases in muscle size do occur in
nondeficient individuals but increases in strength do not (88). The reason for this has been postulated to involve RNA.
Muscle growth induced by rGH depends on increases in the rate and translation of existing RNA, whereas muscle growth
resulting from exercise depends on the synthesis of new RNA (7). Thus, rGH use results in increases in muscle size but
not strength (88). Other limited effects of rGH administration include minimal gains in lean body mass in athletes who use
rGH and do not have a large fat mass. In athletes who do have a large fat mass, rGH use does lead to increases in lean
body mass.
Given such large doses, the resulting side effects are not surprising. In adolescents, the administration of rGH causes
gigantism due to overstimulation of the open physes ( 53). In adults, side effects include acromegaly that results in
overgrowth of a variety of organs, bones, facial features, fingers, toes, and coarsening of the skin; diabetes; coronary
heart disease; cardiomyopathy; congestive heart failure; hypertension; thyroid disease; peripheral neuropathy;
decreased libido; impotence; menstrual disorders; osteoporosis; abnormal growth of melanocytic nevi; decreases in
HDL-cholesterol and apolipoprotein A-1; and a shortened life span ( 7,27,53,89). Some of the side effects of rGH use may
be irreversible even after discontinuation of the hormone. Other consequences of rGH use can be quite serious ( 27,53).
For example, acromegaly can lead to cardiac failure, which is one of the major causes of death in individuals with this
syndrome (53). Although the availability of synthetic rGH has ostensibly precluded the possibility of contracting
Creutzfeldt-Jakob disease, it should be noted that cadaver-originated hGH may still be available on the black market.
Therefore, the possibility of contracting this disease from hGH that is sold as rGH is still a very real danger ( 7). Other
risks in obtaining rGH involve quality and purity of the drug as well as legitimacy. In fact, the U.S. Drug Enforcement
Agency estimates that 30% to 50% of rGH products are phony ( 93).
Human Chorionic Gonadotropin
Human chorionic gonadotropin (hCG) is a hormone that is used for its multifaceted properties involving a complicated
relationship with both exogenous and endogenous testosterone ( 94). hCG is used by male athletes to promote
endogenous testosterone production. Its use is even considered equivalent to exogenous testosterone administration by
the IOC (50,95). The same cellular response that enables LH to stimulate endogenous testosterone production also
enables hCG to do so (94). hCG is also used to prevent testicular atrophy and shutdown during prolonged periods of
exogenous AAS use. Furthermore, the simultaneous administration of hCG and AAS leads to normalization of the ratio of
testosterone to epitestosterone (T/E ratio), a measurement that is used to detect the presence of exogenous AAS.
Without the coadministration of hCG and AAS, the T/E ratio would be greater than the internationally agreed limit, which
is 6:1, and AAS would be detected. Treatments with hCG and clomiphene do not alter the T/E ratio ( 50). For women who
take hCG to promote ovarian steroidogenesis, hCG is not as effective as in men and probably has little if any effect on
their athletic performance ( 94,96,97). Also in women, the presence of high levels of hCG does not necessarily indicate
that exogenous hCG has been taken, because this hormone can be found in the urine during normal or abnormal
pregnancy.
Erythropoietin and Blood Doping
Endogenous and recombinant erythropoietin (EPO and rEPO, respectively) have similar structures—one polypeptide
chain of 166 amino acids with two disulfide bonds attached to four polysaccharide chains—with the exception that rEPO
has a “heterogeneous carbohydrate moiety” ( 98). The molecular mass of EPO is 18,000 Da. EPO is the human
hematopoietic hormone that regulates the production of RBCs in bone marrow ( 98,99). RBCs carry oxygen to skeletal
muscle and aid in the maintenance of acid-base status ( 100). When renal oxygenation is decreased, oxygen-sensor cells
in the kidney stimulate EPO release ( 98,99). The plasma half-life of rEPO is 20 hours when administered subcutaneously
by injection, and its effects have been known to last for 2 weeks ( 99). Blood doping, as defined by the IOC, is the
administration of blood, RBCs, and related blood products to an athlete; the use of rEPO would fall into this prohibited
category. Therefore, the terms “rEPO administration” and “blood doping” are used interchangeably throughout this
section (95).
The athletic community, especially in sports in which endurance is a major key in winning, has been using rEPO for years
for its obvious effects on the circulatory and oxygen energy system ( 30). More RBCs lead to increased total hemoglobin,
hemoglobin concentration, hematocrit, and RBC mass (30,98). These changes lead to an increased oxygen-carrying
capacity of the blood (each gram of hemoglobin carries approximately 1.34 mL of oxygen), which consequently increases
oxygen delivery to working muscles, enhances V O 2max, and thereby enhances endurance performance ( 30,98,99 and
100). The ability of rEPO to increase RBC mass over several hours is extraordinary when it is realized that even a 5%
increase in RBC mass usually takes months of adaptation to endurance training ( 100).
Improved submaximal performance also occurs after rEPO intake and stems from the reduced physiologic strain, which is
characterized by a lower heart rate, lower venous and arterial lactate, higher venous and arterial pH values, and lower
ratings of perceived exertion after rEPO doping ( 30,100). In one study of the effects of rEPO, 15 recreationally trained
men received 20 to 40 IU of rEPO per kilogram injected three times each week for 6 to 7 weeks. The rEPO use led to a
linear increase in hemoglobin levels (0.28 g per week), which were 11% greater after 6 weeks of administration; an
increase in V O2max; and a 17% increase in treadmill run time to exhaustion ( 101). Administration of rEPO may also
improve performance in distance races. It has been shown that an increase in RBCs resulting from blood doping
decreases 10-km run times by approximately 69 seconds, 3-mile run times by approximately 24 seconds, and 1,500-m
run times on a track by approximately 5 seconds (102,103 and 104). Ergogenic responses to rEPO administration vary
from person to person and depend on physiologic factors such as training state, level of fitness, and genetics ( 100).
Although the benefits of rEPO use to counteract the effects of exercising in high altitudes seems obvious, there have
been many studies that show these effects may be limited ( 100). The effects of high altitude on humans seem opposite to
the effects of rEPO administration: reduced oxygen pressure in breathable air leads to decreases in arterial oxygen
tension, which in turn decreases the oxygen-carrying capacity of the blood and leads to a decline in arterial oxygen
content (100). Given such diametrically opposed effects, it would seem that blood doping via rEPO administration would
counteract any negative effects of altitude on the circulatory and oxygen energy system. However, studies have shown
blood doping to have a decreasing impact on V O2max as altitude increases (100,105,106 and 107). At altitudes between
sea level and 2,500 m, blood doping may counteract the oxygen-depleting effects on V O2max (105). Between 2,500 m and
3,800 m, blood doping may ameliorate but does not completely prevent decreases in V O 2max (106). Finally, blood doping
may have minimal or no impact on VO 2max at altitudes higher than 3,800 m ( 107).
On the other hand, administration of rEPO has definite ergogenic benefits for athletes exercising in heat ( 100). Because
rEPO enables greater oxygen-carrying capacity of the blood, a given submaximal exercise can be performed with
decreased muscle blood flow (100). In heat, this would decrease the competition between circulatory oxygen delivery and
circulatory heat dissipation, allowing the latter to be more effective ( 100). In one study involving heat-acclimated men,
300 mL of RBCs were administered 2 to 4 days before and after the subjects walked in the heat while either normally
hydrated or, on another day, dehydrated by 5% of their body weight. The increased RBCs resulted in lowered heart rates,
sweating thresholds, and core temperatures; an increased sweating sensitivity; and an overall thermoregulatory
advantage in either condition ( 108). It was concluded that blood doping results in a thermoregulatory advantage that is
greatest for heat-acclimated individuals and slight for unacclimated people ( 100).
Although rEPO seems to have positive effects (e.g., enhanced heat dissipation), it also has many adverse effects. Major
side effects stem from the use of improper dosages of rEPO. The amount of rEPO that is normally prescribed, for
example to cure renal anemia, would add up to only a few milligrams over 1 year of treatment ( 98). Since athletes
typically use ergogenic aids in dosages that are several times those usually prescribed, the probability exists that there
may be individuals who are using dangerously high levels of rEPO. Such levels could stimulate large increases in RBC
mass, an effect that is dose dependent, resulting in dangerously high hematocrit levels ( 109). Because hematocrit
increases above 30% force blood viscosity to rise exponentially, there would also be a dramatic rise in blood viscosity
(110). This would lead to an increase in vascular resistance, which would make the heart contract more forcefully to
circulate the blood. Moreover, because viscosity tends to increase with dehydration, there would be a potentially
increased risk of coronary and cerebral occlusions, thrombosis, and pulmonary emboli ( 18). Additional side effects of
rEPO administration include hyperkalemia, hypertension directly related to rEPO dosage, flulike symptoms, and inhibition
of the endogenous production of EPO ( 99,100).
Dehydroepiandrosterone
Dehydroepiandrosterone (DHEA) is an androgen steroid produced primarily in the adrenal glands from acetate; it is the
major adrenal steroid of young adults. In 1996 the U.S. Food and Drug Administration banned the sale of DHEA for any
indication because of insufficient evidence of safety and value. Since that time it has become a popular OTC nutritional
supplement (111). DHEA in its free, sulfated, and lipoidal forms is the most abundant steroid secreted by the adult human
adrenal (99). Although a small amount of DHEA is converted to the more potent androgens testosterone and
dihydrotestosterone, as well as androstenedione in peripheral tissues, the true role and physiologic functions of DHEA
have yet to be fully uncovered. In fact, although DHEA is most often referred to as an adrenal androgen because it can
be converted in the periphery to testosterone, DHEA itself does not interact with androgen receptors but with separate
DHEA-specific receptors (112). Studies show that at the lowest doses DHEA has effects on neurologic and immunologic
tissues, suggesting that these two types of sites may be physiologic targets. DHEA also affects cardiologic and metabolic
functions as well as tumor growth, but such actions require higher doses and may reflect “pharmacologic” activities
(99,112,113). It has been proposed that DHEA's pattern of activity represents a new class of steroid hormones, the
“regnantoids” (112).
Research investigating the erogeneity of DHEA has been somewhat limited. However, there is a considerable amount of
anecdotal support from athletes in a variety of sports who proclaim its athletic enhancing qualities. It has been
hypothesized that supplementation with DHEA aids, maintains, or increases testosterone levels; reduces body fat
accumulation; reduces the risk of atherosclerosis with aging; and possibly protects against certain cancers ( 113,114 and
115). One study actually helped confirm some of the purported beneficial effects ( 116). Untrained healthy men (mean
age, 24 years) were given 1,600 mg of DHEA per day for 28 days. Although testosterone levels were not significantly
affected, both DHEA and androstenedione levels were increased. There was also a 31% reduction in percent body fat
and a decrease in serum cholesterol levels. A double-blind, placebo-controlled study done in 1993 using
etiocholanedione, a metabolite of DHEA, found that doses of 32 mg per kg per day also produced significant weight loss
in subjects (117). Furthermore, animal studies fully support this ergogenic effect.
The underlying physiologic mechanism of weight loss with DHEA use is not known. One researcher summarized DHEA
supplementation evidence that purportedly showed the underlying cause to be an increase in mitochondrial respiration
(118). However, most of the animal studies involved high doses of DHEA administered over a period of weeks to months.
Furthermore, although DHEA has clear antiobesity actions in obese animals, studies on humans have failed to show
changes in either body fat or weight ( 119,120).
Even at high doses (50 times the suggested OTC supplement dose), no dose-limiting side effects of DHEA have been
reported (121). Long-term effects are yet to be determined, but users report few adverse effects overall, and most of
those are secondary to androgen excess. Notable irreversible side effects include virilization or voice-deepening, hair
loss, clitoromegaly, and hirsutism in women and gynecomastia in men (53). Potential adverse consequences of DHEA
use include tumorigenesis, specifically hepatic tumors, hepatomegaly, elevation in liver enzymes, increased cardiac risk
factors in women (altered glucose tolerance and increased lipid levels), elevated prostate-specific antigen concentrations
in men, acne, and other androgenic side effects ( 122,123,124 and 125). Furthermore, some researchers believe that
unopposed prolonged estrogen and testosterone secretion may increase the risk of uterine and prostate cancers ( 126).
Whether DHEA is a member of a previously unreported and distinct class of steroid hormones that exerts unique
physiologic actions is still debated. However, research reveals that there is truth to its potential ergogenic effects,
especially at higher doses ( 112), although research regarding such effects in athletes is lacking. Although the
manufacturers of OTC nutritional supplements purport effects with doses between 50 (the physiologic dose in young
adults) and 200 mg per day, the erogeneity and the safety of long-term use of DHEA in humans, as with many other OTC
supplements, have not been shown.
Dihydroxyacetone Pyruvate
Dihydroxyacetone pyruvate (DHAP) is a relatively new supplement on the public sports scene that has been touted by
manufacturers as an ergogenic aid that improves endurance exercise capacity, augments weight and fat loss, serves as
an antioxidant, and lowers plasma lipid levels ( 127). DHAP is a combination of dihydroxyacetone and pyruvate in a 3:1
ratio. Both are three-carbon metabolic byproducts of carbohydrate metabolism (glycolysis) ( 128).
There are two major studies that help support manufacturers' claims of enhanced endurance performance by prolonging
time to exhaustion with DHAP supplementation. The first study found that 100 g of DHAP (75 g of dihydroxyacetone and
25 g of pyruvate) per day, for 7 days, increased arm ergometer endurance time by 20%, compared with placebo, at 60%
of VO2max (129). The second study found that the cycle ergometer endurance time at 70% V O2max in subjects who took 100
g of DHAP per day for 7 days and who consumed a high-carbohydrate diet during that period was improved by 20%
(130). The underlying physiologic mechanism was believed to be enhanced glucose uptake or extraction by the
exercising muscle, because there did not appear to be a difference in preexercise muscle glycogen storage between the
placebo and control groups. Although the results of these studies tend to show significant ergogenic effects with chronic
supplementation, animal studies suggest that the acute effects of DHAP supplementation actually worsen aerobic
endurance capacity (131). Rats infused with DHAP during motorized treadmill running actually fatigued much earlier, with
their run time to exhaustion decreased by approximately 67%. The results of the two human studies cited support a
potential ergogenic effect with prolonged supplementation, but acute supplementation appears to be detrimental to
performance. Clearly, more studies are needed to confirm these findings in well-trained athletes.
Initial research has also supported the claim that DHAP supplementation may effectively augment weight loss and, more
importantly, fat loss in humans. Two studies were conducted involving morbidly obese women who were placed on
restricted diets and supplemented with DHAP. After 21 days, these obese women had a statistically significant greater
weight loss than the control groups (132,133). The supplemented groups respectively lost 16% and 37% more weight,
and 23% and 48% more body fat, than the controls. Although the differences between the groups were statistically
significant, the average differences in weight lost were actually relatively small. For example, in one of the studies the
control group lost an average of 5.6 kg of weight and 3.5 kg of fat, while the supplemented group lost 6.5 kg (16% more)
weight and 4.3 kg (23% more) fat (133). In a subsequent study, further support for DHAP's ergogenic effects was
reported. Again, a morbidly obese group of women were placed on a 21-day hypocaloric diet, which was followed by
another 21 days of hypercaloric refeeding containing DHAP. They were compared with a control group who were given
no DHAP supplementation (134). The treatment group gained 1.8 dg (36%) less weight and 1 kg (55%) less fat than the
placebo group. Again, the differences between the groups were relatively small. From these results, it was concluded that
supplementation with DHAP accelerates weight loss under hypocaloric conditions and decreases weight gain and
reaccumulation of body fat in obese women fed a hypercaloric diet.
Critics of these initial findings are quick to point out their lack of generalization. Because all of the subjects were morbidly
obese women confined to bed while housed in a metabolic ward, it is difficult to ascribe these results to the population at
large (127). Additionally, the doses given to the subjects (28 to 90 g per day) were considerably larger than the
commercially prepared dosages (0.5 to 1.0 g). Finally, the bioelectrical impedance testing used to assess body fat
percentages in these studies is limited in its ability to assess adiposity in obese individuals and has an error margin of
2% to 4%, so it not be a useful tool for measuring the small, short-term changes in body composition seen in the
individuals in these studies ( 135,136).
More recently, a 6-week study compared a DHAP-supplemented group and a placebo group of overweight men and
women who engaged in an exercise program three times per week (137). A significant decrease in body weight (1.2 kg),
body fat (2.5 kg), and percent body fat (from 23% beforehand to 20.3% on posttesting) were found in the
pyruvate-supplemented group, whereas there were no significant changes in these parameters in the placebo group.
This study suggests that ingestion of 6 g of pyruvate for 6 weeks, in conjunction with an exercise program, significantly
decreases body weight and fat mass. This lends further support to the belief that pyruvate can truly be used as an
ergogenic aid.
It is widely advertised that there are no side effects associated with DHAP use. However, in both of the human exercise
performance studies, the subjects experiences gastrointestinal side effects that included excessive abdominal gurgling
(borborygmus), flatus, and diarrhea ( 129,130). However, the commercially available doses found in the OTC formulations
of DHAP (0.5 to 1 g) are probably not large enough to induce similar side effects, because those subjects were given
doses of 100 g (127).
Because the ergogenic effects were measured on untrained subjects and there are as yet no studies that demonstrate
ergogenic effects of pyruvate when taken in the smaller doses suggested by the manufacturing companies, it does not
appear there is any substantive research to support the claims that pyruvate is an ergogenic aid or an effective weight or
fat reducer in athletic populations. Therefore, claims that small doses of this substance are effective ergogenically or that
pyruvate decreases body weight and fat in trained, nonobese individuals should be considered speculative at best ( 127).
Creatine Monohydrate
Creatine monohydrate is today not only the popular ergogenic aid but also one of the most researched
performance-enhancing supplements. It is commonly used by high school, college, professional, and Olympic athletes.
Creatine was first introduced as a potential OTC ergogenic aid in 1992. Since then its use has grown significantly. In fact,
the NCAA study of substance use and abuse habits of college student-athletes found that 13.3% of those surveyed
reported using creatine ( 138). Creatine is an organic compound made by the liver, kidneys, and pancreas from three
amino acids: glycine, methionine, and arginine. In addition to being synthesized by the body, creatine is also obtained
through consumption of meat and fish products. Approximately 1 g of creatine per day is made in the body, and another 1
g per day is consumed in the diet ( 139). Creatine is transported from synthesis sites to the skeletal muscles. In the
muscle it exists in two forms: as free creatine, and as creatine phosphate, which makes up two thirds of the total creatine
in the body.
Creatine appears to play a major role in energy production during quick bursts of activity. In fact, during explosive
sprinting exercise, the energy supplied to rephosphorylate adenosine diphosphate (ADP) to adenosine triphosphate
(ATP) is largely determined by the amount of phosphocreatine stored in the muscle ( 140,141). Basically, when muscles
contract, ATP is used as the fuel for movement. ATP provides energy by releasing one of its phosphate molecules,
thereby becoming transformed into ADP. Because muscle has only enough ATP stored to perform high-intensity muscle
contractions for about 10 seconds, more ATP must be synthesized for the muscle to continue contracting. Essentially,
phosphocreatine gives up its phosphate molecule to ADP to create additional ATP. Thus, the ability to regenerate ATP
depends, to some degree, on the supply of phosphocreatine in the muscles ( 138). In fact, phosphocreatine is a major
source of muscular energy during STHIX bouts lasting from approximately 2 to 30 seconds ( 142). As phosphocreatine
stores become depleted during these explosive exercises, performance is likely to deteriorate rapidly because of the
inability to resynthesize ATP at the required rate ( 143). Studies suggest that increasing muscle creatine content through
supplementation may increase the availability of phosphocreatine and actually accelerate the rate of ATP resynthesis in
myocardial and skeletal muscle metabolism during and after STHIX. Additionally, creatine supplementation is thought to
buffer the intracellular hydrogen ions that are associated with lactate production and muscle fatigue ( 144,145,146,147
and 148). These effects should significantly influence the amount of energy generated during brief periods or repeated
bouts of high-intensity exercise, thereby increasing the force of muscular contractions, prolonging anaerobic exercise,
and theoretically improving repetitive sprint performance capacity.
Creatine is purported to increase strength, produce greater and faster lean-tissue muscle gains, increase energy,
improve sprint performance, delay fatigue, and aid in fat loss. Research indicates that, to maximize creatine stores, a
“loading phase” of supplementation with 20 to 25 g of creatine monohydrate per day for 2 to 7 days is necessary. Studies
creatine loading increases total creatine content by 15% to 30% and intramuscular phosphocreatine stores by 10% to
40% (149). After this “loading phase,” a “maintenance phase” of 3 to 5 g per day is all that is needed to maintain these
levels. Any extra supplement ingested is excreted by the kidneys.
A number of studies add support for creatine's performance-enhancing benefits. Research has shown improvement in
strength, power, sprint performance, and work performed during multiple sets of maximal-effort muscle contractions. For
example, one study reported an increased amount of work performed during five sets of bench press and jump squats
after a loading phase of creatine (25 g per day for 7 days) ( 150). Other studies have shown significant improvements in
single-effort sprint performance for sprints lasting 6 to 30 seconds ( 151,152). Another study reported that sprint
performance during a series of 300- and 1,000-m runs were significantly improved with a loading phase of 30 g per day
for 6 days (143). Furthermore, a study testing off-season college football players found significant increases in repetitive
sprint performance (in the first five of twelve 6-second sprints with 30 seconds' rest between sprints) and isotonic lifting
volume from maximal-effort repetition tests on the bench press, squat, and power clean ( 153). Thus, the reported
ergogenic effects include increased one-repetition maximum and/or peak power, improved performance on the vertical
jump and repetitive jump, increased work during repetitive sets of maximal-effort muscle contractions, enhanced sprint
performance in sprints lasting 6 to 30 seconds, improved repetitive-sprint performance, and improved high-intensity
exercise performance in events lasting 90 to 600 seconds. Studies in support of these hypotheses indicate that creatine
loading may improve high-intensity exercise performance in a variety of athletic activities such as rowing, running,
cycling, swimming, and resistance exercise ( 143,148,150,151,154,155,156,157,158,159,160,161 and 162).
Not all studies investigating the ergogenic value of creatine supplementation have reported enhanced exercise
performance. In fact, several field studies reported a lack of significant ergogenic effect after creatine supplementation
(162,163,164,165,166,167,168,169,170,171 and 172). Overall, creatine supplementation appears to be less ergogenic
when initial loading regimens are less than 20 g per day for 5 days, when low-dose regimens (2 to 3 g per day) without a
loading period are used, and when the period of time between crossover experiments to allow complete washout of
exogenous creatine is less than 5 weeks. In addition, studies tend to show that creatine does not enhance endurance
exercise or affect performance in sprints lasting 6 to 60 seconds when prolonged recovery periods of 5 to 25 minutes are
given between sprint trials ( 30).
Purportedly, the only side effect of creatine monohydrate supplementation in clinical investigations has been weight gain
(142,149). However, clinical investigations have reported modest elevations in serum creatinine, blood urea nitrogen,
creatinine, creatine kinase, lactate dehydrogenase, and aspartate aminotransferase ( 173,174). The significance of these
elevations is unknown, but they appear to normalize with cessation of creatine monohydrate supplementation.
Additionally, there is concern as to whether creatine supplementation may cause long-term suppression of endogenous
creatine synthesis, liver damage, increased renal stress, increased thermal stress, dehydration, and muscle strains and
pulls. Repeated anecdotal reports by numerous athletes, trainers, and physicians seem to strongly support the idea that
supplementation with creatine monohydrate has caused some of these significant side effects, most specifically muscle
pulls (particularly in the hamstrings and biceps), dehydration, and severe muscle cramping (Chief Iron Bear, Special
Olympics Symposium, Raleigh, NC, personal communication, July 1999).
Although there is a good deal of literature regarding the ergogenic qualities of creatine monohydrate, there is little
evidence evaluating the adverse health effects and medical safety of short- and long-term supplementation. To eradicate
the disparity between the scant side effects reported in the literature and the notable side effects reported by numerous
athletes, trainers, and physicians, further unbiased clinical research needs to be completed. Until then, creatine
monohydrate's widespread use will undoubtedly continue to flourish in the athletic arena, especially because it appears
to be an effective ergogenic aid that is presently allowed by athletic governing bodies.
CONCLUSIONS
In the future, many changes must be made in current drug testing policies if they are to effectively prevent the use of
prohibited ergogenic substances. This most surely means an increasing reliance on more invasive techniques, including
blood testing. Because these practices increase the degree of invasiveness and further impinge on the constitutional
rights of athletes, they will undoubtedly create additional medical, legal, moral, and religious concerns. The controversy
surrounding basic rights and drug testing will continue, because the good of the many may indeed outweigh the rights of
the not-so-few athletes who choose to use drugs to artificially enhance their athletic performance. In an age when genetic
engineering and cloning loom in the background, the only certainty for the future of drug testing in sports may be that
technology will continue to dominate, as new drugs of abuse, newer methods of detection, and ingenious methods of
evasion are developed.
It would be unrealistic to believe that our present methods of detection are even close to foolproof. There have been
numerous testimonies by athletes who have successfully evaded the doping control system ( 175). In fact, our present
methods of detection may be perceived as “a vain attempt to preserve what is beautiful and admirable in sports” ( 176).
However, studies indicate that drug testing can be an effective means for deterring drug use, especially when it is
performed intensively, year-round, out of competition, and with no advanced notice ( 25,177,178). Although education and
rehabilitation programs remain an integral part of present drug deterrence policies, collectively they still do not prevent
athletes from using banned substances. To truly be effective, the doping control community needs to be as tenacious in
its commitment to prevent drug use as society is in rewarding the win-at-all-costs philosophy in sports. This might entail
the creation of penalties for use of banned ergogenic aids that are equally as offensive and intolerable as their use is
attractive. As an example, a track and field athlete who is caught using ergogenic substances at the Olympic Games
would not only be banned for life from the sport for the first offense but would also disqualify his or her country from the
competition. This means that athletic programs and sports governing bodies need to be more vehemently committed to
terminating drug use. This would naturally include increased financial resources, a higher priority on education and
prevention, and unified enforcement of sanctions. Unfortunately, it seems that there is a significant proportion of athletic
interests that allow individuals to gain supraphysiologic advantages from drug use and do not want stricter penalties or
enforcement. Instead, they prefer the false appearance that all athletes are competing on a level playing field.
We must weigh the increased monetary costs of extensive doping control programs against the cost to society if we do
not attempt to level the playing fields. The unethical agendas of a significant proportion of athletes and athletic programs,
as well as society's tendency to value winning as a priority, continue to mandate drug testing in sports. Many who support
drug testing believe that it remains a necessary evil and that it is athletes' responsibility as society's role models to live
up to a higher ethical standard. They argue that the relative decline in positive drug test results stands as an affirmation
that the sentinel effect is working ( 25).
On the other hand, there are those who view drug testing in athletics as an unnecessary invasion of Fourth Amendment
rights and an ineffective tool for its purpose of identifying those who use drugs to gain an unfair advantage in athletic
competition (179,180,181 and 182). They argue that drug use and doping procedures in this age of “big-money” sports
have risen to a new level ( 183). Some believe that drug testing will always be one step behind the latest ergogenic
breakthrough and that the large sums of money spent on its development and implementation would be better spent on
prevention programs (181). Sadly, the ultimate cost of drug testing may be paid by those men and women who hold to the
ideals of fair competition without the use of banned substances or doping methods.
The science of drug testing is continually evolving, and there are significant technologies on the horizon that may make it
possible to detect biologic markers of lifetime drug use. However, it is uncertain whether drug testing procedures will ever
be comprehensive enough to thwart those wishing to circumvent the process. The only constant in this biochemical
playing field is that it may never be level. We cannot and should not rely on or expect science to cure what is a societal ill
(3).
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10 Special Concerns of the Pediatric Athlete
10
SPECIAL CONCERNS OF THE PEDIATRIC ATHLETE

MOREY S. MORELAND
Special Considerations of Growth and Development

Fractures in Children: Strains and Sprains
Mechanism
Acute Trauma
Management
Sprains and Strains
Treatment
Overuse Injuries
Anatomy and Growth Considerations
Medical Considerations
Stress Fractures
Osteochondrosis and Osteochondritis Dissecans
Anterior Patella Pain Disorders
Evaluation and Treatment
Spine and Sports
General
Trauma to the Spine
Scoliosis
Kyphosis
Scheuermann Kyphosis
Spondylolysis and Spondylolisthesis
Chapter References
The unique quality of growth potential imparts special characteristics to the musculoskeletal system of children and
adolescents. Indeed, it is the special property of tissues in “transition,” with the ability of creating newer and larger
structures (bones, muscles, tendons, and ligaments), that requires the clinician to understand the specific demands of
sport on these tissue structures. The treating clinician also must understand how these unique characteristics relate to
the implicit healing capabilities of injured children. Therefore, in diagnosing and treating injuries to children it is
fundamental to understand that the child is not just a small adult—although, as noted by Dr. Seuss, the opposite may be
true. This chapter looks at various common pediatric injuries and disorders and examines their relationship to sports
activities in a manner that addresses the special concerns and difficulties of children as they relate to the potential
mechanisms of injury and their diagnosis and management.
SPECIAL CONSIDERATIONS OF GROWTH AND DEVELOPMENT
From birth to the completion of adolescence, the child undergoes a remarkable change in size and body proportion.
Height increases approximately 3.5 times, weight increases 20 to 25 times, and muscle mass increases about sevenfold
(1). The attainment of these increases is not uniform but follows a generally declining growth velocity curve. The notable
exception is the adolescent growth spurt; this period of rapid growth occurs during the ages of 10 to 14 years in girls and
13 to 17 years in boys ( Fig. 10.1). In addition to size changes, body proportions related to the center of gravity change
with respect to head size, truncal length, and leg length ( Fig. 10.2). In infants and young children, the center of gravity is
located in the midtrunk with a proportionally long trunk and short legs, whereas the adolescent attains a nearly adult form
with a center of gravity centered at L-4 and more equally proportioned leg, truncal, and head length ( 2). With increased
interest in organized sports, the problems of differing body size among participating children has necessitated careful
classification and monitoring to ensure that the larger body mass and velocity attained, for example, by older children do
not increase their chances for injury or confer an unfair competitive advantage. The lack of such monitoring remains a
problem for unsupervised playground sports activities.
FIGURE 10.1. Height velocity: single whole-year increment (50th percentile for boys and girls). This chart compares only
the means for boys and girls from the Tanner study; the standard deviations have been removed. The relative velocity for
boys (7.3 cm) is greater than that for girls (6.5 cm) during the maximal year of growth. The data indicate a rapid
deceleration after birth and a relatively short period of acceleration during adolescence. (From Lowey GH. Growth and
development of children, 7th ed. Chicago: Yearbook Medical Publishers, 1978, with permission.)
FIGURE 10.2. Height proportion. Ventral aspect of the body at intervals from the sixth fetal month to maturity. Body
lengths are reduced to the same scale, and the transverse plane of gravity is represented by a transverse line. The
relatively longer upper-body height at earlier ages may be seen. The distance of the center of gravity above the soles is
expressed as an index or percent of stature and maintains a fairly constant ratio, ranging from 55.0 to 59.0 during the
whole of the developmental period. (Modified from Palmer CE. Studies of the center of gravity in the human body. Child
Dev 1944;15:99–180, with permission.)
There also are physiologic differences in children throughout the span of their growth. Compared with adults, children
require more oxygen for a given activity and rely on anaerobic metabolism less during periods of increased muscle
activity. They have a less efficient thermoregulation system with fewer sweat glands ( 3), and they have higher heart rates
and lower cardiac stroke volumes. Tests of strength and endurance show progressive increases in the last half of
childhood ( 4). Neuromuscular development is evident also in faster audio and visual reaction times ( 5) and in reaction
and speed of movement (6).
Finally, and considering the uniqueness of the child's musculoskeletal system and possible response to injury, the
specific specialized anatomic structures of growing bone must be considered. Although the bone substance of children is
the same as that of adults, biomechanically the bones of children have more flexible and elastic qualities, and, especially
in the younger child, they are less brittle in their behavior. In addition, in children the growth plate (physis) is most
commonly considered the “weak link” in resisting forces, although tendon attachments into growing bones (apophysis),
should also be considered vulnerable. These areas and their injury constitute a large percentage of what is commonly
considered significant injury in children's sports. However, reporting variances make actual determination of the
epidemiology of such injuries difficult. As might be expected, reported injury rates vary depending on the sport. Garrick
and Requa have looked at injury rates for participants in high school sports ( Fig. 10.3), as reported by trainers over a
2-year period; there were a total of 1,197 injuries ( 7). As may be seen in this figure, the percentage of injuries requiring
more than 5 days lost to a sport was only 31%. The sport-specific injury rates also rose with increasing age. In a study of
Pop Warner League football players, injury rates rose, from 2.8 per 100 players at ages 9 to 12 years, to 10.1 per 100 for
ages 11 to 14 (8). More organization, longer practice and playing times, and acquisition of advanced skill levels probably
play a role in controlling this rate. These factors are especially important in view of the fact that at these ages the skeletal
system is becoming mature, losing its cartilaginous weaker zones, and increasing muscle bulk, which on an anatomic
basis should have a protective effect. Knowledge of the types of injury likely to cause symptomatic problems for the
pediatric athlete, therefore, must include an understanding of the level of maturity of the athlete and the level of demands
placed on the participant by the sport.
FIGURE 10.3. Injury rates in youth football. (From Goldberg B, Rosenthal PP, Nicholas JA. Injuries in youth football. Phys
Sportsmed 1984;12:122–132, with permission.)
FRACTURES IN CHILDREN: STRAINS AND SPRAINS
Skeletal trauma accounts for 10% to 15% of all childhood injuries, and fractures of cartilaginous physis account for about
15% of all fractures in children ( 9,10). In general, fracture rates for all locations in bones in children are slightly higher
than in adults except for elderly women. Overall, fractures in children account for 18% to 20% of all skeletal trauma, and
sprains and dislocations account for approximately 45% ( 11).
Mechanism
Children's bones and, to some extent, their soft tissues are more flexible than adults', allowing for greater energy
absorption and deformation by any external force. The periosteum surrounding the child's bone is thicker and retains a
considerable capability for growth and remodeling. Fractures can occur because of twisting, bending, or direct blows, and
fracture patterns are reflective of these forces. For example, twisting produces a torque that often leads to a spiral
fracture pattern, bending results in a short oblique pattern, and direct blows cause a transverse pattern ( 12) (Fig. 10.4).
Because of relative elasticity, greenstick and incomplete fractures are commonly seen, as are buckle fractures.
FIGURE 10.4. Schematic of tibia (3-year-old child) showing various types of fractures. (A) longitudinal; (B) transverse;
(C) oblique; (D) spiral; (E) impacted; (F) Comminuted. (G) Bowing (plastic deformation); (H) greenstick; (I) torus. (From
Ogden JA. Skeletal injury in the child, 2nd ed. Philadelphia: WB Saunders, 1990, with permission.)
Disruptions of the physeal plate are usually classified by five types ( Fig. 10.5), as initially described by Salter and Harris
(13). In these injuries, the fracture line either goes through a portion of the growth plate (types 1, 2, and 3) or crosses it
(type 4). In severe compression-type injuries, a crushing of the plate (type 5) may occur. In addition to serving a useful
function for classification, the type of epiphyseal fracture implies various types of injury mechanism: shear or rotation for
type 1; bending for types 2 and 3; bending with compression for type 4; and compression alone for type 5. It is important
to identify the pattern of the fracture, because the potential for permanent damage of the growth mechanism increases
with each type in the classification. In other words, less disruption usually occurs with type 1, and there is a higher
probability of disruption with type 5 ( 14).
FIGURE 10.5. Salter-Harris classification of physeal injuries. The injuries are divided by the plane of the fracture line
relative to the physeal growth plate. (From Staheli LT. Fundamentals of pediatric orthopaedics. New York; Raven Press,
1992, with permission.)
Acute Trauma
Acute trauma, severe enough to produce a fracture, usually occurs as a result of a fall or a contact or collision between
sport participants. In this instance, severe pain, inability to use the extremity, deformity, and swelling readily point to the
diagnosis. The anatomic location of these findings—at the end of a bone (epiphysis), in the middle of a bone (diaphysis),
or in the junctional area in between (metaphysis)—may give the examiner further information on the likelihood of growth
plate injury. Deformities about joints may represent either frank dislocation or complete separation of the epiphysis at the
growth plate. Radiographic examination is the single most helpful test for all musculoskeletal injuries. It should always
include anterior-posterior (AP) and lateral views—or, at the least, two views with 90-degree difference in orientation—to
adequately find and define the fracture. Occasionally, oblique views are helpful, particularly for short oblique and
nondisplaced fractures. Because the skeleton of each child is constantly changing with respect to maturation, it is helpful
to obtain comparison x-ray films of the opposite extremity so as to gain understanding of the normal skeletal pattern for
that patient. This is particularly true because more or less of the cartilaginous anlage of the bone will be ossified and
therefore visible on the radiograph. The appearance of secondary centers of ossification, although reasonably
predictable by skeletal age, are somewhat variable in relation to chronologic age. Therefore, comparison films may be
helpful in determining what is normal for a particular child. In injuries without significant angulation and injuries around
joints, soft tissue swelling, seen clinically and perhaps radiographically, may be helpful in assessing the location of the
injury. For example, ligamentous injuries or injuries to a joint that distention of the joint capsule suggest intraarticular
hemorrhage or soft tissue hemorrhage, or both; this helps determine the location and probability of either fracture or soft
tissue disruption.
Acute trauma must be differentiated from chronic or repetitive trauma because the former is more likely to produce a
sudden onset of severe disruption, whereas chronic injury often represents repetitive, less well-defined events or onset.
Acute injuries in sports most commonly involve the hand and wrist, ankle, knee, elbow, and shoulder and hip, in that
order. The relative frequency depends on the nature of the sport. For example, hand and finger injuries are more
common in baseball than in soccer. However, in soccer, ankle and knee injuries are much more frequent. An accurate
physical examination that attempts to localize as closely as possible the anatomic area of maximum deformity, swelling,
and pain increases the likelihood of getting the appropriate x-ray studies. It also increases the likelihood of initiating a
proper focus of attention so to adequately diagnose the problem and begin appropriate therapy.
Common pitfalls in diagnosing trauma problems in children include the failure to appreciate the cartilaginous injury (e.g.,
a Salter I fracture or a fracture through the cartilaginous portion of the epiphysis). Often these injuries are mistakenly
diagnosed as sprains because no frank fracture is seen radiographically. True sprains are less common in children than
in adults. Injuries surrounding joints should raise a strong suspicion of cartilaginous injury and not be assumed to be “just
a sprain.” Conversely, because trauma seen both in organized activity and in free play activity is so common among
children that symptoms of pain and swelling are often ascribed to an injury or a traumatic event, one should keep in mind
that their symptoms could also represent an infection or a tumor. Careful history and follow-up are helpful to differentiate
the nature of the symptoms.
Management
Careful assessment of the injured player is the first and foremost consideration for any acute injury. Surveying for other
injuries and preventing further injury also are of high priority. With most injuries it is important to evaluate whether there
is a fracture or instability, or both, and, if so, whether it is an open or a closed fracture. Open fractures involve any break
in the skin in or around the fracture site and require the application of a sterile dressing. Closed fractures are those in
which the skin is intact. Initial field management involves immobilization with a splint in cases of extremity fracture or with
a backboard for suspected spine trauma. Splinting should be done in a position satisfactory for transportation and in a
position in which a reasonable normal anatomic alignment can occur. After radiographic confirmation of the diagnosis,
the fracture or dislocation may need reduction, which is done under intravenous sedation, regional anesthesia, or, in
some cases, general anesthesia. Open fractures usually need debridement and irrigation in addition to reduction.
Several unique features of children's fractures are helpful in the healing process. Because of the growth potential of the
growth cartilage and periosteum, children's fractures tend to heal rapidly. In addition, because children are constantly
making new and larger bones, they can correct angular deformities easily—a feature not present in most older
adolescents and adults. Such remodeling may be seen in distal forearm fractures, as in Figure 10.6. The remodeling
process in younger children may take up to 1 or 2 years, but it does not normally interfere with function. One
disadvantage of managing children's fractures is the difficulty of monitoring activity levels during recovery. Cast
immobilization is usually maintained for 6 to 10 weeks, depending on the location and nature of the fracture. However,
after cast removal, a period of rehabilitation of muscle strength and motion is necessary, as is mechanical strengthening
of the fracture site, which may take 6 months or longer. Obviously, return to sports activities requires this rehabilitative
phase to be complete, and this fact is often frustrating for the young athlete, coaches, and parents. Nonunion of fractures
is rare in children, and malunion with shortening or angulation can usually be avoided with careful follow-up.
FIGURE 10.6. Nine-year-old girl who sustained fractures of the radius and ulna in a fall. A: Early radiographs at 1 month
after fracture, showing early bone remodeling of the fracture. B: Radiographs at 4 months, showing further remodeling of
the metaphysis and straightening of the bones.
Healing periods become somewhat longer the closer the child is to adulthood, and for that reason there has been interest
in internal fixation of fractures in the adolescent. Internal or external fixation of fractures reduces hospitalization time and
facilitates ambulation, but careful rehabilitation and monitoring of fracture healing before resuming sports is still
necessary. This is particularly true of femur fractures in the adolescent who is close to reaching skeletal maturity. Such a
procedure may be seen in Figure 10.7. Additionally, fractures that occur around joints or through the epiphysis (types 3
and 4) may require very accurate reduction to reconstruct the joint surface and accurately reapproximate the growth
plate. To achieve this open reduction, internal fixation is frequently necessary. These fractures carry the biggest risk of
potential long-term problems because of growth arrest or because of an irregular joint surface that leads to subsequent
degenerative joint disease. This often needs to be brought to the attention of parents and coaches.
FIGURE 10.7. A and B: Radiographs of 11-year-old boy, who fell while playing soccer, sustaining a fractured left
midshaft femur. C and D: One month after placement of an intramedullary rod for stabilization of the fracture to allow
crutch walking during healing.
As indicated previously, not all injuries lead to significant acute symptoms, but they may have longer-term consequences.
Figure 10.8 shows the result of an ankle injury sustained by a 13-year-old baseball player while sliding into second base.
He had moderate swelling over his left medial malleolus and could walk with pain. The initial radiograph showed little
more than a slight irregularity at the distal tibial physis. He was casted for 4 weeks, had an uneventful recovery, and
returned to sports in 3 months. However, a year and a half later, it was noted that the lower portion of his ankle was
turning in; his x-rays showed a varus deformity of the distal tibia. The initial injury had been a type 5 epiphyseal injury
with very little instability or deformity, but the proliferating cells of the epiphyseal plate had been damaged and
subsequently failed to grow on the medial side, while the lateral portion and the fibula continued to get longer. This
required a surgical procedure to arrest further fibular growth and lateral tibial growth and to realign the tibia. Fortunately,
this event occurred near the end of growth and no significant leg length discrepancy occurred.
FIGURE 10.8. Radiographs of a 13-year-old baseball player who was injured while sliding into second base. There was
swelling and tenderness over the medial malleus. A: Epiphyseal plate disruption of the medial portion of the distal medial
epiphysis. The leg was casted and no attempts at reduction were made. B: Radiographs taken 18 months later, showing
angular growth disturbance of distal tibia with fibula overgrowth. C: Two years after injury, radiographs show operative
correction with distal tibial osteotomy and completion of growth arrest of distal fibula and tibia.
Sprains and Strains
Although contusions are undoubtedly the most prevalent of all injuries in children who compete in sports, just as they are
in adults, true sprains of ligament and strains of muscle are uncommon. This is especially true for younger children, but
not for adolescents, who begin to reflect injury patterns similar to those of adults. There are two anatomic reasons for
this. First, children tend to have a much higher degree of ligamentous laxity, which allows accommodation of relatively
greater excursions than are possible for adults. Second, children appear to have a greater ability to sustain stretching of
soft tissues. Descriptions of ligament injury (sprains) are commonly classified as mild, moderate, and severe: mild sprains
are those in which only minor microscopic disruption occurs, with little clinical evidence of increased laxity; in moderate
sprains, microscopic injury is notable, with swelling and increased excursion or laxity, but the fibers remain in continuity;
and severe sprains are those with gross injury and disruption of the ligament, severe swelling, and potential loss of joint
stability revealed on clinical testing. Ligaments have a higher resistance to failure when rapid, small loads are applied to
them, and they have decreased resistance to failure with slow loading of large loads (e.g., larger body mass).
Similarly, strains that involve an injury to the muscle-tendon complex are rarely seen in the younger athlete. When they
do occur, they may appear as pain and swelling in the substance of the muscle or at the muscle-tendon junction. Short of
violent injuries, tendon rupture is rare in the substance of the tendon. However, occasionally avulsion of the tendon bone
attachment manifests as pain with point tenderness and loss of function due to pain on use of the muscle-tendon
complex. These injuries usually involve a sudden deceleration of a forcefully contracting muscle, such as may occur
while kicking a soccer ball or striking the ground with the foot. Such an injury can cause severe groin pain due to injury of
the attachment of the rectus femora in front of the hip joint. Such injuries usually are associated with a specific forceful
event and need to be distinguished from multiple small, repetitive injuries that may lead to chronic changes at the tendon
enthesis.
Treatment
Treatment for ligamentous injuries is tailored to the type of injury, but in all instances it is designed to allow for the fibers
of the ligament to heal as close as possible to their natural length and thus to provide for subsequent stability. In mild
injuries, rest until symptoms have abated, with avoidance of subsequent stress to the ligament structures for 4 to 6 weeks
until healing is complete, is usually satisfactory. For injuries in which the ligament has been stretched but is still in
continuity (moderate injury), immobilization for several weeks, followed by protective mobilization, is usually sufficient. In
most instances of complete disruption, treatment to that for moderate sprains provides for adequate healing. The role of
remodeling and subsequent growth of ligamentous structures in children is poorly defined.
Strains of the muscle-tendon complex can usually be managed by temporary immobilization for comfort and rest without
stressing the complex for 2 to 3 weeks, followed by rehabilitation and stretching. A program of increasing resistance
exercises is exceptionally helpful for building up muscle strength. As in all sports activities, recovery from injury and
return to previous competitive levels of activity require a graduated program of increasing participation.
OVERUSE INJURIES
Once thought to be found only in elite and highly trained athletes, the effects of repetitive, subacute trauma to connective
tissues producing symptoms are seen with increasing frequency in young adults. These same symptoms are also
recognized in children who do not participate in organized sports but participate vigorously in normal play activities.
Symptoms of pain, particularly while performing an activity or immediately after an activity, are often a reflection of
microtrauma that usually occurs in the muscle-tendon complex. The symptoms themselves most likely are the result of
the inflammatory response to microdamage to the tissues caused by repetitive stress. Primary anatomic sites where this
may be seen include tendon-bone junctions and muscle-tendon junctions in the growing portion of the bone to which the
tendon attaches (apophysis or epiphysis).
Anatomy and Growth Considerations
As has already been mentioned, developing tissues of children require special consideration when analyzing the cause
and location of injury to the musculoskeletal structures. The origins of muscles near the growth apophysis of the iliac
crest, for example, or along the ischial tuberosity, can be sites of irritation or frank inflammation. Because these sites are
the anchor points for the contractile unit working distally, repetitive, forceful stresses are believed to be the initiating
events of the inflammatory response, which, in fact, is the first phase of the repair process. At the other end of the
contractile apparatus, the distal anchor point is also commonly involved in much the same manner. The insertion site of
the tendon and the bone represents a complex, graded interdigitation of fibrous tissue into the cartilage of bone by
histologically evident Sharpey fibers. These attach to the periosteum, and a direct linkage of the collagen into the cortex
through four distinct zones representing mineralization of the fibrocartilage occurs. This stepdown attachment may serve
a protective role in transmitting forces from the flexible tendon to the rigid bone structure ( 15). The blood vessels
supplying the tendon and periosteum at the attachment appear to be completely separate from those supplying the
chondroosseous structures in the apophysis and epiphysis ( 16). Therefore, the exact mechanism that initiates
inflammation as the result of microtears of the tendon near its insertion and which vessels might produce an inflammatory
response in the chondroosseous structure are unknown.
Complicating this issue in children is the fact that the “growth plate” for the tendon may be at the tendon-bone junction.
Therefore, this active area of myelogenesis and fibrogenesis leading to modeling and remodeling may be the unique
feature that leads to such notable anatomic changes as are seen in Osgood-Schlatter disease of the tibial tubercle, and
Sever's disease of the heel apophysis. These two processes are commonly classified as osteochondrosis, but they are
distinctly related to stress and inflammation. Little Leaguer's elbow, which is an irregularity occurring along the common
origin of flexors of the forearm, and Sinding-Larson-Johansson syndrome, an irritation at the inferior pole of the patella
occasionally leading to ossification within the ligament, are processes that represent a true apophysitis and are unique to
children. In some manner yet to be determined, these processes represent the results of unique injury to growing tissues
in children.
Medical Considerations
As with many other injuries to the musculoskeletal system in children, symptoms of overuse tend to be more common as
the child reaches preadolescence. Whether this represents an anatomically unstable period for the skeleton or is related
to growth or significant increase in structural demands, or both, is unclear.
Sever's Disease
In Sever's disease heel pain, originally described as an injury ( 17), is the presenting symptom during or after activities
and may be bilateral. The clinical findings of point tenderness over the posterior aspect of the os calcis is common;
rarely, this tenderness may extend onto the plantar surface or dorsally along the tendo Achillis. Micheli and Ireland found
that soccer was the sport most likely to cause the problem, followed by basketball and gymnastics ( 18). The average age
at diagnosis in their series was 11 years plus 10 months for boys and 8 years plus 8 months for girls.
Treatment follows the same plan for overuse syndromes in general and includes rest until symptoms are relieved,
followed by a gradual, progressive rehabilitation program with return to activities. Many authors, including Micheli and
Ireland, believe that the rapid growth period and increased activities during the growth spurt lead to tight tendons.
Therefore, stretching of the gastrocnemius-soleus complex and strengthening of the dorsiflexion movements of the ankle
are recommended. It should be noted that the x-ray appearance of fragmentation of the apophysis, as seen on the lateral
radiograph, probably represents normal variation in the pattern of calcification of the ossification center rather than
abnormal calcification or abnormality. The addition of a quarter-inch lift under the heel serves as a stress reducer and
may help decrease the symptoms. Rarely are nonsteroidal antiinflammatory drugs (NSAIDs) necessary or helpful.
Osgood-Schlatter Disease
First reported in 1903 simultaneously by Osgood in Boston and by Schlatter in Zurich, this common condition manifests
as pain and swelling over the proximal tibia at the site of insertion of the infrapatellar tendon. Symptoms may begin after
a direct blow or fall onto the region, or they may be present after sports activities. Most observers, including Osgood,
believed that these symptoms were representative of microevultions from the insertion of the quadriceps mechanism ( 19).
In a survey of 389 adolescent athletes, Kujola et al. found Osgood-Schlatter symptoms in 21% of those participating in
athletics, compared with only 4.5% of those in a nonathletic group ( 20).
The clinical symptoms are pain after activities or a hypersensitivity and swelling anteriorly under the knee. Physical
examination confirms tenderness and a variable increase in the prominence of the proximal tibial tubercle. Radiographs
usually show no bony abnormalities, although soft tissue swelling may be present ( Fig. 10.9). In the older adolescent or
adult, a separate, nonunited fragment may occasionally be seen. The treatment is rest, usually begun by having a brief
period of splinting. Graduated stepwise return to sports may be possible, although a basketball type of knee pad may be
helpful for preventing accidental direct trauma. Modification of normal activities of knee bending (e.g., stair climbing,
jumping), may be necessary for patients to remain asymptomatic. Contact sports may prove too difficult because of the
chance of recurrent direct trauma. Hamstring stretching and isometric quadriceps strengthening may be helpful in
rebalancing the muscle forces about the knee. The natural history of this disorder is for the symptoms to disappear with
maturity, particularly with closure of the apophyseal plate anteriorly. This often leaves a slight tibial prominence, which is
usually asymptomatic. On rare occasions, there may be a small separate ossicle in the tibial tubercle that may remain
painful into adulthood and may require excision.
FIGURE 10.9. Lateral radiograph of a 12-year-old with complaints of anterior knee pain with jumping sports and with
kneeling, showing a tibial apophysis that is slightly prominent but otherwise normal. Fragmentation of this apophysis is
not always present in patients with Osgood-Schlatter disease.
Sinding-Larson-Johansson Disease
This is not a true disease process, but merely an expression of multiple microtraumas to the infrapatellar tendon at the
knee. The pain and tenderness manifests nearer the patella than in Osgood-Schlatter disease, and radiographs in
patients with long-standing symptoms or frequent recurrent symptoms may show multiple calcifications of the inferior pole
of the patella. Treatment is the same as for Osgood-Schlatter disease, and jumping activities and sports may have to be
curtailed. Occasionally, excision of the bony ossicle is helpful in patients whose symptoms are recalcitrant to rest and
gradual rehabilitation.
Little League Elbow (Epicondylar Apophysis)
Frequent throwing activities may produce a valgus stress about the elbow that traumatizes the medial epicondylar
attachments of the origin of the flexors of the wrist and fingers. Small fibrous disruptions of this tissue lead to
inflammation and pain. This process seems to occur more commonly in 10- to 14-year-old boys and usually involves the
throwing arm only. Pain on palpation of the medial epicondyle, coupled with the history, usually indicates the diagnosis.
Radiographs may show some fragmentation and irregular ossification of the medial epicondyles. Rarely, repeated trauma
to the medial epicondyle region and associated swelling produce compression of the ulna nerve. Treatment of Little
League elbow involves rest and gradual supervised return to throwing activities. Changing the throwing style and limiting
the number of innings pitched is usually effective. Little League elbow may be best equated with tennis elbow in its
anatomic location and symptom complex. It should be distinguished from osteochondritis dissecans involving the medial
condyle or the lateral capitellum region (Panner's disease), in which irregular ossification of the joint surface occurs ( Fig.
10.10). These conditions are discussed separately later, but they are also found frequently in pitchers ( 20).
FIGURE 10.10. A 14-year-old boy with pain in the elbow after prolonged throwing activities, showing irregular ossification
of the capitellum (Panner's disease). Ossification of the lateral epicondyle may be delayed or may form in an irregular
fashion in patients with Little League elbow.
Stress Fractures
The common cause of the overuse symptom complex involving soft tissues is repetitive microstrains that produce
microscopic tissue damage. The subsequent reactive and reparative process produces the symptoms and what few
findings are present. The same process occurs with microfractures due to repetitive stresses in bone. Stress fractures in
children are less common than in adolescents or adults. Hulkko and Orava surveyed 368 patients with stress fractures
and found fewer than 10% among children younger than 16 years of age and 32% among those age 16 to 19 years ( 21).
In addition, the distribution of stress fractures is somewhat different in children. Stress fractures of the tibia represent
about 50% of the total number of stress fractures. Fractures in the spine (pars interarticularus) are more common in
children, particularly gymnasts and football players ( 23). Metatarsal stress fractures seem to be more common in
adolescents than in adults ( 22). The diagnosis requires a high degree of suspicion aided by a careful history of activities,
including a history of changes in training, training frequency, and training techniques. Localized tenderness may be
present, and plain radiographs may show periosteal new bone and thickening if the symptoms have been present for a
sufficient period—usually longer than 1 month. A bone scan may be helpful, and those patients with suspected stress
fracture should have normal plain radiographs taken.
Treatment consists of rest, avoidance of sports activities, and a carefully supervised return to activities in a stepwise
manner. Occasionally in the very symptomatic patient, a brief period of casting may be necessary to begin the healing
process. Tibial stress fractures may take longer than 6 months to heal completely, and some pars interarticular fractures
may never heal, although they may become asymptomatic. Based on the presumption that too much activity too fast as a
cause of this problem, careful training techniques may be important in both treatment and prevention. Ruben and Lonyon
showed that bone response to training loads results in increased strength for 2 weeks and then in the third week may
show decreased mineral content (24). Based on these same findings, it may be advisable to combine a 2-week, intensive
training period with at least 1 week of decreased training to allow bone strength to catch up and match muscle strength.
OSTEOCHONDROSIS AND OSTEOCHONDRITIS DISSECANS
A variety of disorders occur in children in which pain is a primary symptom and radiographs show an irregular ossification
of the underlying epiphysis or secondary center of ossification. Because most of these disorders appear to involve the
osseous and chondral portions of the bone at the articular ends, the general term osteochondrosis has been applied.
Most of these disorders have been given an eponym associated with the individual who originally described the process.
Most of these processes occur during periods of rapid growth of the skeletal system, leading some authorities to
postulate that many may be related to hormonal dynamics. Disturbed circulation has been shown to lead to avascular
necrosis in some portion of the epiphysis ( 25). Such an avascular process is clearly implicated in those entities involving
the proximal femoral epiphysis (Legg-Calvé-Perthes disease) and Kohler's disease of the tarsal navicula. As noted
previously, irregular ossification of the calcaneal apophysis appears to show a fragmented calcification, but this does not
seem to be related to true avascularity and usually proceeds to a normal closure to the ossified portion of the apophysis.
The role of trauma in the production of osteochondrosis is difficult to evaluate because of the frequency of its occurrence
in children. In addition, histologic and pathologic confirmations have not shown specific fracture patterns. Direct trauma
was suggested as an inciting mechanism by Douglas and Rang ( 26). An inflammatory response once thought to be
infection is most likely a reparative response. Bony repair of the process eventually occurs with healing, although not
always with an epiphysis that is symmetric with the normal site.
Legg-Calvé-Perthes Disease
Originally described in 1913 after roentgenograms became available, this process appears to occur in children age 4 to
11 years. It usually manifests as limping or as thigh or knee pain. More common in boys, it can be bilateral, although it
rarely has its onset in both hips simultaneously. Radiographs show variable irregularity of the capital femoral epiphysis,
subchondral fractures as evidenced by radiolucency, and eventual fragmentation of the femoral head as seen on both the
AP and frog-leg lateral radiographs ( Fig. 10.11).
FIGURE 10.11. Nine-year-old boy with Legg-Calvé-Perthes disease of the right hip, showing shortening of the femoral
neck and enlargement and fragmentation of the femoral head.
The best method of treatment remains controversial, although some form of reduced activities, including walking and
jumping, is common to all forms of treatment. Avoidance of weight bearing with crutches during the acute phase may be
helpful, and an abduction cast or brace may be effective in keeping the femoral head located under the acetabulum
(“containing” the femoral head) during the reparative process. Similarly, operative procedures designed to change the
direction of the femoral head into the acetabulum, or to change the acetabulum over the femoral head to improve
containment, have been used. The purpose of these therapies is to allow healing to occur, a process that takes 1 to 3
years depending on the age of the patient. The goal is to produce a femoral head that is as round as possible and is
contained within the acetabulum and to allow a range of motion that is as normal as possible with fit of the femoral head
in the acetabulum as good as possible. Often some flattening and enlargement of the femoral head occurs during the
healing process and may have implications for joint degeneration in the future. Because of the length of time necessary
to heal this lesion, prolonged absence from running and jumping sports may be necessary. Although this process is not
caused by sport participation per se, the diagnosis should be kept in mind when a child presents with limping or with hip,
thigh, or knee pain.
Kohler's Disease
This painful condition of childhood often manifests with pain over the dorsal medial aspect of the foot after or during
activity. It is most common in the 3- to 10-year-old age group. The characteristic finding on AP and lateral radiographs is
collapse and narrowing of the navicula with increased bone density. Over the course of 1 to 2 years, restoration of the
navicula to near-normal size occurs in most patients ( 27). During that time, the use of orthotics to support the medial side
of the foot, together with modification of sports and play activities, facilitates resolution of this benign condition. Early use
of cast immobilization may be helpful in accelerating the relief of symptoms ( 28).
Osteochondritis Dissecans
The term osteochondritis, once used for all cases of osteochondrosis, has remained the current term of choice for those
epiphyseal irregularities that involve the subchondral area immediately beneath the articular cartilage and most often the
articular cartilage itself. Osteochondritis dissecans probably represents a specialized form of osteochondrosis in which
the underlying pathology represents an area of focal avascular necrosis of the subchondral region of the supporting
articular surface with subsequent repair. An infectious etiology has not been supported in the literature, and the
inflammatory response thought to be part of the process undoubtedly represents true tissue repair. Trauma has been
suggested as a cause, but Mubarak and Carroll found that no such specific association could be made ( 29). Genetic
predisposition for a variation in the ossification patterns of normal development may play a role ( 30). There are three
primary locations where the lesions are characteristically found: the medial femoral condyle of the knee, the posterior
medial surface of the talus, and the anterior-lateral portion of the humeral capitellum. These appear radiographically
either as a radiolucent line or as an elliptical, irregular area of ossification representing an isolated osteochondral unit,
usually 1 to 2 cm in size depending on the joint involved ( Fig. 10.12).
FIGURE 10.12. Osteochondritis dissecans of the knee in a 12-year-old with intermittent right knee symptoms of pain.
Irregular ossification and radiolucency in the subchondral region of the medial condyle may be seen (arrow).
The natural history of the healing of these lesions depends in part on the age of the patient, the symptoms at the time of
presentation, and the radiographic appearance. Pappas classified this process into three categories based on age ( 31).
Category I involves young children up to the beginning of adolescence, defined as age 11 years for girls and 13 years for
boys. The epiphyseal and articular regions have a considerable amount of growth remaining at this age, and lesions are
sometimes not well developed. They occasionally are found as incidental findings on radiographs taken for other injuries.
Category II includes the adolescent age group, which is characterized by a period of rapid growth. Symptoms in this
group are likely to occur especially with frequently repeated sports activities. They may involve not only pain in the knee
joint but swelling, representing an effusion into the knee joint. Some of these patients have distinct symptoms of an
osteochondral fragment, as evidenced by locking or catching. In addition to the radiolucent area seen on routine
radiographs, improved visualization may be seen on other projections, particularly the intercondylar notch view of the
knee. Tomograms of the joint may delineate the extent of the bony involvement. Magnetic resonance imaging evaluation
often clarifies the extent of the bone and cartilaginous involvement. Category III represents the postadolescent or adult
period; these patients also may have a gradual onset of symptoms, but they are even more likely to have some degree of
separation of the fragment and formation of loose bodies. In these individuals, the symptom complex often includes
recurrent episodes of pain, swelling, and occasionally locking of the knee.
Knee Treatment
In younger children (category I), tenderness in the anterior joint line may be diagnostic of the problem of osteochondritis
dissecans. In early involvement, frank radiographic changes may be less extensive and less apparent. If there is no
history of locking and full range of motion of the joint exists, immobilization for a period of 3 to 6 weeks may eliminate the
symptoms. Afterward, modification of sports activities may be necessary along with rehabilitation of the muscles. Most of
these patients do well without further intervention. In those adolescent patients (category II) who have symptoms of long
duration and well-established radiographic lesions, immobilization may be tried. If radiographic healing does not occur or
if significant effusion or locking is present, then a more complete evaluation, including radiography, magnetic resonance
imaging, and arthroscopy is important. Arthroscopic findings of a partially separated subosteochondral fragment may
require drilling to reestablish circulation and/or pin fixation to reattach the fragment, if it is large enough. A completely
free fragment or loose body should be removed. It is much less likely for lesions in category III (adult) patients to heal,
and some form of fixation or excision, or both, is usually necessary. Restriction of athletic activities to allow
reconstruction of the bony integrity or fibrocartilaginous filling-in of the defect is an important part of the rehabilitative
process, as is rehabilitation of the muscle-tendon complex.
Ankle Treatment
The ankle is less commonly affected by osteochondritis dissecans than is the knee, and the condition is usually
somewhat more subtle in its production of symptoms. Diffuse ankle pain and swelling after physical activity may occur.
Occasional locking or snapping of the ankle is noted. Routine AP and lateral radiographs may show the lesion; however,
linear tomograms are often necessary to see the specific lesion well. Forms of therapy similar to those described for the
knee are applicable to this process.
Panner's Disease
Involvement of the anterior and lateral portions of the capitellum of the elbow may be the result of multiple, repeated
loads associated with frequent throwing ( 31). It is postulated that repeated microfractures of the supporting subchondral
region allow for collapse and subsequent separation of the cartilaginous surface. This commonly occurs in the younger
ages (categories I and II) and is more common among boys (32). It is to be distinguished from medial epicondylitis, which
is usually also caused by throwing but produces symptoms on the opposite side of the elbow. Radiographically,
fragmentation is common. In addition to the subchondral radiolucency that occurs, and particularly in long-standing
processes, loose body formation is frequent, giving rise to locking and catching symptoms with elbow motion. In the
milder forms, treatment consists of immobilization and a splint until symptoms have subsided (usually 3 to 6 weeks),
followed by moderation of sports activities, especially throwing. This may require a change in sport emphasis (e.g., giving
up the position of pitcher), at least until radiographic resolution occurs. For elbows with an effusion or a history of locking,
a magnetic resonance imaging study or arthrogram may be helpful. Arthroscopic evaluation and debridement may be
necessary both for diagnosis and for removal of loose bodies.
Reports of upper-extremity problems in young gymnasts with either Panner-like lesions in the capitellum or epiphyseal
changes in the distal radius ( 33) may demonstrate the need to be more aware of potential problems in a variety of sports
that put increased repetitive stresses on the upper extremities.
ANTERIOR PATELLA PAIN DISORDERS
The patellofemoral articulation at the knee is an exceptionally important part of locomotion and therefore plays a role in
almost all forms of sports activities. The extensor mechanism of the knee involves a complex muscle-tendon relationship
in which a sesamoid bone, the patella, facilitates the biomechanical function of active extension. It also plays an indirect
role in controlled flexion of the knee. The patella generally is guided through flexion and extension by the articular
congruity of its various facets and by the femoral condyles while riding in the lateral condylar groove. Because of the
attachment of the infrapatellar tendon into the proximal tibial apophysis and the direction of pull of the quadriceps muscle
mass, both of which are slightly lateral to the intercondylar groove, there tends to be an angular force created about the
knee. This valgus force was described by Curveilhier as a Q angle (quadriceps angle) ( 34) (Fig. 10.13). The direction of
the femoral groove helps determine the stability of the patella passively, but dynamic stability comes from both the medial
and lateral retinacular fibers that attach to the patella but also broadly into the deep fascia on the lateral and medial sides
of the proximal tibia. Any mechanical conditions that increase the Q angle will produce increased pressure during
articulation, particularly over the lateral condyle and the lateral facet of the patella. In severe malalignment problems,
especially those occurring after traumatic disruptions of the medial retinacular structures, the patella may actually
dislocate laterally.
FIGURE 10.13. The Q-angle measurement of patella-femoral-tibial alignment, as described by Cruveilhier (1791–1874).
(From Talbott JN. A biographical history of medicine: excerpts and essays on the men and their work. New York: Grune &
Stratton, 1970, with permission.)
Even though younger children and preadolescents often have increased genu valgus as part of their normal
developmental alignment pattern, anterior patellar pain and symptoms of instability are unusual. A prospective study of
children and adolescents with patellofemoral pain shows that fewer than 10% of these patients had symptoms before the
age of 13 years (35). Indeed, patellofemoral pain in younger children may represent more of a soft tissue overuse
problem, whereas in the older child or preadolescent, in whom patellar tracking problems may become more apparent,
articular cartilage may occur.
Evaluation and Treatment
Children who have suffered a specific traumatic event involving the knee, especially if it involved frank dislocation of the
patella, usually have a dramatic history and clear findings indicating injured tissue with swelling, pain, and perhaps a
laterally displaced patella. However, chronic patellofemoral problems most often manifest as diffuse anterior knee pain in
the patella without a dramatic event. These symptoms are often made worse by participation in specific sports activities
or other activities of daily living.
In younger patients, these symptoms may be difficult to elucidate, but by the time patellofemoral problems appear as a
common problem in the adolescent age group, the symptoms are better defined. Occasionally, there is a sense that the
knee gives out or catches, but this is pseudolocking and rarely represents true interarticular locking episodes. With most
patellofemoral pain problems, an effusion in the joint is rare. Point tenderness at the edge of the patella, especially on the
lateral side, is common. Actively ranging the knee through an arc of motion from extension to flexion will give the
examiner an idea of the direction of tracking of the kneecap in the groove. Evaluation of the Q angle may be helpful in
determining abnormal tracking or positioning. A valgus knee deformity may contribute to the malalignment in the older
adolescent. The side-to-side excursion of the patella when it is pushed in the extended knee may help to determine the
glide of the patella in addition to increased laxity. If pushing the patella gives the patient the sense that there is instability
or produces an increase in pain, their symptoms should be reproduced and an “apprehension sign” elicited. Subpatella
crepitus, thought to indicate softening of the cartilage of the subchondral area of the patella, is a common finding even in
the normal knee. Most patients with nontraumatic patellar pain syndrome have bilateral symptoms, although commonly
one knee is more involved than the other.
Treatment is aimed at symptomatic management by modification of the demands on the knee in the short term and
attempts at rehabilitation of the quadriceps mechanism in the long term. Reducing the demands on the knee often
involves not only modifying sports activities and gymnastics but reducing other daily activities that produce significant
knee use, such as stair climbing, hill climbing, and frequently getting up and down out of chairs. Tight hamstrings must be
stretched to reduce some of the forces across the patella. It may be advantageous to strengthen the vastus medialis
specifically to help support the medial aspect of the patella and to prevent lateral tracking. Quadriceps strengthening
should be accomplished through short-arc exercises using no more than 25 to 30 degrees of flexion to full extension in
order to minimize compressive loads on the patella. The key to successful treatment of most adolescent patellofemoral
problems is a regular and consistent dedication to this program. Elastic knee braces designed to support the patella from
the sides may be helpful in some cases. Unless there is a significant tracking problem, most patellofemoral pain
symptoms can be managed symptomatically. Patients can usually return to most sports activities in the long term. The
symptom complex may have a tendency to wax and wane over several years, but it usually responds to intermittent use
of a program of reduced activities and to increased stretching and strengthening exercises of the thigh muscle. For those
individuals with severe tracking problems, especially frank dislocation, or with such poor mechanics about the knee that
abnormal forces are being brought to bear, a surgical realignment procedure done either from above or from below the
patella may be necessary to ensure normal knee function.
SPINE AND SPORTS
General
The spine represents a complex composite of supportive elements in which the vertebral bodies, their facets, lamina, and
spinous processes are supported by ligaments and an extensive paravertebral muscle system. The growing spine has
some of the same risks for injury as an adult spine—with the added caveat that secondary centers of ossification and
growth plates exist in the vertebral bones, just as they do in immature long bones, and may be injured or affected by
external or environmental forces. It is generally accepted that younger children have proportionally longer trunks and
therefore a longer spine length than extremity length, although this proportionality changes with the attainment of
adolescence and adulthood. Also, younger children have more flexible spines, in keeping with their generalized
ligamentous flexibility as demonstrated in other joints throughout the body. The normal coronal plane alignment is
straight (assuming equal leg length), while the sagittal plane alignment shows a normal cervical lordosis, a thoracic
kyphosis, and a lumbar lordosis. Very young infants and toddlers have reduced lumbar lordosis, and juveniles in the 8- to
12-year-old age group often exhibit increased functional lordosis in the lumbar spine. These are normal variations.
In contrast to adults, back pain in normal children is rare with the exception of Scheuermann kyphosis and spondylolysis
(discussed later). Potentially more serious problems, such as fractures, infections, or tumors, should be considered when
examining the child who presents complaining primarily of back pain. Back pain with peripheral radiation of symptoms
into the lower extremities should also be taken as a potentially serious implication for neurologic abnormality. Otherwise,
children and adolescents occasionally present with back fatigue, generalized muscle pain, and discomfort that may or
may not be sports related. This is more likely to be interscapular and paravertebral. It often is associated with excessive
sports participation in much the same manner as other overuse problems. Occasionally, children and adolescents who sit
for long periods while playing a musical instrument, typing, or doing computer work present with interscapular pain that is
usually related to fixation of the shoulder muscles in order to stabilize the arms, leading to fatigue symptoms.
Trauma to the Spine
Significant injury can occur to the spine in children participating in sports; although these injuries are rare, the outcomes
can be disastrous. With closer supervision of the level of sports activities and avoidance of high-risk behaviors such as
tackling with the head in football (“spearing”), the risk of significant problems has been reduced ( 36). The two highest-risk
areas are football and gymnastics or trampoline-like activity ( 37). Significant injuries include fracture or dislocation with or
without neurologic injury. The cervical spine may be most liable to injury because of its relative lack of support. All
complaints referable to the back or spine that appear to be related to a specific injury should be given serious
consideration for a thorough evaluation.
One special circumstance related to the cervical spine and sports activities involves spinal instability at the C1-2 level in
patients with Down syndrome (trisomy 21). Instability of this specific level has been estimated to occur in 10% to 15% of
these children, although most patients are asymptomatic ( 38). Because of the asymptomatic nature of the problem,
questions have been raised about a particular need to assess children with Down syndrome who are participating in
sports. Recommendations of the American Academy of Pediatrics include the following:
1. All children with Down syndrome should be evaluated with lateral roentgenograms of the C1-2 region in flexion,
extension, and neutral position.
2. If signs of increased stability are present radiographically and neurologic symptoms are present, surgical
stabilization should be considered.
3. If radiographic instability exists and no symptoms are present, then follow-up examinations should be performed as
often as yearly or sooner, and the child should not participate in contact sports, diving, or gymnastics.
4. Because the natural history and the potential for developing radiographic signs if no instability exists, children in
whom no radiographic abnormality is seen should be examined at intervals of 2 to 3 years. In light of the low
frequency of occurrence and the very rare reported complications of participation in sports by children with Down
syndrome, these guidelines might seem restrictive, but until further natural history data and information are
forthcoming, they should be followed.
Scoliosis
Classically, scoliosis is defined as lateral bending of the spine. Because in the coronal plane the spine is usually straight,
theoretically any bending from the zero position would represent a “scoliosis,” although up to 10 degrees of angulation is
generally accepted as being within normal limits and not constituting a true scoliosis. Although scoliosis may be caused
by a wide variety of abnormalities, the most common type encountered in children who are participating in an otherwise
normal sports activity is idiopathic scoliosis. This scoliosis has an unknown cause and occurs in otherwise healthy
children. Often it appears for the first time during the adolescent growth spurt. Other causes of scoliosis, such as
neurologic abnormalities in children with cerebral palsy or congenital scoliosis in children with an underlying osseous
defect presenting from birth, occasionally are seen in children participating in sports. Although muscular imbalance is
thought to play a role in the development of scoliosis in patients with neuromuscular difficulties, the cause of idiopathic
scoliosis is not known. In the vast majority of children, small curves do not progress during the adolescent growth spurt;
however, some do, and progression is somewhat more likely in girls than in boys. There are no clinical or radiographic
indicators that can be used to predict progression, so frequent repeated examination at 6- to 8-month intervals during the
years of remaining growth are necessary to monitor potential changes indicating a progressive deformity. In spite of the
curvature of the spinal column, the spine retains its normal biomechanical integrity, so most children with scoliosis may
participate fully in all activities and are encouraged to do so to help maintain muscle strength and spinal flexibility. There
are no known activities that either increase or decrease the progression of the curve. Anatomically, the curve can
commonly be located in the thoracic region, the lumbar region, or both ( Fig. 10.14). Although the characteristic deformity
is a lateral bending of the spinal column, scoliosis is anatomically a three-dimensional deformity. Changes occur in the
sagittal plane, as seen by flattening (usually in the thoracic spine) and also by a twisting or a rotation that occurs in the
transverse plane of the body. It is the twisting that causes the apparent rib hump when the patient bends forward.
FIGURE 10.14. Adolescent idiopathic scoliosis in a 14-year-old girl as seen from the back, showing lateral bending and
deviation of the spine and trunk that give an imbalance to the trunk. This curve is in the thoracolumbar region and is
convex to the left.
The only two known effective therapeutic interventions are the use of a body brace, called a thoracolumbosacral orthosis
(TLSO), and surgery. The primary goal of brace therapy is to control the curve while it is still mild to moderate and
prevent it from becoming severe. Children must demonstrate a progression of the curve to a significant level and must
have growth remaining for the brace to be effective. Brace wearing is done most of the day and night during the
remaining portion of the growth spurt, which may involve as much as 1 or 2 years. Full participation in sports may occur
during brace treatment. In many instances, participation can occur with the brace on, but if this interferes with the sport
activity or is an endangerment to other participants, sports activities may take place without the brace. This is especially
true for competitive sports, for which the brace may be removed during practice and for competitions without any
detrimental effects. In those children who require surgery, there is usually a period of 8 months to 1 year after the surgery
during which sports participation is not allowed or is limited. After the spine fusion is complete, the patient may again
return to most sports activities. Although flexibility may be mildly disturbed in those who undergo surgery, most return to
normal activities without limitations.
Kyphosis
The term kyphosis is often used in the pathologic sense and means an increased bending in the sagittal plane. Although
normal kyphosis exists in the thoracic spine, an increase in this bending (hyperkyphosis) may produce a noticeable
deformity. The presence of “poor posture” is often a concern of the parents of teenagers. It is usually caused by
hyperkyphosis that is flexible, often positionally related, and fully correctable with an effort on the part of the patient to sit
or stand in an erect manner. This is a common teenage habitus with no known consequences for permanent deformity
despite parental concerns. The condition is also known as “functional round back.” It usually responds to careful
encouragement of the adolescent and improves with maturation. Occasionally, extension exercises of the paravertebral
muscles may be helpful, particularly in nonathletic individuals, but sports participation should be encouraged.
Scheuermann Kyphosis
Scheuermann kyphosis represents a hyperkyphosis or excessive kyphosis, usually in the thoracic region, that involves
actual structural changes in the endplates of the vertebral bodies. The cause is unknown, although its occurrence seems
to be limited to the growing spine. There is usually an associated wedging of the vertebrae ( Fig. 10.15). The deformity
may be quite noticeable cosmetically. Most commonly it is associated with back pain, particularly during activities. If the
symptom complex is mild and only occasional and the deformity is not very noticeable, a program of extension exercises
and a moderation of activities may manage symptoms. At the completion of growth, the symptoms usually disappear
spontaneously, probably associated with closure of the growth plate. In those patients who have a more significant
deformity and whose symptoms are fairly constant during the day, the best management scheme may be with a
specialized TLSO for a period of 1 to 2 years. Again, the symptoms usually disappear fairly rapidly with bracing and the
deformity is at least partially corrected in many cases. In those with severe deformities frequently accompanied by
marked symptoms, it may be necessary to perform surgical stabilization for improvement. Sports participation is
encouraged for all patients except those who have recently undergone surgical correction. Otherwise, the long-term
outcome for patients with Scheuermann kyphosis is satisfactory.
FIGURE 10.15. Scheuermann kyphosis in an 11-year-old boy with back pain and “poor posture.” In addition to the
kyphosis, endplate irregularities (Schmorl nodes) in the lower vertebral bodies and wedging of the vertebrae in the upper
thoracic region may be seen.
Anatomic disturbance of the portion of the vertebral bodies located posteriorly between the superior and inferior facets
may produce structural and symptomatic problems in some patients. This area, known as the pars interarticularis, may
show a defect on AP, lateral, or oblique radiographs of the lumbar spine. The defect often is bilateral, although on
occasion it may be seen on one side only. These findings are noted usually after the child or adolescent has presented
with midline low back pain; occasionally symptoms of posterior or lateral thigh pain also accompany the back pain. This
problem is not found in children younger than 4 years of age. It has an incidence of 4% at age 6 years and 6% in adults
(39). Spondylolysis refers to the mere presence of the defect in the pars interarticularis area, while spondylolisthesis
refers to a slippage or forward movement of one vertebral body onto another. The most common level of involvement is
the L5 vertebra with forward slipping of the body of L5 on S1 ( Fig. 10.16). Occasionally, similar involvement is seen also
at the L4 or L3 level. The slipping process is gradual and may exist in a small portion of the adult population who are
unaware that they have spondylolisthesis. Therefore, not all instances of pars interarticular defect are symptomatic.
Trauma may play a role in the etiology of this problem, because there is an increased incidence among gymnasts and
among interior linemen in professional football.
FIGURE 10.16. Spondylolisthesis of L5 on S1 (sacrum) in a 16-year-old with low back pain that initially occurred only
after sports activities but became more constant with time. Lateral radiographs show forward slipping of the vertebral
body of L5 on S1 (sacrum). The arrow marks the defect in the pars interarticularis.
The clinical presentation, in addition to the presence of back pain, may include evidence of hamstring tightness or a
limitation in motion on a straight leg raising test. Flattening of the lumbosacral region on standing may suggest
displacement and the presence of spondylolisthesis. X-ray studies, as noted previously, often show a defect in the pars
interarticularis and will clearly show the presence of slippage if it is occurring. Treatment is tailored to the specific
problem at the time of presentation. If the onset is acute and symptoms seem related to a specific activity, the
radiographs may show a well-defined defect in the pars and a bone scan may show evidence of increased activity in this
region. In such a patient, an acute injury may be assumed; it may respond to the application of a lumbar brace (modified
anterior-opening TLSO). The healing of such defects has been described ( 40). Other children with a more long-standing
symptom complex or a more notable radiographic defect may respond symptomatically to the application of a brace for a
3- to 6-month period. If they remain asymptomatic, they may undergo a rehabilitation process that includes hamstring
stretching and abdominal muscle strengthening. They may return on a gradual basis to sports activities. They should be
monitored symptomatically, because very mild spondylolisthesis rarely progresses. For those with more severe slippage
or documented radiographic progression, surgical stabilization and fusion may be necessary. As with rehabilitation from
other spinal surgeries, there is an excellent chance for return to most sports play and for full participation in normal
activities once satisfactory fusion has been obtained (8 months to 1 year).
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11 The Aging Athlete
11
THE AGING ATHLETE

ROBERT E. LEACH
Elements of Athletic Performance

Age-Related Tissue and Organ Changes
Patterns of Injury
Muscle Strains
Tendon Injuries
Joint Strain
Articular Cartilage Problems
Rehabilitation
Climatic Conditions
Chapter References
The proposed title for this chapter was “The Geriatric Age Athlete.” Geriatrics is defined as the care and study of old age.
Since I personally do not know the exact definition of “old age,” I prefer to call this section “The Aging Athlete.” The term
“Master's Age athlete” might seem more appropriate, but in one sport (e.g., women's gymnastics) the Master's Age may
start at 25 years while in others it begins at age 40 or even older. This chapter is largely concerned with those athletes in
the over-60 age group, but the discussion is applicable to many of those between 30 and 60 years of age.
“I am 70 years old, look 60, feel 50, and beat a 40-year-old in tennis yesterday.”
Great! More power to you. But if you think your body is the same as it was when you were 40, you either were in terrible
shape when you were 40 and have been working out every day since then, or you are successfully ignoring what is going
on in your own body.
The optimistic part of the above statement is that the 70-year-old is active, is playing sports, and feels great. Every day
there are more people age 60 years and over who are doing just that. We all know the statistics. People are living longer.
Roughly 20% of the U.S. population will be 60 years of age or older in the year 2020. That is potentially 60 million
people. Because an active older population exists, we now have Master's national competitions in sports such as tennis,
golf, track and field, swimming, volleyball, and rowing, as well as age-related leagues in basketball, softball, hockey, and
soccer.
What are some reasons for this increased athleticism on the part of the Master's Age group? People 60 years old and
older have more time to engage in physical pursuits that are pleasurable. Most stay physically active because of the
enjoyment this provides. In later years many have the financial resources to enjoy more activities after having previously
worked to pay off mortgages and educate children. Some stay active primarily to maintain health. More people are aware
from various medical studies that the segment of the population who stay active and in good cardiovascular shape live
longer, have less illness, and use fewer health dollars on hospitalization ( 1,2,3,4 and 5). There may be many and diverse
reasons for being physically energetic in the later years.
However, there are certain factors that must be understood by all health care professionals who care for these older
athletes. Treatment and rehabilitation may have to be tailored to certain specific demands and capabilities. The over-60
athlete is different from an athletic 40-year-old, and health care providers must recognize and deal with this fact ( 6).
Prevention of injuries may be of even greater importance in this age group than in the younger age group, because the
sequelae of injury may be more difficult to manage and longer-lasting in the older patient.
ELEMENTS OF ATHLETIC PERFORMANCE
Let us briefly examine certain elements of athletic performance such as speed, quickness, strength, agility, balance,
coordination, endurance, mental toughness, and experience. On that list it is obvious that only in the last two elements is
it possible that the older athlete may gain some edge. Even then, if the older athlete has not been competing at a high
level, mental toughness is not equal to what it once was, although it does have the possibility of staying the same.
Quickness and speed are definitely lost with age, although people who train continuously may lose these elements more
slowly than those who do not. Strength gradually declines, but it appears to be one aspect that can be relatively
maintained through much of life, provided that the athlete works at improving strength by doing resistance exercises
(7,8). Agility and balance are often related to the strength of certain muscle groups, and frequent use of these muscle
groups helps to maintain both. As for coordination, these elements can be maintained to a greater degree if they are
continually practiced. Endurance remains reasonably constant over time, with a gradual slow decline that is accentuated
rapidly if training is stopped.
AGE-RELATED TISSUE AND ORGAN CHANGES
As they say, “Do you want the good news or the bad news first?”
There are major changes in both the cardiac and respiratory systems with age. Between age 25 and age 85, there is a
gradual decline of 30% of the resting stroke volume of the heart and an accompanying decline in the maximum heart
rate, which together produce a reduced cardiac output. The ability of the heart to return to a baseline rate after exercise
is slowed over the years. The lungs show a gradual decrease in maximal oxygen consumption (V O 2max), an increase in
tidal volume, an increase in residual volume, and a decrease in lung compliance. Each of these changes in the
cardiorespiratory systems has negative effects on athletic performance.
However, with cardiovascular training done under supervision, the function of both heart and lungs can be improved. The
rate of decline in oxygen consumption can be slowed significantly by endurance training, and both cardiac output and
maximum heart rate can be increased to more than the expected age result with training ( 9). This ability to positively
affect both heart and lung performance can be seen even at older ages in persons without previous training.
The changes that occur in the connective tissue with aging include a decrease in elastin and a thickening of the
basement membrane. The collagen cross-links increase, which makes the collagen stiffer. Because ligaments and
tendons are composed primarily of collagen, this means that both ligaments and tendons become stiffer and therefore
weaker. Woo et al. found that by 50 years of age the linear stiffness and ultimate load of the anterior cruciate ligament is
markedly decreased (10). If all knee and ankle ligaments had similar findings, we might be facing a major problem.
Fortunately, those ligaments that are subject to continued stress seem to retain their strength better than the anterior
cruciate, which is only intermittently stressed. Tendons are constantly stressed in athletic performance and are subject to
chronic and acute problems in the older athlete. Degenerative changes that occur within the tendon may lead to acute
rupture or to development of tendinosis as a result of repetitive use in various sports. Other tissues largely composed of
collagen, such as joint capsules, are subject to the same structural damage. These changes may manifest primarily by a
decrease in joint motion, particularly after injury, surgery, or disuse.
Some of the tendon changes with aging can be improved. Connective tissue does not age at the same rate from person
to person. Genetic inheritance and continued activity influence the situation. People who were considered loose jointed
as young adults may maintain a higher degree of mobility with activities as they grow older. Even those who were more
tight jointed can increase their capsular range of motion (ROM) and musculotendinous flexibility, as shown by the work of
Taylor et al. (11). They demonstrated that slow sustained stretching can increase the flexibility of the Achilles,
hamstrings, adductors, and other muscle-tendon units ( Fig. 11.1). Munns' work demonstrated that, after 12 weeks of
exercise and dance, subjects age 65 to 88 years showed significant improvement in motion of the ankle, knee, wrist,
shoulder, and neck when compared with controls ( 12). Aging is inevitable, but not all connective tissue need deteriorate,
and certainly not everybody's tissue becomes stiffer at the same rate.
FIGURE 11.1. Hamstring stretch.
In humans, muscles show a decreased fiber heterogeneity and some functional denervation with age. Protein synthesis
is decreased, which leads to decreased muscle mass and a decrease in strength ( 13). There are concomitant decreases
in speed of movement and in power that are detrimental to athletic performance.
Much of this change was originally thought to be inevitable, because the early studies involved mainly aging runners who
had not performed progressive resistance exercises. They did not maintain their muscle strength at high levels. Later
studies showed that strength can be maintained at remarkable levels and even gained late in life ( 14). The excellent work
done by Fiatarone et al. on patients in their late eighties and early nineties demonstrated that strength of the quadriceps
muscle could be improved to a mean gain of 175% when the subject performed regular resistance exercises over a
12-week period (15). These strength gains produced functional improvement, including the ability to rise out of a chair
without pushing off with the hands. Stair climbing was made easier, and balance when walking a straight line became
better.
Some other tissue changes that occur with age are more difficult to influence. The knee meniscus gradually loses its
water content; some cellular death and decreased proteoglycan production occurs, and there are changes at the
meniscocapsular junction. Each of these changes makes the meniscus more likely to tear. The intervertebral disc loses
some of its water content, and there is a decrease in cellularity with changes in the matrix. This makes the disc softer and
less resilient with increasing age. Joint articular cartilage may show some cellular death and changes in the matrix with
proteoglycan loss. There may be cracking and fissuring of the joint surface, and in many patients this leads to major
osteoarthritic changes. However, the majority of the population does not have major joint osteoarthritis, so without prior
joint injury there is not an inevitable loss of articular cartilage function.
Bone loss, particularly in postmenopausal women, is a severe public health problem. Although this happens also in men,
it occurs at a later age and to a lesser degree. Physical activity, particularly weight-bearing and resistance exercise,
helps to decrease the bone loss of postmenopausal women. Activity at early ages for both men and women may help to
drive calcium phosphate into the skeleton, and this early mineralization may provide a buffer that is helpful in later life,
when the expected loss of bone from nontreated postmenopausal osteoporosis in women may occur.
Taking all of these body changes into account, it is recognized that the process of aging poses some risk for the athletic
population. However, an active lifestyle and physical fitness promote many positive changes in the tissues and are good
for general health and longevity ( 16). Health care professionals must learn how to prevent injuries in older athletes and
keep them active. When injuries do occur, they must recognize those treatment options that are most appropriate for this
particular population group.
PATTERNS OF INJURY
Four basic areas of injury are frequently seen in the older athlete: muscle strains (the most common type) and problems
with the tendons, joint capsules, and articular cartilage. With tendons, the most likely diagnostic possibilities are chronic
tendinosis and acute or chronic rupture. The joint capsule is most likely to be injured by inadvertent excess joint motion.
The articular cartilage can be affected either by a primary problem such as osteoarthritis or, as is highly likely with an
athletic population, by a previous injury to the joint ( Fig. 11.2).
FIGURE 11.2. Degenerative arthritis of the knee 18 years after meniscectomy.
Muscle Strains
This group of injuries can be divided in those acute muscle strains that are caused by a single traumatic episode and
those more chronic occurrences, such as delayed-onset muscle soreness, that happen when a muscle is subjected to
greater stress than it has normally been used to. Any muscle group can be involved depending on the associated athletic
activity, but the most common muscles causing problems for older athletes are those of the back and abdomen, the
hamstrings, and the quadriceps. Prevention of these muscle problems is very important. With age, there is a tendency for
people to use their muscles less, and they lose strength and endurance. People who are engaging or want to engage in
athletic activity should strengthen the appropriate muscle groups. We often think of improving our cardiovascular
conditioning for sports, but it is also essential to improve muscle strength in order to continue playing sports.
Maintenance of muscle strength benefits performance and is protective to the muscles and the attached tendons, as well
as the ligaments and joints of the extremity, because the strengthened muscles help to absorb energy.
The treatment of acute muscle strains in older adults is not dissimilar to that in younger persons. There is a tendency on
the part of the older athlete to emphasize rest, but this should really be only for a day or two. After that time, as with a
younger person, a program of gentle stretching should be started, staying within the limits of pain and then moving on to
the usual active strengthening of the muscle. One worry is that active people will return to sport too quickly. An older
person who has reduced muscle strength and then suffers an acute strain that causes further weakening may start from a
lower level of strength than originally. This might cause a predilection for repeated injury. Regaining athletic normal
strength is very important.
Tendon Injuries
Both tendinosis and acute or chronic rupture of tendons are common in people in the 35- to 55-year-old age range. After
age 55, there is a diminution in these problems that may be related to decreased use and or to less stress applied to the
muscle-tendon unit. In the older age group, it seems as if the weaker muscles give before the tendons do; this may be
reasonable because it is easier to correct strained muscles than to repair damaged tendons.
With a chronically afflicted tendon, a definitive diagnosis and treatment are essential not only to decrease pain and allow
the person to stay active but also so that measures may be instituted to decrease the possibility of rupture of the tendon.
Common areas of tendon problems in older athletes include the Achilles, the rotator cuff, the wrist extensors at the elbow,
and, to a lesser extent, the thigh adductors. The pattern of pain is the same as in the younger athlete, although there is a
tendency on the part of the older athlete to downplay pain and to say that the situation is occurring because he or she is
older. We must make patients realize that chronic pain that is exacerbated by activity and does not go away is important
whether one is 32, 48, or 66 years old. Achilles tendon and rotator cuff problems not only involve the tendon but also
lead to weakening of the attached muscles. These two areas are notorious for progressing to chronic tendon rupture or
an acute rupture superimposed on a degenerated tendon.
With rest the symptomatology usually decreases, but adequate rest is about 6 weeks. By rest, I mean abstaining from the
inciting activity. In some instances this may be enough to cause tendon healing, but nature may be aided by guided
stress—that is, by using the muscles that are attached to the tendon. I recommend that patients start doing progressive
resistance exercises at very low resistance levels and gradually increase the repetitions. As repetitions increase without
pain to a reasonable level, the patient gradually increases the resistance. The concept is the gradual increase in stress
will help the tendon repair itself. Although this happens in many instances, in some cases it does not occur and more
aggressive treatment (e.g., surgery) is needed.
The role of steroid injections and nonsteroidal antiinflammatory medications (NSAIDs) must be explored. The NSAIDs are
helpful in relieving pain and are useful particularly as a means of decreasing acute pain. When acute pain has been
alleviated, appropriate physical therapy may be started. Care must be taken in returning the patient to athletic activity
because the NSAIDs may mask pain. I believe it is appropriate to use NSAIDs to decrease pain or to allow someone to
play with a condition that is not very painful and in which the pain is not increasing. However, the use of medication to
mask pain that is gradually increasing with the same activity is potentially dangerous.
With regard to injecting the shoulder for rotator cuff disease or the elbow for tennis elbow, I prefer to avoid steroid
injections whenever possible. A variety of other therapies and modalities may be used to decrease pain, particularly
those that are proactive. If a condition continues to be painful, the painful area may be injected in acute tennis elbow or
rotator cuff tendinitis. However, in all such instances when a steroid is injected into or near a painful tendon, I tell the
patient that for a period of 12 days the tendon is going to be weaker than usual and that he or she must not return to
athletic activity during that period. Then the usual measures to increase muscle strength are started in an attempt to
stimulate tendon repair. I have injected patients several times for the same condition, but my personal rule is not to inject
more than twice in a 2- to 3-month period. In my opinion, people who have had multiple injections into an area of
diseased tendon and who then subject it to the stress of athletic activity are at increased risk for rupture.
Joint Strain
Joint capsular strains may occur as the result of doing a usual activity repetitively or, more commonly, as a result of doing
an unaccustomed activity, particularly during the early phases of taking up a new sport. This is commonly seen in the
shoulder in sports such as tennis, swimming, canoeing, and rock climbing. It often happens when an older athlete in
reasonably good physical condition takes up a new sport and performs it vigorously early on, without having worked into
shape for that particular sport. It may also happen when someone who is playing a sport forgets to do the usual warmup
and pursues the activity more vigorously than usual. It is more likely in a competitive situation than when the person is
simply having fun and would back off when a problem began to develop. Joint capsular strains may be difficult to
differentiate from strains of the muscle surrounding the joint. Usually, the differential diagnosis can be made because it is
the extremes of motion that are painful and the tenderness is located directly over the joint capsule. The basic treatment
is rest from the offending activity with the possible use of NSAIDs, followed by appropriate exercises to regain a full
ROM.
In older athletic patients who have performed a particular sport for a long time and in some people who have chronic
injury, some of the ROM of the knee, shoulder, or hip may be lost. When the athlete then tries to perform a physical
activity that requires a full ROM, pain or tearing of the capsular tissues may be experienced. Afterward, it may be difficult
to regain a full ROM, and sometimes one is not exactly sure what the present full ROM should be. A history of the
situation before the injury helps, as does looking at the ROM on the normal side. With any joint extremity injury, the
muscles gradually become weaker, so as the patient is regaining ROM he or she must also strengthen the muscles so
that they can be protective of the joint in the future. Whenever a joint is being rehabilitated, work should be done on both
the protagonist and the antagonist muscles; otherwise, a particular group of muscles may become very strong while
others are proportionately weaker, possibly causing problems in the future. For example, the internal rotators in tennis
players may become strong and may cause a small internal rotation contracture of the shoulder, resulting in problems
playing tennis or other sports ( Fig. 11.3). With the multiplicity of athletic activities now available, many older people are
involved in several sports or take up a new sport after age 50; in addition, they may become so involved in one sport that
musculoskeletal problems result.
FIGURE 11.3. Stretching shoulder, showing tight medial capsule from tennis.
Articular Cartilage Problems
With aging there is a gradual increase in the number of people who have osteoarthritis, particularly of the hip and knee.
Osteoarthritis can occur de novo or in response to previous problems. This is particularly so with the knee, a joint that
may become symptomatic after age 50, 60, or 70 because of previously sustained injuries or surgery, or both. In a
common scenario, someone who had a medial meniscectomy as a young person starts to have degenerative symptoms
20 to 30 years later (see Fig. 11.2). This can be devastating in terms of athletic activity. In many an anterior cruciate
ligament can be successfully reconstructed to allow the athlete to return to full activity, but the future course is uncertain.
Although the knee has been mechanically stabilized, the reconstructed cruciate is not the same as nature's own. The
knee motion may not be precisely the same, and this may lead to problems in the future. In any event, the number of
patients who come in with knee or hip problems and want to continue athletic activities is great, and health care
professionals must be prepared to handle this situation.
A physical examination is done to establish a base with regard to motion and muscle strength, and appropriate x-ray
studies are obtained. In most instances, the degenerative process has not advanced enough to require a total knee or
hip replacement. Counseling against certain activities and allowing others may be helpful. This is not always simple. A
person who is a good tennis player but has a bad knee may seem a good bet to become a bike rider or a swimmer.
However, the patient may find these latter sports boring or may simply be unable to do them well. One tries to continue
the patient in the same long-performed sport.
The physical modalities employed for therapy are the usual ones. Attempts should be made to maintain or increase the
joint ROM and to strengthen the muscles around the affected joint. NSAIDs may be used judiciously. I tell patients that if
they use an NSAID and play their sport, they should not have increased pain the next morning. If pain does not improve
over the course of the day to its status before use of the NSAID and participation in the sport, they have pushed too hard.
It is difficult to make patients understand that these medications are not curative but simply keep inflammation down and
decrease pain. They must realize that the degenerative changes in the joint will continue.
The question as to whether to inject corticosteroids into an osteoarthritic joint is an interesting one. Years ago I made a
simple therapeutic decision. I understand that in acute synovitis caused by rheumatoid arthritis the intraarticular injection
of steroids is helpful. I recognize that many people with osteoarthritis have synovitis secondary to debris, and a steroid
injection may help these people for a period of time. However, I will not use an injection as a means of allowing people to
continue playing sports. I believe that in all likelihood both the action of the steroid and the increased physical activity
that it may allow will cause an exacerbation of the primary problem, which may lead to an earlier severe deterioration of
the joint articular cartilage. Each physician must come to terms with what he or she thinks is reasonable with regard to
intraarticular steroid injections.
There are so many people in the 60+ age group with symptomatic osteoarthritis of the knee that doctors feel great
pressure to find a solution. One currently popular remedy, particularly in the lay press, is the use of
viscosupplementation. Basically, this is the injection of some type of hyaluronan into the symptomatic joint in a series of
three to five injections given once a week ( 17).
Much literature is available, and even more unsubstantiated claims are put forth by various manufacturers and lay
writers. At this point, prevailing medical opinion, including that of the American College of Rheumatology and the
American Academy of Orthopaedic Surgeons, states that the injections appear to be safe and as effective in reducing
pain as acetaminophen, but there is no evidence that they are chondral protective or increase the synthesis of articular
cartilage. Until better double-blind, long-term studies are performed, this particular treatment will continue to be
controversial.
With regard to damaged joints, it is helpful to have the patient work on strengthening the muscles, both for power and for
endurance. Appropriate physical activity and maintenance of joint ROM is important in people who have osteoarthritis.
Patients must learn to warm up before playing and to follow that with some gentle stretching of the involved joint and the
muscle-tendon units that cross it. In some instances it is helpful to apply cold to an involved joint after physical activity.
Heat is helpful in decreasing muscle pain or soreness after activity, but I find its use overrated with regard to joint
problems.
As noted later, people with medial degenerative joint disease may benefit from the use of an unloading knee brace.
There does come a time when symptoms increase and function decreases. In an active person, the question of total joint
replacement must be raised at that point. This should be considered primarily to reduce pain, for which it has been
proven effective. However, some people who successfully have a reduction in pain want to continue to be athletic. The
decision as to whether one should play a sport after a total joint replacement can be reached only by agreement of both
patient and doctor. The patient with a total joint replacement must recognize that by playing sports the odds are that the
joint will fail at an earlier time than otherwise. However, patients have a right to make that decision, provided they are
properly informed. Patients who want to continue sports activities should inform their physicians of that fact before any
surgery, so that the surgeon can adequately explain the risks. It goes without saying that patients in this category must
work extra hard to increase their muscle strength in the hope that it will have some protective effect.
Nonsteroidal Antiinflammatory Drugs
The easy availability of NSAIDs has distinct pluses and one definite minus. On the plus side, many people who have
chronic but relatively minor musculoskeletal problems can continue to be active and to enjoy sports. The potential
complications of gastrointestinal distress and bleeding are probably outweighed by the benefits of decreasing pain and
pleasure through activity. However, the use of these medications may cause some people to overuse arthritic joints,
which may hasten the deterioration of a previously damaged joint. The alternatives to medication use are to have an
early operation or to stop the sport. If a person is able to play a sport by taking NSAIDs, neither of these choices seem
reasonable. That decision is best left to the patient.
That there is some abuse of these medications is obvious from the many people who have complications. The older
athlete must recognize that the inability to control pain with NSAIDs is clearly a bad sign. If he or she is having to
increase the number of NSAID doses taken for the same amount of physical activity, that is a bad sign. If there are
physical signs such as swelling, decreased motion, or increased limping while one is taking NSAIDs, that is also a bad
sign. When these signs occur, it is time to reexamine the use of medications and return to a physician to see about an
alternate plan.
Because many Master's Age athletes take NSAIDs and some undergo surgical procedures, it is essential that the doctor
note these facts while taking a history. Many older athletes have become accustomed to easy bruising as a result of
taking aspirin or NSAIDs and forget to mention that they take those medications. Patients who are about to undergo
surgery should be taken off these medications for 7 to 10 days before the surgical procedure.
Bracing
Some years ago my doubles partner and I played in the finals of the senior tournament against an opponent who had a
brace on his right knee and a counterforce strap around his right forearm and had been seen applying ice to his right
shoulder. Yet, he played exceedingly well and only my partner's pinpoint accuracy brought us through. Senior players
often use braces and other musculoskeletal aids to continue playing sports. If the physician believes that use of such a
device could help the patient, it may be tried; if the patient thinks that it does help, it should be continued.
Knee braces used to unload the medial joint surface are effective in decreasing pain particularly in those patients who
have medial compartment osteoarthritis. Many people who continue to be athletically active use such braces. The
unloading brace must be properly prescribed and fitted. For many Master's Age athletes it prolongs sports activity. If pain
gradually increases during use of the brace, it is time for new medical appraisal. There is always the question as to
whether it is better to brace an osteoarthritic knee or to carry out an operation such as an osteotomy or knee resurfacing
procedure. This is an individual consideration that can be handled only by the doctor and the individual patient.
Many active people use counterforce braces for tennis elbow, patellar tendonitis, or adductor strains. Doctors and
patients alike believe that they are effective in decreasing pain. So long as the patient can continue to play without
increasing pain or a reduced status the next morning, the use of these braces should be encouraged. If pain gradually
increases and the level of performance goes down, then the situation should be reconsidered. Neoprene sleeves used as
a type of counterforce brace around the thigh for hamstring strains or adductor injuries are effective in allowing people to
play with less pain. Another area in which older athletes often have chronic problems is the ankle. Many have mildly
unstable ankles that can be helped with ankle supports. It is often a question of finding a particular support that is helpful;
if the device is effective, it solves the question. If it is not, secondary surgery should be considered. The older athlete has
fewer years ahead to play sports, and anything that can be done to relieve pain and allow activity is reasonable to try.
In the Master's Age athlete, these adjuncts to treatment may be considered more often than in a younger athlete, for
whom aggressive rehabilitation and even early surgery may come more quickly to mind. The use of a groin strap or ankle
brace that allows senior players to remain active while continuing rehabilitation makes a huge difference in their outlook.
Few Master's Age athletes have trainers or therapists who are caring for them on a daily basis, and the use of some
appliance may help them in getting through these injuries and in dealing with chronic conditions.
Surgery
With the high incidence of hip fractures in elderly people and the number of total hip and knee replacements that are
performed on people older than 50 years of age, orthopaedic surgeons are accustomed to doing surgery on older people.
The concept of performing a rotator cuff repair or debridement or a meniscectomy on a 60-year-old athletic person is not
a real problem. The caveats of doing surgery on the older athlete are the same as those for the younger athlete. The
physician must be aware of prior medical problems that will influence the surgery, postoperative care, and rehabilitation.
The taking of a detailed history from an athletic aged person is just as important as it is for an infirm elderly accident
victim. Many people in the over-60 age group are taking medications. Taking antihypertension medications is
exceedingly common, and to many patients this is not different from taking morning vitamin pills. Aspirin taken for heart
prophylaxis or NSAIDs taken for muscular aches and pains are ubiquitous in Master's Age athletes and pose a potential
problem with bleeding from operative sites.
The condition of the tissues being operated on or through is paramount in any surgical procedure. In the younger athlete
there is usually little to worry about, but in the older athlete this may be a problem. A 67-year-old with a rotator cuff
rupture who has had previous symptoms may have tissues of different quality than those of a 38-year-old with an acute
rupture of the rotator cuff. This does not mean that surgery cannot be performed on the older patient, but the surgeon
must be prepared for tissue problems. The patient too must be prepared for all eventualities. A 65-year-old patient being
operated on for the primary purpose of being restored to athletic condition must be aware of what one can logically
expect from a particular operation. A surgeon may remove the torn posterior horn of the medial meniscus or repair a
ruptured Achilles tendon in a 62-year-old athletic person with the expectation of a good result, but both patient and
physician must understand what constitutes a good result in that particular person.
There is a question in older athletes as to what operations can be performed with legitimate expectations of returning the
patient to certain sports activities. Many tennis players, golfers, and skiers have knee and hip problems that necessitate
a total joint replacement. Virtually all surgeons would say that a total joint replacement is not aimed at returning the
patient to participation in such sports. Yet, participation may be essential in the life of that particular person. There is a
special obligation on the part of the surgeon to explain to the athletic patient what the possible outcomes are, both good
and bad, after a total joint replacement and resumption of an athletic life. The possibility and even probability that the
prosthetic device may become loose earlier than one would expect in a nonathletic patient must be explained and
understood. There is equally an obligation on the part of the patient to listen, understand, and then make a decision
based on the doctor's advice and his or her own desires.
Rehabilitation may be the biggest problem for both the surgeon and the patient. The loss of muscle mass and strength as
a consequence of long-standing pain in a joint means that intensive and long-term physical therapy will be essential. The
relief from pain will ease this therapy, but the patient must understand before the operation that rehabilitation is likely to
be a long, somewhat slow, gradually improving process. Because of chronic pain, muscle strength may have fallen below
a critical level that impairs not only athletic activity but normal activities; gains in strength through rehabilitation may
produce some striking rewards for these patients.
It does not make sense to withhold surgical procedures from older athletic patients when such surgeries might routinely
be performed on younger athletic patients—provided that the procedure can be properly accomplished and the patient
can be depended on to complete rehabilitation after surgery. To spend an extended period on nonoperative treatment of
a problem that might be treated operatively in a younger patient does not seem fair to the older athlete. If there is no
operative procedure that will help the Master's Age athlete return to activities, then so be it. To withhold a procedure
simply because the patient is older is unreasonable.
REHABILITATION
Rehabilitation of the Master's Age athlete presents several unique problems and perhaps some advantages. It is
probable that many of these athletes have more time to spend on rehabilitation than do their 25- to 55-year-old
counterparts. They may be more focused and more likely to follow instructions than younger age athletes are. If the
rehabilitation setting includes other Master's Age athletes, there is a possibility that the social interaction will be good and
the patients will be encouraged to work even harder. Having had prior experience with other injuries, older patients may
follow instructions to the letter and not return to activity too quickly. The Master's Age athlete realizes that rehabilitation is
important and vital to his or her ability to return to having fun.
The other side of the coin is that such patients may miss the activity they have been doing and for that reason may focus
on it too much. This can make interactions among doctor, patient, and rehabilitation specialists difficult. In addition, the
Master's Age athlete may start a rehabilitation program with less muscle mass and less flexibility in the joints and muscle
tendon units.
For years muscle strength in older persons was ignored or it was accepted that Master's Age athletes were weak and
would stay that way. Recent work has shown that muscle strength in older individuals can be improved markedly—not to
the levels of younger age athletes, but to good levels ( Fig. 11.4 and Fig. 11.5).
FIGURE 11.4. Back extension exercise.
FIGURE 11.5. Partial sit-up for abdominal muscles.
Muscle strength is vital not only to the athletic prowess of these older individuals but to their ability to function well in life
and avoid injury caused by falling. The older athlete may be getting by with decreased muscle strength even as he or she
continues to participate in tennis, golf, or skiing. Previous injuries may have caused decreased ROM of the joint, resulting
in muscle strength that is decreased but still allows the individual to play at a certain level. If another problem arises
causing further pain and decreased activity, muscle strength may then fall below the level required for athletic function
and may result in a decrease in activities of daily living. Thus, muscle strength becomes a main arbiter of the ability to
play sports.
Programs to increase muscle strength in the older athlete must be precise. Many older athletes need to start exercising
at lower levels of resistance, and these levels must be established at the beginning of treatment. Realistic expectations
must be set. Usually, one begins with low weights and gradually increases the repetitions; increments of weight are
increased more slowly than in the younger age group. The weight increases may be on the order of 1 to 2 pounds rather
than the 5- to 10-pound increments often used for younger athletes.
The established ROM of the joint being exercised must be considered. In an arthritic but functioning knee joint with a loss
of 7 degrees of full extension, it would be harder to increase quadriceps strength ( Fig. 11.6). The inability to gain full
extension does not allow the muscle to develop maximal tension. A painful joint may make it difficult for the doctor or
therapist to find a way of increasing strength while not increasing pain, but stratagems must be devised to allow therapy
to continue.
FIGURE 11.6. Knee press for knee extensors.
The use of rubber tubing in various lengths and tensile strengths is helpful for strength training in the older athlete. The
athlete can carry the tubing around, find a place to hook it up, and judge the amount of tension by the ability to work the
tubing without pain. It allows the patient to exercise more than once a day. It may be difficult to figure out how to use the
tubing precisely for certain muscle groups, but resourceful therapists can teach these techniques ( Fig. 11.7).
FIGURE 11.7. External rotation of the shoulder using an elastic cord.
It may be difficult to determine where to perform progressive resistance exercises. The available facilities—home, health
club, hospital, or outpatient therapy department—must be taken into account. Cost is a factor. Long-term physical
therapy is often not covered by the health insurance system. Membership in a health club may be a boon to
rehabilitation. Many clubs have special rates for senior citizens and special times when older athletes can go and feel
more at ease with others of the same age.
Stretching in the over-60 age group is a necessity for function and for athletic performance. There is great variation in the
ability of older athletes to stretch muscle-tendon units and joint capsules. Some of this is based on personal genetics and
some on prior injury. The Achilles, hamstrings, and adductor muscle-tendon units are often tight and are frequently
injured in older athletes ( Fig. 11.8). Attention should be paid not only when there has been an injury but on a preventive
basis.
FIGURE 11.8. Adductor stretch.
Many sports require good shoulder ROM, and loss of motion causes pain and decreased function, which can be
confused with a rotator cuff injury. With age most people lose back motion in flexion and extension. That combined with
weaker muscles can make many athletic activities more difficult.
An acute or chronic injury may bring an older athlete with an examination in showing loss of flexibility or motion in certain
muscle-tendon units. One should take that opportunity to set up a program that is both injury specific and sport specific.
Gains may be slow, but stretching that is carried out over a lifetime may add years of injury-free pleasure for the athlete.
All athletes should know that a few minutes of warmup are required before stretching. A program of stretching four to six
times a day, plus a few minutes of warmup, represents a significant portion of time. The senior athlete, however, may
have the time to follow such a program. It must be emphasized that the stretching is gentle and that pain is not part of the
process. Some older athletes must learn to be content with holding what they have rather than making gains.
Physical therapy modalities are often used in athletes of any age, sometimes as a substitute for the active work that is
needed on muscles, tendons, and joints. Most athletes enjoy application of these modalities and of heat or cold. One
must be careful in older athletes. Even those people who are playing sports may have decreased circulation in certain
areas that may be compromised by the application of heat, cold, or direct pressure.
CLIMATIC CONDITIONS
Both heat and cold can be major problems for athletes of any age but particularly for the Master's Age athlete. Of these
conditions, heat is more likely to be dangerous to the participant. Heat and its co-conspirator, humidity, cause the person
playing sports to have an increase in core body temperature. To prevent the core temperature from rising to a dangerous
level, the person perspires: it is the evaporation of fluid from the skin that takes heat away from the body and helps to
decrease the core body temperature. The athlete must have enough fluid in the body to allow perspiration to form.
Therefore, the intake of water and/or one of the commercially available carbohydrate and electrolyte drinks is critical. The
combination of increased body temperature and potentially decreased fluid volume due to sweating may lead to heat
illness, heat stroke, and cardiovascular collapse.
Heat illness is more likely to be serious in the older athlete, although in any age group it could be fatal. However, the
older athlete has less margin for error. If the adverse climatic condition is superimposed on a cardiac dysfunction or
kidney problem, the situation is more severe. Older athletes must be particularly careful about stressing themselves in
hot weather. Fluid intake must be high throughout the activity period. If the activity lasts longer than 1 hour, the fluid
should include some electrolytes, the most important of which is salt. Any feeling of lightheadedness, incoordination, or
fatigue beyond that which is normally expected must bring an immediate stop to whatever sport activity is going on. Most
Master's Age athletes are aware of heat problems, particularly when doing things for fun or practicing. It is at the time of
competition that good sense may not prevail.
In cold weather the most common worry for the older athlete is the inability to warm up easily and the possibility of major
muscle strains. Of much greater potential import, however, is hypothermia, a condition in which the core body
temperature falls to less than 35°C (95°F). This leads to excessive fatigue, decreased coordination, and decreased
muscle strength; disaster ensues unless help is immediately forthcoming. An older athlete could be in a situation such as
the following. He is out hiking on a temperate (62°F) day and progressing up a mountain. Perhaps he is wearing a light
T-shirt with a light windbreaker in reserve. The activity of walking up the mountain produces heat, and he is comfortable.
At this point a climactic change could occur whereby the temperature drops by 25°F as the sun becomes obscured, the
wind rises, and a light drizzle begins to fall. The increased muscle activity of hiking, which produces heat, also gradually
depletes energy. This combination of the gradual heat loss and energy loss, combined with the slowly cooling weather,
can bring on hypothermia. The person must immediately get into a warm, dry situation before more serious
consequences occur. The onset of hypothermia is more insidious than the onset of heat problems, and the potential
effects of hypothermia can be warded off temporarily by people doing physical activity that increases body heat
production. Yet, if this activity continues over an extended period and protection is not available from cold, wind, or
moisture, then hypothermia may ensue.
The point is not that individuals in the Master's Age group are more likely than younger persons to have a heat-related
problem or hypothermia, but the effects of these problems can be more severe in the older person, particularly if there
are any underlying medical problems. The senior athlete is probably more likely to avoid dangerous climatic situations
because he has heard about them and may be more attuned to the possibilities. He or she is probably less likely to risk
life by trying to carry on despite severe heat or hypothermic conditions.
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71-year-olds. J Appl Physiol 1991;71:2004–2011.
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Sports Med 1990;18:300–309.
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NJ: Enslow Publishers, 1981:167–178.
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Appl Physiol 1988;64:1038–1044.
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17. Lohmander LS, Dalen N, Englund G, et al. Intra-articular hyaluronan injections in the treatment of osteoarthritis of the knee: a randomised,
double blind, placebo controlled multicentre trial. Hyaluronan Multicentre Trial Group. Ann Rheum Dis 1996;55:424–431.
12 Special Concerns of the Female Athlete
12
SPECIAL CONCERNS OF THE FEMALE ATHLETE

MARY LLOYD IRELAND
SUSAN M. OTT
Sports of Participation
High School
Collegiate
Olympic
Injury Rates
National Collegiate Athletic Association
Epidemiologic Study by Sport
Cheerleading
Sports Differences
Gender Differences
Growth and Puberty
Orthopedic Considerations
Specific Joints
ACL Injuries
Consensus Statement—Anterior Cruciate Ligament Injuries in Females
Specific Body Locations
Lower Leg
Foot and Ankle
Shoulder
Elbow
Wrist and Hand
Stress Fractures
First Rib
Back Conditions and Fractures
Psychological Considerations
Nutrition
Fluid Intake
Diet Composition
Eating Disorders
Osteoporosis
Gynecologic and Obstetric Considerations
Normal Menarche
Delayed Menarche
Menstrual Abnormalities
Menstrual Abnormalities and Nutritional Disorders
Exercise and Pregnancy
Breast Development
Protective Devices
Breast Problems
Conclusions
Acknowledgments
Chapter References
Physiologic, anatomic, and psychologic differences between women and men create certain unique patterns of illness
and injury. Appreciation of these special situations enables the practitioner to sharpen diagnostic skills and improve
treatment of the female athlete. Unique illnesses are related to nutritional and hormonal balance, which include anorexia
nervosa, bulimia, athletic amenorrhea, iron deficiency anemia, hormonal imbalance, pregnancy, and postmenopausal
osteoporosis (1,2,3 and 4).
The majority of injuries are related to participation in the sport rather than the gender of the athlete ( 5,6,7,8 and 9).
Anatomic differences in lower extremity alignment, less upper-extremity strength, hormonal imbalance, and nutritional
disorders increase chances for overuse injuries in women. Stress fractures in amenorrheic runners and upper-extremity
injuries in underdeveloped prepubertal gymnasts are common. There is an increased incidence of patellofemoral (PF)
disorders and anterior cruciate ligament (ACL) injuries in women ( 10). Prospective and epidemiology studies are needed.
Differences shown diagrammatically are the wider pelvis, increased flexibility, less developed musculature, less
developed vastus medialis obliquus (VMO), narrower femoral notch, genu valgum, and external tibial torsion in women
(Fig. 12.1A). The male extremity alignment is a narrower pelvis, more developed thigh musculature, VMO hypertrophy,
less flexibility, wider femoral notch, genu varum, and internal or neutral tibia torsion ( Fig. 12.1B). Dynamic movement
patterns demonstrate more clearly the excessive lower-extremity rotational malalignment in women ( Fig. 12.2). Doing a
single leg, step down squat, the female exhibits hip adduction, femoral rotation, and knee valgus, whereas men exhibit
straight hip over knee and foot. These dynamic movement patterns demonstrate the hip over knees and loss of control
and poor core stability in women. Thoracic, lumbar spine, and pelvic alignment and core strength provide the important
stable base from which movement patterns occur. Often, women have an anterior pelvic position, excessive lumbosacral
lordosis, and an extended thoracic spine. Viewing the skeleton from the side, the normal posture is seen with head
forward, normal lumbar lordosis, and alignment without rotation ( Fig. 12.3). In the anteriorly rotated pelvis, compensation
in the lumbar and pelvic positions occurs. There is excessive lumbar lordosis, hip adduction and internal rotation, knee
valgus, external tibial torsion, and forefoot pronation. This altered pelvis position creates malrotation, resulting in PF
disorders and movement patterns leading to knee injuries. It is important to recognize this anteriorly rotated position so
prevention programs can be instituted ( 11).
FIGURE 12.1. A and B: The lower extremity alignment that may predispose to certain overuse problems involving the
hips and knees and especially ACL and patellofemoral injuries. Women have a wider pelvis, increased flexibility, less
developed musculature, hypoplastic vastus medialis obliquus, narrow femoral notch, genu valgum, and external tibial
torsion. Men have a narrower pelvis, more developed thigh musculature, vastus medialis obliquus hypertrophy, less
flexibility, wider femoral notch, more tendency toward a genu varum, and internal or neutral tibial torsion. (From Fu FH,
Stone DA, eds. Sports injuries: Mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:154,
with permission.)
FIGURE 12.2. This step down off a box maneuver well shows dynamic differences in the man on the left and woman on
the right. The man is straight in alignment, with hip over patella over foot. The woman demonstrates hip adduction,
femoral internal rotation, knee valgus, and a compensatory external rotation and pronation of the foot. (Copyright 1999 by
M.L. Ireland.)
FIGURE 12.3. The sequence of displacements from an anterior pelvic tilt includes forward pelvic rotation, femoral internal
rotation, medial displacement of the femoral range of rotation, genu valgus, genu recurvatum, subtalar eversion, and
forefoot or rearfoot pronation. (From Hruska R. Pelvic stability: influences lower-extremity kinematics. Biomechanics
1998;5:24, with permission.)
With the increased awareness of the importance of fitness and the passage of Title IX, ensuring equal rights for male and
female athletes in federally supported institutions, the numbers of women participating in structured competitive and
recreational athletics has skyrocketed during the past several decades. The history of women competing at various levels
(e.g., local, national, and international) shows the growth and interest ( 12,13). With this dramatic increase in participation,
injury patterns and rates must be studied.
SPORTS OF PARTICIPATION
High School
The number of sports in organized sports has been increasing at the high school, college, and Olympic level. At the high
school level during the 1997–1998 season, total participation by high school athletes for men was 3,763,120; women,
2,570, 333; coed, 19,322, for a total of 6,352,775. When these figures are broken down into percentages, 59% of the
athletes participating in sports are men and 41% are women ( 14).
The National Federation of State High School Associations has documented the number of teams and participants. This
documentation includes male participants, female participants, some combined teams, and girls playing on boys' teams
and boys playing on girls' teams. The top 14 teams based on participation are shown ( 14) (Table 12.1).
TABLE 12.1. 1998 HIGH SCHOOL ATHLETICS PARTICIPATION: HIGH SCHOOL ADAPTED SPORTS
PARTICIPATION
The sport of highest participation overall is football with 971,335 participants on 13,243 teams. In football, 779 females
participate on 160 teams. The most frequent sport by number of participants for women was basketball (454,000),
followed by outdoor track and field (395,955), volleyball (373,219), fast-pitch softball (333,374), and soccer (246,687).
The order of participants for men is football (971,335), basketball (544,463), track and field (471,175), baseball
(449,897), and soccer (309,484). By the state participation, the breakdown is shown by the order of participation of the
females (14) (Table 12.2).
TABLE 12.2. SCHOOL ATHLETICS 1997–1998: STATE PARTICIPATION
Collegiate
The National Collegiate Athletic Association (NCAA) has kept epidemiology statistics for injury and number of
participants ( 9). During the 1998–1999 season, participation by division in all sports were as follows: men, Division
I—85,494, Division II—47,501, Division III—78,278; women, Division I—59,191, Division II—30,241, Division III—56,400.
The numbers of participants were recorded for all sports, including emerging sports—rowing and squash for men and ice
hockey, squash, synchronized swimming, and water polo for women. For women, the totals were 145,832 and for men
211,273. If football is excluded, the numbers are close to equal, with the totals being 154,745 for men and 145,832 for
women (9) (Fig. 12.4).
FIGURE 12.4. Total number of college athletes (1989–1999). Since 1989, the number of collegiate participants in the
NCAA are shown, comparing men, men who do not participate in football, and women. The numbers are most similar if
football athletes are eliminated. Data taken from NCAA participation studies.
At the collegiate level, the sports of participation and championship recognized by the NCAA are men and women ( 151),
men only (3), and women only (10) (Table 12.3).
TABLE 12.3. SPORTS OPPORTUNITIES BY GENDER: OLYMPIC
Olympic
Olympic sports that are for women only are rhythmic gymnastics, softball, and synchronized swimming. Men's Olympic
sports are baseball, boxing, ski jumping, Nordic combined skiing, and wrestling. Sport biomechanics of the men's or
women's sports create uniquely different patterns and different incidence of injury ( 15) (Table 12.4).
TABLE 12.4. SPORTS BY GENDER: OLYMPIC
The ratio of female to male participants in the Olympic Games has increased during the last century. In 1900, there were
15 women and 1,206 men. In 1960, there were 610 women and 4,738 men. In 1992, 2,708 women and 6,659 men
participated. In 1996, 3,684 women and 7,060 men participated.
INJURY RATES
National Collegiate Athletic Association
Since 1982, the NCAA Injury Surveillance System has been published with detailed injury information in 16 sports ( 9).
Women's sports are softball, field hockey, and rowing. Men's sports are spring football, football, wrestling, ice hockey,
water polo, and baseball. The six sports in which both men and women compete are gymnastics, volleyball, basketball,
cross country, soccer, lacrosse, swimming and diving, track and field, and golf. Data were not collected for track and field
or swimming and diving. Owing to differences in equipment for men's and women's competition, gymnastics and lacrosse
comparisons must be made carefully.
Using the 1997–1998 NCAA data, for women, the highest overall injury rate in collegiate sports is soccer, followed by
spring soccer, gymnastics, lacrosse, basketball, fall lacrosse, softball, field hockey, volleyball, and spring volleyball. The
men's sports of spring football and fall lacrosse had the highest injury rates for both men and women ( 9) (Table 12.5).
There was a nearly equal occurrence of injury in practice and games in women's and men's soccer, lacrosse, softball,
football, and baseball. However, there is a trend toward more injuries occurring in practice. In the remainder of the
surveyed sports, the trend toward more injuries occurring during practice than during competition is even more
pronounced.
TABLE 12.5. INJURY RATES PER 1,000 ATHLETIC EXPOSURES AND PERCENTAGE IN PRACTICE AND GAMES5
The average injury rates from data collected by the NCAA from 1992–1998, except for 1996–1997 season, when data
were not collected, for women, the highest rate of injury was in gymnastics, followed by soccer, spring soccer, and
basketball. ( 9) (Table 12.6). For men, the highest injury rates occurred in spring soccer, spring football, wrestling, and
soccer. Although the data are adjusted to rates per 1,000 athletic exposures, it should be noted that in this comparison,
data for fall lacrosse, spring soccer, and spring volleyball were collected only during the 1997–1998 year. Knowledge of
injury rate and timing of occurrence allows the practitioner to plan coverage.
TABLE 12.6. AVERAGE NCAA INJURY RATES PER 1,000 ATHLETIC EXPOSURES AND PERCENTAGE IN
PRACTICE AND GAMES6
The type of injury for each of the NCAA sports for which data were collected was analyzed. ( 9) (Table 12.7). The
categories analyzed included contusion, tendinitis, incomplete ligament sprain, incomplete muscle tendon strain,
complete muscle tendon strain, fracture and stress fracture, concussion, heat exhaustion, and inflammation. The
incidence of incomplete sprains for the 1997–1998 data was highest in men's spring soccer, followed by men's spring
football, women's spring soccer, wrestling, and women's gymnastics ( 9). In previous studies, women's gymnastics has led
several diagnostic categories; however, for the 1997–1998 data, men's fall lacrosse and spring football have a higher
injury rate.
TABLE 12.7. NCAA INJURY RATE BY TYPE OF INJURY7
Overall injury rates comparing sports that have regular-season and off-season formal training periods were compared.
For men's and women's lacrosse and women's soccer, the rate of injury comparing the fall and spring seasons were
relatively similar. Spring football and men's spring soccer had higher rates of injury than the regular seasons of those
sports. Women's regular-season volleyball had a higher rate of injury than the spring season ( 9).
The rate at which a particular body part was injured was also analyzed ( 9) (Table 12.8). The ankle was the most
commonly injured joint. The injured body parts for all 21 sports are shown for comparison in this table.
TABLE 12.8. NCAA INJURY RATE BY BODY PART*
Epidemiologic Study by Sport
There are many studies comparing incidence of injury among men and women in similar sports ( 7,8,16,17). Using the
National Athletic Injury Illness Reporting System, Whiteside ( 8) reported the order of highest to lowest incidence of
injuries was basketball, gymnastics, softball in women (compared with basketball), gymnastics, and baseball in men.
Men's and women's basketball had the highest relative injury frequency. Women had a relatively higher frequency of
ankle injuries and fractures in basketball and gymnastics.
Injury type and rate were compared among six varsity sports at Indiana University during the 1977–1978 season ( 16).
The highest injury rate was found in gymnastics (40%), with the most injuries occurring during practice, in tumbling, and
in younger women. Most of the basketball injuries occurred on defense while guarding.
The ankle is the most commonly injured joint in many series (6,8,9,16). In 19 female collegiate sports, injury rates were
most common in basketball, followed by volleyball, field hockey, gymnastics, and track and field ( 18). In this survey of
361 colleges and universities, the injury-contributing factors, in order of frequency, were improper training methods,
inadequate facilities, and poor coaching techniques.
CHEERLEADING
The number of participants in cheerleading has skyrocketed over the last 10 to 15 years. Correspondingly, so have the
number of injuries due to cheerleading. In 1980, 4,954 emergency room visits were attributed to cheerleading injuries. By
1986, that number had risen to 6,911 and had climbed to approximately 16,000 by 1994 ( 19). Even more concerning is
that cheerleading accounted for 56.5% of the catastrophic injuries occurring in high school and college female athletes
from the 1982–1983 season through the 1997–1998 seasons ( 19).
The injury risk (injuries per 1,000 athletic exposures) in games and practices are 0.67 in college and 0.17 in high school
(9,20,21). Injuries cause more time loss in cheerleading than all other sports ( 22). In a survey of cheerleaders, 84% of
participants sustained knee injuries, averaging 35 days out of practice ( 23). Despite the number of injuries occurring in
cheerleading activities, it is recognized as a sport only in Michigan and West Virginia. The National Federation of State
High School Associations considers cheerleaders as spirit groups whose purpose is to serve as support groups for
interscholastic athletic programs within the school ( 19). The major factor in the rate of serious injuries occurring in
cheerleading is its change from a purely support and spirit activity to a pseudogymnastics activity. Pyramids, basket toss
stunts, tumbling and minitrampoline activities are responsible for most of the catastrophic injuries noted in cheerleading.
It is important for coaches to have proper training in spotting and in teaching tumbling skills if gymnastic stunts are to be
performed. It is also important for appropriate safety equipment, such as mats and spotting belts, to be in place if
cheerleaders are to tumble or perform pyramid stunts. The American Association of Cheerleading Coaches and Advisors
offers safety certification; however, this certification is not mandatory. Several states have instituted rules for
cheerleading regarding the use of minitrampolines, the allowable height of pyramids, and banning basket toss
maneuvers. (19)
SPORTS DIFFERENCES
Differences in sport biomechanics, equipment, and training create certain specific injury patterns. The repetitive
maneuvers of ballet, gymnastics, cheerleading, dance, and ice skating create circumstances for unique injuries. Injury
surveys compare rates of injury for men and women who participate in basketball, soccer, lacrosse, and gymnastics
because these are the four NCAA sports for which data have been collected and in which both men and women compete
(9). Important differences between men's and women's lacrosse and men's and women's gymnastics should be made
clear. In lacrosse, there are differences in the sticks used and the protective equipment used for men's and women's
competition. In men's lacrosse, protective padding and helmets similar to those used in football are worn, and in women's
lacrosse, no protective equipment is worn.
In gymnastics, men compete in six events: vault, floor exercise, high bar, parallel bars, pommel horse, and still rings. In
women's gymnastics, the athletes compete in four events: vault, uneven parallel bars, balance beam, and floor exercise.
Gymnastic balance beam maneuvers may cause unusual injuries due to the apparatus ( Fig. 12.5). In one collegiate
gymnast, repetitive landings on the balance beam caused recurrent medial dislocations of the left great toe, one of which
was open, from landing with the beam between the great and second toe, causing the first metatarsophalangeal (MTP)
dislocation. Medial stress views show severe instability of the left first MTP joint ( Fig. 12.6A). Following a season of
buddy taping of the toes, surgical reconstruction of the joint was performed. Intraoperative stress testing shows severe
lateral instability of the left first MTP joint ( Fig. 12.6B). There are reports of profiles and injuries in specific sports, which
include female rowers (24), professional ballerinas ( 25), and swimmers (26). Summarization of physiologic profiles
provide excellent information ( 27,28,29).
FIGURE 12.5. Gymnastic apparatus of the balance beam, which is unique in women's sports, can result in certain
unusual injuries. (From Fu FH, Stone DA, eds: Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore:
Williams & Wilkins, 1994:157, with permission.)
FIGURE 12.6. A and B: A collegiate gymnast sustained several injuries when landing on the beam. The force between
her great and second toe on her left foot caused several medial dislocations, one of which was open. A: Medial stress
radiographs of both great toes medially show the severe medial instability without fracture. B: Clinical stress test
immediately before surgery. Note the previous scar from open dislocation (arrow). The patient required reconstruction of
the lateral structures of her left great toe. ( A, Copyright M.L. Ireland, M.D, 1999; B from Fu FH, Stone DA, eds. Sports
injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:157, with permission.)
GENDER DIFFERENCES
The diagnosis and treatment of the athletic woman has been reviewed in detail ( 4,30). Excellent comparative studies of
the genders have been done in the military setting ( 27,31,32 and 33). Athletic women in the Navy were found to have
more success than nonathletes in areas of stamina, strength, and self-discipline ( 33). Compared with men, women were
found to be capable of equal efficiency and aerobic metabolism at the United States Military Academy ( 27). In a random
review of 74 female and 74 male cadets, an increased incidence of stress fractures were found in women ( 31). Eleven
women and no men sustained stress fractures. Women had double the incidence of men's lower extremity injuries.
However, men required an extra week to resolve their lower-extremity injuries and required twice as much time to reach
maximal improvement from back injuries as compared with women. Physiologic differences in men compared to women
occur in aerobic fitness and resistive training. Compared with men, women midshipmen improved their fitness level more
rapidly (34). Stress-related injuries were seen more often in women. As the women acclimated to the Naval Academy,
similar numbers of serious injuries were seen. There is a comprehensive review of data comparing male and female
athletes in areas of body composition and physique, muscle characteristics, strength, and cardiovascular endurance
capacity (29).
Growth and Puberty
Puberty occurs over an average period of 4.5 years, with accelerated growth, breast development (thelarche at 9.8
years), breast and hair development (adrenarche at a median age of 10.5 years) and beginning of menses (menarche at
a median age of 12.8 years). Blood hormone concentrations follow the production of follicle-stimulating (FSH) and
luteinizing hormones (LH), which rise moderately, followed by a rise in estradiol androgens from the adrenal gland and,
to a lesser degree, ovaries, causing pubic and axillary hair growth. Gonadal estrogen proliferates the endometrium, and
menarche occurs (35). The age at menarche has been decreasing over the years. Timing of puberty is multifactorial,
including genetic, geographic, light exposure, general health nutrition, and psychological factors ( 35).
A girls' growth spurt occurs 2 years earlier (at age 11 and 12 years) than that of a boy ( 36). During the year of a girl's
growth peak, the rate of growth doubles, with an increase in height of 6 to 11 cm. The peak occurs 2 years after breast
budding and 1 year before menarche (36). Skeletal growth is usually complete within 2 years after menarche.
Tanner staging assesses pubertal development and is divided into five stages ( 35) (Table 12.9). Breast development
correlates with a bone age of 11 years and menarche with a bone age of 13 years. It is important to assess puberty to
diagnose disorders such as hypothyroidism, precocious puberty, delayed puberty, hypogonadism, and short and tall
stature. The Tanner staging consists of development of breast ( Fig. 12.7A) and pubic hair (Fig. 12-7B). Breast
development and distribution of the type of pubic hair is correlated with median age ( Table 12.9).
FIGURE 12.7. A and B: Tanner staging assesses development of breasts (A) and pubic hair (B) in five stages. (From
Speroff L, Glass RH, Kase NG. Clinical gynecologic endocrinology, and infertility. Baltimore: Williams & Wilkins,
1994:377–379, with permission.)
TABLE 12.9. TANNER STAGING
After age 10 to 12 years, there are significant differences in all aspects of physical performance. Women reach
physiologic and skeletal maturity before men and achieve peak height velocity before men as well ( 37). It is important to
keep these changes in mind when caring for the young female athlete going through the changes of puberty. In 18 to 22
year old athletes, the amount of body fat in women is 22% to 26%, and in men, it is 12% to 16%. In men, androgens
create greater lean body weight. In women, estrogens contribute to the greater amount of fat. Detailed summaries of
different sports comparing the genders include body composition, somatotype, muscle fiber, strength and cardiovascular
endurance capacity, and maximal oxygen. Similarities in highly trained male and female athletes are lower-body strength
(per unit of body weight), cardiovascular endurance capacity, body composition, and muscle fiber type. In women, a
sedentary lifestyle after puberty may significantly contribute to the differences physiologically ( 29).
Gender differences in body composition and structural variables have been studied ( 28). Differences are similar in
athletic women compared with athletic men, and nonathletic women compared with nonathletic men. Total lean body
mass is greater in men. Similar male and female ranking for fatness and leanness were reported, with the lowest in
runners and gymnasts, and highest in participants in basketball, volleyball, and field events.
Work capacity studies show that, compared with men, women have more fat and less muscle, but only slight differences
in the aoVO2max when expressed relative to body size and composition ( 38). Males have greater hemoglobin and higher
red blood cell levels. In general, females are highly trainable and demonstrate the same physiologic training changes as
males. The effects of aerobic exercises on training in symptomatic women with mitral valve prolapse were reviewed ( 39).
Aerobic exercise was found to be a positive influence in the management of symptomatic women with mitral valve
prolapse.
Women, like men, can experience significant increases in strength, power, and muscular endurance ( 40). Although the
degree of upper-body strength and development are less in women compared with men, sound strength training
principles can decrease these differences as based on ratios to body weight. However, upper-body strength in women,
even with training, has, in some studies, remained only 30% to 50% of their male counterparts. Lower-body strength
comes much closer to parity. The development of strength is usually the weakest link in the physiologic profile of the
female athlete (29).
ORTHOPEDIC CONSIDERATIONS
Specific Joints
Knee
Injury Rates
PF disorders and ACL injuries are more common in women compared with men (9,41,42 and 43). The knee is often
injured in collegiate sports. The injuries can be matched to the sport ( 9) (Table 12.10). The knee injury rates were
categorized into the structures involved, such as ligaments (collateral, anterior cruciate, posterior cruciate), torn cartilage
(meniscus), and patella or patellar tendon. The collateral ligaments were most frequently injured in spring football,
wrestling, men's spring soccer, and football. In comparable sports, the ACL injury rate per 1,000 athletic exposures was
higher for women in gymnastics (0.33 to 0.00), basketball (0.22 to 0.07), spring soccer (0.1. to 0.00), lacrosse (0.29 to
0.27) and soccer (0.32 to 0.14). In fall lacrosse, men injured the ACL more frequently than women (0.46 to 0.34). In
sports, spring football has the highest rate of knee injury for the 1997–1998 data. Women's gymnastics has led this
category in the past. Women's gymnastics lead other women sports with involvement of the ACL. The uniqueness of the
sport and its apparatus, biomechanics, and the gymnast's body habitus, strength, ligamentous laxity, and alignment are
factors that contribute to this increased injury rate.
TABLE 12.10. NCAA KNEE INJURY RATE BY SPORT*
Patellofemoral Stress Syndrome and Alignment.
Anterior knee pain is common in women. The differential diagnosis is lengthy ( Table 12-11) (44). Categories include
inflammatory (bursitis, tendinitis, synovitis), mechanical [subluxation, dislocation, PF stress syndrome (PFSS), plica], and
miscellaneous. The term chondromalacia, or softening of the articular cartilage, is a pathologic diagnosis; clinically, the
use of the term PFSS is suggested. Excellent reviews of chondromalacia exist ( 45,46).
TABLE 12.11. DIFFERENTIAL DIAGNOSIS: ANTERIOR KNEE PAIN
PF stress syndrome is commonly seen in women who have microtraumatic forces, alignment abnormalities, forefoot
pronation, and tibial torsion. For comparison, normal alignment is shown ( Fig. 12.8A). Abnormal alignment or miserable
malalignment syndrome creates excessive forces laterally, subluxing and rotating the patella. These forces include a Q
angle exceeding 15 degrees, increased femoral anteversion, hypoplastic VMO, external tibial torsion, forefoot pronation,
and heel valgus (Fig. 12.8B). This malalignment is commonly seen in cheerleaders, gymnasts, dancers, and track
athletes. A swimmer has exhibited miserable malalignment syndrome, as seen on front ( Fig. 12.9A) and side (Fig. 12.9B)
clinical views. Also, a runner was seen for anterior knee pain. Standing femoral anteversion is shown with the patellas
pointed (Fig. 12.10A).Although standing alignment is relatively straight, when the patient does a single leg squat, one
can see the excessive hip adduction and internal rotation, creating medialization and rotation of the femur relative to the
patella rotation and lateral elevation of the patella ( Fig. 12-10B). PF disorders are best treated with back, hip, and
quadriceps strengthening; avoidance of knee extension machines and full squats; knee sleeves, if desired; orthotics for
weight-bearing sports; and nonsteroidal antiinflammatory medications. Surgical intervention should be a last
consideration for PFSS, plica, and miserable malalignment syndrome.
FIGURE 12.8. A and B: Patellofemoral disorders are common in women. A: Normal alignment with normal Q angle
measured from anterosuperior iliac spine central portion of the patella, patella to tibial tubercle of less than 15 degrees,
and normal musculature of developed vastus medialis obliquus create forces that centralize the patella, resulting in
normal patellofemoral tracking. B: Miserable malalignment syndrome consists of increased femoral anteversion,
excessive Q angle, external tibial torsion, and foot pronation. All of these factors cause lateral patellar subluxation. (From
Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins,
1994:159, with permission.)
FIGURE 12.9. A and B: This miserable malalignment syndrome is frequently seen in women. Clinical example of
collegiate swimmer from the front, (A) showing 20 degrees of genu valgum, external tibial torsion, hypoplastic vastus
medialis obliquus, heel valgus, and pes planus with forefoot pronation. (B) Hyperflexibility of 20 degrees of
hyperextension is seen from the side in a clinical view. (From Fu FH, Stone DA, eds. Sports injuries: Mechanism,
prevention, and treatment , 2nd ed. Baltimore: Williams & Wilkins, 1994:159, with permission.)
FIGURE 12.10. A and B: Standing alignment shows internal rotation of the femur with patellas pointing toward one
another. The alignment is relatively straight; however, there is femoral anteversion as well as internal tibial rotation. A:
Dynamically shown when the individual is asked to do a mini squat on a single leg. B: The patient compensates to stay
balanced with increased internal rotation of the hip and external rotation of the tibia. This medialization of the femur and
rotation is a cause of anterior knee pain and maltracking. (Copyright M. L. Ireland, 1999.)
A symptomatic medial plica is commonly seen in the same population who suffers from PFSS. An inflamed medial plica is
tender to palpation over the medial femoral condyle, just medial to the medial patellar facet. The plica may become thick
enough to sublux over the medial femoral condyle and cause a snapping sensation. A symptomatic plica is treated
conservatively, the same way PFSS is treated, and once again, surgical intervention in the form of arthroscopic excision
of the plica should be performed only when conservative care has failed.
Anatomically, the articular surface of the patella is the thickest of all and consists of medial, lateral, superior, and inferior
nonarticulating facet (Fig. 12.11). Great variability in the size and shape of patellar facets, the depth of the trochlear
groove, and dynamic muscle forces result in clinical PF disorders. The contact areas and facets of the PF joint have been
well identified. Aglietti et al. ( 47) determined the contact areas based on the degree of flexion ( Fig. 12.12). The greatest
contact area and pressure occurs at 90 degrees of flexion. Patellar tracking is dependent on bony anatomy, alignment,
muscular development, and on the type of loading with machines or sport.
FIGURE 12.11. Articular surface of the patella demonstrates the anatomy of mediolateral odd patellar facets and the
nonarticulating inferior and superior facets. (From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and
treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:160, with permission.)
FIGURE 12.12. Patellofemoral contact areas are shaded at 0, 30, 60, 90, and 120 degrees of flexion in this right knee
diagram. Femur (lateral to the left and medial to the right) and patella (lateral to the right and medial to the left) are
shown. (From Aglietti P, Insall JN, Walker PS. A new patellar prosthesis. Clin Orthop 1975;107:175, with permission.)
Patellar Instability: Radiographic and Clinical Assessment
Because PF disorders and ACL injuries are more common in women, attention to specific radiographic views is key
clinical assessment. Routine views are anteroposterior (AP), lateral, femoral notch, and bilateral patellar sunrise.
Radiographic measurements and reviews of chondromalacia are important in the understanding of PF disorders ( 45).
Measurement of length of a patella-to-patella tendon less than 0.8 is termed patella alta and greater than 0.8 is termed
patella infera. A basketball athlete complained of anterior pain and swelling of her knee. Patella alta was demonstrated
on AP view (Fig. 12.13A) and lateral view (Fig. 12.13B). The patella-to-patella tendon ratio is 0.5, and the Hughston
patellar view shows lateral subluxation ( Fig. 12.13C). The subject of these views returned successfully to competition
with a quadriceps strengthening program and use of a neoprene sleeve with lateral pad.
FIGURE 12.13. A–C: Routine plain radiographs include AP, lateral, and patellar views. Views of this left knee
demonstrate patellar alta. A: On the AP view, the patella is significantly superolateral. B: On lateral view, the
measurement of the ratio of the patella to the patellar tendon is 0.5, confirming patella alta. Normal ratio is 0.8. C:
Hughston sunrise patellar view shows the lateral patellar subluxation, which is mildly symptomatic in this basketball
athlete. (From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams
& Wilkins, 1994:160, with permission.)
ACL Injuries
Injury Rates
A recent review article summarizes the epidemiology of ACL injuries ( 17). Comparing the NCAA results from the first 5
years, 1989–1993 to 1994–1998, the ratio of female-to-male ACL injuries per 1,000 athletic exposures was 4:3 times
greater in basketball and 2:4 times to 2:8 times in soccer.
At the collegiate level, injury rates in women's basketball were 0.29 for the 1989–1993 season and 0.30 for the
1994–1998 season. In men's basketball, injury rates were 0.07 for the 1989–1993 season and 0.10 for the 1994–1998
season (48). In soccer, injury rates for women were 0.31 for the 1989–1993 season and 0.33 for the 1994–1998 season.
In men's soccer, the injury rates were 0.13 for the 1989–1993 season and 0.12 for the 1994–1998 season. Injury rates
are recorded at the collegiate level in six sports in which men and women compete. These sports are gymnastics, track
and field, swimming and diving, soccer, basketball, and lacrosse. The ACL was injured in women more than three times
more often in basketball, and more than two times more often in soccer than in men, as measured by rates per athletic
exposure (9). In spring soccer, the ACL injury rate for females was 0.10, whereas no men in spring soccer sustained an
ACL injury (Fig. 12.14). In women, the highest rate of ACL injury was 0.33, which was in the sport of gymnastics. In that
survey, no male gymnast sustained an ACL injury.
FIGURE 12.14. ACL injury rate by sport, 1997 to 1998.
ACL injury rates in sports that have both a regular season and a formal off-season training regimen have been recorded.
Rates are significantly higher in off-season competition for men's lacrosse and football, and women's volleyball. The ratio
of off-season injury to in-season injury in men's lacrosse is 1.93; men's football, 2.1; and women's volleyball, 3.5.
Men's fall lacrosse, men's spring football, and women's spring volleyball had increased rates of ACL injury during the
regular seasons of these sports. For soccer and women's lacrosse, the regular season had a higher rate of ACL injury
(9).
Olympic and Professional Sports
Male and female basketball injuries at the professional level were compared ( 43). Women were found to sustain more
injuries, more sprains, and to have increased knee and thigh injuries than men. The most common injury involved the
ankle. Women's injury frequency was 1.6 times greater than that of men.
An epidemiologic survey of athletes invited to the U.S. Basketball Olympic Trials in 1988 showed that knee injuries ( p <
.0001) occurred more often in females compared to males and that females required surgery ( p < .0007) more often than
males (40). Of the 64 women, 17 required arthroscopy and 8 sustained an injury to the ACL. Of the 80 men, 3 sustained
an injury to the ACL, whereas 3 required arthroscopy only. Factors contributing to this increased incidence of injury at the
professional level ( 43) include differences in training, strengthening, weight lifting, type of shoes, type of floor, and
lower-extremity alignment. Further investigation and prospective studies to determine why knee injuries involving the ACL
are so common in women are needed. Factors contributing to ACL injury can be divided into intrinsic, extrinsic, and
combined.
Radiographic and Clinical Assessment
Femoral notch views are good for outlining the size, shape, and contour of the notch and the articular surface. In the
past, a narrow notch shape and size has been suggested as a contributing factor to ACL injuries. Letters can be used to
classify the shape of the notch. The A-shaped notch on the right is commonly seen in ACL injuries. Other shapes are H,
reverse U, or C (Fig. 12.15). A recent study has been performed to assess notch width index and rates of ACL injury to
determine whether or not notch size is predictive of risk of ACL injury. The results of the study show no difference in
notch width index among patients who did and did not tear their ACLs, and a symmetry of notch width between left and
right knees regardless of ACL status. The study also showed that although women tend to have smaller notches than
men, the difference was not statistically significant ( 49).
FIGURE 12.15. A proposed contributing factor to anterior cruciate ligament tears is the uniqueness of notch shapes.
These have been seen as reverse C or U, H, and A in shape. The more narrow A shape and a low notch to femur ratio on
notch views are common with ACL tears. (From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and
The elastin and collagen tissue in women may contribute to completeness of ACL tears and scar formation. Owing to
their less muscular development and their lower-extremity alignment differences, women rely more on the ACL and less
on muscular control. Ligamentous reconstruction should be considered in the ACL-dominant woman because she is at
high risk for significant meniscal and articular surface injury.
A former cheerleader with bilateral ACL injuries jumped from the stage during a play. She felt her knee give way and she
could not move. AP (Fig.12.16A) and lateral ( Fig. 12-16B) radiographs showed an anterolateral knee dislocation. She
had been disqualified from sports but not all school activities. Her ACL was torn. Intraarticular structures and posterior
cruciate ligament (PCL) were normal. She developed a deep vein thrombosis. After 6 months of anticoagulation, she
underwent ACL reconstruction.
FIGURE 12.16. A and B: These films of a knee dislocation are an example of the severe injuries that can occur in
cheerleading. This athlete fell from the top of a mount, sustaining an anterior knee dislocation. (Copyright 1999, M.L.
Ireland.)
A female soccer player was injured in a noncontact mechanism. She was noted to have significant lateral knee pain on
the examination that was consistent with a torn ACL. A sagittal magnetic resonance imaging (MRI) scan with T1-weighted
images showed incontinuity of the ACL (Fig. 12.17A). This was confirmed at the time of surgery with a complete
midstance ACL tear (Fig. 12.17B). The T2-weighted sequences confirm a lateral bone bruise of the midportion of the
distal femur, (Fig. 12.17C) and posterior aspect of the tibial plateau ( Fig. 12.17D).
FIGURE 12.17. A–D: MRI scan (sagittal views) confirms complete anterior cruciate ligament tear (A) documented by
arthroscopy of a mop end tear of the anterior cruciate ligament lying anterior to the notch. (B). Bone bruise is seen best
on the T2-weighted sequences of the distal lateral femoral condyle (C) and posterior aspect of the proximal lateral tibial
plateau (D). (Copyright 1999, M.L. Ireland.)
Factors Contributing to Anterior Cruciate Ligament Injury and Intervention Programs
The factors contributing to ACL injuries can be classified into intrinsic (not changeable), extrinsic (changeable), and
combined (potentially changeable) ( Table 12.12). Gender variations and movement patterns do exist. Intrinsic factors
include alignment, joint hyperextension, physiologic rotatory laxity, ACL size with its associated notch size and shape,
hormonal influences, and inherited skills and coordination. Extrinsic or changeable factors include strength, conditioning,
type of shoes, and motivation. Combined or potentially changeable factors are proprioception, neuromuscular order of
firing, and acquired skills. The dynamic movement patterns and coaching command of stay in a “get down position” when
landing or rotating is recommended. The get ready position of hip and knee flexion, hips over knees over toes should be
taught. The coaching command “stay down” gives the athlete a more effective and safer starting position.
TABLE 12.12. FACTORS CONTRIBUTING TO ACL INJURIES
Rehabilitation programs are similar for men and women; however, certain factors have been noted in the rehabilitation
programs for women (50). The type of graft used for ACL reconstruction depends on surgeon preference, not gender of
the patient. Readiness of the knee for ACL reconstruction is key.
Electromyelography (EMG) and videoanalysis find differences in activation of muscles and landing patterns comparing
men and women. Female athletes land with a quadriceps activation pattern ( 51). In another study, they landed less flexed
at the hip and knee, and in more knee valgus ( 52). There is ongoing research on contribution from muscle fatigue ( 53)
and muscle firing patterns (54,55).
Preseason screening programs measuring static physical factors have been designed ( 56). However, these studies have
not proved helpful in predicting ACL injury. Preseason screening of movement patterns and assessment by Sahrmann
exercises have resulted in the reduction of ACL tears over the past 5 years ( 57).
Use of a program including Sahrmann exercises and Swiss ball has reduced ACL injury rates. (B. Kola, personal
communication, 1992). The functional movement patterns incorporate standing, seated, and prone positions ( Fig. 12.18)
to maximize brain to body awareness. The program includes steady position for balance and hip strengthening ( Fig.
12.18A), seated with multiple perturbations for balance and core stabilization ( Fig. 12.18B) and prone for hip and back
strengthening (Fig. 12.18C).
FIGURE 12.18. A–C: Use of Swiss ball in rehabilitation enables the combination of balance and functional movement
patterns. In the single leg minisquat, pick-up-the ball, which is put in several different positions, is shown. A: Balance
while seated on the ball with feet on another smaller ball creates opportunity for core stability and perturbation to regain
balance. B: Prone wheelbarrow-type walking allows for perturbation of balance, strengthening of the gluteals on the right
side (C). (Copyright, 1999, M. L. Ireland.)
ACL Research Projects
Some prospective studies have been performed (58), but more research is needed. Studies analyzing differences in
noninjured female volleyball and basketball athletes showed only one statistically significant difference in isokinetic
strength testing and no differences in ligamentous laxity ( 59). This difference was with greater peak extension and higher
hamstring-to-quadriceps peak torque ratio in trail leg at 60 degrees per second in volleyball players. KT 1000 (Medmetric
Company, San Diego, CA) testing showed no statistically significant anterior displacement comparing legs or sports.
Further investigation with high-speed video, taping, force plate analysis, and EMG of lower-extremity musculature is
needed. A plyometric jumping training program was conducted for female athletes. After training, women showed
increased jump heights, increased hamstring strength, decreased peak landing forces, and decreased knee abduction
and adduction moments. After training, the women showed peak torque ratios similar to those of male athletes ( 60). This
factor is significant in that as the hamstring strength is increased, there is less strain on the ACL and this strengthening
program could impact the number of ACL injuries in female athletes.
Researchers and clinicians involved in answering the questions of why women have increased rates of ACL injury over
their male counterparts believe that the answer is most likely multifactorial. Training, laxity, hormonal influences, and
anatomic differences play a role. Researchers have noticed that women tend to be in a more upright position, with less
hip and knee flexion with their body weight more forward with their knees in a more valgus position when landing jumps,
as demonstrated in Fig. 12.19. Why women tend to assume this position with their knees is a question that has yet to be
answered. Does this more upright position predispose women to the so-called point of no return ( Fig. 12.20) valgus
external rotation injury? . Clearly, more research should be conducted in this area in order to find answers to these
questions and also to find methods of intervention to try to prevent ACL injury in female athletes ( 52).
FIGURE 12.19. Injury to the left knee as observed from the back and left side of the athlete. She has just rebounded and
stops to change direction to avoid the defending player. She lands in an upright position with less knee and hip flexion,
and forward-flexed lumbar spine. After the ACL fails, she falls forward and knee valgus rotation and flexion increase. She
is unable to upright herself and regain pelvis control to avoid ACL injury. (Copyright 1999, M. L. Ireland.)
FIGURE 12.20. This picture demonstrates a safe landing position compared to the “point of no return” as this basketball
athlete sustains an ACL tear. (Copyright 1999, M.L. Ireland.)
Consensus Statement—Anterior Cruciate Ligament Injuries in Females
The majority of the ACL injuries sustained by women are of a noncontact mechanism. The American Orthopaedic Society
for Sports Medicine (AOSSM), the National Athletic Trainers Association (NATA), NCAA, and the Orthopaedic Research
and Education Foundation (OREF) sponsored a consensus conference to address the issue of noncontact ACL injuries
and to define risk factors and directions for future research. The members of the symposium concluded that at-risk
situations for noncontact ACL injury include deceleration, cutting or changing directions, and landing. Shoe surface
coefficient of friction may increase the risk of ACL injury. There is no evidence that knee braces prevent ACL injury.
There is no consensus regarding the role of the notch in ACL injury owing to difficulties in obtaining reliable and
reproducible measurements. There are insufficient data on ACL size as measured by notch size to support ligament size
is related to risk of injury. There is no consensus regarding hormonal influences on the ACL or if fluctuating hormonal
levels in females predispose ACL injury. There is no basis for modification of participation during various phases of the
menstrual cycle or manipulation of sex-specific hormones to prevent ACL injuries (Griffin LY et al, Non-Contact ACL
Consensus Symposium, Hunt Valley, Maryland, June 10, 1999).
SPECIFIC BODY LOCATIONS
Lower Leg
Leg pain is a common complaint among athletes and most often results in a diagnosis of shin splints or medial tibial
stress syndrome (MTSS). Although MTSS is common, a stress fracture should always be ruled out when evaluating an
athlete with lower-leg pain. Athletes may also develop an exertional compartment syndrome. Women with exertional
chronic calf compartment syndrome are more susceptible but respond less well to operative fasciotomy compared with
men (61).
Foot and Ankle
Bunions (hallux valgus) are commonly encountered in the female athletes. Correction for cosmetic reasons should not be
performed because a painful, although straight, great toe may result. Modification of the type of shoe worn is the
mainstay of treatment (62). Severe clinical bunion abnormalities are commonly seen but are usually asymptomatic. A
Morton foot with a short first metatarsal can result in a severe but painless hallux valgus, as in the dancer shown in Fig.
12.21. Symptomatic stress fractures of the tibial (medial) sesamoid can mimic bunion pain. A workup with plain films in a
track athlete showed diffuse radiolucency on dorsiflexion sunrise sesamoid views ( Fig. 12.22A). Increased activity on
bone scan (Fig. 12.22B) confirmed the diagnosis.
FIGURE 12.21. Bunions of hallux valgus are quite common in women, especially dance athletes. Standing AP views of
both feet show hallux valgus, lateral subluxation of great toe and sesamoids, and short first metatarsal. (From Fu FH,
Stone DA, eds.Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994;167,
with permission.)
FIGURE 12.22. A,B: In runners, great toe pain, especially with pain in the plantar aspect, can be a sesamoid fracture.
(A) Sunrise views show radiolucency of tibial ( medial) sesamoid compared to fibular sesamoid ( lateral) on right foot
(arrow). (B) Bone scan confirms a stress fracture of the sesamoid left foot. This was treated with padding, avoidance of
running; healing occurred at 8 months clinically. (From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention,
and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:167, with permission.)
Stress fractures should also be considered. In dance athletes, a second metatarsal stress fracture can occur at the
Lisfranc joint (63). Stress fractures of the tarsal navicular cause pain in changing areas of the midfoot and need to be
diagnosed early for predictable healing to occur. Oblique radiographs and computed tomographic (CT) scan should be
performed if tarsal navicular fracture is considered ( 64).
In ballet athletes, posterior impingement of the os trigonum can result in local pressure on the flexor hallucis longus. Pain
in the posterior ankle is elicited by resistive testing of great toe plantar flexion. A cone lateral view before ( Fig. 12.23A)
and after (Fig. 12.23B) os trigonum excision is shown. Pain-free resumption of ballet activities was possible after surgery.
FIGURE 12.23. A–B: Ballet athletes who complain of posterior ankle and great toe pain can have a symptomatic os
trigonum fracture. A: A large os trigonum is seen in this ballet athlete, who is having difficulty in doing repetitive en pointe
maneuvers. Nonunion and pressure on flexor hallucis longus result in posterior ankle pain and great toe flexion
weakness. B: Surgical excision of this lesion, as shown by postoperative lateral radiograph, resulted in a complete cure.
(From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams &
Wilkins, 1994:165, with permission.)
Tendon problems of the foot are common in women. Posterior tibial tendinitis is seen commonly in dance athletes with
pes planus and in gymnasts. Tendon problems are more common with the cavus foot. Accessory ossicles may be
symptomatic at tendon insertions. This condition caused pain on eversion in this soccer athlete. A peroneus brevis
accessory ossicle can be symptomatic. The os vesalianum in Fig. 12.24, as shown preoperatively, required excision
owing to persistent pain.
FIGURE 12.24. Symptomatic secondary ossification center at the base of the fifth metatarsal in this soccer athlete
required excision. Os vesalianum (arrow) was excised with uneventful return to full activities. (From Fu FH, Stone DA,
eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:166, with
permission.)
Tibiotalar impingement syndrome results from repetitive axial loading sports. Osteophyte formation of the distal tibia and
dorsal talar neck causes loss of dorsiflexion range and anterior pain ( Fig. 12.25A). Arthroscopic removal of osteophytes
and partial synovectomy allow a return to sport with improved motion ( Fig. 12.25B).
FIGURE 12.25. A: Tibiotalar impingement syndrome is seen in a forced dorsiflexion lateral view with an osteophyte on
the neck of the talus with convexity instead of concavity. Impingement of the tibia and talus results in anterior
compartment synovitis and limited dorsiflexion range. B: Arthroscopic synovectomy and debridement of osteophytes has
been successful. Resector and tibia are shown on upper side and talus (arrows) on the bottom. (From Fu FH, Stone DA,
eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:165, with
permission.)
The ankle is the most commonly injured body part, and inversion ankle sprains are a common athletic injury. Although
these injuries are usually treated with few sequelae, chronic instability can develop. A basketball athlete began with an
ankle sprain in high school and continued to have problems with lateral instability as a college player. Stress films of her
ankle are shown (Fig. 12.26A, talofibular view; Fig. 12.26B, anterior drawer view). She underwent a lateral ankle
reconstruction after her college career. Her examination under anesthesia shows her severe instability ( Fig. 12.26C).
Talar dome fractures can also occur during an inversion or eversion injury to the ankle. The radiographs in Fig. 12.27 (A,
AP view; B, lateral view) show an example of a lateral talar dome fracture. The lateral talar dome fracture should be
included in the differential diagnosis of an ankle sprain that fails to respond to the usual care. Also in the differential
diagnosis for an ankle sprain that fails to respond to conservative care is chronically subluxing peroneal tendons. The
athlete reports of popping over the lateral ankle with eversion.
FIGURE 12.26. A–C: Collegiate basketball athlete had sustained numerous severe ankle sprains. Her radiographs show
a severe talar tilt and anterior drawer ( A and B). At the time of her lateral reconstruction, clinical talar tilt demonstrates
the only stabilizing structures are the skin laterally (C). (Copyright 1999, M. L. Ireland.)
FIGURE 12.27. A and B: Ankle views show a depressed talar dome fracture with the overlapping radiolucency seen on
the AP view (A) and the indented displaced talar dome fracture seen on lateral view (B). (Copyright 1999, M. L. Ireland.)
High ankle sprains are common in gymnasts, in part due to the nature of their sport. Gymnasts do not wear shoes and
land aerial maneuvers frequently, thereby predisposing them to ankle injuries. Although inversion injuries are most
common, frequently a forced dorsiflexion injury from landing short results in a tibiofibular syndesmosis sprain or high
ankle sprain. The time until the patient can return to sports is longer with this type of sprain.
Shoulder
With generalized laxity, sport-dependent problems involving the shoulder occur. The vicious circle of physiologic
instability, rotator cuff weakness, pain, posterior tightness, and further imbalance results in persistent pain and
dysfunction in overhead activities or in extremes of range of motion ( Fig. 12.28). In girls, joint laxity and decreased
strength can cause shoulder problems.
FIGURE 12.28. Vicious circle of shoulder pain occurs in women, especially when there is a physiologic instability that
may be multidirectional, with rotator cuff weakness, subsequent pain, posterior tightness, further weakness, and muscular
imbalance. (From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore:
In competitive diving, the forces involving axial loading on water entry and extreme ranges of motion during the
gymnastic portion of diving maneuvers result in combined rotator cuff and instability problems. Use of the shoulder as a
weight-bearing joint can lead to long-term dysfunction. In gymnastics, the shoulder is commonly injured ( 6,9,65). A
sport-specific strengthening program may prevent significant injuries.
Restoration of normal range of motion and strength with proper sport biomechanics is the goal.
In swimmers, increasing joint distraction and repetitive microtrauma, “impingement syndrome,” and pain are common
(66). The exact diagnosis should be documented by noting the structure involved, and the severity and acuteness of the
injury. Treatment is strengthening, relative rest, and evaluation of biomechanics. A 13-year-old competitive swimmer with
a 6-month history of vague shoulder pain had physiologic ligamentous laxity of her bilateral shoulders. The examiner
subluxed her shoulder anteriorly and then reduced the humeral head back into the glenoid ( Fig. 12.29A and Fig. 12.29B).
Associated generalized laxity and multidirectional instability are common in swimmers, gymnasts, dancers, and
cheerleaders.
FIGURE 12.29. A and B: Thirteen-year-old swimmer has multidirectional physiologic laxity. Stabilization of the acromion
allows for translation anteriorly (A) and translation posteriorly (B). (Copyright 1999, M. L. Ireland.)
A right-hand dominant discus thrower who was involved in a meet threw the discus, and she felt acute pain in her right
shoulder and the inability to move her arm. Radiographs ( Fig. 12.30A) revealed a posterior dislocation. Closed reduction
was performed in the emergency room. The patient underwent arthroscopy, with the findings being acute posterior
labrum tear, producing severe posterior instability ( Fig. 12.31B). Open posterior capsulorrhaphy was performed. At
1-year after surgery, she has no complaints, is stable posteriorly, and has not been allowed to return to discus throwing.
With acute posterior dislocation with significant intraarticular findings, acute reconstruction should be considered. In
multidirectional instability without one traumatic incidence, avoidance of surgery and rehabilitation is key.
FIGURE 12.30. A and B: Discus thrower sustained an acute dislocation of her shoulder seen in axillary view (arrows
point to glenoid rim posteriorly). A: Arthroscopy documents the posterior superior glenoid labrum tear. B: Reverse
Bankart open posterior reconstruction was performed. (Copyright 1999, M. L. Ireland.)
FIGURE 12.31. Displaced Salter II fracture of proximal humerus in a 13-year-old cheerleader (A). Closed reduction and
percutaneous pinning was performed (B). (Copyright 1999, M.L. Ireland.)
It is important to conduct repeat examinations and understand the psychological status and physical demands of the
patient with multidirectional instability. Although arthroscopic techniques have provided the option of thermal capsular
modification, the question about who needs what procedure remains unanswered. Studies do not have long-term
follow-up. In individuals whose shoulders are equally pathologically unstable in multiple directions, one should not
counsel a patient that the shoulder can be made normal with surgical intervention. It has been stated there is nothing that
cannot be made worse with surgery (Jack Hughston, personal communication). In the multidirectional instability shoulder
patient who does not have proper strengthening core balance, particularly the scapula, the arthroscope and thermal
wand should not be utilized for at least a year or until one is sure they understand the individual and that she has failed
her rehabilitation program.
In the skeletally immature individual, pain and deformity at the proximal humerus indicate a fracture. A cheerleader was
continuing to do back flips in a restaurant parking lot and sustained a Salter II fracture of the proximal humerus ( Fig.
12.31A). Closed reduction and internal fixation were performed ( Fig. 12.31B). Postoperatively, she did well and resumed
cheerleading, including gymnastics, in 4 months. Proximal humerus stress fractures as in throwers' shoulders through the
growth plate are not as common in female as in male athletes.
Elbow
Women have an increased valgus-carrying angle and ligamentous laxity compared with men. Owing to the increased
lateral pressures and less upper-extremity strength, repetitive axial loading activities are common.
Osteochondritis dissecans with resultant loose body formation should be considered in axial loading sports. A
fourteen-year-old gymnast reported that her elbow locked. Arthroscopy revealed several osteocartilaginous loose bodies
in the anterior compartment (Fig. 12.32A).The fragment of the capitellum was loose. Loose bodies were removed, and
capitellar debridement was performed (Fig. 12.32B). The largest loose body is shown at the time of arthroscopic removal
(Fig. 12.32C). She resumed gymnastics 8 months after surgery, with the understanding her elbow may be reinjured or
become arthritic.
FIGURE 12.32. Osteochondritis dissecans of the capitellum is shown with posterior compartment loose bodies (A).
Arthroscopic assessment revealed a loose fragment on the capitellum, as shown by the needle (B). Loose bodies in the
posterior compartment are visualized and were removed (C). (Copyright 1999, M. L. Ireland.)
Severe injuries can occur in cheerleading. A girl sustained an elbow dislocation when she landed short from a
double-back stunt. Attempted reduction by personnel at practice was not successful. AP and lateral elbow radiographs
showed a posterolateral dislocation ( Fig. 12.33A). A physical examination revealed absent radial pulse and pain, an
ecchymotic area medially, and severe elbow swelling ( Fig. 12.33B). An emergency arteriogram (Fig. 12.33C) showed
absent filling of the brachial artery, although collateral filling was present. The hand was viable. Surgical exploration
revealed an entrapped brachial artery. A cephalic vein patch to the brachial artery was required to restore normal
vascularity.
FIGURE 12.33. This cheerleader sustained a dislocation of her right elbow when she landed from a double-back stunt. A:
AP and lateral films in the emergency room show the posterolateral dislocation. Attempts at her practice site had been
made to reduce the elbow. B: Examination revealed a pulseless upper extremity. Notice the ecchymotic area
anteromedially. C: The brachial artery by arteriogram showed no filling of the brachial artery at the elbow proximal and
distal. Distal is at the top as seen by the radiograph on right. Surgical intervention with a cephalic vein patch to restore
normal vascularity in the upper extremity was required. Despite counseling, she returned to cheerleading 6 months later
with 10- to 140-degree range of motion in the elbow and full pronation and supination. ( B from Fu FH, Stone DA, eds.
Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:171.) ( A and C:
Copyright 1999, M.L. Ireland.)
Wrist and Hand
Wrist pain is a frequent complaint in gymnasts, and it can also occur in participants in racquet sports, golf, weight lifting,
martial arts, biking, and softball. Contact injuries resulting in fracture can occur in any of these sports and can also occur
in ice hockey, lacrosse, and field hockey. Overuse injuries are more common in gymnastics, golf, racquet sports, biking,
and weight lifting.
In gymnastics, the upper extremity becomes a weight-bearing joint, predisposing it to injury. Studies have indicated that
73% of gymnasts experience wrist pain (67). Etiologies of chronic wrist pain in gymnasts and other athletes include tears
of the triangular fibrocartilage cartilage complex, ulnar impaction syndrome, dorsal wrist capsulitis, distal radius physeal
injury, dorsal wrist ganglion, and stress fracture ( 68). In gymnastics, there is a phenomenon called a grip lock that is a
source of injury unique to the sport. Previously seen in men participating in high bar, it is now seen in women using the
uneven parallel bars. With the emerging similarities between men's high bar and uneven parallel bar routines, women
have begun wearing doweled grips to protect their hands. Grip lock occurs when the dowel grip becomes locked on the
bar as the gymnast moves through a skill with increasing momentum (69). This phenomenon results in forces being
transferred to the distal radius and can result in fracture. The forces transferred to the distal radius from routine wear of
doweled grips is a potential etiology for chronic wrist pain in gymnasts. Golfers, racquet athletes, weight lifters, and
bikers can fall prey to repetition axial loading syndromes. Injuries to the triangular fibrocartilage complex, fractures of the
hook of the hamate, tendinitis, and carpal tunnel syndrome are sources of wrist pain in these athletes. Bicycle athletes
may suffer from ulnar nerve compression at Guyon canal ( 68).
Stress Fractures
There are several populations of female athletes who are at increased risk for stress fracture. In the military population,
stress fractures were found to be more common in female cadets compared with male cadets (32). The association of
menstrual irregularity and stress fractures in collegiate female distance runners has been established ( 70). Several
series report increased incidence of stress fractures in women ( 71,72,73,74 and 75). The association of stress fractures
with low bone density, amenorrhea, and poor nutrition has been established ( 30,43,45). The association of nutritional
habits and the incidence of stress fractures in ballet dancers were reviewed ( 76). Specific health concerns of female
runners have been addressed ( 30,77).
A detailed nutritional and gynecologic history must be obtained in female athletes presenting with stress fractures. Bone
densitometry should be performed after a second stress injury. Appropriate treatment is mandatory. The plan must be
monitored and include diet and nutritional analysis, hormonal, calcium, and vitamin D replacement ( 1,3,30,78).
First Rib
Fractures of the first rib are most commonly associated with major trauma; however, stress fractures of the first rib have
been reported in female rowers (79). In a ballet athlete, a delayed union ( Fig. 12.34) occurred. The only mechanism of
injury was repetitive lifting by her partner. Treatment was directed toward improvement of the dancer's nutrition and her
hormonal status, with avoidance of the specific lifting maneuvers that led to the injury. Resumption of full activities
occurred at 8 months following the injury.
FIGURE 12.34. A ballet athlete sustained a left first rib fracture that went onto a delayed union. Notice the rounded edges
of the proximal fragment. (From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed.
Baltimore: Williams & Wilkins, 1994:172, with permission.)
Wrist Fractures
Distal Radius Epiphyseal Fractures
Young gymnasts have been reported to have stress changes of the distal epiphysis ( 80). Repetitive axial compression
forces on the distal radius can cause epiphyseal reactions or fracture. A Salter I distal radius fracture occurred in both
wrists in a 10-year-old gymnast (Fig. 12.35). The metaphysis shows increased bone density, and the epiphysis shows
widening. The fractures healed uneventfully. However, radial growth arrest with subsequent ulnar overgrowth can occur.
Clinical and radiographic examinations should be performed until skeletal maturity is reached.
FIGURE 12.35. Bilateral wrist pain consistent with Salter I stress fracture of the distal radial epiphysis. The sclerosis and
widening are more noticeable on the left than the right in this skeletally immature athlete. (Copyright 1999, M. L. Ireland.)
Even in the skeletally immature individual, navicular fractures occur. A gymnast complained of right wrist pain for three
weeks. She had tenderness in the anatomic snuffbox. Radiographs showed a midwaist navicular fracture ( Fig. 12.36).
FIGURE 12.36. Acute midwaist navicular fracture is seen in this skeletally immature right wrist of a gymnast . (From Fu
FH, Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins,
A collegiate gymnast complained of wrist pain for 3 months. A workup with normal plain views marked at the area of
maximal tenderness (Fig. 12.37A), tomograms (Fig. 12.37B), and a bone scan (Fig. 12.37C) confirmed the diagnosis of
distal radius stress fracture with localized cyst. Successful treatment included dorsal taping blocking full dorsiflexion and
relative rest.
FIGURE 12.37. Repetitive landing on the wrist in a dorsiflexed position resulted in wrist pain in this gymnast. Plain
radiographs frequently are negative. Marked AP view before tomograms (A), and oblique tomograms (B) show a cystic
distal radius stress fracture confirmed by (C) bone scan. Increased activity in the dorsal central aspect of the right radius
is shown. (From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore:
Spondylolysis
Repetitive flexion extension activities can result in stress fractures of the pars interarticularis or spondylolysis. The
workup of persistent back pain and a positive hyperextension test should include AP, standing lateral, and oblique
radiographs. The radiolucent defect in the pars interarticularis is best seen on oblique view ( Fig. 12.38A). Increased
activity on oblique view bone scan at the third lumbar level confirms the diagnosis of spondylolysis ( Fig. 12.38B).
Acquired spondylolysis does not progress to spondylolisthesis. In these athletes, spondylolysis and sciatica can occur
simultaneously in a single patient. If there is nonunion of the pars interarticularis, posterior spinal fusion successfully
eliminates pain. (Micheli LJ, personal communication 1984).
FIGURE 12.38. An acute pars interarticularis defect in a cheerleader who had a positive hyperextension test is shown on
oblique marked radiograph (arrow) (A). The acuteness of the spondylolysis is confirmed by increased activity on bone
scan at L4 level (B). (From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed.
Baltimore: Williams & Wilkins, 1994:79 with permission.)
Pelvis
Stress fractures can occur through the apophyses of the pelvis. Specific bony tenderness over the origin of the muscles
of the pelvis should alert the examiner to a bony problem. A 13-year-old dancer and cheerleader was having medial groin
and buttocks pain for 3 weeks. Radiographs revealed an ischial tuberosity and nondisplaced fracture ( Fig. 12.39). She
had reduction of her activities and returned to dance uneventfully in 2 months. She has had no further problems. She had
been increasing her practice activities.
FIGURE 12.39. Ischial apophyseal fracture occurred in this cheerleader presenting with buttock and medial groin pain
(arrows). (Copyright 1999, M. L. Ireland.)
Femoral Neck
There should be a high index of suspicion for fracture in track athletes with persistent groin pain. An iliopsoas or adductor
strain could be a femoral neck stress fracture. A middle distance and cross country track athlete complained of left hip
pain for one month. She was amenorrheic and did not eat meat or drink milk. AP ( Fig. 12.40A) and lateral ( Fig. 12.40B)
radiographs showed cortical reaction of the inferior and posterior femoral neck. An initial bone scan showed increased
activity (Fig. 12.40C). This compression side fracture was treated conservatively with non–weight bearing, swimming,
nutritional counseling, and oral contraceptives. The fractures healed in 6 months clinically and radiographically, as
shown on AP view (Fig. 12.40D). On the compression side, femoral neck stress fractures can be treated nonoperatively.
If the fracture is on the superior or tensile side, percutaneous pinning before fracture displacement is recommended.
FIGURE 12.40. A collegiate middle distance and cross country track athlete had pain in her left hip for 1 month. Plain
radiographs showed (A) AP view with thickened medial cortex and radiolucency and (B) a lateral view with periosteal
reaction posteriorly. The stress fracture on the compression side inferiorly can be treated nonoperatively. Tension or
superior femoral neck fractures should be more aggressively treated with pinning before displacement. C: A bone scan
showed significant increase in activity in the inferior neck . D: Follow-up radiographs 6 months following documentation of
the fracture showed femoral neck periosteal reaction. (From Fu FH, Stone DA, eds. Sports injuries: mechanism,
prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:174, with permission.)
Tibial Fracture
The tibia is a common site for stress fractures. Use of marked views over the area of maximal tenderness to look for
periosteal reactions is helpful. If plain films are negative, a bone scan will confirm the diagnosis.
The midthird anterior cortex stress fractures is important to recognize. Clinically, point tenderness and anterior tibial bow
suggest this unique stress fracture. Plain radiographs of AP ( Fig. 12.41A), lateral (Fig. 12.41B), and cone-marked lateral
view at point of maximum tenderness (Fig. 12.41C) confirm the diagnosis. This type of fracture is commonly seen in
basketball athletes with varus and anterior bow of the tibia. Conservative management usually results in healing, as in
the patient shown in Fig. 12.41, after 6 months. However, electrical stimulation or operative management has also been
suggested.
FIGURE 12.41. This female basketball athlete sustained a stress fracture in the midthird anterior cortex of the left tibia.
AP (A) and lateral view (B) show the healing fracture 4 months after onset of symptoms. C: A metallic marker on lateral
view at point of maximum tenderness helps confirm that the radiolucency seen is at the level of patient's pain.
Conservative management in this patient resulted in complete healing. (From Fu FH, Stone DA, eds. Sports injuries:
mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:176, with permission.)
Fibular Fractures
Repetitive loading, such as tumbling, floor routines, cheerleading, and gymnastic maneuvers, may result in fibular stress
fractures. Pain localization to the lateral fibula and radiographs showing significant increased cortical thickness and a
very small medullary cavity are the usual findings in athletes with fibular stress fractures. Tibiofibular views with the
marker at the area of maximal tenderness suggest a fracture (Fig. 12.42A). Note the prior, now asymptomatic, healed
fibular stress fracture just proximal to marked level in the collegiate cheerleader shown in Fig. 12.42. A bone scan
revealed intensely increased activity at the level of maximal tenderness ( Fig. 12.42B). Successful treatment included
compressive support and avoidance of tumbling activities for 3 months.
FIGURE 12.42. This collegiate cheerleader was evaluated for pain in the lateral calf. A: A marked view revealed
periosteal reaction at the midthird of the fibula. Notice the periosteal reaction just superior to level of symptoms . The
patient had a documented stress fracture of the fibula at this level 6 months before her new onset of symptoms. Notice
the narrow intramedullary cavity. B: A bone scan showed increased activity more intensely at the distal fracture level
shown on the left compared with the normal lower extremity on the right. (From Fu FH, Stone DA, eds. Sports injuries:
Metatarsal Fractures
The most common metatarsal stress fracture occurs in the second metatarsal, followed by the third metatarsal. This track
athlete had a second metatarsal stress fracture ( Fig. 12.43). With localized swelling and tenderness over the diaphysis
and callus on plain radiographs, the diagnosis was easily established.
FIGURE 12.43. A callus is seen in this healing second metatarsal stress fracture in a female track athlete. On plain films,
radiolucency of the fracture line can be seen with abundant callus, which was palpable and painful over the second
metatarsal diaphysis. (From: Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed.
Baltimore: Williams & Wilkins, 1994;177, with permission.)
Tarsal Navicular Fractures
One must consider a stress fracture of the tarsal navicular in an athlete with midfoot pain, which may change in location.
A 19-year-old collegiate basketball player had complaints of pain and had tenderness dorsally and plantarly in her
midfoot when she began college basketball. The increase in training and footwear changes were contributing factors.
Oblique plain radiograph fractures show a medial longitudinal radiolucency consistent with a stress fracture ( Fig.
12.44A). The specific views that should be used are the oblique and coned views ( 64). A bone scan showed increased
activity bilateral in the navicular area ( Fig. 12.44B). A CT scan showed bilateral stress fractures ( Fig. 12.44C). The
patient underwent open reduction and internal fixation (ORIF), and bone grafting ( Fig. 12.44D). She returned to
basketball 6 months later.
FIGURE 12.44. This collegiate basketball player reported pain in the midportion of her left foot. Radiographs show a
longitudinal medial navicular stress fracture (arrow). A: Bone scan confirms bilateral stress fractures, asymptomatic on
the right. B: CT scan shows the fracture to be communicating with the plantar aspect of the talonavicular joint shown on
the right. The asymptomatic right navicular fracture does not communicate with the plantar surface. C: The films after
open reduction internal fixation and bone grafting are shown. D: The patient has continued to play basketball. The right
navicular fracture remained asymptomatic for 4 years. (Copyright 1999, M. L. Ireland.)
Back Conditions and Fractures
Scoliosis
Scoliosis is more common in women than in men. Larger scoliotic curves are more prevalent in women, with smaller
curves having the same incidence (82). The female-to-male ratio in curves rated at 21 degrees is 7.2:1, 11 to 20 degrees
is 5.4:1, and 6 to 10 degrees is 1:1. In reviewing the age distribution, the ratio with the incidence is the same in patients
younger than 8 years of age. In patients older than 8 years of age, the female incidence is 4.6 per 1,000 and the male
incidence is 0.2 per 1,000 ( 83). The etiology of scoliosis is multifactorial ( 84). Sources include ligament insufficiency,
collagen abnormalities, muscle imbalance with unequal fiber distribution, and vestibular influences.
A skeletally immature 11-year-old cheerleader had a 16-degree left lumbar curve with more pronounced rotation seen in
posterior anterior view ( Fig. 12.45). This patient had not previously been diagnosed with scoliosis ( Fig. 12.46). A
posterior-anterior (PA) standing radiograph shows significant thoracolumbar scoliosis. She underwent instrumentation
and fusion.
FIGURE 12.45. Sixteen-degree left lumbar scoliosis with significant rotation is shown in this radiograph. (Copyright 1999,
M. L. Ireland.)
FIGURE 12.46. This severe thoracolumbar curve in this nonathlete necessitated stabilization, instrumentation, and
fusion. (Copyright 1999, M. L. Ireland.)
Spondylolisthesis
Standing lateral views are necessary to assess posterior spinal stability for spondylolisthesis. This collegiate gymnast
had a 5-year history of occasional back pain. Standing lateral view showed L-5 to S-1 grade IV spondylolisthesis,
indicated by dotted lines ( Fig. 12.47A). Oblique views showed two old radiolucencies in the pars interarticularis at L-5
(Fig. 12.47B). This gymnast had previous back problems but had none at the time of presentation. She reported only
limited to lateral calf pain. A bone scan showed increased activity in the fibula ( Fig. 12.47C) but no increased activity in
the lumbar spine (Fig. 12.47D).
FIGURE 12.47. Standing lateral views are necessary to assess posterior spinal stability. A: Standing lateral view of
collegiate level gymnast shows a grade IV spondylolysis at the L-5 to S-1 level (linear arrows). B: Oblique view shows
two levels of pars defect at the L-5 level (arrows). Patient was evaluated for pain in her fibula. She mentioned prior
history of back problems, and a lateral radiograph was obtained. The patient was disqualified from continued collegiate
competition owing to subsequent low back pain and neurologic complaints. The bone scan shows increased activity in
the fibula consistent with a stress fracture (arrows) (C) and no increase in activity in the lumbar spine (D). (From Fu FH,
Stone DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:180,
with permission.)
Spondylolysis at different levels from a spondylolisthesis may also occur. In a cheerleader, an acute spondylolysis is
shown in this oblique marked view ( Fig. 12.48A). A bone scan showed increased activity at the marked level of pain but
not at L-5 to S-1 level. An old grade I spondylolisthesis is shown two levels lower than her acute pars injury ( Fig. 12.48B).
FIGURE 12.48. An old spondylolisthesis can be seen at a different level from an acute spondylolysis. A: A marked
oblique view at the level of pain is two levels above an old symptomatic grade I L-5 to S-1 spondylolisthesis seen on (B)
lateral view level. Note the radiolucency of posterior elements L-5 to S-1 without significant slippage. (From Fu FH, Stone
DA, eds. Sports injuries: mechanism, prevention, and treatment, 2nd ed. Baltimore: Williams & Wilkins, 1994:181, with
permission.)
Vertebral Body Fracture
A vertebral body fracture at L-5 occurred when a collegiate gymnast fell in a hyperflexed position from the top of the
uneven parallel bars. A cone view better shows the fracture, which showed increased activity on bone scan ( Fig. 12.49A).
Anatomic variants or a limbus vertebra may look similar. A positive technician bone scan was helpful to establish the
diagnosis and better counsel the athlete on the timing of a return to sport. A standing lateral view showed marked
lordosis 1 month after injury ( Fig. 12.49B).
FIGURE 12.49. This collegiate gymnast fell from a top uneven parallel bar in a hyperflexion mechanism. A: A cone view
shows superior vertebral body fracture (arrow). B: A standing lateral view 1 month following injury shows excessive
lordosis and healing of the L-5 fracture. (From Fu FH, Stone DA, eds. Sports injuries: mechanism, prevention, and
Pedicle stress fracture has been reported in a ballet athlete ( 85) and documented by CT scan. (Fig. 12.50A). Lateral
views showed radiolucency in posterior elements. The CT scan confirmed this diagnosis. ( Fig. 12.50B) There have also
been cases of multiple vertebral body compression fractures in elite gymnasts. These are chronic injuries due to the
repetitive nature of the sport and are considered stress fractures.
FIGURE 12.50. A pedicle stress fracture occurred in this ballet athlete. A: A standing lateral view shows posterior
element radiolucency (arrow). B: A CT scan confirmed the pedicle fracture. (From Fu FH, Stone DA, eds. Sports injuries:
PSYCHOLOGICAL CONSIDERATIONS
Girls who participate in athletics have improved self-confidence, overall performance, and well-being. Immediate positive
reinforcement is possible when girls actively engage in sports ( 30,86,87). Young women who understand their motives for
being involved in sports relate rewarding experiences. When maturity occurs, these goals may change and priorities are
modified in some female athletes ( 86). However, there are concerns regarding the intensity and ramifications of injury on
elite athletes in figure skating and gymnastics ( 88). Concerns regarding lasting injury and illness exist. Follow-up of a
women's collegiate gymnastic team showed that half of the athletes had not fully recovered from their injuries 3 years
after stopping competition (89). Participating and excelling in athletics can be used as a springboard for dealing with
stress, competition, and challenges in both professional and personal spheres of life ( 42).
NUTRITION
Adequate nutrition is of paramount importance for the athlete's health and successful performance. Reviews of nutritional
concerns in adolescent girls ( 90) and older athletes (91) have been addressed. Particularly in the female athlete, diets
are often poorly balanced or contain inadequate nutritional components ( 30,92,93 and 94). Studies comparing men and
women in similar sports have emphasized major differences in caloric intake and diet type. Collegiate basketball players
were compared showing that men had twice the caloric intake. Nutritional supplements had a significant effect on the
total nutrient intake in women ( 92). Compared with men, female skiers and marathoners consume fewer calories and
have reduced intake of vitamins, proteins, and carbohydrates ( 95).
Poor diet can result in deficiency in the intake of carbohydrates, iron, calcium, and zinc. Low calcium intake is associated
with low bone density, stress fractures, and subsequent problems with osteoporosis ( 95,96). Carbohydrate deficiency can
result in glycogen depletion and an increased onset of muscular fatigue. Zinc deficiency can result in increased injuries
from microtrauma as well as changes in immune function. Iron deficiency can contribute to anemia and to poor thermal
regulation, especially during exposure to cold.
Common nutritional problems contributing to poor performance are inadequate intake of fluids ( 97) and carbohydrates
(98), and excess fat intake (30,97,98,99 and 100). Nutritional counseling for female athletes to stress the importance of
proper ratios of food groups and other nutrients is needed. Nutritional educational programs are essential for
improvement of the food choices and overall health in the female athlete ( 95,97).
Fluid Intake
Fluid loss of only 1% of body weight during activity produces a state of dehydration. Fluid depletion can occur in as little
as 30 minutes (101). Simple weighing of athletes before and after activity to determine fluid loss is necessary. To
maintain physiologic hydration, 16 ounces of fluid must be consumed for every pound lost in excess of body weight
multiplied by .03 (101). Fluid intake schedules and discussions of the best hydration fluids have been published
(95,97,98,100,101).
Diet Composition
Meals high in complex carbohydrates, such as starches of bread, whole grain cereals, pasta, legumes, and vegetables
like potatoes are required to support all sports activity. Carbohydrates are a primary fuel for anaerobic work and the
limiting fuel for aerobic endurance work ( 98). Many female athletes harbor the belief that starchy foods cause obesity
(97). These athletes deprive themselves of starches, then suffer from increased injury and are prone to binge on
high-sugar, high-fat snacks. High-carbohydrate menu patterns of 60% carbohydrates should be made available for the
athlete (95,97,98,102).
Iron and calcium ingestion are of particular importance in female athletes. Calcium intake may need to be increased in
athletes with amenorrhea. Women have decreased blood volume, lower iron stores, decreased oxygen-carrying capacity,
lower dietary iron intake, increased iron loss, and absorption compared with men ( 37). For these reasons and owing to
inadequate intake associated with normal menstruation, iron deficiency anemia is very prevalent in females ( 103,104).
Recognition of iron deficiency anemia and treatment with supplements and dietary counseling are necessary ( 105).
Screening for anemia in all athletes is recommended. In adolescent athletes with a serious commitment to exercise
performance, screening of serum ferritin levels to determine a preanemic iron deficiency has been suggested ( 105).
Weight, body fat standards, and height and weight standards are used as training goals for athletes. The coaching and
medical staff must be aware of the proper methods to assess ideal body weight. It is best to employ standards that
determine progress toward an improved percentage of body fat. Methods for assessing body fat and guidelines for
setting standards can be found in nutritional sports references ( 101,106). Athletes carry more lean mass per height than
the general population. Weight for height standards can be misleading ( 97). The athlete should be performing at ideal
body weight. Contribution to compromised performance and behavior or to the eating disorders of anorexia nervosa and
bulimia occurs when unrealistic body weight and body fat percentages are given by an uneducated member of the
coaching or medical staff. Education of the athlete, the coaches, and the medical staff on athletic nutritional needs is
mandatory. Consultation with dietitians familiar with needs of a particular sport can result in significant improvements in
performance and decreases in injury and illness rates.
Eating Disorders
Eating disorders are underdiagnosed and exist in epidemic proportions in female athletes. Estimates are that anorexia
and bulimia affect as many as one third of athletic women (107). The athlete, family, coaches, and medical staff should
be aware of the very high incidence of eating disorders and nutritional misconceptions among adolescent girls. According
to the American Psychiatric Association's definition, eating disorders are gross disturbances in eating behavior, typically
beginning in adolescence or early adult life ( 108). Bulimia is fear of fatness but weight does not decrease below normal
weight. Episodes of binge eating and vomiting are common in bulimia. Anorexia nervosa is a disorder with features of
refusal to maintain body weight over minimal normal weight for age and height, intense fear of gaining weight or
becoming fat, a distorted body image, and amenorrhea. Anorexia is a misnomer because loss of appetite is rare. Bulimia
and anorexia nervosa can exist in a single patient.
In the athletic setting, frequent body weight measurements and teammate observation help identify underlying problems.
Denial of eating disorders is common. Cures are rare, so that early diagnosis of eating disorders is critical to the hope of
reestablishing a nutritionally sound and normal patient.
OSTEOPOROSIS
Hormonal replacement and weight-bearing exercise in the premenopausal stages reduces bone loss. Weight-bearing
activities in postmenopausal women appears to increase mineral content of bone ( 109). Weight-bearing exercise
increases or maintains bone mass, but does not produce a large increase in bone mass ( 110). Regularly maintained
athletic programs for adult women may reduce the rate of bone mass loss that occurs with age and especially
postmenopausally (111,112,113 and 114). Patients with anorexia nervosa have reduced bone density that may be
permanent. Bone density and mineral content in amenorrheic and eumenorrheic athletes and nonathletes have been
quantitated. Further work on bone density is being conducted to develop normal values for single as well as dual photon
densitometry normal values.
The female athlete triad is defined as amenorrhea, disordered eating, and osteoporosis. Each of the components of the
female athlete triad are discussed in separate sections of this chapter; however, it is important to recognize the triad as a
multifactorial problem. Activities such as dance, cheerleading, gymnastics, figure skating, and distance running that
emphasize a prepubertal body type, perfectionism, and thinness; have revealing clothing; and are subjectively judged are
at risk for developing this disorder. Pictures of Christy Henrich, a former national gymnastics team member who died of
anorexia nervosa, demonstrated the seriousness of this disease ( 88) (Fig. 12.51A and Fig. 12.51B). Young athletes who
are approaching puberty appear to be at increased risk ( 115). The best treatment is prevention, and it is important to
recognize the triad through preparticipation physicals, screening, and counseling.
FIGURE 12.51. Christy Henrich is shown when she was competing at the elite level in gymnastics. A: She did not make
the Olympic team. B: She died of anorexia nervosa, and her picture several months before her death is shown.
(Reprinted with permission from AP/Wide World Photos, 50 Rockefeller Plaza, New York, NY 10020.)
GYNECOLOGIC AND OBSTETRIC CONSIDERATIONS
Hormonal balance, menarche, menstrual disorders, and menopause are unique considerations in the female athlete.
Normal Menarche
Puberty is the transition period between the juvenile state and adulthood, when the adolescent growth spurt occurs and
when secondary sexual characteristics appear. Fertility is achieved and profound psychological changes take place. It is
also the time when many young athletes are initiating or finding their skills. In both men and women, there has been a
trend toward early onset of puberty over the last 150 years. This is thought to result from improvement in socioeconomic
conditions, nutrition, and general health. Although general trends vary, the average age of menarche in the United States
is approximately 12.3 years. It appears that the more critical factor in the time of menarche is the percentage of total body
fat, although critical height-to-weight ratios have been described also ( 116). Any factor affecting this critical percentage,
the body fat ratio, can alter normal menarche. Owing to multiple factors including variations in weight, accelerated activity
level, and individual differences, athletes are at great risk for delays in menarche or alteration in menstruation. Breast
development also occurs when the estrogen production in the normal hypothalamic pituitary gonadal axis occurs. Poor
nutrition and hormonal imbalance can alter normal development.
With the onset of puberty, the normal menstrual cycle occurs. Production of estrogen feeds back to the
hypothalamic-pituitary axis to stimulate production of FSH and development of follicles within the ovary. The surge of LH
at midcycle results in ovulation, followed by an increase in progesterone production in the luteal phase of the cycle, and
subsequently, menses.
Delayed Menarche
Delayed age at menarche and increased incidence of oligomenorrhea and amenorrhea have been associated with
training ( 117). Menarche in athletes appears to be delayed when compared with nonathletic women ( 118,119).
Premenarchal training does delay the onset of menses but not other pubertal changes ( 109).
Menstrual Abnormalities
Menstrual irregularities and nutritional abnormalities interrelate to increase the frequency and severity of injuries and
illnesses. Differences in body composition between men and women may affect performance in environmental extremes
(120). Whereas the average woman has a smaller surface area than her male counterpart, her ratio of body surface area
(BSA) to weight is greater. In hot climates, women gain heat faster and have a smaller mass to store it in. In air
temperature below skin temperature, women lose heat faster. In cold environments, increased subcutaneous fat
enhances insulation in women, but the increased BSA-to-weight ratio in women allows greater heat loss, so that men and
women with an equal percentage of body fat demonstrate no differences in metabolic rate, rectal temperature, or skin
temperature.
Gynecologic concerns and menstrual dysfunction have been reviewed ( 78,121). Decreased resting metabolic rates have
been documented in amenorrheic runners (122). Unique gynecologic situations in the female dancer have been
published ( 123). Women athletes with menstrual irregularity have an increased incidence of muscle injury ( 76).
Premenopausal individuals with irregular menses are at increased risk for musculoskeletal injury ( 71). There have been
recent studies showing that there are estrogen receptors within ligamentous structures such as the ACL. Estrogen
inhibits type I procollagen synthesis and proliferation fibroblasts in vitro at physiologic estradiol concentrations ( 124).
Other studies have attempted to link the phase of menstrual cycle to risk of injury to the ACL, and in one study, there
appeared to be more ACL injuries during the ovulatory phase of the menstrual cycle ( 125). Clearly, further research
needs to be done in this area to answer the question of what are the in vivo effects of estrogen on the ACL, and larger
studies are needed to review the phase of cycle in relation to ACL injuries.
Drinkwater et al. (126) and Lutter (77) reviewed the health concerns of women runners, including concerns about
menstrual abnormalities and pregnancy. An association of athletic amenorrhea, major affective disorders, and eating
disorders in runners has been suggested ( 127). The common occurrence of menstrual dysfunction in adolescents who
are involved in intensive athletic activity or who limit their nutritional intake excessively has been established ( 128).
Excessive exercise can alter body weight, decreasing the percentage of body fat, which, in turn, decreases estrogen
production. In this situation, the hypothalamic pituitary ovarian axis is affected, and anovulation, abnormal bleeding, and
amenorrhea occur. The association of menstrual dysfunction with low bone density has also been established
(96,126,129). Lowered estrogen levels and decreased calcium binding in the bony matrix can cause osteoporosis ( 121).
Oligomenorrheic runners have been noted to have decreased bone density compared with eumenorrheic runners ( 130).
Hypothalamic amenorrhea in dieters and athletic amenorrhea has been treated with estrogen replacement. Controversy
exists over whether routine use of oral birth control pills should be implemented early in the treatment of athletic
amenorrhea (41).
An excellent summary of indications, contraindications, benefits, and negative effects of oral contraceptives is presented
by Kulpa (131). The athlete must understand the importance of taking birth control pills regularly to prevent breakthrough
bleeding and to report any side effects such as calf tenderness, chest pain, severe headaches, or visual symptoms. The
basic problem of decrease in percentage body fat is not addressed.
Controversy exists about whether the use of oral birth control pills increases bone density. Use of birth control pills in the
perimenopausal period may maximize genetic bone density ( 131). Runners who had never taken oral contraceptives
were twice as likely to sustain stress fractures as runners taking birth control pills for more than 1 year ( 70). A definite
decrease in the incidence of stress fractures in female athletes, particularly in gymnasts and cross country runners, has
occurred with the use of oral birth control pills at the University of Kentucky (Hager D and Caborn D, personal
communication 1992).
Athletic performance may be affected by the phases of the menstrual cycle. Exercise performance and muscle glycogen
content are enhanced during the luteal phase ( 121,131,132 and 133) Record-breaking performances have occurred in all
phases of the menstrual cycle.
Menstrual Abnormalities and Nutritional Disorders
The relationship between food intake, activity, leanness, and menstruation has been investigated. There are reviews of
menstrual dysfunction of athletic women ranging from basic principles to evaluation and treatment literature ( 134,135 and
136). Other problems seen in athletic women are iron deficiency anemia and the association of affective disorders and
eating disorders ( 103,127). The causes of athletic amenorrhea continue to be debated and investigated. Low body fat
and low weight have been shown to be a significant contributor to athletic amenorrhea ( 137,138 and 139). The
association of the intensity of the athletic activity with changes in the menstrual cycle have also been explored
(117,140,141). Stress and nutrition are critical factors in the development of menstrual abnormalities ( 142). Interaction
between diet, particularly dietary fiber intake, decreased bone density, and menstrual dysfunction has been postulated
(71). Reviews of athletic amenorrhea discuss its causes, complications, and management ( 143). Hormonal therapy and
greater calcium intake have been suggested to treat the condition ( 143).
The interrelationships of diet and athletic activity, menstrual status and bone density in collegiate women have been
reviewed (16,107,126,144). An abnormality in one of these areas can result in increased illness and injury rates, with
stress fractures as an example.
Exercise and Pregnancy
Special consideration of exercise during pregnancy has been outlined in various articles
(42,145,146,147,148,149,150,151 and 152). When women who exercise routinely become pregnant, continuation of the
same baseline program appears to be safe and should be encouraged. Women who have not exercised before
pregnancy can begin an exercise program cautiously with the physician's permission. Guidelines for exercise in the
pregnant and postpartum state have been set. Regular exercise is defined as a minimum of three periods of exercise per
week. Strenuous exercises should be limited to 15 minutes. Exercise should not be performed in a hot or humid
environment or when the expectant mother is febrile. Maternal temperature should not exceed 38°C. Conditioning during
pregnancy is encouraged, but it should be carried out in accordance with prior exercise patterns. Avoidance of jumping
and loading activities lessens the risk of injury associated with presence of the hormone relaxin, which stretches the
ligaments. No supine exercises should be performed until after 4 months of gestation. The maternal heart rate should not
exceed 140 beats per minute. Appropriate warmup and cool-down periods, as well as the use of liquids, is suggested. In
the postpartum period of 4 to 6 weeks, women have been cautioned against exercise, although more research should be
conducted in this area. In summary, for mental and physical health, during pregnancy, exercise according to the
above-mentioned guidelines is suggested.
Breast Development
Hindle (153) concisely reviewed the subject of the breast and its protective devices. The breast is composed of essential
fat and sex-specific fat. There is no true change in breast size with exercise programs or with pectoralis-specific
strengthening.
The breast is an endocrine end organ composed of fat, suspensory ligaments, and ducts. The nipple is the end organ
that receives the lactiferous, or mammary, ducts, and it is the most prominent part of the breast. Changes in weight and
genetics influence breast size and shape. The development of the mammary gland occurs by hormonal influence,
including estradiol growth hormone, hydrocortisone, insulin, oxytocin, progesterone, prolactin, and thyroxine. The
glandular tissue responds to the menstrual cycle by changes in size and mitotic activity. Except for the period of
pregnancy, the terminal duct units remain in a resting state.
Protective Devices
Sports Bras
Sports bras have design features of firm support of the breast, limitation of breast motion, and material that does not
abrade the skin. The repetitive motion of exercise requires soft material to protect the nipple from abrasion or irritation.
Small-breasted women attain comfort with a compression bra, whereas large-breasted women require an encapsulation
bra. Sports bras are recommended for women with larger breasts in order to limit motion to 2 cm in the vertical plane. The
features important in a sports bra are the following: circumferential support, crisscross or Y construction, unstretchable
straps, breathable material, no seams at the nipple area, no hooks or fasteners, and individualized fit. A sports bra
should be comfortable during exercise and at rest.
Breast Problems
Breast Trauma
Breast discomfort related to sports activity is common. Use of sports bras and appropriate padding is beneficial. Nipple
irritation caused by friction is common, and abrasions can result. Treatment is accomplished with local padding and
lubricants. Breast trauma from contact is uncommon. When direct significant contact occurs, hematoma formation and
prolonged pain can result. The recommended treatment is analgesics, support, and the avoidance of repetitive contact.
Fibrocystic Disease
Fibrocystic disease is characterized by fibrous and cystic changes within the breast parenchyma. Because approximately
70% of women in the United States have this disorder, it is actually more unusual not to be affected by fibrocystic
change. The precise cause of fibrocystic change remains unknown. Xanthines contained in caffeine and chocolate may
accentuate the breast tenderness experienced by the individuals with fibrocystic change. Many female athletes are
troubled with this disorder and experience cyclic breast discomfort. This discomfort can be relieved with the use of
supportive bras and the restriction of caffeine in the diet.
Galactorrhea
Discharge from the nipples (galactorrhea) may be seen in normals. It also may be associated with irritation of the breast
nipple or with the presence of a pituitary microadenoma. A pituitary microadenoma is a noninvasive lesion in the pituitary
gland, which causes an increase in the production of prolactin. Elevated prolactin levels inhibit normal menses and cause
galactorrhea. Female athletes who present with a combination of amenorrhea and galactorrhea should be evaluated for a
pituitary microadenoma.
CONCLUSIONS
Appreciation of the unique situations that exist for female athletes will improve their care and treatment. Medical
personnel who have these added insights in their armamentarium can make diagnoses more efficiently and institute
treatment earlier. The epidemic of knee injuries in women is of concern and requires further research. The high incidence
of hormonal and nutritional imbalances increases the risk of stress fractures. These imbalances are common in the
female athlete. Nutritional, gynecologic, and psychological balance is vital to a healthy athlete. The eating disorders of
anorexia nervosa and bulimia exist in epidemic proportions and treatment programs for these serious disorders must be
instituted promptly. Certainly, encouragement of female participation in sports is beneficial to all, especially the athlete.
The healthy female athlete can best be served by health professionals who appreciate these special and unique
concerns.
ACKNOWLEDGMENTS
Special thanks to Carolyn Large, Transcriptionist; Lonnie Wright, B.A., Manager, Library Services, Central Baptist
Hospital, Lexington, Kentucky; Sharon Wallace, R.D., D.Sc., Chief Clinical Dietitian, Central Baptist Hospital, Nutrition
Consultant for University of Kentucky Athletic Association; David Hager, M.D., Obstetrics and Gynecology; Tom Adler,
PhD, Information Systems Manager, Kentucky Sports Medicine; Jesse Pace, B.S; Cathy Truda, Administrative Assistant,
Kentucky Sports Medicine.
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13 Disabled Athlete
13
DISABLED ATHLETE
HENRY H. P. HO
Classification
Wheelchair Athletes
Physiologic Response to Exercise
Wheelchair Design
Injury Profile
Shoulder Injuries
Elbow and Wrist
Hand and Finger
Special Medical Problems
Pressure Sores
Thermoregulatory Disorder
Urinary Tract Problems
Autonomic Hyperreflexia
Drug Problems
The Mentally Retarded Athlete
Injury Profile
Amputee Athletes
The Blind Athlete
The Deaf Athlete
Conclusions
Chapter References
At the turn of this century, sports remains the prerogative of the able-bodied population. Records of sports participation
by the disabled were scattered and limited. Perhaps the only exception were those of the deaf individuals. Their
involvement in organized sports can be dated back to 1924, when the Comité International des Sports des Sounds
(CISS) was formed and organized the First International Silent Games in Paris ( 1). It was not until the end of World War
II when a significant change in the situation occurred. The war ended, and a large number of disabled veterans returned
to their own countries. Providing rehabilitation and recreation for these disabled ex-servicemen became a new impetus
for the change. Although he recognized the physical impairment and psychological dependence of the paralyzed
patients, Sir Ludwig Guttman introduced archery as a therapeutic measure to rehabilitate them ( 2). Therefore, the Spinal
Injuries Centre of the Stoke Mandeville Hospital was established in Aylesbury, England in 1944. The First Stoke
Mandeville Game for the Paralyzed was held in 1948, with 16 participants, including 14 men and 2 women, all belonging
to the former British Military Force.
Guttman's concept had a lasting influence on the development of wheelchair sports. Independent initiations in the United
States were also reported. The first wheelchair basketball game was played by war veterans at Corona Naval Station in
1945. The First National Wheelchair Basketball Tournament was held in Galesbury, Illinois in 1949 by Tim Nugent. The
National Wheelchair Basketball Association was also formed in this year.
In Europe, Guttman organized The First International Competition for Wheelchair Athletes in 1952 and the British team
competed with a team from the Netherlands. The International Stoke Mandeville Game Federation (ISMGF) was also
formed in the same year. In 1960, the First International Game for the Disabled was held in Rome (Paralympics) under
the auspice of ISMGF, with 400 wheelchair athletes representing 21 nations competing in the games. This event marked
the beginning of the Paralympics, which is held every 4 years in the same site after the Olympic Games. The 1964
Games were held in Tokyo, the same place where the Summer Olympic Games were held. The Paralympic Games in
1968 was not held in Mexico City, partly because of an administrative problem and partly because of the worry that high
altitude would add greater stress to the disabled athletes. Instead the games were moved to Tel Aviv. The games were
held in Heidelberg in 1972 and in Toronto in 1976, when for the first time in history, blind and the amputee athletes were
invited to join the competition. The Toronto games attracted 38 countries to participate, with more than 100,000 paid
spectators. In 1980, the games were held in Arnhem, and cerebral palsied athletes were invited to compete in this year.
There was no united games held in 1984. The VII World Wheelchair Game was held in Stoke Mandeville, whereas the
International Games for the Disabled were held in New York. Fortunately, the 1988 Paralympics reunited once again and
were held in Seoul. Since then, the Paralympic Games return to the former style, with the 1992 and 1996 games held in
Barcelona and Atlanta, respectively.
Concurrent with the development of sports for the paralyzed athletes, athletes with other types of disabilities also
established international governing bodies to foster their interest and to promote sports opportunities for their members.
This included the International Cerebral Palsy Society in 1968, which changed to Cerebral Palsy-International Sports and
Recreation Association (CP-ISRA) in 1978. For the blind athletes, the International Blind Sports Association (IBSA) was
formed in 1981. Another organization is the International Sports Federation for Persons with Mental Handicap
(INAS-FMH), which was formed in 1986. Attempts at coordinating the various international organizations for selected
types of disabilities have been made in the past. The first effort was in 1964, when the International Sports Organization
for the Disabled (ISOD) was formed to act as an international umbrella organization for all disabled. However, ISOD
ultimately became the international organization for amputees, the disabled skiers, and les autres (the French word
meaning “the others”). The second attempt was made by the establishment of International Coordinating Committee
(ICC) in 1982 with representatives from ISMGF, IBSA, ISOD, and CP-ISRA. This group was later joined by CISS and
INAS-FMH. ICC served as a fragile alliance of international sports federation, and in 1987, during a meeting in Arnhem, it
was decided to replace the ICC with a new international sports organization. In 1989, the International Paralympic
Committee (IPC) was formed (3). The final exchange of power from ICC to IPC was set to occur after the 1992 Barcelona
Paralympics. Since then, the IPC has been recognized as the sole international coordinating entity for disabled athletes
worldwide.
In the United States, corresponding national organizations for the various types of disabilities have also been formed
(Table 13.1). During the past 2 decades, we have witnessed a rapid growth of sports opportunities for athletes with
disabilities. This has occurred in part due to the effort of the numerous disabled sports organizations. Another key
contribution was made by federal legislation. Compared with other countries, the United States Government has used
more legislation to protect the disabled population with respect to sports participation. The Federal Rehabilitation Act of
1973 was an important move to provide equal opportunities for otherwise qualified individuals who have disabilities to
participate in federally funded programs ( 4). The Education of the Handicapped Act of 1975 further enhanced the
opportunities of students with disabilities to participate in physical education programs organized by schools or other
education institutes. The Amateur Sports Act of 1978 was another breakthrough in the provision of sports for disabled
athletes (5). As a result of enactment of the Amateur Sports Act, the United States Olympic Committee had to be
reorganized to include a Committee on Sports for the Disabled (COSD) in 1983. Membership of the COSD consists of
two representatives from each of the major national organizations in sports for the disabled. These are group E members.
COSD helps coordinate the various national organizations in disabled sports and also improves opportunities for the
disabled athletes. It also promotes programs for the young disabled athletes and helps increase awareness and
acceptance of disabled athletes by the public.
TABLE 13.1. CHRONOLOGY OF DISABILITY SPORT ORGANIZATIONS IN THE UNITED STATES
CLASSIFICATION
Classification remains one of the most important issues in sports for the disabled population. Even in the able-bodied
sports arena, classification has been present for many years to accommodate the differences in gender, so that men
compete separately from women. Although in some power sports like weight lifting, boxing, wrestling, and judo, in which
differences in muscle mass are believed to put an athlete in an unequal term to compete, a classification system based
on body weight is necessary. Among disabled athletes, another basic difference is their variation in ability to move ( 6).
Therefore, classification is important to ensure fairness in competition. Players are awarded for their athletic skills and
performance rather than their functional abilities.
Much controversy existed in the classification of disabled athletes. The traditional classification was a medical
classification developed by ISMGF for the spinal cord–injured athletes. This was an anatomic classification based on the
level and completeness of the spinal cord lesion. The athletes were assigned to one of the seven classes according to
manual testing of muscle strength over the upper and lower extremities, as well as trunk balance. This classification was
soon followed by classifications of other international as well as national organizations, which devise their own medical
classification system for their own athletes with other types of disabilities. In recent years, there has been a trend to
evolve toward more integrated competition, in which athletes of different type of disabilities compete alongside each
other in the same event. For instance, persons with cerebral palsy, amputees, les autres, and blind athletes compete
together in the swimming event. Major drawbacks become evident when using the medical classification in this situation.
On the one hand, it creates too many classes within each event. On the other hand, there may not be enough entrants in
each, defeating the competitive spirit of the game. The medical classification also fails to take into account other factors
that can affect the athlete's performance. These factors include spasticity, sensation, and deformities ( 7). Spasticity
generally places an athlete in an unfavorable condition in most sports, although in wheelchair sports, strapping for
spasticity may help improve trunk balance. Sensation offers definite advantage to athletes in whom position sense is
preserved. Joint deformities can be congenital or iatrogenic, such as surgical fusion. The limitation in joint movement may
adversely affect performance of the athlete.
As a result of dissatisfaction with the medical classification, functional classification emerges. This classification places
great emphasis on the quality and quantity of active muscle mass, as well as testing the athlete's sports-specific tasks.
The athletes are then classified according to the limitation of function for a specific sport. The functional classification for
the wheelchair basketball was used in the VII World Game in 1984 ( 8). Each player is placed into one of the four classes
based on the level of trunk function and sitting balance as observed on the wheelchair. In the 1992 Paralympic Games in
Barcelona, a sports-specific functional classification was used for the first time ( 9). Although functional classification has
gained popularity in recent years, several inherited problems are present in this classification. This classification depends
on the cooperation of the athlete to perform sports-specific tasks. Faking by the athlete is possible in order to gain
advantage in the classification. Another problem is related to the effect of training. Training does affect function;
therefore, a well-trained athlete may be penalized when compared with a new athlete who has not yet achieved his
functional potential ( 7). The issue of classification is never static, and continued research in this field will help refine the
system of classification in the future.
WHEELCHAIR ATHLETES
Wheelchair athletes encompass a diversified group of disabled individuals, including those suffering from spinal cord
injury and lower limb amputation, as well as a portion of cerebral palsy and les autres athletes. Wheelchair sports have
the longest history among sports for the disabled, as was mentioned previously. Common wheelchair sports include
archery, basketball, road racing, shooting, slalom, swimming, table tennis, tennis, track and field, weight lifting, and
others. Physical disability tends to limit an individual's ability to exercise, and the resulting sedentary lifestyle is known to
increase the risk of medical problems. Regular sports participation has the benefit of improving joint flexibility; maximizing
strength and endurance of muscles; reducing medical complications such as obesity, ischemic heart disease, and
osteoporosis; improving self-esteem; counteracting depression; and encouraging social integration. Wheelchair athletes
have fewer physician visits ( 10) and hospitalizations ( 11) when compared with nonathletes.
PHYSIOLOGIC RESPONSE TO EXERCISE
The cardiovascular response to exercise in spinal cord– injured individuals is related to the level of the spinal lesion. In
general, the higher and more complete the spinal cord damage, the lower is the cardiopulmonary reserve of the
individual. In addition to the impairment of the somatic nervous system, which controls the voluntary muscles, the function
of the autonomic nervous system is also affected. With a high thoracic lesion (T-1), the sympathetic innervation to the
heart is lost. Interruption of the adrenal innervation (T-5 to T-9) also results in loss of catecholamine response from
adrenal secretion. This produces a diminished or hypokinetic circulatory response to exercise. The maximum heart rate is
decreased and depends on the intrinsic sinoatrial rhythm. Besides the loss of chronotropic reserve, the venous return is
also reduced. This is due to venous pooling of blood in the paralyzed limbs. In a high cervical lesion (C-3 to C-5), the
innervation of the diaphragm by the phrenic nerve is also lost. Therefore, the function of the thoracic pump in assisting
venous return is also abolished. This results in a reduction in diastolic filling of the ventricle and the stroke volume is
decreased. The reduction in heart rate and stroke volume results in decreased cardiac output during exercise. Therefore,
spinal cord–injured individuals are prone to circulatory strain and myocardial ischemia. The reflex increase in blood flow
to metabolically active muscle by the sympathetic innervation is also lost. This results in a relative dependence of
anaerobic metabolism for energy production and the accumulation of lactic acid as well as other waste products. The
smaller muscle mass used in arm exercise and the production of lactic acid cause early muscle fatigue and limit exercise
performance (12).
Although arm exercise is more stressful to the cardiovascular system when compared with leg exercise, training and
exercise are still important in improving the fitness of spinal cord–injured individuals. It is believed that the effect of
training is mainly on peripheral muscular adaptation rather than on any significant central cardiovascular conditioning.
Muscle fatigue tends to occur before the cardiovascular and pulmonary systems are driven to high enough output and
long enough duration to stimulate sufficient central training effect ( 12). Muscle adaptions known to occur after arm
training include an increase in peak moment, peak power, average power, and work per contraction during isokinetic
testing (13). An increase in aerobic fitness is reflected in an increase in maximum power output, longer endurance,
greater peak oxygen intake, and larger respiratory minute volume ( 14). This effect cannot be brought about by ordinary
daily wheelchair propulsion. Hooker et al. ( 15) have shown that a minimum of 70% maximum heart rate reserve is the
minimal intensity needed to elicit a training effect in spinal cord–injured individuals.
WHEELCHAIR DESIGN
Sports wheelchairs differ from regular wheelchairs in that their design is directed toward performance and safety. These
chairs must satisfy the requirement of optimal maneuverability, quick turning, and rapid acceleration ( 16). Comfort is
usually sacrificed. Armrests and handles are eliminated. The frame is narrowed, and the seat is lowered and moved
forward. The footrest is usually rigid, and there is no brake. In order to accommodate for the speed requirement in racing
chairs, one of the most obvious changes is to decrease the weight of the chair. Whereas the standard wheelchair weighs
approximately 20 kg, a modern racing chair weighs as little as 6 to 7 kg. The diameter of the drive wheels is increased,
whereas the push-rims are smaller. This decreases the mechanical advantage to allow for a greater drive ratio and
speed. Pneumatic tires with as much as 100 pounds of air pressure are used to reduce surface contact with the ground
and thus rolling friction. The drive wheels of the race chair have an inward camber in which the bottom of the wheels are
farther apart than the top. This improves the efficiency of the push while reducing the possibility of the athlete's arm being
injured by bumping against the wheel ( 13,16). In order to overcome air resistance, the seat of a race chair is lowered.
The front of the seat is kept higher than the rear, and the seat is reclined slightly backward. This configuration serves to
minimize the angle of hip flexion and maximize the angle of knee flexion ( 16).
Safety measures built into the race chair design include plastic wheel guard covers to protect the athlete's finger from
catching the spokes of the wheel. Padded push rims are used to reduce the risk of nerve entrapment around the wrist
region. Anti-tip coasters at the rear of the chair reduce the chance of tipping over. A roll bar beneath the foot platform
prevents the chair from folding in the event of a spill. Strapping can increase stability and prevent the trunk from falling
off the front especially during downhill travel.
INJURY PROFILE
Since the introduction of competitive wheelchair sports in 1948 by the late Sir Ludwig Guttman, the number of wheelchair
athletes has grown dramatically each year. Concurrent with the increase in popularity of wheelchair sports came the
problem of athletes injured during the game or during practice. However, there is a dearth of data concerning the pattern
of injuries in this group of athletes. Most of the research at present consists of cross-sectional studies of selected group
of athletes based on a reporting system.
In 1985, Curtis et al. (17) reported on 128 athletes with 291 injuries. The most common injuries were soft tissue injuries
(33%), blisters (18%), and skin lacerations (17%). For the sporting events that lead to injuries, the three highest risk
sports were track and field (26%), basketball (24%), and road racing (22%).
Ferrara et al. (18) found 50 injuries in 19 elite wheelchair athletes in a 1-year interval. The upper extremity was the most
common site of injury, accounting for 58% of cases. This was followed by the lower extremity (22%), and the neck and
spine (18%). Thirty-two percent of these injuries were classified as major, with loss of more than 22 days of practice of
competition, whereas minor injuries accounted for 57% of the cases. Acute trauma due to either a fall or a collision with
another chair or another object was the cause of injury in 49% of cases. Repetitive stress or overuse contributed to 35%
of the injuries.
McCormack et al. (19) reported on 90 wheelchair athletes with 346 injuries. The most common body parts injured were
the hand (20%), shoulder (16%), and fingers (11%). Seventy-one percent of athletes used protective equipment in which
gloves were most popular. Despite the potential serious consequence of their injury, only 31% of injured athletes sought
medical assistance.
Taylor et al. (20) found no difference in the number of injuries between elite and nonelite athletes. There was no
correlation between training variables (distance pushed per week, amount of speed training, number of weight-training
sessions, and length of time involved in wheelchair racing) to the occurrence of injury. However, there appears to be a
relationship between the recurrence of injury and restarting training before the pain from injury had subsided. This factor
may perpetuate the problem of overuse injuries in these athletes.
Hoeberigs et al. (21) studied 19 marathon wheelchair athletes who raced 7 consecutive days during the race and found
that spills from the wheelchair were common. Problems related to climatologic condition were another frequent complaint.
Wilson et al. ( 22) reported on a pediatric group of wheelchair athletes and found an injury pattern similar to that in the
adult group.
Shoulder Injuries
The incidence of shoulder injuries in wheelchair athletes have been well documented in several studies ( 18,19,21,22,23
and 24). Unlike the able-bodied counterpart, the shoulder of the wheelchair athlete behaves as a weight-bearing joint
especially during transfer. Common shoulder problems include rotator cuff impingement syndrome and myofascial pain
syndrome (23).
Bayley et al. (25) found that 33% of paraplegics complained of shoulder pain, with 24% suffering from shoulder
impingement syndrome. The average time of onset of impingement syndrome after spinal cord injury was 13 years. The
patients who had lower cervical or upper thoracic injury had a higher incidence of impingement. This may be due to
unrecognized damage to the shoulder girdle at the time of injury or because the lower paraplegic can support the upper
torso partially with the abdomen or spinal muscle, so as to relieve the shoulder girdle from some of the weight.
Arthrograms performed on those patients with impingement syndrome showed that 65% of these patients had a rotator
cuff tear. Arthritis of the acromioclavicular joint and avascular necrosis of the humeral head were found in some patients.
Burnham et al. (26) believed that muscle imbalance was one of the causes of shoulder impingement in paraplegic
athletes. Isokinetic tests of shoulder strength showed that although the paraplegic's shoulders were stronger than the
nondisabled control athletes, the paraplegics were relatively weak in adduction as compared with abduction. The group
with impingement syndrome also demonstrate weaker adduction, and external and internal rotation function.
Biomechanically, the oblique pull of the shoulder adductors (e.g., latissimus dorsi, teres major, pectoralis major) and the
rotators (e.g., subscapularis, infraspinatus, and teres minor) act as shoulder depressors against the abduction of the
deltoid, which also pull the humeral head cephalad and so encroach on the subacromial space. Therefore, shoulder
strength imbalance can lead to impingement in these patients.
The heightened demand on the shoulder by the wheelchair-bound individual is also believed to intensify the problem of
shoulder pain in these patients. Because wheelchair propulsion is necessary for mobility, many patients rarely get
enough rest and time for recovery even after the onset of shoulder pain. Some dedicated wheelchair athletes who train
intensively and engage in various sports throughout the year may aggravate the problem further. Another precipitating
factor is the habitual placement of the shoulder in the impingement position. Shoulder flexion and abduction are
commonly used for reaching objects, as well as in performing certain sports activities like shooting basketball. This
impingement position places further strain on the shoulder. Repeated axial loading of the shoulder during transfer is
another factor that stresses the rotator cuff. Pressure readings as high as 2.5 times the arterial pressure have been
recorded in the subacromial space ( 25).
Treatment of these patients should start with prevention. The impingement position, such as using a declined instead of
an inclined bench press and doing short arc latissimus pull down, should be avoided as much as possible ( 26).
Strengthening of shoulder adductors, and internal and external rotators are also important, as discussed earlier. Careful
scheduling of the training program to allow adequate rest of the athletes is also beneficial. Radical alteration of the
training program during the learning of new technique should be avoided in order to allow the athletes to have ample time
to become accustomed to the new demand on their shoulders. Stretching exercises to improve flexibility of the shoulder
muscles are helpful to prevent injury. In the event of documented impingement syndrome, conservative management in
terms of rest, physiotherapy, and the administration of nonsteroidal anti-inflammatory drugs are the mainstay of
treatment. Surgical decompression of the subacromial arch with repair of the rotator cuff can be performed
arthroscopically but are reserved for resistant cases only.
Elbow and Wrist

Improper wheelchair propulsion technique can result in overuse injuries of the elbow and wrist, leading to flexor and
extensor tendinitis of the wrist. Similar injury can occur at the triceps insertion onto the olecranon process. This injury
may occur during the lock-out position, when the weight is in the so-called up position and the elbow snaps into
extension (27).
Compression neuropathies are common among wheelchair athletes. Compression of the median nerve at the wrist (i.e.,
carpal tunnel syndrome) is most common. This is followed by entrapment of the ulnar nerve at the wrist (i.e., in Guyon's
canal) and at the elbow (i.e., in the cubital tunnel) ( 28). Electrodiagnostic studies help confirm the clinical diagnosis and
pick up subclinical cases of neuropathies. The incidence of carpal tunnel syndrome in paraplegics increases with the
length of time after paralysis ( 28,29 and 30). Over half of the patients had bilateral involvement ( 31). However, the
prevalence of carpal tunnel syndrome in wheelchair athletes seems to differ little from that found in the general
paraplegic population ( 31,32). The etiology of carpal tunnel syndrome appeared to be related to repetitive trauma to the
wrist during propulsion of the wheelchair. Increased pressure in the carpal canal during forceful extension of the wrist as
in many daily activities can be another cause ( 29).
Treatment includes padding of the push rim to avoid trauma to the wrist. Use of splintage, nonsteroidal anti-inflammatory
drugs, and steroid injection into the carpal canal are other modalities of treatment. Surgical decompression should be
considered for patients who failed conservative treatment.
Hand and Finger
In a study of 90 wheelchair athletes, McCormack et al. ( 19) found that hand and fingers are among two of the most
common sites of injuries, with an incidence of 21% and 14%, respectively. Acute sprains, abrasions, and lacerations can
occur when the fingers are caught between the rim and spokes of the wheelchair, brakes, sharp edges, or by contact with
tires (33). Blisters may be caused by repetitive contact of the hand with the push rim. The hypothenar eminence of the
hand is particularly subject to abrasions and blisters ( 34). The same mechanism can cause injuries of the
metacarpophalangeal joint of the thumb. Chronic instability of this joint develops as a result of the recurrent injury to the
ulnar collateral ligament.
Injuries can be prevented by using a padded push rim and protective gear like gloves and tape. Spokes should be
covered with plastic wheel guard covers. The lane-width should be maximized in track events in order to avoid collision.
Blisters should be managed carefully to avoid secondary infection. Callus over the thenar eminence can be softened with
cream containing salicylic acid. Light abrasion with pumice stone or sandpaper may prevent the accumulation of
thickened skin (35).
SPECIAL MEDICAL PROBLEMS
Pressure Sores
Decubitus ulcers occur as a result of shear forces and prolonged pressure over insensate skin, most frequently the
sacrum and buttock. Sports that favor the development of pressure sores include road racing, track, and basketball. The
design of the sports wheelchair in which the knees are kept higher than the buttocks also increases the pressure over the
ischial tuberosities and sacrum ( 33). Moisture and sweat around the buttock during exercise aggravate the risk further.
Because pressure sores are notoriously difficult to heal and costly to treat, prevention is important. A high index of
suspicion is necessary. Skin over pressure area should be scrutinized regularly before ulcers develop. Use of a
competition wheelchair should be reduced to a minimum beyond actual competition. Custom-molded seats may also help
dissipate pressure over the buttock area ( 36). Athletes should learn to relieve pressure over the ischial tuberosities by
shifting the body weight with the arm at regular intervals. To reduce skin maceration, moisture-absorbing clothing should
be used. General nutrition and personal hygiene should be improved to combat against sore development.
Thermoregulatory Disorder
Spinal cord–injured athletes are prone to temperature regulation problems during exercise. The magnitude of impairment
is related to the level and completeness of the lesion. The higher and more complete the spinal paralysis, the greater the
thermoregulatory dysfunction (37). The causes of the disturbance stem from the impairment of the sympathic nervous
system, leading to loss of vasomotor and sudomotor control over areas of insensate skin. Reduced afferent input to the
hypothalamic thermoregulatory centers results in diminished effector drive for thermoregulatory response. Finally, the
loss of skeletal muscle pump from the paralyzed lower limb results in venous pooling and a state of relative hypovolemia
during exercise. Dehydration in this situation further compromises the thermoregulatory mechanism. As a result, spinal
cord–injured athletes had a higher core temperature in the warm environment and a lower temperature in cold conditions.
Hyperthermia
Hyperthermia poses a particular threat to spinal cord–injured athletes who engage in long duration sports under high
ambient temperature like wheelchair marathon. The spinal cord–injured athletes dissipate heat by evaporative heat loss
from the arm. Sweating below the level of the spinal paralysis may be deficient or inappropriate ( 38), and the athletes
have to rely on dry heat exchange. Organizers should start the race early in the morning, when the road is not hot.
Shaded areas should also be provided. Athletes should have adequate hydration throughout the game, because thirst
has been shown to be an inadequate stimulus to maintain fluid level in the body. Dehydration will raise the core
temperature further during exercise. Light clothing also helps dissipate heat. Adequate training and acclimatization has
also been shown to help the athlete compete at a higher environmental temperature ( 38).
Hypothermia
Hypothermia can be a threat in cold, rainy, or windy conditions. Although the athlete's core temperature can be
maintained during exercise, problems arise after cessation of the race when heat production decreases. Because of the
disruption of the autonomic nervous system, shivering may not occur. The skin will remain vasodilated, hyperemic, and
soaked with sweat, resulting in accelerated heat losses. Aluminium foil blankets are ineffective in this situation. Wet
clothing should be replaced with dry attire. Plastic sheets wrapped around the extremities or a warm shower are useful
means to conserve body temperature. For slow competitors who cannot generate enough heat during a long race, it is
advisable to take additional clothing to protect the body against heat loss.
Urinary Tract Problems
At one time, spinal cord injury was associated with a high mortality rate. The most common cause of death was renal
failure. Improvement in management of urinary problems has decreased the mortality and morbidity rates of these
individuals ( 39).
An understanding of the normal physiologic control of bladder function is important. The micturition reflex center is
located in the pontine region of the brainstem. Efferent impulses from the pontine micturition center travel down the
spinal cord to the detrusor motor nuclei located at the S-2, S-3, and S-4 levels of the spinal cord. The S-2 segment
innervates the external urethral sphincter, whereas the S-3 and S-4 segments innervate the detrusor muscles of the
bladder. Spinal cord injury below the brainstem may result in detrusor–sphincter dyssynergia because bladder
contraction occurs with simultaneous contraction of the external urinary sphincter. The result is urine retention with high
bladder pressure (40). Reflex micturition can be initiated by tapping the bladder. The residual urine can be excreted by
gentle compression of the bladder at the suprapubic region.
With low lesion of the spinal cord, which damages the detrusor motor nuclei, the bladder reflexes are lost and the
external urethral sphincter becomes flaccid. Micturition is possible by increasing intraabdominal pressure (Valsalva's
maneuver) or manual expression (35).
Several methods are available to drain the bladder, but because bladder dysfunction varies from patient to patient,
management should be individualized. Current methods include indwelling catheters, intermittent catheterization, and
external collecting devices ( 40). Each method has its own advantage and complications. Urodynamic studies are helpful
in characterizing the function of the lower urinary tract, whereas renal ultrasound and intravenous pyelogram can
demonstrate the function of the upper urinary tract. Both of these techniques are useful in planning appropriate
treatment.
Urinary tract infections are common among spinal cord–injured patients. Conditions that precipitate infection include
catheterization, overdistention of bladder, large residual volume after voiding, high voiding pressure, reflux, stone
formation, and outlet obstruction. An asymptomatic bacterial infection requires no treatment unless there is reflux.
Symptomatic urinary tract infection should be treated with a course of antibiotics. Measures to reduce the risk of urinary
tract infection include maintaining good urine drainage, improving personal hygiene, daily cleansing of urine bag with
sodium hypochloride, using a clean wheelchair cover cushion, and having adequate fluid intake.
Autonomic Hyperreflexia
Autonomic hyperreflexia is an acute syndrome resulting from massive unopposed sympathetic discharge. Autonomic
hyperreflexia commonly occurs in persons with spinal cord lesions at or above T-6 ( 39), where loss of supraspinal
inhibitory control of the greater sympathetic splanchnic outflow occurs. The incidence is said to be as high as 80% in
those who are susceptible. In most cases, they are unrecognized or misdiagnosed by those who are unfamiliar with this
condition (41).
The proposed mechanism for autonomic hyperreflexia is a noxious stimulus that travels along the spinal cord until it is
blocked at the level of the spinal lesion. This afferent stimulus then synapses with the sympathetic neuron in the
intermediolateral gray column, causing widespread sympathetic hyperactivity. The most common noxious stimuli include
bladder distention and catheter insertion. Gastrointestinal stimuli from fecal impaction and enemas can also lead to
autonomic hyperreflexia. Even tight garments have been accused of causing autonomic hyperreflexia. The clinical
features of autonomic hyperreflexia include paroximal hypertension, sweating, flushing, nasal congestion, headache, and
bradycardia. Autonomic hyperreflexia can cause life-threatening situations, including seizures, cerebral hemorrhage,
coma, and even death.
Most patients with autonomic hyperreflexia respond to conservative treatment by removing the offending stimuli. Simple
measures, such as having the athlete sit down, are also useful. Pharmacologic treatment is reserved for resistant cases
(treated with nifedipine) or as prophylaxis against recurrent attacks (treated with phenoxybenzamine). Intentional
induction of autonomic hyperreflexia as a method of sports performance enhancement has been used by some
wheelchair athletes. Burnham et al. ( 42) demonstrated a 9.7% improvement of race time with this method. However,
blood pressure reaching dangerously high levels has also been recorded in the boosted state. Therefore, the risk
associated with such practice may outweigh its benefit.
Drug Problems
Prescribed Medications
Medical problems associated with wheelchair athletes frequently require the use of medications. Drugs commonly used
include anticonvulsants, antispasmodics, analgesics, antibiotics, and bronchodilators. Sports physicians should be
familiar with the side effects of these drugs and the drug reactions that may occur when combining various groups of
medications. Of particular concern are medical drugs on the list of banned substances. Although it is not frequent,
medical regimens occasionally need to be altered to control side effects. For example, beta-2 agonists ( 36,43) may cause
unsteadiness and trembling, whereas some anticonvulsants may cause sedation and decrease the athlete's reaction time
and concentration power. The sports physician must be flexible in his or her approach ( 44).
Illegal Drugs
As the level of competition increases among wheelchair athletes, use of ergogenic aids has been speculated for some
years. Beginning in 1986, all first-place winners in weight lifting in the World Championship Stoke-Manville Games in
England were tested for steroid use ( 27). Drug testing has become part of the international scene in sports competition
for the disabled. Existing Olympic-type protocols will be followed.
THE MENTALLY RETARDED ATHLETE
The Special Olympics is the largest organization involved in promoting sports training and competition for the mentally
retarded athletes. In July 1968, the First International Special Olympic Games were held in Chicago under the direction
of Eunice Kennedy Shriver. More than 1,000 mentally retarded athletes from 26 states and Canada participated in the
competition (45). Mentally retarded individuals of 8 years of age or older are eligible to participate in the Special
Olympics. The Special Olympics is officially approved by the United States Olympics Committee to be one of the two
organizations in the United States entitled to use the name “Olympics.” Each year, the organizers of the Special Olympics
arrange games at local, state, and national levels. International summer and winter games are held once every 4 years.
An estimated two million athletes participate in the Special Olympics worldwide ( 46). Official summer sports include
aquatics, basketball, bowling, equestrian events, gymnastics, soccer, softball, and volleyball. Official winter sports
include floor and poly hockey, figure and speed skating, and Alpine and cross country skiing ( 44).
In general, mentally retarded individuals have a lower fitness level than the average population. Because of a sedentary
lifestyle, they have a higher risk of cardiovascular problems and obesity. Their muscle strength and endurance are also
lower (47). They are also prone to other medical disorders. For this reason, a preparticipation examination is especially
important. The leaders of the Special Olympics mandated that all athletes must have a current certificate of fitness before
participating in the competition. According to Hudson ( 48), conditions most commonly encountered include impaired
visual acuity (50%), decreased muscle flexibility (37%), and cardiac murmur (5%). Down's syndrome was found in 9% of
the athletes. In another preparticipation examination by Robson ( 49), Down's syndrome (28%) and epilepsy (11%) were
the two most common medical conditions.
Down's syndrome is a unique disorder associated with multiple orthopedic problems that may affect an individual's
participation in sports. These problems include metatarsus primus varus, pes planus, genu valgum, patella instability,
slipped capital femoral epiphysis, dysplasia of hip, scoliosis, and atlantoaxial subluxation ( 50). The incidence of
atlantoaxial instability among individuals with Down's syndrome has been reported to be 10% to 20% ( 51). The instability
is due to laxity of the transverse ligament, which holds the odontoid process (C-2) against atlas (C-1), as well as
congenital abnormalities of the odontoid process ( 50,51). This can result in compression of the spinal cord. The
neurologic manifestations of spinal cord compression include neck pain, torticollis, increased clumsiness, walking fatigue,
a sudden preference for sitting games, and a change in bowel or bladder function. These problems are often
accompanied by signs such as hyperreflexia, Babinski's sign, clonus, hemiparesis, and quadriparesis. Posterior column
involvement may produce loss of vibration or positional sense, cerebellar ataxia, and cutaneous sensory loss ( 52). There
is usually delay between onset of symptoms and diagnosis because children with Down's syndrome are mentally
retarded and do not vocalize their complaint. Therefore, although no reported cases of neurologic complications caused
by atlantoaxial instability occur in the history of the Special Olympics, the American Academy of Paediatrics Committee
on Sports Medicine laid down several guidelines in 1984 when dealing with athletes suffering from Down's syndrome
(53):
1. All children with Down's syndrome who wish to participate in sports that might produce head and neck trauma
should have lateral x-ray study of the cervical spine in neutral, flexion, and extension positions.
2. If the distance between the odontoid process of the axis and the anterior arch of the atlas exceeds 4.5 mm,
atlantoaxial instability is present. Contact sports or sport that might put stress on the neck such as soccer,
basketball, high jump, gymnastics, equestrian events, the butterfly stroke in swimming, a diving start in swimming,
diving, skating, and skiing ( 54) to have to be restricted.
3. A repeat x-ray study is not indicated for those who have a normal finding in the first study.
4. Patients with symptomatic atlantoaxial instability should be restricted in all strenuous activities, and operative
stabilization of the cervical spine must be considered.
5. If no atlantoaxial instability is present on stress x-ray study, the athlete can participate in all sports and no follow up
is required. The British have a different strategy on atlantoaxial instability in patients with Down's syndrome. In
1985, the British Orthopaedic Association advocated that children with Down's syndrome should not be encouraged
to take part in any competitive sport that is likely to place considerable strain on the cervical spine ( 55).
Cardiac abnormalities are another common disorder found in Down's syndrome. The most common cardiac defects are
endocardial cushion defects, ventricular septal defects, and atrial septal defects. Patients with these problems need
consultation with a cardiologist before participation in sports ( 56).
Injury Profile
The injury profile of mentally retarded athletes has been determined in several studies. In a longitudinal study of the
Hawaii Special Olympic Summer Games over a 4-year interval by Batts et al. ( 57), the overall incidence of injury and
illness was 3.87%. The most common injuries sustained were abrasions and muscle strain. The knee was the most
frequently injured joint. Track and field and softball account for more than 90% of injuries. Most medical conditions
encountered were minor, with gastrointestinal discomfort, heat illness, epistasis, and conjunctivitis being more common.
The most severe medical condition encountered was epilepsy, which occurs in athletes with preexisting seizure
disorders. In another study by Birrer ( 58) on New Jersey State Special Olympics, the overall injury rate was 2.8%. All of
these injuries were minor. Owing to the high ambient temperature, heat-related injuries were common. These injuries
included sunburn and heat exhaustion. McCormick et al. ( 46) reported a 3.5% incidence of injury and illness encountered
during a 3-day local Special Olympics event in Galveston, Texas. Track and field has a higher calculated risk compared
with other sports. Athletes with Down's syndrome also had a 3.2 times greater risk of injury than other athletes. During a
7-day United Kingdom Special Olympic Games in 1989, Robson ( 49) reported the highest injury and illness rate of 13%.
However, this includes injury and illness that occurred during competition as well as during training and other
recreational events.
These studies suggested that sports participation should be safe for mentally retarded athletes because their risk of
injury is similar to that of able-bodied athletes. Bearing in mind the complexity of the preexisting medical conditions in
some of these athletes, medical coverage is essential. Medical records of each of the participants should be readily
available for the team physician. Because heat predisposes these athletes to injury, the Special Olympic Games should
be held at the cooler time of the year. Plenty of water and shade should also be provided. Although most of the injuries
sustained by the mentally retarded athletes were minor, medical personnel should be competent to handle more severe
problems like seizure.
AMPUTEE ATHLETES
Amputee athletes include those with partial or complete loss of one or more limbs. The conditions that lead to limb
amputation include congenital defects, traumatic amputation, tumor, and various medical conditions. Depending on the
degree of disability and the rules of the game, amputee athletes may compete with or without a prosthesis, or they may
use a wheelchair.
Exercise and sports for amputees serve to toughen the stump, improve the circulation, prevent atrophy of muscles, and
correct alignment of the body to enhance a better gait. Furthermore, research for better prosthesis for competition may
lead to advances in material and fitting for all amputees ( 59).
General problems encountered by amputee athletes who compete with a prosthesis include injury to the stump. A poorly
fitted prosthesis can cause superficial skin abrasion, ulceration, and secondary infection. By comparison, a well-fitted
prosthesis, especially one on the lower extremity, can put much strain on the joint above the prosthesis, leading to
premature osteoarthritis. Acute injury to the ligaments or even fractures can also occur ( 60).
Amputee sports include track and field, swimming, volleyball, table tennis, archery, and bowling. But the most extensively
studied sport is alpine skiing. Amputees may ski with one leg and two outrigger ski poles (called Tri-track) or they may ski
with a prosthetic limb and two skis. Advances in the development of adaptive equipment, including outrigger skis, flip
skis, canting wedges, ski bras, sit skis, and mono skis, allow more severely disabled athletes to enjoy sports and in a
safer manner (61). The injury rate for skiers with a disability is comparable to that of the able-bodied skier ( 62,63 and 64).
Disabled skiers also sustain less severe injuries with less fractures and lacerations, whereas abrasions and bruises are
more common (63).
The most common site of injury was over the knee (62,63). Because a knee injury can be very disabling, especially to
lower limb amputees, prevention is important. Equipment consideration includes the ski binding system. This should be
frequently checked and lubricated to ensure proper release in the event of a fall. For amputees who ski without a
prosthesis, lateral canting is sometimes necessary to compensate for a shift of body weight. This consists of a canting
wedge inserted between the boot and the ski in order to adjust the medial or lateral tilt of the boot ( 61).
The outrigger device, which attaches to the ski pole in tri-track ski, can be a dangerous device. The sharp edge can
cause lacerations on the face, trunk, and limbs. Therefore, all skiers using this device should learn how to displace his or
her limbs to a safe position during a fall.
As mentioned earlier, stump problems including abrasions and pressure sores can occur for skiers who ski with a
prosthesis. The use of a forward cant to increase the forward inclination of the body may shift the pressure over the
stump, causing accelerated skin breakdown. This can be prevented by using a well-padded insert over the socket. For
amputees who ski without a prosthesis, the stump may be exposed to intense cold, leading to frostbite. Frequent
checking of the stump is recommended (65).
Quadriceps muscle weakness is common among amputee skiers. The rate of ski injuries increase steadily throughout the
day as fatigue accumulates. Both anaerobic and aerobic exercises can strengthen the muscles and condition the body
during the ski season, which will help to reduce ski injuries.
THE BLIND ATHLETE
Although blind athletes are legally blind, they range from complete to incomplete loss of vision. To be eligible to compete
in this group, the individual should have a visual acuity of 20/200 or less, or have a field limitation from 5 to 20 degrees
for the better eye. The range of sports include goalball, beepball (a kind of baseball with battery inside the ball emitting a
sound), power lifting, judo, wrestling, track and field, distance running, swimming, tandem cycling, gymnastics, golf,
skiing, and speed skating.
The main problem encountered by blind athletes is the lack of spatial orientation during movement. This problem can
lead to fall or collision with other athletes or with an obstacle. Sports injuries such as abrasions, lacerations, and
fractures are common. Burnham et al. (23) reported a high incidence of lower limb injuries in blind athletes during the
1988 Seoul Paralympic Games. Most of these injuries were musculoskeletal strains of the thigh region. Specific
measures adopted to avoid injuries are necessary in certain sports to ensure safe participation. In distance running, a
sighted guide is employed. The blind athlete may choose to hold hands with the guide, to tether together with a rope, or
to touch the guide's elbow from time to time (66). Sprinters in track and field run individually to avoid contact with others.
Orientation is provided by a sound source at the finish line. Nordic skiing requires that the blind athlete have a guide
also. Both the athlete and the guide must wear identifying bibs to alert the skiers. The guide uses verbal command and
touch to instruct the blind skier. With this method, most blind skiers can learn the essential technique and become
proficient enough to ski with two tracks.
Not all sports for the blind required alteration of the original game. There have been occasions in which blind athletes
successfully compete with able-bodied counterparts. Wrestling is a good example of integrated sport ( 66). Each year, an
estimated 5,000 sighted wrestlers compete against blind wrestlers.
THE DEAF ATHLETE
Deaf athletes must have at least 55 decibel (dB) hearing loss in the better ear. Profound deafness is usually due to
sensorineural defects rather than conduction defect ( 59). If there is no concomitant damage to the semicircular canals or
vestibular apparatus, the deaf athlete will have no equilibrium or balance problem.
The major difficulties that confront deaf athletes are difficulties in recognizing signals and communicating with team
members in team sports. These difficulties can be partly compensated by the use of visual signals instead of audible
signs by the referee, and to maximize their visual cue and sign language when communicating with their teammates ( 34).
Because most of the deaf athletes have no other disabilities, the range of sports that they engage in is similar to that of
able-bodied counterparts. In fact, the group of deaf athletes represent the best opportunities for integration with the
able-bodied sports structure. The injury sustained by the deaf athletes are also similar to the able-bodied population.
CONCLUSIONS
Sports for the disabled have evolved from the original concept as therapeutic exercise in rehabilitation of the spinal
cord–injured patient to the current goal of pursuit of excellence as in Paralympics, as well as participation by all as
emphasized by the Special Olympics. The sports for the disabled movement have witnessed a rapid growth in the last
few decades. This is brought about by the increase in the awareness of society in realizing the potential of the disabled
individuals and accepting them as playing a vital role in society. The government also recognized the importance of
sports for the disabled, and over the years, it has established federal legislation to stipulate equal opportunities for sports
participation by the disabled. Traditional segregation of disabled athletes according to their physical disabilities has led
to the emergence of numerous organizations for various groups of disabled athletes. Although at times they are marked
with rivalry within each group, their contribution in promoting sports for the disabled has been well recognized.
Technologic advances have also helped improve the performance of disabled athletes by refining their adaptive
equipment. Notable examples include lighter and faster racing wheelchairs, better designed prosthesis for amputees, and
the mono ski for paraplegics. Increased emphasis on high performance has also attracted more professional coaches
and athletic trainers to engage in the training of disabled athletes. The influx of more science-based and effective training
methods will help excel the performance of the elite disabled athletes. The media has also been more supportive in
promoting sports for the disabled. Stories on disabled athletes are reported in the sports section of the news, and major
sports events are covered by the media.
Throughout the development of sports for the disabled, sports physicians and the members of the sports medicine team
have provided the preparticipation medical screening, management of sports injuries, classification of disabled athletes,
and research on sports medicine of the disabled athlete ( 33). As the new millennium begins, the medical profession is
faced with more challenges. Medical screening is essential to ensure that disabled athletes are medically fit for sports
participation. However the rights of the patient have to be considered when advising those at risk with regard to sports
participation. The Americans with Disabilities Act of 1990, which eliminates the discrimination of individuals with
disabilities, also gives the disabled athletes the legal right to challenge the decision of sports participation based on
medical ground (4). The medical profession is advised in this situation to maintain good physician–patient relationship, to
follow the established screening standard and inform consent, and to protect the health and well being of the patient ( 67).
Another problem related to screening concerns the use of drugs. As the level of competition escalates in sports for the
disabled, the problem of doping is likely to increase. Sports physicians have the responsibility to differentiate between
prescribed medication that are commonly used by these athletes and ergogenic aids. The use of these doping agents
among elite athletes with disabilities should be prevented through education, as well as refinement of the drug screening
test.
Research on disabled athletes is limited and includes physiologic function, fitness testing, and response to training
among the various groups of disabled athletes. Biomechanical analysis, such as wheelchair propulsion and gait analysis
of amputees, mechanism of sports injuries and the psychological aspect of disabled athletes have also been studied.
More research is required to examine specific types of sports, the various factors that affect the athlete's performance,
and the prevention of injury in these athletes.
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14 Baseball Injuries
14
BASEBALL INJURIES
RUSSELL S. PETRIE
JOHN J. KLIMKEWEICZ
CHRISTOPHER D. HARNER
Throwing
Biomechanics of Throwing
Proper Pitching Technique
Shoulder Injuries
Adult Shoulder Injuries
Elbow Injuries
Vascular Injuries
Head and Neck Injuries
Lumbar Spine
Hitting
Sliding
Catching
Fielding
Summary
Chapter References
Baseball is considered America's national pastime and has recently developed a large international following. In 1981,
there were 4.5 million amateur baseball players in the United States ( 1), but baseball skills also are required in softball,
which is the largest team sport in the country, with 40 million league players ( 2). Players of all ages enjoy the sport, and
52% of the participants are younger than 12 years of age ( 1). Many youngsters begin playing at age 6 or 7 years and
dream of playing professional baseball as adults.
Baseball is a noncontact sport with minimal protective gear. Therefore, it is commonly considered a safe sport. In fact,
the relative incidence of injury in baseball is last among common competitive sports, with 1.6 injuries per 1,000
practices/games (3). Because of the large number of participants, however, baseball ranks second only to football in total
number of injuries and fatalities ( 4). In 1981, the U.S. Consumer Product Safety Commission estimated that more than
900,000 injuries occur annually in baseball and that 35% of these injuries require emergency room visits ( 5). From 1973
to 1981, there were 183 baseball-related fatalities nationwide, with 40% of the fatalities in the 5- to 14-year-old age group
(6).
This chapter addresses baseball injuries as they occur during different aspects of the game: throwing, hitting, sliding,
catching, and fielding. Particular attention is focused on the mechanism, diagnosis, and prevention of injuries. Special
mention also is made of vascular compromise and head and neck injuries.
The demographics of the injuries vary between the Little League and the more organized collegiate and professional
levels. At the Little League level, the impact of the ball is responsible for the greatest number of injuries, accounting for
almost 60% of the injuries reported in one study ( 7). Overuse injuries are also common in this age group. Facial injuries
appear to be the most common area of involvement, followed by the hand and fingers and shoulder regions. Injuries
sustained by impact with the ball were more common on defense (68%). In contrast, at the collegiate level, 58% of the
injuries occurred in the shoulder region, with rotator cuff tendonitis being the most frequent complaint. At this level strains
(23%), sprains (19%), and contusions (17%) account for the majority of injuries ( 8).
THROWING
Biomechanics of Throwing
Overhead throwing is an elaborate, synchronous progression of body movements that starts in the legs and trunk,
involves the upper extremities, and concludes in the rapid propulsion of the ball. It is essential to remember that the
throwing mechanism is a total body activity. Parameters that determine the effectiveness of a thrower include (a) velocity,
(b) accuracy, (c) spin production, and (d) endurance. A high level of neuromuscular control is required to ensure that the
above-mentioned parameters are achieved. Synchrony of muscular contractions and neurologic control throughout the
body are essential to produce an effective throwing motion. Effectiveness also necessitates repetitive performance at a
level that maximally stresses the physiologic limits of the upper extremities' anatomic components. A delicate balance
exists between mobility and stability of the joints of the upper extremities while throwing, and maintenance of this fragile
balance is paramount. The intricate interactions between static restraints (i.e., bone, capsule, and labrum) and the
dynamic restraints (i.e., muscle) permit the versatile motion, precise positioning, and tremendous force that are
imperative in efficient throwing. Small aberrations in the mechanisms that control stability have a significant and
cumulative effect on upper extremity function and increase the risk of crossing the fine line between maximal throwing
effectiveness and injury.
Multiple investigators have studied the complex biomechanics of throwing ( 9,10,11,12,13,14,15 and 16). Although the
mechanics of throwing seem to differ slightly between player positions, in essence, the motions are quite similar. The
majority of throwing studies have concentrated on the pitcher, because (a) the motion is more constant, (b) the collection
of photographic and electromyographic (EMG) data is easier, and (c) pitchers frequently injure their arms.
The baseball pitch is divided into five stages: stage I is the stance phase, stage II is the windup or preparation phase,
stage III is the cocking phase, stage IV is the short propulsive phase of acceleration, and stage V is the follow-through
and deceleration phase (Fig. 14.1).
FIGURE 14.1. Phases of the baseball pitch. The baseball pitch is divided into five stages: stance, windup, cocking (early
and late), acceleration, and follow-through.
From a virtual standstill, a professional pitcher will accelerate a 142-g baseball to a release velocity of more than 90 mph
in just 50 msec. Tremendous tensile, compressive, and rotational forces must be created and dissipated in the upper
extremities to achieve this action. Therefore, a detailed description of the throwing motion will help clarify how this force
is generated, transmitted, and dissipated.
In the stance phase, the pitcher stands facing the batter with his or her shoulders parallel to the rubber. The pivot foot
(right for right-handers) is positioned on the rubber. In the windup phase, the body mechanics are quite individual. In
general, windup begins with the stride foot (left for right-handers) coiling backward, away from home plate, and the arms
swinging overhead. At this time, the position of the fingers on the ball is finalized while screened by the glove. The pivot
foot rotates on the rubber as weight is transferred to it. This phase ends with the ball leaving the glove hand and the body
balanced on the pivot foot. The EMG activity of the shoulder girdle and upper extremities is low during windup.
Cocking is divided into early and late stages. Early cocking starts with extension of the pivot leg, thus propelling the
stride leg, nondominant upper extremity, and trunk forward. The gluteus maximus of the pivot leg is important in providing
this propulsion. Temporarily, the dominant upper extremity lags behind the rest of the body. The upper trapezius
upwardly rotates the scapula to place the glenoid in a stable position for the abducting humeral head. The deltoid and the
supraspinatus concomitantly abduct the humeral head. The elbow is flexed by the brachioradialis muscle. This phase is
terminated as the stride foot contacts the ground. Early cocking pain is not typical in throwers, and aberrations in
neuromuscular controls are seldom noted.
During late cocking, rapid forward motion of the trunk is noted ( 10). The dominant shoulder rotates forward. Inertia and
gravity act on the arm in horizontal abduction, external rotation, and adduction; however, the arm does not move in the
direction of these forces. Large torques are generated at the elbow and shoulder joints to overcome the inertial and
gravitational forces. Static and dynamic restraints combine to stabilize both joints against these forces. In this position,
the primary anterior stabilizer of the glenohumeral joint is the anterior inferior glenohumeral ligament ( 17). The pectoralis
major and latissimus dorsi muscles appear to act as a dynamic sling to augment the inferior glenohumeral ligament ( 17).
The scapulothoracic muscles protract and rotate the scapula upward to produce a stable platform for the humeral head,
thus enhancing maximal humeral external rotation. During this phase, the elbow is experiencing considerable valgus
stress that is localized to the medial stabilizers. Sometimes symptoms of anterior instability of the glenohumeral joint and
medial instability of the elbow are demonstrated during this phase, secondary to an imbalance of the stabilizing
mechanism (13).
The acceleration phase begins with maximal shoulder external rotation and terminates with ball release. The acceleration
of the arm is coincident with the deceleration of the rest of the body, producing efficient transfer of energy to the arm and
ball (10). A large glenohumeral joint compressive force (860 Nm), which has a stabilizing effect, is demonstrated during
this phase. Synchronous muscular contraction about the glenohumeral joint balances the requirements of stabilization
and rapid motion. The pectoralis major, latissimus dorsi, and subscapularis muscles concentrically contract, propelling
the humerus into rapid internal rotation. The humeral internal rotation torque is 14,000 inch-pounds with an angular
velocity of 6100 degrees per second ( 2,10,12). The pectoralis major and the latissimus dorsi muscles are the primary
propellers of the arm, whereas the subscapularis muscle functions as a steering muscle to position the humeral head
precisely in the glenoid. The internal rotation force is then transmitted to the forearm through the elbow. A large valgus
stress is created at the elbow as the internal rotation force is transferred to the forearm and hand. Static stabilization at
the elbow is absorbed by a tension force at the medial collateral ligament and compressive force in the radiocapitellar
joint. Dynamic stabilization is augmented by the wrist and finger flexors and pronator muscles that originate from the
medial epicondyle. Elbow extension reaches a maximum angular velocity of 2200 degrees per second ( 10,12). Generally,
athletes note symptoms of elbow or shoulder dysfunction during this phase of throwing. Typical problems include (a)
anterior subluxation of the shoulder, (b) medial ligamentous instability at the elbow, (c) ulnar neuritis pain, and (d)
“catching” pain from posterior compartment pathology.
Follow-through is after ball release. The trunk and dominant lower extremity rotate forward. The shoulder continues to
adduct and internally rotate to 30 degrees, while elbow motion terminates at about 50 degrees of flexion with the forearm
pronated (2,10,12). The decelerating arm and body must absorb the remaining kinetic energy not transferred to the ball.
Deceleration is estimated to be –500,000 degrees per second at the elbow and shoulder, with an external rotation torque
of approximately 15,000 inch-pounds at the humerus ( 10,16). Deceleration of the arm is accomplished by simultaneous
contraction of opposing muscles around the shoulder and elbow. The trapezius, serratus anterior, teres minor, latissimus
dorsi, supinators, and extensors of the wrist and fingers all play essential roles. Posterior compartment elbow pathology
and injury to the posterior glenohumeral joint stabilizers commonly become apparent during this phase.
In summary, the throwing motion requires the rapid transmission of large amounts of kinetic energy through the upper
extremities. The resultant kinetic energy in the throwing arm has been estimated to be 27,000 inch-pounds, which is four
times the energy in the leg during a soccer kick ( 10). This produces huge torques in the musculoskeletal components
involved, putting them at great risk for injury.
Proper Pitching Technique
The best way for a thrower to avoid injury is through conditioning techniques, proper body mechanics, and a vigorous
warmup. McConnell (18) stressed the importance of proper pitching technique:
It is possible to perfect baseball skills and at the same time avoid injury. . . . Very seldom do we hear of a player who
executes a play properly, being injured. The man who knows how to throw, and uses this knowledge in throwing,
doesn't pull a muscle in his arm.
The lessons learned from professional pitchers can be applied to all players on the team. John Sain, an ex-Major League
pitcher and a pitching coach for the Atlanta Braves organization, believes that the most important lesson about proper
body mechanics is throwing the ball in a natural way ( 19). This applies to all players, whether the ball is thrown from the
outfield or the mound. When an outfielder throws the ball, he or she first takes a step backward and then lands on the
opposite forefoot with the knee slightly flexed. A pitcher should do the same. When a pitcher overthrows to get more
speed on the fastball, he or she tends to hyperextend the knee and land on the heel. This places sudden, large forces on
the shoulder during the cocking phase of throwing. Also, all motions should be in the direction that the pitcher is throwing.
This is most easily accomplished by planting the stride foot in the direction of the pitch.
When throwing in a natural fashion, the forearm is supinated during the cocking phase. With a smooth follow-through,
the forearm moves from supination to pronation easily as the elbow extends. With deceleration of the upper extremity,
the forearm should be in pronation.
The arm should be kept in shape throughout the year; however, many pitchers throw their first ball of the year just before
the season begins. Sain has an excellent year-round conditioning program. During each week of the off-season,
professional pitchers throw for 5 days at half speed and then take 2 days of complete rest. The number of pitches should
not exceed 120 per day. During the season, in a 4-day rotation, the workout as shown in Table 14.1 is recommended.
These same principles apply to Little League throwers.
TABLE 14.1. PITCHER'S IN-SEASON PITCHING PROGRAM
An off-season weight-training program should be built around light weights to build endurance, especially in the rotator
cuff musculature. Both the anterior and posterior shoulder muscles should be included. Most people tend to forget the
posterior shoulder muscles when weight training. Furthermore, strength in the legs and trunk is important for proper body
mechanics. Emphasis also should be placed on flexibility.
Adequate warmup is essential to prevent injury. A total body warmup should be followed by general body stretching,
including the legs, trunk, and upper extremities. Always warmup to pitch, do not pitch to warmup.
Finally, many people believe that side-arm pitchers place less stress on their shoulders. This is probably not true.
Shoulder abduction is about the same for the over-the-top and the side-arm pitchers. Side-arm pitchers simply bend their
trunks and extend their elbows more.
Shoulder Injuries
Injuries to the shoulder account for the majority of injuries to adult baseball players ( 20). Most of these injuries occur
during the throwing motion. A professional baseball pitcher may play 30 to 40 games in a season. He or she may throw
as many as 200 pitches in a game, many of these at high velocity ( 21). Although amateur pitchers may not play as many
games in a season, they still try to throw the ball as fast as possible while maintaining accuracy. It is not surprising that
shoulder pain is a frequent complaint among baseball pitchers.
Clinical assessment of shoulder injuries in athletes should not focus attention on the shoulder joint too quickly, because
other disease processes may be overlooked. One must always be aware of other potential causes of shoulder pain when
obtaining a history and physical examination from an injured player. Systemic phenomena, such as rheumatoid arthritis
and calcium pyrophosphate crystalline disease, can result in shoulder pain. Pain also can be referred to the shoulder
from the hand (e.g., carpal tunnel syndrome), neck (e.g., radicular symptoms), or chest (e.g., angina).
The history should be meticulous, including the patient's age, sex, and chief complaint. Loss of velocity, accuracy, and
distance usually alert the thrower to injury more serious than usual aches and pains. The impact of the injury on the
patient's activities of daily living may provide as many clues to the diagnosis as the impact of the injury on sports
performance. A relevant review of systems and family history can aid in diagnosis of systemic diseases. Pain is a
subjective symptom, but careful assessment can provide insight into disease pathology. The duration, anatomic location,
and character of the pain should be specifically assessed. In addition, the presence of night pain and analgesic
requirements should be considered. The temporal relationship to sports activity and the postural relationship to arm
motion should be obtained from the patient with shoulder pain. For example, a pitcher who complains of anterior shoulder
pain during the cocking phase of the throwing motion usually has anterior shoulder instability and possibly impingement.
The pitcher who has pain during the follow-through phase may have posterior shoulder instability. The onset of night
pain, especially when lying on the affected side, may indicate a rotator cuff tear. Pain with overhead activities is
indicative of impingement syndrome.
The physical examination of the shoulder consists of several phases: visual inspection, palpation, range-of-motion
testing, neurologic appraisal, vascular assessment, and general physical evaluation. Visual inspection includes
examining the skin and the contour of the entire shoulder girdle. Special attention should be given to areas of swelling or
muscle atrophy. Side-to-side differences should be recorded with knowledge that there are some normal changes that
occur in the throwing arm. For example, the musculature is usually hypertrophied and the scapula is often displaced
slightly inferiorly in the throwing arm. Palpation should be performed from the neck to the fingers on all sides of the upper
extremities. Magnetic resonance imaging (MRI), computed tomography (CT), and other diagnostic tests are used only to
reinforce the physical findings. The differential diagnosis of shoulder pain in the throwing athlete is shown in Table 14.2.
TABLE 14.2. DIFFERENTIAL DIAGNOSIS OF SHOULDER PAIN IN THE THROWING ATHLETE
Adult Shoulder Injuries
Neurologic Injury
Degenerative joint disease of the cervical spine can be confused with shoulder pathology. Many patients with this
condition initially complain of shoulder pain, but neck pain is usually present on careful questioning. Physical
examination supplemented with cervical spine x-ray studies enables one to localize the pathology correctly.
Thoracic outlet syndrome (TOS) refers to the compression of the nerves and vessels of the upper extremities as they
pass under the clavicle and between the scalene muscles over the first rib ( 22,23,24 and 25). Symptoms are usually
vague, making the diagnosis difficult. Typically, there is a long period of time from the onset of symptoms until the
diagnosis is made. There is usually a history of paresthesia and pain that radiates down the lateral side of the neck, then
moves into the shoulder and the medial side of the arm, and finally continues into the ring and little fingers. Physical
findings are usually subtle. Although it is not specific for TOS, the Adson test is positive if there is a diminution of the
radial pulse when the arm is abducted, the head is rotated toward the involved side, and a deep breath is held. TOS also
is suggested if the patient experiences numbness and tingling when the hands are rapidly opened and closed with the
upper extremities elevated (Roos test). TOS is discussed in greater detail with other vascular injuries, later in this
chapter.
Chronic neurologic injuries of the shoulder can present in baseball players of all ages. The neurologic examination
should include complete sensory evaluation, testing of reflex arcs, observation for atrophy, and strength testing. The
sympathetic system also should be tested for signs of reflex sympathetic dystrophy. Commonly, the throwing athlete has
a long history of achy shoulder pain during the cocking phase.
Suprascapular nerve palsy is defined as injury to the suprascapular nerve and has multiple reported etiologies including
ganglion cysts, tumors, entrapment of the nerve in the suprascapular notch or spinoglenoid notch, and trauma
(26,27,28,29,30 and 31). This section focuses on the history, examination, etiology, and treatment as it relates to the
athlete. Symptoms from this problem often are present for months to years before diagnosis ( 27). Most commonly, this is
either because the onset of symptoms is insidious with a slow decline in function and the athlete does not perceive a
problem until well into the course of the injury. Alternatively, injury to the suprascapular nerve is often not considered,
because many other more common reasons for shoulder pain are considered prior to considering this diagnosis.
The suprascapular nerve is a mixed peripheral nerve and therefore has motor fibers to the infraspinatus and
supraspinatus and sensory fibers to the acromioclavicular (AC) and glenohumeral joint but not to the skin ( 27). As such,
the earliest symptom is typically vague aching in the posterolateral section of the shoulder, often with radiation into the
neck. Atrophy of the infraspinatus and supraspinatus is variably present. Diagnosis requires a high index of suspicion.
This injury is found in overhead power athletes, particularly in volleyball players ( 31) and baseball pitchers ( 32).
The exact etiology of this disorder in the overhead athlete remains controversial. Both traction and compression
mechanisms have been suggested (28,29,31). Treatment, at least initially, is nearly always nonoperative, focusing on
external rotation strength. Athletes refractory to appropriate rehabilitation may require decompression of the nerve
surgically at one of two typical sites of compression ( 27,33,34).
The suprascapular nerve arises from the 5th and 6th cervical nerve roots with an occasional contribution from the 4th
cervical root. The nerve passes behind the brachial plexus and parallel to the omohyoid muscle deep to the trapezius
traversing laterally to the superior edge of the scapula and through the suprascapular notch ( 27,32). It then passes
beneath the suprascapular artery above the transverse scapular ligament before giving off two motor branches to the
supraspinatus muscle and sensory branches to the glenohumeral and AC joint ( 27,32,35). The nerve continues laterally
around the spinoglenoid notch beneath the infraspinoglenoid ligament to innervate the infraspinatus muscle ( 27,32,35).
Multiple sites of entrapment or injury have been proposed. The most commonly recognized are the suprascapular notch
(2), where the nerve becomes compressed beneath the transverse scapular ligament and around the spinoglenoid notch
from either a traction or a compression injury mechanism ( 35). Other sites have also been proposed based on anatomic
dissections (35). Ringel et al. (34) have proposed that three additional sites of compression potentially exist: (a)
proximally as the exiting 5th and 6th cervical nerve roots and upper trunk of the brachial plexus pass between the fascia
of the anterior and middle scalene muscles; (b) more laterally, the nerve is compressed between the fascia of the
subclavius and the omohyoid; or (c) between the supraspinatus and the base of the coracoid process.
The etiology of the nerve injury at the transverse scapular notch is reasonably well accepted as direct compression or
entrapment of the nerve beneath the transverse scapular ligament that traverses the superior aspect of the
suprascapular notch. In contradistinction, the etiology of nerve injury at the spinoglenoid notch is less definite ( 27,35). A
traction mechanism has been proposed. As the forward momentum of the humerus must be slowed, it is theorized that
eccentric contraction of the infraspinatus muscle causes traction and subsequent injury to the nerve. Additionally local
trauma causing microemboli and subsequent occlusion of the vasovasorum has also been proposed. More recently, the
local anatomy has been revisited. Sandow et al. ( 31) have proposed the supraspinatus and infraspinatus muscles create
a myofascial sling as they converge just lateral to the spinoglenoid notch. This strong fibrous sling is pulled medially
during abduction and external rotation, compressing the infrascapular nerve as it rounds the spinoglenoid notch.
This injury results from repetitive trauma over time and is always considered chronic in nature. Neurogenic atrophy with
fatty infiltration consistent with denervation atrophy and rupture of muscle fibers has been shown by light microscopy
(29).
Pain is the most consistent presenting symptom. However, the location and distribution of the pain is not characteristic.
As such, confusion with impingement syndrome, microinstability, and even cervical radiculopathy may occur. Most
athletes complain of insidiously progressive vague pain in the posterolateral shoulder during the acceleration phase of
throwing, but radiation into the neck and chest occur as well ( 26,27,30,32).
Physical examination early on in the disease course may be very unremarkable. Pain with compression at the
spinoglenoid notch or suprascapular notch are variably present and nonspecific. The most convincing sign on physical
examination is atrophy of the supraspinatus or the infraspinatus, although the infraspinatus is nearly always more
affected. Supraspinatus atrophy is often masked by the overlying trapezius atrophy and, therefore, is often less apparent.
Hama et al. (29) developed the “infraspinatus” test to aid in the diagnosis. This examination involves testing external
rotation strength of the affected shoulder against gravity. A person should be able to lift at least 3 kg against gravity while
lying on the unaffected side ( 29). A routine series of radiographs of the shoulder should be obtained, including an
anteroposterior (AP) in the plane of the shoulder and axillary lateral, scapular, and AC joint views to rule out other
sources of shoulder pain.
The diagnostic workup depends on the clinical suspicion. If the diagnosis of nerve entrapment is considered a likely
possibility, then coaxial EMG is indicated to rule out suprascapular nerve palsy. EMG findings of decreased muscle
activity and prolonged latency times confirm the diagnosis ( 26). An MRI with or without intraarticular gadolinium should
also be considered because many of these patients have additional shoulder pathology that requires attention. Reports
of tumors and other space-occupying lesions causing suprascapular nerve palsy have been published.
Diagnostic injection with local anesthetic at the suprascapular or spinoglenoid notch can be helpful in making and or
confirming the diagnosis. This is especially helpful if EMG findings are negative or equivocal ( 27). Treatment initially is
nonoperative, focusing on rest and nonsteroidal antiinflammatory drugs (NSAIDs), if needed. Rehabilitation should
involve rotator cuff strengthening, focusing on external rotation strength. Attention should be focused on both the
supraspinatus and infraspinatus muscles, realizing that the infraspinatus muscle is usually affected more. Three to six
months of nonoperative treatment is considered an adequate trial, after which surgical intervention can be entertained.
The success of nonoperative treatment appears to be related to a change or significant decrease in activity. Athletes
wishing to return to high-level competition may fail when they attempt to return to play.
Operative intervention focuses on releasing the site of injury. As mentioned earlier, there are potentially five sites of
compression. However, two sites are implicated most often. This includes compression at the suprascapular notch
beneath the transverse scapular ligament or around the spinoglenoid notch as the nerve enters the infraspinous fossa to
innervate the infraspinatus muscle.
Traditional teaching asserts that results of surgical decompression are quite variable with greater improvement in the
patients affected by entrapment at the suprascapular notch than the spinoglenoid notch. This has been challenged
recently (31,32). Relief of pain is more predictable than return of muscle function and strength. Nearly 81% of patients
have lasting pain relief after the index procedure ( 27). Return of muscle function is more variable and is perhaps due to
fatty infiltration into the muscle as a result of long-standing denervation. Additionally, muscle tearing may lead to fibrosis
that further inhibits return of full strength. However, with reduced pain, many athletes are able to return to their former
level of play. Recurrence of symptoms can occur as a result of scar formation. Neurolysis has been effective in treating
this complication (27).
Injury to the spinal accessory nerve results in trapezius muscle atrophy with symptoms of pain and weakness during
shoulder abduction. Winging of the scapula, caused by long thoracic nerve palsy, is demonstrated by pushing against a
wall with the arms outstretched. Range-of-motion and strength testing are important in making a correct diagnosis. A
herniated nucleus pulposus can cause nerve root compression in the neck with pain radiating down the arm in the
distribution of the affected nerve. Strength and reflex testing are important to determine the severity of the functional
impairment and the location of injury.
Persistent valgus stress to the medial side of the elbow, induced by throwing, may incite inflammation of the ulnar nerve
in the cubital tunnel. During flexion, the ulnar nerve elongates an average of 4.7 mm and can translate over 7 mm
medially because of the medial head of the triceps ( 36). The presenting clinical symptom is pain about the medial elbow,
occasionally radiating distally along the ulnar aspect of the forearm into the hand. Numbness and tingling of the ring and
little fingers are sometimes present. Additional symptoms include clumsiness, heaviness, and problems with grasp,
especially after throwing. One must be aware of possible concomitant medial elbow instability when a throwing athlete
complains of cubital tunnel symptoms.
Examination elicits tenderness over the cubital tunnel, and the tunnel may feel thick and “doughy.” Tinel sign may be
localized to the cubital tunnel. Neurologic abnormalities in the distribution of the ulnar nerve include hypoesthesia,
interosseous wasting, and dry skin. Ulnar neuritis, in which the symptoms are mild and intrinsic atrophy is absent, usually
responds well to conservative treatment. Rest and ice, along with splint immobilization for 2 to 3 weeks, have been
helpful in reducing acute symptoms. Steroid injections into the cubital tunnel are not recommended, and surgical
intervention is usually not required. Surgical decompression may be indicated in chronic relapsing cases or when
intrinsic atrophy and weakness are present.
AC problems commonly begin with an acute injury, such as shoulder separation. In fact, follow-up of AC joint sprains
reveals a significant number of residual symptoms, with second-degree sprains probably resulting in the highest
incidence (65%) (37). Regardless of the severity, most athletes with a shoulder separation can return to their sport in a
few weeks. However, some athletes develop degenerative joint disease (DJD) of the AC joint. The diagnosis is made by
careful palpation of the AC joint for tenderness and crepitus. The AC joint and the surrounding area are usually painful
with motion, especially horizontal adduction, which loads the clavicle. AC joint DJD can mimic other shoulder problems
such as impingement syndrome. Initial treatment should include antiinflammatory medications and steroid injection. If this
fails, distal resection of the clavicle yields good results. Arthroscopic resection also is an accepted approach, with results
similar to the open procedure. Baseball players treated with distal clavicle resection have returned to competition with no
loss of function, strength, or motion ( 38).
Impingement Syndrome
The most common injuries that occur in the shoulder from throwing result from the constant irritation of anterior shoulder
structures (1). Impingement is defined as compromise of the space between the coracoacromial arch and the underlying
rotator cuff. The coracoacromial arch includes the coracoid, the coracoacromial ligament, the AC joint, the acromion, and
the subacromial bursa. These structures make up the roof over the anterior glenohumeral joint. The supraspinatus
tendon and the tendon of the long head of the biceps brachii are the most commonly compressed structures. When the
humerus is flexed and internally rotated, the insertion of the supraspinatus tendon is brought under the coracoacromial
arch and abnormal contact can ensue. This is especially true when the space between the acromion and the humerus is
further compromised by anterior acromial osteophytes. The athlete initially complains of pain in the anterior shoulder
during the acceleration phase or sometimes during the follow-through phase. Initially, the pain resolves after a short
period of rest. However, the condition relentlessly progresses if the offending activity is not stopped. With time, the pain
becomes more intense, especially with forward flexion and internal rotation (Hawkin impingement sign). Physical
examination reveals tenderness with palpation of the anterior acromion and a positive impingement sign and test. Neer
(39) divided the impingement syndrome into three stages. Stage I is characterized by edema and hemorrhage of the
bursa and cuff. The symptoms are reversible with rest, NSAIDs, and rotator cuff stretching and strengthening exercises
performed in nonimpingement positions. Because the insertion of the supraspinatus and biceps tendons lie anterior to
the coracoacromial arch with the shoulder in a neutral position, any activities that require forward flexion should be
restricted until symptoms resolve. In the majority of cases, stage I impingement resolves within 2 to 4 weeks. Stage II
impingement is characterized by irreversible changes of the rotator cuff, predominantly fibrosis and tendinosis. It persists
longer and may take 3 months to improve. At this stage, surgical intervention may be required. Stage III impingement is
characterized by partial or complete tears of the rotator cuff. Classic teaching is that the patient needs to have 3 to 6
months of nonoperative treatment before any surgery can be recommended. This is not always realistic and must be
modified based on the throwing athlete's skill level and demands, in addition to the surgeon's comfort with impingement
procedures. Current techniques of arthroscopic subacromial decompression and distal clavicle resection minimize the
athlete's down time (4 to 6 weeks).
Impingement may also occur in throwing athletes at the deep surface of the supraspinatus tendon on the posterior
glenoid rim. Walch et al. ( 40) characterized these athletes as having pain on full external rotation and between 90 and
150 degrees of abduction. Supraspinatus weakness or evidence of impingement was noted in most cases. External
rotation of the involved shoulder averaged 15 degrees more on the affected side in four of thirty patients. These changes
can be affected by anterior glenohumeral laxity.
Rotator Cuff Disease
Rotator cuff disease has extrinsic and intrinsic etiologies ( 41). The extrinsic causes are forces acting outside the rotator
cuff that cause injury to the tendons. Impingement syndrome, which Neer ( 42) implicated in 95% of rotator cuff tears, is
an example of extrinsic rotator cuff disease. Extrinsic causes of rotator cuff disease also include instability of the
glenohumeral joint. Jobe et al. ( 43) have shown that muscle activity becomes abnormal about the shoulder as it begins to
subluxate. In an attempt to stabilize the shoulder girdle, the scapula becomes fixed, the rotator cuff muscles attempt to
substitute for the lost scapulothoracic motion, and muscle overuse and fatigue occur. If this condition persists, muscle
fatigue leads to abnormal shoulder kinematics and contributes to instability. A downward spiral then ensues. Eventually,
instability results in the humeral head impinging on the coracoacromial arch. This situation is different from that of pure
impingement, and a careful evaluation for shoulder instability is required. These patients occasionally report that the
shoulder feels as though it is moving anteriorly. However, anterior shoulder pain is usually the only complaint. Careful
physical examination reveals the subtle anterior instability. MRI or MRI arthrogram may show an avulsion of the
anteroinferior labrum from the glenoid (Bankart lesion). Along with demonstrating the Bankart lesion, arthroscopy can
show anterior labral fraying (the only lesion in some cases). A small posterolateral humeral head compression fracture
(Hill-Sachs lesion) also may be present. Conservative treatment results in improvement of the symptoms in most cases.
Because impingement is present, all exercises must be performed with the affected upper extremity in nonimpingement
positions, as described later. Both the rotator cuff and the scapular rotator muscles are weak and must be strengthened.
In this group of patients, an anterior acromioplasty only makes the instability worse. Surgery to reconstruct the anterior
labrum and capsule may be required if physical therapy fails.
Intrinsic causes of rotator cuff disease include traction injuries and primary cuff degeneration not related to impingement
syndrome. There is a critical zone of hypovascularity at the insertion of the supraspinatus tendon ( 44,45). The majority of
rotator cuff pathology occurs in this area. Uhthoff et al. ( 46) showed that most tears of the rotator cuff begin on the
articular side of the tendon, which supports a role for intrinsic etiologies of rotator cuff disease. Nirschl ( 47) wrote of
angiofibroblastic changes occurring in the tendon with secondary development of rotator cuff calcification, erosion, and
impingement. Undoubtedly, both extrinsic and intrinsic factors play a role in rotator cuff pathology.
Motion of all four joints (sternoclavicular, AC, scapulothoracic, and glenohumeral) is essential to normal shoulder
kinematics. This can be assessed both actively and passively. Differences between active and passive motion can be the
result of neuromuscular deficiency such as a rotator cuff tear. Motion should always be compared with the contralateral
shoulder. Brown et al. (48) found that major league pitchers have different ranges of motion between the shoulders. In the
pitching arm, with the shoulder in abduction, there is 11 degrees less extension, 15 degrees less internal rotation, and 9
degrees more external rotation. Therefore, comparison with the contralateral arm should be done with this variance in
mind.
Throwing a baseball subjects the rotator cuff to many insults (impingement, traction, and contusion), which can result in
failure of the tendon fibers. Repeated, small episodes of partial rotator cuff tearing can occur. The incidence of partial
rotator cuff tears rises with age. In a series of 233 patients with rotator cuff tears, Neer et al. ( 49) found 97% to occur in
individuals older than 40 years of age. These patients commonly present with a long history of intermittent shoulder
tendonitis that likely represents tendon fiber failure. Most full-thickness rotator cuff tears occur in a tendon that is already
weakened by earlier pathology. Eventually, the patient experiences increasing shoulder pain that may wake him or her up
at night, especially when sleeping on the affected shoulder. Elevation of the arm in the scapular plane against resistance
becomes increasingly difficult, partly because of the tear and partly because of disuse atrophy. Samilson and Binder ( 50)
found the most common symptoms of complete rotator cuff tears to be pain, weakness in shoulder elevation, and
subacromial crepitus. Partial rotator cuff tears are characterized by less severe symptoms. Nonoperative treatment of
rotator cuff tears includes rotator cuff-strengthening exercises performed with the arm at the side, NSAIDs, avoidance of
precipitating activities, and steroid injections. Surgical repair in competitive athletes has had disappointing results. In a
recent study, only 56% of patients were able to return to their former competitive level after surgical repair. Only 32% of
the throwers were able to return to collegiate or professional sports at the same level ( 51).
Proper rehabilitation of the rotator cuff is essential for a full recovery from shoulder injury. All internal and external
rotation exercises must be performed with the arm at the side to eliminate pain from impingement. To strengthen the
external rotators, the patient is instructed to lie on the side of the uninvolved shoulder with a small weight held in the
hand as shown in Fig. 14.2A. The shoulder is externally rotated, and the patient is then instructed to lie supine and a
small weight is held in the hand as the patient internally rotates the shoulder (see Fig. 14.2B). These exercises also can
be easily performed with elastic bands that have a progressive resistance to elongation. The scapular stabilizers can
best be strengthened with a variation of the standard push-up. At the top of the exercise, the body is pushed as far from
the floor as possible. This activity protracts the scapula, strengthening the stabilizers. Stretching exercises also should
be performed. These exercises should be supervised to ensure that the patient stretches only those muscle groups that
are tight and does not place the shoulder in positions that may aggravate the pathology.
FIGURE 14.2. Rotator cuff strengthening exercises. A: External rotators. B: Internal rotators.
Anterior Instability
Although frank dislocation of the shoulder is extremely rare, subluxation is much more common in the throwing athlete
secondary to chronic overuse. Davidson et al. ( 52) provided a case report of a professional pitcher with a strongly
positive shoulder relocation test who had impingement of the posterior aspect of the supraspinatus tendon, a type II
SLAP (superior labrum anterior to posterior) tear, and evidence of anterior instability. His subacromial space appeared
completely normal on examination. He responded well to anterior capsulolabral reconstruction and was able to return to
pitching.
Posterior Instability
Posterior shoulder instability is often unrecognized in throwing athletes. Pure dislocation of the joint is rare, but
subluxation is not. There are two different mechanisms that can result in posterior instability. In the first situation,
improper pitching technique causes repetitive microtrauma to the posterior capsule. The follow-through phase of the
throwing motion is characterized by intense contraction of the shoulder muscles to decelerate the upper extremity. At this
time, the shoulder is in the vulnerable position of flexion, adduction, and internal rotation. This creates high stresses in
the posterior capsule. Repeated microtrauma, resulting from poor pitching technique, causes posterior capsule weakness
and eventual humeral head subluxation. In the second situation, a single traumatic event initiates the instability. For
example, a player falls on the outstretched throwing arm and has immediate posterior shoulder pain. After the pain
subsides, throwing velocity and endurance decrease. This is accompanied by pain during the follow-through. Through
either mechanism, the posterior capsule can become attenuated. Complete tears of the capsule from the glenoid, which
commonly occur anteriorly, are less common posteriorly.
Patients with posterior shoulder instability complain of pain in the posterior shoulder, sometimes radiating along the
scapula. However, anterior shoulder pain is occasionally noted in these patients. A careful physical examination
demonstrates the true pathology. Usually, the patient has pain with forward flexion, adduction, and internal rotation, and
it may be possible to demonstrate the instability in this position. The best way to feel the subluxation is to place the
patient on the examination table in a supine position. The examiner puts his or her hand over the humeral head and
positions the shoulder, as described earlier. A posteriorly directed force applied to the humeral head results in a palpable
instability. During examination for glenohumeral instability, the examiner must always be aware of the patient's
generalized ligamentous laxity. This is especially critical in the adolescent athlete ( 50). Radiographic examination may
reveal a posterior glenoid spur ( 51). However, this lesion is extracapsular (20) and of questionable significance.
Some athletes can voluntarily sublux their shoulder. These patients have reached the last stage in the spectrum of
instability patterns and do not have an associated psychological component. They should be treated like any other
patient with posterior instability. This is in contrast to the patient with intentional shoulder dislocation and drug-seeking
behavior.
Rehabilitation results in symptomatic improvement in two thirds of the cases ( 42). Rehabilitation should be well
supervised and last for as long as 6 months. Throwing technique also should be examined to eliminate any activity that
may be placing additional stress on the posterior capsule.
Glenohumeral Degenerative Joint Disease
Osteoarthritis of the glenohumeral joint is rare in the throwing athlete. Radiographic findings include joint space
narrowing, subchondral sclerosis, peripheral osteophytes, and cystic changes. Inciting factors in young individuals
include trauma and avascular necrosis of the humeral head.
Biceps Tendon Injury
The biceps tendon may be difficult to palpate. Examination is performed by slowly internally and externally rotating the
shoulder, feeling for the intertubercular groove of the humerus. Relaxation of the deltoid muscle may make this easier.
Numerous stress tests have been described. All involve forced supination or flexion of the forearm trying to elicit pain in
the bicipital groove.
Biceps tendon subluxation can be a source of anterior shoulder pain. O'Donoghue ( 54) described differences in the
bicipital groove that can lead to subluxation. A shallow groove was more prone to subluxation with the internal and
external rotation that occurs during the throwing mechanism.
Superior Labral AP Lesions
In 1984 Andrews et al. (55) reported on a series of throwing athletes with labral pathology just anterior to the biceps
insertion and theorized that injury to this area may occur as a result of high-deceleration forces in the biceps as the
elbow is extended during the follow-through phase of throwing. The lesions Andrews described were localized primarily
to the anterior portion of the labrum; however, there was a subset of patients that had lesions both anterior and posterior
to the biceps attachment (53). In 1990 Snyder et al. ( 56) provided what is now considered the classic description of the
superior labral anteroposterior (SLAP) lesion. Snyder also described an acute traumatic mechanism of injury in which
detachment of the biceps anchor and glenoid labral complex occurred after as a result of a fall onto a flexed and slightly
abducted upper extremity (54).
Patients with a SLAP tear often give a history of prolonged shoulder pain and discomfort before diagnosis ( 54,55). Nearly
all athletes complain of pain with throwing and about half will have catching or popping ( 54). Diagnosis can be
problematic. O'Brien ( 57) has described the active compression test for diagnosing and distinguishing labral tears and
AC joint abnormalities. With the arm forward flexed to 90 degrees, adducted 10 degrees, and the hand pronated with the
thumb pointed to the ground, a downward force is placed on the arm. This test is repeated with the hand supinated
(thumb up). Pain felt “in the shoulder,” as interpreted by the patient, with the hand supinated and not in the pronated
position is a positive result and suggestive of labral pathology. This must be distinguished from pain felt “on the shoulder”
in the region of the AC joint and pain with hand in both the pronated and supinated positions ( 56).
Imaging of the shoulder with conventional radiographs has been of little use in diagnosing this entity. They are routinely
obtained to rule out other causes of shoulder pain and should consist of AP, axillary, and scapular-Y views. MRI has
emerged as perhaps the most sensitive and specific examination for diagnosing labral pathology ( 57,58). The addition of
intraarticular gadolinium has enhanced the sensitivity and specificity of the MRI examination ( 57). MRI is preferred over
CT-arthrography owing to the superior imaging of soft tissues by MRI, which allows evaluation of other potential shoulder
pathology. Patients can have concomitant rotator cuff tears as well as Bankart lesions that may require attention ( 58).
Snyder described four basic types SLAP lesions. Type I: fraying of the biceps anchor and labral complex but the
peripheral labral edge remained firmly attached to the glenoid and the attachment of the biceps tendon to the labrum was
intact. Type II: detachment of the superior labrum and biceps anchor resulting in instability of the complex. Type III: a
bucket handle tear of the superior labrum. The central portion is displaceable into the joint, the labrum remains firmly
attached to the underlying glenoid and to the biceps tendon. Type IV: similar to type III except the tear extends into the
biceps tendon. Type II tears were the most common (41%) followed by type III (33%) (56).
Treatment is primarily surgical ( 55). By the time patients present, they have often tried nonoperative modalities. Surgical
treatment is dictated by the type of lesion present ( 55). Types I and III are typically debrided ( 55,60). Types II and IV are
amenable to reattachment using an anchor technique ( 59). Postoperative regimens consist of early gentle passive
range-of-motion (ROM) exercises that are slowly progressed over 4 to 6 weeks. Gentle isometric strengthening is then
initiated and progressed to a formal rehabilitation program. Return to gentle throwing is allowed at 3 to 4 months.
Surgical treatment has been successful in alleviating pain and returning athletes to play ( 59).
In the authors' laboratory, it has been shown that the biceps tendon can stabilize the glenohumeral joint in a simulated
dynamic shoulder model (61). When superior labral lesion was created, the stabilizing effect of the biceps tendon during
the late cocking phase of throwing was eliminated in the model. EMG studies in pitchers with unstable shoulders show
increased activity in the biceps muscle during this same phase of the throwing motion. This implies the biceps muscle
plays a role in stabilizing the glenohumeral joint in the thrower with anterior instability.
Microfracture and Macrofracture
The humerus is subject to enormous forces during the throwing mechanism. Several authors have found that the torques
on the humerus during throwing are larger than the torque required to fracture the humerus ( 10,62). Axial compressive
forces on the humerus from muscular contraction are thought to be protective in preventing fracture. Although they are
rare, these forces can result in stress fractures ( 62) or overt fractures (63). When an athlete reports proximal humerus
pain, the physician is obligated to rule out a stress fracture. The authors have seen two cases of humeral fracture
preceded by upper arm pain humerus fractures.
Overt fractures of the humeral shaft have also been reported in several series of amateur baseball players. These
fractures most commonly occur at the junction of the middle and lower thirds of the humerus and are spiral in
configuration (64,65 and 66). Although both an internal and an external rotatory force involved in the overhead throwing
motion have been described as the mechanism responsible for this particular injury, the external rotation fracture pattern
is most common. These forces reach a maximum in the acceleration phase of the throwing motion when these injuries
are thought to occur by rotatory tensile overload ( 67). Professional and collegiate players seem protected from these
injuries secondary to the adaptive cortical remodeling that occurs over time with increased amounts of conditioning and
play. Factors related to the occurrence of this injury include muscular fatigue, amateur level, irregular practice habits, and
dysfunction or lack of coordination of muscular antagonists in the arm. Treatment for these injuries is generally
nonoperative with functional bracing. Radial nerve injuries, while uncommon, have been reported with these fractures.
Their presence has not affected the overall outcome of these patients, because complete recovery has been
demonstrated with conservative management at one year from the time of injury (64). The need for operative treatment of
these injuries is rare.
Pediatric Shoulder Injuries
Micheli (69) has noted several risk factors that predispose the pediatric athlete to injury. These include training errors,
anatomic malalignment, repeated trauma to growing cartilage, and associated disease states.
Little League shoulder was first described by Dotter ( 70). This entity, further characterized by Adams ( 71) consists of pain
in the shoulder occurring at the end of a hard throw. The onset can be insidious or acute and usually does not
immediately stop the pitcher from throwing. Radiographs typically show uniform widening of the proximal humeral
epiphysis compared with the contralateral shoulder. There is no evidence of displacement although Cahill et al. ( 72) feel
that the repeated trauma of pitching results in disruption of the epiphyseal plate, thus causing fracture. They suggest that
stress fractures result either from the large torque generated in the cocking and acceleration phases of throwing or from
the distraction force generated during acceleration. Other etiologies also have been proposed ( 70,72). In all cases, the
condition is self-limiting, with the pain relieved by rest.
A young pitcher who complains of shoulder or upper-arm pain should be examined for other pathology as well. In this age
group, musculoskeletal tumors are most commonly benign. A simple bone cyst is a solitary cystic defect of bone. The
classic location of this lesion is in the proximal humerus of young children, and the most common reason for clinical
presentation is a fracture through the weakened bone. Radiographs reveal a well-defined lucent area in the bone with a
thin sclerotic margin (Fig. 14.3). A pseudoloculated appearance can be present. When observed over time, the lesion
appears to migrate away from the growing epiphysis. Treatment includes observation for small lesions and cast
immobilization for lesions associated with fracture. Large lesions require steroid injection or bone grafting to ensure
healing of the cyst.
FIGURE 14.3. Simple bone cyst in the proximal humerus of an adolescent. AP radiograph reveals a well-defined
radiolucent area in the humerus with a thin sclerotic margin.
Elbow Injuries
Baseball players can sustain a plethora of injuries to the elbow. The repetitious, high-velocity nature of the baseball
throw induces chronic stresses at the elbow and particularly predisposes the elbow to overuse syndromes.
Biomechanically, efficient throwing necessitates rapid forceful extension of the elbow, accompanied by significant valgus
stress and finally pronation of the forearm. The angular velocity of the elbow while throwing can exceed 3000 degrees
per second. The normal valgus angle of the elbow in extension may specifically bias the medial aspect of the elbow to
overuse injuries. The velocity and force required in repetitive throwing contributes to inflict microtrauma on the elbow and
its stabilizers. Commonly, overuse injuries are encountered when the body's physiologic ability to heal lags behind
incessant microtrauma. Each age group and proficiency level normally demonstrates specific injury patterns. Therefore,
even though the throwing motion is similar in all ages, the typical sites of injury are much different when comparing
immature and mature throwers. Four distinct areas are vulnerable to throwing stresses: (a) medial tension overload, (b)
compression overload to the lateral surfaces, (c) posteromedial shear stresses, and (d) extension overload to the lateral
restraints (73) (Fig. 14.4). In the mature thrower, the weakest link is the ligamentous and bony surface, as opposed to the
physis in immature throwers.
FIGURE 14.4. Forces at the elbow during throwing include medial tension, lateral compression, and posteromedial shear.
Adult Elbow Injuries
The differential diagnosis of adult elbow injuries is shown in Table 14.3.

TABLE 14.3. DIFFERENTIAL DIAGNOSIS OF ADULT ELBOW INJURIES
Medial Tension Overload
A significant tension force is absorbed by the medial elbow restraints during the late cocking and acceleration phases of
the throwing cycle. The resultant force presents as tension on the medial epicondylar attachments of the flexor muscle
origin and medial collateral ligaments. Chronic microtrauma to these structures can result in inflammation of the
musculotendinous attachments on the medial epicondyle or scarring and attenuation of the medial collateral ligaments,
with possible rupture.
Inflammation of the medial epicondyle presents with pain and tenderness and positive provocative tests (pain with
resisted wrist flexion and pronation). Initial treatment entails ice, rest from throwing, phonophoresis, and the
administration of NSAIDS. Recalcitrant cases sometimes need local steroid injections at the site of maximal tenderness.
Once symptoms have abated, a systematic regimen of strengthening exercises is helpful.
Inflammation and scarring of the medial collateral ligaments, secondary to insidious microtrauma, is much more
demanding clinically. Diagnosis is difficult, with the athlete typically reporting pain distal to the medial epicondyle during
late cocking and acceleration. Associated ulnar neuritis symptoms may be present. Throwing velocity is decreased, and
the athlete will have problems when accelerating the ball more than three quarters normal velocity. Physical examination
demonstrates deep tenderness at the site of the ligaments. Instability tests require sensitive fingers to detect subtle
medial instability. Stress radiographs are technique dependent and are helpful only when positive.
Treatment of these injuries depends on the integrity of the medial collateral ligament complex and the degree of joint
instability. Most cases of medial ligament sprain resolve with conservative treatment, including ice, rest from pitching,
phonophoresis, and the administration of NSAIDS. Once acute symptoms subside, a strengthening protocol of the
forearm flexors and pronators and a progressive throwing program are started as symptoms permit. Infrequently, chronic
microtrauma of the ligament causes a complete rupture with resultant medial instability. The history includes multiple
bouts of medial elbow pain that have responded to conservative treatment. Suddenly, a single episode of “giving way”
occurs, representing ligamentous rupture. Treatment depends on the goals of the athlete and the degree of instability.
However, surgical reconstruction for acute ruptures of the medial collateral complex is usually necessary in high-level
throwers.
Lateral Extension Overload
Lateral extension overload presents during the acceleration phase of throwing when rapid forearm pronation initiates a
tension stress to the lateral musculotendinous origin. Repeated stress may induce lateral epicondylitis; however, the
lateral ligamentous complex is rarely involved. Treatment is similar to that described for medial epicondylitis.
Posteromedial Shear
Posteromedial shear with posterior compartment damage is common in adult throwers and develops in two phases of
throwing. During late cocking and follow-through, the posterior compartment must absorb and dissipate the
posteromedial shear force that develops. This force commonly induces three types of pathology: (a) posteromedial spurs,
(b) pure posterior spurs, and (c) osteophytes on the floor of the olecranon fossa. All three of these sites may contribute to
loose body formation. Treatment is initially conservative with attention to symptomatic control. Chronic posterior
impingement and loose body symptoms usually necessitate arthroscopic removal of spurs and loose bodies.
Pediatric Elbow Injuries
Young throwers tend to have more elbow injuries than shoulder injuries ( 73). The term “Little League elbow” has been
routinely used to describe a group of pathologic entities in and about the elbow joint in immature throwers. Each of these
conditions, in fact, is a specific elbow injury with an individual personality as to prognosis and treatment. The typical
problems in immature throwers include (a) medial epicondylar fragmentation and avulsion, (b) delayed or accelerated
apophyseal growth of the medial epicondyle, (c) delayed closure of the medial epicondylar physis, (d) osteochondrosis
and osteochondritis of the capitellum, (e) deformation and osteochondrosis of the radial head, (f) hypertrophy of the ulna,
and (g) olecranon apophysitis with or without delayed closure of the olecranon apophysis ( 65,75,76,77,78 and 79). Many
investigators have implicated these maladies to be secondary to the biomechanical throwing stresses placed on young,
developing elbows (60,80,81 and 82). Exceptional forces are absorbed and transmitted by the elbow during throwing.
These forces include traction, compression, and shear localized to the medial, lateral, and posterior elbow, respectively
(74). Any or all of these forces may contribute to the alteration of normal osteochondral development of the elbow ( 83).
The cornerstone to successful treatment of Little League elbow is a timely, accurate diagnosis of the specific injury. A
meticulous history and physical examination are the essential tools in achieving this goal, routine radiographs excluded.
The use of special tests such as the arthrogram, CT scan, and MRI are often necessary in a confirmatory role rather than
a diagnostic one.
Two of the most common abnormalities in the immature thrower are medial tension injuries and osteochondritis dissecans
(OCD) of the capitellum. The differential diagnosis of pediatric elbow injuries is shown in Table 14.4.
TABLE 14.4. DIFFERENTIAL DIAGNOSIS OF PEDIATRIC ELBOW INJURIES
Medial Tension Injuries
The most common reports in immature throwers involve the medial aspect of the elbow. The athlete reports a triad of
symptoms, including progressive medial pain, decreased effectiveness, and decreased throwing distance. The most
common cause of the dysfunction is a subtle stress fracture involving the medial epicondylar physis. Radiographs usually
are negative; however, an irregular medial epicondylar epiphysis occasionally is apparent. The salient physical finding is
tenderness of the medial epicondyle. Generally, acute symptoms subside with rest, ice, and NSAIDS. A flexibility,
strengthening, and progressive throwing protocol is helpful after cessation of symptoms. Residual deformity and delayed
fusion of the epicondyle is not common.
If a more vigorous valgus stress is absorbed while throwing, an avulsion fracture through the medial epicondylar physis
may occur. Sudden medial pain, point tenderness, and a flexion contracture are typical. Radiographs most often
demonstrate a minimally displaced epicondylar fragment, although at times substantial displacement is apparent ( Fig.
14.5). Treatment depends on the amount of epicondylar displacement. Although controversy exists, the authors advocate
an anatomic surgical reduction and do not accept any degree of medial epicondylar displacement.
FIGURE 14.5. Displaced medial epicondylar fragment in the joint of immature thrower.
Medial ligamentous ruptures in immature throwers seldom occur. These instabilities are much more prevalent in mature
throwers, who have accumulated years of insidious microtrauma and scarring of the medial collateral complex. Treatment
is usually conservative, involving initial immobilization followed by functional bracing and, finally, gradual rehabilitation.
This rehabilitation protocol includes symptomatic control, ROM exercises, and strength training. Surgical reconstruction
of the medial collateral ligament complex is rarely indicated.
Lateral Compression Injuries
OCD of the capitellum typically presents in young throwers between 13 and 16 years of age. They complain of dull lateral
elbow pain associated with a flexion contracture and occasional locking. Radiographs demonstrate a focal island of
subchondral bone demarcated by a rarefied zone, with or without loose bodies ( Fig. 14.6). OCD can usually be
delineated from Panner disease (osteochondrosis) of the capitellum by age (patients with Panner disease are younger
than 7 to 12 years of age) and radiographic presentation. Treatment of OCD is determined by lesion location, size,
fixation, and condition of the articular cartilage. Type I lesions that are intact with no evidence of displacement or articular
fracture require rest and splinting for 3 to 4 weeks, followed by ROM exercises. Protection of the elbow is continued until
radiographic evidence of healing is apparent. Type II lesions present with fracture or fissuring of the articular surface and
with partial displacement of the nonvascular fragment. Partially detached Type II lesions usually require elbow
arthroscopy to evaluate the articular surface. Two modes of treatment are common: in situ pinning (large fragment) and
removal and burring of the base of the lesion (small fragment). Type III lesions are completely detached, and loose body
symptoms may be present. The avascular fragment is usually hypertrophied and rounded. The crater is obscured by
fibrous tissue and is subsequently smaller than the fragment. Treatment requires arthroscopy, removal of the fragment,
and burring of the crater. Late sequelae of OCD include loose bodies and residual deformity of the capitellum. Residual
elbow disability is common.
FIGURE 14.6. Osteochondritis dissecans of the capitellum in an immature thrower.
Vascular Injuries
Diagnosis of vascular compression injuries in the throwing athlete is difficult. The symptoms are usually vague, and
physical findings are often subtle. In addition, these injuries are relatively uncommon.
The anatomy in the shoulder can create a tethering effect on third portion of the axillary artery where the anterior and
posterior circumflex arteries arise when the arm is in the extreme extension, abduction, and external rotation. This excess
force on the axillary artery can result in thrombosis more proximally or an aneurysm at this site over time. Several reports
exist documenting digital ischemia attributed to a more proximal aneurysm in athletes that required initial thrombolysis,
followed by saphenous vein grafting combined with ligation of the circumflex vasculature or vein patch angioplasty in
more limited defects (84,85). These athletes presented with digital pallor, cyanosis, discomfort, and ulceration attributed
to ischemic compromise. When suspected, arteriography and plethysmographic studies of the digital arteries are
indicated because distal pulses and duplex scanning are often normal.
Vascular examination includes a number of tests for vascular compression in addition to skin examination and pulse
palpation. Vascular injuries in athletes are related to chronic throwing effort. McCarthy et al. ( 87) evaluated 17 baseball
players for vascular upper extremity conditions: 7 had TOS and the remaining 10 athletes had hand ischemia. The
athletes with TOS had complaints of decreased endurance or severe finger ischemia from emboli (one athlete). All of the
pitchers had a measurable loss of pitch velocity and were unable to pitch for more than three innings. Forearm pain,
throwing arm heaviness, and hand coldness were present in some pitchers. Loss of pitching control was not a symptom.
Physical diagnosis revealed a diminished pulse or a loud bruit in all but one athlete. Doppler ultrasonography and duplex
scanning confirmed the presence of arterial compression in more than 90% of the athletes. Most of the athletes had
compression of the subclavian artery behind the scalene musculature. Sometimes these injuries are the result of
subclavian artery aneurysm with thrombosis. In this case, embolization can occur to the hand. Fortunately, these arterial
injuries are rare. Compression of the subclavian artery can occur at the thoracic outlet by either a cervical rib or a
hypertrophied scalene musculature ( 25,87). Treatment of TOS includes avoidance of all exacerbating activities and a
carefully supervised program of muscle strengthening for the entire shoulder girdle. Postural training also may have a
positive effect. Surgical decompression of the thoracic outlet can be approached in many ways ( 21,23,24 and 25,87).
Compression of the posterior humeral circumflex artery ( 88), the suprascapular artery, or the subscapular artery ( 86) also
can result in localized symptoms.
Rohrer et al. (90) examined 92 extremities in three groups: professional pitchers, nonpitching professional players, and
nonathlete controls. They found 83% of the extremities had some compression of the axillary artery by the humeral head
when the shoulder was in the position of abduction and external rotation. However, greater than 50% arterial
compression was present in only 7.6% of the extremities, and a significant difference was not present among the three
groups.
Itoh et al. (89) have documented circulatory disturbances in the throwing hand of baseball pitchers, resulting in finger
pain, ulcers, and cyanosis. They proposed that the digital arteries sustain repeated compression and traction with ball
release because they are entrapped between Cleland ligament and a hyperextended proximal interphalangeal (PIP) joint.
With surgical release of Cleland ligament good recovery of circulation and return to throwing is possible. Pitchers who
commonly throw the split-finger fastball may be particularly prone to developing circulatory disturbances in their throwing
hands. This may be related to the extreme angular displacement between the index and long fingers required to perform
this pitch.
Blunt Chest Trauma
There has recently been increased attention focused on isolated, yet serious, injuries in baseball secondary to blunt
trauma caused by a baseball's impact on the chest wall. The force and timing of this impact, along with the relative
compliance of the chest wall, appear to dictate the severity of the injury. These injuries can range from transient apneic
episodes to fatal arrhythmia. Maron et al. ( 89) recently reported on 25 fatalities (patients aged 3 to 19 years) secondary
to blunt chest trauma. Eighteen of these deaths involved softball or baseball injuries and were cardiac in origin.
Structural injury to the heart can result in myocardial contusion that can lead to, in rare instances, cardiac arrhythmia
(90). These arrhythmia often occur shortly after the injury but have been reported as late as 1 week from the time of injury
with stress testing. Because contusions result in areas of myocardial necrosis and hemorrhage, creatine phosphokinase
(CPK) values, electrocardiographic (ECG) tracings, and echocardiography are helpful in diagnosing this condition.
Exercise stress testing has been recommended before the patient returns to sports.
Nonstructural injury or commotio cordis is thought to result from mild to severe chest trauma that alters the hemodynamic
and electrophysiologic status of the heart, leading to fatal arrhythmia without gross myocardial damage on autopsy
(90,92). Both the timing and location of the impact must be precise to trigger a fatal ventricular arrhythmia. The force of
the chest trauma has been thought to be less important than the timing. Trauma must occur in narrow temporal window
between 15 to 30 msec before the peak of the T wave was necessary to cause this fatal arrhythmia in animals. Others
have studied the impact of the components of the baseball in inducing these injuries, hypothesizing that soft-core
baseballs may decrease the incidence of these injuries. Conflicting reports have arisen from these studies, and it is
thought that adequate coaching techniques designed to decrease chest trauma may be a more effective way of
preventing these injuries.
HEAD AND NECK INJURIES
Baseball, although not considered a contact sport, results in surprisingly high numbers of head and neck injuries.
Approximately half of baseball fatalities are the result of head and neck injuries ( 4). The U.S. Consumer Product Safety
Commission estimates that 170,000 baseball-related injuries occur each year to the face, predominantly the mouth and
the eyes (5). Head injuries are especially common in the 5- to 14-year-old age group, accounting for 40% of all baseball
injuries (5). Numerous studies have found baseball to be the leading cause of youth sports-related head injuries ( 6,93).
The mechanisms of head and neck injury in baseball include ball impact, collision trauma, and sliding accidents. Between
40% and 70% of baseball-related youth eye injuries occur from being hit by a pitch while batting ( 6,93,94). Bony trauma
to the teeth, jaw, facial bones, nose, orbit, and skull also can result from being hit. Ocular injuries seen in baseball
include lid lacerations, foreign bodies, hyphema ( Fig. 14.7), vitreous hemorrhage, retinal detachment, optic nerve
damage, and blindness (6,93,94). Head-first sliding has been described as causing neck hyperflexion injuries that can
result in quadriplegia ( 1). Neurologic sequelae, including subdural hematomas, also can result from head trauma during
baseball.
FIGURE 14.7. Hyphema. Blood in the anterior chamber of the eye in a batter hit by a pitch. (Courtesy of JB Jeffers.)
Careful physical examination of a baseball player who has sustained a head or neck injury is essential. Clinical
assessment must define the cause, type, location, and extent of injury. In every instance of significant head trauma, the
neck should be stabilized in a rigid cervical collar until the integrity of the spine is established. Types of traumatic head
and neck injury include concussions, contusions, skull fracture, epidural hematomas, subdural hematomas, and spinal
fractures. Any loss of consciousness, sensory change, motor deficit, neck stiffness, or altered mental status, other than a
transient concussion with rapid recovery of all senses, should be aggressively pursued with a careful neurologic
examination and further diagnostic tests to determine the extent of involvement. Significant facial soft tissue injury
suggestive of bony involvement should be evaluated with appropriate diagnostic radiographs. When ocular involvement
is suggested, a thorough eye examination, including evaluation of fundi, visual fields, acuity, and eye movements, is
necessary to determine the extent of injury. Table 14.5 reviews important aspects concerning the examination of a patient
with suspected head or neck injuries.
TABLE 14.5. HEAD AND NECK INJURY ASSESSMENT
Baseball is being targeted as a sport that should require total head and face protection. Little League and professional
baseball organizations require the use of batting helmets, base-running helmets, and catchers' helmets with face masks.
Facial and ocular injuries resulting from baseball impact are largely preventable. The National Society to Prevent
Blindness estimates that 90% of ocular injuries resulting from sports are preventable and thus recommends that baseball
batters and base runners be required to wear face guards ( 5). Much effort is being channeled into the research and
development of protective equipment, including a polycarbonate face guard (Home Safe-Face Guards Inc., Salem,
Virginia) (Fig. 14.8) and improved energy-absorbing capabilities of baseball headgear ( 99).
FIGURE 14.8. Commercially available polycarbonate face guard attached to a batting helmet to reduce head and face
injuries. (Courtesy of Home Safe Face Guards, Inc.)
LUMBAR SPINE
Although lumbar spine problems and lower-back pain are not unique to the sport of baseball, their influence on
performance is substantial. Trunk stabilization is a key element in both throwing and hitting a baseball. Pain and referred
pain alter the biomechanics of these activities and can lead to poor functional performance and further injury if they are
not alleviated. A recent survey of a collegiate baseball team over the course of three seasons revealed that lower-back
injuries account for approximately 15% of reported injuries. The majority of these injuries involved spondylolysis and
lower-back strains, and almost half of these injuries resulted in lost playing time for recovery and rehabilitation ( 95). At
the Little League level, lower-back pain is far less common and consists mainly of muscular strains as a direct result of
athletic participation and spondylolisthesis ( 7). Infielders and pitchers at all levels seem more prone to developing
lower-back problems. Surprisingly, at the Major League level, a very low incidence of lower-back problems exists in
catchers despite what intuitively appears to be a high-risk position ( 96).
The biomechanics of swinging a bat have been thoroughly analyzed, and proper technique emphasizes a transfer of
energy from the lower to upper extremities by way of the trunk musculature. The lower-extremity muscles appear to be
crucial to the generation of power in the swing and are most active in the preswing phase of hitting ( 96). In contrast, the
upper extremity appears to be more involved with the positioning of the swing. Trunk musculature, which includes but is
not limited to the erector spinae and abdominal oblique muscle groups, is most active in early swing phase and is
instrumental in rotation of the pelvis and power transfer in the swing. Alteration of these mechanics as a result of
lower-back pain results in uncoupling of the motions between the upper and lower extremities, resulting in poor timing
and lack of power in the swing.
The presence of pathology in the lumbar spine often results in compensation by the dominant throwing shoulder or
elbow, thus placing them at increased risk for injury. The trunk musculature is intimately involved in proper pitching
mechanics. EMG studies have supported the role of contralateral paralumbar and abdominal oblique musculature in
resisting what has been described as a “controlled falling” phenomenon of the pitcher toward his or her dominant side.
This activity is greatest during the cocking and acceleration phases of throwing and allows one to obtain maximum power
and efficiency ( 96,97 and 98). This aspect of trunk support, so crucial to proper pitching mechanics, places these players
at risk for nondominant paralumbar muscular and sacroiliac injury. It is often magnified in the presence of poor
mechanics.
The diagnosis and treatment of lower-back pain follows standard treatment algorithms centered on conservative and
preventative measures (97). Careful neurologic and imaging examinations to exclude more serious neurologic injury,
especially in the presence of trauma, are indicated. Proper mechanics in both pitching and hitting a baseball, with
emphasis on the trunk musculature in off-season conditioning programs and workout routines are essential to preventing
injuries to the lower back.
HITTING
The ability to hit a baseball hurled 60 feet 6 inches at speeds greater than 90 mph is a skill that requires coordination,
strength, quickness, and judgment. Most batting injuries result from being hit by a pitch. Soft tissue trauma and fractures
can occur at the site of impact. Such injuries to the head and face were described earlier. In addition, batting injuries can
occur during the swing itself as a result of either a full, uncontrolled swing (patellar dislocation) or direct impact with the
bat handle (hook of the hamate fracture).
Gross (101) described a series of five softball players who dislocated the patella of their trailing legs while taking a full,
uncontrolled swing. When the batter begins to swing, a valgus force is placed on the knee of the trailing leg, with the foot
fixed by cleats into the ground. As the quadriceps contracts with the trailing leg in flexion, the tibia rotates externally with
respect to the femur. Thus, the patella can be subluxed laterally out of the femoral sulcus with a resultant rupture of the
medial capsular structures ( 101). Radiologic evaluation of the patellofemoral joint is made with standard knee views (AP,
lateral) and with axial “sunrise” views of the knee in varying positions of flexion. The treatment of acute patellar
dislocation is relocation, immobilization (up to 3 weeks) to control pain, and intensive quadriceps rehabilitation and
subsequent conditioning. Braces and tape to prevent recurrences may be effective but have not been studied. In the
majority of cases, surgery can be avoided, but osteochondral fractures, which are unstable, should be ruled out.
Isolated fractures of the hook of the hamate can occur while batting. In a series of 62 patients with hook of the hamate
fractures described by Stark et al. ( 103), more than 80% of the fractures occurred while swinging a baseball bat, golf
club, or tennis racquet. When a baseball bat is gripped, the butt of the bat is located over the distal and ulnar aspect of
the hook. Thus, if the centrifugal force of the swinging butt can overcome the grasping power of a right-handed batter, the
end of the bat can fracture the hook of the left hamate. Patients with hook of the hamate fractures usually report a dull,
aching pain on the ulnar aspect of the wrist that worsens with passive or active extension. On physical examination, grip
strength is usually decreased and palpation over the hook results in increased pain. Radiographically, most of the
fractures can be diagnosed on a carpal tunnel view or a special oblique view of the supinated wrist. When the fracture is
not apparent on either of these types of roentgenograms, a bone scan or a CT scan ( Fig. 14.9) with the hands in the
praying position should be made. There are many reports of acute hook of the hamate fractures that fail to heal after
immobilization of the hand and wrist (103,104,105 and 106) or after open reduction and internal fixation ( 107). Because
of the ligamentous and muscular attachments to the hamate, Stark et al. ( 103) suggest that movement of the fingers and
thumb tends to cause motion at the hamate fracture site and, therefore, prevent union even when the wrist and hand are
immobilized. Thus hook resection is the treatment of choice and reliably eliminates symptoms, lessens the likelihood of
subsequent sequelae, and returns most players to their previous level of activity in 8 weeks ( 102,108,109).
FIGURE 14.9. Hook of the hamate fracture. CT images of left (left) and right (right) carpal bones. Fracture of the hook of
the hamate is seen in the right wrist.
SLIDING
Baseball sliding involves sprinting along a baseline and converting a vertical stance to a horizontal stance to arrive at a
base while avoiding a fielder's tag. The two primary sliding techniques are head first and feet first.
Corzatt et al. (111) kinematically analyzed the head-first and feet-first sliding techniques of professional baseball players
during game situations with high-speed cinematography. The act of sliding was divided into four distinct phases. In phase
1 of the feet-first slide (sprint phase), the base runner accelerates in the horizontal direction. Body lean is approximately
70 degrees from horizontal, and the runner keeps the center of gravity ahead of the striding foot. In phase 2 (sliding
position), the base runner leans back and the arms move behind the player in anticipation of the airborne and landing
phases. In phase 3 (airborne phase), the position of the feet-first slide is characterized by extension of the lead leg, with
the trail leg flexed beneath and a semierect trunk posture. In phase 4 (landing phase), the runner hits the ground. In
feet-first sliding, base contact is made with the extended leg, whereas body contact is made with the buttocks, lower
back, and posterior thighs. In head-first sliding, forward lean is increased to approximately 30 degrees from horizontal
and the body position is lowered to assume a crouching position. The airborne phase of the head-first slide is much less
distinct than in the feet-first slide and involves a prone position with arms forward and legs extended. Base contact is
made with the forward arms, whereas body contact is made with the chest and anterior thighs.
Sliding is responsible for a large proportion of injuries in baseball and softball. Investigators have estimated that 41% to
71% of all softball injuries occur while sliding ( 111,112). The mechanisms of sliding injuries include (a) shear force of the
infield surface (abrasions and contusions), (b) rapid deceleration against a stationary base (ankle and hand fractures,
ankle and hand ligamentous injuries, and knee ligamentous injuries), (c) collision injuries with a fielder (head injuries,
fractures, and sprains), and (d) rapid acceleration from a standing position (hamstring pulls). Wheeler ( 112) investigated
55 sliding injuries during competitive softball games and found the following injury frequencies: ankle injuries, 46%; ankle
fractures, 36%; knee injuries, 7%; and upper extremity injuries, 11%. Vertebral fractures can occur as a result of rapid
deceleration against a stationary base or collision with a fielder. Most sliding injuries occur during the landing phase
(phase 4) owing to the significant forces acting against the body during impact with the ground and the base. However,
injuries can occur during the other phases of sliding as well ( Table 14.6). Hamstring muscle strains during the sprint
phase of base running are common baseball injuries and are discussed in more detail later in this chapter. It is unclear
whether feet-first sliding or head-first sliding results in a greater relative incidence of injuries; however, head-first sliding
injuries tend to be more severe (1,111).
TABLE 14.6. SLIDING INJURIES
Preventive measures to reduce the incidence of sliding injuries in baseball include making sliding illegal, the use of
base-running helmets, instruction on proper sliding technique, improved musculoskeletal conditioning, and the use of
recessed bases or break-away bases. Some Little League associations have disallowed head-first sliding or sliding
altogether until the child has reached a certain age. However, this is impractical to the majority of participants and fans in
a sport as steeped in tradition as baseball. Furthermore, making sliding illegal may result in increased collisions and
thrown ball injuries. Instruction and practice of proper sliding technique can be beneficial in organized settings such as
Little League baseball ( 113). Aspects of proper sliding technique include keeping the lead foot (feet-first slide) or lead
hand (head-first slide) elevated, starting the slide at the correct distance, maximizing body surface contact area, and
avoiding last-minute hesitation ( 1,113). At home plate, ankle injuries during sliding are less frequent because the base
runner slides over, not into, the base ( 86). Hence, recessing second and third bases, as is done with home plate, could
reduce the number of sliding injuries; however, poor visualization of the bases by umpires is problematic. Janda et al. ( 2)
demonstrated significant prevention of softball sliding injuries through the use of break-away bases by prospectively
studying 633 games played on break-away base fields and 627 games played on stationary base fields ( Fig. 14.10). A
total of 45 sliding injuries occurred on the stationary base fields (1 injury for every 13.9 games), whereas two sliding
injuries occurred on the break-away base fields (1 injury for every 316.5 games). In a 1,035-game follow-up study on
breakaway base fields, only two sliding injuries occurred (1 injury for every 517.5 games) ( 114). Although break-away
bases cost roughly twice as much as stationary bases, Janda et al. estimated that mandatory use of break-away bases
by recreational softball leagues could save $2.0 billion per year in acute care medical costs. It also was believed that
break-away bases did not detract from the flow of the game or base visualization by umpires.
FIGURE 14.10. Break-away base. Anchored and detachable portions of a break-away base designed to reduce sliding
injuries. (Courtesy of DH Janda.)
CATCHING
Catching of the thrown baseball is an exacting task that requires excellent hand–eye coordination. The catcher is
considered to play the most physically demanding position in baseball because he or she is constantly getting up and
down from a squatting position, receiving pitches, making throws, chasing foul balls, and avoiding collisions with the ball,
bat, and base runner.
The mechanisms of catching injuries include chronic repetitive catching impact (digital ischemia); acute collisions with a
base runner, ball, or bat (head injuries, fractures, and sprains); and meniscal lesions in the older catcher from constant
squatting.
Catchers are predisposed to vascular injury in the gloved hand because of the sizable impact forces involved in catching
150 to 200 pitches per game, many of which exceed velocities of 90 mph ( 115). Sugawara et al. (117) demonstrated the
presence of digital ischemia using angiograms and thermography in eight baseball players who presented with coolness
and numbness in the index fingers of their catching hands. Physical examination of the involved hand demonstrated
paleness, cyanosis, and a positive digital Allen's test. Thermograms and angiograms revealed an occluded index digital
artery located at the distal interphalangeal joint more frequently than the proximal interphalangeal joint.
Lowry et al. (118) assessed 21 professional catchers and one collegiate catcher with Doppler flow studies and a modified
digital Allen test. These investigators found that only 41% of the catchers had normal left index finger circulation
(catching hand), whereas 95% of the catchers had normal right-hand circulation (noncatching hand). Furthermore, the
nine catchers with normal left-finger circulation reported the frequent use of a thick glove below their catcher's mitt. To
assess the incidence of digital ischemia among baseball players, Sugawara et al. ( 117) surveyed 578 junior high school,
high school, and college baseball players in Japan. The researchers found an increased frequency of digital ischemia
among those positions involving the most repetitive catching: catchers and first-base players. They also found an
increased incidence of digital ischemia in players with more accumulated experience.
Measures to reduce the incidence of catching injuries in baseball include hand padding, improved mitt design, protective
equipment, and instruction on proper catching technique. Enhanced mitt padding or the use of a thick glove under the
mitt may reduce the vascular changes in the catching hand that result from repetitive impact. Protective equipment is
essential to avoid collision injury from a ball, bat, or base runner. Proper equipment for the catcher includes a padded
mask, a helmet, a throat protector extending from the lower aspect of the mask to the clavicle, a chest protector, a
protective groin cup, and well-fitting shin guards that include patellar shielding ( 117). Instruction for the catcher
concerning proper tagging technique can reduce the number of base- runner collision injuries, and instruction concerning
proper catching stance can reduce the number of bat and ball impact injuries. Protection of the noncatching hand, by
placing it behind the back in one-handed catching or cupped behind the glove hand in two-handed catching, is also
essential to avoid injuries from foul tips and wild pitches ( Fig. 14.11).
FIGURE 14.11. Catcher in protective gear, which includes padded glove, padded mask, helmet, throat protector, chest
protector, groin cup, shin guards, and patellar shielding. Proper catching technique includes protection of the
noncatching hand.
FIELDING
Fielding of fly balls and ground balls requires coordination, judgment, and sudden running. It is essential to the success
of the team in the field.
The mechanisms of fielding injuries include (a) collision with players or the ballpark fence (head injuries, fractures, and
sprains), (b) ball trauma from uncaught balls (head injuries and fractures), and (c) explosive bursts of muscle activity
(muscle strains).
Strain of a muscle group from sudden activity after a period of inactivity is a common baseball injury. An acute strain is
the result of a single violent force applied to the muscle and can be classified into three degrees, depending on the
extent of injury (Table 14.7). Even a mild muscle strain can be distressing and debilitating to a competitive baseball
player. However, it is essential that the muscle–tendon unit be given protected time to heal so that complete recovery
and prevention of subsequent injury is ensured ( 119,120 and 121).
TABLE 14.7. GRADING OF HAMSTRING MUSCLE STRAINS
Preventive measures to reduce the incidence of fielding injuries in baseball include stretching exercises ( 121), good
communication between players to avoid player collisions, and warning tracks around the outfield fence to avoid wall
collisions.
SUMMARY
Baseball is a fun and challenging sport enjoyed by players of all ages. Although not a particularly dangerous sport,
baseball results in a substantial total number of injuries due to its large participation. A good history and thorough
physical examination, augmented by selected diagnostic tests, usually result in the appropriate diagnosis. Definitive,
early treatment of injuries with close follow-up and the allowance of time for healing results in good recovery and return to
activity. An understanding of the mechanisms of injury associated with throwing, hitting, sliding, catching, and fielding is
helpful in the prevention of injuries. Emphasis on good conditioning and proper technique will not only improve
performance but also prevent injury. Through better understanding of the mechanism, diagnosis, treatment, and
prevention of injury, it is possible to enhance the careers of players and make baseball an even safer sport.
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15 Basketball
15
BASKETBALL
DELMAS J. BOLIN
CRAIG BENNETT
Epidemiology of Basketball Injuries

Children, High School, Collegiate Men and Women, and Professional
Physically Challenged Athletes
Evaluation, Management, and Return to Play for Specific Injuries
Head and Neck
Hand, Wrist, and Upper Extremity
Chest
Spine
The Lower Extremity
Prevention and Conditioning
Conclusions
Chapter References
Basketball has evolved over the past 25 years from an inadvertent contact sport to today's highly physical game.
Dramatic rule changes, including the addition of the “slam dunk” and the three-point shot, have contributed to the sport's
dramatic rise in popularity. Basketball is now played throughout the world and is a featured Olympic sport. In the past 15
years, women's basketball has also grown in popularity. Women's division I and professional league games are now
regularly televised. Wheelchair basketball has emerged as a featured sport in the paralympics. At the youth and high
school levels, there is greater opportunity for participation by both boys and girls than ever before.
Rule changes have changed not only the game but also the player. Today's basketball players are taller, stronger, and
faster. With more agile athletes and physical play, the sports physician must be aware of the athlete's injury risk at each
level of competition, from youth leagues to professional. Coaches and teams increasingly look to athletic trainers and
team physicians not only for diagnosis and treatment but also for efficient rehabilitation and fast return to play. The sports
medicine team must possess knowledge of the utility and safety of ergogenic and prophylactic devices, as well as
sport-specific training regimens being touted as helpful in preventing injury.
EPIDEMIOLOGY OF BASKETBALL INJURIES
Children, High School, Collegiate Men and Women, and Professional
There have now been several epidemiologic reports of basketball injuries at various age and skill levels. A review of the
sports epidemiology literature reveals marked variations in injury definitions, exposure time, and data collection methods
that often lead to contradictory results.
Youth and high school basketball injuries have been studied extensively. Yde and Nielsen ( 1) studied adolescent injuries
in soccer, handball, and basketball. They found statistically similar injury rates for boys and girls. Finger injuries from ball
contact and ankle sprains were common. Prebble et al. ( 2) prospectively followed sports injuries over a 6-year period at a
rural emergency room. Basketball accounted for 17% of 6,013 sports injuries. The ankle was the site most frequently
injured (33%), followed by the finger (19%) and the face (16%). Ankle sprain was the most common injury. Two thirds of
injuries occurred in boys and men. The majority of these injuries were in patients aged 10 to 19, and 53% occurred in
conjunction with school-related activities. Nearly three quarters of the injuries were considered minor and expected to
resolve after 2 weeks.
Moretz and Grana (3) looked at injuries among boys and girls on a high school team over two consecutive seasons. The
injury rate for girls was 0.72 injuries per player, more than four times the rate for boys. The highest percentage of injuries
occurred during activity without the ball. The ankle was the most frequently injured site. No injury in the study required
surgery.
Prospective studies in Texas high school basketball programs have appeared. The results from the study of 100 Texas
high school basketball teams are similar to other studies. The most common injuries among girls and women were
sprains (55%), contusions (15%), and dental injuries (14%) ( 4). A second prospective study compared the injury patterns
of girls and boys teams ( 5) (Fig. 15.1).The injury rate was similar, and both girls and boys were eight times more likely to
be injured during a game than at practice ( 3,4). The ankle and knee were the first and second most commonly injured
body areas, respectively. Female basketball players had a significantly higher incidence of knee injuries and were nearly
four times more likely to injure the ACL and require surgery ( 3). With the exceptions of more serious ACL injuries and the
greater number of injuries occurring in female basketball players, the musculoskeletal injuries appear to be specific to
basketball, rather than specific to gender ( 6,7).
FIGURE 15.1. Injury distribution of male and female high school basketball players. (Adapted from Messina D, Farney W,
DeLee J. The incidence of injury in Texas high school basketball: a prospective study among male and female athetes.
Am J Sports Med 1999;27:294–299, with permission.)
At the collegiate level, trends are similar to the high school population, with injuries of the ankle and knee being the most
common sites of injury (8,9). The number and severity of knee injuries, including ACL rupture, is greater in female
athletes (10,11).
Zelisko et al. ( 12) compared injuries in men's and women's professional basketball over two consecutive seasons.
Women sustained 60% more injuries than men. The most common injury was to the ankle in both men and women,
representing about 20% of the total injuries in both groups. As seen at lower levels of competition, women experienced a
greater number and severity of knee injuries ( 12). A retrospective study of National Basketball Association (NBA) injuries
over 8 years found that injury rate and pattern were not significantly influenced by position. Fowards averaged 9.8
injuries per player; guards, 8.3 injuries per player; and centers, 7.8 injuries per player ( 13).
Physically Challenged Athletes
Wheelchair basketball places athletes at particular risk for injury ( 14). It requires intermittent bursts of high-intensity
propulsion and maneuvering, as well as overhead activity for shooting, passing, and rebounding. Activities of daily living
(ADLs) also place constant demands on the upper extremity. Not surprisingly, the wheelchair athlete is at particular risk
for upper extremity overuse syndromes (15). Weakness of external rotators and abductors have been implicated in
subacromial impingement (15). Compensatory thoracic kyphosis, with concomitant internal rotation of the shoulder and
scapular protraction, may further limit overhead shoulder motion ( 16). In one series of elite female wheelchair basketball
players, 52% reported shoulder pain; however, only 11% believed that it limited performance in the previous week ( 17).
In this series, pain was more correlated with ADLs, transfers in particular, rather than sports or leisure activity. In
addressing shoulder injuries, the sports medicine team should address biomechanical and strength issues in
rehabilitation. A longer course for recovery might be expected secondary to inability to appropriately rest the extremity.
Although shoulder injuries are most common, elbow, hand, and wrist complaints are frequently seen ( 18). Repetitive
high-intensity propulsion can place stress on the palmar surface of the wrist and hand, leading to compressive
neuropathy. In a survey study, 33 wheelchair basketball tournament participants were queried for symptoms of carpal
tunnel syndrome. Of the 33 athletes, 70% had histories consistent with exercise-exacerbated carpal tunnel syndrome that
was confirmed by electrodiagnostic studies ( 18). The history of overuse injuries should be sought and taken seriously
when evaluating and treating these athletes.
EVALUATION, MANAGEMENT, AND RETURN TO PLAY FOR SPECIFIC INJURIES
Head and Neck
A 1989 National Association of Athletic Trainers (NATA) survey of high school athletes found that the head and face
were involved in 10% of basketball injuries ( 19). Basketball is second only to baseball in the number and severity of
sports-related ocular ( 20) and oral traumas (21). Significant neurotrauma is rare and is discussed in Chapter 48. Facial
lacerations, ocular trauma, orbital and nasal fractures, and dental trauma are the most commonly seen facial injuries.
Facial Lacerations
Facial lacerations usually occur over bony prominences of the superior orbit and zygomatic arch. Lavage, topical
antibiotic ointment, and Steri-strips are usually sufficient to close most wounds. If suture is required, 5-0 or 6-0
monofilament should be used to close the skin with minimal tension and left in place no longer than 5 days ( 22).
Through-and-through lip lacerations should be closed from inside out after copious irrigation. Absorbable chromic suture
should be used to approximate the mucosal edges first, followed by closure of the muscle and subcutanous layers.
Monofilament is then used to close the skin edges. If contact with the teeth caused the laceration, risk of infection is high
and copious irrigation and oral antibiotics are recommended ( 22).
Eye
There are an estimated 100,000 sports-related ocular injuries each year ( 23). In some regions, basketball is the most
common cause of ocular trauma (24). Over 17 months, 5.4% of NBA injuries involved the eye ( 25). More than half the
injuries occur during rebounding or during offensive play. Most injuries were caused by fingers (36%) or elbows (29%).
The most common injuries were abrasions, lacerations, or contusions. Other common injuries are corneal abrasions and
orbital fractures.
Evaluation of eye injuries begins with inspection for pupil alignment, reactivity, and symmetry. The eyes should track
symmetrically. Palpation, direct and consenual light reflexes, and funduscopic examination should be performed. Training
room ophthalmoscopy offers a very limited view of the retina and optic disk. A red reflex suggests normal transparent
structures. Visual acuity and peripheral vision fields should be checked. Fluoroscein examination can reveal corneal
defects (22). A slit lamp permits a much more thorough evaluation of anterior structures but is usually not available in the
training room.
Corneal abrasions typically present with pain, photophobia, and a foreign body sensation. Diagnosis is made by
fluorescein staining. Small defects are self-limited and may be treated with topical medications ( 22). Patching does not
speed resolution (26), but nonsteroidal drops lessen symptom severity and may allow faster return to play ( 27).
Globe impact by flying elbows or fingers may cause a blow-out fracture of the thin medial wall or orbit floor ( 22). Orbital
contents may become entrapped in the fracture, leading to enopthalomos and diplopia. Blow-out fractures have been
reported after apparently innocuous injury ( 28). Other signs and symptoms include pain and, occasionally, subcutaneous
emphysema around the eye. Initial radiographs can be negative, and computed tomography (CT) may be required for
diagnosis. Management is controversial, and surgery is often required ( 22). The athlete should avoid the Valsalva
maneuver and blowing the nose; positive pressure may force air into the orbit, increasing the intraocular pressure and
promoting retinal ischemia ( 22).
Significant ocular injury, such as retinal detachment ( 22) and optic nerve avulsion ( 29), can have permanent sequelae
and may be easily missed on superficial examination. Opthalmologic consultation should be strongly considered in
players with persistent pain, diplopia, or decreased vision. Eye injuries may be prevented by light, well-fitting
polycarbonate lenses that protect the eye and dissipate impact forces ( 24).
Nasal Fractures
Head-to-head contact, such as occurs when rebounders flail their elbows, is a common cause of nasal fractures. On
examination, there may be marked deformity. Palpation reveals crepitance and mobility of fractured bones. Topical
phenylephrine should be applied to shrink the nasal mucosa for inspection. Bleeding can be controlled by compression. If
this fails, local application of pledgets soaked in epinephrine (1:1000) are often effective. Septal hematoma should be
ruled out. Septal abscess or pressure necrosis can destroy the cartilaginous septum and result in disfigurement ( 30).
Nasal fractures are usually managed by realignment under anesthesia. Return to play before complete healing is usually
possible if a well-fitting and well-secured nose protector is worn ( 22).
Dentoalveolar Trauma
A Scandinavian study found that dental injuries represented 6.7% of all basketball-related injuries over a 5-year period
and were usually the result of contact with another player. Half of injuries occurred during games. The most common
injuries were tooth fractures and avulsions ( 31).
Dental fractures involving only the enamel do not require urgent care unless the tooth has sharp edges or is sensitive to
changes in temperature. Fractures with exposed dentin are typically very sensitive. Temporary treatment with zinc oxide
and eugenol may permit the athlete to return to play ( 22).
Tooth avulsions from contact or net entanglement have been reported ( 32). The tooth can be rinsed with saline or tap
water but should not be scrubbed. Survival of the tooth depends largely on vital periodontal root surface fibers and time
to reimplantation (22). If transfer is necessary, the tooth can be stored in the mouth, milk, saline, or Sav-A-Tooth
containers. The tooth should be reinserted as quickly as possible, because tooth vitality decreases significantly after 30
minutes. Once reimplanted, the athlete should bite down on gauze to seat the tooth. Splint stabilization of the avulsed
tooth to adjacent teeth is usually required for several weeks ( 22). In all cases of dental trauma, the athlete should be
referred to a dentist as soon as possible.
Custom-molded plastic mouth guards may significantly decease the dental injuries from basketball. In a survey of 1,020
high school basketball players, only two minor injuries occurred in the 43 athletes wearing mouth protectors. In contrast,
32% of the 977 players not wearing mouth guards suffered oral injuries, representing nearly a 7-fold increase ( 33).
Custom-molded plastic mouth guards are better fitting, less bulky and more comfortable to wear. The players can easily
speak, breath, and drink, which increases compliance ( 34).
Hand, Wrist, and Upper Extremity
The majority of the injuries to the upper extremity in basketball involve the hand and wrist, and most are the result of falls
or secondary to impact with the ball ( Fig. 15.2). Shoulder and elbow injuries are less common and are usually associated
with falls or collisions ( 5). Most hand injuries occur at the proximal interphalangeal joint (PIP) and metacarpophalangeal
joint (MCP) (35).
FIGURE 15.2. A: The lateral radiograph of the nondominant wrist of a college basketball player who was undercut after
shooting a jump shot reveals a transscaphoid perilunar dislocation. Note the volar tilting of the lunate bone. B: AP
radiograph of the same wrist. Note the fracture through the waist of the scaphoid (S) with rotation of the proximal
fragment and the dissociation between the capitate (C) and the lunate (L).
Injury to the wrist is usually associated with falls on outstretched hands. A common scenario is a player being undercut
while in the act of shooting or rebounding. Both bony and ligamentous injuries can occur. Players who present with
radial-sided wrist pain at the anatomic snuffbox after a fall may have a scaphoid fracture. Scaphoid fractures are prone to
nonunion, which is a function of their vascularity ( 36). The blood supply of the scaphoid runs distal to proximal; more
proximal fractures take longer to heal and have greater risk of nonunion. Initial radiographs are normal in 5% to 15% of
scaphoid fractures. Technetium bone scan or CT scan performed 72 hours after the injury can confirm a fracture when a
rapid diagnosis is necessary ( 37). With a high index of suspicion and negative radiographs, the wrist should be
immobilized in a short-arm thumb spica cast. Angulated or displaced fractures require open reduction and internal
fixation (38).
Ligamentous injuries disrupt the complex articulation motion patterns of the wrist, and if they are left untreated, can lead
to early degenerative arthritis. Scapholunate dissociation is the most common ligamentous injury of the wrist and is best
seen on clenched-fist posteroanterior (PA) radiograph ( 37). The mechanism of injury is similar to scaphoid fracture.
Instability may be elicited through the Watson test. The examiner's thumb is placed on the proximal pole of the scaphoid,
with the wrist in ulnar deviation. As the wrist is radially deviated, if there is scapholunate instability, pain and occasionally
the click of dorsal scaphoid subluxation is felt ( 39). Regardless of the injury, initial management includes splinting, ice,
and antiedema measures. Definitive care should be sought at the earliest opportunity (see Chapter 55).
Hand and Fingers
PIP and MCP joint sprains represent 90% of all basketball hand injuries ( 1,37). When evaluating the hand and fingers,
active and passive range of motion and assessment of stability should be performed. Stability is maintained by four major
retaining ligaments. Collateral ligament sprains typically occur by angulatory stress. If radiographs are normal, most
injuries are treated with immobilization for 1 to 2 weeks and then buddy taping for variable periods. The athlete can return
to play, but there is risk of reinjury ( 37).
Ball impact can load the PIP joint axially, resulting in dorsal dislocation of the middle phalanx. Longitudinal traction and
exaggeration of the deformity usually achieve reduction. Reduction may be blocked if the joint capsule, volar plate,
collateral ligaments, or flexor tendons become interpositioned ( 40). The joint is usually immobilized in 15 degrees of
flexion for 3 weeks and then buddy taped for 3 additional weeks ( 37). Volar plate injuries can result in pseudoboutonnière
deformities (41).
Tendon Injuries
Injuries to the tendons and their attachments must be recognized promptly to prevent long-term sequelae. Mallet fingers,
the avulsion of the extensor tendon off of the distal phalanx, commonly occurs when the basketball impacts and forcefully
flexes the actively extended distal interphalangeal (DIP) joint. On examination, there is a flexion deformity at the DIP, and
the athlete is unable to actively extend the joint. The DIP should be examined for stability and a true lateral radiograph
obtained to rule out fracture. The DIP is usually splinted in full extension with a plastic Stack splint, allowing full motion at
the PIP joint (42).
Boutonnière deformity results from rupture of the extensor tendon's central slip at the insertion into the base of the middle
phalanx. The acute injury may be missed, and delayed treatment is associated with deformity. Examination reveals the
inability to extend the PIP joint fully. In cases in which pain limits motion, a diagnostic digital block may clarify the
diagnosis. Treatment involves splinting the PIP joint in full extension allowing unrestricted motion at the MCP and DIP
joints. The splint can usually be padded, allowing the player to return to play early ( 42).
Phalangeal Fractures
The treatment of phalangeal fractures depends on their location. Distal fractures can be managed with splinting that
includes the DIP joint. Nondisplaced fractures of the proximal phalanx can be treated with buddy taping and return to play
when the patient tolerates (37). Follow-up radiographs should be obtained to ensure adequate reduction is maintained.
Middle phalangeal fractures are often unstable secondary to volar and dorsal forces from tendonous insertions, which
tend to displace and rotate the fracture segments. If the fracture can be reduced but remains unstable, alignment can be
maintained by percutaneous pinning ( 43).
Chest
Injuries to the chest wall are few and are usually contusions resulting from elbow impact. Contusions of the breast in
female basketball players can produce significant pain for a short time. Treatment is usually short-term use of ice and
nonsteroidal antiinflammatory agents (NSAIDs) and compression with a sports brassiere. Traumatic manubriosternal joint
subluxations associated with basketball have been reported in the chiropractic literature and are fortunately rare ( 44).
Radiographs may be helpful in cases of severe injury in which rib fracture or pneumothorax is suspected.
Spine
During the 1996–1997 season, low-back injuries accounted for 7.1% of all orthopedic problems ( 45). Soft tissue injuries
such as contusions, and lumbar muscle strains or sprains were the most common types. Serious injury such as herniated
disc, spondylolysis, and spinal stenosis are rare ( 46).
Repetitive jumping and extension maneuvers, such as with “posting up,” load the neural arch and can lead to stress injury
of the pars interarticularis (spondylolysis). Young, immature athletes are at particular risk. Evaluation reveals low-back
pain exacerbated by twisting and hyperextension. There is no radicular signs. Standard radiographs, including obliques,
may demonstrate a fracture (46). With a high index of suspicion and negative radiographs, a single photon emission
computed tomography (SPECT) scan may confirm the diagnosis. If a true stress fracture is identified, athletes are placed
in a lumbosacral orthosis for 3 months (47). This orthosis limits hyperextension and allows healing. After bracing,
rehabilitation for lumbar stabilization and hamstring flexibility is undertaken ( 46).
The Lower Extremity
Overuse Injuries
Basketball's repetitive jumping, pivoting, and combination of rapid acceleration and deceleration predisposes its players
to overuse injuries. The most common overuse injuries seen in basketball players are patellar tendonitis (jumper's knee),
Achilles tendonitis, posterior tibial tendonitis (medial shin splints), and peroneal tendonitis. Many of these injuries occur
early in the season secondary to poor conditioning. A key to effective treatment of these problems is primary prevention
with sport-specific training, which is discussed later.
Jumper's knee refers to tendonitis of the knee extensor mechanism. It is often associated with patella alta or a history of
Osgood-Schlatter or Sinding-Larsen-Johansson disease. High eccentric loads are placed across the knee on landing
from the jump (Fig. 15.3). On examination, there is tenderness at the distal pole of the patella at the origin of the patellar
tendon or at its insertion in the tibial tubercle. Hamstrings tightness and weak hip flexors are associated signs. Treatment
involves proper training to strengthen the hip flexors and eccentrically condition the quadriceps and hamstring flexibility.
Relative rest and modalities, including ice, ultrasound, and iontophoresis or phonophoresis, are helpful. If there is
patellar pain secondary to patellar subluxation, patellar taping can relieve symptoms and aid healing ( 48) (Fig. 15.4).
Pool therapy minimizes the effect of gravity and can be helpful in eccentric quadriceps training ( 49).
FIGURE 15.3. A: Normal radiograph of knee with patellar tendinitis. B: Patella alta and calcifications following patellar
tendon tear. C: MRI of patellar tendon tear demonstrating midsubstance tear and patella alta and large knee effusion.
FIGURE 15.4. X-ray study of acute patella dislocation in a college basketball player before reduction.
The Achilles tendon experiences tensile loads eight times the body weight with running and much higher loads with
activities such as basketball ( 50). The Achilles tendon is prone to mucoid degeneration at the watershed area 4 cm
proximal to the calcaneal insertion ( 51). Overuse is associated with anatomic malalignment, cavus feet, and tight
gastrocnemius, soleus, and hamstrings. Relative rest, ice, stretching, NSAIDs, and orthotics are the mainstays of
treatment (52). Rupture can occur and is usually associated with a pop, extreme pain, a palpable defect, and a positive
Thompson test (Fig. 15.5). Longitudinal tears have been reported in basketball players, and MRI can be helpful if there is
diagnostic uncertainty ( 53). Players can be managed conservatively with a non–weight-bearing short-leg cast with the
ankle plantarflexed for 8 weeks, followed by aggressive rehabilitation. Elite athletes often undergo surgery for true
ruptures. Neither treatment speeds return to play, which can take 9 to 12 months, but conservative treatment is
associated with a slightly higher rate of rerupture ( 52).
FIGURE 15.5. Achilles' tendon tear in a 30-year-old former college basketball player. Note obvious swelling in ankle and
defect in Achilles' tendon.
Shin splints is the lay term describing irritation of fascial insertion of the soleus and posterior tibialis fascia on the
posteromedial tibia. Palpation of the medial tibia reproduces pain. Radiographs are usually negative, and bone scans
may be necessary to rule out a stress fracture ( Fig. 15.6). Rest followed by gradual return to activity is the mainstay of
treatment. Stretching, local modalities, supervised rehabilitation, and custom orthotics may be helpful in returning the
athlete to play. In chronic cases, surgery may be necessary for symptom resolution ( 54).
FIGURE 15.6. Right tibial stress fracture in a college basketball player.
Anterior Cruciate Ligament Injuries
Basketball movements place the anterior cruciate ligament (ACL) under constant stress with high-intensity running,
cutting, pivoting, jumping, and deceleration ( 55). The are multiple mechanisms of injury. Noncontact injuries are
discussed later. In men, ACL tears are more likely to result from mechanisms involving contact ( 56). Blows to the lateral
aspect of the knee result in valgus and rotational stress, placing the ACL under tension. On landing, as during
rebounding, hyperextension, eccentric contraction of the quadriceps, and varus stress can place the ligament under
excessive tension (55).
Treatment of ACL tears can be surgical or conservative. For athletes who want to participate in running, jumping, and
cutting sports, such as basketball, surgical reconstruction is usually required. Patellar tendon (bone-tendon-bone) grafts
are most commonly used, and graft selection does not influence outcome ( 57). Partial tears can be treated with bracing
and functional rehabilitation. A supervised rehabilitation program is part of both conservative management and recovery
after surgery. Strong quadriceps and hamstrings, as well as proprioceptive retraining, are essential to promote dynamic
stabilization of the knee joint. The patient can return to play usually 6 months after surgery ( 58).
Women and Anterior Cruciate Ligament Injuries
It is well established that women suffer ACL tears more commonly than do men (11,56,59). In a study of NCAA women
basketball players, women were four times more likely than men to have an ACL tear ( 56). In contrast to men, the
mechanism of injury in women in more than 50% of cases was one of noncontact. The combination of deceleration and
change of direction, either internal or external rotation, was the common noncontact mechanism of injury ( Fig. 15.7).
FIGURE 15.7. ACL tear in a female college basketball player.
The explanation for the difference in injury rate among men and women is likely multifactorial. Multiple hypotheses have
been advanced, including training deficiencies (hamstring and quadriceps ratio, proprioception) ( 60), skill level,
shoe–surface interface, estrogen effects on ligamentous laxity, and femoral notch width ( 56).
Hamstring:quadriceps strength ratios are less in women than in men, which may allow increased forward translation of
the tibia and greater stress on the ACL during deceleration ( 61). Skill level has been implicated as causative. A 3-year
survey of elite Norwegian women soccer players attributed a nearly 50% drop in injuries per week to increased skill level
(62). In contrast, ACL injury rates in the NCAA among women remained constant over a 5-year period ( 56). The
menstrual cycle has been reported to influence ACL injuries. Wojtys et al. ( 63) found a higher incidence of ACL injuries
during days 10 to 14 (follicular phase) than during days 15 to 28 (luteal phase). The contribution of intercondylar notch
width remains controversial. A prospective study of 902 high school athletes showed that athletes with noncontact ACL
tears had a smaller notch width index (NWI) and that women on average had smaller NWI than men ( 64). A smaller study
of division I athletes in multiple sports failed to demonstrate gender differences in ACL injuries or NWI ( 65). Further study
is needed to describe clearly the increased risk of ACL injury in female athletes.
Ankle and Foot
Most basketball-specific studies list the ankle as the most common site of injury, and the sprain as the most common
injury type (2,3,5). Inversion mechanisms damage the lateral ankle supporting ligaments, the anterior talofibular,
calcanofibular, and posterior talofibular ligament. Diagnosis is straightforward, and the prognosis for return to play
depends on the grade of the sprain. Ankle stability is assessed by the anterior drawer and talar-tilt tests. Treatment
involving antiedema measures, ice, NSAIDs, and rehabilitation should be instituted as soon as possible. Peroneal,
posterior tibialis, and anterior tibialis muscle strengthening exercises, as well as proprioception retraining, are an
essential but often neglected means of reducing the risk of reinjury ( 66).
Stress fractures of the metatarsals are seen frequently in basketball players ( Fig. 15.8). Biomechanical risk factors
include flatfoot and prolonged pronation during gait ( 67). Fractures of the middle metatarsals constitute 90% of
metatarsal stress fractures. Treatment is activity modification and 4 weeks in a hard-soled shoe or removable boot. The
sole should be stiff, to prevent motion (extension) of the metatarsals during the toe-off phase of gait. After cast removal,
rehabilitation involves gentle stretching and graded return to activity ( 68).
FIGURE 15.8. AP radiograph demonstrating a complete fracture of the second metatarsal neck at the site of a previous
stress fracture. Note the buildup of callus around the fracture site.
Basilar fifth metatarsal stress fractures can present problems. Fracture of the proximal third are common in sports with
significant running and jumping ( 69). Successful conservative treatment with strict non–weight-bearing casting for 6 to 8
weeks has been reported (70,71), but there is a high incidence of nonunion ( 72). Surgical management with
intramedullary screw fixation has been successful if conservative treatment fails ( 73). Primary surgical management
appears to hasten return to sports ( 74).
Tarsal navicular stress fractures can be challenging. Patients often present with the insidious onset of forefoot pain, and
their condition is treated conservatively as a forefoot sprain. Diagnosis is often delayed an average of 4 months because
of vague symptoms. A high index of suspicion is required; plain radiographs are usually normal. Bone or CT scanning
may be necessary to make the diagnosis. Treatment with non–weight-bearing casting for 6 weeks followed by
rehabilitation is the treatment of choice ( 75,76). Complications include nonunion and chronic pain, which can be
debilitating ( 76).
PREVENTION AND CONDITIONING
From the earlier discussion, it is clear that inadequate warmup and individual muscle group weaknesses contribute to
many basketball-specific injuries. Prevention of these injuries and, indeed, rehabilitation after them must address the
deficits and implement basketball-specific training. Appropriate strength and endurance achieved during the off-season
may lead to fewer injuries and perhaps faster return to play after injury.
Before play, the athlete should be adequately warmed up. The benefits of a set stretching regimen include injury
prevention and increased muscle contractility ( 77). Effective regimens include both active warmup to raise muscle
temperature and static stretching to relax the muscles and allow more forceful contraction ( 78). Pregame or prepractice
stretching can be monotonous; the program should be tailored to be basketball specific, resulting in adequate warmup of
the muscle groups that will be used in competition. Such programs have been published ( 78). Regardless of which
program is chosen, it should start at a moderate pace, gradually increase in tempo, and provide a thorough stretch.
Good conditioning is the foundation of injury prevention. Specific training regimens for men's and women's basketball
have been published that are tailored for the different goals of off-season and in-season preparation ( 79,80). Off-season
training should be focused on building strength. Basketball specific goals should be set to improve weak areas, increase
overall strength, and develop explosive strength of the legs ( 79). Ideally, strength programs should be similar to strength
movements required in the sport. For example, basketball-specific squats place the feet closer together, matching their
position for the jump shot. Squats can be performed alternating the speed, depth, and weight to increase power, speed,
and the explosive takeoff necessary to improve the vertical leap ( 81).
In the preseason period, the focus shifts to building endurance by training the metabolism. Often, this involves
substantial amounts of running. In game play, however, high-intensity work lasts 35 to 45 seconds until the ball changes
possession or a foul is called. Sprint conditioning can be tailored to match game requirements, including the integration
of shuffling, backpedaling, and forward sprinting to preset positions on the court ( 82).
When the season begins, goals shift to maintaining skill performance and fitness. Traditional conditioning programs
during in-season practices can be altered to combine fitness with skill work, such as with shooting drills ( 83). Weight
room time is usually minimized in favor of practice time ( 79). If an appropriate strength base has been achieved during
the off-season, plyometric training can be added to traditional fitness programs. Plyometric training involves maximal
contractions in response to rapid stretching ( 80). Programs usually begin after 2 months of strength training and progress
from general to more focused and specific exercises. At the end of one 14-week program, athletes added an average of
2.1 cm to the vertical leap and lowered their 20 m and 40 m sprints by 0.047 and 0.115 sec respectively ( 80). Although
plyometrics may be of use in improving performance during the season, no data yet support its role in injury prevention.
CONCLUSIONS
Although most basketball injuries are minor, most basketball players are in exceptional physical condition. Many of the
injuries can be prevented with appropriate training leading up to and during the basketball season. Good technical
coaching and vigilance by officials can prevent further injuries. Substitution of tired athletes will further prevent those
injuries that more easily occur as a result of fatigue.
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16 Bicycling
16
BICYCLING
MATTHEW J. MORELLI
DAVID A. STONE
Road Rash
Lacerations
Contusion
Fractures
Concussion
Eye Injuries
Sun Burn
Overuse
Mechanical Failures and Hazards
Bicycle Size and Fit
Conditioning
Conclusions
Chapter References
The sport of cycling has grown in popularity over the past decade. Today's interest in cycling is not limited to competitive
racing alone ( Fig. 16.1). Cycling has become a popular form of exercise and recreation. With this increase in cycling
comes an increase in injuries. Injuries to the cyclist normally fall into one of the following categories: acute, chronic,
overuse, or traumatic. Some of the cyclist's injuries can fall into more than one of the above-mentioned categories.
However, some cyclists' injuries can be attributed to mechanical problems, or they may be related to improper fit, size, or
adjustments to the bicycle itself. A majority of cycling injuries can be avoided with proper training, bicycle maintenance,
proper size, fit, and adjustments.
FIGURE 16.1. Photo of Thrift Drug Classic, Pittsburgh, PA.
ROAD RASH
This injury is an abrasion caused by a crash or fall from the bicycle ( Fig. 16.2). The skin is abraded and can become a
deep wound. There are three degrees of abrasion-type injuries: first-degree injuries are superficial, second-degree
injuries leave some or partial thickness damage to the skin, and third degree is full-thickness damage to abraded areas.
The first-degree abrasion needs to be cleaned out with all debris (i.e., gravel, sand, or dirt) removed from the skin and
tissue. This may require one to use hydrogen peroxide and gauze to scrub the area clean. If packed in the tissue a scrub
brush may be required. Once clean, the wound should be cared for by using a petroleum-based medicated ointment and
can be covered with a non-stick sterile dressing. Second-degree abrasions and wounds normally respond to the same
care as first-degree wounds. However, if an alternative is needed then the use of silver sulfadiazine cream could be
administered (1). Third-degree wounds require more attention, and if they do not respond to the above-mentioned
treatments, then skin grafting may be a last resort.
FIGURE 16.2. Example of road rash on a cyclist's thigh.

LACERATIONS
Lacerations also occur from falling off or crashing bicycles. A laceration is an open wound with jagged edges. This may
result from falling into another bike or equipment from a bicycle striking the rider as he falls. The cyclist may also receive
a laceration when striking the ground. Common sites for lacerations include the hands, arms, legs, head, and face.
Lacerations need to be cleaned, and then the physician needs to determine if suturing is needed. Some lacerations can
be avoided by wearing protective equipment such as gloves, a helmet, and possibly sunglasses or eyewear. It is
important to remember that all open wounds should be kept clean and the bandages changed regularly. Wounds should
be observed for signs of infection, and the patient's tetanus injection status should be reviewed.
CONTUSION
A contusion is usually the result of collisions or falls. A contusion is the compression of soft tissue. This injury can result
in hemorrhage and may be marked by ecchymosis. Depending on whether the contusion is deep or superficial, the
athlete may return immediately or within a few days. Rest, ice, compression, and elevation, along with stretching and
range-of-motion (ROM) exercises, are often all that is needed to manage these injuries. Some contusions can be
prevented with the use of helmets, gloves, and other protective equipment.
FRACTURES
Fractures of the upper extremity are common in cyclists; however, the possibility of a lower-extremity fracture must
always be considered. The upper extremities are at greater risk because they are used to break falls and avoid collisions.
The most common sites are the hand, wrists, clavicle, and olecranon. The hand is the first anatomic part in contact with
the ground if the rider tries to break the fall. This places the metacarpals at risk from impact. Also, the hand may be run
over by another cyclist or may get entangled in the bicycle of the fallen rider or another rider passing by. The wrist is also
at risk for the same reasons as the hand. It would not be uncommon for a fallen cyclist to sustain a fracture of the
navicular, lunate, or distal radius. These injuries need to be evaluated, diagnosed, and treated properly to avoid such
complications as Kienböch's or Presier's disease. Fractures of the hand and wrist need to be immobilized initially to
facilitate healing. However, they can be treated with a soft molded cast to allow for training or competitive riding. Usually,
this is accomplished with a silicone cast. The cast must allow the rider to manipulate both the handlebars and the brakes.
To help prevent such fractures, the cyclist should try to avoid using the hands to break falls.
The olecranon is another common fracture site. A fracture to the olecranon process can occur when the bicycle suddenly
slides out from underneath the cyclist, causing the athlete to strike his elbow on the road surface. Most commonly, this is
due to loose debris on the course, bad weather conditions such as rain, or a first ride on an unfamiliar course. These
fractures require x-ray evaluation and proper immobilization to facilitate healing. Displaced fractures require surgery.
Even if a fracture does not occur from such an event, olecranon bursitis may result. Olecranon bursitis should not keep
the cyclist out of action.
A fracture of the clavicle is a more common injury in the fallen cyclist. As the rider falls or wrecks, he or she may use the
arm to break the fall. After the hand strikes the ground, the force is transferred through the hand, wrist, forearm, humerus,
and finally, to the weak and vulnerable clavicle. Clavicle fractures may be simple or compound. Most can be treated with
a figure-of-eight brace or strap.
A cyclist may also sustain a shoulder dislocation in a wreck or fall. In this situation, a direct blow to the shoulder or the
arm being forced into a position of external rotation or abduction causes the humeral head to displace or dislocate. Signs
and symptoms include a flattened deltoid with decreased ROM, in particular, internal or external rotation. The athlete
frequently holds or cradles the affected arm in a position of comfort. A fall directly on the elbow or a direct blow to the
shoulder may result in a shoulder separation or acromioclavicular (AC) sprain. These injuries usually present with pain
and deformity over the AC joint and can be difficult to treat in cyclists.
CONCUSSION
Concussions occur when the cyclist strikes his head during a fall. They are common in both road cycling and mountain
biking. Head injuries can be avoided or decreased in numbers and severity by wearing a helmet ( 2,3). In the Unite
States, since 1986, all competitive cycling events require the use of a helmet ( 4). As a result, race-related head injuries
have declined (4,5 and 6). A study by Thomas et al. showed that cyclists who did not wear a helmet were at greater risk
of suffering a head injury and were at sevenfold greater risk of losing consciousness than a cyclist who wears a helmet
(5,7,8).
Concussions have been categorized into three classes: first-degree concussion—mild, second-degree
concussion–moderate, and third-degree concussion—severe. The state of unconsciousness increases with severity. In a
first-degree, there is no loss of consciousness and the athlete may feel stunned or dazed. With a second-degree
concussion, there is loss of consciousness of up to 5 minutes. In a third-degree concussion, there is loss of
consciousness for up to and greater than 5 minutes. Memory may also be affected. The cyclist may also suffer from
dizziness and tinnitus, which also increases in severity. There may even be an unsteadiness that is varied or mild in a
Grade II and marked to severe in Grade III.
No athlete with a suspected concussion should be allowed to return to activity until cleared by a physician and no signs
or symptoms are present. Return to cycling should be slowly progressive because physical exertion often triggers any
postconcussive symptoms. When the athlete is free of complications, full training and competition may be continued.
EYE INJURIES
The cyclist can sustain numerous eye injuries. An orbital hematoma (black eye) can occur from a collision or fall when
something strikes the area surrounding the eye. These injuries can be treated with a cold pack or ice. If any distorted
vision or bleeding is present, a physician may determine further evaluations and treatments. Floating bodies such as dirt,
gravel, sand, and insects may get in the eye. The eye should be flushed with saline solution or cold water to remove the
object. Never use fingers to remove the object. Some debris can be rubbed or moved in the eye, causing a corneal
abrasion. Signs and symptoms are severe pain, watering eyes, and an eyelid in spasm. The eye should be covered with
a patch and the cyclist sent to a physician for further evaluations and treatments. A corneal abrasion can be confirmed
with a fluorescein strip. Referral to an ophthalmologist may be needed.
A direct blow to the athlete's eye can result in a retinal detachment. The detachment may be painless. Signs and
symptoms include seeing specs or dots, a sensation of flashing lights, blurred or fuzzy vision, or a curtain falling down on
field of view. This injury requires immediate ophthalmologic evaluation. A direct blow to the eye may also cause a
hyphema, a collection of blood in the anterior chamber, another injury that can be serious and result in permanent
damage if it is not taken care of promptly. A globe or orbital fracture can also occur with a direct blow. If such an injury is
suspected, refer the athlete to an ophthamologistist as soon as possible.
Some eye injuries can be avoided with proper care and protective eyewear such as sunglasses.
SUN BURN
Cyclists are in the outdoors, and their legs, arms, neck, and face are extremely susceptible to the sun and burning. A
cyclist should wear clothing that covers the neck and arms, if weather permits, or use sunscreen to avoid sunburn. The
sun can also contribute to dehydration, especially when clear skies, high temperatures, and high humidity cause cyclists
to sweat profusely as they train or compete. Proper hydration starts several days before and continues after events.
During an event, an athlete should try to drink about 8 ounces of water or fluid every 20 minutes during and past 1 hour
of exercise to maintain hydration and to keep sustained maximum effort. One should never wait until the sensation of
thirst to drink; at this point, too much fluid has been lost through sweat and exercise.
Dehydration and sun can cause heat-related illness such as cramps, heat exhaustion, and heat stroke. Cramps can be
the result of dehydration and rapid loss of fluid without replacing the fluids. Heat exhaustion is also caused by excessive
fluid loss. With heat exhaustion, there is gradual weakness, excessive sweating, and possible nausea. Pale gray, clammy
skin is noted. The athlete needs to be removed from sun and competition, and fluids must be replaced. Heat stroke
results from a failure to dissipate heat. These athletes may present with headaches, weakness, or syncope. Symptoms
include rapid pulse, a high temperature, and hot, red, dry skin. On the course, these athletes should be placed in the
shade and immediately cooled. During transport to the hospital, the athlete should be immersed in cold water and ice
should be applied. Intravenous fluids should be started as quickly as possible.
Heat-related complications can be avoided with proper hydration, lightweight clothing, and acclimations to the
environment or conditions.
OVERUSE
Saddle sores and chaffing normally occur on the buttocks or inner thigh of cyclists. They may be caused by a lay off in
riding time or the beginning of the season at which time the skin is not acclimated to these conditions. Proper wound care
is essential to healing and fast return to cycling. The use of properly padded cycling shorts and ointments or powder to
decrease the amount of friction is the key to prevention. If the sores should open, antibiotic creams or gels maybe
needed to prevent infection. Folliculitis, an infection or irritation of hair follicles, is common in cycling. An area with hair
that is short or shaved that is rubbed repeatedly by clothing is associated with this condition. Cyclists who shave their
legs increase the risk of folliculitis in the thigh and buttock regions, and added protection is often needed in these areas.
The combination of decreasing friction and the use of powder or lubrication creams or ointments is advised to prevent
these conditions (1,9).
Cyclists can experience several neuropathies related to hand placement on the handlebars. The ulnar nerve is at risk
due to the pressure and force applied through handlebars and brakes. This condition usually results in numbness and
tingling and decreases strength in the fourth and fifth fingers of the hands ( 1,9,10). This problem should alleviate with
rest but can last from days to weeks. The cyclist and the bicycle should be carefully examined if signs or symptoms
persist. The frame size, stem length, seat heights, and saddle adjustments all need to be checked and adjusted
accordingly (see section in this chapter on bicycle size and fit ). The median nerve may be compressed under the same
circumstances as the ulnar nerve, resulting in the production of symptoms in the thumb, index, and middle fingers instead
of the ring and fifth fingers. This is caused by constriction or narrowing of the carpal tunnel space or direct pressure on
the median nerve. Bicycle fit must be addressed with emphasis on improper hand placement. Not gripping the
handlebars as tightly or relaxing the hands when the ride permits can decrease the incidence and severity of these
injuries. Stretching and forearm and wrist strengthening can also help. However, if the signs and symptoms persist, then
the athlete should be evaluated.
With the growing popularity of clipless (cleat step-in) pedals ( Fig. 16.3), the incidence of foot neuropathy has decreased.
However, this injury can be caused by other factors other than tight toe straps. The cyclist may be wearing the wrong size
shoe or one in which the toe box is not wide enough to allow the forefoot to spread as pressure is exerted on the pedal.
Improperly aligned cleats may also contribute, leading to poor positioning of the foot through the pedal stroke ( Fig. 16.4).
Treatment often consists of correcting the mechanical aspects and decreasing riding and riding time until the neuropathy
alleviates.
FIGURE 16.3. Clipless pedal for a road bicycle.
FIGURE 16.4. Example of how a shoe mounts to clipless pedal. Note that the ball of the foot is over the axle of the pedal.
Metatarsalgia, which is caused by abnormal pressure being exerted on the bottom of the foot, can also occur from the
same factors as peripheral neuropathies. Metatarsalgia is characterized by pain beneath the metatarsal heads
exacerbated by palpation in particular at the second and third metatarsal heads. Both peripheral nerve and metatarsalgia
injuries are associated with improper seat height, resulting in excessive or extreme pressures on the foot.
Improper fit of the bicycle's frame size, seat height, and saddle may cause penile or pudenal nerve symptoms. This injury
is characterized by the cyclist experiencing numbness or tingling in the scrotum or penile shaft areas. These symptoms
may be intermittent at first and become more permanent if the lack of treatment increases. Mechanically, the seat height
needs to be checked to be sure that it is correct. The saddle should be examined to be sure that it is either horizontal
(level) or even slightly tilted upward to help ease these symptoms and eliminate the injury. An entirely new saddle or
saddle style may be needed to correct this problem ( Fig. 16.5). Riding and riding time may need to be decreased or
discontinued completely until the signs and symptoms resolve. If this injury is not taken care of immediately or correctly,
permanent damage may result. There has been concern that this neuropathy could lead to impotence and other penile
and urinary dysfunctions ( 1,9,10).
FIGURE 16.5. Photo of cycling saddle. Note the cut-out portion at the posterior aspect of this particular saddle. This
helps reduce the pressure in the pudenal area of the cyclist.
Some lightly trained and competitive cyclists may experience a rare vascular injury called external iliac artery
endofibrosis (EIAE). Pain or cramps in the buttocks, thighs, or calves characterize EIAE. The cyclists may also
experience the sensation of the swollen leg with maximal effort or strenuous cycling. EIAE is a progressive stenotic
intimal thickening of the external iliac artery. Cyclists who are experiencing these signs and symptoms need to be seen
and evaluated by a physician as soon as possible. Three methods may be needed to confirm this diagnosis: ( 1)
ultrasound and continuous-wave Doppler of the lower limb, ( 2) systolic humeral and posterior tibial arterial pressures
measured with an oscillometer method, and (3) arteriography with femoral Seldinger technique ( 11,12). Treatment for
professional cyclists normally requires surgery because this is their career or job. Nonprofessionals can switch to other
sports or activities in the hope that the lesions will decrease or stabilize. If they do not improve, surgery remains an
option (11,12).
Cyclists are prone to overuse injuries owing to training errors, musculoskeletal imbalances, or poorly fit bicycles. Iliotibial
band syndrome is caused by overtraining, a tight iliotibial band, or incorrect seat height. It is often accompanied by
trochanteric bursitis and is characterized by pain and point tenderness over the greater trochanter. In some cases,
crepitus or clicking may be audible. Iliotibial band syndrome can also produce symptoms at the knee joint or its insertion
site on the tibia. Signs and symptoms include pain with motion at the lateral femoral epicondyle or Gerdy's tubercle.
Management consists of iliotibial band stretching, ice massage, nonsteroidal antiinflammatory drugs, and in some cases,
a corticosteroid injection, especially for a bursitis that is not responding to conservative treatment. Even in cyclists,
orthotics may be of benefit.
Patella femoral pain, chondromalacia, and infrapatella tendinitis are all seen in cyclists. Patella femoral pain is commonly
referred to as bikers knee, and is associated with several factors: patella malalignment, increased Q angle, a saddle that
is too low or forward, or poor cleat adjustment or alignment ( 1,9,10). These factors all cause poor biomechanics and
result in pain. Treatment includes correcting the mechanical factors related to the bicycle and then proper strengthening
of the vastus medialis to ensure proper tracking of the patella. McConnell taping may also help decrease the signs and
symptoms. Icing and stretching may reduce symptoms. Patellar tendinitis presents with pain at the proximal or distal pole
of the patella that increases with the extension of the knee, especially against resistance. Examination also produces
tenderness over the tendon and its insertion. The mechanical factors usually associated with patella tendinitis are
incorrect seat height and improper saddle fitting. The cyclist should decrease the intensity of rides and the resistance
that they are pedaling against by using lower gears and higher cadence until symptoms permit return to increased
training.
Achilles tendinitis and plantar fasciitis are overuse injuries that can be caused by training errors or riding with the seat
height too low. Plantar fasciitis may also be caused by old or worn out biking shoes. The shank or rigid sole of the biking
shoe becomes more pliable causing excessive flex in the shoe and results in poor biomechanics. Achilles tendinitis is
marked by pain in the Achilles tendon and occasionally the insertion. It is increased with plantar flexion, toeing off, or
standing on toes and pedaling. Plantar fasciitis usually presents with pain at the plantar fascia insertion of the medial
calcaneus. Treatment and management for both Achilles tendinitis and plantar fascitis is similar, consisting of therapeutic
exercise for the foot and ankle, ice massage, and nonsteroidal antiinflammatory drugs. Both may benefit later from use of
orthotics, night splints, and rarely, injections. The cyclist can aid recovery by decreasing riding time and intensity. Riding
at a higher cadence with low resistance may also help ( 1,9,10).
Handlebar height and reach can cause a cyclist to experience trapezius and levator scapula pain or spasm. The pressure
placed on the arms and shoulders normally causes these problems. If the handlebars are too far and too low, the cyclist
has to over reach to grab the bar and thus places increased stress on these muscles. Ensuring that the handlebar is
placed at the correct height and the stem is the proper length to ensure proper reach ( 1,9) can rectify this problem.
MECHANICAL FAILURES AND HAZARDS
According to a report entitled, Bicycle Use and Hazard Patterns in the United States by the U.S. Consumer Product
Safety Commission, released in June, 1994, the most frequently reported problems involved bicycle chains breaking or
falling off, brakes failing, and various components such as handlebar and brake components coming loose ( 13). Bicycle
maintenance is vital for safety; without it, parts failure and injuries are inevitable.
Spoke injuries (Fig. 16.6), which can potentially be fatal, can also be avoided with maintenance. The two most common
mechanisms of spoke injuries include spokes coming off or free of the rim or something causing the forceful dislodging of
a spoke. Maintaining the proper tension in the spokes will prevent rim damage, which causes wobbling or shaking of the
entire wheel and tire. Unfortunately, it is difficult to avoid completely having objects on the road caught in the wheel and
spokes. It is best to be aware of your surroundings and steer free of loose debris ( 1,9,14).
FIGURE 16.6. Photo of broken spoke. (Damaged spoke at the 6 o'clock position on the rim.)
Brakes and components can wear down, and if these parts are not taken care of, malfunction can lead to failure and
serious potential injury. With aggressive off-road use, or big descent, the pads may misalign. The cables that actuate the
brakes and derailleurs can stretch out, causing too much slack. Poorly maintained cables also result in brake
dysfunction. Frayed cables can break if they are not replaced, causing the rider to loose brakes or shifting ability.
The bicycle chain can cause a variety of hazards. The chain needs to be lubricated regularly to ensure smooth pedaling
and shifting. A dry or rusted chain can derail and lodge between the rings. Chains must maintain tension in order to
operate correctly. If the chain is loose or too stretched from wear, it can pop off or get lodged in the chain rings. Checking
the chain for the above-mentioned conditions can prevent failure or breakage. Injury can also be avoided by ensuring
that loose items do not get caught in the chain. Toe straps and shoelaces that are not secured properly or removed from
harm's way can get caught in the chain, resulting in serious injury.
BICYCLE SIZE AND FIT
The frame size is the single most important aspect of the bicycle, and proper size is vital to safety, performance, and
risk-free biking. The frame needs to be tall enough and long enough. LeMond states it the best, “The key is to find a bike
that is as small as possible vertically, while being long enough horizontally that it doesn't bunch you up” ( 15). The rider
should have 1 to 2 inches of clearance between the crotch and the top tube of the bicycle frame ( Fig. 16.7). A mountain
biker should have 2 or 3 inches of clearance to allow for more maneuverability and changing terrain. After choosing the
proper frame size, the saddle has several dimensions that need to be attended to. Saddle height is important and
possibly the number one error resulting in overuse injuries. The knee should be slightly bent, not hyperextended or flexed
forward. Burke states that “proper seat height is determined by putting the pedals at 6 and 12 o'clock positions with the
ball of the foot on the pedals; there should be about twenty-five to thirty degrees flexion of the extended leg”( 16).
FIGURE 16.7. Rider demonstrating the way to determine proper top tube clearance. Note the 1 ½ to 2 inches of the
clearance between the tire and the floor.
The saddle needs to be adjusted fore and aft. Neutral positions can be obtained by putting the crank arm at 3 and 9
o'clock. A plumb line or long straight edge should start at the front of the patella and drop perpendicular to the ground.
Some cyclist or off-road riders may be 1 to 2 cm behind the end crank arm ( 1,15).
The saddle may now be adjusted for tilt. The saddle should be level or slightly upward for men and level or slightly
downward for women. Once again, use of a yardstick to check adjustments is helpful. Stem length directly affects reach.
Burke suggests that a plum line dropped from the tip of the rider's nose should bisect the middle of the stem ( 16).
LeMond also suggests that with cranks at the 7 and 10 o'clock positions, there should only be 1 or 2 inches between
knees and elbows, with the elbows bent at 65- to 70-degree angles ( 15). Burke states “you could do this by the reach
method,” in which the top of the elbow is placed at tip of saddle and with fingers extended should touch handlebars ( 16).
Handlebar height is adjusted in relation to the saddle height. Saddle height should be corrected first. For shorter riders,
the bars should be 1 to 2 inches below the top of saddle. Taller riders may wish to lower the bars as much as 3 to 4
inches to allow for longer torso or arms. Mountain bikers should generally follow the 1- to 2-inch standards. You can use
a plumb line straight edge from top of the saddle and then measure down to the handlebars. LeMond adds that handlebar
width should be as wide as the cyclist's shoulders. However, a smaller width results in more agile steering ( 15).
Crank arm length should be evaluated based on the guidelines provided by Burke ( 16):
160mm for a height of 5 feet and under

165mm for a height between 5 feet and 5 feet, 5 inches
170mm for a height between 5 feet, 5 inches and 6 feet
175mm for a height between 6 feet and 6 feet, 4 inches
180mm for a height greater than 6 feet, 4 inches
The last measurement to check is foot position. The cyclist's foot should strike the pedal axle with the ball of the foot.
There should be no toe in or toe out positioning of the foot ( Fig. 16.8). The cleats should be adjusted to allow neutral
contact and alignment. Some pedals today are designed with “float,” which means some slack in the tension mechanism
allows cleats to be more forgiving to bad rider mechanics. Cleats can also be posted with spacers to help correct
biomechanics for a rider with a pronated or supinated foot.
FIGURE 16.8. Proper cleat alignment and foot position. Balls of feet over axle of pedal with no toe in or toe out.
Finally, cycling shoes need to be checked regularly. Like running shoes, they can break down. Be sure that the shoe
maintains its rigid sole without any abnormal flex. The cyclist needs to replace shoes that wear or begin to flex. Comfort
can be added to any cycling shoe by trying insoles that provide some cushioning.
CONDITIONING
Conditioning for cycling has been addressed by Rhyan ( 17), who described a program calling for a series of microcycles
focusing first on muscle hypertrophy, then muscle strength, and finally, endurance. The emphasis of the lifting program
should be on muscular development and balance between both sides of the body, with attempts to simulate the sport as
much as possible. Aerobic capacity should be developed by overdistance training. If the usual race time is 60 minutes,
then overdistance training involves 75- to 120-minute rides using a so-called slower-than-race pace. Interval training is
also recommended, using 2- to 5-minute intervals with short work-to-rest ratios of 1:0.25,1:0.5, and 1:1.
CONCLUSIONS
Bicycling can be fun and a rewarding sport or form of exercise. The correct size, fit, and equipment are important ( Fig.
16.9 and Fig. 16.10). Maintaining the bicycle, roads, courses, and trails we ride plays an important role in preventing
injuries. Intrinsic risk factors such as conditioning, proper nutrition, and hydration can improve enjoyment and
performance and potentially avoid injuries.
FIGURE 16.9. Proper bicycle fit. Rider in the neutral or upward position.
FIGURE 16.10. Proper bicycle fit. Rider in the sprint position.
CHAPTER REFERENCES
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3. Buccin RV, Wasserman RC. Helmet protection from head injuries among recreational bicyclists. Am J Sports Med 1990;18:96–100.
4. Patterson MQ, Thompson DC. Cycle helmets and the prevention of injuries. Recommendations for competitive sport. Sports Med
1998;25:213–219.
5. Thomas S, Acton C, Nixon J, et al. Effectiveness of bicycle helmets in preventing head injury in children: Case-control study. Br Med J
1994;308:173–176.
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12. Abraham P, Chevalier J-M, Saumet JL. Echography of external iliac artery endofibrosis in cyclists. Am J Sports Med 1993;21:861–863.
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17 Boxing
17
BOXING
LYNDON B. GROSS
History
Amateur Versus Professional
Preparticipation Evaluation
Vital Signs
Head, Eyes, Ears, Nose, and Throat
Face/Mouth
Pulmonary
Cardiovascular
Abdomen
Skin
Musculoskeletal
Neurologic
Laboratory Evaluation
Boxing Injuries
Hand/Wrist
Shoulder
Cervical Fracture
Ocular Injuries in Boxing
Mechanism of Injury
Types of Ocular Injuries
Rare Injuries
Forces in Boxing
Acute Brain Injury
Death
Subdural Hematoma
Subacute Subdural Hematoma
Chronic Subdural Hematoma
Acute Epidural Hematoma
Intracerebral Hemorrhage
Diffuse Axonal Injury
Cerebral Edema and Ischemia
Concussion
Chronic Traumatic Boxer's Encephalopathy
Neuropathology of Chronic Traumatic Boxer's Encephalopathy
Epidemiology of Chronic Traumatic Boxer's Encephalopathy
Risk Factors for Chronic Traumatic Boxer's Encephalopathy
Potential Preventive Measures in Chronic Traumatic Boxer's Encephalopathy
Pros and Cons of Boxing
Chapter References
Bibliography
HISTORY
A historical overview of the ancient origin of boxing has been published by Unterharnscheidt and others ( 1,2 and 3).
Boxing was introduced into the 23rd Olympic games in 688 B.C. Boxers were divided into two classes, either older or
younger than 18 years of age without consideration of weight or experience. Apparently no ring was used, there was no
time limit, no rest period, blows could be landed anywhere, kicking was allowed, and there was no grace period if a boxer
was knocked down. Matches continued until one fighter could no longer continue or until he acknowledged defeat. The
origin of boxing in ancient Greek and Rome can be divided into three periods. The so-called period of soft thongs
extended from Homeric times to the end of the 5th century B.C. Soft thongs were long pieces of leather believed to be
made of tanned ox hide that were wrapped around the forearm and hand in order to protect the knuckles and hand ( Fig.
17.1). Boxing became more brutal with the identification of the second period called the period of sharp thongs, lasting
from the 4th century bc until the 2nd century A.D. during the Roman Empire. Sharp thongs consisted of leather gloves
extending over the forearm and hand, with a hard leather ring encircling the knuckle ( Fig. 17.2). Although the purpose of
a soft thong was to protect the boxer's hand, the purpose of a sharp thong was to inflict more punishment. Boxing
reached its low point during the third phase entitled the period of the Roman caestus. A caestus was a type of hard thong
that had iron or lead spikes present at the knuckle region ( Fig. 17.3). The caestus obviously was intended to inflict great,
if not fatal, punishment on the opponent.
FIGURE 17.1. Soft thong. These were thought to be made of tanned ox hide and were wrapped around the knuckles and
hand for protection.
FIGURE 17.2. Sharp thong. Hard leather covered the knuckles. Sharp thongs were meant to inflict more damage on the
opponent.
FIGURE 17.3. Roman caestus. This device was intended to inflict brutal, if not fatal, punishment to the opponent.
Boxing was apparently banned around 400 A.D. for unclear reasons. It made a brief come back at the time of the Italian
Renaissance only to again fall into obscurity until it was revived in Great Britain in the 18th century. It became popular
shortly thereafter in the United States. The modern era of boxing was actually ushered in with the Queensbury rules in
1867. These rules included the use of padded boxing gloves, 3-minute rounds with 1-minute rest periods, banning of
wrestling, prevention from hitting an opponent who had been knocked down and mandating that a boxer must rise
unaided within 10 seconds following a knockdown. Other than decreasing the length of a boxing contest in recent years
the nonmedical aspects of the sport have not changed significantly in the last 100 years. On the other hand, significant
progress has been made in both medical understanding and medical input into boxing in recent years. This chapter
outlines the current state of boxing viewed from a medical standpoint.
AMATEUR VERSUS PROFESSIONAL
Amateur and professional boxing have many similarities but also many significant differences ( Table 17.1).
Administratively, the amateur sport is much more organized with centralized authority under one national governing body
termed USA Boxing, Inc. (4). This organization has a strong central authority with uniform rules and regulations to govern
all aspects of amateur boxing nationally. Theoretically, every aspect of the amateur sport should be the same in all
states. The detailed amateur organizational structure and working guidelines were developed with boxing safety as a top
priority. Professional boxing on the other hand has no centralized authority, and therefore, rules and regulations vary
from state to state. In addition, professional boxing is governed by world sanctioning organizations such as the World
Boxing Association (WBA), World Boxing Council (WBC), and the International Boxing Federation (IBF), which have their
own rules that often conflict with state regulations. Recently, the Association of Boxing Commissions, which includes all
state boxing commissions, has implemented changes that unify the rules that govern championship professional boxing
matches. Although this is a far cry from the demands for a national boxing authority to monitor professional boxing, it is a
step in the right direction. Amateur boxers carry “medical passports,” which provide information on their prior bouts and
any injuries sustained. Professional boxers have no such document, leaving state officials sometimes without adequate
documentation of a boxer's true status. To provide closer medical supervision in the professional ranks, certain states
have implemented strict regulations to achieve more accurate documentation of a boxer's status. New York, a leader in
this issue, mandates annual examinations and an ancillary test before issuance of professional fighting permits. In
addition, medical examiners in this state have the authority to suspend boxers based on the number of knockouts or
consecutive losses. The New York Boxing Commission has also empowered the ring side physician to terminate fights at
any time, giving him or her absolute authority over the referee. Regulations such as these should be made universal to
standardize professional boxing.
TABLE 17.1. AMATEUR VERSUS PROFESSIONAL BOXING DIFFERENCES
The optimal result in a professional contest is to render the opponent neurologically incapable of continuing the match.
The scoring system is heavily weighted toward encouraging hard head blows with a resultant knockdown or knockout. As
a result of this scoring system, it is exceedingly rare for a boxer to be judged the winner of a round if he has been
knocked down. In contrast, amateur boxing does not seek to reward a boxer for scoring a knockdown blow. In the
amateur ranks, all blows are weighted equally in the scoring system so that landing a knockdown blow does not enhance
a boxer's score card any more than landing a light body blow. The end result is that the amateur competitor tends to
emphasize defense and boxing skills over the pursuit of a knockout.
Amateur contests are of considerably shorter duration than are professional contests. Professional contests contain
anywhere from 4 to 12 three-minute rounds, with a veteran professional always scheduled to box at least 10 rounds. In
contrast, amateur bouts are limited to three rounds of 2- or 3-minutes' duration. On very rare occasions, an amateur may
box five rounds of 2-minutes' duration. The total number of hard head blows landed is presumably less in the shorter
amateur contest. Amateur boxers must always wear a headgear, whereas professionals do not. The purpose of the
amateur headgear is to reduce the impact force on the head, and to reduce the chance of facial cuts and ear injuries.
Headgear does appear to decrease the incidence of cuts, but a significant reduction in head impact force probably does
not occur. The use of a headgear gives the amateur boxer a false sense of security in terms of blunting the effects of
hard head blows. Amateur officials are much quicker to terminate a contest in which one boxer is out classed or hurt than
are professional officials. Any head blow that stuns an amateur in the slightest is grounds for a standing eight count.
Three standing eight counts in one round, or a total of four over the course of the three-round match, automatically
terminates the contest in amateur boxing. For professional championship boxing matches, in which the rules have been
unified, only the referee may stop the bout. In addition, only a knockdown warrants a mandatory eight count and there is
no three-knockdown rule in effect. This generally allows the professional boxer to “weather the storm,” thereby absorbing
much more punishment. Any facial laceration is generally grounds to terminate an amateur contest, whereas generally
only if the laceration is affecting the boxer's vision will it be used as a reason to stop a contest in the professional ranks.
Amateur boxing emphasizes uniform restriction periods for any boxer who has had his match terminated because of hard
head blows. Amateur boxing does not recognize the terms TKO (technical knock out) and KO (knockout) but prefers the
euphemisms RSCH and RSCM. Any amateur sustaining an RSCH (referee stops contest due to head blows) is given a
30-day mandatory suspension from any further boxing competition or gym sparring. An RSCM (referee stops contest for
medical reasons) with unconsciousness lasting less than 2 minutes results in a 90-day suspension, whereas an RSCM
with unconsciousness lasting more than 2 minutes results in a 180-day suspension. If an RSCH or RSCM occurs a
second time within 90 days from the end of the suspension period for the first RSCH/RSCM the mandatory suspension
times are even longer. An RSCH occurring within 90 days after the first RSCH results in an additional 90-day
suspension; an RSCH after an RSCM is also an additional 90 days. An RSCM following an RSCH is given a 180-day
suspension, whereas an RSCM following an RSCM results in a 365-day suspension. These suspensions are noted in the
amateur boxers' medical passports, making it difficult for the suspension to be ignored. Similar initial suspensions are
codified by many but not all state boxing commissions for the professional sport. Because of the absence of national
guidelines and communication channels at the professional level, a boxer's suspension in one state may not be known or
upheld by another state. This allows a boxer to jump from state to state to avoid medical disqualification. A national
database for the professional pugilist is needed to ensure reciprocity among the state boxing commissions. All amateur
boxers, and professional boxers in most states, are required to provide medical clearance at the end of their suspension
periods before resuming boxing. For amateurs, notification of medical clearance is forwarded to the national office.
Dissemination of notification of medical clearance is not as structured at the professional level. How well this process
really works at the local level for either amateur or professional boxing is unknown. Many state boxing commissions do
not have a codified upper age limit for competition, whereas amateur boxers have a demarcation point at age 32. After
this age, an amateur can only compete at the local level in masters competition against similarly aged individuals.
Tournament competition past the local level does not exist for masters. This rule effectively serves to discourage amateur
boxing after this age. Finally, no individual is allowed to compete at the amateur level after having sustained any type of
retinal tear or detachment, even if it has been adequately repaired. Further competition at the professional level following
successful retinal repair is considered acceptable in many situations.
The amateur boxing establishment feels very strongly that the documented neurologic sequelae of professional boxing
not be extrapolated to include amateur boxing (5,6 and 7). There is, however, no randomized study of amateur boxers
comparable to Roberts' study on professional boxers ( 8,9). The general consensus is that amateur boxing does not
involve the same degree of neurologic risk as is present in professional boxing. However, work by Kaste ( 10) and Casson
(11), in particular does cast doubt on the safety of amateur boxing. Similarly, McLatchie ( 12) studied 20 amateur boxers
and noted an abnormal clinical neurologic examination in seven, abnormal EEG in eight, and abnormal
neuropsychological testing in nine. No controls were included in this study. In a study of military boxing, Enzenauer noted
that 68% of all injuries were due to head blows and reported one death and one case of unilateral blindness ( 13). Most
studies that have specifically addressed the neurologic risk in amateur boxing do report much less neurologic
abnormalities than in professional boxers. Thomassen compared the neurologic, electroencephalographic, and
neuropsychological examinations of 53 amateur boxers and 53 soccer players ( 14). He found no significant differences
between the two groups, concluding that modern amateur boxing did not lead to serious or permanent brain damage.
However, the median age of the boxers in this study was only 36 years. Brooks reported the results of
neuropsychological testing in 29 active amateur boxers and also found no evidence of cognitive impairment compared
with a matched control group (15). A similar report by Porter demonstrated no evidence of neuropsychological impairment
in 20 competitive amateur boxers and a matched control group ( 16). Heilbronner also reported normal
neuropsychological testing following active competition in 23 amateur boxers ( 17). Jordan reported finding no
abnormalities on magnetic resonance imaging (MRI) scans of a small group of active amateur boxers examined after a
knockout (18). In a very comprehensive look at amateur boxing, Haglund studied a group of Swedish amateur boxers and
compared them to controls participating in other sports ( 19,20,21,22 and 23). No differences were noted on neurologic
examination, computed tomography (CT), or MRI scanning. There was a difference between the groups in
electroencephalography (EEG) and neuropsychological testing, which might indicate slight brain dysfunction in some
amateur boxers (22). Haglund concluded that no evidence of chronic brain damage could be elicited in modern-day
Swedish amateur boxers.
An objective assessment of amateur boxing leads one to conclude that it probably does not involve the same degree of
neurologic risk as seen in the professional sport. This is an understandable conclusion because the competitions are
much shorter and the likelihood of terminating a contest owing to head blows is much greater in the amateurs. The
usefulness of other amateur initiatives such as the wearing of a headgear and existence of medical passports awaits
further proof. Longer follow-up is required before the true risk of current-day amateur boxing can be definitively stated. At
present, it seems prudent to accept that some degree of risk for development of chronic traumatic encephalopathy or of
acute brain injury does exist for amateur boxing but not to the same degree as is seen in professional boxing.
PREPARTICIPATION EVALUATION
Many physicians who provide preparticipation clearance for boxers, either amateur or professional, are unaware of the
peculiarities particular to the boxing evaluation. Recent literature from the Walson Army Community Hospital has
incorporated United States of America Amateur Boxing Federation (USAABF) guidelines and current sports medicine
literature to formulate preparticipation evaluation guidelines for the health care professional involved in performing
examinations (24). Recommendations made in the remainder of this section are based on these guidelines. Although
differences exist between the evaluation of amateur and professional boxers, these differences are subtle and are
mentioned when clarification is necessary.
The prefight examination is generally performed on the day of the competition. The history and physical examination
should be performed in a private, quiet, well-lit room, with a desk or table on which the boxer and physician may sit. The
participant should be attired in shorts. On occasion, the promoter or state boxing commissions expect the physician to
conduct the examination in a crowded, noisy environment, with boxers queued up waiting to be examined. This type of
arrangement should be resisted by the physician. The history and physical examination are performed to screen for
individuals who are at risk for injury and to prevent them from participation. As with nearly all physical examinations, the
history is perhaps the most crucial element. The past medical history is designed to assess the major aspects of an
individual health history. There are many conditions that are congenital or acquired, that are acute or chronic, and that
warrant disqualification, and these conditions are shown in Table 17.2. As evidenced by this list, previous surgery, as
well as chronic medical conditions, may be contraindications to participation. A detailed family history may alert the
physician to inherited conditions that may predispose the participant to injury. The information gained from this history
may help direct the physical examination and laboratory assessment. The remainder of the history is directed toward
detecting specific disqualifying conditions through the review of systems. The boxer is asked about any prior history of
knockout or concussive episodes in or out of the ring. Any complaints referable to the neurologic, ocular, or
musculoskeletal systems should be specifically brought out. The boxer's general demeanor should be scrutinized. Any
slurring of words or abnormal movement should be addressed. Any abnormalities that are found require further
investigation before clearance.
TABLE 17.2. BOXING DISQUALIFYING CONDITIONS
Vital Signs
Monitoring of vital signs represents the only portion of the physical examination that can be performed by a trained
nonphysician. Visual acuity, height, weight, and blood pressure should be obtained on each individual. The participant's
blood pressure should be appropriate for his age. For children younger than 10 years of age, blood pressure of 130/75
mm Hg is the upper limit of normal (25). For youngsters between 10 and 15 years old, 140/80 mm Hg is the upper limit,
and for adults 150/100 mm Hg is the upper limit of normal (25). Minor degrees of hypertension do not preclude
competition, but blood pressure greater than or equal to 150/100 mm Hg in any age group requires disqualification until
further evaluation. The physician should be aware of the artificially elevated pressure readings that can be seen in
heavier boxers with large arms. A thigh cuff can be used to accommodate for the increase in arm girth. Pressures as high
as 160/95 mm Hg are accepted in these individuals. Essential hypertension that is well controlled is not a
contraindication to competition. If the boxer's blood pressure is elevated on the initial examination, he should be given an
appropriate amount of time to rest and relax in an attempt to lower the pressure. If he is consistently hypertensive, the
contest should not take place and referral for hypertensive evaluation is advised.
Head, Eyes, Ears, Nose, and Throat
Any bruising or swelling about the head or face should be noted. Lacerations that are not well healed are grounds for
failing the examination. Participants in competitive boxing are required to have adequate vision. Visual acuity of less than
20/60 without glasses or contacts is an absolute criteria for disqualification ( 26). Current medical literature, the USSABF,
and various state boxing commissions recommend that all boxers have a complete ophthalmologic examination before
starting boxing careers and annually after this because certain pathologic conditions may exist and go undetected
(26,27,28,29 and 30). A complete ophthalmologic examination is not required for preparticipation clearance. Certain
conditions, such as congenital glaucoma, history of retinal detachment, absence of an eye, or significant decreased
acuity in one eye (greater than 20/200), are strong indications for disqualification. Scleral hematomas are common and
not necessarily grounds for failure. Anisocoria should be noted, if present, and acquired anisocoria requires investigation
before permitting participation. Congenital anisocoria is not a contraindication to boxing. The preparticipation status of
the ears must be documented. The tympanic membrane should be examined to ensure that they are intact. A tender or
swollen nasal septum may indicate a fracture or impending fracture and requires further investigation before clearance.
Face/Mouth
The physician should examine the mouth for any loose teeth and tender areas. Broken or loose teeth and severe cavities
require referral to a dentist. Although the problem is not a criterion for disqualification, in the primary care setting, these
individuals should be have proper dental care before release for competition. Previous dental work and prosthesis should
be noted before participation. As mentioned earlier, any lacerations or open skin lesions that are not healed are grounds
for disqualification.
Pulmonary
Pulmonary symptoms are rare in active boxers. The chest should be examined for any deformity, pulsation, or retraction.
Documentation of any abnormalities should be noted, but rarely are they a reason to disapprove a match. Controlled
asthma is not a contraindication to competition, but both amateur and professional governing bodies have policies
regarding the medications used in the treatment of asthma ( 26).
Cardiovascular
Although cardiovascular symptoms are rare in active boxers, the physician needs to perform a careful and thorough
examination. The purpose of this examination is to identify those individuals with conditions that are a relative or absolute
contraindication to boxing participation. The physician must combine a thorough history and physical examination to rule
out conditions that predispose an individual to sudden cardiac death. The frequency of sudden death in athletes is
extremely low, and no more common that in any other population (31). The causes of sudden cardiac death in athletes is
generally age related. In athletes younger than 30 years of age, congential anomalies of the major coronary arteries
account for 35% of sudden death, hypertrophic cardiomyopathy contributes to 22% of those deaths, and a multitude of
other conditions account for the remainder. In the athlete older than 30 years of age, coronary atherosclerosis accounts
for 97% of cases of sudden death (31,32).
The past medical history should focus on previous workups and diagnosis. Absolute contraindications to boxing include
the following: history of cardiac surgery, third-degree heart block, hemodynamically significant valvular heart disease,
coarctation of the aorta, persistent patent ductus arteriosus, and significant coronary artery disease ( 26,33). It should be
noted that this list is not all inclusive, and individual cases should be discussed with a cardiologist. Relative
contraindications include mitral valve prolapse and significant arrhythmias. Mitral valve prolapse requires individual
consideration. Athletes with mitral valve prolapse and a history of exertional syncope, exertional chest pain, or sudden
cardiac death in a primary relative should be prohibited from boxing pending a comprehensive cardiac evaluation.
Paroxysmal supraventricular tachyarrhythmias, including Wolf-Parkinson-White syndrome should not prevent an athlete
from participation, but cases should be discussed with a cardiologist.
The review of systems should allow the physician to detect those athletes who are at risk for sudden cardiac death. The
following areas should be examined, including a history of syncope or presyncope, fatigue, dizziness, dyspnea,
palpations, or history of sudden death in a primary relative. Positive answers to any of these questions should raise the
physician's suspicion for possible underlying heart disease.
The physical examination should be performed in a quiet setting so subtle abnormalities may be discovered.
Documentation of any murmurs should be noted, and any diastolic murmur or systolic murmur greater than 3/6 warrants
further evaluation before participation. An irregular pulse indicates an underlying problem, which is reason to cancel a
match pending further investigation.
Abdomen
The abdomen should be examined for organomegaly and areas of tenderness. Specific disqualifying conditions include a
single testicle, a single kidney, or the presence of a large or symptomatic inguinal or incisional hernia. An enlarged
spleen, as might be seen in mononucleosis, is rarely found but is a contraindication to participation in contact sports. The
examination should also include inspection of previous traumatic and surgical scars. Jaundice should be noted and
further workup performed before participation. The standard inguinal hernia examination is not necessary in this setting.
Skin
The physician must examine the entire integument. Boils, impetigo, herpes, and pediculosis are contraindications to
boxing. Pustular acne is a relative contraindication to contact.
Musculoskeletal
The physician should note symmetry, general strength, flexibility, and range of motion. Particular emphasis should be
placed on the cervical spine. A neck profile (assessment of cervical strength and range of motion) should be completed
before participation. Evidence of joint laxity, instability, or radicular symptoms with range-of-motion testing warrants
further investigation. The hands, elbows, and shoulders should be examined for any swelling, tenderness, or instability.
The physician must pay close attention to the hands because they are the most common area for boxing injuries. Any
deformity, swelling, or tenderness of the hands, specifically at the knuckles or wrist, should be looked for. Metacarpal
fracture, extensor tenosynovitis, or capsular synovitis are capable of limiting a boxer's performance and may be grounds
for disapproval in some cases. Tenderness of the rib cage may indicate a fracture, which could result in pneumothorax
with further injury.
Neurologic
All boxers should have a complete neurologic examination incorporating a past medical history, review of central nervous
system symptoms, and a comprehensive neurologic examination. The history may often alert the physician to occult
neurologic compromise and vulnerability before subtle physical signs are apparent. Initial questions should explore any
history of seizures, neurosurgery, concussions, headaches, changing behavior, awkwardness, disequilibrium, irritability,
confusion, memory lapses, personality changes, diplopia, or other visual changes. A positive answer in any of these
areas, even in the face of a normal neurologic examination, requires further evaluation before training or competition can
commence.
At present, there are no data to suggest that pharmacologically well-controlled seizure disorders require restriction from
contact sports; however, most physicians would caution these individuals from participating in boxing owing to the
potential for neurologic injury ( 34,35). There is a consensus that posttraumatic seizure disorders are an absolute
contraindication to any further competition in contact sports ( 33,36). In addition, most physicians would agree that a past
history of third-degree concussion or multiple second-degree concussions, previous neurosurgery, and subdural or
epidural hematoma should preclude an individual from boxing ( 33,34 and 35).
The neurologic examination should consist of a mental status check, cranial nerves testing, cerebellar testing, and reflex
examination. This examination takes only a few minutes but should pick up any obvious focal signs. Any focal signs or
subtle abnormalities detected require restriction from contact until further evaluation can be completed. A neurologic
examination may or may not identify early signs of chronic traumatic boxer's encephalopathy (CTBE).
Laboratory Evaluation
In addition to the history and physical examination, laboratory tests may be indicated. Most practitioners would agree that
routine laboratory tests in an asymptomatic population are not warranted ( 26,33). Any diagnostic studies should be
ordered only as indicated. For professional boxing, several state commissions have mandated human immunodeficiency
virus (HIV) testing for the purpose of excluding boxers, presumably so that the fighter can continue to fight when
bleeding. Although the risk of HIV transmission has been judged to be low in all sports, the rational for this policy is
questionable from a medical and public health standpoint. The guidelines for amateur boxing require no HIV testing but
adhere to the guidelines with respect to bleeding injuries during competition. These guidelines are to stop the competition
when an athlete is bleeding and for that athlete to receive care as soon as practical. The injured individual may not
resume participation until all bleeding is halted and wounds dressed.
BOXING INJURIES
No current sport presents more controversy with regard to the safety or dangers incurred than the sport of boxing. Public
opinion has caused a debate as to the safety of this sport, placing this issue in prominent focus. The condemnation of
boxing by various medical associations impedes any attempts to improve the safety standards in this sport and also
perpetuates the profession's ignorance with regard to the safety or dangers of the sport ( 37,38 and 39). The goal of the
field of sports medicine is to minimize the incidence of injuries without unacceptably altering the nature of the sport. It is
hoped that the sports medicine model will identify training techniques, conditioning patterns, and potential types of
injuries and effect changes in these areas to shape a safer sport. For this reason, studies need to be instituted to assess
the risk, incidence, and pattern of injuries in boxing.
Only a few large population-based studies assessing boxing injuries have been conducted ( 6,40,41 and 42). The majority
of these studies have focused on documenting the safety of amateur boxing as compared with professional boxing
(6,40,42). This comes from the belief that amateur boxing is safer than professional boxing owing to the safety measures
employed. Most of these studies have focused on injuries primarily during competition and have ignored training and
sparring injuries. The injuries most commonly seen are predominately to the head, face (including the eye, ear, nose, and
mouth), and the musculoskeletal system. The following sections present a discussion of the injuries particular to boxing.
In order to improve the safety of this sport at all levels, more structured studies need to be performed. Our understanding
of the injury risk in the sport of boxing, either professional or amateur, will be greatly enhanced by well-constructed
epidemiologic studies. These studies should provide meaningful and constructive conclusions.
MUSCULOSKELETAL INJURIES
Musculoskeletal injuries other than the hand and wrist are not very common in boxers but can occur. Occasionally, a
rotator cuff tear will be seen. This author has also seen a case of acute anterior dislocation of the shoulder occurring in a
boxer. Rarely, lower-extremity injuries such as ligament or meniscal injuries can be seen if the boxer pivots incorrectly
with his foot firmly planted on the canvas. This section discusses the most common musculoskeletal injuries particular to
boxing starting with the more frequent injuries.
Hand/Wrist
The most common musculoskeletal injuries in boxing involve the hand and wrist ( 43). Although few studies exist to
document the incidence and pattern of injuries in boxing, most show the hand and the wrist as the having the highest
incidence (6,40,42). A 10-year prospective study at the U.S. Olympic Training Center during training and competition
demonstrated that upper-extremity injuries accounted for the majority of injuries (32.9%) and that hand and wrist injuries
accounted for more than half (62%) of all upper extremity injuries ( 6). Most hand and wrist injuries are related to direct
impact and occur more frequently during competition than while training. Injury to this area can prematurely end a boxer's
career. Considering the nature of this sport, it is surprising that more hand and wrist injuries are not seen. The following
typical injuries are most commonly seen.
Thumb
First Metacarpophalangeal Ulnar Collateral Ligament Tear
The first metacarpophalangeal ulnar collateral ligament tear is analogous to skier's thumb and is due to forcible
abduction of the thumb. The ulnar collateral ligament can be partially or completely torn by any extreme valgus stress to
the thumb (Fig. 17.4). Injuries to the ulnar collateral ligament of the metacarpophalangeal joint of the thumb are relatively
common in boxing. Conventional boxing gloves allow the thumb to be abducted, resulting in a potentially injurious
situation. Maintaining a secure clenched fist prevents this injury, but such concentration is not always possible in the heat
of competition. Use of thumbless gloves, which prevent the thumb from being forcibly abducted, should diminish the
occurrence of this injury. However, no studies are available to document this effect. When an incomplete rupture is
present, treatment consists of a period of cast immobilization in a short-arm spica cast for 4 weeks. After this period of
immobilization, active and passive range of motion can be started, and grip strength can begin by the sixth week.
Nonoperative treatment of partial ligament injuries results in a stable and painless thumb. Complete ulnar collateral
ligament tears that result in metacarpal phalangeal instability are generally treated with surgical repair. Postoperative
splinting is continued for 6 weeks, and unrestricted usage is allowed at 3 months. The functional results of operative
treatment are excellent, resulting in a stable, painless thumb in the vast majority of cases. Chronic instability may be
treated with ligament reconstruction, although if secondary arthritic changes are seen, arthrodesis is recommended.
FIGURE 17.4. A complete rupture of the ulnar collateral ligament. This is due to forced abduction of the thumb, which can
occur with a standard boxing glove when the thumb is not attached to the remainder of the glove.
First Carpal Metacarpal Injury
Injury in this location represents either traumatic synovitis, subluxation, or fracture of the first metacarpal base. These
injuries are caused by striking the opponent's head with the radial side of the fist. Attention to proper punching technique
and adequate glove padding will decrease the occurrence of the injury. Traumatic synovitis is treated by avoidance of
further boxing or heavy bag punching until symptoms subside. Subluxation of the first carpal metacarpal joint, or a
Bennett fracture, is best treated by stable fixation to overcome the deforming forces of the abductor pollicis longus ( Fig.
17.5). Of paramount importance is that a stable union is obtained between the ulnar-volar fragment attached to the volar
ligament and the main portion of the shaft. Methods of stabilizing this fracture dislocation are multiple, but all are based
on reduction of the fracture and rigid fixation until healing occurs.
FIGURE 17.5. Bennett fracture. A fracture of the base of the first metacarpal can occur when the unpadded thumb strikes
the opponent's head.
Wrist
Second-Fourth Carpal Metacarpal Injury
Injuries in this location can be either a traumatic synovitis, subluxation and dislocation, or fracture of the metacarpal
base. The most common site of involvement is at the second and third carpal metacarpal regions, either alone or in
combination. Although they are relatively rare, fractures or dislocations of the carpometacarpal joint are often missed on
initial evaluation because of inadequate radiographs. This occurs due to poor-quality radiographs or positioning during
radiography. These injuries are due to direct impact loading at the metacarpal heads. Subluxation or dislocation at the
carpal metacarpal level probably results from landing a direct blow with the wrist in slight volar flexion. These injuries can
be diminished by proper wrapping or taping of the wrist region. Synovitis is best treated by rest. Subluxation or
dislocation are best treated by closed reduction and percutaneous pin fixation. Fractures in this region are treated by
closed technique if they are nondisplaced and by open reduction internal fixation if they are displaced. Carpometacarpal
injuries associated with carpal bone injuries often require open reduction, repair of torn ligaments, and internal fixation.
Recurrent injury can lead to a build up of bone termed carpal-metacarpal bossing. Symptomatic bony prominence may
need surgical intervention.
Conventional Sprain
This injury is due to stretching or tearing of the dorsal wrist capsule or ligaments. Symptoms include vague pain or
swelling in the wrist. No fractures are visible by x-ray study. Treatment is rest and proper wrist taping with resumption of
boxing activity.
Scaphoid Fractures
Fracture of the scaphoid can be either a troublesome or a benign problem for boxers ( 44). The boxer may or may not
recall a specific episode during which the fracture occurred. Symptoms may be very mild and indistinguishable from
minor wrist sprains. Frequently, the boxer will not seek medical attention for several weeks or months after the injury. An
established nonunion may be present by the time a boxer presents for treatment. Often, the nonunion is only minimally
symptomatic or completely asymptomatic. If symptoms are not present, the boxer usually elects not to treat the nonunion
so that his career is not interrupted. The long-term consequences of not treating a symptomatic scaphoid nonunion are
carpal instability and degenerative arthritis of the wrist.
Scaphoid fractures are classified as acute stable, acute unstable, delayed union, and nonunion. Treatment of scaphoid
fractures depends on the chronicity and stability of the fracture. Any boxer with snuffbox tenderness with negative
radiographs should be treated as if an acute stable fracture is present, with a thumb spica cast for immobilization. This
should be followed by repeat examination in 7 to 10 days. If tenderness persists, despite negative radiographs, treatment
should continue and further diagnostic studies should be obtained. Symptomatic acute stable fractures should be treated
with a long-arm thumb spica cast for 6 to 8 weeks, followed by a short-arm thumb spica cast until the fracture is healed.
Alternatively, early internal fixation is an option, and this may limit postoperative immobilization. Delayed unions that are
stable can be treated with cast immobilization in combination with other forms of treatment, including electrical
stimulation. Symptomatic acute and delayed unstable fractures require open reduction and internal fixation. Symptomatic
nonunion of the scaphoid that is stable may be treated with bone grafting and internal fixation, whereas unstable
nonunion requires realignment, bone grafting, and internal fixation. Scaphoid nonunion with accompanying degenerative
changes may require salvage procedures.
Knuckle
Second to Fourth Metacarpophalangeal Sagittal Band Tear
These injuries are very common in boxers and are often referred to as boxer's knuckle ( 45). They are due to direct impact
loading at the knuckle region. The most common location is at the second metacarpophalangeal level, followed by the
third, and less frequently, the fourth. Pathology consists of a stretch or tear of the extensor mechanism sagittal bands.
Symptoms include tenderness and swelling at the knuckle joint. If the tear is large enough, the extensor tendon may
subluxate or dislocate to the side opposite the tear. Minor stretches of the sagittal bands are best treated conservatively,
whereas complete rupture requires surgical repair. This injury tends to be recurrent in boxers. Prophylactic avoidance
measures include adequate taping and padding of the knuckle region. Increased padding in both sparring and
competition gloves should also decrease the occurrence of this problem.
Second to Fourth Metacarpophalangeal Dorsal Capsular Tear
The clinical appearance of metacarpophalangeal dorsal capsular tear is similar to that of the sagittal band rupture.
Occasionally, a distinct rent in the capsule is palpable. This injury results from a tear of the sagittal bands and the oblique
fibers of the hood, usually the radial side. Failure to treat this type of injury may result in ulnar subluxation of the extensor
mechanism with associated loss of finger extension and ulnar deviation of the digit. Treatment of acute tears is by direct
surgical repair of the defect ( 45). There have been case reports of successful treatment by cast immobilization with the
metacarpophalangeal joint in full extension for 4 weeks ( 46). This conservative treatment is more likely to be successful if
the diagnosis and treatment occur immediately after injury. If diagnosis is delayed and primary repair is not possible, then
reconstructive procedures are required to centralize the extensor mechanism. Prophylactic avoidance mechanisms are
identical to those used for a sagittal band disruption.
Metacarpal Fracture
Fracture of the neck or shaft of metacarpals results from axial loading against a clenched fist. The second or third
metacarpals can be involved following properly thrown punches, and the fourth and fifth in improperly thrown punches. A
direct blow with impact occurring at the prominent second or third knuckle joint can produce this type of fracture despite
the fact that the second and third metacarpals are less mobile than the more ulnar metacarpals and are supported by the
thenar eminence (47). These anatomic considerations would tend to diminish the risk of fracture, but generated forces
can occasionally overcome these protective features. The commonly labeled boxer's fracture, a dorsally angulated
fracture of the fourth or fifth metacarpal neck, is more appropriately termed street fighter's fracture ( Fig. 17.6). It is due to
improper punching technique in which the blow is delivered in a round house manner with impact occurring at the
relatively unsupported mobile fourth and fifth metacarpal phalangeal joint level ( Fig. 17.7).
FIGURE 17.6. A dorsally angulated fracture of the fifth metacarpal neck, commonly known as a “boxer's fracture,” is more
appropriately entitled a “street fighter's fracture.”
FIGURE 17.7. Cartoon strip on the left demonstrates an improperly thrown punch with forces concentrated at the fifth
metacarpal. This type of blow can produce a “street fighter's fracture.” The strip on the right depicts a properly thrown
punch, which can fracture the second or third metacarpal.
Most authors would agree that rotational or lateral deviation deformity of the metacarpal should be corrected. However,
the amount of deviation that can be accepted varies with the metacarpal involved. There is universal agreement that any
rotational deformity is not acceptable and must be corrected, because it is directly responsible for residual functional and
cosmetic problems. Treatment varies from closed reduction and casting, to percutaneous pinning and casting, to open
reduction and internal fixation ( 48,49,50 and 51).
Shoulder
The shoulder is the second most common area for musculoskeletal injury in a boxer ( 6). There is a higher incidence of
shoulder injuries in the novice boxer as compared with the experienced boxer. These injuries are musculotendinous
strains, shoulder subluxations, and dislocations. Many novice boxers are exposed to such injuries because of poor
technique, insufficient glenohumeral stability, and inadequate upper-limb strength. Most shoulder injuries involving the
experienced boxer are overuse and impingement-type injuries. Apparently, the relative level of experience determines
the type and frequency of shoulder injuries experienced by boxers.
The initial treatment for overuse injuries is directed at decreasing pain and restoring strength and motion. Pain relief is
achieved by avoidance of aggravating activities and use of cryotherapies and nonsteroidal antiinflammatory medications.
It is the opinion of most sports medicine physicians that cortisone injections are not indicated in the youthful athletic
population because of possible damage to tendons. On relief of initial pain and restoration of strength and motion, guided
rehabilitation is used to identify any aberrant techniques used by the boxer and to correct them. An initial episode of
instability is treated with immobilization until the pain subsides, then a rehabilitation regimen designed to strengthen the
dynamic stabilizers of the shoulder is instituted. This program is successful in preventing recurrence in most boxers.
Recurrent instability is treated operatively with open or arthroscopic procedures.
Cervical Fracture
Although the fear of cervical fracture is ever present whenever a boxer is knocked down or out, its occurrence is actually
quite rare. Any unconscious individual should be treated as though a potential neck injury is present, but in boxing, the
actual presence of cervical fracture is very unlikely. To this author's knowledge, only three cases of cervical fracture due
to boxing have been reported in the English literature. Kewalramani reported one case of a hyperextension injury
resulting in a C-6 fracture with associated quadriplegia ( 47). No details of the fracture or of its mechanism of production
were given in this report. Strano reported one case which he believed to represent an isolated anterior vertical arch
fracture of C-1 occurring as a result of long-term boxing exposure ( 52). The signs and symptoms were not classic for a
C-1 arch fracture, and the published CT scan raises the question that the finding may well have been a congenital
anomaly rather than a fracture. Jordan also reported one boxer who was believed to have sustained a nondisplaced C-3
lateral mass fracture due to boxing ( 53). No mention of neck pain was given in the report, and the boxer received no
cervical immobilization because the injury was deemed to be stable.
As previously stated, acute injuries to the spine are rare in boxing, but any boxer who is unconscious should be treated
as though he has a cervical fracture until proven otherwise. All spine injuries should receive immediate immobilization of
the involved area and prompt transfer to a medical facility. Resuscitation equipment should be available at ringside at all
fights. Any spinal injury of magnitude can end a boxer's career, and rehabilitation to this sport is moot.
OCULAR INJURIES IN BOXING
Earlier authors relying on anecdotal experience have tended to downplay the frequency or seriousness of ocular injury in
boxing. Blonstein wrote that serious ocular injuries were rare in amateur boxers, noting only four cases of detached retina
and making no mention of serious anterior chamber pathology during a 40-year period in which he cared for British
amateur boxers (54). Whiteson also wrote that retinal injury was rare among professional boxers ( 55). However, more
comprehensive ocular studies in boxers have confirmed that the incidence of minor and major boxing-induced ocular
injury is actually quite high ( 27,30,56,57 and 58). Elkington surveyed the ophthalmologic society of the United Kingdom
and reported that 47% of ophthalmologists had examined at least one boxer with an eye injury ( 59). Fifty-six percent of
the survey injuries were said to be retinal detachments. Giovinazzo performed a dilated ocular examination on every
seventh professional boxer applying for a license within the state of New York over a 2-year period ( 27). A total of 74
asymptomatic boxers were examined. They found at least one ocular injury in 66% of the boxers examined and vision
threatening injuries in 58% of the boxers examined. The early lack of awareness of boxing-induced ocular injury was due
to the subtle or nonexistent clinical symptoms of the injuries, failure to perform an adequate ophthalmologic examination,
and general ringside physician inability to diagnose accurately ocular pathology when present. Giovinazzo has pointed
out that an adequate ocular examination in a boxer should be performed by a licensed ophthalmologist and should
include visual fields and acuity, anterior chamber slit lamp examination, applanation tonometry, gonioscopy, and dilated
examination of the retina, including indirect ophthalmoscopy with scleral depression ( 27).
Mechanism of Injury
Blunt trauma to the globe produces ocular injury by one or a combination of mechanisms termed coup, contrecoup, or
equatorial expansion (29,60). Coup injury is the result of a direct blow producing local injury at the point of impact. Direct
blows to the globe produce local injury of the lids and cornea, whereas blows that strike the globe from the less protected
infratemporal direction affect the sclera, ciliary body, and peripheral retina. Contrecoup injury refers to that occurring at
some point distal to the site of a direct blunt trauma. The ocular injuries resulting from a contrecoup force are due to
shock waves that originate at the site of impact and that traverse the globe, producing injury at the interface of tissue of
different densities ( Fig. 17.8). Injury due to blunt ocular trauma causing compression of the globe in an anteroposterior
direction with obligatory expansion along the equatorial plane is termed equatorial expansion injury ( Fig. 17.9).
Equatorial expansion causes traction on the peripheral retina in the region of the vitreous base, leading to a tear or
detachment of the retina.
FIGURE 17.8. Depiction of force transmission with coup and contrecoup sites of injury indicated by the black dots.
FIGURE 17.9. Equatorial expansion of the globe caused by compression in the anterior posterior direction.
Types of Ocular Injuries
Both anterior and posterior chamber pathologies are seen in boxing. Anterior chamber pathology may include corneal
abrasions, injury to the lens, subconjunctival hemorrhage, ciliary body injury, and angle recession among others.
Posterior chamber injury includes all types of injuries to the retina or vitreochoroid complex.
Angle recession
Palmer examined the anterior chambers in 55 former professional boxers at an average of 33 years from retirement and
documented angle recession in 8% (61). Of note, no boxer demonstrated glaucoma as a consequence of the angle
recession. Chronic glaucoma has been reported to occur in 7% to 9% of patients following traumatic angle recession.
The onset of the glaucoma may take up to 10 years to be evident after the angle recession. A similar incidence of 9%
angle recession was also documented by Giovinazzo ( 27). In a 1989 study based on the examination of 286 boxers
performed by 22 ophthalmologists, Sills documented angle recession abnormalities in 39% ( 58). This study included
angle recessions as small as 10%. In a study by Wedrich on 25 asymptomatic amateur boxers, angle abnormalities
accounted for 20% of the pathologic changes seen in the anterior compartment ( 30). It is generally believed that angle
recession must be at least 90 degrees before glaucoma will develop and usually must be 180 degrees. If the Sills data is
adjusted to eliminate any angle recession less than 90 degrees, then the incidence of angle recession falls to 4.5%. In
the Wedrich study, angle abnormalities up to 90% were found in 16% of the boxers. Interpreted correctly, it would appear
that the chance of a boxer developing glaucoma later in life as a result of his occupation is real but low. Only a long-term
study of former boxers will answer the question concerning the frequency of secondary glaucoma.
Lens Abnormalities
Palmer noted the presence of cataracts in 12 of 55 professional boxers examined ( 61). The majority of the cataracts were
of the nuclear sclerotic type. Giovinazzo documented a 19% incidence of cataracts in his study of 74 professional boxers
(27). Seventy percent of these cataracts were posterior subcapsular. Only one of the boxers in this group had visual
impairment due to the cataract, but the possibility exists that vision may well decrease as these individuals age. A similar
incidence of lens changes were documented in a study by Wedrich, in which 16% of the boxers examined showed
changes (30). No boxers in this study demonstrated any visual impairment due to these changes. Smith examined a
group of 118 professional boxers over an 18-month period and documented a 10% incidence of cataracts with 66% being
posterior subcapsular (29). Smith postulated that the posterior subcapsular cataracts were due either to transmission of
contrecoup forces or to equatorial expansion. In addition, Smith pointed out that he had examined other boxers with
significant visual impairment due to cataract formation. Sills' study of 286 boxers, an expansion of the study population
used by Giovinazzo, documented cataract formation in 10% of the boxers or 7% of the eyes ( 58). Only 5% of the eyes
with cataracts had uncorrected vision reduced to less than 20/40. Steroid use has been associated with an increased
incidence of posterior subcapsular cataracts. Whether the prevalence of posterior subcapsular cataracts in boxers is in
any way related to steroid usage is unknown.
Retina
Injury to the retina in boxing is common and may result in blindness if not appropriately treated ( 27,60,62). Maguire
reviewed the records of the retina service of the Wills Eye Hospital over a 31-month period and documented seven
professional and two amateur boxers with evidence of retinal detachment in eight and retinal tear in one ( 60). Symptoms
of retinal detachment included decreased visual acuity, peripheral field loss, light flashes (photopsias), and floaters
(entopsias). All nine of these boxers had presented because of visual symptoms. Maguire noted that of the eight retinal
detachments, six were secondary to a retinal dialysis, which is a linear tear along the vitreous base. Maguire believed
that all retinal tears were definitely caused by blunt trauma to the eye. Five of the patients also had evidence of a definite
posterior vitreous detachment. Three had evidence of vitreous hemorrhage, and two had an avulsed vitreous base which
is known to be pathognomonic for blunt trauma.
Giovinazzo evaluated 74 asymptomatic professional boxers with a complete dilated ocular examination over a 2-year
period (27). Twenty-four percent showed evidence of a retinal tear. An additional 4% had very small atrophic holes in the
retina. All of the involved eyes had evidence of vitreous traction. Two patients had retinal detachments. The probability of
retinal tears correlated with increasing number of bouts and increasing number of loses. Giovinazzo pointed out that after
six bouts, the incidence of retinal tears rises, and after 100 bouts, nearly all of the boxers in the study had evidence of at
least a peripheral retinal tear. In Smith's study of 68 boxers undergoing a dilated retinal examination, 13 (19%) had
evidence of vitreoretinal pathology with five showing evidence of a retinal tear ( 29). Sills' study of 286 boxers showed
evidence of peripheral retina involvement in the form of either atrophic holes, tears, dialysis, or detachment in a total of
13% (58). The majority of these boxers demonstrated atrophic holes or tears, with only three of the group demonstrating
a retinal detachment. In a study by Wedrich, there was a 24% prevalence of retina tear formation in asymptomatic
amateur boxers (30). These retinal tears were classified as horseshoe tears and atrophic holes. There were no cases of
retinal detachment seen. It would seem that amateur boxers appear to have the same risk of developing retinal tears as
professional boxers.
Macular Injury
Involvement of the important central retinal macular area may result in severe central visual loss. Four of the retinal
injuries in Maguire's study involved the macular region. Giovinazzo documented macular pathology in 8% of boxers. Sills
documented macular pathology in 1.7% of boxers examined. No macular pathologic changes were observed in the
amateur boxers examined by Wedrich. This difference may be the result of the use of headgear, which may reduce the
velocity of the hitting glove to below the critical limit necessary to produce retinal edema.
RARE INJURIES
Very rare, practically unique injuries, have been reported in boxers ( 63). Niezgoda reported a case of
pharyngoesophageal perforation secondary to blunt neck trauma following a boxing match ( 64). Solar plexus knockout,
heart knockout (commotio cordis), and carotid sinus knockout have also been mentioned in the literature. Their
occurrence is exceedingly rare.
FORCES IN BOXING
The production of injury to the brain and its coverings is complex because the mechanism involves the effect of both
direct impact of the gloved fist with the skull and the relative motion of the brain and skull in response to this impact.
These factors have been studied experimentally in both humans and animals by scientists interested in preventing brain
injury in automobile and other accidents, as well as in boxing and other sports. Anatomically, the brain is suspended
within the skull by attachments of its blood vessels and some nerve fibers to its tough elastic covering, the dura mater,
and by the cerebrospinal fluid that lies between the two inner coverings of the brain, the arachnoid membrane and the pia
mater. This suspension allows some movement of the brain within the skull. Brain injury in boxing results from either
linear or angular acceleration of the head, or from impact of the boxer's head on the ring mat ( 63,65) (Fig. 17.10). The
skull moves faster than the brain because of the inertia of the brain, and as the skull comes to rest the brain continues to
move in the direction of the supplied force. This may produce injury by structural coup, contrecoup, and concussion
mechanisms. A direct blow such as a straight jab tends to produce linear acceleration of the head, whereas tangential
blows such as hooks or upper cuts produce angular acceleration. Angular acceleration can result in a head force three to
four times greater than that produced by linear acceleration. Gurdgian believed that translational acceleration produced a
pressure gradient in brain and cerebral spinal fluid, resulting in brainstem shear forces in the region of the foramen
magnum (66). Ommaya stated that similar gradients are produced with angular acceleration ( 67). Conversely, Gennerelli
used a primate model to suggest that concussive injury was due to diffuse axonal injury of the entire brain ( 68).
FIGURE 17.10. Schematic demonstrating angular (rotational) acceleration, linear acceleration, and injury due to head
impact on the mat.
The forces generated by head blows in boxing are revealing. Using the Gadd Severity Index, a numeric measure of the
severity of head motion, Johnson has shown that in a realistic boxing situation, a safe level of force on the head can be
exceeded by a factor of four (69). Schwartz reports that head blows can generate acceleration moments on the head as
high as 120 Gs (70). This force is said to be equivalent to that of an unrestrained passenger striking his or her head on
the dashboard in a low-speed auto collision. Atha performed a particularly revealing study in which a top-rated
professional heavyweight boxer punched an instrumented dummy ( 71). The peak force on the dummy head reached 0.63
tons with 53 Gs of head acceleration. Atha stated that the generated force was equivalent to that produced by a blow
from a 13-pound padded wooden mallet swung at 20 mph. Clearly, the force impact due to boxing head blows is
disturbingly high.
The most effective way of diminishing head trauma is to ban head blows in boxing. This approach has been adopted by
at least one boxing club in Denmark (72). However, this is not a practical solution in North America and would not be
accepted on a large scale. More practical potential interventions to decrease head forces have included the mandatory
use of headgear and larger gloves. Evidence to support the efficacy of either of these interventions is not available ( 73).
Headgear is mandatory in all amateur competitions and sparring sessions. Professionals use headgear only in sparring
sessions. In a study in which very small head forces were generated, Schmid demonstrated a 15% to 25% reduction in
head acceleration with the use of a headgear ( 74). However, it is very unlikely that a similar reduction in head
acceleration can be achieved in an actual boxing match in which a significantly higher force is generated ( 73,75).
Competition gloves in both amateur and professional boxing weigh 10 ounces versus 16 ounces for sparring gloves. The
increased padding of larger gloves is reported to blunt the forces imparted to the head. Support for this position does
exist experimentally. However, concussion and knockdowns are not rare events in the gymnasium despite the use of
headgear and 16-ounce gloves. It is this author's opinion that concussive blows are primarily related to punch
acceleration and to the effective body weight imparted to the punch. When the entire hip region and upper torso are
thrown into the punch, there is an increase in the force generated ( 76). The forces generated by hard head blows appear
to be higher than the threshold for brain injury. Any potential decrease in force generation by use of bigger gloves or
headgear does not appear to be large enough to bring the punch force below the threshold for head injury.
Consequently, use of these interventions may provide the boxer with a false sense of security concerning his
susceptibility to head injury. In an attempt to promote safety and decrease the potential for injury generated by the forces
to the head, rule changes have been suggested by the organization that regulates amateur boxing. These changes
include the limitation on the number of rounds, increased power of the referee to terminate the match in which one
competitor is clearly outmatched, and better medical control over boxers who have had concussions before they return to
the ring. There are no federal controls for professional boxing in the United States despite efforts to establish them. This
situation results in less of an effort to promote safety with regard to head injuries in the professional ranks.
ACUTE BRAIN INJURY
Death
Contrary to popular misconception, the occurrence of death as a direct consequence of acute boxing injury is not as high
as in several other sports ( 41,77,78,79 and 80). The incidence of boxing fatalities has been reported to be 0.13 per 1,000
participants compared with 0.3 in college football, 0.7 in motor cycle racing, 1.1 in scuba diving, 5.1 in mountain climbing,
5.6 in hang gliding, 12.3 in sky diving, and 12.8 in horse racing ( 77,81). From 1918 to 1983, 645 deaths world wide have
been reported as an acute result of either professional or amateur boxing. From 1945 to 1983, 353 deaths are recorded;
from 1970 to 1981, 50 deaths; from 1979 to 1983, 28 deaths; and from 1984 to 1997, only 42 deaths ( 80,81). These
findings appear to show a slight decrease in the acute fatality rate in boxing. Most acute deaths in boxing are due to the
sequelae of acute subdural hematomas with diffuse brain swelling. Whether the deaths are the result of a single blow or
a multitude of blows is not documented but it is the author's opinion that most are secondary to multiple head blows over
one or more rounds. High-speed photography has demonstrated that most knockouts occur before the boxer actually hits
the canvas (3). Further head damage can be sustained if the head strikes the canvas.
Better refereeing should decrease the incidence of acute death. No boxer should be allowed to continue fighting in a
groggy or concussed state. It is at this time that a boxer is most vulnerable to further head damage. The referee must
appreciate that lack of defense, leaning against the ropes, drowsiness, lethargy, or wobbly legs all signify a concussed
state in which the boxer has diminished control over body tone and neck musculature, resulting in the generation of
larger coup and contrecoup head forces as the unsupported head is accelerated with each blow.
Subdural Hematoma
Acute subdural hematomas are found in up to 75% of individuals who have died acutely as a result of boxing injury. The
subdural hematoma is due to tearing of bridging veins connecting the brain with the superior sagittal sinus in the dura
mater. Subdural hematomas are frequently associated with cerebral edema. The boxer is typically drowsy or unconscious
from the moment of impact. Occasionally, a short lucid interval may intervene between the offending blows and onset of
symptoms. Clinical signs include stupor, coma, and ipsilateral pupillary dilatation. Brain herniation with resultant death
can result without emergency treatment. A CT scan shows a collection of blood. The primary goal of treatment is to
prevent or minimize neuronal injury. Emergent burr hole drainage is required, if the hematoma is large enough, to relieve
pressure. If the injury is associated with cerebral edema, increased intracranial pressure is reduced by the use of
mannitol, which dehydrates the brain ( 53). Further reduction of intracranial pressure is achieved through the use of
hyperventilation ( 53,84). This lowers the arterial carbon dioxide concentration of the blood, reducing cerebral blood flow.
The insertion of a subarachnoid screw is employed to monitor intracranial pressure and thus detect increases in that
pressure before further clinical neurologic deterioration occurs. Permanent neurologic damage is common even if the
boxer survives.
Subacute Subdural Hematoma
Occasionally, several hours or a few days will pass before symptoms are obvious. The injured boxer will complain of
headache, confusion, slowed thinking, or seizure. Coma may develop with a progressively downhill course similar to that
of acute subdural hematoma. Treatment is similar to the acute injury. Any boxer sustaining a knockout should be closely
observed for several hours. Appropriate instructions should be given to his handlers so that treatment will be rendered if
symptoms do occur.
Chronic Subdural Hematoma
This injury is seen much less commonly than an acute subdural in boxers. Symptoms are those of headache, confusion,
seizure, personality change, or paresis occurring weeks or months after a bout. Treatment is varied depending on the
size and location of the clot.
Acute Epidural Hematoma
This is a rare injury in boxing resulting from rupture of the middle meningeal artery. There is an associated skull fracture
in up to 75% of individuals. Symptoms include drowsiness progressing to coma and hemiplegia. Treatment is surgical.
Intracerebral Hemorrhage
This injury is due to mechanical forces that cause differential movement between the brain and skull, resulting in coup
and contrecoup forces propagated through the brain. The hemorrhage may consist of small petechiae or large clots
occurring anywhere in the brain (85). In boxers, the injury is more unusual than subdural hematoma but more common
than acute epidural hematoma.
Diffuse Axonal Injury
This unusual injury is due to widespread disruption of axons, which probably occurs at the time of impact or shortly
thereafter (68). The extent of injury may be additive with additional bouts. Prognosis for recovery is not good.
Cerebral Edema and Ischemia
This process may occur alone or following brain contusion or bleeding. It is frequently seen in association with acute
subdural hematoma and may lead to death despite drainage of the subdural. Treatment is directed at lowering the
intracranial pressure by the use of mannitol, hyperventilation, and intraventricular catheter drainage, if necessary ( 53,84).
Concussion
A cerebral concussion is the most common acute neurologic injury occurring in boxing. The definition of concussion
remains controversial because its relationship to structural brain damage remains obscure. The Congress of Neurological
Surgeons defines concussion as a “clinical syndrome characterized by immediate and transient post traumatic
impairment of neural function such as alteration of consciousness, disturbance of vision, or equilibrium, and so forth.”
Concussion can be viewed as an acute posttraumatic loss of neural function with rapid and generally complete return of
function. Controversy arises concerning its classification, etiology, and cumulative effects of multiple concussions and the
presence or absence of structural brain damage as a result of concussion ( 86,87 and 88).
Classification
It is important to grade the severity of a concussion if one believes that a more severe concussion implies more severe
underlying transient or structural brain injury. This correlation would seem to be obvious, but scientific proof is not
conclusive. There are several classifications of concussion that can be found in the medical literature. The Congress of
Neurological Surgeons defines concussion in the following manner:
1. Mild—no loss of consciousness

2. Moderate—loss of consciousness with retrograde amnesia
3. Severe—unconscious for more than 5 minutes
This classification does not appear to be specific enough or encompassing enough to be of much use in boxers. It does
not account for different types of amnesia or for amnestic states occurring in individuals without loss of consciousness.
Parkinson studied slow-motion film strips of 20 boxing knockouts and proposed a classification that is useful for acute
boxing-induced concussion (88):
Stage I—Impairment of memory
Stage II—Added impairment of somatic motor activity
Stage III—Motor activity ceases and respirations are impaired
Stage IV—Respirations cease
Recovery from Stages IV, III, and II to Stage I generally occurred in a matter of seconds but recovery from Stage I can
take minutes to hours. Parkinson stated that most boxing knockouts were Stage II concussions characterized by
clumsiness arising from the canvas, wobbly legs, or inability to defend oneself. A standing eight count may allow a boxer
time to recover from Stage II to Stage I, thus enabling him to continue to fight. The referee should either terminate a
match or, if permissible, give a standing eight count to any boxer who displays Stage II concussive symptoms. Serious
additional acute brain injury can occur if a match is allowed to continue while a contestant is in a Stage II concussive
state. The referee and ringside physician must be able to make this determination.
Jordan has proposed a boxing-specific classification that includes the following ( 89):
Grade I—Transient neurologic impairment without loss of consciousness lasting less than 10 seconds
Grade II—Transient neurologic impairment without loss of consciousness lasting greater than 10 seconds.
Grade III—Loss of consciousness with complete recovery in less than 2 minutes.
Grade IV—Loss of consciousness with complete recovery taking greater than 2 minutes.
This classification provides a practical working scheme for boxing. For example, a boxer who sustains a Grade I
concussive blow should be given a standing eight count in an attempt to recover before the match is allowed to continue.
Etiology and Cumulative Effects
The pathophysiologic mechanism by which head blows lead to concussion is not conclusively known. Neubuerger
proposed a thixotropic cause in which the gel sol equilibrium of the brain is altered due to sudden acceleration ( 90).
Hallervorden also believed that a change produced in the colloid medium of the brain would result in concussive
symptoms (91). Other theories relate to changes in the neural cell membranes or internal cellular components. Whether
the responsible alterations are localized to one area, such as the brainstem or limbic system, or more generalized to the
entire cortex is also conjectural. Current imaging modalities such as CT or MRI do not demonstrate any abnormality in
cases of concussion. EEG studies performed shortly after concussive episodes have been documented to be both normal
and abnormal. Most, but not all authors, believe that structural brain changes are not present in concussion. The
absence of identifiable structural brain change would imply that concussion is due to a reversible, transient biochemical
or mechanical change at the cellular level. Parkinson described a rat model of concussion in which he demonstrated that
mild concussion did not result in permanent deficits. However, Windle presented experimental data suggesting that
concussion was due to changes in the neuronal cell bodies of the reticular formation and that measurable changes in
memory function and rate of information processing persisted after overt concussive episodes ( 92).
It is controversial if multiple concussive blows result in a cumulative effect with manifestations that are more serious than
one isolated concussion. Parkinson's rat study showed that the effect of multiple concussions was not cumulative ( 61).
On the other hand, Windle ( 92) and Gronwall (93) believed that the effects can be cumulative. The unknowns concerning
whether concussion is associated with a structural injury to the brain, whether the injury is reversible and over what
period of time, and whether multiple concussions are cumulative in their effect are important in understanding the true
implication of boxing-induced concussion. Any definition of concussion probably should imply the potential for cerebral
damage with the potential for healing and recovery. Lack of information concerning the true nature of concussion makes
it impossible to provide a scientific basis for the recommendation to refrain from boxing for a specified period of time after
one or more knockouts.
CHRONIC TRAUMATIC BOXER'S ENCEPHALOPATHY
The concern relative to chronic neurologic injury occurring subsequent to a career in boxing is the single most divisive
issue surrounding any discussion of the medical aspects of boxing. The polemic of this discussion is frequently strident
and passionate ( 94,95,96 and 97). That a distinct constellation of abnormal clinical signs and symptoms can occur
following a career in the ring is no longer in question ( 9,98,99,100 and 101). Lay expressions used to describe such
individuals were common before any medical description of this problem. Boxing aficionados and fans refer to the
unfortunate ex-boxer suffering from this syndrome as being cuckoo, goofy, slug nutty, cutting paper dolls, punchy, head
case, punch drunk, or stumblebum. The French boxing fan is familiar with the expression sonnes cloche (ringing bells),
the German with weiche birne (soft pair), and the Italian with suonato come una campano (ringing like a bell) ( 102). There
are an equally large number of terms in the medical literature describing the same clinical picture ( 103). In 1928,
Martland provided the first medical description of chronic brain damage occurring in ex-boxers with his classic description
of what he termed the punch drunk syndrome (104,105). This syndrome is referred to in the medical literature under
several other names—dementia pugilistica ( 106), chronic progressive traumatic encephalopathy of boxers ( 107), chronic
traumatic encephalopathy of boxers (108), chronic neuro psychosyndrome ( 108), traumatic encephalopathy (109), and
psychopathic deterioration of pugilists ( 110). This author prefers the term CTBE to describe this unique syndrome and
uses CTBE throughout this chapter when referring to the syndrome.
CTBE is characterized by a varying combination of cortical, pyramidal, extrapyramidal, cerebellar, and psychiatric signs
and symptoms (100,105,107,111,112). The onset of the syndrome is insidious and may first appear after a particularly
severe bout, near the end of a boxer's active career, or not until many years after the boxer has retired. This extremely
varied time of onset as well as varied clinical presentation makes recognition of the early symptoms difficult. It is not
possible to give a single, universal description of the CTBE syndrome because its time of onset, rate of progression, and
clinical manifestations are quite variable. Rather than attempting to describe a single clinical picture, it is more helpful to
consider the syndrome as a variable combination of cerebral, pyramidal, extrapyramidal, cerebellar, and psychiatric signs
occurring in an individual as a result of a career in boxing.
Cortical symptoms include slurred speech, occasional headache, dizziness, and perceived tinnitus, but most important,
variable degrees of dementia. An affected individual demonstrates a decrease in cognitive function, perception,
calculation ability, and memory. Short-term memory for nonsignificant events is first affected but may progress to loss of
both long-term and short-term memory for significant people, events, or places. The ability to perform even the simplest
of tasks such as dressing or other activities of daily living can be lost. The dementia of CTBE can be indistinguishable
from that of classic Alzheimer dementia (AD) ( 113).
Cerebellar signs in CTBE include a general dysequilibrium, particularly in lower extremities. A momentary or continuously
unsteady gait pattern can develop. Tinnitus and dizziness tends to aggravate the dysequilibrium. Pyramidal signs are
generally more subtle but tend to occur early, frequently as the first manifestation of CTBE ( 114). Frequently, a lack of
awareness by the affected ex-boxer does not permit him to appreciate early subtle dragging of a leg or weakness of an
upper extremity. Signs of spasticity, including increased tone, hyperactive reflexes, the presence of the Babinski sign,
and clonus, may develop.
Extrapyramidal signs are a classic finding in CTBE, explaining the occasional confusion in differentiating individuals with
classic parkinsonism from those with CTBE. Extrapyramidal signs seen in patients with CTBE include immobility of the
face, slowing or lack of movement, shuffling gait, rigidity, tremors particularly of the hands and feet, and hypophonia. The
occurrence of these symptoms tends to be somewhat later in the course of the syndrome.
Psychiatric abnormalities also commonly occur. Affected individuals will show varying degrees of personality
deterioration, violent behavior that can approach momentary periods of rage, a generalized lack of awareness, and
intolerance to alcohol consumption. In 1969, Johnson studied 16 ex-professional and 1 ex-amateur boxer at an average
age of 54 years and an average time of 22 years since they last boxed ( 108). He believed that the clinical pictures of
individuals with CTBE could be grouped into five clinical psychiatric syndromes. The psychiatric symptoms may or may
not be progressive and can overlap, with any one individual showing varying degrees of all five clinical syndromes.
These five groups include:
1. Chronic amnestic state—believed to be due to scarring, neurofibrillary tangle, and plaque formation in the
mammilo-thalamic-fornico-hippocampal system in and around the mammillary bodies, at the hippocampal areas,
and deep in the midline in and around the third ventricle. The memory loss is typically for short-term impersonal
data but can be more global.
2. Dementia—a progressive, irreversible disorganization of personality particularly affecting cognitive function.
3. Morbid jealously syndrome—attributed to involvement of the limbic system and typically directed at the boxer's wife
in the form of accusations of infidelity. The jealousy may be heightened by sexual impotency, which is seen later in
the disease process.
4. Rage reaction—believed to be due to involvement of the limbic system and possibly the septum pellucidum. These
reactions are manifested as extreme violence, usually of short duration, which may result in emergency psychiatric
admission or civil incarceration. Intolerance to alcohol magnifies this problem.
5. Frank psychosis—generally typified as delirium and paranoia.
Considering the protean manifestations of CTBE, it is difficult to describe a typical case. However, it is this author's
impression that the earliest findings consist of subtle slurring of speech with minor dysequilibrium such as momentary or
continuously unsteady gait. Inability to perform a tandem gait test may be the first sign of CTBE. Cognitive function is at
first only mildly effected, but progression can lead to severe dementia. Personality changes and symptoms of
parkinsonism tend to develop slightly later in the disease process. End-stage involvement results in a severe combined
AD and parkinsonian picture that can result in permanent institutional placement ( Fig. 17.11). There is no agreement in
the medical literature concerning the degree of progression in CTBE syndrome. Many individuals exhibit only minor
involvement, without any tendency for progression. On the other hand, there are numerous examples of individuals with
relentlessly progressive signs and symptoms. It is this author's impression that symptoms are generally progressive if
affected individuals are followed long enough.
FIGURE 17.11. CTBE can demonstrate a varied course, but a typical scenario is provided.
Although the time of onset and progressive nature may vary, there is no doubt that a distinct encephalopathy due to
boxing-related trauma does exist. Some authors have actually discounted the existence of a distinct CTBE syndrome,
ascribing the pathologic picture to alcohol and drug abuse, genetics, hazards outside the ring, and baseline behavioral
states (55). These extraneous factors can exacerbate CTBE symptoms but do not by themselves explain the problem.
Attempts by medical apologists to downplay the neurologic aftermath of boxing serve only to perpetuate the current
inadequate medical understanding of this problem. Analysis of the current body of knowledge allows us to identify
significant risk factors and potentially to affect a change in these risk factors, thereby improving boxing safety.
Neuropathology of Chronic Traumatic Boxer's Encephalopathy
The neuropathologic changes in the brains of selected ex-boxers shed considerable light on the deleterious clinical
aftermath sustained in the ring. Most, if not all, of the signs and symptoms comprising CTBE can be explained by these
neuropathologic findings. Published literature documenting these neuropathologic changes is not extensive but is
sufficient to identify a characteristic picture. Brandenburg and Hallevorden were the first to describe chronic cerebral
changes found in ex-boxers ( 115). They described the findings in an ex-boxer who had fought as an amateur from age 18
to 29 and who subsequently developed a progressive dementia and Parkinsonian picture beginning at age 38. The brain
was grossly atrophied with microscopic vessel degeneration. Widespread neurofibrillary tangles and senile plaque
formation were noted. The authors interpreted these findings as being consistent with posttraumatic dementia and
Parkinsonism, distinct from typical AD. Grahmann and Ule also reported the case of an individual who had boxed as an
amateur and in the booth from age 15 to 25, who subsequently developed dementia, pyramidal, and extrapyramidal signs
beginning at age 46 ( 116). Grossly, this brain showed evidence of atrophy and ventricular hypertrophy with a cavum
septum pellucidum. Neurofibrillary tangles, without plaque formation, were documented microscopically. In 1959,
Neubuerger reported on one cortical biopsy and one autopsy specimen obtained from two ex-boxers who demonstrated a
severe dementia (90). Both specimens displayed gross cortical atrophy and gliosis. There were no senile plaques or
neurofibrillary tangles.
In 1967, Constantinides reported on an ex-amateur boxer who developed progressive clinical signs of dementia,
parkinsonism, and motor weakness (117). Postmortem examination disclosed brain atrophy and a cavum septum
pellucidum with fenestration. Microscopic scarring, neurofibrillary tangles, and a depigmented substantia nigra were also
observed. Payne provided the first detailed review of postmortem findings in the brains of six ex-professional boxers
(118). All six specimens showed some enlargement of the ventricular system with an associated cavum septum
pellucidum. Three of six cases demonstrated fenestration in the septum. Payne believed that the cavum and fenestration
were secondary responses to an internal ventricular enlargement that caused stretching of the corpus callosum and
consequent separation of the septal attachments. He believed that injury to septal blood vessels during separation would
presumably predispose, or initiate, septal fenestration. All specimens demonstrated a proliferation of the surface layer of
the cerebrum, which was interpreted to represent foci of organized subpial hemorrhage. Macroscopic focal scarring was
found in four specimens, whereas all six showed evidence of focal microscopic scarring. Scarring was believed to be due
to replacement of nerve cells by hypertrophied and hyperplastic astrocytes. This process was found in both the
parieto-occipital lobes and the cerebellum. In summary, Payne believed that the main pathologic features included an
enlarged ventricular system, miniature scars and microscars in the gray matter, focal areas of demyelination in the white
matter, and irregular proliferation of the surface layer of the cortex, all of which were believed to indicate small areas of
focal brain damage. He did not comment on any possible changes in the midbrain. Critics of Payne's work point out that
one subject was very old at the time of death, another had malignant hypertension, and two were chronic alcoholics,
potentially obscuring the true etiology of these brain changes.
The most comprehensive work documenting the neuropathologic findings in boxers' brains was published in 1973 by
Corsellis (119). This eloquent study underscores the anatomic basis for the myriad signs and symptoms present in CTBE
(Table 17.3). Corsellis studied the brains of 12 retired professional and 3 amateur boxers, all of whom had boxed
between 1900 and 1940. He documented a characteristic pattern of cerebral pathology consisting of a cavum septum
pellucidum with fenestration, cerebellar scarring, cerebral scarring, degeneration of the substantia nigra and locus
caeruleus, and Alzheimer neurofibrillary tangles without plaque formation.
TABLE 17.3. CTBE NEUROPATHOLOGY
Normally, the septum pellucidum is composed of two thin sheets of nervous tissue aligned in the midsagittal plane
between the undersurface of the corpus callosum and the dorsal aspect of the fornix. If these two sheets are separated
forming a cavity, it is referred to as a cavum deformity ( 120) (Fig. 17.12). Schwiddle studied a general population sample
of nonboxers and found a 20% incidence of cavum, most occurring later in life ( 121). Corsellis demonstrated a consistent
septal abnormality consisting of a cavum septum pellucidum with fenestration. To confirm further the high prevalence of
septal abnormalities in boxers, Corsellis then reviewed 500 brains, 475 of which were from psychiatrically
institutionalized nonboxers in whom septal abnormalities would be expected to occur with a greater frequency than in the
general population. He found a mean septal cavum width of 1.6 mm in the psychiatric controls compared to 5.17 mm in
the boxers. Furthermore, 77% of the boxers demonstrated septal fenestration compared to only 3% of the psychiatric
controls. The fornix was found to be almost totally detached from the under surface of the corpus callosum. The two
flattened fornical bodies were stretched horizontally over the dorsal surface of the thalamus. The corpus callosum itself
was quite thinned. Corsellis believed that repetitive blows to the head caused differential movement at the septal
attachments on the ventral corpus callosum and dorsal fornix, resulting in cavum formation and fenestration of the
tethered septum. As the ventricles enlarged, the septal tears would further enlarge. However, Corsellis did not believe
that increased ventricular size alone was enough to cause septal fenestration. Other authors have also commented on
the significance of septal changes ( 122,123 and 124).
FIGURE 17.12. A gadolinium-enhanced T1-weighted MRI demonstrating a large cavum septum pellucidum.
Cerebellar scarring was particularly marked on the inferior surface of the lateral lobes, especially in the folia of the
tonsillar region near the edge of the foramen magnum. As many as one half to two thirds of the Purkinje cells in these
folia were lost and the adjacent granular layer was thinned with demyelinization of the associated white matter. Purkinje
cell loss also extended far beyond the limits of gross scarring. Corsellis postulated that these cerebellar changes could
be explained on the basis of multiple bleeds or miniherniations of the tonsils. Corresponding changes were not seen in
the adjacent brainstem. Unterharnscheidt documented similar Purkinje cell and granular layer damage in cats subjected
to repetitive low-intensity head blows ( 3).
Cerebral scarring, particularly in the deep periventricular region, did occur but was not a prominent finding. In 1923,
Martland hypothesized that the primary pathology, in what he referred to as the punch drunk syndrome, was due to
multiple concussive hemorrhages in the deeper portions of the cerebrum, resulting in scarring and atrophy ( 105).
Martland believed that the hemorrhage and subsequent scarring would be found in the region of the corpora striata and
corona radiata but not in the cerebral cortex or cerebellum. Consequently, evidence of old hemorrhage or scarring should
be frequently observed in these areas if Martland's hypothesis is correct. Contrary to the findings in Payne's study, which
do appear to validate Martland's theory, this hypothesis could not be verified by Corsellis' work. However, Corsellis did
document decreased brain weight, increased ventricular size, and thinning of the corpus callosum, all of which would be
expected as a consequence of decreased cerebral size. Interestingly, subsequent work done by Adams, using more
sophisticated tests for iron deposition, has demonstrated a high incidence of old microscopic hemorrhage throughout the
cerebrum (125).
Degeneration and loss of pigmented nerve cells in the substantia nigra was a very common finding in Corsellis' study.
This neuropathologic finding, classically seen in parkinsonism, readily explains the frequent occurrence of Parkinson-like
extrapyramidal signs and symptoms noted in CTBE. The medial nuclear group of the substantia nigra was typically
spared, whereas the intermediate and lateral groups were typically involved. In addition, neurofibrillary tangles were
common in these areas. Similar depigmentation changes were also documented in the adjacent locus caeruleus. How
multiple repetitive trauma leads to depigmentation of the substantia nigra is not known ( 126).
Probably the most striking neuropathologic finding in Corsellis' study was the documentation of diffuse neurofibrillary
tangles without overt senile plaque formation ( Fig. 17.13). Neurofibrillary tangles, accompanied by senile plaque
formation, are a classic finding in AD. Tangles and plaques are found diffusely throughout the cerebrum in AD but are
particularly prominent in the anteromedial temporal gray matter, amygdaloid nucleus, and hippocampus. The
periventricular region is generally spared in AD. In contrast, neurofibrillary tangles, without senile plaque formation are
typically seen in the parkinsonian complex of Guam, postencephalitic parkinsonism, certain types of chronic encephalitis,
and progressive supranuclear palsy. Unlike typical AD, most of the tangles in these latter conditions are localized to the
midbrain, pons, and medulla. In the boxers' brains, tangles were diffusely located throughout the brainstem and cerebral
cortex, particularly the medial temporal gray matter, amygdaloid nucleus, hippocampus, and parahippocampal regions.
The absence of overt senile plaque formation was similar to the findings of Grahmann ( 116) and Constantinides (117).
How cerebral trauma induces tangle formation is not well understood.
FIGURE 17.13. A normal neuronal cell body is depicted on the left. The right picture is the appearance of a typical
neurofibrillary tangle.
Roberts later strengthened the neuropathologic relationship between AD and CTBE ( 127). He used immunocytochemical
methods in preparing an antisera to the proteinaceous substance found in the tangles of AD. This antisera gave an
identical morphologic and immunoreactive profile to the neurofibrillary tangles seen in CTBE. He postulated that these
two conditions shared a common traumatic etiology. The puzzling absence of senile plaque formation observed in
Corsellis' work was eventually explained by additional experiments performed by Roberts. Reinvestigating Corsellis'
original specimens with the help of immunocytologic methods and an antibody to the b-protein present in Alzheimer
plaques, Roberts showed that all CTBE specimens with significant tangle formation also showed evidence of extensive
b-protein immunoreactive deposits. These diffuse occult plaques were not visible with Congo red or standard silver
stains, as used by Corsellis, but were readily identified when Roberts pretreated the specimens with formic acid and
labeled them with antibodies to the b-protein found in Alzheimer plaques. Roberts postulated that the diffuse occult
b-protein immunoreactive plaques of CTBE simply represent a younger version of the diffuse, overt, congophilic plaques
seen in classic AD. Tokuda et al. also demonstrated significant immunocytochemical similarity between the neurofibrillary
tangles and plaques found in both AD and CTBE, providing further proof of a basic connection between the two diseases
(128). In addition, ubiquitin, a protein found in the neurofibrillary tangles of AD and involved in the degradation of
abnormal proteins, has also been found in the tangles of CTBE ( 129). Diffuse tangle and plaque formation are believed
to be the hallmark changes resulting in the clinical dementia of AD, and may well explain the analogous signs and
symptoms of dementia noted in CTBE. The neurofibrillary tangles in both conditions tend to cluster in the temporal lobe.
Current research into the etiology of AD lists trauma as a predisposing factor. Based on this neuropathologic evidence, it
is understandable why the clinical signs of AD and CTBE are very similar ( 113,130).
Brain damage in CTBE is believed to result from a combination of mechanical shearing forces on the neurons and
breakdown of the cerebral blood–brain barrier. Traumatic damage to the cerebral blood vessels could cause leakage of
b-protein into the brain substance, resulting in occult plaque formation. Brayne demonstrated that creatine kinase
isoenzyme (CK-BB), which is normally found in high concentrations in the brain and low concentrations in blood, rose
systemically following amateur boxing competitions ( 131). Interestingly, Rodriquez has demonstrated a diminution in
regional cerebral blood flow, particularly in the parietal and temporal lobes, of professional but not amateur boxers ( 44).
Further evidence of diffuse vascular damage in boxers' brains was also provided in a study by Adams, in which 17 of 22
ex-boxers showed evidence of old hemorrhage either intracerebrally, in the meninges, or in the cerebellum ( 125).
The totality of the pathologic changes provide an explanation for the clinical signs and symptoms in CTBE. Memory
capability is believed to reside in the limbic areas of the brain, particularly in the medial temporal gray matter and
hippocampal formation. Neurofibrillary tangles are numerous in these areas as well as in other limbic areas that
constitute an important control center for memory and cognitive functioning. Extensive cortical scarring, neurofibullary
tangles and plaques would all tend to diminish further cognitive function, thus explaining the Alzheimer-like symptoms
seen in CTBE. The macroscopic and microscopic cerebellar changes can easily explain the coordination problems,
tremors, and irregular movements. Parkinsonian (extrapyramidal) features, including slowness of movement, rigidity, and
blunted facial expression, are explainable by the marked depigmentation noted in the substantia nigra. And finally, the
emotional changes noted so frequently in CTBE can also be explained by the limbic and septal changes described
earlier.
It can unequivocally be stated that although other etiologies such as head injury outside of boxing, alcohol abuse,
degeneration due to old age (AD), or classic parkinsonism can each demonstrate selected clinical and pathologic
features of the CTBE syndrome, only CTBE displays the constellation of cortical, pyramidal, extrapyramidal, cerebellar,
and psychiatric features in association with the five classic pathologic findings of cavum septum pellucidum with
fenestration, cerebral and cerebellar atrophy, depigmentation of the substantia nigra, and diffuse neurofibrillary tangles
with occult plaque formation.
Epidemiology of Chronic Traumatic Boxer's Encephalopathy
The prevalence of CTBE in professional or amateur boxing varies depending on the criteria used to make the
determination. The syndrome is much more common in professional boxers but not unknown among amateurs (132).
Older reports had estimated the prevalence anywhere from 0 to 50%, but documentation of these estimates was not
provided. The best study addressing the prevalence of CTBE in professional boxers is undoubtedly that of Roberts in
1969 (100). He examined a random sample of 224 boxers out of a total population of 16,781 registered with the British
Boxing Board of Control between 1929 and 1955. The boxers had to be British nationals and have at least 3 years of
professional experience to be included in the study. Roberts reported that 37 of the 224 (17%) had definite signs of
encephalopathy that were not explainable by other causes. In 13 of the 37 affected, the signs and symptoms of chronic
encephalopathy were either of a moderate or of a severe degree. Eleven additional boxers also demonstrated an
encephalopathy but the etiology could not definitively be attributed to boxing as other relevant factors or diseases were
also present. The prevalence of full-blown CTBE was definitely related to the length of the boxers careers and their age
at time of review. Roberts noted that if the boxer was older than 50 years of age at the time of review and had had a
career lasting greater than 10 years, the incidence of encephalopathy was 47%, compared with 17% if the boxer's career
was between 6 and 9 years, and 13% if the career lasted less than 5 years. Similarly, for boxers younger then 50 years
old at the time of review, with careers lasting more than 10 years, the incidence was 25% compared with 14% for careers
lasting 6 to 9, and 1% for careers lasting less than 5 years. Of note also were individuals who demonstrated either
isolated dysequilibrium, dysarthria, alcohol intolerance, or isolated pyramidal signs but without a full-blown traumatic
encephalopathy. Roberts found that one or more of these symptoms was present in 74% of retired boxers who were older
than 50 years old at time of review and had had careers lasting greater than 10 years, compared with a 56% incidence if
the career lasted from 6 to 9 years, and 35% if the career lasted less than 6 years.
Roberts also correlated the prevalence of encephalopathy with the actual number of professional bouts that the boxers
were involved in. Similarly to the length of professional careers, the more professional bouts a boxer had, the higher the
prevalence of traumatic encephalopathy. For boxers older than age 50 years of age at review who had had more than
150 professional fights, the incidence of encephalopathy was 50% versus 19% for those who had participated in 50 to
150 fights and 7% for those who participated in less than 50 professional fights.
Criticism of Roberts' work is primarily that his study population is not representative of modern-day boxers, who arguably
compete under improved medical supervision and better overall supervision. Many of Roberts' boxers had competed
before World War II (WWII) at a time when careers tended to be much longer and boxers had many more bouts. There
was a tendency to allow boxers to absorb far more punishment than is currently deemed appropriate. Matches were
frequently longer than is currently permitted, with some bouts lasting longer than 15 rounds. Before WWII, an unknown
percentage of professional boxers also engaged in unregulated, unlicensed matches termed booth boxing. These
competitions could be either staged or competitive in which weight limits were not observed and varying amounts of head
trauma absorbed. Professional sparring, in which a boxer received payment for services, also appeared to be more
common before WWII. Neither professional sparring or booth boxing was considered in Roberts' analysis. Modern-day
studies of boxing encephalopathy have been of a nonrandomized nature, with attention directed to findings on EEG, CT,
and MRI. Kaste studied 14 boxers, six of whom were professional and eight amateur, with neuropsychiatric testing, EEG,
physical examination, and CT scanning ( 10). He documented evidence of cerebral atrophy in four of the professionals
and one of the amateur boxers. Two professionals and seven amateurs showed EEG abnormalities, whereas two
professionals demonstrated abnormal neuropsychiatric testing. One of the boxers, a professional, had obvious
encephalopathic symptoms. Overall, structural or functional abnormalities were found in five of six professionals and four
of eight amateurs. Kaste concluded that there was no evidence to support the view that modern-day boxing is safe from a
neurologic standpoint. Casson reported the CT findings of 10 professional boxers who had been knocked out a few
weeks before their examination (133). No boxer demonstrated acute pathology, but five did have evidence of cerebral
atrophy. The presence of a CT abnormality was directly related to the number of bouts fought by the boxers and not to
the proficiency of the boxer. In fact, better boxers tended to have more bouts and more cerebral atrophy on CT scan.
Casson concluded that the CT findings were due to multiple subconcussive blows. No boxer demonstrated a clinical
CTBE syndrome. Sironi performed CT scans and EEGs on 10 young professionals and found CT evidence of definite
atrophy in two and borderline atrophy in four, as well as definitively abnormal EEGs in three and borderline changes in
four (134). He noted that the CT changes appeared to be related to the number of knockouts sustained by the boxer
rather than to the length of career or number of bouts fought. This is in contrast to most other studies that have
emphasized number of bouts and length of career. Ross performed 38 CT scans and 24 EEGs on 40 modern
ex-professional boxers, looking for brain atrophy as identified by gyral hypertrophy or ventricular enlargement ( 135).
Twenty of the 38 CT scans showed evidence of brain atrophy. He noted a positive correlation between increasing
number of bouts and ventricular enlargement but not with gyral atrophy. He did find that boxers with more bouts tended to
have a greater number of EEG changes. Gyral atrophy did not correlate with the number of times a boxer had been
knocked out. Casson studied 18 modern boxers (13 ex-professionals, two active professionals, and three active
amateurs) with physical examinations, CT scanning, EEG, and neuropsychological testing ( 11). All potential causes of
brain damage other than boxing were criteria for exclusion from the study. CTs were reviewed for evidence of
generalized cerebral atrophy (increased ventricular size, prominence sulci), central cerebral atrophy (increased
ventricles, normal sulci), cerebral cortical atrophy (normal ventricles, prominent sulci), or for a cavum septum pellucidum.
Eight of the professional boxers had an abnormal CT scan, five an abnormal neurologic examination, and seven of 13
studied had an abnormal EEG. All 18 boxers demonstrated abnormal findings on neuropsychological testing. Of note,
four of the five professional champions or highly rated boxers in this study demonstrated CT abnormalities. Six of eight
professionals who had participated in more than 20 bouts had abnormal CT findings compared with two of ten who
participated in fewer than 20 bouts. Casson concluded that CT abnormalities, EEG changes, and abnormal
neuropsychological tests all correlated with increasing number of bouts. There was no correlation with the number of
knockouts. He did not believe that modern-day professional or amateur boxing was safe. Drew compared 19 young
modern professional boxers with ten nonboxing controls using neuropsychological testing and found abnormalities in 15
of 19 boxers compared with two of ten controls (136). He concluded that modern boxers still suffer brain damage.
The body of evidence shows that overt CTBE was a significant problem for professional boxers whose careers spanned
the years before WWII. Although similar conclusive proof of frequent overt CTBE does not exist for modern-day boxers,
much inferential evidence exists to raise the specter that it still may. Almost all recent studies using CT scanning or
neuropsychological testing demonstrate a high frequency of subclinical abnormalities in professional boxers, with similar
but less frequent findings in amateur boxers. Classic cases of overt CTBE continued to be reported, albeit not frequently,
despite modern-day medical care. Long-term clinical follow-up on the individuals who have been reported to have
abnormal CT, EEG, or neuropsychological findings is necessary to determine if full-blown CTBE will develop. In the
meantime, the medical and organizational reform recommendations outlined in this text should be implemented in the
hope that the incidence of CTBE can be reduced in the modern sport of boxing.
Risk Factors for Chronic Traumatic Boxer's Encephalopathy
The majority of the medical literature identifies two proven risk factors for CTBE. First, CTBE is much more common
following a career in professional boxing than after an isolated amateur career. Second, the longer the professional
career, generally translating into more professional bouts, the greater the risk of CTBE ( 100,137,138). It is not difficult to
understand why professional boxing is riskier than amateur boxing. The contests are longer and much more brutal. The
combatants are more skilled, throw harder punches, and absorb far more head trauma than amateur boxers. Sparring
sessions are longer, with harder and more frequent head blows. A professional boxer's livelihood depends on his ability
to absorb head blows. Officiating personnel are much more likely to allow a potentially dangerous bout to continue than
are amateur officials. Because multiple subconcussive blows alone can eventually lead to CTBE longer careers are
inherently more dangerous. A direct correlation is identified between the number of professional bouts and the likelihood
of developing CTBE. There is disagreement concerning the degree of CTBE risk in various boxing weight divisions.
Some authors have stated that heavier boxers are at a greater risk owing to the harder punches thrown. However, this
probably is not true. CTBE is appreciated in ex-boxers of all weight classes. Any boxer, no matter how small, who
receives multiple subconcussive head blows is at risk for development of CTBE. Sluggers who are willing to absorb two
or three punches to land one are potentially at increased risk. Second-rate boxers, or those that frequently work as
sparring partners for better boxers, are potentially at increased risk. Ironically, boxers with an ability to take a punch,
who, therefore, can be expected to win more fights and have longer and more financially productive careers may be at
increased risk. Severe CTBE necessitating permanent institutionalization has been seen in many excellent ring
technicians including many that have held world titles. Boxing legends such as Joe Lewis, Sugar Ray Robinson, Billy
Conn, and Fritzi Zivic are prime examples of very skilled world champions who have, or are suffering, the unfortunate
effects of CTBE.
There is no clear correlation between the number of knockouts sustained by a boxer and the subsequent development of
CTBE. Some authors have observed a direct correlation ( 139), whereas others refute this claim, instead concentrating on
the correlation with multiple subconcussive blows ( 10,11,100). It is clear that CTBE can occur in the absence of a boxer
having been frequently or even ever knocked out. Although it is argued that the incidence of CTBE has diminished since
the inception of stricter medical guidelines after WWII support for this position is not universal. The above-mentioned
work by Ross, Kaste, and Casson performed on boxers whose careers commenced after WWII, raises the specter that
significant evidence of both clinical and subclinical CTBE continues to exist.
Recent research has demonstrated that there may be a genetic susceptibility of certain individuals for the development of
CTBE. Investigators have identified apolipoprotein E (APOE) as a susceptibility gene for late-onset familiar and sporadic
AD. Owing to the similarities between AD and CTBE, Jordan conducted a study to evaluate the relationship between
APOE genotype and CTBE in boxers and to determine if any genetic susceptibility exists ( 140). The human APOE gene
encodes a cholesterol carrier lipoprotein (APOE) produced in the liver and brain. It is polymorphic and occurs in three
common allelic forms designated APOE e2, e3, and e4. This gives rise to six possible genotype combinations. Individuals
possessing the APOE e4 allele show an increased risk of AD in a dose-dependent fashion. In addition, these individuals
have a shift for an earlier onset of the disease. APOE e2 is underrepresented in the AD population and may protect
against AD. Head trauma has been implicated as an environmental trigger for the development of AD. As stated in earlier
sections, CTBE exhibits several features that are similar to characteristics of AD. In the Jordan study, this relationship
was evaluated in 30 professional boxers. Although the APOE genotype frequent of the study population was
approximately the same as that found in the general population, boxers with high exposure with the APOE e4 allele had
significantly greater chronic brain injury scores than high-exposure boxers without the APOE e4. Further research is
necessary, but these preliminary results may suggest that possession of an APOE e4 allele may be associated with an
increased susceptibility for chronic neurologic deficits in high-exposure boxers.
Potential Preventive Measures in Chronic Traumatic Boxer's Encephalopathy
There are a multitude of approaches, if implemented, that could potentially decrease the incidence of CTBE ( 28,141)
(Table 17.4). Foremost is the belief that better medical supervision will improve all aspects of boxing safety, including
decreasing the incidence of CTBE ( 28,142,143). Although there is evidence that acute boxing injuries can be decreased,
the effect on CTBE is as yet unproved. Better medical supervision would take the form of better ringside physicians;
enforcement of mandatory medical layoffs; serial screening with CT, MRI, EEG, and ophthalmologic examinations;
availability of acute life support measures at ringside; comprehensive evacuation plan for the boxing arena; and available
neurosurgical back-up support. Additionally, significant improvements can be accomplished in other aspects of the sport.
TABLE 17.4. POTENTIAL PREVENTIVE MEASURES AGAINST CTBE
Better Medical Supervision
Ringside Physicians
Having a physician sit at ringside who is knowledgeable in both the medical and the nonmedical aspects of boxing is
essential. Not only must the physician be knowledgeable but he must have the authority to intervene without fear of
obstruction by state or local boxing officials, or from the boxer's corner, if he believes that a boxer is in trouble. In many
states. the physician is not authorized to stop a match even if he believes that a boxer is taking too much punishment. In
more progressive states such as Pennsylvania or New York, the physician can mount the ring apron at any time during a
round or rest period to examine the boxer and terminate the contest if he deems it medically necessary. In many
instances, the physician faces a difficult decision in deciding whether to stop a contest or let it continue. The boxer, his
corner, the promoter, and frequently the local governing body may all want the bout to continue. If in the physician's
medical judgment a boxer's well-being is in jeopardy by allowing the contest to continue, then he must stand his ground
and terminate the contest. Repeated Grade I concussion or groggy state behavior is an absolute indication to terminate a
contest. Despite their having spent countless years in the sport of boxing few trainers, promoters, or other lay individuals
have the physician's medical understanding of the dangers inherent in allowing a boxer to become repeatedly
concussed. A situation that has become an obvious and real neurologic danger to the boxer may be perceived as mere
guttiness, guile, or simple ability to take a punch by the lay public. The tendency to repeatedly allow a boxer to weather
the storm must be guarded against. It is not necessary for a boxer to be repeatedly knocked down before a bout is halted
by the physician. Even though a physician's financial renumeration for working a boxing match is paid for by the
promoter, the physician's obligation is first and foremost to protect the medical well-being of the boxer. National
sanctioning bodies and state boxing commissions must be supportive of the physician's decision even if it is unpopular.
The difficulty in deciding to terminate a contest due to excessive head or body blows mandates that the ringside
physician have a thorough understanding of the sport of boxing. Boxing is inherently dangerous and seemingly brutal to
some individuals. The ringside physician must walk the fine, ill-defined line between accepting this reality and protecting
the well-being of the participants. It is only with continued exposure to the sport that the distinction can be appreciated. A
ringside physician must also be knowledgeable with respect to the didactic medical aspects of boxing. He or she should
be introduced and tutored in the sport by an experienced ringside physician. It is unacceptable for the medical coverage
of an amateur or professional boxing show to be provided by a physician who has never attended a boxing match or does
not understand the risks involved. Refereed journal articles, reviews ( 82,102,144,145), chapters (146), and even entire
books on the medical aspects of boxing are available for review ( 58). Unfortunately some physicians who sit ringside for
boxing matches do not possess this knowledge. They are then incapable of knowing when enough punishment is
enough. Frequently, they will err by either allowing a bout to continue too long or by stopping a bout prematurely. Any
competent physician can achieve an understanding of boxing and its medical implications. It should be obvious that a
professional or amateur boxing competition should never be held without the presence of at least one and preferably two
competent ringside physicians. Allied health personnel such as chiropractors or physician's assistants are not qualified to
sit ringside as the sole providers of medical coverage.
Having two physicians present at a competition allows one to attend to any medical needs in the postfight dressing room
while the other remains at ringside to monitor subsequent bouts. The ringside physician should attempt to arrange
appropriate follow-up for suture removal, referral to specialists, and scheduling of tests, if necessary. Facial lacerations
should be repaired by the ringside physician in the dressing room if he is comfortable with suture repair; otherwise,
referral to a local emergency room is necessary.
Mandatory Medical Suspensions
At present, if a boxer is under medical suspension in one state, there is no guarantee that all other states will know of the
suspension or will honor the suspension if the boxer attempts to compete in their state. If a boxer has been knocked out
and is medically suspended in one state, he may attempt to compete shortly thereafter and risk further injury in another
state. Although this situation has lessened as state boxing commissions have improved their communication with each
other, it is still not ideal. At least four states still lack any boxing commission whatsoever. Medical suspensions by one
state boxing commission should be conveyed to all other state commissions and be honored except in rare
circumstances.
Many state boxing commissions have regulations regarding medical suspensions, but they are not always enforced by
the commissions. Enforcement of established medical suspension guidelines should be assiduously performed. Every
state should develop and follow guidelines similar to those of New York or Pennsylvania. In Pennsylvania, if a boxer
sustains a knockout, he is automatically suspended for 45 days. If a boxer loses six straight bouts, he must have an
examination by a commission-approved physician. Before further competition in New York, following a medical
suspension, a boxer must obtain either an EEG, CT scan, or MRI study. Similar guidelines exist in Pennsylvania.
At present, if the imaging studies and neurologic examinations are normal, there is no valid medical rationale that can be
used to determine the optimal length of suspension following head trauma sustained in the ring. Empirically, it can be
argued that a boxer takes a suspension more seriously if it is for at least 30 days. State boxing commissions should have
input from a medical advisory board composed of physicians with recognized expertise in the medical aspects of boxing
in developing guidelines for medical suspension. The medical advisory board should review the results of all
examinations or tests performed at the end of the suspension period before allowing a boxer to commence with further
boxing competition. A prohibition from further boxing during the suspension period also applies to gym sparring.
Practically speaking, enforcement of the sparring prohibition falls completely on the shoulders of the boxer and on his
trainer or manager.
Serial Screening
Although cavum septum pellucidum and cortical atrophy can be visualized on CT or MRI, the presence of an anatomic
structural abnormality does not always imply a functional abnormality ( 24,120,122,147,148 and 149). The lack of a direct
correlation makes the interpretation of serial imaging studies more difficult in boxers with a normal neurologic
examination. If the boxing community were receptive to the concept of barring from competition those individuals with
normal examinations but with abnormal CT or MRI studies, then serial screening would have a significant impact.
Unfortunately, this acceptance does not exist for serial imaging studies or for EEGs ( 150,151). Yearly screening
ophthalmologic examinations would also be quite beneficial to boxers. Subtle retinal changes predisposing to tear, or
existing peripheral asymptomatic tears, can be monitored and the boxer counseled appropriately. The practical concern
with any type of serial imagining or ophthalmological screening is not only boxer compliance, but more important,
determining who will pay for the test. Active boxers frequently cannot afford to pay and managers or promoters are not
always willing. Except for the state of New York, state boxing commissions are not funded to the level that they can
underwrite such an expense.
Acute Life Support
All professional and possibly all amateur competitions should have an ambulance in attendance at the boxing arena. The
ringside physician should make a point to speak to the paramedics before the start of the boxing competition and outline
a plan for intubation or resuscitation, if necessary. Capability to intubate on site and to transport rapidly is essential.
Evacuation Plan and Neurosurgical Support
The ringside physician should also arrange with paramedics and the local hospital for a definite evacuation plan. The
hospital to be used should be identified and informed. Proper neurosurgical support should be available, or if not, then
plans developed for transfer to the closest facility that has such support. Severe neurologic sequelae or even death
following acute boxing head injury is potentially preventable if proper actions are taken immediately.
Decrease Length of Competition
All of the world boxing sanctioning organizations have enacted a rule that decreases the length of championship bouts
from 15 to 12 rounds. This safety feature was presumably enacted in response to public outcry over the dangers of
boxing. Although there is no medical evidence supporting the efficacy of this intervention, it does make common sense.
The last three rounds of a 15-round bout tend to be grueling because both boxers experience fatigue, making them
easier to hit and to hurt. Limiting championship bouts to 12 rounds should involve less risk to the boxers because of
fewer head blows landed. This intervention obviously is germane to only a small fraction of individuals who compete as
professionals. Consideration should be given to further limiting the number of rounds for all professional bouts. This
would not be a popular innovation because both boxers and fans would probably oppose such a rule change.
National Boxing Commission
At present, there is no centralization of boxing authority in this country. Official sanctioning bodies such as the WBA,
WBC, or IBF have not been particularly helpful in leading the movement for boxing safety reform. These organizations
propagate their own existence by collecting large sanctioning fees. By virtue of their sanctioning authority, these
organizations must take responsibility for many of the inappropriate circumstances that have mired the sport of boxing
today. This author believes that national standards to ensure boxing safety should be enacted. Prefight certification,
ringside management, postfight medical suspensions, and yearly screening should be standardized throughout the
country and ideally the world. The enactment of national safety standards probably would require the institution of some
form of federally mandated national boxing commission with real power to enforce developed guidelines. If uniform safety
standards could be enacted nationwide by the existing state boxing commissions, then centralized bureaucracy could be
avoided. However, this author has reservations whether the existing state boxing commissions will ever be funded
sufficiently or can ever work in concert to ensure the type of medical safety guidelines that are necessary. Congressional
hearings have been and continue to be held to explore this issue in boxing. The lobby against mandated federal reform in
boxing is enormous and consists of a sizeable number of promoters, current world sanctioning organizations, and most
state boxing commissions. Unfortunately, the boxers themselves have little or no control over this process.
State Boxing Commissions
Most states have a state boxing commission that is empowered to supervise and administrate boxing regulations in that
state. Unfortunately, many commissions are underfunded and do not adequately monitor boxing safety. Obvious
mismatches as well as poor judging and officiating have been all too standard in boxing. Medical clearance to obtain a
boxing license is often capricious and certainly not standardized from state to state. Common rules to govern boxing,
ensure its safety, and enforce penalties for violating these rules do not exist. Some state boxing commissions are diligent
in their actions, whereas others are either negligent or even nonexistent.
Most commissions support safety in boxing but are either underfunded or uninformed. Judging by the display of boxing
competition in some states, satisfactory medical input to the commissions either is not provided, is ignored, or is simply
not enforced. Comprehensive national boxing safety reform can only be accomplished via the current state boxing
commission system by dramatically increasing their budgets. This would involve a serious reworking of finances at the
state legislative level and would likely be opposed by many groups both in and out of government. Finally, state
legislatures need to reexamine the dual roles that they have given to their state boxing commissions. At present, state
commissions have a dual role of both encouraging and expanding boxing, as well as providing for regulation of the sport
within each state jurisdiction. These two roles can, at times, be in conflict. State boxing commissions must at all times
keep boxing safety as the primary goal.
Trainers, Managers, Promoters, Referees
Enlightened understanding of the dangers inherent in boxing head blows and institution of measures to counteract these
dangers by trainers, managers, promoters, and referees are paramount to any improvement in boxing safety. Any type of
worthwhile mandated safety proposal by either a federal or state regulatory body will be for naught if the boxers' handlers
are not brought into the process. Boxing safety awareness must begin with the trainer. Boxing instruction should
emphasize tactics to avoid being hit by head blows. The willingness to take two or three blows in order to administer one
must be deterred. Trainers should ensure that sparring sessions are safe, specifically that their boxer does not take
undue head punishment, does not routinely spar with bigger men, and does not spar while under medical suspension.
Trainers should guard against routine lengthy sparring sessions in which the boxers are poorly protected and continually
absorb excessive head blows. Amateur trainers should guard against their boxers frequently sparring with professionals.
The discrepancy in talent between these two groups is considerable. Trainers should not condone the practice of
importing second-rate fighters to act as human punching bags for their charge. A trainer should actively discourage a
boxer from continuing with his career if the boxer routinely absorbs undue punishment in either the gym or in competition.
Unfortunately, despite having spent their entire adult lives in the sport of boxing, many trainers are ignorant, or worse,
are indifferent, to the medical dangers that they might potentially deter.
The boxer's manager should work closely with the trainer to ensure his boxer's personal safety. Most professional boxers
have signed 1- to 3-year managerial contracts that obligate their professional services to the manager. The manager
stands to make a profit by appropriately managing his boxer's career. He oversees arrangements to train his boxer and
determines who the opponents will be. It is incumbent on the manager not to overmatch his boxer knowingly by purposely
offering his boxer's services as a mere opponent playing the role of stepping-stone or trial horse to a younger, stronger,
more talented competitor. The manager has a moral obligation to protect the boxer and even encourage his retirement if
it is obvious that the boxer is absorbing too much punishment. Unfortunately, the best interest of the boxer and the
financial interest of the manager can frequently be contradictory.
The promoter's function is to put together and promote or sell a boxing competition. He employs a matchmaker whose job
it is to actually put the matches together. The promoter frequently has legal addendums in the boxer's contract that
dictate that a certain number of the boxer's subsequent future bouts be exclusively promoted by this promoter. Such a
contractual addendum can give a promoter complete control over a boxer's financial future. It is incumbent on the
promoter to treat the boxer fairly. He must ensure that the matchmaker has not overmatched the boxer and that the boxer
is fairly compensated for his performance. Promoters should instruct their matchmakers to refuse to use boxers who have
no chance of winning a match or are known to routinely absorb an excessive amount of head blows.
The referee has a very important role in ensuring a boxer's safety ( 152). He is in the best position to view a boxer's
condition and has the authority to terminate a match at any point. The referee must never allow a boxer to absorb
repeated, unanswered blows. The referee should stop a bout if the boxer is “out on his feet,” as manifested by the boxer's
uncoordination, imbalance, and impaired ability to defend himself. A boxer can be in a concussed state without being
knocked down. Recognition of this condition by the referee is imperative. Failure to appreciate that a boxer is out on his
feet or in a groggy state exposes him to a heightened risk of acute brain injury. If a fighter has lost the ability or will to
continue, the referee should stop the contest without regard for fan approval. A referee's primary function is to ensure a
boxer's safety. Second-guessing a referee's decision to terminate a contest is rarely helpful. The referee should request
a ringside physician's consultation whenever he is in doubt about a boxer's ability to continue. He should never disregard
a physician's recommendation to stop a contest ( 153). On the other hand, he should feel free to stop a contest even if the
ringside physician would allow the contest to continue. One additional unnecessary blow may be all that it takes to result
in serious acute brain injury. It is the responsibility of the state boxing commission to ensure that the referee is
competent. Some referees will consistently be a step behind the action or not clearly appreciate that a boxer is in trouble,
thereby exposing the boxer to unnecessary risk. Referees such as these should be retired by the state boxing
commission.
Managers, promoters, and state boxing commissions should ideally begin discussions toward establishing disability and
pension funds for injured or retired boxers. Precedent for such activities certainly exists in other major sports such as
baseball and football. Discussions on this issue will obviously be complicated and any enactment will be expensive but
certainly would demonstrate a true commitment to improving the quality of life of the professional boxer.
Gloves, Ring Posts, and Headgear
These measures are probably more important in preventing an acute injury than in preventing CTBE. Headgear can
diminish the incidence of cuts but does not decrease the incidence of acute or chronic head injury. Headgear is
mandatory in amateur competition but is never used professionally. Although some fan attraction with professional boxing
would undoubtedly decrease if head gear was used, facial lacerations from punches, butts, and elbows would decrease.
Proper padding of the ring posts and the floor mat should be ensured. Although most knockouts occur before the boxer
hits the canvas, additional coup and contrecoup forces can be generated if the boxer's head strikes the mat or ring post.
Proper padding of these structures can diminish the forces involved.
Ocular Safety Measures
The potential for vision-threatening injuries in boxing has been found to be as high as 58% in professional boxing and
32% in amateur boxing (27,30). Several very good measures have been advocated to decrease the incidence of ocular
injury in boxing (27,29,58). These measures are listed in Table 17.5. A review of this list includes the following:
TABLE 17.5. OCULAR SAFETY MEASURES IN BOXERS
1. An annual ophthalmologic examination should be performed on every amateur and professional boxer. This
examination should include measurement of visual acuity, visual fields, slit lamp examination, intraocular pressure
measurement, gonioscopy, and dilated vitreoretinal examination within indirect ophthalmoscopy. Once an
abnormality is documented, its significance must be addressed by the boxer, his manager, and the state boxing
commissions in conjunction with the treating ophthalmologist. Mandatory yearly ophthalmologic examinations
should be performed in all states.
2. A national registry to document and follow ocular injuries in amateur and professional boxers should be created.
Proper records and documentation would ensure adequate examination of injured boxers. In addition, the national
registry would be helpful in generating a database concerning the true ocular implications of boxing. The absence
of a national database makes it impossible to speak objectively about the real incidence of ocular trauma in boxing.
3. There should be the adoption by state and local licensing agencies of standard safety equipment to minimize ocular
injury. For instance, the use of thumbless gloves may well decrease the incidence of ocular injury. The State of New
York mandates that fighters in all nontitle bouts use thumbless gloves. Unfortunately, no evidence exists to prove
that thumbless gloves decrease the incidence of ocular trauma ( 57). They are used so infrequently that any impact
would be difficult to determine.
4. More education of ringside physicians in diagnosing ocular trauma is necessary. Most ringside physicians are not
qualified, nor do they posses the requisite equipment to perform an adequate ocular examination. Most attention is
paid to periorbital cuts, which are not really very serious from an ocular standpoint ( 154). Temporary visual
impairment due to periorbital bleeding that drips into the eye is easy to appreciate, whereas similar visual
impairment due to retinal injury may elude recognition. It should be the responsibility of the state boxing
commissions, working through their medical advisory boards, to educate ringside physicians properly so that ocular
injury does not go unrecognized.
5. Institution of mandatory minimal ocular requirements for state licensure is essential. The State of New York has
taken the lead in mandating that all boxers should have an uncorrected visual acuity of at least 20/200 or better in
each eye and a corrected visual acuity of 20/40 or better in each eye. The visual fields should be at least 30
degrees centrally in each eye. These minimal requirements would appear to be very reasonable. No boxer should
be allowed to compete if there is evidence of significant angle recession abnormality, lens abnormality, or
peripheral retinal or macular abnormalities. Most serious vision-threatening injuries in boxing can be successfully
treated if care is instituted early. Unfortunately, this time frame of opportunity is frequently before the boxer
experiences clinical ocular symptoms.
Mandatory temporary suspension from sparring or competition should be required for specific ocular injuries.
Controversy still surrounds the issue of continued participation in boxing following successful repair of a retinal tear
or detachment. Clearly, most boxers who have had successful retinal surgery are able to continue to box. A
decision in this regard should be made on a case-by-case basis. Ongoing ophthalmologic evaluation of these
individuals is obviously necessary to ensure that no further damage occurs once their boxing career has resumed.
6. An ophthalmologist should serve on each state and local boxing commission and medical advisory board to assist
in decision on a boxer's eligibility for licensure.
Boxer Education
An effective way to diminish undesirable medical risks inherent in boxing is to educate the boxer himself. This would
seem to be an obvious approach that is applied to all other aspects of public health but rarely, if ever, discussed in
relation to boxing. The task of educating active boxers about the risks that they subject themselves to is not easy.
Professional boxers generally come from the poorer, less educated segments of our society. They are too often unaware
of the risks inherent in their sport and commonly have inadequate personal or social support systems to help them sort
out these risks. Professional and amateur boxers in particular must be educated about the acute and chronic neurologic
and ocular sequelae of their sport. They should clearly understand the causes, prevention, natural history, and proposed
preventive measures with respect to both neurologic and ocular injury. A mature understanding of these risks by the
boxer lessens the legitimate argument that the boxer is no more than a pawn in the public's desire for entertainment.
Boxer education should be an objective of both organized medicine, world sanctioning bodies, and state boxing
commissions. Trainers, managers, and promoters should also be educated as to the medical risks inherent in the sport.
All parties involved should understand that it is likely that better boxing education will result in some professionals
choosing to end their careers voluntarily. Education of parents and their teenage children may also result in fewer young
men choosing to participate in an amateur program. Boxer eduction will also partially offset the argument that boxers are
being exploited by denying them information with which they could make informed individual choice. A national boxing
commission or unified state boxing commissions could be very helpful in disseminating this information.
PROS AND CONS OF BOXING
The risks inherent in boxing and reported interventions to decrease these risks have been outlined in this chapter.
However, any opinion concerning the overall merits or deficiencies of boxing must be made not only on medical but also
on sociologic, moral, psychological, and financial grounds ( 155,156,157,158 and 159). Feelings run deeply about the
sport of boxing from unyielding support to unyielding opposition with a determination to seek its abolition
(38,39,161,162,163,164,165 and 166). Amateur boxing has made a concerted effort to divorce itself from the professional
ranks, arguing with some justification that their sport is not associated with the same risks as the professional level and,
therefore, not deserving of the same criticism. Opponents of all types of boxing argue that even the amateur sport carries
undue risks to the brain and is, in fact, the breeding ground for the professional ranks. Cowart has stated that amateur
boxing is not an end in itself but a means to get to the professional level ( 167). Proponents of boxing argue that the sport
encourages rigorous training, discipline, resolution, alertness, courage, and endurance, and generally builds character.
In addition, boxing competition is reported to provide an orderly controlled environment in which the competitors can
release innate aggression in a more disciplined framework. Finally, boxing is lauded as one of the few avenues to escape
the ghetto for economically disadvantaged minority youths. Opponents of boxing cite its known deleterious cerebral and
ocular effects and consider it brutal, atavistic, uncivilized, and inherently discriminatory, with predominantly
disadvantaged minority youth sacrificing their health for the entertainment and financial reneumeration of the more
privileged, who control interests, and the public. Opponents go so far as to liken boxing to earlier outlawed uncivilized
activities such as gun dueling, bull fighting, cock fighting, pit bull fighting, bear bating, and feeding Christians to the lions.
Sammons eloquently sums up his opposition to boxing when he writes “most scholarly evidence indicates that boxing
success is illusory and short lived, its positive quality greatly overrated. Attracting those who are most dependent on
hope, it is, at best, a low percentage proposition, at worst a cruel hoax that discourages tried and tested means to
success and legitimates violent behavior” ( 158).
Organized medicine has clearly voiced its opposition to boxing ( 37,94,95,96 and 97,168,169,170,171,172 and 173). Table
17.6 lists the organizations that either strongly oppose boxing or have actually called for its abolition. The only medical
organizations that have publically supported boxing are the American Academy of Orthopaedic and Neurological
Surgeons, The American Association to Improve Boxing, and the American Board of Ringside Physicians. Many medical
editorials have called for a physician ban on boxing, citing rationale such as the Declaration of Tokyo, which states that
“the doctor shall not countenance, condone or participate in the practice of torture or other forms of cruel, inhumane or
degrading procedures” (174).
TABLE 17.6. ORGANIZED MEDICAL OPPOSITION TO BOXING
In summary, both amateur and professional boxing are very difficult sporting endeavors requiring significant commitments
to dedication and hard work. The participants, particularly at the professional level, expose themselves to significant
medical risk with respect to neurologic and ocular injury. The boxing establishment is attempting to reduce these risks,
but the effectiveness of these measures is not yet known. Organized medicine generally supports broad condemnation of
boxing, primarily on medical grounds, believing that any libertarian argument to the contrary is either fallacious or
provides insufficient justification to offset the inherent medical risks. As is true with most complex social issues, and
boxing is surely more than simply a medical issue, there is room for compromise. Boxing will simply not be legally
outlawed in the foreseeable future due to its inherent medical risks. By refusing to become involved in the effort to reform
boxing, medical opponents of the sport may unwittingly be shutting themselves out of the debate. In the meanwhile,
diligent medical participants will continue to enhance boxing safety. Ongoing expert care, sophisticated neurologic and
ocular monitoring, and high-quality retrospective and prospective medical studies in conjunction with the institution of
national administrative reform measures will eventually provide an indisputable database that society can use to make an
educated, unemotional decision whether it chooses to continue to support professional and amateur boxing. Ultimately, it
must be society that determines if the objectives of boxing are appropriate for our culture and what level of inherent
medical risk we are prepared to accept as an unfortunate byproduct of this sport.
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18 Competitive Diving
18
COMPETITIVE DIVING
RICHARD L. CARTER
Epidemiology
Mechanisms of Injury
Blunt Trauma
Orthopedic Injuries
Spinal Injuries
Conditioning and Treatment
Conditioning
Psychological Preparation
Treatment
Conclusions
Chapter References
Diving is one of the most aesthetically pleasing sports. It shares similar characteristics with both gymnastics and figure
skating, and thus tends to be a very popular sport in terms of viewing audience during Olympic years. Diving can be
traced back to the 17th century, when gymnasts began performing acrobatic feats over water rather than land. Therefore,
there is a significant similarity between diving and gymnastics, with the exception of the landing, which is done in water in
diving and on dry land gymnastics.
In the early 1900s, there were a minimum of platform and springboard dives that were being performed in competition.
There are approximately five times as many maneuvers that are performed on both springboard and platform today ( 1). In
addition, the difficulty of dives has significantly increased. Often people consider competitive diving to be dangerous
because of the increased difficulty of the dives being performed. On the contrary, it is still a generally safe sport. There
are relatively few injuries, and those that do occur are usually not serious; however, the sport of competitive diving does
have some inherent dangers related to rapid somersaulting and twisting maneuvers, often being done simultaneously,
which can lead to disorientation. Disorientation ultimately can lead to improper impact with the water or, in certain
circumstances, the platform or springboard itself. In addition, there is a significant force generated by the body on impact
because of the change in acceleration of the body.
Because of the complexity of maneuvers, a significant amount of stress is placed on multiple muscle groups of the body,
and these muscles need to be conditioned and exercised to promote adequate strength to mitigate against these forces.
Therefore, conditioning and coaching techniques are significant factors in the prevention of many types of injuries.
This chapter reviews the epidemiology of diving-related sports injuries, with an extensive discussion of specific
mechanisms of injury, which, in turn, leads to a section on conditioning and specific treatment mechanisms. Brief mention
is made of diagnostic modalities, because these also tend to lead naturally into the appropriate treatment options.
EPIDEMIOLOGY
Much of the published medical literature regarding springboard diving concerns recreational injuries. Within this
literature, there is a significant number of head and neck injuries, some of which have lead to death or paralysis.
However, within the competitive diving milieu, there is a significant decrease in these fatal or moribund injuries. Most of
the injuries are less serious ones involving extremities. The difference in injury patterns is related to proper coaching and
learning techniques, which lead to safer performance of complicated maneuvers.
There have been relatively few studies regarding the incidence of competitive diving injuries ( 2,3,4 and 5). These
published studies do indicate an incidence of injury ranging from approximately 90 to 100%. However, the definition of
injury is extremely broad and essentially has included any injury that prevents training for approximately 1 week. One can
easily see that such “injuries” as ear infections increase the incidence reported in the literature. Because of this broad
definition, there is a trend toward increasing numbers of injuries with increasing years of training and competition.
However, there have been no reported differences in injuries between male and female divers. The incidence of injuries
is higher for actual pool training rather than monitored dry land training and clearly is higher for platform diving than
springboard diving.
MECHANISMS OF INJURY
Mechanisms of injuries can be grouped into the following categories: blunt trauma to the head and neck, orthopedic
injuries to the joints of the upper and lower extremities, spinal injuries including myofascial strain, and other
miscellaneous injuries.
Blunt Trauma
Most blunt head injuries are associated with recreational diving. However, blunt trauma can occur in the competitive
diver. For years, divers were taught to keep their arms overhead until reaching the bottom of the pool in an armstand type
of position. However, certain landing techniques have been used by divers in order to improve the aesthetic quality of the
dive, and especially the entry. In competition, judges' scores are most significantly affected by the entry in the water and
a splashless entry is preferable. In order to accomplish this, the divers are now taught to “swim” their arms to the sides or
in front on impact with the water. This technique leaves the head unprotected as the body descends through the water. In
a deep pool, this is not a problem, but in shallow waters such as commonly present in many high school pools of older
age, the depth of the pool is such that this maneuver can predispose to blunt trauma to the neck and face.
Scalp lacerations occur relatively frequently in diving and most usually on inward or reverse type of dives, in which the
diver is leaning toward the board while spinning in that direction ( Fig. 18.1 and Fig. 18.2). These injuries are related to
flawed takeoff techniques and can be prevented only by good board work, which is developed with repetitive land drills
and many lead-up–type dives, such as perfecting a reverse double somersault before attempting a reverse 2½
somersault dive.
FIGURE 18.1. The sequence of an inward 1½ somersault platform dive from the pike position is shown. A: The diver
faces the tower with her hands over her head to initiate the inward spinning motion. The ankles are snapped backward,
while the arms and upper body begin their downward acceleration. After completing the inward revolutions, the diver
prepares for entry. B: Note the head position originates over the tower, but the force of spinning will ultimately place the
diver in a safe position.
FIGURE 18.2. The sequence for a reverse 2½ somersault platform dive in the tuck position is shown. A: The diver faces
the water and initiates reverse rotation by reaching up into the air while rotating her knees upward into her hands. B to D:
As the diver finishes the reverse somersaulting action, he tries to visualize a spot on the water, which signals him to
initiate the correct body alignment for entry.
There are only two cases of fatal head injuries that have occurred in the history of competitive diving. In both cases,
divers were performing reverse 3½ somersault in the tuck position off a platform ( 1) (Fig. 18.3).
FIGURE 18.3. An attempted reverse 3½ somersault dive is demonstrated. A: The diver begins by swinging his arms
behind his back. B: He reaches vertically and brings his knees up to his arms to continue the reverse somersaulting
motion. C: Because of an unfortunate takeoff, the diver strikes his head on the platform. D: His spinning motion is
interrupted, and the diver loses his grasp on his legs as he is projected forward in a disruption of his dive. (Courtesy of
Canapres.) This is actual camera footage of one of only two fatal diving injuries that has occurred in competitive diving.
Most blunt trauma to the head and neck affects the eyes and ears. Perforations of the tympanic membrane are usually
the result of a diver landing directly on the side of the head. This often occurs secondary to disorientation during a
twisting maneuver. A good diver can execute a forward 3½ somersault, which calls for 1260 degrees of rotation. Another
common dive is a forward 1½ somersault with three twists, in which the diver somersaults 540 degrees and twists 1080
degrees (6) (Fig. 18.4). Even more complex feats are now being performed on a routine basis.
FIGURE 18.4. Twisting dives are among the most difficult to learn because the diver is spinning in one direction while
twisting in a totally different axis. A: This diver is shown with her arms in the appropriate position to initiate the twisting
movement. B: These complex dives are practiced with the aid of a twisting belt, which is composed of an inner ring that is
fixed to the diver with a belt and an outer ring that is connected to the spotting ropes, with ball bearings separating each
ring. This allows the rotation to occur. C to E: The vectors for somersaulting and twisting are indicated. (From Frohlich C.
The physics of somersaulting and twisting. Sci Am 1980;242:156, with permission.)
Tympanic membrane perforations have occurred even with well-performed dives. This most likely is associated with rapid
pressure changes secondary to the entry into water and often can occur at greater depths such as achieved with tower
diving (7,8 and 9). Vestibular abnormalities have been reported, and it is not uncommon that the vestibular disturbance
caused by the diving technique is subsequently exacerbated by the rupture of the membrane. If hearing loss is
associated, immediate otolaryngologic evaluation is appropriate. The patient should refrain from entering the water until
there is complete healing of the tympanic membrane so as to prevent subsequent infections.
Otitis externa (swimmer's ear) is also relatively frequent. There are no known pathophysiologic factors associated with
diving per se that predispose one to this disease ( 8,10). Retained external ear canal moisture is the critical variable in
developing this disease, and the condition most often occurs in warmer climates. This condition can quite easily be
prevented with the use of drying agents, such as hydrogen peroxide or isopropyl alcohol placed externally, presuming,
again, the tympanic membrane is intact.
Blunt trauma to the eyes also has been reported. Most of the time, divers have no permanent injuries or changes in
intraocular pressure despite repeated ocular contusions. Retinal detachment can occur infrequently with blunt facial
trauma, especially on contact with the water surface (11,12).
Clearly, visual disorientation can occur with many complex spinning and twisting maneuvers. Spotting techniques such
as enhanced visual cueing on water or other objects, such as the diving board itself, can ultimately improve a diver's
orientation, giving him or her an innate sense of position in the air. As this is developed, divers are less prone to these
blunt eye traumas. The use of spotting gear, both on land and in the water, can also facilitate these spotting techniques
and ultimately diminish the incidence of blunt trauma to the eyes.
Landing flat on the water surface from a tower or 3-meter springboard has rarely been associated with chest and
pulmonary parenchymal contusions. Although the injury may appear to be horrific in nature, most divers are able to return
to practice or competition within 48 hours from the traumatic event ( 1).
Orthopedic Injuries
Upper Extremity Injuries
Shoulder Injuries
Divers frequently injure the shoulder girdle muscles, and in a recent study of United States National Team divers, 80%
were noted to have at least one shoulder injury that inhibited training for a minimum of one week ( 13). Most of these
injuries occur on entry into water, but an occasional injury can occur secondary to the handstand takeoff techniques that
are required for platform diving. These handstand dives require tremendous strength and balance, and the incidence of
shoulder problems occur when joint mobility or stability, or muscular support, are compromised. Shoulder injuries are also
associated with twisting maneuvers. The act of twisting results from throwing one arm across the chest and the other arm
behind or on top of the head. This places the shoulder in an abducted and externally rotated position. This maneuver
may cause irritation of the long head of the biceps tendon ( 1).
Most shoulder injuries and, for that matter, most diving injuries occur on entry to the water. Velocity on entrance is related
to the height of the diving apparatus and the height the diver achieved on takeoff ( 14,15 and 16). The average force on
impact for a 10-meter dive is in the range of 2.0 to 2.4 Gs. (G=9.8m/5 2). LeViet et al. (17) have documented a change in
velocity from 51 km per hour to 33 km per hour at the moment of impact.
Most divers use the entry technique called flat-handing. Just before entry, the hands are brought together with the wrists
dorsiflexed, pronated, and radially deviated. One hand is either clasped by the other or one thumb is clasped by the other
hand (Fig. 18.5). This also involves internal shoulder rotation. On breaking the surface of the water, the arms are pulled
in front or in the lateral plane in a swimming motion in order to displace the water and minimize the splash.
FIGURE 18.5. A diver demonstrating the “flat-handed” entry posture. Note his extremely well-developed shoulder
muscles, which are essential if this technique is to be used. B: The correct position for the multiple finger-clasped hand
for the flat-hand entry. C: A less satisfactory solid thumb clasp grip is demonstrated, which may be more rapidly achieved
in an emergency.
Because the forces upon entry are transmitted proximally, the shoulder absorbs a significant axial load while the humeral
head is superiorly translated. The bony stability is related to adequate scapular abduction. If the position of the shoulder
is compromised, excessive stress is placed on the supporting tissues of the glenohumeral region and can subsequently
result in instability ( 1).
The other predisposing factor to shoulder injury is the flexibility required by divers to perform their technical maneuvers.
Although an occasional single incident is associated with shoulder dislocation, most often it is repetitive microtrauma and
continued abuse of the shoulder, especially with the flat-handing technique, that ultimately affects the anterior capsule or
superior labral attachment causing a superior labrum anteroposterior lesion (SLAP), with subsequent instability. Other
injuries include humeral avulsion of glenohumeral ligaments, labral splints, and acromioclavicular arthritis ( 1).
Acromioclavicular arthritis can occur secondary to the flat-handing technique, especially. If the hand position is lost at the
time of entry into the water, the arm can be forcibly abducted and thrown behind the back, resulting in injury to the rotator
cuff. Inflammation involves the subdeltoid bursa and limits the space beneath the acromion process and, ultimately, may
cause impingement on the coracoacromial ligament ( 12). Finally, proximal triceps tears have been observed, especially
in older divers.
Instability problems are often compounded by secondary traction tendinitis of the supraspinatus, infraspinatus, teres
minor, and long head of the biceps. Articular side partial tear of the supraspinatus muscle is commonly observed
arthroscopically in unstable joints ( 1).
Frequently, divers present with symptoms consistent with recurrent anterior or anterior inferior subluxation. This problem
is related to malposition of the scapula caused by weakness of the serratus anterior, lower trapezius, and rhomboids.
These muscles should be strengthened in functional positions in order to prevent these types of injuries ( 1).
Wrist and Elbow Injuries
Both the wrist and elbow tend to be injured during the entry phase of diving. Once again, this injury involves dorsiflexion
of the wrist, and on impact, there is a force transmitted axially through the elbow into the shoulder. The elbow is locked in
extension, with isometric contraction of the triceps used to prevent flexion. Hyperextension of the elbow can cause injury
to the medial collateral ligament and subsequent instability ( 1). This often can result in a subsequent ulnar neuropathy. In
addition, failure to maintain extension can result in strains of the triceps with distal triceps injuries, occurring more
commonly in age group divers.
Injuries to the wrist occur with repetitive diving. Divers often perform approximately 100 dives per day in a typical practice
session. With the dorsiflexion that occurs at impact, there is impingement of the distal row of the carpal bones, which can
result in either periostitis or stress fractures. In addition, the wrist joint capsules and ligaments can also be injured. The
armstand technique with platform diving also is associated with wrist injuries secondary to hyperextension.
The most common cause of wrist pain in divers includes subtle carpal instability, occasional ganglion cysts, and flexor
carpi ulnaris tendinitis ( 5,17). Sprains of the ulnar collateral ligament or the basilar joint of the thumb may also occur at
impact (1). Direct trauma to the metacarpals and phalanges can occur when the hands strike the board or tower during
the mid-air maneuvers. Soft tissue contusions to the dorsum of the hand can also occur because the inadequate
development of the triceps causes loss of the extended arm position on entry, especially in younger divers. With rapid
flexion of the elbow at impact, the dorsum of the hand can come in contact with the cranial vault.
Lower-Extremity Injuries
Lower-extremity injuries are mostly relatively minor. These injuries usually involve contusions, lacerations, and
occasional fractures of the metatarsals and phalanges related to direct contact with the board or tower. In addition,
lacerations and contusions of the tibial region can occur. Most of the injuries of the lower extremity are secondary to the
takeoff or jumping phases. Patellofemoral symptoms are caused by patellar or quadriceps tendinitis with maltracking of
the patella. The takeoff also has been associated with posterior tibial and Achilles tendinitis, in addition to tendinitis of
the foot and ankle. Ankle and foot sprains and an occasional fracture of the fifth metatarsal can occur if the foot lands
during the approach in an awkward position ( 1). Foot and ankle injuries occur more frequently in dives done in the pike
position because the legs and feet are more exposed ( 18). Osteochondritis may be a growth center problem encountered
occasionally at the knee and, rarely, at the elbow. This is usually secondary to overuse in young divers ( 12). Lesions in
the elbow can occur in children when they go through a significant growth spurt, and especially when performing
maneuvers on a 10-meter platform. It is often best to keep divers off the tower during a rapid growth phase.
Most of the aforementioned injuries can be prevented by learning good board takeoff techniques and also entry
techniques. This can be accomplished only with repetitive simple diving maneuvers done in land drills. Also, one must
begin by performing simple maneuvers and mastering them before proceeding to more complex maneuvers. Other aids,
such as wearing protective tape or splints, especially of the wrists, can often restrict the dorsiflexion stresses, especially
in tower divers (5,11,17).
Spinal Injuries
The most common type of injury sustained by any athlete, but especially divers, is musculoskeletal. The term myofascial
strain syndrome is given to this class of injuries. This injury most frequently occurs during the beginning portion of a
season and is often associated with the paraspinal musculature of the neck and low back. They usually do not proceed to
cause significant neurologic sequelae and are often treated conservatively.
Hyperextension Injuries
On entering the water, especially with back and reverse dives, divers can also improve the entry by “saving the dive.”
This involves continuing the arc of rotation under water. This causes significant hyperextension of the back with
hyperflexion of the shoulder musculature. These hyperextension types of injuries can cause posterior segment pathology
such as at the facet joints and the pars interarticularis ( 1). Superimposed rotational maneuvers with hyperextension also
can exacerbate this condition. Spondylolysis and spondylolisthesis, in addition to facet arthropathy, has been observed
in divers but with less frequency than in gymnasts ( 19,20 and 21). The incidence of spondylosis is higher in platform
divers compared with springboard divers, which is related to the increased stress that occurs from impact of the body
secondary to greater height.
In 1980, Garick and Requa noted that up to one third of gymnastic injuries involved the lumbar spine, and one of the
more common causes was traumatic spondylolysis. The pain associated with this injury is usually dull and aching or
cramping, and persistent. It tends to be mechanical in nature and exacerbated by motion, especially hyperextension, and
occasionally rotation. The pain may initially occur unilaterally. Continued stress to the area can subsequently cause
subluxation and a true spondylolisthesis ( 22) (Fig. 18.6).
FIGURE 18.6. These x-ray studies and myelograms are of a 16-year-old diver with multiple, recurrent episodes of severe
back pain. Conservative treatment failed this patient, who was subsequently referred for neurosurgical consultation. The
patient did suffer some tenderness to palpation over the spinous processes but otherwise had a normal neurologic
examination with the exception of subtle left L-5 nerve root dysfunction. He had a positive straight leg raise maneuver at
30 degrees on the left side only. A: A grade I dislocation (spondylolisthesis) of the L-5 vertebral body on S-1 is exhibited;
the arrowhead designates the break in the pars interarticularis. B: The oblique view accentuates the congenital defect in
the L-5 pars interarticularis (arrowhead). This is an example of the classic broken neck of the scottie dog. C: This lateral
view of the myelogram demonstrates the degree of space between the Pantopaque column in the posterior margin of the
vertebral bodies in which a true herniated disc or a pseudoherniated disc may be hidden.
Hyperextension injury tends to be secondary to repetitive microtrauma, and many of the injuries are recurrent in nature.
Flexion Injuries
The anterior segments (the anterior two thirds of the vertebral body and intervertebral disc) are particularly vulnerable to
compressive forces in divers. The increased load on the spine is secondary to diving from rigid surfaces, the use of
trampolines, and also on impact with the water, especially from greater heights. This increased disc loading occurs
during the press phase on takeoff and at entry, especially in flexion type of dives, such as in the pike position ( 1). The
combination of a flexed or rotated spine during maximum loading is most likely the source of disc injury ( 23) (Fig. 18.7).
There is more anterior stress placed on the lumbar spine in springboard compared with platform competition. This is
related to the upward directed force of the springboard during the press phase of the takeoff. In tower dives, much of the
actual stress is absorbed by flexion of the hips and knees ( 24).
FIGURE 18.7. These x-ray studies and myelograms are of a 20-year-old collegiate diver with a long history of chronic low
back pain who suffered acute injury while performing on a trampoline. He subsequently developed a classic
radiculopathy of the right S-1 nerve root. Conservative treatment failed this patient, who was unable to continue with
workouts. He subsequently underwent a decompressive laminectomy and discectomy at L-5 to S-1. The neurosurgeon
who performed this procedure remarked that this was the second largest disc herniation he had seen in performing over
1,000 operations. A: The anteroposterior view of the x-ray film exhibits a defect in the left articular facet (arrowhead). B:
The oblique view shows the defect more readily (arrowhead). C: The lateral view of the lumbar spine x-ray study
revealed an unsuspected compression fracture of the T-12 vertebral body (arrowhead). This most likely is the source of
the patient's chronic back pain.
Diving-related injuries to the cervical spine occur most often in recreational divers. These injuries are the result of
improper or informal training; poor pool facilities, such as shallow depth; inadequate supervision; and occasional
substance abuse. There have been no reported cases of cervical fractures in the competitive diver ( 1), although cervical
hyperflexion injuries have occurred. With extreme flexion of the cervical spine, there can be compression of the anterior
portion of the spinal cord, especially if there is an isolated segmental spondylotic bar. This problem can be compounded
if congenital cervical stenosis is identified. However, the segmental stenosis is probably more significant than diffuse
global stenosis ( Fig. 18.8).
FIGURE 18.8. These images reproduce the alignment of a 26-year-old diver who suffered pain, paresthesias, and
radicular symptoms in the bilateral C-6 distribution when she entered the water with her neck flexed. She suffered
tenderness of the C5–6 interspinal ligament. The approximate body alignment on entry is illustrated with the arms
posterior to the head and the cervical spine in a flexed position. B: In contrast, this is the appropriate body alignment.
The head is in neutral position, thus protected bilaterally by the arms, which mitigate against the degree of neck trauma.
Hyperflexion is also prevented because true axial loading type forces only are encountered in this alignment.
This rapid flexion across an anterior bar can subsequently produce radicular symptoms and occasional early symptoms
of central cord dysfunction. Any posterior ligamentous laxity of the cervical spine with superimposition of a spondylotic
bar in a congenital canal would also increase the risk of significant cervical damage.
Hyperflexion cervical injuries can be diminished with the use of proper entry techniques. This can be learned with the use
of multiple line-ups. A line-up is essentially nothing more than practicing the final portion of a dive. The diver can stand at
the end of the platform or board and essentially fall forward, bringing the arms overhead into the entry position. In this
way, concentration on the entry alone can be performed without worrying about the intricacies of a complex maneuver. In
addition, strengthening of the paracervical musculature is extremely beneficial.
Although cervical injuries can occur, the spine is indeed protected by the hands and arms at entry. This, however, is
probably not adequate enough to prevent significant stress on the cervical spine in diving from greater heights ( 25). In
1966, Scheider et al. studied the chronic trauma to the cervical spine experienced by divers in Acapulco, Mexico.
Permission was obtained from one of the divers to examine six athletes and to procure subsequently cervical spine x-ray
studies. These divers all had been diving from the 100- or 130-foot perches for many years. The statistics for these
divers are shown in Table 18.1. The site of the perches from which the divers take off is shown in Figure 18.9A. Divers
must project themselves 27 feet outward from the cliff on their dive and then land in 15 to 18 feet of water, depending on
the tide. Aside from an occasional cervical myofascial strain, none of the divers had any significant physical disability and
all were neurologically normal. The lateral cervical spine x-ray studies of the selected six divers are shown in Figure
18.9B, Figure 18.9C, Figure 18.9D, Figure 18.9E, Figure 18.9F and Figure 18.9G. These x-ray studies show significant
spondylotic changes and, in case C, a small compression fracture was also identified. Interestingly enough, two divers (B
and D) showed well-preserved cervical spine architecture. Cases B, C, and D had very similar architecture of the spine.
In cases E through G, at least two vertebral bodies were well fused anteriorly. The divers associated with x-ray studies B,
C, and D entered the water with their hands locked, as illustrated in Fig. 18.9H. Divers whose x-ray studies are illustrated
in E, F, and G did not use this clasping technique. These divers subsequently developed significant axial load to the
cervical spine, not diminished by the arms and hands. Therefore, it is postulated that the newer technique of flat-handing
does presumably help prevent cervical spondylosis to the degree shown in the above-mentioned studies.
TABLE 18.1. STATISTICAL DATA ON MEXICAN DIVERS STUDIED FOR CERVICAL SPINE ABNORMALITIES
FIGURE 18.9. The Quebrada is shown with the 100- and 130-foot perches on the right cliff from which the divers perform.
The diver (circled) is shown at a height two thirds of the way down from the diving platform. B to D: The lateral cervical
spine x-ray studies of these three divers generally exhibit preservation of the intervertebral spaces, a normal-sized spinal
canal, minor degenerative changes exhibited by spurring, and normal vertebral body height, with the exception of C, who
has minimal anterior vertebral body compression. E to G: The x-ray studies of the vertebral bodies of these cervical
vertebrae show a spontaneous fusion anteriorly (white arrows), but again, there was preservation of the intervertebral
bodies and the width of these spinal canals (black arrows). H: The correct method of high diving from these cliffs is to
clasp the hands together. The divers whose spines are shown in B to D used this technique satisfactorily. The divers
whose spine x-ray studies are shown in E to G dove “improperly,” with their hands wide apart, as shown in I, “punching a
whole in the water” and sustaining a blow directly to the head. (Courtesy of RC Schneider, M Paop, and R Alverez.)
Sprains and strains of the thoracic region are relatively common and are associated with twisting and arching during
flight. These tend to be relatively minor and are usually treated conservatively.
CONDITIONING AND TREATMENT
Conditioning
Conditioning for any athlete, including divers, is exceedingly important. Many injuries can be prevented with appropriate
preseason conditioning. In a study of 66 divers conducted in 1981, a total of 89% suffered from low back pain, which is
usually an isolated event, but which sometimes becomes a chronic complaint. Subsequent to this study, a comprehensive
program of exercises was developed ( 26). If a program is to be effective, it must be carried out during the off season as
well. These regimens must stress posture as well as flexibility training.
A vigorous workout often includes performing up to 100 dives during a typical session. Although less dives are performed
when doing platform training, one must still, however, repetitively climb 33 feet into the air after each dive. This involves a
significant aerobic challenge to the body, and therefore, preseason conditioning should involve a degree of aerobic
conditioning. Walking or preferably jogging is an aerobic method that also helps prevent low-back injuries, and is often
prescribed as a course of therapy for those with chronic back pain.
Flexibility also is stressed because of the need to maintain supple joints in order to perform the intricate maneuvers
associated with diving. Because most injuries that occur are relatively minor and are musculoskeletal in nature, these can
be prevented with appropriate flexibility training. In a study by Rosomoff, flexibility and stretching exercises were the only
significant regimen that had a positive impact in the prevention of chronic back pain ( 27). Stretching should be done in a
more static nature, such as flexing gently at the hips to touch one's toes. The stretch should be held for approximately 60
seconds while avoiding the severe, sharp, shooting type pains. Rapid acceleration-deceleration stretching is not an
acceptable form of preconditioning and often in and of itself can lead to injury. Major muscle groups such as hamstrings,
quadriceps, gastrocnemius and soleus muscles, pelvic girdle muscles, and shoulder girdle muscles must be stretched to
maximize their flexibility and the function of their respective joints ( Fig.18.10).
FIGURE 18.10. Push-ups are most the common exercise for conditioning the chest, arms, and shoulder musculature.
Exercises for the pelvic girdle are also appropriate, especially for maintaining appropriate postural alignment during
mid-air maneuvers. Typical Kegel-type maneuvers can be performed in addition to abdominal crunches. It cannot be
stressed enough that the abdominal musculature is probably the most important group of muscles that can diminish the
incidence of low back pain ( Fig. 18.11). Typical preconditioning should involve stressing certain muscular groups on an
every-other-day basis. This will allow the stressed muscles to recover on the off day.
FIGURE 18.11. A sit-up routine or abdominal crunch routine is demonstrated. The hands are placed on the shoulders
and the knees in the bent position. These exercises are effective in strengthening the abdominal muscles.
Weights can be beneficial, but essentially small weights with higher repetitions are most beneficial. This increases the
tone of the muscle without causing significant increase in bulk with subsequent decrease in flexibility. As stated earlier,
shoulder girdle strength is important, especially in the functional position, such that the arms are maintained overhead.
Specific exercise machines, such as the MedX, often can help with isolation and strengthening of low back muscles.
Psychological Preparation
The psychological makeup of athletes is beginning to be addressed more frequently. This is crucial in the diver,
especially in the early phase of learning. A good coach must understand that each diver is an individual, which therefore
will necessitate slightly different coaching strategies. It is imperative that the basics of the diving be taught before
pushing a diver to attempt more complicated maneuvers. As the basics are mastered, this ultimately leads to increased
confidence and subsequently the ability to perform the more technical maneuvers with less difficulty. In addition, pushing
a diver to perform a more difficult maneuver when he or she is psychologically not ready often will predispose the diver to
subsequent fear and trauma. This can lead to literal psychological paralysis and inability to perform under certain
circumstances.
Treatment
Prevention
Most treatment really begins with a discussion on prevention. Prevention of injuries with respect to diving can be divided
into five broad categories: primary physical examination, the aforementioned conditioning exercises, midair diving
techniques, training techniques, and in addition, psychological preparation, as discussed earlier.
Primary physical examination is imperative on at least a yearly basis. If there is a history of repetitive trauma and chronic
joint or spinal pain, an evaluation by a specialist such as an orthopedic surgeon or neurosurgeon may be advised.
Midair Diving Techniques
Midair diving techniques are important in terms of preventing illnesses. Land-based posture exercises such as the Kegel
exercises can help in terms of diminishing the amount of hyperextension that can occur in the spine. This not only can
help prevent serious posterior column spinal injuries, but also diminishes the abnormal forces that can be exerted to the
body with improper alignment at entry.
It is also imperative that divers are taught to spot or use visual cues to diminish disorientation. Many young divers are
considered to be “blind” divers because they close their eyes during maneuvers ( 28). As any well-conditioned gymnast,
diver, or figure skater can demonstrate, spotting techniques diminish disorientation. Visual orientation can be developed
only by performing a dive hundreds of times. Ultimately, cerebellar training occurs, and essentially, a complex maneuver
can be performed without thought. The use of spotting techniques can easily be taught with land-based techniques, such
as spotting gear. The diver must attempt to focus on certain spotting areas, such as the diving board, with
backward-rotating or inward-rotating dives, and the water with reverse or forward-rotating dives.
Training Aids
The most crucial training aid is the coach. There has been a significant improvement in coaching techniques. Their
experience on a first-hand basis has led to improved handling of their athletes.
The coach also must adhere to a strict set of rules. With appropriate supervision and rules prohibiting double bouncing
and preventing multiple divers being on the board at one time, many recreational-type accidents can be prevented. Basic
skills need to be taught at lower levels first, such as on the 1-meter board before proceeding to the 3-meter board and
learning skills on the 1-meter tower before proceeding to the 5- or 10-meter tower.
The use of spotting rigs with trampolines, Port-A-Pit diving boards, and poolside diving boards ( Fig. 18.12) has also been
an important advance. The trampoline has been used for years for training purposes, especially with gymnasts and also
with divers (Fig. 18.12A). Spotting equipment is extremely valuable in terms of developing a confidence in performing
complicated maneuvers but also in terms of cerebellar training and visual orientation techniques. The spotting gear not
only helps the diver but the coach as well. It is easier for the coach to decide when it is appropriate for the diver to
perform these maneuvers at the pool when they have adequately mastered them with the use of spotting gear.
FIGURE 18.12. Use of a poolside trampoline is demonstrated in conjunction with the spotting rig. This diver is supported
in midair while performing a backward 1½ somersault in the layout position. B: The diving coach is used as a
counterweight to support the diver while she performs on the Port-A-Pit diving board apparatus. As the diver lands, the
diving coach will be elevated 8 to 10 feet in the air. C: The most recent application of the spotting rig over water allows
this diver to practice an inward spinning dive without fear of hitting the board.
A more effective training technique is the use of land-mounted diving boards with a Port-A-Pit and subsequent spotting
rigs. The Port-A-Pit is quite similar to the landing gear that pole vaulters or high-jumpers use ( Fig. 18.12B). This gives the
diver an opportunity to learn the dive in the exact manner as one would do at the poolside. However, because there is no
need to enter the water and subsequently return to the board, a dive can be performed multiple times in rapid sequence,
which aids in learning. In addition, a very rigorous workout performing multiple dives can be accomplished in a relatively
short period of time before fatigue can set in. One of the fears a diver must ultimately overcome is that of hitting the
board. Because one can perform the maneuver on a land-based diving board, this fear subsequently can be abolished.
Spotting rigs use both somersaulting and twisting belts. The twisting maneuvers are best learned with the trampoline-type
spotting device (see Fig. 18.4).
The spotting apparatus can also be used in the pool over a 1-meter springboard (see Fig. 18.3C). This is the most
accurate way that a diver can experience the sensation of a new dive with minimization of injury. This device, however, is
not commonly available.
Visual cues are also aided with the use of bubble machines or spraying devices that break up the surface homogeneity of
the water in order to help the diver recognize this visual cue ( Fig. 18.13). Certain bubble machines cause significant
aeration and ultimately cushion the diver on impact. This minimizes the soft tissue injuries of blunt trauma and also helps
the diver conquer fear as these injuries tend to be minimized.
FIGURE 18.13. The amount of bubbles generated by the bubble machine in the area of distribution as shown here (see
text for details).
Other aids that can be used are water polo helmets with ear protectors when learning twisting dives, and Neoprene
wetsuits can also be worn when attempting more complex maneuvers. These aids tend to cushion the blunt trauma
associated with improper landing. Taping of wrists can also help in the prevention of wrist injuries secondary to
dorsiflexion stress.
Medical Treatment
The medical treatment required in most diving-related injuries is usually simple. Most soft tissue trauma is treated
symptomatically with antiinflammatory medications and occasional modality-type physical therapy, such as acute icing of
soft tissue injuries. In general, exercises such as flexibility training also can be administered to treat myofascial injuries.
Lacerations tend to be clean injuries because of the antiseptic properties of chlorinated water. However, the tetanus
status of divers should be ascertained if a diving board or tower platform is struck.
Treatment of other blunt trauma such as tympanic membrane ruptures should begin with the minimization of
contamination of the middle ear structures. Clearly, if the diver is disoriented or has vestibular disturbances, he or she
should not return to practice. Exercises can be performed to minimize positional vertigo if a concussion has been
sustained.
Significant head trauma should be assessed as with any major trauma protocol. The ABCs of physical examination need
to be addressed, and any significant head trauma involving concussions requires immediate neurosurgical evaluation.
Underlying skull fractures are associated with a high incidence of intraparenchymal injury and must be considered in a
patient with loss of consciousness. With the easy availability of computed tomography (CT) scanning, noncontrast CT of
the brain should be taken in patients with significant loss of consciousness. If a patient were to develop a postconcussive
syndrome, return to activity should not occur until complete neurologic recovery has been documented.
Most orthopedic joint injuries can be prevented by teaching appropriate techniques. However, if trauma does occur,
consider treatment with antiinflammatory medications and splinting or bracing as appropriate. If pain persists, then the
exacerbating activity should cease and ultimately an orthopedic consultation is advised. It is imperative that appropriate
diagnosis be made such that subsequent treatment be administered appropriate to the diagnosis.
Myofascial symptoms of the spine tend to be self-limiting and often occur at the initial portion of any training period.
Prolonged complaints of low-back pain, however, should be investigated, because chronic low-back pain, especially in
younger people, is relatively rare. Initial evaluation should include a lumbar spine and potentially cervical spine series.
This must include anteroposterior (AP), lateral, and oblique views, especially when evaluating for pars interarticularis
defects. Presuming no underlying significant pathology is identified on plain x-ray studies, a course of physical therapy
should be instituted (29). It is most appropriate to institute the therapy within a very short time frame between injury and
treatment in order to maximize its effect. Modalities tend to be relatively ineffective with the exception of icing techniques.
If x-ray evaluation reveals an underlying congenital defect, such as congenital spondylolysis or stenosis, these conditions
need to be addressed at that time. Most significant in the cervical spine is segmental spondylosis, because this has a
higher incidence of subsequent spinal cord trauma. Diffuse congenital stenosis is rarely associated with any significant
cervical injuries.
If an orthopedic or neurosurgical evaluation ultimately elicits a classic neurologic entrapment syndrome, further
diagnostic workup is appropriate. At present, magnetic resonance imaging (MRI) is the procedure of choice if one
suspects significant intradiscal or nerve root pathology. Preferably, closed-unit, 1.5-Tesla MRIs should be used for spinal
imaging (Fig. 18.14). If this is not available, or if the MRI quality is less than ideal or does not adequately confirm a
clinical impression, then there is a role for spinal myelography with postmyelographic CT scanning.
FIGURE 18.14. The imaging modality of choice for patients with chronic back or radicular symptoms in who at least 6
weeks of conservative treatment has failed would be the MRI. MRIs, of course, would be performed earlier in the time
course if there was an emergent indication such as bowel or bladder impairment or footdrop (cauda equina syndromes).
These images are T2-weighted MRI scans of a herniated disc. At L-5 to S-1, fast-spin echo sagittal (A) and axial (B)
images demonstrate a large herniated disc (white arrows), the fat–dural interface (large black arrow), compression and
posterior displacement of the thecal sac, and compression of the right nerve root compared with the left (small black
arrows).
Ultimately, the treating physician needs to decide when the injured athlete should return to the sport. Most injuries are
minor and little delay is needed before returning to this activity. However, as alluded to earlier, 90% to 100% of divers
miss at least 1 week of training during their career because of injury.
If significant spinal pathology is identified and there is a significant entrapment syndrome, 80% of these patients will
ultimately respond with conservative treatment within 6 weeks. Presuming symptoms persist and the patient fails
treatment of physical therapy, steroids and potentially epidural steroids, then ultimately, surgery is an option. Newer
techniques include microscopic discectomy and, more recently, minimally invasive microendoscopic discectomy. The
more minimally invasive procedures ultimately should allow the athlete to return to the activity, but roughly 6 weeks of
time should be used for postoperative convalescence. Stretching exercises should begin roughly 2 weeks after surgery in
order to facilitate return to the diving activity. If cervical decompressive procedures are performed, the most common
procedure is that of an anterior cervical discectomy and fusion. Posterior decompressions are also appropriate but are
associated with a higher incidence of chronic neck pain because of denervation of the paraspinal musculature. If an
anterior procedure is performed, adequate bony healing must occur if a fusion is performed. With the advent of newer
plating techniques, the fusion rate has now approached 98% for single level disease and ultimately would not necessarily
preclude a diver from returning to the sport. However, a minimum of 2 months of convalescence would be needed and,
until adequate fusion is demonstrated, divers should not return to the sport. Flexion-extension cervical x-ray studies often
do not show any significant motion but do not necessarily guarantee that arthrodesis has been achieved. Sometimes,
thin-section CT is needed to assess for fusion.
However, if the patient has an underlying segmental spondylotic bar and were to suffer a significant cord injury, diving
should cease in this circumstance and, more likely than not, should not be resumed.
Most concussions tend to be very minor and are not necessarily associated with the classic postconcussive syndrome.
However, if this syndrome does occur, then the patient should not return to the sport until all vertiginous symptoms have
abated. If one concussion occurs, there is a high incidence of subsequent concussions.
Although the sport is relatively free from any significant injury, one must also consider the chronic, long-term effects of
repeated stress. As in any athlete, especially football players, one sees a significant amount of chronic injuries after the
athlete leaves the sport. This is also true with divers. Overuse syndromes ultimately tend to heal themselves because
most divers usually leave the sport and proceed to other avocations. However, there is a relatively high incidence of
degenerative disc disease that can occur in these athletes. Newer techniques, including provocative discography, have
been somewhat controversial but more recently have been more accepted in terms of diagnosing true degenerative disc
disease with or without associated spondylolisthesis. Newer techniques of laparoscopic or open anterior lumbar
discectomy and fusion have led to some preliminarily promising results. There is a very high fusion rate, and often the
patient can be spared a posterior procedure if the disease is isolated to one segment. Ultimately, this can spare the
denervation of the paraspinal musculature and may mitigate against a permanent condition of chronic back pain.
CONCLUSIONS
Diving is a relatively safe sport on the competitive level. Most injuries are those of recreational divers. With a good
preseason conditioning program and adequate coaching, most injuries can be prevented. Coaches need to learn the
most recent diving techniques and also must learn to listen to their divers and learn their specific nuances. Persistent
reports of pain should prompt a coach to refer athletes for further evaluation. This can be done with an athletic trainer, if
available, but ultimately with a physician, if symptoms persist.
If a diver suffers an injury, it is imperative that appropriate healing time be afforded. Coaches must also recognize when a
diver is trying to hide an injury.
Preseason physical examinations are important and often should include a screening series of spinal x-ray studies if
indicated. Recognition of the common mechanisms of injury and ultimately focusing on preventative techniques should
continue to make diving a pleasurable and relatively safe sport.
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19 Cricket
19
CRICKET
THOMAS CRISP
JOHN B. KING
ANSWORTH A. ALLEN
Bowling
Fielding
Foot and Ankle
Lower Leg
Knee
Hip and Thigh
Back
Shoulder
Elbow and Arm
Wrist and Hand
Face and Head
Chest and Trunk
Conclusions
Chapter References
For the most part, cricket is an outdoor team game, with 11 players on a side and with some similarities to baseball. The
International Cricket Conference was unable to provide numbers for worldwide participation, but the Sports Council in
1986 made available some numbers for the United Kingdom. In 1983, 0.5% of the U.K. population—about 650,000
adults—played cricket once a month in the course of the summer, although this number does not distinguish between
formal and informal games, and school games were not included. Thus cricket is the 10th most popular outdoor sport in
the United Kingdom, although it may be diminishing in popularity, because it was equal to angling in 1965, which is now
the number one sport. On a worldwide basis, there appears to be increasing interest, especially in North America; even
Holland now has a national team.
A cricket team contains some specialist bowlers (usually four), some specialist batsmen (usually five), one or two “all
rounders,” and a specialist wicket keeper, who stands behind the stumps. Each member of the team must bat, but only
the specialist bowlers and all-rounders bowl. Because it is not a contact sport, there is a relatively low incidence of injury,
but certain aspects of the game carry specific morbidity.
Although one side bats with two batsmen in play at any one time, all of the players of the other side field. A player from
the fielding side bowls the ball overarm six times, attempting to hit a set of three 28-inch-high stumps that are topped with
two horizontal rods called bails, which are 22 yards away (the pitch). The batsman protects these stumps with a
4-inch-wide bat. At the same time the batsman tries to hit the ball to a part of the field without fielders and then run to the
opposite end of the pitch (changing places with the other batsman), scoring a run. At the end of six balls, play switches to
the other end of the symmetric pitch and another bowler delivers six balls. The batsman may be out when the ball hits his
or her stumps or when, without first hitting the bat, the ball hits the batsman's leg, which is in front of the stumps, but
would have hit the stumps if it had not been stopped (leg before wicket). The batsman is also out if the ball is caught by a
fielder before it bounces or if the ball arrives at the stumps from a fielder before the batsman makes his or her ground
when attempting a run (run out). The batsman may continue to run until the ball has been returned to one or other end,
although if the ball is hit outside the field of play, it counts four (or, if the ball did not bounce, six) runs.
The ball weighs approximately 5.5 ounces and is propelled at speeds of up to 90 mph. It is circumscribed by a line of
stitches called the seam, and this area can be made to bite on the ground as the ball pitches, causing deviation in height
and or direction. The ball can be a major source of injury if it hits the batsman, and at the top level, where bowling speeds
are highest, considerable protection is worn on the head and trunk, along with the mandatory pads on the lower legs and
the “box,” which protects the genital area ( Fig. 19.1). Because the game is played outdoors and almost invariably on a
grass pitch and because the ball is made to bounce before reaching the batsman, variations in bounce and trajectory are
inevitable. It is not, however, approved of to project the ball at the batsman's body full pitch without it bouncing first (the
beamer). Sometimes a bowler will bowl the ball (the bouncer) such that it bounces up toward the head and trunk of the
batsman, who may fend the ball off, perhaps into the hands of a fielder; this certainly may frighten the batsman, even if it
does not cause injury. Repeated use of the bouncer amounts, therefore, to intimidation. Although this is outlawed by the
rules, the two umpires do not always enforce this, and the side with the fastest bowlers may use this technique to soften
up the batsman, who is then more intent on his or her own safety than in scoring runs. The batsman may bat for
prolonged periods and may have to attempt many rapid 22-yard sprints to gain runs during the course of a long inning. In
first-class cricket, it is not unusual in a game that takes place over 3 to 5 days for only one or two batsmen to bat for all
three 2-hour sessions held in 1 day.
FIGURE 19.1. A The dressed batsman. B: The batsman's protective gear. Note the helmet with visor, chest protector,
forearm guard, gloves, box or genital protector, thigh pads (a larger one is on the leading leg), and the pads protecting
the lower legs.
BOWLING
The method of propelling the ball—bowling—hinges on the rule that the elbow must be fully extended at the moment of
release of the ball, and thus throwing is not allowed. The standard method of bowling fast involves a run-up of up to 30
yards, as if throwing the javelin, and in the stride before delivery, the bowler arches the back into extension, fully rotating
(to the right in a right-handed bowler). In the next step—delivery—the bowler strides rapidly while flexing and rotating the
back to the other side (Fig. 19.2). Not surprisingly, this is associated with a high injury rate, especially of the facet joints
of the lumbar spine. The straight elbow makes injury in this area rare, but shoulder problems, for example, rotator cuff
strains and impingement, are common. Because a lot of the bowling speed is generated by the trunk, shoulder injuries
are much more commonly caused by throwing the ball while fielding. Thus players may participate in the game and bowl
freely even though they are unable to throw.
FIGURE 19.2. The bowling positions from the front during coaching. A: The front foot is still to be planted. B: The
delivery is beginning; note the side on stance in this phase. C: The elbow still has to be straightened for the release of
the ball, but note the progress to the face on stance. D: The ball is released, the trunk has swiveled through nearly 180
degrees, and the back has gone from extension to flexion. The positions more extreme during a real throw.
The bowling technique is further complicated by the need to vary the trajectory of the ball. The better bowlers land the
ball on its seam, which tends to make the ball deviate as it bounces. Some bowlers also have the ability to make the ball
swing in flight as do baseball pitchers. Certain variations in arm and trunk action tend to help the ball to swing either left
or right, making hitting the ball more difficult for the batsman but putting more pressure on the bowler's body. There also
are slow bowlers who apply spin to the ball, which may then deviate on bouncing. These bowlers may get wear-and-tear
injuries to the spinning finger.
FIELDING
For the fielder, prolonged periods of relative inactivity may be followed by a sudden sprint to field the ball, which carries a
risk of muscle strains. The shoulder may be cold and unstretched before the fielder makes a rapid throw of up to 80
yards. Some fielders are placed very close to the batsman so they can attempt to catch the ball. Unfortunately, these
fielders are sometimes hit by the ball, thus they may wear a helmet, shin pads, and a box as do batsmen. This protective
gear may provide a false sense of security, causing the fielder to move closer to the batsman than is safe.
A ball that is not stopped by the batsman and does not hit the stumps is collected by the wicket keeper, who stands
behind the stumps. The wicket keeper wears gloves that are similar to a baseball mitt; they are worn on both hands. The
wicket keeper also wears pads on the lower legs to protect him or her from the ball. This is a specialist position that
requires special skills, fitness, and more prolonged concentration than most other fielding positions. The considerable
impact of catching a ball may be repeated 200 times or more in a day, which causes much trauma to the wicket keeper's
hands. Fractures of the fingers are not uncommon. In addition to taking these balls, the wicket keeper is the most likely
person to catch out the batsman when the ball just touches the edge of the bat and is lightly deflected. The agility needed
to catch a ball moving an unpredictable direction and changing height at 90 mph is extraordinary. Knees may be
damaged from prolonged squatting, and recently, a wicket keeper lost the sight in one eye after he was struck by a flying
ball. Although it is common practice for cricketers to be less physically fit than many other athletes, they are subject to
great strains over a long period. The top-class professionals may play cricket every day for 30 or more days without a
break. Thus, it may be that the present trend to greater fitness and conditioning in the national teams may reduce injury
rates. In recent years, a lot of 1-day cricket has been played. The advantage for the spectators is that they see the final
score after 6 to 8 hours of play. However, 1-day play makes swift fielding and the rapid running of single runs more
important, which has caused an increase in fielding injuries in particular, for example when fielders throw themselves
after the ball to stop it from crossing the boundary of the field of play.
The amateur game is less injury prone than the professional game. However, the game is played well into middle age,
and stress on older muscles and tendons can be excessive. The bowling tends to be slower and less dangerous, but the
skill and timing of the batsman may be poorer, and sometimes injury occurs.
FOOT AND ANKLE
There may be a great deal of running, and cricketers, especially bowlers, can suffer the same foot and ankle injuries as
any other runners, including stress fractures of the metatarsals and sesamoids, as well as sesamoiditis. Appropriate
footwear is important, and it may be necessary to wear different cricket boots for batting and fielding. Furthermore, the
condition of the playing surfaces may vary from dry and hard one day to damp and slippery the next. Bowlers may suffer
from chronic bruising of the big toe and its nail caused by pressure from the shoe; some bowlers even cut a hole in the
toe of their shoes to reduce the pressure, although it would seem more logical to wear shoes that fit properly in the first
place. In addition there may be chronic bruising of the heel from the repeated trauma of heel plant in the leading foot
during the delivery stride.
It is common for a bowler to bowl 20 six-ball overs in a day, which results in 120 impacts. On occasion, this practice can
cause a chronic bursa within the heel pad, which responds slowly to rest and physical therapy, and occasionally requires
corticosteroid injection and even surgical excision. Early treatment is easier and involves a good heel pad, but sometimes
the problem is only relieved by a molded heel cup made to fit the bowling shoe. The help of the coach may be needed
because anything that changes the feel of the impact may interfere with the balance in the delivery stride, causing loss of
the essential line and length of the ball.
The toes are at risk while batting from a ball that is delivered fast and to the area of the feet (a yorker). These are difficult
balls to play, and they often hit the toes. Despite the protective gear elsewhere on the body, it is common to wear light
batting shoes to aid quick running. This results in a high rate of major bruising and fractures; these light shoes often have
no protective caps.
The grip of the soles is important, and small studs or spikes, similar to those on golf shoes, are usual for fielding,
although for batting it is common to wear shoes with a molded ribbed sole to give greater mobility.
Ankle strains may occur in fielding, and lateral ligament strains are the most common. It is unusual to tape cricketers'
ankles, and in view of the prolonged play, this may be ineffective anyway. Bowlers with slight weakness of the ankle
ligaments may have to wear a support on the ankle, such as an inflatable ankle stirrup. Bowlers are particularly
vulnerable because of the rotational and lateral strain to the ankle in the delivery stride. However, most ankle strains
respond to physical therapy that has an emphasis on proprioception through wobble board exercises and increasing
strength in the peroneal muscles. As in other sports, taping should not be used as a means of getting the player back to
competition before he or she has fully recovered.
Fielders rarely do enough running to produce Achilles tendon injuries, but fast bowlers do get tendonitis as well as
bursitis around the Achilles. Usually, there is no obvious initiating injury. Instead, there is a gradual onset of pain in the
heel, which at first is ignored and often disappears after warming up. However, the pain increases in severity and
eventually restricts activity. It is not uncommon for stiffness in the morning to be a prominent symptom in severe cases. It
is important to distinguish peritendonitis from tendonitis when the tendon itself is inflamed, which may be the result of a
partial tear. The peridtendonitis usually responds to physical therapy, such as ultrasound and laser, and injections of
corticosteroid next to—not into—the tendon. Tendonitis responds more slowly, if at all, and steroid injection carries a risk
of rupture of the tendon. In resistant cases, the tendon should be examined with diagnostic ultrasound or computerized
tomography (CT) scans. It is important to remember that gout is a possible cause of resistant tendonitis in the age group
of recreational cricketers.
Partial rupture and cystic degeneration, for the most part, require surgery in the form of excision of the paratenon,
longitudinal incision into the degenerate area, and removal of obvious cysts. Small tears do not require repair, but large
ones do. The ankle need not be immobilized, but dorsiflexion should be restricted with a dorsal splint if a repair has been
performed. In rehabilitation, it is essential to limit the proportion of the work cycle that is eccentric.
Bursitis is easily detected on examination, and the deep bursa responds well to steroid injection into the area deep to the
tendon immediately above the calcaneum. The superficial bursa can cause great problems from contact with the back of
the shoe and needs careful treatment (which may benefit from changing the footwear). It may respond to steroid injection,
but there is a danger of skin atrophy if the injection is made too superficially; therefore, this measure should be reserved
for failure of physical therapy, and a small volume of hydrocortisone acetate is used rather than anything more potent.
In the older age group of cricketers, Achilles rupture is common when the players are running in the field, running
between the wickets, or in batting. This happens because the back foot must remain on the ground ( Fig. 19.3). Although
calf muscle strain can occur in all of these maneuvers, complete rupture of the tendon should always be suspected, even
in the absence of an obvious gap in the tendon. A calf squeeze test that looks for a small amount of plantar flexion on
squeezing the bulk of the muscle should be performed.
FIGURE 19.3. The forward defensive stroke, with the weight, head, and bat forward but the back foot locked behind the
crease, so if the ball is missed, the player cannot be stumped.
LOWER LEG
Biomechanical abnormalities of the foot such as excessive pronation can lead to lower leg problems in bowlers and
runners. Compartment syndromes, periostitis, and tibial stress fractures are well documented. Stress fracture should
always be suspected when the player presents with increasing pain on exercise and tenderness at the junction of the
upper and middle thirds of the tibia. Because usual changes found on x-ray study are late, a bone scan should be
performed to confirm the diagnosis. These fractures are more common in the leg impacting on the ground in the delivery
stride. Rest is essential, but if there is an underlying biomechanical foot problem it can be corrected as in other sports by
orthotics. Compartment syndromes and periostitis—often referred to by the players as shin splints—also usually respond
to orthotics. Technique, in particular the position of the front foot on impact, has a large effect on the stress imposed. The
coach must be involved in resistant cases. Keeping the toes of the leading leg pointing forward and not outward helps
keep the body side on the target, which is associated with a lower injury rate to the back than when the body is more
open (front on). However, this means that there is likely to be rotation of the foot after impact as the body follows through.
The bowler must immediately swing off the playing areas (the line between the two sets of stumps), causing torsional
stress to the lower leg.
KNEE
In young bowlers, there is a risk of both Osgood-Schlatter disease and anterior knee pain, arising from the patellofemoral
joint. Reducing the level of activity is often enough to cure the pain. The wicket keeper squats for long periods behind the
stumps and is at risk for both anterior knee pain and patellar tendon problems. Care is necessary to distinguish these
entities. Patellofemoral pain often responds to rehabilitation of the vastus medialis obliquus muscle by terminal knee
extension exercises, except in cases for which symptoms have started in a congenitally bipartite patella. In these cases,
surgery is essential if the player is to continue as a wicket keeper. Patellar tendonitis is commonly gradual in its onset,
although careful questioning may be necessary to elicit the prodromal history predating an apparently acute episode. If
the well-localized pain in the tendon does not resolve with 6 weeks of reduction in activity and nonsteroidal
antiinflammatory drugs (NSAIDs), the tendon must be investigated with ultrasound, CT, or magnetic resonance imaging
(MRI) scanning. Small lesions within the tendon substance close to the bone attachment usually respond to steroid
injection. After such an injection, it is important to avoid stressing the tendon for 1 week afterward to avoid any risk of
further damage to the tendon. Large lesions, especially those near the middle of the tendon, respond only to surgery.
The paratenon must be excised; if not, there will be a secondary peritendinitis. The tendon is palpated, and the pealike
lesions can be easily felt. The fibers are split at that point, and the macroscopically diseased tissue is removed. Because
the removed tissue was not functional, rehabilitation can start with skin healing. Full flexion should be regained by 6
weeks, and further return to sport depends on the speed of recovery of muscle strength. Initial return should be to a
fielding position some distance from the bat, as the close fielders adopt the alert, bent-knee stance during the bowler's
run up.
Twisting injuries causing meniscal and ligament damage occur around the knee from fielding, when a player turns to
chase the ball and when a batsman turns at the end of a run to return for a second run. These are not common. On level
ground and with no contact, it is rare to damage the cruciate ligaments, but occasionally when diving to stop the ball from
crossing the boundary, severe damage is done to the knee. The increasing level of fitness and muscle power of the
players may protect the joints from this kind of damage. More common is wear and tear to the articular cartilage of the
knee in bowlers, especially in the front leg at delivery when the knee is braced and the leg acts as a pivot for the trunk.
This can produce disabling pain, which may be difficult to distinguish from the attritional-type tear of the slightly
degenerate meniscus. A technetium bone scan will show a well-localized increase in activity, and for most players, this is
the end of the bowling career because the recovery from high tibial osteotomy is so variable that surgery is usually
declined, even if it is offered.
HIP AND THIGH
The muscles of the upper leg can be strained from fielding or batting, although this problem can be avoided to a great
extent by well-conditioned muscles, a good warmup, and stretching. Unfortunately, the batsman may wait for a long time
(perhaps hours) before he or she is called to the center to participate, and he or she then must be able to sprint 22 yards
immediately. Clearly, this makes a full warmup impossible, especially when the necessary psychological preparation is
included. Not only do batsmen have to run but they may have to stretch their hamstrings suddenly as they put one foot
right out in front of themselves to get to the pitch of the ball, while the back foot is locked behind the crease. Even the
fielder may find it difficult to remain warm and flexible during long periods of play when the ball does not come near him
or her.
Much more common than these intrinsic injuries are hematomas caused by contact with the ball. The shins of the
batsman are protected by pads, but even with a thigh pad on the side of the thigh most likely to be hit by the ball, there
are large unprotected areas. The most skilful bowlers bowl the ball such that it lands on the seam and can deviate
unpredictably, making it difficult for the batsman to make contact with the bat. Furthermore, as with the baseball pitch, the
ball may swing in flight and find the body or leg rather than the bat. With immediate ice compression and elevation, such
injuries resolve quickly, but if, as is commonly the case, the batsman continues to bat for long afterward, all that can be
done at the time is application of analgesic spray, and definitive treatment is delayed.
Adductor strains, traumatic osteitis pubis, stress fractures of the pubis rami, and groin strain with damage to the conjoint
tendon occur rather rarely in cricketers. A first-class bowler has recently been injured and has become handicapped with
avascular necrosis of the femoral head.
BACK
Because cricket at an amateur level is played into or past middle age, there are many overweight cricket players who
undergo little or no conditioning. These players are likely to suffer back strains. In these relatively minor injuries, physical
therapy such as massage, pulsed microwave, and other forms of heating, along with manipulation are usually effective,
and the batsman may be able to play with a corset or lumbar support, which will reduce mobility only slightly. Emphasis
also should be placed on back and abdominal muscle strengthening in rehabilitation, and the role of weight loss in the
obese should not be forgotten.
Back problems are common, particularly in bowlers ( 2). As described earlier, the technique of bowling is stressful. It has
evolved as the best way of projecting the ball at speed and with the control necessary to test the batsman. Unfortunately,
even with a perfect action, there is the risk of damage to the lumbar spine, in particular from this combination of slight
hyperextension then flexion and rotation at speed. The most common injury is to the short ligaments around the facet
joints. This presents as stiffness, which may start suddenly and reduce movements in all directions Once the acute
episode is past, the bowler may be left with the common symptoms of stiffness that follows immobility, eases with gentle
exercise, and is exacerbated by violent exercise. There is little or no referral of the pain down the leg beyond the
buttocks. Examination reveals reduced extension and side flexion and, in particular, reduction in range and pain on
performing extension and side flexion together. There is tenderness around the area of the facet joint about 2 inches
lateral to the middle on deep palpation.
The acute episode should be treated with physiotherapy aimed at reducing the muscle spasm and increasing movement.
Gentle manipulation may be of use at this stage. In the chronic situation, manipulation and other physical therapy should
be supported by back and abdominal muscle strengthening exercises designed to give a full range of movement and full
muscle power.
Attention to technique is important because recent studies have indicated an increase in incidence of back problems in
bowlers who bowl square on, that is, with the thorax facing the batsman rather than side on, or with the leading shoulder
pointing toward the target. Different bowlers use their back more or less than others, who may get more speed from
shoulder rotation and thus experience fewer back problems. Input from the coach in the rehabilitation phase may be
useful, and prevention requires good education at an early stage.
More severe problems may be caused by spondylolysis in which there is a stress fracture of the pars interarticularis. This
injury is relatively common in fast bowlers. Foster et al. ( 2) showed that 11% of 82 high-performance young male fast
bowlers developed a defect in the year of study. The symptoms are similar to those of a facet joint strain, but this problem
should always be considered. The diagnosis is traditionally made by oblique views of the lumbar spine, which show the
obvious break across the neck of the “Scotty dog.” In these athletes, such views may be inadequate and CT scanning
with reversed gantry angle must be performed. If a bone scan shows considerable bone activity, the patient should be
immobilized and supported. If there is any significant forward slip of the vertebral body or spondylolisthesis and if the
symptoms persist, surgery may be indicated. Bone scanning is not useful in assessing healing, and repeated CT scans
must be performed. Old injuries with no hot spot on a bone scan can be treated like a facet joint strain and are the result
of either a congenital defect in the pars or an earlier ununited stress fracture. Rehabilitation is the same as for facet joint
strain and includes back and abdominal muscle strengthening exercises.
SHOULDER
The most commonly injured joint in cricket is the shoulder, and most injuries occur during throwing. Unfortunately, in
coaching little or no emphasis is placed on injury prevention in this area by encouraging strong rotator cuff muscles. In
the rehabilitation phase following injury even more attention must be given to strengthening and fine-tuning the rotator
cuff muscles, because premature strengthening of the prime movers, for example, the deltoid, the trapezius, and the
pectoralis, may exacerbate the problem. Impingement problems are common.
In cricket a fielder may have to throw the ball up to 80 yards accurately and fast to prevent runs being taken by the
batsman. If he or she is not warmed up or if the throw is disordered, there is a risk of injuring one of the rotator cuff
muscles, usually the supraspinatus ( 4). The ball drops short and the fielder experiences severe pain in the shoulder,
which will recur when he or she throws again. The shoulder must be rested with the addition of NSAIDs. If this is done
promptly, no more than 3 weeks should be lost from the sport. The player may be able to bowl, because this action
involves much lower rotational velocities and, consequently, less strain on the rotators. However, the team must accept
that he or she is “hidden” in the field and so is not called on to throw.
In a severe injury in the acute phase, there may be restriction of all movements on examination, but after 1 or 2 days, the
pain is principally on abduction, causing a painful arc. If the damage to supraspinatus is severe, initiation of abduction
may be lost. Incomplete tears can be differentiated from complete rupture of the tendon by the injection of local
anesthetic into the subacromial space; the pain of a partial tear or severe tendonitis will be obliterated and the
supraspinatus will function normally, whereas no change will be noted if there is a complete tear. There is usually enough
damage in these shoulders for abduction to be lost with a complete supraspinatus tear. Strain of the other rotators can be
differentiated by detecting pain on resisted external rotation (infraspinatus) and internal rotation (subscapularis); the
supraspinatus will cause pain on resisting abduction from the neutral position.
The treatment for complete tears is surgical repair. For incomplete tears and tendonitis, treatment involves stopping the
aggravating exercise (throwing) and physical therapy. As already noted, the rotator cuff must be strengthened before the
major muscle groups, and the player should be discouraged from returning to full activity until the recovery is complete.
Chronic cases may be complicated by subacromial space impingement. This condition may respond to rest,
strengthening of the rotators, or injection of corticosteroid into the subacromial space. If there is no response to these
measures, examination, including arthroscopy, if needed, should be performed to rule out instability (which may be
multidirectional) in the shoulder joint, which can occasionally present as a chronic thrower's shoulder. Decompression of
the subacromial space and excision of the coracoacromial ligament will buy time, but full throwing strength rarely returns.
ELBOW AND ARM
Injuries to the elbow are not common in cricket, although occasional throwing injuries are seen. There may be traction
tears to the flexor mechanism (golfer's elbow) from the acceleration phase of the throw or compression to the lateral
aspect of the elbow. More common is a direct blow to the forearm from the cricket balls, which may cause fracture of the
radius or ulna. These fractures usually occur in the leading arm, and players often wear a forearm guard on the lower
part of this arm to at least soften the blow. The injuries arise when the bounce of the ball is irregular and the ball rises
higher than expected, hitting the arm above the bat.
WRIST AND HAND
The wrist may be damaged when a player falls on the ground while diving to field the ball. The pressures on the wicket
keepers' hands, which suffer repeated microtrauma, acute contusions, and occasionally fractures (particularly when the
hard ball is not taken cleanly in the middle of the hand) were already discussed. In the past, wicket keepers apparently
were known to put a slice of steak inside their gloves to soften the impact of the ball. These days, gloves are made to
withstand the blows, but the 200 to 300 catches made in a day may lead to chronic soft tissue thickening. The gloves
need to be flexible for the ball to be taken cleanly and, therefore, must transmit some of the force of the impact. The
gloves have webs between the fingers to aid catching as well as to reduce the force separating two fingers if the ball is
caught there.
Fielders often stand next to the wicket keeper or in close catching positions to catch any ball that deviates off the edge of
the bat. These balls are traveling fast and can cause significant damage. If taken on the end of the finger, the most
common injury is a mallet deformity, with or without a segment of bone. Many players choose to do nothing more than
tape the finger or fingers, because the more conventional immobilization of the terminal joint interferes with batting.
Intraarticular fractures of the interphalangeal joints and even the base of the proximal phalanges are usually treated by
so-called buddy taping and early mobilization. Blows to the side of the digits cause ruptures of the collateral ligaments or
dislocations. These are again treated by taping and movement.
Balls that wedge between two fingers may cause severe web space lacerations, requiring suture and significant time out
of the game. It is important that full mobility is regained as soon as possible after such injuries, because all players may
be called on to bat and full-finger function is necessary for proper batting. Bellipia and Barton ( 5) claim that the fractures
of the base of the proximal phalanx are the most likely to be stiff. The authors' experience is more in concordance with
that of Sadlier and Horne ( 6), who report some degree of stiffness or deformity in most of these intraarticular fractures.
The best prophylaxis for this is practice, to ensure a good hand-eye coordination, and using in these positions only
fielders whose reflexes are sufficiently quick.
Batsmen's fingers are at risk from the “lifting” delivery that bounces higher than expected and catches the handle of the
bat. Sometimes these balls trap a finger against the bat. Although batting gloves give good protection most of the time,
fractures do occur at the top level of play. Several manufacturers are addressing this problem, but it is difficult to protect
the fingers fully without interfering with the grip on the bat. Because of the need to grip the bat, and despite the risk of
accelerating possible degenerative changes, it is sometimes necessary to inject the joints that remain stiff after bone
healing with a small volume of corticosteroid to reduce inflammation and increase mobility. Exercises to increase range of
movement and strengthen intrinsic muscles help in the rehabilitation process. A number of cricket grounds regularly
provide a hot wax bath to ease the pain and swelling of such chronically injured fingers.
FACE AND HEAD
The bouncer, mentioned earlier, may not cause the batsman to be bowled out, but it is difficult to score from and may
cause bodily harm. At the lower levels of cricket, few bowlers bowl fast enough to make the ball bounce sufficiently high
to cause damage; thus this is a problem largely restricted to the professional game. The hook shot necessary to hit the
ball aimed at the face involves playing across the trajectory of the ball ( Fig. 19.4), and there is thus a higher than usual
chance of missing. If the batsman's technique is not good enough, he or she is likely to miss the ball completely or to
cause the ball to deviate slightly; both result in a hit to the face or body. To avoid such risks, most batsmen wear a helmet
and many have a visor of some kind to protect the face, temples, and skull. Despite these measures, head injuries still
happen and range from fractures of the nose, facial bones, and teeth to lacerations on the face and ears. Hill et al. ( 7)
suggest that injuries to the face and teeth occur most frequently in rugby, followed by soccer and then cricket in the
United Kingdom. Recent changes in the rules restrict the number of bouncers that can be bowled at each batsman and
have made the game a little safer.
FIGURE 19.4. The hook shot to a fast ball at face level. If the ball is missed, the consequences are obvious.
The eye is remarkably vulnerable when the size of the ball is compared with that of a squash ball. Aburn ( 8) reports that
30% of all sports injuries to the eye were from cricket; this was, however, indoor cricket, in which the level of protection
may be different from that of the outdoor sport. Jones and Tullo ( 9) describe five serious injuries, including retinal
detachment and rupture of the globe, mainly brought about by the rising ball already mentioned. The data do not allow
one to estimate the overall incidence of such injuries, but it seems as if they have become less frequent with the
improved head protection.
Also at risk from head injuries are the close in fielders, but in professional cricket the short-leg fielder, who stands within
about 8 feet of the batsman who usually wears a helmet similar to the batter's.
CHEST AND TRUNK
The chest and trunk are at risk from impact from the ball, and the area is often protected by padding at the top level of
play. A few serious incidents have been reported of a blow on the chest stopping the heart. Fortunately, such
occurrences are rare, but they mean that good medical care should be available immediately on site. More common is
severe bruising of the ribs with restriction of the full breathing excursion, and it may be necessary to inject the area with
long-acting local anesthetic to allow the player to continue the next session.
CONCLUSIONS
The game of cricket is not associated with a high level of injury, but certain aspects carry risk. Cricketers are not always
in peak condition, and a greater emphasis on physical fitness would reduce some injuries. In other areas, protective
equipment is essential and is still being developed to protect batsmen in particular. Correct technique is important and
can reduce injury rates; thus coaching can produce cricketers who are not at unnecessary risk. Finally, application of the
laws, especially about intimidation, is essential to minimize risks.
CHAPTER REFERENCES
1.Goodbody J. The (London) Times.

2.Hardcastle P. Lumbar pain in fast bowlers. Aust Fam Physician 1991;20:946–951.
3.Foster D, John D, Elliott B, et al. Back injuries to fast bowlers in cricket: a prospective study. Br J Sports Med 1989;23:150–154.
4.Crisp T. Cricket: fast bowlers back and throwers shoulder. Practitioner 1989;148:560–561.
5.Belliappa PP, Barton NJ. Hand injuries in cricketers. J Hand Surg [Br] 1991;16:212–214.
6.Sadlier LG, Horne G. Indoor cricket finger injuries. N Z Med J 1990;103:3–5.
7.Hill CM, Crosher RF, Mason DA. Dental and facial injuries following sports accidents: a study of 130 patients. Br J Oral Maxillofac Surg
1985;23:268–274.
8. Aburn N. Eye injuries in indoor cricket at Wellington Hospital: a survey Jan 87 through June 89. N Z Med J 1990;103:454–456.
9. Jones NP, Tullo AB. Severe eye injuries in cricket. Br J Sports Med 1986;20:178–179.
20 Dance
20
DANCE
DAVID A. STONE
RUTH KAMENSKI
JULIA (CHUAN-HSIU LIU) SHAW
KATHLEEN M. J. NACHAZEL
STEPHEN F. CONTI
FREDDIE H. FU
Dance Positions
Dance Movements
Occupational Factors
Training Errors
Poor Preseason Conditioning
Inadequate Warmup
Intensity and Duration of Training
Technique Errors
Development of Muscle Imbalances
Lack of Training Specificity
Compensatory Techniques
Anatomic Factors
Somatotype
Femoral Torsion
Genu Recurvatum
Tibial Torsion
Ankle Joint
Biomechanical Factors
Hallux Rigidus
Pes Planus and Cavus
Environmental Factors
The Dancer's Shoe
Dietary and Nutritional Factors
Psychological Factors
Common Injuries and Treatment
Upper Extremities
Spine
Hip
Knee
Tendinitis
Lower Leg
Foot and Ankle
Tendon Disease and Tendon Rupture
Rehabilitation
Chapter References
In recent years, dance medicine has come into the medical limelight. Attention has been directed toward dance in
response to an increased injury rate among both professionals and students. The dancer, like the athlete, has high levels
of physical demands related to movement and impact (1). In addition, types of injuries sustained and measures employed
to treat such injuries are similar to those associated with other athletic activities. Nonetheless, important differences exist
between athletes and dancers. The most obvious is that in dance, aesthetic content and its transmission transcends the
athletic aspect of the activity ( 1). Flexibility, strength, endurance, control, balance, and coordination are essential
requirements for expertise in dance. Performance must appear effortless. Because of such demands, to appear graceful
and beautiful while performing, the classical dancer forces his or her extremities into awkward anatomic positions, which
are potentially injurious ( 2). Professional dancers must, therefore, be cognizant of the fine line between maximizing
versus exceeding their physical limitations. On the one hand, dancers must push to their physical limits to maximize the
range and variety of movement available for expression. Yet, on the other hand, dancers must constantly strive to protect
themselves against the consequences of stressing their bodies beyond the designed physical limits, thus risking injuries
that can interrupt or threaten a career ( 3).
In an attempt to optimize care, it is imperative that the health care provider familiarize himself or herself with factors that
may predispose this population to injury. Recognition and prevention are the keys to a successful rehabilitation and
career longevity.
DANCE POSITIONS
Five basic foot positions exist in classical ballet. All movements begin, pass through, or end in one of the five positions.
One essential requirement for achieving these positions is external rotation (ER), or turnout, of the lower extremity. The
five foot positions are as follows ( Fig. 20.1) (4):
FIGURE 20.1. A: First position. B: Second position. C: Third position. D: Fourth position, anterior view. E: Fourth
position, lateral view. F: Fifth position.
First position: Heels are touching, and legs are ER so that the feet form a straight line from the toes of the right foot to the
toes of the left foot. Both knees are straight.
Second position: Heels are approximately 12 inches apart, with the weight evenly distributed over both feet; legs and feet
are ER, as in first position; and both knees are straight.
Third position: Both legs are ER from the hips, the heel of the right foot is placed in front of the arch of the left foot, the
feet are touching, weight is evenly distributed over both feet, and both knees are straight.
Fourth position: Both legs are ER from the hips; the feet are approximately 12 inches apart, with the right foot opposite
the left and directly in front of it (i.e., the heel of the right foot is in front of the toes of the left); both knees are straight;
and weight is evenly distributed over both feet.
Fifth position: Both legs are ER from the hip, the heel of the right foot is in front of the great toe of the left foot, the feet
are touching at all points, both knees are straight, and weight is evenly distributed over both feet.
DANCE MOVEMENTS
Plié involves a simple bending movement of the knees while bearing weight and maintaining ER of the lower extremities.
Pliés are done in all five positions. There are two types of pliés, demi pliés and grande pliés. Demi pliés involve a slow
partial lowering of the body through a knee bend, keeping the heels on the floor ( Fig. 20.2). Grande pliés, or full pliés, are
performed in a similar manner, except the bend is deeper and the body is lowered to the floor. The heels are kept on the
floor as long as possible while the body is being lowered ( Fig. 20.3) (5,6).
FIGURE 20.2. Demi plié in second position.
FIGURE 20.3. Grand plié in fifth position.

Pointe is another common term. Like plié, pointe can be either demi or full. Demi pointe is when a dancer is dancing on
the balls of his or her feet ( Fig. 20.4). Full pointe, often simply referred to as pointe, is reserved for female dancers only
and requires the use of a specially designed shoe with a toe box ( Fig. 20.5). Pointe involves dancing on the extreme tips
of the phalanges (5,6). The maneuver from which the dancer moves from a flat foot position to a demi pointe or a pointe
position is referred to as releve ( 5,6).
FIGURE 20.4. Demi pointe requires approximately 90 to 100 degrees of dorsiflexion at first metatarsophalangeal joint.
FIGURE 20.5. Full pointe.
Arabesque is a maneuver in which the dancer stands balanced on one leg (the supporting leg) while the other leg (the
working leg) is extended behind the body, parallel to the floor ( Fig. 20.6). The torso is arched forward, and the arms are
extended (6). Pirouettes are complete turns of the body while the dancer balances on one foot ( 6). Pirouettes can be
singular or multiple and may rotate either clockwise or counterclockwise relative to the supporting leg ( 5,6). A battement
is a beating movement of the working leg, usually against the supporting leg. Petite battements are small beating
movements of the foot against the ankle of the supporting leg. Grand battements involve lifting the entire leg into the air
from the hip (6). A jump from one foot to the other when the weight of the body is transferred from the starting foot to the
landing foot is known as a jetté (Fig. 20.7) (5).
FIGURE 20.6. Arabesque at the barre.

FIGURE 20.7. Grand jeté. Photograph by Susan Cook; courtesy of the Pittsburgh Ballet Theatere.
A ballet barre is a railing fastened to a studio wall at a height of approximately 3.5 feet to provide hand support for the
preliminary exercises of the class. The sequence of exercises that begins every ballet class are referred to as barre
exercises (5).
Aesthetically, each dancer strives to achieve an acceptable line. Line is the aesthetic conformation or projected image
created by the shape and portion of the dancer's body as well as the positioning of the head, shoulders, arms, torso, and
legs (6).
Several aspects factor into the etiology of ballet injuries. Often, more than one of these factors is responsible for injuries
sustained by the dancer. Commonly, these injuries are not acute but are chronic in nature, developing subtly over a
period of time. Occupational, training, technique, anatomic, biomechanical, environmental, nutritional, and psychological
factors are among those that contribute to many dance-related injuries.
OCCUPATIONAL FACTORS
The dance profession is a highly competitive yet private one. Dancers are constantly driven by self-imposed demands or
those of teachers, staff, colleagues, and the audience (including the critics) to exceed previous standards. In light of this
drive, dancers often push to or beyond the point of injury. Dealing with injury may be no small task. Many factors
complicate a dancer's response to injury. Medical services are not often readily available, worker compensation may
pose restrictions on the amount of time or money available for rehabilitation, and performances or castings for upcoming
performances often affect injury management. It is often difficult to slow down goal-oriented, motivated people to prevent
further insult or injury. All of these factors may cause the dancer to return prematurely to dance without adequate
rehabilitation, which inevitably contributes to the development of chronic injury ( 7).
TRAINING ERRORS
Poor Preseason Conditioning
Dancers are faced with the dilemma of allowing adequate time for healing and rest following the completion of a season
and return to dance for conditioning before the beginning of a new season. Should the dancer not condition during the off
season, he or she may begin the season in less than optimal physical condition. In such instances, the dancer may be
predisposed to overuse injuries as a result of long and demanding rehearsal schedules. If they are ignored, these injuries
may plague the dancer throughout the season. Off-season conditioning may reduce the chance of injury, enhance
physical performance, increase muscle endurance and strength, and increase joint range of motion.
Inadequate Warmup
In a recent dance survey conducted by Bowling (8), 14% of those surveyed attributed their injuries to insufficient warmup.
Many dancers use class as an opportunity to maintain or adjust technique but do not prepare beforehand. Light exercise
and gentle stretching before class is encouraged. A second concern lies in the difficulty in keeping warm. Some dancers
may not rehearse immediately following class as a result of casting and scheduling of rehearsals. On the other hand,
some dancers may, in fact, rehearse immediately following class but are active only periodically and then only for short
spurts. This problem also arises during performances. Dancers are encouraged to remain active, stretch frequently, and
to clothe properly in an attempt to keep warm. The use of off-stage portable heaters may be helpful during
preperformance warmup, rehearsals, and performances to reduce risk of injury.
Intensity and Duration of Training
A normal day of dance for most professionals consists of approximately a 1.5-hour class before rehearsal. Rehearsals
may run from 4 to 6 hours per day in preparation for upcoming performances. If a dancer is not well conditioned, this
strenuous schedule may result in overuse injuries early in the season. Recovery time during the season may be hindered
by contract obligations, dancing roles, or the fear of losing a dancing role. Ideally, dancers should condition during the
off-season, and at the onset of a new season, rehearsal schedules should build gradually to a full day. Unfortunately, the
ideal is usually not the norm.
TECHNIQUE ERRORS
Development of Muscle Imbalances
Good ballet training should develop muscles of the lower extremities symmetrically. However, in some instances,
excessive training or faulty technique, or both, may result in muscle imbalances, especially about the trunk and
extremities. Downey et al. (9) conducted a preseason screen of company members of the Pittsburgh Ballet Theatre (18
women, 13 men) to identify trends in flexibility, strength, and posture. Results indicated that dancers had reduced
flexibility in the gastrocnemius-soleus and rectus femoris muscles, as well as the tensor fascia latae and the iliotibial
band. Strength deficits were noted in the lower abdominals (primarily in women) and the middle and lower trapezius (both
groups). Hamilton et al. (10) performed isokinetic testing as well as range-of-motion measurements on 28 members of
two different ballet companies (14 men and 14 women) and found the men had imbalances in adductor and abductor
muscles, weakness in the quadriceps and hamstrings, and increased strength in the ankle dorsiflexors and plantarflexors
when compared with controls. Women did not demonstrate quadriceps weakness but were otherwise similar in their test
results. The marked reversal of hip abduction and adduction ratios was believed to be the result of time spent of one leg,
resulting in increased isometric strengthening.
Lack of Training Specificity
Often ballet companies will incorporate modern pieces into their repertoire in addition to performing the classic full-length
ballets such as Swan Lake and The Nutcracker. Dancers who do not routinely train in modern technique may find they
suffer from uncommon aches and injuries associated with the new movement patterns that they must now perform.
Injuries sustained during these rehearsals are often short lived, and the symptoms subside with the cessation of
rehearsals or once the body has adapted to the new movement patterns.
Compensatory Techniques
Although most professional dance instructors have a good understanding of technique, they are often unaware of an
individual dancer's physical limitations. Therefore, the dancer will try to compensate to appear to execute maneuvers with
good technique. Compensation often precipitates faulty technique, which, in turn, precipitates injury.
Ideal turnout involves 90 degrees of ER at each hip ( 7). Although this is ideal, it is rarely, if ever, the norm. Nonetheless,
many dancers can achieve adequate turnout for the basic ballet positions. Turnout involves 55 to 70 degrees of ER at the
hip, approximately 10 degrees of ER at the knee, up to 12 degrees of tibial torsion, and abduction of the forefoot at the
midtarsal joint (7). The need for those who lack adequate turnout to compensate can manifest in a variety of ways.
Increasing the lumbar lordosis will, in effect, decrease the tension on the iliofemoral ligament, allowing for increased ER
at the hip (Fig. 20.8). This, unfortunately, increases stresses in the lumbar spine, predisposing the dancer to stress
fractures or possible spondylolisthesis ( 7,12,13,14 and 15).
FIGURE 20.8. Increased lumbar spine lordosis to compensate for inadequate turnout at the hip.
Another method of compensation is known as “screwing the knees,” which is accomplished by assuming a demi plié
position, placing the feet at a 180-degree angle at the floor and from there, straightening the knees ( 2,14). Such a
maneuver creates a great deal of torque on the knees, producing strain on medial structures that may result in
ligamentous injuries, patellofemoral pain, or possible lateral patellar subluxation ( 2,14).
Rolling in, or pronation of the foot, is another compensatory technique. Rolling in involves eversion of the hindfoot with
forced pronation of the midfoot and forefoot ( 16). The consequence of rolling in is excessive strain on the medial
structures of the foot ( 10,16,17 and 18). Inadequate length in the Achilles tendon can exacerbate this problem ( 12).
Dancers with inadequate length will roll in, thus decreasing tension in the tendon, allowing for increased dorsiflexion at
the ankle joint. Although such a maneuver may result in a deeper plié, it can often lead to an array of problems involving
the medial structures of the foot and the great toe ( Fig. 20.9) (19,20).
FIGURE 20.9. Rolling is often associated with inadequate length in the Achilles tendon and can lead to an array of
problems involving the medial structures of the foot.
Sickling is another faulty maneuver that occurs in demi pointe or full pointe positions and involves either excessive
abduction of the forefoot with valgus at the heel (sickling out) ( Fig. 20.10) or excessive forefoot adduction with the heel in
varus (sickling in) ( Fig. 20.11). Sickling may be a result of careless technique, muscular weakness (especially in the
peroneal muscle group), and poor balance ( 17). Some dancers may sickle out as a method of achieving greater turnout
of the extremity. Others may sickle in, placing increased stresses on the lateral ligaments. Consequences of sickling out
may involve ailments of the medial structures of the foot, whereas sickling in may result in lateral ankle sprains ( 19,21).
FIGURE 20.10. Sickling out is a faulty maneuver involving forefoot abduction with calcaneal valgus.
FIGURE 20.11. Lateral view of sickling in, which is a faulty maneuver involving forefoot adduction with calcaneal varus.
Certainly other faulty techniques occur that result in inefficient movement patterns and subsequent injury. The ones
noted here are simply a few of those commonly seen. The clinician must, therefore, always question technique as a
possible causative factor when dealing with the etiology of injury.
ANATOMIC FACTORS
In the general dance population, anatomic factors are more likely to contribute to dance injuries. However, as training
continues, inability to perform adequately without obvious aesthetic variation or painful struggle is almost always a cause
of attrition. This allows for natural selection of those more anatomically suitable and likely to succeed as professional
dancers. Once a dancer reaches the professional level, anatomic factors may still contribute to injury; however, they may
be more subtle and supplementary to other factors such as technique ( 7).
Somatotype
There may be variation from company to company; however, it appears the current aesthetically ideal body projects sleek
lines formed by a long neck and long limbs, a slightly short torso, and a small head ( 2,12). Likewise, dancers with minimal
body fat are preferred. Because of this, the percentage of fat to body weight in female dancers tends to be below the
tenth percentile of the normal population. ( 22).
Femoral Torsion
Femoral torsion determines the intrinsic amount of external (femoral retroversion) and internal (femoral anteversion)
rotation at the hip. A dancer with femoral retroversion may achieve turnout more easily because this permits ER. Dancers
between the ages of 6 and 11 can influence bone modeling to enhance turnout through static stretching into ER or
positioning of ER during dance ( 22,23). However, after age 11, the femoral neck can no longer be altered by the molding
process of continual pressure. Therefore, after this age, subsequent development and maintenance of turnout is
achieved primarily by stretching of the soft tissue structures about the hip ( 22).
Male dancers typically begin dance at a much later age than girls and may be into adolescence before the onset of
training. These dancers must achieve turnout through natural femoral retroversion and joint flexibility, or they must
achieve this rotation by the stretching of soft tissue ( 22,23).
Genu Recurvatum
Although a slight degree of recurvatum (hyperextension) of the knee is aesthetically desirable in dance, excessive
degrees may present problems. For example, in such a position the posterior capsular structures of the knee may
become painful, especially when dancing en pointe (19). In fact, the dancer en pointe may have difficulty maintaining the
body weight over the foot when the knee excessively hyperextends. This may lead to overuse injuries of the lower leg
and foot (7). Excessive recurvatum may not allow the heels to approximate in first position; thus weight distribution may
be more over the heels rather than over the entire foot. A dancer might compensate by increasing his or her anterior
pelvic tilt, thereby increasing the lumbar lordosis. This position may predispose the dancer to back injury ( 7). Excessive
hyperextension of the knees also may place greater strain on the triceps surae during repetitive jumping and perhaps
contribute to Achilles tendon overuse injuries ( 19).
Tibial Torsion
Normal external tibial torsion is approximately 12 degrees. Excessive torsion (greater than 26 degrees) may result in an
inability to align the knee over the foot during dance maneuvers ( Fig. 20.12). This is especially true during plié (7). The
femur becomes internally rotated over a fixed externally rotated tibia. During plié, as the femoral internal rotation and the
tibial external torsion increase, so does the Q angle, resulting in subsequent patellofemoral and foot problems ( 24).
FIGURE 20.12. Inability to align the knee over the foot during plié as a result of excessive tibial torsion or inadequate
turnout (ER), or both, at the hip.
Ankle Joint
Impingement syndromes in the lower extremities of the dancer are the natural result of forcing the joints into extreme
ranges of dorsiflexion and plantarflexion required for aesthetics and technique in classical ballet ( 21). Anterior talar
impingement syndromes occur during plié and may be a result of years of hitting bottom during plié or laxity in the lateral
ligaments secondary to ankle sprains (17,21). Roentgenographic findings will reveal tibiotalar contact when the foot is in
extreme dorsiflexion (Fig. 20.13). An exostosis may be present on the anterior talar neck or the anterior lip of the tibia
(16,17). Thus, the dancer may lack adequate depth with plié and have pain with such activities.
FIGURE 20.13. Anterior talar impingement during plié demonstration by x-ray.
Posterior talar impingement syndrome occurs with maximal plantarflexion at the ankle, as seen with demi pointe or full
pointe. As the foot approaches the extreme range of plantarflexion, an os trigonum (a large posterolateral tubercle of the
talus) or, less commonly, a large dorsal process of the os calcis may compress soft tissue structures such as the
synovium and joint capsule against the posterior tibia. This may produce a limitation in range of plantarflexion and be
associated with pain. Repeated entrapment of the soft tissue will lead to inflammatory changes, with eventual thickening
and fibrosis ( 16,17). Dancers most often complain of pain with releve or en pointe.
BIOMECHANICAL FACTORS
It is not uncommon for dancers to push to the extremes of their physical limitations to maximize the range and variety of
movements available for expression. Unfortunately, this can lead to altered strength and flexibility patterns, changes in
kinematics, and subsequent injury, especially around the foot and ankle.
Years of dance training or faulty technique, or both, may result in imbalances of strength and flexibility. Inadequate
strength or flexibility may alter function and thus lead to inefficient movement patterns. Inefficient movement patterns may
manifest in improper muscle sequencing, leading to misuse or overdependence on muscles not designed for the desired
action. If training continues in this fashion, it can result in overuse of the inappropriate muscles as well as weakening of
those more appropriate for the desired movement (25).
Functional equinus is often seen in dancers secondary to excessive shortening of the plantarflexor muscles. Such
tightness limits the available range of dorsiflexion necessary to achieve adequate depth with plié and landing from jumps.
In an attempt to increase dorsiflexion at the ankle in the presence of tight plantarflexors, the dancer will compensate by
pronating at the subtalar joint. By virtue of its triplanar axis of motion, the subtalar joint can move in any direction
necessary to compensate for deformity of the lower extremity. In the above-mentioned case, subtalar pronation will allow
for increased motion at the ankle in a sagittal plane ( 26).
Unique to pointe dancing is the occasional forefoot sprain. Overarching of the foot en pointe increases the amount of
stress in the ligamentous and tendinous structures on the dorsum of the foot. This occurs when the line of gravity falls
anterior to the dorsum of the foot rather than through the foot ( 7). Under such conditions, the weak dorsal capsules (now
under tension) at the base of the fourth and fifth metatarsals are easily torn, producing the characteristic sprain at the
tarsometatarsal joints (21). Likewise, increased dorsal stresses decrease stability over time and may lead to subluxation
of the cuboid (19,20,27). Marshall and Hamilton (27) tracked dance injuries during two separate 3-week periods and
reported that cuboid subluxation totaled more than 17% of foot and ankle injuries. Although the two periods of time
examined included 3 weeks of performance and 3 weeks of rehearsal schedules, no significant difference in terms of
incidence of subluxation was noted when comparing the two.
Hallux Rigidus
Approximately 90 to 100 degrees of dorsiflexion at the first metatarsophalangeal (MTP) joint is necessary to achieve full
releve onto demi pointe (see Fig. 20.4) (7,18,21). Hallux limitus or rigidus is usually an acquired condition in dancers, with
an insidious onset leading to gradual stiffening at the joint. Acquired limitus or rigidus may be a result of repeated MTP
joint trauma, causing inability of the first metatarsal to plantarflex ( 18,26). Impingement spurs are commonly seen in this
joint in older dancers and are often a result of direct impingement of bony surfaces in dorsiflexion or from capsular
avulsions associated with sprains ( 21).
Limited motion of the hallux often results in faulty mechanics when attempting to achieve full demi pointe. To accomplish
this, the dancer will roll laterally onto the lesser metatarsals, thereby sickling in (see Fig. 20.11). As mentioned
previously, this faulty maneuver can lead to lateral ankle sprains and malalignment problems ( 18,21).
Pes Planus and Cavus
Although aesthetically favorable, the pes cavus foot ( Fig. 20.14) is often relatively rigid and proves to be an extremely
poor shock absorber ( 7,18,26). A dancer with this condition may have to depend on a forgiving dance surface to assist
with shock absorption. In addition, the dancer must ensure proper technique when dancing (e.g., when landing from
jumps, demi plié) to allow the heels to load and contact the floor. Adequate length in the Achilles tendon must be
maintained.
FIGURE 20.14. Pes cavus foot.
Pes planus is a condition often associated with forefoot varus ( 7). The planus foot allows for excessive pronation.
Excessive pronation can lead to a variety of conditions about the foot and ankle, as well as up the lower kinetic chain.
ENVIRONMENTAL FACTORS
Environmental factors contribute to dance injury as well. In a survey conducted by Bowling ( 8), 25% of those surveyed
perceived the cause of their injuries to be related to dancing on unsuitable stages and flooring (e.g., hard, unsprung
floors) and 14% attributed injuries to dancing in a cold, drafty environment and being insufficiently warmed up.
Dancers often report dance studios to be cold or drafty, making it difficult to properly warm up or to stay warm. In
addition, many dance companies agree to outdoor performances during the summer months. Cool night air may cause
the same problems associated with inadequate warmup. On the other hand, humidity or high temperatures can lead to
dehydration, heat cramps, heat exhaustion, or heat stroke ( 7).
The dance surface is another variable that has great bearing on the dancer's ability to perform adequately. The dance
surface is often thought to act as a silent partner to enhance performance and confidence ( 28). Dancing is an interaction
between two dynamic systems: the dancer and the floor (29). Dance surfaces must provide adequate shock absorption
yet be firm enough to provide sufficient energy return to the dancer to enhance performance and reduce fatigue ( 29,30).
Surfaces that are too firm with little or no give (such as concrete and asphalt) may lead to early muscular fatigue,
because the musculoskeletal system of the lower extremities must act to absorb most of the shock. Once this system fails
to absorb shock adequately, afflictions of the feet and legs (e.g., shin splints and stress fractures) may ensue ( 28,29).
On the other hand, if a dance surface is too soft, this, too, can lead to early fatigue. In this situation, there is adequate
absorption but inadequate energy return to the dancer, thus requiring considerably more effort to perform the desired
movements. An extreme example of such a surface is a sandy beach (29,30).
Therefore, the most important properties of a dance floor are proper surface friction, resiliency, and shock absorption.
For a flooring system to be resilient and shock absorbing, it must perform certain functions. According to Seals ( 28,29), a
dance floor
Should have shock-absorbing qualities.

Should give under impact to some degree and absorb some of the impact energy in doing so.
Should not deform permanently or dent under pressure or impact of normal use.
Should not be so springy that it acts as a trampoline.
Should not be absolutely rigid or hard and should not give the impression of being so.
To achieve these properties, a dance surface must consist of three components: (a) a subfloor or base, such as concrete,
asphalt, or tile; (b) a substructure, such as rubber pads and sleepers or springs and sleepers; and (c) a surface, such as
hardwood flooring or vinyl sheet flooring. Seals ( 28,29 and 30) provided details of specific substructure designs and floor
surfaces.
A final property is surface friction. The friction or traction of the surface is important when the foot is interacting with the
flooring surface. There is a delicate balance between the needed slide and traction during performances and rehearsals
(29). To ensure that dancers will function uninhibited on such a surface, daily care is a must. The surface must be kept
free of a buildup of rosin, body oils, cleaning materials, dust, and other foreign materials that may create uneven surfaces
or lead to slippage problems ( 28,29 and 30).
Many dance companies encounter difficulties when touring. For this reason, many professional companies tour with
portable floors that provide a familiar, uniform surface on which to perform. Still, these floors lack sufficient mass or
thickness to mask a rigid stage floor. Nonetheless, portable floors do provide adequate surface traction and friction
(28,29 and 30).
THE DANCER'S SHOE
The ballet shoe is another contributing factor to dance injuries. A traditional ballet shoe costs' between $40.00 to $75.00
a pair; however, they can break down and wear out after one demanding performance. Each shoe is handmade of satin
and ribbon. The shoe allows for shock absorption by having a stiff cardboard midsole, cotton insole, and a stiff cardboard
outsole. Forming the tip of the shoe is glued canvas to allow dancing on full pointe. Because the shoes are handmade,
there are often irregularities in the construction and fit of each shoe; this in itself can contribute to injury.
Ballet dancers suffer a wide range of foot and toe problems, including blisters, calluses, bunions, first MTP osteoarthritis,
stress fractures, hallux rigidus, sprained ligaments, and plantar fasciitis. Modifications of the ballet shoe can help reduce
the incidence of injury and pain created by the shoe. Simple modifications may include physically stretching or bending
the shoe. Dancers may tape their toes or add extra layers of fabric at the tip of the shoe for extra support and cushioning.
Dancers have many different ways in which to break in the ballet shoes. Some dancers warmup in them by performing
pliés and tondus, and walking around en pointe before class. Some find wetting the toebox slightly before the warmup
helps the shoe form to their foot. Others like to hit the tip of the shoe on the floor or a wall to make the tip less slippery.
Injuries may also occur when the ballet shoes have worn out. The dancer knows the shoe is worn out when it become too
soft and no longer supports them en pointe. Many times, the shoe will collapse, causing the dancer's foot to roll over
when en pointe. In our experience, dancers like to stay with the same company's shoe but often are disappointed with the
lack of consistency of shoes from year to year. Lack of dance shoe durability can contribute substantially to the cost
burden of the ballet company. This often creates an injury that is contributed to by the shoe but cannot be treated with
just standard rehabilitation.
DIETARY AND NUTRITIONAL FACTORS
Because of the current aesthetic ideal, a typical dancer's somatotype calls for thinness. Such a demand may be
responsible for several nutritionally related health problems. Because ballet is not an aerobic activity, dancing in and of
itself does not allow the dancer to reduce or maintain weight. Therefore, many dancers resort to improper dieting
methods that may result in menstrual irregularities, skeletal abnormalities, or serious eating disorders.
A study conducted by Hamilton et al. (31) surveyed 49 female dancers in four national ballet companies in America (65%)
and the Peoples Republic of China (35%). Findings showed that all of the groups reported a delay in menarche and
weighed approximately 14% below their ideal weight for their corresponding height.
Frusztajer et al. (32) studied 55 female dancers and 59 nondancer controls to investigate the incidence of stress
fractures in ballet dancers. Information was gathered through interview questionnaires and medical examination. The
authors found that the majority (%) of the dancers (n=10) with recent stress fractures had weighed less than 75% of their
ideal body weight and showed a greater incidence of eating disorders. This group also showed a lower fat intake and a
higher intake of low-calorie foods.
Nutritional deficiencies may also contribute to fatigue, anemia, and muscle spasm ( 33). In the event of injury, those who
lack sound nutritional habits may find it difficult to build, maintain, and repair tissue ( 33). Given the possibility that quests
for ultraleanness by some dancers may precipitate injury, lead to menstrual abnormalities, or eating disorders, clinicians
and dance instructors alike must attempt to recognize those at risk and seek appropriate professional consultation.
Likewise, if the dancer is asked to lose weight, he or she should be directed to a professional source so that weight loss
can be achieved in a safe and reasonable manner.
PSYCHOLOGICAL FACTORS
The dance profession is a highly competitive yet private one. The road from childhood training to a professional career
can be a long and grueling trip. Many dancers must decide if dance is a career goal at an early age so that they can
develop their skills. Often, young dancers choose to leave home during their formative years to train at certain
prestigious schools. The dance school becomes a surrogate parent, and most of their lives are consumed with
developing enough talent and skill to become a professional. These circumstances may cause some students to become
emotionally fatigued or burned out ( 7). Emotional fatigue can be associated with physical fatigue and inattentiveness,
which may lead to injury (7).
For those whose perseverance and talents allow them to capture the professional ranks, competition and pressures may
present more barriers. Competition for roles and demands from instructors, other company members, the media, or the
dancer themselves may lead to self-destruction on a physical or emotional level. A total of 38% of those surveyed by
Bowling (8) believed their injuries were the result of feeling overtired, rundown, overworked, and under strain and
pressure.
Finally, injury or age may present an inevitable but possibly premature crossroad for the dancer. Dancers may be
presented with a situation in which the instrument of expression—their bodies—cannot function as it used to. The
dancers may feel their bodies are “imperfect” instruments trying to perform in a perfect art ( 7).
Transition from a life of dance to alternative careers can be an anxious time for dancers. A career in dance often begins
early in life and may limit formal education. Because of this and their focused career in dance, many dancers are often
unaware of their capabilities, talents, and potentials outside of dance ( 34). The realization that some professional
assistance may be needed for such an adjustment has led to the birth of the Dancers Transition Center of Canada, which
addresses the stress of giving up professional dance ( 34).
COMMON INJURIES AND TREATMENT
Injuries seen in dance are usually chronic in nature, developing subtly over a period of time. However, on occasion, there
are acute traumatic injuries. The following discussion briefly addresses common injuries seen at specific anatomic
regions. This review is in no way inclusive of all plausible injuries in these areas. It is important to recall the etiologic
factors that contribute to such injuries, as discussed previously.
In general, treatment goals for each injury are directed toward the following ( 35):
1. Pain relief
2. Restoration of full active and passive range of motion
3. Stability of the joint
4. Normal muscular strength, endurance, control, and coordination
5. Proper proprioceptive responses
6. Restoration of confidence in dancing ability
7. Patient education in regard to the musculoskeletal system, immediate first aid care, and injury prevention
In the next section, the specific treatment for each injury is addressed following the introduction of each injury.
Upper Extremities
Injuries to the upper extremities are less common in dance than those of other regions. Male dancers are more subject to
upper-extremity injuries because of the demands of choreography. Men are often required to partner and lift females.
Repetitive lifting in the presence of poor technique, poor postural alignment, and inadequate strength or flexibility can
predispose one to overuse or impingement syndromes, especially at the shoulder. Rarely, a shoulder dislocation or
subluxation may occur. Likewise, ligament sprains of the wrist and hand may ensue when male dancers are catching
their female partners (36).
The treatment includes standard treatment principles. The modalities can be used properly to control inflammation and
pain. Specific stretching and strengthening exercises can be addressed. If it is necessary, the dancer may need to modify
and limit his or her painful movement.
Spine
Cervical region
Cervical problems are less common in dancers. However, sometimes the dancers may develop muscle tension and
spasm over cervical and shoulder girdle region. In severe cases, it may occur as acute torticollis ( 37).
The regimen of treatment is to use modalities such as ice, heat, electrical stimulation, and ultrasound to release muscle
spasm and pain. Friction massage and stretching are usually helpful. Sometimes, it may require manual therapy such as
mobilization and manipulation. However, the dancer needs to be educated for proper postural awareness, self
-stretching, and massage, as well as relaxation technique to prevent recurrence.
Lumbar Region
Spinal injuries in the lumbar area are more common than other injuries and most often are the result of repetitive
microtrauma. Mechanical low-back pain is often seen in dancers and is usually associated with a hyperlordotic posture,
both statically and dynamically ( 13). Such a posture may be a reflection of anatomic alignment and musculotendinous
imbalances, and is nearly always an acquired posture ( 13). Poor technique, for example, hyperlordosis in an attempt to
increase turnout or when lifting female partners, must be addressed. Appropriate soft tissue length (especially in the hip
flexors and thoracolumbar fascia) and muscle strength (especially in the abdominals) are essential.
Spondylolysis ( Fig. 20.15)is probably a result of the repetitive flexion and extension of the spine, resulting in a stress
fracture of one or more pars interarticularis of the lumbar spine ( 13). Findings on physical examination include a
decrease in lumbar flexion and pain with lumbar hyperextension. Often, the dancer complains of pain with unilateral
hyperextension (e.g., when performing an arabesque) on the affected side (10,11,36). One should keep in mind that a
dancer who maintains poor alignment (e.g., hyperlordosis) may be predisposed to facet irritation and impingement. A
differential diagnosis must, therefore, be made to distinguish facet syndrome from spondylolysis ( 38). The presence of a
pars defect or even a grade I spondylolisthesis does not warrant termination of a dance career. These defects are often
the result of a stress fracture, and the condition is usually a fairly stable one. Dance can continue safely, although
possibly with discomfort (13,39).
FIGURE 20.15. Spondylolysis in the professional dancer shown in Figure 20.14.
The treatment is to brace initially to control pain and begin a rehabilitation program focusing on spine stabilization
exercises, abdominal strengthening, hip flexor stretching, and proper body mechanics. On return to dance, movements
such as arabesque must be scrutinized carefully for technical faults. Correcting faulty dance technique, in particular the
“weight back situation” ( 11,13), can prevent recurrences.
Stress Fracture of the Lumbar Spine

The stress fractures occur in the pars interarticularis, most commonly at the level of L-4 and L-5 ( 37). They may be
unilateral or bilateral. The stress fracture with forward slip of the vertebrae can gradually progress to spondylolisthesis. It
is extremely important to detect the condition because missed fractures may not heal. We brace these fractures for a
minimum of 6 weeks and for as long as 6 months. We do not limit physical activity in the brace, but the majority of dance
activity cannot be performed while the dancer is braced. It is also important to assess the dancer's nutrition status to
ensure proper healing. Once the stress fracture shows healing, rehabilitation is progressed to intense abdominal and
trunk strengthening exercises, a lumbar stabilization program, and barre work as tolerated. Emphasis on a Pilates
program in the later stages of rehabilitation is generally appreciated by dancers and helps in the transition back to dance.
Discogenic low-back pain in dance, however, appears to be more prevalent in male dancers and is probably caused by
lifting (13,38). Nonoperative management of such a condition, with cessation of lifting and directed exercise, is preferred.
Bracing may be of value, especially on initial return to dance. Nonetheless, bracing is usually not an option for
performances because of aesthetics. In the event of disabling pain or progressive neurologic loss, the dancer should be
managed like any other patient with a serious herniation ( 13).
Muscle imbalances also may influence pelvic alignment, leading to sacral or innominate rotations, thus causing pain with
static or dynamic activities. Appropriate exercise, manual therapy, and improved dance technique can assist with
correction and maintenance of the correction.
Hip
Anatomic and biomechanical factors at the hip were discussed earlier. Hip injuries are uncommon in dance. In a study of
hypermobility, Klemp and Learmont (40) found only 11 injuries to the hip out of a total of 138 injuries in their study of
hypermobility. All injuries were strains, bursitis or tendinitis. Sammarco ( 41) noted the importance of the iliopsoas in
developpé and the presence of snapping hip with grande plié. Hamiliton et al. (42) noted that students dropping out of
ballet had a higher incidence of impaired turnout of the hip among other musculoskeletal problems. Development of
turnout is extremely important in dance. It is generally accepted that turnout should be measured in the neutral, not frog
legged position. Generally, it is accepted that retroverted hips are more suited to dance, although dancers who begin
training in their juvenile years can develop turnout by developing their femoral neck angle, and the femoral neck angle
becomes more retroverted through growth and development. After the age of 11, the femoral neck angle cannot be
altered through this molding process, and increases in turnout must come from stretching of the hip capsule. Khan et al.
(43) demonstrated that dancers aged 16 to 18 years can continue to increase turnout by small amounts (e.g., 4 degrees)
over the course of a year. Repeatedly stretching the joint capsule with forced turnout can lead to chronic strain and
possible calcification at the acetabular attachment of the capsule ( 22). Hip calcifications were found in retired dancers
much more frequently than the nondancer population in one study ( 44).
Stress fractures of the femoral neck are also important in the differential diagnosis of dancer's hip pain ( 22,39).
Nondescript pain is usually found in the groin, with symptoms increasing at the beginning and the end of class but
minimized during class. Rest usually relieves the pain. Early physical examination reveals no limitations of range, but
groin tenderness is present. Standard x-ray studies do not show a fracture until several weeks or months later. A bone
scan or magnetic resonance imaging (MRI) is usually necessary to locate the area of increased activity ( 22). Progression
of symptoms results in decreased hip flexion, abduction, and ER secondary to pain. Diagnostic tests may be necessary
to rule out other possible conditions such as arthritis, synovitis, infection, or tumor ( 22). A lesser trochanter avulsion
fracture of a dancer involving the iliopsoas insertion has also been described ( 45).
The snapping hip is a common problem among dancers. It is most often seen in women, who report clicking and
snapping over anterior hip while they bring their hips into flexion, ER, and abduction such as developpé at the second
position, grand rond de jambe, or preparation for passé (22,39,46,47 and 48). The snapping may or may not be
associated with pain. The anterior clicking may result as the iliopsoas tendon passes through the anterior hip capsule or
ligament while the hip is brought into flexion, ER, and abduction. However, snapping may also occur at the iliopsoas
bursa and the pectineal eminence. This is often classified as internal coxa saltans. Dancers also experience snapping
over the greater trochanter secondary to thickening of the iliotibial band or the anterior border of the gluteus maximus
muscle. This can be diagnosed by placing the patient on his or her side with the affected hip up and flexing and
extending the hip with palpation of the greater trochanter. The snapping can usually be blocked by applying pressure at
the level of the greater trochanter ( 49). Trochanteric bursitis may also accompany a snapping hip. Pain is accentuated
during certain dance steps such as rond de jambe and when landing from jumps (20). Bursitis of the anterior hip capsule
also may become a problem when the bursae lying between the capsule and the iliopsoas tendon becomes inflamed.
Hip pain in dancers also may be the result of other conditions such as piriformis syndrome, rheumatoid arthritis, or a disc
herniation. Several internal organs also can refer pain to the hip such as the genitourinary system or the female
reproductive system (39). Should examination of the hip render negative findings, a complete physical and diagnostic
studies should be performed to rule out other possible conditions.
Knee
Dancers often encounter knee pain during the course of their careers. Many of these problems are attributed to overuse,
muscle imbalances, poorly sprung dance surfaces, and faulty technique ( 14,19). Mild hyperextension of the knees,
although aesthetically desirable, may result in incorrect weight placement ( 11,19). Posterior capsular structures may
become painful, especially in women when dancing en pointe. Such a condition may place increased strain on the triceps
surae and contribute to Achilles tendinitis ( 19).
Chronic rotational stresses may be present at the knee in dancers who force their turnout. In such instances, there is
increased strain placed on the medial collateral ligament, menisci, and joint capsule. Likewise, patellofemoral disorders
may develop, including lateral subluxation, lateral dislocation, excessive lateral pressure syndrome, or patella femoral
pain syndrome (39,50,51).
Patellofemoral Dysfunction
There are several predisposing factors for patellofemoral dysfunction, such as increased Q angle, muscle imbalance
including tight iliotibial band and weak quadriceps, femoral anteversion and tibial torsion, and faulty technique such as
forcing turnout from the knees ( 11). Achilles tendon tightness is also thought to predispose the dancer to patella femoral
problems either by altering shock-absorbing patterns with jumps or by increasing pronation. Traumatic chondromalacia is
occasionally a sequelae to falls on slippery floors.
Tendinitis
Patellar tendinitis, often associated with Osgood-Schlatter disease in the young participant, is commonly seen in
dancers. Precipitating factors may include repetitive jumping, unyielding surfaces, and/or an increase in total volume of
work (as is often seen during rehearsals for upcoming performances) ( 12,19,51). Hamstring strains and tendinitis usually
result from poor technique, especially dancing in the “weight back” position or “sitting in the hip” ( 11). Most often, the
dancer is injured in second position while performing a grand battement, penché, or arabesque, all maneuvers requiring
the working leg to be raised. Overturning can result in semimembranosus tendinitis.
On rare occasions, traumatic injuries occur about the knee. These injuries are more often the result of neglect to treat
chronic symptoms (e.g., patella tendinitis) rather than a single isolated movement. Nonetheless, traumatic patella
subluxation, patellar tendon rupture, knee ligament tears, and meniscal tears do occur.
Knee surgery is rarely a treatment option in dance. However, in the event of meniscal injuries or major ligamentous
rupture, surgery may be indicated. Some authors reported in earlier literature that it would be almost impossible to get a
dancer back to full dance activities after a knee ligament reconstruction ( 39,45). However, recent medical advances have
provided dancers with a second chance.
Lower Leg
Medial tibial stress syndrome, tibial stress fractures, and anterior compartment syndrome are the most common
conditions seen in the lower leg in dancers ( 30,54,55). Stress fractures may be either posterior medial, as commonly
seen in other athletes, or anterior and transverse. Medial tibial stress syndrome as well as stress fractures are associated
with poor conditioning and sudden increases in volume of dance and intensity of dance, but anterior tibial stress fractures
are often associated with poor technique and sway back knees. When dancers perform on different stages, such as
dance tours or guest appearances with other companies, the change in floor stiffness may also contribute to injury. A
study by Gans (56) investigating the relationship between heel contact and the incidence of medial tibial stress syndrome
in 16 dancers showed that heel-to-floor contact on ascent or descent from jumps did not appear to be related to the
incidence of medial tibial stress syndrome in dancers. However, in those with a history of medial tibial stress syndrome,
Gans noted an increased incidence of what she referred to as double heel strike—the heel is elevated from the floor
between landing and push-off.
Fibular stress fractures are also seen in dancers and are often associated with sickling of the feet, or weakness of the
intrinsic muscle of the feet. Tibial bowing may also contribute to this condition, as may faulty alignment of pointe shoes
(11).
Strains of the gastrocnemius muscle were the most common muscle injury of the lower leg in the study by Klemp and
Learmonth (40).
Foot and Ankle
The foot and ankle are the most common sites of injury in dance. Although injury may be acute, chronic injuries usually
predominate. Chronic injuries are often the result of repetitive impact loading on relatively unyielding surfaces. Other
factors contributing to injury include improper footwear that does not adequately absorb shock, improper technique,
anatomic variation, and on occasion, fatigue ( 14).
Acute injuries at the foot and ankle are most commonly ankle sprains. Injury usually results from forced plantarflexion and
inversion of the hindfoot when landing from a jump ( 16,57), or falling off pointe for girls, or in boys during grande allegro.
Contributing factors include poorly fitting pointe shoes, weakness of the foot or ankle resulting in poor posture, and
incompletely rehabilitated previous ankle sprains.
In addition to ankle sprains, dancers also are predisposed to midfoot sprains, peroneal tendon injuries or subluxation,
fracture of the second and fifth metatarsals (16,58), and avulsion fracture ( 59).
The most common acute fracture is the spiral fracture of the distal one third of the fifth metatarsal (dancers fracture),
occurring when the dancer loses his or her balance on demi pointe and rolls over onto the lateral border of the foot ( 19).
Although such injuries are not commonly seen, high external forces during a fouetté (a turn en pointe or demi pointe away
from the supporting leg while the working leg is thrown outward as the body spins) can cause a lateral malleolar fracture
or fracture dislocation of the supporting leg ( 40). Conversely, fracture of the medial malleolus occurs while the foot is
forcefully everted such as landing a jump with the weight on the medial side of the foot. Classically, the dancer jumps
rapidly into the air, bringing one foot forward in front of the other and lands in a demi pointe position (39).
Interphalangeal joint dislocations occasionally occur in dancers. They are most often the result of direct trauma such as
walking into or kicking a heavy object or stage equipment while in ballet slippers ( 21,53).
Tendon Disease and Tendon Rupture

Although tendinitis can be an acute condition, the frequency of recurrence and the nature of dance tend to make
chronicity more the norm than the exception. Although any tendon about the foot and ankle can be affected in dancers,
the Achilles, flexor hallucis, tibialis posterior, and peroneal tendons are most commonly involved ( 10,14,15,52,53). Faulty
technique, improper dance surfaces, fatigue, the repetitive nature of dance, musculoskeletal imbalances, or a
combination of any or all of the above are usually responsible for the onset and persistence of tendinitis or tendon
rupture. These injuries need not be career-ending. Operative repair ensuring restored physiologic tendon length,
prevention of postoperative complications, appropriate rehabilitation, and dedication on the part of the dancer can lead to
normal function and safe return to dance.
Achilles tendon problems are frequent in dance, and are associated with muscle weakness of the feet, lower leg and,
thigh musculature. Tight-fitting pointe shoes or shoe ribbons that cut into the tendon have also been described as
precipitating Achilles tendon problems. When the gastrocnemius and soleus muscles are tight, dancers have difficulty
with plié, and often have poor weight distribution, resulting in faulty technique ( 11,54).
The flexor hallucis longus tendon passes through a tunnel at the posterior aspect of the ankle immediately adjacent to
the posterior process of the talus. The flexor hallucis longus can function as a dynamic stabilizer of the midfoot and
ankle. The distance the tendon must travel to achieve en pointe to grand plié can be 2 to 3 inches. Rolling in and sickling,
which result in poor en pointe positioning, are often associated with this condition. Dancers eccentrically load the flexor
hallucis longus while landing from jumps. Chronic overuse causes inflammation and irritation (e.g., tenosynovitis).
Longitudinal tearing can then result leading to nodule formation in the tendon and triggering ( 55).
The posterior tibialis tendon is adjacent to the flexor hallucis longus, and assists the dancer en pointe. The common
location of chronic tendon injury is at the point where the posterior tibialis tendon sharply turns around the medial
malleolus to enter the foot. Acute injuries often occur at the enthesial insertion into the navicular. As with the Achilles
tendon, poorly fitting shoes, intrinsic muscle weakness, and frequent jumping may be associated with problems.
The peroneus longus and brevis tendon may develop tenosynovitis from overuse or following ankle sprains.
Occasionally, the peroneal tendons are torn, subluxed, or dislocated over the lateral malleolus. Dancers with tibial
bowing and decreased turnout may force the ankle into eversion, overloading the peroneal musculature ( 56).
Stress fractures are common in dancers' feet. The most common sites are the proximal shaft of the second and third
metatarsals (55,57,58). Although the first two metatarsals bear most of the body weight in demi pointe and pointe, stress
fracture of the first metatarsal is very uncommon unless technique is a problem and intrinsic strength is poor. The
sesamoids, navicular, and distal tibia are also commonly susceptible to stress fracture ( 12,14,16,39). Stress fractures are
most often the result of cumulative microtrauma rather than a single acute traumatic event. Symptoms are mostly seen
with jumps and en pointe. They are also associated with solid wood, concrete, and unsprung floors. Hardaker ( 16)
believes the experienced dancer is less vulnerable than the beginner, because of the gradual adaptive hypertrophy of the
bony structures. However, experienced professionals often sustain stress fractures nearing the end of a long tour that
requires dance on surfaces of varying stiffness. As noted by Harrington et al. ( 59), second metatarsal stress fractures
must be distinguished from stress reactions and synovitis of Lisfranc's joint. Early diagnosis resulted in improved
outcomes in their study. Micheli et al. ( 60) demonstrated that failure to make the diagnosis early can result in poorer
outcomes. Repeated incidence of stress fractures in a dancer should be a red flag for the medical practitioner and
warrants an investigation of nutritional history, menstrual history, and training practices.
Traumatic fractures most often involve the fifth metatarsal neck and distal shaft. It is most often seen in women when
falling off point, but is also seen in male dancers performing grande allegro.
Joint bursae and capsules can also become inflamed and irritated in the dancer's foot. Retrocalcaneal bursitis and dorsal
capsulitis of the first MTP joint are common sites of involvement.
Plantar fasciitis is another common ailment in ballet. The most likely cause of plantar fasciitis is faulty biomechanics
secondary to either a tight triceps surae or an externally rotated lower extremity. As stated previously, one consequence
of forced turnout is excessive strain on the medial structures of the foot from resultant pronation. Wearing shoes that are
too short, especially in association with pes cavus, has also been associated with the development of plantar fasciitis. In
this case, the fibrous aponeurosis assumes a greater share of the force than it can physiologically accommodate ( 61).
Fasciitis also may occur in the dancer with a cavus foot secondary to the inability of this foot type to dissipate forces
adequately.
The extreme dorsiflexion with plié and plantarflexion with demi pointe and pointe can lead to talar impingement
syndromes. Anterior impingement syndrome, involves the impingement of bony or soft tissue between the anterior lip of
the tibia and the talar neck. Posterior impingement syndrome involves the soft tissues, such as the synovium and capsule
in the posterior aspect of the ankle; at times, the flexor hallucis longus (FHL) tendon may be involved. The presence of
an os trigonum or the posterior process of the os calcis ( 58) is an important finding on x-ray study. Hamilton et al. ( 62)
removed the os trigonum in 24 of 32 operative cases of posterior impingement syndrome in their series. In four of these
cases, the os trigonum had been fractured and not healed. They also noted loose bodies, a pseudomeniscus, a posterior
slip of the tibial branch of posterior talofibular ligament, and a posterior medial tubercle as sources of impingement at
surgery.
Cuboid subluxation is a common but poorly recognized condition in dancers. It is caused by dorsal ligamentous laxity
associated with hypermobility of the midfoot. It can also be secondary to landing from jumps and the sequelae of lateral
ankle sprain (27). In general, the incidence of cuboid subluxation is seen more often in female dancers than in male
dancers. Usually, it occurs acutely in male dancers when they land from jumps. Female dancers develop the cuboid
subluxation as an overuse syndrome from repetitive pointe work. Moving from foot flat to demi pointe initially creates a
dorsiflexion moment on the midfoot, which changes to a plantarflexion moment while the foot moves to pointe. Again the
force reverses to a dorsiflexion moment while the foot returns to foot flat. The repetitive forces gradually decrease the
stability of the midfoot and predispose some dancers to cuboid subluxation ( 27).
Sesamoid injuries are fairly common in dance, although in our experience, sesamoid fractures are rare. There are two
sesamoid bones lying within the flexor hallucis brevis tendon beneath the plantar surface of the first metatarsal head. The
medial and lateral sesamoids take the load beneath the metatarsal head and help distribute it. Sesamoiditis is most likely
caused by direct trauma such as landing from jumps. Sometimes prolonged working on a hard surface also cause the
irritation and inflammation of sesamoids.
Hallux valgus may result from heredity, narrow or pointed footwear, overpronation of the foot, excessive rolling in during
plié, and sickling. Einarsdottir et al. ( 63) measured by x-ray the valgus angle in dancers and compared it to a nondancing
control group, and found the difference negligible. Hallux valgus can lead to blistering due to altered weight-bearing
patterns in dancers, especially in women who dance en pointe. Hallux limitus and hallux rigidus are often the result of
degeneration in the first metatarsophalangeal joint. The condition is progressive, and the range of motion of the hallux in
extension is decreased. Ogilvie-Harris et al. ( 64) noted an increased incidence of hallux rigidus in dancers with a longer
second toe in comparison with toes of equal or shorter length. Forcing the foot into demi plié may increase symptoms,
and dancers should be counseled to “listen to their body” and not push through pain.
A variety of skin and nail problems is encountered by the dancer, especially women required to dance in pointe shoes.
Cunningham et al. (65) performed an analysis of the toe box of five different pointe shoes, and found significant
differences in axial compressive stiffness, vertical compressive stiffness, and vertical strength levels between the brands.
They also noted that the most durable or mechanically sound pointe shoe is not always the preferred shoe. Dancers are
often adept at protective tapings and dressings to minimize skin problems.
REHABILITATION
Dance rehabilitation is very similar to rehabilitation of other sports injuries with several important exceptions. Most
important, dancers require greater range of motion for pointe and grand plié than most athletes require for jumping,
running, and cutting. Dance also requires great control of the body to provide the artistic aspects of not just performing
the activity, but also appearing to do so effortlessly. In addition, the dancer's body must appear symmetric and balanced
after treatment is completed. Dancers often rely on Pilates machines as a conditioning and rehabilitation tool rather than
weights or other forms of resistance training. Also, because of the emphasis on leanness in dance, aerobic exercise to
maintain weight is important in the rehabilitation scheme. Caution should be taken not to return the dancer too quickly to
unrestricted dance after injury, despite his or her seeming urgency to do so because of self-imposed demands or those of
the other company members or ballet masters. Inadequate rehabilitation and premature return to dance will likely result in
reinjury or chronic problems, or both. Open communication among the physician, caregiver, dancer, and artistic director
is imperative to ensure timely and safe return to dance.
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21 Emergency Medical Care At Sports Events
21
EMERGENCY MEDICAL CARE AT SPORTS EVENTS

RONALD ROTH
VINCENT VERDILE
Sports Events Coronary Care

The Olympic Games
Sports Events as Multicasualty Incidents
Medical Preparedness for Sports Events
What
Who
Where
When
Common Factors in Emergency Planning
Leadership
Emergency Medical Systems Involvement
Medical Supplies
Medical Personnel
Conclusions
a
Appendix A. Medical Care at Mass Gatherings: Guidelines for Care
Chapter References
Since the mid-1960s, out-of-hospital emergency care has been provided by specially trained emergency personnel as
part of organized emergency medical services (EMS) systems. Over the past three decades tremendous advances have
taken place, particularly in the out-of-hospital care of cardiac and trauma patients ( 1,2,3 and 4). However, little attention
has been directed to the special circumstances surrounding emergency care at sporting events ( 5).
Although most athletic events have personnel dedicated to the care of injured athletes on scene, transportation of the
injured athlete and care of spectators is almost uniformly relegated to local EMS systems. Poor coordination and lack of
preplanning between athletic care personnel and the local EMS system may result in substandard care for the injured or
ill spectator or athlete. The purpose of this chapter is to review the current understanding of the state-of-emergency care
at sports events and to make recommendations about preparedness for EMS systems.
Emergencies at sporting events occur both on and off the field of play. Planning for emergencies at sports events must
include plans for managing sports-related injuries as well as medical emergencies involving spectators ( Appendix A).
Fortunately, unexpected tragedies and catastrophic injuries are rare at sports events ( 6,7,8,9,10 and 11). The majority of
requests for medical care at these events are for minor first aid issues ( 11,12). However, the emergency care team must
be prepared to deal with major events such as spinal cord injury, myocardial infarction, syncope, anaphylaxis, and
cardiac arrest.
Most major sporting events attract sufficient numbers of participants and spectators to constitute a mass gathering (more
than 1,000 people). If the definition of a disaster, from an EMS standpoint, is an event that can result in a quantity of
patients who can overwhelm a local EMS community, then most major sports events constitute a potential disaster
situation.
As might be expected, emergency care for sports events tends to follow a traditional disaster mode of teaching ( 13,14).
Most events involve a finite patient population, spectators plus participants in a confined area. Theoretically, emergency
care providers could make some predictions for issues such as medical supplies, transportation needs, and health
professional staffing. However, such predictions are very difficult. A wide variety of uncontrollable variables, as listed in
Table 21.1, influence the use of emergency care services at sports events. These include weather, age and condition of
participants, and the influence of drugs and alcohol, to list a few ( 5,11,12,15,16,17 and 18). In the past, the medical
literature on emergency care at sports events has for the most part consisted of anecdotal reports of individual
experiences (2,5,7,9,15). Some of the earliest reports concerning medical care of spectators at large events concerned
nonsports events such as rock concerts and conventions. Several authors reported their experiences with outdoor rock
festivals and conventions ( 19,20,21,22 and 23). Although most emergencies at these concerts were minor, alcohol and
drug abuse contributed to the injury patterns reported. Cumulative data suggest that 1.5% of attendees at these types of
events can be expected to request medical care ( 19,20,21,22 and 23). Based on their experience at rock concerts,
Levens and Durham (22) recommended health care coverage consisting of one physician and six first aid personnel for
every 2,000 attendees.
TABLE 21.1. VARIABLES INFLUENCING THE USE OF EMERGENCY CARE SERVICES
Numerous individuals have documented their experience providing emergency care at football stadiums ( 9,11,24). Pons
et al. (11) described their experience of covering the 1978 football season at Mile High Stadium, which at the time had
seating for slightly more than 72,000 fans. The authors provided medical coverage from three first aid stations. During
the season, 298 patients were treated, 35 were transported to the hospital, and 2 were successfully resuscitated from
cardiac arrest. The greatest number of patients were treated during the warmer months of the season.
Rose et al. (9) described their 6½-year experience providing emergency medical coverage for the West Virginia
University home football games, which included 38 games. The stadium seated 65,000 spectators. Onsite care was
provided by Emergency Medical Technicians (EMTs) and paramedics at three advanced life support (ALS) ambulances
and two first aid stations. Two EMS physicians were available by pager within the sports complex. Of the 313 patients
treated in their system, 286 received onsite care and 71 were transported to local emergency departments. The most
common presenting complaint was lacerations and abrasions (20%), followed by bee stings (9%), heat exhaustion
(7.6%), and weakness or dizziness (7%). During their study, seven patients suffered out-of-hospital sudden death. The
authors concluded that EMS with physician coverage of collegiate football games is required and that the 1 paramedic
per 5,000 spectators and 1 physician per 25,000 spectators is sufficient.
In a survey of the 28 National Football League (NFL) teams, Roberts et al. ( 25) found considerable variability in the
facilities, medical personnel coverage, and EMS coverage provided for the emergency medical care of spectators.
Although ALS medications and equipment were present in all of the stadiums, these services were maintained by a
variety of providers, including the stadium itself, private EMS companies, hospitals, and municipal services. All stadiums
used two-way radios for communications, and most also used telephones. At least one ambulance was dedicated to
patient care at each stadium, and golf carts were used for intrafacility transport. The average stadium was staffed with
eight EMTs, seven EMT-Paramedics, three registered nurses, and two physicians ( 25). Recent and proposed NFL
expansions and relocations will certainly challenge local emergency care providers. Individuals responsible for
organizing emergency coverage should find the article by Roberts et al. and several other in the literature, very useful
(9,11,24,25).
SPORTS EVENTS CORONARY CARE
Although the literature reviewed suggests that emergency medical care delivered at sports events tends to be for the
evaluation of minor problems, emergency care providers must also be prepared to treat out-of-hospital sudden death.
Special attention to the resuscitation of patients from sudden death should be a key aspect of all emergency medical care
or planning. Table 21.2 reveals the cardiac death rates for several large public assemblies from the past.
TABLE 21.2. CARDIAC DEATH RATES FOR SEVERAL LARGE PUBLIC ASSEMBLIES
Kassanoff et al. (8) described the life support system that was used at Atlanta–Fulton County Stadium for the evaluation
and treatment of sudden death during the professional baseball season. All stadium security personnel were trained in
basic cardiopulmonary resuscitation (CPR) and were able to communicate a sudden death event to a life support station
via two-way radio. An emergency patient transport cart was developed from a standard golf cart to transport patients from
the spectator area to the life support station. This transport vehicle was equipped with a defibrillator, a monitor, and
oxygen.
During the 1970 season, eight patients were treated at a life support station, seven of whom were believed to have
suffered an acute myocardial event; four patients required resuscitation from either syncope or sudden death. Two of the
four patients were successfully resuscitated and were eventually discharged from the hospital, one neurologically intact.
The authors had access to the data for sudden death from the first 5 years of the stadium's operation. For 27 million
hours of fan exposure, including the 1970 season, 13 episodes of cardiac arrest were documented. Overall, 23% of the
patients were resuscitated. The authors suggested that the low incidence of cardiac death in the Atlanta–Fulton County
Stadium begs the question of the cost-effectiveness of implementing, equipping, and training health care personnel. They
suggested that facilities and personnel that are already in place should be trained to handle basic CPR.
The introduction of automatic external defibrillators (AEDs) in the mid-1980s allowed individuals with little medical
knowledge to quickly deliver life-saving treatment to victims of cardiac arrest. AEDs analyze the patient's underlying
cardiac rhythm and deliver a countershock if ventricular fibrillation or ventricular tachycardia is found. In addition, the
AED unit prompts the user to check for a pulse and for breathing and to initiate CPR.
Weaver et al. (26) trained security personnel in CPR and the use of AED units for Expo '86, held in Vancouver, Canada.
Of the six cardiac arrests that occurred during the 22-month event, two patients were defibrillated by lay personnel and
survived. The authors suggested, based on their Expo '86 experience, that lay personnel trained in the use of AED units
represent an ideal approach to managing sudden cardiac death at large public gatherings.
Sudden cardiac death of athletes has occurred at sporting events. Concussion of the heart (commotio cordis) has been
reported to occur as a result of being struck in the chest with a baseball, hockey puck, or other projectile
(27,28,29,30,31,32 and 33). Sudden death of athletes during training and competition, secondary to structural
abnormalities, arrhythmias, and atherosclerotic coronary disease, has also occurred ( 34,35 and 36).
THE OLYMPIC GAMES
The application of the scientific process is a relatively new occurrence in evaluating the medical care provided at sports
events. Reports published after the 1996 Centennial Olympic Games in Atlanta, Georgia, provide some insight into the
injury and illness patterns seen at large sports events ( 5,18,37,38 and 39). However, the lack of standardized definitions,
indications, and methods prevents meaningful comparison and trend analysis ( 5).
Preparations for the Atlanta Olympic Games demonstrated how a systematic approach could be applied to the planning
and analysis of emergency care for sports events ( 5). The task was to plan for the health and safety of more than 5
million visitors and 10,000 athletes. The 6-year planning process included public health activities, surveillance, EMS, and
medical disaster planning.
Medical care was coordinated with local public health agencies; local, state, and federal agencies; and local EMS
personnel. Medical care was provided at a polyclinic located in the Olympic Village, at 24 competition venues, and at 11
noncompetition venues ( 37). Overall 44,142 medical encounters were recorded in log books. Among the 10,715 patients
treated by physicians, spectators accounted for the largest number of visits (32.5%), followed by volunteers (30.6%) and
athletes (16.8%). Wetterhall et al. ( 37) calculated a physician treatment rate of 4.2 per 10,000 in attendance, with a range
of 1.6 to 30.1 per 10,000. A total of 432 patients were transferred to hospitals. The majority of emergency transports were
for spectators or volunteers. The diagnosis for transported patients included heat-related illness (10%), injuries (22.9%),
and other medical-related illnesses (67.2%). Of those persons with medical illness, more than half were transported for
cardiac disorders: 23 patients were admitted for chest pain, and 8 had confirmed myocardial infarction ( 38). Of the three
patients with cardiac arrest, two were successfully resuscitated at the scene and transferred to a hospital. The authors
suggested that these findings underscore the importance of having advanced cardiac life support capability within each
venue and coordinating onsite medical services with experienced EMS, transportation systems, and local hospitals.
Scientific evaluation of the medical care provided at the 1996 Summer Olympics provides insight into the complex
delivery of medical care at large sports events. The researchers noted significant differences in types of medical
problems and use rates between spectators, volunteers, and athletes ( 18). In addition, their findings corroborated the
need to coordinate services with local emergency care providers, disaster planners, and local, state, and federal health
officials.
SPORTS EVENTS AS MULTICASUALTY INCIDENTS
The mass gathering of spectators and athletes at sports events is often viewed as a planned disaster by local health care
officials (18). The events often disrupt the daily activities of local public safety services, hospitals, and local government.
As previously mentioned, many officials charged with providing emergency care at sports events model their responses
to parallel those used in disasters. Although catastrophic occurrences are rare at sports events, there have been several
reports of medical care responses at such occurrences. Although the information provided is anecdotal and the incidents
are unique, a review of the medical care responses is worthwhile.
The bombing incident in Centennial Park during the 1996 Olympic Games highlighted the need for officials to plan for a
multicasualty incident. The bomb blast occurred in the early morning of July 27, after the local spectator care station had
closed. The number of initial casualties was so large that local first responders (police and fire) assumed responsibility
for evacuating injured persons to local hospitals ( 37). A total of 106 people were seen in emergency departments for
injuries resulting directly from the bomb explosion. There was one death from the bombing, and one journalist sustained
a cardiac arrest near the bomb scene (18).
Although the Olympic bombing represents one of the most recent and most publicized multicasualty incidents at a sports
event, disasters have occurred at several other sporting venues. In 1985, a chair lift collapsed at the Keystone Ski Resort
in rural Colorado, throwing 60 of the 372 passengers to the ground from heights of up to 50 feet. The remaining 312
people were left stranded on the chair lift for up to 3 hours. The initial medical care was delivered by the ski patrol and 12
volunteer physicians and nurses who were present on the slopes ( 40,41).
A total of 49 patients were first triaged to the medical clinic at the base of the mountain after immobilization and oxygen
therapy were initiated. Transportation was accomplished by snowcat, snowmobile, or toboggan. Once at the medical
clinic, advanced trauma life support measures were carried out, including placement of chest tubes in six patients with
clinically apparent pneumothorax ( 40). Rotocraft and ground vehicles were used to deliver patients to hospitals. The
authors suggested that the successful triage, treatment, and transportation of these patients from a remote location was
possible only because of advanced planning and the participation of the regional trauma system ( 40).
Another multicasualty event that occurred at a major sports event took place in Pittsburgh during the annual Three Rivers
Regatta Formula I Boat Race (42). This 3-day event in 1988 attracted 440,000 spectators, and 135,000 were estimated to
be present on the day of the boating accident. At the event, spectators generally lined up on the riverbanks and bridges
or sat in bleachers provided to watch the race. City of Pittsburgh EMS units, including river rescue teams, and EMS
medical command physicians were stationed throughout the racecourse area to facilitate access to both spectators and
Formula I drivers. Four river rescue teams made up of three EMT paramedics each (two teams also had a physician) and
two mobile and three stationary EMS teams composed of one physician and three EMT paramedics each were
strategically placed during the race. A total of 7 EMS physicians and 27 paramedics were available for patient care.
Communication was coordinated through an onsite command center, which was linked to the citywide communication
network, including area hospitals.
During the 50-lap race, one of the Formula I boats traveling at approximately 45 mph veered from the racecourse just
after a turn and went into a crowd of approximately 800 spectators. The 1,100-pound boat came to rest on the shore after
striking 24 spectators. The onsite medical teams provided an overall assessment of patients and injuries.
Physician-directed triage accomplished the initial treatment and disposition of 24 patients to five hospitals (four of which
were level I trauma centers) in 32 minutes. A physician and paramedic accompanied six of the eight most seriously
injured patients to the hospital and used interventions such as intravenous catheters and military antishock trousers
(MAST) during transport. A total of nine ground ambulances were employed.
Of the 24 individuals injured, 12 were children. A total of 10 were admitted to the hospital, 6 of whom required emergency
surgery. There was one fatality. The authors attributed the success they had in expeditious triage, treatment, and
transport of these patients to extensive preplanning; availability of adequate personnel, supplies, and ambulances;
integrated communication systems; and the presence of EMS physicians for patient triage and treatment ( 42).
Disasters do not necessarily result from catastrophic events. Ellis et al. ( 15) described their experience of providing
medical coverage for the Pittsburgh Marathon in 1986. The 26.2-mile course had 2,900 runners and an estimated
500,000 spectators on an unusually warm day (30°C [86°F]) with a wet bulb-globe temperature of 25.5°C (78°F). The
medical teams at the 24 field aid stations along the racecourse and at the finish line were composed of 54 emergency
and sports medicine physicians, 180 nurses, 141 EMT paramedics, 30 podiatrists, and 86 athletic trainers and physical
therapists. The medical team had hundreds of volunteers to support its efforts, including recorders, escorts, and research
assistants. Each field aid station was equipped with ice, oral rehydration fluids, intravenous fluid therapy, dextrose
solutions, and rectal thermometers. The oral fluids and medical therapies and the weather advisory system were in
compliance with the recommendations of the American College of Sports Medicine ( 43). Communications for the
marathon medical team were coordinated by volunteer ham radio operators.
This sports event, coupled with the unusually warm temperature on race day, accounted for an inordinately high number
of patients seen by the medical team. A total of 658 runners (25%) required medical attention, and 52 (8%) needed
transport to a hospital. Of the total number of patients treated, 379 (58%) were cared for at the finish line and the
remainder were seen on the racecourse, most commonly (78%) between miles 16.2 and 22.8. A total of 228 runners
dropped out of the race for unknown reasons. The authors concluded that a marathon provides a unique opportunity to
practice disaster management, particularly if the weather conditions are extreme. They recommended having 50% of the
medical personnel and equipment dedicated to the finish line area and 80% of the remaining personnel and materials at
field aid stations located 1 mile apart between miles 16 and 23. The health care team must be capable of providing ALS
therapy, including the determination of hypothermia/hyperthermia and fluid electrolyte disorders ( 15).
Although the potential for a large-scale disaster is always looming at any sports event, one must not neglect the perhaps
more common phenomenon of isolated spectator or athlete injury or illness. A number of reports in the literature deal with
mostly isolated, athlete-related injuries from projectiles or simply from the playing style ( 44,45 and 46). Ocular (47,48),
dental (49,50), and head and neck (51) trauma are common recurring injuries to athletes, particularly those who play
hockey, baseball, or lacrosse. Little has been written about isolated spectator injuries for those who attend either
high-contact sporting events or sporting events with the potential for projectile-type injuries.
MEDICAL PREPAREDNESS FOR SPORTS EVENTS
Based on what has been reviewed, the vast majority of illnesses and injuries seen at sports events are relatively minor in
nature. On the other hand, the overall prevalence of death from cardiovascular disease and the fact that more than half
of such deaths occur outside of the hospital necessitate a well thought-out medical coverage plan for sports events.
Disasters can and do occur at sporting events, and emergency care providers must be prepared.
Although it is difficult to recommend one single plan to fulfill every medical coverage need, there are some basic
questions that should be asked when preparing for emergencies at sporting events. These questions are what, who,
where, and when.
What
First, what is the event? What is the injury potential for the event? Predictably, some events will have more injuries and
illnesses on than off the field ( 44). Contact sports with players going at high rates of speed can be expected to produced
more injuries than individual performance sports. Events with large crowds, simply by virtue of their number, have the
potential to generate more medical emergencies. In addition, alcohol consumption by spectators, the ability of spectators
to be mobile, and increased ambient temperature influence the number of people presenting for medical care ( 12). Before
developing a strategy for providing care at sports events, planners should determine whether a similar event has been
held previously. Articles in medical and EMS literature, as listed in Table 21.3, may provide some background and
prevent “reinventing the wheel” ( 12).
TABLE 21.3. PUBLISHED REPORTS OF EMERGENCY MEDICAL CARE AT SPORTS EVENTS
What are the responsibilities of the emergency care providers? Are the emergency care providers responsible for
providing equipment, personnel, and transportation? What authority does the provider of medical care have?
Finally, what is the budget for emergency care supplies, and how will care providers be “paid” (e.g., money, souvenirs,
free tickets)?
Who
Who will be participating in the event? Will the participants be amateurs or professionals? What is the average age of
participants, and what is their expected level of conditioning? How many participants will be involved, and will they have
their own trainers or physicians? Will the event include disabled participants or spectators, elite athletes, dignitaries or
other VIPs? What accommodations are necessary to meet the needs of this population?
Who is expected to attend the event? For most sports events, a wide age range of spectators can be expected. However,
large numbers of younger spectators may have a higher number of problems related to alcohol and drugs, whereas an
older group of spectators may have more cardiac-related events ( 12). Are estimates available regarding the number of
spectators that will attend the event? The most difficult situations are open events where spectators can come and go as
they please (12).
Emergency planners should also learn what beverages will be available for spectators and participants. At warm-weather
events, adequate amounts of water should be made available free of charge. Spectators are often reluctant to stand in
line to purchase water. This may lead to casualties secondary to dehydration and heat illness. Planners at events at
which alcohol will be available must be prepared to manage alcohol-related illnesses and injuries.
Where
Where will the event take place? Will it be held in an indoor stadium or at multiple outdoor venues? Access and
transportation issues are uniquely affected by the location of an event. Also to be considered is whether the spectators
will be seated (e.g., in a stadium) or roaming around a venue. For outdoor events, is shelter available in case of bad
weather?
Emergency care planners must identify and develop contacts with the local hospitals, EMS agencies, and government
entities. Are there local laws and regulations that may regulate coverage of sporting events and mass gatherings?
When
When will be event be held? During what season of the year will it occur, and what time of day? These factors may
influence the start time of the event. Historical weather data can often be obtained from local weather services.
Emergency planners must be prepared for weather extremes. Over the 14-year history of the City of Pittsburgh Marathon,
which is held on the first weekend in May, weather conditions during the race have ranged from 0°C (32°F) and snowing
to 30°C (86°F) and sunny. Many other factors may influence the date and time of an event, such as holidays, television
coverage, local traditions, and the dates of other related events.
The weather can influence the number of casualties among both spectators and participants. Temperature is only one of
the factor to be monitored. Wind, humidity, and cloud cover also influence the heat-related stress for athletes and
spectators. The Centennial Olympics revealed how heat and humidity can combine to influence the use of medical care
facilities at sports events ( 18). In addition, major weather or factors such as lightning, hurricanes, tornados, and floods
must be considered in susceptible areas.
COMMON FACTORS IN EMERGENCY PLANNING
Leadership
As in most organizations, health-related or otherwise, the medical coverage of a sports event requires medical
leadership. A physician with experience in out-of-hospital medicine would be an ideal leader, but the head of the medical
care team should at least be a physician with expertise in sports medicine. There are training programs that offer
experience in EMS and others that offer fellowships in sports medicine ( 52). Less ideally, the medical leadership could
take the form of a medical advisory committee that leads by consensus. The medical leadership of some EMS systems is
structured in this fashion.
The physician leadership should determine the optimal way to provide medical care at a sports event, based on
experience, the current medical literature, and the resources available. The equipment, personnel, and treatment
protocols must all be medically sound and subjected to regular postevent review. Event-day information (e.g., weather
conditions, attendance, potential dangers from the sports event itself) should be taken into consideration and should
provide the impetus for change in the medical coverage plan.
Another responsibility of the medical leadership might be to develop educational programs or materials for spectators
and competitors to prevent illness or injuries during the sports event. Factors such as lightning precautions, hot or cold
weather precautions, and the location of health care facilities within the stadium or park could serve to minimize the
numbers and types of injuries encountered during the sports event.
Emergency Medical Systems Involvement
Every day, EMS providers respond to emergencies involving acutely ill or injured persons. Prehospital care providers,
acting as physician surrogates, perform life-saving interventions as part of their routine practice. It is critical to involve the
EMS system of the locality of the sports event in the medical care plan. The level of commitment of course depends on
the nature of the sports event and the number of participants and spectators.
For large crowds (more than 1,000 spectators), it would make the most sense to have an ambulance dedicated to the
sports event with no other outside patient care responsibilities. This ambulance and crew would be responsible for caring
for participants and spectators who become ill or injured. If the size of the spectator crowd grows, additional EMS crews
may be committed to the event. If it is feasible to have an onsite physician involved with large sports events, then the
nurses and EMT paramedics can function under direct physician input. In the absence of a physician, the prehospital
providers would need to function from protocols that may or may not require communication with the physician before
implementation.
Almost all of the studies reviewed in this chapter reflected a reliance on the EMS system for the successful operation of
the medical care team. Whether it be ground ambulance service, air medical service, or a combination of both, it is
imperative to have the support and commitment of the EMS system in any medical care coverage plan for a sports event.
In addition, it behooves the organizers of events and the medical leadership providing the care to familiarize themselves
with the local EMS disaster plan. It is of great mutual benefit to hold mock disaster drills in the stadium or convention hall
to test the local disaster response and to familiarize the disaster team members with the sports event facility.
Medical Supplies
It is difficult to speculate on the amounts and types of medical supplies that will be needed for a sports event. There is no
equation that can take into consideration the number of spectators and participants and the incidence of certain types of
injuries or illnesses and then provide a medical supply recommendation. The variable nature of sports events and the
environments in which they occur make the task of predicting requirements for supplies very difficult.
The provision of ALS medical therapies seems to be essential. Physicians, nurses, and EMT paramedics staffing a sports
event without ALS supplies could offer nothing beyond basic CPR. Airway equipment, cardiac resuscitation medications,
and intravenous catheters and solutions are the minimally essential medical supplies. The quantity of each that is
needed obviously depends on the anticipated number of patients. For the City of Pittsburgh Marathon, the EMS team
keeps a running tabulation of the quantity of supplies put out on the racecourse each year, what is used, and how many
runner-patients are treated. In 1992, for example, 320 patients (less than 10% of the registered marathon participants)
were treated along the racecourse or at the finish line. A total of 15 patients received intravenous crystalloid fluid
resuscitation, 2 received 50% dextrose and water, and 7 received both. This type of data at least provides a general idea
of what may be needed from year to year. Usually the EMS team overestimates the medical supplies needed each year
by a small percentage so as to be prepared for any untoward events ( 15).
Medical Personnel
Several authors have attempted to predict the medical personnel needed for a given event based on the number of
spectators or participants ( 9,16,53,54). This method does not take into consideration the various types of sports events,
the environmental conditions, or the risk of injury from the different sporting activities. These estimates are a place to
start, however, when developing a medical care team. In addition to the prehospital providers enlisted, the roles of
physicians, nurses, or other health care providers must be determined.
The City of Pittsburgh Bureau of EMS and the EMS physicians from the University of Pittsburgh provide medical care for
the Three Rivers Stadium and the University of Pittsburgh football stadium for the home football season. The stadium
medical coverage for each facility is responsible for both spectators and participants, although the football teams usually
have preidentified team physicians. Three Rivers Stadium has seating for 59,000 spectators, while the University football
stadium seats 56,000.
The medical team for the Three Rivers Stadium coverage consists of 2 EMS physicians and 10 paramedics, with two
dedicated ambulances at the stadium. The EMS physicians and four of the paramedics are stationed in the single first aid
room that provides for the spectators almost exclusively. Another six paramedics are located on the playing field, with the
primarily responsibility to care for ill or injured players. All medical personnel share a dedicated radio frequency that can
be accessed by the stadium security radio communication system. The City of Pittsburgh EMS system can be called on
for additional ambulances and EMT paramedic support as necessary.
The University of Pittsburgh football stadium configuration for medical care is similar to that for the Three Rivers Stadium.
Two or three physicians, eight paramedics, and three dedicated ambulances are present for each home football game.
The single aid station is staffed with one physician and two or three paramedics. The other paramedics are placed in
pairs throughout the stadium in positions that provide optimal access to spectators and participants. Physician
rendezvous with the paramedics to assist in patient care as needed. All medical personnel share a dedicated radio
frequency that can be accessed by the stadium security communications system.
Thus far, there have been no mass casualty incidents at any of the football games in Pittsburgh. The emergency medical
care plan described here has served the needs of the spectators and participants extremely well, with both basic and
ALS care delivered. Furthermore, integration of the plan into the local EMS system has provided excellent reserve
paramedics and ambulances when the need has arisen.
CONCLUSIONS
This chapter reviewed the current understanding of emergency medical care at sports events. Because most of the
medical literature is retrospective and anecdotal, it is difficult to propose specific guidelines for medical coverage. The
information that can be garnered from descriptive studies is useful, but the paucity of qualitative research techniques in
these reports leaves one with merely suggestions. Published reports from the Centennial Olympic Games in Atlanta
begin to apply a scientific approach to the coverage of sports events.
Planning for medical coverage of a sports event is analogous to disaster preparedness planning and as such should
include some of the mainstay features. Leadership, communication, personnel, and supplies must all be detailed in any
successful medical plan. Developing an emergency medical care plan for a sports event offers unique challenges that
must be met if public needs are to be successfully addressed. Organizations such as the National Association of
Emergency Medical Services Physicians and the American College of Sports Medicine stand to lead the way in the
development of policies and procedures for the emergency medical care of sports events.
APPENDIX A. MEDICAL CARE AT MASS GATHERINGS: GUIDELINES FOR CAREa
I. Objectives for Medical Care

A. Mandatory: All mass gatherings should have provisions for emergency medical services to evaluate, treat, and
transport patients who develop illness or injuries that are threats to life or limb. The following objectives must be
met at all events.
1. Basic first aid and life support should be provided by someone trained to at least the level of basic
emergency medical technician (EMT). Basic aid should be available to anyone at the public gathering, within
4 minutes after being taken ill, when the site is at full capacity.
2. Advanced life support resuscitation and immediate treatment of acute medical emergencies should be
provided, within a maximum of 8 minutes after anyone is taken ill, when the site is at full capacity. This
support could be provided by paramedics under medical control or by physicians appropriately trained and
equipped.
3. The ability to evacuate the patient to a definitive care facility within 30 minutes should be provided.
B. Optional: Those sponsors wishing to have additional care available may provide for the evaluation and
treatment of nonemergency illnesses and injuries (e.g., sprains, lacerations). This would allow the spectator to
return to the event after evaluation and treatment. The following objectives may be adopted.
1. Medical evaluation and treatment for nonemergency problems should be provided by licensed physicians,
with attention to appropriate documentation on medical records.
2. Triage and medical evaluation of a presenting complaint involves medical judgment as to whether the
complaint is an emergency or a nonemergency and recommendations for follow-up. This should be done by
a licensed physician, with appropriate documentation on medical records.
II. Aspects of medical care: In order to accomplish the mandatory objectives, appropriate planning must be done by
sponsors with regard to the following.
A. Communication: Adequate communication must be available
1. To the public: To understand how to call for medical help and what medical services are available within the
facility
2. Within the facility: Adequate communication among security, medical, and transport personnel so that they
can be dispatched promptly to an area of need within the facility
3. With an area-wide emergency medical services (EMS) system: Adequate communication with area-wide
emergency medical dispatch, base-station hospitals, additional paramedic units, and the like.
B. Transportation: Adequate transportation and access must be provided
1. For medical personnel to get to the injured patients
2. For patients to be transported promptly to a definitive care facility
C. Emergency medical personnel: The number and type of emergency medical personnel to accomplish the
objectives will depend on the event and facility involved. Factors to be considered when planning or the number
of personnel include age of anticipated audience, length of event, density of crowd, movement of crowd, type of
event, design of facility, weather, indoor versus outdoor event, availability and use of alcohol or other drugs, and
location of nearest EMS facilities.
III. Guidelines for Meeting Objectives: Although the number and type of medical personnel may vary depending on a
number of factors, the important point is that they be considered adequately in the planning process to accomplish
the stated objectives. The following guidelines are provided as one method that sponsors may use to fulfill the
desired objectives.
A. Mandatory Objectives
1. In most circumstances the most practical method of providing emergency medical care for potential threats to
life and limb is to ensure that paramedics or paramedic/EMT teams are available within the facility. Two
paramedics or one paramedic/EMT team for each 10,000 people is recommended. These teams should be
placed strategically throughout the facility so that they can promptly respond to a communications system
call from anywhere within the facility.
2. Paramedics should be familiar with the EMS services available in the area. They must be state certified. It
should be noted that paramedics are not licensed to practice medicine. Therefore, in order to provide
advanced life support (paramedic) services at events, appropriate arrangements must be made with
paramedic provider agencies and the base-station hospital. Paramedics are not capable of providing the
optional objectives listed. They should not be treating nonemergency medical problems or rendering medical
judgment regarding patient complaints unless they are under the direct supervision of a physician.
B. Optional Objectives
1. If the sponsor wishes to provide the optional capabilities described, the services of a physician are
recommended. It must be emphasized, however, that the provision of these optional services alone will not
necessarily accomplish the mandatory objectives (emergency services for threats to life and limb).
C. Mandatory and Optional Objectives
1. If the sponsor wishes to provide evaluation and treatment of medical problems as well as emergency medical
services for threats to life and limb, teams of physicians and prehospital care providers should be utilized.
We recommend one to two physicians for every 50,000 people and two EMTs/paramedics or one
paramedic/EMT team for every 10,000 people. These teams should work together as coordinated units to
provide both the mandatory and the optional services. A system of record keeping and storing of medical
records is mandatory. Clinical equipment and designated facilities to care for both emergency and
nonemergency problems must be provided in order for health care personnel to adequately use their skills.
2. Physicians should be licensed in the state in which the event occurs. Preferably, they should be board
certified in emergency medicine; if this is not possible, then they should be certified in advanced cardiac life
support and advanced trauma life support. They must be familiar with the EMS system and base-station
hospitals in the area. Registered nurses may be able to aid in accomplishing these objectives. Whenever
possible, they should be certified emergency nurses and certified in advanced cardiac life support.
a
These guidelines have been approved by the Arizona Chapter of the American College of Emergency Physicians (ACEP). They are presented
for evaluation and discussion. They have not been approved by the national ACEP Board of Directors. Reprinted by permission from Sanders
AB, Criss E, Steckl P, et al. An analysis of medical care at mass gatherings. Ann Emerg Med 1986;15:515–519.
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22 Equestrian Sports
22
EQUESTRIAN SPORTS
DAVID M. JENKINSON
SARAH W. JENKINSON
History
Biomechanics, Disciplines, and Diversity
Racing: Flat Track, Steeplechase, and Harness
Polo
Rodeo and Western Riding
English Riding
Driving
Miscellaneous Competition Events
Recreational Activities
Epidemiology
Age
Sex
Areas of Injury
Types of Injury
Specific Injuries
Neurologic Injuries (Head and Spinal Cord)
Spine
Pelvis
Upper Extremities
Lower Extremities
Medical Issues
Toxicology and Drugs
Safety and Conditioning
Conditioning
Skills and Knowledge
Equipment
Medical Services
Conclusions
Chapter References
There is no doubt that horse sports are extremely dangerous, particularly those involving riding or jumping at high
speeds. Riders have long accepted accidents and injuries as “part of the game,” and “get right back on the horse that
threw you” is the catchphrase. Accidents happen because each horse is an individual, with its own personality, and
although the basic nature of horses remains the same, it can be markedly influenced (for good or ill) by handling and
training. Accidents and injuries are more likely to occur if a rider of limited skill, ability, or knowledge is paired with a
horse whose level of training or personality is beyond the rider's scope. If the rider is not wearing appropriate and safe
attire, the results may be that much worse. It is only in the last few decades that books about horses and riding have
done more than gloss over safety for the rider; previously, most information on injuries and accident prevention was
dedicated to the welfare of the horse.
HISTORY
Before domestication, the horse was first used as a source of food, being hunted by Paleolithic humans some 25,000
years ago (1). Not long after domestication (2000 to 3000 bc), horses were used for war, and they continued to be
valuable allies well into World War II. Training for war spawned many of the horse sports seen today. As early as 1450
bc, the Greeks introduced both horse racing with riders and chariot racing into the Olympic Games ( 1). These evolved
into the horse racing events we know today—on the flat track (as in the Kentucky Derby), the steeplechase (over jumps),
and harness racing. The competition known as 3-day eventing (or “combined training”) has a direct link to the military; it
started as a test of training and endurance for the cavalry and now has become a popular competitive sport. As a source
of transportation and labor, the horse had no equal until the advent of the engine. Various breeds were developed to
make horses more efficient at certain tasks: heavy draft breeds to pull enormous loads, lighter riding breeds with smooth
gaits for swiftness and easy riding, small tough pony breeds to work and thrive where the living is hard, fancy-stepping
elegant breeds to pull coaches and carriages, and many more.
As the need for horses in daily transportation, agriculture, and war declined, their popularity as a source of sport and
recreation rose, and their former occupations were modified for pleasure and competition. The stagecoach and the
delivery wagon have been replaced by competitive driving events, the military cavalry training is now 3-day eventing, and
the cowboy's art with horse and rope can be seen at rodeos across the United States. Foxhunting still exists in various
forms around the world, but it too has been modified into the show-ring sport of “hunters and jumpers.” Polo is an ancient
sport carried into the modern day, still a fast and furious competition. Millions of people participate in horse sports and
horse-related activities each year in the United States. This can involve a pony ride at the zoo, a trail ride on a dude
ranch, a horse kept in a backyard and ridden on weekends, lessons taken once or twice a week at a local stable, a
serious competitor riding daily as practice for showing throughout the summer, a professional trainer riding five horses
each day, a ranch hand moving livestock, or a jockey racing in several races a day. Humans have invented innumerable
ways to employ and enjoy the horse, and detailing them all would fill several volumes.
The human race has been magnetically attracted to the horse throughout history. Consider the words of Xenophon in 400
bc: “The horse is such a thing of beauty, none will tire of looking at him.” It is impossible to extinguish the passion true
horsemen feel for their horse, their beauty, and the development of their prowess, and there is a spiritual cathartic
process when our nature is combined with theirs ( 2). Riding is fundamentally a partnership between human and horse,
and the satisfaction lies in the subtle communication and interaction between the two ( 3). The horse is a fascinating
animal, combining immense power with gentleness, speed with patience, and the fear-driven instincts of a prey animal
with an amazing ability to trust. Despite the inherent dangers of horse sports, millions of people climb aboard a broad
back and are carried away, physically, emotionally, and spiritually. As Robert Smith Surtees put it, “There is no secret so
close as that between a rider and his horse” ( 4).
BIOMECHANICS, DISCIPLINES, AND DIVERSITY
This section is intended as a brief overview of the more common riding styles and horse-related activities and the factors
that contribute to injuries particular to each sport.
Racing: Flat Track, Steeplechase, and Harness
Although there are many classes of races, the objective is the same: the first horse under the wire wins. A horse can run
at a top speed of 40 to 45 mph, and because there are up to 12 horses in a race, the consequences of a fall can be
traumatic. The potential for injury is greatest with steeplechasing, because it involves jumping 4½-foot fences, some with
6-foot ditches in front, at a 30-mph gallop ( 3). The horse may hit a fence and catapult the rider to the ground, or the
horse may fall with or onto his rider. If the fall happens at the front of the pack, the jockey also stands a good chance of
being kicked or stepped on as the rest of the horses go by. Harness races are run at a trot or pace. Although the
incidence of driver injury has not been well documented, there is great potential for serious injury should a collision
occur. Jockeys and drivers must wear helmets that meet or exceed standards set by the racing commissions.
Polo
Polo is a team sport, with four horses per team. It is played at a gallop, with many quick changes of direction and speed.
Mallets are used to whack a small, hard ball into the goal. Riders may be injured by another's mallet or by collisions or
falls. Helmets are mandatory, as are knee, knuckle, and shin protection, and facemasks are becoming commonplace ( 5).
Rodeo and Western Riding
In the past, early sports medicine advances in rodeo were slowed by the disregard for orthotic concerns, inadequate
self-treatment, and a lack of onsite preventive care. Injury awareness is increasing, however, as is the use of taping,
elbow braces, forearm padding, mouth guards, and neck braces (6).
Bronc Riding: Saddle and Bareback
The rider needs to stay on his bucking horse for 8 seconds. Bareback riders wedge a hand into rigging strapped around
the horse's middle, but the horse is otherwise free. Saddle bronc riders hold a rope attached to a halter on the horse's
head. In both events, the rider must keep one hand free and may not touch the horse with it at all. The legs are used in a
swinging motion from the horse's shoulders to ribs and therefore cannot be used for gripping. Some riders wear neck
rolls, similar to “cowboy collars” seen in football, and the riding arm may be braced or taped. Head protection is almost
never worn.
Roping and Steer Wrestling
There are several roping events in rodeo, but all involve a mounted rider or riders chasing a calf or steer, getting a rope
on it, and bringing it to a standstill. In two events the rider must also dismount, grab the animal, and tie three of its legs
together. There can be major trauma to the hand if it gets caught between the rope and the saddle. In steer wrestling (or
bulldogging), a rider gallops after a steer, dives off the horse and onto the steer, and, by grabbing its head and horns,
pulls the steer to the ground. Both are timed events. Usually no safety gear is worn other than gloves.
Barrel Racing
This is a timed event in which the rider must run a cloverleaf pattern around three barrels and back as fast as possible
without knocking a barrel over. Barrel horses are typically very high energy. Because the sport mixes speed with
extremely tight turns, a horse may lose its footing and fall, or the rider may cut too close to the barrel and hit it with a
knee or shin. Although knee and shin guards may be worn, helmets usually are not.
Reining and Cutting
Cutting is a test of a horse's “cow sense.” The rider selects a cow from a small group and separates it from the bunch.
The horse then takes over and then must keep that cow from returning to the herd. This involves many quick starts and
stops, ducks and dodges, and the rider must stay with the horse but not interfere. Reining is a sport of speed and
precision that demonstrates a horse's training and handiness and the rider's accuracy in riding a figure. There are set
patterns involving circles, spins, and short fast runs with sliding stops. Both cutting and reining require a rider who is well
balanced on a horse and supple enough to absorb the quick changes of speed and direction. As with almost all western
riding, helmets are not worn.
English Riding
Hunters and Jumpers
Both of these activities take place in an enclosed ring or arena. Riders negotiate a course of 8 to 12 jumps, up to 4½ feet
in height and 4 feet in width, depending on the level of competition. Each course consists of twists and turns between
jumps, but jumper courses are judged on speed, making the result of a misstep more dangerous. Jumps are designed to
fall apart if they are hit, and points are deducted for knocking off rails (poles). Hunters also ride in “flat” classes, in which
horses are ridden in a group and do not jump (see Miscellaneous Competition Events ). A helmet must be worn for
competition, but an ASTM/SEI-approved helmet is not required. In fact, because of the uncomfortable fit and unattractive
appearance of most approved models, the nonapproved helmets seem to be preferred by competitors and even judges
(7).
Three-Day Eventing (Combined Training)
Eventing, also called combined training, is what is seen in the Olympic Games. It is also the sport that made Christopher
Reeve a quadriplegic, despite his correct and appropriate use of safety equipment. At the lower levels (horse trials or
three-phase), it consists of dressage, cross-country, and stadium riding (similar to jumpers), normally run on 1 or 2 days.
At the upper levels, it is run on 3 days because there are additional endurance tests for the horse and rider team. Of the
three phases, cross-country has the greatest potential for injury. Depending on the level of competition, riders must
gallop 1,500 to 4,000 m at speeds of 300 to 600 m per minute and tackle up to 40 jumps averaging 4 feet in height and
spread. The terrain may be uneven and hilly, and the jumps are solid and designed not to fall apart if hit. Mandatory
safety equipment includes a helmet, a body protector vest, and a medical armband ( 8).
Dressage
Dressage is to riding as figures are to skating and dance is to gymnastics. The word dressage means “training,” and the
sport involves various paces, figures, and movements executed by the horse and rider with precision and accuracy. It is
sport and art combined to display the horse's full athletic potential. Although dressage does not generally involve great
speed or jumping, and is usually practiced in an enclosed ring or arena, and there is still a potential for injury. Too many
dressage riders do not wear helmets because they are not jumping, because they feel that their horse is “bomb-proof,” or
because they assume that they ride too well to fall off. However, horses still retain the ancient fear of a predator in the
shadows, and even the best trained and seasoned horse can spook violently and unpredictably.
Driving
Driving encompasses everything from a farm horse pulling logs out of a woodlot, to an Amish buggy used for daily
transport, to fancy show horses in competition in the ring, to the Budweiser Hitch. There are myriad things a horse can
pull, but all driving involves the horse's overcoming the natural fear of being chased. The classic western movie scene of
the runaway buckboard is a very real danger, and, apart from the driven version of eventing, drivers and their passengers
very rarely wear any safety equipment at all. Although the horse and buggy may seem an anachronism in today's
fast-paced world, there are small communities that still rely on the horse as their primary source of transportation. In the
United States, the Amish and Mennonite drivers are most commonly seen, and as the density of automobiles increases
on the roads they travel, so does the frequency of buggy-auto collisions. The large, heavy draft horses used for farm
work can weigh 2,000 pounds (900 kg) and stand more than 7 feet tall (2 m) at the shoulder. Though they are normally
the gentle giants of the horse world, even a minor mishap can have drastic results simply because of their size and
power.
Miscellaneous Competition Events
There are so many different styles of riding and breeds of horses throughout the world that it would be impossible to
touch on them all. Endurance sports are becoming popular. These may include 25- to 100-mile endurance rides, “ride
and tie” competitions, the modern pentathlon, and even the new EcoChallenge. These events test the horses'
conditioning as well as the riders' fitness and horsemanship. There are many kinds of riding competitions that are judged
as “rail classes”—that is, a group of horses are ridden at various gaits, with the judging emphasizing everything from the
rider's ability to the horse's way of going. In two disciplines in particular, western riding and saddleseat, riders classically
do not wear helmets in competition, not even small children. Although one would think that competitions would be
designed to prove whose horse is faster or better trained, or which rider is the most skilled, many horse shows have
become nothing but beauty pageants, and fashion often counts for more than safety and common sense.
Recreational Activities
The most common use of the horse today is for individual pleasure and recreation. The casual weekend rider, the child
taking weekly lessons at a local stable, and the backyard horse owner probably make up the majority of the ridership in
the United States. Unfortunately it is just this population that is hardest to quantify in terms of injury rates and— with the
possible exception of the lesson-taking child—impossible to regulate in terms of safety. Even those riders who must
compete in a helmet might not do so at home or in practice, and because many people who keep a horse just for trail
riding also ride western, there is little incentive to wear a helmet.
EPIDEMIOLOGY
To begin this section one should keep in mind that equine sports have been considered dangerous since ancient times,
to wit the old Arab proverb: “The grave yawns for the horseman” ( 9). The horse is a massive animal, weighing 1,000 to
1,500 pounds (500 to 680 kg) or more, that can travel with a rider at 30 mph (50 kph) or more ( 10,11). With the average
saddle height at 6½ feet (2 m) and the rider's head height at almost 10 feet (3 m) ( 12), a fall is a dynamic event unrivaled
in nonmotorized recreational sport. The force of a kick, supplied through a steel-shod hoof, exceeds 10 kN ( 13). Because
of such large forces involved, equestrian injuries should be initially considered “ballistic” or high-energy injuries. Indeed,
in some studies, horse trials have a higher rate of injury and death than motorcycle racing ( 5,14).
In the United States, horseback riding is an extremely popular sport. Approximately 30 million people ride at least once a
year, and at least half of them ride on regular basis ( 15,16 and 17). The U.K. riding community exceeds 3 million, half of
whom are children (18). In 1990, the U.S. Centers for Disease Control and Prevention (CDC) estimated the incidence of
horse-related injuries to be 18.7 per 100,000 ( 19). Although the various riding disciplines have some differences in their
injury statistics, use of the National Electronic Injury Surveillance System (NEISS) database revealed that in 1987–1988
there were an estimated 92,763 emergency room visits relate to riding. Between 45% and 75% of the injuries resulted
when the rider fell from the horse ( 12,15,17,20).
Because of wide variation in the way horses are used for sport and pleasure and the different reporting systems (from
discipline or professional society reviews to emergency room reports), a review of the literature can paint quite a
confusing picture. However, such a review clearly documents the hazards of riding ( 17,21,22,23,24,25,26,27 and 28) and
on closer inspection does reveal some basic patterns.
Age
The American Horse Council estimated that 258,434 youths were involved in 4-H horse and pony programs in 1994 and
13,000 youths were members of United States Pony Clubs (29). Earlier the same organization estimated there were 1.2
million horse owners in the United States who were younger than 20 years of age ( 30). In 1985, Hammett noted that “in
the two-year study of the estimated 13,428,000 hours of horse activity by 18,408 U.S. Pony Club members age 6 to 21 in
scheduled supervised programs, there were 64 accidents resulting in 88 injuries” ( 31).
In 1996 a review of the United States NEISS database showed that approximately 25,000 emergency department visits
were made by individuals younger than 25 years of age as a result of horse-related injuries ( 32). Approximately 2,300 of
these patients were admitted to the hospital ( 33). The total cost of these horse-related injuries was estimated at more
than $88 million, and the average cost per injury at $7,400 ( 34).
When data from worldwide studies of horse-related injuries by age group are reviewed for both pediatric (USPC, VISS)
(35,36,37 and 38) and all ages (NEISS, CHIRPP) (39), two peaks become clear (Fig. 22.1). The first peak is the 10- to
14-year-old age group (20.2% to 48.1% of participants injured), and the second peak is the 25- to 40-year-old age group
(13.1% to 39.6% injured). Although it is difficult to compare data from such varied studies, these results are certainly
consistent with the overall trend seen in the literature.
FIGURE 22.1. Age versus percent injured. (Data from references 9 [NEISS 1992–1996 (USA)], 35 [CHIRPP 1995 (CAN)],
36 [VISS 1995 (AUS)], 37 [Chitnavis 1996 (UK)], 38 [USPC 1982–1996 and 1997 (USA)], and 39 [NEISS 1997 (USA)].)
Sex
There appears to be a marked sex-related difference in injury rates. The highest accident rates occur among young and
inexperienced children and teenagers, a group in which girls predominate ( 40,41,42,43,44,45,46,47,48,49,50,51,52,53 and
54). Their accident incidence is out of proportion to the numbers involved ( 48,55,56,57 and 58). Girls and women
dominate the riding population up through the young adult age group, and they also surpass male riders in rates of injury.
Men have a higher rate of injury among those age 25 years and older, which may reflect the male-dominated professions
such as racing and rodeo sports.
Areas of Injury
Thirteen studies were reviewed and the cumulative results tabulated. The studies were done between 1976 and 1999;
they covered pediatric and adult populations and a fairly wide variety of horse activities. Although the disparity in the
studies is evident, Figure 22.2 shows that the upper extremities are the primary site of injury, followed closely by the
lower extremities, head, and spine.
FIGURE 22.2. Areas injured. (Data from references 24 [Press—UK Nat. Jockey], 31 [B-H Youth 82 and 83], 35 [CHIRPP],
38 [AMEA—USPC 1997], 39 [NEISS 1995], 45 [B-H NPS 1978–1983 and B-H USPC 1982–1990], 103 [Paix 1999—Aus
Ct], 104 [Whitesel TB Jocks 1976], 105 [B-H AMEA Jockey Inj. 1997], 106 [Costa-Paz Polo], 107 [Hobbs], and 108
[Whitlock BJS M-1999].)
Types of Injury
When seven studies were compared for injury types, it was found that contusions and abrasions made up the majority of
the injuries sustained. Fractures were also common, especially in jumping and speed sports. Closed head injuries
represented slightly less than 10% of total injuries; although this percentage is down from 20 years earlier ( 37), it is still
significant ( Fig. 22.3).
FIGURE 22.3. Types of injuries. (Data from references 9 [NEISS], 24 [Press], 31 [B-H Youth], 35 [CHIRPP], 38 [USPC
1997], 45 [B-H NPS], and 109 [Whitesel].)
SPECIFIC INJURIES
Neurologic Injuries (Head and Spinal Cord)
For planning purposes western European, North American, and Australian neurosurgical services can expect at least one
severe riding head injury per month per million of local population served ( 52,53,59,60 and 61).
Head trauma can occur in any aspect of horse handling, not just riding. Kicks present the greatest chance of serious
injury, but closed head injury or fracture can be the result of a blow from the horse's head, or if the handler is pushed or
dragged to the ground or into other objects. Most horses do not understand their strength relative to that of humans, and
a horse who does can be very dangerous indeed. Mounted injuries are usually the result of a fall. The rider may be
dragged and may sustain repeated, multiple occipital injuries to the head. This is caused when a foot or leg is caught in
the stirrup due to failure to wear a heeled riding boot ( 54,62). If the rider is thrown clear, he or she may still be struck by
another horse if riding in a group (e.g., racing, foxhunting, group trail rides).
Becker's principle (63), that the proportion of head injuries in a sport reflects the degree of head-forward stance adopted,
holds in riding and ensures that head injury complicates much riding trauma ( 53,57,58,60,64,65). Skull penetration and
deformation and brain acceleration (linear, radial, and rotational about all three spatial axes) with associated brain tissue
shearing, cavitation, and hemorrhage are all consequences of riding head injury ( 66).
In the past, the cumulative effects of repeated head injury were a major feature of the racing scene, with
punch-drunkenness particularly notable among steeplechasing jockeys ( 67). Since the early 1960s, aggressive medical
surveillance, improved and mandatory head protection, the recording of injuries, and the routine review of the medical
status of each rider before each race and before provision of any compensation have greatly reduced this hazard ( 67,68
and 69).
Spinal injury is traditionally the most feared of riding injuries ( 67,70,71,72 and 73). Racing injuries are usually limited to
primary fracture by direct blows to the spinous and transverse processes, with secondary flexion injuries occasioning
stable compression, crush, or blowout fractures of the vertebral bodies ( 69,70,74,75 and 76). However, hunting and
cross-country accidents can apply any vector to the spine and may involve hyperflexion, extension, and lateral flexion
and rotation ( 76). In adults, spinal cord injury usually results in actual fracture and dislocation, commonly of the lower
cervical segments or the dorsolumbar junction, although spontaneous reduction may occur before the time of radiologic
examination (76). Odontoid fracture should always be suspect ( 77). Spondylosis in the elderly enhances these hazards,
and spinal stenosis is a complicating factor of acute spinal injury ( 76). The anatomic peculiarities, mobility, and elasticity
of the spine in childhood are reflected by the infrequency of radiologic spinal fractures and the devastating high cervical
flexion injuries of those younger than 8 years of age ( 78).
Adult-style lower cervical cord injuries occur in the 8-to-16-year-old group, but again radiologic abnormality may be
absent (78,79). The phenomenon of delayed onset of clinical spinal cord injury is a particular problem in children ( 78).
Initial rapid recovery from immediate motor and sensory symptoms is followed, after a period of apparent normality, by
the progressive development of total cord transection. Cord percussion–induced segmental vasoparesis (traumatic
failure of local cord bloodflow autoregulation) compounded by sympathoparesis (loss of peripheral sympathetic
vasomotor tone due to focal central cord contusion) and consequent systemic hypotension appear to be responsible.
Such a child should be kept horizontal until a detailed medical review can be made. Transient, immediate sensory and
motor symptoms must be asked for after any child falls from a horse and must be recognized as being of the utmost
gravity. As always, it is prudent to presume spinal cord injury after every major incident until proven otherwise.
After a head injury, alteration of consciousness, or limb symptoms, no rider should mount again before a formal medical
review has been performed (80,81 and 82). The keeping of individual riding and accident records, following the example
of the Jockey Club, is recommended (69,80,81).
In the past paraplegia, repeated injury, and the specter of the punch-drunk jockey were all features of the racing scene
(68,83). The introduction of mandatory safety measures has led to a progressive decline in the incidence of serious injury
and disablement without any decrease in the quality, competitiveness, or excitement of the races ( 67,68,69,84). Racing
provides an example of major problems openly recognized, continuously reviewed, and progressively contained that
could be followed with advantage by many other disciplines ( 69). In the United Kingdom, the role of the Jockey Club is
now under review. Whether any alternative system or organization could match this record remains to be seen.
Spine
The cervical spine is particularly vulnerable to injury. It is mobile, and the likelihood of damage is enhanced by the
disparity in the movements of the unsupported skull on the cervical spine. The skull may be likened to a heavy ball on the
end of a chain. The force created by its movement falls on the two vulnerable junctions: that of the skull with the cervical
spine and that of the mobile cervical spine with the fixed thoracic spine. The danger of dislocation is increased by the
minimally oblique alignment of the facets, which present little resistance to dislocation ( 85).
A force exerted through the crown of the head is transmitted through the skull to the cervical vertebrae and results in
crushing of the vertebrae and extrusion of vertebral body and disk material posteriorly into the cervical cord ( 85). A rider
who leans forward on the horse, either out of fear and inexperience or as in jumping, is most likely to be pitched headfirst
onto the ground if the horse should stop suddenly or buck. Reflex usually puts the rider's arm or arms out to break the
fall, but should the arms be blocked in some way, the head usually takes the brunt of the impact. The rider can also be
thrown onto his or her head and outstretched arm ( 53,58,84) (Fig. 22.4). Secondary spinal (usually flexion) injury is
compounded by rotation at the dorsolumbar junction ( 75,76,86) (Fig. 22.5).
FIGURE 22.4. This rider is being thrown onto his head and is attempting to protect himself with outstretched arms, a
mechanism that frequently results in a fractured clavicle or upper limb. (Photograph courtesy of Stewart Newsham.)
FIGURE 22.5. When the pelvis and thorax rotate in opposite directions, there is rotation at the dorsolumbar junction on
impact, with the possibility of a fracture dislocation at that site. (Photograph courtesy of Stewart Newsham.)
Pelvis
“Major fractures of the pelvis are generally associated with a high energy impact. The fractures caused by horse riding
accidents were comparable in type and severity to those resulting from high velocity road accidents and falls from
buildings.... In particular, these injuries are associated with a high risk of massive retroperitoneal hemorrhage, which is
potentially fatal, and injuries to the bladder, urethra and rectum, which must be recognized early” ( 87) (Fig. 22.6).
FIGURE 22.6. A rider is crushed during a race. The leg and pelvis of the rider are barely visible under the horse. Such
crushing is associated with internal injury, pneumothorax, or contusion/laceration of abdominal viscera. (Photograph
courtesy of Stewart Newsham.)
Disruption of the symphysis pubis has also been reported. In one study, riders were astride horses that bucked
repeatedly. The pubic arch was brought down violently on the pommel (front) of the saddle, splitting the arch and
dislocating the sacroiliac joint ( 87).
Upper Extremities
As can be seen in Figure 22.2, the upper extremities are the most common sites of injury. Most injuries are the result of a
fall from a horse (e.g., rider “thrown,” horse falling with the rider). In falling, the rider may extend one or both arms,
resulting in fractures, sprains, dislocations, and various contusions or lacerations. Clavicle fractures and shoulder
dislocations are common to jump jockeys and eventers (24,88). Wrists, hands, and fingers may be injured in a fall,
crushed (i.e., stepped on), bitten, or injured by rein or rope entanglement ( 6). In British studies, the incidence of hand
injuries was recorded 0.6% to 4.3% (53,54). In a study of U.S. collegiate rodeo riders, 12% of injuries were to the hand,
and 63% of those occurred during roping events. Roping exposes the metacarpophalangeal area to contusions, sprains,
and abrasions from rope use (6). It can also result in thumb fractures, avulsions, and amputations if the roper mishandles
the rope and allows the thumb to be trapped between the rope and the saddle horn when “dallying” (anchoring the rope
to the saddle horn after roping the steer). Similar injuries can occur when a lead rope or reins are wrapped around the
hand or fingers (6,18,37,89) and the horse pulls back suddenly or is frightened into running off.
Lower Extremities
Lower extremities are the third most likely sites of injury (see Fig. 22.2). Toes and feet get stepped on; knees and shins
can be banged on barrels, gateposts, or trees while riding. When riding in a group there is a danger of being kicked by
another horse, with the lower thigh, knee, and lower leg being the most vulnerable. In a fall from a horse, a foot caught in
the stirrup can result in fractures and dislocations. Broken feet and ankles are common in harness racing drivers because
of the angle at which they sit, with feet and legs in front of them and slightly elevated. A fall with the horse can also cause
crushing injuries.
Medical Issues
The rider can be crushed or compressed between the horse and ground, with a blunt or “burst” injury to the chest,
viscera, limbs, or head. The injury is caused by the horse's mass, which is traveling at variable speed (see Fig. 22.6) (5).
Nonpenetrating chest trauma, as from a kick, has been reported to cause intraventricular conduction delay and heart
block (90,91).
Within the abdomen, ruptured liver and spleen plague the young, and disruption of the aorta and great vessels can occur
at any age, although such injuries are uncommon in children. Of intrathoracic injuries, pneumothorax commonly
compounds crushing and rib fractures. Soft tissue injuries are accepted as commonplace; referral to a physician usually
reflects the personality of the individual rider or parents. Skin laceration, abrasion, and superficial cold injury
(panniculitis) usually go unreported ( 5).
Vascular Injuries
Neck injuries are not uncommon and are usually musculoskeletal. Although rare, trauma to the neck arteries may initially
go unnoticed yet have catastrophic consequences. Internal tears can allow arterial blood to dissect the layers of the
arterial wall and block the lumen. If the blockage is severe, it can lead to cerebral ischemia and infarction ( 92).
Infections
Pubescent girls who wear nylon and tight pants can experience troublesome intertrigo, thrush, and urinary tract
infections. Panniculitis occurs in the winter months ( 93). More serious infections can be transmitted through bites. “In
addition to staphylococcus and streptococcus infections, horse bites may involve Bacteroides spp., Clostridium tetani,
and rabies. The most recent CDC report on cases of rabies in domestic animals showed 63 cases of rabid horses in the
United States, with 20 of these cases occurring in Texas” ( 94). Rabies especially poses a hazard to veterinarians during
the investigation of its early choking symptoms ( 5).
Other zoonotic diseases that can be transmitted from horses include salmonellosis, anthrax, histoplasmosis,
leptospirosis, cryptosporidiosis, brucellosis, and encephalitis. As in influenza, humans and horses are end-host targets
for the migratory bird–borne group A arboviruses of the equine encephalitides: eastern, western, and Venezuelan.
Melioidosis is endemic in Southeast Asia ( 5).
Toxicology and Drugs
Although toxicity problems related to horses have not been well documented, the potential for poisoning of one form or
another certainly exists. A look through a horse-supply catalog illustrates the volume of fly sprays, medications,
anthelmintics, and miscellaneous health products that are available. Fly sprays are usually pyrethrin or permethrin
based, although “natural” sprays containing citronella or oil of pennyroyal are gaining favor. The most common wormers
contain ivermectin, fenbendazole, pyrantel, moxidectin, or oxibendazole ( 95,96 and 97).
Phenylbutazone (“Bute”) is a very common nonsteroidal antiinflammatory drug prescribed by veterinarians ( 98). It can be
found in many barns as a normal part of the equine first aid kit, and more than one person has been known to take some
when human analgesics were not available. In 1991, Newton and Rose reported a case of equine phenylbutazone
poisoning in a racetrack worker ( 98). He had taken 17 g in a 24-hour period (the average therapeutic equine dose is 2 g
[98]) and developed grand mal seizures, coma, hypotension, respiratory and renal failure, and hepatic injury ( 98).
Another common item is dimethyl sulfoxide (DMSO), which is used as a topical rub for strained tendons and arthritic
ailments. It is sometimes mixed with cortisone to be applied to arthritic joints, or with nitrofurazone to be used as a sweat
or poultice ( 99). It is readily available in catalogs and farm stores ( 95,96 and 97).
SAFETY AND CONDITIONING
Conditioning
Perhaps the key to learning to ride well and safely is the rider's level of fitness. Riding requires general aerobic
endurance, a sense of rhythm, strength, agility, and flexibility. A rider is agile when all joints are working freely and
moving with ease. Agility can be limited by a body's structure: the way the joints are built; the arrangement of tendons
and ligaments; the length, elasticity, and expandability of muscles; and being overweight ( 99). Agility is also influenced
by age, outlook, level of conditioning, degree of fatigue, outside temperature, time of day, and warmup or lack thereof. A
rider needs to be able to coordinate a fine-tuned interplay of all the muscles, often using cross-movements (e.g., right leg
and left elbow). Speed of action and reaction must be quick yet controlled. To achieve an adequate level of fitness, riders
should do aerobic conditioning and strength training as well as regular riding. Working once a week will at best maintain
a training level. Training and conditioning several times a week is a better goal, with periodic increases in frequency and
duration to maintain aerobic endurance ( 99). As with any other sport, a warmup should be done before the main workout,
especially in cold weather. Stretching exercises done before mounting should be followed by light limbering and
stretching while walking and trotting the horse during the horse's warmup time. In our experience, a strong and fit person
is also less likely to be injured in the day-to-day care and handling of horses, including all the heavy lifting their care
requires.
Skills and Knowledge
This factor is harder to define. There are lists of dos and dont's in virtually every manual about horses, but the only way
to learn what a horse is and how to understand and ride one is to do it, as much as possible. All riders, regardless of their
level of expertise, can benefit from riding lessons. The novice needs more supervision, however, and should get help in
all aspects of horse handling from a skilled and knowledgeable horseman. A young, inexperienced, or timid rider paired
with a young, inexperienced, or headstrong horse is a recipe for disaster ( 25,100).
Equipment
Great strides have been made in the development of better safety gear for the rider, and slowly the strange social stigma
attached to the wearing of such equipment is waning. The mandating of its use in many organized events is helping to
reduce the more serious consequences of a fall or other mishap. Basic safe attire for riding includes a properly fitted
ASTM/SEI-approved helmet with the chin strap clipped snugly, close-fitting pants, and a boot with a small heel and a
smooth sole. Also recommended would be gloves that provide a good grip (usually leather), a body protector vest,
quick-release stirrups on the saddle (and any stirrup must be ¼ to ½ inch [6.5 to 12.5 mm] wider than the rider's boot),
and no loose or dangling jewelry ( 100,101). Different disciplines have more specialized equipment as well (e.g., shin
guards, “cowboy collars”), and even the rough and tough rodeo cowboy should realize that preventing injury means more
time doing what he loves best (6). Whatever tack or equipment is on the horse must be correctly fitted, in good repair,
and appropriate to the task at hand.
Medical Services
Equestrian events, particularly those involving speed and jumping, should have advanced medical services on hand (i.e.,
paramedics or physicians or both). The medical professionals must be experienced in handling severe trauma, notably
major limb fractures, head injuries, and spinal injuries. Equipment for spinal and fracture immobilization, intubation, and
intravenous care should be available, as should supplies for more minor medical emergencies such as asthma or allergic
reactions. Plans and means of transport must also be available for evacuation to a trauma facility. For rough-terrain
events such as eventing or endurance rides, four-wheel drive vehicles and helicopter service must be available for
remote evacuations (102).
CONCLUSIONS
Sports medicine professionals need to be aware of the unique combination of speed, power, and interspecies
cooperation that provide both the danger and the exhilaration of equestrian sports. Riders and their horses are an
athletic team, and should be treated as such, for there is much more to riding than just sitting on a horse. At competitions,
medical personnel should be available onsite and prepared for high-energy “ballistic” injuries, especially in
steeplechasing, eventing, and similar events.
Although horseback riding in any form can be dangerous, accidents and injuries can be minimized or prevented with care
and attention to detail. Proper attire, including an ASTM/SEI-approved helmet, heeled boots, and a safety vest for speed
and jumping, should be worn routinely. Safe and prudent handling of horses, using good quality, well-maintained
equipment and enlisting the aid of a suitable professional, can go a long way toward reducing the rate of accidents and
injuries.
It is to be hoped that the equestrian and medical communities together can continue to assess the factors that promote or
prevent injury in horse sports. Accurate record keeping, the continuing development of safety gear, and education of the
riding public in general are the challenges that confront us.
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23 Fencing
23
FENCING
JULIE M. KNOWLES
REBECCA JAFFE
MARLENE ADRIAN
Rules of Play
Epidemiology
Acute Injuries
Overuse Injuries
Fencing Environment
The Fencer
Techniques
Training, Conditioning, and Rehabilitation
General Concepts
Sport-Specific Training Techniques
Mental Training
Rehabilitation
Sport-Specific Treatment Concerns
Evaluation and Treatment of Emergencies
Special Supplies
Rules Influencing Medical Care
Conclusions
Acknowledgments
Appendix A. USFA Fencing Treatment Form
Appendix B. USFA Injury Initial Evaluation Form
Appendix C. Fencingspecific Training Chart
Appendix D. Personnel Responsibilities for Medical Coverage
Appendix E. USFA Injury Waiver and Drug Testing Form
Chapter References
Fencing is a sport of European ancestry with origins in weapons of war and dueling. The latter could be thought of as a
combination of war and sport, because the duelists did not fight to the death but only to save their honor. A cut across the
cheek was a common trademark of dueling with the sword as late as the 20th century. Today, the sport involves blunted
weapons and a linear fencing area in which two people attempt to score touchés (contacts of the weapon to the body) on
each other (Fig. 23.1). It is a sport of intense physical and mental activity, and the two opponents are within 6 feet (2 m)
of each other most of the time.
FIGURE 23.1. Fencing is a sport in which two people attempt to score touchés on one another by using blunted weapons
on linear fencing area.
The U.S. competitions and rules are governed by the United States Fencing Association (USFA); fencing's National
Governing Body, which is recognized by the U.S. Olympic Committee; and the International Fencing Federation, or
Federation Internationale d'Escrime (FIE). The USFA was founded as the Amateur Fencers League of America in 1891.
The technical rules established by the FIE are, in most cases, the same rules adopted by the USFA and therefore are the
rules used to govern fencing in the United States. These rules address such issues as equipment and technique, safety,
injury timeouts, and drug testing.
The USFA also is the official body that chooses the national teams to represent the United States in international
competitions, including world championships. Point-awarding competitions (North American circuit and national junior
and senior championships) are offered for the purpose of selecting these teams. International competitions include world
cups, world championships (junior and senior), the Pan American Games, the World University Games, and the Olympic
Games.
Three weapons are used in fencing: the épée, the foil, and the sabre ( Fig. 23.2). Each weapon has its own design and
rules of play. All three weapons are fenced by men in international contests, but only the foil and épée are fenced by
women in the Olympic Games, but all three weapons have World Cup events. National, sectional, and divisional
USFA-sanctioned competitions are offered in all three weapons to both men and women. There are children's events
(under 14 years and under 17 years), junior events (under 20 years), open events, and senior events (40 years and
older). University and high school leagues also exist and are governed by the appropriate athletic governing bodies. In
the schools, female competitions have been limited to the foil. There have been, however, instances when women have
fenced on the male épée and sabre teams, because there were no women's teams with these weapons.
FIGURE 23.2. The three weapons used in fencing are the épée (top), the sabre (middle), and the foil (bottom).
Another form of fencing competition is designed for athletes with physical impairments. National and international
wheelchair fencing require that the participants fence from a sitting position. These competitions are governed by the
relevant national and international disabled sports organizations.
Fencing is offered throughout the United States in many major cities and in some remote towns through recreation
programs, private clubs, health and sport clubs, and fencing clubs. The fencing club is known as a fencing salle, and the
fencing coach, if a graduate of a fencing school, is known as a fencing master (maistro).
Fencing equipment is usually provided by the schools and by the facilities offering novice classes. After the class stage
and as the fencers begin to compete and become members of a club, students usually must purchase their own
equipment. The mask, weapon, glove, and uniform (exclusive of the shoes) cost approximately $200. If the equipment is
certified for international competition, the price is approximately $500, which includes three weapons. All the equipment
sold in the United States must meet the fencing standards approved by the FIE for safe fencing. All pertinent equipment
must be properly inspected by the technical committee before competition. Most teams and competition sites have
equipment specialists (armorers) as part of their entourage to ensure that the equipment meets FIE safety standards
(Fig. 23.3). Because scoring is based on electrical contact, the armorer also ensures that the equipment has been
assembled in such a way as to avoid a malfunction or misrepresentation of the electrical scoring system.
FIGURE 23.3. The armorer is the individual who officially inspects fencing equipment to ensure the athletes' safety.
Fencing equipment and wear has been designed with the athlete's safety in mind. For all three weapons, the protective
jacket must overlap the knickers (or uniform of Kevlar-type material), a plastron is mandatory, and women must wear
breast protectors. The glove must cover at least one half of the forearm so that the opponent's weapon cannot enter the
sleeve. All masks must be checked by an instrument with a spring-loaded point before competition to ensure that the
mask cannot be penetrated by the opponent's blade. This instrument must be able to withstand a 12-kg force ( 1).
To prevent injury, there are rules governing the methods by which one fences. It is strictly forbidden for a fencer to
perform any abnormal motion, such as severe hits or opponent collision, that may be construed as discourteous and
dangerous (1).
RULES OF PLAY
Fencing has several courtesies, including saluting of the opponent and the director (official) at the beginning of each
match and shaking hands with the opponent afterward. The mask, weapon, and clothing of both fencers are evaluated by
the director before the start of the bout. The fencers assume the ready position (en garde). The referee says “Fence,”
and fencers fence until the referee says “Halt.” When there have been five touchés scored by one fencer, the bout is
ended and that fencer is declared the winner. During some competitions and at later stages of a large competition,
fencers must win with a margin of two touchés in two of three bouts, to a maximum score of 6 in each bout.
The area of fencing is a linear strip (piste) approximately 5 feet (1.5 m) wide and 47 feet (14 m) long ( Fig. 23.4). The
fencers exchange a series of offensive attacks and defensive actions consisting of advances, retreats, lunges, and
flèches in which the feet are usually at right angles to each other and the legs are in continual semiflexion or vigorously
extending (Fig. 23.5). Defense involves retreats and arm flexion movements. Attack arm actions are primarily elbow and
wrist extension and lateral or circular movements of the hand and forearm.
FIGURE 23.4. The piste is the linear strip on which fencers compete.
FIGURE 23.5. A series of attacks and defensive actions produces vigorous extremity movements, and mechanical
stresses are common in the sport of fencing.
Because of the rules and target area for valid touchés, the actions of the arm when using the foil are more restrictive than
with the other two weapons. Only the torso is a legal target. Lunges are prominent in the foil strategy. The rule of
right-of-way results in a rather definite pattern of attack—defend—attack—defend before a hit (contact) is made.
Right-of-way refers to the need of a fencer to initiate an attack before the opposing fencer does.
In the sabre competition, the target is expanded to include the head and arms. In addition, the cutting edge of the blade
may be used to score a touché. For these reasons, there is a greater variety of arm actions than with the foil. The flèche
is used more extensively than the lunge. The right-of-way rule also applies to the sabre.
The total body is the legal target in the épée, and no right-of-way rule exists. Both fencers can score a touché
simultaneously as long as it is done within 1/25 second. As with the foil, only the point of the épée can be used to score a
legal touché. Lunges are used, but the fencers rely frequently on their quickness or reaction time, and some do not often
lunge.
EPIDEMIOLOGY
Acute Injuries
Because of the nature of the sport, fencing produces a wide diversity of acute injuries. A 2-year study was performed by
the USFA's medical commission to investigate the actual frequency and distribution of such injuries. This study was
conducted from 1988 to 1990 at all North American Circuit (NAC) events and two national championships (each weapon
has three NAC events and nationals). During this time, 586 injuries were reported by the fencers to official medical
personnel, in most cases a certified athletic trainer. Only 323 of the 586 reported injuries were acute injuries requiring
medical attention. (Non acute injuries included sinusitis and diarrhea.) All acute injuries requiring medical treatment were
documented on the Fencing Treatment Form IQ (Appendix A). In addition, for any significant injury that required
stabilization, transport, and possible future medical treatment, the Injury Initial Evaluation Form was also completed
(Appendix B); this form was reviewed by the physician onsite or on call whenever possible.
Relationship Between Acute Injuries and Weapons
To determine whether the differences in injury ratio (type of injury and body part injured) for each weapon (men's foil,
women's foil, men's épée, women's épée, men's sabre, and women's sabre) were the result of chance alone or whether
the results were caused by significant differences between groups, a statistical analysis using a chi-square and Cramer's
V value was performed.
When weapons were compared with body parts injured, a statistical significance was found among the variables ( p =
.0177); however, the Cramer's V value indicated that this relationship was not strong (V = .32618). It was concluded that
the body part injured may depend on the type of weapon. When comparing the weapon with the type of injury,
researchers found the p value to be .0838 and Cramer'sV value to be .18098, indicating no statistically significant
relationship between these two variables.
Distribution and Types
Of all injuries reported during the study almost 33% were sprains (more than 50% of which occurred during men's épée
events). Strains were the second most common injuries (23.8%), followed by heat-related disorders (17.9%), contusions
(6.2%), fractures and complete tendon ruptures (1.2%), and other miscellaneous systemic disorders (0.3%) ( Table 23.1,
Fig. 23.6).
TABLE 23.1. TYPES OF ACUTE FENCING INJURIES (%)
FIGURE 23.6. Percentage of acute injuries in men's and women's fencing. Numbers are based on men's and women's
fencing combined. (Graphs courtesy of D. Grygo.)
Comparing all six weapons, men's épée accounted for the most injuries, 45.8%. Men's sabre represented 20.7% of all
injuries, and men's foil, 10.5%. This may be partially attributed to the fact that the épée has a much larger target area
than the sabre or foil. Furthermore, the épée is of greater stiffness and weight compared with the other weapons.
Of the three women's events, women's foil represented 15.2% of the total injuries, compared with 6.8% for épée and
0.9% for sabre. This may be accounted for in part because more women compete in women's foil than in women's épée
or sabre.
Location
In terms of body part, a significantly higher number of injuries occurred at the ankle (15.8%) compared with the other 23
sites observed (Table 23.2, Fig. 23.7).
TABLE 23.2. LOCATION OF FENCING INJURIES (%)
FIGURE 23.7. Percentage of acute injuries by body part in men's and women's fencing. Numbers are based on men's
and women's fencing combined. (Graphs courtesy of D. Grygo.)
The total body (systemic) was the location for the second most frequently treated acute disorders (usually heat related) at
10.5%, followed by the hand (8.4%) and the knee (8%).
Types of Acute Injuries
Because of the planted, flexed, and externally rotated valgus-stressed position of the trail leg, acute injuries such as
medial collateral ligament sprains, medial meniscal tears, lateral subluxating patella, groin strains, ruptured Achilles
tendons, and eversion ankle sprains have been observed. Quadriceps strains, blisters, and nail contusions have been
noted in the front leg. Because the trunk is a target area for all three weapons (in addition to the upper extremities for the
sabre and épée), more contusions and lacerations are seen in this area.
Gender Differences
Over one academic year, men's and women's collegiate fencing injuries were monitored and compared. When adjusted
for exposure time, no significant gender differences were found. Approximately 0.10 injuries per 100 person-hours were
noted in men's fencing, compared with 0.18 in women's fencing. There were 0.43 disability days per 100 person-hours
associated with these injuries for men, compared with 0.21 days for women. Overall, 28% of men participating in fencing
were injured, compared with 50% of women (2).
Overuse Injuries
Because of the nature of the sport and its unique positioning, fencers are prone to sprains and strains as well as overuse
injuries in multiple body parts. Fencers must maintain balance while holding their weapons in a prepared position for
extended periods. Inflammatory syndromes, usually tendonitis about the wrist and hand, are often seen. Fencers may
experience muscle cramping when they are forced to compete several times in a short period of time. Whether this is
caused by muscle fatigue or by electrolyte disturbances from sweating is unclear.
Fencers also are subject to back problems. Most of these involve the trunk extensor musculature. Lumbosacral strains
are seen. It is important to emphasize a strengthening program for the back to avoid unnecessary injuries.
Lower-extremity injuries are most frequently seen. They may occur in many different circumstances. When competing on
a raised piste, the fencer is at risk for ankle sprains caused by imbalances and falling off the platform. Iliotibial band
syndrome can result from the stance required. There have been cases of osteochondritis dissecans of the patella
attributed to the angle at which the knee must be maintained and the repeated microtrauma caused by the trail leg in
valgus stress while the leg is externally rotated ( 3). This must be kept in mind if a fencer presents with anterior knee pain.
The diagnosis is made by magnetic resonance imaging or arthroscopy.
Because the fencing footwear is not supportive, the legs are prone to overuse injuries. The hyperpronated stance leads
to an increase in plantar fascitis, posterior tibialis tendonitis, shin splints, stress fractures, and possibly periostitis of the
navicular.
The asymmetric development of the body may make fencers prone to non–sport-related injury. Both the weapon-side
upper extremity and the forward lower extremity test stronger isometrically and dynamically ( 4).
MECHANISMS OF INJURY
Injuries are a result of many factors related to the environment, the fencer, and the technique performed. In addition, the
interrelationships among these components of fencing make the cause of injury complex.
Fencing Environment
The surface on which the fencer moves must be kind to the feet and joints. Sometimes the piste is set on concrete, which
causes heel bruises and trauma to the joints. If the footwear and the fencing surface are not matched to provide optimum
friction (traction), the fencers' feet may slip or stick. In either case, a fall or tearing of soft tissue is possible. Contusions,
muscle strains, and ligamentous sprains can result.
The piste is often elevated during the final round of a competition. This creates a risk of falling, and greater injury can
occur. In some cases, the copper strip may be torn, the base may be uneven, and sections may separate from each
other. Prevention of injuries caused by these problems rests primarily with the facility director. Adequate standardization
of surfaces must be provided so that the fencer can select the proper footwear.
The environment also must have adequate space between pistes and between the piste and the scorer's table. Weapons,
clothing, and other articles must be out of the way of fencers. Again, proper enforcement of the rules and commonsense
behavior will reduce the possibility of injuries.
The Fencer
Injuries are caused by improper training and conditioning. Fencers must develop adequate strength, cardiovascular
conditioning, balance, and coordination to compete throughout a tournament. Those who do not become fatigued or lose
their balance while fencing have a lower risk of injury. Fencers who stretch their bodies to the point needed for a bout
during fencing training and preevent warmups have a lower risk of straining the muscles and other soft tissues when
going all-out on lunges and other movements performed during competition.
The major mechanism of injury is the inability of fencers to tolerate the forces exerted on their bodies. Their own
muscular force, the force of gravity, the acceleration forces of body segments, and the impact forces (foot to piste or
weapon to body) must be less than what the human body can tolerate without trauma. Some actions require singularly
high forces, and there are also repetitive lower forces that cause accumulated trauma; both must be conditioned for.
Techniques
The techniques of fencing can be categorized with respect to the sites receiving the greatest forces and being at the
highest risk. However, fencers do not always perform these techniques in exactly the same way. Novices, in particular,
may not perform according to the description of a technique. Therefore, a biomechanical analysis of how the fencer
moves his or her body parts is necessary to obtain knowledge of how the technique is being performed. Leg extension
mobility at the hip, alignment of the knee over the foot to prevent torsion, extension at the elbow, hand movement about
the wrist, and alignment of the trunk are the movements that must be analyzed in each fencer ( Fig. 23.8). To reduce the
risk of injury, these movements must be performed properly.
FIGURE 23.8. There are many upper-extremity, trunk, and lower-extremity movements in fencing that can be
biomechanically evaluated to confirm proper technique and prevent injuries.
Inadequate strength, power, and flexibility create trauma because of the high acceleration rates and repetition of
movements. Balance, agility, and coordination conditioning must be part of a fencer's training so that the fencing
movements will be made optimally with a reduction in extraneous forces.
TRAINING, CONDITIONING, AND REHABILITATION
General Concepts
Because of the complexity of the sport, fencing training and conditioning should be divided into three categories: general
conditioning, mental exercise, and sport-specific training. In terms of general conditioning exercises, researchers have
shown that cardiovascular fitness and strength influence fencing performance ( 4,5 and 6). Others have suggested that
technique, speed, and agility are the essential characteristics for elite performance ( 7).
A general conditioning and training program is essential not only for good performance but also for injury prevention. This
program should include at least the following components: (a) warmup phase; (b) stretching; (c) power and strengthening
exercises; (d) aerobic and endurance activities; (e) sport-specific activities; (f) warmdown; and (g) relaxation techniques
to promote mental control and speed fatigue recovery time ( 8).
As stated previously, the sport-specific skills and mental training components are important and warrant special
consideration. Also, strength and endurance workouts are extremely beneficial. The movement pattern in fencing
promotes muscular asymmetry; for example, elbow flexion strength of the weapon hand and strength and muscle mass of
the forward leg have been shown to be significantly higher than in the contralateral limb ( 4). Because many injuries are
caused by muscular imbalance, it is essential that a total-body strength program, including trail leg strengthening, be
implemented.
There are three main types of strength and power exercises that should be incorporated into the program: isometrics,
isotonics, and isokinetics. All exercises should be executed both eccentrically and concentrically. The intensity,
frequency, and duration of the exercises as well as the age and gender of the fencer should also be considered.
Although power training at a limb speed equal to competition speed would be optimal, this is often difficult to achieve.
Most isokinetic equipment does not exceed a speed of 400 degrees per second, whereas maximum human limb velocity
usually averages between 900 and 1,100 degrees per second ( 9). Therefore, a suggested protocol for isokinetic power
training would be concentric, full-velocity spectrum speeds and one midrange eccentric speed ( 9,10,11 and 12). The
same muscle groups should not be exercised more often than every other day, and exercises should be performed until
the muscle is at a point of 50% fatigued instead of the traditionally established methods of repetitions and sets ( 13).
Women and youth should undergo a different weight-training program from men. Compared with men of equal size and
weight, women possess approximately 50% as much strength; the difference is primarily in the upper body ( 14,15).
Because of the musculoskeletal immaturity of youths, modifications should be made in their isotonic training. The
following guidelines should be incorporated into a weight-training program developed for youth. Only one to three sets of
6 to 15 repetitions should be performed, no more than two to three times a week, with at least 1 day of rest between
sessions. The program should emphasize full-range, submaximal, concentric lifting. Until the technique is perfected,
youths should lift bars or machines without added weight. When 15 repetitions can be properly executed, weight can be
added in 1- to 3-pound increments ( 8,16).
In fencing, the body must be able to generate quick bursts of high-level energy (anaerobic) and also to maintain
submaximal motions for extended periods (aerobic). Therefore, to avoid injury from premature fatigue, endurance
activities must be included in the conditioning program. A combination of interval training (repetitions of 5- to 10-second
bursts of maximal work with 30- to 60-second rest periods) with aerobic workouts (minimum of 20 minutes, 70% to 80%
maximum heart rate intensity, 3 to 4 days a week) is suggested (17).
Sport-Specific Training Techniques
Although many injuries occur during competition, some injuries also occur during practice. Often these injuries can be
avoided if proper training and conditioning are done. Many fencers do not train in a regular or scientific manner. They do
not keep records of their level, frequency, or duration of training or competition. The following training principles and
techniques are based on programs that coaches and highly skilled fencers have used. It is believed that participation in
such a program will reduce the risk of injury to fencers.
Training intensity, duration, and frequency should be individually prescribed. The training program must be both general
and specific, because fencing is a unilateral-type sport. Without general training, the fencer develops asymmetrically.
The asymmetric body does not have the balance and harmony required for intense competition.
Training must be done in an environment that is kind to the body, and the fencer should not train at a level that causes
pain or undue discomfort. The training should consist of adequate rest days and hard workouts interspersed with regular
workouts. Rests should be given before competitions. Cross-training principles can be used to motivate the fencer and
prevent staleness. Cross-training also can be an injury-prevention strategy.
Charting or record keeping is one of the proven ways to evaluate the adequacy of the fencer's training table ( Appendix
C). For all types of fencing activities, the number of minutes should be recorded as well as the intensity of the activity.
The intensity of each activity can be estimated using a perceived exertion scale. This scale can be a three-point scale
(i.e., easy, moderate, and hard), a five-point scale (easy, moderate, slightly hard, hard, and maximum), or another type of
scale. Both general and specific training activities as well as competition results should be recorded. The type of
information kept within these categories can follow that shown in Appendix C or can be modified to fit the individual
athlete or coach. For example, specific conditioning might include only three categories: footwork, handwork, and total
bodywork.
Records of competition identify the limitations of the training program. The number of touchés scored by the fencer and
the number scored by opponents in competition can be recorded as a ratio. Comments concerning opponents' styles and
one's own weaknesses should be recorded. The competition record can be used to modify the training program. If the
fencer did not have enough stamina, cardiovascular activities should be increased. If the fencer lost balance and could
not perform techniques correctly at the appropriate times, then emphasis should be given to improving balance and
reaction time.
Mental Training
Each day time should be spent on mental exercises. These exercises include visual imagery, autogenic training, and
relaxation techniques to aid the fencer in improving concentration, reducing stress, speeding injury recovery, and
improving overall technical performance. Not only does this training help promote mental conditioning, but it also helps
the elite fencer gain an emotional and physical edge.
Rehabilitation
Rehabilitation after fencing injuries follows the same general guidelines as rehabilitation from other sports-related
injuries. Application of the specific adaptations to imposed demands (SAID) principle is imperative. Rehabilitation and
functional tests before return to play must be specifically geared toward the athlete's sport, weapon, and age.
The two basic treatment regimens used in sports rehabilitation are therapeutic modalities and exercise. Modalities are
used primarily in the early stages of rehabilitation to enhance the fencer's exercise program ( 18). The therapeutic
exercise program actually helps restore injured tissue to its previous level of function ( 19). Rehabilitation should include
exercise of the uninvolved body parts while treating the involved body part. This minimizes the chance of injuring
deconditioned areas when the athlete returns to play.
The athlete must undergo functional testing before he or she is allowed to return to fencing. Normally, sport-specific
activities can begin during the rehabilitation program when the affected limb has 70% of the strength and 75% of the
balance and proprioception of the contralateral limb. However, because of the pronounced asymmetry usually found with
fencers, this may be difficult to access. These functional activities should encompass all aspects of the sport, such as
jumping, hopping, lunging, and squatting.
Actual return to sport should not be allowed until the athlete (a) has passed a functional test at a level equal to at least
90% of that in the contralateral limb; (b) has 100% proprioception compared with the contralateral limb; (c) has 90% of
the peak strength, total work, and average power of the contralateral limb; (d) uses proper protective equipment as
indicated; and (e) has passed a clinical examination.
SPORT-SPECIFIC TREATMENT CONCERNS
Evaluation and Treatment of Emergencies
The fencing instrument is sharp when broken and may inflict lacerations to an opponent's clothing and skin. Basic first
aid measures should be employed. Preventing further hemorrhage is paramount.
Foreign bodies in the eye are frequently experienced. A scratch must be delineated from a foreign body that remains
imbedded in the cornea. It is wise to numb the eye before evaluating the situation. Next, gross inspection for a foreign
body should be done. If one is discovered, then thorough rinsing of the eye should be accomplished. If the foreign body
remains in place and the facilities are adequate, one may attempt to flick the foreign body out of the cornea with a sterile
needle tip. If the foreign body does not move, it would be best to patch the eye and send the athlete to a specialist who
can use a slit-lamp for removal. The risk of corneal puncture is real. Fluorescein examination with a blue light would be
the next step, looking for a persistent defect in the cornea. If an abrasion is noted, then conservative management with
antibiotic cream and patching is appropriate. One must decide on an individual basis whether the athlete, with adequate
numbing, can complete the competition before definitive treatment is rendered.
Puncture wounds caused by a weapon have been reported. There have been a few cases of brain injury and death from
a weapon that penetrated the face shield. At least two immediate deaths have occurred ( 20). In these cases, the basic
precepts of advanced trauma life support would be the most appropriate steps to follow (e.g., managing the patient's
airway first and foremost). Case reports have been published of survival after penetration of the brain by a foil, which left
the athlete with a permanent amnesia; these emphasize the importance of rendering all possible life support to the
athlete and transporting seriously injured patients quickly to sophisticated facilities ( 21).
As with most sports, the support personnel (coaches and referees) are older and under a great deal of stress. These
individuals may have cardiac complaints, which should be taken seriously and evaluated and treated quickly. Basic life
support (airway, breathing, and circulation) should be immediately initiated if someone complains of chest pain and then
loses consciousness.
Many of the sporting arenas are quite warm. The gear worn by fencers makes them prone to heat injury. Athletes should
be kept well hydrated, and perspiration and weight should be monitored carefully.
Special Supplies
It is important that the physician or ancillary medical staff be properly prepared with additional supplies beyond the usual
medical supplies carried by a trainer. An eye kit—including topical anesthetic, fluorescein with a blue light, a fine needle,
topical antibiotics, and patches—should be available. A sterile suturing kit with skin and subcuticular sutures should be a
part of the medical supplies, as should topical antibiotics. A handheld electric cautery device is helpful for subungual
hematomas. Intravenous fluids, oral rehydration fluids, and ice should be available in case of heat-related problems. A
vacuum splint kit may be helpful for the stabilization of fractures.
Rules Influencing Medical Care
In international competition, an FIE medical committee or “doctor on duty” is present at all events. If an accident occurs
during a fencing bout, the injury must be confirmed by the committee or doctor. The referee of the competition then allows
the athlete an injury break lasting no more than 10 minutes. The break can be used for treatment of that specific injury
only. If the doctor believes the athlete cannot safely continue, he or she advises the director of this decision. Fencers
who are in an individual competition may be asked to withdraw. If it is a team competition, the fencer may be replaced
during that event, but may fence other events on same day if approved by the same physician. At no time during the
course of the same day can another injury break be taken for the same injury. Muscle and heat cramps are not
considered for injury timeouts (1).
Care also must be taken when using tape or other medical supplies and devices. If tape or other devices must be used
on the weapon hand, or on any other area near the equipment or target area where its use might be interpreted as an
attempt to alter the electrical current and interfere with proper scoring, it may be appropriate to have the athlete approved
for competition by the referee or rules committee before the start of the event ( Fig. 23.9). During national events, the
USFA recommends that at least a full-time certified athletic trainer and one on-call physician be available during the
entire competition. Specific duties of the athletic trainer, the physician, and the local organizing committee hosting the
event have been outlined by the USFA ( Appendix D). In addition, all athletes are asked to sign waivers of liability and
agreement to drug testing (Appendix E).
FIGURE 23.9. Tape or electrical treatment devices, such as this electrical stimulator, should be cleared by the rules
committee so that their use is not interpreted as an attempt to alter electrical current and hence interfere with proper
scoring.
CONCLUSIONS
Proper conditioning is a key to injury prevention in fencing, especially because pronounced muscular imbalances are
common to the sport. Proper techniques and mechanics and proper equipment are important for injury prevention. The
positions and techniques involved in fencing contribute to some of the sport's common injuries, such as medial collateral
ligament sprains of the trailing knee, ankle sprains, plantar fascitis, and stress fractures.
A variety of acute injuries may be seen, and they can occur throughout the body. More injuries are seen with men's épée
than with any other type of fencing. Sprains are the most common type of injury, and the ankle is the body part most
frequently injured.
It is essential to have qualified medical personnel at all fencing events. At least one full-time athletic trainer and one
part-time or full-time on-call physician should be present. All health care providers working at fencing competitions should
be well versed in the management of medical emergencies, including puncture wounds, fractures, and eye injuries.
Rehabilitation of fencing injuries is similar to that of other sports-related injuries. The SAID principle applies, and
sport-specific activities must be incorporated in the exercise regime. Functional tests before return to fencing are
essential.
ACKNOWLEDGMENTS
The authors acknowledge D. Hammond, D. Grygo, and C. M. Richards for their assistance in the preparation and review
of the manuscript.
APPENDIX A. USFA FENCING TREATMENT FORM
APPENDIX B. USFA INJURY INITIAL EVALUATION FORM

APPENDIX C. FENCINGSPECIFIC TRAINING CHART
APPENDIX D. PERSONNEL RESPONSIBILITIES FOR MEDICAL COVERAGE
The duties of the local organizing committee shall include the following.
1. Coordinate medical coverage through the assistance of the USFA's Medical Commission.
2. Notify the area hospital when and where the fencing event is going to be held.
3. Provide food, housing, and transportation reimbursement for the trainer and physician. If a local athletic trainer
and/or physician cannot be obtained or if the USFA/local organizing committee chooses to bring in a
trainer/physician from outside the area, the trainer/physician must also be supplied with a vehicle for local
transportation and medical purposes.
4. Mail the completed treatment report forms and initial evaluation forms to both the USFA Headquarters and the
Medical Commission.
5. If the trainer or physician engaged is not familiar with fencing, the local organizing committee along with a fencing
official shall instruct the medical personnel as to their duties.
6. Events with a higher number of entrants require additional staffing. Each event should have at least 1 physician and
1 trainer present at all times (Nationals = 3 trainers, 2 physicians, minimal).
7. Notify USFA headquarters of all serious injuries or injuries requiring hospital transport.
8. Notify the trainer and physician of the ambulance response time, transportation time, and give the medical staff a
map of the area including competition site, hotel, and hospital.
9. Find a suitable training room area in close proximity to the actual competition. Communication devices between the
training room, physician, and committee are recommended.
10. Medical personnel should be provided with adequate medical supplies. An example of supplies used for a 4day
tournament follows:
80 rolls (2 cases 1 ½ white tape)

8oz. can tape spray
4 ace wraps (4'')
8 oz. hydrogen peroxide
box 100 knuckle BandAids
pack 100 sterile 3'' × 3'' gauze
1 bottle (100) aspirin
1 bottle (100) Tylenol
4oz. tube bacitracin
rubber gloves
eye wash
crutches
5 rolls prewrap
pack (minimum 100) midsize supermarket plastic bags and biohazard bags
400 cups
2 10gallon water coolers
ice
20 treatment report forms
20 initial evaluation forms
11. Contact the local medical groups and licensure committee to confirm temporary medical practice of outofstate
medical personnel.
The duties of the athletic trainer shall include the following:
1. Provide prevention and immediate care of injuries to athletes and supportive staff.
2. Arrange for transportation of injured persons to the hospital.
3. Make necessary referrals to the physician.
4. Bring their own standard trainer's kit.
5. Maintain treatment reports and initial evaluation forms.
6. Notify the local organizing committee of all serious injuries or injuries requiring hospital transport.
7. All medical personnel (including physicians) are responsible for their own malpractice insurance; however, because
the services are of a volunteer nature, in some states the Good Samaritan Law may ocver emergency care of
injuries.
The duties of the physician shall include the following:
1. Fulfill the role as described in the rules and regulations involving the determinations if an injury is a result of trauma
(i.e., rule out cramps).
2. Determine and make a record of all interruptions of combat granted.
3. If a 10min request is denied, the physician must issue a warning and subsequently notify the bout committee, as a
repetition of the offense will result in exclusion.
4. In addition to the above requirements in the rules of fencing, the physician must provide emergency treatment of
injuries as necessary or as requested by the athletic trainer.
APPENDIX E. USFA INJURY WAIVER AND DRUG TESTING FORM
ENTRY CANNOT BE ACCEPTED UNLESS STATEMENTS BELOW ARE SIGNED
DOPING CONTROL AGREEMENT: I understand that the drug testing program is implemented at all USFA point events.
Any athlete competing in these events is subject to drug testing during the competition. I understand that the detection of
use of banned drugs would make me subject to suspension by the USFA and the USOC for at least six months. By
registering for this competition, I am consenting to a drug test if selected and am subject to penalties if declared positive
for a banned substance. If selected, I am aware that failure to comply with the drug test will be cause for the same
penalties for those who are positive for a banned substance. I know that I may call the USOC Drug Hotline (800)
2330393 for any questions about medications and banned substances or practices.
FENCER'S SIGNATURE ___________________
PLEASE BE AWARE THAT MANY NONPRESCRIPTION MEDICATIONS HAVE BANNED SUBSTANCES. ANY
ATHLETE WHO IS TAKING ANY MEDICATION VERIFY WITH THE USOC HOTLINE 18002330393 THAT THE
MEDICATION DOES NOT CONTAIN A BANNED SUBSTANCE. THE USOC MAINTAINS A CURRENT LIST OF
RELATED MEDICATIONS.
WAIVER OF LIABILITY: Upon entering this North American Circuit tournament, sponsored by the USFA, I agree to abide
by the rules of the USFA, as currently published. I understand the appreciate that participation in sport carries a risk to
me of serious injury, including permanent paralysis or death. I voluntarily and knowingly recognize, accept, and assume
this risk and release the USFA, their sponsors, event organizers, and officials from any liability. The undersigned certifies
that the individual for which this entry is submitted is a current competitive member of the USFA or another recognized
Fencing Federation from which the fencer has a current FIE card.
FENCER'S SIGNATURE __________________ DATE ________
ATHLETES UNDER18 YRS. OLD: I have explained to my son/daughter the aforementioned stipulated conditions and
their ramificatinos and I further consent to his/her registration for this USFA competition under abovestipulated
conditions.
SIGNATURE OF PARENT/GUARDIAN DATE
MEDICAL PROBLEMS: Please indicate any significant or special medical problems that you have (e.g., diabetes,
asthma, etc.) that the organizers should be aware of:
CHAPTER REFERENCES
1. U.S. Fencing Association. USFA rules. Colorado Springs: United States Fencing Association, 1990.
2. Lanese R, Strauss R, Leizman D, et al. Injury and disability in matched men's and women's intercollegiate sports. Am J Public Health
1990;80:1459–1462.
3. Gray WJ, Bassett FH. Osteochondritis dissecans of the patella in a competitive fencer. Orthop Rev 1990;19:96–98.
4. Nystrom J, Lindwall O, Ceci R, et al. Physiological and morphological characteristics of world class fencers. Int J Sports Med
1990;11:136–139.
5. Roi GS, Fasci A. Survey of requests for medical assistance during fencing matches. Ital J Sports Trauma 1988;10:55–62.
6. Stewart KJ, Perecto AR, Williams CM. Physiological and morphological characteristics associated with successful fencing performance. J
Hum Ergol (Tokyo) 1977;6:53–60.
7. Vander LB, Franklin BA, Wrisley D, et al. Physiological profile of national class NCAA fencers. JAMA 1984;252:500–503.
8. Grana WA, Lombardo JA, Sharkey BJ, et al., eds. Advances in sports medicine and fitness. Chicago: Year Book Medical, 1990.
9. Parker MG. Characteristics of skeletal muscle during rehabilitation: quadriceps femoris. Athletic Train 1981;4:122–124.
10. Hageman PA, Gillaspie DM, Hill LD. Effects of speed and limb dominance on eccentric and concentric isokinetic testing of the knee. J
Orthop Sport Phys Ther 1988;10:59–65.
11. Thomee R, Renstrom P, Grimby G, et al. Slow or fast isokinetic training after knee ligament surgery. J Orthop Sports Phys Ther
1987;8:475–479.
12. Weltman A, Tippett S, Janney C, et al. Measurement of isokinetic strength in prepubertal males. J Orthop Sports Phys Ther
1988;9:345–351.
13. Timm KE. Investigation of the physiologic overflow effect from speed-specific isokinetic activity. J Orthop Sports Phys Ther
1987;9:106–110.
14. Klafs CE, Arnheim DD. Modern principles of athletic training. St. Louis: CV Mosby, 1977.
15. Kuland DN. The injured athlete. Philadelphia: JB Lippincott, 1982.
16. Duda M. Prepubescent strength training gains support. Phys Sportsmed 1986;14:157–161.
17. Rothman J, Levine R, eds. Injury prevention and rehabilitation. Philadelphia: WB Saunders, 1992.
18. Torg JS, Vegso JJ, Torg E. Rehabilitation of athletic injuries: an atlas of therapeutic exercises. Chicago: Year Book Medical, 1987.
19. Allman FL. Rehabilitation of sports injuries: a practical approach. In: Ryan AJ, Allman FL, eds. Sports medicine. San Diego: Academic
Press, 1989.
20. Crawford AR. Death of a fencer. Br J Sports Med 1984;18:220–222.
21. Squire LR, Amaral DG, Zola-Morgans S, et al. Description of brain injury in the amnesic patient N. A. based on magnetic resonance
imaging. Exp Neurol 1989;105:23–35.
24 Football
24
FOOTBALL
ROBERT O. BLANC
DERYK G. JONES
Epidemiology
Protective Equipment
Head and Neck
Concussion
Facial Injuries
Cervical Spine Injuries
Shoulder
Brachial Plexus Injuries
Acromioclavicular Joint Injuries
Contusions
Glenohumeral Instability
Rotator Cuff Injuries
Elbow
Forearm, Wrist, and Hand
Lumbar Spine
Hip
Thigh
Knee
Ligament Injuries
Lateral Ligaments
Menisci
Patellofemoral Joint
Foot and Ankle
Chapter References
Football remains the most popular collision sport in the United States. Participants include children, adolescents, and
adults at all levels of competition. With its inherent high rate of injury, large numbers of players in this sport are affected
by missed participation time or more significant morbidity each year. Many studies have evaluated football injuries and
led to significant improvements in equipment, conditioning, and rule changes that have decreased the incidence of
certain types of injuries. Despite these improvements, the game has evolved with bigger, faster, stronger athletes and
unfavorable playing surfaces contributing to maintain the high rate of injury.
EPIDEMIOLOGY
The study of Mueller and Blyth from 1974 estimated approximately 1.2 million high school and college football
participants ( 1). The number of football-related injuries was estimated at 600,000 per year ( 2,3). Because of the
magnitude of this problem, studies to evaluate football injuries are important in helping to recognize conditions that
increase or decrease the athlete's risk of injury. The existing literature, however, contains widely varying estimates of the
likelihood of football-related injury, from 10.5% to 81.1%. A number of methodologic problems in the literature make
comparing data and drawing conclusions difficult. These have been well described by Thompson et al. ( 4).
Differences in the definitions of injury, injury severity, population at risk, and exposure time, as well as differing methods
of collecting the information, complicate interpretation of the data. The definition of an injury used for collecting data
influences the injury rates reported in studies. One method uses time lost from practice or games. This definition is
limited in that an injury that is completely disabling to a player at one position may allow full participation by a player at
another position. Another limitation is that some injuries may be excluded despite being significant. An example is a
concussion that resolves and allows participation before a practice or game is missed. In an effort to account for these
limitations, DeLee and Farney ( 3) expanded the definition of injury to include (a) any incident that requires the athlete to
miss all or part of a single practice or game; (b) any incident that is treated by a physician; and (c) all head injuries
reported to the trainer. Their study reported an injury rate of 0.509 per athlete per year. This rate is similar to those
reported by Prager et al. ( 5) (42.1%), McLain and Reynolds ( 6) (62%), and Lowe et al. ( 7) (32.1%). Consistent with other
reports (8), the risk of injury during a game in this study was much higher than the risk during practice. In the DeLee and
Farney study, 56% of the injuries occurred during games, even though the majority of time was spent in practice ( 3).
The type and location of injuries have been consistent among most studies ( 5,8,9,10,11,12 and 13). The knee (20%),
ankle (18%), and shoulder (11%) are most often injured. The most common types of injuries are sprains (45%) and
contusions (21%) (3).
Player position has also been reported in relation to overall risk of injury, as well as risk of specific types of injuries.
Andresen et al. (14) and Prager et al. (5) found that running backs (43%), tackles (18%), guards (12%), and ends (10%)
sustained the greatest percentage of injuries. However, running backs and quarterbacks had the highest relative risk of
injury. Players at certain positions are more likely to sustain certain injuries. Linemen often sustain medial collateral
ligament (MCL) knee injuries, while defensive backs are more likely to sustain significant cervical spine injuries ( 15,16).
Andresen et al. (14) reported the activity at the time of injury. Tackling (32%) caused the highest percentage of injuries.
Blocking (26%), carrying the ball (19%), and being blocked (10%) caused the next highest percentages. Fewer injuries
were sustained while running, receiving, and passing.
The distribution of injuries during a game has been reported by several authors ( 9,14,17,18). One report (14) showed that
the lowest number of injuries occurred in the first quarter (13%). The highest number of injuries occurred in the third
quarter (31%), followed by the second quarter (29%) and the fourth quarter (27%). The distribution during the season
was also recorded in this study. Most injuries occurred during the first half of the season, with the peak rate at
midseason.
PROTECTIVE EQUIPMENT
Improvements in football equipment have helped to limit the number and severity of injuries in the sport. Ensuring the
correct fit and maintenance of the equipment is essential to allow proper protection. The basic equipment consists of a
helmet; shoulder, hip, thigh, and knee pads; and a mouthpiece ( Fig. 24.1). These are required by National Collegiate
Athletic Association (NCAA) rules. The National Operating Committee on Standards for Athletic Equipment (NOCSAE)
establishes guidelines for equipment maintenance and reconditioning and is responsible for approval of helmets. As
helmets age or are modified, however, they may fail to meet these standards. One study showed that 75% of randomly
selected 3-year-old helmets failed the NOCSAE test ( 19).
FIGURE 24.1. A: Shoulder pads. B: Shoulder pads with cowboy collar.
General helmet design consists of a hard plastic, outer shell and inner pads, or air- or fluid-filled cells to cushion the
head. The older suspension-type helmets were found to be inferior after the webbing material stretched with wear. This
allowed contact between the head and shell on impact ( 20) (Fig. 24.2).
FIGURE 24.2. A: Suspension and padding from 1995. B: Current padding system.
Before fitting, an initial inspection of each helmet should be made. The outer shell and inner padding should be checked
for cracks. Screws and rivets should be tightened and checked for cracks at these sites. Air pockets should be filled to
recommended levels.
After inspection the helmet should be fit ( Fig. 24.3). The player's head should be examined for any significant variation
that may require special fitting or a special helmet. The player should be fit with a hair length that will be worn throughout
the season. Instruction in proper donning of the helmet, by pulling the earholes apart with the fingers and pulling the
helmet into place, should be next. The fit should then be inspected for any gaps between the head and pads, and
adjustments should be made to ensure a snug fit on all sides. In the back, the helmet should cover the base of the skull
but not impinge on the cervical spine with full neck extension. At the forehead, the anterior rim should rest about 0.75
inch (19 mm) above the eyebrows. The jaw pads should fit snugly against the cheeks, and the chin strap should fit tightly.
The examiner should attempt to rotate and rock the helmet on the athlete's head. The helmet should move only slightly.
Pressure should then be applied to each side of the helmet. There should be no significant gapping between the pads
and the head with pressure applied.
FIGURE 24.3. Fitting the helmet. A: Measuring the head circumference for helmet fitting. B: Inspecting for gaps between
head and pads. C: Evaluating earholes and ensuring appropriate fit. D: Evaluating the helmet at the base of the skull. E:
Checking for excessive movement.
Facemasks are selected based on player position, protection required, and player preference. Quarterbacks, receivers,
and backs require an unobstructed view, whereas linemen require more facial protection. Eye shields can be attached to
prevent eye injuries while allowing unobstructed vision.
Mouth guards have been required in high school football since 1962 and in NCAA football since 1973. Mouth injuries
decreased 50% after the adaptation of these rules ( 21). In addition, the mouth guards dissipate the shock of blows the
chin, which decreases the rate of jaw fractures. Another significant benefit is protection against concussions.
Shoulder pads should also be examined carefully before player fitting. Cracked pads, loose rivets or screws, and worn
straps should be addressed. The player's size from shoulder to shoulder should be measured and the appropriate size
pads selected. Shoulder pads are also position specific, with quarterbacks and receivers using smaller pads that allow
greater range of motion. Other players use larger pads that offer more protection. When assessing fit of the pads, the
axilla straps should be tightened and the laces tightened so that the pads meet but do not overlap. The pads should
extend just beyond the lateral aspect of the shoulder, and they should cover the sternum and clavicles anteriorly and the
scapulae posteriorly. The player should be able to raise the arms overhead without causing impingement of the inside
rim of the pads on the neck. There should be an overall snug fit that allows little motion between the pads and the player.
Additional accessories for further protection may be attached to the shoulder pads. Neck rolls and collars are advocated
for players with a history of “stingers,” to limit neck motion. Rib pads may be attached to the shoulder pads or suspended
over the shoulder. These allow added protection for quarterbacks and others with rib injuries. Back plates allow further
posterior protection. Linemen and linebackers may need additional arm protection to decrease the repetitive trauma at
the upper arm. Additional upper extremity protection includes padded gloves commonly worn by linemen to decrease the
rate of hand injuries. Elbow pads and skin protection are also commonly used by players, especially in games played on
artificial turf.
Hip pads should be fitted to cover the iliac crests, greater trochanters, and sacrum. These commonly fit in a girdle that
may also have pockets for thigh pads. Knee pads are fit into pockets in the pants.
Protective equipment may also include shoewear. Certain shoes and types of cleats have been identified to cause an
increased injury rate. In addition, a protective metal plate in the sole of the shoe (to limit dorsiflexion) may be used by a
player with turf toe. Ankle taping, braces, and high-top shoes have been used for players with ankle injuries. Some
studies have shown lower injury rates when ankles were prophylactically taped. Others have advocated laceup ankle
supports to allow better maintenance of support, because they allow periodic retightening ( 22). Ankle protection remains
a controversial area with several different practices.
One of the most controversial areas of protective equipment concerns prophylactic knee braces. Because of the high
incidence of knee injuries, especially MCL injuries, knee braces with a lateral hinged support were developed. These
braces decrease injuries by limiting valgus stresses on the knee. There has been evidence to support a decreased rate
of MCL injuries in defensive players ( 23). However, at least two studies have reported an increased rate of injury with
prophylactic braces ( 24,25). Because of the lack of proof of efficacy and the potential for causing harm, no
recommendation or requirement for widespread use of braces can be made.
HEAD AND NECK
Concussion
An estimated 250,000 head injuries occur due to football each year in the United States. Twenty percent of high school
football players are estimated to sustain a concussion each year ( 26). Concussions occur while players are tackling
(43%), being tackled (23%), blocking (20%), or being blocked (10%) ( 26). With the potential morbidity and mortality of
complications of these injuries, it is essential that each team physician have a clear understanding of their management.
One of the most commonly used definitions of concussion is, “a clinical syndrome characterized by immediate and
transient posttraumatic impairment of neurologic function, such as alteration of consciousness, disturbance of vision,
equilibrium, etc., due to brain stem involvement” ( 27). Many grading systems are used for concussion evaluation. The
most commonly used system was developed by Cantu (27). This system uses duration of loss of consciousness and
retrograde amnesia for grading severity ( Table 24.1).
TABLE 24.1. CONCUSSION SEVERITY
After the initial management, a decision concerning when to allow return to play must be made for each athlete with a
concussion. Awareness of the potential complications is necessary to make this decision. The so-called second impact
syndrome was described in 1984 to occur when an athlete sustains a second head injury before symptoms associated
with the first concussion have resolved. It is characterized by visual, motor, and sensory changes and difficulty with
thought and memory processes (28). The mortality rate is approximately 50%, and the morbidity rate near 100% because
of diffuse cerebral swelling. Avoidance of this complication forms the basis of management strategies for concussions.
Another complication is postconcussion syndrome. This consists of headache, dizziness, fatigue, irritability, and impaired
memory and concentration. This syndrome may persist for days, weeks, or months.
Grade 1 concussions, which account for 90% of cases, involve no loss of consciousness and a period of posttraumatic or
retrograde amnesia lasting less than 30 minutes. This type is the most difficult to recognize, and many players attempt to
continue playing after “having their bell rung.” Treatment should include removal from play and observation on the
sideline. After headache, dizziness, impaired concentration, and retrograde amnesia have resolved for a brief period,
return may be considered.
A grade 2 concussion is associated with loss of consciousness for less than 5 minutes and a period of posttraumatic
amnesia lasting more than 30 minutes but less than 24 hours. Initial management is similar to that for grade 3
concussions. However, if the period of unconsciousness is brief and there are no neck or peripheral neurologic
complaints, removal on a spine board may not be necessary.
Grade 3 concussions are the most severe. Loss of consciousness lasts longer than 5 minutes, and posttraumatic
amnesia lasts longer than 24 hours. All unconscious athletes should be treated as though they have a concurrent
cervical spine injury. The neck should be immobilized and the player removed on a spine board until the player regains
consciousness and a full examination or radiographs can rule out the possibility of cervical spine injury. All players with a
suspected neck injury, whether conscious or not, should have their helmet and shoulder pads left on ( Fig. 24.4). There is
a reported 50% incidence of further neurologic injury with improper handling in unstable neck injuries. The facemask may
be removed to allow better access to the airway. If the athlete is in respiratory distress and better access is needed, then
the shoulder pads and helmet may both be removed while the head and neck are held in a neutral position. Opening of
the airway is performed with the jaw lift technique, by lifting the mandible forward. If this is not adequate, the head tilt–jaw
lift technique may be used with careful attention not to overextend the cervical spine. The athlete should be taken for
cervical spine radiographs immediately. After this, a computed tomographic scan of the head should be obtained to rule
out severe intracranial contusion or hematoma. It is often recommended that athletes with grade 3 concussion be
admitted overnight for observation.
FIGURE 24.4. Log roll to a spine board. A: Chief of the team immobilizes the head and neck, while the support team
concentrates on the lower body. Members of the support team should be positioned at the shoulder, hips, and lower legs.
B: The chief initiates the move while immobilizing the head and neck at all times as the injured player is turned. C: The
player is positioned on the center of the spine board while the chief continues to immobilize the head and neck. (From
Vegso JJ, Lehman RC. Field evaluation and management of head and neck injuries . Clin Sports Med 1987;6:1–15, with
permission.)
After the initial management of a concussion, the physician needs to make a decision concerning when to allow the
player to return to competition. Considering the potential consequences of second impact syndrome, one should err on
the side of conservatism. Guidelines for return to play are based on the grade of the concussion and the player's history
of any prior concussions ( Table 24.2).
TABLE 24.2. RETURN TO PLAY GUIDELINES
Currently used return-to-play guidelines are based on clinical observations rather than findings from research
experiments. Studies objectively evaluating the changes in cognitive function and equilibrium that are known to occur in
head-injured patients may allow formation of a more scientific basis for these guidelines. One study compared
head-injured athletes to controls with postural stability and cognitive assessments ( 29). The results showed differences
between the groups in postural stability but not in neuropsychological testing. Based on the timing of return to normal
function, the authors recommended keeping athletes from competition for a minimum of 3 days after a mild head injury.
Facial Injuries
As football equipment has evolved to include the use of facemasks and eye shields, there has been a decrease in facial
injuries. However, such injuries are still frequently seen by the team physician. Abrasions, contusions, and lacerations
should be carefully evaluated to rule out more significant ocular or maxillofacial injury. When facial lacerations occur,
they should be irrigated and closed with small sutures with little tension. Through-and-through skin to oral mucosa
lacerations should be closed in layers. Absorbable suture is used for the mucosa, muscle, and subcutaneous layers
before the skin is approximated. Facial sutures should be removed within 5 days to avoid suture marks. Football is a
high-risk sport for ocular injuries, which are often caused by fingers to the eye. A basic evaluation should include an
adequate history, a visual acuity test, a check of pupillary responses, and extraocular movement testing. The most
common sports-related injuries are corneal abrasion, traumatic iritis, traumatic hyphema, and orbital fractures. Basic
initial treatment before referral may include a small amount of crushed ice placed gently on the eye for severe swelling. If
an open globe injury is suspected, a plastic shield should be taped over the eye and the patient should be transferred for
emergency ophthalmology evaluation.
Despite facemask protection, nasal injuries occur in football. Common signs and symptoms of nasal fractures include
epistaxis, nasal airway obstruction, asymmetry, crepitus, periorbital and subconjunctival ecchymosis, and septal
hematoma. Initial management involves ensuring a secure airway and controlling the bleeding by external pressure or
intranasal packing. Evaluation of the intranasal structures may be allowed by spraying 0.25% phenylephrine
hydrochloride to shrink the mucosa. Septal hematoma, a collection of blood between the cartilage and
mucoperichondrium, should be ruled out; this injury manifests with bluish-red bulging in the nasal vestibule. Players
should be referred for realignment and counseled about possible deformity. Return to play is allowed with protective
gear.
Mandible fractures also occur in football players as a result of blows under the facemask. Pain, tenderness, and swelling
are suggestive. Management includes securing an airway, ice, immobilization, and referral for definitive diagnosis and
treatment.
Cervical Spine Injuries
Cervical strains, sprains, fractures, dislocations, and neurologic injuries occur commonly in football players. Careful
evaluation to differentiate minor injuries from potentially catastrophic ones is imperative. The initial management of these
injuries by trainers and team physicians may be life-saving.
The most common cervical injury in football is probably the acute strain. Overloading or stretching of the
musculotendinous unit causes torn muscle fibers. Commonly involved muscles are the sternocleidomastoid, trapezius,
rhomboids, erector spinae, scaleni, and levator scapulae. Initial pain followed by tenderness, swelling, and decreased
motion is typical. Management should include ice, rest, and antiinflammatory medications.
Cervical sprains are injuries to the intervertebral ligaments and joint capsules. These injuries may have a similar clinical
appearance to cervical strains, but without specific point tenderness over a muscular structure. A severe sprain may
result in cervical instability. Initial management of neck pain should include removal from play and evaluation for any
significant injuries. Pain and decreased range of motion should arouse suspicion. Any neurologic findings should prompt
immediate immobilization and transfer to a hospital for further evaluation. If no fractures are present on initial
radiographs, flexion and extension lateral views should be obtained to rule out instability. Repeat films after 10 to 14 days
may be necessary, because spasm may limit motion after the acute injury. Athletes with instability may require surgical
treatment. Otherwise treatment should include rest, ice, and a brief period of immobilization. Return to play may be
considered after full, painless range of motion has returned.
Cervical spine fractures and dislocations with resulting neurologic injury are the most dreaded injuries in football. These
injuries have been the subject of much research in attempts to identify risk factors and mechanisms of injury. With this
knowledge, changes in the game have been made to decrease the rate of injury.
Data from 1971 to 1975 gathered by the National Football Head and Neck Registry revealed 77 deaths and 99
permanent quadriplegias as a result of football injuries. A total of 259 cervical fracture-dislocations occurred ( 16). In
Pennsylvania and New Jersey during 1975 a total of one death, eight quadriplegias, and three other cervical spine
fractures occurred (30). These alarming data prompted critical review and comparison with previously collected data from
1959 to 1963 (31). A dramatic increase in neck injuries with a decrease in head injuries was reported. It was concluded
that improvements in protection of the head by the helmet had decreased the rate of head injuries but allowed changes in
techniques of tackling. The head-first tackling technique (“spearing”) was determined to be responsible for most of the
injuries, because it places the cervical spine in an unfavorable position (see Fig. 24.2). Axial loading of the cervical spine
causes more efficient transmission of force to the cervical vertebrae, resulting in fractures and dislocations. In a study by
Torg et al., 51 films of injuries allowed determination of the mechanism of injury, and axial loading was found to be the
mechanism in each case (32). After presentation of these data, the NCAA and the National Federation of High School
Athletic Associations implemented rule changes banning spearing in 1976. Within 2 years, dramatic reductions in
cervical fractures, dislocations, and quadriplegias were realized. Quadriplegias decreased from 34 cases in 1976 to 5
cases in 1984 (32). With the axial loading mechanism accepted as the usual mechanism for catastrophic spine injury, it
was expected that continued player education and coaching in proper techniques would be the best protection against
injury. A survey of high school players from 16 high schools in one state, however, reported that 29% of the players
agreed it was within the rules to tackle with the top of the helmet ( 33). The relationship between player education and
injury is suggested by the reported high rate of cervical spine injuries in this state.
Of the eight quadriplegias occurring in 1975 in Pennsylvania and New Jersey, six of the players were defensive backs
(30). From the 1971 to 1975 data, 73% of the college players and 52% of the high school players rendered quadriplegic
were defensive backs. Special teams (13%) and linebackers (10%) were next most affected positions in the high school
data (16). Players in these positions make a large number of tackles and are often involved in high-speed collisions.
These players should be targeted for coaching in proper tackling techniques.
Other means of prevention should also be used. A resistance strengthening program for the neck musculature may be
helpful. The neck muscles are usually small with poor strength, and increasing their strength may help stabilize the spine
during contact.
If a player does sustain a suspected neck injury, an immediate on-the-field evaluation is mandatory. Initial management
is critical, because a neurologic injury can be worsened by improper handling of the athlete. An assessment of the
airway, breathing, and circulation should be performed first, because the player may have an airway obstruction or
neuromuscular cause for airway compromise. The player should not be moved while a determination is made whether
there is loss of consciousness, neck pain, extremity pain, or motor or sensory loss. A player who is supine should be left
in that position with the helmet and shoulder pads on. If the player is prone, a careful, well-supervised log roll should be
performed. Enough people should participate so that the athlete's body can easily be rolled over as one unit, and one
person should carefully immobilize the head and neck with their hands and forearms. For transport, the player should be
immobilized on a spine board.
A detailed physical examination, including a complete neck and neurologic examination, should be performed. If there
are any neurologic findings, or if any significant neck pain or loss of motion is present, the athlete should remain
immobilized and be immediately taken to the hospital. There, under controlled conditions, the helmet and shoulder pads
may be carefully removed, maintaining neutral neck position. Cervical spine radiographs should include anteroposterior,
lateral, and odontoid views. Oblique views and flexion and extension lateral views may be indicated. Adequate
radiographs should be obtained or the patient should remain immobilized and further studies ordered. Fractures,
dislocations, or other signs of instability should be ruled out. A magnetic resonance imaging study should be obtained for
most patients with neurologic findings.
Transient quadriplegia from cervical spinal cord neurapraxia is another cervical spine injury occurring in football players.
This is thought to occur with hyperflexion or hyperextension injuries, usually in athletes with cervical stenosis. This
syndrome includes sensory changes of burning pain, numbness, tingling, and loss of sensation, as well as motor
changes ranging from weakness to complete paralysis. Neck pain is usually absent. Recovery is complete and usually
takes 10 to 15 minutes, but it may take up to 48 hours. A survey of 503 NCAA football teams in 1984 estimated that 1.3 of
every 10,000 athletes had experienced cervical cord neurapraxia ( 34). Current reports do not suggest that sustaining this
injury predisposes a player to a higher risk of permanent neurologic injury. There is an association with narrowing of the
spinal canal, and evaluation should include imaging studies to rule out congenital anomalies, instabilities, disk disease,
and spinal stenosis ( 34). After initial treatment as for any potentially catastrophic neck injury, a full evaluation should be
pursued. Management after the resolution of symptoms, including decisions regarding return to play, must be
individualized. Preventive measures include education in tackling technique and neck-strengthening exercises.
SHOULDER
Shoulder injuries are common in football. In several studies, shoulder injuries were among the top four injuries, ranging
from 10% to 13.3% of all injuries (3,9,10). The mechanism in the majority of these injuries is acute trauma related to
tackling, being tackled, or blocking. Fractures of the clavicle, scapula, or humerus; brachial plexus injuries;
acromioclavicular injuries; contusions; and exostoses are examples of injuries in this area. Instability may result from an
acute dislocation or subluxation, or it may occur after chronic insults, such as posterior instability in an offensive lineman
resulting from blocking techniques.
Brachial Plexus Injuries
Stingers, burners, and pinched nerves are very common in football players. In one prospective study of Division I players
the incidence was 7.7% (34). In another study of Division I players, 49% sustained these injuries during their 4-year
career (36). Yet another study, of Division III players, reported that 65% had experienced stingers during their career
(37). Defensive backs were shown to have the highest incidence in one prospective study ( 35).
The most commonly proposed mechanism is ipsilateral shoulder depression and contralateral neck deviation causing
traction injury to the upper brachial plexus (C-5 and C-6) ( Fig 24.5). Others suggest that some burners are the result of
neck extension and ipsilateral shoulder deviation that causes nerve root compression in the intervertebral foramina ( 38).
Still another suggested mechanism involves compression of the fixed brachial plexus between the shoulder pad and the
superior medial scapula when the pad is pushed into Erb's point ( 39). Presentation usually involves burning pain,
numbness, and tingling from the shoulder to the hand after a collision. Any neck pain or bilateral symptoms should be
considered a cervical spine injury and evaluated as such. Initial evaluation should include checks for a full, painless
range of motion of the neck. Upper-extremity sensory and motor testing should be next. Attention should be paid to the
deltoid, biceps, and external rotators, which are the muscles most often affected. When full, painless range of motion and
normal strength have returned, the athlete may return to play. The degree of neurologic injury varies widely, and the time
for recovery may be from several minutes to months. Extra shoulder padding and protective equipment (e.g., neck rolls)
are used on return to play.
FIGURE 24.5. Mechanism of Injury to the brachial plexus (burners). (From Zarines B, Prodromos LC. Shoulder injuries in
sports. In: Rowe CR, ed. The shoulder. New York: Churchill Livingston, 1988:411–433.)
Acromioclavicular (AC) joint injuries are also common in football. In a study of a Division I NCAA football team over a
5-year period, 8.1% of their 283 injuries were AC joint injuries ( 13). In a study at the U.S. Naval Academy of AC joint
injuries in athletes, 41% were the result of football ( 40). The mechanism usually described is a force applied to the
acromion with the arm adducted. This may occur when a player is being tackled and the point of the shoulder is driven
into the ground. As the scapula is being driven downward and medially, the clavicle levers on the first rib and the AC
ligaments and coracoclavicular ligaments may be disrupted ( 41). An indirect mechanism, with the force transmitted from
the upper extremity upward across the glenohumeral joint, driving the scapula upward and medially, has also been
described (41).
The classification scheme of Rockwood is useful for communication and for directing treatment ( Fig. 24.6). The history
usually confirms the typical mechanism of injury. On physical examination, tenderness at the AC joint, decreased range
of motion of the shoulder, and the typical deformity for types III and higher should be noted. Treatment of types I and II is
nonoperative, with the use of a sling for several days to weeks, activity modification, and isometric exercises, followed by
range of motion and progressive resistance exercises. A modified Kenny Howard sling has been associated with skin
breakdown over the distal clavicle. Treatment of type III injuries remains controversial; most surgeons favor initial
nonoperative management, with some exceptions. Operative treatment is recommended for types IV, V, and VI AC joint
injuries. For chronic symptomatic AC separations, the modified Weaver-Dunn procedure is often advocated. In this
procedure the distal clavicle is excised and the coracoacromial ligament is transferred to reconstruct the coracoclavicular
ligaments, with additional fixation to protect the reconstruction.
FIGURE 24.6. Classification of acromioclavicular injuries. Note that type III and above are associated with
coracoclavicular disruptions. (From Rockwood CA. Injuires to the acromioclavicular joint. In: Rockwood CA, Green DG,
eds. Fractures in adults. 2nd ed. Philadelphia: JB Lippincott, 1984:871.)
Contusions
Contusions are second only to sprains as an injury type, with an incidence of 21% to 30.1% ( 3,9,10,11). Around the
shoulder these injuries are very common and may have painful sequelae. Two complications of these soft tissue injuries
are tackler's exostosis and myositis ossificans. Tackler's exostosis occurs at the anterolateral proximal humeral cortex
after repeated injuries cause periosteal stripping and new bone formation. Myositis ossificans may also occur, but it is
separated from the cortex, occurring in the muscle belly. Both conditions should be recognized early and treated with ice,
compression, and possibly aspiration. Symptomatic lesions may ultimately require surgical excision for pain or possibly
for elbow contracture (42,43).
Glenohumeral instability represents a broad spectrum of injury. The most obvious degree is dislocation. In Pritchett's
study of injuries reported to insurance companies, 1.5% of all injuries were shoulder dislocations ( 11). The report of
Canale et al. on the injuries sustained by a Division I college football team listed 2.1% of all injuries as shoulder
dislocation/rotation injuries ( 13).
The mechanism of injury is often a blow to the abducted, externally rotated arm for anterior dislocations ( Fig. 24.7) or,
less commonly, a blow to the adducted, internally rotated arm for posterior dislocations. Improper tackling techniques
have been noted as a cause of anterior dislocation ( 42). More subtle anterior instability may occur in quarterbacks, as in
throwers in other sports. Posterior instability may also occur secondary to repetitive loads on the adducted, internally
rotated arm, as sustained by offensive linemen using pass blocking techniques. Prevention of instability may take several
forms. Correction of poor tackling techniques may prevent some injuries. An appropriate shoulder-strengthening program
with avoidance of certain exercises, such as the bench press with posterior instability, may be helpful. Rehabilitation
consists of strengthening of the internal and external rotators of the shoulder. Despite these measures, recurrent
instability can be disabling for a football player, and surgical treatment may be necessary ( Fig. 24.8). Open capsulolabral
reconstruction is usually suggested in the contact athlete, although arthroscopic stabilization may play a role in selected
cases.
FIGURE 24.7. Improper tracking technique can result in anterior shoulder dislocation. Note the position of the arm, which
is completely abducted, creating a lever that can result in a large moment across the shoulder. From Zarines B,
Prodromos LC. Shoulder injuries in sports. In: Rowe CR, ed. The shoulder. New York: Churchill Livingston,
1988:411–433.)
FIGURE 24.8. Hill-Sachs fracture in a fullback who suffered an anterior dislocation when he fell while blocking.
Rotator Cuff Injuries
Rotator cuff injuries are unusual in the younger population typically involved in football. Quarterbacks, like other throwing
athletes, are most likely to sustain these injuries. A study by Blevins et al., however, reported traumatic cuff injuries in
football players documented surgically ( 44). The mechanism can be repetitive microtrauma or an acute injury. Pain with
overhead activities and with throwing are typical complaints. All of these patients should be carefully evaluated for
anterior instability with secondary impingement, which is more likely in this age group ( Fig. 24.9).
FIGURE 24.9. Partial-thickness rotator cuff tear in an offensive lineman.
Rehabilitation with strengthening of the rotator cuff, deltoid, and scapular stabilizers is often successful in patients with
cuff-related complaints. Posterior capsular stretching is also important. Complete tears and some contusions and partial
tears, as noted by Blevins et al. ( 44), can be managed successfully with surgery.
ELBOW
The incidence of elbow injuries in football players is difficult to estimate because most series include them with other arm,
forearm, and wrist injuries. Canale et al. ( 13) listed 1.4% of the injuries to a college football team as occurring to the
elbow. Dislocation may occur after a fall on the outstretched upper extremity. The most commonly proposed mechanism
of injury is levering of the humerus out anteriorly as the olecranon is locked in the olecranon fossa in full extension.
O'Driscoll described a posterolateral mechanism that may be more common ( 45). After a careful neurovascular
examination, a dislocation may be reduced and radiographic evaluation and splint immobilization should follow.
Medial collateral ligament injuries resulting in valgus instability also occur in football. Pain and tenderness at the medial
elbow are typical. Associated arthritic changes and loose bodies may develop. Rehabilitation for valgus instability
generally consists of rest followed by supervised stretching and strengthening. If this is unsuccessful, surgical
reconstruction of the ulnar collateral ligament with a graft through bone tunnels may be necessary. Rehabilitation after
elbow dislocation follows a brief period of immobilization, then protected range of motion. Subsequent problems after
dislocation have been reported to be infrequent in the past but are increasingly recognized ( 45).
FOREARM, WRIST, AND HAND
The forearm, wrist, and hand are commonly injured in football. From 10.4% to 21% of all injuries have been to this region
(8,9,10,11 and 12). These relatively unprotected parts of the body are often brought into contact with helmets, pads,
cleated shoes, and the ball.
Contusions of the dorsum of the hand and metacarpal fractures are common and should be differentiated. Ice,
compression, and protective padding should be used for contusions. Stable metacarpal fractures may be treated with a
hard cast for practice and a soft cast for games, to comply with rules. Unstable fractures should be treated with internal
fixation and return to play with protective padding. In a study by Rettig et al., the average time lost from play was found to
be 12 days for nonoperative treatment and 22 days for operative treatment ( 46).
The scaphoid is the most commonly fractured carpal bone, and these injuries are common in football players. The usual
mechanism is a fall on the outstretched hand with an extended wrist. Pain and tenderness in the anatomic snuffbox are
suspicious, and radiographs should be evaluated carefully. Negative radiographs with a suggestive examination should
prompt repeat films, because the fracture line may become evident later. Nondisplaced fractures are treated in a short
arm–thumb spica cast with a soft cast for games. Return to play for some skilled position players may be difficult.
Displaced fractures, delayed unions, and nonunions are managed with internal fixation and possibly bone grafting ( 47).
Another common hand injury in football players is a tear of the thumb ulnar collateral ligament, which is called
gamekeeper's or skier's thumb. In a contact sport, the outstretched thumb is particularly vulnerable. Forced abduction of
the thumb is the mechanism of injury. Inadequate treatment may result in difficulty in activities that require pinch.
Radiographs should rule out associated avulsion fractures. Partial tears of the ulnar collateral ligament are stable to
radial stress and should be treated in a thumb spica cast for 3 weeks, with additional protection afterward ( 48). Complete
injuries demonstrate instability on radial stressing of 30 degrees greater than the uninjured side. The interposed adductor
tendon (Stener lesion) often prevents healing of the ligament, necessitating surgical repair ( 48). Again, 3 weeks in a
thumb spica cast followed by additional protection is required. Linemen may be able to return to play with protection, but
skilled position players may have more difficulty.
Injuries to the phalanges and interphalangeal joints are particularly common in football players. Injuries should be
evaluated with stressing of the interphalangeal joints and radiographs when the possibility of fracture exists. Most sprains
are treated with buddy taping and range-of-motion exercises. Certain injuries should be specifically looked for because of
their potential for loss of function and deformity. Terminal extensor tendon insertion avulsion (mallet finger) may occur
after the player is struck by the ball, with pain, swelling, and inability to extend the distal interphalangeal (DIP). These
injuries should be managed with splinting in extension for 6 to 8 weeks unless a fracture involving 25% of the articular
surface is present, in which case open reduction and internal fixation should be performed.
A painful, swollen proximal interphalangeal (PIP) joint should be tested for ability to extend against resistance. If this
ability is not present, a central slip avulsion (traumatic boutonnière) should be suspected. Treatment is with extension
splinting of the PIP with the DIP free for 6 to 8 weeks.
An avulsion injury of the flexor digitorum profundus tendon (jersey finger) may occur when a player grasps an opponent's
jersey. The player is unable to flex the DIP joint. The injury should be managed with surgical repair. The urgency of the
repair depends on the degree of retraction of the tendon.
LUMBAR SPINE
Football necessarily places the lumbar spine under considerable stresses, and injuries to this area are common. Studies
have suggested that 30% of college and 12% of National Football League (NFL) players lose playing time because of
these injuries (49). The reported incidence ranges from 4.9% to 8% of total injuries ( 3,11,13). Acute excessive loads may
cause injury, but repetitive lesser stresses inherent to certain blocking and tackling techniques may also cause injury.
Offensive linemen are particularly susceptible, apparently because of repetitive extension loads sustained when coming
out of a stance for blocking. Weight lifting may also be contributive, especially squats ( 50,51).
Contusions and strains are the most common injuries (52). These are generally managed with activity modification and
rehabilitation. A stretching and strengthening program is usually successful for these injuries.
Spondylolysis, a defect in the pars interarticularis, is also a common condition in football players. Incidences of 15% in
college players ( 53) and 50% in college linemen ( 54) have been reported. Many cases, however, are asymptomatic and
usually go undetected. It is generally accepted that repetitive extension loads are a cause of this condition ( Fig. 24.10).
Players with back pain and spondylolysis should participate in a rehabilitation program until symptoms subside before
returning to play ( 55). A player with unresponsive symptoms or with neurologic findings may be evaluated with further
imaging studies.
FIGURE 24.10. Stress reaction of pars interarticularis.
Spondylolisthesis is forward slippage of one vertebrae of the next, usually L5 on S1. Grades 1 and 2 (less than 50%
slippage) without evidence of progression or neurologic findings are managed like spondylolysis. Higher-grade slips,
progression, and neurologic findings warrant further evaluation and possible surgical treatment. Bracing is advocated by
some in certain situations. A rehabilitation program should include hip flexor stretching to decrease lumbar lordosis.
Back pain and radiculopathy may be caused by disk herniation ( Fig. 24.11). Initial nonoperative treatment is usually
successful (56). Unresponsive or progressive signs or symptoms may necessitate surgical treatment.
FIGURE 24.11. Magnetic resonance image of acute herniated disk in a football lineman.
HIP
Hip injuries made up 2.4% and 2.5% of the total football injuries in two series ( 3,13). Most injuries are contusions,
although the uncommon fracture or dislocation can have disastrous consequences. Avulsion fractures around the hip
occur in younger players.
A contusion over the iliac crest (“hip pointer”) is probably the most common injury to the hip area. This injury should be
managed with ice and compression initially. Later, range-of-motion exercises and protective padding are used for return
to play. Avulsion fractures occur at the anterior superior iliac spine (sartorius), anterior inferior iliac spine (rectus
femoris), ischium (hamstrings), lesser trochanter (iliopsoas), and iliac crest (abdominals). Unless displacement is severe,
these injuries are managed with protected weight bearing, ice, and activity modification. Progressive range of motion and
strengthening are initiated as pain resolves. Return to play is allowed when full, painless range of motion and strength
have returned.
THIGH
Quadriceps contusions are common, occurring in 6.7% of the injuries in one study ( 13). The mechanism is usually a
direct blow from a helmet or shoulder pad as a player is being tackled. Pain, tenderness, swelling, and an antalgic gait
are typical. A classification scheme based on the initial range of motion and gait abnormality was proposed by Jackson
and Feagin (57). Initial treatment consists of attempts to decrease hemorrhage with ice, compression, and protected
weight bearing. Some advocate strapping the knee in full flexion to limit edema and hemorrhage and maintain motion.
Early pain-free range of motion is important, but overly aggressive therapy may be detrimental by increasing the
hemorrhage. Return to play is allowed once range of motion and strength have returned to normal. Ryan et al. ( 58)
reported results in West Point cadets. Disability averaged from 13 to 21 days depending on severity. Myositis ossificans
can be a problematic complication of these injuries. Risk factors appear to be severity of the initial injury and inadequate
treatment. Severe contusion can also lead to compartment syndrome. A high index of suspicion should be maintained.
Those players with classic symptoms should be evaluated with compartment pressure measurements and, if necessary,
fasciotomies should be performed.
KNEE
Between 22% and 36.5% of all football injuries occur to the knee, making it the most commonly injured joint ( 2,3,8). One
study of college players determined the risk of knee injury to be 6% to 22% per year. Football players have a 5.8 times
higher incidence of knee injuries than the general population ( 3). Knee injuries account for significant time lost from
participation as well as a large portion of the medical expenses resulting from football injuries ( 11).
The structure most commonly injured is the MCL (Fig. 24.12), followed by the menisci and the anterior cruciate ligament
(ACL). The mechanism of injury and the position played often suggest which structures are injured. Interior linemen,
offensive backs, and linebackers were found to be most susceptible in one study ( 59) (Fig. 24.13). Linemen often sustain
MCL injuries after being blocked in the side of the knee or when a player rolls onto the lateral leg, causing a valgus
stress. Receivers and defensive backs may be more likely to sustain a noncontact ACL injury. Rapid deceleration and
cutting can place excessive strain on the ACL ( Fig. 24.14). Running backs often sustain contact injuries while being
tackled. The direction of the blow to the leg can often suggest which ligaments have been injured.
FIGURE 24.12. The most common mechanism of injury to the medial collateral ligament is seen when a player gets
struck by an opposing player on the outside lateral aspect of the knee, which produces valgus force with tearing of the
medial collateral ligament. (From Tria AJ, Hosea TM. Diagnosis of knee ligament injuries: an illustrated guide to the knee.
New York: Churchill Livingston, 1992:87–99.)
FIGURE 24.13. Grade III medial collateral ligament sprain that occurred after valgus injury to the knee in a college
lineman.
FIGURE 24.14. Partial anterior cruciate ligament tear in a college linebacker.
Owing to the high incidence and severity of knee injuries sustained by football players, there have been considerable
efforts toward prevention. Rule changes have been made to protect the knee during blocking. The effects of playing
surfaces and shoes have been investigated ( 60,61). The use of prophylactic knee braces, however, remains the most
often studied, yet controversial topic concerning prevention. Most studies have design flaws that make reaching firm
conclusions difficult ( 62). Several clinical studies reported a decreased rate of MCL injuries ( 63,64 and 65), while two
studies reported an increased rate of injuries ( 66,67). In addition, biomechanical data suggest that prophylactic knee
braces offer limited protection to the MCL and ACL under valgus knee stresses ( 68,69,70 and 71). Therefore, there
continues to be no clearcut support for or against the use of prophylactic knee braces based on the current literature.
The effect of artificial turf on the rate of knee injures was reported using NFL data from the 1980s. A higher rate of MCL
injuries among linemen and a higher rate of ACL injuries among special teams players were documented ( 61). It has
been suggested that a higher coefficient of friction between the surface and the shoe leads to more forces being
transmitted to the knee (14). Matching shoes to the playing surface may help offset this effect.
Aside from equipment issues, prevention of knee injuries is directed toward conditioning of the athlete. Strengthening of
the quadriceps and hamstrings is emphasized. Maintaining balance between these groups and maintaining flexibility are
also important.
Ligament Injuries
Like other injuries, knee ligament injuries should be evaluated on an individual basis. A player at one position or level of
play may tolerate an injury that another player cannot. Treatment options should be well understood by the player and
family in this sometimes complex decision-making process.
MCL injuries are the most common knee ligament injury in football players, with linemen most often affected. Physical
examination confirms tenderness over the MCL and increased laxity with valgus stress at 30 degrees of flexion. Injuries
are graded as 1, 2, or 3. Grade 1 injuries demonstrate no disruption of the ligament fibers and no increased laxity on
examination. There is tenderness over the ligament. Management includes weight bearing as tolerated, with return to
play after full range of motion and strength are achieved. Grade 2 injuries involve a partial disruption of ligament fibers
and demonstrate increased laxity with a firm endpoint on examination. Grade 3 injuries represent complete ligament
disruption and increased laxity with no endpoint on valgus stress. There are often associated injuries to the menisci and
ACL with grade 3 injuries. Treatment for isolated MCL injuries is now generally nonoperative, with bracing and
rehabilitation. Return to play is allowed after tenderness and swelling have resolved and range of motion and strength
have returned. Braces are often used on return to play.
Lateral Ligaments
Lateral injuries are less common than MCL injuries and may result from a blow to the medial knee. They are often seen in
combination with more extensive posterolateral corner or cruciate injuries, and a high index of suspicion should be
maintained for these injuries when lateral instability is noted. Varus stressing at 0 and 30 degrees is used for basic
evaluation. Mild injuries may be treated nonoperatively with bracing and rehabilitation, but the threshold for surgical
treatment should be much lower than for MCL injuries. Early primary repair of significant injuries has yielded superior
results compared with reconstruction for chronic instability.
Although MCL injuries are more common, ACL injuries are the most common knee injury requiring surgery. In one study,
63% (37/59) of the knee injuries requiring surgery were ACL disruptions ( 3). The mechanism is frequently a noncontact,
deceleration, rotational injury. Valgus, hyperextension, or varus contact injuries may also cause ACL rupture. Associated
collateral ligament or meniscal injuries are common, especially with contact injuries.
Most players report hearing or feeling a “pop” at the time of injury, and hemarthrosis usually develops within minutes.
Physical examination findings also include a positive Lachman test with a soft endpoint. A positive pivot-shift test may
also be present, especially with chronic insufficiency.
Management of ACL injuries may be operative or nonoperative depending on many variables. Functional instability often
results in players who require the ability to accelerate, decelerate, and cut. However, some players are able to tolerate
an ACL-deficient knee. Injury to the collateral ligaments and menisci may also determine the need for surgery.
Nonoperative management includes aggressive rehabilitation with hamstring strengthening to limit anterior tibial
translation. A functional knee brace is used on return to play. One prospective study evaluated 43 athletes with isolated
ACL injuries who attempted return to play with rehabilitation and bracing. Seven of the nine football players were able to
return to play. Most athletes, however, experienced recurrent buckling of the knee and ultimately required reconstruction.
In 17 of 29 knees at surgery, meniscal tears were discovered, suggesting that there is a significant risk of sustaining
further damage to the knee with return to play ( 72). Operative treatment includes reconstruction using autograft or
allograft tissue. Return to play is usually possible in 6 to 9 months, although some athletes have returned earlier.
Posterior cruciate ligament (PCL) injuries are much less common than injuries to the MCL or ACL. The true incidence is
difficult to determine because isolated PCL injuries often go undiagnosed. The incidence has been reported to be from
8% to 23% of all knee ligament injuries ( 73,74,75 and 76). During the NFL's predraft physical examinations, a consistent
2% incidence of players with isolated PCL laxity is found ( 77).
Several mechanisms of injury exist. The most common is a direct blow to the anterior tibia with the knee flexed ( Fig.
24.15); however, hyperflexion, hyperextension, valgus, or varus stresses can also cause injury to the PCL (see Fig. 24.5).
Isolated injuries can occur, but there are often other associated injuries ( Fig. 24.16). Initial findings vary but may be less
severe than with ACL injuries. The posterior drawer test at 90 degrees is most sensitive, and posterolateral instability
should also be ruled out. Isolated injuries with minimal laxity are managed with rehabilitation including,
quadriceps-strengthening exercises to decrease posterior tibial translation. Avulsion fractures should be treated with
internal fixation or reconstruction. Combined injuries and those with functional instability are managed with surgical
reconstruction.
FIGURE 24.15. Potential mechanism of PCL injury includes direct contact with an anterior force applied to the proximal
tibia.
FIGURE 24.16. Posterior cruciate ligament tear in a college linebacker.
Knee ligament injuries are very common and can be career-threatening in football players. Delays in diagnosis,
inadequate treatment, and unrealistic expectations can increase time lost from play. With early accurate diagnosis and
carefully individualized treatment plans, however, most athletes can return to their sport.
Menisci
Injuries to the menisci are common among football players. Most injuries result from a twisting injury to the knee, and
often in association with a ligamentous injury. Catching, pain, swelling, and joint line tenderness are common findings.
McMurray's test may be positive. Symptomatic players usually require arthroscopic treatment to return to competition
quickly. Partial meniscectomy may allow early return to play, but at the possible increased risk of later arthritic changes.
Meniscal repair, however, requires prolonged absence from participation. These issues should be addressed on an
individual basis preoperatively.
Patellofemoral Joint
Dislocations of the patella are often the result of noncontact injuries. The mechanism usually involves external rotation,
quadriceps contraction, and extension of the knee. Several anatomic variations in lower-extremity anatomy may
predispose some people to an increased likelihood of patellar instability. These include femoral anteversion, genu
valgum, and patella alta. The initial examination findings may include a tense hemarthrosis and medial parapatellar
tenderness. Associated MCL and ACL injuries should be ruled out. Initial management includes rest, ice, compression,
and immobilization. Range-of-motion and quadriceps-strengthening exercises with particular attention to the vastus
medialis obliquus should follow. A knee sleeve or patella taping is often recommended on return to play. Some players
have continued disability and eventually need surgical treatment.
Patellar tendonitis is a common overuse injury involving inflammation of the tendon at the inferior pole of the patella.
Although more commonly associated with jumping sports such as basketball and volleyball, it occurs frequently in football
players as well. Typical complaints include anterior knee pain that is worsened with jumping or the use of stairs. Patella
alta may be a predisposing factor in some players. Tenderness at the inferior pole of the patella with the knee in
extension is the main physical finding. Nonoperative treatment is successful in most players and includes hamstring
stretching, quadriceps strengthening, bracing, oral antiinflammatory agents, and avoidance of repetitive jumping and
certain knee extension exercises. For those with persistent complaints, operative excision of degenerative tendon may be
necessary and is usually successful.
Fat pad syndrome (Hoffa disease) is another cause of anterior knee pain in football players. Repeated trauma to the
anterior knee may lead to fibrous changes in the patellar fat pad. Pinching of the fat pad between the femoral condyles
and tibial plateau may cause pain in extension. Players with genu recurvatum are more susceptible. Tenderness medial
and lateral to the patellar tendon is characteristic. Treatment with ice, activity modification, stretching and strengthening,
and padding is usually successful. Unresponsive cases may be treated with arthroscopic debridement of the thickened
fat pad.
FOOT AND ANKLE
Ankle injuries were the second most common injuries in two studies, at 18% and 13.7% ( 3,13). Most injuries are sprains
sustained when cutting and changing directions and involve supination of the foot, causing injury to the lateral ligament
complex. Another mechanism involves pronation with external rotation of the talus. This may occur when the athlete's
body is twisted away from the injured side or when another player falls on the posterior aspect of a downed player's leg
(Fig. 24.17). Differentiation between a lateral ankle sprain and a “high” ankle sprain or syndesmosis injury is important.
Syndesmosis sprains have been shown to require much longer rehabilitation time ( 77,78) (Fig. 24.18). In addition, if
radiographs suggest widening of the syndesmotic space, surgical treatment is indicated.
FIGURE 24.17. Calcification of syndesmosis after recurrent ankle sprain in a college running back.
FIGURE 24.18. Mechanism for external rotation injuries to the ankle. A: With the foot fixed to the ground, the athlete's
body is twisted away from the injured side. B: The player's foot is externally rotated when he receives a blow to the lower
leg. (From Boytim MJ, Fischer DA, Neumann L. Syndesmotic ankle sprains. Am J Sports Med 1991;19:294–298.)
Treatment includes protection, rest, ice, compression, and elevation. Limited immobilization is sometimes used for severe
sprains. Rehabilitation should include strengthening and proprioception exercises. On return to play, braces, taping, and
high-top shoes may be used for protection. Surgical reconstruction is reserved for those with symptomatic chronic lateral
instability.
Turf toe is a condition involving injury to the first metatarsophalangeal (MTP) joint complex. This injury has been
increasingly recognized since the 1970s. The use of lightweight, flexible shoes on hard artificial turf has been credited
with increasing the frequency of this injury. In one study, 83% of patients reported that their initial injury occurred on
artificial turf ( 79). The usual mechanism is forced dorsiflexion of the first MTP joint, which causes stretch of the plantar
structures and impaction of the proximal phalanx on the dorsal metatarsal. This often occurs when a player falls on the
posterior aspect of another player's leg ( Fig. 24.19). Pain during push-off, swelling, decreased motion, and tenderness at
the dorsal or plantar aspect of the joint are typical. Radiographs should be evaluated to rule out associated fractures,
including fractures of the sesamoids. Early treatment is with protection, rest, ice, compression, and elevation. Taping and
use of a stiff-soled shoe offer protection for return to play. These injuries may cause prolonged time lost from athletics.
Hallux rigidus and hallux valgus may be late sequelae of this injury. Clanton and Ford reported a 50% incidence of
persistent symptoms at 5-year follow-up of 20 athletes (80).
FIGURE 24.19. Mechanism of injury for turf toe. Forced dorsiflexion of the first metatarsophalangeal joint commonly
occurs when a player falls across the posterior aspect of another player's leg. (From Rodeo SA, O'Brien S, Warren RF, et
al. Turf toe: an analysis of metatarsophalangeal joint sprains in profession football players. Am J Sports Med
1990;18:280–285.
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25 Golf
25
GOLF
PETER J. CAREK
Equipment
Golf Swing
Setup
Backswing
Downswing
Follow-Through
Epidemiology of Golf Injuries
Back
Shoulder
Elbow
Wrist and Hand
Knee
Foot and Ankle
Head
Yips
Medical Issues
Conditioning
Chapter References
Golf probably began in Scotland in the 1400s, although there are some traces of golf being played as early as 1350. The
first golf course in the United States opened in 1888. Currently, golf has gained popularity both as a sport with millions of
participants and as a spectator sport involving further millions of individuals.
In many sports, the opponent directly affects the player in regard to performance and injury. Because there is no direct
contact with the opponent and a high level of cardiovascular fitness is not required, golf is classified as a noncontact,
low-intensity sport. The underlying etiology of golf-related injuries usually involves the swing, the equipment, or an object
other than the ball (e.g., a tree root) that is struck with the club.
EQUIPMENT
The golf club and ball are the basic equipment used in the game of golf. As defined by the United States Golf Association
(USGA), the club is “an implement designed to be used for striking the ball and generally comes in three forms: woods,
irons, and putters distinguished by shape and intended use (not by composition).” The form and make of the club, shaft,
clubhead, and clubface shall not be substantially different from usual tradition and custom and are specified in the rules
of golf (1). The golf ball is subject to rules governing its weight, size, spherical symmetry, initial velocity, and overall
distance standard.
In addition to being the predominant pieces of equipment in the sport, the golf club and ball are frequently implicated in
traumatic injuries. Although golf clubs are indirectly involved in most golf-related injuries, they are commonly directly
involved in significant trauma, especially in children who are struck as they inadvertently enter the swing zone ( 2). Being
hit by a club and being hit by a ball accounted for almost two thirds of golf-related injuries reported by 300 patients
presenting to several emergency departments over a 6½-year period ( 3). Along with the tee, the golf ball has been
reported to cause significant inadvertent injuries ( 4,5).
The golf shoe has evolved to serve as both a comfortable walking shoe and a stabilizing medium of contact between the
golfer and the golf course. Based on a study by Williams and Cavanaugh ( 6), who examined the ground-reaction forces
and center-of-pressure patterns created during the golf swing, the following design criteria for golf shoes was
recommended: modification of the outsole configuration, replacing the raised heel with a continuous heel wedge;
alteration of the placement and inclination of cleats; incorporation of a valgus wedge insert in each shoe; and use of
different designs for the right and left shoes, which they were shown to have totally different functions. Pförringer and
Rosemeyer (7) also suggested an asymmetric design with elimination of spikes and reconfiguration of the sole to support
the course of movements rather than impede them.
GOLF SWING
The fundamental objective of the golf swing is to hit the ball a specific distance and direction in a certain trajectory.
Fundamentally, the golf swing can be divided into four stages: setup (address), backswing, downswing, and
follow-through. The setup consists of assuming the proper grip and body position. The backswing begins as the club
moves away from the ball and torque develops in the hips, torso, and shoulders; it ends when the clubhead reaches the
top of the swing. Some authors identify the period when part of the body starts the downswing while the club is still in the
backswing as the “transition stage” ( 8). This “stage,” as described, may not occur in every golfer. Once the clubhead
begins its downward path and the stored torque is used to increase clubhead velocity, the downswing stage is occurring
and continues through impact as the clubhead strikes the golf ball. After impact, the follow-through stage begins. The
purpose of the follow-through is to decelerate the club and complete the swing without using excessive effort from the
muscles.
The golf swing has been extensively reviewed by authors attempting to improve performance, associate the phases of
the swing with specific injuries, or reduce the risk of injury ( Table 25.1) (8,9,10,11,12,13,14,15 and 16). Based on their
previous descriptions, the stages of the golf swing for a right-handed golfer are reviewed here.
TABLE 25.1. PHASE OF THE GOLF SWING AND ASSOCIATE MOVEMENTS AND RESULTING INJURY
Setup
There are three basic grip types: the Vardon, the interlocking, and the 10-finger ( 15). The Vardon grip, named after Harry
Vardon, is by far the most popular in golf today. The player overlaps the last finger of the right hand between the second
and third fingers of the left hand. The interlocking grip takes the last finger of the right hand and interlocks it with the
second finger of the left hand. The 10-finger grip is achieved by placing all ten fingers on the club. The hands are close
together, but there is no interlock or overlap of the last finger on the right hand. Although the grip alone rarely causes
injury, gripping the club too tightly and rapidly pronating the forearms in the downswing may lead to medial epicondylitis,
or “golfer's elbow” (17).
After assuming the proper grip and aligning perpendicular to the path of the ball, the golfer flexes the knees, hips, and
neck (Fig. 25.1). The wrists are radially and ulnarly deviated. The feet are shoulder-width apart and the weight is on the
balls of the feet. The buttocks may move slightly backward to maintain balance, placing more weight toward the heels.
FIGURE 25.1. The setup, with the golfer standing perpendicular to the path of the ball.
Backswing
After addressing the ball during the setup, the golfer is prepared to begin the “active” stages of the golf swing ( Fig. 25.2).
As the club starts the backswing, the right foot applies an anteriorly-directed shear force and the left foot applies a
posteriorly-directed shear force. The knees, hips, shoulders, and lumbar and cervical spine rotate. As the left hip rotates,
the left foot rolls inward to the right, placing a valgus stress on the left knee. At the height of the backswing, the wrists
deviate radially, the left thumb hyperabducts, the left wrist radially deviates, the right wrist dorsiflexes, and the left thumb
extends.
FIGURE 25.2. The backswing is the first active stage of the golf swing.
Downswing
This stage begins as weight is being shifted in the direction of the target ( Fig. 25.3). The purpose of the downswing is to
generate clubhead velocity. The forward weight shift initiates the unwinding of the torso with a transfer of energy through
the shoulders, into the arms and hands, and ultimately to the clubhead and the ball. A double pendulum model has been
proposed to explain the mechanics of clubhead speed generation ( 8,15). The upper pendulum is formed between the
shoulders and the wrists. The lower pendulum is formed from the wrists to the clubhead. As the golfer shifts more weight
onto the left foot, a counterclockwise torque is generated. As this torque is passed through the legs, thighs, and buttocks,
additional forces are added. The culmination of stored energy in the upper body and generated energy in the lower
extremities is unleashed to cause a counterclockwise acceleration of the upper pendulum. The lower pendulum is quiet
until the shaft of the club is roughly horizontal with the ground, approximately at midswing. Then the wrists, which had
been radially deviated, begin to release and allow the transfer of energy into the shaft of the club. These movements are
powered by the pectoralis major, subscapularis, and latissimus dorsi of both shoulders. The delay between the swinging
of the upper and lower pendulums allows the clubhead to achieve its greatest possible velocity ( 18).
FIGURE 25.3. The downswing generates clubhead velocity prior to impact.
Impact begins at the instant before contact, when the clubhead has attained its maximum velocity, and lasts until the
instant that the ball has completely left the club. The head of the club and the ball are in contact for approximately half a
millisecond (0.0005 seconds). At impact, the weight is shifted to the left side so that 80% to 95% of the weight has been
transferred. Valgus stress occurs on the right knee. Impact velocity requires well-formed latissimus dorsi and triceps
muscles along with equal “drive” from both sets of rotator cuff muscles. Driving power involves the buttocks, quadriceps,
hamstrings, and low back. Both wrists are under compression as the left elbow extensor mass contracts.
Follow-Through
The follow-through is the period that begins immediately after impact and lasts until completion of swing ( Fig. 25.4 and
Fig. 25.5). After impact, the left forearm supinates, the right forearm pronates, and the lumbar and cervical spines rotate
and hyperextend. Hip rotation is completed as weight is transferred to left side of body with rotation of the knees to the
left and inversion of the left ankle. The subscapularis, with coordinated reduced input from the latissimus dorsi and
pectoralis muscles of both arms, continues to be active, decelerating the swing. While the knees rotate, the right knee
flexes and the left knee everts. As the club decelerates, the golfer may hyperextend the back into a reverse “C” position.
FIGURE 25.4. The follow-through begins immediately after impact.

FIGURE 25.5. A: The reverse “C” (“modern” golf swing) follow-through position may cause lumbar strain. B: An upright
follow-through posture (“classic” golf swing) results from releasing the upper body, causing less lumbar strain.
A significant amount of lumbar strain may be caused by the reverse “C” position, which occurs as weight is being
transferred under a stationary head (often termed the “modern” golf swing) (see Fig. 25.5A). Some golfers release the
upper body during the follow-through, resulting in an upright posture (often termed the “classic” golf swing) (see Fig.
25.5B).
EPIDEMIOLOGY OF GOLF INJURIES
Compared with other popular sports, golf is not considered to be associated with a significant number or severity of
injuries. Several studies and reports have attempted to quantify golf-related injuries ( 10,11,14,19,20 and 21). These
studies are difficult to interpret and may not be applicable across the population of golfers because of several limitations:
self-reported information obtained retrospectively through nonstandardized surveys, low response rates, and unclear
demographic information regarding respondents, including lack of data on preexisting conditions. Nevertheless, these
studies provide initial information regarding golf-related injuries.
Most injuries in golf are associated with either repetitive swings and overuse or poor swing mechanics ( Table 25.2)
(10,11,20,21 and 22). Among professional golfers, a number of injuries are reported to occur secondary to contact with an
object other than the ball during a swing ( 10). Thøriault et al. ( 21) noted that overuse injuries were slightly more frequent
than injuries involving a single trauma.
TABLE 25.2. MAIN CAUSES OF GOLFRELATED INJURIES
With a few exceptions, the anatomic distribution of injures by body segment is fairly similar across studies of professional
and amateur golfers (Table 25.3). In both populations, the back is commonly injured. In the studies that examined gender
differences, the overall distribution of injuries by anatomic site demonstrated a similar pattern between men and women
(10,11,21). The only difference noted was an increased frequency of injuries to the upper limbs, compared with the spine,
in female golfers; male golfers were more likely to sustain an injury to the spine rather than the upper extremities. In a
study published in a popular golfing magazine, Jobe and Yocum ( 19) reported that the back was the most common site of
injury in 412 amateur golfers, followed by the shoulder, elbow, and knee.
TABLE 25.3. GOLF-RELATED INJURIES BY ANATOMIC SITE
Many of the previously mentioned studies failed to determine either preexisting conditions or risk factors that might
predispose a golfer to injury. In the study by Batt ( 20), a significant number of golfers had “incidental injuries,” defined as
other ailments compromising an individual's golf performance. These types of injuries were more commonly reported than
were injuries received while actually playing golf (42.4% versus 37.3%). Almost half of these reported incidental injuries
involved the back. Because low back pain has a lifetime prevalence of 60% to 80% in industrialized countries, golfers
presenting with low back pain may have an underlying etiology that is being exacerbated by the repetitive motion
involved in the golf swing ( 23,24). In a prospective study by Burdof et al. (25), no significant increase in back pain
incidence was found, and none of the subjects with back pain attributed their pain to playing golf. This finding implies that
golf may not be the dominant risk factor accounting for the onset of back pain. In a prospective, longitudinal study of
athletic injuries occurring to students in grades 7 to 12, no injuries were found among 128 golfers ( 26). In this study, an
injury was defined as any complaint by an athlete that required the attention of an athletic trainer. Therefore, many of the
injuries previously directly attributed to the golf swing may have had other primary causes.
Back
Large lateral-bending shear, compression, and torsional forces have been found to affect the lumbar spine during the
golf swing and may predispose the lower back to injury ( 27,28 and 29). The shear forces were greater in the amateur
population and also were associated with wider standard deviation, possibly owing to greater variations in the amateur
swing patterns. Professional golfers usually exhibit a classic weight shift from the right to the left side when changing
direction between the backswing and follow-through, which protects the back. In contrast, amateur golfers commonly
swing from the top, or reverse pivot, causing the upper torso actually to lean away from the ball at impact, increasing
stress on the back.
A myoelectric analysis revealed that the left external oblique, the left rectus abdominis, and the left L3 paraspinal
muscles initiate the takeaway, whereas the right-sided muscles lead from the top of the backswing through impact. Peak
muscle forces occur during this period. Anterior muscles continue to contract during the follow-through, while the
paraspinals are essentially inactive. The right-sided external oblique and rectus muscles of the abdomen develop a
higher peak activity than the left, while the activities of the paraspinals are almost symmetric. Watkins ( 30) demonstrated
that the trunk muscles are important in stabilizing and controlling the loading response for maximal power and accuracy
in the golfer's swing.
Hosea et al. (27) demonstrated that the magnitude of the forces on the lumbar spine during the golf swing is sufficient to
produce pathologic changes over time. Low back pain most likely develops secondary to the repetitive and increased
rotational and compression forces on the lumbar spine at the top of the backswing and the subsequent uncoiling and
hyperextension through the downswing and follow-through. Twisting has also been associated with the development of
low back pain (31,32). The compression load on the lower back generated during the golf swing is more than eight times
body weight and places considerable pressure on the posterior elements. These changes would most likely occur at the
intervertebral disk, the pars interarticularis, and/or the facet joints.
The history and physical examination provide valuable information in the initial care of the golfer who presents with low
back pain (Table 25.4) (24). As noted earlier, the loads placed on the lumbar spine during a golf swing and associated
lumbar muscle activity may predispose a golfer to muscle strains, herniated nucleus pulposus, spondylolysis, and facet
arthropathy with associated spinal stenosis ( 29,32,33 and 34). Major trauma, age older than 50 or younger than 20 years,
history of cancer, constitutional symptoms, risk of spinal infection, pain worsening when supine, recent bladder or bowel
dysfunction, saddle anesthesia, and severe or progressive neurologic deficit are critical “red flags” that require additional
study (35). Additionally, Lord et al. ( 36) noted 19 cases of stress fractures of the ribs in golfers and suggested that this
condition may be more common than previously realized and may be incorrectly diagnosed as recalcitrant back strain.
Others have noted lower rib stress fractures in golfers ( 37).
TABLE 25.4. COMPARISON OF COMMON CAUSES OF LOW BACK PAIN
Acute lumbosacral strain manifests as discomfort in the lower back that is first noted during or after activity. Patients with
acute lumbosacral strain typically complain of mild to moderate low back pain that is worsened with movement and
relieved by rest and lying still ( 38). Tenderness over the affected soft tissue area is noted on physical examination. No
significant abnormalities are noted on radiologic examination.
Herniated disks in the lumbosacral spine may also cause low back pain in golfers. Although low back pain is a common
complaint in the general population, sciatica is uncommon, affecting only 2% to 3% of all patients with low back pain ( 38).
Sciatica is present in 95% of patients who have a symptomatic herniated nucleus pulposus. If sciatica is absent, a
clinically significant herniation is almost excluded ( 39,40). Patients with herniated nucleus pulposus present with low back
pain radiating down the leg and associated paresthesias or motor deficits. The sciatic pain usually radiates below the
knee into the foot, because 95% of lumbar disk herniations involve the L4-5 or L5-S1 intervertebral disk space. On
physical examination, signs of nerve root impingement are found.
Facet arthropathy or facet syndrome refers to back pain originating from the facet joints ( 41). Extension, especially when
coupled with lateral flexion or rotation to the painful side, reproduces or increases the back pain.
Spinal stenosis refers to any narrowing of the spinal canal or neural foramen; it is usually associated with osteoarthritic
changes of the lumbosacral spine and may involve the facet joints ( 42). Presentations suggestive of spinal stenosis
include radicular symptoms and neurogenic claudication. Lumbar extension usually exacerbates the pain. Degenerative
changes and neural foraminal stenosis can be noted on plain radiographs.
Spondylosis (disruption of the neural arch without forward displacement) and spondylolisthesis (anterior displacement of
one vertebral body on another) are defects in the pars interarticularis and usually represent a stress reaction secondary
to repetitive loading of the lumbar spine ( 29,42). Patients may present with low back pain secondary to degenerative
changes and increased stress on the ligamentous structures. Pain is usually exacerbated by hyperextension. Lateral and
oblique plain radiographs usually are able to demonstrate these lesions. Treatment is conservative if symptoms are
minimal and no neural impingement is detected.
In addition to lumbosacral strains and disk herniations, the golfer may present with back pain caused by an underlying
etiology that is exacerbated by the golf swing. Rheumatic disease, infections, tumors, endocrine disorders, and referred
pain may present as back pain worsened during the golf swing ( 43).
There is rarely a need for additional diagnostic studies in golfers with low back pain, because 90% of patients recover
from limitations within the first 4 weeks after symptom onset. Further diagnostic studies are dictated by the presence or
absence of “red flags.” Initial treatment includes “active” rest (activity to pain tolerance), flexibility and strengthening
exercises, use of acetaminophen or nonsteroidal antiinflammatory drugs (NSAIDs), and therapeutic modalities (i.e., heat
or ice) with or without physical therapy. Although several of these treatments may help some patients, the literature
supports the use of all forms of exercise (e.g., McKenzie extension exercises, Williams flexion exercises) as beneficial in
the treatment of back pain (44,45 and 46). The main goal for acute care is to maintain or retain activity tolerance ( 35).
Bed rest has not been shown to be an effective treatment option ( 44). Finally, the swing should be reviewed and
recommendations for decreasing the amount of stressful movements on the lumbosacral spine (i.e., hyperextension
movements) should be made.
Shoulder
Because golf is not considered an overhead sport, the incidence of acute shoulder injuries is relatively low. The shoulder
appears to be at greatest risk for injury during extremes of motion. The nondominant or lead arm is usually involved. The
phase of the golf swing and the specific complaint of the golfer can often provide information regarding the underlying
cause of the problem (Table 25.5) (47). Predisposing factors for shoulder injuries from the repetitive stress of the golf
swing include constitutional factors, insidious trauma, acute trauma, postinflammatory changes, postinfection sequelae,
tumors, congenital defects, and other factors such as impingement syndrome, labral tears, rotator cuff tears, previous
shoulder surgery, symptomatic previously placed staples and screws, and reflex sympathetic dystrophy ( 48).
TABLE 25.5. CAUSES OF SHOULDER DISCOMFORT IN GOLFERS BY SWING PHASE AND ANATOMIC AREA
The contributions of the shoulder muscles to the golf swing have been extensively studied. The subscapularis appears to
be the most active muscle throughout the swing ( 49). The rotator cuff muscles on both sides show equal amounts of
activity, indicating that the left shoulder of right-handed golfers does not provide more “drive” than the right shoulder.
Pink et al. (50) demonstrated that certain muscles of the shoulder act during specific stages of the swing: the
infraspinatus and supraspinatus predominate at the extremes of shoulder range of motion, the subscapularis and
pectoralis major during the downswing, the latissimus dorsi during the forward swing, and the anterior deltoid during
forward swing and follow-through. Finally, Kao et al. ( 51) found that the muscles associated with scapular movement and
stabilization (i.e., levator scapula, rhomboids, serratus anterior, and trapezius) are active during and contribute
significantly to the biomechanics of the golf swing.
Impingement syndrome, with associated rotator cuff tendinitis or rotator cuff tears, is common in golfers who present with
shoulder pain. Impingement syndrome refers to the irritation of the rotator cuff tendons secondary to abnormal contact
against the undersurface of the acromion ( 52). These injuries result from acute rotator cuff overload, intrinsic rotator cuff
degeneration, or chronic overuse, which is a significant cause of impingement. Often, subtle instability leads to recurrent
subluxation, rotator cuff abnormalities, and subsequent impingement ( 53). However, athletes may also present with pure
and isolated impingement without any instability. Repetitive overuse of the shoulder yields definitive rotator cuff
pathology (48). The examination of the shoulder should include tests for rotator cuff weakness and glenohumeral
instability as well as provocative testing for impingement.
The golf swing places an increased load on the acromioclavicular (AC) joint ( 47). Each golf swing places the arm in an
adducted position and may result in spur formation under the AC joint, impingement of the rotator cuff on spurs, or
bursal-side partial cuff tears. Degenerative joint disease occurs, leading to decreased range of motion and additional
shoulder problems. Localized tenderness over the AC joint and exacerbation of the discomfort with cross-body adduction
are often noted (54).
Once a diagnosis has been established to explain the shoulder discomfort, treatment that emphasizes rehabilitation
should be instituted. After the a period of acute treatment with restricted rest, ice, and elimination of the traumatic
process, range-of-motion and strengthening exercises are prescribed. The strengthening exercises should concentrate
on both the rotator cuff muscles as well as the muscles responsible for scapula stabilization (i.e., serratus anterior and
rhomboids). If this therapy is not effective, local corticosteroid injection or surgical consultation may be required.
Acute shoulder injuries in the golfer are uncommon. An avulsion injury to the conjoined tendons of the latissimus dorsi
and teres major muscles has been described in a golfer after a period of markedly increased participation ( 55).
Elbow
The predominant elbow injury in the golfer is medial epicondylitis (golfer's elbow). This injury may result from the golfer's
“hitting fat” (repetitiously striking the ground before the ball), which causes abnormal forces to be transferred to the lead
or nondominant elbow. Tenderness to direct palpation and elicitation of pain with resistant palmar flexion of the wrist are
noted on examination.
Lateral epicondylitis occurs more frequently in the trailing or dominant arm of golfers ( 21,22). This condition develops as
a result of sudden or repeated concentric muscular activity of the extensor carpi radialis longus and brevis. Localized
tenderness to the lateral epicondyle and exacerbation of the discomfort with grasping of the hand or extension of the
middle finger are findings on physical examination that are consistent with lateral epicondylitis.
Conservative treatment for both medial and lateral epicondylitis includes restricted activity, stretching and strengthening
exercises, and NSAIDs. Rarely, splinting is needed. Exercises should focus on increased forearm muscle strength,
flexibility, and endurance ( 56). In addition, altering swing technique, changing equipment, and using an elbow support
may assist in decreasing the force transmitted to the elbow. If this therapy is not effective, local corticosteroid injection or
surgical decompression may be required.
Wrist and Hand
Injuries to the wrists and hands are commonly seen in golfers and may be attributed to the mechanical stress and
range-of-motion extremes these structures undergo during the golf swing ( 57,58 and 59). During the backswing, the
right-handed golfer hyperabducts the left thumb and radially deviates the left hand ( 59). At the top of the backswing and
during the initiation of the downswing, the right wrist dorsiflexes. At impact, the left wrist moves from a position of radial
deviation through neutral to slight ulnar deviation, while the right wrist moves from a dorsiflexed, radially deviated
position to a more neutral position with slight ulnar deviation. Significant force is transferred from the clubhead to the
hands and wrists at impact. During the follow-through, the motion of the wrists subsides as the left forearm supinates and
the right forearm pronates, creating the “rollover” action of the hands, with the right wrist regaining the extended position.
DeQuervain disease is a tenosynovitis of the abductor pollicis longus and extensor pollicis brevis tendons as they pass
through the first dorsal compartment of the wrist. This overuse injury is caused by a tight grip of the club and the ulnar
and radial deviations associated with the swing ( 60). A positive Finkelstein test, which consists of pain over the common
sheath of the first dorsal compartment with the wrist ulnar deviated, assists with the diagnosis. Conservative treatment
includes modified activity, splinting, stretching and strengthening exercises, and use of NSAIDs. If this therapy is not
effective, local corticosteroid injection or surgical decompression may be required.
The golf swing is associated with other forms of tendinitis of the wrist ( 61). Extensor carpi ulnaris tendinitis is
characterized by tenderness directly over the extensor carpi ulnaris tendon and the sixth dorsal compartment of the wrist.
Symptoms are exacerbated by forced ulnar deviation and flexion of the wrist. Tendinitis of the flexor carpi radialis tendon
causes pain and tenderness over the volar aspect of the wrist. The pain is often reproduced by resisted pronation of the
wrist. Flexor carpi ulnaris tendinitis commonly manifests as painful wrist motion and tenderness along the flexor carpi
ulnaris tendon sheath. Stenosing tenosynovitis of the digital flexors occurs as the result of thickening of the proximal
portion of the flexor tendon sheath with associated synovitis. Symptoms include pain, locking, and triggering of the
involved digit.
Intersection syndrome is a localized inflammation of the peritendinous or bursal tissue at the intersection of the abductor
pollicis longus, the extensor pollicis brevis, and the radial wrist extensors just proximal to the wrist's dorsal retinaculum
(62). Significant soft tissue swelling with marked crepitus 6 to 8 cm proximal to Lister's tubercle may be found.
These overuse-type injuries are treated similarly to DeQuervain disease. Conservative treatment includes rest, splinting,
stretching and strengthening exercises, and NSAIDs. If this therapy is not effective, local corticosteroid injection or
surgical decompression may be required.
Flexor tenosynovitis and carpal tunnel syndrome result from repetitive grasping and wrist motions. Repetitive digital
flexion in an individual unaccustomed to such activity can induce significant tenosynovitis of the digital flexors ( 61). Pain
may be aggravated by finger motion. Median nerve compression with associated findings of median nerve irritability (i.e.,
Tinel sign or Phalen maneuver) may occur. Conservative treatment includes rest, splinting that immobilizes the wrist and
metacarpophalangeal joints, and NSAIDs ( 61). If median nerve symptoms persist or predominate, a corticosteroid
injection into the carpal tunnel may be effective. At least 6 weeks of conservative therapy should be attempted before
proceeding with carpal tunnel release and flexor tenosynovectomy.
A fracture of the hook of the hamate bone may result from the clubhead's striking against a stationary object during a full
swing (63,64,65,66,67,68 and 69). The stress of the impact is transmitted up the shaft to the hand, causing the fracture in
the upper hand. The nondominant wrist is typically affected ( 67). On physical examination, tenderness over the hamate
near the proximal portion of the hypothenar eminence (the hook of the hamate is 1.5 cm distal and lateral to the pisiform),
painful abduction of the small finger against resistance, decreased grip strength, and ulnar nerve symptoms may be
noted (62). A carpal tunnel view and computed tomography scans are helpful in the diagnosis of this injury. Despite early
diagnosis and prompt treatment with immobilization, fractures of the hook of the hamate often progress to nonunion.
Treatment of symptomatic nonunions consists of excision of the fragment.
Other wrist and hand fractures in golfers are rare. A stress fracture of the ulnar diaphysis thought to be the result of
supination together with overuse of the hand flexor muscles was reported in a golfer ( 70).
Excessive ulnar deviation during the golf swing causes compression to the triangular fibrocartilage complex (TFCC) ( 71).
Wrist pain has been attributed to tears and thickening of the TFCC ( 72). Because this structure functions as a major
stabilizer of the distal radioulnar joint and the ulnar carpal joint and acts as a shock absorber in the transfer of axial
loads, the TFCC is exposed to stresses that may cause injury. Discomfort with ulnar variance is associated with TFCC
perforation ( 73). Persistent wrist discomfort from a TFCC injury requires further evaluation and possible surgical
intervention.
Hypothenar hammer syndrome results from single or repeated episodes of blunt trauma to the palm of the hand causing
damage to the ulnar artery and associated discomfort ( 74). Although this is considered an occupational injury, the
syndrome has been reported in golfers ( 76).
Knee
The knee is an uncommon site for golf-related injuries. The relative incidence of knee injuries in golfers is about 9%. The
most stressful phase of the golf swing, for the knee, is the downswing ( 77). Although meniscal tears and patellofemoral
problems are commonly believed to be acute knee conditions associated with golf, golfing also may exacerbate
underlying knee conditions ( 78,79). In a study of 35 golfers with knee pain ( 79), a torn meniscus was found to be the most
common cause (17 cases); the other causes were osteoarthritis (10 cases), lateral meniscus tear (4 cases),
chondromalacia of the patella (2 cases), and loose bodies (2 cases). Because of the low-impact nature of golf, most knee
injuries should initially be treated conservatively, with restricted activity, NSAIDs, and a program of flexibility and
strengthening exercises.
Foot and Ankle
The principal movement in golf occurs during the swing; it is a lateral move in the frontal plane and involves a rotational
motion that takes place along a longitudinal axis ( 6,80). The right foot of the golfer performs a rocking movement during
the swing, and at the end of the swing the player rests first on the anteromedial edge of the big toe, and finally on the tip
of the toe. A weight shift occurs from the medial to the lateral edge of the left foot, and there is a supination of the left foot
and ankle. This movement may terminate in a buckling of the foot, with the foot resting on the lateral edge.
Excessive rolling of the ankle during the follow-through stage of the golf swing may result in ligamentous injury ( 80). The
lateral ligamentous complex (anterior talofibular, calcaneofibular, and posterior talofibular ligaments) of the left ankle are
at risk for this type of injury. Acutely, treatment is aimed at controlling swelling and pain while protecting the joint from
further injury. After initial treatment, management centers on restoration of the range of motion, strength, flexibility, and
proprioception.
Because golfers may be expected to walk several miles while completing a round of golf, they are at risk for the common
problems associated with weight-bearing activity. Blisters, contact dermatitis, tinea pedis, Morton neuroma, hallux rigidus,
hallux valgus, plantar fasciitis, Haglund deformity, and Achilles tendinitis may be found in golfers who complain of foot or
ankle pain or discomfort ( 80,81).
Head
Numerous reports have been published implicating golf clubs as the cause of significant head injuries, especially to
children and often including ocular trauma ( 2,4,82,83,84,85 and 86). Golf has been shown to be one of the sports most
commonly associated with head injuries that require referral to a regional neurosurgical center ( 87). Lindsay et al. ( 88)
demonstrated that children are predominantly involved in head injuries that require referral to a regional neurosurgical
center. McGuffie et al. ( 89) found that 22 of 23 children presenting to an emergency room for head injuries over a
3-month period were injured while observing another person playing golf (only 3 were injured while playing golf on a golf
course). The most common injury was scalp or facial laceration. A compound depressed skull fracture and an acute
extradural hematoma were reported.
Yips
The “yips” are a convulsive-like twitch that occurs during putting ( 90,91,92,93 and 94). This malady, which is golf specific
and affects an estimated 12% of golfers, is an involuntary movement that occurs during the execution of focused, finely
controlled, skilled motor behavior. The movements emerge particularly during putting and are less evident during
chipping or driving. The affected golfer is often unable to complete the putting stroke successfully, regardless of the
length or ease of putt. Symptoms worsen with the intensification of anxiety, and increasing percentages of affected
golfers report worsening of symptoms with practice (46%), periods of increased stress (77%), or tournament play (99%)
(93). Older golfers, golfers who have played for a long time, and golfers with obsessional thinking patterns are commonly
affected. In a study by Sachdev (94), the contention that the “yips” is not an anxiety disorder or a neurosis was
supported, although the role of anxiety and arousal in its manifestation was recognized. To date, no beneficial treatment
has been reported. Possible treatments include hypnosis and use of a different putter, grip, or style. Specifically,
recommended compensatory strategies include putting cross-handed, using a longer putter, putting “sidesaddle,”
changing the head position, and altering visual fixation ( 93). No beneficial effects have been reported with anxiolytic drug
therapy.
Medical Issues
Golf is associated with several other types of injury and medical conditions ( Table 25.6) (95,96,97,98 and 99). The
greatest risks to golfers result from exposure to lightning, heat, and sunlight ( 95). Lightning can cause cardiac arrest with
asystole. High air temperature combined with high relative humidity creates the conditions necessary to induce
heat-related illnesses, including heat cramps, heat exhaustion, or heat stroke. Exposed areas of skin are predisposed to
sunburn and ultimately to accelerated changes and malignant processes.
TABLE 25.6. MEDICAL RISKS AND CONDITIONS AFFECTING GOLFERS AND GOLF COURSE EMPLOYEES
CONDITIONING
To date, the benefit of a conditioning program to reduce the risk of injury and improve the performance of individual
golfers has not been studied. Specific preventive techniques have been recommended ( Table 25.7) (15). Additionally,
golfers should be reminded to participate in a regular program of physical fitness to potentially reduce the risk of injury
and to improve their overall health.
TABLE 25.7. PREVENTIVE TECHNIQUES SUGGESTED TO REDUCE RISK OF INJURY
Golfers should participate in some form of moderate physical activity daily. Continuous heart rate monitoring of a group of
golfers demonstrated an average rate of 108 beats per minute, or activity at 35% to 41% of maximal oxygen consumption
(100). A program of moderate physical activity could decrease the risk of injury and improve performance as well as offer
protection from the mortality and morbidity associated with cardiovascular disease.
To complete the conditioning program, golfers should be encouraged to regularly perform flexibility and strengthening
exercises (101,102). Stretching exercises should incorporate the lumbosacral spine, shoulders, elbows, and wrists. The
rotator cuff muscles, the scapular stabilizing muscles (i.e., serratus anterior and rhomboids), wrist extensors and flexors,
lumbosacral extensors and flexors, and the muscles of the lower extremities should be the focus of a strengthening
program. Based on the limited absolute strength demands of golf, the golfer should be instructed to use a program
emphasizing an increased number of repetitions with lighter weights.
Before a practice session or round of golf, the player should use a warmup routine. This routine should incorporate
stretching of the lumbosacral spine, shoulders, elbows, wrists, and lower extremities. In addition, the golfer should begin
with low-intensity swings of one or two clubs, increasing intensity during the warmup period.
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26 Gymnastics
26
GYMNASTICS
PATRICK E. GREIS
JEFFERY R. WEISS
ROBERT T. BURKS
Events and Equipment

Women's Apparatus
Men's Apparatus
Potential Sources of Injury
Epidemiologic Studies
Injury Recognition and Treatment
Upper-Extremity Injuries
Wrist Injuries
Elbow Injuries
Shoulder Injuries
Knee Injuries
Low Back Injuries
Ankle Injuries
Foot Injuries
Chapter References
Gymnastics as a sport has experienced a variable level of popularity over the last several decades. Although its roots in
the United States can be traced back to the mid-1800s, its popularity was increased by its exposure during the Olympic
Games in 1972 (1,2). Since that time, the number of private establishments has increased to allow participation by a
large number of young children and adolescents. These young competitors may remain active as they mature, but few
find their way to the elite ranks of the Olympics. However, continued participation at the high school and collegiate level
account for a significant group of athletes competing at the upper levels of the sport.
Statistics on participation by both men and women at the high school and collegiate level are available from several
sources (2,3 and 4). The National Federation of High School Associations has tracked participation by both boys and
girls since at least 1970 (3). From their data, the number of boys participating at the high school level peaked in 1972, at
40,530 participants in 1,861 schools. This number has continuously declined, and 2,618 boys from 204 schools were
participating during the 1996–1997 season. Girls' participation at the high school level peaked at 84,943 during the
1978–1979 season but declined to 21,725 during the 1996–1997 season. These numbers can be compared with the
numbers of girls and boys participating in other sports in 1996–1997, such as basketball with 544,025 boys and 447,687
girls, football with 957,057 boys, or soccer with 296,587 boys and 226,636 girls. Although gymnastics remains a popular
sport at the high school level, the number of the athletes participating is clearly less than in some of the more popular
sports today.
At the collegiate level, the number of both men's and women's teams has declined over the last 15 years ( 3). Sixty-seven
(22%) of 308 Division I colleges fielded a women's gymnastics team in 1997, compared with 99 (36%) of 277 schools in
1982. Men's teams have likewise declined, with 21% of Division I teams fielding gymnastics teams in 1982 and only 8%
(25/308) sponsoring a team by 1997. With this decline in teams, the number of athletes competing has likewise declined
at the Division I level ( Fig. 26.1). During the 1981–1982 season, 1,052 men competed, compared with 379 during the
1996–1997 season. For women, 1,059 gymnasts competed during the 1981–1982 season, compared with 985 in
1996–1997. Although fewer teams were fielded in women's gymnastics during the 1996–1997 season, team size has
increased over the years and therefore the numbers for women have not declined as markedly as for men.
FIGURE 26.1. The number of men and women participating at the Division I collegiate level has decreased since the
early 1980s.
Despite the declines in numbers of athletes participating, many schools have maintained very active and competitive
teams with athletes competing at the very highest level. Because of the drive of these athletes to compete nationally, and
because of the prestige in winning National Collegiate Athletic Association (NCAA) events, training schedules at the
collegiate level are often as demanding as for athletes competing at the elite Olympic level. With the emphasis on
performing gymnastic maneuvers to perfection and on performing increasingly difficult gymnastics maneuvers, injuries in
this sport are common and occur with frequencies that may surpass those of other sports.
EVENTS AND EQUIPMENT
The disciplines in men's and women's gymnastics are separate ( 4). Although there is some overlap in equipment usage,
the manner and style in which the apparati are used are also different.
Women's Apparatus
The four disciplines of women's gymnastics include the vault, uneven bars, balance beam, and floor exercise. Each event
is judged and scored based on standard scoring criteria. Each event has specific expectations and requirements that
must be performed to score well. The events are performed sequentially, and the scores for each event are tallied to
obtain an overall winner as well as individual event winners.
Vault
The vaulting horse in women's gymnastics is 120 cm tall, 35 cm wide, and 160 cm long. It is positioned with its long axis
perpendicular to the runway. The runway is 1 m wide and a maximum of 25 m long. Vaults are scored on the Code of
Points text, which gives the relevant value of each skill performed. Height, distance traveled, number of twists, and the
landing all play a role in scoring.
Uneven Bars
The uneven bars consist of a low and high bar. The low bar can be adjusted to 140 ± 3 cm, while the high bar must be at
228 ± 3 cm. The bars can be a maximum of 150 cm apart from each other. The gymnast moves in a routine between the
low and high bar, with releases and regrasps, saltos, circle swings, and flight elements. Each routine should flow without
pause and must have two release elements before the landing.
Balance Beam
The balance beam routine must last between 70 and 90 seconds and must cover the entire length of the beam. The
balance beam stands 120 cm high and is 10 cm wide and 500 cm long. Scoring for this event is based on requirements
that must be performed on the balance beam, including an acrobatic series and a gymnastics series. These maneuvers
should be performed as though the gymnast were performing on a floor instead of a strip of wood 10 cm wide.
Floor Exercise
The floor exercise in women's gymnastics is choreographed to music and lasts from 70 to 90 seconds. The entire floor
area should be covered during the routine. The elements of the floor exercise include two acrobatic series, one with at
least two or more saltos in different directions. The exercise area for the floor exercise is 40 feet by 40 feet.
Men's Apparatus
The men compete in six disciplines: the pommel horse, still rings, vault, parallel bars, high bar, and floor exercise.
Floor Exercise
Like the women, the men compete in the floor exercise. Again, the area of the floor exercise mat is 40 feet by 40 feet.
The performance during the men's floor exercises lasts between 50 and 70 seconds and is not set to music. Much of the
scoring is based on acrobatic tumbling maneuvers.
Pommel Horse
The pommel horse is 115 cm tall, with the horse itself being 35 cm wide and 160 cm long. The two pommel handles stand
between 40 cm and 45 cm apart. The gymnast covers all three areas of the horse, allowing only his hands to touch the
apparatus.
Still Rings
The ring towers on which the rings are supported are 575 cm tall. The cable and straps to which the rings are attached
are 300 cm long and 50 cm apart. The still rings routine includes at least two handstands and one element of strength
held for 2 seconds. Deductions are taken for unnecessary swings or instability during any maneuver.
Vault
Once again, individual vaults are categorized in the Code of Points, the official text that gives the value for each skill
performed. The men's vault is 135 cm tall, 35 cm wide, and 160 cm long. The long axis of the vaulting horse is in line with
the runway, which is 1 m wide and a maximum of 25 m long. Height, distance, acceleration through the vault, and a
landing with no additional steps are all important in scoring for this event.
Parallel Bars
The parallel bars are 195 cm high. Each bar is 350 cm long, and the two bars can be adjusted to be placed between 42
and 52 cm apart. The routine on the parallel bars consists primarily of swing and flight elements. More difficult skills
require that the gymnast lose sight of the bar for a moment, such as during double front or back saltos.
Horizontal Bar (High Bar)
The high bar is 275 cm tall, with the horizontal bar being 240 cm long and 2.8 cm in diameter. The routines consist
exclusively of swinging movements with releases and regrasps of the bar. Dismounts often include multiple somersaults
and twists before landing.
Potential Sources of Injury
All of the events in both women's and men's gymnastics are tests of both skill and precision with regard to executing
maneuvers and landings. The high impact that occurs during many of the release and landing portions of these events,
as well as the pounding that both the upper and lower body endure, can be a source of acute or overuse injury. Because
perfection on each of the events is the goal, overuse injuries are not uncommon as the athlete attempts to perfect a
series of maneuvers. In addition, because of the desire to perform maneuvers of increasing complexity, training for and
learning such maneuvers can be a cause of injury. In an effort to minimize risks during training sessions, the apparatus
may be positioned closer to the floor or placed between elevated pads, as seen in Figure 26.2A and Figure 26.2B. Loose
foam padding placed in the landing area, as seen in Figure 26.2C, helps limit potential injuries during landing of difficult
maneuvers.
FIGURE 26.2. The balance beam can be placed close to floor level (A) or between pads (B) to limit the potential for
injury. C: Loose foam landing pits provide a safe landing area as new maneuvers are learned.
EPIDEMIOLOGIC STUDIES
A significant amount of epidemiologic data concerning gymnastics injuries were generated during the 1980s and 1990s
(5,6,7,8,9,10,11 and 12). Much of this literature deals with female collegiate and club athletes. Although design flaws,
reporting inaccuracies, and the inherent difficulties in defining injury are common to many of these studies, they do
provide useful insight into injury patterns.
In 1987, McAuley et al. reviewed the literature available at the time on the topic of injury in women's gymnastics ( 10).
They concluded, among other points, that injury rates increased as the skill levels increased, that the floor exercise
produced the most injuries, and that the lower extremity was the most frequently involved site of injury.
In 1989, Caine presented data on 50 high-level competitive young gymnasts ( 11). Injury rates per 1,000 hours of
exposure were reported; an injury was defined as any gymnastics-related event that resulted in the gymnast's missing
any portion of a workout or a competition. During 40,127 hours of training, an overall injury rate of 3.66 injuries per 1,000
hours was recorded. Forty-three of the 50 gymnasts sustained an injury, and the first several months of training resulted
in a higher injury rate than later periods in the year. Lower-extremity injury accounted for 63% of the cases; 20% of the
injuries occurred in the upper extremities, and 15% in the spine and trunk. Nonspecific pain (40%) was the most common
injury, with sprains and strains accounting for 37% of the injuries. However, it should be noted that five fractures and one
dislocation were recorded, and that serious injury is certainly a problem in this group of athletes. Floor exercises
accounted for 35% of the injuries, balance beam 23%, uneven bars 20%, and vaulting 14% ( Fig. 26.3).
FIGURE 26.3. Injuries by event in women's gymnastics.
In this study, injury severity was classified according to time lost in days. Using this classification, 23% of injuries resulted
in 2 days or less of practice loss, and 41% of injuries caused 1 week or less time lost. Approximately 25% of injuries,
however, resulted in more than 3 weeks of time lost, representing significant injury. Finally, this study found that 58% of
new injuries were of the sudden-onset variety, and 42% had a gradual onset. In contrast, only 17% of reinjuries had a
sudden onset. This emphasizes the fact that many gradual overuse injuries can be chronic or recurrent in nature. In many
ways, this study reflects the findings of much of the other literature available. Although variations do occur among the
published reports, trends in Caine's study ( 11) seem to recur.
Additional findings on the epidemiology of injuries in women's gymnastics have been reported from the University of
Utah. Sands et al. (12) described a 5-year study of the University's Division I Collegiate Women's Gymnasts Team. The
definition of injury in this study was “any damaged body part that would interfere with training.” The reason for this
definition was that injured body parts may not completely prevent a high-level gymnast from training; instead, they may
interfere with parts of training only. For example, a sprained ankle may prevent training in landing maneuvers or the floor
exercise, but it would not preclude work on the uneven parallel bars. The number of injuries per training exposure was
reported; a training exposure consisted of a practice or a meet. This study demonstrated that gymnasts at the Division I
collegiate level trained with an injury approximately 71% of the time, and that a new injury could be expected
approximately 9% of the time. Injuries were often graded as unknown or repetitive stress syndrome type injuries, and
these accounted for 38% of total injuries and 31% of new injuries reported. The low back was the most commonly
recorded site of new injury (approximately 15%). The shin and ankle represented the second most commonly affected
areas. The authors of this study also noted that injury occurrence increased during times when training and performance
of full routines occurred. This led them to suggest that additional precautions should be taken during these periods and
that equipment changes such as additional padding around apparatus should be considered.
The NCAA Injury Surveillance Survey for the 1997–1998 women's gymnastic season ( 13) reported injuries per athletic
exposure, with an athletic exposure being equal to one game or practice. Practice injury rates were 7.2 per 1,000 athletic
exposures in 1997, compared with a 13-year average of 7.9 injuries per 1,000 athletic exposures. Competition resulted in
12.1 injuries per 1,000 athletic exposures. Injuries in practices accounted for 87% of all injuries. Sprains (33%), strains
(23%), and contusions (11%) were the three most commonly reported injuries. Fractures (acute and stress) accounted for
8% of injuries. The ankle (21%), knee (15%), and lower back (8%) were the three most common body sites. Head and
neck trauma accounted for 7% of injuries.
The event during which a competitor was most likely to have an injury was the floor exercise, followed by the uneven
bars, balance beam, and vault. Most injuries occurred when the athlete was performing a maneuver unassisted without
the help of a spotter, and the most common time an injury occurred was during the landing portion of an event.
INJURY RECOGNITION AND TREATMENT
Given the precision, timing, and skill required to perform many gymnastic maneuvers, repetitive training is often
necessary to master the various skills. Unlike many other sports, these maneuvers are often practiced in real time. With
this comes repetitive stress and chance for injury. Although training during the season does have variations in intensity,
the desire to perform new skills is often constantly pushing gymnasts to the limits of their ability. This can result in
overuse injury while perfecting maneuvers and routines, and it can result in acute injury when mistakes are made while
learning the routines. Again in contrast to many other sports, both the upper and lower extremities are exposed to high
stresses and pounding, and gymnasts are subject to both acute and overuse injuries of these areas.
UPPER-EXTREMITY INJURIES
All parts of the upper extremity, from the skin on the hands to the muscles of the shoulder, are exposed to high stresses
during gymnastics (14,15). Damage to the skin of the hands and wrists, although bothersome, is rarely serious. This,
however, is not an uncommon problem, and it can impede the athlete's ability to practice or compete. Blistering and
tearing of the palm and wrist may occur at any time, but is often an early-season phenomenon. Keeping wounds clean,
applying chalk, using grip locks on the bars ( Fig. 26.4), and taping can often minimize or prevent lost time. Over the
course of a season many gymnasts develop protective thickening of the skin, with calluses that allow for continuous
training.
FIGURE 26.4. The use of grip locks can improve holding power and minimize skin damage on bar routines.
Wrist Injuries
In the 1996–1997 Injury Surveillance Survey of the NCAA, 3% of injuries were of the wrist ( 13). However, wrist pain in
gymnasts has been reported to occur in 46% of high-level club athletes and 79% of collegiate athletes ( 11,15). This is
probably secondary to the weight-bearing nature of the wrist: forces exceeding two times body weight cross this joint
during many maneuvers. These high loads can lead to many problems. Recognition that these stresses in the immature
athlete may damage the distal radius physis has led several investigators to examine this problem. In 1985, Roy reported
on 21 young gymnasts, average age 12 years, who presented with wrist pain mainly on the dorsal aspect ( 16). He
described radiographic changes in 11, which included widening of the growth plate of the distal radius epiphysis, cystic
changes, an increased irregularity of the metaphyseal region, and a beaked appearance of the distal aspect of the
epiphysis. When these radiographic findings were seen, the prognosis for a speedy recovery was poor; 5 of the 11
gymnasts took at least 6 months to become asymptomatic. When no radiographic changes were seen, 7 of 10 wrists
were symptom free within 2 to 4 weeks. Treatment in this group consisted of prompt abstinence of weight bearing on the
affected wrist as soon as possible after the onset of symptoms. The author recommended educating coaches about the
entity so that young athletes are treated early on. After a period of rest, during which the gymnast may do
non–upper-extremity maneuvers, the wrist is taped to prevent maximum or excessive dorsiflexion. Regular vaulting is
withheld for 3 to 4 weeks after recovery to allow for gradual stressing of the injured joint. With prompt recognition, stress
injury to the distal radius epiphysis should lead to minimal downtime.
The long-term consequences of increased stress on the immature wrist have been described. Several authors have
examined the relationship between the repetitive stresses placed on the distal radius and positive ulnar variance ( 17,18
and 19). In 1994, De Smet et al. noted a marked increase in ulnar length in both adult and immature elite female
gymnasts (17). They concluded, as have others, that repetitive injury and compression of the wrist lead to a premature
closure of the distal radius growth plate and secondary ulnar overgrowth. In 1997, DiFiori et al. looked at nonelite
athletes and found ulnar variance to be more positive in gymnasts, when compared with age-predicted norms ( 18).
Radiographic findings consistent with stress injury were seen in 25% of those studied.
The importance of injury to the distal radius epiphysis with resultant ulnar positive variance lies in the fact that the ulnar
positive condition has been associated with ulnar impaction syndrome, damage to the triangular fibrocartilage, and
degenerative changes of the ulnar head, lunate, and triquetrum. Concern about the long-term effects on the wrists of
young gymnasts remains. However, its occurrence in the competitive athlete may not be totally preventable.
Although stress reaction or fracture of the distal radius epiphysis has gained significant attention, other causes of wrist
pain in gymnasts have been documented, including dorsal capsular strain, damage to the triangular fibrocartilage
complex, ganglia, and ligamentous injuries. Depending on the presenting complaints, the site of pain, and the results of
diagnostic tests, each entity will require specialized evaluation and treatment.
The pommel horse has been implicated as the main contributor to wrist injuries in male gymnasts. During the pommel
horse exercise, the gymnast uses the wrist as a rigid structure to support his body weight. The wrist is subjected to
high-intensity impact and stress from repetition. During a front scissors maneuver, the wrist may bear loads averaging 1
to 1.5 times body weight (20). The duration of the exercise and the force generated during a dismount maneuver increase
the risk of injury.
Dorsal wrist pain described as an intense pain across the dorsum of the wrist exacerbated by hyperextension is most
likely a capsulitis. The onset of dorsal wrist pain is usually insidious and tends to increase with activity ( 21). Pain may
occur with vaulting, floor exercise, or pommel horse maneuvers during which the wrist is forced into hyperdorsiflexion
with compression or torsion (22). The treatment for dorsal wrist pain involves the use of therapeutic modalities, flexibility
stretches, and strengthening of the wrist musculature ( 23), as well as a dorsiflexion wrist block. Blocks placed around the
dorsal aspect of the wrist just distal to the midcarpal junction prevent the wrist from moving into full extension. In the
immature athlete, care must be taken to distinguish this entity from distal radius stress fracture.
Scaphoid fractures are uncommon in gymnasts, but the usual mechanism of injury is a compression force with the wrist
held in hyperextension; though the forces applied in this position are usually subthreshold, their continued application
may result in a stress reaction. Scaphoid fractures can also occur from a fall on an extended wrist and an extended arm,
as when a gymnast falls off an apparatus and does not tuck or roll for protection. Surgical treatment of acute injury should
be considered to minimize immobilization time and to encourage predictable healing with near-normal range of motion.
Another source of wrist pain is ulnar impaction syndrome. Mandelbaum believed that the location of this pain was
different in male and female gymnasts, with men having pain on the dorsal aspect of the wrist toward the ulnar side and
women on the ulnar side of the wrist but not on the dorsal or palmar aspect ( 15). Both men and women in this study felt
pain during compression of the wrist, but none complained of pain with distraction. Pain was most prevalent in men
during the pommel horse and was related to weight bearing on the wrists. Women had pain primarily while vaulting.
Treatment for these wrist injuries initially focuses on activity modification along with ice and use of nonsteroidal
antiinflammatory drugs. After the pain cycle has been eliminated, stretching and strengthening can be initiated. Gradual
return to sports with cryotherapy after completion of practice is most beneficial. For patients with dorsal wrist pain, taping
may be beneficial.
Elbow Injuries
Elbow injuries account for approximately 5% of the total number of injuries in gymnasts; during the 1997–1998 NCAA
season, they accounted for 6% of the injuries in women's gymnastics ( 13). The usual mechanisms of acute injury were
missed moves, falls from apparati, or incorrect dismounts. The most common acute injuries in one study of immature
athletes were fractures and dislocations ( 24). The most common chronic problems are triceps tendinitis, medial and
lateral epicondylitis, and osteochondritis dissecans.
Priest described 41 separate elbow injuries in 30 acutely traumatized elbows in gymnasts; 41% of these injuries were
fractures to the medial epicondyle, and 39% were dislocations ( 24). It should be noted, however, that this patient
population was young, averaging only 13.6 years of age. During analysis of these injuries, Priest found that 60%
occurred when no spotter was present. There were twice as many injuries sustained on a thin mat or on the bare floor
compared with thicker mats. Priest was unable to determine which apparatus caused the most injuries or which tricks
caused elbow injuries. Twelve percent of all elbow injuries occurred during a dismount maneuver. Treatment of these
injuries includes prompt recognition, relocation or open reduction with internal fixation of displaced fractures, and early
range-of-motion exercises to prevent stiffness. Loss of extension is often preventable if early treatment includes
emphasis on regaining this motion.
Osteochondritis dissecans of the capitellum is another problem occurring in the elbow that has been well recognized
among gymnasts. Several studies have examined this entity in the female athlete. Jackson et al. ( 25) described 10 cases
of osteochondritis dissecans of the humeral capitellum in seven high-performance female gymnasts. All seven of these
gymnasts underwent arthroscopy for curettage, drilling, or removal of loose bodies. Although this surgical treatment led
to improved symptoms, return to competitive gymnastics was not routine, and a number of these gymnasts were unable
to compete because of continued complaints. The authors concluded that early definitive diagnosis of persistent elbow
pain should be a priority in young female gymnasts. There is hope that magnetic resonance imaging (MRI) might provide
for earlier detection of osteochondritis dissecans of the capitellum, which could improve both conservative and operative
management outcomes. Early recognition treated with either activity modification or surgical treatment might allow for
healing of these lesions and an improved functional outcome. Baumgarten et al. demonstrated that removal of loose
bodies and abrasion chondroplasty was successful in returning 13 of 16 young athletes back to their sport, including 4 of
5 gymnasts (26).
Another study, by Singer and Roy, described seven cases of osteochondritis of the capitellum occurring in five
high-performance female gymnasts between the ages of 11 and 13 years ( 27). The authors recommended that if
radiographic abnormalities were present, cessation from gymnastics for 6 to 8 weeks, until all symptoms had cleared,
was appropriate. However, if loose bodies were already present, then arthroscopic excision was warranted.
After an acute dislocation or fracture which has been treated, or after a surgical procedure such as an arthroscopy for
removal of loose bodies in the treatment of osteochondritis dissecans, gymnasts must be able to demonstrate full range
of motion at the elbow joint as well as full strength in the surrounding musculature before contemplating return to the
gymnasium. Gymnasts should be able to support their own body weight for an adequate length of time without pain. They
should progress slowly back to their regular gymnastics routine, concentrating first on support moves and working up to
more difficult tricks.
Overuse problems can also occur at the elbow joint. Medial epicondylitis is common in both male and female gymnasts,
because weight bearing on the upper extremity places a significant amount of force on the common flexor mass ( 28). The
main mechanisms of medial epicondylitis in male gymnasts are power moves, such as the iron cross on the rings, and
grasping the high bar with the wrists in a flexed position. Both of these maneuvers increase the force needed in the flexor
muscle mass. A gymnast also may suffer medial epicondylitis while performing the floor exercise. Most tumbling passes
are performed with the wrist in maximal hyperextension, which fully stretches the flexor mass.
Triceps tendinitis, sometimes termed “jumper's knee of the elbow,” can develop after irritation of the triceps tendon as it
attaches distally into the olecranon process. The most frequent mechanism of injury is the repeated exertion of great
force in the triceps to propel the body. This occurs usually during the vault and floor exercises; the gymnast flexes and
then rapidly extends the elbow, creating large forces on the triceps tendon. In vaulting, gymnasts commonly produce
force on the upper extremities in excess of 2.5 to 3.5 times their body weight ( 22).
The treatment of overuse injuries such as epicondylitis and triceps tendinitis include appropriate rest, antiinflammatory
drugs, stretching, and eccentric strengthening and conditioning. After acute inflammation has subsided, appropriate
stretching before competition and appropriate cryotherapy after gymnastic activities usually help symptoms abate. An
eccentric conditioning program, however, may be vital to eliminating symptoms altogether and must be emphasized for
those athletes with recurrent problems. Counterforce bracing may be helpful in the treatment of epicondylitis and may be
used as the gymnast begins training again after symptoms have diminished.
Shoulder Injuries
Shoulder injuries are more common in male than in female gymnasts. In one study of women's collegiate gymnastics
injuries between 1986 and 1991, the shoulder was the most commonly injured joint. Shoulder injuries accounted for
approximately 6% of the injuries during the 1997–1998 women's gymnastic season ( 13). The most common shoulder
injury appears to be a supraspinatus strain or tendinitis. Events such as the still rings produce significant stress on the
shoulder musculature. The use of the dowel grip increases the force across the shoulder by allowing the gymnast to
reach higher velocities. These forces are controlled by eccentric rotator cuff contractions. Muscle strains of the rotator
cuff are particularly common in younger gymnasts, whose upper-body strength may not be adequate.
Impingement-type symptoms occur frequently in both male and female gymnasts. The symptoms can represent a primary
problem caused by overuse or a secondary problem resulting from either glenohumeral instability or functional scapular
instability. Gymnasts often demonstrate increased range of motion in the shoulder, and complaints of instability are often
related to hypermobility of joints combined with poor technique and poor muscle tone and strength. Acute dislocation
events are usually the result of missing a trick or falling from the apparatus.
The treatment of primary impingement type symptoms includes rotator cuff exercises emphasizing internal and external
rotation strengthening in both eccentric and concentric manners. Scapular stabilization programs are also helpful and are
aimed at giving the glenohumeral joint a solid base from which to work. Acute inflammation of the rotator cuff is treated
with relative rest, antiinflammatory drugs, and cryotherapy. Occasionally at the collegiate level and above, an in-season
subacromial injection of cortisone is considered; however, its use should be judicious in nature, recognizing that
long-term effects on the tendon of such injections are not fully understood.
In the ligamentously lax individual with a multidirectional instability pattern, pain may be the presenting finding. However,
a complaint of shoulder slipping may also be made. Again, an appropriate shoulder strengthening program and a
scapular stabilization program are appropriate. Many of these patients improve and their instability symptoms abate.
For the athlete who has an acute traumatic dislocation after a fall, conservative measures may be employed if it is the
first dislocation of that joint. A relative period of immobilization for several days to 2 weeks is instituted, followed by an
aggressive strengthening and range-of-motion program. After full pain-free range of motion and near-normal strength
have been demonstrated, the athlete can return to activity, realizing that there is an increased risk of recurrent
dislocation. Depending on the time of season, acute stabilization may be considered for those patients who have
experienced an acute traumatic anterior dislocation. The results of arthroscopic repair after first-time dislocation appear
promising and the Bankart lesion is usually amenable to direct repair. Although other sports are able to employ braces to
eliminate the vulnerable position for dislocation (abduction and external rotation), braces are unacceptably restricting in
gymnastics and therefore are not used. Recurrent dislocations are treated with an appropriate operative intervention.
Knee Injuries
Epidemiologic studies have indicated that the lower extremity is the body area most commonly injured in gymnastics.
There is some discrepancy as to whether the knee or the ankle is more commonly affected, but both occur with high
frequency. Knee injuries accounted for 39 (15%) of 257 of injuries reported during the 1997–1998 NCAA women's
gymnastics season (13).
Acute injuries to the knees are often linked to dismount maneuvers because the forces are many times greater than
during other landings. Because scoring procedures in gymnastics award the highest scores to complicated dismounts,
attaining a higher score often involves increased risk. During dismounts, the gymnast should be educated not to land on
the fully extended or hyperextended knee, which may result in rupture of the anterior cruciate ligament (ACL). Instead,
the knee should be in a slightly flexed position. Epidemiologic studies have demonstrated that women are at increased
risk for ACL injury compared with men, and ongoing investigations as to the reasons for this discrepancy continue ( 29,30
and 31). Multiple injuries including posterior cruciate, medial collateral, and lateral collateral ligament injuries do occur.
Although they are less frequent than isolated ACL tears, falls during dismounts can result in severe hyperextension
injuries, resulting in knee dislocation. Treatment of these injuries should follow standard protocols, which include prompt
reduction, evaluation of neurovascular structures, treatment of any associated vascular injuries, and appropriate
treatment of the ligamentous injuries depending on the injury pattern and severity.
One must be careful to rule out fracture as a cause of significant knee pain after an injury. Although ligamentous injury is
more common, plateau fractures and proximal metaphyseal fractures can occur, and their treatment is distinctly different
from that of the routine cruciate injury. Burks et al. ( 32) described the case of a 14-year-old female gymnast who injured
her right proximal leg in class I competition. Initial radiographs of the knee and tibia on the day of injury and 3 days later
were unremarkable. Because the diagnosis was in question, however, an MRI scan was performed. This study revealed
a fracture of the proximal tibia extending into the metaphyseal region through the physis. The authors emphasized that
although MRI is not advocated as a screening tool, its results can be significant when the diagnosis remains in question.
Patella dislocation or subluxation is also a common problem. Andrish monitored 28 male and 142 female gymnasts for 78
months (33). During this time, a total of 170 knee injuries were recorded, 9.4% of which were patellar subluxations or
dislocation. The most common mechanism was a twisting injury with the femur internally rotated on a fixed tibia followed
by a sudden burst of quadriceps activity. This injury was usually seen during a dismount procedure or a vault.
Predisposing factors for patella subluxation include an increased Q angle at the knee, patella alta, weakness of the
vastus medialis, and a shallow patella sulcus. The young female gymnast often presents with genu valgum, medial
femoral rotation, proximal tibial vara, and external tibial torsion. This combination produces an increased Q angle and
can result in a lateral subluxation of the patella ( 34).
Acute patellar dislocations without osteochondral fracture are often treated conservatively, especially in the skeletally
immature athlete, in whom distal patellar realignment is an unattractive option because of an open proximal tibial physis.
Acute dislocations with large osteochondral fragments should be treated acutely with arthroscopy, repair of the
osteochondral fracture if possible, or removal if it is small. Controversy exists over whether a first-time patellar dislocation
should be treated with a realignment procedure. In the absence of significant anatomic abnormalities, first-time
dislocators may do well with nonoperative care. This should include early icing and antiinflammatory medication to limit
swelling, followed by a functional rehabilitation program that emphasizes quadriceps strengthening, including the vastus
medialis obliquus. Consideration of a lateral patellar support brace should be given. With recurrent dislocations or
subluxation events, a realignment procedure is warranted. These procedures should be aimed at correcting anatomic
abnormalities as determined on both radiographic and clinical examination. Factors such as patella alta, an increased Q
angle, a tight lateral retinaculum, and injury to the medial patellofemoral ligament should all be addressed at the time of
surgery.
Patellar tendon ruptures are a rare injury in gymnastics. Donati reported on a 21-year-old gymnast who ruptured both
patellar tendons simultaneously while vaulting ( 35). Before this injury, she apparently had no symptoms. Treatment
consisted of acute surgical repair. Patellar tendon rupture is uncommon in young athletes who are skeletally immature.
However, distal physeal separation with avulsion of the patellar tendon can occur ( Fig. 26.5). Lepse et al. described a
14-year-old male gymnast who sustained bilateral simultaneous tibial tuberosity fractures while attempting a forward flip
(36). On completing the trick, the gymnast fell to the floor and was unable to stand. Radiographs demonstrated bilateral
displaced avulsion fractures of the tibial tuberosities which were subsequently treated with open reduction and internal
fixation. The authors used screw fixation and noted that the patient did go on to premature closure of the tibial apophysis,
but the effects remained subclinical because of his limited remaining growth. In the younger patient population, other
repair techniques may be required, including suture fixation or the use of smooth pins that can be removed and may help
prevent premature closure of the tibial tubercle physis.
FIGURE 26.5. A: Tibial tubercle avulsion may be seen in the immature athlete. B: Repair can be performed with suture
fixation through drill holes.
Chronic knee injuries in gymnasts include generalized patellofemoral pain and inflammation, patella tendinitis,
Osgood-Schlatter disease, and quadriceps tendinitis ( 37,38 and 39). Weiker monitored 873 gymnasts for a 9-month
season and found that the most common problem was patellofemoral pain, most often the result of forceful leaping from a
hyperflexed knee (8). Patellofemoral pain in the young gymnast can be brought on simply by the repetitive activities of
gymnastics. This symptom is often treated with antiinflammatories, relative rest, and stretching and strengthening
exercises. Generalized patellofemoral pain is frequently a self-limited problem. However, it may plague athletes off and
on throughout the course of their careers. Its cause is probably multifactorial, and continued evaluation may be
necessary to identify and treat specific causes.
Long practice sessions and numerous repetitions during practice stress the patellar tendons. When tendinitis ensues,
pain at the inferior pole of the patella, especially in extension, and difficulties with exercises that require forceful
extension of the limb may occur. Although the process can be self-limiting, it should be treated with appropriate
stretching exercises, the use of antiinflammatory medications, postpractice cryotherapy, and an infrapatellar compression
strap. In more chronic and severe cases in the adult athlete, patellar tendinitis can be disabling. MRI or ultrasonography
can be useful in detecting degenerative areas within the tendon as it inserts onto the patella. When symptoms persist
with no relief from conservative measures, surgical treatment has been employed with reasonable success. Debridement
of the involved area of tendon along with trephination of the surrounding tendon and drilling or microfracturing of the
inferior pole of the patella can be helpful in these situations. Histologically, the patellar tendon may show areas of mucoid
degeneration and scarring. Excision of the diseased portion of the tendon, allowing regeneration of the area with new
collagen tissue, may be considered when conservative measures have failed and the athlete is unable to continue
because of the pain (Fig. 26.6).
FIGURE 26.6. A: Open patella debridement may be necessary in the treatment of refractory patellar tendinitis. B:
Excision of degenerative tissue may allow for repair and healing.
In the adolescent athlete, pain over the tibial tubercle is often a hallmark of Osgood-Schlatter disease. Tibial tubercle
apophysitis can occur from overuse and is treated with relative rest and stretching exercises along with antiinflammatory
medication. Although the condition is usually self-limited, severe discomfort should be taken seriously, and curtailing of
exercises must ensue. Unabated activity despite pain may result in avulsion of the tibial tubercle and is a complication
that can be avoided if symptoms are treated early.
In addition to problems that involve the extensor mechanism of the knee, strains of the flexor musculature are common.
Caine found that strains accounted for 17.7% of all injuries recorded, and these most often were found in the lower
extremity (11). The frequency was higher during the first hour of practice, and Caine attributed this to improper warmup
and stretching before practice. Gymnasts possess increased flexibility compared with the normal population. However,
the demands placed on them during gymnastics maneuvers are also much greater than in the normal population. Proper
stretching and warming up before high-intensity workouts should obviate many of these problems.
Most commonly strains occur during a vault run or floor exercise. During the sudden burst of energy, the hamstring is
placed under maximal stretch when the hip is forced into flexion and the knee is forced into extension in forward striding
movements. The hamstrings act to decelerate the extension moment of the knee. If the muscle is not adequately
stretched, a strain may result at the musculotendinous junction. Treatment of hamstring strains starts with good
prevention techniques. Again, the gymnast should be required to warm up adequately and to stretch before practice and
competition. If a strain does occur, therapeutic modalities and stretching should be used as tolerated. Immediate
cryotherapy on the day of injury is helpful in limiting the swelling. Strengthening of the hamstrings should emphasize
endurance and low-weight activities. Full return to activity is limited until the athlete is pain free and has near-normal
flexor strength.
Low Back Injuries
Low back injuries have long been recognized as a significant cause of disability in gymnasts ( 40,41,42 and 43). The
NCAA surveillance surveys have listed this as the third most commonly injured body part, with 8% of injuries occurring
due to low back problems (13). In another large review of female gymnasts, approximately 12% of injuries sustained by
gymnasts were to the spine (6). Low back complaints are frequent, and the causes of continued low back pain have
garnered significant attention.
Because flexibility is important in gymnastic performance, gymnasts attempt to gain always-greater ranges of motion.
Performing at these end ranges of motion may predispose gymnasts to injury. It is believed that the demands placed on
the gymnast's low back, including hyperflexion, hyperextension, and twisting, cause repetitive microtrauma and
macrotrauma that result in damage to the lumbar spine. Conditions in gymnasts that have been reported with a fairly
consistent frequency included spondylolysis of the lumbar spine, spondylolisthesis, and injuries to the endplates of the
disks (40,41,42,43 and 44).
In evaluating a gymnast with new-onset lumbar pain, it is common to see decreased range of motion, pain with
hyperextension, and decreased flexibility in the lower extremities. Although mechanical back pain is often what is
considered first, other, more serious entities must be considered and a reasonable level of diligence must be kept to
ensure that more serious conditions are not missed.
Spondylolysis, a fracture of the pars interarticularis, can occur both as an acute event or with repetitive microtrauma.
Gymnasts can also become acutely symptomatic even when the condition is chronic in nature. Treatment remains
controversial with regard to acute injury. The importance of determining whether spondylolysis is acute or chronic is
debated. However, treatment goals are the same, namely the restoration of a pain-free range of motion and normal
function. In the acute setting, a bone scan may be considered to determine whether there is an acute fracture ( Fig. 26.7).
If there is marked increased uptake consistent with an acute fracture, some would advocate bracing in an effort to
promote healing. In the young adolescent population, this is a reasonable course and bracing should continue until the
patient is asymptomatic, after which a rehabilitation program designed to regain motion and strength is instituted. In the
adult population, the need for bracing is somewhat more controversial. Although many would suggest that a period of
immobilization based on symptoms is appropriate, prolonged bracing is unlikely to result in high rates of union, and
therefore the treatment is aimed at getting the patient pain free. After resolution of the acute pain, a stretching and
strengthening program is instituted along with a Mackenzie-type back program to allow a gradual return to activities.
FIGURE 26.7. A: An L-5 pars defect is seen radiographically. B: Single photon emission computed tomographic (SPECT)
scanning increases the sensitivity of the bone scan in identifying pars defects.
Other injuries that can occur to both the lumbar and upper thoracic spine include acute disk space injuries. Swärd et al.
reported on two young female gymnasts with vertebral ring apophysis injury and subsequent disk degeneration after
traumatic injury (44). If these injuries are recognized early, activity modification and bracing may prevent more long-term
sequelae.
In the younger population with low back pain, infection must also be ruled out as a source. Persistent back pain in the
child is inconsistent with malingering, and a cause for the pain should be determined. Bone scanning or MRI may be
helpful if the diagnosis cannot be made on plain radiographs.
Rehabilitation after spine injury can take a significant amount of time because of the demands placed on the spine during
gymnastics. The goal of rehabilitation should be good trunk stability, flexibility, and a solid base of support. Care should
be taken not to cause an increase in pain in either the low back or the extremities during conditioning.
Functional strengthening can be achieved by performing manually resisted trunk and lower-extremity proprioceptive
neuromuscular facilitation patterns. Lower-extremity patterns include non–weight-bearing diagonals, resisted crawling,
bridging, and plantigrade movements. Resisted trunk movements may include lifts for the upper extremity, low trunk
rotations, and rowing. Exercises that emphasize abdominal strengthening and low lumbar strengthening are instituted.
Extension of the lumbar spine should be progressed without introducing pain. Once the patient is pain free in the prone
position, he or she should be encouraged to attempt increased extension while standing. The ultimate goal is to achieve
a back walkover so that maneuvers on the balance beam and floor can be done without pain. Progression should
proceed with increased extension allowed only to the point of discomfort. Once back walkovers can be completed without
any exacerbation of pain, the athlete can be progressed to hand springs and gradually to full participation.
Ankle Injuries
Ankle injuries are one of the most common injuries occurring in both men's and women's gymnastics. Because of the high
stresses that occur during landings and acrobatic maneuvers on the floor exercise, ankles are at increased risk in many
aspects of gymnastics. The 1997–1998 NCAA Women's Gymnastics Injury Surveillance Survey placed ankle injuries as
the number one problem among women gymnasts (13). Although for the most part these consist of common sprains of
the anterior talofibular and calcaneal fibular ligaments from inversion-type movements, injury to the posterior tibialis
tendon, Achilles tendon ruptures, injury to the peroneal tendons and tendon sheath, and associated fractures about the
ankle can occur. One must be careful not to dismiss an acute ankle injury as a simple sprain before a careful examination
is performed.
The treatment of common ankle sprains from inversion injury has been extensively studied in the sports literature. During
forced inversion of the ankle, the anterior talofibular ligament and the calcaneal fibular ligament are often injured. This
results in acute pain and swelling over the anterior lateral aspect of the ankle due to disruption of the ligament fibers. On
careful examination, tenderness along the anterior portion of the lateral malleolus and down onto the talus is often
demonstrated, along with swelling, pain with inversion, and a positive anterior drawer sign. In the acute setting, a
functional rehabilitation program has been recognized to allow early return to sport with good results and a low incidence
of recurrent instability. Immediate and acute treatments include ice, elevation, compression, and antiinflammatory drugs.
Immobilization usually is not necessary. However, protection from recurrent injury is necessary during the acute and
painful phase. With severe injuries, crutches with partial weight bearing and a lateral ankle support brace are often
employed until the swelling and pain of the initial injury subside. As discomfort diminishes, full weight bearing is allowed
as tolerated, with cessation of use of the crutches as soon as the gymnast is comfortable.
Rehabilitation starts immediately, with early range of motion movements performed in a protected fashion to prevent
stiffness and scarring. During this phase, care must be taken to prevent reinjury, which can occur as a result of muscle
weakness and lack of proprioception after injury. A lateral ankle support brace is often worn. Early exercises often
include stationary bike, stair stepper, leg press, and deep-water jogging and running exercises. This allows for
dorsiflexion and plantar flexion without recurrent inversion injury. When the patient is able to walk without discomfort,
ankle-specific exercises can be started. Some of the exercises that are specific for inversion ankle injuries include
strengthening of the peroneal tendons, Achilles stretching, and exercises aimed at improving proprioception.
Specific exercises that are used after ankle injury include isolation of the peroneal muscles in both concentric and
eccentric strengthening exercises. An elastic resistance band program is often instituted during this phase when the
patient is fairly pain free but has yet to regain full strength and mobility. At the same time, more aggressive straight line
exercises can be instituted, including treadmill on an incline and light straight-ahead jogging. Proprioceptive exercises
can be performed in the closed chain position with the use of a biomechanical ankle platform system (BAPS; CAMP,
Jackson, Michigan). The BAPS board can also be used to increase range of motion as it helps create proprioceptive
awareness. Initial use of this device is done in the sitting position with a small ball under the board to work on
proprioceptive function. Larger balls can be used to improve range of motion, and patient can progress to the standing
position as pain diminishes and strength improves.
When the gymnast is pain free in straight-ahead activities and is able to perform both concentric and eccentric
strengthening exercises without difficulty, a more vigorous functional rehabilitation program is started. Goals of functional
rehabilitation include performing side-to-side movements and gaining strength during jumping and landing activities.
Often, a minitrampoline is used at first, with the athlete performing jumping and landing activities in a controlled fashion.
When the gymnast is able to perform these activities, tumbling can be started with protective gear. Ankle taping along
with a lateral ankle support brace is often employed early on, and routines are limited to activities that minimize twisting
maneuvers. Over time, full activities are allowed, including twisting maneuvers, takeoffs for the vault and landing, and full
tumbling routines.
Sequelae from severe inversion ankle injuries can be numerous. Although many athletes return to practice and
competition in an uncomplicated fashion over the course of days to weeks, some are persistently bothered by residual
symptoms of a severe ankle sprain. Residual problems can include scarring at the anterior lateral corner of the ankle joint
with continued talar impingement in dorsiflexion ( 45). Treatment here is initially aimed at aggressive dorsiflexion
stretching along with plantar flexion stretching. Occasionally, a local injection of steroid can help with pain related to
postinjury scarring. In resistant cases, ankle arthroscopy with debridement or open excision of scar tissue at the
anterolateral corner is successful in treating refractory anterolateral impingement pain on dorsiflexion after a severe
ankle sprain.
Other associated injuries with a severe inversion sprain include lesions of the talar dome. Acute osteochondral fractures
can occur; they may or may not be evident on plain radiographs. For the gymnast who continues to be bothered with
anterolateral pain despite an appropriate rehabilitation program, a workup for lesions of the anterolateral talus must be
considered. Plain radiographs may show evidence of an osteochondritis dissecans type of lesion, but they often are
negative. In this setting, an MRI is helpful for detecting occult chondral and osteochondral lesions of the anterolateral
talus. Treatment includes arthroscopic or open debridement of loose fragments and drilling of in situ osteochondritic
lesions. Depending on the exact pathology, recovery can take from weeks to several months.
Additional problems after an inversion injury can include persistent posterolateral pain. Care must be taken to rule out
injury to the peroneal retinaculum, which can cause tendon subluxation or pain. This entity must be considered in the
athlete who has had an inversion injury with pain that is atypical and centered on the posterior aspect of the fibula. For
the gymnast who continues to have pain posteriorly, examination in the prone position to look for peroneal subluxation is
warranted, and an MRI may be necessary to evaluate the peroneal tendons for tenosynovitis, tearing ( Fig. 26.8), or injury
to the retinaculum that allows for increased translation or subluxation of the peroneal tendons. Injuries that are
recognized acutely may be treated with immobilization with the peroneals in a reduced position. However, chronic injuries
with continued tendon subluxation require surgical treatment with repair of the posterior peroneal retinacular sheath.
FIGURE 26.8. Fluid around the peroneal tendons and injury to the tendon substance can be visualized with magnetic
resonance imaging.
Achilles tendon rupture is rare in the young age population from which many gymnasts are drawn but has been reported
(46,47). Barron and Yocum (47) described the case of a 30-year-old female gymnast with unrecognized Achilles tendon
rupture associated with ipsilateral medial malleolar fracture. It is necessary in athletes with severe injuries or injuries to
the ankle that have unusual or significant increased swelling or pain to perform a careful examination of all the structures
about the ankle to avoid missing these less common entities.
Other entities that have been described in gymnasts include injury to the posterior tibial tendon sheath ( 48), fractures of
both medial and lateral malleoli, and osseous injuries to both the talus and the calcaneus. Again, careful examination of
the ankle along with a high index of suspension usually leads to the correct diagnosis.
In addition to acute injuries, which occur commonly to the ankle, chronic injuries can occur in the form of tendinitis, other
soft tissue inflammation, and stress fracture ( Fig. 26.9). Achilles tendinitis is a relatively common problem in gymnasts.
The repetitive nature of the sport, especially during practice and in the learning phase of routines, increases the risk of
overuse injury. Problems associated with the Achilles tendon are often attributed to dismounts and tumbling. The
treatment of Achilles tendinitis should emphasize an aggressive stretching program, use of antiinflammatory medications,
and, in some more severe cases, rest from the tumbling and landing aspects of gymnastics. In severe cases, a gentle,
pain-free, non–weight-bearing stretching program is instituted, followed by weight-bearing stretches after pain subsides.
A 90 degrees dorsiflexion ankle-foot orthosis can be considered for nighttime use; this provides for continuous stretch on
the Achilles to prevent shortening and contracture. Night splinting may be instituted in both acute and chronic cases.
After cessation of acute inflammation, rehabilitation is centered on maintaining maximal Achilles tendon length through a
stretching program together with strengthening of the gastrosoleus complex through weight training. Protective measures
can include taping of the ankle in some plantar flexion in an attempt to relieve stress on the Achilles tendon during
landing and tumbling exercises. However, long-term success in the management of this problem requires regaining
musculotendinous length and strengthening of the muscle tendon complex through both concentric and eccentric
strengthening programs.
FIGURE 26.9. Fibular stress fracture seen on magnetic resonance imaging (MRI). Plain films were suggestive of stress
fracture at the time of MRI. Pain had persisted for several weeks with increasing intensity.
Foot Injuries
Injuries to the foot are not uncommon in gymnasts owing to the repetitive landing maneuvers required. Major traumatic
injuries to the foot include subtalar dislocation, Lisfranc fracture dislocations and sprains, and other acute fractures of the
metatarsals and toes (49,50). These are usually associated with major miscues or falls from an apparatus. Appropriate
recognition and treatment is vital, because delayed diagnosis of these injuries can result long-term problems.
Chronic and subacute injuries to the foot include plantar fasciitis, stress fractures, and capsulitis of the forefoot joints.
Treatment of plantar fasciitis should include an aggressive Achilles and midfoot stretching program, use of
antiinflammatory drugs, and night splints as necessary ( 51). Gymnasts have approximately three times the normal
population's incidence of plantar fasciitis, probably because of the repetitive nature of practice, especially in tumbling and
the vault run (38).
Rehabilitation of plantar fasciitis may be difficult. The normal course of rehabilitation would include therapeutic modalities
and rest, night splints, flexibility and strengthening exercises, and functional return with the use of orthotic devices to
correct any biomechanical deficiencies. However, in gymnastics there is little, if any, true rest period, because the sport
is conducted 12 months a year. The use of an orthotic device may not be an option, because most gymnasts perform in
their bare feet. The best treatment is to screen athletes for significant tightness of the posterior calf and ankle
musculature and to insist that all athletes take the proper time to stretch before the start of practice sessions and
competitions. Prevention of this problem is often much easier than treatment after it becomes a chronic issue.
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27 Ice Hockey
27
ICE HOCKEY
JEFFREY MINKOFF
STEVEN STECKER
GERARD P. VARLOTTA
BARRY G. SIMONSON
Nature of the Game

Mechanics of Skating
Components of Skating
Kinematics and Kinesiology of Skating
Acceleration and Skating Velocity
Epidemiology of Injury and Contributing Implements and Forces
Rink Design and Injury
Kinesiology and Injury Potential
Hockey Participants and Injury Epidemiology
Surgical Consequences of Hockey in the National Hockey League
Psychological Considerations in Aggression and Injury
Role of Fitness: Relation to Performance and Injury
Hockey Penalties
The Hockey Rink and Collision Injuries
Protective Equipment in Hockey
Helmet
Facemask
Half-Face Visor
Neck Protectors
Skates
Sticks
Other Equipment
Injuries
Head and Face
Lower Extremity
Upper Extremity
Dermatologic Disorders
Soft-Tissue Injuries
Musculotendinous Strains
Other Soft-Tissue Injuries
Visceral Injuries
Chapter References
Ice skating appears to have originated in Northern Europe during the Renaissance; animal bones served as skate blades
(1). Although the precise origins of ice hockey are obscure and mired in controversy, it is at least clear that the game was
conceived and played originally in Eastern Canada near the midportion of the 19th century ( 2). Pashby (1) cited Sagard
(1939) as having reported that the origins of ice hockey are traceable to 17th-century Huronia (Ontario, Canada), where
a wooden ball was pushed along the ice with curved sticks. Derivatively, hockey is probably a homonymic descendant of
the old French word hoquet, meaning “shepherd's staff.” Like its cousin of North American origin, basketball, ice hockey
saw the creation of professional leagues within a few decades after its conception and entered the registry of Olympic
Games before the outbreak of World War II (Antwerp in 1920) ( 2).
Although traditionally ice hockey has been considered a sport predominantly of northern latitudes, it has substantially
invaded the more temperate regions, especially North America. Writing in 1999, Kahn ( 3) indicated that more ice hockey
rinks had been built and more franchises awarded at various professional levels in Florida in the previous 5 years than in
many northern states. Two of us (JM and BGS) are associated with the medical team of the Florida Panthers and are
appreciative of the trend.
NATURE OF THE GAME
Pashby (1) explained that sequential changes in the evolution of ice hockey increased risk to the players. The
introduction of the forward pass and a center red line increased the speed of the game and its collision energies. The
center red line is a part of the “icing” rule, whereby opposing players are made to race each other to the end boards
trying to reach the puck first, often with collision. In Olympic hockey, there is no red line and there is “nontouch” icing (P.
Flatley and J. Norton, New York Islanders and former Olympians, personal communication, 1991).
Curved sticks appeared (Fig. 27.1) and in 1950 begat the slap shot ( 4), in which pucks are driven at speeds well over
100 mph; the curved stick also taunted the goalies with rising, dropping, and curving pucks, adding danger to the
unprotected faces and throats of the netminders. Recognition of the progression of dramatic injuries evolved slowly;
measures to reduce their severity began almost 70 years after the Ontario Hockey Association, forerunner of the National
Hockey League (NHL), was founded in 1890. In 1959, a professional goalie began to use a molded mask for protection in
games (Fig. 27.2A). Although not completely effective, it was a beginning. Today, ice hockey is an aggressive contact
sport in which opportunity for injury derives from numerous sources.
FIGURE 27.1. Right and left curved sticks showing variability in (A) geometry, (B) blade curves, and (C) blade taping.
FIGURE 27.2. A: Facemasks in evolution from 1960s (left) to early 1980s (right). (Courtesy of Chico Resch.) B: Hockey
Equipment Certification Council and Canadian Standards Association approved helmet with faceshield (left) and metal
cage (right). (Courtesy of Cooper Canada, Toronto, Canada.)
MECHANICS OF SKATING
Components of Skating
The kinematics of the skating motion are evident in all the ice skating sports (e.g., ice hockey, speed skating, figure
skating), as well as in non-ice skating activities such as cross-country skiing, rollerblading (in-line skating), and
skateboarding. Ice hockey is unique among all these activities by virtue of its combination of forward power skating,
frequent stops and starts, lateral agility, and backward propulsion.
The ice, the skate, and the technique of skating are among the factors that must be scrutinized in a discussion of skating
dynamics. The quality and composition of the ice surface affect skating resistance and energy expenditure. Ice may vary
in topographic smoothness, surface water, and density, with each of these factors having a potential influence on speed,
power movements, and agility.
Assessment of the skate is important because it is the moderating link between the power generator (lower extremity of
the skater) and the ice surface. In order to attempt alteration of a technique to maximize performance, the biomechanics
and kinematics of an individual's skating characteristics must be analyzed. Skaters of different body types and training
demonstrate great variability in skating efficiency.
Variability of the ice surface can have an impact on the effectiveness of skating, because the coefficient of friction of the
ice surface can be as low as 0.004 or as high as 0.0200 ( 5,6). Hence, the condition of the ice influences the speed and
stability of players, any propensity for ruts in the surface, and the control and path of the puck. The ambient temperature
may influence the condition of the ice with respect to its density, resistance, and coefficient of friction. Higher air
temperatures and humidity may elevate the latter by 0.001 to 0.002, thereby reducing skating velocity and encouraging
skater fatigue (6). The puck tends to bounce more on warmer ice. The San Jose Sharks arena maintains an ice
temperature of –8.9°C (16°F) for ice hockey and –5.5°C (22°F) for figure skating ( 7). The colder ice lends to increase
skater speed, whereas the softer ice at higher temperatures allows the blade of the figure skater to penetrate more
deeply for enhanced stability. Canadian rinks tend to have “better” (harder and smoother) ice than do those in the United
States. Rinks that share basketball and other sports tend to have less desirable surfaces, as do those in warmer
climates, where cargo doors may be left open for deliveries and other purposes.
As indicated, the skate is a vital and moderating link between the ice surface and the skater. Technology and design
modifications have improved the skate boot, blade, and assembly. The skate consists of a leather or composite material
boot, ankle support, toe box, heel counter, rigid sole, skate blade housing, and blade ( Fig. 27.3). Each of these
components has an effect on comfort and efficiency of skating.
FIGURE 27.3. Bauer hockey skate boot with Tuuk V2 blade. Note the narrowing of the blade from the distal one third of
the blade proximally. a, heel counter; b, toe box; c, rigid plastic sole; d, skate blade housing; e, metal blade; f, Achilles
guard; g, pad tongue. (Courtesy of CanStar, Toronto, Canada.)
Historically, the first ice skates evolved from a blade attached to a walking boot. The first skate blades were made of
bones from animals endemic to Scandinavia ( 8). By the late 1880s, the metal blade was attached to the boot by means of
a wooden support. Eventually, a pure metal blade assembly was used, adding considerable weight to the skate and
reducing skating speed ( Fig. 27.4). With the progression of technology, a tubular skate blade was developed around
1975. This evolution considerably lightened the weight of the skate, facilitating an increase in skating speed.
FIGURE 27.4. Evolution of ice hockey skates (clockwise from lower left): (A) skate circa 1910; (B) skate permanently
mounted to a leather boot circa 1920; (C) “tube skates” with pointed back of the blade; (D) tube skate circa 1950 with
plastic over the back of the blade; (E) modern skate with plastic blade holder. (Courtesy of Chico Resch.)
Although the evolution of blade design had unburdened the work of skating by the 1970s, acral promontories remained
which could lacerate or puncture players. In 1977, stimulated by the North American hockey community to develop a
safer blade, the Association of Standardization and Testing of Materials (ASTM) worked toward development of an
appropriate standard for skates. After several years of diligence, standards were developed (in 1981 and 1986) that
reduced the potential for skate blade injuries (see Fig. 27.32). As an aside to the improved safety design, a very
lightweight plastic and metal blade assembly was developed that improved skating speed and maneuverability even more
than had its predecessors.
FIGURE 27.32. Impact methodology for facemasks including impact sites perpendicular and at 45 degrees from center.
Visual fields (laterally, 90 degrees; superiorly, 45 degrees; and inferiorly, 60 degrees) must be unimpaired. From Dixon,
ISO Draft, 1991.
At the international level, the International Olympic Committee (IOC) supported research by the Ice Skating Conditioning
Equipment Corporation to investigate the blade and boot design of figure skates ( 9). This research led to a confirmation
of variables in skate design that affect performance, such as edge sharpness, blade geometry (including thickness and
taper of the blade and rocker radius), and the boot-to-blade angle.
In cross-section, the skate has two edges separated by a hollow ( Fig. 27.5). The depth of the hollow can be shallow or
deep in accordance with the sharpening technique. A deeper hollow results in a sharper blade edge that cuts deeper into
the ice, thereby increasing push-off power while compromising smooth stops. Conversely, a more shallow hollow
compromises the skater's ability to engage the ice surface, thereby reducing agility and push-off power. Players have
position-related and personal preferences with respect to how much hollow is ground into the blade by the rotating stone
wheel sharpener used to modify the hollow. Goalies, for example, like less hollow so as to avoid catching an edge when
scrambling from side to side in front of the net ( 7).
FIGURE 27.5. Skate blade in cross-section showing two edges (inner and outer) and hollow.
Skaters are perpetually mindful of their blade “edges.” Edges influence the stability, agility, and power of the skater. The
inside edge contacts and penetrates the ice during the push-off and glide phases ( Fig. 27.6). The outer edge of the skate
blade is used predominantly in effecting stops and turns ( Fig. 27.7). A dull or angled edge will not penetrate the ice
effectively, resulting in the loss of an edge during turns or an ineffective stop ( Fig. 27.8).
FIGURE 27.6. Skater using left inside edge for push-off. (From Stamm L. Laura Stamm's power skating. Champaign, IL:
Leisure Press, 1989, with permission.)
FIGURE 27.7. Skater using left outside edge for agility (turns and crossovers). (From Stamm L. Laura Stamm's power
skating. Champaign, IL: Leisure Press, 1989, with permission.)
FIGURE 27.8. Skater losing right inside edge. (From Stamm L. Laura Stamm's power skating. Champaign, IL: Leisure
Press, 1989, with permission.)
In a geometric modification of the skate blade (see Fig. 27.3), its width was narrowed to increase the amount of force per
unit area in contact with the ice; the increased force facilitates penetration of the ice by the blade, and thereby increases
the power of the stroke, while reducing the frictional resistance of the blade (A. Mullen, CanStar Corporation, Division of
Research and Development, personal communication, 1991). This design modification is theoretically sound, but there
remains a technical difficulty in sharpening the skates to create an adequate hollow flanked by edges of appropriate
height (M. Pappas, former NHL equipment manager, personal communication, 1991).
The skate blade is created with a radius of curvature (the rocker), which may be modified by skate sharpening ( Fig. 27.9).
The rocker radius has reciprocal influences on the ability and stability of the skater. Elite and professional players have
anecdotally reported an increase in their agility when using a rocker of decreased radius (7-foot or 9-foot “greater rocker”
(see Fig. 27.9A); increased stability has been reported when using an increased radius (11-foot or 13-foot flatterblade)
(see Fig. 27.9B). The magnitude of the rocker varies among skate models and manufacturers. It may be questioned
whether there is a “critical” radius whereby stability is compromised in the quest for agility. Centering of the rocker is
critical for optimal skating performance. If the center line is too far anterior or posterior, then turning, starting, stopping,
passing, and shooting abilities may be affected.
FIGURE 27.9. A: Photograph of skate blade with a 7-foot radius rocker (“greater rocker”). B: Photograph of skate blade
with a 13-foot radius rocker (flatterblade). Arrows indicate ice contact.
Kinematics and Kinesiology of Skating
The biphasic skating motion in ice hockey is illustrated in Figure 27.10. The nomenclature identifying the phases of the
skating cycle varies among authors. The terminology used by Stamm ( 10) includes the wind-up, the release, the
follow-through, and the return (recovery) phases. The glide (single-support) phase occurs during the return phase of the
contralateral leg (see Fig. 27.10G, Fig. 27.10H). At a comfortable skating speed, the single-support (glide) phase
constitutes 82% and the double-support (wind-up, release, and follow-through) phases constitute 18% of the skating
cycle. Acceleration occurs through the double-support phase and for 50% of the single-support phase ( 11).
FIGURE 27.10. Skating motion for right lower extremity: (A, B, and C) wind-up phase; (D and E) release phase; (F)
follow-through phase; (G and H) recovery phase; (I and J) glide phase. (From Stamm L. Laura Stamm's power skating.
Champaign, IL: Leisure Press, 1989, with permission.)
Ice skating differs from other types of human locomotion, specifically in the push-off phase. In skating, the direction of the
push-off skate is perpendicular to the direction of travel of the opposite glide skate ( Fig. 27.11; see Fig. 27.10I, Fig.
27.10J). There is a decrease in plantar flexion force developed at this phase of the cycle as compared with bipedal
terrestrial gait (6,12). The push-off action of skating is a catapult-like action, with the power output being generated from
the muscular action of the hip (adductors and extensors) and from knee extension. The overall force of the muscle
contraction of the lower extremity (in the form of a leg press) is summated during propulsion ( 6,9,12,13,14 and 15) (Fig.
27.12). Peak forces during the push-off phase reach values up to 140% of body weight ( 6) and have a bearing on the
frequency of observed hip muscle strains. The kinematics of skating is summarized in Table 27.1.
FIGURE 27.11. A: Push-off skate (right foot). B: Push-off skate is perpendicular to glide skate (left foot).
FIGURE 27.12. Power sources per segments are the external movements and forces (except gravity) per link. (From Van
Ingen Schenau GJ, Cavanaugh PR. Power equations in endurance sports. Biomechanics 1990;333:865–881, with
permission.)
TABLE 27.1. THE KINEMATICS OF SKATING
The wind-up phase (see Fig. 27.10A, Fig. 27.10B, and Fig. 27.10C) follows the end of the recovery phase with
touchdown of the swing skate to the ice. The center of gravity is located directly in line with the ipsilateral ankle joint in
the sagittal plane. In the frontal plane, the center of gravity is just anterior to the ankle joint and fosters dorsiflexion of the
ankle and flexion of the knee and hip.
During the release phase (see Fig. 27.10D, Fig. 27.10E), contractions of the gluteus maximus and gluteus medius,
semitendinosus, biceps femoris, and triceps surae result in a progression of the hip and knee toward full extension,
abduction, and external rotation. The ankle is in the neutral position. The center of gravity shifts toward the contralateral
(glide) extremity. The skate is fully on the inside edge.
The follow-through phase (see Fig. 27.10F) completes the powerful push-off with full extension of the hip and knee and a
final forceful plantar flexion of the ankle.
During the recovery phase (see Fig. 27.10G, Fig. 27.10H), the hip and knee flex to about 40 and 90 degrees,
respectively. The hip rotates internally and the ankle is maximally dorsiflexed. The end of recovery of the ipsilateral leg
should correspond to the release phase of the contralateral lower extremity.
The push-off phase (wind-up, release, and follow-through) in skating is handicapped by the absence of the rapid,
powerful plantar flexion developed by the triceps surae that occurs in other bipedal activities, such as running and
jumping (6). The reduction of muscularly controlled ankle motion takes its toll in maneuverability and speed. The precise
contribution of plantar flexion to skating power and speed has not been determined. Many players at all levels do not
tape their skate boot to their skin pads, so as to avoid a reduction in their final thrust, thereby sacrificing safety for
performance (see later discussion). Technical modifications of the skate boot that allow an increase in dorsiflexion and
plantar flexion of the ankle potentially allow greater propulsion and an increase in skating velocity.
Acceleration and Skating Velocity
Acceleration relates to the location of the center of gravity, which varies throughout the skating cycle. During the glide
phase, it is located above the ankle joint of the stabilizing leg and then moves anteriorly as acceleration is generated by
the push-off leg (6). The lateral trajectory of the center of gravity follows a sine wave pattern, as it does in ambulation.
The amplitude of displacement is about 25 cm with higher stroke frequencies, and it increases up to 50 cm at lower
stroke frequencies as the result of a prolonged glide phase ( 6,12,16) (Fig. 27.13). Acceleration in skating occurs when
the center of gravity is anterior to the support foot and when the push-off lower extremity is externally rotated to establish
an appropriate angle between the blade and the ice surface ( 15) (Fig. 27.14). The angle between the skate blade and the
ice is considered to be of importance. In fact, it has been suggested ( 10) that the application of the blade to the ice at
precisely 45 degrees is critical to the achievement of maximum skating thrust. Not only blade design, but freedom of
ankle and subtalar motion influence of the contact angle ( 17,18). In addition, Marino and Weese ( 11) determined that the
achievement of a maximally accelerated velocity without a compromise in skating balance was accomplished with a quick
internal rotation of the push-off lower extremity during the recovery phase and a quick propulsive thrust during the
push-off phase.
FIGURE 27.13. Ice cuts (solid line) and trajectory of the center of gravity (broken line) for (A) higher and (B) lower stroke
frequency. Direction of travel is noted (arrow).
FIGURE 27.14. A: The angle between the push-off leg and the ice determines the effectiveness of the push-off. (From
Van Ingen Schenau GJ, de Boer RW, de Groot G. Biomechanics of speedskating. In: Vaughan CL, ed. Biomechanics of
sport. Boca Raton, FL: CRC Press, 1989, with permission.) B: Side view of the push-off angle. C: Front view of the
push-off angle. ( B and C from Stamm L. Laura Stamm's power skating. Champaign, IL: Leisure Press, 1989, with
permission.)
An increase in velocity has been shown to be directly related to an increased stride rate ( 19,20). Stride length does not
have an effect on velocity ( 6,16,19). Hence, the power and acceleration of skating result from the product of the stroke
frequency and the mechanical work done per stroke.
The highest rate of acceleration and the shortest skating time to cover a 6-m distance have been shown to correlate
highly with factors other than increased stride rate alone ( 21). These factors include an increased forward lean of the
torso at the touchdown of the swing skate, a reduction of the single-support phase of the skating cycle, and precise
placement of the swing skate directly below the hip joint at the start of the wind-up phase. Increased acceleration is the
result of a decreased leg angle at takeoff of the skate blade (approximately 45 degrees; see Fig. 27.14) at the end of the
follow-through phase, a decreased hip flexion angle at touchdown of the skate, and an increased stride rate ( 6,10,22,23).
The variables that contribute to increased acceleration are summarized in Table 27.2. Double-support time, stride length,
hip and knee angle at push-off, lower extremity push-off angle, hip flexion angle at touchdown, and angle of the skate
blade at push-off did not correlate with increased acceleration ( 15,20).
TABLE 27.2. SUMMARY OF ACCELERATION VARIABLES
When considering all kinematic parameters, elite skaters differ from skaters at lesser levels by achievement in the
following categories:
1. Smaller knee angle early in the wind-up phase of push-off (approximately 90 degrees)
2. Significantly greater amount of work per stroke and a slightly higher stroke frequency
3. Greater knee extension velocity
4. A rapid, but powerful push-off
5. A push-off angle of 45 degrees
The best of the elite performers can be identified by their ability to achieve superior scores on items 2, 3, and 5 ( 6). The
ability to accelerate distinguishes the elite hockey skater from those of lesser skating ability. Overall, faster skaters show
more precise push-off mechanics, with an effective glide perpendicular to the push-off direction. These factors maximize
the power output of the skater's lower extremity.
A specific category of skating acceleration is the start. Few studies have evaluated the effectiveness of the hockey start.
There are three basic ice hockey starts: the standing forward start ( Fig. 27.15A, Fig. 27.15B), the crossover side start
(Fig. 27.16A, Fig. 27.16B), and the thrust and glide start. Disagreement in the published literature exists as to the most
effective start. The backward skating stride and start, the forward skating crossover start, and backward and forward
starts have not been evaluated in the academic literature. Descriptions of each can be found in detail in Stamm's Power
Skating (10).
FIGURE 27.15. Forward start sequence. A through G: Note the precise blade-to-ice angle at push-off and the quick,
powerful knee extension. H: Forward start ice cuts (solid arrows) and direction of travel (broken arrows). (From Stamm L.
Laura Stamm's power skating. Champaign, IL: Leisure Press, 1989, with permission.)
FIGURE 27.16. Crossover side start sequence. A through G: Note the precise use of the left outside and right inside
edges. H: Closeup of crossover side start. I: Ice cuts for crossover side start (solid arrow) and direction of travel (broken
arrow). (From Stamm L. Laura Stamm's power skating. Champaign, IL: Leisure Press, 1989, with permission.)
EPIDEMIOLOGY OF INJURY AND CONTRIBUTING IMPLEMENTS AND FORCES
The National Collegiate Athletic Association (NCAA) Injury Surveillance System (ISS) has been in place since 1982. It
reports injuries as a randomly sampled cross-section of the NCAA institutions. The injuries are expressed as a ratio per
1,000 exposures; an “exposure” represents participation in a game or practice and is not necessarily related to the
quantity of time in participation.
The NCAA ISS data from the 1989–1990 academic season revealed that injuries were recorded twice as often in ice
hockey games as in practices, despite the fact that there were approximately four practices for each game ( 24). Roughly
a quarter of the injuries were recurrences or complications of previous injuries. Almost 70% were contact injuries, the
preponderance of which resulted from contact with another player. The most frequently injured body parts were the knee,
the shoulder, and the groin. Surgery was an infrequent sequel to injury.
NCAA ISS data for the 1998–1999 season revealed little alteration of the trends that existed in the previous decade. The
rate of injuries per 1,000 exposures was 16.97 for games and 2.06 for practices. With respect only to games, the “new”
injury rate was 14.44, compared with 2.13 for all reinjuries to an area. Contact with another player remained the leading
cause of injury. Forwards sustained many more injuries than did defensemen or goalies. The shoulder, knee, and groin
areas remained among the predominant sites of injury. Head injuries (1.70 per 1,000 exposures) ranked third among all
sites injured in games, mostly accounted for by concussions. No periorbital injuries were recorded, a testimony to the
protective value of facial visors and cages. Face protectors of varying description became a standard for both the
Canadian Amateur Hockey Association (CAHA) and the Amateur Hockey Association of the United States (AHAUS) in
the 1970s (25).
The National Hockey League Injury Surveillance System (NHLISS) is predicated on game and practice exposures, similar
to the NCAA ISS (26). Data from the 1996–1997 and 1997–1998 seasons were collected from the 26 participating clubs.
Of trends appreciated in the 2-year study period, there were fewer injuries during the third period of play (28%) than
during the first or second period. The reason is not clear. When comparing injury severity measures based number of
days or games missed, it must be remembered that NHL players play up to four or five games per week, whereas the
game schedules of the NCAA and other organized leagues are less condensed. The injury rate per 1,000 exposures for
the two seasons studied was slightly less than 12.0; half of these were injuries that resulted in no games lost, and one
quarter cost 10% or more of the regular season (more than eight games).
Despite the progressive increase in use of head and face protectors over the previous decade, the face and scalp
remained the most frequent category of injury in the NHL (30.5%). Although the knee accounted for only 9.5% of injuries
(about 1 knee injury per 1,000 exposures), it accounted for the highest proportion of missed games (18%); groin injuries
accounted for the second highest proportion (9%).
With regard to stick-related injuries in the NHL, slashes accounted for the greatest number of injuries resulting in missed
games, whereas hooking accounted for the highest mean number of games missed. Among injuries resulting from body
contact, body checks were the most frequent cause, followed by boarding, charging, tripping from behind, elbowing, and
kneeing as causes of the highest proportion of mean games missed ( 26).
In a review of injuries sustained in international competition, Lorentzon et al. ( 27) reported an injury rate of about 80 per
1,000 game-hours. Contusions and sprains were the most common injuries. The primary causes of missed games and
practices were checks (31.6%) and contact with other players (42.1%). As in the NCAA study, forwards were injured more
often than defensemen, and goalies were injured least often. In Thomson's survey of amateur hockey in Ontario ( 28),
forwards and defensemen were at equal risk from the atom to the senior level, but the former were more likely to be
injured by a stick and the latter by a puck. Among the most recent and comprehensive ice injury surveys (1995) was that
reported by Biasca et al. ( 29). It compared injury patterns of the NHL, Canadian Juniors, and some European leagues.
The conclusions were that for all leagues the preponderance of injuries occurred during games. Knee sprains accounted
for the majority of games missed, followed by shoulder sprains, and then by groin and back strains. They found that face
protectors had reduced the incidence of facial and eye injuries, but concussions and cervical spine injuries remained
unreduced and possibly were escalating.
Players skating at speeds of 20 to 25 mph or more may collide with each other, with the hard side boards of the rink, with
the ice, or with the goal posts (which were immovable until the mid-1980s). Injuries also may be caused by impact with
implements of the game—from the frozen, 6-ounce, vulcanized-rubber puck; to skate blades; to the blades, heels, and
handle butt ends of the hockey sticks ( Fig. 27.17).
FIGURE 27.17. Photograph of professional player's fist. Note the numerous old lacerations over the knuckles
(arrowheads).
Rink Design and Injury
Rink design is an issue in regard to the flow of the game and the injuries that may occur. The end boards and side
boards are critical components in concussions, cervical spine fractures and dislocations, and numerous other injuries.
The goal is situated close to the end boards, and the lane between them is a site of congestion and injuries ( Fig. 27.18).
Amateur rinks have moved the goal further from the end boards to create a wider lane than that customary in NHL
hockey rinks (approximately 3 m [10 feet]). The NCAA ISS revealed that the highest rates of game injury are sustained
not behind the goal (1.42 per 1,000 exposures), but in the corners and between the blue line and the face-off circle (4.47
each).
FIGURE 27.18. There is a narrow lane (especially in the National Hockey League) between end boards and the goal net.
As discussed by Keating and Norris ( 14), two basic rink designs have evolved worldwide. One, the North American
variety, is smaller (26 by 61 m [85 by 200 feet]) and is characterized by tight corners. A second design, which
predominates in Europe, is larger (30 by 60 m [98 by 197 feet]) and has corners with a large radius of curvature.
Commensurate with their respective dimensions, the North American rink is better geared for tight checking games and
many spectators, while the European variety is geared for wide-open skating.
Keating and Norris concluded on the basis of videotape reviews that most injuries (or at least most of the severe injuries)
occur along the rink's end boards and in the corners. On this basis, they proposed that the corners be modified to form a
continuous, smooth curve; that the goal be moved further away from the end boards; and that the blue line also be moved
further out. A national standard for rinks has been established in Germany (defined under the German Standards Code
DIN 32 927), and a provincial one has been established in Ontario by the Ontario Hockey Association.
Kinesiology and Injury Potential
As has already been suggested, the speed achieved by players is an important contributor to injury potential. Daly et al.
(30) used high speed cinematographic methods to determine that senior amateur players achieved velocities of about 30
mph. Fallen players can achieve velocities of up to 12 mph while sliding. If deceleration occurs by cranial impact on the
boards, for example, the impact can cause serious injury to the cervical spine ( Fig. 27.19).
FIGURE 27.19. Loading apparatus testing cervical spine impact with test dummies. (Adapted from Bishop PJ, Wells RP.
Cervical spine fractures: mechanisms, neck loads, and methods of prevention. In: Castaldi CR, Hoerner EF, eds. Safety
in ice hockey. Philadelphia: Association of Standardization and Testing of Materials, 1989:71–83, with permission.)
By virtue of its acquired speeds, sharp edges, and condensed, frozen form, the ever-dangerous hockey puck can invoke
serious injury. Puck speeds have been measured at velocities as high as 90 mph for senior amateurs and up to 120 mph
for professionals (30). Puck impact forces have been estimated to be capable of exceeding 1,200 pounds ( 27, 30).
Among all types of shots in hockey, the slap shot is considered the one most likely to drive the puck to maximum velocity.
The acceleration derives from the weight shift of the body, the snap of the wrists at release, and a kinetic contribution
from the stick blade, with its vital components of curve and flexibility. The stick blade is made to contact the ice a foot or
two in advance of contact with the puck. The blade is therefore made to bow, storing potential energy. This is
transformed into a kinetic form on contact with the puck, at which time the bowing reverses precipitously, helping to “slap”
the shot (7).
According to Sim et al. (30), stick angular velocities during puck shooting are in the range of 20 to 40 radians per second,
which not only can drive the puck to impact forces in excess of 1,200 pounds but can inflict significant injuries to players
in its path. As a result of assertions of many players and trainers of NHL teams, the aluminum stick, recently introduced
and suspected as the cause of more dramatic slashing injuries, was subjected to scrutiny. Studies undertaken by Haas
(31), however, revealed that no greater amount of force was delivered by aluminum sticks than by conventional (wooden)
sticks. Carbon-graphite sticks with aluminum shafts have become quite popular ( 7).
Forces generated by power skating per se, even in the absence of contact, can predispose to musculotendinous injuries
(usually of the groin) or to knee sprains. Dynamic force plate analysis during simulated power push-offs demonstrated a
vertical thrust reaction in the 300-pound range, a posterior thrust in the 150-pound range, a lateral thrust in the 80-pound
range, and vertical twisting forces in the 40 to 80 inch-pound range ( 30). These forces help explain the incidence of groin
pulls. A synopsis of the relative contributions of the implements and forces of ice hockey to injuries, collated from several
studies, is provided in Table 27.3.
TABLE 27.3. MECHANISMS OF ICE HOCKEY INJURIES
It can be seen from Table 27.3, adapted from the study of Sim et al (30), that the skate was responsible for 3% to 5% of
injuries. For the 1998–1999 academic year, the NCAA ISS reported that contact with a skate accounted for a game injury
rate of 1.49 per 1,000 exposures. The senior author (JM) has witnessed only two significant skate blade injuries. One
was a partial amputation of a finger and the other a deep laceration of the popliteal fossa that spared the vital popliteal
neurovascular structures. Several severe skate blade slashes to the necks of players have been reported ( 32) (see later
discussion).
The fiercely competitive and contact nature of ice hockey leaves room only for the intrepid and for those with a physical
makeup that can withstand incessant pounding. There are few injury-prone elite participants. However, there are many
whose styles of play predispose them to higher rates of injury (accident proneness). This style is often hard to
characterize or alter, even under the observant eye of an experienced coach. Game strategy incorporates purposeful
collisions of one player into another, otherwise known as “checking.” Body checking is a vital component of the game. It
may be instigated with any magnitude of force so long as it is done from a position at the front or side of the recipient
using the torso (including the shoulder) ( Fig. 27.20) or the hip (known as a hip check) ( Fig. 27.21).
FIGURE 27.20. A and B: Purposeful collisions (shoulder checking). (Courtesy of Paul Bereswill.)
FIGURE 27.21. Hip check. (Courtesy of Paul Bereswill.)
In North American hockey, fisticuffs are a common and accepted (although penalized) aspect of the game. With the
exception of occasional nasal, zygomatic, malar, and hand fractures, fighting rarely results in injuries more severe than
facial lacerations.
A first offense for fighting in the NCAA results in a one-game suspension; a second offense results in a two-game
suspension, and third offense costs the player the remainder of the season. Fighting in the Olympic Games results in
disqualification from the tournament (P. Flatley and J. Norton, New York Islanders and former Olympians, personal
communication, 1991).
Hastings (1974) reported that fighting produced only 3% of the injuries in his series ( 33). We have observed that most
fighting injuries are facial lacerations, but facial and tooth fractures as well as hand (see Fig. 27.17) and wrist fractures
are not unknown (see also Chapter 17). Lacerations on the knuckles of the hand are usually sustained when the
opponent's teeth penetrate the skin. Naturally, these wounds are dirty; they should be thoroughly irrigated, painted with
antiseptic, and not sewn closed; antibiotics should be administered. Perhaps more worrisome than bacterial infection in
this era is the concern that open, bleeding wounds may provide a portal for infection with viral diseases such as human
immunodeficiency virus or hepatitis. Fighting is a concern in this regard. Nevertheless, the chance of such an infection's
being acquired as a result of contact sports is virtually nil. Both sporting clubs and medical organizations have created
guidelines for the handling of blood in the sports environment.
Hockey Participants and Injury Epidemiology
It is well known to most sports enthusiasts that hockey has both professional and amateur participants. Among amateur
associations worldwide, divisions of players are made according to age, citizenship, checking and nonchecking
participation, and geography. This is true of the AHAUS (now USA Hockey) and the CAHA. These organizations have
Senior groupings (older 30 years of age and younger than 30 years of age, checking and nonchecking) and Junior
groupings (19 years of age and younger). The latter include multiple groupings for boys by age: Midget (15 to 17 years),
Bantam (13 to 15), Pee Wee (11 to 13), Squirt (9 to 11), Mite (7 to 9), and Minimites (5 to 7). Girls have fewer groupings
(Senior, 19 and under, 15 and under, and 12 and under), and there is a Women's group; neither the women's nor the
girls' groups have checking. In Canada, the smallest participants are designated Atoms (equivalent to the Minimites and
Mites), and they have no checking. There are numerous regional affiliate organizations, industrial leagues, and college
and high school classifications adding to the complexities of groupings ( M. Rudolf, Director of Officials, AHAUS,
personal communication, 1991).
The divisional breakdown by age is an important procedure for avoiding catastrophic mismatches in size and weight and
for surveying injury patterns, which can be used to alter the game toward increased safety.
Among the earliest comprehensive studies of hockey injuries was that of Marchant et al. ( 34). It reviewed a 10-year
experience (1963–1973) of the British Columbia Amateur Hockey Association in the era before helmets and face masks
were used. Over the 10 years, injury rates per 1,000 participants declined from 0.874 to 0.199 for Pee Wees, from 3.64 to
0.610 for Bantams, from 4.37 to 0.784 for Midgets, and from 16.72 to 4.03 for Juniors. As might be expected in the
absence of helmets and face protectors, 70% of injuries were lacerations, dental injuries, and fractures. Concussions
were not uncommon; they were primarily a result of board and ice collisions (80% combined). Protective equipment
evaluation revealed many difficulties with quality, fit, and condition. Poor fit was particularly noted in helmets (42.2%),
mouth guards (38.2%) and skates 14.8%).
The revelation of injury formats by studies such as that of Marchant et al. ( 34) stimulated the creation of annual injury
reviews. The annual reviews began in 1975, just as helmets and face masks were introduced. The AHAUS annual
reports revealed a reduction of the injury rate from 8.9% in the 1975–1976 season to 6.5% in the 1987–1988 season.
However, the anatomic distribution of injuries had changed, with an expected reduction of injuries above the shoulders.
Unfortunately, the incidence of spinal injuries, often with paralysis, had risen to epidemic proportions, and the incidence
of ocular injuries had also risen in older players, for whom there was no mandate with respect to face protection ( 34).
There have been other excellent, comprehensive surveys of injury patterns in amateur hockey. One such study was
undertaken by Thomson (28) as a representative of the Hockey Development Center of Ontario. Using detailed
questionnaires, he gleaned injury information from 1,558 amateur teams, with details on 1,025 injuries.
The study showed an average of 2.1 injuries per team per season, which involved 11.4% of the players, and an injury
rate that was 55% greater during games than during practices. However, analysis by player division painted a more
enlightening picture ( Table 27.4).
TABLE 27.4. YEARLY INJURY RATE
Despite the apparent alarming rates for junior- and university-age players, the industrial/recreational group players had
the highest injury rates when exposure was factored into the analysis (3.6 times higher than the average).
Bruises, contusions, and muscle pulls represented about 40% of injuries; fractures represented 15%, and dislocations
and separations 13%. The most often injured body areas were the shoulder (22%); the knee (16%); and the head/face,
arm/wrist/hand, and leg (8% each). Specifically, shoulder separations and dislocations or knee sprains were the most
common entities (22%). These injuries were caused by body checks (26%), collisions (16%), hitting the boards (12%),
being hit from behind (11%), and sticks (11%).
Returning to the point, it was clear that the described patterns are to some extent a function of the level of the player. Of
the factors considered (e.g., dislocation/separation of the shoulder), 9 of 22 were of value in discriminating levels of play.
By way of example, the Atoms class of play had a negative correlation with shoulder dislocation, whereas Junior class
had a positive correlation. Both groups had positive correlations for equipment failure. Further development of such
analyses may result in level-specific reductions in injuries.
Overall, Thomson's analysis pointed the hockey world toward prevention. It showed that ice quality and officials played
no significant role in injury predilection when the current rules are used. Being hit from behind caused 11% of injuries
despite the illegality (as of a 1985 ruling) of such actions. The boards accounted for 12% of injuries, raising the issue of
board alteration discussed later under spinal fractures. Body checks accounted most for injuries produced by collision
(26%), and injury rates were substantially higher for checking versus nonchecking teams. Of the more than 50
concussions, 84% were caused by checking, being hit from behind, and other collisions. About 30% were attributed to
helmet failure (despite the use of helmets approved by the Canadian Standards Association [CSA]). Equipment failure
was implicated in 20% of all injuries, primarily because of poor quality of manufacture or design). In-depth research of
this type on equipment must be continued.
The cry for prevention, particularly with regard to youth hockey, was trumpeted throughout the 1980s and 1990s. A study
by Stuart et al. (35), was published in 1995, at which time almost 20,000 USA Hockey youths were registered in leagues.
This prospective study was constructed to discover the literal impact of checking on injuries in youth hockey. This
single-season study, encompassing Bantam, Pee Wee, and Squirt players, revealed the injury rate to be highest among
Bantams. This group demonstrated the greatest variation in weight and height among those studied. Nevertheless, any
adverse influence clearly attributable to checking in these groups was subtle at best. The authors concluded that hasty
rule changes to stop checking remain unsubstantiated. Roberts et al. ( 36) reported in 1999 that for tournament youth ice
hockey, body checking for boys was introduced at the Pee Wee level. Brust et al. ( 37) had recommended the elimination
of youth violence and body checking and the promulgation of rule enforcement and good sportsmanship. Roberts et al.
(36) studied the influence of violent contact on the Junior Gold players of Minnesota (1996). Junior Gold is equivalent to
high school club level but is under the sponsorship of USA Hockey. In a “fair play” tournament concept, competing teams
have points added for remaining beneath a predesignated limit of team penalties on a per-game basis. In this study, the
quantities of injuries and penalties levied during the regular season were compared with those noted during the “fair play”
competition. In the tournament period, the injuries were roughly 20% of those in regular play, and the penalties were
barely more than 50% of those recorded in nontournament play. The obvious conclusion is that many injuries are
preventable and that incentives and rule changes can influence the ravages and medical costs attributable to youth
hockey.
Surgical Consequences of Hockey in the National Hockey League
A sport with as much contact, violence, and ballistic movement as is seen in ice hockey is bound to produce injuries
requiring more than conservative treatment. In a survey of NHL players, 80 (38%) of 213 respondents had undergone
surgery for injuries sustained subsequent to joining the NHL ( 38). Among players who had been in the league for less
than 5 years, 20% had required surgery; this incidence rose to 60% for 6 to 10 years and 76% for 10 and 17 years of
NHL play.
Psychological Considerations in Aggression and Injury
The introduction of protective equipment has been a blessing with respect to head and face injuries. The helmet and
facemask, however, have been implicated in the creation of additional violence within the game of ice hockey. Players
wearing this gear feel confident and invincible and charge with abandon, having no respect for the possibility that their
opponent, armed with similar protection, can be seriously hurt by high sticks, slashes, or cross-checks ( 39).
Nevertheless, this attitude must be one that is cultivated, for the same violence that marks North American hockey is not
so much a part of the European game, where the same type of protective gear is available and worn. Parayre ( 39)
indicated that many “Old Guard” coaches, mentors, and television sports commentators wean young players on phrases
that die hard, such as “Take him out of the play,” “Protect the goalie at all costs,” and “Don't let them intimidate you.”
In the spirit of these teachings, an aggressive attitude, disrespectful of injury, replaces propriety. According to Walsh
(40), the American College Hockey Coaches Association rendered a unanimous opinion at its 1988 annual meeting that
the use of the full face protector has promoted excessive violence in the sport. Walsh claimed, “There is a lack of respect
by the player for himself as well as his opponent. It is human nature . . . to consider himself as a battering ram.” As
indicated earlier, however, we believe that this attitude is culture and training dependent. The learning of aggression is
begun at a very tender age.
In the study of Pee Wee players, comparing participation with and without body checking, Regnier et al. ( 41) reported
that “hostile penalties” (such as for charging and cross-checking) were more numerous when checking was permitted
(7.7 penalties per game) than when checking was not permitted (4.8 penalties per game). Penalties for high sticking were
twice as frequent in the presence of checking. A comparison of checking and nonchecking Pee Wee leagues in Quebec
(1985–1986) revealed a fracture rate 12 times greater in the former group. Body checking caused 88% of fractures, the
majority of which (58%) involved the clavicle. Body checking was again banned in Quebec for Pee Wees in 1987.
Gerberich (42) studied high school players in Minnesota, asking each to prioritize their reasons for playing. When
“ridding of tension” was selected as either the first or second choice, the player ran a four times greater risk of
concussion (42). In a study of high school ice hockey players, Smith et al. ( 43) asserted that those with high quantities of
ice time were more likely to be injured, and, perhaps of greater interest, those with a pattern of low vigor or high fatigue,
as demonstrated by the Incredibly Short Profile of Mood States (ISPOMS), had a significantly increased incidence of
injury. Fatigue or low vigor was perceived to be a manifestation of depression or high life stress or both.
Reynan et al. (25) raised the issue as to whether the additions of head protection and faceguards have contributed to the
incidence of spinal cord injury. Gerberich ( 42) interviewed high school players and found that 89% thought they were less
apt to be injured if wearing a face protector. Sixty-four percent acknowledged a greater likelihood that they would engage
in contact, and a similar percentage thought masks gave them more protection. In 1988, the American College Hockey
Coaches Association demonstrated a unanimous accord that full face protectors promote violent play ( 25). Reynan et al.
(25) suggested that only since the combined use of helmets and face shields has there been a notable increase in
cervical spine injury rates. On the other hand, and contemporaneously, LaPrade et al. ( 44), prospectively interpreting
injury-exposure ratios of Division I NCAA teams, found no trend toward increased head and neck injuries when helmets
and face protectors were worn.
An interesting psychosocial statement about hockey was made by the study of Frank and Gilovich ( 45). Based on the
socially accepted premise that black is bad (e.g., “blacklist” or “blackball”), these researchers undertook to study the
potential influence of black uniforms in the NHL. They discovered a strong correlation between blackness of uniforms and
the number of team penalties. Teams that switched to black uniforms from other colors began to register more penalties.
Assuming a validity to the trends demonstrated, it remains unanswered whether black uniforms instill aggression into
players, referees call more penalties on black-uniformed players, or management personnel who select black uniforms
have an aggressive attitude that is passed on to team members.
Widmeyer and Birch ( 46) studied hockey performance and its relation to “aggressive penalties” (those involving stick or
body contact) in the NHL over four seasons spanning 15 years. It was discovered that a significant correlation existed
between points accumulated per game and aggressive penalties incurred during the first period of play. The study
implied (without statistical significance) that aggression was often employed as a reaction to losing. Widmeyer and Birch
cited Cullen and Cullen's 1975 finding that winning college hockey teams were more aggressive both when the score was
close and when it was very disparate.
It is evident that there are multiple psychosocial elements of aggression affiliated with the game of hockey. To reduce
serious injuries, these elements must be altered in the formative years, or the game itself must be dramatically altered.
Role of Fitness: Relation to Performance and Injury
Muscular Fitness
Ice hockey is practiced with a skating format known as “power skating” (as opposed to “speed” or “figure” skating). The
long, flat blade of the speed skater is ill-suited to maneuverability, and the short, front-ratcheted blade of figure skating is
designed for grace and maneuverability. The hockey blade evolved as a compromise between these functions, offering
both speed and maneuverability.
Muscle test profiling of sports and teams generally characterizes strength or work performed by an isolated joint or the
ratios of muscles controlling that joint. Recognizing the combined importance of explosive knee extension and hip flexion,
extension, abduction, and adduction, Minkoff ( 47) sought to pursue ratios not previously considered for correlations to
performance. The results of these correlations are reviewed in Table 27.5.
TABLE 27.5. CORRELATIONS OF SKATING ATTRIBUTES TO MUSCLE TESTING
Minkoff noted the cinematographic work by Holt in 1977, which revealed that faster skaters had a wider left leg stride and
a longer right leg stride. Also, the early training of many skaters involves primarily counterclockwise skating ( 47). Agre et
al. (48) found none of the right-to-left lower-extremity strength differentials reported by Minkoff ( 47). However, Minkoff
found no obvious differentials of significance when evaluating isokinetic strength about a given joint, only when working
with strength ratios of one joint to another.
With respect to standard ratios about a given joint, Minkoff ( 47) found that the hamstring:quadriceps ratios of hockey
players were similar to those of other athletes (about 0.6). However, the ratio of knee extension to hip flexion
distinguishes hockey players and accents again the importance of the hip in this sport. For almost two dozen American
League baseball players, this ratio averaged 0.62, but for the professional hockey players it averaged 0.79, and for
hockey All-Stars the average was 0.89 (47).
Cardiovascular Fitness
The subject of fatigue is important in hockey, a game that is intermittently continuous and in which much energy is
expended in leverage, checking, and inefficiency of style in addition to that expended by skating alone. Fatigued players
commit more errors, predisposing to injury, and defensemen in particular “chase the play,” committing more penalties
(hooking and tripping) in an effort to thwart the puck carrier.
In his study of professional hockey players, Minkoff ( 47) concluded that their mVo amax levels were lower than those of
endurance athletes, and that they correlated poorly with performance success. He further concluded that the mVo amax
breakpoint of these players was a more significant evaluator of their function.
Sim et al. (49), drawing on the studies of several workers, disclosed that the mean oxygen consumption of ice hockey
players was 55%, which is 10% to 15% lower than that reported for endurance athletes, but that their anaerobic capacity
was increased to fairly high levels (although less than in sprinters or swimmers).
Citing Green et al. (23), Sim et al. (49) indicated that forwards play about 20 minutes per game. The time is divisible into
14 to 21 shifts, each with just under 40 seconds of continuous playing time at an average speed of 8.5 mph.
Montgomery (8) phrased these demands of the game somewhat differently. He indicated that hockey shifts last between
30 and 80 seconds with 4 to 5 minutes of intershift rest. The obvious implication of these figures is that hockey is neither
a wholly aerobic nor a wholly anaerobic sport. “Players must enter into a season conditioned rather than playing into
shape,” is a commonly practiced myth; once the season is under way, strengthening, cardiovascular training, and skills
development activities must not be abandoned. There is evidence that shorter shifts would reduce lactate buildup and
allow for restoration of high-energy phosphate bonds with preservation of valued glycogen reserves ( 8). Glycogen is
often depleted significantly after a game. Back-to-back games can lead to severe energy problems, especially in the
absence of nutritional counseling ( 8).
Cox et al. (50) indicated that today's elite hockey players are getting bigger and manifest better levels of physiologic
fitness. Finely trained aerobic and anaerobic energy pathways are necessary, the latter possibly dependent on the
former. Since the work of Montgomery (8), there has been little additional information contributed about the physiology of
ice hockey. Nevertheless, there is some to review. Not only have the players become bigger, but also their grip strength
and Vo2max were found to have progressively increased, with a leptokurtic distribution, over a decade of study ending in
1991 (50). In view of the relatively short shifts, during which are accomplished large quantities of work at high speeds,
anaerobic ability has become a greater focus. Lactate accumulation clearance programs have become quite common
among elite ice hockey players. Cycling for at least 20 minutes at 130 S after games is a prototypic program. The
benefits are probable, but unproven. Dehydration would doubtless eliminate any possible benefit from such a program.
Dehydration of more than 2% inhibits temperature regulation and impairs performance physiology. It has become a
bigger problem since helmets and face guards, which further challenge heat dissipation, have become the rule rather
than the exception.
Visual Fitness
In his study of a championship NHL team, Minkoff ( 47) found several tests of visual function that correlated significantly
with success in hockey. Composites of eye test scores related strongly to shooting accuracy, as did tests of visual span.
Visual span correlated strongly to face-off success. Only three players of those studied scored the maximum on both
tests; two of them were goalies, the third was the team's leading scorer. Concurrent testing of a professional baseball
team (a slower sport visually) revealed no maximum scores among those tested. Furthermore, maximum stereoscopic
scores were found among all past and present hockey All-Star players ( 47).
Hockey Penalties
In a large epidemiologic study of all levels of amateur hockey in Canada, Thomson ( 28) determined that 17% of injuries
were associated with penalties. This was in accord with Sutherland's report, cited by Montgomery ( 8), in which 25% of
injuries were associated with penalties.
The Hockey Rink and Collision Injuries
Peculiarities of the hockey rink may ultimately contribute to injuries. Contrary to general expectation, there are limited
standards for design and construction of professional rinks. In North America, rinks need only be at least 60 feet (18 m)
wide and 160 feet (49 m) long (2). The goal cage must be at least 10 feet (3 m) away from the end of the backboards
(see Fig. 27.18). Depending on the width of this passageway, the frenzy of activity and the numerous collisions that occur
behind the goal increase the potential for injury ( 8) (Table 27.6).
TABLE 27.6. CAUSES OF INJURY IN ICE HOCKEY
Moore noted that scrambles behind the net resulted in 7% of injuries ( 8). Montgomery referred to a report by Sutherland
that activity around the net (not just in front of it) accounted for 42% of the injuries in his study ( 8). The material and yield
characteristics of the boards also have potential for modifying the character and severity of injuries resulting from
collisions. The height of the boards has not been designed by scientific intent to reduce injuries ( Fig. 27.22). In many
rinks today, there are Plexiglas extensions of the boards that ascend several feet above them. These extensions permit
abutment of the face or head into their rigid panels by boarding and cross-checking maneuvers ( Fig. 27.23 and Fig.
27.24).
FIGURE 27.22. The ledge of the side boards–glass interface is an area of potential serious injury.
FIGURE 27.23. Plexiglas abruptly ends at the penalty box and players' bench areas, leaving an area of potential serious
injury (viewed from players' bench).
FIGURE 27.24. Injury can occur to a player who is checked from behind into the rigid Plexiglas panels.
PROTECTIVE EQUIPMENT IN HOCKEY
Hockey is a sport in which injuries are sustained by virtually every body part. At the inception of the sport, equipment was
scant and the thrust for development of protective wear did not accelerate until the 1970s, after the initial epidemiologic
studies began to elucidate vulnerabilities and injuries. The manufacturers and organizations that test and approve
equipment around the world have responded by producing progressively better equipment that offers not only greater
protection, but, in many instances, better function ( Fig. 27.25). Other factors of importance include fit, weight, ventilation,
motion, durability, unimpeded vision and hearing, and economic reality ( 51,52). Hockey equipment is expensive, and
products of varying quality are available. Particularly for helmets and face gear, fit is critical. No less critical is the
condition of the equipment, including the effects of aging, perspiration, and repeated percussion. Failure to replace
outgrown or poorly maintained equipment risks a trade-off between parsimony or imprudence and a serious risk of injury.
The maximum protective equipment available to skaters and goalies can be seen in Fig. 27.26. Areas of incomplete
protection can be seen in Fig. 27.27.
FIGURE 27.25. Graphic representative interaction of standards associations (ISO, CEN, SSA, ASTM, HECC, CSA) and
hockey associations (CAHA, NHL, AHAUS, NFHS, NCAA, USOC) for equipment certification. (Note that the NHL
presently does not directly interact with the standards and equipment certification organizations.) AHAUS, Amateur
Hockey Association of the United States (now USA Hockey); ASTM, Association of Standardization and Testing of
Materials; CAHA, Canadian Amateur Hockey Association; CEN, European Standards Organization; CSA, Canadian
Standards Association; ETL, Equipment Testing Laboratories (Independent) (USA); HECC, Hockey Equipment
Certification Council (USA); ISO, International Standards Organization; NCAA, National Collegiate Athletic Association;
NFHS, National Federation of High Schools; NHL, National Hockey League; SSA, Swedish Standards Association;
USOC, United States Olympic Committee.
FIGURE 27.26. Maximum protective equipment for (A) skaters and (B) goal tenders. Note the junction of the shoulder
pads, elbow pads, and gloves in the upper body. Pants, shin pads, and skates are confluent. (Courtesy of Cooper
Canada, Ltd. Toronto, Canada.)
FIGURE 27.27. A: Incomplete protection of the lateral arm. B: Incomplete protection of the dorsal forearm. C: Incomplete
protection on the volar surface of the elbow and forearm.
Helmet
An awareness of severe head injuries received in hockey in Sweden in the 1950s prompted the Swedish Hockey
Association to conduct surveys that led ultimately to compulsory use of helmets in 1963 ( 53). The early helmets were
flimsy in construction and deficient in protection. In the late 1950s, for example, leather helmets lined with felt were in
vogue. These were followed by compression-molded plastic and leather helmets and then by injection-molded plastic
(54) (Fig. 27.28).
FIGURE 27.28. Early helmets: Sears sports helmet circa 1890 (upper left); leather helmets circa 1940s with minimal
protection (upper right and middle row); and compression-molded plastic helmet (lower left). (Courtesy of Dave Beaune,
Toronto, Canada.)
In 1965, the CAHA mandated the use of helmets for all juvenile and younger players. In 1969, CAHA requested the CSA
to establish a standard for helmets ( 55).
In 1973, responding to outcries about head injuries, the CSA published a standard for the manufacture of hockey helmets
(56). In the 1970s, modern plastic helmets with suspension liners met the early CSA standards ( 54). Although there was
general accord that the CSA standard was a safety improvement over preexisting helmet designs, there were questions
about its merits. Many design factors had to be considered, including peak forces, peak acceleration, and kinetic energy
absorbed. Organizations responsible for testing, such as the CSA and National Operating Committee on Standards for
Athletic Equipment, perform testing using different methods ( 56). Countries other than Canada have their own testing
protocols and standards. Bishop et al. ( 56) explained the two basic components needed for a “safe” helmet: first, a firm
outer shell is needed to diffuse forces from the site of impact; second, an energy-absorbing liner is required to decelerate
impact forces to a tolerable level.
On the issue of impact testing for helmets, Johnson ( 57) stated that the Gadd Severity Index, which is based on the
Wayne State Curve (gravitation acceleration as a function of time), is among the most popular methods of evaluating
injury hazard. This index, as well as other popular ones (e.g., the head injury criterion), address only frontal blows. There
are no corresponding indices for rotational acceleration. Johnson, in Sweden, and investigators in North America used
head forms with triaxial accelerators to record impact phenomena, which they then related to the indices to ascertain
danger levels. Johnson contended that dropping the head form onto an anvil ( Fig. 27.29) was a more physiologically
realistic test format than dropping an object onto the head form ( 57). The ASTM Performance Specification for Ice
Hockey Helmets (specification F 1045-87) in the United States also uses an evaluation in which head forms are dropped
(58). Instead of the wooden head form used by Johnson, Morehouse (58) selected a magnesium alloy (Z-90) for its
reliability. This points up the complexity of considerations entering into the evaluation of safety levels of hockey products
worldwide today.
FIGURE 27.29. Helmet impact test apparatus of drop-head type. From Dixon, ISO Draft, 1991.
Morehouse (58) explained that Gadd derived a maximum safe level of 1,500 units (effective acceleration divided by time),
beyond which there is a risk of concussion. The ASTM standard deals with “G max” rather than the Gadd Severity Index.
However, Morehouse cited the work of Calvano and Berge that established a correlation between the two: a Gadd
Severity Index of 1,500 corresponds to a G max of 225. The ASTM selected a G max of 275 for its helmet standard ( 58).
Helmets must comply with this protection value by being tested in multiple sizes, multiple times, with impacts at each of
six designated sites on the helmet. Chin straps are also tested by loading them with suspensory weights. They must not
break before adding 50 N and must release before 550 N; elongation must not exceed 25 M ( 58) (Fig. 27.30).
FIGURE 27.30. Chin strap loading apparatus with suspension weights. From Dixon, ISO Draft, 1991.
Hoerner (52) made the point that hockey helmets must be able to absorb kinetic energies ranging from a player's high
mass (weight) and low velocity (speed) to the puck's low mass and high velocity without compromising defense at either
of these extremes or at levels between the extremes. This principle is partly exemplified by motorcycle crash helmets.
These helmets are lined with polystyrene beads within a Styrofoam pad to absorb the energy of high-mass, high-speed
collisions. However, for lower-energy impacts, such as those occurring in hockey, Jones reported an increased incidence
and degree of concussion with the use of this type of helmet ( 59).
Drafts for an international standard for headgear under International Standards Organization (ISO) supervision and with
the cooperative efforts of standards organizations from various nations ( 57,60,61) are underway (Fig. 27.31). Unlike the
head forms of Johnson's studies (wooden) and of Morehouse's ASTM studies (magnesium alloy), the head form for the
international standard is made of a rubberized epoxy. This standard, unlike that of the ASTM, calls for the use of the
Gadd Severity Index limit (1,500). The gravity-drop form of testing has been adopted. Chin strap testing has a format
similar to that described earlier ( 61).
FIGURE 27.31. Areas of concern and dimensions for helmet design. (From Dixon, ISO Draft, 1991).
Facemask
Puck speed can exceed 100 mph and impact forces of up to 1,200 pounds can be generated ( 49), so the need for face
protection in hockey is apparent. Nevertheless, almost 70 years of professional hockey had been played before an NHL
goalie sought to protect himself by using a molded face plate (see Fig. 27.28). These face plates were better than no
protection, but they allowed facial contact when hard shots were fired. Some of the early polycarbonate face plate models
had large windows for the eyes. Sticks or pucks could enter these windows even when wire-mesh face protectors were
used. In Sweden, some standards for faceguards were finally approved in 1972. New, more elaborate standards awaited
the creation of the Swedish Hockey Association in 1978 ( 53). In North America, there were no standards for facemasks
before 1977; a preliminary standard was established in that year, and modifications have been made several times since
(55,62).
ISO drafts are currently under consideration for ISO-approved face masks ( Fig. 27.32) (62). See Table 27.7 for types of
facemasks and description of function. Performance tests for facemasks must ascertain the following: areas of facial
coverage, penetrability (through orifices), impact tolerance, and preservation of vision (through a complicated battery of
visual tests) ( 55,57,62).
TABLE 27.7. TYPES AND FUNCTIONS OF FACE MASKS
Half-Face Visor
In 1988, the American College Hockey Coaches Association voted unanimously in favor of half-shields rather than
full-face masks, claiming that the latter serve as an instigation to increased violence and result in more dangerous
injuries (40). Walsh (40) pointed out that half-shields are used in European hockey and in Canadian college and major
junior hockey. Smith and Bishop ( 63) tested visors as well as full-face protectors. They found that polycarbonate visors
allowed facial contact at puck impact velocities of 22.4 m per second (50 mph) or greater. The findings of Roy and Dore,
cited by Smith and Bishop (63), established mean and expected maximum puck velocities for various age levels ( Table
27.8). It is evident that the visor permits facial contact at the expected maximum velocity achieved by a 13-year-old
player, and certainly at the mean velocity achieved by a 14-year-old.
TABLE 27.8. SHOOTING SPEEDS OF ICE HOCKEY PLAYERS

Although visors may not be wholly protective of the eyes and face for all consequences of impact, they are at least of
value in reducing the incidence of facial lacerations ( Fig. 27.33). Reporting on observations of elite Swedish players,
Lorentzon et al. (27) noted that those who used a visor had 52% fewer lacerations about the face. The use of visors is
currently increasing among collegiate players and among many industrial and recreational league players. Furthermore,
thus far no player wearing a visor has suffered a blinding injury ( 64).
FIGURE 27.33. Areas of coverage for protective visors. From Dixon, ISO Draft, 1991.
Neck Protectors
The use of neck protectors has become increasingly popular. In the past, neck protectors were used fairly routinely by
goalies; more recently, they have been used by forwards and defensemen to prevent skate cuts around the neck (see
later discussion) (Fig. 27.34). A movement to create standards for neck protectors has been started. Standards for throat
protectors were set by the Swedish Hockey Association in 1987 ( 53). The area to be protected is demonstrated in Figure
27.33.
FIGURE 27.34. Neck protector recommended to reduce cut injuries, not presently designed to prevent impact injuries.
Skates
By the beginning of the 20th century, metal had replaced wood and the skate blade was attached permanently to the boot
(see Fig. 27.4A, Fig. 27.4B). The solid metal blades and runner were heavy and clumsy. Within a few decades, the metal
runners and blades had been streamlined for increased skating speed and made taller so that the puck would be less
likely to contuse the foot within the boots. By the mid-20th century, the blade had become tubular (hollow), allowing
greater speed by virtue of its reduced weight (see Fig. 27.4C). Later, tubular models were also canted for improved
acceleration. These skates had a special liability, in that the exposed back end of the blade acted as a weapon,
especially after repeated sharpenings of the blade. By 1960, bumpers had been designed to cap the pointed blade end
so as to avoid some of the fatalities known to have occurred ( 65). Vegso and Lehman (32) were the first to report on
deaths caused by neck slashes from skate blades since the single fatality reported in 1955 by Demp. Modifications by the
ASTM had improved skate blade safety in the 1980s, but fatal lacerations of the neck remained a threat because of the
high tangential velocities, and the consequent kinetic energy of almost 200 J, that could be achieved by the skate and
blade. In 1987, Vegso and Lehman (32) described three incidents, two of which were fatal. The victims collectively
sustained lacerations of the external carotid artery, the subclavian and jugular veins, the apex of the pleura, the strap
muscles, the trachea, and the thyroid. Other than in amateur hockey, neck protectors are uncommonly used. Today,
skates have either a safety guard (when the skate blade is open in the back) or a heel guard (when the skate is totally
closed in the back) (see Fig. 27.4D).
By the early 1970s, the all-metal blades and runners were giving way to plastic assemblies into which blades were fixed
(see Fig. 27.4E). These models were even lighter than those before them, fostering another escalation in skating
velocity. Unfortunately, many of the assemblages broke, representing a measure of danger. The ASTM was requested to
create guidelines for quality and safety. They did, and, in 1986, the new guidelines included a mandate that the plastic
portion of the blade assembly must extend 3 mm beyond the front and rear of the runner for safety.
With respect to skates, there are two basic concerns. The first is their ability to protect the foot from lacerations and
impacts. This has been accomplished to some extent by elevating the boot adequately above the ice and by the creation
of molded skate boots with various guards (e.g., for the Achilles tendon). The second basic concern is the achievement
of comfort and support while allowing an adequate range of motion of the ankle for maximum performance. Hoshizaki et
al. (18) evaluated motion and stability of the ankle for several power-skating activities by testing a variety of skates and
concluded that the type of skate used could, in fact, limit ankle and hindfoot range of motion, thereby reducing
acceleration, although the molded skates did not substantially restrict motion in these areas. The fit of the skate is,
naturally, of critical importance.
Sticks
From forerunners made exclusively of wood, hockey sticks have evolved into eclectic instruments made of wood,
Fiberglas, aluminum, and plastic in various combinations. Certain dimensions of the sticks have been standardized, but
certainly not all (see Fig. 27.1). Many players wrap tape around the blades of their sticks, claiming it assists their
effectiveness. No studies have been done to ascertain the merits of taping.
Sticks have figured significantly in the production of injuries. Sticks represent a danger when they are used above the
shoulder (high sticking), for slashing, for tripping, or for cross-checking. Furthermore, breakage of the stick (usually at the
angle of the shaft and blade) creates a danger because the loose, jagged segment may become a missile if the break
occurs during the act of shooting. Players must immediately drop a broken stick so that the handle cannot act as a
pointed lance.
Other Equipment
Because much of the early equipment, such as pants and gloves, was adapted from lacrosse and cricket, their specific
protective value in hockey was deficient. The evolution of hockey equipment can be seen in Figure 27.35, Figure 27.36,
Figure 27.37, Figure 27.38, Figure 27.39, Figure 27.40, Figure 27.41, Figure 27.42 and Figure 27.43. The evolution of
modern hip, pelvis, and thigh protection, as exemplified by Cooperalls (Cooper Canada, Ontario, Canada), took several
decades (54) (see Fig. 27.43).
FIGURE 27.35. Elbow pads from the 1920s (bottom) made of horse or deer hair rolled and sewn into the leather; 1940s
elbow pads (middle) with protective olecranon cap; and 1980s elbow pads (top) with a short forearm protector made of
plastic and foam. (Courtesy of Chico Resch.)
FIGURE 27.36. Hockey gloves in evolution. The 1930s model (right) had deer hair and dried sugar cane sewn into the
leather. Palms were sewn flat onto the glove. The 1940s glove (middle) was made with plastic forearm protector. The
palm was better contoured to hold the stick. The modern glove (left) is made of lightweight, dense foam. (Courtesy of
Chico Resch.)
FIGURE 27.37. The 1990s hockey glove with shortened forearm protection. It should be used in conjunction with an
elbow pad that has an extended forearm piece. (Courtesy of Cooper Canada, Toronto, Canada.)
FIGURE 27.38. Forearm protectors circa early 1900s made of metal riveted to a nonprotective glove. (Courtesy of Philip
Pritchard, Hockey Hall of Fame, Toronto, Canada.)
FIGURE 27.39. Shoulder pads circa 1920 (left) and 1940 (right) made of leather sewn onto melton. Shoulder pads circa
1970 (top), made of foam and plastic, offered more protection. (Courtesy of Chico Resch.)
FIGURE 27.40. A: Modern shoulder pads made of lightweight plastic and foam providing adequate shoulder and chest
protection. Posteriorly, the shoulder pad should be continuous with the pant. B: Modern shoulder pads made of thin foam
and plastic with adequate coverage but inadequate protection. (Courtesy of Cooper Canada, Toronto, Canada.)
FIGURE 27.41. Cricket shin guards circa 1920 used for ice hockey. (Courtesy of Dave Beaune, Toronto, Canada.)
FIGURE 27.42. Shin pads circa 1930s (left) were made for hockey with leather sewn onto melton. Dried sugar cane was
used as struts for tibial protection. Modern shin pads (right) provide increased protection of the patellar tendon, patella,
peroneal nerve area, and calf. (Courtesy of Chico Resch.)
FIGURE 27.43. A: Pants circa 1930s with dried sugar cane struts sewn into pants. (Courtesy of Dave Beaune, Toronto,
Canada.) B: Modern pants with maximum protection. (Cooper Canada, Ltd., Toronto, Canada.)
Today protective material is tested for resilience by automatic puck-delivery systems with impacts recorded by special
video systems (54). Such sophisticated testing methods are expected to increase the protective nature of equipment so
as to avoid catastrophic injuries such as commotio cordis. (Fig. 27.44). Though this injury is uncommon, Kaplan et al. (66)
reported on two deaths from commotio cordis that came to be evaluated by the medical examiner. Both players were 15
years of age. In both cases, the players were wearing a chest protector, and in both there was no evident damage to the
heart on autopsy. The protector worn by each of these players had a thinner area within it, composed of 0.7-cm
closed-cell plastic foam. The fatal puck had hit this thinner area. The cause of ventricular arrhythmia and/or cardiac
arrest induced by puck impact to the chest is not precisely known. It appears that blows sustained to either the anterior or
lateral aspects of the precordial region are capable of causing death. Implicit in the findings is the question of whether an
alteration of material or design might be preventive ( 66).
FIGURE 27.44. Newspaper reports of the death of a 15-year-old boy who sustained a traumatic cardiac arrest as the
result of a puck impact to the chest. Reports such as these underscore the need for the regulation of equipment.
INJURIES
Several injury categories are of particular concern, including head and brain injuries, spinal injuries (especially cervical
spine injuries), ocular injuries, and groin strains (by virtue of their frequency, not their severity).
Head and Face
In the 1989–1990 NCAA ice hockey season, only about 6% of injuries involved the head, face, eyes, ears, or nose; most
of these were concussions. Face guards, almost evenly divided between plastic and metal, apparently served a great
protective function ( 24).
Lacerations about the head and face are common. Studies have clearly demonstrated that face shields prevent many of
them (27).
With the exception of lacerations, the most common serious traumatic head injuries are concussions ( 67). In accordance
with criteria listed by Sim et al. ( 68), any evident loss of consciousness exceeding 10 seconds indicates a grade IV
concussion and implies brain damage. Any player who is unconscious from a head injury should be presumed to have a
cervical spine injury (68).
Nagobads' unpublished investigations from the early 1970s, cited by Sim et al. ( 49), were the first formal studies of head
injuries in ice hockey. Thirty percent of 97 injuries caused primarily by sticks, pucks, and collisions (in that order) were
concussions or fractures, even though 87 of the injured players were wearing helmets.
Bull (67) described numerous fatal and near-fatal catastrophic injuries in nonhelmeted players of yesteryear caused by
impacts with ice, sticks, and boards that resulted in skull fractures and/or epidural and subdural hemorrhages. According
to Bull (67), fractures and head injuries resulting in sudden or near-sudden death have been curtailed in the era of the
helmet (mandated even in the NHL for all players entering the League since 1980). He also cautioned, however, that
even helmeted players are subject to these injuries, particularly when poorly designed helmets are worn. Even the most
effective helmet is of limited value if it is improperly fitted or is cross-matched with a face shield from a different
manufacturer.
The attending physician must have a view of play that allows observation of injuries and their mechanisms, easy access
to the ice to facilitate emergency treatment, and a full array of the medical equipment needed to carry out treatment.
Logistic issues, such as the availability of ambulances, hospitals, and special consultants, should be settled at the outset
of the season. In instances of choking or apnea, it must be remembered that false teeth or even gum may have been
dislodged from the mouth into the trachea (67). In one instance of loss of consciousness with apnea and cyanosis
experienced by one of us, a video replay revealed that the mechanism was not a head injury but a collision that drove the
handle of the player's own stick into his solar plexus. In another personal experience, a player hit the boards with his face
and chest, lost consciousness for a moment, and became dyspneic. Absent breath sounds presaged x-ray findings of a
complete unilateral pneumothorax (in conjunction with a clinical concussion).
Head injuries are a frightening component of ice hockey. Helmets offer limited protection. Fortunately, the majority of
head injuries are not terribly serious. The traumatic brain injury, known as the concussion, is the most commonly
observed variety. It is an injury that results in an alteration of cerebral function consequent to a direct or rotational force
(69). It may be manifested by lightheadedness, vertigo, cognitive or memory dysfunction, tinnitus, blurred vision,
difficulties in concentrating, amnesia, headache, nausea, vomiting, photophobia, or disturbance of balance ( 69). Although
the list is long, the presence or persistence of any of these findings is a reason to preclude participation.
Tenger and Lorentzon (70) studied concussion among Swedish elite ice hockey players by both prospective and
retrospective methods. Twenty percent of all players had had at least one concussion during a career in an era in which
all players wore helmets and face protectors. It was concluded that the chance of a player's sustaining a concussion in a
given year was 5%. In the 1995–1996 NHL season, the concussion injury rate was between 1.15 and 1.56 per 1,000
exposures.
To date, there remains an incomplete understanding of the pathobiology of cerebral concussion. What is known is that
head injury produces an imbalance of the ratio between cerebral cell fuel utilization and the rate of cerebral blood flow.
There exists a type of double jeopardy, whereby the demand for glucose is increased while, concurrently, the cerebral
blood flow is reduced. This occurrence heralds a cascade of metabolic disorders that leave brain cells vulnerable to
damage or death. This vulnerability can produce the formidable second impact syndrome, to which teenagers are
particularly susceptible. Avoidance of catastrophic consequences, such as the second impact syndrome, depends on
avoidance of head injury susceptibility (i.e., participation) for the duration of the metabolic crisis. This duration has not
been delineated accurately. Positron emission tomography studies have revealed that metabolic dysfunction persists
after head injuries in humans from a few weeks to more than 1 year (69).
The team physicians and trainers are vital to the welfare of the players because they are charged with the detection of
those signs and symptoms that determine whether a player can safely continue participating or must be removed from
play for evaluation and observation. To most effectively implement their caretaker roles, members of the medical team
must frequently update their protocol for the handling of head-injured players. Each must be trained in the knowledge and
mechanics of his or her responsibilities in order to be properly prepared for a crisis. All necessary support staff and
equipment must be kept instantly available, and the latter must be maintained in good order. An emergency plan, by
which a player may be promptly evacuated to a nearby hospital, must remain extant throughout games and practices.
It is beyond the scope of this chapter to detail all considerations in the evaluation of a head-injured player. However,
some salient points are reviewed. Airway, respiration, and pulse are the obvious priorities: if they are compromised, the
neck must be stabilized before any cardiopulmonary resuscitation is administered. In particular, this is an issue in the
unconscious player in whom a cervical injury must be presumed.
An attribute of ice hockey is the common presence of face guards (visors or cages), which are attached to the helmets
and are mandated in the NCAA but optional in the NHL. Presently, the face guards are secured to the helmets by screws,
whereas formerly the attachment was by clips. There is neither an existing protocol nor any instrument suggested to
facilitate removal of the half-visor, should it obstruct access to the oronasopharynx. Removal of the helmet is forbidden
when a cervical spine injury cannot be ruled out. Horodyski et al. ( 71) demonstrated a significant alteration of cervical
alignment when a helmet is removed from a supine player wearing shoulder pads. LaPrade et al. ( 44) demonstrated that
helmet removal in the supine player wearing shoulder pads resulted in a significant degree of lordosis in the midcervical
spine, the segment with the greatest predilection for injury.
Fortunately, half-visors are unlikely to obstruct access to an airway. Although the fastening screws are removable, it
would take too much time to remove them in an emergency. Emergency Medical Services, often available in the arena,
maintain an array of endotracheal and nasotracheal tubes. Team physicians should have large-bore (14- or 16-gauge)
needles to penetrate the tracheal cartilage, if necessary. On the other hand, full visors are clearly an obstruction to an
airway. However, simply by cutting a restraining strap, these visors can be expeditiously flipped up to expose airway
portals.
Poorly fitted and poorly secured helmets are commonly observed in ice hockey. Paradoxically, loose fitness can facilitate
a helmet's removal, with virtually no risk to the cervical spine. Sim et al. ( 68) stated that hockey helmets are less tightly
fitted than football helmets, so removing them to maintain an airway is less risky than leaving them in place. Regardless
of any such paradox, a firmly fitting helmet is the standard of safety recommended to minimize the risk of a traumatic
brain injury. Players seeking the protection ostensibly offered by a firm fit can take advantage of additional, posterior
helmet straps and sliding bilateral side panels, both of which minimize rocking and shifting of the helmet ( Fig. 27.45).
FIGURE 27.45. A: Adjustable screws for tightness of helmet; screws hold on half-visor (itech). The oropharynx may be
accessible without its removal, but there is no way to rapidly remove screws and shield. B: Attempt to improve helmet fit
posteriorly to prevent the back from sliding up.
In evaluating a head-injured player on the ice, universal standards must be invoked. It has already been stated that the
first priorities are to determine the patency of the airway and the status of the cardiovascular system. However, as
cautioned by Vegso and Lehman ( 32), the initial state of the player is not necessarily a reliable indicator of either the
pathologic diagnosis or the severity of the injury. The on-ice evaluation should include an immediate assay of facial
expression, orientation, amnesia, and, when possible, gait. An observation of a total lack of motion in the extremities may
signify a cervical spine injury. Certainly, an unconscious player should be presumed to have such an injury ( 69). Level of
consciousness is typically evaluated in accordance with the Glasgow Coma Scale, with scores higher than 11 suggesting
a good prognosis. Retrograde amnesia is usually associated with more significant injuries. Nystagmus, which is most
frequently detected by the initial observer, may be seen transiently after a rotational or shearing injury to the brainstem.
Facial paralysis may indicate the presence of a basilar skull fracture ( 69).
The majority of medical persons confronted with on-the-field decisions about head-injured players are neither
neurologists nor neurosurgeons. Hence, the complex stratifications that various organizations have created to define
grades of concussion are not practical for the orthopedic surgeon or other types of covering physicians in an emergency
field circumstance. In an attempt to simplify classification and decision making, the American Orthopedic Society of
Sports Medicine (AOSSM) sponsored an extensive multidisciplinary workshop in December, 1997 ( 69). in the simplest
terms, the decision to be made is whether to (a) rush the player to the nearest hospital with all necessary support, (b)
remove the player from the field to a quiet area for further evaluation, or (c) remove the player from the field to a quiet
area and then allow a return to play after careful evaluation.
When the player has demonstrated an ability to follow commands and a cervical injury appears to be unlikely, the player
may be assisted to a sitting position. This may help reduce the confusion and other manifestations associated with
increased intracranial pressure. Standing may be permitted if improvement is ongoing. Evaluation for upper motor neuron
disorder, sensory and motor function, and coordination must be accomplished. If the player's condition seems
satisfactory after 15 minutes, he or she should be subjected to physical rigors, such as running, sit-ups, push-ups, or
deep knee bends, that may raise intracranial pressure and thereby reincite symptoms. Reclining in a supine position, with
feet elevated, may produce the same effect. Even if the player passes all of these evaluative measures and is permitted
to return to play, he or she must be tested at regular intervals during the remainder of the competition.
The absence of gross physical findings does not rule out the presence of brain damage. Disorders of mental faculties
may be the only good clue to the presence of pathology that should preclude participation. Players with acute head
trauma typically manifest such disorders. In addition, many players have manifested postconcussion syndromes, whereby
they “just do not feel right” or experience persistent headaches, fatigue, insomnia, or other manifestations not previously
experienced by them. A family member or friend may be the only one aware of the change in the player's demeanor.
Neuropsychological testing has become a gold standard of evaluation for mental impairment resulting from concussive
injuries to the brain. The evaluation normally comprises a battery of tests. For such testing to be of maximum value in the
postinjury period, baseline tests, performed before the season or earlier, should be available for comparative analysis. In
the acute injury setting it is common to test within 24 hours after the suspected concussion, and then again after about 5
days (69). Condensed, field versions of neuropsychological testing protocols have been created. The most popular
version is the Standardized Assessment of Concussion—Sideline Evaluation of the Athlete (SAC). The SAC incorporates
measures of orientation, memory, and concentration. It can be administered on the sideline, even by a trainer. It is
printed on a pocket-sized card and has proven (but not unerringly) accuracy in the diagnosis of concussion, even if the
player appears to be asymptomatic (69).
The bottom line in attempting to simplify the rules pertaining to handling of players with a perceived traumatic brain injury
is that the presence of any symptoms on the field should ordinarily preclude a return to play. If there has been no loss of
consciousness, nor any evident signs or symptoms, after 15 minutes of observation that includes provocative physical
testing, a same-day return to play may be considered with continuing vigilance.
Face, Mouth, and Mandible
Initiation of protection against injury in hockey (as well as other sports) took place in 1969 when the F-8 Committee of
ASTM was formed to set standards for protective equipment; it antedated by 4 years the creation of the Committee of
Safety and Protective Equipment of USA Hockey. In the early 1970s, C.R. Castaldi proposed a mandatory mouth guard
rule to AHAUS, and in 1974 face protector designs were adopted as standard equipment ( 72).
Bull (67) made the important point that behind every facial laceration is a potential fracture. Lacerations over the cheek
area may overlie malar, zygomatic, or even orbital fractures.
Mandibular fractures are not uncommon in hockey, and they most often require surgical treatment with internal fixation. A
sense of malocclusion is often a clue, in addition to whatever pain is present. Although the “toothless” hockey player is a
fading visual cliché, dental injuries have been a hockey tradition.
Sane et al. (73) studied maxillofacial and dental injuries among all registered ice hockey players in Finland between 1979
and 1982 (108,921 players) and between July 1984 and December 1985 (62,182 players). Full facemasks were made
mandatory beginning with the 1979–1980 season. In the first study period, 11.5% of 6,885 injuries involved the
maxillofacial and dental regions. Sticks were the primary culprits (54.1% of cases), and pucks were the second major
cause (14.2% of cases). About 65% of these maxillofacial and dental injuries required prosthetic or endodontic treatment.
Crown fractures were the most common injuries (51.7%). Serious bone fractures represented 7% of the series. Full-face
cages substantially reduced the incidence of injuries to the areas in discussion ( 73).
With head and face trauma, three particularly serious sequelae are of concern. The first is brain damage. The second is
cervical spine pathology, including fractures and dislocations (with paralysis). The third is permanent loss of vision due to
an ocular injury.
Neck and Spinal Fractures
In our experience, serious spine fractures are a rare occurrence. In almost 20 years of an association with NHL teams,
we have encountered several fractures of the transverse processes of the lumbar spine and a single instance of a
fracture-dislocation of the cervical spine with quadriparesis.
Despite this relative paucity of spinal trauma, Reid and Saboe ( 74) reported approximately 200 sport-related spinal
fractures occurring over a 7-year period. Hockey accounted for 3% of these injuries, but almost 70% of the
hockey-related fractures were associated with a permanent paralysis. Of the fractures diagnosed, 50% were of the
cervical spine. The mechanism of injury was consistently the same: the player hit either the boards or, before the era of
displaceable posts, the goalposts. Checks from behind often enhanced the impact ( Fig. 27.46). Helmeted individuals
were protected against severe concussion but not against axial loading of the cervical spine with the neck in neutral or
slight forward flexion (the usual fracture positions) (see Fig. 27.46B).
FIGURE 27.46. A: Checking from behind (illegal) with potentially catastrophic results. B: A helmeted player striking the
boards with axial loading of the cervical spine.
The magnetic breakaway fixation, introduced in the latter part of the 1980s then abandoned in 1991 for flexible rubber
posts, reduced the threat of injury from collisions with goalposts ( Fig. 27.47). To reduce board injury, the boards can be
better padded or made more resilient; the development of a potential space between the boards and the Plexiglas
extension could inhibit face and head collisions. Reid and Saboe ( 74) did not confirm the contentions of those who blame
facemask pulling for a rising trend of cervical fractures in ice hockey. However, according to Sim et al. ( 49), Tator et al.
(75) feared that helmet and facemask protective apparatus may be associated with an increasing frequency of cervical
spine injury based on an increased number of cases noted, starting in 1980.
FIGURE 27.47. Flexible rubber posts were established beginning with the 1991 season.
Tator et al. ( 75) state that there had been no reports of spinal injuries to hockey players in the English-speaking medical
literature before 1984. Nevertheless, the Committee on Prevention of Spinal Cord Injuries due to Hockey was formed in
1981. By March 1987, 117 hockey-related spinal injuries had been registered. The preponderance of victims (64%) were
in the 11- to 20-year-old age group; 80% of the incidents involved the cervical spine. Slightly more than 50% of those
with injury to the spinal cord (52.1%) suffered a permanent sensory or motor loss, and five players died. Almost 65% of
the injuries were sustained as a result of a collision with the boards. The predominant causes were being pushed,
checked, or tripped, with more than 20% of episodes involving pushing or checking from behind. Almost all of the injured
players in the series by Tator et al. ( 75) were helmeted, and most were wearing facemasks. In 1985, the CAHA initiated a
prohibition against pushing and checking from behind.
About 50% of the cervical spine injuries in the study of Tator et al. ( 75) involved the region between C-4 and C-6, with
burst fractures and fracture-dislocations predominating ( Fig. 27.48). Bishop and Wells ( 76) indicated that when the top of
the crown of the head strikes an immovable object, axial compressive loading of the cervical spine results. They studied
this phenomenon using anthropometric test dummies propelled in free flight against a rigid barrier and recorded the
results by high-speed photography. The protocol was performed with both bareheaded and helmeted dummies (multiple
types of helmets) and with the neck in both neutral and slight forward flexion. It was determined that once the head came
to rest, inertial movement of the torso continued, causing an “S”-shaped inflection of the cervical spine. Helmets did little
to alleviate loads on the neck. Using the formats represented in Figure 27.19 and computing the expected influences of
anticipated spinal ligament tension and spinous process compression, Bishop and Wells determined the high probability
of lower cervical vertebral failure ( Table 27.9). These calculations were made on the basis of impact at 1.8 m per second,
knowing that impacts at 3.1 m per second always cause cervical fracture and that hockey impacts can exceed 1.8 m per
second. Note the risk to failure with axial loading at the C-5 level, where fractures are most frequent.
FIGURE 27.48. Relatively uncommon burst fracture of C-1 (Jefferson fracture) in a junior hockey player.
TABLE 27.9. DYNAMIC FAILURE LOADS IN COMPRESSION FOR CERVICAL VERTEBRAE
Although padded helmets effectively protect the brain from serious injury with the collision types in discussion, it would
require padding several inches thick to prevent or deter cervical fractures, an obviously impractical consideration. In
seeking clues that would help prevent spinal catastrophes, Tator et al. ( 75) made some keen observations. These are
excerpted in Table 27.10 in the left column.
TABLE 27.10. CAUSES OF CERVICAL SPINE INJURIES IN ICE HOCKEY
Helmets and shields have been implicated as causative agents by virtue of their widespread acceptance just before the
onslaught of spinal injuries. However, their role in injury production is more likely psychological, producing a sense of
invincibility for the North American style of hockey player. Daly et al. ( 30) referred to the work of Smith and Bishop ( 63),
who used a biomechanical model, both with and without a helmet, to simulate axial loading to the cervical spine. It was
concluded that the helmet does not increase the risk of cervical spine trauma. In Europe, spinal injury is apparently less
prevalent, despite the use of protective gear. This raises the issue of instruction in learning the game and in developing
an attitude of play that is respectful of spinal trauma.
In 1988, the Committee on Prevention of Spinal and Head Injuries produced a videotape for universal distribution entitled
“Smart Hockey.” A neck-strengthening protocol, detailed in a brochure entitled “Neck and Spinal Conditioning for Hockey
Players,” has also been disseminated by the Committee. Professional players, who wear a minimum of supracervical
protective equipment, have suffered little in the way of spinal trauma, perhaps by virtue of their neck strength or their
know-how. Neck strengthening for female and younger (preadolescent) male players is likely not to be productive from
the standpoint of protection. Bishop et al. ( 76) warned that the evolution of approval criteria to be met by helmet-mask
protectors has resulted in a relatively heavy apparatus designed to avoid a forward offset; this weight may predispose to
cervical spine injuries. The weight of the apparatus on a weak young neck fosters fatigue of the neck muscles, adding a
flexion movement to the neck.
“Uncrowding” rinks by altering their dimensions may help prevent these injuries to a degree, but it may be more practical
and productive to concentrate on the padding, height, and shape of the side boards. The several inches of padding that
is excessive weight for helmets might be applied to the boards (if puck caroming can be controlled). If the boards were
lowered, sloped away from the ice from bottom to top, and curved for helmet deflection, cervical risk might be reduced. If
the Plexiglas were recessed away from the boards, there would be more potential space to allow dissipation of impact
velocity. In any case, preventive efforts should be directed at the attitude and gamesmanship of players and at altering
the energy absorption properties of the collision surfaces.
If a spinal fracture or dislocation should occur, proper control of neck movements is imperative, although no consensus
has been reached (Table 27.11). It is important in transporting the player to avoid manipulation of the disrupted area.
After an airway has been assured by whatever means necessary, including tracheotomy, the spinal segment should be
immobilized with the use of sandbags or supported by immediately available implements, such as hockey gloves and
cerclage taping. It is best not to implement traction in the absence of x-ray control. To get the player off the ice ( Fig.
27.49), we recommend the scoop stretcher, which separates longitudinally into two parts, each with a shovel-like scoop.
The two shovel-like portions are slid beneath the player and then closed, with no need to lift the player at all.
TABLE 27.11. ONFIELD (ICE) TREATMENT OF CERVICAL SPINE INJURIES
FIGURE 27.49. Scoop stretcher: (A) open; (B) closed.
Probably the best preventative measures for soft tissue and bony injuries to the neck include a major program of neck
strengthening (Fig. 27.50), avoidance of lowering the head anywhere near the boards to avert skeletal catastrophes, and
the use of a neck protection device to prevent puck impacts and skate lacerations.
FIGURE 27.50. Neck-strengthening exercises.
Cervical fractures and dislocations are not the only serious neck injuries. Laryngeal fractures are also potentially life
threatening. Stridor, hemoptysis, subcutaneous crepitus, and loss of the “Adam's apple” promontory are the most flagrant
signs of this fracture. A tracheotomy is sometimes necessary. A cross-check at the cervical level or garroting from behind
(Fig. 27.51), with stick across the front of the neck, are causes that are preventable by rule application or neck
protectors. Bull (67) referred to the personal experience of McGrail, who reported six laryngeal fractures over an 18-year
period with an NHL team. In 1997 and 1998 reports, Tator et al. ( 77,78) provided an update of cervical spine traumatic
injuries related to ice hockey. Almost 60 cases had been added to their registry since their report of a few years
previously. For the entire collected series of 241 cases, the 16- to 20-year-old age group accounted for more than 50%;
the 11-15 year-old age group was the runner-up, with an incidence of 17.5%. Impacts with the boards accounted for just
over 70% of the incidents, regardless of whether the victim was pushed or checked from behind (36.6%). In 1995, USA
Hockey moved the goal line farther away from the boards and instituted a penalty rule for checking an opponent who is
not in possession of the puck.
FIGURE 27.51. Garotting from behind.
Eye Injuries and Protection
Eye damage with visual loss or compromise is one of the most worrisome consequences of sports accidents. It is among
the greatest concerns among NHL physicians. In the absence of face protectors, pucks and sticks all too frequently inflict
eye injuries that either compromise vision or blind the player outright ( Fig. 27.52). Avoidance of such damage may be
accomplished only by the use of eye protection devices. In 1977, a banner year for the advancement of eye protection in
ice hockey, the ASTM F-8 Committee on sports equipment issued a standard for face protection in hockey, as did the
CSA; the net result was a dramatic decrease in the incidence of eye injuries in both amateur and professional hockey
(13). Nevertheless, ocular pathology attributable to hockey has remained an epidemic that has been underappreciated by
its participants. Further progress toward ocular safety in ice hockey has been made grudgingly. Improvements have
come largely through the crusading efforts of two ophthalmologists, Tom Pashby in Canada and Paul Vinger in the
United States, who have pioneered protective reforms in their respective countries.
FIGURE 27.52. Professional hockey player without a facemask was hit in the right eye by a puck and sustained a
hyphema. Retinal hemorrhages and partial loss of central vision were the consequences. The player may go on to
develop secondary glaucoma as a result of damage to the ciliary body.
In 1974, statistics presented by Pashby ( 1,79) demonstrated that eye injuries in hockey had become an unchecked
epidemic. Twenty eyes had been blinded, primarily from sticks and mostly in players age 11 to 15 years.
In 1975, Pashby and Vinger joined forces. Polycarbonate and heavy wire mesh face protectors were produced.
Facemasks were mandated 2 years later by AHAUS for all but Junior A and B players. The CAHA issued a similar
mandate in 1977. The Hockey Equipment Certification Council (HECC) was also formed in 1977 ( 72). Results of the
ongoing eye injury survey in Canada for the 1976–1977 season demonstrated an altered pattern. The 12 cases of blind
eyes during that season occurred only among players who wore no masks and were older, mostly past 16 years of age.
Studies in subsequent years of the decade showed a persistent trend of reduced blindness and a rising average age of
the afflicted; those with face protectors remained essentially immune. The predominance of stick-inflected serious injuries
decreased as puck-induced injuries increased ( 1,79).
Vinger (72) stated that before the institution of mandatory eye and face protectors two thirds of all injuries in hockey were
eye and face injuries. By the end of 1980, the CAHA and AHAUS had each mandated full-face protectors fastened to
helmets for all players including goalies. At about the same time, new players entering the NHL were required to wear
helmets, but without specifications and without a requirement to wear face shields. A chronologic summary of ocular
injuries in relation to blindness is presented in Table 27.12.
TABLE 27.12. OCULAR INJURIES AND BLINDED EYES AMONG CANADIAN hOCKEY PLAYERS
Jones (59) stated the issue of the eye injury with cynical accuracy: “The belief that 'it will never happen to me' is
common.” In 1977, Wilson et al. surveyed players at all levels of play and determined that only 3% of college players and
9% of professionals considered a mask acceptable ( 80). They concluded that a mandate was needed.
An epidemiologic survey questionnaire was distributed to the 225 players in the NHL in 1987 ( 38). The players were
asked to prioritize their concerns about injuries to various body parts. Of the 90 players responding, 40% ranked knee
ligament injuries as their primary concern. Only 14% of players ranked head and face injuries first, and only 0.5% placed
their concern for their eyes first. From a medical standpoint, the priority of concerns is the inverse of what was expressed
by the players. Two important conclusions can be drawn this study. First, players are undereducated about the import of
such injuries and about treatment results when injuries to these areas occur. Second, the failure of education has been a
major obstacle to the routine donning of helmets and face protectors when such equipment is not specifically mandated
by rules governing the hockey organization of which the player is a member (e.g., the NHL, amateur leagues for older
players).
Pashby (1,79) offered the following suggestions to reduce the sequelae of hockey violence in general and of eye injuries
in particular. He asserted that rink sizes should be standardized and that the distance between the end board and the
goal should be lengthened from 10 to 13 feet (3 to 4 m) to obviate collisions due to congestion. These parameters,
including rink dimensions of 61 by 30.5 m (200 × 100 feet), are stipulated in the rulebook of the International Ice Hockey
Federation ( 81).
Based on more than 30,000 responses to questionnaires, parents of hockey-playing children in Canada agreed on the
following:
1. Skills only should be taught before 10 years of age.

2. There should be no all-star hockey before age 11.
3. There should be no slap shooting before age 12.
4. There should be no body checking before age 13.
5. More appropriate leadership in prevention should be demonstrated by junior and professional teams.
6. At least one practice should take place for each game.
7. Referees should be less inhibited in calling penalties.
8. Players should serve out all penalties and not be released even when a goal is scored.
An additional recommendation offered by the Minister of Fitness and Amateur Sport of Canada in 1989 was to give full
responsibility for play conduct to the coaches, as an inducement to mellow any thoughts of teaching aggression ( 1).
The goal in developing prophylactic eye devices is the dissipation and diffusion of potentially damaging forces away from
the soft ocular structures and toward the less vulnerable bony orbit and periocular soft tissues. Rampton et al. ( 82)
provided an interesting perspective with regard to ocular protection based on a study performed in the emergency
department of a treatment facility in northern Ontario. The ice hockey players treated included both young and old, male
and female, and elite and nonelite players. This study revealed that full facial visors prevented injuries to the nose and to
structures cephalad to it. Persons wearing half-visors, however, demonstrated the same distribution of injuries as players
wearing no specific face protection. Adult players sustained injuries more often, and they tended not to wear face
protection. Male players had a much greater proportional quantity of injuries than female players did, despite the
progressive rise in female participation in recent years. Pashby ( 1,79) recommended full-face protection, which is
mandatory for all players younger than 14 years of age in Ontario and for all players in Quebec. Half-face protectors are
successful in preventing eye injuries but not in preventing injuries to the face below the eyes. Sticks do the most frequent
damage, and their tips are able to negotiate the interval between the face and the visor ( 82). Recommended sports eye
protection is listed for three sports in Table 27.13.
TABLE 27.13. RISK LEVEL FOR EYE INJURY IN CERTAIN SPORTS, AND RECOMMENDATIONS FOR PROTECTIVE
WEAR
There are those in the NHL who would argue not only that the introduction of helmets and facemasks is an invitation to
increased use of the stick and to other violence directed toward the head (see later discussion on neck trauma and
equipment) but also that the wearer has an increased sense of invulnerability and may demonstrate increased
aggression in charging the goal and elsewhere in the game. An increased risk of cervical sprains and fractures has also
been ascribed to facemasks, because upward leverage on the mask can result in hyperextension injuries. The absence
of any mandate to wear face protection in the NHL has initiated the creation of special rules governing their use, such as
an instigation penalty for players with protection who taunt unprotected players into aggressive retaliatory acts.
Lower Extremity
Knee
Hockey players sustain the full gamut of knee injuries, ranging from torn menisci to torn cruciate and collateral ligaments.
It is the mechanisms by which these injuries are commonly caused that are characteristic of ice hockey. As indicated by
Bull (67), the basic mechanism in ice hockey is almost invariably contact, whereas in sports with greater degrees of foot
fixation (e.g., cleats), many meniscal and ligament injuries are sustained in the act of cutting (noncontact). Paradoxically,
it is the absence of foot fixation that often enables hockey players to function with moderate instabilities not withstood in
other sports. In any case, when the hockey player is skating with the knee in flexion (which is the case for most of the
stride), the knee is exposed to collisions with the knees or thighs of opponents. A hit is usually received on the lateral
aspect of the knee, spraining the medial side of the joint and often tearing the anterior cruciate ligament as well as the
medial capsule. Derotational braces and strengthening suffice for lesser degrees of disruption, but surgical
reconstruction is needed for severe ligament disruptions. Sometimes a player's knee is hit from the front, causing a
hyperextension injury. Although an effusion and missed playing days are the rule, ligamentous disruption is rare.
Magnetic resonance imaging often reveals bone bruising on the anterior aspect of the femoral condyle. A
hyperextension-blocking brace and physical therapy are the usual treatments.
Ankle and Foot
Ankle sprains are infrequent in ice hockey because of the rigidity of the skate boot. However, entrapment of the skate
blade by the ice or against the boards as the pronated ankle is abducted and externally rotated by the player's inertia not
infrequently produces a low-grade syndesmosis injury. McConkey ( 83) indicated that ankle syndesmosis injuries occur by
a different mechanism than those associated with common ankle sprains. Derotational braces and strengthening may
lead to lesser degrees of injury, but surgical reconstruction is needed for severe ligamentous disruptions. Knee ligament
injuries account for a substantial percentage of player-days missed in ice hockey, nearly 20% according to the NHLISS
for 1996–1998 (26). The mean number of games lost from knee injuries represented almost 10% of the season (more
than 7 games) for the 1996–1997 and 1997–1998 seasons. Anterior cruciate ligament injuries accounted for a mean of
9.63 games missed, followed by lateral collateral ligament injuries (8.25 games). Medial collateral ligament injuries were
the most frequently reported sprains of the knee, accounting for a mean of 6.66 games missed for the two seasons.
Fractures of the ankle are relatively uncommon, but bursal enlargements over malleoli that have repeatedly received
impacts from pucks are common.
In lacing skates, it is usual to make the distal and upper laces very tight, while leaving the throat area lacing looser for
flexibility. The tightness of the upper boot lacing sometime causes extensor tenosynovial reactions and even painful
venous thromboses of the superficial veins. Some players leave the skate tongue everted for greater flexibility. This has
led to an incidence of lacerated extensor tendons caused by skate blades ( Fig. 27.53).
FIGURE 27.53. Representation of the mechanism of extensor tendon laceration. Note that the top two eyeholes of the
player's skates are not laced and the tongue is not taped to the anterior shin pad.
Fractures of the feet are relatively common and are almost invariably the result of impact by the puck. The most
commonly fractured bone is the navicular ( Fig. 27.54). If the fracture is not displaced, players often “play through the
pain.”
FIGURE 27.54. Fracture of the medial side of the navicular (arrow) due to puck impact.
On occasion, a player slides and hits the boards with the blade portion of the boot. Although severe injuries are
uncommonly encountered, Figures 27.55 demonstrates a dramatic consequence. Such injuries stimulate thoughts about
modifying the design of the boot.
FIGURE 27.55. Professional hockey player with a comminuted and displaced fracture of the left calcaneus. A and B:
Clinical postoperative photographs. C and D: Preoperative radiographs. E: Preoperative computed tomographic scan. F
and G: Postoperative radiographs.
Upper Extremity
Common Shoulder Afflictions
Acromioclavicular (AC) separations are among the most common injuries sustained by postadolescent and adult hockey
players. In an NHL locker room, finding players with two normal AC joints is the exception rather than the rule ( Fig.
27.56).
FIGURE 27.56. Professional hockey player who sustained an acromioclavicular separation with an associated fracture of
the distal end of the clavicle (arrowhead).
A testimony to the common involvement of the AC joint in hockey is the study by Norfray et al. ( 85). Professional and
amateur hockey players were evaluated radiographically. It was determined that 35 (45.5%) of 77 evaluated professional
players demonstrated radiographic abnormalities of the clavicle or AC joint or both; 31% of the abnormalities were
confined to the AC joint. Clavicular fractures were more common than ligamentous disruptions among young teenage
amateurs, while the reverse was true in amateurs between 18 and 21 years of age.
The injury is commonly caused by the transmission of force to the AC joint via impact of the outstretched abducted arm or
of the point or back of the shoulder against the ice or the boards. The AC joint may be separated with or without an
associated fracture of the portion of clavicle or acromion adjoining it (see Fig. 27.56B). Almost regardless of the grade of
the separation, operative intervention as a primary treatment is rarely, if ever, needed. This is in accord with the study of
Glick et al. (86) in which 35 unreduced AC dislocations in athletes (more than 50% of which were in football players) were
observed for an average of 3 years. Of these patients, 70% returned to their specific sport within 4 weeks, and the
majority were uninhibited by symptoms other than weakness. A tardy excisional arthroplasty (with resection of the distal
end of the clavicle) can be performed if severe pain or significant restriction of arm elevation in abduction results from the
impinging hypertrophy of the dislocated clavicular head. Players with a low-grade separation typically miss up to a few
games. Players with a grade III separation typically miss 3 to 6 weeks of games. Restoration of strength, especially of
horizontal abduction, takes weeks to accomplish. This is an important arc of function in ice hockey because it is used by
players to displace or hold off opponents in struggles along the boards ( Fig. 27.57; see Fig. 27.15A). Because the
mechanisms by which the injury is sustained are a function of transmitted forces rather than direct impact to the joint,
protective equipment is not preventive. Subcutaneous dislocations of the AC joint warrant open reduction and fixation
with repair of the detached or torn overlying musculature. For the lesser grades of AC separation, the rule is to initiate
motion and strengthening as soon as pain permits. Elevation of the arm is easiest to initiate in a pool, where buoyancy
may assist and where the column of water provides a gentle resistance against which to strengthen.
FIGURE 27.57. Horizontal abduction is used frequently in hockey to push opponents during interactions along the
boards.
Shoulder (glenohumeral) dislocations and subluxations are common in ice hockey, but they are an infrequent cause of
missed player-days. Thomson (28) reported shoulder dislocations and separations to be among the three most frequent
groupings of injuries in his analysis of more than 1,000 injuries in amateur players. Hovelius ( 87) reported an 8%
incidence of recurrent dislocation among the most elite of Sweden's divisions. Taking into consideration that most hockey
players are “left handers” (the left is the bottom hand on the stick), Hovelius undertook to study the relevance of this fact
to dislocation. He concluded that 80% of the operative repairs were performed on the left shoulder, but that this was not a
representation of the distribution of unstable shoulders (dominant versus nondominant). Glenohumeral instability is a
disruptive pathology that forces most hockey players to seek a surgical solution. For goal tenders, it is potentially career
threatening, especially if the glove hand extremity is the one involved. Even if a reconstruction of the shoulder is
performed, any resulting loss of external rotation and extension in the abducted arm will limit the defensive capacities of
the goalie.
Sternoclavicular Joints and Ribs
Not as common as AC joint injuries are injuries to the sternoclavicular joint ( Fig. 27.58). These are sustained by players
who hit the boards chest-first while experiencing a sudden retraction of the shoulders from a hit to the back. These
injuries, along with injuries of the ribs and costochondral junctions, are treated by abstinence from play and by supportive
and symptom-relieving measures, after it has been ascertained that the underlying viscera are unimpaired. Special
protection, offered by flack jackets, is recommended on the player's return to contact participation.
FIGURE 27.58. Sternoclavicular injury (arrow) in a professional hockey player. Pain and swelling were noted after the
player was checked into the boards chest-first.
Elbow
Apart from simple contusions and impact injuries to the elbow, the more common significant afflictions are olecranon
bursitis and hyperextension and/or valgus injuries to the capsule. Either may be caused by falls on the ice or elbow-first
collisions into the boards. In addition, leveraged forces through the player's stick by an opponent can cause capsular
injuries. Standard elbow pads are not always helpful in preventing concussive damage and are of no help in leverage
injuries.
Olecranon bursitis is sometimes acute, but more often it is chronic. The pressure from an enlarged, tense bursa can be
painful, but it rarely precludes play. Aspiration should be considered only for severe pain or restricted motion or to rule
out the presence of infected contents. In most cases, the bursal inflammation subsides after the season without a need
for surgical excision.
Hyperextension and valgus injuries can be disabling enough to cause a loss of playing days. Shooting the puck, pressing
the stick against the ice, and pushing opponents away are painful motions. Hyperextension-blocking braces with hinges
or straps are often helpful in providing stability and allaying pain. Therapeutic modalities and strengthening exercises
accelerate a return to function. Surgery has never been necessary in our experience.
Hand and Wrist
The variety of hand and wrist injuries incurred by ice hockey players is too large to cover. Fractures of the metacarpals
occur from slashes and fisticuffs (Fig. 27.59). Carpal fractures and dislocations derive from falls on the flexed or
extended wrist. But perhaps the most traditional hand injury is the “gamekeeper's thumb.” Bull ( 67) indicated that this
injury can result from fighting, but more particularly it is caused by falls with stick in hand, whereby the stick imparts a
radially directed force that ruptures the ulnar collateral ligament of the metacarpophalangeal joint. Surgery is frequently
necessary to restore maximum function, but spica immobilization is sometimes adequate for partial tears when there has
been no concurrent bony avulsion. Specially contrived splints of plastic or Fiberglas may be used to permit the player to
continue performing.
FIGURE 27.59. Fracture of fifth metacarpal neck (boxer's fracture): the unwanted result of fisticuffs.
DERMATOLOGIC DISORDERS
Contact dermatitis is a relatively common entity among hockey players. It is manifested as either an acute or a chronic
inflammatory disorder of the skin secondary to irritation. Such irritant skin reactions in athletes are usually caused by
physical and mechanical agents. In hockey players, the excessive sweating beneath protective equipment results in an
eczematous dermatitis (Fig. 27.60), fondly referred to as “the gonk” ( 88).
FIGURE 27.60. A and B: Dermatitis caused by excessive sweating under protective equipment.
SOFT-TISSUE INJURIES
Musculotendinous Strains
The incidence of strains in NCAA hockey was 54 per 1,000 exposures, or about 17% of injuries, for the 1989–1990
season (24). In the NHL, the predominant strain is the groin or adductor pull. In the 1986–1987 NHL season, with 21
teams and almost 400 players, 4,470 player-days were lost to injury, 12% of which were attributable to lower-extremity
strains. Of these, approximately 80% were groin strains. Groin pulls produced an average of 7 player-days missed per
injury, with a range from 1 to 49 days (89). Strains of the hip flexors, hamstrings, quadriceps, and abdominal muscles
combined accounted for only 63 player-days missed. NHL data for the years 1993–1995 revealed groin injury rates of 0.8
to 1.0 per 1,000 exposures, but the rates were 1.5 times greater for games only, as opposed to a composite of games
and practices. For the same interval, each initial groin injury resulted in a mean loss of approximately 2 player-days. The
number of missed days rose virtually exponentially with each subsequent recurrence. When recurrences happened, the
mean interval between the index injury and the first or second reinjury was 3 to 5 weeks. Recurrent groin injuries appear
to be more likely after 26 years of age (John Powell, personal communication). Since 1993, there has been an apparent
change in the frequency pattern of groin injuries. From 1993 through the 1997–1998 season, there were groin injury
spikes during the preseason. From 1993 through 1995, the spike was bimodal, but it has not been so since then.
The abdominal suprainguinal posttraumatic hernia is a relative of the groin strain. It is common in ice hockey and
represents a virtual epidemic in soccer. In soccer, it most often appears precipitously with a single initiating event. In ice
hockey, however, it typically develops insidiously, often seemingly as a proximal extension of an adductor strain. Both
entities are to be distinguished from osteitis pubis. The sports hernia in the suprainguinal area is usually terribly
disabling. A resolution of symptoms from this entity by noninvasive techniques is, at the least, inordinately protracted.
The 1990s demonstrated an expedient reduction of symptoms as a result of a herniorrhaphy, allowing players to return to
competition within 2 to 3 months. Davidson ( personal communication) conveyed early successes in the NHL using the
herniorrhaphy. After the inception of major league soccer, in the wake of the 1994 World Cup, numerous players have
undergone variants of this operation, many bilaterally, and many others more than once or twice on a given side.
Presently, there exist controversies regarding which operative variant (if any) is best and whether to add adductor
releases or other local procedures to the herniorrhaphy. Magnetic resonance imaging has been notoriously unsuccessful
in depicting pathology associated with the suprainguinal hernia.
The groin muscles are critical force generators for the power starts of ice hockey, making them particularly susceptible.
The occurrence of a pull has been thought to be instigated by factors including tight muscles, inadequate warmup,
weakness and/or fatigue, and muscle imbalances. The player typically experiences a popping or tearing sensation and
for one to several days is unable to use the muscle effectively. Work by Nikolau et al. ( 90) suggested that muscle
strength returns rapidly but that pain and inflammation impede its functional use. For this reason, some physicians
prescribe antiinflammatory drugs, which may actually delay regeneration of injured muscle tissue ( 91). Generally, most
symptoms dissipate within a few weeks, but there is a high susceptibility to recurrence of strain owing to progressing
immature collagen within the injured site and weakness and inflexibility of the recovering muscle.
Before a player is allowed to return to competition, the preinjury (normal) level of strength of the muscle and the
extremity, as well as full flexibility, must be restored ( Fig. 27.61). Ekstrand and Gillquist demonstrated that persistent
muscle weakness results in a higher rate of strain recurrence ( 92).
FIGURE 27.61. Graphs depicting the relationship between extension and flexion of uninvolved extremities: (A) after
rehabilitation; (B) after injury.
The role of strength (or a strength ratio) as a protector was implied by the study of Merrifield and Cowan ( 93), who
performed preparticipation isokinetic tests on players and related the results to subsequent injury. All players who
sustained groin pulls were among those who had demonstrated strength deficits of the hip muscles of at least 25% in the
involved versus the uninvolved extremity.
Restoration of strength is not as simple a concept as first it might appear. The entire extremity often becomes
deconditioned in the wake of (or as a predisposition to) injury. Restoration of general strength as well as specific ratios
(47) is the goal of the rehabilitation program. Common formats of abductor-adductor strengthening are not wholly
adequate for rehabilitation of groin pulls in ice hockey players. Common abductor-adductor variable resistance machines,
for example, work the muscles only with the hips flexed, and only through limited arcs. In hockey the adductors are often
used with the extremity extended and widely abducted relative to the plane of the body. This movement is often best
simulated by pulley systems, the Eagle multihip machine, and other closed kinetic chain formats. Once recovery has
been achieved, and in general to prevent such injuries, the following practices should be maintained: (a) maintenance of
strength, for reasons discussed previously; (b) maintenance of general conditioning to achieve increased blood flow,
enhanced delivery of nutriments, and resistance to fatigue; and (c) warmups before participation, including low-intensity
activity and nonballistic stretching. The result of warmups is increased muscle heat with greater viscosity of muscle
elements and an associated stress relaxation requiring greater forces to tear the muscle ( 94).
Other Soft-Tissue Injuries
Hematoma, in one form or another, is a common injury despite use of protective pads over the predilected sites ( Fig.
27.62). The two most characteristic and disability-producing sites are the anterior or lateral thigh (the “Charley horse”)
and about the iliac crests (the “hip pointer”). The former is usually a result of an opponent's knee hitting the thigh, the
latter of slashes or impacts of the hip against the ice or boards. When a hematoma in the thigh is small, it is common to
hear trainers refer to a Charley horse as a “Chuck's pony.” When the hematoma is large, thigh pain is moderate and knee
flexion is severely curtailed.
FIGURE 27.62. Left rectus abdominis hematoma on computed tomographic scan (arrowheads) in a junior hockey player.
Immediate rest, ice, compression, therapeutic modalities, antiinflammatory medication, and gentle active range of motion
exercise are the usual early treatment formats. When defiant of a program of relative rest, youths are particularly prone to
develop myositis ossificans, especially if repeated blows to the thigh are sustained over a period of time. On occasion, a
player complains of vague discomfort in the hip, associated with stiffness, but has no obvious Charley horse. If a hand is
placed on either side of the thigh (medial and lateral), a shock “fluid wave” initiated by sudden movement of one hand
can be subtly detected by the other hand. Repetition of the test on the contralateral thigh reveals virtually no sensation of
a fluid wave in the “receiving hand.”
Hip pointers, or collections of blood within or around the periosteum of the iliac crest, are quite painful, especially when
they result from collision contact. It is common to see players wearing large foam rubber sheets or pads beneath their
standard hip pads to avert or protect against hip pointers. Because of the level of pain, it has been an all-too-frequent
practice to inject the site with steroids so that the player can resume participation. Sometimes collections can be
aspirated to gain relief. Both the Charley horse and the hip pointer are indicators of the inadequacy of existing protective
equipment.
Visceral Injuries
Of the viscera, the spleen is the most vulnerable in ice hockey. The left upper quadrant is unprotected from elbows and
from the blades and butts of sticks. The spleen can also be injured by crushing blows to the rib area. Injuries to the
spleen range from subcapsular hematomas (Fig. 27.63) to the surgical emergency of rupture with massive bleeding.
Splenic rupture is a life-threatening injury. There is virtually no professional team physician of tenure who has not known
at least one player who required a splenectomy.
FIGURE 27.63. Subcapsular hematoma on computed tomographic scan (arrowheads) in an adult men's hockey league
player.
Less often, perinephric bleeding is diagnosed ( Fig. 27.64). Injury of a kidney is usually heralded by frank hematuria.
Serial urinalysis, abdominal radiography, and an excretory urogram are among the diagnostic tests that may be
implemented to rule out damage (68). Preexisting splenomegaly, as from mononucleosis, predisposes to rupture. When
splenic abnormalities are suspected, they are best evaluated by computed tomography. Players with a history of
mononucleosis and those whose preseason physical examination reveals splenomegaly may be screened and monitored
by sonography (65). Hemoptysis and dyspnea have been observed after chest contusions that produced bleeding within
the lungs. Testicular hematomas (Fig. 27.65) have been witnessed after puck or stick contact.
FIGURE 27.64. Perinephric hematoma on computed tomographic scan (arrowheads) in a junior hockey player who was
cross-checked from behind. Initial complaints were of back pain and hematuria.
FIGURE 27.65. Testicular hematoma (large arrowheads) demonstrated on ultrasound in a Midget-level hockey player
after he was struck by a puck. Small arrowheads indicate the testicle.
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28 Skating: Figure, Speed, Long Distance, And In-Line
28
SKATING: FIGURE, SPEED, LONG DISTANCE, AND IN-LINE

DAVID L. MULLER
PER A. F. H. RENSTROM
Historical Background
Orthopedic Injuries
Foot
Lower Leg and Ankle
Knee
Hip and Thigh
Back
Shoulder
Elbow and Wrist
Hand
Nonorthopedic Injuries
Epidemiology
Biomechanics and Technique
Prevention
Equipment
Conditioning
Sport-Specific Treatments
Chapter References
Skating of all types has gained increasing popularity in recent times. The number of skaters has increased to millions of
people per year. In-line skating has experienced the greatest growth, but there has also been widespread media
coverage of figure and speed skating as popularized by the Winter Olympic Games. These sports have traditionally been
popular in countries with naturally occurring ice. Interest has also increased in countries that have built artificial ice tracks
and skating rinks. Now, with the explosion of in-line skating popularity, skating injuries once exclusive to colder climates
are being seen in all areas of the country. The types and frequencies of injuries seen vary among different skating events
and between recreational and competitive skaters. The development of highly technical training programs has led to
better understanding of skating biomechanics and injury risk and prevention.
Figure, speed, long-distance, and in-line skating involve different equipment, skating surfaces, and techniques and
therefore expose skaters to unique patterns of injuries. Figure skating involves several different events, including singles,
pair skating, and ice dancing. Both singles and pair events emphasize acrobatic jumps, placing great torque on the
landing leg, leading to both overuse and acute traumatic injuries. Ice dancing emphasizes foot work and coordination and
does not generate high levels of rotational forces. Speed skating involves great strength, endurance, and technique.
Although speed skating has traditionally been a relatively safe sport, short track skating has added a component of acute
injuries caused by pack skating and tight turns that have led to many falls. Injury risk and pattern related to the clap skate
(see later discussion) are not well defined.
Long-distance skating, most common in Scandinavian countries and in the Netherlands, involves traveling long distances
on frozen lakes and canals (Fig. 28.1).Skating is a popular sport in countries with ice on lakes during the winter season.
In a national survey in Sweden, 33% of the population had skated during a 6-year period ( 1). Most were recreational
skaters, and 50% had participated in long-distance skating. Long-distance skating injuries are usually related to poor ice
conditions and harsh climate.
FIGURE 28.1. Long-distance skating is both a recreational and a competitive sport in Scandinavian countries. Pack-style
races are common in this sport.
In-line skating is one of the most rapidly growing sports in the United States and Europe. Most participants are
recreational skaters who use bike paths and roads for general fitness and fun. In-line skating in the summer is well suited
for cross-training for a number of winter sports. Racing events and roller hockey are becoming more popular. The smooth
motion of in-line skating is believed to place little stress on joints, but frequent falls on hard pavement cause many
injuries. Padding and prophylactic bracing are crucial in in-line skating to decrease the incidence of fall-related injuries.
HISTORICAL BACKGROUND
Many theories exist regarding the origin of skating. One possibility is that skating originated from skiing, and that skates
evolved merely as miniature skis. Another theory suggests that an accidental slip on a piece of bone across the ice led to
the development of skating (2). Nevertheless, the origins of skating have been noted in archaeological discoveries in
Asia and Europe and from Scandinavian and Icelandic legends that date back more than 3,000 years. Drawings depict
prehistoric hunters traveling on snow and ice with pieces of bone and wood on their feet.
Primitive forms of skates were made of shank or leg bones that were fastened to the feet by leather straps. The word
skate is derived from the Dutch word schaats, which can be further traced to old German and French words meaning
“shank bone” or “leg bone.” Eventually, animal bones were replaced by wood and finally by iron, a true advance in
skating technology. A wood carving from the 15th century shows that iron skate blades have existed for at least 600
years (3). The most significant advance was the invention of all-metal skates in Philadelphia in 1848. These provided
superior fixation to the foot by eliminating the wooden foot plate that was often too loose and fell off or was too tight and
cut off circulation.
Initially used as a form of travel, early skating did not entail a push-off and glide technique. Apparently, this technique is
from the Netherlands and was characterized by a sideward push-off technique using sharp “whetted iron blades.”
Skating competition started before the 17th century. The famous Elfstedentocht in Holland was first held in 1763. It is a
long-distance race that visits 11 cities and covers more than 250 km. In 1985, a total of 16,176 skaters participated, and
almost 75% completed the race (3). The race is currently limited to 16,000 skaters.
The first skating club was formed in Edinburgh, Scotland, in 1742. Individuals had to prove various technical skills to gain
membership (2). The first speed skating world championships were held in 1891 in Amsterdam.
Since the development of artificial ice, colder climates, still water, and minimal snowfall are no longer prerequisites for a
strong skating community. Therefore, many nationalities are now evident in elite skating competitions. The first artificial
ice rink was built in 1876 in London. Madison Square Garden, which opened in 1879 in New York City, is the oldest
American skating rink.
The oldest record of a skating injury is found in The Life of Saint Lidvinia, written by Brogman in 1498. Saint Lidvinia
suffered a fracture while skating and, according to the book, was confined to bed for the rest of her life ( 2).
Roller skating dates back to the 1700s. Myth has it that a Dutch skater, frustrated by the hot summer months, strapped
wheels onto his shoes (4). The old street rollers were popularized in the United States in the 1860s and remained
essentially unchanged until 1965, when polyurethane wheels and precision bearings were introduced. These provided a
quiet, smooth ride with better traction, speed, and maneuverability, and their introduction was responsible for the
increased popularity of roller skating in the 1970s. By 1979, approximately 57% of teenagers and 12% of adults
participated in roller skating in the United States ( 5). Participation decreased through the 1980s coincident with the rise
in popularity of in-line skating.
In-line skates were developed in 1980 as a means of off-season training for ice hockey. In 1984 marketing was directed
at the general fitness crowd, resulting in 4 to 5 million in-line skaters in 1991. This number grew to more than 26 million
by 1997.
ORTHOPEDIC INJURIES
Both acute and chronic injuries are noted in skaters of all types. The recreational skater is more apt to sustain an acute
injury in a fall or collision rather than an overuse injury, whereas competitive figure skaters are susceptible to an equal
number of acute and overuse injuries. Speed skaters are less likely to sustain acute injuries related to falls, as noted
previously. The following is a representation by anatomic area of the types of injuries that are commonly seen in skaters.
Foot
All skaters are aware of the problems poorly fitting skates can cause. Toe numbness and foot pain may simply be related
to narrow boots. Outdoor skaters may be more susceptible to frostbite in skates that are too tight. Bursitis and callosities
are common in skaters. Well-fitting and often custom-made boots are necessary to prevent these painful and annoying
injuries. Doughnut-shaped pads and boot modifications can distribute pressures over bony prominences. Davis and
Litman (6) evaluated 45 competitive figure skaters and found that 40% had intermittent foot pain severe enough to limit
training, and 69% had hammer toe deformities. These were usually multiple and bilateral. Hard corns were noted in most
skaters.
Stress fractures are the most common foot injuries. Pecina et al. (7) reported on seven foot stress fractures in competitive
skaters. Two involved the tarsal navicular; two, the base of the fifth metatarsal; two, the fourth metatarsal; and one, the
second metatarsal. Most healed with rest, one underwent open reduction and internal fixation, and two were successfully
treated in short leg casts. The tarsal navicular stress fracture is often overlooked. The diagnosis is secured with a bone
scan, tomogram, or magnetic resonance imaging scan. Smith (8) reported that most figure skaters do well with decreased
jumping activity until the stress fracture heals; however, some skaters must be forced to rest from skating if they are not
willing to modify their skating regimen. Orthotics can occasionally help redistribute forces within the skate boot to help
prevent further injury.
Lower Leg and Ankle
The lower leg and ankle are common areas of injury in all types of skaters. Problems include stress fractures, tendonitis,
tendon subluxation, bursitis, shin splints, compartment syndromes, sprains, fractures, and dislocations.
Stress Fractures
The series of 42 world-class figure skaters reported by Pecina et al. ( 7) included a total of nine stress fractures. Of these,
one involved the fibula and one the tibia. The skater with the tibial stress fracture noted a sudden increase in training
jumps associated with occurrence of this injury. Stress fractures usually heal well with rest; some need immobilization
and time. The exception is the “dreaded black line” type of fracture on the shaft of the tibia, which can be resistant to
usual treatment methods (9). These fractures should be taken seriously and treated aggressively (i.e., up to 12 weeks in
a cast) and sometimes require surgery. Shock-wave treatment is now being tried and seems promising. Although not
proven, electric stimulators may shorten healing time.
Tendinitis
Poorly fitting skates can lead to inflammation over the tibialis anterior and extensor hallucis longus tendon. If left
untreated, this may progress and lead to chronic tendinitis. The condition initially presents as “lace bite” and can be
treated effectively with padding taped both medial and lateral to the tendons at the ankle joint to relieve the pressure
caused by the skater's boot (10). This condition usually resolves quickly if treated early.
Achilles tendon injuries are common in skaters. Figure skaters are at high risk, because tremendous forces are
generated in the Achilles tendon as it works eccentrically in the landing of jumps. Older figure skaters are at increased
risk for partial tears as the tendon degenerates and weakens with age. Adequate stretching and warmup are helpful in
preventing these injuries. A heel wedge can often improve symptoms.
The plantar flexed nature of the skate can lead to Achilles peritendinitis. Pain is often located at the insertion of the
tendon into the tuberosity of the calcaneus. Pain may be relieved by activity. Tenderness often radiates proximally
several centimeters up the tendon. Retrocalcaneal bursitis should be considered in the differential diagnosis. Treatment
includes rest initially, then muscle stretching and strengthening, and antiinflammatory medication. Casting for a short time
may be necessary. Occasionally, ultrasound and electric stimulation may be used.
Although rare, peroneal tendon subluxation has been reported in figure skaters. Conservative treatment is preferred, but
surgical reconstruction of the tendon sheath, in combination with deepening of the groove in the fibula, may be
necessary.
Speed skaters are at risk for medial tibial stress syndrome (shin splints). Treatment includes decreased training until
symptoms improve, followed by a program of gradually increasing stretching and strengthening exercises.
Bursitis
Fluid-filled bursas can develop over prominent areas such as the medial and lateral malleolus and the anterior tibial
tendon; they may contain up to 30 mL fluid ( 8). They are usually caused by excessive pressure from tight-fitting boots.
Boot modifications are usually successful in improving these painful areas.
Exertional Compartment Syndrome
Compartment syndrome occasionally occurs in competitive skaters. Individuals usually complain of severe pain after a
heavy workout, often in the anterior compartment of the leg. These symptoms occasionally manifest acutely and should
be treated as a surgical emergency by performing compartment releases after measurement of elevated pressures. In the
nonacute setting, increased pressure can be caused by muscle hypertrophy or thickened muscle fascias, or both. In
these patients, it is necessary to measure pressures before and after an exercise routine that creates typical pain.
Compartment releases may be necessary if elevated pressures correlate with symptoms and conservative treatment has
failed. The athlete should be warned of a possible 10% to 15% loss of strength after compartment release.
Sprains, Fractures, and Dislocations
Garrick reported an incidence of one ankle sprain in 36 competitive figure skaters ( 11). Davis and Litman found that
skaters using heavier and stiffer boots were more prone to ankle sprains ( 6). It is not known whether this is a
cause-and-effect relationship.
Ankle fractures and dislocations can occur in competitive skaters but are infrequent. More commonly these injuries are
seen in beginner skaters, in-line skaters, and those with poorly fitting equipment. They should be managed with
appropriate radiographs and treatments not discussed in this chapter.
Knee
Knee pain is common in all types of skaters. Acute injuries such as ligamentous disruption and meniscal injuries do
occur, but overuse syndromes are by far more common. Injuries such as osteochondral fracture or osteochondritis
dissecans should be in the differential diagnosis; they should be ruled out by careful physical examination and
radiographic studies.
Patellar tendinitis, or jumper's knee, is the most frequently seen overuse injury in the competitive figure skater. Its course
can develop quickly and lead to lengthy lost training time. In the adolescent, a high incidence of Osgood-Schlatter
disease is evident. Patellofemoral pain or anterior knee pain, patellar subluxation, and bursitis also should enter the
differential diagnosis in these athletes. Smith et al. ( 12) studied 46 junior elite figure skaters and showed that adolescent
skaters with anterior knee pain, jumper's knee, Osgood-Schlatter disease, or isolated patellofemoral pain had less
quadriceps and hamstring flexibility than similar skaters without knee pain. A stretching program designed for these
individuals decreased the knee pain in 9 of 14 skaters. Approximately 75% of all adolescent skaters evaluated needed
improved flexibility, regardless of the presence of knee pain.
Speed skaters frequently develop knee pain related to dry-land and off-season sports, including cycling, running, and
weight lifting. Meniscal tears can occur in speed skaters as a result of twisting falls. Such injuries may be more prevalent
in short-track speed skating, where they are caused by catching an edge during falls into corners of the hockey rink.
Hip and Thigh
Cramer and McQueen (13) identified four causes of groin injuries in figure skaters: muscle imbalance between hip
adductors and gluteus medius, forcible push-off adducting the hip, forced external rotation of the adducted leg, and
forced adduction of the hip. The differential diagnosis includes strain or tendinosis in rectus femoris, adductor longus, or
iliopsoas muscles. The most common site is the adductor longus. A detailed physical examination and history often lead
to the proper diagnosis of these injuries. Prevention by stretching during warmup is imperative for all types of skaters.
As reported by Garrick (11) and Smith and Micheli ( 14), overuse injuries of the hip are rare. Femoral neck fractures
represent a rare but serious injury that is more frequently seen in recreational skaters than in competitors.
Toron et. al. (15) reported a case of bilateral diaphyseal femoral stress fractures in a 5-year-old who participated in
in-line skating with his father for 3 hours, twice a week for 6 weeks. Healing occurred with rest after 5 weeks.
Back
Both figure skaters and speed skaters have a high incidence of back pain. Smith and Micheli ( 14) noted that 6 of 19
competitive figure skaters reported back pain in a retrospective analysis. This study found that 5 of 15 girls with scoliosis
by physical examination, an unusually high incidence compared with that in the general population (15%). The question
of joint laxity and scoliosis arises in this group of athletes known for their flexibility. Low back pain is related to repeated
jumping, hyperextension, and lifting and twisting in pairs skaters and is a problem for dancers and gymnasts as well. The
authors believed that low back pain was related to tight lumbodorsal fascia as a result of an overgrowth syndrome in
which soft tissues become taut secondary to skeletal growth. They also noted that most of these skaters had no
stretching regimen in their training routines.
Speed skaters, because of the repetitive movements and the extreme forward flexed position of the skater's trunk, are
prone to chronic low back problems. Specific strengthening of the lumbar musculature is important in prevention. Speed
skaters occasionally use heat retainers to keep the lumbar musculature warm during outdoor training and competition.
Shoulder
Shoulder injuries are infrequent in ice skaters. Lifting injuries in pairs skaters can lead to rotator cuff strain and tendinitis,
but again these are uncommon. Clavicle fractures are reported in the recreational skater ( 16). Shoulder dislocations,
proximal humerus fractures, and acromioclavicular injuries are reported to account for 5% to 12% of in-line skating
injuries (17,18).
Elbow and Wrist
Wrist, forearm, and elbow injuries have become epidemic in in-line skating; 45% to 88.8% of reported injuries involve the
wrist, forearm, or elbow (17,18). Almost all injuries to the elbow and wrist are fractures. These are caused by direct
trauma to the elbow or by a fall onto the outstretched hand. Direct trauma to the elbow may cause traumatic olecranon
bursitis or olecranon fractures. Most olecranon fractures require surgical treatment. Falling onto an outstretched hand
with the wrist and elbow extended is the most common mechanism of injury in the inexperienced skater. The position of
the wrist at the time of impact can determine whether the wrist or elbow is injured. If the wrist is dorsiflexed more than 40
degrees, then a distal radius fracture or scaphoid fracture is produced. If the wrist is dorsiflexed less than 40%, then a
radial head or capitellar fracture is produced ( 19). The incidence of these injuries could be decreased by instruction for
beginning skaters, protective gear, and avoidance of crowded facilities and poor skating surfaces. Nevertheless,
“splint-top” fractures occur even with the use of wrist guards. Cheng et. al. ( 20) reported four cases of open forearm
fractures that occurred at the proximal border of wrist guards.
Hand
Most hand injuries in ice skating are lacerations caused by a skate blade. These usually occur in recreational skaters
who skate in crowded public facilities. Competitive skaters at risk for these injuries are short-track skaters and pairs
skaters. Protective gloves would prevent many of these lacerations. In-line skaters are at risk for abrasions from falls
onto pavement. Most of these problems can be prevented by routine use of wrist guards, which protect the palm.
Nonorthopedic Injuries
Competitive and recreational ice skaters are exposed to cold weather conditions. Training and conditioning can be
compromised in cold weather. Bergh (21) showed that lowering of the muscle temperature by 2° to 6°F decreases
maximum aerobic effort as well as maximal isometric and dynamic muscle power. Hixson (22) showed that Olympic
athletes perspire during training and competition despite subzero temperatures. Dehydration and decreased blood
volume in muscles can be a contributing factor in acute and overuse injuries. Adequate fluid replacement is important for
the competitive skater in outdoor conditions.
Frostnip is a superficial blue-white discoloration of the skin with associated insensitivity, usually found on exposed skin
areas such as the face. Often the athlete does not recognize its presence. Treatment includes rewarming of the affected
area. Frostbite is a deeper affliction of the skin layers and is painful. Initial treatment is rewarming and increased activity.
Blisters can result from frostbite and involve tissue loss. Clear blisters indicate a superficial injury and can be debrided.
Hemorrhagic blisters indicate a deeper injury; they should be left intact because debridement can lead to progression of
the zone of injury.
EPIDEMIOLOGY
Several reports have been published on the epidemiology of figure skating injuries. Various results have been reported,
depending on the skating population studied. These studies indicate that competitive, recreational, and novice skaters
are at risk for different types of injuries.
Williamson and Lowdon ( 23) reported on the injuries seen in the local emergency department during the 2-month period
following the opening of a public skating facility in an area previously without a rink. They found an injury risk of 1 per
1,000 visits. Sixty percent of the injuries were fractures, of which 80% involved the upper extremities and 50% were distal
radius fractures. The rest of the injuries were lacerations, 66% of which involved the hand. Approximately 75% of patients
had skated fewer than 10 times, and only 8% had received formal instruction.
Garrick (11) reported on the population of injured athletes referred to his clinic, which deals primarily with recreational
athletes. Figure skating was the ninth most common sport involved. Approximately 85% of the figure skaters were female,
and 63% were between 13 and 18 years old. Overuse injuries slightly outnumbered acute injuries, and fractures
represented only 8% of the injuries. The knee (30%), ankle (25%), and back (10%) were most commonly injured.
Several studies have looked specifically at competitive figure skaters. There has been an increased incidence of injuries
in these skaters because of the increased demands of training time and the increased difficulty of maneuvers practiced.
These athletes skate up to 6 hours per day, 50 weeks per year. Emphasis has shifted to triple jumps, which are
performed at all levels. Missed triple-jump landings can cause tremendous rotational forces on the landing leg. Repeated
practicing of the same maneuver leads to repetitive microtrauma and overuse injuries.
Brock and Striowski (24) looked at 64 nationally ranked Canadian skaters and found that 45% sustained a significant
injury over a 1-year period. Overuse and acute injuries were equally seen; 60% of the acute injuries occurred during
jumps. The overuse injuries were believed to be caused by the minimal time spent stretching. Smith and Micheli ( 14)
looked at injuries throughout the careers of 19 competitive skaters and found 52 overuse injuries and only 8 acute
injuries. The most common problem was low back pain, which was believed to be secondary to tight lumbar fascia from
an overgrowth syndrome. Both studies found few serious injuries, especially compared with sports with similar training
demands, such as gymnastics. The authors believed that the majority of overuse injuries could be prevented with better
warmup and flexibility exercises.
Ice dancers and pairs skaters are exposed to additional risks because of the potential for contact with their partners. As
noted, the demands of ice dancing are different from those of pairs skating. Smith and Ludington ( 25) looked at injuries in
elite pair skaters and ice dancers in a prospective study. They found 33 significant injuries in 48 skaters over a 9-month
period. The female pair skaters were at highest risk, with a rate of 1.9 significant injuries per skater per year.
No epidemiologic studies have been published on speed skating injuries. Because participants compete two at a time in
time trials, the sport has remained relatively safe from acute injury. Collisions are rare, and falls are infrequent. However,
the popularity of short-track pack racing may change this. The potential for collisions and lacerations is much greater,
and protective equipment will play an important role in injury prevention. The speed skating motion is thought to provide
little stress to the bones and joints of the lower extremities, but the sustained forward flexion trunk position is a cause of
back pain. Boot-related problems of tendinitis and calluses are common overuse injuries. The violent movement during a
sprint can cause adductor strains or skate blade lacerations. However, most injuries seen in competitive speed skaters
occur during off-season training with weight lifting, running, or cycling.
Injuries among long-distance skaters are not uncommon. In a study in Sweden ( 26), an incidence of 2.2 injuries per 1,000
skater-days was found, which is similar to that reported in downhill skiing. In interviews with 4,000 members of a skating
club in Stockholm, it was found that 20% had sustained an injury during long-distance skating. The upper extremities and
head were the most common locations. A total of 18% were head injuries, indicating that a helmet should be worn.
Femoral neck fractures were otherwise the most common serious injury. Most of the skaters were 30 to 65 years old, with
a mean age of 55 years, which explains the high number of hip fractures. Most injuries are sustained during falls related
to poor ice conditions. The most common causes are cracks in the ice and over-ice, a phenomenon in which a thin
surface layer of ice has not bonded to the underlying ice. A skater's blade can penetrate the thin surface layer, leading to
falls. These can cause severe hand and facial lacerations from the sharp shards of ice.
The number of skaters and injuries sustained in in-line skating has sharply risen. The National Electronic Injury
Surveillance System in the United States reported 28.9 million skaters and 102,911 injuries in 1996, with an injury rate of
0.356% per skater. This injury rate puts in-line skating seventh in frequency of injury among all recreational sports in the
United States. (27). Adams et al. (17) prospectively evaluated emergency room observation, in-field observation, and
in-field survey of in-line skaters. Acute injuries included fractures or dislocations (48%), abrasions (22%), contusions
(21%), lacerations (20%), blunt head trauma (6%), and blunt abdominal trauma (1%). However, only 2.6% of surveyed
skaters who had had an injury sought medical care in an emergency room. Loss of balance, inability to stop, surface
irregularities, and collisions were the most frequent mechanism of injury. Distal radius fractures account for about 50% of
fractures incurred by in-line skaters ( 18,28,29,30). Lower-extremity injuries account for fewer than 16% of total injuries,
although occasionally they can be severe ( 18,28,29).
BIOMECHANICS AND TECHNIQUE
Most recreational skaters have little concern for power, work per stroke, center of gravity, or hip and knee angle.
However, proper biomechanics and technique are crucial to the success of a competitive skater. Speed skating has been
the most extensively studied discipline, because improvements in times by fractions of seconds can drastically alter race
outcomes. The skating technique of speed skaters and figure skaters is remarkably different. Recognizing these
differences can help in the understanding of injury patterns related to these sports.
A knowledge of the different techniques used in the three events of figure skating (singles skating, pairs skating, and ice
dancing) is necessary for proper care of the injured skater. Each event stresses different skills and exposes the skater to
different types of injuries. Singles skating involves forward and backward maneuvers, footwork, jumps, and spins.
Increasing emphasis in competitions has been placed on difficult and dangerous jumps. Now, skaters even at the novice
level spend a significant amount of time practicing triple jumps. These jumps require great rotational speed to complete
the revolutions, but rotational speed must be decreased before landing. This is done by extending the arms and the
non-landing leg away from the axis of rotation to decrease the moment of inertia just before landing. Opening out a
fraction of a second too early or too late can place significant rotational forces on the landing leg, leading single fall
injuries or to overuse syndromes from repeated microtrauma.
Pairs skating requires skills similar to those of singles skating, except that the jumps and spins must be precisely
coordinated with a partner. Spins can be done side by side or about a common axis of rotation. Pairs skating also
involves lifting maneuvers and throws. In the lifts, the male partner lifts the female skater high above the ice. Both spins
and lifts increase the risk for skate blade lacerations. In the throw jumps, the man throws the woman into the air, where
she completes two or three revolutions; greater height and distance in throws improves the scores received in
competitions. This leads to even greater axial loading and rotational forces on the landing leg and is responsible for the
high incidence of injuries among female pairs skaters. The lifts and throws require upper-extremity strength in the male
partner, placing him at risk for overuse injuries including rotator cuff strains and tendinitis.
Ice dancers concentrate on speed, precision, coordinated footwork, and body lean. The spins are shorter and the lifts are
smaller than in pairs skating, and there are no throws. Couples are judged on artistry, form, symmetry, and music
interpretation. The rotational forces encountered in the lower extremities are much less than in pairs skating. The
dancers are still at risk for injuries caused by contact between partners.
Techniques in speed skating are related to the event. Olympic or metric-style races use time trials in which two skaters
race simultaneously against the clock. The races are carried out on 400-m outdoor tracks, and they vary from 500 to
10,000 m for men and from 500 to 5,000 m for women. Collisions and falls are infrequent, as are acute traumatic injuries.
In short-track skating, four to seven skaters compete in each heat on a 111-m oval indoor track. These races are
characterized by explosive pack starts and tight, crowded turns. Short-track speed skating has become popular because
special outdoor tracks are not needed; the races are run in standard indoor rinks. This has broadened the accessibility of
speed skating.
Speed skating involves a powerful start and long skating strokes with constant repetition. The body position of a speed
skater is illustrated in Fig. 28.2. The goal of a speed skater at any level is to improve efficiency and speed by maintaining
the trunk position as parallel to the ice as possible throughout a race. Variations in body position and anthropometric
measurements have been shown to exist between less competitive skaters and elite skaters; the less competitive skaters
are more upright (31,32) (Fig. 28.3). Multiple factors are important for efficiency in speed skating. Factors such as air
friction, ice friction, weather, and air pressure influence times and thereby drastically influence race outcomes ( 3). Air
pressure and resistance are reduced at high altitudes. The air pressure at the Medeorink in Alma Ata, Kazakhstan, which
is at 1,700 m, is reduced by 20%. Maximal oxygen consumption has been shown not to be drastically altered at this
altitude in the shorter race distances ( 33). These near-optimal climatic conditions coincide with the high number of world
records set at the Medeorink.
FIGURE 28.2. Elite speed skaters maintain a parallel trunk position during the entire race. Skins are worn to minimize
wind resistance.
FIGURE 28.3. The trunk position of these long-distance competitive skaters is more upright then that of an elite Olympic
skater. Hats, gloves, masks, and goggles are worn for protection from cold weather.
As mentioned earlier, in-line skating was developed as an off-season training tool for ice hockey. In-line skating
techniques can be modified to resemble those of various winter sports such as speed skating, figure skating, ice hockey,
cross-country skiing, and downhill skiing. This allows winter athletes to customize their off-season training and optimize
the benefits for their specific sport. In this fashion, in-line skating can be used to improve both technique and
conditioning.
Use of in-line skating to cross-train for Nordic skiing has become more popular as the skating technique has emerged in
that sport. Ski poles can be used with the double-pole push-off technique to more closely simulate Nordic skiing. The
weight transfer, edging, and turns of alpine skiing can be practiced with in-line skates on sloped surfaces. Some ski
areas now have paved trails serviced by ski lifts for skiing with in-line skates in the summer. Recreational in-line skating
has undergone a popularity explosion in the United States and is now a common form of general fitness training.
During the off-season, skaters train on roads, streets, or bike paths using in-line skates. Most injuries are caused by
uneven skating surfaces. Stones, potholes, sand, and wet pavement cause many falls. Downhill terrains are challenging
because high speeds can be obtained and braking is more difficult than with ice skates. The skaters stop by using friction
bumpers on the back of the skate that are pushed against the pavement with the hip flexed and the knee extended in
front of the skater ( Fig. 28.4). Many skaters prefer to use a T-stop when traveling at faster speeds. To T-stop, the braking
leg is dragged behind the skater with the skate perpendicular to the direction of travel. Both breaking techniques are
difficult and cannot stop the skater suddenly. In-line skate manufacturers are trying to develop better breaking systems.
Almost all injuries are related to collisions or falls on hard pavement, so in-line skaters require padding and prophylactic
bracing.
FIGURE 28.4. Stopping with a friction bumper (A) or by a T-stop (B) requires practice to help avoid high-speed falls and
injury.
Long-distance skaters in Scandinavia travel on unfamiliar ice surfaces over lakes, seas, and canals. The technique
involves a more upright body position (see Fig. 28.3), often using a pole or stick for balance, support, and speed. These
skaters often carry ice spikes and rope in case they fall through the ice.
PREVENTION
Equipment
Improperly fitted equipment can lead to injury. The myth of weak ankles is an equipment-related phenomenon. Figure
skates, speed skates, long-distance skates, and in-line skates are all quite different.
Figure-skating boots provide good support and a snug fit ( Fig. 28.5). The boot is in slight plantar flexion with a raised
heel. The skate blade is approximately 4 mm wide and has a slight crown or rock along its entire length. The inner and
outer edges are sharp with a slight hollow between them ( 34). The front of the blade is molded with a toe pick for starting
and spins.
FIGURE 28.5. A properly fitted skate can prevent many of the foot and ankle injuries to which figure skaters are
susceptible.
The leather boots of speed skates are low cut and provide less ankle support than other skates ( Fig. 28.6). With
increasing speed, some long-track skaters are adopting molded skates for better ankle support. The speed-skating blade
is designed for maximal contact with the ice; it is 38 to 40.5 cm (15 to 16 inches) long and flat along the length of the
blade. The blade is 2 to 3 mm wide and is sharpened without a hollow. Competitive speed skaters wear tight suits, called
skins, for minimum wind resistance during a race (see Fig. 28.2). The skins are thin, and there is a risk of exposure to
cold weather.
FIGURE 28.6. The speed-skating boot is low cut, providing minimal ankle support. The long blade is designed for speed.
Clap skates, or klapschaats, have emerged as the latest technology to significantly improve performance. Since their use
in competition, many world records have been broken. The idea of clap skates is not new, but new materials and
technology have allowed them to become an advantage. The blade of a clap skate is attached to the forefoot with a pivot
point. Most are single axle; some have multiple axles. The rear of the blade lifts off the heel to allow the skate blade to
remain in contact with the ice for a longer portion of the skating stroke. The blade then springs back (“claps”) to its
original position.
The introduction of short-track skating has necessitated changes in the design of the speed skate. The boots are more
rigid and are custom molded; they are made of composites (Kevlar, carbon fiber, plastics, epoxy resins) with a leather
boot top. The short-track skate has a rock or crown along the length of the blade. The blade is not centered under the
boot, but is positioned just to the left of center in both the right and left foot. The heel post is higher, which allows a more
acute angle between the skate and the ice surface, for tighter turning. These two adaptations ensure that the boot does
not contact the ice, resulting in a fall. Elite skaters bend both blades to the left to allow tighter cornering. In short-track
skating, protective equipment is essential. A helmet is required, as are cut-proof gloves, knee pads, shin pads, and
protective eyewear. Neck guards have been introduced to prevent lacerations. Short-track skating races are performed in
indoor hockey rinks equipped with standard corner padding to cushion the falls of the skaters.
The long-distance skater often wears a winter boot on which he or she straps the blades of a skate. As noted,
long-distance skaters carry ice spikes and rope. These skaters should wear helmets and elbow and knee pads for injury
prevention.
The boots of in-line skates are made of either leather or molded plastic and are similar to hockey skate boots. Special
racing skates are made that have a low-cut boot and a longer blade, similar to speed skates. The wheels are
approximately 1 cm in width and are arranged in a single line. Recreational skates have three or four wheels (depending
on the shoe size), and racing skates have five wheels ( Fig. 28.7). Because of uneven wear, the wheels should be rotated
every 40 to 50 miles and should be replaced when worn out. The hard plastic brake extends from the heel behind the
wheels and needs to be replaced when worn down.
FIGURE 28.7. A: In-line skates are usually made of molded plastic and provide good ankle support. B: Racing skates are
lower cut and have an additional wheel for speed.
Protective equipment is an essential part of in-line skating ( Fig. 28.8). Although the incidence of head injuries is low, the
risks are great, and helmet use is recommended. Wrist guards are recommended at all times because of the high
incidence of wrist fractures. The guards have internal metal splints that help prevent wrist dorsiflexion. Elbow and knee
pads also protect against injury. Studies show that 16% to 75% of skaters do not wear protective gear. ( 17,28,35,36). A
survey of skaters revealed the following reasons for not wearing equipment: lack of perceived need (47%), too hot (38%),
uncomfortable (38%), cost (16%), and undesirable appearance (16%) ( 37).
FIGURE 28.8. The in-line skater should be adequately equipped with protective gear. A helmet, wrist guards, and elbow
and knee pads can prevent serious injury.
Adams et al. (17) showed that only 2% of in-line skaters wore four recommended pieces of equipment (helmet plus wrist,
elbow, and knee protectors) simultaneously. Eight percent of the skaters who were wearing wrist guards sustained injury,
compared with 26% of those not wearing wrist guards. Of five patients with head trauma, none was wearing a helmet.
Women were more likely to wear protective gear than men (79% to 57%). Scheiber et al. ( 36) determined that there was
a 13-fold increased risk of wrist injury without wrist guards. Nevertheless, as previously noted, wrist guards can be
associated with a “splint-top” fracture; in a series of four such injuries, all were open fractures ( 20).
The American Academy of Pediatrics (38) and the American Academy of Orthopaedic Surgeons (AAOS) ( 39) have
published position statements recommending proper safety equipment, proper stopping techniques, adequate warmup,
obedience to traffic rules and signals, and avoidance of crowded streets, walkways, and roads with debris and defects.
In-line skater safety education should be integrated into patient education programs by all health care providers. The
broad accessibility of in-line skating and the rapid growth in participation make prevention of injuries a particularly difficult
challenge for health care professionals. Risk factors include easily achievable high speeds, difficult stopping techniques,
and the hazards presented by the public pathways or roads that in-line skaters share with pedestrians, cyclists, and
motor vehicles.
Most studies recommend the use of protective equipment and report that it is underused. However, use of protective
equipment alone is not a guarantee of injury prevention. The importance of instruction for beginning skaters should be
pointed out. The following recommendations for in-line skaters are suggested based on information from the AAOS ( 15),
and other available information:
Wear complete protective gear.

Learn the basics.
Anticipate hazards.
Avoid public roads, if possible, and obey road rules if you must use public ways.
Skate in safe areas and under good conditions.
Do not skate while being towed.
Make sure to use highly visible clothing, and use fluorescent clothing and lights when it is dark.
Conditioning
Proper warmup and training routines are crucial for prevention of injury in all types of skating. Kjaer and Larsson ( 40)
evaluated the physiologic profile of elite Danish figure skaters. Maximal oxygen uptake was high in these athletes and
was comparable to that of athletes in other endurance-related sports. Elite Canadian skaters outperformed the Danish
skaters, which suggests that other factors may be related to performance. This study showed a lower injury rate than was
shown in a comparable Canadian study, possibly because of more time spent by the Danish athletes on warming up and
stretching (75 versus 12 minutes per week).
SPORT-SPECIFIC TREATMENTS
Figure skaters, speed skaters, long-distance skaters, and in-line skaters are at risk for numerous overuse and acute
injuries. Treatment for these injuries has been previously described. Most overuse injuries can be prevented by proper
warmup, stretching, and conditioning. To avoid overuse injuries, tendinitis, and stress fractures, skaters should gradually
increase training duration and intensity. Properly fitting skates are crucial to avoiding foot and ankle injuries. Many acute
injuries can be prevented by wearing protective equipment, especially in short-track and in-line skating. Skating for a
well-trained, well-equipped, experienced individual with appropriate protective equipment is a rewarding, enjoyable, and
relatively safe sport.
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3. van Ingen Schenau GJ, DeBoer RW, De Groot G. Biomechanics of speed skating. In: C. Vaughan, ed. Boca Raton, FL: CRC Press,
1989:121–167.
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5. Bregenzer RJ. AC Nielson Company News: international marketing research. Northbrook, IL: AC Nielson, July 30, 1979.
6. Davis MW, Litman T. Figure skater's foot. Minn Med 1979;62:647–648.
7. Pecina M, Bojanic I, Dubravcic S. Stress fractures in figure skaters. Am J Sports Med 1990;18:277.
8. Smith AD. Foot and ankle injuries in figure skaters. Phys Sportsmed 1990;18:73–86.
9. Micheli LJ. Stress fractures in athletes. Paper presented at the Sports Symposium, Burlington, VT, 1991.
10. Cummings T. Lace-bite padding. Phys Sportsmed 1984;12:166.
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12. Smith AD, Stroud L, McQueen C. Flexibility and anterior knee pain in adolescent elite figure skaters. J Pediatr Orthop 1991;11:77–82.
13. Cramer LM, McQueen CH. Overuse injuries in figure skating. In: Casey MJ, ed. Winter sports medicine. Philadelphia: FA Davis,
1990:254–268.
14. Smith AD, Micheli LJ. Injuries in competitive figure skating. Phys Sportsmed 1982;10:36–47.
15. Toren A, Goshen E, Katz M, et al. Bilateral femoral stress fractures in a child due to in-line (roller) skating. Acta Pediatr 1997;86:332–333.
16. Murphy NM, Riley P, Keys C. Ice-skating injuries to the hand. J Hand Surg [Br] 1990;15:349–351.
17. Adams SL, Wyte CD, Paradise MS, et al. A prospective study of in-line skating: observational series and survey of active in-line
skaters—injuries, protective equipment, and training. Acad Emerg Med 1996:3:304–331.
18. Calle SC, Eaton RG. Wheels in-line roller skating injuries. J Trauma 1993:35:946–951.
19. Frykman G. Fracture of the distal radius including sequelae—shoulder-hand-finger syndrome, disturbance in the distal radioulnar joint, and
impairment of nerve function: a clinical and experimental study. Acta Orthop Scand Suppl 1967;108:1–26.
20. Cheng SL, Rajaratnam K, Raskin KB, et al. “Splint-top” fracture of the forearm: a description of an in-line skating injury associated with the
use of protective wrist splints. J Trauma 1995;39:1194–1197.
21. Bergh U. Human power at subnormal body temperatures. Acta Physiol Scand Suppl 1980;478:1–39.
22. Hixson E. Injury patterns in cross-country skiing. Phys Sportsmed 1981;9:45–53.
23. Williamson DM, Lowdon IMP. Ice-skating injuries. Injury 1986;17:205–207.
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25. Smith AD, Ludington P. Injuries in elite pair skaters and ice dancers. Am J Sports Med 1989;17:482–488.
26. Eriksson E, Lofstrom B, Raf L, et al. Injuries from long distance lake skating. Nord Idrettsmedisinsk Kongress Proc Beitostolen Norway
1977:142–149.
27. National Injury Information Clearinghouse. National Electronic Injury Surveillance System, 1992–1996. Washington, DC: United States
Consumer Product Safety Commission, 1996.
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29. Ellis JA, Kierulf JC, Klassen TP. Injuries associated with in-line skating from the Canadian hospitals injury reporting + prevention program
database. Canadian Journal of Health 1995;86:133–136.
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31. van Ingen Schenau GJ, De Groot G. On the origin of differences in performance level between elite male and female speed skaters. Hum
Movement Sci 1983;2:151.
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Biomech 1986;2:175–185.
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physiology. Basel: S Karger, 1976:165–177.
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Williams & Wilkins, 1985:516–531.
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29 Judo And Karate
29
JUDO AND KARATE

JOSEPH F. FETTO
Origins
Differences Between Judo and Karate-Do
Basic Forms of Grappling
Injuries
Prevention and Treatment
Anticipation
Environment
Supervision
Preparation
Conditioning for Martial Arts
Specific Traumas
Head and Neck
Face and Teeth
Chest
Abdomen
Testes
Lumbar Vertebrae
Extremities
Conclusions
Chapter References
The prevention of injuries is the ideal toward which sports medicine strives. It is through the identification and control of
factors that cause injuries that this goal can be achieved. It is in this context that this chapter discusses the sports of judo
and karate-do.
Although the type, prevalence, and incidence of injuries vary from sport to sport, the analysis of injuries occurring in a
specific sport such as judo or karate-do can be performed in a logical and standardized, rather than anecdotal, manner.
Such a process creates an injury profile for a specific sport. Defining a given sport's injury profile can provide insight into
the etiology of injuries associated with that sport. Out of such data comes the means to efficiently identify a given
athlete's potential for injury, a potential that represents a mismatch of that athlete's physical attributes versus the
requirements of a given sport.
The concepts on which this approach is predicated are as follows ( Fig. 29.1):
FIGURE 29.1. Types of trauma and their possible outcomes.
(a) injuries are an unavoidable aspect of sports participation; (b) they occur for a variety of reasons; (c) some injuries go
on to recovery, while others go on to chronic disability. The critical questions to be answered are
1. Why do specific injuries occur?

2. Can they be anticipated?
3. How can one prepare for their occurrence?
4. Can their incidence be reduced?
5. Can their consequences be modified?
6. Can some injuries be prevented altogether?
Temporarily setting aside from consideration psychological factors such as motivation, discipline, and so on, sports
injuries can be studied as events occurring within a mechanical system. This system, although organic, alive, and able to
respond, is still subject to the same laws of physics and mechanics as those governing inorganic systems. As such,
injuries represent mechanical failure of the system. This failure may occur in one of two modes. It can be either the result
of a single event in which acute, excessive stress is applied to an otherwise normal system (i.e., fracture or sprain). Or it
can be the result of repeated submaximal stresses producing a fatigued state within the system (i.e., stress fracture or
tendonitis) ( Fig. 29.2). In either type of failure, if the organic system has not been totally overwhelmed by the trauma (in
which case death ensues), it will attempt to respond. The intensity and extent of its response are determined by the
magnitude of the injury. In a biologic system this reaction is called an inflammatory response. It is the system's attempt to
initiate healing of the injury. It can be thought of as a nonspecific reflex action of the body responding to a stimulus
(injury).
FIGURE 29.2. The vicious circle of injury brought on by system failure as a function of either acute overload or repetitive
submaximal stress.
The inflammatory response mechanism involves chemical, hormonal, and cellular events. These are manifested as pain
(dolor), swelling (tumor), and redness (rubor).The intensity of these events may be modified by immediate medical
intervention, with modalities such as rest, ice, elevation, and compression as well as definitive, specific treatment choices
dictated by the nature of the injury at hand. In any case, the outcome of a period of injury-imposed rest (removal of
stress) is a lowered tolerance and, therefore, increased vulnerability to being injured again. If nothing is done to restore
or increase the system's tolerance limit to its preinjury state, the injured athlete has a significant likelihood of initiating a
pattern of reinjury and chronic disability ( Fig. 29.3A). This pattern has been described as the “vicious circle of injury.”
FIGURE 29.3. A: Increased risk of reinjury is a direct consequence of reduced tolerance caused by rest of the injured
part. B: Conditioning is the result of the controlled application of stress at a frequency, intensity, and duration that can be
tolerated by the system, permitting adaptation and increasing the maximum tolerance level achieved before the onset of
fatigue.
A consequence of this model is the effect of training (the controlled application of stress to a biologic system) on injury
prevention and postinjury recovery. Unlike the inorganic system (e.g., an airplane wing), which is destined to ultimate
failure, the organic system, if given the opportunity, has the potential to adapt to applied stresses. Stress, in this way, can
be considered a stimulus. When it is applied at a frequency, intensity, and duration that permit adaptation before fatigue
failure occurs, the result is a raised level of tolerance (conditioning) and hence a reduced vulnerability to injury (see Fig.
27.3B).
This model also has two important corollaries. First, it provides a methodology by which training techniques can be
evaluated and refined in terms of achieving a desired goal. Second, it demands that individual variability (e.g., age, sex,
body type, anatomy) be considered when evaluating the appropriateness of various training techniques and routines for a
given individual or group of individuals.
This approach permits the identification of potential areas of vulnerability to injury. A specific activity (sport, level of play,
or position within a given sport) can be analyzed for its prerequisites (e.g., strength, flexibility, cardiovascular
endurance). In turn, a composite of which specific attributes may be required to permit successful participation and
lessen the likelihood of injury can be created. This concept of comparing the individual against the anticipated demands
of the chosen activity has been referred to as profiling. This model lays a logical foundation for sports medicine to
achieve its ultimate goal of injury prevention and provides a template for the creation of exercise prescriptions.
With this preamble, a more productive discussion of judo and karate-do injuries and their prevention can be undertaken.
ORIGINS
To have a thorough understanding of the traditional and technical aspects of a sport, it is necessary to have an
appreciation of both its cultural and historical origins and its evolution. Judo, karate-do, and sumo are combat techniques
that evolved in Japan in a unique way. All of them were derived and developed from individual fighting techniques used
in historical times.
Judo, originally called jujitsu, was initially developed in the latter half of the 16th century, when samurai knights grappled
with each other in battle. At that time, Japan was in the midst of civil wars. In the early 19th century, the Teno (emperor)
system was established in Japan after a series of civil wars, and Jigoro Kanoh (1860—1939) rose to become the master
of jujitsu. At the same time, he made a comparative study of the techniques of jujitsu as taught in the various schools. He
picked out what was best among those schools and developed a technique that enabled the most effective mental and
physical training. Kanoh called his technique judo and his training odokan, meaning that the disciplinary principles should
be extended and highly respected.
Karate-do is a martial art that was developed in the Okinawa Island area at the southern tip of Japan. Since ancient
times, Okinawa has had a fist combat technique called te (hand). During the latter half of the 14th century, there was an
interchange of information on the fist-fighting arts with the Chinese via trade routes. This contact was said to have had an
important influence on the conventional te arts of Okinawa. About the time that the Teno system was established on the
mainland of Japan, previously unknown Okinawan martial arts were introduced and spread gradually all over Japan. It
was in 1901 that the name karate was first formally used. However, it is officially called karate-do, meaning that it should
not be interpreted as merely a form of combative technique but as a discipline that aims to develop a mentally and
physically mature person through mastery of the integral arts used in self-defense.
Today, judo and karate-do are played throughout the world. Judo is a recognized Olympic sport. Through Western
involvement in Southeast Asia, it has become popular in Europe (especially France) and in the United States. It has, as a
result of this involvement, expanded to include a significant number of female participants. Karate-do, unlike judo, is
usually considered more of a fighting and self-defense activity than a competitive sport. This is reflective of its greater
emphasis on contact through strikes, blows, and kicks, as opposed to the grappling techniques of judo.
DIFFERENCES BETWEEN JUDO AND KARATE-DO
Judo and karate-do are similar combative sports in the sense that two players, who wear a training suit stipulated in the
rules, stand facing each other and fight to win the match. However, there is a fundamental difference in the essentials of
the respective arts (1,2,3,4 and 5). Judo requires grappling, and karate-do involves contact from a distance, employing
strikes, kicks, and blows.
The natural posture in judo is as follows. The distance between the ankles is approximately 1 foot, and the body weight is
equally distributed on both feet. No particular strain is applied to the four extremities. The participants should look and
stand straight. Either the left or right leg may be put forward by one sole length when the participant moves in any
direction. He or she walks smoothly, rubbing the floor lightly with the sole of the foot. In contrast, the natural posture of
karate-do can vary. The feet may be placed shoulder-width apart, with the knees flexible. The player faces forward and
stands straight. The player may also stand with the feet touching lightly or with the feet two shoulder-widths apart. In
accordance with the distance between the players, the whole body bends, extends, rotates, or propels at an accelerating
speed. The purpose of such motion is to increase the attacking or defending effect.
BASIC FORMS OF GRAPPLING
In judo, the players grapple with each other by gripping the uniform of their opponent with one hand, with the other hand
at the middle of the sleeve ( Fig. 29.4). By doing this, the player can perform a pushing, pulling, or turning action most
effectively. According to the present form of judo, each player grapples with his or her partner with both hands and tries
to apply the attacking technique or to dodge an attack. The player throws the opponent, keeps the opponent on his or her
back for 30 seconds, strangles the opponent just short of unconsciousness, or applies damaging stress to the opponent's
joints. Therefore, the action consists of throwing, pressing, strangling, or joint-attacking techniques.
FIGURE 29.4. The players demonstrate the basic form of grappling used in judo.
In karate-do, two players face each other standing at a distance. They never grapple with each other ( Fig. 29.5), but
there are many patterns of how to hold the arms. In one case, the hand is closed to form a fist, and in another, it is open
and loose. There are many kinds of winning techniques in karate-do. Basically, the sport consists of thrusting and hitting
with the upper extremities, kicking with the lower extremities, and striking with the elbows as well as receiving techniques
for defense against an enemy attack. Except for the receiving techniques, karate-do essentially aims to strike a sensitive
area of the other player while moving swiftly from the confronting posture. Such a technique requires a bending and
jumping movement with the whole body. The winning technique is judged effective when the strike is made at the
aimed-for spot on the other player. There are no throwing, pressing, strangling, or joint-damaging techniques in
karate-do.
FIGURE 29.5. The basic form of karate-do is shown; players face each other at a regulation distance.
INJURIES
Every sport and activity has an inherent risk of injury. No study to date has reported the absolute incidence of injury
among judo and karate-do players. It is noted in Japan that judo ranks after skiing, baseball, karate-do, field athletics,
and skating in frequency of injured athletes reporting to hospitals ( 6). This is similar to the American experience, which
ranks judo far below contact sports such as football, rugby, and hockey and similar to wrestling. The latter has an
expected incidence of significant injury occurring in approximately 10% of participants (significant injury is defined,
according to the American College of Sports Medicine, as one causing absence from sport participation for 24 or more
consecutive hours). The types of injury reported in judo and their frequency are sprains (56.5%), dislocations (21.7%),
fractures (19.2%), and other (3%). The regions of the body most frequently reported injured, in order of incidence, are the
knee, ankle, shoulder, elbow, lumbar spine, wrist, neck, toes, and fingers. The incidence of toe and finger injuries is
believed to be highly underreported by most individuals familiar with the sport ( Fig. 29.6). The remaining injuries include
chest and abdominal contusions, concussions, and rare intracranial hemorrhages.
The limited available data on karate-do demonstrate a greater than 50% incidence of injuries occurring among
tournament participants, an obviously experienced group ( 7). In one tournament, injuries occurring among 70 participants
were as follows: extremities, 18; head and neck, 11; trunk, 8; thigh and leg (hematomas), 8; hand and fingers, 5;
concussion, 2; and eye, 1 (6). Both judo and karate-do have reports of hematuria and myoglobinuria after competition
and from training sessions.
These injury profiles reinforce the fact that judo and karate-do are dissimilar sports, in both the type and the frequency of
injuries that they engender. More data exist on injuries resulting from specific techniques for judo than for karate-do. The
incidence of injuries in judo as a function of specific techniques is illustrated in Figure 29.6. When comparing matches
against free exercise, injuries in judo occur somewhat more frequently during match competition. The defense techniques
in judo usually cause more injuries than the attacking techniques do ( Fig. 29.7). The defending player in karate-do also is
more frequently injured.
FIGURE 29.6. The nine judo techniques most frequently responsible for causing injuries. (From Mifune T. Canon of judo.
Tokyo: Seibundo-Shinkosha, 1956. Courtesy of Horiyasu.)
FIGURE 29.7. The nine judo techniques most frequently responsible for causing injuries, depending on whether the
player is using an attacking or defense technique. (From Mifune T. Canon of judo. Tokyo: Seibundo-Shinkosha, 1956.
Courtesy of Horiyasu.)
Injuries are commonly caused by throwing techniques. Attacking players using the shoulder throw (seoi-nage) and back
drop (tai-otoshi) techniques sustained more injuries when they were unsuccessful and were subsequently crushed under
the defending players (Fig. 29.8 and Fig. 29.9). The defending players were most often injured when subjected to the
attacking techniques of the inner thigh (uchi-mata), major outer reaping (o-sotogari), or sweeping loin (marai-goshi) (Fig.
29.10, Fig. 29.11 and Fig. 29.12). These injuries were the result of throwing of the defending player or the catching of the
extremity between the two players.
FIGURE 29.8. The shoulder throw (seoi-nage) is the technique responsible for the highest number of injuries in judo
(20.9%).
FIGURE 29.9. The back drop (tai-otoshi) is the second leading cause of judo injury (10.4%).
FIGURE 29.10. The frequency of judo injuries from use of the inner thigh (uchi-mata) technique (9.6%) is close to that of
the back drop.
FIGURE 29.11. The major outer reaping (o-sotogari) approach of judo is demonstrated.
FIGURE 29.12. The initial phase of the sweeping loin (harai-goshi) technique of judo is demonstrated.
During throws in the high circle (tomoe-nage), both attacking players, as they were crushed, and defending players, as
they were thrown, suffered a similar number of injuries ( Fig. 29.13). The crab-claw throw (kani-basami) resulted in a
smaller percentage of injuries (Fig. 29.14). However, this particular technique has been under vigorous discussion as one
to be prohibited, because of the severity of lower-extremity injuries (triad lesions: complete anterior cruciate sprains;
medial collateral ligament sprains; and medial meniscus tears) caused by this throw even when it is executed properly.
FIGURE 29.13. The rigors of the judo move of throwing in the high circle (tomoe-nage) are demonstrated.
FIGURE 29.14. The crab-claw throw (kani-basami) technique is responsible for a small percentage of judo injuries
(3.5%).
Groundwork techniques (mat work, or ne-waza) produce few injuries except for occasional severe muscular strains of the
torso. During exercise and training, instances of olecranon, acromioclavicular, and minor trochanteric bursitis have
occurred in connection with forward rotation of the body, whereas cervical strains are generated by backward rotation.
Depending on the skill of the receiver, contusions of the hypothenar aspect of the hand; compression-disruption of the
ankle mortises, the calcaneus, and the talus; and contusion of the lateral malleolus also have been observed.
Stand-up throwing (tachiwaza) can frequently cause strain, fracture, and dislocation of the toes and the foot. A difficult
problem occurs when actual rotation movement is applied to the half-bent knee, resulting in a serious ligament sprain or
subluxation-dislocation of the patellofemoral joint.
When a judo player is thrown and falls to the floor onto the shoulder, an acromioclavicular separation can occur. If body
distortion is involved, the player may also suffer a clavicular or rib fracture. If a judo player takes a violent fall backward,
he or she may hit the occipital region, resulting in concussion or acute subdural hematoma. This was seen in the
neurosurgical department at the University of Tokyo ( 6).
The strangling technique is often applied during mat work. The player being strangled can fall into temporary
unconsciousness. This mechanism is explained by the sudden oxygen deprivation of the brain caused by compression of
the common carotid artery bilaterally.
In the articular technique (usually applying a hyperextension force), disruption of ligaments with resultant dislocation is
caused by excessive application of force. According to Norton and Cutler ( 8), serious injury of this sort is most likely to
occur at the knee and shoulder. The elbow is directly attacked quite often, but the defenders usually yield before
dislocation of the elbow occurs. This is because of the continuous, rather than sudden, manner in which correct
technique applies stress to the elbow joint.
Frequently, the toes suffer minor injuries, and contusions, sprains, fractures, and dislocations are significantly
underreported.
The rare cases of reported fatalities caused by strangling have involved players with preexisting heart conditions or liver
dysfunctions.
Studies have attributed judo injuries to several factors ( 1): (a) poor technique with excessive force (61.7%); (b)
inexperience with the technique employed (17.4%); (c) insufficient physical strength or conditioning for the level of
activity attempted (14.8%); and (d) inadequate equipment, environment, and supervision (6.1%). These statistics are
used to explain the occurrence, causes, and mechanisms of injuries that occur in the sport of judo. Attention has
traditionally been concentrated on training methods that enhance technical skill, particularly in defense techniques.
The receiving technique is a defensive move against a good throw executed by the opponent. Norton and Cutler ( 8)
concurred with this analysis of injuries in judo. According to their explanation, the receiving, or defensive, technique is the
absolute essential first step in judo training. It is indispensable. Notwithstanding these reports, the fact remains that many
players become discouraged early in their experience with judo as a result of suffering injuries that occurred because of
not only poor technique but also because of fatigue or inadequate physical condition, or both. Both judo and karate-do
require quickness and repetitive movements over an extended period.
In addition to acute trauma, overuse syndromes are frequently encountered. Because overuse conditions are not
dramatic—although they are incapacitating—they are grossly underreported by judo and karate-do participants. These
injuries include tendonitis of the lateral extensor musculature of the forearm (secondary to sustained grip activity), rotator
cuff and shoulder girdle strains, paraspinal strains (secondary to throwing and lifting techniques), and hamstring strains
(secondary to sweeping and rapid extension moves involving the lower extremities). The explosive, repetitive loading of
the muscle group brings on each of these conditions. Therefore, preparation must emphasize sufficient flexibility
(stretching) and aerobic conditioning along with strengthening exercises so that the athlete can withstand the sudden and
sustained output of energy and effort required by the sport. Experience has shown that proper and successful execution
of the movements requires quickness, agility, and flexibility.
In 1978, comparison of anthropomorphic data of judo veterans with average adult Japanese men showed three points of
variance: strength of back muscles, girth of the chest, and side-step quickness. A similar attempt to profile karate-do
players seemed to show a bias in favor of their having shorter reaction times. These data are of interest but cannot be
relied on to predict success. However, DeMeersman and Ruhling ( 9) evaluated the physiologic effect of a specific
training regimen. Their conclusion was that judo training enhanced cardiorespiratory function. This result, although also
observed in Canada by Taylor and Blassard ( 10), did not clearly show an advantage over the results achieved in other
sports. More data are required before a more complete profile for judo and karate-do can be constructed. Because of the
explosive and sustained output of energy and effort required by judo and karate-do, players must have adequate stamina
to avoid premature fatigue and increased vulnerability to injury.
PREVENTION AND TREATMENT
Prevention depends on anticipation, environment and equipment, supervision, and preparation.
Anticipation
Understanding how winning is accomplished in a given sport aids in the anticipation of injury-producing situations.
Winning in judo is determined by the accumulation of a greater number of points than the opponent or by ending a match
by pinning or choking out the opponent. Performing specific techniques of bringing the opponent to the mat, performing
near-pinning movements, and successfully executing escapes or reversal maneuvers awards points. The number of
points awarded also is reflective of the technical excellence with which the execution of a given maneuver is performed,
in adherence with specific defined parameters of the sport. Therefore, success in judo depends on a combination of
technical skill, endurance throughout the match, and sufficient strength to execute attack and defense maneuvers well.
In karate-do, winning is also determined by point accumulation. Points are awarded according to the specific style of
karate-do being performed (noncontact, limited contact, or full contact). Here, quickness and agility are paramount,
endurance is important, and strength is a lesser prerequisite for success.
Judo techniques consist of overthrowing, holding, strangling, and joint articular maneuvers. Each of these can be divided
into a large number of subtechniques. The common general training methods are as follows. The beginner must first
become accustomed to the atmosphere of judo and get rid of excessive tension. Furthermore, he or she must learn the
manners of judo. When the athlete stands, he or she must master the natural posture without fail. Then, the player must
repeatedly practice smooth and quick movements in any direction, while keeping the sole of the foot in contact with the
floor. The overthrow must be started with a simple movement. Its series of steps must be understood fully by analysis of
the motion in detail. This exercise must be done repeatedly, because the mastering of these basic actions is
indispensable to safety in the contact training that comes later. One-on-one training with players who do not know the
basic techniques well is highly dangerous and frequently ends in injury; this must be strictly prohibited. The remaining
aspects of beginning training for judo players are concerned with the aggressive method of overthrow and the receiving
technique. The properly executed receiving technique protects the player who is being overthrown from injury. For the
holding technique, the application and evading methods must be practiced.
When the correct technique has been learned from solitary practice, the player may practice the attack and receiving
techniques with a partner, after they have agreed on the exercise contents. At the beginning, the player should avoid
performing the techniques with full strength. The free practice (rando-ri) must be done with a partner. It is recommended
that this free practice exercise be done with a more experienced player to help with learning the correct technique. After
the basic action has been learned, other kinds of overthrow and holding techniques must be mastered in the same way.
The player tries to distort the opponent's posture and simultaneously to apply his or her own technique in response to the
opponent's movement. In this way, the forte or special technique of a player is developed. Free practice with a partner
becomes the mainstay of the exercise, and the full-force practice is repeated. At the same time, the technique is
perfected through the practice matches.
The art of karate-do is theoretically identical to that of judo. However, the technical aspects are different. Roughly
speaking, there are three schools of karate-do. In the first school, a technical motion must be stopped shortly before it
comes in contact with the opponent. In the second school, only the thrust technique against the face is prohibited;
otherwise, contact with the body of the other player is allowed. In the third school, the player must wear protective gear
during the match while technique is applied directly by the other player ( Fig. 29.15). Various standard postures and
footwork must be learned, and the purposes and advantages of each must be considered. Then, the motions of the
hands and feet must be learned. After all these steps are mastered, the self-practice must repeat the respective
techniques such as the thrust, strike, hit, kick, and receiving movements. In karate-do, throwing and strangling are
prohibited in principle. While receiving, however, a player may try tripping or throwing to attempt to thwart the opponent.
After repeated practice, players become accustomed to the techniques, after which the following two practice methods
are applied. First, one player carries out the various movements in succession alone. This is the practice of kata form. If
two players try to apply the karate-do movements against each other with full force, there is a danger of causing injury.
Therefore, it is indispensable to learn fully a series of kata forms. The second practice method is called jumite and
involves the combination of techniques employed by two players. Here, the players agree in advance on which moves to
practice. For the free technique, combinations of movements are used, and the players make no agreement in advance.
The latter is equal to the free practice method (rando-ri) of judo.
FIGURE 29.15. Two karate-do players are pictured in action wearing full protection.
Environment
The traditional training facility of judo or karate-do is called the dojo. The training and matches for judo are carried out on
straw mats (tatami) put down over a wooden floor, whereas karate-do is usually performed without mats. These setups
have obvious inherent hazards. Western programs usually use padded mats (4 by 6 feet or 4 by 8 feet) connected by
Velcro on four sides. A training hall floor should be founded on a spring base. The standard allocation is three tatami
mats per player. In all cases, both judo and karate-do are performed in bare feet. Therefore, to avoid foot trauma, the
need for meticulous care, maintenance, and cleanliness of the exercise facility is obvious. The dojo should be well lit and
well ventilated. Proper recommended lighting is 150 to 300 lux for training and 200 to 500 lux for match purposes.
The training uniform is called the gi (pronounced “gee,” with a hard “g” sound). It is composed of a loose-fitting jacket and
pants fastened by a cloth belt. The belt color is used to designate the level of proficiency of the athlete.
These seemingly reasonable prerequisites have led, however, to a philosophic schism among advocates of these sports.
For example, in karate-do, one camp advocates the use of protective equipment during learning and training sessions in
order to avoid injuries. These devices, they believe, should be used in one-on-one practice to protect the face, abdomen,
hands, back, and ankles. Purists, however, believe that to achieve the maximum potential benefit of a training session it
is necessary to employ “total effect of training” through the use of severe environmental surroundings, and they
discourage the use of protective gear.
At present, both judo and karate-do are popular internationally as sports for physical education and the art of
self-defense. Women are increasingly engaged in these traditional male activities. Both these sports were developed
from martial arts, and even when they are handled as sports the original military spirit remains. However the names of
judo and karate-do are applied, they are not to be thought of as simply military combat activities. Do means “the way” or
“disciplinary principle.” Through the practice of politeness, fraternity, calmness, modesty, seriousness, courage, and
other human qualities, judo and karate-do attempt to address the total person. Together with the aesthetics of the sport,
importance is given to the development of mental skills such as the powers of observation, patience, and the ability to
focus attention. Above all, good manners are emphasized as an essential part of both sports' traditions. The player is
taught always to respect the senior or more experienced player. At the match, the player must wear the training uniform
(gi) correctly. Before and after the match, the players sit down formally and make a bow to each other, expressing mutual
respect.
The Oriental philosophy that human integrity must be maintained while learning and practicing the techniques is strongly
evident. The overt and intentional inclusion of these concepts gives a greater dimension to the sports of judo and
karate-do than is usually encountered in general physical education or Western sport activities. However, this spirit of
commitment to the whole person sometimes leads to dangerous or, at best, unwise training environments. For example,
to foster patience and self-control, some advocates of the sports have suggested that winter practice be carried out on
frigid early mornings and summer practice in the heat of the midday sun. It is alleged that in both cases the mental
discipline to overcome these unbearable environments and the strength and positive spirit gained are more important
objectives than the mere improvement of the techniques.
The positive physiologic effects of athletic participation have been reported on numerous occasions in Western medical
literature. However, a tremendous amount of evidence also exists concerning the adverse effects of severe climatic
conditions on physiologic systems and their performance. Therefore, enthusiastic adherence to the Oriental philosophy
must be tempered with judicious management of environmental conditions in the training hall. In this way, injuries arising
from the environment itself and those that may occur as a result of impaired performance secondary to suboptimal
climatic conditions (e.g., excessive heat, cold, humidity) should be avoided.
Supervision
Because injuries do occur and the goal is to minimize their occurrence, frequency, and consequences, supervision of
sports activities is a critical factor in establishing a safe environment for the athletes. Supervision has three aspects:
preseasonal, intraseasonal, and interseasonal. Supervision is mandatory for training and competition, and it requires a
multitude of skills and expertise. This section outlines an ideal program of supervision. Limitations of resources and
personnel obviously force choices to be made in executing an individual program. An attempt is made to underscore the
relative importance of each factor and thereby to assist the reader in selecting optimal choices when faced with the
reality of a limited amount of available resources on which to draw.
It is absolutely imperative that there be a clearly designated person to direct the program. This person may also embody
other responsibilities, as outlined later. Supervisory responsibilities may be delineated between those concerned with
medical issues and those pertaining to specific issues of training, training techniques, and competition ( Fig. 29.16).
Certainly, these are complementary and not mutually exclusive areas of concern. Both areas must be serviced by
individuals with not only a thorough knowledge of their specific area of responsibility but also a familiarity with the areas
for which the other members of the supervisory team are responsible. For optimal function, open, frequent, and candid
communication among these individuals is an absolute necessity.
FIGURE 29.16. The two components of sports supervision.
A complete medical program requires, at the barest minimum, involvement of a person or persons who have completed a
certified first aid course through a recognized agency (e.g., American Red Cross, local medical center educational
program, American College of Sports Medicine). This person should be present at all training sessions and must be
present at all competitions. He or she must be designated as a central figure responsible for identification, management,
and triage of injuries. Ideally, the person responsible should be a physician, a certified athletic trainer, or someone with
established, recognized competence in the area of sports medicine. He or she should have an established and posted
plan for the management of medical situations (emergent, urgent, and follow-up), including (a) steps to be taken in the
event of an emergency; (b) location of first aid equipment; (c) name, location, and phone number of program supervisor;
(d) name, location, and phone number of local emergency transport service (e.g., 911); (e) name, location, and phone
number of local emergency room or emergency treatment center; and (f) name, location, and phone number of physician
affiliated with the program or telephone number of local emergency room director.
Preparation
Knowledge and familiarity with judo and karate-do assists in the anticipation of injuries. A proper and adequate
environment and use of high-quality equipment will prevent unnecessary injuries. Good supervision encourages safe
participation. Injury prevention must be taken care of before attention can be focused on preparation of the player.
Training for judo and karate-do is traditionally divided into three distinct phases— kata (learning), rando-ri (free practice),
and jumite (advanced practice)—each of which should be further broken down into warmup, play, and cooldown periods.
Match competition may be attempted only after training has been established and techniques have been learned. The
key tenet of judo and karate-do training is that defense (receiving technique) must be mastered before offense training
can be started.
The learning of form includes understanding the intent and proper application of the specific techniques. It starts with the
repetitive practice of basic movements. Then a training partner is introduced onto the mat. Movements are then
repeatedly practiced with the partner. Next, the players agree on what techniques to practice and actual execution is
attempted. Overthrowing and pressing are carried out with the partner only after kata has been completed. In karate-do,
this phase does not always involve a partner.
The free practice of judo and karate-do is a training method by which well-rehearsed and mastered basic forms are tried
freely on a partner. After the combination of various techniques is learned, practice matches are conducted to master the
entirety of the sport.
Advanced practice involves two players who have agreed on what moves to practice; they then engage in learning
through mutual execution of the techniques. This also is referred to as the agreed combination technique. More
advanced training involves the free combination technique, which is, in effect, mock competition.
Each of these levels of practice has the express purpose of mastering techniques. To minimize injury during training,
players must learn warmup and cooldown routines. The warmup must be performed before initiation of the formal practice
session. It involves flexibility and light aerobic (cardiovascular) exercises. Every player should be analyzed in regard to
his or her inherent musculoskeletal flexibility or lack thereof. Accordingly, the athlete should be guided through a logical,
formal program of stretching movements for the torso and lower extremities (11). It is important to give special attention to
individual needs and to keep in mind any previous trauma. Nonimpact or low-impact aerobic activity (calisthenics)
provides excellent cardiovascular preparation for a training session.
At the conclusion of a training session, it is equally important for the athlete to engage in a cooldown period, which
includes cardiovascular and stretching components. Usually, the warmup and cooldown segments should consist of 10 to
15 minutes of stretching and 5 to 10 minutes of cardiovascular exercise.
CONDITIONING FOR MARTIAL ARTS
Martial arts require speed, power, flexibility, isometric strength, and balance. Competition may require participation in
four or more bouts in one day, requiring an endurance component to performance. Although strength is not considered
an important component for performance, it may enhance some aspects of performance such as defense and grappling
(13). Rutamess (13) described a training program for jujitsu that incorporates an aerobic component and strength
component, with suggestions for core exercises and sports-specific exercises to enhance performance. The program
follows the concept of periodic intense loading and unloading cycles. Shirley ( 14) described a similar program for
Taekwondo training, with a bigger emphasis on strength training and a detailed analysis of the side kick.
SPECIFIC TRAUMAS
Head and Neck
Even if the head sustains an impact from throwing in judo or from being kicked in karate-do, it is not necessarily an
emergency unless the player is unconsciousness or shows evidence of brain damage, including violent headache or
vomiting. A concussion or blood clot must be suspected in players who cannot stand, have an impaired state of
consciousness, respond slowly, or do not respond to their name. In such cases, when no neck injury is suspected, the
patient must be laid down with the head turned laterally and positioned lower than the feet to encourage draining from the
bronchial tree during the observation and transportation. Pulse rate, blood pressure, and respiration must be checked. If
the athlete's condition is found to be stable, he or she is moved to a room and lies quietly while observation is continued
for a time. If the base of the tongue drops backward and respiration is impaired due to a disturbed state of
consciousness, the mouth must be opened, the tongue pulled forward, and an oral airway inserted. The patient must then
be transported to a medical facility. Even when consciousness has been regained, transportation to the hospital should
be considered if the patient complains of violent headache or if vomiting occurs. Of course, if convulsion or
unconsciousness lasts longer than 10 minutes, rapid transfer to the hospital must take place. Generally, if the initial state
of unconsciousness continues for more than 10 minutes, some type of brain damage, which is demonstrable in 25% of
the cases on a scan, has probably occurred. A fracture of the skull seldom happens when the head strikes a tatami.
However, an acute subdural hematoma sometimes does occur from the rupture of a parasagittal-bridging vein.
If choking is caused by the strangling technique and is followed by unconsciousness, cerebral hypoxia results from the
circulatory disturbance. The patient should be placed on the back with the head lower than the feet. Usually,
consciousness is recovered in about 10 seconds.
A blow to the head is often accompanied by trauma to the cervical vertebrae and neck region. A cerebral vertebral
fracture causes violent pain. If pain is distributed over the upper extremities, a cervical fracture is likely. It also is
necessary to check for any spinal cord damage involved in these fractures; symptoms include diaphragmatic respiration,
numbness in the region below the upper extremities or chest, trouble in stretching out or bending the forearm, and
paralysis of the lower extremities. The patient should be laid down and carefully transferred to a stretcher. The position of
the head and neck should be fixed with sandbags or a cervical collar before transfer to the hospital is attempted.
Face and Teeth
In karate-do, trauma to the face and teeth and lacerations to the oral cavity are frequently sustained. Fractures of the
nasal cartilage, zygomata, and upper and lower jaws require surgical treatment; local treatment is not possible. However,
resultant nasal hemorrhage with bleeding in the oral cavity must be treated immediately. This hemorrhage may occur
after a blow to the nose or face, even without fracture or damage to the teeth. For a severe nasal hemorrhage, the patient
should be laid in the lateral posture to prevent blood flow into the larynx, which could block the respiratory pathway. If
available, clean gauze soaked with epinephrine diluted to about 1:100,000 and a 1% lidocaine solution should be
inserted into the nostrils to compress the region, thus stopping the bleeding. The nasal membrane is rich in small vessels
and is prone to bleeding. Most nasal hemorrhages occur at Little's area in the external nasal region; pieces of clean
gauze should be applied at that point. If no medication is available, gauze packing can be used alone. If nasal
hemorrhage is slight, the patient should lie down quietly. A towel should be placed on the upper face, including the base
of the nose. Bleeding in the oral cavity, fractures of the jaw, broken teeth, and laceration of oral membranes can be
caused by a blow from the hand to the lower face. The blood that is caught in the oral cavity and mixed with viscous
saliva may eventually move into the upper respiratory passage and cause blockage; pieces of broken teeth can also
block respiration. Therefore, the injured patient should be laid down in a lateral, side lying position, and foreign material
should be removed from the oral cavity. A piece of gauze soaked with epinephrine and lidocaine may be packed at the
bleeding site. The medical supervisor may have the patient gargle with a hydrogen peroxide solution. After the acute
condition is somewhat abated, the patient should be transported to an oral surgeon. It is imperative that all loose or
broken teeth be saved and transported with the patient.
Chest
Rib fractures may occur in karate-do practice performed without chest protection and occasionally in judo practice. Local
pain is strong at the region of the fracture, particularly during respiration. The injured person should be laid on the back
in a suitable place. Pain is usually alleviated by slight elevation of the upper body. Do not bandage the chest.
Abdomen
Trauma to the abdomen may occur in karate-do matches. If the player is hit severely in the abdomen, impairing the state
of consciousness, or if the player is found in a shock-like state with complaints of violent pains in the abdomen, damage
to internal organs must be suspected. Pain in the right abdominal region leads to suspicion of liver damage. Left
abdominal pain may indicate splenic damage or rib fracture. The patient should be placed in the most comfortable
position and then transported to the hospital at once. Oxygen inhalation therapy and intravenous drip infusion are
desirable on such occasions, if available.
Testes
In karate practice, the testes are sometimes kicked in error. Violent pain occurs instantaneously, which spreads to the
upper abdominal region. Furthermore, there is accompanying nausea and vomiting, and the patient suffers, in some
cases, from transient shock conditions. However, it is seldom that the testes or ancillary area is burst open. Some
bleeding at the scrotal region and edema are usually observed. Prompt recovery from shock is usually achieved by
keeping the patient in a quiet, head-down position. Cooling of the affected area is recommended. If the scrotum has
swelled significantly, a hematoma may be present. The patient should be sent to a urologist for further evaluation.
Lumbar Vertebrae
Trauma to the lumbar vertebrae often occurs in judo practice, because players must lift or throw their opponents while
also twisting their bodies. During mat work, the body has to be bent in forced postures. Fracture dislocation of the lumbar
vertebrae rarely happens, but a lumbar sprain can occur during preliminary exercises or matches. Therefore, violent and
severe lumbosacral discomfort may manifest during these activities. It is recommended that the patient be placed supine
on a solid surface with a pillow behind the knee and the hips flexed approximately 45 degrees. This position gives the
most pain relief. If there are symptoms of spinal cord injury (e.g., paralysis of the lower extremities), the sides of the trunk
must be fixed with pillows or sandbags and a backboard used for immediate transport.
Extremities
If the player complains of intense pain in the joints in any of the extremities, it is safe to assume that a sprain, dislocation,
or fracture has occurred. Accurate diagnosis and treatment must be made at a local emergency facility. The basic
treatment is the application of a splint that protects and fixes the injured area in the position in which it was found.
Restoration of alignment is to be undertaken only by people competent to do so. For this purpose, the practice hall or
athletic facility should be equipped with various sizes of splints, triangular cloths, and slings. An inflatable air splint is
useful for handling fractures of the extremities or severe ligament injuries; it is recommended that one should be
prepared in advance and readily available. After the injured region has been fixed in a proper fashion, the patient should
be promptly transferred to hospital for further evaluation and treatment.
CONCLUSIONS
Judo and karate-do are dissimilar sports. However, their training and supervision can be managed with common logic.
These sports encourage and reward flexibility, endurance, and agility. As such, they are excellent tools for achieving
fitness. However, they also engender potentially injurious activities. Learning of the techniques of these sports must be
well supervised. Their mastery requires rigorous adherence to a formalized program of training that does not allow
competition until mastery of techniques has been well demonstrated.
CHAPTER REFERENCES
1. Matsumoto Y. Coaching of judo. Tokyo: Daishudan-Shoten, 1975.

2. Nakamura R. Judo. In: Japan Amateur Sports Association, ed. The report of researchers on sports medical science in Japan, No. 2. Tokyo:
1981:167–184.
3. Oyama M. This is karate. Tokyo: Japan Publication Trading, 1974.
4. Roth J. Black belt karate. Rutland, VT: CE Tuttle, 1974.
5. Smith RW. A complete guide to judo. Rutland, VT: CE Tuttle, 1958.
6. Kodama T. Sports injuries and their prevention. Int Congress Sports Sci 1964:1:1–50.
7. McLatchie G, Davies JE, Caulouey JH. Injuries in karate: a case for medical control. J Trauma 1980;20:956–971.
8. Norton NL, Cutler C. Injuries related to the study and practice of judo. J Sports Med Phys Fitness 1965;7:149–173.
9. DeMeersman RE, Ruhling RO. Effects of judo instruction on cardiorespiratory parameter. J Sports Med Phys Fitness 1977;17:169–183.
10. Taylor AW, Blassard L. A physiologic profile of the Canadian judo team. J Sports Med Phys Fitness 1981;21:160–174.
11. Anderson B. Stretching. New York: McGraw-Hill, 1974.
12. Glover B. Family fitness guide. New York: McGraw-Hill, 1991.
13. Rutamess NA. Weight training for jiu jitsu. Strength and Conditioning 1998;20:8–15.
14. Shirley ME. The taekwondo side kick: a kinesiological analysis with strength and conditioning principle. National Strength and Conditioning
Association Journal 1992;14:7–8,72–78.
30 Canoeing and Kayaking
30
CANOEING AND KAYAKING

DAVID M. JENKINSON
SARAH W. JENKINSON
History
Biomechanics
Rowing versus Paddling
Boat and Blade
Water Environment
Racing Disciplines
The Stroke: Canoeing
The Stroke: Kayaking
Epidemiology
General Population
Injury Data
Injuries
Shoulder
Elbow and Wrist
Back Injuries
Pelvic Injuries
Chest and Abdomen
Neurologic: Head and Neck
Eyes
Ears
Mouth and Face
Lower Extremities
Dermatologic Problems
Infectious Diseases
Problems Related to Environmental Conditions
Drowning
Conditioning
Summary
Chapter References
Most North Americans are first exposed to paddle sports by those noisy old aluminum canoes at summer camp. Those
who have never paddled a canoe immediately think of the Native American paddling a birch bark canoe across a mirror
lake. Others think of the sealskin kayak that the Inuit uses to paddle across the lonely frozen north. Most people in the
United States would not think of the people of the early Polynesian culture, who used the outrigger canoe to island-hop
their way across the Pacific Ocean—or of the great ornate dragon boats of the Chinese cultures. The point is that every
society and culture across time has used a human-powered watercraft with an independent paddle for transport. This
chapter updates these images to elucidate the dynamic sport that makes up modern paddle sports.
HISTORY
As the world entered the machine age, what once was a utilitarian boat evolved into a tool for sport and recreation.
Flatwater canoeing and kayaking became popular leisure sports in the United States and Europe at the end of the 1800s.
Increasing interest in the sport led to the development of a racing community, and in 1924 the International Canoe
Federation (ICF) was formed in Europe to promote the racing of canoes and kayaks ( 1).
The Olympic connection of canoeing and kayaking began in 1936, when flatwater racing was first introduced at the
Eighth Olympic Games in Berlin. Although the longer distances were dropped in later years, ICF sprint racing has been a
medal sport ever since. Whitewater slalom racing is a relatively new Olympic sport. It was first introduced on the Olympic
stage in 1972 at the Munich Games. However, because of concerns about the expense of building an artificial
racecourse, as was done in Munich, the sport was not seen again until the 1992 Olympic Games in Barcelona and in the
1996 Olympic Games in Atlanta (2). Whitewater slalom racing was initially dropped in 1996 because of concerns about
expense, but it was reinstated in 1998 after strong lobbying by the international paddling community. Currently, both
flatwater sprint and whitewater slalom racing are scheduled for the 2004 Olympic Games in Athens.
Various terms are used to describe the world of paddle sport. In most of the Americas the term canoe is used to describe
a specific type of boat that is paddled with a single-blade paddle (i.e., the old family canoe). The term kayak to describes
a boat that is paddled with a two-bladed paddle from the seated position (i.e., the “Eskimo kayak”). The sports are usually
referred to as canoeing, kayaking, canoe and kayak, or by the specific subdiscipline (e.g., sprint kayak). In other parts of
the world, the all of paddle sports combined may be referred to as canoeing, regardless of the type of boat being used,
and a boat that looks like the old family canoe it is called a “Canadian canoe.” This inconsistent terminology can cause
problems in researching the sport.
BIOMECHANICS
Rowing versus Paddling

There are two major differences between rowing and paddle sports (canoe and kayaking): the type of blade and the
attachment of the paddle to the boat. In rowing the oar has a single blade, but in kayaking the paddle has a double blade;
canoeing uses a single-blade paddle, but it is held in a different manner. In rowing the oar is attached to the boat via a
mechanical oar lock, whereas in canoeing and kayaking in the paddle is never attached to the boat but is held by the
paddler. These differences produce some interesting biomechanical considerations. For example, the rower is able to
generate much higher forces per stroke but cannot as high a stroke rate as a canoer or kayaker. In addition, the oarlock
provides certain stability to the boat, allowing a sliding seat to be added to shells. The addition of the sliding seat allows
a greater contribution of lower extremities to the stroke, whereas in paddle sports there is a minimal contribution from the
legs and the stroke power comes mostly from the trunk and upper body. In addition, instead of sliding on the long axis of
the boat, paddlers rotate their torsos ( 3,4), potentially causing a certain degree of increased axial and boat instability.
Boat and Blade
Paddle sport is divided into two disciplines: kayaking and canoeing.
In kayaking, athletes usually sit in their boats with their feet up in front of them and paddle with a double-bladed paddle.
The blades have traditionally been “offset” or in different planes (usually 45 to 80 degrees); the control hand,
predominantly the right hand, rotates (extends) in order to rotate the blades into proper orientation to the water. The
boats have a top deck, and the kayaker is usually sealed in the boat by means of a fabric or neoprene spray skirt,
although “sit-on-top” kayaks have no cockpits.
In canoeing, athletes may be sitting or kneeling (on either one or both knees), and they use a single-bladed paddle. The
boats themselves maybe either “open” (no top deck) or “decked” (with top deck, cockpit, and spray skirt). The control
(top) hand rotates the single-bladed paddle in order to control the direction of the craft.
Water Environment
Canoe and kayaking activities can be further divided into three broad categories: flatwater, ocean, and whitewater
paddling. Flatwater paddling includes ICF sprint boats, ICF marathon boats, United States Canoeing Association (USCA)
marathon canoes, recreational and tripping canoeing, canoe sailing, * and kayak (canoe) polo.† Ocean paddling includes
sea kayaking, surf skis (sit-on-top), surf kayaks, and outrigger canoes. Whitewater paddling includes slalom racing,
wildwater racing, whitewater rodeo competition, recreational whitewater paddling, and extreme whitewater steep creek
paddling.
Racing Disciplines
Paddling has a worldwide popularity; in fact, canoeing is actually the national sport of several European countries.
Although flatwater sprint racing and whitewater slalom racing are the two most recognized racing forms of the sport owing
to their Olympic Games exposure, paddle sports includes a wide variety of racing variations. Disciplines that have races
and world championships sanctioned by the ICF are wildwater downriver racing, canoe sailing, canoe polo, and ICF
marathon. Other sports with race series and championships are kayak and canoe whitewater rodeo, outrigger canoe,
dragon boat, surf ski, and USCA marathon canoe‡.
Sea kayaking is a tremendously popular recreational sport in the coastal areas of the world. “Long-distance” ocean
paddling races have become popular both by themselves and in combination with triathlons and multidiscipline extreme
races.
The relatively new competitive sport of whitewater rodeo is a combination of whitewater recreational paddling or “play
boating” and elements of squirt boating. Whitewater rodeo is analogous to freestyle or aerial skiing. In this sport a
paddler in a short whitewater kayak or canoe (either open or decked) uses certain stationary river rapid features to
perform spectacular surfs, spins, flips, cartwheels, and so on, in front of a panel of judges. The discipline is unique
because of the extreme and rapid changes of position and high proprioceptive demands made of the paddler.
The Stroke: Canoeing
The basic forward stroke of canoeing has the most variations. In competition it is performed from a “high kneel” position
(one knee down) in sprint racing, from a full kneeling position (both knees down) in whitewater open and decked canoes,
and from a seated position in USCA open marathon canoes.
A basic stroke can be separated into four phases: entry, propulsion, exit, and recovery ( 5). In the entry phase, the stroke
is begun by trunk flexion and rotation. The lower arm is extended and the shaft hand is semipronated parallel to the axis
of the canoe; the elbow of the upper arm slightly bent, and the center of gravity is slightly forward. The blade is angled as
it enters the water; the best blade angle at entry for sprint is 35 to 40 degrees ( 5). During the propulsion phase of the
stroke, the flexion of the trunk is diminished while it is rotated back to neutral. The arms “pull” through the stroke, until the
lower hand reaches the area of the hip. At this point the upper hand may ulnar deviate as the lower wrist flexes to change
the angle of the blade in the water from a power stroke to a turn or J-stoke. In the exit phase, as the paddle clears the
water, the trunk is extended. During recovery, the lower arm is flexed and lifted, with the lower elbow moving outward
from the body, while the upper arm is dropped toward the inside of the canoe. During the return movement, the trunk
again begins to flex ( 6).
Another aspect in the biomechanics of paddling a canoe is the idea of paddle side changing. In sprint canoeing, the
paddler never switches sides, whereas in USCA Marathon canoeing the paddler switches sides every few strokes. In
whitewater canoeing, the canoeist may either change sides (switching) or keep the same hand placement and simply
rotate the trunk enough toward that side to paddle stroke (cross-stroking). Information is lacking on whether asymmetric
muscle development in canoeists (7) plays a role in injuries. This would appear to be more of an issue in those
disciplines in which paddlers do not switch paddle sides.
The Stroke: Kayaking
The biomechanics of the kayak stroke are clearly much more symmetric. Although it looks to the uninitiated as if only the
arms were propelling the boat, the stroke is actually an intricate coordination of trunk, shoulder, arm, wrist, and hand
(5,6,8). In the entry phase, the stroke is begun by leaning forward and rotating the trunk. The shoulder on the stroking
side is dropped, while the uppermost arm is flexed. In the propulsion phase of the stroke, the rotation of the trunk
decreases. The shoulders are initially set in the same lateral plane, but as the stroke proceeds the active shoulder moves
forward. The elbow of the lower arm, stroke side, is now flexed, and the paddle passes close to the boat. The pushing
action is initiated by the shoulder girdle of the upper arm (opposite side from the stroke) and is continued by the arm on
that same side of the body. In the exit phase, the paddle clears the surface, the trunk rotates, inclining away from the
water. During the recovery phase, the lower arm is now flexed to 90 degrees, and is lifted, keeping clear of the body and
returning to the start position.
In all kayak variations—sprint, whitewater, sea kayak, and sit-on-tops—the stroke is preformed in the seated position.
The major difference among the disciplines is in the position of the knees. In ICF flatwater racers (sprint and ICF
marathon), the knees are held close together with the feet in a neutral to slightly externally rotated position. In whitewater
and sea kayaking, the knees are as wide apart as possible, with more external rotation of the feet. In most kayaks a foot
bar, foot peg, or bulkhead is used to brace the feet. Sprint boats may have either a fixed or rotating seat. In whitewater
kayaking, not only is the seat fixed but also the paddler is held in place with additional “hip pads” to further anchor the
pelvis in the boat.
EPIDEMIOLOGY
General Population
According to data compiled from the 1995 National Survey on Recreation and the Environment (NSRE) ( 9), of the total
number of paddlers in the United States, 14 million individuals canoe, 2.6 million kayak, and 15.2 million are rafters. The
24.8 million combined figure takes into account an overlap among paddling disciplines of 7 million people. The 1995
NSRE showed that the number of people who paddle a canoe, kayak, or raft in a given year represents 12.1% of the total
U.S. population age 16 years and older. When canoeing and kayaking are combined, it is the third most popular
watercraft sport, behind motor-boating and water skiing and ahead of sailing and jet skiing ( Table 30.1). A regional
breakdown revealed that paddling is most popular among those living in the midwestern region of the country (13.7%),
followed by the northeast (12.1%), the south (11.9%), and the west (10.7%). In terms of actual numbers of paddlers, the
south had the most (8.12 million), followed by the midwest (6.54 million), the northeast (5.14 million), and the west (4.48
million). The sport is more popular among men than women, and the 16- to 24-year-old age group has the greatest
percentage of participants ( Table 30.2 and Table 30.3)
TABLE 30.1. PERCENT OF U.S. POPULATION 16 YEARS AND OLDER PARTICIPATING IN OUTDOOR
RECREATION, BY ACTIVITY, 1994–1995
TABLE 30.2. NUMBER AND PERCENT OF U.S. POPULATION PARTICIPATING IN OUTDOOR RECREATION BY
ACTIVITY AND GENDER, 1994–1995
TABLE 30.3. NUMBER AND PERCENT OF U.S. POPULATION PARTICIPATING IN OUTDOOR RECREATION BY
ACTIVITY AND AGE, 1994–1995
Injury Data
The absence of reliable statistics has long plagued paddle sport participants, athletes, coaches, researchers, and
medical personnel ( 10). Many studies have simply overlooked canoeing and kayaking, and others suffer from
inconsistent survey methods, missing data, limited sample populations, and various other problems. As a result, it is
difficult to assess something as basic as the rate of growth of canoe and kayak participation, let alone injury data.
The United States Coast Guard has released boating injury statistics for 1997 and 1998 on the World Wide Web ( 11,12).
In 1998, 115 deaths and 80 injuries were reported to the Coast Guard; 105 of the deaths were from drowning, and 42% of
those injured were admitted to hospital ( 12). The 1998 data showed that 57% of all injuries were caused by hypothermia.
The data were not separated according to subdiscipline (e.g., flatwater versus whitewater, type of boat).
The American Canoe Association (ACA) (13,14,15 and 16) and the American Whitewater Association (AWA) ( 17,18) are
two groups that have tried to analyze and extract lessons from the record of fatal accidents in recreational whitewater
paddling. Even though the data were derived from various sources, including word of mouth, an increasing trend in the
number of deaths was noted (Fig. 30.1). The greatest increase in the death rate of 1997 apparently occurred among
rafters and inexperienced canoers and kayakers ( 18). The increase in deaths among experienced boaters appeared to
be related to high water levels that year and to marked advancements in boat designs and in the skills of experienced
paddlers: “In 1986 a large group of paddlers suddenly graduated to class 5.0 rivers. Ten years later, in 1996, a large
number of boaters suddenly started paddling class 5.1 and 5.2 extreme runs, especially steep creeks. At the top of the
skill curve, a larger than normal group of pioneers seem to have pushed through the next barrier resulting in the suddenly
large number of accidents in class 5 whitewater and an unusual number of high profile boaters dying” ( 18) .
FIGURE 30.1. Annual whitewater fatalities. Accidents including rafters.
In 1995, Edwards did an injury survey of 30 international kayakers ( 19) in which he found that the most injured area was
the shoulder (53%), followed by the back (20%)( Fig. 30.2). Further investigation found that 54% of the kayakers had
impingement syndrome (Fig. 30.3). These shoulder data are consistent with a 1997 pilot screening study done on USA
Canoe Kayak Junior slalom athletes, of whom more than 52% were found to have active shoulder injuries. But instead of
simply impingement and its various forms, the junior slalom athletes had a mixture of injuries (impingement syndrome
alone represented 23%), as well as instability combined with impingement (27%) (D.M. Jenkinson and S. Grindel,
USACK Junior Shoulder Pilot Study, unpublished data, 1997).
FIGURE 30.2. Areas of injury in sprint kayaking.
FIGURE 30.3. Types of shoulder injuries.
INJURIES
Shoulder
Numerous studies have shown that the shoulder is one of the most common areas injured in members of the paddling
community, and impingement syndrome is the most common shoulder injury (1,6,19,20 and 21). Impingement syndrome,
both acute and chronic, is a cause of lost training and poor performance. In the canoe stroke, the top arm is placed in a
position that can cause structures of the shoulder to be pinched on a repetitive basis. By the very nature of the canoe
stroke, the subacromial bursa and supraspinatus tendon are prone to impingement by the acromion process and
coracoacromial ligament.
The kayak stroke also offers ample opportunity for an impingement type of injury pattern. The kayak paddler's stroke
abducts and elevates to shoulder level, causing rotator cuff structures to be pinched on a repetitive basis. This condition
can become chronic, because persistent inflammation can lead to fibrosis. Rotator cuff degeneration and tear, however,
are very rare in this athletic population.
Pelham et al. reported anecdotal concerns in the flatwater community the shoulder injuries and impingement syndrome
were less common before year-round weight training was instituted ( 22). Berglund and McKenzie reported some
concerns about certain overhead weightlifting practices as well ( 1). They further stated, “The mechanism responsible for
this condition is overuse resulting in microtrauma causing local inflammation often associated with edema. A major factor
in the development of this syndrome is the muscular hypertrophy common in these athletes” ( 1). In addition, several
authors have questioned whether the early season or the lack of proper warmth, or both, have led to an increased risk of
injury (1,20,23).
Berglund and McKenzie noted that, when canoeists were tested with an isokinetic dynamometer, flatwater paddlers had
exceptional strength in the movements of external and internal rotation of the shoulder. They suggested that, to prevent
shoulder injuries, one should strive for a ratio of external to internal strength of 0.7 ( 1).
One of the most devastating injuries a boater can suffer is anterior-posterior glenohumeral dislocation or subluxation. In
contrast to most sports, an improperly performed high-brace, roll and static turning stroke puts the paddler in the classic
externally rotated, abducted position. Quick identification and field reduction of anterior dislocation, by properly trained
medical personnel, is a key to minimizing sequelae.
Heinrichs suggested that posterior rotator cuff strain is a relatively common injury and that posterior capsule instability is
occasionally seen in whitewater slalom kayakers ( 24). There are even anecdotal reports of posterior dislocation suffered
by whitewater kayakers who reach forward for the next stroke only to plant the paddle into a fixed position, thus forcing
the humeral head into the posterior medial capsule.
Relatively little has been written about the role of shoulder instability in paddle sports, specifically the whitewater
disciplines (slalom, recreational, and rodeo). In a pilot study done in 1997 (D.M. Jenkinson and S. Grindel, USACK Junior
Shoulder Pilot Study, unpublished data), 27% of junior slalom athletes showed symptomatic instability (instability
impingement syndrome [25]) (Fig. 30.4). In 1991, Heinrichs commented that “chronic shoulder instability may be an
underlying cause of rotator cuff tendonitis” ( 24) and that any conditioning or rehabilitation program must include a
shoulder stability program ( 26).
FIGURE 30.4. 1997 USACK Jr. survery.
Elbow and Wrist
Elbow and wrist injuries present another problem for boaters. Although medial and lateral epicondylitis are relatively rare
in whitewater sports, flatwater athletes often suffer from these conditions.
A common injury in paddling is overuse of the wrist extensors. This repetitive overuse injury of the wrists can range from
medial nerve palsy to general extension tendonitis ( 19,20). In one study, 23% of long-distance canoe racers developed
wrist extensors tenosynovitis. “This is an overuse injury often seen with the initiation of on-the-water training:
Traditionally, long distances are done early in the season and this excessive use can lead to an inflammatory condition”
(1). The dominant hand was much more likely to be affected; the type of boat or angle of blade had little effect in this
study. It appears that rough water and windy conditions can cause an increase in this injury, because the athlete is
forced to grip the paddle aggressively to control the boat ( 1,27).
A lesser problem is that of DeQuervain tendonitis, which affects about 10% of paddlers ( 19). Possible solutions including
changing the diameter of the paddle shaft for canoe or kayak paddles and changing the offset (the “feather”) of the kayak
paddle blade, from the traditional 80- to 90-degree angle to the newer 45-degree offset.
Flexor tendonitis is more common in the canoe paddler who must flex the lower wrist in order to steer the boat. Again,
environmental conditions such as rough water or wind can play a role in the development of this injury. A cross-wind
forces exaggerated wrist flexion in the J stroke, and overuse initiates an inflammatory response. Also, use of a tight grip
for prolonged periods during long paddle sessions can result in median nerve entrapment at the wrist. Tendon
hypertrophy may also play a role in the development of this exercise-related carpal tunnel syndrome. Often a looser grip
and a paddle with a different shaft diameter help this condition ( 1).
Forearm compartment syndrome is occasionally seen when concerted effort is accompanied by an aggressive grip. The
athlete has restricted wrist flexion, tight and painful flexor compartments, possibly some hand numbing, but normal
peripheral pulses. Although acute discomfort should resolve fairly rapidly, this condition can interfere with training. A
series of forearm stretches, combined with massage and change in paddle shafts can be beneficial, as can relaxing the
grip somewhat (1).
Back Injuries
The large muscles of the upper and lower back and shoulders provide the power in all canoe and kayak strokes, and
paddlers are subject to frequent back strain ( 20,28). Numerous studies have reinforced the value of preevent stretching
for all boaters (20). In most cases the athlete can benefit from increasing hamstring flexibility and abdominal
strengthening. In kayaking, transient back pain can be helped with added lumbar support (a “back band”).
Biomechanically, attention should be paid to improving trunk rotation on the catch phase of the forward stroke, rather
than leaning forward from the waist. The more serious injuries in this area occur in the weight room, where maximal lifts
generate tremendous forces in the thoracic and lumbar regions. The most common injuries are to the rhomboid,
trapezius, latissimus dorsi, and serratus anterior muscle groups. Disk herniation and neurologic involvement are rare in
these athletes, but for back pain that does not resolve disk herniations and spondylopathologies ( 29) should be ruled out.
Pelvic Injuries
Overuse injuries to the lower extremities are relatively minor. Boaters occasionally suffer from ischial tuberosity bursitis.
Flatwater kayak paddlers spend a great deal of time sitting on a hard seat, and with the rotation associated with each
stroke considerable pressure is transmitted to the ischial tuberosities. Compression of the sciatic nerve in the buttock
with numbness to the foot is a chronic complaint. Modifications of the seat with padding or even drilling holes in the seat
to relieve pressure may help. Ice massage, hamstring stretching, physiotherapy, and nonsteroidal antiinflammatory drugs
(NSAIDs) are useful therapeutic tools; corticosteroid injections into the bursa may be necessary to resolve this injury ( 1).
Chest and Abdomen
Hypertrophic cardiomyopathy is the most common cause of sudden death in young athletes ( 30). It is a congenital
disease involving hypertrophy of the left ventricular wall, mostly the septum. The abnormal heart muscle can cause
malignant ventricular arrhythmias and death. This congenital disease may be contrasted to the “athlete's heart,” in which
left ventricular hypertrophy is seen as an adaptive response to exercise ( 31). Although most studies have noted an
increase in wall thickness, three studies showed not only wall hypertrophy but also an increased septum wall thickness in
canoe athletes (30,32,33). Pelliccia et al. commented that this unique echocardiographic change may be caused when
canoeists, “working against high resistance, generate greatly increased cardiac output by performing a combination of
isotonic and isometric exercise” ( 30). Although hypertrophic cardiomyopathy is extremely rare, any cardiac symptoms,
including accentuated dyspnea, dizziness, and syncope, must be investigated vigorously, keeping in mind that any
finding of septum wall hypertrophy may be adaptive rather than pathologic.
A rarer occurrence is that of intermittent vascular obstruction of the axillary vein ( 34). In this case the marked hypertrophy
of the shoulder girdle muscles causes compression of the axillary vein.
One case study reported on a canoeist who presented after 10 days of abdominal and back pain. An ultrasound
examination and ultrasound-guided needle aspiration demonstrated a rectus sheath hematoma. After conservative
treatment, the paddler resumed full participation ( 35).
Paddlers can also be subject to blunt trauma from a missed stroke, boat edges, other boats, and so on. This can result in
contusions, broken ribs, or even puncture wounds of the abdomen or legs. In addition, several reports have been
published of another rare overuse injury in paddlers, rib stress fractures ( 36).
Neurologic: Head and Neck
Head and neck injuries, although relatively uncommon in flatwater canoeing, are a significant consideration in whitewater
boating. The combination of gradient, water volume, and rocky river channels make blunt head trauma, loss of
consciousness, and/or neck hyperextension injury a possible consequence in case of an upset or roll. Hence the
recommendation that all whitewater canoers, kayakers, and rafters wear helmets ( 37). Any loss of consciousness on the
water always mandates immediate cervical spine precautions and evaluation by a physician.
“Exercise-induced syncope is a fairly common problem. It is the result of global cerebral ischemia due to failure of
cerebral perfusion. Perfusion failure during, or shortly after, a prolonged exertion, such as hard endurance training, may
be related to cutaneous vasodilation while muscle blood vessels are still dilated, compromising cardiac output and
resulting in syncope. Migrainous attacks (effort migraine) can occur after athletic effort of any kind. Many effort migraine
attacks have only parts of the classic migraine. Severe headache, scotomas, occasional hyperventilation and nausea
usually occur immediately after exertion. Focal neurologic deficits are seldom seen. The symptoms may be precipitated
by dehydration, excessive heat, hypoglycemia and unaccustomed altitude. Effort migraine is more common in untrained
athletes and tends to decrease provided physical fitness improves and other precipitating factors are avoided” ( 1).
Eyes
In addition to infections, mentioned previously ( 38), ocular trauma is common during associated waterside travel in
whitewater and wilderness boating. Frequently corneal abrasion occurs from surrounding vegetation during scouting or
portaging. Occasionally lid laceration or corneal hemorrhage can occur during scouting, falls, or rolls ( 39). Contact
lenses may be worn during whitewater and wilderness boating, but the risk of loss during upset and recovery requires
one or two backup devices.
Paddlers are also threatened by the development of pterygium, a overgrowth of connective tissue that can extend over
the conjunctiva. This condition is promoted by exposure to wind, water, and sunshine. Several cases of this condition
have been reported in paddlers ( 1), and excision of the lesion is necessary. Routine eye protection is recommended for
all paddlers.
Ears
Formation of exostoses is a threat unique to extended-season whitewater boaters and sea kayakers ( 40,41). This
condition, although known to physicians, has only recently gained recognition among the boating community itself. If the
condition is recognized early enough, watertight earplugs can frequently slow progression of the disease. Tympanic
membrane perforation has been reported in whitewater boaters after forcible submersion events (D.M. Jenkinson and M.
Roush, unpublished injury data, 1999 World Slalom Championships).
Mouth and Face
Blunt trauma to the face and teeth are always a concern in whitewater boating. Dental trauma usually occurs when a
boater lets go of the end of the paddle during an upset. Canoe polo provides a new aspect of a team sport in that the
athletes are at risk of injury from other competitors' paddles and boats. More severe facial trauma or fractures can occur
during upsets in kayaking or canoeing. The possible use of face shields and proper control of the paddle could minimize
this possible injury; “Hold it, don't eat it” is a common admonishment.
Lower Extremities
Overuse injuries to the lower extremities are, by nature of the sport, relatively minor. Boaters occasionally suffer from
quadriceps strains, hamstring pulls, iliotibial band syndrome, patella-femoral syndrome, patella tendonitis. A whitewater
boater in an improperly fitted boat can sometimes develop a transient numbness and tingling. This lower-extremity pain is
usually caused by vascular insufficiency or occlusion from extreme flexion of the foot and knee in combination with
general decreased flexibility and improper outfitting. Modifications in the outfitting of the boat and a general program of
stretching usually resolve this problem quickly. Fractures of the femur, lower leg, ankle, and foot have all been reported
during whitewater entrapment situations or falls during scouting. Sprint (high-kneel) canoe paddlers are subject to
peripatellar pain in the “down” knee, and a chronic bursitis in this area has been reported. Modification of the boat with
special padding can resolve this injury ( 1).
Dermatologic Problems
Dermatologically, canoers and kayakers are exposed to a wide variety of skin pathologies. They range from simple
overuse blisters (21) on the hands, heels, and buttocks to allergic dermatitis from exposure to the Fiberglas, Kevlar, and
other complex materials and resins that make up the boats. Breakdown of the dependent derma is a very real threat to
long-distance paddlers ( 1). Lacerations are common occurrences during scouting and portaging. The on-water conditions
warrant special attention to sun protection. Sunburn, sun poisoning, and skin cancer are important concerns to long-time
boaters. In addition, overgrowth of calluses on the hands can be a serious problem; occasional paring can easily keep
this condition under control.
Infectious Diseases
Kizer found that 10% of boaters reported developing diarrhea and other symptoms of gastroenteritis during boating trips
(21) (Fig. 30.5). Foreign wilderness travel can also expose boaters to an assortment of fungal and parasitic infections of
the skin and gastrointestinal tract. Numerous infections have been reported in the literature, including malaria ( 42),
schistosomiasis (43,44), pulmonary blastomycosis (45), onchocerciasis (38), and Staphylococcus aureus infection
(42,43,44,45 and 46). No boater should drink untreated water. Other simple steps in infection prevention (e.g., simple
laceration and blister care) are frequently overlooked. One study found that 47% of whitewater boaters were not currently
immunized against tetanus (21). Some wilderness organizations are debating whether guides and instructors need to
have hepatitis immunization.
FIGURE 30.5. Whitewater recreational activities.
Problems Related to Environmental Conditions
Heat produced during exercise in a hot, humid environment cannot readily be dissipated from the body. Therefore, during
prolonged exercise in the heat there is a risk of developing fatigue secondary to hyperthermia. When accompanied by
dehydration, heat exhaustion may lead to hypovolemia, inability to provide both skeletal muscle and skin with oxygenated
blood in required rates, and heat stroke ( 47). This disorder is a potentially lethal condition characterized by disturbed
consciousness and organ damage.
The introduction of high-tech drysuits and synthetic clothing has extended the recreational paddle sport season well into
the late fall and early spring. In southern states, rowing and whitewater boating are year-round sports. The elite Olympic
racer must train and paddle all year round. In the north, sea kayakers frequently “break ice” to start their season.
Hypothermia is always a threat. Most cases of hypothermia occur in 4.5° to 15.5°C (40° to 60°F), rainy weather,
especially in the unprepared paddler. A sudden immersion can cause hyperventilation, bronchospasm, and cardiac arrest
due to the shock of cold water ( 48). Longer exposure results in loss of thermoregulation ability and hypothermia.
Therefore, when the water is cold, all paddlers are advised to wear adequate clothing and a personal floatation device
(PFD) and to ensure that their boats have enough buoyant support. Although drowning is uncommon among elite
paddlers (a major Swedish flatwater racing club had only two drownings in 30 years [ 1]), it must be given serious
consideration as a risk when paddling on cold water.
Drowning
And lastly a word about one of the obvious complications of paddle sport, accidental death and drowning. Most
accidental deaths can be broken down into two categories: inexperienced boaters without proper training and not
wearing a PFD, and experienced boaters in a boat or body entrapment situation. Some simple lessons are important in
preventing serious consequences:
1. Never boat alone.

2. Make sure your boat is in good repair with the appropriate safety equipment.
3. Wear your PFD.
4. Never use alcohol before or during boating.
5. Good swimming skills and good physical condition are important.
6. If you are new to the sport, get some training in the basic techniques and rescue skills.
7. And for the experienced boater: know your skills and limits.
Many local YMCAs, local paddling clubs, or university clubs are a good place to get the basic training at low or no cost.
CONDITIONING
Any canoe and kayak conditioning and rehabilitation program must concentrate on some fundamentals. A good baseline
aerobic fitness is a must, especially for speed and endurance. Even though slalom, rodeo, and other activities are
considered to be more anaerobic than aerobic, baseline aerobic conditioning is important.
In the past, a number of authors have been concerned about inappropriate strength training ( 1,20,21,22 and 23). A good
general program must be balanced to work not only on developing the large power muscles but also on strengthening the
rotator cuff and the scapular stabilizers. Regardless of discipline, all canoers and kayakers need to pay special attention
to scapular protraction and retraction. It is crucial for a boater not only to generate and maintain power output but to do
so with the glenohumeral joint in a balanced and nonpathologic state.
Flexibility is the third key to any training or injury prevention program. Special attention should be paid to the lumbar and
hamstring regions. Numerous authors have proposed that lumbar and hamstring flexibility is important in the prevention
and rehabilitation of low back injuries ( 1,19,20,21,22,23 and 24). But clearly flexibility is not limited to the low back;
paddlers must pay attention to the shoulders, forearms, and wrists as well.
SUMMARY
Few sports come in as many variations as canoeing and kayaking. From a multiweek expedition paddle trip across
Canada's Northwest Territory to a final run down an Olympic slalom course that lasts only 100 seconds, all of these
variations harken back to those original images we all have of canoe sport: a boat, a paddle, and a paddler.
*Another unique event is canoe sailing, which, although it is a well-recognized international sport, actually involves little or no paddling.
†Kayak (canoe) polo is a hybrid event in which small kayaks are used to play a variant of water polo, usually in a large swimming pool or, rarely,
an outdoor body of water.
‡ICF marathon differs from USCA marathon. ICF marathon uses boats similar to sprint boats and is extremely popular in Europe. USCA
marathon canoeing uses an open canoe and is an extremely popular sport in Texas and other regions of United States.
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31 Lacrosse
31
LACROSSE
LESLIE S. MATTHEWS
RICHARD Y. HINTON
NANCY BURKE
The Game
History
Rules
Equipment
Conditioning
Injury
Epidemiology
Mechanisms
Prevention
Management
Conclusions
Chapter References
Lacrosse is a fast-paced team sport played by men and women at the youth, high school, collegiate, club, and
professional levels. Considered North America's oldest sport, the game has rich historical roots in many of America's
Native Indian cultures. Lacrosse was played to resolve tribal conflicts, heal the sick, and develop strong, skilled warriors.
Interest in the modern game has exploded, and lacrosse now rivals soccer as the fastest growing youth sport in America
(1,2). Today, almost 100,000 boys and girls participate in high school lacrosse, and another 100,000 play in youth
recreational leagues. In addition, there are more than 400 men's and approximately 250 women's college teams
participating at the varsity or intercollegiate club level. In just the past 5 years, the number of high school women's
programs has doubled. There is also growing interest on the international level. In 1998, 11 nations fielded teams at the
Men's International Lacrosse Federation World Championships, and nine international women's teams competed in the
International Federation of Women's Lacrosse Associations Championships. A number of countries have also introduced
“soft lacrosse,” a noncontact coed version of the game ( 2).
From its beginning, the game has been played with a stick that has a stringed pocket at one end, resembling a crosier ( la
crosse, a symbol of pastoral office). Field players use their sticks (crosses) to pass, catch, and run with the ball. The
game rewards stick skills, speed, and endurance, not brawn. Full-field sprints, precision passes, and quick player dodges
are the routine in both the men's and women's games. The speedy changes of direction involving players, sticks, and ball
create a unique set of physical demands, training requirements, and potential injury situations for lacrosse participants
(Fig. 31.1).
FIGURE 31.1. Lacrosse is a high-speed field sport that demands quick starts and stops, which may lead to
lower-extremity strains and sprains. (Photograph courtesy of Bill Welch.)
THE GAME
History
Legends tell of baaga'adowe (early Indian form of lacrosse) contests involving hundreds of participants per side played
on fields of 1 to 15 miles in length ( 3). The original game was rough and required endurance, often being played over a
2- or 3-day period with little rest. The first literary reference to the game was made in 1636 by Jesuit missionary Jean de
Brebeuf, who wrote of a game played by the Huron Indians near Ontario, Canada ( 3). French Canadians became avid
players, and the Montreal Lacrosse Club was formed in 1856. In 1867, W. George Beers developed standards for field
dimensions, number of players per team, and basic procedural rules. Later that same year, an American Indian team
generated considerable interest while touring Great Britain. Subsequently, lacrosse clubs were formed near London and
Liverpool, and in the following year the English Lacrosse Association was formed ( 2,3,4,5 and 6).
In the United States, New York University fielded the first college team in 1877. Interest spread throughout New England,
and Harvard, Princeton, and Columbia formed teams. The Intercollegiate Lacrosse Association was formed in 1878.
Intercollegiate lacrosse has grown to more than 350 teams participating in National Collegiate Athletic Association
(NCAA) Division I, II, and III varsity programs. In 1995, only the men's NCAA Basketball Final Four championship game
outdrew lacrosse as the NCAA contest with the largest attendance ( 2). Lacrosse was a men's sport in the Olympic
Games of 1928, 1932, and 1948. More recently, it was an exhibition sport at the 1984 Los Angeles Olympic Games. The
Men's World Championships were initiated in 1967 by the International Lacrosse Federation in Toronto and are now
hosted on a rotating international basis every 4 years. The first Women's International World Cup was played in 1982,
and this competition is now held every 4 years. There are similar international competitions for both boys and girls
(under-19 teams).
Women's lacrosse was first played at the Saint Leonard's School in Scotland during the 1890s ( 7). An attempt was made
to start women's lacrosse in the United States in 1914 at Sweet Briar College in Virginia, but it was not until 1926 that
women's lacrosse was well established at the Bryn Mawr School in Baltimore, Maryland ( 7). The United States Women's
Lacrosse Association was established in 1931.
US Lacrosse was founded in 1998 as the single national governing body of the sport. This association has unified a large
number of previously existing men's and women's lacrosse organizations and provides a leadership role in levels of
amateur lacrosse throughout the United States. Located in Baltimore, Maryland, US Lacrosse houses the Lacrosse
Museum and National Hall of Fame, publishes Lacrosse magazine and Lax Mag for Kids, and directs a number of
development and educational programs. Nationwide, there are more than 50 regional chapters of US Lacrosse serving
almost 1 million enthusiasts.
Box lacrosse is an indoor spinoff of field lacrosse that is played on artificial turf in an arena the size of an ice hockey rink
(8). The sticks and goals are smaller than those used in field lacrosse, and the rules allow a great deal more physical
contact (8) (Fig. 31.2). Box lacrosse has been played predominately in Canada, but in 1986 the National Lacrosse
League was formed as a professional indoor league in the United States ( 2). In 1998, there were seven American teams
and one Canadian team. The indoor season runs from January to April, and additional expansion plans for the league
are underway.
FIGURE 31.2. Professional box lacrosse is played indoors and allows more contact than the outdoor field game.
(Photograph courtesy of Bill Welch.)
Rules
Until the mid-1930s, men's and women's lacrosse games were played under the same rules and with little protective
equipment. At that time, men's lacrosse began to evolve into a true contact sport, whereas the women's game remained
more traditional in its emphasis. Field size, number of players per side, and procedural rules are different in the men's
and women's games. However, for the sports medicine specialist, the biggest difference is the much greater amount of
player-to-player and stick-to-player contact allowed in the men's game. As a result, the men's game requires the use of
helmets, shoulder pads, and heavy protective gloving.
Men's Lacrosse
Men's lacrosse is played by 10 players: 3 attackmen, 3 midfielders, 3 defensemen, and a goalie. Each team must keep at
least four players (including the goalie) in its defensive half of the field and three in its offensive half. The attackmen's job
is to score goals. Their play, usually restricted to the offensive end of the field, involves short bursts of speed and
dodging changes of direction. They need excellent stick skills and tend to be smaller, quicker athletes. The midfielders
cover the entire field of play; their job is to move the game from the offensive to defensive and back again. Speed,
stamina, and distance passing skills are essential. Defensemen, who tend to be larger players, use longer sticks to keep
check on opposing attackmen. The goalie needs good hand-eye coordination and strong leadership skills ( 8). The
playing area for men's field lacrosse is 110 yards (100 m) long and approximately 60 yards (55 m) in width. The goals are
80 yards (73 m) apart, and there is a playing area of 15 yards (13.5 m) behind each goal, permitting more action behind
the goal than is seen in ice hockey ( 9) (Fig. 31.3). The goal consist of two vertical posts 6 feet [1.8 m] high joined by a
crossbar 6 feet [1.8 m] long. A goal (1 point) is scored when the ball passes from the front completely through the
imaginary plane formed by the goal line, goalposts, and top crossbar. Regulation playing time in college lacrosse games
is 60 minutes, divided into four periods of 15 minutes each. High-school teams usually play 12-minute periods. A referee,
umpire, and field judge supervise play.
FIGURE 31.3. Diagram of the field of play for men's lacrosse. (From US Lacrosse: Parent's guide to the sport of lacrosse,
4th ed. Baltimore: US Lacrosse, 1998, with permission.)
Play begins with a faceoff, in which the ball placed at the field's center, between the sticks of two crouched opponents,
who try to direct the ball to their teammates. After gaining control of the ball, the team moves it toward the opponent's
goal and tries to score. If a player throws or carries the ball out of bounds, the opposing team gains possession. One
exception to this rule occurs when a loose ball goes out of bounds as a result of a shot taken at the goal. In this situation,
the ball is awarded to the team whose player is closest to it at the exact time it crosses the boundary line.
There are two methods for substituting players in lacrosse. The regular method follows that used in basketball, with the
player entering the game whenever play has been suspended by an official. The other method is known as “substitution
on the fly” and is similar to that in ice hockey, with substitution of players occurring while the game is in progress. One
player at a time may enter the game after a teammate leaves the playing area through a special substitution near the
center line ( 9,10).
Although body and stick checks are part of men's lacrosse, the governing rules help prevent injury. Body checking of an
opponent is legal only so long as that opponent has possession of the ball or is within 5 yards of a loose ball. Contact
must be from the front or side and must be above the waist and below the shoulders. A player can use his stick to check
his opponent's stick when the opponent has possession of the ball or is within 5 yards of a loose ball. The opponent's
gloved hand, while on the stick, are considered part of the stick and can legally be checked.
Penalties in lacrosse are similar to those in ice hockey: players who violate the rules must, under most circumstances,
serve time in a penalty box. This forces the violator's team to operate with one less player than the other team, giving the
losing team a decided advantage. There are two types of penalties in lacrosse: personal fouls and technical fouls.
Personal fouls are more serious and consist of the following ( 9,10):
Illegal body checking: hitting an opponent from the rear, at or below the waist, or when he is not in possession of
the ball or within 5 yards of a loose ball.
Slashing: striking an opponent on the arm, shoulders, head, or any part of the body except the gloved hand that is
holding the stick. Slashing may also be called when, in the opinion of the referee, a check is malicious or
uncontrolled.
Cross-checking: using the portion of the handle between the player's hands to check or push the opponent.
Clipping: obstructing an opponent below the knee with the stick, hand, arms, feet, legs, or body.
Unsportsman-like conduct: using threatening, profane, or obscene language to an opposing player or official, or an
act considered unsportsman-like by the official.
Illegal crosse or gloves: using a stick or gloves that do not conform to required specifications.
The penalty for a personal foul is suspension of the offending player from the game for a period of 1 to 2 minutes.
Technical fouls are less serious than personal fouls and consist of the following:
Interference: interfering in any manner with an opponent who does not have possession of the ball, thus preventing
his free movement on the field.
Holding: grasping an opponent's stick or any part of his body in any manner.
Pushing: shoving an opponent with the hand, arm, or any other part of the body, unless he has possession of the
ball or is within 5 yards of a loose ball.
Withholding the ball from play: lying on a loose ball on the ground or trapping it with a stick longer than is necessary
to control the ball and to pick it up with one continuous motion.
Screening: moving into and making contact with a defensive player with the purpose of blocking him from the man
he is defending.
Offsides: having fewer than three men in the offensive half of the field or fewer than four men in the defensive half
of the field.
The penalty for a technical foul is a suspension from the game for 30 seconds if the offending team does not have
possession of the ball at the time the foul is committed. If the offending team has possession of the ball at the time the
technical foul is committed, it simply loses possession to the opposition.
Women's Lacrosse
Women's lacrosse is played by 12 players: a goalie, 5 attackers, and 6 defenders. There are no fixed boundary lines,
and the field of play is determined by natural terrain. An area 120 by 70 yards (110 by 64 m) is preferred ( 9) (Fig. 31.4).
On the attack, the first home and second home positions are the main scorers and play makers. The defensive and attack
wings are responsible for moving the ball from defense to offense. On the defense, the point and coverpoint mark the
opposition's first home and second home. The center and third home cover much of the field and should have good
speed and endurance. As in men's lacrosse, the goalie's job is to protect the goal and orchestrate the defensive effort.
FIGURE 31.4. Diagram of the field of play for women's lacrosse. (From US Lacrosse: Parent's guide to the sport of
lacrosse, 4th ed. Baltimore: US Lacrosse, 1998, with permission.)
The women's game begins with a draw, in which the ball is placed between the sticks of two standing players at the
center of the field. The ball is flung into the air as the crosses are pulled away from each other. After gaining control of
the ball, the team moves it toward the opponents' goal in an effort to score. Traditionally, and contrary to the offside rule
in the men's game, there have been no restrictions on the movement of the 12 players in women's lacrosse teams.
However, in an effort to decrease potential injury situations and to open up play, the women's collegiate game did adopt
a restraining line rule in 1998. This limits the number of players who can be behind the restraining line (a line 30 yards
[27.5 m] in front of the goal) at any one time to seven offensive and eight defensive ( 11).
Contact to the body with the crosse or body is not allowed. A player may gain possession of the ball by dislodging it from
an opponent's stick with a stick-to-stick check. The player must be one step in front of her opponent to stick-check, and
the check should be to the head, not the handle, of the stick. All legal checks must be directed away from an imaginary
6-inch bubble around the head of the player. An offensive player must not protect the ball so close to the body or face as
to make a legal check impossible. The collegiate women's game consists of two 30-minute halves; high-school games
are 50 minutes, with two 25-minute halves.
The penalty for fouls is the award of a free position. For major fouls, the offending player is placed 4 m behind the player
who was fouled, and for minor fouls she is placed 4 m off in the direction from which she approached before the foul was
committed. The major fouls in women's lacrosse are the following ( 9,11):
Blocking: occurs when contact is initiated by a defender without giving the opponent a chance to stop or change
direction.
Charging: occurs when a player barges or backs into an opponent, or pushes with the hand or body.
Dangerous shot: an uncontrolled shot at the goalie or another field player.
Misconduct: unsportsman-like conduct.
Slashing: deliberate, reckless swing of the crosse.
For longer than three seconds: standing within the 8-m arc (see Fig. 31.4) unless closely guarding another player.
Free-space obstruction: occurs when a defender is not closely guarding her opponent and is obstructing another
player in the free space to goal area.
Minor fouls in women's lacrosse are the following:
Goal circle fouls: movement of player other than the goalie into the goal circle.
Warding off: illegal guarding of the ball from the opponent with the use of the crosse, hand, or body.
Empty crosse check: checking an opponent's crosse that does not contain the ball.
Equipment
The lacrosse ball is made of solid rubber, is white or orange in color, and is comparable in size to a tennis ball or
baseball. The crosse is made of wood, laminated wood, plastic, or other synthetic material. It has an elongated, netted
pocket at the distal end. The men's crosse is between 40 inches (1 m) and 72 inches (1.8 m) in length, with the exception
of the goalie's stick, which may be of any length. The inside measurement of the head of every stick, except the goalie's,
is between 6.5 and 10 inches (0.165 and 0.25 m). Attackmen usually use shorter, smaller sticks to aid them in ball
control. Midfielders also use relatively small sticks, whereas defensive midfielders and defensemen prefer longer sticks to
enhance reach and blocking abilities. The women's crosse must be 36 to 44 inches (0.9 and 1.2 m) in length, the head of
the crosse must be between 7 and 9 inches (.18 and .23 m), and the pocket must be strung traditionally, with no mesh
(which is allowed in the men's stick). In the women's game, the top of the ball, when the ball is dropped in the pocket,
must remain even with or above the side walls. The men's pocket can be slightly deeper and allows more secure cradling
of the ball (9,10 and 11).
The men's game requires that each player wear a helmet and gloves ( Fig. 31.5). The helmet is designed to provide
protection from ball, stick, and incidental body contact. The helmet is equipped with a facemask, a chin pad, and a
cupped four-point chin strap. All helmets should be approved by the National Operating Committee on Standards for
Athletic Equipment (NOCSAE). The use of the head in contact is strictly prohibited. Hard-capped helmets (see Fig. 31.5),
similar to kayak helmets, have largely replaced the more traditional slatted designs. They are lighter and fit more snugly
than the older helmets, and many players find their cosmetic appearance appealing. Although they provide a more solid
design, the newer helmets are not without potential problems. The facemasks are bolted on, and in cases of airway
compromise and suspected cervical spine injury a decision must be made as to whether to remove the helmet or use a
bar cutter. In the newer helmets, the facemask may be closer to the face than it is in the older helmets, which may lead to
more facial contusions and cuts. There is concern that there may be an increase in minor concussive incidents
associated with the increased use of hard-capped helmets. Gloves are similar to those worn by ice hockey players but
are much more flexible. Alterations of the gloves, including removal of palms or fingers to enhance tactile sensation, are
prohibited.
FIGURE 31.5. Fully equipped, young, male lacrosse player wearing the newer, hard-capped helmet design. (Photograph
courtesy of Bill Welch.)
At the college level, shoulder pads are required equipment for all players except the goalie, and many players choose to
wear rib, arm, and elbow pads. Athletic supporters and protective cups are also strongly recommended. Brightly colored
mouth guards are required of all players. A throat protector attached to the lower end of the mask is a required piece of
equipment for the goalie, as is a chest protector in both the men's and women's games.
The only mandated protective equipment for women's field players is a mouthpiece ( Fig. 31.6). Close-fitting gloves, nose
guards, soft headgear, and eye guards are optional, and their merits in the women's game are under debate. As of 1999,
there are two models of protective eyewear that meet the standards of the Eye Safety in Sport subcommittee of the
American Society for Testing Materials. They are LAX Vision and Coverpoint, both from the Leader Company
(Boucherville, Quebec, Canada) ( 11) (Fig. 31.7). A number of new, more protective glove designs are being investigated
by equipment manufacturers and by the US Lacrosse Women's Sport Science Division.
FIGURE 31.6. For women lacrosse players (other than the goalie), the only mandatory protective gear is the mouthpiece.
(Photograph courtesy of Bill Welch.)
FIGURE 31.7. Example of elective, protective eyewear used in the women's game. (Photograph courtesy of Bill Welch.)
Conditioning
Next to the basic skills such as throwing, catching, and cradling, the most important requirement for consistent success in
lacrosse is a well-conditioned athlete. Proper conditioning is a prerequisite for development of individual skills, full-field
concepts of team play, and injury prevention. Proper training not only decreases a player's incidence of injury but can
also substantially raise his or her level of play. Speed, quickness, and explosive power, all qualities important in lacrosse,
were once thought to be solely the province of genetic gift. Athletes are now discovering that through various training
techniques these characteristics can be enhanced as effectively as the more traditional areas of endurance and strength.
A solid, year-round training program allows preseason practice time to be spent on individual and team skills rather than
a crash course in fitness.
Four areas of conditioning are involved: stretching, cardiovascular condition, weight training, and transfer training. There
are a few fundamental concepts that apply to each of these areas. The most important is the overload principle, which
states that for conditioning to occur an athlete must be presented with, and overcome, a progressively greater stress.
This increasing stress may come in the form of increased intensity, duration, frequency, or volume of work. Next is the
idea of specific adaptations to imposed demands (SAID). For example, an attackman's preseason running program
should emphasize short sprints and burst, whereas a midfielder's program should include longer sprinter intervals to
more closely duplicate the full-field demands of that position. A lacrosse training program should be divided into
off-season, preseason, and in-season segments. The off-season should be used to develop strength and an aerobic
endurance base. About 8 weeks before practice, the preseason program emphasizing explosive power and duplication of
sports demands should start. As games begin, a lower-intensity maintenance program should be continued.
Diligent training benefits all players, not just the male high school or collegiate player of exceptional talent. The player
who lacks some of the “natural gifts” can close the gap through proper conditioning. Because of hormonal differences,
female players will not increase their muscle mass as much as male players, but strength, coordination, and speed will
certainly improve. The young lacrosse player will also derive such benefits from a properly supervised program.
Stretching
More than 30% of the injuries in lacrosse are of a noncontact nature. A large percentage of these are musculotendinous
strains incurred during quick accelerations, stops, and changes of direction. Stretching helps decrease these injuries by
increasing the elastic, accommodating nature of the musculotendinous unit. Stretching after activity helps remove
metabolic waste products and decreases postexercise soreness. Stretching should be performed daily year-round, as
well as before and after running, practices, or games. Individual stretches should be performed in a long, slow, relaxed
manner (20 to 30 seconds each), with each stretch repeated at least twice. All major muscle groups should be stretched
in a well organized routine.
Cardiovascular Conditioning
During an off-season program, a player must establish an aerobic base by working out for 30 to 45 minutes, three times
weekly, at 60% to 80% maximum heart rate. As the endurance program progresses, the intensity, duration, and
frequency should continually increase. In addition to running, cross-training activities such as high-impact aerobics,
intense basketball, and squash are beneficial.
As the season approaches, the running routine needs to duplicate more closely lacrosse-play and position-specific
demands. Interval training does this most effectively. Variables within such a program are the work-rest ratio, the type of
rest period, the distance of each work bout, the total training distance, and the number of sessions weekly. The athlete
should start with longer work bouts (0.25 to 0.5 mile [400 to 800 m]) and then progress to shorter, more intense ones. In
general, the work-rest ratio should be determined by the distance run: 800 m or longer, 1:1 work-rest ratio; 200 to 400 m,
1:2; less than 200 m, 1:3.
The athlete should gradually progress to a total work distance of 1.5 to 2 miles (2.4 to 3.2 km). To enforce an overload,
the work-rest ratio, running intensity, number of sets, and number of repetitions may be increased. As the season
approaches, rest periods should progress from total rest to walking to jogging.
Strength Training
The object of strength training for lacrosse is to build coordination and explosive power, not weighty bulk. Multijoint,
coordinated lifts such as squats, power cleans, and snatches are excellent, and rotational, full-range lifting motions are
important. Developing power in the large muscles of the thighs and buttocks is the key. The muscles in the abdomen and
lower back must also be developed to transfer lower-extremity strength to the upper body. Detailing of specific lifts is
beyond the scope of this chapter, but general suggestions include emphasizing technique and coordination rather than
the sheer amount of weight used; concentrating on combination lifts; lifting through a full, controlled range of motion; and
stretching before and after lifting. Weight-lifting programs in skeletally immature players must be well supervised; the
focus should be on good technique with more repetitions and less weight, and the programs should not be competitive in
nature.
Transfer Training
Transfer training consists of various bounding and leaping techniques that are the bridge between traditional conditioning
and lacrosse play. These exercises truly overload and shock the neuromuscular system, so they should be performed
only after good flexibility, strength, and endurance bases have been built. They are best performed during the preseason
segment of training and should not be performed more than twice weekly. They should be continued at a rate of once per
week rate during the season.
Hill Training
Hill training is divided into three phases. Uphill running should be performed in a very bounding nature, emphasizing
knee lift and hip and arm drive. The downhill phase of the running forces the neuromuscular system to adapt to a longer
stride length. Emphasis should be placed on stretching each stride as far as possible. At the bottom of the hill, the player
should be moving at top speed. Such speed is applied in a 50-yard flat-out sprint.
Plyometrics
These exercises enhance explosive muscular power by putting muscle groups at maximum stretch (cocking them) and
then calling on them for quick reaction. These jumps, leaps, bounds, and exaggerated skips are done with 100%
intensity, coordinating the entire body to explode for maximum vertical leap, horizontal bound, or lateral distance.
Lacrosse players need to concentrate on techniques for legs, hips, and trunk ( 12).
INJURY
Epidemiology
As part of their ongoing Injury Surveillance System, the NCAA has tracked data on men's and women's collegiate
lacrosse injuries since the early 1980s ( 13,14). This information forms the foundation of knowledge concerning the
epidemiology of lacrosse injuries. Data are gathered on a nationally representative sample of Division I, II, and III schools
and include information on seven women's and nine men's sports. This NCAA database allows a relative risk assessment
between sports. Injury is defined as reportable if an incident meets the following criteria: (a) it occurs as a result of
participation in an organized intercollegiate practice or game; (b) it requires medical attention by a team physician or
trainer; and (c) it results in restricted sports participation for 1 or more days. To establish injury rates, data are expressed
as the number of injuries per athletic exposure. An athletic exposure is defined as participation by one athlete in one
game or practice in which he or she is exposed to potential injury. Injury rates are expressed as number of injuries per
1,000 exposures.
When compared with soccer, wrestling, football, and gymnastics, both men's and women's lacrosse are relatively safe
sports (Fig. 31.8 and Fig. 31.9). Women's lacrosse injury rates are consistently in the lower third and men's rates are in
the middle third of the 16 investigated sports. The injury burden for women's lacrosse is substantially lower than that for
the men's game. This relative female-gender protection is greater than that seen in women's basketball, soccer, or
gymnastics. In men's lacrosse, the game injury rate (15.7 per 1,000 exposures) is almost four times that of practice
sessions (3.8), but in women's lacrosse the game injury rate only doubles (7.2 per 1,000 exposures, compared with 3.5 in
practice) (see Fig. 31.8). These data reflect the fact that women's and men's lacrosse have fundamental rule differences:
the women's game is essentially a noncontact sport, and the men's game is a collision one. The greater increase
between game and practice injury rates for men probably reflects the greater intensity and frequency of hard, purposeful
contact in game situations.
FIGURE 31.8. Game and practice injury rates, 1996 to 1997. (From National Collegiate Athletic Association. Injury
Surveillance System, 1996–1997: men's lacrosse. Overland Park, KS: NCAA, 1997, with permission.)
FIGURE 31.9. Injury severity, 1996 to 1997. (From National Collegiate Athletic Association. Injury Surveillance System,
1996–1997: men's lacrosse. Overland Park, KS: NCAA, 1997, with permission.)
The three most common injuries for women collegiate lacrosse players are strains (37%), sprains (18%), and contusions
(8%). The ankle (16%), upper leg (16%), and knee (13%) are the most commonly injured body areas. For men, strains
(30%), sprains (30%), and contusions (15%) are most common; and the upper leg (17%), ankle (16%), and knee (10%)
are most often injured. Over the past 10 years, shoulder injuries have been ranked within the top three categories of
areas injured for men, but these injuries occur very infrequently among women. The high rates of upper leg injuries reflect
the high frequency of strain in two joint muscles, but also the fact that the thigh region is completely unpadded and open
to contusion. For both genders, most injuries (44.6% for women, 39% for men) are minor, resulting in only 1 to 2 days of
lost participation. Injury rates are higher on artificial turf than on natural grass (8.0 versus 6.6 per 1,000 exposures,
respectively, for women; 17.9 versus 14.3 for men). For both men and women, injury rates are higher during the
preseason than during season play, and there are no substantial differences in injury rates among Division I, II, and III
programs (13,14).
The National Center for Catastrophic Sports Injury Research collects nationally representative data on major high school
and collegiate sports injuries ( 15). Catastrophic injuries are defined as injuries that (a) are fatal; (b) are nonfatal but result
in permanent disability; or (c) are serious by their nature, such as spinal fractures. Injuries are defined as either direct
(those that result directly from participation in the skills of the sport) or indirect (those that are related to systemic failure
as a result of exertion during participation). Over the past 16 years, there have been only two catastrophic high school
lacrosse injuries (one fatal, one serious), both involving the cervical spine. In the collegiate game, there have been five
direct catastrophic injuries (two nonfatal, three serious) and one indirect fatal incident.
As mentioned earlier, the question of mandating protective gear in the women's game is a subject of considerable
debate. Isolated case reports (16,17,18 and 19) have detailed face, orbit, and finger injuries among women players that
might have been prevented by the use of protective equipment. However, there is an argument that the addition of such
gear would change the fundamental noncontact nature of the women's game and actually lead to higher injury rates. A
national high school study ( 20) found that although the unprotected head and face were susceptible to injury, 75% of
these incidents were very minor, resulting in 0 to 1 day of lost participation time. The NCAA data ( 13) revealed a head
and face injury rate of 2.2 per 1,000 exposures, and a 1990 high school study from New York ( 21) found a seasonal
incidence of 0.4% for facial and head injuries causing more than 2 days' lost participation time. Other researchers ( 19)
have argued that the protective bubble rule in women's lacrosse (described earlier) does not provide adequate
protection. A 1991–1992 study from Australia ( 19) found that 22% of women players sustained head or face contact at
least once per game. Efforts underway to standardize protective eyewear for the women's game are hindered by the
relatively small market and the special visual needs of the game. Currently, there are insufficient data to assess the true
nature of head and facial injuries in women's lacrosse. In the meantime, lightweight headgear, protective goggles, and
close-fitting gloves are optional, not mandatory, equipment.
Mechanisms
The fast-paced combination of players, sticks, and ball makes for a unique set of injury mechanisms for lacrosse
participants. Injuries may generally be classified as noncontact or contact. Contact injuries may be further divided into
those involving player-to-player, stick-to-player, ball-to-player, and surface-to-player situations. Injuries often occur when
players are focused on a skill task, such as scooping a ground ball or firing a shot on goal, and not on body protection
(Fig. 31.10).
FIGURE 31.10. Injury may occur when players are focused not on bodily protection but on a specific task such as
scooping a ground ball. (Photograph courtesy of Bill Welch.)
Noncontact Injuries
Studies (13,22,23) have found that 30% to 40% of lacrosse injuries are noncontact in nature. Passing, shooting,
checking, and scooping ground balls require full-body, twisting motions, often performed at high speed and with rapid
change of direction. Such demands lead to a relatively high rate of groin, hamstring, and low back strains. As in other
cutting-and-turning field sports, noncontact anterior cruciate ligament injuries are a concern. As in other field sports, and
in the older club-level player, Achilles' tendon ruptures are not uncommon. These injuries usually involve fatigue and an
uncoordinated, eccentric contraction activity. At lower levels of play, uneven field conditions may predispose to ankle
sprains.
Compared with other throwing and racquet sports, lacrosse is relatively free of upper-extremity overuse conditions such
as shoulder impingement or elbow epicondylitis. Likewise, overuse conditions commonly seen in immature throwing
athletes are unusual in young lacrosse players. The full-body throwing motion and long crosse lever arm allow
generation of high ball speed without substantial stress on the upper extremity.
Women's Lacrosse
In a study of high-school and collegiate women's lacrosse, Koerner found that most injuries occur in “on-goal” situations
(24). In women's lacrosse, a large number of players can cluster near the goal. It appears that this proximity of players is
a major risk factor for injury. Other common injury situations are transitional midfield and ground ball play. Attack players
have a higher rate of injury than do defensive players. It appears that right-wing attack has the highest rate of injury ( 14).
The two most common mechanisms of head and facial injuries are inadvertent stick-to-face contact during a stick check
and ball-to-face contact when a long pass is misjudged ( 20,24). Players must be coached to not cradle the ball close to
the face in an effort to preclude legal stick checks from defensive players. Officials must enforce rules that prohibit this
practice. Insurance data from US Lacrosse (K. Clarke, personal communication, Lacrosse Foundation loss history,
updated. Interoffice correspondence from K&K Insurance Group, Inc., June 6, 1995) revealed that 30% of women's
injuries were noncontact in nature, 47% were related to stick or ball contact, and only 18% were related to body-to-body
contact. In contrast, 54% of the injuries among male players resulted from body-to-body contact.
Men's Lacrosse
In men's lacrosse, the contact injuries can be divided into four categories of contact: body-to-body, stick-to-body,
ball-to-body, and body-to-playing-surface.
Body-to-Body Contact
Body contact occurring in men's lacrosse can vary from simple shield blocking to high-speed body-to-body contact.
Protective gear worn in the men's game is primarily designed to protect the athlete from stick, ball, and incidental body
contact injuries. In high-energy situations, substantial injuries may occur not only to the player receiving the blow but also
to the player delivering it. Upper-extremity injuries are more commonly the result of contact, rather than noncontact,
mechanisms. The shoulder girdle is particularly vulnerable. Shoulder pads are mandatory at most levels of play, but they
are not designed to protect the shoulders as football shoulder pads are. Lacrosse shoulder pads are not cantilevered but
rest across the top of the shoulder. Clavicle fractures and acromioclavicular joint separations are two of the most
commonly seen injuries.
Lacrosse rules allow stationary “picks” (like those in basketball), but a player's feet must not leave the ground. This
upright posture exposes the neck and upper torso to contusions. As a result of body contact, fracture of one or more ribs
is not an infrequent finding. For reasons that are not entirely clear, abdominal injuries appear to be rare in lacrosse. One
case of pancreatitis, thought to be the result of a direct blow to the abdominal area, has been reported ( 22). Injuries to the
spleen appear to be rare.
Concussions are the most frequently encountered head injury resulting from body contact ( 25). Although all lacrosse
helmets must meet NOCSAE standards, they are not designed to protect against high-speed head-to-head contact.
Helmets also provide no protection for the cervical spine in head-to-head or head-to-body contact. Inappropriate head
contact is a primary cause of the few catastrophic injuries that have occurred in lacrosse.
Stick-to-Body Contact
Fractures of the hand, wrist, and shoulder girdle are the most serious types of trauma encountered as a result of
stick-to-body contact (Fig. 31.11). Fractures in the shoulder girdle region usually occur from the violent stick-to-body and
cross-checking contact of illegal checks and can include clavicle fractures and, rarely, first rib fracture. Direct stick-to-arm
contact, as when an offensive player carries the stick in one hand and uses the opposite forearm to ward off an
opponent's blows, can also result in forearm fractures. Full-arm protective pads can reduce the number of such fractures.
FIGURE 31.11. Example of stick-to-body contact in the men's game. (Photograph courtesy of Bill Welch.)
Men's lacrosse players are required to wear protective helmets and facemasks; consequently, they experience fewer eye
and facial injuries from stick-to-body contact than do female players, who are not required to wear such equipment.
Nevertheless, helmets and facemasks do not protect against all head or facial injuries. Injuries can occur when a stick
edge slips between the facemask bars or when a stick hits the parietal area of the skull despite the presence of a helmet
(25). NCAA rules now mandate the use of brightly colored mouth guards for all players so that officials may more readily
monitor compliance.
Ball-to-Body Contact
Of all lacrosse injuries, 10% result from ball-to-body contact. Injuries to the neck and throat area are potentially the most
serious (26). Even protective equipment such as a helmet and mask may not prevent all ball-to-body trauma such as
facial lacerations and eye injuries. A loose-fitting or inadequately strapped helmet can be forcefully displaced against the
face by a ball, resulting in contusion or laceration. The mandatory use of a four-point chin strap mechanism may help
prevent such situations.
In men' lacrosse, only the goalie is required to wear a protective cup in the groin area. Therefore, the other players are at
risk for testicular injuries, especially in close play around the goal area.
The potential for injury to officials and spectators must also be mentioned. Errant shots have been known to strike
inattentive spectators. Limiting pedestrian traffic and erecting barriers behind the goal are helpful preventive steps.
Body-to-Playing-Surface Contact
As in all other field sports, lacrosse players are at risk of falling or being knocked to the ground, which can result in a
variety of injuries. Some of the most common injuries are turf burns, prepatellar and olecranon bursitis, and contusions
about the unprotected knee. Players falling or being blocked to the playing surface can also sustain a wide variety of
upper-extremity injuries: wrist fractures, elbow dislocations, acromioclavicular joint separations, and glenohumeral
dislocations.
Prevention
There is a basic framework from which the prevention of lacrosse and all other athletic injuries should be initiated. This
involves viewing injury as a disease model and applying the concepts of the Haddon interventional matrix ( 27,28).
Application of these ideas has been integral in decreasing the injury burden in motor vehicular incidents, pedestrian
trauma, occupational overuse syndromes, childhood poisoning and injury, and other situations. The field of sports
medicine has lagged behind in using these concepts to more effectively direct injury prevention efforts. These concepts
are discussed in the following paragraphs in general terms, and some lacrosse-specific interventions are suggested.
The disease model of injury begins with the triad of agent, host, and environment ( Fig. 31.12). This model was first
applied to infectious disease in the 1700s and led to a basic understanding of disease transmission and prevention.
Within this framework, various characteristics of the infectious agent, the susceptible host, and the predisposing
environment contribute to the presence and severity of disease. This model was first applied to injury in the early part of
the 20th century, when motor vehicle and plane crashes were studied. In an injury, the agent is not a bacteria or virus but
rather the energy that is exchanged during an injury incident; the host is the involved athlete; and the environment
includes the social milieu and the physical surroundings of play. Each ingredient may vary and contribute differently to
injury outcome. For example, the high-speed body-to-body contact allowed in the men's game represents a much larger
energy exchange than the stick-to-stick check contact allowed in the women's game. Accordingly, the rate of injury,
particularly to the upper body, is much higher in the men's game. Environmentally, higher rates of skin abrasions and
noncontact ligamentous injuries of the knee are seen on artificial turf, but higher rates of ankle sprains may be seen on
uneven, poorly maintained natural fields. The host factors that contribute to lacrosse injuries include poor physical
conditioning, overaggressiveness in play, poorly rehabilitated injuries, and age and size mismatches in youth play.
FIGURE 31.12. Disease model of injury.
Using the disease model, lacrosse injuries can be viewed not as random, uncontrollable accidents but as predictable,
preventable incidents. For example, it is known that preseason injury rates are higher than those in-season ( 13,14).
Accordingly, teams may need to spend more time with off-season conditioning and prepractice and postpractice
stretching during the preseason period to decrease injury rates. It can also be predicted that, even at the youth level,
game injury rates will be considerably higher than practice injury rates. Therefore, emergency medical coverage should
be available at games, even though it may not be financially practical for most practice situations. Because the rate of
minor finger injuries is predictably higher than the rate of shoulder injuries in the women's game, discussions of protective
gear for women may include the merits of protective gloves, but not the use of shoulder pads such as those used in the
men's game.
The Haddon matrix (29) is used to design injury intervention programs. It views agent, host, and environmental factors in
the temporal context of preinjury, injury, and postinjury events. Within this framework, potential intervention opportunities
may be defined and targeted. An example would be an acromioclavicular sprain (shoulder separation) in men's lacrosse.
A player's risk of such injury may be less if the shoulder girdle mass and strength have been increased by a year-round
weight-lifting program. A youth playing for a coach who emphasizes aggressive body checking with the shoulder may be
at higher risk for this injury than one who is coached in a less aggressive manner. Given the same energy exchange, a
player wearing a quality protective shoulder pad might not injure the joint, whereas a player without shoulder pads might
sustain a substantial injury; this is an example of an event factor. Hitting a larger, faster moving player is also an event
characteristic that leads to increased energy exchange and a higher chance of shoulder separation. Finally, postevent
factors might include a player who returns to play too quickly after an initially moderate injury and therefore is at risk for a
more severe injury if hit in the shoulder again. If postinjury first aid and appropriate rehabilitation measures are directed
by an athletic trainer, the consequences of the injury may be less than those for the player who has no such medical
supervision. Other general examples are given in Figure 31.13 (29).
FIGURE 31.13. Haddon matrix for designing injury prevention efforts.
It must also be remembered that the likelihood of success of a preventive intervention is inversely related to the amount
of effort required to implement the intervention. At lacrosse summer camps, heat illness is more effectively avoided by not
scheduling play time in the heat of the day than by expecting kids to hydrate adequately during midday play. Mandatory
use of a throat drop-guard on the bottom of a female goalie's facemask is more effective in preventing throat trauma than
coaching and expecting players not to fire shots directly at the goalie.
Rule changes (9,10 and 11), such as mandatory mouthpiece wear and NOCSAE standardization of helmets, are also an
important avenue for injury prevention. Rule changes that limit both unnecessary contact in “unprotected” situations and
purposefully elevating a player off his feet in the crease area are aimed at decreasing injury in the men's game. Future
areas of consideration may include standardization of shoulder pads and mandatory shoulder pad use at the youth and
high school levels. As helmets shift to the hard-capped variety, players and coaches must be diligently educated in the
fact that the helmet provides no protection for the cervical spine and that inappropriate use of the head has been a
primary cause of the few catastrophic injuries that have occurred in lacrosse. In the women's game, rules changes now
prohibit defensive players in the shooting space when an opposing player is taking a shot on goal and limits to 3 seconds
the time a free-floating defensive player can spend in the 8-m arc ( 11,21). In the women's college game, the restraining
line rule limits the number of offensive and defensive players that can be positioned across the restraining line at any one
time (11,21). These changes have opened up play and also decreased injury-causing congestion about the goal area. In
1995, stick checking became illegal for female school players up through the seventh grade ( 11). This ruling was made in
an effort to encourage the development of sport fundamentals before introducing advanced and potentially dangerous
maneuvers such as stick checking. As women's lacrosse continues to grow, the merits of optional versus mandatory
facial and hand protection will need to be addressed more fully. To do so will require the continued gathering of
descriptive injury data to assess the burden of these injuries and the effects of interventional efforts. Player education,
coaching changes, and rules enforcement may be an effective and much more acceptable means of preventing these
injuries than the mandatory use of more protective gear.
As mentioned earlier, an important concept in injury prevention is to decrease the consequences of an initial injury
through appropriate emergency care and injury rehabilitation. It is imperative that every lacrosse organization have a
well-understood emergency medical plan. Such a plan involves a coordinated effort of players, parents, coaches,
emergency medical personnel, team physicians, and local hospitals. Every possible situation should be imagined, and
appropriate responses should become automatic. Contact with local emergency medical services providers is imperative.
These individuals should know the exact location and quickest routes of travel to the practice and game fields, what time
games and practices are usually held, the age group of the team members, what (if any) medical personnel normally
attend games and practices, and to which hospital patients should be transported in an emergency. At the youth and high
school levels, coaches must know who will call for emergency help, whom to call, the location of the nearest and always
available telephone, which players have special medical needs, and which family members should be contacted in case
of injury. Plans should be written down and be a part of each team's records. If an emergency arises, all of the
surrounding circumstances should be recorded in detail. This information may aid health professionals in future
treatment, and it may prove invaluable if medicolegal questions arise ( 30).
Management
Chronic Contusion and Myositis Ossificans of the Lateral Arm
This problem is most commonly seen in male attackmen who use the arm in a protective posture to ward off defensive
stick checks (Fig. 31.14). Prevention is key, and attackmen should be encouraged to wear protective arm pads that
extend from the deltoid distally to the glove. Rule changes may be considered to make such protection mandatory. Once
the arm has been injured, a bubble pad made of hard Plastazote-type material is effective in decreasing repetitive injury.
Myositis may be established via plain radiographic films or a bone scan.
FIGURE 31.14. Guarding arm position of an attackman, which may lead to chronic upper-arm contusions. (Photograph
courtesy of Bill Welch.)
Abrasions, Turf Burns, and Prepatellar Bursitis
There is no protective padding or even uniform coverage of the knee area in men's or women's lacrosse ( Fig. 31.15).
Falls and skids on artificial surfaces are particularly problematic. Abrasions must be aggressively cleaned and protected
to avoid secondary infection. Application of petroleum gels or the use of tube stockinets over the knee area provides
some protection without hindering mobility. A large prepatellar bursitis can be managed by draining it and then using a
pressure dressing and oral antiinflammatory drugs. In cases associated with abrasions, septic bursitis must be
considered and ruled out by clinical examination, aspirate, Gram stain, and culture.
FIGURE 31.15. The unprotected knees are subject to contusion on hard or artificial playing surfaces. Note that these
players are wearing the older, slatted-helmet design. (Photograph courtesy of Bill Welch.)
Ball-to-Body Contact
The lacrosse ball is made of extremely hard rubber and can be propelled at more than 100 mph (134 kph). Injuries to the
face, throat, and neck are potentially serious. Since 1983, both men and women goalies have been required to wear drop
shields from their helmets. As mentioned previously, there are many considerations in adopting protective headgear in
the women's game. Ball speed is not as high, and current rules encourage attack players to shoot away from, not at, the
goalie. Coaches must ensure that transitional players have excellent stick skills and master the long pass. Research
(20,24) has pointed to misjudged long passes as a primary cause of ball-to-face injury in the women's game. For men, the
incidence of testicular injuries resulting from a blow to the groin area by a lacrosse ball could potentially be reduced or
eliminated by the wearing of protective cups by all players, not just the goalie.
Contusions and Fractures of the Forearm and Hand
Injuries to the forearm and hand are fairly common in both the men's and women's game. In the men's game, the hand is
considered part of the stick and can legally be stick-checked. The well-padded men's glove provides protection from most
incidents but is inadequate for some high-energy checks. Fractures can involve the phalanges, metacarpals, radial and
ulnar styloids, and even the long-bone shafts. Modern gloves are more supple on the volar surface than the older-style
gloves, and players are now less likely to cut out the fingers to gain better stick control. Enforcement of the “gloves may
not be modified” rule also has increased. The combination of these two factors appears to have resulted in a decreased
rate of phalangeal fracture. For fractures of the metacarpals or styloids, an orthoplast splint, fabricated to fit inside a
lacrosse glove, may be used to allow the player to return to competition at an early date.
Although women's rules forbid stick checking to the hands or handle area of the crosse, inadvertent contact is common.
Gloves are not mandatory, but the use of a low-profile protective glove is gaining popularity ( Fig. 31.16). These gloves
may decrease superficial injuries and contusions but may not prevent fractures. As discussed earlier, more protective
glove designs are being developed.
FIGURE 31.16. Example of lightweight, protective gloves worn electively in the women's game. (Photograph courtesy of
Bill Welch.)
Acromioclavicular Separations
Acromioclavicular separations are probably the most common major contact injury in lacrosse, and their incidence has
increased as the men's game has become more of a collision sport. These injuries can result from body-to-body or
body-to-playing-surface contact. Unlike football shoulder pads, lacrosse shoulder pads are not cantilevered in design.
They lie directly on the shoulders, and even the more sturdy types do little to protect from full-body contact.
Dominant-side shoulder separations are particularly disabling for attackmen. Their stick work requires repeated
cross-body adduction of the arm in an elevated position, which heavily loads the acromioclavicular joint. Plastazote
bubble pads placed under the shoulder pads are effective in shielding the acromioclavicular joint from direct contact ( Fig.
31.17).
FIGURE 31.17. Player receiving a bubble pad for acromioclavicular separation. Note the bilateral upper-arm contusions
on this attackman. (Photograph courtesy of Bill Welch.)
Anterior Cruciate Ligament Injury
The high-speed, “plant and cut” activity that is necessary in lacrosse is poorly performed by knees with deficient anterior
cruciate ligaments. As in other field sports, women may be at a higher risk for anterior cruciate ligament disruption.
CONCLUSIONS
The sport of lacrosse has a rich tradition and a bright future. Today, it is one of the fastest growing team sports in
America. Its combination of player speed, sticks, and ball make for a unique set of potential injury situations and training
demands for lacrosse participants. The available injury data suggest that, compared with most field sports, both men's
and women's lacrosse are relatively safe games. Rule changes, equipment improvements, and new coaching techniques
should help to decrease injury rates further. There is a need for prospective collection of injury data, particularly at the
youth and high school levels. Analysis of such data will lead to a better understanding of the mechanisms of lacrosse
injuries and permit assessment of the effectiveness of preventive interventions. Such data collection requires a
cooperative effort of the game's governing body and medical and public health personnel, as well as the support and
interest of lacrosse players, coaches, officials, and enthusiasts.
CHAPTER REFERENCES
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2. US Lacrosse. Lacrosse: America's first sport. An introduction and participation overview. Baltimore: US Lacrosse, 1998.
3. Vennum T Jr. The creator's game: a brief history of Native American lacrosse. Baltimore: US Lacrosse, 1994.
4. Morrill WK. Lacrosse, rev. ed. New York: Ronald Press, 1966.
5. Scott B. Lacrosse: technique and tradition. Baltimore: Johns Hopkins University Press, 1976.
6. Weyand AM, Roberts MR. The lacrosse story. Baltimore: H & A Herman, 1965.
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8. McCue FC. Box lacrosse. In: Larson LA, ed. Encyclopedia of sport science and medicine. New York: MacMillan, 1971;325–326.
9. US Lacrosse. Parent's guide to the sport of lacrosse, 5th ed. Baltimore: US Lacrosse, 1998.
10. National Collegiate Athletic Association. 1999 NCAA men's lacrosse rules. Overland Park, KS: NCAA, 1998.
11. US Lacrosse. 1999 women's rules: official rules for women's lacrosse. Baltimore: US Lacrosse, 1999.
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13. National Collegiate Athletic Association. Injury surveillance system, 1995–1996: women's lacrosse. Overland Park, KS: NCAA, 1995.
14. National Collegiate Athletic Association. Injury surveillance system, 1996–1997: field hockey. Overland Park, KS: NCAA, 1996.
15. Mueller FO, Cantu RC. National Center for Catastrophic Sports Injury Research: fifteenth annual report, fall 1982–spring 1997. Chapel Hill,
NC: NCCSIR, 1997.
16. Lapidus CS, Nelson LB, Jeffers JB, et al. Eye injuries in lacrosse: women need their vision less than men? J Trauma 1992;32:555–556.
17. Livingston LA, Forbes SL. Eye injuries in women's lacrosse: strict rule enforcement and mandatory eyewear required. J Trauma
1996;40:144–145.
18. Mayer NE, Kenney JG, Edlich RC, et al. Fractures in women lacrosse players: preventable injuries. J Emerg Med 1987;5:177–180.
19. Vinger P. Why women's lacrosse players should wear helmets. Lacrosse 1993;March:8–9.
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what is being done to protect players. Lacrosse 1993;May/June:13–17.
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23. National Collegiate Athletic Association. Injury surveillance system, 1996–1997: men's lacrosse. Overland Park, KS: NCAA, 1996;
24. Koerner RA. Head and facial injuries in women's lacrosse: incidence, type, and causes [master's thesis]. Temple University, 1983.
25. Rimel RW, Nelson WE, Persing JA, et al. Epidural hematoma in lacrosse. Phys Sports Med 1983;11:140–144.
26. Nelson WE, Crampton RS, McCue FC, et al. Syncope, bradycardia, and hypotension after a lacrosse shot to the neck. Phys Sports Med
1981;9:94–97.
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32 Nordic and Alpine Skiing
32
NORDIC AND ALPINE SKIING

GLORIA M. BEIM
Alpine Skiing
Injury Incidence
Trends in Alpine Ski Injury
Nordic Skiing
Powder Skiing and Helicopter Skiing
Ski Jumping
Extreme Skiing
Epidemiology of Alpine Skiing Injuries
Head Injuries
Spine and Spinal Cord Injuries
Hip Injuries
Femur Fractures
Knee Injuries
Tibia Fractures
Ankle Injuries
Shoulder Injuries
Elbow Injuries
Wrist and Hand Injuries
Skier's Thumb
Fatalities in Skiing
Adolescent Skiing Injuries
Injury Prevention
Super Sidecut Skis
Ski Boarding
Ski Falling Techniques
Snowboarding
Conclusions
Acknowledgment
Chapter References
Skiing has been used as a mode of transportation for as long as 5,000 years. Scandinavian skis have been found to date
back to 2000 B.C. In the United States, recreational skiing has become popular only in the last 70 years and began to
increase after the 1932 Winter Olympic Games in Lake Placid, New York. In 1935, there were approximately 10,000
Alpine skiers in the United States. In 1987, there were an estimated 14.5 million in the United States and 200 million
worldwide. With this exponential increase in skier participants, both recreational and competitive, it is not difficult to
imagine the impact of skiing-related injuries on the medical community. In addition, with all of the changes in the sport,
the types of injuries have changed throughout the decades. With the increasing popularity in telemarking, ski jumping,
freestyle ski jumping (moguls, aerobatics, and ballet), extreme skiing, and the relatively recent introduction of
snowboarding, injury types and incidences have changed from those associated with traditional Nordic and Alpine skiing.
This chapter covers many of these winter sports, the types of injuries encountered, treatment options including surgical
indications, and prevention of many of these injuries.
ALPINE SKIING
Injury Incidence
Skier injury rates are generally underestimated because of unreported injuries. In the literature skiing injuries are
reported as number of injuries per 1,000 skier-days. In the 1950s, the reported incidence was as high as 5 to 8 injuries
per 1,000 skier-days. Values reported in the 1980s were between 2.4 and 3.8 injuries per 1,000 skier-days, some authors
estimated as many as 10 injuries per 1,000 skier-days ( Table 32.1). Currently there are between 200,000 and 500,000
skiing injuries per year in the United States and 5 million skiing injuries per year worldwide. The decrease in injuries over
the past two decades has been attributed to improved ski equipment, ski area design and maintenance, and safety
innovations (Fig.1). Compared with other sports, the injury incidence in skiing is relatively low; however, the types of
injuries in skiing may be more severe. For instance, the injury rate per 1,000 participants is 810 in football and 30 in
tennis, compared with 3 to 4 per 1,000 skier-days in skiing.
TABLE 32.1. INCIDENCE OF ALPINE SKI INJURIES
FIGURE 32.1. This figure illustrates the overall injury rate change (increase in mean days between injuries [MDBI]) found
in Vermont study of 18 seasons of ski injuries. (From Johnson RJ, Ettlinger CF, Shealy J. Skier injury trends, 1976–1990.
In: Mote CD, Johnson RJ, eds. Skiing trauma and safety: ninth International Symposium. ASTM STP 1182. Philadelphia:
American Society for Testing and Materials 1993;11–22, with permission.)
Davidson and Lahotis retrospectively reviewed injuries at two California ski resorts over a 9-year period ( 1). The overall
injury rate was estimated to be 2.6 injuries per 1,000 skier-days, for a total of 24,340 injuries over nine seasons at two
resorts. The rate of injuries decreased slowly over the period studied. The knee was the most commonly injured body part
(35% of all injuries).
Trends in Alpine Ski Injury
Tremendous effort over the past several decades has been focused on the prevention of skier injuries. Safety prevention
measures include tuned-up ski equipment, binding design, slope maintenance, and the skier-responsibility code. Modern
ski equipment, especially the design of the modern ski boots and release binding systems, has contributed to the major
decline in injury in Alpine downhill skiing. There has been a marked decline in lower-extremity injuries, to approximately
50% of the incidence of 20 years ago. However, the incidence of upper-body injuries has changed very little for Alpine
skiers (2). In addition, with the ever-increasing popularity of snowboarding, ski mountain clinics are certainly not short of
upper-extremity injury visits.
In the 1960s and 1970s, tibia fractures were the most common injuries seen. With the advent of more advanced binding
release systems, however, knee ligament injuries have become the epidemic in ski injuries ( Fig.2). Newer ski boots block
rotation of the ankle and transfer large torsional forces proximally. The first rotational axis above the ski is the knee, and
these torsional forces stress the knee ligaments.
FIGURE 32.2. Comparison of incidence in ski injuries of different parts of the body registered at Watterville Valley, New
Hampshire, over a 15-year period. (From Young LR, Lee SM. Alpine injury at Watterville Valley: 1989 update. In: Mote
CD, Johnson RJ, eds. Skiing trauma and safety: eighth international symposium, ASTM STP 1104. Philadelphia:
American Society for Testing and Materials 1991:125–132, with permission.)
NORDIC SKIING
Nordic or cross-country skiing is a very popular sport and can be quite demanding physically on both recreational and
competitive levels. Because of the high endurance and strength demands of Nordic skiing, overuse injuries are common,
and acute injuries also can occur.
The knee is the most common joint injured, with the same mechanism of injury as Alpine skiing. Fewer isolated anterior
cruciate ligament (ACL) injuries and more combination injuries of the ACL and the medial collateral ligament (MCL) occur
in cross-country skiing. Glenohumeral dislocations are the most common shoulder injuries; they are caused by catching
of poles in snow or underbrush, which causes a violent abduction–external rotation force on the shoulder.
Acromioclavicular separations are the next most common shoulder injuries in cross-country skiing.
Low back pain is a common overuse injury, especially on the competitive level. Eriksson et al. reported on 87 top skiers
in Sweden and made the following conclusions. (a) Low back pain was the most common complaint and overuse injury
among junior and young senior elite male and female cross-country skiers. (b) Classic-style skiing induced most of the
back pain—among men predominantly the diagonal style and among women both the diagonal and double poling ( Fig.
32.3 and Fig. 32.4). No skiers had back pain under conditions of packed powder or ice, compared with more powdery
conditions in the back country. Unlike Alpine skiers at lift-serviced areas, where 10% of injuries are caused by collisions,
these types of injury mechanisms are rare in back-country telemark skiers.
FIGURE 32.3. General movement pattern: the classic or diagonal stride (A), the double pole technique (B), and (C) the
kick double pole technique. (From Casey J, Foster C, Hixon EG, eds. Winter sports medicine. Philadelphia: FA Davis,
1990, with permission.)
FIGURE 32.4. General movement patterns in recently evolved ski skating techniques: the marathon skate (A), the V2
skate (B), and (C) the V1 skate. (From Casey J, Foster C, Hixon EG, eds. Winter sports medicine. Philadelphia: FA
Davis, 1990, with permission.)
A common injury is the MCL injury with or without ACL injury (Fig. 32.5). This occurs with an externally rotated and valgus
stress application to the knee due to a fall. The fact that the heel is releasable on the telemark binding allows the skier to
absorb some of the stress in the ankle and forefoot ( Fig. 32.6). This may account for the decrease in severity of knee
injuries in Nordic compared with Alpine skiing. Seventy-five percent of Alpine skiers with an acute knee injury have
damage to the ACL with either the MCL or one of the menisci. The telemark binding design allows for greater range of
movement of these joints because the heel is not fixed to the ski.
FIGURE 32.5. An Alpine skier with the most common injury type: grade III knee ligament sprain. (From Jorgsholm P,
Bauer M, Ljung BO, et al. Downhill skiing is developing: snowboard and telemark skiing give new injury pattern.
Lärartidningen 1991;88:1589–1592, with permission, and by permission of Fredrik Johansson, medical artist.)
FIGURE 32.6. Examples of typical cross-country ski bindings and heel fixation devices presently in use. (From Renströ P,
Johnson RJ. Cross-country skiing injuries and biomechanics. Sports Med 1989;346–370, with permission.)
POWDER SKIING AND HELICOPTER SKIING
Helicopter skiing is the ultimate in untracked untouched powder skiing. Most people who undertake this extreme type of
athletic adventure are experienced skiers who are able to adapt to deep powder conditions. Ekeland et al. reported on
injuries specific to powder skiing ( 5). They found that there was a lower injury risk for powder skiers than for skiers on
groomed slopes. This is probably due to the higher skiing ability of powder skiers. The authors admitted, however, that
their results might not be completely accurate in that many of the advanced skiers on ungroomed slopes may not report
their injuries. Inexperienced skiers have a greater risk of injury while skiing in powder conditions than on groomed slopes.
The authors concluded that the types of injuries occurring in powder skiing were similar to those found in skiers on
groomed slopes. The injury risk seemed to be less in powder skiing, probably because of the higher ability of the skiers
attracted to this challenge of skiing performance.
SKI JUMPING
Ski jumping is a very exciting sport involving precision and high velocity. Although one would expect a higher incidence
of injury with this particular sport, the rates are actually similar to those of recreational Alpine skiing owing to the strict
regulation of jumpers and jumping facilities in the United States and internationally.
The technique of ski jumping begins with the skier at the top of a ramp or contoured ground ( Fig. 32.7), referred to as the
inrun (6). On the 90-m inrun, the skier crouches low with the arms held tightly by the sides, reaching speeds of up to 60
mph. At the base of the inrun, the skier assumes a flight position by pressing the body over the skis. This position
generates lift. The skier lands with one leg in front of the other in a telemark-type landing.
FIGURE 32.7. The landing hill is convex near its top, the knoll, and concave near its bottom, the transition. The height of
the starting gate at the top of the inrun is set so that the majority of jumpers will land on the straight (i.e., steep) portion of
the landing hill (between the normal point [P] and the critical point [K]) so that the transition begins. When jumpers fail to
land on the steep middle portion of the landing hill, they land with greater impact and risk a serious fall. Jumpers who fall
on the steep portion of the landing hill merely slide down the hill, dissipating their kinetic energies. In a ski-jumping
competition, the winner is determined on the basis of total style and distance points awarded for each of two official
jumps. If jumpers exceed the critical point (i.e., “outjump” the hill) during one of these two rounds of jumping, the starting
gate is lowered and the round is restarted. (From Wright JR, McIntyre L, Rand JJ, et al. Nordic ski jumping injuries: a
survey of active American jumpers. Am J Sports Med 1991;19:615–619, with permission.)
There is very little evidence in the literature regarding ski jumping injuries. Wright et al. performed a retrospective review
of types and frequencies of injuries sustained by Nordic ski jumpers over a 5-year period ( 7) (Fig. 32.8). They found that
the injury rates for competitive Nordic ski jumping were similar to those reported for recreational Alpine skiing and that
serious injuries were infrequent. Injury rates for non–World Cup and World Cup competitions were 4.3 and 1.2 per 1,000
skier-days respectively. Sixty-one percent of injuries occurred in the upper extremity and 26.1% in the lower extremity.
None of the injuries sustained during the study period resulted in any degree of permanent disability. The authors found
that the injuries were linked to weather and to design and grooming of the ski jumping hill.
FIGURE 32.8. Anatomic distribution of Nordic ski jumping injuries. (From Wright JR, McIntyre L, Rand JJ, et al. Nordic ski
jumping injuries: a survey of active American jumpers. Am J Sports Med 1991;19:615–619, with permission.)
EXTREME SKIING
Speed, jumping, and danger are the essential ingredients of extreme skiing. Skiers find the most technical and
dangerous lines among trees, through chutes, and off rock ledges while traveling down slopes with pitches of about 50
degrees. This sport has become more popular in the past decade in the United States. Since 1991, the U.S. Extreme
Skiing Championships have been held at Crested Butte, Colorado. Approximately 200 men and women compete for the
title each year in order to advance to the World Extreme Skiing Championships in Valdez, Alaska. During the
competition, skiers are judged on aggressiveness, degree of difficulty, control, fluidity, and form. The more dangerous the
chute, or the higher the jump, the more points are scored. As one can imagine, many serious injuries can occur. Many of
the injuries seen during these competitions are of high energy, such as hip dislocations and long bone fractures.
Relatively few injuries occur in elite athletes during competition, compared with less technically advanced skiers trying
out the same dangerous terrain during the rest of the season.
EPIDEMIOLOGY OF ALPINE SKIING INJURIES
Head Injuries
Head injuries are not uncommon in skiing, accounting for up to 10% of all skiing injuries. Davidson and Lahotis reviewed
their 9-year statistics at two California ski resorts and found a total of 2,187 head injuries, with an average of 243 head
injuries per year ( 1). This was 8.9% of all injuries during the study period. After two celebrity deaths in the 1997–1998 ski
season, public awareness of the use of helmets escalated and helmet sales in ski shops increased as much as 300% by
the end of that same ski season (Beim, unpublished data from 10 randomly-selected ski equipment retail stores on the
Western Slope of Colorado). Opponents to the use of helmets have concerns about reduced visibility and comfort.
However, when skiing near obstacles such as trees and other skiers, helmet wear should decrease the incidence of
major head trauma in skiers. Many athletes involved in other mountain sports (e.g., rock climbing, mountain biking)
currently advocate the use of helmets, and the number of helmets seen on the ski slopes appears to be similarly on the
rise.
Spine and Spinal Cord Injuries
Spine and spinal cord injuries are among the most devastating and expensive injuries seen in skiing. Lifetime costs for
these patients and their families often exceed $500,000, and the emotional devastation is not quantifiable ( 8). Prall et al.
conducted a retrospective study of 126 patients over a 10-year period from several ski areas to clarify the incidence,
patterns, and injuries associated with spinal injuries caused by skiing ( 9). They found that the incidence of spinal injuries
was relatively low compared with the overall incidence of ski injuries: 0.001 versus 3 per 1,000 skier-days, respectively.
Although the overall incidence of injury among skiers has decreased by 66% over the past two decades, the rates for
head injury and spinal injuries have not declined ( 10,11). Spinal injuries, in contrast to injuries of the lower extremities,
are distributed equally among skiers of all skill levels. These authors, like others, found that seriously injured skiers,
including those with spinal injuries, usually are skiing at or below their skill level and that speed is the preeminent factor
in virtually all of these accidents ( 12,13 and 14). The lower cervical region and the thoracolumbar junction were most
commonly involved. Most fractures were of the compression type (38%). The authors suggested that the cervical injuries
resulted much more frequently from skier-skier collisions than from noncontact falls. Thoracolumbar vertebral injury was
more likely to be associated with torso injury, whereas cervical injuries were more commonly isolated. Reid et al. found
that 36% of spinal patients had neurologic deficits and 60% had serious associated injuries ( 15). Myles et al. found that
44% of spinal injuries were associated with neurologic deficits ( 14).
Kip and Hunter retrospectively reviewed cervical spinal fractures in Alpine skiers over a 5-year period at two Colorado ski
areas (16). They reported on 18 cervical fractures, which accounted for approximately 0.1% of all skiing injuries during
the study period. Sixteen of the 18 fractures occurred in men, and the average age was 40.8 years (range, 20 to 73
years). Thirty-three percent of these injuries were treated symptomatically with a soft collar. Five patients had neurologic
involvement, including two patients with lasting quadriparesis. Forty-four percent of patients had associated injuries, and
there was one death attributed to a cervical fracture. The authors found that those patients who were involved in
collisions with immovable objects had more severe injuries and a greater chance of neurologic involvement.
Hip Injuries
Hip fractures and dislocations occur in skiers of all ages. The type of injury differs depending on the age of the skier and
the energy pattern of the fall. In elderly osteoporotic skiers, intertrochanteric and intracapsular fractures may be seen
after relatively minor falls at low speeds. In younger skiers, higher-energy falls and collisions with trees or other obstacles
may result in severe hip injuries. In the 1997–1998 ski season in Crested Butte, Colorado, there were five posterior hip
dislocations, one hip fracture-dislocation, and two intracapsular hip fractures ( 16A). This was calculated as rate of 0.016
serious hip injuries per 1,000 skier-days. The care of these patients should follow current orthopedic recommendations,
and the natural history of the injury, including the incidence of osteonecrosis, should be discussed with the patient.
Femur Fractures
Femur fractures occur in high-velocity skiers. The incidence is approximately 0.4% of all skiing injuries. Thirty percent are
a result of collisions with either stationary objects (e.g., trees, ski lifts) or moving objects (e.g., other skiers,
snowmobiles). The fracture type seems to be dependent on the age of the skier. In the 3- to 18-year-old group, spiral
fractures are seen; in the 19- to 45-year-old age group, direct-impact, high-energy fracture patterns are seen; and in the
group older than 45 years of age, are often seen after trivial falls, such as twisting while getting off of a chair lift.
Optimal treatment of most closed femoral fractures is surgical in nature. My preference for adults is closed reduction and
intramedullary nailing. One must be quite aggressive surgically for a proximal femur fracture, and expedient if the fracture
is intracapsular in the young patient. Displaced intraarticular distal femur fractures can be treated with open reduction
and internal fixation, and supracondylar fractures can be treated with a reconstruction intramedullary nailing. Again, the
specifics of surgical treatments of various femur fracture types are beyond the scope of this chapter, and the reader is
referred to other trauma or fracture references.
Knee Injuries
The knee is the most commonly injured structure in Alpine skiing accidents. Many authors have supported this statement
with reports that 25% to 30% of all injuries occur in the knee, and more than 9 out of 10 knee injuries involving the
ligamentous structures (17,18 and 19). Of the four primary ligamentous structures in the knee, the two most commonly
injured in skiing accidents are the MCL and the ACL, either isolated or in combination with each other ( Fig. 32.2).
Isolated meniscus tears also occur, especially in the more extreme skiing, where axial compression and rotational forces
are accentuated at the knee. Patellar fractures, patellar dislocations, and patellar tendon ruptures also occur, but they
are relatively uncommon compared with the ligamentous injuries.
Anterior Cruciate Ligament Injuries
With the boot design changes of the 1960s, there was an immediate decrease in tibia fractures and an increase in ACL
injuries. There is currently an epidemic of knee ligament injuries. Ski boots have newer designs that block rotation of the
ankle and transfer large torsional forces to the knee ( Fig. 32.3). With the ankle splinted in a rigid plastic boot, the first
rotational axis above the ski is the knee joint. Ski boots with higher, stiffer ankle support and firm, cambered composite
skis were developed to allow more rapid changes of direction. There has been almost threefold increase in knee injuries
since 1972, with ACL injuries currently accounting for approximately 10% of all skiing injuries ( 20) (Fig. 32.9).
FIGURE 32.9. This figure illustrates the injury rate decrease (increase in mean days between injuries [MDBI]) for grade I
and II knee sprains (left) and the increase (decrease in MDBI) for grade III knee sprains (right) in a Vermont study of 18
seasons of ski injuries. (From Johnson RJ, Ettlinger CF, Shealy J. Skier injury trends, 1976–1990. In: Mote CD, Johnson
RJ, eds. Skiing trauma and safety: ninth international symposium. ASTM STP 1182. Philadelphia: American Society for
Testing and Materials, 1993:11–22, with permission.)
Seventy-five percent of knee injuries that develop an effusion have an ACL tear ( 2). Most ACL tears are isolated in these
cases, yet 23% have associated meniscal tears. ACL/MCL combined injuries occur 50% of the time and are more
commonly lateral meniscal tears (lateral tears are nine times more common than medial ones). Of the 25% of effusions
without ACL tears, 90% ultimately require operative intervention for tibial plateau fractures, meniscal tears, or other
intraarticular pathology ( Table 32.2).
TABLE 32.2. INCIDENCE OF ANTERIOR CRUCIATE LIGAMENT INJURIES IN ALPINE SKIERS
The mechanism of injury involves catching the inside edge of the ski, which results in a valgus–internal rotation of the
femur, stressing the knee. The ACL, MCL, and meniscus are at risk. Landing on the ski tail after a jump with one ski
shooting forward is another mechanism for ACL injury. Beginners may tear the ACL by sitting back on their skis to gain
control, one ski shooting forward. This mechanism produces strong quadriceps contractions that result in tibia
subluxation on the femur, tearing the ACL.
Injuries to the ACL in skiers appear to occur most commonly at the femoral attachment. This is in contrast to other sports,
in which most tears occur in the midsubstance (21,22 and 23).
Indications for surgery in an isolated ACL tear in the active athlete engaged in pivoting sports should be stronger than in
a more sedentary individual who would consider activity modification. There authors advocate ACL reconstruction in
patients with meniscal pathology, especially if the meniscus is torn in the vascular zone and is amenable to repair. Timing
of ACL reconstruction is controversial. Hughston stated that the inflammatory environment that exists in the immediate
postinjury phase can be detrimental to the rehabilitation of the knee (J.C. Hughston, personal communication, 1997.)
Many authors recommend reconstruction of the ACL when the knee has a reduced effusion, satisfactory range of motion,
and an excellent quadriceps contraction. ACL reconstruction is an elective procedure, and the surgeon at home who will
be monitoring the patient postoperatively should often be considered as the primary choice for performing the procedure.
Graft choices for ACL reconstructions include the central third of the patellar tendon (ipsilateral or contralateral),
semitendinosus/gracilis, quadriceps tendon, and allograft. There is much controversy in the literature regarding the
optimal ACL graft, and this discussion is beyond the scope of this chapter. Increasing evidence suggests that the
gracilis/gracilis graft may be the best graft choice, because of the newer fixation techniques that are available and less
morbidity associated with graft harvest ( 24).
Medial Collateral Ligament Injuries
MCL injuries account for 15% to 20% of all skiing injuries and 60% of knee injuries in skiers. Tears are commonly
isolated, but they may occur in association with other ligamentous injuries. Associated meniscal pathology is rare.
Isolated MCL injuries should be treated nonoperatively with early range-of-motion exercises, isometric quadriceps
strengthening, and dynamic bracing. Progressive physical therapy can begin once full range of motion has been
achieved, followed by functional rehabilitation and return to skiing.
Lateral Collateral Ligament Injuries
Isolated lateral collateral ligament (LCL) injuries are uncommon in skiers. Several authors have reported an incidence of
approximately 4% of all knee injuries and approximately 1% of all injuries ( 25,26). The injury occurs when the skier
catches the outside edge of the ski, directing the tip of the ski to turn in across the opposite ski, resulting in a forced
internal rotation–varus load ( 27). Tears of the lateral side of the knee often occur in combination with injuries to other
structures in the knee such as the posterior cruciate ligament (PCL), the ACL, and the posterolateral corner. Fractures of
the tibial plateau must also be sought.
In general, isolated lesions of the LCL are treated nonoperatively, similar to MCL injuries. Range-of-motion and
quadriceps strengthening exercises should be initiated immediately, along with functional bracing and antiinflammatory
modalities. Surgery usually is reserved for combination injuries that do not have as favorable a prognosis with
nonoperative treatment.
Posterior Cruciate Ligament Injuries
PCL injuries in skiing are rare. Most series have reported that they represent fewer than 1% of all knee injuries ( 27). Most
reported PCL injuries have occurred secondary to a direct collision with a fixed object such as a tree. Less often, the
patient gives a history of hearing a “pop”; such patients are usually able to bear weight, unlike those who have ruptured
an ACL. Therefore, a careful examination is crucial to make the diagnosis of a PCL injury. Examination of the
posterolateral corner is also important when a PCL injury is suspected. Controversy still exists in the literature regarding
operative treatment of isolated PCL injuries. Several studies have reported satisfactory short- and long-term functional
results with nonoperative treatment (28,29 and 30). Other studies have suggested that nonoperative treatment of isolated
PCL insufficiency results in increasing early degenerative changes over time, as well as increasing complaints of
discomfort and pain (31,32 and 33). Symptomatic clinical instability is rarely a significant problem, and bracing is
generally not necessary. To date, there are no long-term prospective studies to indicate whether early operative
reconstruction of the PCL is warranted. The only exception is the early repair of PCL avulsion fractures, which should
undergo open reduction and internal fixation in a timely fashion.
Meniscal Injuries
Meniscal injuries appear to occur in a different pattern in skiing compared with nonskiing injuries. Palette et al. studied
the incidence and patterns of meniscal injury associated with acute ACL tears in 75 skiers and 75 athletes in nonskiing
sports (34). They demonstrated that 31 of 75 skiers had an associated meniscal injury, compared with 47 of 75 nonskiers.
This was a strong trend yet not statistically significant. The nonskiers had a higher incidence of major meniscal tears that
required repair or partial meniscectomy. The location of the meniscal tear was significantly different in that the incidence
of isolated lateral meniscal injury in skiers was higher than in nonskiers. The skier group was more likely to have a
longitudinal tear of the posterior horn of the lateral meniscus. In both groups, lateral meniscal tears were more likely to
require conservative treatment or partial meniscectomy and medial meniscal tears were more likely to be repaired than
excised. The indications for ACL reconstruction are expanded in the face of an associated meniscal tear that is
repairable.
Knee Braces
There have been many studies regarding the use of knee braces for prophylaxis, after knee injury and after surgical
reconstruction of the knee. There has been a great lack of scientific knowledge about the biomechanical and physiologic
function and effects of braces, and controversy continues as to whether to recommend bracing after a knee injury or
reconstructive surgery. Many authors have stressed the importance of afferent proprioceptive impulses for knee stability
in patients who have had an ACL injury ( 35,36,37,38 and 39). The current belief, based on the literature, is that knee
braces mainly influence the afferent input and proprioception from the ACL-deficient knee to the central nervous system
in high-loading situations (e.g., skiing). Nemeth et al. studied six expert downhill skiers with ACL injuries and different
degrees of knee instability to measure changes in electromyographic (EMG) activity of lower-extremity muscles in a
slalom course with and without a custom-made functional knee brace ( 40). They concluded that use of the knee brace
caused an increased afferent input from proprioceptors, resulting in an adaptation of motor control patterns in the injured
knee. However, there is much controversy regarding the mechanism of obtaining this proprioceptive input. Some have
recommended that an inexpensive neoprene knee sleeve can provide the same proprioceptive impulse as an expensive,
custom-made functional knee brace.
Reports on prophylactic bracing in runners by Osternig and Robertson revealed that EMG activity in knee flexors and
extensors was decreased in 42% of all braced versus nonbraced comparisons, and there was increased activity in 17%
(39). They also suggested that neuromuscular control is altered with prophylactic braces. These data suggest that the
brace does not have a proprioceptive influence. Prophylactic knee braces used during collegiate football did not produce
a reduction in ACL injuries ( 41). Most authors do not recommend prophylactic knee bracing for skiing in the intact knee.
Tibia Fractures
There has been an 80% decline in tibia fractures in the past 25 years. This is probably the result of use of boots with
higher support. Children younger than 10 years of age and elderly persons have not shown any decrease in tibia fracture
incidence despite the change in boot design. Johnson et al. ( 2) reported 87 tibia fractures in 1990. This accounted for
18% of all fractures and 3.6% of all injuries in skiers and was equivalent to 0.13 per 1,000 skier-days.
Treatment of tibia fractures depends on the nature and location of the fracture, the age and medical condition of the
patient, and the preference of the orthopedic surgeon. Some surgeons still prefer to cast patients with simple midshaft
tibia fractures, whereas others prefer intramedullary nailing for almost all fractures if the patient is a good surgical
candidate. Tibia fractures that are intraarticular, whether tibia plateau fractures or pilon fractures, certainly warrant
surgical intervention if any displacement is involved. An in-depth discussion of surgery for these types of fractures is
beyond the scope of this chapter. However, I have seen a number of tibial shaft fractures with associated displaced tibial
plateau fractures in skiers. I have treated them all aggressively, either with intramedullary nailing of the shaft fracture and
open reduction and internal fixation of the tibial plateau or with a hybrid external fixator, with excellent results.
“Boot-Top” Tibia Fractures
With the advent of higher, more supportive boots in which the top reaches the midshaft of the tibia, stresses are
transferred to the strong midthird of the bone and away from the weaker metaphysis. This has decreased the incidence of
tibia fractures by 80% in the last 25 years. However, in those younger than 10 years of age and in elderly persons with
osteoporotic bone, the risk for tibia fractures has not decreased significantly.
Boot-top tibia fractures are caused by bending forces and are not prevented by bindings. There has been a constant
incidence over the past three decades despite newer designs of boots and bindings ( Fig 32.10). Some 35% to 50% of all
tibia fractures in skiing are of this type. As mentioned earlier, the indications for operative versus nonoperative treatment
have many variables and require subjective decisions by the orthopedic surgeon; their discussion is beyond the scope of
this chapter. In the scenario of a closed tibia fracture I always give the patient both nonoperative and operative options
for treatment, but I am generally more aggressive to recommend intramedullary nailing in the young, active skier who is
interested is accelerated rehabilitation and maintenance of the strength and flexibility of the muscles and joints of the
lower extremities. Open tibia fractures are common in skiing, especially extreme skiing. With these injuries, immediate
surgical intervention is indicated with insertion of an intramedullary nail or open reduction and plating after thorough
irrigation and debridement of the wound and fracture site.
FIGURE 32.10. Representing the most common ski binding, two-mode release capability releases in twist at the toe, twist
at the heel. Multimode release capability releases in additional directions, including backward lean at the toe, twist at the
heel, and lateral shear and lateral roll. (From Eriksson E, Johnson RJ. Exercise and sports medicine sciences reviews.
Philadelphia: Franklin Press, 1981, with permission.)
Ankle Injuries
The incidence of ankle fractures has decreased significantly since the early 1940s with the evolution of the hard plastic
boot. In 1942, the reported incidence of ankle fractures was 46%; by 1976 this had declined to 7% ( 42). In other sports
such as snowboarding, where the incidence of ankle injuries is higher than in skiing, indications for surgical versus
conservative treatment are based on the type of fracture, the amount of displacement, the age and medical condition of
the patient, and the preference and personal experience of the orthopedic surgeon. Further discussion is beyond the
scope of this chapter, and the reader is again referred to the literature.
Recurrent dislocation of the peroneal tendons at the ankle occurs in sports such as skiing and soccer ( 43). Karlsson et
al. found satisfactory functional results in 87% of their patients who underwent surgical reconstruction of the superior
peroneal retinaculum (44). They found that conservative treatment was not an option in patients with recurrent peroneal
tendon dislocation, because of persistent symptoms of instability and pain. The surgical technique was nicely illustrated
by Karlsson et al. (44). Patients were allowed to return to their sport once they had regained full range of motion in the
ankle and normal ankle strength, which usually took between 4 and 6 months.
Shoulder Injuries
Injuries to the shoulder are common in skiing. Shoulder injuries during Alpine skiing have been estimated to account for
4.5% to 10% of all Alpine skiing injuries. The shoulder is the most commonly dislocated joint in skiing, and fractures
about the shoulder complex represented 15% of skiing fractures according to Johnson and Pope ( 45). Because of the
relative decrease in lower-extremity injuries over the past several decades, there has been a resultant increase in the
ratio of upper-extremity to lower-extremity injuries (45,46,47,48,49,50 and 51). Kocher and Feagin (52) noted that this ratio
increased from 1:4 to 1:2 over an 11-year period from 1982 to 1993. Epidemiologic data have estimated upper-extremity
injuries to account for 30% to 42% of all ski injuries ( 45,50,53). The most common upper-extremity injury is an injury to the
thumb's ulnar collateral ligament, known as “skier's thumb” (see later discussion).
Kocher and Feagin retrospectively reviewed shoulder injuries acquired in skiing accidents during three seasons at one
ski resort in Jackson Hole, Wyoming ( 52). Their overall injury rate was 4.44 injuries per 1,000 skier-days. Injuries to the
upper extremity represented 29.1% of all injuries, and the shoulder accounted for 39.1% of upper-extremity injuries, or
11.4% of all injuries recorded. The male-female ratio of these patients was 3:1, and the mean age was 35.4 years. The
mechanism of injury was most often a fall (93.9%), followed by a collision with another skier (2.8%), pole planting (2.3%),
and collision with a tree (1%). The most common shoulder injuries were rotator cuff strains (24.2%), anterior
glenohumeral dislocations/subluxations (21.6%), acromioclavicular separations (19.6%), and clavicle fractures (10.9%).
Other shoulder injuries included greater tuberosity fractures (6.9%), trapezius muscle strains (6.4%), proximal humeral
fractures (3.3%), biceps tendon strains (2.3%), glenoid fractures (1.5%), scapular fractures (1%), humeral head fractures
(1%), sternoclavicular separations (0.5%), acromion fractures (0.3%), posterior glenohumeral dislocations (0.3%), and
biceps tendon dislocations (0.3%).
Treatment of all of the above injuries is beyond the scope of this chapter and should be addressed on an individual basis
depending on multiple factors as described previously.
As with all skiing injuries, the numbers presented are probably low, and the true incidence is difficult to determine. For
example, skiers with a history of shoulder instability may have multiple episodes of subluxation during their skiing
careers, and many do not visit the clinic on the day of injury and therefore go unreported.
Elbow Injuries
Elbow injuries are relatively uncommon in skiing. However, dislocations and distal humerus fractures can occur with
high-energy falls and collisions with obstacles (e.g., trees, rocks, other skiers or snowboarders). Treatment of these
injuries should follow standard orthopedic practice.
Wrist and Hand Injuries

Wrist Fractures
Distal radius fractures and carpal fractures occur in Alpine skiing but are much more common in snowboarding (see later
discussion).
Intersection Syndrome of the Wrist
Intersection syndrome is a disabling condition that affects the first and second extensor compartments of the wrist.
Tendinitis and tenosynovitis in these compartments can cause pain, swelling, and crepitus several centimeters proximal
to Lister's tubercle. This has been seen in extreme powder skiing such as helicopter skiing. Dragging, jamming, and deep
pole planting with excessive repetition can cause this syndrome. Palmer in 1994 described “bugaboo forearm” in powder
skiers (54). It can also occur in weight lifting, rowing, and canoeing. Exacerbating maneuvers may include wrist extension
and radial and ulnar deviation. Early treatment consists of rest, ice, nonsteroidal antiinflammatory drugs, splinting, and
even corticosteroid injections. Alterations of the ski pole including shortening and narrowing the pole grip diameter may
reduce the recurrences. Use of the strap in order to help lessen the stress on the extensor compartments may also be
effective (55).
Skier's Thumb
Skier's thumb is an acute tear of the ulnar collateral ligament (UCL) of the metacarpophalangeal joint of the thumb ( Fig.
32.11). The chronic injury pattern in the UCL of the thumb was first described by Campell as an occupational trauma,
“gamekeeper's thumb,” seen in gamekeepers who repetitively snared rabbits ( 56). The forced abduction and extension of
the thumb can cause a tear of the UCL in skiers ( 57). The UCL injury represents 40% to 85% of upper-extremity injuries
in skiers. Most series underreport this entity. It often occurs in advanced skiers. The lowest incidence occurs in skiers
who use the simple strap handle without a bottom platform. Saber-type ski pole handles have no pole straps and a
conforming grip. Skiers using this type of ski pole handle have a two times greater incidence of acute UCL injury. In 1962,
Stener described a lesion associated with a UCL injury in which the ruptured ligament displaces and folds back
proximally to the adductor aponeurosis ( 58). A displaced ligament proximal to the adductor aponeurosis cannot
spontaneously regain its original position, which is necessary for healing. At least 50% of grade III injuries have
accompanying Stener lesions. The metacarpophalangeal joint of the thumb is a diarthrodial joint. The UCL is the major
stabilizing structure on the ulnar side. The adductor muscle inserts by the adductor aponeurosis into the dorsal aspect of
the joint capsule and by the adductor tendon onto the base of the proximal phalanx and the ulnar sesamoid. The UCL is
located deep to the adductor aponeurosis, coursing from its origin at the metacarpal head in a distal volar direction to its
insertion at the base of the proximal phalanx.
FIGURE 32.11. A telemark skier with the most common jumping injury type: ulnar collateral ligament rupture of the thumb.
(From Jorgsholm P, Bauer M, Ljung BO, et al. Downhill skiing is developing: snowboard and telemark skiing give new
injury pattern. Lärartidningen 1991;88:1589–1592, with permission, and by permission of Fredrik Johansson, medical
artist.)
Clinical diagnosis of the acute UCL tear is performed by placing a radial stress on the metacarpophalangeal joint of the
thumb both in full extension and in approximately 20 degrees of flexion. This examination may be difficult in certain
patients due to pain and apprehension. Therefore, some advocate diagnostic tools such as magnetic resonance imaging
(MRI) (59,60) or ultrasound ( 61,62 and 63), and others recommend performing the clinical examination after a digital
anesthetic block has been administered. Plain radiography may reveal small avulsion fractures, yet these findings may
not indicate a need for surgical intervention.
Ultrasound examination is more cost-effective than MRI, but accurate diagnosis can be very technician dependent ( 60).
Ultrasound examination is done in both the longitudinal and transverse planes in order to identify the location of the UCL
in relation to the adductor aponeurosis. In Hoglund's study, ultrasound correctly diagnosed a displaced UCL in 82% of
cases (32/39), a diagnostic result that compares favorably with those obtained by other methods, including MRI ( 63). In
four cases, the ultrasound examination suggested a more severe lesion than was found at surgery, and in three cases, a
lesser injury was suspected than later was revealed at surgery. Hergan et al. pointed out pitfalls in ultrasound diagnosis
of UCL injury of the thumb (60). They noted that ultrasound is able to illustrate the position of the torn UCL correctly in
approximately 90% of cases. However, errors can be caused by a dislocation of the palmar joint capsule to the ulnar joint
space, by a scalloping of the adductor aponeurosis due to the displaced UCL, or by scar tissue. The authors
recommended MRI whenever a nondisplaced UCL tear is suspected by ultrasound.
Treatment of grades I and II UCL tears are agreeably conservative in nature, with casting or splinting. Complete tears of
the UCL with retraction of the ligament proximal to the adductor aponeurosis (Stener lesion) is generally considered an
indication for primary repair. Several techniques have been described, including ligament-to-ligament repair (if an
intraligamentous injury is present), pull-out wires, connecting drill holes, direct suture to the periosteum, and repair with a
bone anchor (64,65,66,67,68 and 69).
Fatalities in Skiing
The actual rate of death in skiing in the United States, not including heart attacks, avalanches, and lift-related deaths, is
approximately 20 to 30 per year, or 0.2 deaths per 100,000 skier-days. This is low in comparison to other sporting
activities, such as water sports (2.8 per 100,000), and in comparison to automobile-related fatalities (26.6 per 100,000)
(12). The typical skier fatality occurs as a result of moving out of control at high speeds and colliding with a stationary
object, such as a tree, causing a massive head injury. Morrow et al. found that 81% of the 16 skiers who died over six ski
seasons at a Vermont ski resort were men, with a mean age of 29.7 years ( 70). The incidence was 0.66 deaths per 1
million skier-days. Shealy also found the fatally injured skier to be predominantly male (83.1%), with an average age of
27.4 years (12). Most fatalities are caused by head injuries (60%), and 76% of the deaths resulted from collisions with
trees. Most cases do involve a collision of the skier with a stationary object such as a tree, rock, or lift tower. The major
factors leading up to these collisions include high speed and loss of control. Morrow's study also suggested that fatigue
was a factor, because all of his recorded fatalities occurred in the afternoon. Most fatalities also occur in advanced-level
skiers rather than in beginners according to Morrow's experience. Sherry and Clout examined ski-related deaths over a
period of 32 years (1956 to 1987) in an Australian ski area providing both downhill and cross-country skiing ( 71). They
found 29 deaths, 8 of which were trauma-related; the incidence was 0.24 per 1 million skier-days.
Adolescent Skiing Injuries
The rate of ski injuries in the pediatric population has not been well documented in the literature until recently. Deibert et
al. prospectively studied injuries in children and adolescents over a 22-year period at two Vermont ski areas ( 72). They
found an overall incidence of 2.79 per 1,000 skier-days; there were 2.69 injuries per 1,000 skier-days in adults, 2.93 in
adolescents, and 4.27 in children. During the last 8 years of the study, the authors found the most common injuries to be
the grade III ACL sprain in adults, the UCL sprain of the thumb in adolescents, and knee contusions in children. They
found a decrease of 58% for injuries in children from the beginning of the study in 1972 to its end in 1994, compared with
a decrease of 43% of injuries overall. There was a 10% decrease in tibial fractures and an 8% increase in
upper-extremity fractures in children. In adults, there was an 89% decrease in tibial fractures and a 280% increase in
ACL injuries. The authors found that higher binding-release values were related to an increase in spiral tibial fractures,
and they concluded that the use of properly functioning modern equipment can decrease the rate of injury, particularly in
children.
Despite a decrease in the overall injury rate in skiing over the past few decades, serious injuries are increasing both in
number and in relative frequency ( 73,74). As mentioned earlier, it is estimated that each year there are approximately 20
to 30 Alpine skiing deaths in the United States, of which a small number occur among skiers younger than 18 years of
age (12). Shorter et al. retrospectively studied patients admitted to a pediatric intensive care unit for serious Alpine skiing
injuries over a 5-year period ( 75). They identified 38 patients with serious injuries, 58% of which were caused by
collisions with stationary objects. Thirty-four of the 38 patients were boys or men (age range, 5 to 18 years). Only three of
the patients were wearing helmets. There were no deaths in this study, but during the study period four pediatric deaths
were reported in New Hampshire and Vermont. Head injuries were the most common injury (71%). Fifteen of the 27 head
injuries were skull fractures (6 of which were depressed). There were 13 extremity fractures, 8 facial fractures, 6
abdominal injuries, 5 thoracic injuries, and 2 spinal injuries. One third of the patients had multiple injuries, and 26% had
long-term sequelae. The average cost for treatment was $22,000. The authors concluded that prevention efforts must
target excessive speed and loss of control and that because of the number of head injuries helmet use should be
aggressively encouraged.
INJURY PREVENTION
Most ski injuries occur between noon and 1 o'clock in the afternoon, or between 2 and 4 o'clock in the afternoon. In
addition, skier injury has been attributed to skier fatigue, poor visibility, number of skiers on the slopes, and failure of
binding release. The last factor alone has been associated with 44% of skier injuries, due to improper adjustment and
maintenance.
Many factors may decrease the incidence of injuries in skiing. One of the most important, as in many sports, is preseason
conditioning. Skiing requires high demands of fitness, including strength, flexibility, and endurance. Strength and
conditioning of the quadriceps and hamstrings as well as the hip abductors is important in preventing many
lower-extremity injuries, and endurance training is invaluable in preventing injuries that may result from skier fatigue.
Many skiers are subjected to sudden altitude changes and can develop symptoms of high altitude sickness. High altitude
produces euphoria in some but can cause dysphoria and illness in others ( 76). The revenue loss in Colorado from
altitude illness in travelers is estimated to be more than $35 million annually. Altitude illness syndromes can range from
acute mountain sickness (AMS) with symptoms mimicking a hangover, in 15% to 30% of Colorado resort skiers, to high
altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). HAPE is a noncardiogenic pulmonary
edema that occurs in 5% to 10% of those with AMS. HACE, possibly an end stage of AMS, can lead to death as early as
24 hours after the development of AMS. Some of the best preventative measures include slow ascent to altitude (if
possible), aggressive hydration, and avoidance of alcohol consumption, especially during the first several days of
acclimatization. For people who are at a higher risk for development of high altitude sickness, a prophylactic dosing of a
diuretic such as acetazolamide may be recommended by the skier's family physician, beginning 24 hours before
ascending to altitude and continuing for 2 to 3 days after arrival. Acetazolamide works by inhibiting carbonic anhydrase in
the kidney and lung, resulting in a slight metabolic acidosis. Acetazolamide reduces symptoms by speeding
acclimatization and decreases susceptibility to AMS. It is thought to reduce the incidence of HAPE and HACE as well.
Hypothermia can play a role in injury or sickness, and wearing multiple layers of clothing is recommended for prevention
of this uncomfortable and sometimes dangerous condition.
Bright clothing is a wise choice in fashion on the slopes, so that the skier is more visible to another skier or snowboarder
traveling at potentially high speeds.
Ski instruction is important to learn the basics of skiing and skiing safety. However, several authors have noted that
skiing instruction is not related to safety unless it is coupled with a significant amount of skier experience ( 77,78 and 79).
Frequent equipment tuneups are essential in preventing injury from equipment failure during the act of skiing. Failure of
binding release has been associated with 4.4.% of skier injuries due to improper adjustment and maintenance. The
releasable binding systems now available are quite technical, and an experienced mechanic should assist the skier in
gaining the appropriate setting. These settings are based on the skier's weight, skiing ability, and type of binding used.
Each manufacturer has a specific scale and chart to determine the appropriate setting. Finch and Kelsall reviewed 15
published studies examining the effectiveness of bindings and their adjustment ( 80). They found that all of the articles
included anecdotal or informed opinion, and all but one focused on equipment design. Most of the evidence suggests
that currently used bindings are insufficient for the multidirectional release required to reduce the risk of injury to the
lower limb, especially at the knee. The optimal adjustment of bindings has been shown with a testing device to be
associated with a reduced risk of lower-extremity injury. However, the adjustment of bindings has been shown to be
inadequate for the average skier, especially for children's bindings. The standard of the manufacture of bindings and
boots must continue to be biomechanically studied and improved in order to reduce injury.
A properly tuned ski—that is, correct edge sharpness and wax type for the type of snow conditions—may also reduce
injuries. Proper care of skis over the summer months includes releasing spring tension in the bindings, cleaning and
oiling the bindings, and coating the base of the skis with a protective wax to reduce drying of the bases and rusting of the
edges. A breakaway strap on the ski pole can prevent injuries in the upper extremities when a pole is caught up in terrain
such as trees, roots, rocks, or ice.
Super Sidecut Skis
Super sidecut skis, also known as shaped skis or parabolic skis, have become popular, and there has been concern
about an increased incidence of ski injuries with the use of these modern skis. Skiing Magazine reported an increase
from 6 types of shaped skis to 40 different models between the 1995–1996 and the 1996–1997 ski seasons. Currently,
retail ski shop purchases of these types of skis represent 50% to 90% of all of their new ski purchases ( 81).
Advertisements in ski magazines imply a quicker learning curve and better turning performance with super sidecut skis,
leading to improvement of the skier's ability to enjoy the sport.
Johnson et al. did an epidemiologic study to look for any changes in the injury incidence with shaped skis ( 82). Anecdotal
reports from experienced skiers indicate that shaped skis lead to certain difficulties in normal ski terrain. Some have
noted that it is difficult to make short-radius skidding turns to control speed. Some skiers believe that it is difficult to ski
directly down the fall line without the ski's becoming unstable, and others have reported problems with the ability to
maintain directional stability after landing from a jump. Johnson et al. found that, in the one ski season studied in a
Vermont ski area, 18% of the control population used shaped skis, yet 36% of the injury group were using shaped skis,
meaning that shaped skis were overrepresented among the injured skiers. Their data revealed that skiing injuries
associated with shaped skis occurred at a higher rate than expected in comparison to conventional skis and that expert
skiers using shaped skis had a higher than expected incidence of ski injuries. Although there were not enough numbers
in this study to obtain statistical significance, the injury trends presented certainly warrant further study as these skis
continue to gain in popularity.
Ski Boarding
Ski boards were introduced in 1991. They are a shorter and wider version of Alpine skis, 63 to 90 cm in length (compared
to 150 to 240 cm for Alpine skis). Like snowboarding, ski boarding does not require poles, and the bindings do not
release. But, as with skiing, there is independent leg action, and regular Alpine boots are used ( 83). Ski boards require
more speed than conventional skis, and the injury incidence is still unknown. Ski boards were introduced to a large
television audience during the 1998 ESPN Winter X-Games in Crested Butte, Colorado. During the practice sessions for
this event alone, there were two significant injuries: one tibia fracture requiring operative treatment and a three-level
compression fracture of the thoracic spine.
Ski Falling Techniques
Ettlinger et al. prospectively monitored injuries occurring at a Vermont ski area over a 22-year period in order to identify
the incidence and types of skier injuries ( 84). Using videotape documentation and other data, 1,400 ACL injuries were
observed during the study period. The authors identified two common mechanisms of ACL injury: the phantom-foot injury
mechanism and the boot-induced ACL injury mechanism. The authors performed a study to determine whether training
could help reduce the risk of ACL injuries and found that there was a 62% decline in serious knee sprains in the group
who received training.
The phantom-foot injury profile includes several elements that the authors believed must all be present at once to cause
an ACL injury: (a) uphill arm back; (b) skier off balance to the rear; (c) hips below the knees; (d) uphill ski unweighted; (e)
all weight on inside edge of downhill ski tail; and (f) upper body generally facing downhill. The combination of these
elements results in a lever from the ski that points in a direction opposite that of the human foot, causing rotational and
torsional forces significant enough to injure the ACL ( 84).
The boot-induced ACL injury mechanism occurs during hard landings by off-balance skiers. The skier, after beginning a
jump off balance to the rear, rotates one arm upward and rearward and fully extends the contralateral knee. When the
skier lands, the tail of the ski hits first. By the time the ski directly under the boot heel contacts the snow surface,
everything that can be stretched in the lower extremity has been stretched and everything that can be compressed has
been compressed. With no capacity remaining to absorb the jarring impact of the boot heel, the stiff back of the modern
Alpine boot is able to drive the tibia out from under the femur, thereby tearing the ACL ( 84).
Jorgensen et al. tested the effect of an instructional ski video on the behavior and injuries of 763 downhill skiers ( 85).
The video informed the skiers on how to get started in downhill skiing and on injury prevention. Outcome parameters,
including adjustment of bindings and injury risk, type, and consequence, were registered by a questionnaire after the
skiers returned from their ski vacations. The authors found a 30% reduction of injuries among those who had watched the
instructional video. This value was found to be statistically significant, and the authors concluded that the instructional ski
video was able to change the behavior of the downhill skier and reduce the risk of injury.
SNOWBOARDING
Snowboarding has been one of the fastest growing winter sports, now representing an estimated 20% to 30% of all
lift-ticket holders at ski areas that allow snowboarding. In the 1989–1990 season there were an estimated 100,000
snowboarders in the United States This number increased to an estimated 2 million by January 1995. A lot of evidence
suggests that snowboarders and skiers have different injury rates and different types of injuries. There are currently three
major ski resorts in the United States that do not allow snowboarding.
Primitive forms of snowboarding were first described in the 1920s. One of the earliest production snowboards was
designed and developed by Sherwin Popper during the 1960s in Michigan. These early snowboards, called “snurfers,”
were made of wood and had “skegg” or fin on the bottom for tracking in deep powder. Since then, snowboards have
evolved into boards constructed similarly to Alpine skis, with Fiberglas bodies, plastic bases, and steel edges, making
them appropriate for groomed trails as well as back-country powder. Snowboarding boots are available in hard or soft
designs. The hard-shelled boots provide rigid ankle support, but the hybrid boot has a more flexible upper shell for
increased maneuverability. The soft-shelled boots provide less ankle support, and there is a higher incidence of ankle
injuries when these boots are used. Snowboarding bindings are nonreleasing, and snowboarders do not use ski poles.
Snowboarders stand sideways, similar to surfers and skateboarders, with the rear foot at 90 degrees to the long axis of
the board and the front foot positioned between 45 and 90 degrees to the long axis ( 87,88). Turns are performed by
shifting the body weight to the front foot and allowing the tail of the board to swing outward ( 89). Snowboarding injuries
appear to occur at a lower mean age (19.6 to 21 years) and in a higher percentage of men (74% to 90%) compared with
Alpine skiing injuries ( 42,87,90,91 and 92). Furthermore, beginners are the largest fraction of injured snowboarders.
Davidson and Laliotis found injuries in beginner snowboarders to occur at a rate of 49%, compared with 18% of skiers
(93). They also found that upper-extremity injuries were increased compared with those in skiers, and snowboarders
were almost ten times as likely to injure the wrist as their Alpine skier counterparts (19% versus 2%). The wrist was the
most common injury zone in the total population of injured snowboarders and accounted for a third of all injuries in
beginner snowboarders ( Fig. 32.5). Other differences that were statistically significant between snowboarders and skiers
are listed in Table 32.3.
TABLE 32.3. STATISTICALLY SIGNIFICANT DIFFERENCES BETWEEN SNOWBOARDING AND SKIER INJURIES
Pigozzi et al. reported on 106 snowboarding injuries and found 45.1% of injuries occurred in the upper extremities ( 94)
(Fig. 32.12). They recommended guards to protect the upper extremities during descent on a snowboard. Chow et al.
reviewed 355 injuries in snowboarders who presented to a rural hospital emergency department in California ( 95). It was
estimated that snowboarders comprised 20% to 25% of participants on the ski slopes but 45% of the emergency
department visits. They found 81% of the injuries to occur in men (mean age, 19.8 years). Snowboarders were injured in
the upper extremities 58% of the time, compared with 32% for skiers. Of the upper-extremity injuries seen, wrist injuries
were most common. Skiers injured their lower extremities more frequently than snowboarders (35% versus 16%,
respectively).
FIGURE 32.12. A snowboarder with the most common type of injury: fracture of the wrist. (From Jorgsholm P, Bauer M,
Ljung BO, et al. Downhill skiing is developing: snowboard and telemark skiing give new injury pattern. Lärartidningen
1991;88:1589–1592, with permission, and by permission of Fredrik Johansson, medical artist.)
Kirkpatrick et al. studied injuries to the foot and ankle in snowboarders ( 96). They studied 3,213 snowboarding injuries
from 12 Colorado ski resorts over a 7-year period. They found that 15.3% of the total injuries occurred in the ankle and
1.8% in the foot. Ankle injuries included 44% fractures and 52% sprains; 57% percent of the foot injuries were fractures,
and 28% were sprains. They found no significant correlation between boot type (soft, hybrid, or hard) and overall foot or
ankle injury rate, but there were significantly fewer ankle sprains in those wearing hybrid boots and fewer fractures of the
lateral talar process in those wearing soft boots. The lateral talar process fractures represented 2.3% of all snowboarding
injuries and 34% of all ankle fractures. This type of talus fracture has been termed “snowboarder's ankle” ( 97). Fracture
of the lateral process of the talus is an unusual fracture of the foot. It is often not apparent on plain radiography and can
easily be misdiagnosed as a sprain of the anterior talofibular ligament. The combination of softshell boots and aerial
maneuvers increases the incidence of this type of fracture. Computed tomography can confirm the diagnosis, and early
operative management is often indicated to decrease the risk of subtalar degenerative joint disease. McCrory
recommended the following treatment protocols for a “snowboarder's ankle” ( 97):
Type I (undisplaced fracture measuring less than 2 mm): short leg cast and partial weight bearing for 6 weeks
Type II (large displaced fracture): open reduction and internal fixation
Type III (large comminuted fracture): excision of fragments if exact restoration of anatomy if not obtainable
CONCLUSIONS
Over the past several decades, there has been an increase in the number of participants in winter sports such as Nordic
and Alpine skiing. The number of overall injuries appear to have been on the decline owing to advances in ski equipment
design and improved maintenance of ski areas. The rate of serious injuries, however, has increased. This may be a
result of increased numbers of skiers and snowboarders moving too fast and out of control. The increased popularity of
snowboarding has many skiers wondering whether snowboarders are a source of increased skiing injuries as a result of
collisions. To date, there are no studies to accurately answer this question. Prevention of injury is an important aspect of
skier and snowboarder education, and injury rates may decrease as knowledge is gained from ongoing epidemiologic
studies.
ACKNOWLEDGMENT
The author thanks Erik Klemme for his extensive expertise in the art and mechanics of skiing and his assistance in the
preparation of this chapter.
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33 Power Lifting, Weight Lifting, and Bodybuilding
33
POWER LIFTING, WEIGHT LIFTING, AND BODYBUILDING

THOMAS C. NAMEY
PETER J. CAREK
Definition of the Specific Sports
Equipment
Science of Strength Training
Nutrition and Diet
Medical and Physiologic Adaptations to Weight Training
Considerations for Health and Disease
Strength-Training Injuries
Back
Shoulder
Elbow
Groin and Thigh
Knee
Ankle and Foot
Children and Strength Training
Women and Strength Training
The Elderly Population and Strength Training
Chapter References
The use of weight training, whether training for the specific sports of weight lifting, power lifting, and bodybuilding or as
part of the overall conditioning regimen of athletes of other sports, has steadily increased in the United States over the
past several years. Strength training is being used not only in an attempt to excel in the chosen sport but also as an
adjunctive modality in the rehabilitation and prevention of injuries. The numerous benefits of a solid weight-training
program need to be defined, and potential uses have yet to be discovered.
As with any other sport, specific injuries occur with regularity in the weight-lifting sports. Although the true frequency of
injuries that occur while training and competing for these sports has not been well documented, the incidence of injuries
occurring during general strength training is surprisingly low and comparable with several other sports ( 1,2 and 3). With
the increased popularity, the primary care physician as well as the sports physician will undoubtedly be presented with a
growing number of weight-lifting associated injuries. To treat these injuries effectively, the physician must be familiar not
only with sports injuries in general but also with the injuries commonly seen in the strength athlete.
Competitions involving weight lifting and demonstrations of strength have been present since the beginning of
humankind. Using various forms of strength development, early humans used rocks, stones, or irons to determine who
was the strongest. A “scientific” approach to weight training was begun by Milo of Crotona (sixth century B.C. ), a six-time
Olympic champion, who used a growing calf in a form of progressive resistance training, lifting it on his shoulders every
day until it was full grown.
Until the late 19th century, weight lifters were delegated to act as strongmen in shows and circuses, where they could
demonstrate their strength and skill. During the late 1800s, weight lifting as a sport was born in Europe with the
organization of the first European Championship in Rotterdam (1896) and the first World Championship in Vienna (1898).
Weight lifting also was included as a competition during the first modern Olympic Games (1896).
Since the establishment of the International Weightlifting Federation (IWF) in 1905, numerous weight-lifting associations
have formed and several other sports involving demonstrations of strength and muscular hypertrophy have been created
(i.e., power lifting and bodybuilding). The popularity of these newer forms of strength sports has surpassed that of the
original form of weight lifting.
In recent history, the superiority of the Eastern European countries and the former Soviet Union in international
weight-lifting competitions was used as a psychological weapon during the Cold War as a gauge of political and ethnic
supremacy. Furthermore, several Third World countries have used their citizens who excel in international competitions
as a means to increase the country's exposure and, possibly, prominence in the world.
The international popularity of the strength sports remains significant and appears to be increasing. Historically, these
sports have been popular in the Eastern European community and the former Soviet Union. Whether the changing
political climate in that area of the world affects participation is yet to be seen.
DEFINITION OF THE SPECIFIC SPORTS
The goal of these sports is to demonstrate strength in a controlled and regulated manner, whether lifting a one repetition
maximum or exhibiting muscular hypertrophy. The rules and regulations associated with these sports are determined by
the specific governing bodies, who also determine the eligibility of the participants and the levels of competition ( Table
33.1).
TABLE 33.1. GOVERNING BODIES AND LEVELS OF COMPETITION OF THE SPECIFIC STRENGTH-TRAINING
SPORTS
The sports that demonstrate strength and power by lifting one repetition at maximum weight within three attempts (i.e.,
weight lifting and power lifting) consist of the successful completion of specific lifts. The participant is allowed to set the
weight at the level at which he or she will begin to compete, similar to high jumpers and pole vaulters setting the height of
their initial attempt. Each lift has specific guidelines for approved completion, and each is associated with sites
susceptible to injury.
Olympic weight-lifting competitions consist of the completion of two lifts: the snatch and the clean-and-jerk. To perform
the snatch, the weight is lifted from a position in front of the lifter's legs to above the head, with the elbows in full
extension. The bar must pass with a continuous movement along the body. This lift may be accomplished with either a
split or squat move as the lifter maneuvers himself or herself underneath the lifted weight.
The clean-and-jerk consists of two distinct moves. The weight is pulled from the floor to the shoulders, while either
squatting or splitting the legs. The bar may rest on the clavicles, on the chest above the nipples, or on the fully bent
arms. After recovery to a standing position, the weight is then lifted over the head until the arms are vertical and the
elbows are fully extended.
Power-lifting competition consists of three lifts: bench press, squat, and dead lift. For the bench press, the barbell is held
with the elbows fully extended while the athlete lies supine on the bench. The lifter lowers the weight to the chest and
raises it again to the elbow-extended position. The squat involves supporting the barbell, while standing, on the
shoulders posterior to the neck, with the top of the bar not more than 3 cm below the top of the deltoid. The weight is
lowered by flexing the knees and hips until the thighs are parallel to the floor. Once cleared by the referee, the lifter must
recover to an upright position with the knees locked. During the dead lift, the barbell is lifted from a position in front of the
lifter's legs as the individual stands, without raising his or her hands, until the knees are locked in a straight position and
the shoulders held in an upright position.
Although each specific lift predisposes several anatomic sites to injury, the bench press and its mandatory equipment is
associated with an increased risk of serious injury. A significant number of injuries and deaths occur during the
performance of bench pressing, especially in the unsupervised, home setting ( 4,5).
EQUIPMENT
Although the equipment used for training varies considerably among individual athletes, the equipment used for the
strength sports in competition is standardized. The purpose of the modifications is to allow for safe, effective, and fair
means of demonstrating strength and power.
The free weights and bars have several unique design features. The plates have a larger caliber hole, and the bar has
smaller caliber ends compared with nonstandardized equipment, allowing for a rapid exchange of plates and ease of
balance. The grip area is knurled to create a secure, nonslip surface.
Designed more for athletes not involved with a specific weight-lifting sport, the numerous weight machines (e.g.,
Universal and Nautilus) do offer several advantages over the free weights ( Table 33.2). The disadvantage of weight
machines is that the supporting musculature used during the balancing of the barbell is not given the opportunity to
develop if machines are used exclusively.
TABLE 33.2. COMPARISON OF BARBELLS AND MACHINES
Accessory equipment, including lifting belts, joint wraps, lifting shoes, proper clothing, and hand protection (e.g., gloves,
chalk, and wrist straps) are often used during training to reduce the risk of injury and to allow maximal work. Many of
these items are legally used during competition, as long as they meet specific criteria.
Weight-lifting belts have been shown to support indirectly the spinal column and musculature of the lower back by
maintaining or even increasing intraabdominal pressure ( 6,7).The effect may reduce back muscle and disk compressive
forces while improving lifting safety ( 8). This additional support is especially pronounced during squatting moves and in
lifters without optimally conditioned torso musculature. A competitive lifting belt is 12 cm wide and one layer thick. The
benefits in terms of improving performance are not well known, and several world records have been set by individuals
who have opted not to use one.
Joint wraps, allowed only around the knee and wrist joints under IWF rules, are usually composed of inexpensive, thin
material of specific width and length wrapped circumferentially around the specific joint. Although limited data exist as to
their effectiveness, justifications for their use include keeping the joint warm, providing external support to the joint,
preventing skin-to-skin sticking around the knee during squatting, limiting the range of motion of the wrist joint, and
providing comfort and confidence to the weight lifter ( 9). On the other hand, joint wraps may be partially responsible for
the formation of hematomas and varicosities of the lower extremities. In addition, they may cause the development of
blood pooling and vascular collapse, hemodynamic changes that when combined with the other physiologic changes that
occur with weight lifting could ultimately result in acute complications, such as syncopal episodes.
Weight-lifting shoes need to provide a firm, snug, nonslip foundation. The shoes should have a small, wide heel to
prevent side movement, providing better balance than a continuous incline wedge-type shoe. A thin, solid sole does not
provide an exaggerated platform from which to lift tremendous weights. The presence of a solid heel counter with the
addition of a strap around the arch are modifications that create additional support.
Proper clothing, in addition to being a marker of team membership, is essential for comfort and safety. The weight-lifting
suit, which must adhere to the specific rules of the sport, should be lightweight, firm fitting, and supportive. T-shirts, worn
under the suit, are both popular and legal under most rules. The use of athletic supporters or approved lifting briefs is
essential, although the use of garments with legs or ones that act as girdles, are illegal.
Gloves and chalk are used in an effort to improve the security of the grip during a lift attempt and to protect the hands
from blister and callus formation. Chalk, usually in the form of baby powder, pool hall chalk, liquid chalk, resin, talc, or
magnesium carbonate, maintains a dry grip and is often added to the body and attire to dry extra moisture. The
effectiveness of these items is not known.
Straps are used during training sessions to improve the grip, especially while attempting heavier weights. These straps
are wrapped around the hand, wrist, and bar to assist in securing a strong grip. Excessive training with straps may be
deleterious and result in a weakened grip strength, adversely affecting performance in competition, during which they are
not allowed. Straps also may disrupt proper position of the hand, wrist, elbow, and shoulder during clean-and-jerk
movements and cause delay when the athlete attempts to move out from under the weight during a missed lift.
SCIENCE OF STRENGTH TRAINING
Many variables are involved in the successful completion of a weight-lifting movement. Two basic variables, strength and
power, are commonly considered to be similar terms, yet each has a specific definition and a vital role in weight-lifting
sports.
“Strength” is defined as the ability to develop force against an unyielding resistance of unrestricted duration ( 10). It is the
maximal amount of weight that can be lifted during one complete repetition of a particular movement, using the force
generated by a specific muscle group ( 11). To lift maximal weight, the individual consciously and unconsciously performs
several neurophysiologic actions to increase the amount of force he or she is able to generate: (a) recruitment of
additional motor units and muscle fibers, (b) initiate movement while the muscle is at an optimal length, (c) fire involved
motor units in a synchronous fashion, and (d) relax the antagonistic musculature ( 11,12). Strength is the variable that is
probably measured to a greater extent during a power-lifting competition.
In contrast to strength, “power” is defined as the amount of work performed during a specific period of time, that is, work
rate (11). It is a function of both the amount of muscular force exerted and the rate of body or limb movement. If the work
performed is mechanical and the force applied is constant, power simply equals force times the first derivative of distance
with respect to time, or force times speed (1). Power is important in Olympic-style weight lifting because an element of
quickness and speed is present as the participant attempts quickly to lift and lunge under the bar as it is raised. The
element of power is demonstrated because weight lifters have the highest power outputs and vertical jumps of all athletes
(13). Power also is an important factor while training for sports other than the strength-training sports. Power as an
important variable in power lifting has not been demonstrated. During the action of weight lifting, isometric and isotonic
contractions of involved muscle groups occur ( 10). Isometric action is a contraction of muscle that occurs without a
change in the total length of the muscle. Because no movement occurs, no work is performed. In regard to strength
development and injury risk, this form of muscular contraction is the most efficient in terms of repetitions per yield of
strength development and has minimal risk of injury. This form of exercise is specific for the muscle length and joint angle
at which it is performed.
Isotonic contraction is a contraction of the muscle that is associated with changes in total muscular length; therefore,
work is performed (10). If relevant loads are chosen, a frequency of five to six repetitions per session appears to provide
the best results in terms of strength development. Muscles performing isotonic exercises do not encounter constant
resistance through the entire range of motion and most of the improvement noted with training or limitation of maximal
lifts occurs at the weakest point along the strength curve for the particular muscle group and joint.
Isokinetic contraction, an additional form of muscle action, is a contraction that occurs at a constant velocity. An
isokinetic exercise is an accommodating resistance type in which the muscle experiences the same relative resistance at
all points in the range of motion to maintain a constant speed ( 10). This form of exercise is used primarily during
rehabilitation and may be associated with submaximal strength gain.
In addition to these forms of muscular actions, muscle contractions may be considered either concentric or eccentric.
Concentric weight training refers to a muscle contraction that causes a shortening of muscle length, and positive work is
performed. Eccentric muscle contraction refers to an increase in muscle length during contraction. This form of action
produces negative work and is usually associated with an increased risk of injury and muscle soreness.
NUTRITION AND DIET
Strength-training athletes, as a result of their unique body composition and rigorous training schedule, have specific
nutritional and dietary requirements ( 13). To maintain a positive energy balance, weight lifters require a larger amount of
caloric consumption per day than would be expected of individuals of similar size and weight (2,500 to 8,000 kcal per
day). This added caloric intake takes into account the obligatory increased energy demand required by these athletes
who possess a greater lean body mass, with its associated increased amount of muscle tissue, which requires a greater
amount of total calories at rest than fat.
The increased caloric consumption is achieved through ingestion of various amounts of carbohydrates, proteins, and
fats. Carbohydrates are the preferred metabolic fuel used during anaerobic exercise and should constitute approximately
50% to 60% of total caloric intake. Proteins provide a minimal amount of the total energy requirement during training if a
regular diet is followed. Athletes in a heavy weight-training cycle or in the process of losing weight may require additional
protein (1.5 to 2.0 g/kg body weight per day compared with a maintenance intake of 0.8 g per kg per day) to account for
tissue injury (breakdown) that requires repair and resynthesis. Fats are concentrated aerobic fuel (9 kcal per g of fat
compared with 4 kcal per g of both carbohydrates and proteins) and should constitute 20% to 30% of total caloric intake.
Minerals and vitamins, which function as coenzymes, enzyme cofactors, and structural material and in gas transport and
muscle contractions, are often used and abused by athletes. The scientific basis for mineral and vitamin supplementation
remains unclear, and specific recommendations depends on individual needs. The intake of supplements ensures
adequate intake. No proven benefit has been demonstrated from the ingestion of megadoses of vitamins and minerals,
and in reality, they may be associated with adverse effects. An example of such an adverse effect is the deposition of
oxalate with increased intake of ascorbic acid, which may lead to nephrolithiasis if dehydration occurs. A significant
problem with most athletes is maintaining an adequate volume status, especially during times of unusual environmental
conditions or intense training. To maintain an appropriate level of hydration and electrolyte balance, especially in lieu of
an obligatory plasma volume expansion associated with some forms of training, the weight-training athlete should
consume sufficient fluids that are supplemented with the appropriate minerals, especially potassium.
In addition to vitamins and minerals, other medications and chemicals are used on a regular basis as ergometric aids in
an attempt to improve performance. Amino acids and proteins are taken in large quantities to increase synthesis of lean
body mass, particularly muscle. This action is based on anecdotal evidence and myths, with no supportive data present.
Although they have been banned by most competitive associations, anabolic steroids and growth hormones are used to
promote protein synthesis. Although data support the enhancement of strength using one repetition maximum
measurement, these chemicals are associated with numerous adverse side effects, including alterations in the blood lipid
profile and changes in psychological mood; their use should be strongly discouraged ( 14,15). Furthermore, the use of
drugs used to counteract the short-term side effects of anabolic steroids could lead to additional complications ( 16).
MEDICAL AND PHYSIOLOGIC ADAPTATIONS TO WEIGHT TRAINING
Several physiologic parameters are influenced by weight training, and numerous misconceptions exist pertaining to
possible harmful effects on measurements such as blood pressure and body composition. During dynamic resistive
exercises, both systolic and diastolic blood pressures rise, with recordings reaching 450/310 mm Hg during a double-leg
press (17). In contrast, normal or even slightly lower blood pressures result with prolonged training, even in individuals
who initially had elevated blood pressures ( 18). The use of an appropriately sized blood pressure cuff in these
disproportionally large individuals is mandatory to ensure reliable and reproducible measurements. An increase in blood
pressure may be the result of other factors that are unrelated to the physiologic response to resistive training ( Table
33.3). Increases in stroke volume, muscle mass and strength, and insulin sensitivity, and decreases in heart rate and
body fat are possible mechanisms by which resistive exercises lower blood pressure ( 19)
TABLE 33.3. FACTORS CAUSING SIGNIFICANT BLOOD PRESSURE INCREASES IN WEIGHT LIFTERS
Although it is elevated during the strenuous activity of training and composition, the heart rate of weight lifters is typically
lower at rest than that of the average adult. When calculating the double product during acute resistive exercise, using
the increased heart rate and markedly elevated systolic blood pressures, the result indicates a significantly increased
oxygen demand on the myocardium.
Aerobic fitness or power, usually measured by maximum oxygen consumption in liters of oxygen per minute or milliliters
of oxygen per kilogram per minute, may demonstrate small to moderate increases with high-volume weight training
compared with sedentary individuals ( 13,20,21 and 22). Training specifically to improve aerobic power and endurance
using typical methods such as jogging and the stationary bicycle ergometer compromises maximum anaerobic power
and, subsequently, reduces weight-lifting performance ( 24). On the other hand, interval training programs or high-volume
weight training can increase Vo 2max with little or no compromise in strength and power compared with typical aerobic
endurance training.
Beneficial alterations in blood lipid profiles, with declines in total cholesterol, low-density lipoprotein (LDL) cholesterol,
and the ratio of total cholesterol to high-density lipoprotein (HDL) cholesterol, have resulted from high-volume weight
training, such as performed by bodybuilders ( 24,25). These favorable effects may be altered with anabolic steroid use
(24).
The body composition of most weight lifters and, as would be expected, most bodybuilders, appears to demonstrate an
average or increased lean body mass with an associated decrease of percent body fat ( 13,21,22,26). This characteristic
of strength-training athletes, although needing further study, indicates that a program of intense resistive exercise
maintains and may decrease the percentage of body fat in addition to increasing muscle mass.
Weight training results in changes in measures of pulmonary functioning. Weight lifters have group mean values for vital
capacity (VC) and maximum breathing capacity measures of 10% to 20% greater than the values predicted from height
and age tables (13). In particular, individuals suffering from exercise-induced asthma (EIA) (also known as
exercise-induced bronchospasms) usually are able to train and perform competitively in weight lifting because the
symptoms associated with EIA have a longer duration of exercise demand before onset than the time required to perform
the necessary lifts. Pulmonary problems, such as spontaneous pneumothorax, are more often associated with running
and only infrequently reported with weight lifting, despite the increase in intrathoracic pressure that occurs.
CONSIDERATIONS FOR HEALTH AND DISEASE
Weight lifting and weight training are associated with several specific medical problems. These problems arise from the
exaggerated demands placed on the internal organs and external structures during training and competition. Many of
these conditions actually reflect an appropriate physiologic response to conditioning rather than a pathophysiologic
process.
The incidence of hypertension among competitive weight lifters and bodybuilders is well known but may be related to risk
factors separate from the sport itself (Table 33.4). Hypertension is a relative contraindication to weight training. Once it is
controlled, hypertension should not pose a threat to the health of an individual who chooses to lift weights and may act as
an adjunctive therapy, actually reducing blood pressure ( 18,28).
TABLE 33.4. CONTRAINDICATIONS TO WEIGHT LIFTING AND WEIGHT TRAINING

The athletic heart, a condition associated with increased diastolic dimensions of the left ventricle, thickness of the left
ventricular wall, and calculated left ventricular mass, commonly occurs with long-term athletic training. It is often difficult
to distinguish from pathologic forms of hypertrophy, such as hypertrophic cardiomyopathy, a leading cause of sudden
death in young athletes ( 33). An increase in the thickness of the left ventricle results from hypertrophy of cardiac muscles
and is thought to be a compensatory mechanism caused by an increased vascular resistance (afterload) that occurs
during resistive-type exercises. In comparison, endurance-trained athletes have increased left ventricular dimensions
(i.e., end-diastolic volume) caused by an increase in plasma volume (preload). In mild forms, the increased wall thickness
is a natural result of athletic training. Markedly elevated measures of wall thickness, especially septal wall thickness and
mass-volume ratio, are present in such conditions as asymmetric septal hypertrophy (ASH) and idiopathic hypertrophic
subaortic stenosis (IHSS) ( 30). These conditions are noted on physical examination by the presence of an enlarged
heart, an S4 gallop, or a systolic murmur that is accentuated by standing or the Valsalva maneuver. Weight lifters, as a
population, do not experience as great an increase in echocardiographic-measured left ventricular wall thickness as
athletes in the endurance sports of rowing and cycling or in individuals with ASH or IHSS ( 30,31). Although left
ventricular hypertrophy is noted, it is accompanied by normal relative diastolic volume and function, consistent with
physiologic hypertrophy ( 32).
Weight lifters also experience difficulties associated with the exaggerated demands placed on the venous vascular
system, including lower extremity varicosities, phlebitis, and hemorrhoids. Hemorrhoids, a complication of the increased
venous pressure occurring during a Valsalva maneuver, are best treated symptomatically and can be improved with a
diet rich in fiber and an adequate fluid intake.
In addition, headaches (also known as weight lifter's cephalgia) and syncope occur commonly. The headaches, which
appear to be a variant of the exertional headache, also may be associated with other forms of intense physical activity.
These headaches have an abrupt onset, are of brief duration (4 to 6 hours), and begin during periods of exertional
activity (33,34). The etiology of these episodes has yet to be delineated. Although potentially serious etiologies are only
occasionally present, other causes of severe headache have been reported and should be considered ( 33,34 and 35).
Treatment usually consists of cessation of activity and use of a nonsteroidal antiinflammatory drug (NSAID).
Syncopal episodes appear secondary to a seemingly mandatory Valsalva maneuver performed while attempting maximal
lifts. The decrease in venous return of blood associated with the use of several pieces of ancillary equipment may
exacerbate the dramatic decline of cardiac output that causes these episodes. The abrupt loss of consciousness may be
associated with severe injuries as a result of the falling weight and are best prevented by attempting to continue regular
breathing throughout the entire performance of the lift.
Dermatologic problems, including hematomas, abrasions, and calluses, occur because of the need for a firm, nonslip grip
and various maneuvers required to lift immense weights. These problems are usually treated on a symptomatic basis but
are best dealt with by avoiding them initially through proper preventive measures such as the use of gloves while
training.
Several other medical conditions have been noted to occur in weight lifters, but only through anecdotal reports. These
problems include aortic dissection ( 36), rhabdomyolysis (37), chest wall deformities (38), and posttraumatic syringomyelia
(39). The incidence of these injuries is not well documented.
As with other sports, the preparticipation examination for weight lifting must be sport specific. A comprehensive medical
history should be performed, including questions concerning previous medical problems, unusual symptoms (i.e.,
episodes of syncope, dyspnea with exertion and chest pains), and previous injuries. A family history must include
questions pertaining to the occurrence of sudden death or other congenital heart disease in close relatives. The physical
examination should highlight areas of concern noted in the history as well as the shoulders, lower back, and knees.
Contraindications, both absolute and relative, are similar to those found in other strenuous sports ( Table 33.4).
Specific event coverage consists of proper preparation to ensure prompt and effective medical treatment of the injured
athlete. Proper preparations include adequate supply of medical equipment ( Table 33.5) and prepared medical
personnel, alert local medical consultants, authority pertaining to medical disqualifications, and clearance from
participants to allow emergency medical treatment.
TABLE 33.5. CATEGORIES OF MEDICAL SUPPLIES REQUIRED FOR ADEQUATE EVENT COVERAGE
STRENGTH-TRAINING INJURIES
Training for weight lifting and the other strength sports of power lifting and bodybuilding is truly sport specific, unlike
other sports that use strength training in an attempt to improve performance in a dissimilar activity. Because training is
sport specific, the incidence of weight-training injuries is less than in many of the other sports.
Injuries that occur with weight training, like with most sports, can be divided into acute (i.e., sprains and strains) and
chronic or overuse (i.e., tendinitis). A strain is a stretching or tearing of a musculotendinous unit, and a sprain is a similar
type injury occurring to a ligament or other stabilizing connective tissue structure. A sprain generally results in pain with
passive movement of the involved joint, whereas a strain produces pain with active movement of the joint. The
classifications, symptoms, and initial therapy of sprains and strains is similar ( Table 33.6). Sprains of varying severity
display differences in the amount of laxity and presence of an end point on physical examination when the structure is
stressed (Table 33.7).
TABLE 33.6. CLASSIFICATIONS AND IMMEDIATE CARE OF SPRAINS AND STRAINS
TABLE 33.7. LIGAMENTOUS INJURIES
Numerous underlying mechanisms have been incriminated as etiologies for these types of injuries and include
inadequate warmup or stretching; improper technique; trying out an untested new technique; maximum effort, usually
during competition, far exceeding that previously attempted; losing concentration; not completely rehabilitating from a
previous injury; or coaching failure ( 40,41). The risk of these injuries can be significantly decreased if the proper
preventive measures are taken: proper warmup; flexibility training; balanced strength training, using simultaneous
development of agonist-antagonist muscle groups; and proper coaching.
Chronic or overuse injuries, usually seen as tendinitis, occur as a result of repetitive microtrauma to a specific structure
that accumulates with time until a threshold is surpassed, resulting in macroscopic injury with symptoms and dysfunction.
Overuse injuries frequently occur as a result of overtraining; a sudden increase in training frequency, duration, or
intensity; inadequate training, leading to muscular imbalance between agonist-antagonist muscle groups; poor technique;
a decrease in flexibility; and failure to rehabilitate fully after an injury. These injuries require accurate diagnosis, not only
to target the symptomatic problem but also to determine underlying abnormalities that may leave the athlete vulnerable to
further injury or reinjury. Treatment of overuse problems usually consists of active rest, continued aerobic training of
some form, and correction of the underlying mechanism ( Table 33.8). These injuries are best treated by adequate
prevention, which includes proper warmup, flexibility training, appropriate coaching, periodization of training, and
restoration of proper technique.
TABLE 33.8. CLASSIFICATION AND MANAGEMENT OF OVERUSE INJURIES
The NSAIDs prescribed for both acute and chronic injuries are some of the most frequently prescribed medications in the
United States. Although the superiority of clinical efficacy of any of these medications is difficult to distinguish, the
differing pharmacologic properties provide some rationale for specific choices. Because the antiinflammatory dose is
greater than the dosage needed for analgesia, an adequate yet safe dosage must be prescribed, depending on the goal
of therapy. In addition to the well-known side effects of this group of drugs, specific NSAIDs differ in their effects on the
repair rate of tissue, with some increasing the strength of healing ligaments with short-term administration ( 42,43).
Therefore, the drug of choice to be used in a majority of these conditions provides both analgesic and antiinflammatory
action at safe dosages, can be taken on a simple dosing schedule (no more than twice daily), has a low frequency of
adverse effects, and has a favorable effect on healing.
The return of the injured athlete to activity depends on several variables: presence of symptoms, with and without activity;
adequate rehabilitation of injured structures; and improvement in any preexisting biomechanical abnormalities, including
increased flexibility and correction of muscle-strength imbalances. During the rehabilitation process, the athlete may
continue to remain active and continue aerobic conditioning, if possible, and strength training on unaffected muscle
groups.
Back
The lumbosacral spines of weight lifters are often asked to support a tremendous amount of weight, not only acutely but
also cumulatively over an extended period of time during training sessions and competitive seasons. Competitive weight
lifters have been shown to have a greater incidence of radiographic changes to their lower spine than athletes in other
sports. Except in the case of fractures, no correlation between these radiographic changes and lower back pain could be
found, because the incidence of lower-back pain is less than the incidence of radiographic changes ( 44,45 and 46). Many
of these x-ray findings were noted in asymptomatic male weight lifters who had normal physical examinations ( 46).
The true incidence of lower-back injuries in competitive weight lifters is not well known, although it may be less than
previously reported ( 47,49). Studies suggesting an increased rate of injuries to the lower back were noted in adolescents
(2,49), and the rate was comparable with that of high school football players ( 2).
Sprains, strains, and other soft tissue injuries of the lower back are the most common cause of lower-back pain in weight
lifters (2). These injuries usually result from a sudden reaching or twisting motion associated with sharp, stabbing,
localized pain. The neurologic examination is unremarkable, and radiographs demonstrate no acute findings. Other
causes of lower-back pain, including discogenic and nondiscogenic, should be excluded ( 50,51). Initially, these injuries
are treated with rest and ice for the first 24 to 36 hours and mild NSAIDs. Physical therapy is initiated immediately and
emphasizes improvement or maintenance of a full range of painless motion, followed by a program of stretching and
strengthening exercises. Chronic low-back problems result from improper rehabilitation following prior injury, weak
abdominal musculature, increased lumbar lordosis, tight hamstring muscles, and leg-length discrepancies.
Weight lifting, along with several other sports that require repetitive hyperextension of the lumbosacral spine, has an
increased incidence of spondylolysis ( Table 33.9) (52,53). Spondylolysis can either be a congenital or acquired defect of
the pars interarticularis related to a stress-type reaction or a stress fracture (also described as a fatigue fracture of the
pars interarticularis ( 54). It develops following microtrauma caused by repetitive hyperextension of the lumbar spine. This
problem often presents as subacute, unilateral, well-localized low-back pain, which is exacerbated by activity and
hyperextension. It is often associated with the hyperlordotic position, although not as frequently as is spondylolithesis.
On physical examination, the pain is reproduced with lumbar hyperextension and the one-leg lumbar extension test. Tight
hamstrings and decreased flexibility are found in approximately 80% of these individuals ( 55). This defect usually occurs
at the level of the fifth lumbar vertebrae ( 56). Lumbosacral radiographs that include obliques are necessary to ensure
accurate diagnosis, because a significant number of these lesions are not seen on regular anteroposterior (AP) or lateral
views (56). If symptoms persist despite normal plain radiographs and conservative therapy (e.g., active rest,
antiinflammatory medications, and physical therapy), a bone scan may be necessary to assist with the diagnosis. In
addition, a bone scan will help differentiate an acute defect from an old lesion ( 57).
TABLE 33.9. INCIDENCE OF SPONDYLOLYSIS BY PLAIN RADIOGRAPHS IN SELECTED SPORTS
If a defect is detected, the treatment consists of restricting activities that exacerbate symptoms, especially ones that
result in compressive loading of the lumbar spine; selective bracing; and an individualized exercise program. Return to
activity is determined by relief of symptoms and progression of muscular development and flexibility. The bone scan may
remain positive for several months after adequate healing secondary to remodeling. A fibrous union is common. The
long-term significance of a spondolytic defect has yet to be defined, although a recent review implies that a fairly benign
course with an incidence of low back pain no more frequent than the general population ( 58).
Spondylolithesis is the favored displacement or slipping of one vertebra over another and is usually associated with
either a pars defect or elongation. This defect usually occurs at the junction of the fifth lumbar vertebrae and sacrum.
Spondylolithesis and spondylolysis usually have similar presentations and mechanisms of injury, although the
epidemiology of spondylolithesis is not as well known. The classification of this defect determines the treatment ( 59)
Grade I and II lesions (i.e., less than 50% of the AP diameter of the vertebral body and no neurologic symptoms) can be
treated with a conservative exercise program and careful observation for progression of symptoms. The exercise
treatment should include an emphasis on flattening of the lumbar lordosis, stretching of the hamstrings, and
strengthening of the abdominal musculature. Conservative therapy in this group of individuals, especially adolescents,
has results similar to those who underwent surgical stabilization ( 60). When the athlete is asymptomatic, he or she is
allowed to return to full activity without restrictions, because there is no definite evidence that athletic activity increases
the risk of further slippage, especially following an adequate rehabilitation program.
Grade III through IV lesions (i.e., slippage over 50% of the AP diameter of the vertebral body) mandates a
discontinuation of sports that require repetitive hyperextension or axial loading, specifically weight lifting. The athlete may
engage in sports that do not require axial loading or repetitive hyperextension (e.g., bicycling and swimming).
Progressive slippage or continued low-back pain, or both, in spite of a conservative rehabilitation program, neurologic
symptoms that are not cleared by physical therapy, and cosmetic deformity that is unacceptable are indications for
surgical referral.
Although the incidence of intervertebral disk problems occurring in weight lifters is not well known, the frequency of
radiographically demonstrated reduction in disk height is increased ( 45). These problems are the result of extreme
loading and abnormal rotational forces, usually occurring in the lower lumbar spine. Disk degeneration occurs with aging
as the disk loses hydration and elasticity, becoming more fibrotic ( 61). The greatest changes occur between the ages of
25 and 35 years of age, a period of life when most lifters are constantly increasing the peak compressive forces applied
to their spines (62). The most common cause of this degenerative process is thought to be mechanical ( 62).
Symptoms of degenerative disk disease and an associated bulging or herniation of the nucleus pulposus include
lower-back pain exacerbated by coughing, radiation of pain into the lower extremity, paresthesias, and neurologic
deficits. On physical examination, a pattern of specific dermatome involvement, symptoms (i.e., paresthesias and
radiation of pain) reproduced or exaggerated by stretching of the sciatic nerve (some form of a positive straight leg test),
and loss of spinal reflex of appropriate level are found. The differential diagnosis of these findings include lumbar spinal
stenosis and nondiscogenic causes of sciatica, such as piriformis syndrome, sacroiliitis, iliolumbar syndrome, facet
syndrome, quadratus lumborum syndrome, trochanteric bursitis, and ischiogluteal bursitis ( 50,51). These causes of
nondiscogenic low-back sciatica often accompany pain associated with intervertebral disk disease.
Conservative treatment may be begun if symptoms are stable and of recent onset. Aggressive conservative treatment,
including adequate pain control and physical therapy, has been shown to treat herniated nucleus pulposus of the lumbar
intervertebral disk successfully compared with surgical intervention, even when a radiculopathy is present ( 63). Following
initial presentation, there should be a period of relative rest in which no overhead lifting or axial loading exercises are
attempted until symptoms dissipate. Once he or she is asymptomatic, the athlete may begin rehabilitative exercises that
concentrate on back flexibility, focusing on extension and abdominal muscle strengthening isometrically or in short arc
crunches without contracting the hip flexors ( 64). Biomechanical factors, such as poor resting and lifting postures and
muscular imbalances, are corrected. If symptoms progress or are unrelieved with conservative therapy, referral for further
diagnostic evaluations and treatment is warranted.
Shoulder
Most injuries of the shoulder in strength-training athletes are the result of strains and overuse problems of the
musculature, which include the rotator cuff, biceps, and deltoid. These injuries are usually secondary to poor flexibility,
muscle-strength imbalances, and overtraining. Power lifters, as a group, especially demonstrate less flexibility in
shoulder movements (64). Unless a complete macroscopic tear of a muscle has occurred, treatment consists mainly of
relative rest, proper medication, and rehabilitative exercise, as has been previously discussed.
Impingement syndrome occurs in weight lifters and involves the rotator cuff musculature (e.g., strains and tendinitis) and
associated structures (e.g., bursitis). This syndrome is related to muscular insufficiency or imbalance between the
anterior and posterior muscle groups of the rotator cuff or glenohumoral instability. Symptoms occur when flexion of the
shoulder as the arm is internally rotated causes the muscles of the rotator cuff to rub against the inferior aspects of the
acromion process and coracoacromial ligament, resulting in both chronic and acute injury, from tendinitis and bursitis to
an acute rupture. This particular movement is replicated during the physical examination in an attempt to elicit symptoms
and is the commonly performed test of impingement.
The rotator cuff muscles may be individually injured by specific mechanisms ( 40). Subscapularis injury is usually the
result of forced or repetitive abduction and external rotation. Injury to the posterior musculature, mainly the teres minor
and the infraspinatus muscles, is secondary to forced or repetitive adduction and internal rotation. These muscles are
often neglected during strength-training regimens, leading to muscle strength imbalances. Resisted abduction or forced
adduction, which occurs with the snatch maneuver, causes injury to the supraspinatus.
These injuries present with a deep, aching shoulder pain exacerbated by overhead activity. Localization of the pain is
often difficult, and occasional radiation to lateral shoulder and arm may occur. Further radiation of symptoms may
indicate a nerve compression. The duration of the symptoms vary, and the incidence of chronic shoulder pain is frequent.
On physical examination, point tenderness may be present over the involved musculotendinous unit or bursa. The pain of
tendinitis or muscle strain is reproduced with specific muscle testing, as in the use of the supraspinatus, or empty can,
test to isolate tension in the supraspinatus muscle. Glenohumoral joint instability is demonstrated by documenting
passive subluxation of the humeral head on the glenoid fossa and reproducing symptoms by performing apprehension
tests. Weakness of the posterior musculature may be present. A positive impingement sign, either the Neer impingement
test or the Hawkin sign of impingement, may be present. Plain radiographs are performed to demonstrate suspected
fractures or dislocations, although they usually provide little additional information to a thorough physical exam. Magnetic
resonance imaging (MRI) may be helpful if a completed tear of the musculature is suspected.
Conservative treatment is usually instituted before obtaining the more elaborate diagnostic studies. If therapy, active rest,
NSAIDs, and rehabilitative exercises that concentrate on flexibility and correcting muscle-strength imbalances fail to
improve symptoms, further diagnostic studies and possible referral are indicated. Return to activity is determined by
resolution of symptoms, return of full range of painless motion, and acquisition of balanced strength.
Condensing osteitis is a dense thickening of the clavicle caused by inflammation and overuse that frequently occur in
weight lifters (41). On plain radiographs, sclerosis and enlargement of the medial end of the clavicle is apparent with a
normal sternoclavicular joint. Conservative therapy is indicated with activity as limited by pain.
Osteolysis of the distal clavicle has been associated with weight lifting and weight training ( 66). This injury probably
results from excessive stresses being concentrated on the distal part of the clavicle and the acromial process during
weight lifting, leading to microfractures of the subchondral bone and subsequent repair. It presents as pain and
tenderness of slow onset in the area of the acromioclavicular joint and is usually first noted while bench pressing. The
pain worsens without loss of glenohumeral motion. Subluxation of the acromioclavicular joint does not occur.
Characteristic radiographic signs include osteoporosis, loss of subchondral bone detail, and cystic changes in the distal
part of the clavicle in varying degrees ( 66,67 and 68). Joint scintigraphy may be necessary to confirm the diagnosis.
Treatment is conservative with NSAIDs and physical therapy. Surgery is indicated if initial therapy fails to improve
symptoms but generally not before 6 to 12 months of treatment.
Elbow
The elbow, because of its importance in the proper execution of several of the major lifts, is the site of numerous reported
injuries, although epidemiologic data are limited. Documented injuries involving the elbow and associated structures
include ulna neuritis, ruptured biceps (distal) and triceps, and other undefined elbow pains, including brachialis and
anconeus injuries, intraarticular difficulties, and nerve impingement ( 68). Depending on the specific injury and severity,
early range of motion exercises are important to maintain full functioning of the joint.
Medial and lateral epicondylitis result from heavy repetitive forearm activity, causing microtrauma to either the extensor
or flexor conjoined tendons of the wrist, leading to inflammation and pain. The classic signs of these conditions on
physical examination include tenderness over the involved epicondyle and pain exacerbated by either active flexion or
extension of the wrist against resistance. This injury is best treated with relative rest, NSAIDs, and a proper strengthening
and flexibility program with postexercise cold application. A proximal forearm brace may offer some relief. Surgical
release of the conjoined tendons is rarely necessary.
Complete tendinous ruptures of the biceps and triceps are fairly uncommon injuries but have been reported in weight
lifters (68,69). Rupture of the triceps insertion on the olecranon process has been seen primarily during the snatch and
the bench press, with its deceleration stress and eccentric contraction. The mechanism of injury that causes rupture of
the biceps tendon is probably similar. Complete ruptures usually are fairly apparent on physical examination with
dependent ecchymosis; the defect is noted along the musculotendinous unit and there is little or no resistance on specific
muscle testing. These injuries frequently require surgical repair.
Repeated or old trauma to the ulnar nerve as it traverses just lateral to the medial epicondyle may result in an ulnar
neuropathy. Significant trauma to the nerve may occur secondary to compression of the nerve between the heads of the
flexor carpi ulnaris muscle, subluxation of a taut nerve over the medial epicondyle (hypertrophied triceps further promote
subluxation of the nerve across the medial epicondyle), lack of full flexibility, partial rupture of the surrounding tissue, and
direct trauma to the nerve itself ( 41,70). The individual usually reports medial elbow pain, radiating distally along the
ulnar aspect of the forearm, and paresthesias along the distribution of the ulnar nerve. A Tinel's test at the elbow may be
present (40). Weakness of grip, atrophy of the hypothenar eminence and adductor pollicus muscle, and a Wartenburg
sign also may be present ( 70).
If it is diagnosed early, an ulnar neuropathy may be treated nonsurgically with rest (immobilization if needed), NSAIDs,
vitamin B6, and a thorough rehabilitative exercise program. If problems persist despite conservative therapy, surgical
release may be necessary. Full recovery and return to previous level of activity is expected.
Compartment syndromes of the arm, although rare, occur as a result of overuse, usually involving the triceps and biceps
muscles (71). These problems present as significant pain along the length of the muscle, representing expansion of the
tense facial tissue as a result of the swelling of underlying tissue. Neurologic changes may occur, including paresthesias
and motor weakness secondary to ischemic muscle and compression of peripheral nerves. This syndrome is associated
with severe pain and muscle weakness on passive stretch of the muscles involved ( 72). Compartment syndromes can be
adequately treated if diagnosed early with rest, ice, NSAIDs, and physical therapy; otherwise, release by fasciotomy,
often emergently, is required.
Violent dislocations of the elbow occur often in the weight-training sports. An acute dislocation should be quickly reduced
to prevent further soft tissue and neurovascular damage, which are commonly associated with this type of injury. Before
reduction, a neurovascular examination should be well documented and radiographs should be taken to determine the
presence of coexisting fractures.
Proper forearm, wrist, and hand functioning are an integral part of proper weight-lifting technique. With their importance,
they lend themselves to be particularly susceptible to injury, especially when lifters fail to get their elbows around in the
clean maneuver, forcing the elbow into the knees while the wrist is hyperextended and loaded ( 41).
The wrist sprain is the most common injury of these structures and is usually the result of hyperextension. Although it is
occasionally difficult to distinguish a sprain from a strain, initial management is the same for both: rest, ice,
immobilization, and NSAIDs. Radiographs are usually recommended to detect possible fractures and dislocations,
particularly scaphoid features and scapholunate dissociations.
Fractures and dislocations of the ulna and radius have been reported in weight lifters, although the incidence of such
injuries is unknown (73,74 and 75). Many of the reported fractures are stress fractures involving the ulna. If a fracture is
suspected (well-localized tenderness, palpable periosteal elevation, pain with distant stress of the bone, no improvement
of symptoms following a short-term period of rest) and plain radiographs are normal, a bone scan is indicated. These
fractures can be treated with restricted activity and immobilization until healing occurs.
Forearm compartment syndromes, which have been noted in the weight-lifting sports, are the result of repetitive use and
activity (76). This injury is associated with forearm pain, especially noted with passive dorsiflexion. Treatment consists of
rest, ice massages, immobilization, and NSAIDs. If symptoms worsen or are associated with neurovascular compromise,
fasciotomy may be required.
Nerve entrapment syndromes, caused by a mechanical compression within a confined anatomic space or unusually thick
peritendinous tissue pressing a nerve against bone or ligament, occur within several anatomic tunnels of the wrist ( 41).
These tunnels are the radial, pronator, cubital, carpal, and ulnar at the wrist (Guyon canal). The sport's techniques
require tremendous weight to be placed on the extended wrist, increasing risk of developing these problems. Following
prompt and accurate diagnosis, this condition is best treated with rest, immobilization, ice massages, and NSAIDs. If
symptoms persist with prolonged or worsening neurovascular compromise, surgical decompression is indicated.
Wrist ganglions are considered to be herniations of the joint capsule or synovial sheath of the tendon and frequently
occur about the wrist joint. Ganglions usually develop following a sprain on the dorsal aspect of the wrist. Unless they are
symptomatic, treatment of wrist ganglions is not necessary.
The most frequently encountered problems of the hands occur as the result of callus formation. Calluses are the result of
the shearing forces produced while gripping the knurled bar. They are vulnerable to tears and cracks, with subsequent
exposure of the underlying dermis and infection of the surrounding tissue.Treatment of torn calluses consists of properly
protecting the underlying skin. Because the lack of elasticity predisposes the callus to tearing, the best preventive
measure against this complication entails the use of an emery file to reduce the callus, especially following bathing, and
the application of a lanolin hand lotion to help maintain the skin's elasticity.
Groin and Thigh
Acute injuries to the large musculature associated with the hip and knee occur with weight lifting. The hamstrings are
particularly susceptible to acute strains for several reasons: lack of flexibility; strength imbalance between quadriceps
and hamstrings; strength imbalance between hamstrings in both legs; and activities that cause excessive fatigue of the
hamstrings (41). Initial treatment consists of rest, ice massages, elevation, and compression, with additional treatment
targeted at correcting the underlying abnormalities. Firm-fitting shorts, such as used by cyclists, may provide additional
support during rehabilitation.
In dealing with such sites of susceptible injury, it is important to perform the proper preventive measures: attention to
balanced strength, proper flexibility exercises, adherence to the principle of specificity of training to acclimate the
muscular to specific demands, biomechanical abnormalities, and proper warmup and cooldown. Recurrent injuries to
these muscle groups probably reflect a combination of the above-mentioned abnormalities in addition to inadequate
rehabilitation of previous injuries.
Knee
Contrary to commonly held beliefs and previous recommendations ( 77), weight lifting is not commonly associated with an
increased risk of knee injury (2,78). In fact, proper strength training maintains (and may increase) the stability of the joint
and its ligaments (79,80). Compared with athletes of other sports who demonstrate increased ligamentous laxity following
a period of their selected activity, performing a session of squats resulted in no change in the AP laxity noted in the knee
joint as measured by a mechanical device (81). When knee injuries do occur, they are usually the result of factors other
than the biomechanical aspects of the lifts themselves: inadequate warmup or stretching, improper technique, poor
flexibility, attempting new or unfamiliar techniques, performing maximal efforts, or participating in other activities besides
weight lifting (41,68). The initial treatment of knee injuries, as with other soft tissue problems, consists of rest, ice,
elevation, and protection of the area from further injury. After the initial phase of therapy, treatment is aimed at correcting
underlying abnormalities.
Patellar tendinitis results from excessive, repetitive contractile forces of the quadriceps, causing microscopic tears of the
musculotendinous unit. This repeated stress and loading, which also inhibits the healing process, ultimately leads to
inflammation, pain, and dysfunction. This condition is worsened by activities that encourage full range of active motion of
the knee joint, which places immense stress on the tendon and associated structures, for example., squats, squat
snatches, and squat cleans.
Patella tendinitis usually presents as pain just below the inferior aspect of the patella. The pain initially is present
following activity, and may progress to pain at the onset of activity that diminishes with warmup. Severe tendinitis is
distinguished by the presence of constant pain and swelling. Treatment is similar to that described for patellofemoral
problems, with the possibility of an increased benefit of using eccentric exercises early in the strengthening problem. The
use of a patellar-tendon band may provide further support and relief.
The patellofemoral syndrome, with the associated arthroscopic diagnosis of chondromalacia patellae, is a degenerative
process that results in the softening of the hyaline cartilage on the undersurface of the patella and the articulating
condyles of the femur (articular cartilage). Several factors predispose the weight lifter to this condition: (a) malalignment
of the thigh and the lower leg, resulting in an increased Q angle; (b) abnormally small or high-riding patella; (c) deformity
of the patella or femur; and (d) tight hamstrings or iliotibial band. This condition symptomatically presents with anterior
knee pain with active flexion, weakness, subjective feelings of apprehension associated with subluxation, tenderness
about the patella and the patellar facets, hypermobile patella, and patella crepitus. Treatment of this condition consists of
rest and ice during the acute phase, followed by active rehabilitation including stretching and strengthening, specifically
in arcs of motion that do not produce symptoms, and selective bracing ( 82). Isokinetic rehabilitative strengthening
programs afford a definite advantage in patellofemoral syndromes.
Bursitis, true inflammation of one or more of the bursae that surround the knee joint, is caused by either the repetitive
compressional forces created by the large muscle groups during flexion and extension, instability of the knee joint
secondary to osteoarthritis and previous internal derangement, or direct trauma to the bursae. Localized treatment with
ice massages and protection from further injury in addition to the administration of NSAIDs are the therapies of choice. A
local injection of a corticosteroid and anesthetic provide almost immediate relief and is indicated for both severe bursitis
or more prolonged pain refractory to physical modalities and oral agents. The condition most often overlooked is
anserine bursitis, a cause of chronic or acute medial compartment pain. The pes anserine bursa is inferior and slightly
anterior to the inferior insertion of the medial collateral ligament. Pes anserine bursitis is a common sequela of improper
technique in performing both squats and repetitive power cleans.
Ligamentous injuries about the knee primarily involve the medial and lateral collateral ligaments and usually are the
result of excessive knee rotation, abnormal valgus or varus stress, hyperflexion, or hyperextension. These injuries
present as localized pain, swelling, and tenderness over the involved structure. Stress placed on the ligament may or
may not exacerbate the symptoms, depending on the presence of a partial versus a complete tear of the ligament. These
injuries are treated initially with rest, ice massages, and protected motion. Complete tears of these structures require
evaluation by a specialist. Complete return to previous level of activity is expected, and with proper rehabilitative
exercises, these structures are strengthened with weight training and aerobic exercises such as bicycling.
Meniscal and cruciate ligament injuries (also known as internal derangements of the knee) are usually the result of a
direct blow to the knee, forced hyperextension, or an abnormal twist. They also may develop secondary to chronic but
repetitive minor injury. These injuries commonly present as acute onset of pain (especially following an audible “pop” or
“snap”), a swelling that occurs immediately or within a few hours of the injury, an inability to fully extend or flex the knee,
pain with walking or standing, or the sensation of joint instability. Injuries of this type are usually associated with a
significant effusion, which if immediately aspirated, reveals a hemarthrosis; they should be radiographed to assist with
the diagnosis and determine the presence of possible fractures. Arthrocentesis and joint fluid analysis assists in the
differentiation of possible etiologies of the effusion, because rheumatic syndromes, such as Reiter syndrome, may also
present with acute onset knee with effusion. The presence of a hemarthrosis is highly correlated with the tearing of the
cruciate ligaments. Initial therapy includes protecting the joint from additional injury and providing adequate relief, usually
with an NSAID. Patients with partial anterior cruciate tears are frequently rehabilitated successfully without surgery.
Complete or recurrent tears usually require surgical intervention, but significant rehabilitation must follow, and current
surgical technique for repair almost always precludes competitive lifting for 12 months.
Particular attention to strengthening the hamstrings is one important goal, and a strength ratio with the quadriceps
femoris of 2:3 or even 3:4 is desired. Musculotendinous tears and ruptures of the patella tendon, gastrocnemius tendon,
and distal insertions of the hamstrings have been reported in weight lifters. These injuries are often believed to occur at
sites in the tendon weakened by overuse. Partial tears can usually be treated conservatively, whereas complete tears
require surgical evaluation.
Ankle and Foot
Fortunately for weight-lifting athletes who require a solid foundation from which to lift the tremendous amount of weight,
ankle and foot injuries in their sports are rare. The incidence of ankle sprains is rare, contrary to the incidence of this
injury in other sports. A number of injuries occur from dropped weight plates or from wearing of overnight shoes, which
causes entrapment of the peroneal nerve.
CHILDREN AND STRENGTH TRAINING
Although recent research has demonstrated short-term programs in which prepubescent athletes can increase strength
without risk of significant injury ( 83,84 and 85), studies on long-term weight training; weight training in less-supervised
programs; and the effects of weight training on strength, injury prevention, and improved performance are lacking.
Anecdotal reports on strength training in pubescent athletes often detail significant musculoskeletal injuries, including
epiphyseal fractures, ruptured intervertebral disks, and low-back bony disruptions, especially when performing the major
lifts (49,74,86). The true incidence of these significant injuries is not well known, even though several studies have
attempted to quantify the injury rate. Considering the flaws associated with the limited data on the incidence of injuries in
adolescent weight lifters, the incidence of injury in this group of athletes compares favorably with the incidence of injuries
in other sports (1).
The sports of weight lifting, power lifting, and bodybuilding are gaining increased popularity among teenagers. The
number of teenagers joining established associations is increasing, with the USWF reporting close to 600 teenage
members and the USPF reporting more than 3,000 teenage members. Approximately 8,500 adolescents are formally
involved in the sport of bodybuilding.
With the increased popularity of these sports among the pediatric population, the American Academy of Pediatrics has
established the following recommendations ( 87):
1. Strength training programs for prepubescent, pubescent, and postpubescent athletes should be permitted only if
conducted by well-trained adults. The adults should be qualified to plan progress appropriate to the athletes' stage
of maturation, which should be assessed objectively by medical personnel.
2. Unless good data become available that demonstrate safety, children and adolescents should avoid the practice of
weight lifting, power lifting and bodybuilding, as well as the repetitive use of maximal amounts of weight in
strength-training programs until they have reached the Tanner stage 5 level of developmental maturity.
WOMEN AND STRENGTH TRAINING
Women participating in weight training and competing in weight lifting and bodybuilding has become a common
occurrence, despite the outdated notion that strength is solely a masculine quality. The involvement of women in the
strength-training sports has created an interest in the relative strength of females compared with males. If static
measures of strength are used, absolute strength in females is less than that of males ( 88). These differences in strength
decrease if anatomic and physiologic variations are considered ( 89). Gains in strength and hypertrophy of musculature
are expected with training in females, although not to the extent found in males ( 90).
Although the benefits of a successful weight-training program in males is well documented, the benefits of such a
program in females are not as well known. Some of the benefits females appear to gain from weight training are
increased lean body mass and improved psychological profile, including being somewhat less anxious, neurotic,
depressed, angry, and confused and more extroverted, vigorous, and self-motivated than the general public ( 91).
Furthermore, the density of bone in weight lifters is increased, and whether this alteration results in a decreased
incidence of osteoporosis in later life is not known.
Intense weight training may have several deleterious effects on female physiology, particularly on normal menstrual
functioning. Exercise-associated amenorrhea (EAA) is found in patients who engage in various endurance sports.
Although the exact incidence is unknown, EAA also has been associated with competitive female bodybuilders and is
probably found in other strength-training women involved in intense training ( 92).
THE ELDERLY POPULATION AND STRENGTH TRAINING
National and international weightlifters usually obtain their maximal lifts between the ages of 28 and 34 years. As a
seemingly dependent variable of the aging process, a decline in measurable strength occurs. Although total strength may
decrease, the ability to increase strength and of the muscle to hypertrophy through a proper program of resistive
exercises appears to be maintained, even in the very old ( 93,94). Gains in strength during a power-lifting training
program were demonstrated by a 50-year-old retired competitive Olympic-style weight lifter ( 95). The effect of a regular,
long-term program of strength training on the decline of strength with age is not known but may be similar to the slower
decline in aerobic fitness with aging noted in individuals who maintain a regular program of endurance exercise ( 95).
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34 Racquet Sports
34
RACQUET SPORTS
MARC R. SAFRAN
The Different Sports

Epidemiology of Racquet Sports Injuries
Distribution of Orthopedic Injuries in Tennis
Shoulder
Elbow
Hand and Wrist
Forearm
Central Region Injuries (Back and Trunk)
Other Regions
Biomechanics of Tennis Strokes in Influence on Injury
Serve
Forehand
Backhand
Footwork
Unilateral Arm Dominance, Adaptations, Asymmetry, and Injury Production
Exercise Physiology of Tennis and other Racquet Sports
Tennis
Other Racquet Sports
Equipment and its Evolution
Racket
Strings
Shoes and Court Surface
Tennis Balls
Squash and Racquetball
Contusions and Abrasions
Eye
Heat Illness
Shoulder
Elbow
Wrist
Back
Hip
Knee
Leg
Ankle
Foot
Badminton
Shoulder
Elbow
Wrist
Back
Thigh and Groin
Knee
Leg
Ankle
Foot
Treatment Pearls
Indications for Surgery of Common Injuries
Shoulder Pain—Instability, Impingement, and Rotator Cuff Tears
Medial and Lateral Epicondylitis
Wrist
Achilles Tendon Rupture
Conclusions
Acknowledgments
Chapter References
Racquet sports are enjoyed throughout the world and are increasing in their popularity. These sports include tennis,
racquetball, badminton, and squash. The increasing popularity of these racquet sports and consequent rise in injuries
has resulted in an increasing concern in the world of sports medicine. At present, there is very little information regarding
racquet sports injuries. Most of the literature on racquet sports injuries is descriptive with case series and case reports.
There are very few studies evaluating the epidemiology and pathophysiology of injuries in racquet sports. What
information does exist about sports specific injury has concentrated on tennis injuries, and as such, this topic is the focus
of this chapter.
Although many “experts” believe that limitations in motor development prevent children from learning and playing tennis
and other racquet sports until the age of 7, it is not uncommon to see boys and girls start in organized racquet sports
instruction as early as 5 years. Indeed, with the increased popularity of all of these sports, especially with the visibility of
professional tennis and the success of many young tennis stars, a growing number of preadolescents and adolescents
have been drawn to the courts. Furthermore, with the vast amount of money involved, particularly in tennis, the impact on
young, aspiring racquet sports competitors leads to greater pressure to practice, higher expectations of performance and
increasing demands on the human body. Even still, year-round involvement in training, competition, and tournaments is
the norm. It is intuitive then, that these factors would combine to result in a greater susceptibility to injury.
The investigation of the specific musculoskeletal demands in racquet sports has shown adaptive responses to the
stresses of performing these sports. These adaptations have been described as being both beneficial and deleterious.
Positive adaptive changes include improved motor control, muscular power, and speed. Negative adaptive changes
include reduced flexibility and motor imbalance. These negative changes have proven to be important factors in the injury
process. Poor physical condition and poor technique may also be factors in injury patterns in the athlete.
An understanding of the biomechanics of the individual racquet sports and the stresses placed on the court participant
can be as helpful as a careful examination in the diagnosis and treatment of these injuries. Factors including a player's
physical condition, previous injuries, skill level, stroke mechanics, and intensity of training must be considered when
evaluating a racquet sports athlete. Other important factors include equipment variables such as string type and
tightness, grip size and type, racquet composition, thickness, length and head size, footwear and court surface.
Once accurate identification of the injury and its cause are made, proper treatment and rehabilitation can begin. It is
important to remember that many of these injuries are overuse injuries, and the treatment involves relative rest,
strengthening, and review of stroke mechanics to help prevent recurrence.
This chapter is written to provide the reader with an overview of the epidemiology of racquet sports injuries, a discussion
of the biomechanics of each of the tennis strokes and how they relate to injury, a review of the exercise physiology of
tennis, a discussion of tennis equipment and its evolution, a discussion of the management of some tennis-related
injuries including indications for surgery for common tennis injuries. and finally, a review of what is known about
badminton, squash, and racquetball injuries. With this information, the reader will have a better understanding of the
injuries, and be able to better evaluate, treat, rehabilitate, and prevent future injury.
THE DIFFERENT SPORTS
Tennis is by far the most popular of all of the racquet sports, especially in the United States. It is estimated that over 20
million people participate in tennis in the United States at least once a year, with more than 5 million playing tennis at
least twice a month (1). The United States Tennis Association, whose members play tennis competitively, had a
membership of 530,000 in 1999 (2).
Tennis is an individual, noncontact sport played on a court 78 feet long with a net 3 feet in height dividing the court in two
equal parts. The court is 27 feet wide for singles, with one player on each side of the net. Doubles is played with two
players on each side of the net, with the court being 36 feet wide. The racquets measure 27 to 29 inches long, although
the maximum length allowed is up to 32 inches. There is no weight restriction of the rackets, although current technology
has resulted in rackets weighing 7 ½ to 13 ounces. Strings are made from resilient gut or nylon. The tennis ball is hollow,
composed of inflated rubber and covered with fabric. The ball measures 2 ½ inches to 2 5/8 inches in diameter and
weighs 2 to 2 1/16 ounces. The ball may travel at a velocity of up to 140 mph on the serve and 85 mph on the return. The
court surfaces may be hard court, clay and other composite surfaces, grass or carpet. Tennis is usually played outdoors,
although it may be played indoors, usually on carpet.
The International Badminton Federation estimates that 1 billion people play badminton worldwide. Badminton is a very
popular sport, especially in China, Indonesia, and Malaysia. It is estimated that almost 10 million people in the United
States played badminton at least once in 1998 ( 3), although this number includes social backyard games. It is estimated
that nearly 1 million people play badminton more than twice a month ( 4). There are only 2,000 members in the USA
Badminton Association (5).
Badminton is an individual, noncontact sport played on a court 20 feet wide and 44 feet long, with the court evenly
divided in two, lengthwise, by a net 5 feet high at the center. Opponents are on opposite sides of the net. This sport is
usually played indoors on a wood floor. The shuttlecock is made of 16 feathers with a fixed base. The shuttlecock is
almost cone shaped, 2 ½ to 2 3/4 inches long with a diameter of 2 1/4 to 2 5/8 inches at one end and 1 to 1 1/8 inch at the
other, and it weighs between 4.7 and 5.5 g. The racquets are much lighter than the tennis racquet (3 to 3.7 ounces). The
rackets are 26 3/4 inches in length. The head length cannot exceed 11 3/8 inches. The shuttlecock may travel up to 200
mph in world class adult play.
The United States Squash Racquets Association estimates that 18 million people play squash worldwide. Although there
are 7,500 members in the US, 500,000 play at least once a year, and less than 150,000 play regularly ( 6).
Squash is a sport played in an indoor enclosed court. The North American type court is more narrow than the
international sized court and measures 16 ½ feet by 32 feet enclosed by a ceiling that is used in play. The ball now most
commonly used internationally is soft, measures 1 3/8 inches in diameter, and weighs 0.826 to 0.865 ounces. Racquets
measure 27 inches in length and weighs 7 ½ to 9 ounces. The strung racquet head measures 7 ½ × 8 ½ inches, although
larger head racquets are now available. The ball velocity has been measured at over 110 mph after direct contact ( 7).
The players are in close proximity in singles and especially in doubles.
Racquetball was invented in 1949 in the United States by a person who sought a fast-paced game that was easy to learn
on a handball court. Racquetball has grown to a total of approximately 7 million players a year in the United States, and 8
million world wide (8). More than 1.5 million of the participants are estimated to play at least twice a month ( 4). There are
20,000 members of the United States Racquetball Association (USRA).
The racquetball court is enclosed with a ceiling, which is used in play. The court is 40 feet in length and 20 feet in width.
The height of the front wall is 20 feet, while the back wall is equal to or greater than 12 feet. The racquet cannot exceed
22 inches in length. The ball is soft, weighs 1.4 ounces, and has a diameter of 2 1/4 inches. The ball has been shown to
travel consistently at 127 mph during high competitive play after a direct hit ( 9). The players are in close proximity, both
in singles and doubles.
EPIDEMIOLOGY OF RACQUET SPORTS INJURIES
The true understanding of racquet sports injury requires information about the frequency of occurrence over a defined set
of time, the frequency of injury in a defined population, and distribution of these injuries (the epidemiology). Again,
although much is written about tennis and the other racquet sports, good studies evaluating the incidence and
prevalence of injury are lacking. The following is a review of the incidence, prevalence, and distribution of injuries in the
different racquet sports and the studies comparing the sports. Population-based incidence studies have been limited to
the sport of badminton.
A population-based study of badminton injuries revealed 208 injuries presenting to community hospitals out of a
population of 10,032 badminton players, or approximately 20 per 1,000 players ( 10). In another population based study
from Denmark of people presenting to a “casualty ward,” the incidence of injuries among players younger than 18 years
old was 28 per 1,000 per year, whereas for those 18 to 25 years old, the incidence was 45 per 1,000 per year, and for
those older than 25 years old, the incidence of injury was 42 injuries per 1,000 people per year ( 11). Badminton injuries
have been reported to account for 1% ( 12) to 4% (10) of all sports injuries ( 13). Jorgensen identified 0.85 injuries per
year in badminton as compared with 0.56 per year with tennis, with an injury rate of 2.9 injuries per 1,000 hours of
badminton play as compared with 2.8 injuries per 1,000 hours of tennis play ( 14). Further, men sustain injuries more
frequently (0.9 injuries per season and 2.8 injuries per 1,000 match hours) than women (0.78 injuries per season and 2.1
injuries per 1,000 match hours) ( 14). In Sweden, badminton had an injury rate of 2 to 5 injuries per 1,000 players ( 15,16).
The incidence of severe eye injuries in badminton has been estimated at 16 per 100,000 participants as compared with
squash at 19 per 100,000 participants ( 17).
In racquetball, there are no population based studies available, although one study reported 70 new cases of injury
presenting to a university student health clinic over a 15-month period ( 18), with 54% involving the head and face. One
retrospective study reported 157 injuries in 141 racquetball players with 57% involving the head and face ( 19). Of the 75
nonfacial injuries, 33% of injuries were ankle sprains, whereas less than 10% of the injuries were ankle fractures, elbow
fractures, and foot sprains, and less than 5% were elbow sprains, knee sprains, shoulder sprains and back spasms ( 19).
In squash, again there are no population-based studies available. Most reports of squash injury discuss eye injury
(17,20,21,22,23,24,25,26,27 and 28) and sudden death (7,29); however, a retrospective telephone survey revealed that
44.5% of players interviewed reported an injury ( 30). Players older than the age of 40 years are considered to be at
greatest risk of injury (30). Contusions, abrasions, and lacerations are the most common injuries ( 30). Of the orthopedic
injuries in this retrospective study, strains were the most common injury, followed by ligament injuries (ankle sprains),
inflammation, and tendon injury (30). For eye injuries in squash, the incidence ranges from 5.2 to 33.3 per 100,000
(31,32,33,34 and 35).
In tennis, there are also no population based studies available, although researchers have attempted to determine the
incidence (9.1%) ( 36) and prevalence (40% to 50%) ( 36,37 and 38) of tennis elbow. However, in evaluating different
studies of tennis injuries, most injuries are sport specific, although relative rates do seem to vary by age, ability, and
gender (see further discussion later). Hutchinson studied injury rates for 6 years during the USTA Boys' National
championships and found that 21% of the athletes sustained new or recurrent injuries that required evaluation by the
medical team (39). The incidence rate was 9.9 per 100 athletes and 21.5 per 1,000 athletic exposures ( 39). The
incidence of injury (defined as lost time from practice or play) for high school tennis players has been estimated at 3.5
injuries per 1,000 players for males and 5.8 per 1,000 female players ( 40). Another 8-year study of high school injuries
that resulted in a player missing 1 or more days of practice or play revealed an injury risk of 0.29 for girls and 0.13 for
boys, and 0.35 injuries per female tennis player and 0.14 injuries per male tennis player ( 41). A 1-year prospective
collegiate injury study identified an incidence of 0.16 injuries per 100 person-hours in male tennis players as compared
with 0.10 injuries per 100 person-hours for female tennis players ( 42). Winge noted an incidence of 2.3 injuries per
player per 1,000 hours of play when 100 elite tennis players were prospectively studied during the 1984 Danish outdoor
season (43).
Comparative data of injury rates among the different racquet sports and injury rates in other sports is sparse. In one
study, tennis accounted for only 0.3% and badminton for 0.1% of the total of 1,576 injuries in a population of school-aged
children (44). The rate of injury in tennis was 0.01 injuries per 1,000 participant hours as compared with 0 for badminton,
5.68 in track and field, and 1.05 in football ( 44). Tennis accounted for less than 1% of all injuries in Irish children ( 45). In
an ambitious, 2-year prospective high school injury study, Garrick found that the injury rate for tennis was 0.07 for women
as compared with 0.03 for men, and was 0.06 for female badminton participants (46). Chard and Lachmann performed an
8-year retrospective study of racquet sports injuries that presented to a sports injury clinic in England ( 47). The authors
found that 59% of injuries were squash related, 21% were tennis injuries, and 20% were associated with badminton ( 47).
This is to be considered in light of the fact that there are considered similar numbers of participants in these three sports
in England. The authors related the predominance of squash injuries to the fact that this sport has higher physical stress
and increased risk of contact as compared with tennis and badminton. Lower limb injuries predominated in all three
sports, and tennis had a significantly greater percentage of upper extremity injuries as compared to the other two.
Furthermore, tennis was responsible for more low back injuries (43%), including disk herniation, as compared to squash
(35%), and badminton (25%), with the latter two sports having less severe strains ( 47). A recent population based study
in England and Wales revealed a rate of new injuries of 5 per 1,000 occasions of participation in squash over a 1-year
period, as compared with 3 per 1,000 in badminton, and 2 per 1,000 in tennis which can be compared with rugby, which
had 50 new injuries per 1,000 occasions of participation over the one year studied ( 48).
The National Electronic Injury Surveillance System (NEISS) combines injury statistics for squash, racquetball and
paddleball. In 1998, there were estimated to be 8,983 injuries due to squash, racquetball, and paddleball treated in
emergency rooms in the United States, as compared with 22,665 tennis related injuries in the same period ( 49).
The results of injury studies in tennis players have shown some variability as to the distribution of injuries ( 39,43,50,51
and 52). However, they all seem to identify a certain pattern of injury with respect to location and type of injury. Injuries to
the back, neck, and groin occur at a number roughly equal to that of upper extremity problems (shoulder, elbow, and
wrist). Overall, leg injuries (hamstring, knee and ankle) occur approximately twice as often as upper extremity injuries.
Virtually all of the previous studies evaluating patterns of injuries in tennis players have focused on men ( 39,43,51,52 and
53). Yet, the number of women participating in sports, including tennis, has risen dramatically since the 1970s. In
general, injury patterns are observed to be more sport specific than gender specific. Nevertheless, female athletes tend
to have more frequent patellofemoral problems. Furthermore, women have less upper extremity strength and potentially
begin competition at a lower level of physical conditioning than men. Thus, female tennis players may have an increased
incidence of overuse and stress-related injuries related to poorer physical conditioning and an increase in injuries of the
shoulder and elbow secondary to the comparatively less upper body strength.
A preliminary study by Safran and Hutchinson ( 54) compared injury patterns in elite junior athletes (both men and
women) during a 3-year period (1996 to 1998) at the USTA Tennis Championships ( 54). Sixteen- and eighteen-year-old
boys sustained more new injuries during the USTA National Hardcourt Championships as compared with girls at the
USTA Girls' 16's National Championships over the 3 years studied ( Table 34.1). However, there was no significant
difference in the overall rate of injury (new and recurrent) between boys and girls ( Table 34.1). Boys and girls had a
similar rate of lower extremity injury, both in incidence and prevalence; however, the amount of lower extremity injuries
was disproportionately greater in girls as compared with boys ( Table 34.2 and Table 34.3). Injuries to the abdomen, back
and groin were significantly fewer in females as compared with males. Both boys and girls have a high rate of injury to
the back and shoulder, whereas girls have more injury to the feet, leg or calf, and wrist. Boys sustain more injuries to the
ankle, groin, and hand. For both boys and girls, strains predominated, followed by inflammation and sprains. Boys have a
greater incidence of contusion, abrasions, and lacerations.
TABLE 34.1. INCIDENCE (NEW INJURIES ONLY) AND PREVALENCE (NEW AND RECURRENT INJURIES) OF
INJURY DURING THE 1996–1998 USTA NATIONAL CHAMPIONSHIPSa
TABLE 34.2. INCIDENCE OF INJURY BY LOCATIONa
TABLE 34.3. PREVALENCE OF INJURY BY LOCATIONa

The author has found in his study of Girls' 16's USTA National Championships participants over the last 4 years, and the
Boys' USTA National Championships more recently, that those who are injured during the national championships play
and practice more often per year than those who were not injured during the same tournaments. Girls injured during the
1998 tournament played and practiced 11% more often per year than those who were not injured, and boys injured during
their 1998 nationals played and practiced twice as much per year as those who were not injured ( 55). Eighty-nine percent
of injured girls jogged and 77% lifted weights as part of their training program as compared with uninjured girls, of whom
82% jogged on the average 10% less mileage than the injured girls and only 50% lifted weights ( 55). There was no
difference between injured and uninjured boys for running or weight lifting.
During the 1998 USTA Girls' 16's and Boys' 16's and 18's National Championships, Safran and Hutchinson administered
a validated tennis questionnaire ( 56) to assess the prevalence of injury in these elite junior players. Only 23% of girls and
45% of boys noted no injury that kept them from playing for 1 week or more, whereas 53% of females and only 29% of
boys noted more than one tennis injury in the past ( 55). Table 34.4 reveals that low back pain was the most common
ailment that has kept elite junior boys and girls from play ( 55). Pain in the front of the shoulder was the next most
prevalent injury in girls, followed by dominant wrist injury, nondominant wrist, and elbow pain. Boys noted similar rates of
injury to the elbow and dominant wrist, and pain in the front and back of the shoulder ( 57).
TABLE 34.4. PREVALENCE OF INJURY OR PAINa
Hutchinson et al. found that lower extremity injuries were most common, as were overuse injuries (39). Those authors
noted that lower extremity injuries occurred twice as frequently as upper extremity injuries, whereas central injuries were
not different in incidence from upper extremity injury ( 39). Back pain (strain) was the most common injury in boys
participating in the USTA Boys' 16's and 18's National Championships, followed by the thigh or hamstrings (strains), and
shoulder inflammation ( 39). Sprains, particularly of the ankle, were the most common injury, followed by muscular and
tendinous strains (39). Nonmusculoskeletal injuries identified include heat illness, cramping, and bee stings ( 39).
Reece et al. studied injuries for 4 years at the Australian Institute of Sport and found that lower extremity injuries occurred
in 59% of the cases, with upper extremity and central injuries occurring with equal frequency ( 52). Winge prospectively
studied 104 elite tennis players at the Danish Tennis Championships and noted 46% of injuries in the upper extremity,
with only 39% of injuries in the lower extremity and 11% of injuries in the back, with an overall prevalence rate of 30
injuries per 100 athletes ( 43).
Similar information regarding the epidemiology of injuries in young participants in the other racquet sports does not exist
in the English literature.
DISTRIBUTION OF ORTHOPEDIC INJURIES IN TENNIS
Shoulder
The shoulder girdle is especially prone to injury because it has to accelerate and decelerate the arm maximally while
maintaining precise control over the racquet at ball strike. A tennis player performs repetitive motions that generate
high-magnitude forces about the shoulder during the various tennis strokes. Owing to the repetitious nature of these
forces, it is difficult to maintain the balance between motion and stability in the shoulder. The strokes and their inherent
forces are discussed later as part of the biomechanics of the tennis strokes, including the serve, forehand, and
backhand. Furthermore, high forehand and backhand volley strokes and overhead smash also place large stresses on
the shoulder and rotator cuff.
The shoulder is the most frequently affected part of the upper extremity, with rotator cuff inflammation being one of the
most common injuries in tennis players and racquetball players of all levels ( 57,58). Rotator cuff inflammation usually
occurs as a result of chronic repetitive swinging of the racquet, including overhead serving. Pain from rotator cuff
inflammation is associated with shoulder abduction such as with serves, overhead smashes, high backhand volley, and
the follow-through with the backhand stroke. Investigators have found that 50% of adult tennis players complained of
shoulder pain at some time (57,58). Lehman found that 24% of junior tennis players complained of shoulder pain
currently or in the past (57). A survey of participants in the 1998 USTA Girls' 16's National Championships, 35% noted
shoulder pain currently or in the past (56% of these were anterior shoulder pain, 15% posterior shoulder pain, and 31%
both anterior and posterior) ( 57). For the 16- and 18-year-old participants at the 1998 USTA Boys National
Championships, 25% noted previous or current shoulder pain (38% anterior shoulder pain, 30% posterior shoulder pain,
and 32% noted both anterior and shoulder pain) ( 55).
It is usually the older players that may have rotator cuff impingement, rotator cuff tear, or shoulder degenerative change
including the glenohumeral or acromioclavicular (AC) joint, or both. In contrast with the older player, the young player's
rotator cuff symptoms are more often secondary to instability of the glenohumeral joint ( 59,60). Instability may result in
labral degeneration or tears. Other shoulder injuries include humeral periostitis ( 61) and bicipital tendinitis ( 52).
Less common shoulder injuries have also been described in the young tennis player ( 62). Traction apophysitis of the
shoulder is similar to Osgood-Schlatter disease of the knee. It is an overuse injury caused by repetitive microtrauma at
the insertion of the supraspinatus muscle into the greater tuberosity, or the subscapularis muscle into the lesser
tuberosity of the humerus. Proximal humeral physeal injury in junior badminton players has also been reported ( 63).
Slipped capital humeral epiphysis was initially described by Dotter in 1953 ( 64,65). It occurs secondary to shear and
distraction caused by rotational forces about the shoulder. Widening of the physis or slight slippage may be seen, but
severe slippage is not usually present.
Tennis shoulder refers to a drooping, internally rotated shoulder caused by long-term overhead arm use contributing to
generalized laxity of the shoulder capsule and musculature ( 58,66). This is more common in professional players or those
who have played for many years (58). This may potentiate rotator cuff symptoms due to the protracted scapula not
allowing the acromion to rotate sufficiently out of the way from the greater tuberosity ( 58,59). Drooping of the shoulder
may also be associated with thoracic outlet syndrome ( 58,59). Although the shoulder is not an uncommon site for overuse
or injury in adolescent tennis players, the findings consistent with tennis shoulder are not commonly reported ( 67). This is
probably because the young shoulder has not yet experienced enough repetitive traction stress to lead to permanent
stretching and drooping.
Acute shoulder injuries are uncommon in tennis, though shoulder dislocations and AC Joint separations may occur from
collisions with the wall in squash and racquetball or as the result of a fall in any racquet sport.
Elbow
Lateral epicondylitis (tennis elbow), medial epicondylitis, and injury to the medial epicondylar apophyseal growth plate in
skeletally immature players are common injuries about the elbow seen in tennis players ( 62,68,69). Owing to the rapid,
repetitive arm movements required in the other racquet sports, medial and lateral epicondylitis has been reported in
badminton, squash, and racquetball. These injuries are associated with chronic repetitive overload. On the lateral aspect
of the elbow, epicondylitis involves the extensor carpi radialis brevis but may involve the entire lateral mass. Although its
name suggests inflammation, microscopic examination suggests that inflammation is not really involved. Repetitive
microtraumatic injury is believed to result in microtears of the muscular origin. Focal degeneration and healing with
vascular and fibroblastic proliferation suggests that this is a degenerative process ( 70,71). Lateral epicondylitis occurs
more frequently in recreational tennis players, particularly those with poor mechanics of the backhand ( 72). Medially, the
medial epicondylar growth plate, the flexor mass, or the medial collateral ligament may be involved. Medial epicondylitis
occurs much less frequently than lateral epicondylitis, although it tends to occur in higher level tennis players ( 72). It has
been noted that an incidence of tennis elbow in world class athletes ranges from 35% to 45% ( 73,74). This incidence is
much lower in elite junior athletes ( 39,43), supporting the opinion that tennis elbow is related to age ( 36). In addition,
small avulsion fractures may occur because of the anatomy of the adolescent elbow. Nonunion of the medial or lateral
epicondyle has rarely been seen. Ulnar collateral ligament injuries in the tennis player are uncommon.
In the author's survey of participants in the 1998 USTA Girls' 16's National Championships, 25% noted elbow pain
currently or in the past, whereas 22% of participants at the 1998 USTA Boys National Championships reported previous
or current elbow pain (55).
Hand and Wrist
Hand and wrist complaints are common in tennis players, especially in women. Further, nondominant wrist pain is
common in players using two-handed backhands. In the study of participants in the 1998 USTA Girls' 16's National
Championships, 29% noted dominant wrist pain and 25% noted non-dominant wrist pain currently or in the past. For the
male participants at the 1998 USTA Boys National Championships, 19% noted previous or current dominant wrist pain
and 6% noted nondominant wrist pain (55).
Tendinitis of the wrist may develop in elite players who place a lot of spin on their shots or in novices with mechanically
improper technique (50,75). Wrist extensors are most frequently involved, but flexor tendons may be involved as well
(76). DeQuervain stenosing tenosynovitis is one of the most common tendon problems seen in the tennis player ( 75,76).
This usually occurs due to shearing within the fibro-osseous sheath from repeated ulnar deviation. Insertional tendinitis
of extensor carpi radialis longus and brevis tendons commonly occurs in tennis players at the base of the second and
third metacarpals and is usually associated with carpal bossing. Extensor carpi ulnaris tendinitis is primarily due to
overuse or technique flaws, and often it is associated with triangular fibrocartilage tears or ulnocarpal impingement ( 77).
It is often seen in the nondominant wrist of players with two-handed backhands, possibly due to the overuse during the
backswing. Extensor digitorum communis tendinitis, particularly to the index and little fingers due to their oblique course
across the wrist, is often seen in tennis players. Tendinitis of the extensor pollicis longus uncommonly occurs in tennis
players as the tendon passes Lister's tubercle. Tendinitis at the insertion of the dorsal interossei into the proximal
phalanges may occur in tennis players from repeated gripping ( 75). Occult dorsal ganglions may be the most common
cause of radial wrist pain in the tennis player ( 75).
Recurrent dislocation of the extensor carpi ulnaris tendon has been reported in tennis players associated with
hypersupination and ulnar deviation, such as with a backspin slice, low forehand or slice, or topspin service motion
(76,78,79).
The evaluation of the wrist also should consider the possibility of a fracture of the hook of the hamate (from abutment
with the bottom of the grip) (80,81), injury to the triangular fibrocartilage complex ( 75,76), ulnocarpal impingement (75,80),
chondromalacia of the pisiform ( 75,82,83), ulnar nerve compression in Guyon's canal ( 80), ulnar artery thrombosis
(76,84,85), median nerve entrapment in the carpal canal ( 75,76,80), and triquetrolunate ligament injury ( 75); however,
these are less common causes of wrist pain in tennis players. Wrist fractures and dislocations have been reported with
all the racquet sports from falls, although collision with the wall may also be a mechanism of injury.
Digital nerve compression, particularly of the index finger, may occur at the radial digital nerve due to pressure between
the metacarpal head and the racquet handle ( 75,76,86).
Forearm
Stress fractures of the ulna of the nondominant forearm in adolescents, as well as distal radius and ulna fractures of the
dominant wrist have been reported and should be kept in mind when evaluating the tennis player with forearm and wrist
pain (87,88,89,90 and 91). These injuries to the nondominant forearm occur in players who use a two-handed backhand.
Fig. 34.1 is an magnetic resonance imaging (MRI) scan of the forearm of a top 10 professional female tennis player,
revealing a stress fracture of the ulna.
FIGURE 34.1. Stress fracture ulna. This is an MRI of the nondominant forearm of a top-25 female professional tennis
player who changed her backhand to a two-handed backhand with a large amount of topspin 8 months before evaluation.
This player had 6 months of pain and tenderness at the junction of the middle third and distal third of her forearm before
the MRI. The MRI reveals marrow (arrows) and surrounding edema, confirming the diagnosis of stress fracture of the
nondominant ulna.
Central Region Injuries (Back and Trunk)
Overuse injuries of the central region are common in the racquet sports athlete. It has been reported that 38% of
professional male tennis players reported missing at least one tournament because of low back pain ( 92). In the elite
junior tennis survey, 47% of girls and 31% of boys noted low back pain currently or in the past ( 55). Sward found 50% of
randomly selected elite players had a history of low back pain of at least 1 week's duration and 46.7% had abnormal
radiographs of the lumbar spine ( 93,94 and 95).
There are a variety of sources of low back pain in the tennis player. High demands placed on the lower back and trunk
combined with low flexibility patterns result in frequent overuse injuries ( 51,69,80,96). The three areas most often
involved are (a) the posterior midline paraspinal musculature (used in the service motion, when charging the net, or when
dropping straight back for a volley); (b) The peripheral trunk musculature, that is, the quadratus lumborum or oblique
muscles (used during the service motion or in ground strokes); and (c) the rectus abdominus (tears in this muscle may be
associated with hitting overhead strokes or serves) ( 50). Other potential causes of low back pain include intervertebral
disk degeneration and herniation, facet impingement, and spondylolysis due to the repetitive hyperextension and rotation
of the spine (97).
Injuries to the abdominal muscles occur frequently during serves, particularly to the nondominant rectus abdominus
muscle and obliques ( 98). Open-stance forehand strokes are purported to be the cause of the increasing incidence of
abdominal muscle injury as well.
Racquet sports place unique stress on the soft tissues of the lower leg. This is due to the amount of time players spend in
the ready position (on the balls of their feet with their knees bent slightly), the extreme ranges of motion that the ankle
and foot must go through, and the ballistic nature of these movements ( 99). In young tennis players, lower-extremity
overuse injuries are about twice as frequent as upper-extremity or central region overuse injuries ( 39). This
predominance has been identified in squash and badminton as well ( 47). Lower-extremity injuries are common for two
reasons. First, each of these sports involves repeated short bursts of activity with quick stop-start and sharp lateral
movements and accelerations, which place high demands on the lower extremities. Second, athletes may be less flexible
and weaker in specific anatomic areas, including the lower extremity, which may predispose them to overuse injuries
(51,96).
Hip and Thigh
Leg muscle strains may be acute or chronic in nature ( 100). Acute injuries tend to occur later in the match, when the
muscle is fatigued or when there has been inadequate preparticipation warmup and stretching. Chronic muscle strains
usually occur secondary to inadequate rest or rehabilitation from an initial injury.
The most common areas for strains in the thigh are the adductor muscles (groin pulls) and the hamstrings ( 101).
Adductor muscle strains usually result from sudden changes in direction, particularly when attempting to stop lateral
movement by sliding or posting the lead foot ( 101,102). Slipping on clay courts, resulting in “the splits,” may also strain
the adductor muscles. Hamstring tears may occur at either end of the muscle and are usually associated with explosive
acceleration, for example when sprinting or charging toward the net. Hip flexor strains have not been found to occur as
commonly in the young tennis player as compared with the older tennis player. Quadriceps strains, and potentially
ruptures in the older athlete, are known to occur, particularly when a player slides on clay courts with the knee flexed and
then the player tries to extend the knee forcefully ( 80).
Knee
Statistics from the USTA national teams reveal the fact that 19% of all injuries are knee injuries, with 70% of the injuries
being traumatic and 30% overuse (103). Lehman reported an incidence of anterior knee pain in 16% of tennis players,
with an incidence of 7% for boys and 11% for girls under the age of 14 years ( 104). Owing to the sudden changes in
direction, repetitive stop-start activity, lunging, and jumping involved in tennis, the patellofemoral joint is susceptible to
overload and overuse injuries. This may be commonly manifested as Osgood-Schlatter syndrome (tibial tubercle
apophysitis) in young racquet sports players ( 103), patellar (jumper's knee) and quadriceps tendinitis in adults
(69,101,103), and patellofemoral syndrome or chondromalacia patellae in children and adults ( 69,101,103).
Acute knee injuries, such as knee sprains and meniscal tears, are less common in tennis and the other racquet sports as
compared with basketball, football, volleyball, or skiing, but they can occur secondary to the twisting demands of the
sport on the knee (105). Knee ligament and meniscal injuries are more common in squash, badminton, and racquetball
than in tennis ( 15,47,69,101,103,106). This may be because of the frictional characteristics of the wood court in squash
and racquetball as compared with the different surfaces in tennis. Medial collateral ligament injuries are the most
common injuries, although ruptures of the anterior cruciate ligament have been reported ( 47,103). Patellofemoral pain is
more common in tennis as compared with the other sports (47,69,101,103). Patellofemoral pain may be related to the
sudden start and stops of these sports, as well as lunging and jumping. The author has found an unusually high rate of
chondral injury of the trochlea in tennis players, similar to that of basketball players, presumably due to the factors noted
earlier. Patellar dislocations have also been documented in tennis, racquetball, and squash ( 47,101,103). Less common
causes of knee pain in tennis players include prepatellar bursitis, pes anserine tendinitis, semimembranosus tendinitis,
and iliotibial band syndrome ( 103,107). Isolated popliteus musculotendinous injuries are uncommon in any sport
including racquet sports. However, the mechanics of lunging with the trailing knee flexed and externally rotated puts the
popliteus musculotendinous unit at risk for injury. Fig. 34.2 is an MRI of a touring professional male tennis player who had
symptoms of posterolateral knee pain for several months with an exacerbation when lunging (twisting injury to the flexed
knee) for a ball during a half volley due to popliteus tendinitis ( Fig. 34.2).
FIGURE 34.2. Popliteus tendinitis. This is an MRI of the knee of a top-25 male professional tennis player with
posterolateral knee pain following a twisting injury to his flexed knee. There is edema of the popliteus insertion into the
lateral femoral condyle (arrow) and edema of the lateral femoral condyle. (Courtesy of George C. Branche III, M.D.)
Leg
Muscle cramps of the calf are very common (101). Gastrocnemius muscle strains are common and occur during
repeated, explosive accelerations of the leg, such as while sprinting or jumping. These strains and injuries to the Achilles
tendon occur when a foot that has been plantarflexed is suddenly forced into dorsiflexion while the knee is in full
extension (108,109). This happens during the serve when the first step forward is made and during ground strokes as
forward and lateral lunges are executed ( 110). “Tennis leg” is described as a strain or partial tear of the gastrocnemius at
its medial origin ( 69,108,109,110,111 and 112). Tennis leg tends to occur in players 30 to 45 years of age. Less
commonly, soleus injuries may occur and are seen with sliding on clay courts with extreme ankle dorsiflexion with
concurrent knee flexion (113).
Achilles tendinitis and Achilles tendon ruptures may be seen in tennis players, although not as frequently with racquetball
and squash (101,109,113,114). A sudden increase in activity, including changing surfaces from hard court to clay, or the
effect of long-term repetitive stress on the tendon may lead to the development of microtears or degeneration of the
tendon. Achilles tendinitis can be chronically debilitating and is often associated with recent change in the amount or
intensity of play, especially on clay courts ( 43). Once again, most injuries are acute exacerbations of chronic injuries.
Achilles tendon ruptures are common in older racquet sports participants, usually over 40 years of age, due to the
sudden bursts of speed that are necessary in each of the racquet sports. Achilles tendon ruptures have been estimated
to occur with an incidence rate of 5.5% ( 114).
Shin splints, or periostitis, is an overuse injury seen frequently in all the racquet sports, although there appears to be a
predominance when participants play tennis on hard courts ( 109,113). Furthermore, changes in training habits, or an
increase in play or running may account for the increased incidence of these injuries in tennis players ( 113). Stress
fractures of the tibia and of the distal fibula also infrequently occur in tennis players ( 113).
Ankle
Ankle sprains are the most common macrotrauma injury in tennis as well as the other racquet sports
(10,30,64,69,101,109,113). Each of these sports demand frequent running and pivoting, and stopping and starting
movements, as well as lunging, and jumping. As a result, high twisting forces about the ankle result. Most injuries occur
during twisting while the ankle is in plantarflexion, resulting in lateral ankle sprains.
Foot
Foot injuries in tennis players may include stress fractures, plantar fasciitis, blisters, abrasions, heel bruises, calluses,
corns, warts, and “tennis toe” (101). Stress fractures in racquet sports athletes occur most commonly at the base of the
fifth metatarsal, the metatarsal diaphysis, lateral process of the talus, and occasionally, the navicular neck ( 101). Older
racquet sports participants with poorly cushioned footwear with absent medial arch support may be prone to plantar
fasciitis or rupture of the plantar fascia ( 101,109,113,115). Tennis players are particularly susceptible to this injury owing
to the great amount of time spent on the balls of their feet while making quick changes in direction ( 113). A heel bruise is
an intracutaneous hemorrhage located at the plantar aspect of the heel and is seen more commonly in older players ( 80).
The etiology of this injury is the increased impact seen during the landing phase of jumping or running activities. Hallux
rigidus, degeneration of the first metatarsal phalangeal joint with dorsal exostosis, occurs frequently in tennis players
owing to the excessive dorsiflexion of the first toe during play ( 109,113). Players have pain during push-off.
Tennis toe is an injury to the great toe or second toe due to impaction of the toe onto the toe box of the shoe ( 101,109).
The injury frequently occurs as the athlete makes a quick stop after charging toward the net. The impaction of the toe
onto the anterior aspect of the shoe can lead to subungual hematomas, nail bed injuries, or jammed joints at the distal
interphalangeal, proximal interphalangeal or metatarsophalangeal joints. Shoes with a small, tight toe box may be
associated with tennis toe. The court surface and shoe design determine traction and the impaction of the toes; hardcourt
and wood surfaces are associated with greater traction than grass or clay courts, and consequently, toe impaction is
more common with hardcourt or wood surfaces (99). Tennis toe is also associated with improperly sized shoes,
loose-fitting shoe laces, or long toenails or digits ( 80,101). Fortunately, tennis toe is infrequently seen in the young
racquet sports player (39). Calluses and corns develop owing to increased pressure at bony prominences of the foot. Soft
corns develop between the toes as a result of toe condylar prominence and moisture of the feet. Fungal infections, such
as athlete's foot, are also frequently seen in tennis players owing to the moisture that accumulates from prolonged play
with rapid foot movement.
Other Regions
Skin
Tennis is usually played outdoors in the sun, frequently with the participants wearing short sleeved shirts and shorts or
skirts. This can potentially result in prolonged exposure to the sun, in addition to excessive perspiration. The result of
these conditions is the potential to develop skin cancers (basal cell carcinoma, melanoma), sunburn, sun sensitivity,
keratoses, and fungal infections. Repeated and severe skin injury, particularly repeated sunburn and sun exposure, are
related to basal cell carcinoma, squamous cell carcinoma, and melanoma. Blocking the sun's rays may potentially reduce
the risk of developing these sequelae. This can be done by staying out of the sun or with clothing as a barrier. Although
there are data to support the benefit of sunscreen as a way to help prevent keratoses, melanoma, basal cell carcinoma,
and squamous cell carcinoma, some controversy still exists ( 116,117,118,119,120,121,122,123,124,125 and 126). There
is much publicity and public awareness about skin cancers and the potential benefit of sunscreen. This likely accounts for
the fact that when asked, 90% of participants at the Girls' 16's USTA National Championships stated that they used
sunscreen always or some of the time, whereas 69% noted that they used hats always or some of the time during play
(55). On the other hand, only 65% of the participants at the Boys USTA National Championships used sunscreen all or
some of the time while playing and 75% of them use a hat all or some of the time while playing ( 55). The decreased use
of sunscreen among men as compared with women has also been identified in the general population ( 121).
Poison ivy and bee stings are also common occurrences in tennis players ( 39,127).
Eyes
One area of potential injury, both acute and long term, that is often neglected in the discussion of tennis injuries is the
eye. Acute injury to the eye has been reported. The etiology of acute eye injuries is being hit directly in the eye by the
ball when rushing or being up at the net, or when looking back at the players' doubles partner as the partner hits the ball.
The tennis ball functions as a projectile that may cause injury to the orbit or blunt injury to the eye, resulting in hyphaema
(blood in the anterior chamber), iris dialysis that may cause chronic glaucoma, retinal detachment, concussion cataract,
lens dislocation, and commotio retinae ( 17,23,24,28,128,129,130 and 131). Although the tennis ball is larger and moves
slower than a squash ball, its hollow interior allows it to distort on contact with the orbital rim to impact on the eye within
the orbital aperture (23,24,26). Tennis is a sport known to result in these injuries; however, the relative risk is
approximately 5% to 12% of all sports causing eye injury ( 17,24,28).
Potentially of greater concern is the development of age-related cataracts. It has been shown repeatedly in
well-controlled studies that a risk factor for the development of age related cataracts is increased exposure to sunlight
(132,133,134,135 and 136). Tennis is a sport that is played, for the most part, outdoors and usually in the sun. There
have been no studies comparing the rate of cataract development in tennis players with age-matched, nontennis playing
controls (or the general population). Furthermore, it has not been proven that sunglasses prevent cataracts, although
research suggests that the use of sunglasses may be of some benefit. Only 7% of participants in the Girls' 16's 1998
USTA National Championships note that they use sunglasses all or some of the time, whereas 11% of boys participating
in the Boys USTA National Hardcourt Championships use sunglasses with similar frequency ( 55). The discrepancy
between the percentage of players using sunscreen to prevent skin cancer and not using sunglasses to prevent cataracts
may be due to the lack of public awareness or attention regarding cataracts.
Heat Illness
Tennis players compete in conditions that range from comfortably warm to oppressively hot. The 1994 Australian Open
was played in temperatures of more than 100°F, with the center-court surface air temperature regularly approaching
130°F (137).
Of all the relatively infrequent nonorthopedic problems that may afflict tennis players, heat illness needs attention owing
to its potentially devastating consequences and the fact that it may be completely preventable. Heat-related illness, such
as heat cramps, heat syncope, heat exhaustion and heat stroke, caused by the environmental conditions of temperature
and humidity in which long matches are played, with little or no shade and limited access to water, have been
documented in tennis (138). This is potentiated by the fact that sometimes during tournaments, several matches are
played in 1 day. Further still, this factor is even more important in preadolescents, because it has been shown that they
have poor heat tolerance and may not acclimatize as effectively as adults ( 139,140,141 and 142). During tennis play, a
player's metabolic rate increases substantially ( 143). Most of the energy liberated is released as heat. Thus, players are
faced with an ongoing physiologic challenge to dissipate heat effectively and maintain body core temperatures near
98.6°F. If adequate fluid intake is not maintained a player's thermoregulatory capacity is diminished ( 144,145,146,147
and 148). This situation is further exacerbated in hot, humid conditions ( 149) and may result in heat illness.
There are many preventive measures that may be taken to reduce the risk of heat illness. These precautions include
playing at cooler times of the day; drinking fluids the day before the match (“water loading”); drinking water or electrolyte
solutions during the match, even if the player does not feel thirsty; wearing light, cotton-based clothing; seeking shade
whenever possible; using rest times on court changeovers and between sets; and stopping if symptoms of
light-headedness, dizziness, nausea, weakness, cramps, or autonomic behavior occur ( 50,138). Furthermore, players
should not be allowed to return to play until they have replaced the weight lost through perspiration water loss and are
completely recovered from their symptoms.
Currently, the Women's Tennis Association (WTA) Sports Sciences and Medicine Department has developed rules
regarding tennis play in extreme weather conditions, while the Men's Professional Tennis Tour (ATP) is considering
similar rules. Heat stress is measured by a heat stress monitor or a combination of air temperature and humidity. When
the heat stress exceeds a particular level, start of play is delayed, or a longer break period during play is instituted to
reduce the risk of heat illness.
BIOMECHANICS OF TENNIS STROKES IN INFLUENCE ON INJURY
The majority of tennis injuries are due to overuse. The high demand of repetitive strokes on the body often results in
these overuse injuries in tennis. The mode of injury to the musculotendinous units is almost always eccentric in nature,
whereas upper-extremity ligamentous injuries are most often microtraumatic in origin. The tennis serve, forehand, and
backhand strokes have been studied in detail, and each places unique demands on different joints of the body. Each of
these strokes has been divided into stages. These stages are discussed and correlated to the potential for injury
production in the player.
The kinetic chain is defined as the transferring of force efficiently from the ground through the proper sequencing of body
parts through the legs, hips, trunk, and upper extremity to the racquet. Each successive body segment moves faster than
the previous one, resulting in maximal racquet acceleration. The sports with repetitive overhead motion, such as baseball
and volleyball, have injuries to the upper extremity that are similarly seen in tennis players. However tennis, because of
the racquet, differs from these sports because of the weight and long lever arm effect that is created at the time of ball
impact. The racquet provides a mechanical advantage to help create power for each stroke, but may also help increase
stresses to the upper extremity during the acceleration and follow-through stages, especially the serve and overhead
smash. Muscles appear to stabilize the arm as a rigid extension of the racquet during ground strokes (forehand and
backhand). The racquet–forearm unit accepts the transfer of energy from the shoulder and trunk as they rotate and as
body weight shift occurs.
The game of tennis, as played at present, is described as a power game. Hitting with power means that the tennis player
must optimize the action between the larger body parts to hit at high velocity and still allow the upper limb to maintain
good control over the racquet ( 150).
Impact and shock to the forearm and elbow musculature is related to grip tightness. The tighter the grip is held, the more
shock vibrations are transferred to the elbow ( 151,152). It has also been shown that high-level players do not grip the
racquet as tightly or for as long as lower level players for both backhand and forehand strokes ( 152,153 and 154).
Serve
To become proficient in tennis, the player needs to master a number of strokes, although it is the serve that is often
considered the most important facet of the game (155,156,157 and 158). The serve is controlled by the player, and
although it seems that it should be easy to master, the complex motions requiring both upper and lower limb coordination
to produce a fluid service action may create many problems of technique. One limb must rise slowly to push the ball to an
optimal hitting height while the other upper limb and racquet must swing in a complex pattern to hit the ball with both
power and control. Median and peak muscular activity levels in the shoulder and forearm muscles are higher during the
service action than during other strokes, indicating that the serve is the most strenuous stroke in tennis ( 159).
The power of the tennis serve stems from the transference of force from the ground through the lower extremities to the
trunk and on to the upper extremity and racquet, which functions as an extension of the upper extremity. This is also true
for developing force and power with forehand and backhand strokes. This coordinated transfer of force is referred to as
the kinetic chain ( 157,160). A fluid motion or rhythm of this transference of force is of paramount importance to optimize
power in the serve and minimize the risk of injury.
The service motion has been separated into four main stages ( 161,162 and 163). The service motion has many
similarities with throwing mechanics and thus may produce clinical syndromes with signs and symptoms similar to those
seen in baseball pitchers. Despite the similarities of the mechanics of pitching and serving, there are differences. The
four major phases of serving are the windup, cocking, acceleration, and follow-throug ( Fig. 34.3).
FIGURE 34.3. Tennis serve phases. The tennis serve can be divided into four phases: The preparation phase, cocking
phase, acceleration phase, and follow-through phases. See text for details.
The windup phase begins with the tennis player standing with the shoulders in line with the intended direction of the
serve and ends with ball release or toss. Body weight is usually on the forward foot. The nondominant arm is used to toss
the ball up in the air in front of the body first by lowering the limb with the wrist extended and then lifting the hand forward
overhead by forward flexing the shoulder and extending the elbow. At the same time, the dominant shoulder is being
extended, externally rotated, and slightly abducted while flexing the elbow submaximally to bring the racquet in a looping
fashion to behind the back. Body weight is being shifted posteriorly, although foot movement to the foot up or foot back
position (see later) usually begins in this stage. Furthermore, the trunk and dominant shoulder rotate toward the dominant
arm. The knees begin to flex, as do the dominant hip and both ankles. The spine begins to flex laterally and extend.
During this phase, the lower extremities prepare for the build up of power that occurs in the cocking phase and is
transmitted during the acceleration phase. This stage has a low propensity for injury owing to the slow, controlled motions
being well within physiologic range and muscular contraction being concentric ( 164).
The second phase, cocking, begins with ball release and ends with the racquet in the “back scratch” position and the
dominant shoulder (the one holding the racquet) in maximal external rotation. This phase is characterized by a gradual
building of power, a sort of coiling up before transfer and release of energy along the kinetic chain to the racquet and ball
impact. During this phase, energy is stored by prestretching muscles. After the ball is released, the nondominant arm
slows its forward elevation and elbow extension while the racquet continues to loop behind the back. To do this, the
dominant shoulder continues to abduct and externally rotate. Furthermore, there is a high degree of muscle activity in the
wrist extensors and triceps, acting eccentrically to position the wrist, forearm, and elbow ( 161).
The first 75% of this phase, early cocking, ends when the lower extremity begins to concentrically contract and drive the
body up (161). In this part of this phase, the knees, ankles and dominant hip continue to flex as the shoulder moves to 90
degrees of abduction and external rotation. The shoulder motion is mostly concentric during this part of the second
phase. The spine continues to flex laterally and hyperextend owing to concentric muscle function. The ranges of motion
continue to be within physiologic range, and thus, injury during this portion of the serve is still uncommon.
The latter part of this phase, late cocking, the player's shoulder remains in 90 degrees of abduction and maximal external
rotation while the force generated by the lower extremity pushing off the ground travels up the kinetic chain to the trunk
and eventually to the upper extremity. In the elite tennis player, the shoulder may appear to be at 120 to 180 degrees of
external rotation, although this is usually due to the combined rotations of the glenohumeral and scapulothoracic joints in
addition to hyperextension of the spine as the lower extremities drive the forces up. Most of the power buildup during this
stage is generated from a combination of vertical and anterior ground reaction forces through ankle plantarflexion, knee
extension, and racquet-side hip extension ( 156,158,165). The knee extension drives the racquet-side hip and shoulder
upward (158), while the racquet itself moves inferiorly (the result of forced shoulder external rotation). The elbow is flexed
approximately 63 degrees during this phase ( 156,158). Furthermore, the trunk is uncoiled, which is to say, concentric
contraction with trunk rotation and lateral flexion away from the dominant side and nondominant hip internal rotation.
Players may use a foot back or platform stance, or they may use a foot up or pinpoint stance.
With the platform stance, both feet are approximately shoulder width apart during the serve, which tends to result in a
more anteriorly directed contribution of ground reaction force and a less vertical component. With this stance, the player
does not elevate the racquet as high when serving, although it allows the person to be in a position to approach the net a
little more quickly ( 166). With the pinpoint stance, the player's back foot slides forward to meet the front foot during the
serve. There is a larger contribution of vertical ground reaction force, which allows for greater ball velocity, and as the
ball is contacted at a higher level, there is less likelihood of a fault serve in the net ( 166).
Although it may appear that a player jumps during the serve, it is usually the result of forces generated by the closed
kinetic chain that result in a carry over of momentum ( 158). This open kinetic chain may allow the unrestricted rotation of
the pelvis to facilitate further range of motion and more powerful rotation of the trunk.
The late cocking phase has the potential for injury to the shoulder. While the shoulder is in maximal external rotation, the
anterior shoulder capsule, and more specifically, the anteroinferior glenohumeral ligament, is under tension to their
physiologic limits. The upward driving force from the lower extremity forces the shoulder into greater external rotation,
subjecting the anterior capsuloligamentous structures to forces of up to 40% body weight ( 167). This maneuver can
compromise the dynamic stabilizers, namely the subscapularis, latissimus dorsi, and pectoralis major, because the force
couples within the shoulder decrease with increased abduction ( 168). This may result in glenohumeral subluxation,
secondary impingement, overuse musculotendinous injury and muscle imbalances. As a result, it may also result in
inefficient muscle function and less power development ( 163). Other areas of potential injury include musculotendinous
injury at the calf, quadriceps, and groin during the generation of force while the lower extremities extend as well as injury
to the intervertebral disks and pars interarticularis from hyperextension and rotation of the spine ( 169,170). Wrist
extensor muscles have increased activity in the late cocking phase, subjecting them to injury during this phase as well
(161). Players who have a large loop during the swing behind the back place increased stress on the medial side of the
elbow (37).
The third phase is the acceleration phase, which begins with internal rotation of the dominant shoulder and ends with ball
contact with the racquet. This stage of the service motion represents the accumulation and release of the power and
forces generated by the athlete's dynamic kinetic chain. The propagation of power, starting from ground reaction forces
sequentially moves up each body segment from the lower extremities, to the hips/pelvis/trunk/abdomen to the upper
extremity. Specifically, there is a resultant velocity increase in successive segments from the knee joint to the hip, the
shoulder, the elbow, the wrist, and finally to the head of the racquet as the time of impact approaches ( 158,171).
In this phase, the glenohumeral internal rotators and adductors are concentrically contracting in a very powerful fashion
because they have reached maximal preloading to propel the racquet forward. Shoulder internal rotation has been shown
to provide 37% of the total forward momentum at the moment of ball impact, the highest of any measured movements
(172), and 17% of the total power of the serve ( 156). The horizontal shoulder flexion is followed by elbow extension and
wrist flexion due to concentric muscle contraction ( 161). The elbow contributes 21% of the total kinetic energy and 15%
of the force in serving (173), mostly from elbow extension and forearm pronation. The forearm moves from approximately
15 degrees of supination in the cocking phase to approximately 70 degrees of pronation at contact with the pronating
motion beginning just before ball contact ( 50,161,172,173). The wrist is in extension and ulnar deviation at impact ( 75).
The biceps and scapular stabilizers (rhomboids) are eccentrically contracting, as are the brachialis and wrist extensors.
The lower extremities have already transferred the energy to the trunk and upper extremity, although the lower extremity
musculature is still active to help stabilize the trunk and prepare for energy absorption of landing. The trunk is flexing
laterally toward the nondominant side and forward flexing. Most muscular prime movers of the upper extremity do not
produce maximal activity levels at impact but during the upward acceleration phase of the stroke before impact ( 171,174).
Muscular injury in this phase due to overload exists in many locations including the abdominal muscles (obliques and
rectus abdominus), as well as the rotator cuff, other glenohumeral internal rotators and adductors, elbow extensors, and
wrist flexors. Also, valgus stress to the medial elbow occurs during this phase, which may result in injury to the
flexor-pronator muscles of the elbow or the ulnar collateral ligament of the elbow. Hypersupination and ulnar deviation,
such as with a slice or topspin serve motion, may result in dislocation of the extensor carpi ulnaris tendon at the wrist
(79). An injury somewhere within the kinetic chain may result in injury to another area within the kinetic chain owing to
attempts to compensate for the injury while trying to maintain power.
The final serving phase is the follow-through. This stage starts just after ball contact with the racquet and ends with the
completion of the stroke. The predominant muscle activity is eccentric as the athlete is absorbing the energy and
decelerating the racquet and upper limb. The follow-through results in the arm being horizontally adducted, extended to
neutral and internally rotated at the shoulder, and pronated at the forearm to end diagonally across the athlete's body
(158,172).
The posterior shoulder muscles, specifically the infraspinatus muscle, are most commonly injured during this phase
because they slow the shoulder internal rotation by eccentrically contracting ( 175). The whole rotator cuff may be injured
as it attempts to maintain the humeral head within the glenoid and offset the distraction forces during follow-through.
Furthermore, the biceps may become inflamed owing to overuse as it functions to slow the forearm pronation and elbow
extension and assists the rotator cuff in maintaining glenohumeral stability ( 161). The posterior shoulder capsule may
also be subjected to excessive tension secondary to distraction forces, especially if the rotator cuff is dysfunctional.
Posterior glenohumeral capsular tightness may result, as is evident by the decrease in internal rotation as discussed
earlier. Decreased internal rotation may result in increased anterior and superior translation of the humeral head during
the late cocking and acceleration phases ( 176). This anterosuperior translation may result in instability, impingement, or
labral injury.
The scapula is fully retracted in the early phases and translates to full protraction by follow-through for a distance of 18
cm. This large amount of scapular motion, particularly protraction during follow-through, combined with infraspinatus
contraction to decelerate the shoulder and arm motion, potentially puts the suprascapular nerve at risk for injury at the
spinoglenoid notch ( 177).
Kibler and Chandler reported biomechanical data on three elite male tennis players during the serve ( 50). The peak
velocity of a tennis racquet during a tennis serve ranged from 62 to 72 mph, with resultant ball velocities of 83 to 125
mph. This speed is achieved in 0.2 to 0.3 seconds from the late cocking until ball contact. The shoulder was observed to
be internally rotating at 1,140 to 1,715 degrees per second to achieve these speeds during this phase. The elbow is
flexed as much as 120 degrees at late cocking and extends to 15 to 20 degrees at ball impact. This results in an
extension velocity of approximately 900 to 1,000 degrees per second during the acceleration phase. Hip and trunk
rotation is approximately 300 degrees per second. Forearm pronation has been recorded to be 350 to 900 degrees per
second as measured 0.1 second before ball impact, and this increased to 1,300 degrees per second 0.1 second following
impact, whereas wrist flexion has been recorded at 1,087 degrees per second at 0.1 second before ball impact ( 173,178).
Early in the acceleration phase, the medial elbow is subjected to significant valgus forces. Repeated forceful wrist flexion
at impact may result in medial epicondylitis ( 80). The range of motion of the wrist during the serve is an arc of 90 to 100
degrees of flexion and extension. It has also been noted that 10% of the force and 15% of the energy involved in service
motion is dissipated across the wrist joint ( 75).
The position of the ball at the peak of its toss is a major factor that may disrupt the rhythm of the serve. Plagenhoef
showed that many elite players struck the ball just after the ball reached its peak and began to drop ( 179). At this point, it
has been shown the player has eight times more time to hit the ball as compared to tossing it 1.2 meters higher than the
sweet spot (near center of the racquet face) ( 180). Players fit the ball toss to the swing in such a manner that the position
of the ball at impact with the racquet does not require excessive hyperextension and lateral flexion of the spine, if the
potential for injury is to be minimized ( 156). If a player is maximally extended, that is the body upright, the shoulder fully
elevated and abducted, and the elbow and wrist extended, allows the player to contact the ball at maximal height. Players
who hit the ball at a greater height are able to hit it at higher velocities and yet still not serve a fault ( 158,181).
Other potential causes for overuse injury during the serve include (a) incorrect grip: causes off-center contact with the
ball; (b) improper stance: may result in under or overrotation of the body, making the upper body more responsible for
force production; (c) hitch in the backswing: causes loss of momentum gained during the backswing, then the player must
use more upper body force to make up for momentum loss to produce power on the serve; (d) stiff arm serve: loss of ball
control and result in increased force absorbed by the wrist, elbow, and shoulder; and (e) excessive pronation: trying to
increase the pronation to get more spin may result in excessive rotation of the upper limb and injury to supportive
structures of the wrist, elbow, and shoulder.
Forehand
The forehand stroke is divided into three phases: racquet preparation, acceleration, and follow-through ( Fig. 34.4). The
first and third phases do not produce many injuries; however, the wrist extensor muscles reveal predominant activity
throughout all phases of the forehand ( 161). The majority of injuries occur from the mechanics and forces in the
acceleration phase. The conventional forehand stroke is typified by the upper extremity functioning as a single unit–the
elbow and wrist move minimally during the acceleration and follow-through phases. Many world-ranked players, and now
many juniors attempting to imitate the professionals, play with an “open-stance” forehand ( Fig. 34.5). Not much research
has been performed evaluating these recent changes. With the open-stance stroke, individual segments of the upper
limb are used to generate racquet velocity.
FIGURE 34.4. Forehand phase. The forehand can be divided into three phases: The preparation phase, acceleration
phase, and follow-through phases. See text for details.
FIGURE 34.5. Photo of open-stance forehands.
In the first phase, racquet preparation, the player starting in the set position moves the racquet back on the dominant
side until the racquet motion stops. The backswing begins with flexion of the knees and hips. Deceleration of the body
may stretch the muscles, allowing for storage of energy. The player's body weight starts forward and is shifted posteriorly
as the torso leans slightly backward over the back leg ( 182). The shoulders, hips, and trunk are rotated from parallel to
the net toward the racquet side to end with the shoulders nearly perpendicular to the net.
The open-stance player pivots on his or her back foot, which is followed by backward movement of the elbow in
synchrony with the shoulder. The elbow is then raised by shoulder abduction, then the player externally rotates the
shoulder. The shoulder is only slightly abducted. The elbow is bent slightly during this phase with the open-stance
forehand. Thus the racquet and forearm rotate around the elbow and shoulder ( 182).
The standard forehand is characterized by the racquet moving back in synchrony with the shoulder turn and the elbow
somewhat fixed in a slightly flexed position. The shoulder is further externally rotated. The shoulder abducts and extends
with this stroke, more than with the open-stance forehand. The elbow is slightly flexed, although more extended than with
the compact open-stance backswing. Thus, the racquet and forearm rotate around the shoulder and not the elbow ( 182).
The backswing for both types of forehands often is in a looping motion, although the degree of looping varies according
player preference. It has been shown that those players using a circular backswing averaged a higher racquet head
velocity as compared with a straight backswing ( 183). The racquet head is usually held higher than the elbow. The wrist
is hyperextended with both forehand preparation phases, such that the forearm and racquet are not aligned.
The second phase, acceleration, begins with forward racquet motion and ends at ball contact. This is where the majority
of differences exist between the two forehand strokes. With both strokes, the front knee stays flexed while the back knee
extends to start transmission of ground reaction force along the kinetic chain. This maneuver also transfers body weight
forward. Further, with both forehands, the hips extend and the racquet-side shoulder elevates while the trunk rotates and
laterally flexes. Rotation of the trunk and lower limb drive increase shoulder rotation gradually over the forward swing,
allowing for ball impact and resulting in 10% of the final racquet velocity. At the end of this phase, the shoulders are
aligned parallel to the net with both forms of forehand ( 182).
The angle of the shoulder in relation to the body remains constant during the open-stance forehand as compared with the
decreased angle (forward flexion and adduction) during the traditional forehand. During this phase, the elbow is gradually
extended in the open-stance forehand with some flexion just before impact as compared with the traditional forehand, in
which it remains stiff throughout this phase. The open-stance forehand has a significantly higher maximum elbow
extension velocity as compared with the standard forehand.
The wrist angle decreases from the backswing position for both styles as the racquet trails the forward moving limb until
just before ball impact. The open-stance forehand players have increased wrist flexion velocity at impact that results in
an increased racquet head speed. This increased racquet head speed is the result of an increased linear velocity due to
the sequential pattern of end points (elbow, wrist, racquet tip) being further away from the axis of rotation (the shoulder)
(158). The result of this greater racquet head speed is greater ball speed. The wrist is in extension and ulnar deviation at
impact (75). The elbow moves approximately 11 degrees (46 to 35 degrees flexion) during the forehand stroke ( 50). The
knees, hip, trunk, shoulder, and wrist positions are the same between the two styles of forehand at ball impact.
The biceps is active in this phase, helping the pronator teres as a force couple ( 173). The wrist flexor and extensor
muscles function to stabilize the wrist.
Depending on the foot position, the trunk may rotate 60 (traditional forehand) to 90 (open-stance forehand) degrees ( 50).
Furthermore, with the open-stance forehand, the trunk is rotated earlier than with the traditional forehand. The early
rotation reduces the contribution of the trunk to the production of racquet velocity. However, the increased trunk rotation
arc puts more prestretch on the trunk muscles, resulting in increased rotational acceleration and rotational forces that
may be the cause of the increased number of abdominal muscle strains seen at present with open-stance forehands.
This is potentiated by the player stepping around a backhand shot to hit an “inside-out” forehand. In order to maintain
racquet speed, the player must compensate by increasing arm acceleration. This uncoupled motion, with the more
extreme position of the racquet in the hand and limitation of shoulder motion, may result in repetitive overload of the
medial elbow and anterior shoulder. This may result in medial epicondylitis, ulnar collateral ligament injury of the elbow,
and anterior shoulder capsuloligamentous injury ( 50,184). Furthermore, those players who attempt to hit a lot of topspin
on their forehand may develop medial epicondylitis ( 69).
Contact with the ball should occur anterior to the player, allowing for maximal energy transfer to the ball. This body
movement increases the trunk's contribution to energy transfer to the ball and thus reduces the demands on the extremity
(184).
The third phase, follow-through, begins just after ball contact and ends at the completion of the stroke. Both strokes are
similar, with deceleration of the shoulder forward elevation and adduction, elbow flexion, and forearm pronation as the
upper limb and racquet complete a smooth upward motion. A recovery step is made by the rear leg, which is brought
forward to a position level with the front foot, which prepares the player for the next shot.
Other potential causes of injury during the forehand include (a) improper ball contact [such as hitting late {behind the
body} or not entering phase one soon enough]: may result in attempts to accelerate the racquet faster, causing injury to
the trunk or upper limb including medial epicondylitis, anterior shoulder muscle injury, and wrist injury; (b) hitting off the
back foot: the inefficient transfer of energy along the kinetic chain, and loss of forward momentum results in the upper
limb doing most of the work and in similar injuries as described in (a); (c) excessive wrist movement during swing, such
as when attempting a heavy topspin, results in increased stress to the muscles of the wrist (e.g., wrist flexor tendinitis,
DeQuervain tenosynovitis), forearm, and elbow (e.g., medial epicondylitis); (d) distorted follow-through: results in
off-center hits and a twisting moment to the wrist, forearm, elbow and shoulder, producing musculotendinous injury to
these structures; and (e) a low forehand or backspin slice forehand by using a lot of wrist motion, ulnar deviation, and
hypersupination: may result in recurrent dislocation of the extensor carpi ulnaris tendon at the wrist.
Backhand
There are two common types of backhand strokes–the one-handed backhand and the two-handed backhand. Both types
of backhand strokes are divided into three phases, similar to the forehand: racquet preparation, acceleration, and
follow-through ( Fig. 34.6A, Fig. 34.6B, Fig. 34.6C, Fig. 34.6D, Fig. 34.6E and Fig. 34.6F). Again, the first and third
phases do not produce many injuries, although the wrist extensor muscles are highly active in all phases of the backhand
stroke (161). The majority of injuries occur from the mechanics and forces in the acceleration phase. Many authors have
noted that the two-handed backhand is associated with a lower incidence of tennis elbow because the helping arm
appears to absorb more energy and changes the mechanics of the swing ( 68,165,185).
FIGURE 34.6. Backhand phases. The one-handed backhand (A–C) and the two-handed backhand (D–F) can be divided
into three phases: the preparation phase, acceleration phase, and follow-through phases. See text for details.
Phase I, racquet preparation, begins with the first motion of the backswing and ends with the first forward motion of the
racket. The backswing begins with flexion of the knees and hips, which may apply a stretch to the muscles, allowing for
storage of energy. The player's body weight starts forward and is shifted posteriorly as the torso leans slightly backward
over the back leg ( 182,186). The shoulders, hips and trunk are rotated from parallel to the net toward the nonracquet
side. At the end of this phase, the shoulders are overrotated beyond perpendicular to the net while the hips are nearly
perpendicular to the net.
With the one-handed backhand, the player pivots or steps back with their back foot, which is followed by trunk rotation.
The shoulder moves in synchrony with trunk rotation. The upper limb motion is characterized by shoulder horizontal
adduction, internal rotation and forward elevation, some elbow flexion, forearm pronation, wrist radial deviation, and
slight extension (185). The non-dominant upper limb grips the throat of the racquet lightly to assist the backswing. The
large trunk rotation is important to generate high racquet head speeds as part of the kinetic chain ( 187). The backswing
for the one-handed backhand often is in a looping motion - though the degree of looping varies by player preference. It
has been shown that those players using a circular backswing averaged a higher racquet head velocity as compared with
a straight backswing and thus is a finding in many high-level players ( 183). The racquet and racquet hand are usually at
the level of the nondominant shoulder, which is slightly higher than the racquet side shoulder.
The two-handed backhand is characterized by a more straight backswing and less looping motion due to the constraints
of the nondominant hand holding the racquet. The nondominant hand holds the racquet above the dominant hand, on the
grip or shaft. The dominant forearm is held in more pronation than with the one-handed backhand stroke ( 185). At the
beginning of this phase, the two-handed backhand player also pivots or steps back with his or her back foot, which
follows trunk rotation. The shoulders move in synchrony with trunk rotation. The upper limb motion is characterized by
dominant shoulder horizontal adduction, internal rotation with little or no forward elevation, elbow flexion (less than with
one-handed), increased forearm pronation, and wrist motion to ulnar deviation and flexion. For the nondominant upper
extremity, the shoulder extends and externally rotates, the elbow flexes, the forearm supinates, and the wrist
hyperextends and the ulnar deviates. The racquet head is usually held near the level of the nondominant elbow, well
below shoulder level.
With both backhand strokes, the forearm and racket are not aligned. Players with symptomatic AC joint arthritis of the
dominant shoulder have pain during this phase of the backhand.
The nondominant wrist hyperextension and ulnar deviation with the two-handed backhand place excessive stress on the
triangular fibrocartilage complex (TFCC), resulting in tears and ulnar-sided wrist pain. Extensor carpi ulnaris tendinitis is
also frequently encountered in the nondominant wrist of players with two-handed backhand strokes, possibly owing to the
extreme position of ulnar deviation during the preparation phase ( 75).
The second phase, acceleration, begins with the forward motion of the racquet and ends with ball impact. This stroke
begins with pushing off from the back leg, starting the transmission of ground reaction force from the lower extremity by
ankle plantarflexion, knee extension, and hip extension. The force is transmitted along the kinetic chain with trunk
rotation and lateral flexion to the racquet side, moving the body weight and momentum forward. The front knee stays
flexed, and with both styles of backhand, contact with the ball occurs in front of the body ( 186,187). The shoulders rotate
with the trunk. The trunk has been shown to rotate 60 degrees with the backhand stroke ( 50). As the racket moves
forward, at the initiation of the acceleration phase, the dominant shoulder drops ( 185).
With the one-handed backhand, five body parts are used before impact and more strength is required ( 150,188). With
the two-handed backhand, only two body parts are used to swing the racket to impact, because trunk rotation is the major
contributor to forward force generation in this phase ( 150,188).
With the one-handed backhand, the dominant shoulder abducts, externally rotates, and extends slightly from the
adducted, internally rotated, and slightly forward flexed position. The elbow extends from an average 48 degrees flexion
to 30 degrees (thus not fully extended), and is stable at impact ( 50). This is important because only 15% of racquet head
speed is generated by trunk rotation, forward motion of the body, and upper arm movement. Elbow extension alone
accounts for approximately 25% of the generation of racquet head speed. Thus, if the elbow is fully extended to generate
racquet velocity, this position may increase the likelihood of injury ( 187). The pronated forearm supinates during this
phase, regardless of the spin placed on the ball, to align the racquet face for impact. The wrist is extended throughout
this phase and is in slight radial deviation ( 75).
With the two-handed backhand, the dominant shoulder abducts and rotates externally while the elbow extends, although
not fully, and is stable at impact. Dominant forearm pronation is maintained, although slightly reduced, throughout the
acceleration phase, whereas pronation is increased in the nondominant forearm. There is greater pronator teres muscle
activity with the two-handed backhand technique during this phase, suggesting the dominant forearm has more pronation
than with the single-handed technique ( 153,185). It has been shown that as the racquet begins to move forward, the force
of the nondominant arm may impart a rotation (due to nondominant forearm pronation) to the racquet that must be
counteracted by increased pronator muscle activity in the dominant arm. This increased pronation of the nondominant
forearm is suggested to be the cause of nondominant ulnar stress fractures in the two-handed backhand tennis player
(88). Both wrists maintain their position throughout this phase.
Lateral epicondylitis (tennis elbow) is reported to be more common with one-handed backhand technique as compared
with a two-handed backhand. This may be due to the increased risk of poor mechanics with a one-handed technique.
Muscle activity in the dominant wrist extensors is similar when comparing the two strokes ( 185). Thus, stroke mechanics
during this phase is believed to be a major implicating factor for the development of tennis elbow, especially when the
player starts with the stroke high, prepares late, hits off the back foot and with a leading elbow, the forearm in less
pronation, and the wrist hooked in ulnar deviation ( Fig. 34.7A and Fig. 34.7B) (68). It has been shown that novice tennis
players develop tennis elbow more often than expert or more advanced players ( 68,74,189,190 and 191). The poor form
described in the above-mentioned stroke mechanics occurs more frequently in inexperienced players ( 175). Furthermore,
it has been shown that expert players have their wrist extended an average 23 degrees just before ball impact and that
they extend their wrist further at impact (192). In contrast, novice players strike the ball with their wrist in 13 degrees of
flexion with their wrist moving into further flexion at impact ( 192). Thus, it appears that the novice players hit the
backhand while eccentrically contracting the extensor muscles of the wrist. This form, when performed repetitively,
especially with off-center ball impact, subjects the wrist extensors to recurrent microtraumatic injury of the forearm
extensor musculotendinous unit at the lateral epicondyle, resulting in lateral epicondylitis. Other factors associated with
the development of tennis elbow include excessive use of spin, lack of strength, and lack of coordination ( 188).
FIGURE 34.7. Backhand Forms. Correct form of the backhand (A). Incorrect or poor backhand form illustrated (B) reveals
body weight back, hitting off the back foot, leading with the elbow, the wrist in palmarflexion.
Another cause of injury with a one-handed backhand includes chopping the ball. When attempting excessive slice or
backspin with a one-handed backhand, excessive wrist action results in ulnocarpal impingement or abutment with the
potential for a TFCC tear and musculotendinous injury to the forearm, lateral elbow, and posterior shoulder.
The final backhand phase, follow-through, begins at ball impact and ends with the completion of the swing. This phase is
often further subdivided into early follow-through, the first 25% of the phase, and late follow-through, the last 75% of the
phase. During this phase, there is a smooth upward racket movement, with completion of trunk rotation, continued
shoulder abduction and external rotation, elbow extension, and wrist extension until forward motion is completed. There
is some slight ulnar deviation of the dominant wrist with the one-handed stroke ( 186). With the two-handed backhand,
some players supinate the dominant forearm while the nondominant forearm continues to pronate, which may be the
mechanism of stress fracture of the nondominant ulna ( 88). The trunk rotates more with the two-handed backhand
because the nondominant shoulder must rotate more completely with the follow-through ( 97). Furthermore, the
two-handed backhand also puts the lumbar spine at increased biomechanical risk when reaching for a wide ball. The
obligatory trunk rotation with the two-handed backhand, coupled with a relatively fixed pelvis for hitting a wide ball, can
cause a greater stress on the lumbar spine because forced rotation is applied to a relatively fixed pivot point ( 97).
Footwork
The earlier portion of this section discussed the importance of the kinetic chain in the development and transference of
ground reaction forces to the upper extremity, the racquet, and the ball. It discussed upper body biomechanics, because
this is what differentiates tennis from other sports. However, before the athlete can hit the ball, he or she must get there
and set the body in the appropriate position. This is commonly described as “footwork.” Tennis places great demands on
the lower extremities and on the cardiovascular system owing to the sudden bursts of running, stopping, cutting, pivoting,
lunging, and jumping. The repetitive bursts of these actions place potentially excessive demands on the bones,
ligaments, muscles, and tendons of the lower extremities to absorb these forces.
These lower extremity injuries may be acute, including subungual hematomas (tennis toe), ankle sprains, Achilles tendon
ruptures, strains of the gastrocnemius, shin splints (periostitis), knee sprains, meniscal tears, patellar dislocations,
hamstring strains, quadriceps strains, and groin strains. Lower-extremity overuse injuries due to the demands of tennis
include stress fractures, plantar fasciitis, Achilles tendinitis, patellar tendinitis, Osgood-Schlatter syndrome, and
patellofemoral pain syndrome (i.e., excessive lateral patellar compression).
Unilateral Arm Dominance, Adaptations, Asymmetry, and Injury Production
Because tennis is a unilateral arm dominant sport (in most players), the potential exists for flexibility and muscular
strength imbalance. In general, the specific physical demands placed on the racquet sports player increase with
extended playing time and with the increased skill required at higher levels, as has been shown repeatedly in tennis
(51,96). Most of these demands are directed at anatomic areas that are sports specific, including the shoulder, arms,
back, trunk, hips, and legs in tennis, as described earlier in the previous biomechanics section. Large demands are
placed on the shoulder in terms of the range of motion, loads, and velocity required. The forearm, elbow, and wrist
experience substantial rotational forces when hitting the ball that are increased by the extreme hand and grip positions of
current playing styles. The back, trunk, and hips are of vital importance in tennis. They act as a center of rotation and
transmit the forces generated in the legs to the shoulders and arms. The abdominal muscles and the intrinsic trunk
muscles are most important in this respect.
Skeletal adaptations to tennis have been well documented. Jones et al. ( 193) found an increase in bony diameter and
cortical thickness of the distal humerus in the dominant arm of professional tennis players as compared with the
nondominant arm. Buskirk et al. (194) and others (195) reported muscular hypertrophy in the dominant arm of ranked
tennis players. In a more elaborate and detailed study, Krahl et al. ( 196) performed a radiologic study of the forearm and
hand of professional tennis players. They found an increase in bone density and bone diameter, as well as length in the
dominant arm as compared with the nondominant arm (196). Using volumetric displacement techniques, Noffal and Elliott
(197) identified hypertrophy and increased mass of the dominant arm, forearm, and hand in tennis players as compared
with the nondominant arm.
As the athlete continues to play these racquet sports, the musculoskeletal system adapts to these sport-specific demands
through altered flexibility, strength, muscle balance, and endurance. These adaptations have been demonstrated by
numerous authors in tennis (50,51,53,62,67,69,96,195,198,199,200 and 201). Flexibility measurements in tennis players
were significantly lower in sit-and-reach, dominant shoulder internal rotation, and nondominant shoulder internal rotation
tests compared with those in athletes who do not throw and do not play tennis. Tennis players were also shown to be
more flexible in the external rotation of both shoulders ( 51,53,96,195,200). Patterns of reduced flexibility, in dominant
forearm pronation and supination and in nondominant hip internal rotation, have also been demonstrated
(50,51,53,96,195,200). These flexibility differences suggest that adaptations take place in response to the repetitive,
short-duration, high-velocity, and high tensile demands of tennis. Muscle weakness patterns have also been identified in
tennis players (51,198). Chandler et al. and others identified increased dominant shoulder internal rotation strength as
compared with the nondominant shoulder, whereas there was no difference between dominant and nondominant
shoulder external rotation strength ( 198,200,202). Notably, weaknesses occur in the upper extremities (shoulder and
forearm) and in the central region (back and hips). It is surmised that the athlete's adaptive changes may be creating
biomechanical deficits that predispose the athlete to injury with continued, increased use. For example, rotator cuff
weakness and imbalance, as well as weakness of the scapular stabilizer muscles, can place the athlete at risk of
shoulder instability and rotator cuff pain due to overuse or impingement, or both. Furthermore, weakness in the lumbar
extensor muscles can also lead to an imbalance with the abdominal flexors, which may increase the risk of lower back
problems or abdominal strains. In addition, increased grip strength of the dominant hand has been repeatedly identified
in tennis players (195,203,204,205 and 206).
In a study of trunk muscle strength, elite junior tennis players have significantly more abdominal muscle strength than low
back strength (207), whereas this imbalance does not exist in the general population ( 208). Sward (209) found that 10%
of elite tennis players displayed a pelvic tilt of greater than 1 cm difference between iliac crests, and that 77% of players
had asymmetry of the back in forward flexion due to asymmetric muscle development and a mild scoliosis. Sward ( 209)
found that elite tennis players had greater trunk extension as compared with athletes who do not play tennis, whereas
trunk flexion was nearly the same between the two groups, confirming the strength imbalance in tennis players.
Andersson (210) found that tennis players have greater muscle strength in side bending on the nondominant side. Fig.
34.8 is an example of a top-ten male professional tennis player with hypertrophy of his rectus abdominus muscles on the
side contralateral to his dominant shoulder. This could be expected, especially in a player with a powerful serve, owing to
the repetitive, powerful lateral and anterior flexion of the trunk during the late cocking and acceleration phases of the
serve.
FIGURE 34.8. Abdominal muscle hypertrophy. This is an abdominal MRI of a top-10 male professional tennis player.
Notice the left rectus abdominis muscle hypertrophy (arrow) of this right hand dominant player.
Increased external rotation of the shoulder, loss of internal rotation of the shoulder, and a lack of flexibility of the pronator
and supinator muscles are adaptations that could be considered as normal efforts to control the high forces generated in
tennis. However, these adaptations appear to create biomechanical inefficiencies and cause functional alterations that
decrease optimal performance and increase injury risk, as discussed earlier ( 51). The importance of these adaptations is
highly suggestive. Anatomic adaptations occur even in young players, so young age is not a protective factor ( 50).
Furthermore, they occur in anatomic areas that have a high incidence of injury, indicating a relationship between these
changes and injury patterns.
Bone adaptations can have a negative effect, resulting in pathologic reactions to overuse. Examples of bony adaptation
include reports of stress fractures of the metacarpals ( 211,212), ulna (Fig. 34.1) (88,90,91), humerus (213), distal radius
(89), and lateral process of the talus ( 214) in tennis, the proximal humeral physis in badminton ( 63) and tennis (62,64,65),
and humeral shaft periostitis in tennis ( 61). Although there have been no reported cases of stress or overt fractures of the
acromion in tennis players, there has been a report of a stress fracture of the acromion after a subacromial
decompression (215).
EXERCISE PHYSIOLOGY OF TENNIS AND OTHER RACQUET SPORTS
Tennis
The metabolic and strength demands imposed upon athletes in these racquet sports have been studied. Tennis includes
intermittent bouts (300 to 500 bursts of effort during a match) of varying intensities and duration that are interrupted by
many pauses (216). Although tennis is characterized by periods of high intensity exercise in high-level players, the
overall metabolic response resembles prolonged moderate intensity exercise or submaximal exercise ( 143).
In tennis, metabolic functioning has been characterized as being approximately 90% anaerobic and 10% aerobic, varying
slightly based on the level of play and competition ( 51,216). The anaerobic activity had been further subdivided as 70%
alactic and 20% lactic anaerobic ( 217). Thus, metabolic specificity in the sport of tennis dictates that the alactic
anaerobic energy system is the primary system used. The relative duration of these three energy systems indicates that
the first 10 to 15 seconds of maximal exercise is alactic anaerobic. Recovery from this alactic anaerobic work, particularly
alactic oxygen debt, can take place during low-intensity exercise or short rest periods. Within 20 seconds, 50% of the
depleted adenosine triphosphatase (ATP) is restored; within 40 seconds, 75% is restored; and in 1 minute, 87% of the
ATP is restored (218). This is reinforced by Chandler's finding of length of time of points played during the men's and
women's finals at the 1988 United States Open Tennis Championships ( 219). He found that for the men 59% of points
lasted less than 10 seconds and only 19% last more than 20 seconds, while for women 62% of points lasted less than 10
seconds and only 13% lasted more than 20 seconds ( 219). Chandler also found that for men, the average rest between
points was 28 seconds (12 after point, 42 seconds at the end of the game without changing sides and 128 seconds with
court change). For women, the average rest period was 16 seconds (11 seconds after points, 24 seconds at the end of
the game without changing sides and 100 seconds with changing sides) ( 219).
The maximal oxygen uptake of top male players is approximately 60 mL per kg per minute, whereas in high-level women,
it is 50 to 55 ml per kg per minute ( 220,221). The heart volume of high-level male tennis players may reach 13 mL per kg,
whereas in women, it is approximately 12 mL per kg (221). Heart rates during recreational competitive tennis matches in
children average 171 beats per minute, whereas in adults (average age 35 years), the heart averages 154 beats per
minute (221). For professional male tennis players, the average heart rate during match play is 141 beats per minute,
whereas for women it is 149 beats per minute (221). Morgans found that in a 1-hour singles match, participants reached
an average 61% of maximal heart rate reserve, whereas in doubles, they reached only 33% ( 222). During rallies, heart
rates have been found to reach 80% to 90% of predicted maximum, although this depends on the intensity of play and
conditioning of the player ( 223,224 and 225).
Tennis players can expect to lose between 0.5 and 2.5 L of water during each hour of play, depending on the
environment, intensity of play, acclimatization, aerobic fitness, hydration status, age, and gender ( 142,146,147,148 and
149,221,226). Electrolyte losses during training that need special attention include potassium, sodium, magnesium,
chloride, iron, and zinc ( 221). Although carbohydrate-electrolyte drinks do not appear to affect performance directly
during average-length tennis matches, they can maintain blood glucose concentrations throughout match play, which
may have an effect during a particularly long match ( 227,228 and 229). During long matches, endurance levels approach
that of other endurance sports. In these situations, performance can be enhanced with carbohydrate drinks owing to the
sparing of glycogen and reduced lipolysis and oxidation of fatty acids, which is less economical for energy production
and utilization ( 228,230,231,232,233,234 and 235,). Burke and Ekblom (236) showed that ingesting carbohydrates during
tennis skill testing increased power by 11.6% and concluded that carbohydrate ingestion results in maintaining power,
with the ball being hit harder and less shots hit into the net. Another benefit of carbohydrate drink ingestion is the effect
on cognitive function. The maintenance of blood glucose levels can decrease the amount of error and maintain skill
levels by influencing brain function and improving mental performance and coordinative capacities ( 228). Lastly,
carbohydrate-electrolyte sports drinks can allow for replenishment of lost electrolytes and help prevent dehydration
(141,142,229,237). The energy requirements of play and training necessitate a daily caloric consumption of 2,000 to
4,000 kcal (221,228).
The repeated short bursts of energy in tennis may improve aerobic endurance and cardiovascular fitness ( 51,205,238). It
has been shown that the values for the aerobic–anaerobic threshold are much higher in high-level male and female
tennis players compared with healthy, untrained individuals of the same sex ( 221,239,240). In fact, one study showed
that tennis players who play or train 4 to 5 hours every week have a physical performance capacity similar to that of an
untrained individual who is 20 years younger ( 221).
Other Racquet Sports
Squash and racquetball place a high demand on the aerobic system for energy delivery during play and recovery
(241,242). In addition, these sports require bursts of intense, anaerobic physical activity involving the lactic anaerobic
energy system. The average squash match may last 40 to 115 minutes and may require 2,000 or more running steps
(243). Blanksby (244) found that the heart rate response in squash players reached a steady state by the ninth minute
and persisted throughout the activity. Noakes found that in a 90-minute squash game, rectal temperatures may rise by
1.6°C, reaching a final value of 39 degrees, with body fluid losses of about 2 L and heart rate of 160 beats per minute
(245). The metabolic response to squash is very similar to that measured during moderate- to high-intensity running
(245). Aerobic demands may exceed 80% of maximal oxygen uptake, although the game also places a significant
anaerobic demand on players ( 246). Singles and doubles racquetball play has been shown to meet the American
College of Sports Medicine criteria for developing aerobic fitness ( 247). Badminton is a highly aerobic sport that also
places a significant anaerobic demand on players. For each of these racquet sports, players must possess appropriate
levels of local muscular endurance, strength, power, flexibility, and speed, combined with agility, balance, and
coordination ( 241). Furthermore, the benefit of carbohydrate-electrolyte drinks on physical performance and endurance,
mental cognition and alertness, and reduction of fluid loss, as discussed earlier, likely applies to these other racquet
sports as well.
EQUIPMENT AND ITS EVOLUTION
Most of the advances in tennis technology, and similarly in squash, have occurred with the racquet. Changes have
occurred in racquet size, composition, and playing characteristics. These changes have had a major impact on the nature
of play at all levels.
Racket
Modern tennis is believed to have originated in 1883, with the original tennis racquets being made of wood and strings
made from cat gut or steel. The wood frame had been the mainstay of racquet composition, with only few exceptions until
the 1970s (Fig. 34.9). There were attempts at steel racquets with wood handles in the early 1900s as well as some
experimentation with different sizes and shapes of frames in England, but these did not become popular. Metal
(aluminum and steel) tennis racquet frames were introduced in the mid 1960s ushering in an era that displaced the wood
frame. Since the 1970s, there has been an explosion of technologic change in the composition of tennis racquets from
metal to fiberglass, and then to graphite, boron, ceramic, magnesium, and kevlar ( Fig. 34.10). The most recent entry are
the titanium racquets, which are predominantly graphite frames with small amounts of titanium at high stress points in the
frame (248). Many current racquets combine two or more materials. Furthermore, there are different types of graphite and
carbon fiber composites with differing material properties. Different racquets use different fibers as well as different
amounts of these fibers and materials, resulting in racquets with varying degrees of stiffness. The reasons to change
racquet composition include the goal of reducing the weight of the racquet while increasing its durability and strength,
and to increase the power of the stroke as well as to reduce injury. Theoretically, a racquet that dampens vibration and
reduces shock impulse (force of contact at impact) to the athlete's arm may reduce injury. This may be accomplished by
using lightweight materials in the composition of the racquet or by increasing the size of the head to increase the sweet
spot and thus reduce the effect of off-center hits ( 188). It has never been shown that injury rates or severity are reduced
by racquets that dampen vibration or reduce the shock (impulse). However metal racquets, which do not dampen
vibration well, have been identified as a risk factor for the development of lateral epicondylitis ( 36). Recent research has
shown that graphite composite racquets do reduce the vibrations more than most other materials, whereas ceramic and
boron are stiffer and do not appear to dampen vibration as well. The increased stiffness of racquets, including those with
a heavy and wide-body design, reduces vibration, although the frequency of vibration to the forearm is increased and the
increased impact shock transmission may be longer (248). To play with lighter racquets, the player must swing harder,
which has several effects on the racquet and player. These effects of the harder swing with lighter racquet include
increased impulse or shock at impact, increased change of racquet velocity at impact, and increased frequency of
vibration. On the other hand, lighter racquets are easier to swing longer and the player may thus be susceptible to injury
from overuse (188,248). Again, the effect on injury has not been proven scientifically.
FIGURE 34.9. Racquet evolution—wood frames. These are examples of four wood tennis racquets starting in the early
1900s until the mid-1960s. Notice the change in head size and shape.
FIGURE 34.10. Racquet evolution—composite frames. These are examples of four nonwood tennis racquets beginning
with one of the first metal racquets, a popular metal composite, the first oversized racquet, and a more recent oversized
composite racquet.
The shape of the racquet has also undergone change, although not as dramatically as the composition. It is generally
accepted that the smoother the transition between the widest part of the racquet head and the handle of the racquet, the
more inherently stiff the racquet becomes ( Fig. 34.11). There also have been changes in the shape of the head from oval
to a more square shape. The shape affects the stiffness, but weight and strength of wood racquets made the shapes
prohibitive before the use of graphite in tennis racquet technology. Looking at the profile of the racquet, a few changes
have been made. These changes include the thickness of the frame, resulting in a stiffer racquet and tapering of the
thickness along the frame, affecting the flexibility and the vibration of the frame ( Fig. 34.12) (249,250). Furthermore, the
stiffer racquet may reduce twisting with off-center hits ( 188). Again, increased stiffness may provide more power with
each shot and reduce vibration; however it may also promote shock transmission to the body and thus increase the
susceptibility to injury, while flexible racquets tend to dampen the shock. Other changes include initially moving the
center of the head and center of percussion toward the handle, increasing power ( 248). Current racquet design attempts
to move the maximal power point toward the center of the racquet away from the throat, because this is where most
people attempt to hit the ball on the strings. Unfortunately, at present, there are no data that supports or refutes any
effect of these changes on the risk of injury.
FIGURE 34.11. Comparison of racquet head size of standard wood and new oversized frame. This photo compares a
standard 1960s to 1970s wood racquet and a current oversized composite frame. Notice the new frame with oversized
racquet head that is more square on top, the smoother transition from the racquet head to the shaft and grip, larger
stringing area, and overall increased length of the racquet and head.
FIGURE 34.12. Comparison of racquet width. This photo compares a standard 1960s to 1970s wood racquet and a
current oversized composite frame. Notice the increased width of the new composite frame as compared with the
standard wood frame, resulting in increased frame stiffness.
Racquet head size is another racquet “shape” that underwent dramatic change with the introduction of the Prince
oversized racquet. Since then, most racquets made are midsize or large size ( Fig. 34.11). Both versions increase the
maximal hitting zone as well as the sweet spot, reducing the off-center hits. Increased racquet head size has been shown
to reduce arm vibration (250,251). International Tennis Federation rules provides a limit to the size of the racquet head
and maximal string length (248). The increased head size theoretically reduces the shock to the forearm and elbow
musculature and may potentially reduce injury. Although there has been a fair amount of research that supports the
advantages of both sizes, there is no clear-cut performance advantage and no effect on injury rates have been identified
solely due to the use of these racquet types. The definition of the “sweet spot” of the racket varies among the tennis
manufacturers as well as how it is measured (248). Thus, studies to compare the significance of sweet spot size on injury
prevention are difficult to perform. There appear to be as many anecdotes about tennis elbow and sore shoulders being
caused by the racquets as there are about these conditions being cured by the racquets.
Racquet length is another recent change ( Fig. 34.11). Racquets are being manufactured at 0.5 to 1.5 inches longer than
the standard racquet length. The maximal allowable racquet length is 29 inches. The longer racquet has been shown to
result in more powerful shots. However, the longer racquet results in a longer lever arm for the upper limb. Thus, small
increases in weight or force at the racquet head potentially results in large stresses to the shoulder, elbow, and wrist.
Some promoters of the long body racquet suggest that the increased length is easier on the arm because there is more
racquet length to absorb shock and vibration before it reaches the hand. However, the effect of increased racquet length
on injury is unknown.
An important aspect of racquet selection involves the size of the grip to be used by the performer. Nirschl ( 175,191) has
recommended that the grip size on the racquet should correspond to the distance between the tip of the ring finger to the
proximal palmar crease with the ruler placed between the ring and long fingers. Too small a grip makes the player
squeeze the handle too firmly to maintain control over the racquet head at impact. Holding the grip more tightly has been
shown to allow for increased transmission of vibrational forces to the elbow, theoretically resulting in tennis elbow.
Prolonged need for increased grip tightness may cause fatigue from overuse. A grip size that is too large causes a player
to have less feel for and control over the racquet. Both too small and too large grips have been implicated in the etiology
of tennis elbow (36). Grips traditionally have been made of leather. Cushioned grips have been shown to reduce impact
shock and vibration transfer from ball impact and have become more popular ( 252,253).
Composite racquets are lighter than the original wood racquets. As a result, racquet weights have decreased by 50% in
the last 10 years. Titanium racquets are the lightest tennis rackets that have ever been produced. The strength of these
newer composite racquets, including titanium and aluminum, allows a lighter weight racquet to be used without sacrificing
stroke power or control (254). The lighter and stiffer racquets allow players to play the power game longer with less
fatigue, begin the power game earlier in life, and continue into later years of life. However, lighter racquets may allow the
player to play longer, resulting in more repetition, and thus overuse injuries may occur. Alternatively, if players play the
same amount with lighter racquets as compared with the heavier racquets, then fatigue may be lessened and injury may
be reduced. Thus, the effect on injury is not clear at this time. The author does recommend lighter racquets for players
who are rehabilitating from upper extremity injury.
Strings
Strings have undergone an evolution from steel strings to gut and nylon, and now the most popular string is a synthetic
gut. Steel strings were very durable, but the rapid destruction of tennis balls resulted in the decline of their use in
competition and recreational tennis. Gut strings are more elastic and have a soft feel with decreased energy being
transmitted to the forearm of the player (248). However, gut strings wear out rapidly and are costly. Nylon strings have
intermediate elasticity, with some types of synthetic strings having properties very similar to gut strings, but they last
longer. At higher string tensions, nylon strings lose their elasticity and have an effect of being more stiff longer ( 248).
Multifilament, synthetic strings are filled with many tiny filaments that have a softer feel. It is theorized that these tiny
filaments stretch more than a monofilament string or strings, with a core string surrounded by fewer filaments, resulting in
reduced stiffness, reduced impact and potentially less vibration transmission. Kevlar strings are relatively inelastic and
are not as popular as the other synthetic multifilament nylon strings ( 248). Titanium strings have been introduced on the
market, although their purported benefit is unclear to the author. To the knowledge of the author, the effect of string types
on injury patterns or incidence have not been studied.
String tension has been the subject of much research and debate. The ideal string tension has varied from the extremely
high tension of the Bjorn Borg era to a more moderate tension favored by most players at present. There is laboratory
evidence that at lower string tensions (looser strings), the ball stays on the strings longer and come off the strings at a
higher velocity. It is believed that the force of impact of the ball is spread out over a longer time. With looser strings, the
strings will deform more and the ball will deform less. Thus, less energy will be absorbed from the ball, which then
reduces the force exerted on the body and potentially reduces the risk of injury. However, the difference in terms of
demands on the tennis player is negligible. Similarly, there has been no demonstrable evidence that string tension is a
variable in causing or preventing tennis-related injuries.
Dampers placed in the strings have no effect on elbow and forearm pain ( 255). Although these string dampers quickly
decreased the high-frequency string vibrations, the lower frequency frame vibrations were not affected ( 255).
Shoes and Court Surface
Sports shoes have undergone as much a technologic transformation as tennis racquets in the last 20 years. Tennis
shoes are very important to the player owing to the quick start and stopping, cutting, pivoting, and jumping that are part of
the game. Many of the innovations, such as sole cushioning systems (e.g., air, special polymers), variable lacing
patterns, deepened heel cups, reinforced toes, and additional supportive mechanisms, have no research basis to prove
the superiority of one type over another. However, tennis players may benefit from wearing shoes that are made
specifically for tennis. The shoes should be properly fitted with the socks the player plans to use while playing. Often,
players use a thick pair of socks or two socks to afford padding and protect the underlying skin. The shoes should have a
fairly wide heel and good heel counter for rearfoot control, and a heel thickness of 5/8 to 1 ½ inches. The traction surface
of the heel should be shock absorbent and of a nonslip material ( 256). The heel cup should fit snugly, which helps
prevent the foot from slipping forward in the shoe. The shoe should have a medial arch support that is appropriate for the
individual's arch. There needs to be good lateral support for the forefoot. The toe of the shoe must not create pressure
and should conform to the general shape of the foot. The vamp (upper front) of the shoe must never constrict or cause
pressure across the metatarsal area or instep. The rolled heel is an important innovation to absorb shock when the leg is
stretched forward and the heel strikes the ground ( 80). The high heel counter is purported to reduce Achilles tendon
rotation and thus injury ( 114).
Court surface, style of play, and foot structure should be considered when selecting a tennis shoe ( 256). A competitor
who plays mostly from the baseline requires a shoe that has more sidewall support to stabilize the foot during the quick
lateral, side-to-side movements that are necessary. The baseline player also needs good support for forward and rear
forces in addition to the extra sidewall support. The serve and volley player generates tremendous levels of forward
forces in the forefoot or toe box area of the shoe. Without the appropriate shoe, these players are susceptible to
developing tennis toe (subungual hematoma of the toe). Appropriate shoewear for these players includes a large toe box
to provide adequate room so the toe will not slam against the end of the shoe.
Very seldom are custom orthotics necessary for the average player. Their shock absorption functions are not high, and
foot control can be better maintained by flexible joints and muscular strength in the legs.
Natural rubber outersole provides excellent traction on all court surfaces. Polyurethane soles do not provide as much
traction as natural rubber, and they are usually only recommended for high traction court surfaces that provide
exceptional footing, such as indoor carpet, where too much traction may result in injury. Lighter weight shoes, with less
support, are more applicable to clay or composite courts, rather than hard courts ( 254).
Court surfaces have influences other than those regarding shoewear and type. Different court surfaces can alter the
demands that are placed on the tennis player. In general, clay courts and some synthetic courts slow the ball down and
produce a higher bounce, allowing for longer points and longer matches. Because more strokes are hit in trying to impart
more speed to a slower ball, there may be extra strain on the arm and back. The softer surfaces cushion the knees and
legs, reducing knee pain, particularly for arthritic knees, and the likelihood of shin splints and lower-extremity stress
fractures. However, since the softer surfaces result in longer matches, the extra running may put more demands on the
legs, resulting in muscular fatigue, and there may be more muscle strains from sliding on the soft surfaces. Achilles
tendinitis occurs more commonly when switching to clay courts after playing predominantly on hard courts. Most synthetic
courts and hard courts speed the ball up and keep the bounce lower, creating shorter points. However, because of the
speed of the ball, more impact forces may be placed on the racquet and arm. Similarly, the quick pace of the points on
the harder surface may cause increased stress on the legs, such as shin splints and lower-extremity stress fractures
(257). This is particularly true when starting the hardcourt season after playing on clay courts for a prolonged period of
time. Grass courts place an increased stress on the upper extremity owing to the frequency of irregular ball bounces and
an increased ball speed. The player must compensate for the fast moving ball that may bounce awkwardly and change
their stroke mechanics to hit the ball. During prolonged practices and match play, this difference in repetitive stress is
evident.
Tennis Balls
Tennis balls have undergone less change than many of the other equipment variables. Pressureless balls are not used
very often at present. Pressureless balls are preferred on clay courts and at high altitudes; however, they are very heavy
and do not bounce well on hard courts at sea level. The tennis ball is hollow, composed of inflated rubber, and covered
with fabric and is pressurized. The ball measures 2 ½ to 2 5/8 inches in diameter and weighs 2 to 2 1/16 ounces. The ball
has not had many recent changes, although there are proposed changes. Softer balls with similar properties to current
tennis balls may reduce injury in a way similar to softer strings in the racquet, with the ball staying on the strings longer
(248). Conversely, harder balls are being considered for play on clay courts. Harder balls increase the speed of play, and
the ball bounces higher on clay ( 248). Last, a larger tennis ball, approximately 7% to 8% larger than the standard ball,
became legal on January 1, 2000. It is not used for the professional tours. The goal of the larger ball is to slow the game
on faster surfaces (hard court, grass), and potentially make tennis easier for recreational players by being easier to hit
longer (248). The effect of these changes in the ball on injury is unclear at this time. Used or “dead” balls (i.e., loss of
some pressure) require more stroke energy to achieve a comparable amount of speed as compared with new balls. The
player has a tendency to stroke the ball harder and overhit the shots. This increases stress on the upper extremity and
back, and may result in an overuse injury.
SQUASH AND RACQUETBALL
There is less research on the musculoskeletal aspects of racquetball and squash as compared with tennis. However, the
demands of these two sports reveal many similarities to tennis. The major musculoskeletal demands in racquetball and
squash in the upper extremity are to the shoulder, elbow, and wrist due to the repetitive fast swinging of the lighter
racquets with more whipping or snapping motions to attain power for the swing. The squash and racquetball swings are
swifter and more compact than the tennis swing. However, the lower extremities are most frequently injured, especially
the knee and ankle, which are subjected to the greatest stresses owing to the rapid starting and stopping, cutting, and
pivoting on predominantly wood surfaces that provide excellent traction ( 30,47,243). Young players appear to sustain
more fractures, while older players tend to sustain more cartilage and tendon injuries ( 30). Further still, more experienced
players appear to sustain more serious injuries and more orthopedic injuries, whereas less experienced players sustain
more numerous injuries but less severe injuries, such as lacerations ( 30). Squash and racquetball participants are more
likely to sustain acute injuries, as opposed to the predominance of overuse injuries with tennis and badminton ( 47).
Contusions and Abrasions
In squash and racquetball, owing to the enclosed nature of the court and the close proximity of the players, there is a
greater risk of acute contact injury as compared with tennis and badminton. Contusions, abrasions, and fractures can
occur in racquetball and squash owing to contact with the ball, the opponent, the opponent's or partner's racquet, the
walls, and occasionally, the player's own racquet. Contusions that occur to the trunk or extremities due to the impact by
the ball sting and are painful but usually are superficial. Local swelling is usually small. Early return to play is the rule.
Contusions that occur due to racquet impact may, however, have more damaging consequences. These injuries may
involve deeper structures and may actually tear muscle or cause fractures, especially around the face and head. Pain
may be significant enough to stop play. Gradual return to normal use is usually advocated. Experimental work on
direct-blow muscle contusions reveal that optimum healing takes place by regeneration of muscle tissue ( 258). This
process may take 3 to 4 weeks and will result in excessive scar tissue if too much tension is placed on the repair site
early in recovery (258). Lacerations about the face, eyelid, and eye also occur due to contact with the racquet—either the
opponent's or the player's own ( 17,21,22,23 and 24,30,32,34). Facial lacerations and eye wounds account for 36% of all
squash injuries (30).
Eye
The most dangerous injury that occurs in all racquet sports is damage to the eye, either by direct contact with the ball or
racquet. As such, eye injuries related to indoor racquet sport have received more extensive review in the literature than
injuries to other body systems. Eye injuries are more common with racquetball and squash as compared with tennis and
badminton due to the confined nature of the court and because the players are not separated by a net
(22,31,32,130,131). Both the racquetball and squash ball function as missiles of high velocity and kinetic energy ( 24). In
fact, the squash ball can be hit at a velocity of approximately 140 mph, which has four times the energy of a 22 caliber
bullet (259). Both balls have been shown to be capable of conforming tightly into the orbital cavity on direct impact,
creating tremendous direct and concussive forces on the fragile eyeball and orbit ( 23,24). Eyeguards are mandatory in
the United States and have been shown to reduce the risk of eye injury in racquetball and squash ( 130,260,261). The
mechanism of contact with the ball or opponent's racquet is usually the player looking back at the opponent or ball as the
opponent hits the ball, although it may also occur from a bounce off the wall, such as when a ball is being played off the
side or back walls (17,22,23,28,34,262). Another mechanism of eye injury occurs when a player rushes to the wall to
chase a drop shot and immediately turns to run back ( 24). Experience does not reduce the risk of injury ( 23,32,34). In
racquetball, the racquets are shorter and the courts are larger; thus, the players are at a lesser risk of being hit by the
racquet as compared with squash (23). Hyphemas, which result from direct contact between the racquet or ball and the
eye, may be effectively treated in the acute stage but may be associated with cataract, retinal detachment, or retinal
hemorrhages (17,20,21,22,23,24,25,26,27 and 28). Increased risk of future glaucoma may occur with these injuries ( 33).
There is a suggestion that racquetball eye injuries are less severe in nature than those associated with tennis and
squash because the ball is softer and more pliable and its elasticity allows it to conform to the orbital rim, diffusing its
force (22).
Regular glasses do not protect the eye in these sports. In actuality, they may increase injury to the eye either by
shattering, or if they are shatterproof, they may rotate out of the frame and lacerate the eye ( 21,259). The optimal
eyeguards are wraparound polycarbonate lenses with eyeguard rims that are posterior to the orbital rim, antifog coated,
and have secure stabilization to the back of the head ( 23,24,33,263). It has been estimated that there may be a 25% risk
of eye injury in a lifetime of a participant who regularly plays squash without eye protection ( 17).
Heat Illness
The sports of squash and racquetball require sudden, sharp side-to-side and front-to-back movement patterns and great
endurance in a confined space, often in conditions of high temperature and humidity. Because of the high aerobic nature
of squash and racquetball, especially in indoor courts with poor ventilation, there is a significant cardiovascular and
thermal stress to the body (264). Heat-related illness, such as heat cramps, heat syncope, heat exhaustion, and heat
stroke may result (138,264). As stated earlier, this is particularly important in preadolescent athletes because they have
poor heat tolerance and do not acclimatize as effectively as adults ( 139,140,142). Cardiovascular stress and heat illness
potential are discussed in more detail in the Exercise Physiology section of this chapter.
Shoulder
Shoulder pain occurs less frequently in racquetball and squash players compared with tennis players. Although these
sports do not require an overhead service motion, overhead shots, such as smashes or lobs, are needed in both sports.
However, rotator cuff inflammation (impingement, tendinitis, instability) occurs more commonly in racquetball owing to
lengthy ceiling rallies in this sport. The AC joint is susceptible to injury due to falling or impact with the wall, resulting in
sprains and separations.
Elbow
Lateral epicondylitis is the most common upper-extremity injury in racquetball and squash players. As with tennis, poor
technique and faulty grip may play a role in the development of this problem. Furthermore, racquet technology is
changing in both of these sports, and racquet type, size, and strings may also play a role in this malady, especially if a
recent change was made before the onset of symptoms.
Medial elbow pain is very common in squash and racquetball players owing to the snapping mechanism of kill shots and
to the lighter racquet. Contact with the wall may also cause extra valgus force. Injuries sustained include medial
epicondylitis, ulnar collateral ligament injury with secondary findings of lateral and posterior elbow pain and ulnar nerve
irritation.
Traumatic hemorrhagic olecranon bursitis may infrequently occur due to falling or diving for the ball in these sports.
Repeated microtrauma may also result in nonhemorrhagic olecranon bursitis. Elbow sprains and fractures may also
occur due to falling or contact with the wall ( 19).
Wrist
Racquetball and squash require a snapping motion of the wrist as part of the normal stroke. This puts stress on the
tendons and ligaments of the wrist that may result in an overuse injury. The chronic overstretching or recent initiation of a
new motion or technique will result in the wrist pain. This is often manifested as tendinitis about the wrist. Often, this pain
is in the wrist extensor tendons, either in the dorsal compartment or at the distal insertions. DeQuervain tenosynovitis is
also common among racquetball and squash players. Intersection syndrome, a peritendinous bursitis that occurs when
the musculotendinous junction of the first extensor compartment overlaps, or intersects, with the second compartment, is
particularly common in squash players. Review of the player's stroke mechanics, particularly the backhand, may provide
insight into the cause of this problem and help in the resolution of the symptoms. The stroke mechanics of these sports
are also believed to be the etiology of anterior interosseous nerve syndrome of the forearm.
Ligamentous injuries and fractures are not as common as tendinitis and may occur as a result of a fall or being hit by a
racquet. TFCC tears may result from a fall, although the stresses that occur during a squash swing have also been
implicated in these injuries. Subluxation of the extensor carpi ulnaris tendons has been associated with both racquetball
and squash.
Injuries including fracture of the hook of the hamate, ulnar artery compression and thrombosis, and chondromalacia of
the pisiform-triquetral joint due to abutment of the butt of the racquet on the base of the hand may occur in these sports
(76,82,83). Carpal tunnel syndrome has also been reported in racquetball players ( 265).
Back
Overuse, overreaching for the ball, hyperextension, and bending to hit the ball are motions that have been implicated in
the high incidence of low back pain amongst squash players ( 30,243,262,266). These motions may produce flexion and
rotation stresses to the spine, factors known to result in the commonly seen problem of intervertebral disk prolapse in
squash players (47). These injuries often may be traumatic in origin and have been identified in higher level players ( 47).
Hip
There has been a report of development of degenerative hip disease in elite squash players necessitating retirement or
curtailment of activity by the third decade of life ( 262). The question remains as to whether this is caused by the sport or
a childhood hip problem, such as slipped femoral capital epiphysis or Legg-Calve-Perthes disease, that guided the
athlete to squash as a sport that they could play while having a residual hip deformity until the eventual hip arthritis
develops and limits the player.
Knee
Knee injuries may occur in any racquet sport, but they are of particular concern in racquetball and squash, in which
nearly every type of knee injury may occur (105). Patellofemoral pain is the most frequently encountered condition in
persons playing racquetball and squash ( 105). This injury is usually insidious in onset due to the rapid starts and stops,
cutting, pivoting, jumping and lunging that define these sports. The frequent pivoting maneuvers in racquetball and
squash, particularly on wood floors with excellent traction, predispose players to meniscal and ligamentous injuries ( 105).
Older players are particularly susceptible to symptomatic meniscal tears due to propagation of degenerative tears.
Ligamentous injuries are relatively uncommon in these sports; however, with increasing use of play on bare, unvarnished
floors, the improved traction increases the risk of injury to knee ligaments, especially the anterior cruciate ligament ( 267).
Leg
The classic and most common injury in the leg is cramps of the calf musculature. The explosive bursts necessary in these
sports, especially when ankle plantarflexion is combined with knee extension, places the gastrocnemius-soleus group at
risk. In players 30 to 45 years of age, this may result in a partial tear of the medial head of the gastrocnemius, also called
tennis leg ( 30,108,243). Players usually feel a sudden onset of pain in the upper to middle third of the calf, and note that
it feels like they were shot or hit in the leg by the ball or a block of wood. Fortunately, these injuries are self-limited, and
take about 6 weeks to resolve. In older players (those older than 40 years of age), Achilles tendon ruptures occur
(20,243). This is a more severe injury. These patients note a snap and inability to push off on the affected foot. Return to
play is prolonged after this injury, regardless of whether it was treated surgically or in a cast. Achilles tendinitis is an
uncommon entity in racquetball and squash players. When Achilles tendinitis does occur, it is usually secondary to
overuse or recent change in training or play habits.
Ankle
Ankle sprains are one of the most common injuries in racquetball and squash due to the sudden changes in direction and
jumping necessary for these sports (19,30,243,262). Chronic, recurrent ankle sprains usually occur secondary to
incomplete rehabilitation. Ankle fractures have been reported ( 19).
Foot
Blisters, calluses, and tennis toe are common complaints of racquetball and squash players. Plantar fasciitis is the most
commonly seen orthopedic condition of the foot in these athletes, and the injury responds well to rest, stretching of the
calves and heel cups, and rarely necessitates injections or surgery. Less commonly, foot sprains occur due to the sudden
changes in direction (19).
BADMINTON
Although badminton is one of the most widely played sports in the world, it has received little attention with regard to
sports medicine research and study. Badminton is an individual, noncontact sport requiring jumps, lunges, quick changes
of direction, and rapid arm movements. Most injuries in badminton are due to overuse, although acute injuries,
particularly to the lower extremity, are common (10,14,268). Overall, lower-extremity injuries are the most common,
followed by upper extremity injuries and then back injuries ( 10,14,15,268). Much of the power for play comes from the
upper extremity—shoulder, elbow, and wrist—placing greater strain on these structures, resulting in overuse injuries from
repetition.
The badminton shuttlecock can travel over 200 mph, and as a result, it may function like a missile, causing injury. In
badminton, contusions and abrasions and eye injuries have been reported from the uncommon contact with the
shuttlecock, partner, or the partner's racquet ( 10,23). There have been reported cases of eye injury in badminton,
although eye protection is not mandatory ( 10,17,21,23,129,268,269 and 270). In fact, it is suggested that badminton is the
third most common cause of eye injury in sports in England, responsible for 11% of all sports eye injuries ( 24). It has
been generally assumed that a badminton shuttlecock does not have the destructive power of a squash ball. However, it
has been shown that the shuttlecock can produce an injury of equal severity ranging from hyphaema to retinal
detachment (10,17,21,23,129,268,269 and 270). Owing to the aerobic nature of badminton with the sudden stops and
starts and long play, muscle cramps are common in male players ( 271).
Shoulder
Shoulder pain due to overuse occurs occasionally in the badminton player. This occurs less commonly than with tennis
players. Although this sport does not require an overhead service motion, overhead shots, such as smashes or lobs, are
needed. As such, rotator cuff inflammation (impingement, tendinitis, instability) does occur. Furthermore, it has been
shown that the greatest force producing movement is internal and external rotation of the shoulder for the forehand and
backhand. This biomechanical technique can result in stress fractures of the proximal humeral epiphysis in the junior elite
badminton player, as has been reported ( 63).
Elbow
Lateral epicondylitis is a common upper extremity injury in badminton ( 14,47,268,271). This is usually believed to be an
overuse injury.
Wrist
Badminton requires a snapping motion of the wrist as part of the normal stroke. This maneuver puts stress on the
tendons and ligaments of the wrist that may result in an overuse injury. This is manifested as tendinitis about the wrist.
Often, this is in the wrist extensor tendons, either in the dorsal compartment or at the distal insertions as well as flexor
tendon inflammation. DeQuervain tenosynovitis also occurs in athletes in this sport ( 76).
Ligamentous injuries and fractures are not as common as tendinitis and may occur as a result of a fall or being hit by a
racquet (15). TFCC tears may result from a fall. Fracture of the hook of the hamate, chondromalacia of the
pisiform-triquetral joint, and hypothenar hammer syndrome (i.e., occlusion of the distal ulnar artery at the level of the
hamate bone) due to abutment of the butt of the racket on the base of the hand may occur ( 76,272).
Back
Musculoskeletal back pain due to overuse, overreaching and lunging for the shuttlecock, hyperextension and bending to
reach low have been implicated in low back pain among badminton participants ( 14,268).
Thigh and Groin
Quadriceps and groin strains are particularly common in badminton players owing to the leaping and lunging required in
this quick sport (14,271).
Knee
Knee injuries may occur in any racquet sport, including badminton, owing to the pivoting and jumping required ( 105).
Patellofemoral pain is the most frequently encountered condition in persons playing badminton ( 14,47). This is usually
insidious in onset due to the rapid starts and stops, cutting, pivoting, jumping, and lunging that predominates this sport
(14). Knee ligament injuries occur infrequently owing to the motions mentioned earlier ( 14,15,47).
Uncommon acute knee injuries identified in badminton include patellar dislocation, patellar fracture, and meniscal tears
(14,47).
Leg
Achilles tendon injuries in badminton may be due to a combination of factors. These factors include the special footwork
involving a fast forward movement and stopping with a forceful heel strike, eccentric work by the gastrocnemius muscle
alternating with concentric gastrocnemius function seen with backward or combined back and sideways jumps and
backward running. These movements produce alternating, rapidly changing high tension in the Achilles tendon.
Achilles tendinitis is a particularly common entity in badminton players secondary to overuse or recent changes in
training or play habits ( 14,271). As with racquetball and squash, the explosive bursts necessary for play places the
gastrocnemius-soleus muscle group at risk. In players 30 to 45 years of age, this may result in a partial tear of the medial
head of the gastrocnemius muscle, which is also called tennis leg ( 15,108,268). In players older than 40 years of age,
Achilles tendon ruptures occur (11,13,14 and 15,271).
Ankle
Ankle sprains are one of the most common injuries in badminton owing to incorrect placement of the foot dictated by the
sudden changes in direction and jumping necessary ( 10,11,13,15). Chronic, recurrent ankle sprains usually occur
secondary to incomplete rehabilitation. Infrequently, ankle fractures have been reported to occur during play ( 15).
Foot
Blisters, calluses, and corns are common complaints of badminton participants, particularly owing to the high friction
court surfaces and low shock absorption of the shoes. Plantar fasciitis is the most commonly seen orthopedic condition of
the foot in badminton players ( 14,271).
TREATMENT PEARLS
This section discusses some of the pearls of evaluation and treatment of tennis injuries in tennis players that I have
learned over the years as a competitive player and tournament physician. Detailed review of the treatment of specific
injuries is not the goal of this section. That topic is discussed in other places in this book. This section includes
information that specifically pertains to tennis players. Much of this information is empirical and based on
experience—the author's and others who care for professional and collegiate players-although scientific support for
these pearls does not exist at this time.
Management of the tennis player, whether junior, professional, or recreational, may require more information than the
usual musculoskeletal examination of the nontennis player with similar maladies. The evaluation of the tennis player
should include information about the type of strokes used for the serve, forehand (closed versus open stance), and
backhand (one- versus two- handed), how much they play per week (singles and doubles), the amount of other sports or
training they do, whether or not they stretch and what areas they stretch, whether they stretch before or after practice or
play, court surface played on, type of racquet (including length of time used, and grip size) and string (include tension),
and any recent injuries. I usually recommend players to bring their tennis racquet to my office so the player can
demonstrate their stroke mechanics and that their grip can be checked. I also keep a racquet in my office in case the
player forgets to bring his or her own racquet, although in this case, grip size cannot be checked. The ideal size can,
however, be measured, as discussed earlier in the equipment section.
Often, players with symptoms may have had another injury along the kinetic chain, clinically apparent or not, and as
result of compensating for another injury, may develop symptoms somewhere else along the kinetic chain. As an
example, a player with patellofemoral pain may develop shoulder or back pain while trying to “play through” the pain and
use the back or shoulder in an excessive or unusual manner. Frequently, I see patients with medial or lateral elbow pain
that have had a recent history of shoulder pain, and visa versa. In participants of the 1998 Girls' 16's USTA National
Championships, 50% of the girls who were injured during the tournament had a significant injury in the year before the
tournament compared with 36% of girls who did not sustain an injury during the tournament ( 273).
Professional tennis does not have a season, and more and more, college tennis is becoming a year round sport as well,
with many of the top collegiate athletes playing summer professional tournaments as an amateur. Thus, these athletes
cannot afford time off to rest an injury. The key to the management of tennis injuries is to prevent them. The way to
prevent injuries in tennis players is to identify risk factors and eliminate those under the player's control. Unfortunately,
other than maintaining hydration during matches, there is very little scientifically proven evidence that clearly identify
preventive measures. Wearing sunglasses and sunscreen may prevent injuries as the athlete ages. Furthermore, there is
enough evidence to suggest that stretching before and after play reduces the risk of injury ( 274,275,276,277 and 278).
Low back pain is a frequent complaint of tennis players, yet when queried, most admit they do not spend time
strengthening their abdominal or low back muscles ( 97). Thus, adding strengthening of these areas to the player's
workout regimen may help reduce these injuries, although again, this has never been proven. Furthermore, strength and
motion asymmetry of the dominant shoulder may produce shoulder pain, as discussed earlier. Eliminating these
asymmetries by increasing shoulder internal rotation motion in abduction and increasing external rotation strength in
abduction and adduction may theoretically reduce the likelihood of shoulder injury or pain, or pain somewhere else in the
kinetic chain. One author has shown that there was a 63% higher incidence of shoulder injury among recreational players
with tennis elbow than among players without a history of tennis elbow ( 279).
Many injuries in tennis players are due to overuse. The author has found in his study of Girls' 16's USTA National
Championships participants over the last 4 years and the Boys' USTA National Championships, more recently, that those
who are injured practice and play more per year than those who were not injured during the respective tournament. Girls
injured during the 1998 tournament played and practiced 11% more per year than those who were not injured. Boys
injured during their 1998 nationals played and practiced twice as much per year as those who were not injured ( 55).
Eighty-nine percent of injured girls jogged and 77% lifted weights as part of their training program as compared to
uninjured girls, of whom 82% jogged on the average 10% less mileage than the injured females and only 50% lifted
weight (55). There was no difference between injured and uninjured girls for running or weight lifting.
When evaluating shoulder pain in all patients, and especially in athletes such as tennis players, the physician must have
clear visualization of the shoulder from behind. This allows examination of the musculature of the infraspinatus and
supraspinatus muscles, assessing for atrophy and thus suprascapular nerve injury, as well as scapulothoracic motion.
Scapular dyskinesis due to weakness of the scapular stabilizers, such as the serratus anterior muscle, often results in
rotator cuff symptoms from outlet impingement (the acromion does not rotate out of the way) or because the rotator cuff
musculature is working harder and inefficiently owing to the fact that the origin (the scapula) is not well fixed to the chest
wall.
When evaluating players with patellofemoral pain, I make sure to assess the feet for pes planus in addition to the usual
evaluation of quadriceps atrophy (assessed by size with the quadriceps muscles contracted), tight hamstrings (popliteal
angle), patellar tracking, and evidence of significant effusions and other intraarticular pathology. Players with flat feet are
treated with off-the-shelf cushioned orthotics that are not, in any way, rigid, in addition to the usual program of hamstring,
calf and quadriceps stretching, straight leg raises, short arc closed chain quadriceps strengthening, and when indicated,
hip abductor strengthening and iliotibial band stretching. These off-the-shelf orthotics are usually sufficient, although they
tend to wear out more quickly when playing on hard courts. If the patient wishes to have custom or longer lasting
orthotics, they should be made from leather. I have treated professional and collegiate players with lower-extremity stress
fractures, in whom the only risk factor was recently (within 3 weeks) starting to use rigid, plastic, custom orthotics.
Furthermore, return to play for athletes with patellofemoral pain should begin with easy ground strokes, avoiding lunges,
jumping, and sudden starts and stops.
Some players complain of pain over the Achilles tendon. This sometimes is actually from abrasion of the skin overlying
the Achilles due to the back of the tennis shoe. Most tennis shoes have a notch in the back to reduce the stress to the
skin over Achilles, but occasionally, this accentuates the abrasion. Taking time away from the shoe, stretching the leather
of the notched area, or wearing a heel lift all can eliminate the symptoms. Otherwise, the player may need to switch
shoes permanently. Players returning to play after Achilles tendinitis or tennis leg (strain of the medial head of the
gastrocnemius muscle) will benefit by beginning play on hard courts (as compared with clay courts) and a heel lift. Using
gradually smaller heel lifts help return the player to the game sooner and more gradually. The athlete should be told to be
patient with Achilles tendinitis because the recovery may be prolonged. Start with stretching of the gastrocnemius and
soleus muscles individually. Use a heel lift for ambulation and return to play. Strengthen the calf muscles as well as
gradual return to play.
Players with tennis toe are managed in the usual fashion acutely. That is, if pain is severe, a hole is made in the toenail
to alleviate pressure. Long-term management and prevention of this problem (including recurrence) involves placing a
cushioned pad on the toe, wearing two pairs of socks for extra padding (make sure the shoe is big enough to do this
comfortably), switching shoes to one with a larger toe box, or having a shoe repair person stretch the leather of the shoe
to increase toe box size.
Tennis elbow, or lateral epicondylitis, is treated in the standard manner of rest, stretching, and strengthening. The author
has found short-term use of wrist extension splints may help rest the wrist extensor muscles if the symptoms are
particularly acute. Care must be taken to educate the patient that this is an overuse syndrome. Of additional importance
are proper stroke mechanics, reduction in tension of the racquet strings, the use of a cushioned synthetic grip, ensuring
proper grip size, conditioning, and the use of the counterforce (tennis elbow) brace. If symptoms persist (length of time
depends on previous treatment and level of player), I recommend an injection with Xylocaine and corticosteroids at the
lateral epicondyle. The author finds that this is beneficial for short-term use and allows the patient to perform appropriate
rehabilitation. If an injection is used, the player's symptoms are severe enough to warrant the recommendation to not play
for 2 weeks. After the symptoms abate, a comprehensive rehabilitation program is initiated, emphasizing strength and
flexibility of the forearm flexors and extensors. Medications and injections are only temporizing factors to reduce the
symptoms. The author recommends that players switch to a stiffer racquet, or string the racquet at a looser tension. The
patient should be encouraged to seek professional instruction to eliminate biomechanical errors in stroke production if
and when they are identified in the office ( 280). Furthermore, if mechanics in the office appear normal but symptoms
return, then the player should seek a tennis professional to ensure that the player is using the proper mechanics. Typical
errors in stroke mechanics include (a) improper weight transfer (hitting off the back foot), (b) hitting with the leading
elbow during the backhand, (c) excessive pronation of the forearm during the serve or the overhead. Also be sure that
the player stretches the forearm muscles before and after play, and ices the lateral elbow for 20 minutes immediately
after play.
When a player returns to play after an upper extremity injury or surgery, they must have full range of motion and strength
of the affected joint. The author recommends that the player start playing with a midsized or oversized light racquet that
does not have a heavy head and has the appropriate grip size. Choosing a racquet that has a light head, in which the
center of weight of the racquet is closer to the grip, will reduce the lever arm of stress to the upper extremity.
Furthermore, the racquet should be strung at a low string tension (at least 3 to 5 pounds less than normal) using real gut
strings or the new multifilament synthetic gut that has no central core string. Strings that are thinner and more elastic also
reduce vibration to the arm and may be of benefit. New tennis balls should be used during rehabilitation because they do
not have to be hit as hard as older balls that are not as lively and require more upper extremity force to hit. If the
diagnosis is rotator cuff inflammation (from impingement, rotator cuff injury or instability), after symptoms abate, return to
play starts just with ground strokes, particularly forehands, avoiding high forehands, powerful backhand shots, serves,
and overhead smashes. These recommendations are based on the theoretical benefits of these individual factors,
although again, they have never been proven to reduce injury.
When recovering from a lower extremity or back injury or surgery, the author recommends playing on softer surfaces,
such as clay or other composite surfaces. Once the player can play on clay or indoor carpet without recurrence of
symptoms, then they may progress to hard courts. Progression from a structured practice situation to competition is the
biggest step of the tennis player's rehabilitation process. This is due to the increased amount of stress and resultant
force on the musculotendinous units during a match situation. During a match, a player works much harder due to the
pressure of the match as compared with practice. As such, a graduated program is necessary to progress from structured
practice sessions to practice matches to tournament play. The athlete must be able to play three consecutive sets in a
practice match without recurrence of symptoms before returning to competition. In overuse injuries, the athlete must be
able to play 5 to 7 consecutive practice days of competitive tennis without recurrence of symptoms before return to
tournament play.
INDICATIONS FOR SURGERY OF COMMON INJURIES
The author's indications for surgery of several common injuries seen in tennis players comprise this section. More
detailed discussion of indications for surgery for these problems are elaborated on elsewhere in this book.
Shoulder Pain—Instability, Impingement, and Rotator Cuff Tears
Players that are younger usually have rotator cuff inflammation due to acquired glenohumeral microinstability. The rotator
cuff functions to help dynamically stabilize the humeral head within the glenoid. With a lax capsuloligamentous complex,
the rotator cuff has to work harder to keep the humeral head centered within the glenoid. The rotator cuff is then
susceptible to overuse injury. Furthermore, when the rotator cuff is fatigued or injured, contraction of the deltoid during
shoulder motion may pinch the rotator cuff and bursa between the humeral head and coracoacromial arch because the
rotator cuff cannot keep the humeral head centered in the glenoid. Thus, management of rotator cuff inflammation in the
young tennis player relies on relative rest; stretching the shoulder musculature; strengthening of the rotator cuff,
particularly the frequently weak external rotator muscles; and antiinflammatory medications. There is no role for
corticosteroid injections in this group. Relative rest allows for the player to try strokes that do not cause pain, usually
forehands (not high forehand), and maintain cardiovascular fitness. Return to play for tennis players with shoulder
instability is based on symptoms. Players who have symptoms despite 6 months of appropriate rehabilitation are
candidates for surgery. This may involve open procedures (rarely is there a true Bankart lesion) such as a capsular shift
or arthroscopic capsular tightening. A full discussion of the advantages and disadvantages of each procedure is beyond
the scope of this chapter. Depending on the evaluation under anesthesia, specifically assessing the total amount and
side-to-side difference of glenohumeral laxity, the author prefers a selective capsular shift or arthroscopic
capsulorrhaphy. Arthroscopic evaluation is also helpful in defining pathology in athletes with shoulder instability ( 281)
including superior labral, anterior to posterior (SLAP) lesions and internal impingement. Care should be taken to not
overtighten the glenohumeral joint, because this will prematurely end the career of the tennis player. Furthermore,
excessive humeral head motion within the glenoid (due to instability) may result in labral tears and degeneration. Isolated
debridement of labral tears is associated with poor results in the overhead athlete because this is a symptom of the
instability, which is usually not the primary problem ( 59,167,282). Partial-thickness rotator cuff tears are often seen in
tennis players with subtle shoulder instability( 59). Isolated debridement of these partial thickness rotator cuff tears alone
has been shown to be ineffective in overhead athletes ( 283).
Rotator cuff inflammation due to impingement generally occurs in players older than 25 to 30 years of age. Management
of these players includes relative rest; stretching the shoulder musculature; strengthening of the rotator cuff, particularly
the frequently weak external rotator muscles; and antiinflammatory medications. Corticosteroid injections may be of
benefit in reducing the pain and allowing the player to perform the exercises. The player must be reminded that the
injection is not the treatment—the exercises and relative rest are the treatment. Relative rest allows the player to try
strokes that do not cause pain, again usually forehands (not high forehand), and maintain cardiovascular fitness. Play is
allowed as symptoms permit but not for at least 1 to 2 weeks after an injection of a corticosteroid. Surgery is
recommended if symptoms persist for more than 3 months despite adequate rehabilitation, relative rest and two
injections. If symptoms recur more than a year after treatment, a second course of treatment may be attempted, with
injections. The author limits a player to three injections in the same shoulder in a single year. Arthroscopic subacromial
decompression is the author's procedure of choice owing to the low morbidity associated with this procedure and
excellent results in tennis players. Isolated debridement of partial thickness rotator cuff tears alone has been shown to be
ineffective in overhead athletes ( 283).
Symptomatic full-thickness rotator cuff tears in the dominant shoulder of the tennis player should be fixed. As noted
earlier, the stress to the shoulder and rotator cuff is very high in the production of tennis strokes. If a player wishes to
continue to play, a torn rotator cuff should be fixed. If the rotator cuff tear is not repaired, it will most likely progress to a
larger tear. Bigliani et al. ( 284) have shown that 83% of club level tennis players who underwent an open rotator cuff
repair had a pain-free shoulder and were able to return to tennis playing at their presymptomatic level, while 95% were
able to return to play. Those players who were unable to return to play had massive (> 5 cm tear) rotator cuff tears. The
results of rotator cuff repair in high-level (professional or collegiate) athletes have not been studied, and thus, these
results may not apply to these athletes. Collegiate and professional baseball players have an unpredictable rate of return
to presymptomatic level of play (285). Nonetheless, the torn rotator cuff in the tennis player should be fixed. This may be
performed open, arthroscopically assisted, or completely arthroscopically. The author prefers arthroscopically assisted
repair with a bony trough in tennis players with small to medium-sized tears or tears without much retraction, whereas
chronic, large or massive tears with significant retraction are managed with open repair.
Medial and Lateral Epicondylitis
My indication for surgery for persistent epicondylitis is when a good conservative treatment program, including rest from
play, completion of an appropriate exercise program, and two to three injections of corticosteroids, does not relieve the
patient's symptoms. A first recurrence of epicondylitis is treated as if the patient was presenting for the first time, although
confirmation of appropriate stroke mechanics is helpful. The author also recommends that the player try changing tennis
racquets to a stiffer racquet or trying a lower string tension before considering surgery. The author prefers the open
technique of excising the granulation tissue, roughening the epicondylar bone, and repairing the muscular hood. Most
authors report success rate of 85% to 95% with surgery. Care should be taken to note that the results of surgery for
medial epicondylitis are not as good when there is associated ulnar neuropathy.
Wrist
DeQuervain stenosing tenosynovitis often responds to conservative management of relative rest, splinting, and
nonsteroidal antiinflammatory medications, although occasionally, injections are necessary to reduce the inflammation.
Surgical decompression of the first dorsal compartment is indicated if symptoms persist in spite of 6 to 12 weeks of
conservative treatment. Return to tennis may be anticipated 8 weeks after surgery.
Acute dislocation of the extensor carpi ulnaris tendon is an uncommon injury in tennis players, although when it occurs,
the author recommends repair or reconstruction of the sheath to regain stability of the tendon ( 79,286). Some authors
recommend cast immobilization (75,287,288), and theoretically, some patients may be asymptomatic. Rowland identified
that acute ruptures undergoing surgery had a considerable gap between the torn edges of the fibro-osseous sheath,
regardless of wrist positioning suggesting surgery is necessary in all cases ( 286). Others believe that surgery is only
necessary in chronic cases due to the fibrous tissue that is interposed between the torn ends, which results in recurrent
subluxation or dislocation. The author has found that this entity is usually problematic in tennis players, and if the
condition is left untreated, it may lead to attritional rupture and recurrent dislocation and thus recommends surgery in all
cases of this problem in tennis players.
Fractures of the hook of the hamate are usually managed with excision in tennis players. Many of these injuries are
stress type fractures and often do not heal with casting. Complications of nonoperative treatment include persistent,
symptomatic nonunion, ulnar nerve symptoms, and tendinitis or rupture of the flexor digitorum profundus tendon to the
little finger (75,80,289). Because of these risks of nonoperative management and the low risk and functional loss
associated with excision of the fragment, the preferred treatment of the author is excision. The patient can return to play
approximately 7 to 8 weeks after surgery.
Achilles Tendon Rupture
When the Achilles tendon is ruptured, the author prefers surgical repair in the competitive tennis player. Nonsurgical
management involves a long leg cast, followed by a short leg cast or walking boot. In the long leg cast, the knee is
initially bent and the foot plantarflexed to attempt to make the tendon ends contact. The advantages of this treatment
include avoiding the risk of anesthesia or general risks of surgery (infection, bleeding or injury to nerves), as well as
avoiding the risk of wound complications. The advantages of surgical repair include placing the torn tendon ends in direct
contact reducing gap scar formation, avoiding the prolonged immobilization in a cast that would otherwise result in stiffer
ankle and stiff knee joints (after surgery the knee is not immobilized and thus does not get stiff), lower risk of re-rupture of
the tendon, and slightly stronger calf muscles. Surgery allows for earlier rehabilitation and, thus, earlier return to play.
CONCLUSIONS
Racquet sports are becoming increasingly popular. In spite of recent advances in epidemiologic research of tennis
injuries (39,51,60,67,201,273), there still is a need for more injury research in all of the racquet sports. What data do exist
show that the athlete is susceptible to injury in these different sports, with injury being sports specific. Although most of
the sports result in similar injury patterns, such as a predominance of lower-extremity injury, there are some differences.
It appears clear that the physical demands of racquet sports are becoming more clearly documented and the adaptive
response to these demands are becoming understood. The adaptive response reveals a common etiology for many of
the injuries in the different sports. This is most often related to repetitive microtrauma with resultant loss in flexibility and
strength. Most of the injuries are overuse injuries to the upper extremity in each of these sports. Tennis and badminton
have a relatively high incidence of lower extremity overuse injuries. Tennis has a high incidence of patellofemoral pain.
On the other hand, racquetball and squash have a relatively high incidence of acute injuries, such as ankle sprains and
knee meniscal and ligament injuries. Each of these sports has a risk of thermal and cardiovascular stress, whereas
racquetball and squash have a higher risk of contact and collision injuries owing to the confined nature of the court and
proximity of the players.
This chapter should provide the practitioner with information that will allow him or her to have a better understanding of
the injuries in the racquet sports athlete, and allow the practitioner to be able to better evaluate, treat, rehabilitate, and
prevent future injury.
ACKNOWLEDGMENTS
The author would like to thank Kendall and staff at Paramount Tennis, Costa Mesa, CA for the tennis racquets to
photograph and Dr. Howard Brody for sharing his time, knowledge, and experience.
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35 Rugby
35
RUGBY
MARK FERGUSON
CLIVE NOBLE
Injury
Epidemiology
Mechanism of Injury
Site of Injury and Sport-Specific Treatment
Head and Face
Cervical Spine and Spinal Cord Injuries
Shoulder
Trunk, Lumbar, and Thoracic Spine
The Lower Limb
Injury Prevention
Conditioning
Chapter References
Rugby is played in more than 100 countries, with the United States alone having approximately 1,500 teams and each
year an estimated 50,000 to 75,000 participants per season ( 1).
Until as recently as 1995, rugby had a unique place in collision and contact sports. No one was supposedly allowed to
“seek or receive payment or other material reward for taking part in the game” ( 2), that is, it was an amateur sport.
Following the advent of World Cup Rugby, the onset of professionalism, strong regional championships, and major tours,
an increasing number of studies into injuries in rugby are being conducted ( 3). This has allowed the medical profession,
since its first misgivings about the safety of the sport in the 1980s ( 4,5), to call for rule or law changes to make the game
safer. Furthermore, as more recent studies with accurate data collection ( 6,7) are being reported, the high incidence of
injury has initiated a greater interest in injury prevention.
Anthropometric and physical performance studies of the various player positions have recognized the highly specific
conditioning aspects of the game.
The object of the game is that two teams of fifteen players each (eight forwards, seven backs) should be carrying,
passing, kicking, and grounding the ball, scoring as many points as possible ( 2). The opposing team prevents the
carrying of the ball by tackling their opponents. A tackle occurs when a player is held by an opponent with his arms, or
brought to the ground.
Players may then compete for possession of the ball. If the player with the ball remains standing, a maul will form. If,
however, the ball goes to the ground the competing players will form a ruck ( Fig. 35.1). Following an infringement of the
laws or if the ball leaves the field of play, play is restarted by either a scrummage or line out, respectively.
FIGURE 35.1. A: The tackled player with the ball attempts to remain on his feet. A maul is then formed as opposing sides
compete for the ball. B: The player with the ball has gone to ground and a ruck will then ensue.
The scrummage is formed by the eight opposing forwards, who bind together in a pyramid formation ( Fig. 35.2). The front
row consists of two props and a hooker. After both sets or packs of forwards have engaged each other, the ball is placed
on the ground between them. The ball is competed for by either hooking the ball backward with their feet or by pushing
the opposing pack off the ball.
FIGURE 35.2. A scrum is formed by the eight forward players in each team binding together in a pyramid formation.
These basic phases of the game represent an archetypal body contact sport. The skills required for tackling, mauling,
rucking, scrummaging, and line out play expose the player to extrinsic and intrinsic forces and their commonly associated
injuries. An extrinsic injury occurs when external forces are applied to the body, for example, striking an opponent in a
tackle, which causes overloading of a tissue's structure. As the playing season has become longer and higher levels of
fitness need to be achieved, an increasing incidence of intrinsic injuries is being seen. Intrinsic injuries occur with
overloading of one's tissue by repetitive overuse of the body. This chapter focuses on injuries caused by extrinsic forces.
A rugby injury is defined as an injury that prevents a player from playing rugby for 7 or more days or that requires medical
treatment (7).
INJURY
Epidemiology
Rugby remains the sport with the apparently highest risk of injury per player per hour ( 8,9,10).
Garraway (6) studied 26 senior rugby clubs in Scotland during the 1993 to1994 season. One in four players sustained an
injury, with 84% of injuries occurring during matches. The 20- to 24-year-old age group sustained 43% of the injuries.
This rate was approximately five times the incidence in the group younger than 16 years of age. The overall injury rate
was 11.64 per 1,000 player hours, with the lower age group rate being 3.41 per 1,000 player hours and the 20- to
24-year-old group being 18.59 per 1,000 player hours. Moderate to severe injuries accounted for 40% of all injuries.
The outcome of all severity's of injury would result in a loss of playing time of an average of 39 days and an absence from
work or school of 18 days (6).
F. Verster, the South African National team doctor noted, however, in reviewing the team's injuries from 1993 to 1995,
that the team doctor or physiotherapist treated 76% of the injuries. Specialist opinion was required in 11% and surgery in
3% of all injuries (unpublished data).
Rates of injury for different age groups were confirmed in other studies ( 8,10,11 and 12). Although only 9% of school
injuries were serious compared with 18% in senior players ( 13).
Mechanism of Injury
Although early studies ( 14,15) found that age and grade of the player did not affect the injury patterns, the reported injury
rate during the 1995 rugby World Cup is disturbing ( 16). The overall incidence for elite players was 32 injuries per 1,000
player hours. This study suggests that the prevalence of rugby injuries rise with the increasing competence of the
players. This may be the result of the increased speed of the game ( 10) and the physical and technical abilities of the
players' (7).
This is further supported by studies showing that the phases of plays in which 49% to 64% of injuries occurred was in the
tackle. Of severe injury episodes 60% occurred during the tackle. In reviewing the circumstances of the tackle in which
injuries occurred, 80% occurred in the player with the lower momentum and 85% of players who were injured were back
line players (17).
Rucks and mauls have the second highest incidence of injury. Foul play can be responsible for 6% to 31% of injuries
(16,18). Most injuries in both senior and grade school levels occur at the beginning of the season. ( 6,8,10,12,19). This
suggests that players are not “match fit” and are more likely to be injured ( 20). Adequate off-season and preseason
training could well reduce the number of early season injuries. There are a reported greater number of injuries in senior
players occurring in the third and fourth quarters of the game ( 18). This may be due to the influence of fatigue on the
incidence of injuries. Newer studies reflecting the improved fitness programs and tactical substitutions allowed in the
modern game are required.
A clear relationship between injury and playing position has not been established. Clark found that the most commonly
injured adult players were the hookers, wings, and fullbacks. Eighthmen, flyhalves, and wings were found by Roux to be
most commonly injured in grade school rugby. Elite players in those positions most likely to be involved in play that
occurs at speed and tackle situations are at greatest risk ( 16).
However, Garraway et al. (17) and Inglis et al. ( 14) found that there was no significant difference in the proportion of
injury episodes according to player position. They found that the major risk factors for injury were the age and expertise
of the player, the pace of play, and the time of season.
SITE OF INJURY AND SPORT-SPECIFIC TREATMENT
Upper and lower limb regions account for 50% to 70% of injuries, with the knee and ankle being the most common joints
involved (6,8,10,11 and 12,14,16,18,21,22). Head, neck, and trunk are less commonly involved. Dislocations, sprains, and
strains of muscle, ligament, and tendons account for more than half of all injuries. Muscle, tendon, and ligament injuries
occur more in senior players, whereas fractures and closed head injuries (concussion) are more common in school boys.
The upper limbs are more at risk for fractures and recurrent injuries are dislocations, sprains, and strains.
Head and Face
Lacerations to the scalp and eyebrow area, and contusions are the most common injuries. These are caused either by
contact with another head or knee or foul play, but are fortunately transient and players are able to return within 7 days.
Fractures of the facial bones are uncommon and account for 3% of all injuries. Most facial fractures occur in the middle
third, that is, the nasal complex and the zygomaticomaxillary complex.
Nasal fractures require immediate treatment to stop the bleeding but usually only require reduction after 7 to 10 days.
This is often delayed to the end of the player's career to perform a final reconstruction owing to the high reinjury rate.
Surgery for uncomplicated zygomaticomaxillary complex fractures is usually performed after 7 to 10 days, allowing return
to sport at 4 to 5 weeks.
Concussion occurs when a moving head impacts against an unyielding object, for example, the ground or an opponent
producing diffuse brain injury. Various mild head injury scales may be used to define the degree of dysfunction ( 23,24). At
present, the International Rugby board recommends a player with documented concussion not to participate in match or
training sessions for 3 weeks if asymptomatic (25).
Neurologic assessment is required if this period is to be reduced and after frequent injuries.
Rugby players, particularly props, locks, and eighthmen, develop characteristic disfiguring auricular haematomas
commonly known as cauliflower ear. An acute hematoma rarely requires aspiration or drainage.
Cervical Spine and Spinal Cord Injuries
The high incidence of spinal cord injuries was first recognized in 1977 ( 26). Subsequent retrospective studies have
reported an effective decrease in spinal cord injuries following changes to the rules of the game ( 5,27,28,29). However,
Scher (30) and Armor et al. (31) have reported that the number of injuries in South Africa and New Zealand respectively
have not decreased. The number of serious spinal cord injuries seen at spinal units varies from 2 to 8.9 per year. Only
Rotem et al. have claimed to have sufficient retrospective data to give an incidence of 1.2 to 0.5 severe cord injuries per
10,000 players.
It is however important to appreciate that in analyzing only those injuries that cause serious spinal cord injury, as many
as 10 severe neck injuries without cord involvement may be missed. There appears to be international differences in the
proportion of serious injuries relating to the different phases of play. With the exception of South Africa and Ireland, most
injuries occur in the scrum ( 7). Front row forwards suffer the majority (85%) of cervical injuries that occur during the
scrum with the hooker being the position at greatest risk of injury. Conversely, back line players suffer the majority of
neck injuries occurring when they tackle (68%) or are tackled (66%) ( 32).
The mechanism and nature of the injury is largely dependent on the phase of play in which the injury occurs. The forces
produced during the scrum exceed the necessary load to cause compression fracture of the vertebral body (4,500
Newtons) or ligamentous injury to the cervical spine (2,000 N) ( 33). The front row produces a force of 6,200 N during
engagement, which decreases to 4,600 N after the scrum is formed or settled.
Injuries occur during engagement, collapsing, crashing, and popping of the scrum ( Fig. 35.3). The most common
mechanism is a hyperflexion trauma to the spine, which frequently produces anterior dislocation with bilateral facet
locking. Cervical injuries can be sustained in tackling by both the tackler and the tackled player. The tackler is brought to
a sudden halt when his head strikes either the ground or commonly the tackled player's thigh. An axial compression force
is applied to a slightly flexed cervical spine, that is, direct vertex impact injury. This can result in compression fractures or
anterior dislocation ( 30,34). Tackled players sustain hyperextension injuries, often with additional rotational stress, in the
high or double tackle situations.
FIGURE 35.3. The collapsed scrum is a potential site for severe cervical injuries.
The ruck and maul, as previously described, are two phases of loose play also responsible for spinal injuries. Cervical
injuries are sustained by forced flexion of the neck running into a maul, with or without the ball, or by the player at the
bottom of a ruck. Scher (30) reported a significant increase in early onset degenerative disc disease in rugby players.
The affected players are more likely to present with signs and symptoms of cervical osteoarthrosis and are at greater risk
of hyperextension injury.
Brachial plexopathy, or so-called burner/stinger syndrome, is occasionally seen in rugby players. They are typically of the
type I traction injury caused by incorrect tackling, imparting a lateral neck flexion and shoulder depression force.
Resolution is spontaneous, and long-term sequelae are rare.
Shoulder
Shoulder injuries are common, accounting for nearly 12% to 15% of all rugby injuries. The tackle is responsible for most
shoulder injuries.
This occurs when the tackled player's arms are caught in the tackle and the resulting fall onto the point of the shoulder
results in either a fracture to the clavicle or an acromioclavicular (AC) separation ( 35). AC separation injuries have been
reported to occur in as many as 45% of certain player groups. The treatment of type III AC separations remains
controversial. At present, these injuries are treated conservatively and only in those that remain symptomatic would a late
reconstruction, preferably at the end of a player's rugby career, be considered.
Glenohumeral capsulolabral injuries are predominantly seen in two forms. Acute anterior dislocations occur in the tackle,
to either the tackler or the tackled player, and when grounding the ball. The arm is forced into abduction and external
rotation either by the weight, or the momentum of the player. Owing to the nature of the game, recurrent dislocations are
common and surgical shoulder stabilization is often required. Subtle instabilities of the shoulder due to repetitive loading
in the tackle are more frequent in the loose forwards.
Trunk, Lumbar, and Thoracic Spine
Rib injuries, comprising fractures and costochondral strains, are infrequently seen, but in front row forwards these injuries
may be disabling often requiring a long recovery period.
The thoracic and lumbar spines have a surprisingly low incidence of injury. Injuries are predominantly myofascial,
although isolated lumbar posterior and transverse process fractures and thoracic disk prolapse have been reported ( 36).
The hip and pelvis seldom sustain acute traumatic injuries. Hip pointers or contusions over the anterior superior iliac
spine seldom require attention.
Repetitive overload syndromes in the form of a groin disruption (Gilmore groin) or sports hernia, bone stress reactions of
the pubic rami, and osteitis pubis are usually the result of poor training techniques or repetitive ball kicking and can be
severe enough to signal the end of a player's career.
The Lower Limb
The knee and ankle joint are the two most common sites of injury (6,8,11,18). These are predominantly ligamentous
sprains and strains, and are of a minor severity.
Medial collateral ligament (MCL) injuries are the most common ligamentous injuries involving the knee. The MCL is the
primary medial structure resisting valgus stress and external rotation. The mechanism of injury is a valgus force at the
knee caused by a tackle from the lateral side or with the lower limb trapped in external rotation and the weight of the
falling body producing a valgus force. Injuries are isolated or combined with tears of the posterior oblique ligament (POL)
or less commonly with either anterior cruciate ligament (ACL) or posterior cruciate ligament (PCL) injuries.
Isolated grade I and II injuries are treated conservatively with initial brace immobilization and protected weight bearing
with crutches. Rapid rehabilitation with a return to sport in 4 to 8 weeks is usually achieved. Grade III injuries with
associated POL injury often require surgical repair, but with early postoperative limitation of movement and a gradual
recovery of knee extension during rehabilitation, rugby training can still begin at 8 weeks. Mild residual medial laxity is
often present but does not limit any rugby activities.
Isolated rupture of the lateral ligamentous restraints is less frequent in rugby.
The majority of PCL tears in rugby are usually caused by a hyperflexion mechanism. Acute level I injuries with isolated
PCL tears and less than 10 mm of posterior tibial translation are managed conservatively. This method of management
has favorable results in players in all positions. Treatment consists of immediate control of pain and inflammation with
nonsteroidal antiinflammatory drugs (NSAIDs) and an aggressive quadriceps strengthening program. The incidence and
significance of patellofemoral and medial compartment arthrosis is still unknown, but may not be as benign as previously
thought.
Level II injuries have more than 10 mm of posterior translation but are stable in full extension are essentially combined
injuries. Acute PCL and MCL injuries can be casted in extension for 4 weeks and then reassessed at 2 months because
these injuries often tighten up. Acute reconstruction using autogenous hamstring grafts or synthetic LARS ligaments
through a single femoral tunnel to substitute the anterolateral bundle and retaining the injured PCL tissue has good early
results. Early surgical intervention is recommended in combined PCL and posterolateral corner injuries.
Chronic level II injuries that remain symptomatic require reconstruction using either a double tunnel or tibial inlay
technique.
Combined level III injuries require immediate surgical reconstruction but often have limitation of movement and the return
to sport is unpredictable.
Meniscal injuries are typically traumatic vertical longitudinal type tears, either isolated or in combination with cruciate
injuries. Young players typically present with a locked knee, most commonly involving the medial meniscus. Arthroscopic
repair with vertical sutures and fibrin clot is preferred in isolated meniscal injuries to improve the success rate of healing
and allow a rapid rehabilitation. The use of bioabsorbable meniscal fixation devices has been reserved for meniscal
repair in association with ACL reconstruction until studies have shown comparable fixation strengths and healing rates.
Owing to the nature of the game, ACL injuries are common in rugby, but surprisingly, no epidemiologic studies exist.
There appears to be a higher rate of ACL injury in back line players. The majority of ACL injuries occur by a noncontact
rotational deceleration mechanism. However, ACL and MCL combinations can occur by a mechanism of forced valgus
and external rotation.
Diagnosis can be made from the typical history and by careful examination. Often only after aspiration of the
hemarthrosis and follow-up examination, if necessary, can the diagnosis be finally made. The routine use of magnetic
resonance imaging (MRI) is not recommended.
Treatment selection for isolated ACL tears in rugby players is not clearly defined at present. However rugby being a level
1 activity, and the majority of player's ages being younger than 25 years, and requiring jumping, pivoting, and hard
cutting, and many hours of participation per year, surgical reconstruction is recommended ( 37). Furthermore, the use of
rigid ACL orthosis bracing is not permitted under current regulations. However, there has been the observation that
certain anthropometric forms of players do tolerate an ACL injury of the knee at a high level of participation in rugby ( 38).
Although there is no ideal time to perform surgical reconstruction of acute injuries, it is generally delayed until swelling
and pain have subsided and almost full range of movement has been restored.
Recognizing that the gold standard for graft selection remains an intact ACL, no clear guidelines for graft preference in
rugby players exists. Recommendations to use quadruple bundle hamstring grafts in forward players who require an
intact extensor mechanism for jumping and pushing and who may sustain direct anterior patella trauma during
scrummaging have possible merit but are unsubstantiated. Often the criterion for graft selection is for a more rapid return
to training in a young, pivotal, elite athlete, suggesting a bone patella tendon bone graft selection. As in all other sports,
no clear consensus has been reached.
Lateral ligament complex injuries of the ankle due to plantarflexion and inversion force are the most common of foot and
ankle problems in rugby. In some countries, prophylactic external support of the ankle is almost becoming mandatory to
decrease the incidence of these ankle injuries. The majority of acute injuries can be treated conservatively and a
favorable outcome can be expected. Chronic functional instabilities need surgical stabilization. A Brostrom/Gould
procedure has good results in back line players who do not tolerate loss of subtalar movement obtained with certain
peroneal tendon augmentation techniques. The various procedures using peroneal or autogenous tendon with bone
tunnels are most often performed in the heavier, less mobile forward players.
INJURY PREVENTION
As rugby begins its first few years of professionalism the emphasis on prevention of rugby injuries has been heightened
and the identification of those risk factors responsible for the majority of injuries has been of benefit, not only to the elite
players but the schoolboy and club players as well. All participants, including the player, coach, administrator, and
trainer, should be actively involved in reducing the risk of injury.
From our epidemiologic studies certain risk factors for rugby injuries have been identified ( Table 35.1).
TABLE 35.1. RISK FACTORS FOR RUGBY INJURY
Coaching must begin with the recognition of different anthropometric and physiologic characteristics between the playing
positions (39). This identifies players that have the physical requirements to perform the skills of a specific position.
Players should only be selected in positions appropriate to their morphology. Furthermore, individualized training
programs for different playing positions can be prescribed. Only since 1991 has conditioning been recognized as an
important aspect in the prevention of injury ( 32). The specific skills of those phases in which most injuries occur, that is,
tackle, ruck and maul, and in which serious injuries are sustained, that is, the scrum, must be understood and practiced.
The learning of correct techniques of tackling situations and scrummaging cannot be overemphasized.
The equipment worn by rugby players is strictly prescribed by the International Rugby Board ( 2). Approved supportive
clothing is listed in Table 35.2. Mouth guards or mouth protectors protect against injuries to the teeth and mouth. Their
use has been shown to be effective in protecting against concussion and injuries to the cervical spine. Custom fabricated
mouth guards are recommended and should be changed regularly ( 40).
TABLE 35.2. ADDITIONAL CLOTHING THE PLAYER MAY WEAR
The use of padded headgear provides protection against lacerations and abrasions and injury caused by impact ( Fig.
35.4). Further studies are required to determine their effectiveness in reducing closed brain and cervical cord injuries.
FIGURE 35.4. The use of padded shoulder supports and head gear is becoming increasingly popular with players but
their use is still optional.
The external knee supports permitted in rugby are most often used in rehabilitation following injury and do not provide
any structural support.
Shoulder padding that is permitted in rugby union does not decrease the incidence of severe shoulder injury but could
lessen the impact on the soft tissue during tackling.
The effectiveness of ankle braces and prophylactic taping in rugby union remains, as in other sports, controversial.
Because taping can only provide limited mechanical support and proprioceptive enhancement, the use of ankle braces
with or without strapping are recommended.
Strict observance of the rules of rugby has ostensibly seen a reduction in the number of injuries. The controlled
management and depowering of the scrum has lowered the incidence of serious neck injuries ( Fig. 35.5). Further
eradication of foul play is required to reduce the incidence of all injuries ( Table 35.3).
FIGURE 35.5. A–C: depict the sequence of phased engagement of the scrum under the referee's supervision. This is
essential to prevent the possibility of a spinal injury due either to vertex impact on engagement or hyperflexion on
collapse.
TABLE 35.3. PREVENTION OF RUGBY INJURIES
Conditioning
Fitness training and the proper development of sports specific skills in rugby have both been shown to reduce the risk of
injury. Following the success of fitness programs for elite players in 1987 in New Zealand and in 1991 to 1993 in England
and Australia, scientific studies have supplied the requirements for rugby conditioning ( 41,42).
Close analysis of the game of rugby has helped in the prescription of a sports specific conditioning program ( 43,44). In
rugby, although the game is played for 80 minutes, the ball is only in play for 20 to 30 minutes. Because rules have
changed since these early studies, the ball may well be in play for longer than 30 minutes. The game consists of between
125 and 160 activity cycles, with 85% of them lasting less than 20 seconds. The recovery periods during a game are
often greater than the preceding period of work. However, if one takes into account the number of rucks and mauls,
which may total between 40 and 100 in a game, 30% of activities have a shorter recovery period than the preceding work
bout. Therefore, strength training and quick recovery are an integral part of a player's fitness program.
The running component of rugby may range from 3,500 to 6,300 meters during a game, with approximately 66% of that at
three-quarter pace, and 33% full-out sprinting in back line players. Forwards are usually running at full speed for shorter
distances. Endurance and speed training are therefore required.
We find different physical performance characteristics and anthropometric attributes within the different playing positions
(45). Forwards are generally taller, possess greater body mass, and more endomorphic than back line players. The back
line players tend to be aerobically fitter, faster, and more agile and possess a higher degree of muscle endurance.
Specificity of fitness training with regard to player's position is required.
We are able to define five groups of players according to their different fitness requirements for the game ( Table 35.4).
TABLE 35.4. PLAYERS MAY BE GROUPED ACCORDING TO THEIR DIFFERENT CONDITIONING REQUIREMENTS
Turnbull et al. (46) emphasizes cycle training or periodization in planning a conditioning program. A rugby year may be
divided into well-defined phases of rest, building up or base, preseason, and competition or season.
In order to monitor the efficacy of a particular training program, physiologic tests should be carried out during the year.
They must be reproducible and be able to evaluate accurately body composition, muscle strength and endurance, agility,
explosive power, flexibility, and fatigue resistance ( 32).
The onset of professionalism has ensured the future of rugby as a worldwide game. Greater scientific evaluation of rugby
specific training methods, incidence and treatment of injuries, dietary requirements and injury prevention is required to
ensure its increasing popularity into the new millennium.
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10. Roux CE, Goedeke R, Visser GR, et al. The epidemiology of schoolboy rugby injuries. S Afr Med J 1987;71:307–313.
11. Davidson R, Kennedy M, Kennedy J, et al. Casualty room presentation and schoolboy rugby union. Med J Aust 1978;1:247–249.
12. Sparks JP. Half a million hours of rugby football. The injuries. Br J Sports Med 1981;15:30–32.
13. Lee AJ, Garraway WM. Epidemiological comparison of injuries in school and senior club rugby. Br J Sports Med 1996;30:213–217.
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15. Seward H, Orchard J, Hazard H, et al. Football injuries in Australia at the elite level. Med J Aust 1993;159:296–301.
16. Jakoet I, Noakes TD. A high rate of injury during the 1995 World Cup. S Afr Med J 1998;88:45–47.
17. Garraway WM, Lee AJ, Macleod DAD, et al. Factors influencing tackle injuries in rugby union football. Br J Sports Med 1999;33:37–41.
18. Davies JE, Gibson T. Injuries in rugby union football. Br Med J 1978;2:1759–1761.
19. Nathan N, Goedeke R, Noakes TD. The incidence and nature of rugby injuries experienced at one school during the 1982 season. S Afr
Med J 1983;64:132–137.
20. Upton PAH, Roux CE, Noakes TD. Inadequate preseason preparation of schoolboy rugby players. A survey of players at 25 South African
schools. S Afr Med J 1996;86:531–533.
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cohort. Br J Sports Med 1994;28:229–233.
22. Myers PT. Injuries presenting from rugby union football. Med J Aust 1980;2:17–20.
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24. Kelly JP, Rosenberg JH. Diagnosis and management of concussion in sports. Neurology 1997;48:575–580.
25. International Rugby Board. Report. Medical advisory committee meeting. January 1998.
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Wales, 1984–1996. Med J Aust 1998;168:379 - 381.
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34. Torg JS, Pavlov H, O'Neill MJ, et al.. The axial teardrop fracture. A biomechanical, clinical, and roentgenographic analysis. Am J Sports
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39. Nicholas CW. Anthropometric and physiological characteristics of rugby union football players. Sports Med 1997;23:375–396.
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41. Blair J. Rugby fitness. Auckland, New Zealand: SETO Publishing, 1990.
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Pietermaritzburg, Natal, South Africa: City Printing Works, 1995.
36 Running
36
RUNNING
DAVID N. M. CABORN
THOMAS D. ARMSEY II
LARRY GROLLMAN
JOHN A. NYLAND
JOSEPH A. BROSKY, JR.
Part 1: Evaluation and Treatment of the Injured Runner

The Act of Running
Etiology of Overuse Injuries
Extrinsic Overuse Injuries
Intrinsic Overuse Injuries
Common sites of Overuse Injuries
Diagnosis
Treatment
Conclusions
Part 2: Organization and Administration of Medical Coverage for Road Races
Organizing Committee
Team Personnel
Communications
Aid Stations
Equipment and Supplies
Fluid Stations
Environmental Considerations
Runner Education
Conclusions
Chapter References
PART 1: EVALUATION AND TREATMENT OF THE INJURED RUNNER
Recreational running has become as much a part of the modern American psyche as cellular phones and fast-food
restaurants. Ever since Frank Shorter's emotional victory in the 1972 Olympic marathon, American's have been taking to
the streets and pavements in ever-growing numbers. Although it is beneficial in a number of ways, recreational running
can result in significant overuse injuries to the musculoskeletal system. It has been estimated that 37% to 56% of the 30
million recreational runners in the United States sustain an annual injury ( 1,2 and 3). Approximately 2.5 to 5.5 injuries per
1,000 hours of running have been reported ( 4,5). Injured male (52%) and female (49%) runners eventually visit a health
care professional ( 5). Although running injuries occur approximately 2 to 2.5 times less frequently than injuries from other
sports, this represents a multimillion-dollar annual expenditure ( 4). It is hoped that through preventive education, this
number can be reduced (2,3).
The Act of Running
Running injuries occur because of the repetitive stresses and increased forces that are placed on the musculoskeletal
system. During running, midstance ground reaction forces are equivalent to a vertical force of approximately 1.5 to 5
times body weight (6). These forces are generated over the 1,100-foot strikes that occur on average per mile and the
5,000-foot strikes that occur in 1 hour of running ( 7). During running, joint shear forces increase to approximately 50
times that of walking (7). With this increased force, it is easy to appreciate how musculoskeletal dysfunctions caused by
small intrinsic or extrinsic abnormalities can be amplified in the progression from walking to running.
Running represents a normal progression from walking, but certain key factors must be appreciated in order to
understand the increased stresses placed on a runner's musculoskeletal system. During running, the stance phase
comprises less than 50% of the total gait cycle. Another major distinction is the presence of a double-float period, which
represents approximately 10% of the total gait cycle ( 8). The double-float period occurs when both feet are off the ground
(Fig. 36.1). On heel strike, the rear foot is inverted, and as the foot becomes loaded, the tibia starts to rotate internally
while the foot is converted from a rigid body support (supinated position) to a shock absorber (pronated position) ( 7).
Pronation refers to a normal combination of rearfoot eversion, ankle dorsiflexion, and forefoot abduction. Supination
refers to a normal combination of rearfoot inversion, ankle plantarflexion, and forefoot adduction. Pronation or supination
that demonstrates excessive displacement or velocity during stance phase may contribute to running injuries. The
subtalar joint functions as a vertical-to-longitudinal torque converter. As the body is propelled forward, the foot becomes
supinated and rigid to provide the maximum propulsion lever effect. Throughout the running gait cycle, the talus follows a
cyclical movement pattern. Compared with walking, running normally presents an increased rate of subtalar pronation,
diminished pronation time, and diminished pronation range.
FIGURE 36.1. Walking and running gait cycles. (From Ounpuu S. The biomechanics of running: a kinematic and kinetic
analysis. Instr Course Lect 1990;39:305–318, with permission.)
All of the major muscle groups show an increase in electromyographic (EMG) activity during running ( 9,10 and 11).
Quadriceps EMG activity increases approximately 172%; hamstrings, 86%; tibialis anterior, 56%; and
gastrocnemius-soleus, 95% ( 8). The major joints of the lower extremity also show increased motion during running. The
hips and knees become eschewed toward flexion, and the ankle demonstrates increased range of motion and specific
modulation changes related to landing strategy. Rear foot strikers represent 80% of distance runners, with 20% being
midfoot strikers (12). During the stance phase of running, the major site of power generation is the ankle. The ankle
performs 1.5 times the work of the knee and 3 times the work of the hip. In other words, the ankle is responsible for 60%
of the running power generation, whereas the knee and hip are responsible for 40% and 20%, respectively. The knee,
however, is the principal power absorber, performing approximately 2 times the work of the ankle and the hip.
Understanding the energy transfer and power generation concepts of the running gait cycle helps improve the recognition
of the underlying etiology of injury. Power generation during the swing phase is contributed primarily from the hip. Power
from hip flexion during the initial swing phase, power for hip extension during the terminal swing phase, and all other
motions are the result of inertia. Energy transfer at the knee and the hip occurs through concentric rectus femoris action
during the initial swing phase and hamstring action during the terminal swing phase, with some evidence of balanced
concentric activity proximally and eccentric activity distally ( 8). Many running injuries take place during the stance phase.
It is during this phase that maximal eccentric muscle activation and power absorption within the musculoskeletal system
occurs. If abnormal pronation occurs during midstance, musculoskeletal stresses may become evident on the medial
aspect of the extremity. In contrast, if abnormal supination occurs during midstance (as seen with a cavus foot),
musculoskeletal stresses may become evident on the lateral side of the foot and knee ( 13) (Fig. 36.2 and Fig. 36.3; Table
36.1).
FIGURE 36.2. Anterior and posterior views of habitus varus.
FIGURE 36.3. Anterior and posterior views of habitus valgus.

TABLE 36.1. SPECIFIC INJURIES SEEN IN THE RUNNING POPULATION
Etiology of Overuse Injuries
Approximately 70% of overuse injuries are seen in runners. The etiology of these overuse injuries can be classified as
either intrinsic or extrinsic ( 1, 14,15 and 16). The majority of overuse injuries in runners are the result of extrinsic factors.
Extrinsic Overuse Injuries
As mentioned earlier, extrinsic injury factors are responsible for the majority of overuse injuries. These injuries are
caused by factors external to the body such as running shoes, running terrain, running surface, and training errors.
Errors in training are by far the most common cause of extrinsic running injuries.
Primary Extrinsic Factors
Running Shoes
Running shoes can affect the type and frequency of injury ( 17). If running shoes become wet or the midsole is worn for
greater than 400 km, the shock absorption capability decreases by approximately 30% to 50% ( 18). In addition, the
proficiency in which running shoes provide effective heel pad containment is important ( 19). Proper heel pad containment
in the normal foot can increase shock absorption by 29.5%, and in the traumatized heel pad, it can increase shock
absorption capability by as much as 48.5%.
Running Terrain
Running terrain refers to the topography of the course. Downhill running causes significant knee stress because the line
of action of gravitational force is positioned posterior to the knee. In addition, downhill running increases the magnitude
of knee flexion, patellofemoral contact forces, net extensor moment, power absorption, and EMG activity of the knee
extensors as they attempt to maintain dynamic stability ( 8). However, studies on the effect of running terrain on
biodynamics are somewhat conflicting. Although certain studies have shown hill running to increase overuse injuries,
others have found no association ( 20,21). Overall, downhill running demonstrates an injury trend towards patellofemoral
pain and iliotibial band syndrome, and uphill running demonstrates an injury trend toward Achilles peritendinitis and
plantar fascitis.
Running Surface
The importance of the running surface in the etiology of injuries should not be overlooked. In certain sporting activities,
the frequency of injury may as much as quadruple depending on the running surface ( 16). Frequent running on asphalt or
concrete surfaces increases mechanical loading. This increase in loading can act on joints, muscles, and tendons,
thereby promoting greater injury rates ( 18). In contrast, running on too soft a surface may cause hypermobility within the
joints, tendons, and muscles, leading to overuse injuries ( 13). Running on uneven surfaces, slippery roads, or banked
tracks may cause a functional leg-length discrepancy. This discrepancy may cause excessive loading on the long leg and
result in an iliotibial band syndrome or trochanteric bursitis.
Training Errors
Errors in training are by far the greatest extrinsic cause of running injury. Training errors may include too much volume,
too much intensity, or inadequate recovery. Clement et al. ( 20) described four categories of training error: (a) persistent
high-intensity training without lower intensity (easy days); (b) sudden increases in mileage and intensity without adequate
rest; (c) single, severe training or competitive sessions; and (d) repetitive uphill-downhill training. Running experience or
speed of training has not been shown to alter the propensity for running injury ( 22). The need for an individualized
balance between training volume, intensity, and recovery must be recognized and maintained.
Intrinsic Overuse Injuries
Intrinsic injury factors are categorized as basic, primary, or secondary. The key intrinsic factors are malalignment, muscle
imbalance, inflexibility, and leg-length discrepancy. Secondary acquired factors such as kinetic chain dysfunction and
prior history of injury also are important. When considering gender, it is important to determine an accurate menstrual
history because amenorrhea may be a cause of recurrent stress syndromes involving not only the bones but also the soft
tissue (23).
Although there are physiologic and metabolic musculoskeletal system changes associated with aging, there does not
appear to be a significant predisposition to injury among this group. Konradsen et al. ( 24), in examining subjects with 30
to 40 years of distance running experience, failed to discover an increased incidence of osteoarthrosis of the hip. Similar
findings have been noted at the knee and ankle ( 25, 26). In childhood and adolescence, bone growth rate exceeds the
rate of growth of the musculotendinous unit. This can result in secondary inflexibility with resultant apophysitis. These
factors provide further justification for the importance of optimal musculotendinous flexibility. Height appears to have no
association with running injury, and reports about weight are conflicting ( 27).
Obtaining a thorough athletic and nonathletic injury history may also be of considerable importance in understanding soft
tissue healing and the potential for complete recovery. However, in the area of soft tissue healing, researchers are just
beginning to obtain a greater working knowledge. In examining specific injuries, certain biodynamic parameters should be
noted. When considering the effect of downhill running on knee and ankle kinematics, it is easy for one to understand
why certain overuse injuries occur. During downhill running, knee flexion, peak extensor moments, patellofemoral
compressive forces, power absorption, and eccentric activation of the knee extensors are increased. Ankle dorsiflexion,
net plantarflexor moments, power absorption, and eccentric activation of the plantar flexors also are increased. Downhill
running by athletes with anterior knee pain results in increased select kinematic and kinetic parameters. Examples of this
include doubled knee flexion angles, tripled peak knee extensor moments and patellofemoral compressive forces,
quadrupled peak power generation, quintupled peak power absorption, and increased eccentric muscular activity ( 8).
The runner with iliotibial band syndrome may present with increased hip adduction, peak hip abductor moments, peak hip
power absorption, peak hip power generation, and increased lower extremity muscular activity.
Primary Intrinsic Factors
Malalignment
The relationship between abnormal pronation and supination during the gait cycle and predisposition to injury has
already been discussed. However, it should be further emphasized that on initial ground impact, a minimal injury effect is
seen. As the runner moves into midstance and push-off, higher forces are generated from increased muscle activity,
resulting in a greater peak load on the tissues ( 28). The important distinction between total pronation displacement and
the rate of pronation is discussed later.
The so-called malicious malalignment syndrome can be seen in certain runners ( 29,30). This syndrome is the
combination of a broad pelvis, increased femoral anteversion, genu valgum with or without genu recurvatum, squinting
patellae, excessive Q angle, tibial varum, and excess pronation of the foot.
Leg-Length Discrepancy
Leg-length discrepancy can be related to sacroiliac (SI) dysfunction, lumbar paravertebral muscle spasm, poor
musculotendinous flexibility, muscle imbalance, or unilateral abnormal pronation or supination ( 31). Leg-length
discrepancy can result in pelvic tilt with secondary lumbar convexity toward the shorter extremity as well as increased hip
adduction, hip internal rotation, and supination. In the longer extremity, excessive pronation, increased knee valgus,
genu recurvatum, hip abduction, and hip external rotation also may be noted. Leg-length discrepancy may result in
iliotibial band friction syndrome, trochanteric bursitis, low-back pain, and stress fractures. A 20- to 30-mm leg-length
discrepancy may be acceptable in a low-demand population. However, in the running population, the repetitive high
loading forces may require that a leg-length discrepancy as small as 5 mm be compensated ( 13,32).
Inflexibility
Structural variations around the foot and ankle that create impingements, traction effects, or decreased mobility can
subsequently predispose the runner to injury. Examples of structural variations include Haglund deformity, tarsal
coalition, and an accessory navicular bone.
Muscle Imbalance
The importance of overall muscular condition remains contentious. However, it is believed that neuromuscular
coordination and ligamentous laxity may be important factors in hypermobility etiologies. Dysfunctions in
musculotendinous strength, flexibility, or coordination may result in increased impact loading forces.
Acquired or Secondary Intrinsic Factors
Kinetic Chain Dysfunction
Steindler (33) and, more recently, Gray ( 34) have discussed the concept of the kinetic chain. The kinetic chain concept
defines the body as a series of interrelated linkages. Anything interfering with the progression and mechanics of force
transfer can lead to compensatory changes in motion within one segment or in a subsequently balancing segment within
the kinetic chain. For example, an individual with a history of an untreated hamstring strain may subsequently develop
problems in the Achilles tendon as the gastrocnemius compensates for the dysfunctional proximal linkage in the kinetic
chain. Dysfunctional mobility and orientation of the SI joint is a common occurrence ( 35). The SI joint remains somewhat
enigmatic and should be carefully evaluated in the static and dynamic state ( 36).
Common sites of Overuse Injuries

Certain overuse injuries are seen at specific joints and locations of the lower extremity. The following section describes
common overuse injuries seen in runners. Epidemiologic data, physical examinations findings, differential diagnoses, and
treatment options are presented.
Knee
MacIntyre et al. (37) conducted a survey of 4,173 running injury cases in 1991. They found that the knee was the most
common site of running injury, comprising 48% of all of the injuries, followed by the lower leg, 20.4%; foot, 17.2%; hip,
6%; upper leg and thigh, 4.2%; and lower back 4.1%. When these injuries were broken down into specific conditions, the
anterior knee pain, which made up 24.3% and 29.6% of the total running injuries in men and women, respectively, was
the most common injury. The following frequencies of injuries are presented for men and women, respectively: iliotibial
band syndrome, 7.2% and 7.9%; patellar tendinitis, 5.1% and 3.1%; medial tibial stress syndrome, 7.2% and 11.4%;
Achilles tendinitis, 4.7% and 27%; and metatarsal stress syndrome, 3.1% and 3.8%.
When considering running injuries to the knee, medical personnel must remember that the knee is the major power
absorber. This power absorption is accomplished primarily through eccentric muscle activation. The knee performs twice
as much work as the ankle or the hip in this capacity. The majority of knee problems seen in runners are extraarticular in
nature. Occasionally, runners report mechanical intraarticular irritation secondary to a plica, an osteochondrotic lesion,
degeneration of the chondral surface of the patella, or in the older population a degenerative meniscal tear ( 37).
Extraarticular anterior knee pain or patellofemoral pain syndrome is the most common knee problem. Hypermobility of the
foot and ankle and malalignment of the hip, knee, ankle, and foot relationships can become manifested in altered
biodynamics with secondarily increased patellofemoral compression or traction effects in the muscles, tendons, and
ligaments. The necessity for a comprehensive static and dynamic biomechanical evaluation has been reviewed.
Frequently, extraarticular knee pain is seen in runners with a malicious malalignment syndrome. In addition, it is often
observed if the runner presents a tight lateral retinaculum; poor vastus medialis obliquus tone; and poor flexibility of the
hamstring, quadriceps femoris, and gastrocnemius-soleus musculature. Furthermore, examination may reveal divergent
insertional levels of the vastus medialis obliquus and the vastus lateralis obliquus muscles, with the more distal vastus
lateralis obliquus insertion creating a fulcrum-type effect, thereby affecting patellar orientation.
When examining the patella, the physician should assess not only patellar height and tracking but also superior, medial,
and lateral patellar glide. Further assessment should include Patellar tilt, J-tracking, and functional Q angle at 0, 60, and
90 degrees of knee flexion. The best functional test for isolating the patellofemoral joint is the single leg squat at
approximately 45 to 60 degrees of knee flexion, as described by Drez ( 38). Anteroposterior and lateral radiographs while
weight bearing, in addition to Merchant views at 30 and 60 degrees of knee flexion, should be obtained to evaluate
patellar subluxation and tilt ( Fig. 36.4).
FIGURE 36.4. Lateral patellar compression.
Specifics of treatment for patellofemoral conditions should include the correction of static and dynamic imbalances
through rehabilitation and conditioning programs. In addition, if excessive static pronation is present neutral orthosis
should be added. Runners who are experiencing an acute patellofemoral syndrome may also benefit from the McConnell
patellar taping protocol ( 39) (Fig. 36.5). Various patellar tendon straps and open patellar neoprene sleeves, with and
without buttresses and dynamic straps, may also be effective. These devices may enhance proprioception at the
patellofemoral articulation ( 40).
FIGURE 36.5. McConnell taping method.
The second most common overuse condition of the knee is iliotibial band syndrome (ITBS). Runners frequently report
pain while running downhill because the iliotibial band impinges on the lateral femoral condyle when the knee is flexed
approximately 20 to 30 degrees. This friction may result in tenderness over the condyle, the bursa (located midway
between the condyle and Gerdy tubercle), the tibia, or Gerdy tubercle itself. Excessive lateral shoewear and functional
rearfoot varus are often seen in runners with ITBS. These runners also present with a positive Ober test, weak hip
abductors, and poor hamstring flexibility. The presence of diffuse pain in this region, however, requires careful evaluation
to rule out the presence of lumbar disk pathology. As with any overuse injury condition, it should be emphasized that the
entire kinetic chain requires evaluation because ITBS may occur in combination with excessive genu varum, decreased
pronation and functional supination, cavus feet, heel varus, and compensatory forefoot abduction. The treatment for ITBS
involves strict counseling regarding running terrain and running surface choices. Runners with ITBS should avoid
cambered roads and hills. Rehabilitation should emphasize flexibility of the iliotibial band, hamstrings,
gastrocneius-soleus, and gluteus maximus musculature. Initially, a 1-inch lateral heel wedge may help alleviate
symptoms. Iontophoresis can provide a local antiinflammatory or anesthetic effect. Ultrasound (US) over this region
should be avoided, because it may exacerbate symptoms. Occasionally, injection or excision as described by Martens et
al. (41) is performed.
Proximal medial tibial pain is the next most common overuse condition of the knee. This condition is often confused with
other pathologies at the medial knee and may precede a medial tibial stress fracture. This condition is discussed later
with stress fracture syndromes.
Pes anserine bursitis has a similar presentation to proximal medial tibial pain; however, the pain is located more
posteromedially near the insertions of the medial hamstring group. This condition often occurs in conjunction with
excessive pronation. Iontophoresis, hamstring stretching, posterior tibialis strengthening, and functional drills that
emphasize eccentric hamstring muscle action are often beneficial. The presence of a medial stress fracture must be ruled
out if any doubt is present.
Quadriceps tendinitis is not usually seen in the running population. If this condition does occur, it should be managed in
a similar manner as anterior knee pain.
A rare condition in runners is popliteal artery entrapment syndrome. This condition is caused by the presence of an
anatomic variation of the gastrocnemius muscle that constricts the artery. Runners with this condition present with
intermittent claudication and decreased pulses of the dorsalis pedis, posterior tibial, and popliteal arteries. Diagnosis is
performed by biplanar arteriography, although magnetic resonance imaging (MRI) may be helpful in evaluating the
specific entrapments. Treatment is achieved through surgical release or arterial grafting.
Lower Leg
Styf and Kormer (42) used microcapillary infusion 133Xe clearance studies on 98 patients with chronic, exercise-induced,
anterior lower-leg pain. They reported that 26 patients had a documentable chronic compartment syndrome, 25 had
anterior compartment tenderness, 16 had posteromedial compartment tenderness, and 13 had a compression of the
superficial peroneal nerve. A total of 42% of these subjects also experienced tibial periostitis. Chronic compartment
syndromes most frequently involve the anterior and anterolateral compartments and, less commonly, the posterior tibial
compartments (43). Evaluation criteria using the slit-catheter method are considered to be positive when
intracompartmental pressures are greater than 15 mm Hg preexercise, greater than 30 mm Hg 1 minute postexercise,
and greater than 20 mm Hg at 5 minutes postexercise. Although more sophisticated catheter systems are available, the
criteria for diagnosis remains the same ( 44). Amendola et al. (45) employed MRI on four patients with chronic
compartment syndrome and noted that the T1 signal increased in 30% of chronic compartment syndrome cases.
However, this method was only 80% sensitive, with high variability. This technique allows simultaneous visualization of
all of the lower-leg compartments. As MRI techniques become more sophisticated, this method may become a useful
diagnostic tool. The use of EMG in biodynamic testing for chronic compartment syndrome is being evaluated.
Runners with a chronic compartment syndrome present with a history of a nonspecific lower-leg fullness and painful
pressure in the region of the involved lower-leg compartment. These symptoms occur at a specific moment during a
training session. These runners also report weakness or paresthesia along the distribution of the involved nerve. Anterior
compartment compression is associated with paresthesia over the dorsum of the foot, whereas posterior compartment
compression is associated with paresthesia over the instep. If the diagnosis is conclusive, the treatment is surgical.
However, stretching activities and the use of an air-stirrup with an anterior tibial pad may help reduce compartmental
pressure changes caused by periosteal traction. D'Ambrosia ( 46) attempted a nonoperative approach for approximately
15 weeks; however, surgical intervention was generally inevitable. Martens and Moeyersoons ( 47) found a 100% failure
rate in patients with compartment syndrome that they treated nonoperatively. Rorabeck ( 48) reported similar results.
Before surgical intervention, the runner should be carefully evaluated for an occult involvement within the deep posterior
or posterior tibial compartments. The omission of this diagnosis is the most common cause of failure following the
surgical release of the anterior or anterolateral compartments. Surgical release of chronic compartment syndromes is
generally performed through a single lateral approach or a combined lateral and medial approach. The lateral approach
provides easy access to the anterior and anterolateral compartments, whereas the medial approach can be used for
easier access to the superficial posterior, deep posterior, and tibialis posterior compartments. When using the lateral
approach, the surgeon may use a relatively large single incision or smaller double incisions to avoid injuring the
superficial peroneal nerve.
Following surgical intervention, Rorabeck et al. ( 49) reported approximately a 92% success rate for pain relief and
improved function. Detmer et al. (50) reported a 90% rate of cure, and Martens and Moeyersoons ( 47) reported a good to
excellent score for 85% of their patients who underwent fasciotomy. A portion of these positive results may represent the
surgical denervation of the periosteum in addition to the actual fascial compartment release.
Postoperatively, patients should receive ice, compression, and elevation to the involved extremity for approximately 48
hours. A gradual return to full weight-bearing ambulation generally takes 2 to 4 days. By the 5th postoperative day, the
patient may begin aquatic therapy, emphasizing range-of-motion exercises, and progressing through closed kinetic chain
functional activities. A dry land functional rehabilitation progression is initiated shortly thereafter, terminating with the
return to full activity by approximately 4 to 6 weeks following surgery.
The shin splint conundrum can be considered to be two distinct etiologies: (a)medial or posteromedial tibial stress
syndrome (MTSS), which is seen generally in those who pronate excessively, and (b) anterior or anterolateral stress
syndrome, which is more common among runners who have diminished dynamic shock absorption capability.
Runners with MTSS present pain over the distal third of the posteromedial tibia. Through cadaveric dissection, Michael
and Holder (51) located this area of tenderness in the soleus and in the investing fascia of the soleus. This finding was
substantiated by bone scintigraphy. Michael and Holder also reported a strong association between excess pronation of
the foot and MTSS. Cadaveric dissections demonstrated that the soleus is medially rotated 90 degrees to its insertion on
the calcaneus. This suggests that the soleus is a primary invertor of the subtalar joint in addition to being a primary
plantar flexor of the ankle ( 51). This information adds to the appreciation of the traction effect it undergoes in the
presence of excess subtalar pronation. D'Ambrosia et al. ( 52) believed that MTSS was attributable to hypermobility in the
posterior tibial musculature, which was most evident with manual muscle testing of the posterior tibialis muscle. Garth
and Miller (53) noted that runners with MTSS may develop a concomitant flexor digitorum longus overuse condition and
weakened intrinsic muscles of the foot secondary to keeping the toes in greater flexion at push-off. Radiographs of
runners with MTSS may show hypertrophy of the medial tibial cortex. Scintigraphy may show myositis and tendinitis,
which are differentiated by an increased blood pool phase.
Conservative treatment is generally aimed at improving flexibility, correcting biomechanical deficiencies, improving shock
absorption, and increasing the eccentric strength of antagonistic muscles. Nonsteroidal antiinflammatory drugs (NSAIDs)
should generally be avoided, because these may mask the progression to a definitive stress fracture. Occasionally,
iontophoresis with dexamethasone and lidocaine (Xylocaine) may alleviate symptoms. Garth and Miller ( 53) mentioned
the use of a special orthosis with a metatarsal pad attachment that facilitates toe-down during push-off. This device may
be indicated if atrophy of the intrinsic muscles of the foot is noted. Surgical intervention for this condition is infrequent in
the United States but is common in Scandinavia. A 2-mm posterior tibial margin surgical release probably serves to
denervate the periosteum. This surgical approach provides 80% to 100% pain relief ( 51).
Achilles tendinitis, although decreasing in frequency remains, a relatively common presentation among runners. The
plantarflexors of the ankle are the major power generators of the lower extremity during running. During running,
dorsiflexion range of motion increases, peak concentric work or power generation more than doubles, and peak eccentric
work or power absorption may quintuple (8). The initial clinical examination should rule out any friction of the Achilles
tendon on the heel counter of the running shoe. Runners who experience Achilles tendinitis often complain of pain that is
exacerbated by uphill running. Two contrasting etiologies may be factors in the occurrence of this condition among
runners: (a) greater shock transmitted through the Achilles tendon because of subtalar hypomobility and (b) greater
torque at the medial soleus because of subtalar hypermobility. Approximately 50% of runners who experience Achilles
tendinitis present bilateral symptoms, primarily at the musculotendinous junction region of the Achilles tendon, which is
several centimeters proximal to the calcaneus. Initially, a “creaking” peritendinitis may be palpated with dorsiflexion and
plantar flexion of the ankle. Over time, this condition progresses to a tendinosis with mucolipid degeneration and fibrinoid
necrosis (Fig. 36.6). Frequently, runners with Achilles tendinitis complain of increased symptoms when getting out of bed
in the morning, difficulty with stair climbing, and decreased push-off while ambulating. Partial tears of the Achilles tendon
are often missed during the initial clinical examination and are characterized by a sudden onset of pain, distinct
tenderness, and localized swelling. These findings help distinguish partial tears from peritendinitis and tendinosis.
Allenmark et al. (54) reported that 82% and 73% of runners with US or MRI-verified partial Achilles tendon tears
continued to have problems at 5 and 10 years after injury, respectively.
FIGURE 36.6. MRI view of Achilles tendon degeneration.
Treatment for acute peritendinitis includes flexibility and eccentric strengthening activities, NSAIDs, iontophoresis, ice
massage, 15-mm heel lifts, and a resting night splint. Furthermore, the runner is counseled regarding training and activity
modifications to diminish stresses at the injured area. If symptoms persist for more than 6 months, surgical intervention is
recommended. Surgery for a partial tear of the Achilles tendon includes excision of scar tissue and granulation tissue, as
well as an osteotomy of the calcaneal tuberosity if a Haglund deformity ( Fig. 36.7) is viewed on a lateral x-ray study.
FIGURE 36.7. Haglund's calcaneal deformity.
In cases in which a Haglund deformity is present, it is common to locate pain and swelling anterior to the Achilles tendon
from the retrocalcaneal bursa. Retrocalcaneal bursitis may respond to conservative local treatments such as
iontophoresis or the injection of a corticosteroid and local anesthetic combination. When retrocalcaneal bursitis is
present in combination with Achilles tendinitis, a surgical approach, as described by Leach and Hammond ( 55), is
recommended. This approach involves a medial incision bursectomy and excision of the posterosuperior angle of the
calcaneus. Leach and Hammond reported an excellent to good rating for 88% of peritendinitis cases, as opposed to in
situ suture (73%), flap (88%), and retrocalcaneal bursal excision (71%). However, a 6% incidence of skin necrosis was
reported with this technique. A posterior longitudinal incision should only be used if there is substantial degeneration
within the tendon or if a medial or lateral approach would not provide adequate visualization of the injured area.
Postoperative management begins with a walking cast locked at 10 degrees of plantarflexion for 2 weeks and progresses
to a shoe with a 1-cm heel lift for 3 weeks. Flexibility exercises and progressive functional training are begun judiciously
following the 2nd postoperative week; however, this period varies with the amount of tissue that was excised.
Runners account for 69% of all stress fractures either through high stresses on normal bone or normal to high stresses
on weakened bone. Grimston et al. (56) reported that the development of stress fractures was not associated with
reduced bone mineral density. Leg-length discrepancy, gait abnormalities, poor running terrain, poor running surface,
and the presence of poorly rehabilitated and conditioned previous injuries can predispose the runner to stress fractures.
Cook et al. (18) believed that only 22.4% of all stress fractures were associated with training errors and that the affected
area was equally distributed throughout the body. These findings, however, contrast greatly with several other reports.
McBryde (44) reported that stress fractures occur mostly in the tibia (34%) but may also occur in the fibula (24%),
metatarsals (18%), femur (14%), pelvis (6%), and other bones (4%). Giladi et al. ( 57) noted decreased medial tibial width
and proposed that this was the biomechanical cause of stress fracture. Scully and Besterman ( 58) documented the
response of bony tissue to stress among military recruits. During weeks 1 and 2, increased osteotropic osteoid formation
takes place, but tissue strength does not increase. Over weeks 3 and 4, tissue strength gradually increases; however, the
rate of strength increase in bony tissue is slower than that for muscle tissue. Scully and Besterman noted that by
eliminating jump training during week 3 of recruit conditioning the incidence of stress syndromes decreased from 4.8% to
1.6%. This supports the concept of an adaptive period of bone remodeling, during which its load tolerance improves.
Stress fractures that occur on the tension side of a bone or in regions of poor vascularity have a poor prognosis. This
type of stress fracture may occur at the anterior tibial cortex, femoral neck (tension side), proximal fifth metatarsal, and
tarsal navicular. Stress fractures generally present a focused pain, in contrast to the rather diffuse pain seen with a
MTSS. The single-leg broad jump functional test is usually positive if a stress fracture is present.
Stress fractures of the femoral neck and of the fifth metatarsal (Jones fracture) often require surgical intervention. The
most common stress fracture occurs at the medial tibia. It is generally managed with an air-stirrup with an anterior pad
until focal tenderness ceases ( Fig. 36.8). A functional rehabilitation progression, including alternative cardiovascular
conditioning and aquatic therapy should be implemented within symptom-free limits, then the runner should be gradually
returned to training activities. Low dye taping may be useful when one is rehabilitating or conditioning the runner who has
experienced a Jones fracture.
FIGURE 36.8. Air-stirrup with anterior pad.
Heel
Runners often report heel pain. The etiology usually involves the plantar fascia. It must be emphasized, however, that
central heel syndrome, calcaneal stress fracture, and nerve entrapment should also be considered.
Plantar fascitis usually represents a microtraumatic tearing of the medial cord of the plantar fascia, and it has been
reported in runners with both cavus and planus feet. Runners with plantar fascitis present decreased static and dynamic
range of motion at the knee, ankle, and first toe, in addition to overall decreased lower extremity strength ( 59). However,
it remains unclear whether these deficits arise as a result of plantar fascitis. It should again be emphasized that the entire
kinetic chain should be evaluated. Runners with plantar fascitis complain of excruciating heel pain with their first step on
arising from bed in the morning. This pain is increased by a sleeping posture displaying a flexed hip, knee, and
plantarflexed ankle. Pain from plantar fasciitis is located at the insertion of the medial cord of the plantar fascia on the
calcaneus. This is contrasted with central heel syndrome, which presents with central heel pain ( Fig. 36.9).
FIGURE 36.9. Non–weight-bearing (A) and weight-bearing (B) views of the heel fat pad.
Treatment for plantar fasciitis may include NSAIDs, iontophoresis, flexibility exercises for the plantar fascia, and
strengthening exercises for the intrinsic muscles of the foot and the muscles of the lower leg. The single most effective
treatment for plantar fasciitis has been the resting night splint, which the authors have used for many years. This
treatment has recently been documented by Wapner and Sharkey ( 60). D'Ambrosia (61) reported good results with
orthotic intervention for runners who pronate excessively but poor results for runners with cavus feet. This finding was
supported by Gross et al. ( 62) in their evaluation of 500 long-distance runners.
For central heel pad syndrome, the injection of the injured area with a corticosteroid is not advised because of
subsequent fat pad atrophy. If surgical intervention is necessary, no more than 33% of the fascia should be released
(63). Approximately 20% of runners with chronic heel pain may have an underlying nerve entrapment ( 64).
Functional nerve disorders deserve consideration when the pain presentation is atypical, such as complaints of radiating
paresthesia or sudden electric shock–type sensations. However, this condition may also present with persistent
toothache-type pain. Close interaction with a skilled electromyographer is necessary to evaluate the signs of functional
nerve entrapment. MRI can be useful in exposing edema within the nerve sheath, as noted with posterior tibial nerve
entrapment.
Diagnosis
As emphasized by Renstrom and Johnson (13), any overuse running injury should be regarded as a manifestation of
kinetic chain dysfunction, and the entire chain must be examined to rule out any asymptomatic injury or dysfunction.
Obtaining a pertinent injury history is an important factor in determining present injury etiology.
The comprehensive evaluation of a runner must include the areas of orthopedic sports medicine, sports physical therapy,
biodynamic, and physiologic concepts. The area of biomechanics that studies the relationship between motion and the
forces affecting motion is biodynamics. In the next decade, an even greater marriage among biodynamic concepts, and
orthopedic sports medicine, and sports physical therapy will occur, as each area recognizes the benefits that can be
derived from the others' expertise (65).
Although any structural assessment should include the entire body, the emphasis of the structural assessment of a
runner should be on the musculoskeletal system of the lower extremities and back. This assessment should include static
and dynamic postural alignment, flexibility, and anthropometry. The data from this assessment provides a basis for
determining the effect of body posture on movement, musculature activity, forces, moments, power, pressure, and
metabolic activity.
Static posture should always be evaluated in the frontal and sagittal planes. Deviations in the transverse plane are more
difficult to identify but must also be considered. The frontal plane should reveal symmetry of the shoulders, pelvis, hips,
knees, and ankles as well as the angle of toeing in or toeing out. Hip anteversion and retroversion, genu varus and
valgus, and the magnitude of subtalar pronation also can be appreciated. A low incidence of running injuries is seen with
genu varus of less than 8 degrees; however, an increased incidence is seen when genu varus is greater than 18 degrees
(66). Excessive pronation may be physiologic or secondary to tibial varus of more than 10 degrees, functional equinus,
talar varus, and forefoot supination ( 66). Sagittal plane analysis assists in the identification of abnormalities in the truncal
posture or carriage of the runner. The segmental relationship of the major joints to a plumb line is well recognized ( 67).
Although static alignment provides clues to identify dysfunction, it must be emphasized that the body is in a constant
state of omnidirectional, triplanar motion. Static postural findings may or may not correlate with those noted during the
dynamics of walking or running. When an evaluation of each subphase of the gait cycle does not reveal abnormal
findings, other means should be used. One interesting concept is to use myriad exaggerated functional activities ( 68). By
using dynamic activities such as excessive knee flexion or “Groucho walking,” excessive trunk rotation, increased pelvic
translation, and increased stride length, deficiencies in flexibility, strength, and stability may be accentuated. Obscure
abnormalities may be further exposed through the technologic capabilities of a biomechanics or biodynamics laboratory.
A comprehensive evaluation of the entire lower quadrant is essential. However, during this evaluation, attention should
be focused primarily on the foot and ankle. Abnormalities in the foot can affect the mechanics of the ankle, knee, hip, and
lower back. Neutral subtalar position is of clinical significance because this is considered to be the position of optimal
function (69). Neutral subtalar position is identified through palpation of talonavicular congruency. There should be a
slight (3- to 4-degree) varus relationship between the bisection of the distal third of the lower leg and the perpendicular
bisection of the calcaneus. The bisection of the calcaneus should be perpendicular to the line of the metatarsals, and the
metatarsal heads should be in line with one another. Integrity of the medial longitudinal arch is assessed by the navicular
drop test, or Feiss line, which is formed by the tip of the medial malleolus, the navicular tuberosity, and the first
metatarsophalangeal joint (70). Normally, the navicular tuberosity should be intersected by the Feiss line.
Neutral subtalar position is considered to be the norm. The two extremes of this continuum are represented by pes
planus and pes cavus. Pes planus, or so-called flatfoot, results in excessive pronation through midstance. Excessively
weighted rearfoot valgus and compensatory internal rotation of the tibia often occur in conjunction with hypermobility of
the subtalar joint during running. This interaction can predispose the runner to injuries at the medial aspect of the lower
extremity. These injuries may include medial tibial stress syndrome; posterior tibial tendinitis; pes anserine tendinitis and
bursitis; and stress fractures of the tibia, fibula, and tarsal bones; Achilles tendinitis; and plantar fasciitis ( 20,71,72). This
is contrasted with the cavus, or high-arched, foot. The cavus foot presents decreased subtalar motion with resultant
decreased mobility of the midfoot and excessively weighted rearfoot varus. The heel of the cavus foot remains in varus at
foot strike, the longitudinal arch is maintained, and the foot remains in a locked, rigid posture. Concurrently, the tibia
remains in external rotation, resulting in a net increase of stress transference from the ground throughout the midstance
phase of running. The reduction of internal tibial rotation increases the stress on the lateral aspect of the foot and lower
extremity; therefore, a pattern of lateral injury is seen. These injuries may include iliotibial band syndrome, trochanteric
bursitis, stress fracture, Achilles tendinitis, peroneal muscle strain, plantar fasciitis, and metatarsalgia ( 29,71,72).
Mobility of the great toe should be assessed with the first ray stabilized. Restriction of the great toe, or hallux limitus, can
affect push-off and promote the development of early arthritic changes, sesamoiditis, and metatarsalgia ( Fig. 36.10).
These problems can be treated effectively with the use of a Morton's extension to assist push-off and metatarsal pads to
unload areas of excessive stress.
FIGURE 36.10. Hallux rigidus.
Diagnostic Imaging
Only recently has image evaluation played a significant role in the evaluation of overuse injuries. Conventional
radiography is obtained to exclude bony pathology; however, 66% of radiographs are initially negative for stress fractures
and only 50% ever develop radiographic evidence of stress fractures related to running ( 73). A stress fracture may
become evident when new periosteal formation, endosteal thickening, or a radiolucent line is observed. Occasionally,
tomograms may be helpful in delineating a tarsal navicular stress fracture. As with any pathologic bony condition,
however, radionuclide imaging is more sensitive than radiography ( 74).
A triple-phase bone scan may be particularly useful in differentiating soft tissue abnormalities masquerading as stress
fracture or vice versa (75). The three phases of a triple-phase bone scan are the angiogram, blood pool, and delayed
image phase. Stress fractures are positive for all three phases of the bone scan. In contrast, shin splints are negative for
the angiogram and blood pool studies. Plantar fasciitis and calcaneal bursitis also present particular patterns that are
distinct from calcaneal stress fractures. The use of serial bone scans to evaluate treatment has been proposed with a
characteristic progression noted from diffuse uptake early in the stress reaction to sharp fusiform demarcation in
advanced stages (76).
The roles of US and computerized tomography (CT) are limited in demonstrating injuries to tendons and muscles, unless
complete discontinuity has occurred ( 77). Standard radiography may be helpful in evaluating accessory ossicle and
osteophyte impingement. In addition, a modified zero radiogram is helpful in the evaluation of the heel pad fibrosepta
when one is attempting to differentiate central heel syndrome from plantar fasciitis.
The role of MRI, although secondary to clinical evaluation, is adding greatly to the understanding of intrinsic bony and
soft tissue pathology. The high intrinsic contrast and spatial resolution of MRI enables a detailed anatomic differentiation
of abnormal and normal structures. These capabilities present tremendous potential applications in the sports medicine
arena. MRI is particularly useful in providing a detailed assessment of intrinsic abnormalities in tendons, especially at the
knee and ankle. However, the use of MRI requires a strong clinical correlation and interaction with a skilled radiologist
because special views may be required. An example of this is the modified coronal oblique imaging for cases of
suspected posterior tibial tendinitis ( 78). The role of MRI in the sequential evaluation of stress fractures and soft tissue
healing has not yet been clearly defined.
MRI has also been useful in the evaluation of entrapment neuropathies. As many as 60% of all entrapment neuropathies
occur among the running or jogging population ( 79). This entity should be considered when atypical, chronic, or
recalcitrant pain exists, particularly around the heel and foot. The etiology of this pain is often dynamic, with the only
finding being edema around the nerve, which is not found at the contralateral extremity ( Fig. 36.11).
FIGURE 36.11. MRI view of tibial nerve compression.
EMG and nerve conduction tests are often unremarkable, unless performed in a dynamic model ( 79). Therefore, standard
EMG and nerve conduction tests that appear to be normal do not preclude a diagnosis of entrapment neuropathy. In
conclusion, radiologic and neurologic studies have a role in the evaluation of a runner's injury, however, they are
considered secondary to a thorough clinical evaluation.
Soft Tissue Extensibility
Flexibility, hereafter referred to as extensibility, and joint range of motion are often used interchangeably, but a distinction
is warranted. Range of motion refers to the amount of movement about a joint. Extensibility refers to the holistic ability of
the soft tissue to elongate through a range of motion ( 80). Maintenance of an adequate range of motion and soft tissue
extensibility following injury is critical, because connective tissue may develop scarring, adhesions, and fibrosis. The
proliferation of shortened connective tissue can result in the development of a chronic muscle strain cycle.
Soft tissue running injuries are specific to the microtrauma caused by repetitive submaximal loading of musculotendinous
structures. Most strains occur at the musculotendinous junction because it is the weakest link of the myotendinous
structural unit (81). Potential etiologies may include increased collagen content, decreased local extensibility, and the
presence of a transitional area of two histologically different tissue types. This is in agreement with the abundance of
strains to the gastrocnemius-soleus complex, hip adductors, and hamstring musculotendinous junction observed
clinically.
Evaluation of soft tissue extensibility should include all major muscle groups of the lower extremities and lower back.
Documentation of initial findings is necessary, and periodic comparison may provide motivation to the runner. Gross
assessment of the lower back and hips may include the sit-and-reach ( Fig. 36.12) and standing fingertips to floor tests.
Specific evaluation of hamstring length can be accomplished by a supine straight leg raise ( Fig. 36.13), a 90-degree hip
flexion-knee extension maneuver (Fig. 36.14), or a seated-knee extension while maintaining a lordotic posture ( Fig.
36.15). Care should be taken to assess lumbopelvic substitutions. Two common tests that assess hip flexor and iliotibial
band extensibility are the Thomas and Ober tests, respectively ( Fig. 36.16 and Fig. 36.17). The standing hip-drop test is
also useful in identifying muscle extensibility and strength imbalances around the hip ( 82) (Fig. 36.18). The hip rotators
may be evaluated in a prone position with the knees flexed at 90 degrees ( Fig. 36.19). Gastrocnemius extensibility can
be determined by passively dorsiflexing the ankle with the knee extended ( Fig. 36.20). Soleus extensibility can be
determined in a similar fashion, but with the knee slightly flexed ( Fig. 36.21). Any side-to-side asymmetry found on
examination may represent an abnormality that necessitates further evaluation ( 83).
FIGURE 36.12. Sit and reach test.
FIGURE 36.13. Supine straight leg raise test.
FIGURE 36.14. The 90-degree hip flexion-knee extension maneuver.
FIGURE 36.15. Seated knee extension.

FIGURE 36.16. Thomas test.
FIGURE 36.17. Ober test.
FIGURE 36.18. Standing hip-drop test.
FIGURE 36.19. Hip rotation assessment.
FIGURE 36.20. Gastrocnemius extensibility assessment.

FIGURE 36.21. Soleus extensibility assessment.
Innovations in biodynamic analysis are rapidly adding to the understanding of the etiology of running injuries. Individuals
that treat runners should stay current with these innovations and implement them when indicated.
Treatment
Functional Rehabilitation
Both acute and chronic running injuries should initially be managed with the traditional rest, ice, compression, and
elevation (RICE) to diminish pain and inflammation ( 84). NSAIDs appear to decrease inflammation and promote
analgesia while enhancing the return to functional activities and preventing reflex inhibition. Adverse gastrointestinal
affects are common with prolonged use of NSAIDs. Because of this, a greater emphasis on local and topical NSAIDs in
the form of lotions, ointments, and sprays will likely appear in the near future. The therapeutic effect of US,
phonophoresis, iontophoresis, electrical stimulation, and cryotherapy for the treatment of pain and inflammation is well
documented (84,85). Iontophoresis is superior to US and phonophoresis in the treatment of relatively superficial soft
tissue inflammatory conditions, especially when osseous tissues are in the proximity. Several combinations of analgesic
and antiinflammatory agents have been suggested, depending on the primary treatment objective ( 86).
As pain and inflammation are controlled, active mobility and extensibility of the involved tissues should be initiated within
symptom-free limits. The exacerbation of any symptom related to the injury site should be interpreted as an indication
that the rehabilitation progression is too rapid, the rehabilitation program was poorly designed, something was missed
during the initial evaluation, or the runner is noncompliant with the program. Because temperature has been shown to
have a profound influence on the viscoelastic properties of connective tissue, a warmup period before the performance of
stretching activities is recommended. Although conventional modalities such as hydrotherapy, hot packs, and US may be
effective in increasing tissue temperature, a 10- to 15-min session of low-to-moderate-intensity stationary cycling or
walking is equally effective.
Traditionally, proper stretching is taught as a low-intensity, long-duration, static stretch. The optimal number of repetitions
and duration of each stretch remains controversial. One recent study that used an animal model found that 80% of total
tissue elongation occurred by the fourth repetition, with the greatest length increase occurring during the initial 12 to 18
seconds of each stretch (87). This study supplies valuable information concerning the mechanical properties of the
musculotendinous unit. However, the study did not account for the added difficulty of stretching muscles that act across
multiple joints, the components of functional muscle groups that present divergent sites of insertion, or the learning of
proper technique.
A recommended stretching routine is three to six repetitions of 15 to 20 seconds' duration, with total repetitions
depending on the functional muscle group being stretched, the ability of the runner to perform the stretch properly, and
the amount of warmup before stretch performance. The amount of force during stretching should be subjectively
moderate. Static stretching is considered to be safe and can be performed practically anywhere without assistance.
Ballistic stretching attempts to improve extensibility by incorporating gentle bouncing into the stretch. The viscoelastic
properties of muscle and the stretch reflex make this technique potentially dangerous if it is performed by poorly
conditioned runners. Ballistic stretching is also potentially dangerous if it is performed on a joint before dynamic
stretching has resulted in maximal range of motion. Because this is considered to be an advanced technique, it should be
performed only after subjectively adequate muscle extensibility has been attained through a static stretching program.
This method of stretching focuses on the reciprocal action of agonist and antagonist rather than on an isolated muscle
group. Dynamic stretching is a useful, but underused rehabilitation tool. It is effective in treating chronic hip adductor,
hamstring, and gluteal strains. Examples of this type of stretching include standing hip flexion and extension ( Fig. 36.22)
and stepping over or under a series of hurdles ( Fig. 36.23). Dynamic stretching has the added beneficial component of
improving joint and muscle kinesthetic and proprioceptive awareness.
FIGURE 36.22. Hip flexion (A) and extension (B) dynamic stretching.
FIGURE 36.23. Hurdle stepping dynamic stretching involves (A) moving over the hurdle in a figure eight motion and (B)
ducking under the hurdle.
Proprioceptive neuromuscular facilitation (PNF) is a skilled method of promoting neuromuscular activity through a series
of quick stretches in functional movement patterns. PNF is frequently used in running rehabilitation programs as a
method of manual resistance and also has been shown to improve extensibility ( 88). The disadvantage of this method of
stretching is that it generally requires the assistance of a trained professional.
In addition to pain control, inflammation control, and the return to improved mobility and extensibility, a cardiovascular
maintenance program should be initiated. An upper body ergometer may be used immediately. The maintenance of
cardiovascular conditioning is an essential component of the total rehabilitation program. As healing progresses,
stationary cycling, stepping, rowing, stair climbing, or cross-country skiing devices may be used. Few running injuries
require absolute rest from activity. It should be emphasized, however, that it is imperative to minimize reinjury risk factors
when planning a rehabilitation and conditioning program. In order to work effectively, specific programs should be
designed to simulate the demands of the runner's training regimen.
Once pain and inflammation have resolved, causative factors have been eliminated, and biodynamic limitations such as
poor musculotendinous extensibility or a leg-length discrepancy have been addressed, a functional rehabilitation plan
can be initiated (89). Eccentric muscle action is an important component of this plan when treating the injured runner. The
intense eccentric action of the knee extensors during the stance phase of running has been closely associated with the
development of tendinitis and muscle injury ( 81). Running incorporates a rapid role reversal of the knee extensors and
the calf musculature from dynamic shock absorbers following impact to propulsive force generators following midstance.
The eventual magnitude of these propulsive forces are largely mediated by eccentric muscle action. The specificity
principle of rehabilitation suggests that because the lower extremity normally functions through the synergistic action of
multiple muscle groups, exercises that enhance this action are desirable. However, there are instances in which select
isolated components (weak links) of the kinetic chain require specific attention such as isolated exercises for the intrinsic
musculature of the feet. A rehabilitation and conditioning program for most runners should emphasize progressive
resistance and range-of-motion squats and multidirectional lunges and step-ups. Each movement is performed for
approximately two to five sets of 10 to 25 repetitions. Progressive resistance is included with these activities; however,
proper technique is obligatory, and each set is terminated at the onset of faulty technique.
Each of the tools previously mentioned as cardiovascular devices may be used to train the anaeorbic capacity of the
runner. The performance of multiple anaerobic “bursts” from 10 seconds to 2 minutes in duration help simulate the
demands of their event. Intervals of shorter duration are more appropriate for sprinters, whereas longer duration intervals
more effectively train the middle or long-distance runner. Cross-country skiing machines most effectively train the hip
extensors and ankle plantarflexors.
Sliding boards provide total lower-extremity rehabilitation with emphasis on the eccentric action of the hip abductors and
adductors, whereas the knee extensors and flexors simultaneously act as hip and knee stabilizers. Running against
rubber tubing resistance can provide variable resistance for strength and stabilization activities in a variety of functional
positions. Each of these activities may be performed for two to five sets of 10 seconds to 2 minutes duration.
The biomechanical ankle platform system (BAPS) (Camp International, Jackson, MI) is an effective rehabilitation tool that
can supplement the rehabilitation plan of most running injuries from initial intervention through terminal rehabilitation and
conditioning. This device was designed with the triplanar motion of the foot and ankle in mind and is useful for
proprioceptive training of this area. This activity is performed for two to three sets of 10 to 30 repetitions. Performing
activities such as these without shoes further strengthens the intrinsic musculature of the foot, thereby improving dynamic
impact dampening (90).
Injured runners who rehabilitate in a manner that closely replicates the demands of their event should progress to a
running program sooner. No matter how well designed a rehabilitation or conditioning program is, neglecting structural
abnormalities of the lower extremity or lower back will probably result in an unsatisfactory outcome. In particular, a
thorough static and dynamic assessment of the feet is encouraged. The emphasis of any rehabilitation program should
be on the promotion of a normal ratio between the agonist and antagonist musculature. For example, runners frequently
present hamstring dominance, and over time, develop a relatively atrophic quadriceps femoris. A proper rehabilitation
program should improve this relationship.
Orthotics
Normally, the relationship between the rearfoot and forefoot is such that when the rearfoot is in a subtalar neutral
position, the forefoot is situated transversely to the long axis of the calcaneus. In pathologic conditions, this condition
may be altered (12). Orthotics may be used to (a) control excess mobility, (b) unload a specific region of the foot, (c)
improve the relationship of the forefoot and rearfoot, and (d) enhance shock absorption.
When treating the excessively mobile foot of a runner who pronates, the physician must determine both the maximal
pronation range of motion and the maximum velocity of pronation that occurs during the stance phase. The maximum
velocity of pronation can be controlled more effectively by orthotics. Fortunately, this parameter is believed to be of more
importance to injury prevention ( 91). Orthotics have been reported to decrease the rate of pronation by 20% to 70%
(91,92). When treating the relatively hypomobile foot of runners who supinate, the physician may find orthotic intervention
that emphasizes shock absorption to be useful. In either condition, posting may be used to improve the forefoot and
rearfoot relationship.
Runners are generally satisfied with their orthotics, although minor adjustments are often necessary. When orthotics are
issued, a dialogue should be maintained to solve problems and evaluate their long-term effectiveness. Further research
regarding orthotic and footwear design using recently developed devices such as capacitive pressure distribution
platforms that can be inserted into the running shoe is recommended ( 93).
Return to Running
Returning the injured runner to his or her preinjury level is a complex process. In addition to safely restoring the
physiologic and psychological readiness of the runner, care must be taken to avoid reinjury ( 94). Communication
between the runner, coach, and health professionals is vital to prevent training errors. Any return to a running program
should be goal oriented. By involving the runner in goal planning, the runner's mental outlook will be improved and
discouragement caused by the initial absence of competitiveness can be diminished ( 95). This involvement also
increases the likelihood that the runner will have confidence in the program and, therefore, be more willing to comply.
Taking these factors into consideration, the concerned personnel can initiate an individualized return to running program
that incorporates variable portions of anaerobic and aerobic training based on the specifics of the runner's event. Initially,
the following program is recommended: a pace progression from slow to fast, a frequency progression from alternate
days to 4 or 5 days per week, and progressive interval training approximately 6 weeks following injury. Before returning to
running, the runner should be advised on proper footwear, the avoidance of certain running terrain such as hills, the
importance of an adequate warmup, and the importance of compliance with the functional rehabilitation, and conditioning
program such as stretching.
Conclusions
As the popularity of running continues to grow, it is likely that an increased incidence of running injuries will occur.
Through the implementation of a thorough static and dynamic clinical examination, the use of innovative imaging
techniques, and the acquisition of physiologic and biodynamic data, researchers' diagnostic capabilities are greatly
enhanced. This information enables the development and optimal use of functional rehabilitation programs, conditioning
strategies, coaching strategies, and orthotics. However, the clinical examination, including a thorough injury history and
open communication, will always be the most important component in the treatment of the injured runner.
PART 2: ORGANIZATION AND ADMINISTRATION OF MEDICAL COVERAGE FOR ROAD RACES
Recreational running is one of the most popular sporting activities in America. The popularity of this sport can be traced
back to Frank Shorter's emotional victory in the 1972 Olympic marathon. With more people becoming involved in
recreational running, the variability of participants seen at competitive road races has increased. It is not unusual, at least
at the beginning of a race, to see professional athletes running side by side with novice runners. The shear number of
participants and the vast disparity in their training techniques have made adequate medical support at road races
essential.
The percentage of runners who will require medical attention as a result of racing depends largely on environmental
conditions and the distance of the run. Injury rates may vary from about 0.1% to 20% of runners treated. The author's
experience with the medical coverage of marathon races in Pittsburgh from 1988 to 1992 has included races run in wet
bulb globe temperatures ranging from 38° to 84°F (2° to 26°C). Injury rates in Pittsburgh have ranged from 9.6% to 21.8%
of runners requiring medical treatment ( 96).
The coordination, training, and supervision of medical personnel is necessary to provide proper medical care to the
runners. The goal of medical support should be to minimize the potential dangers associated with road racing. These
dangers can be minimized through the proper organization of medical personnel, equipment, and supplies. The medical
support staff should also promote runner education, injury prevention, and proper preparation for event participation.
Organizing Committee
The medical support for a road race must include components of both emergency medicine and sports medicine. In
reality, preparing for the medical support of thousands of runners is similar to disaster planning. To ensure optimal care,
the medical support should be recruited early in the planning of the event. A medical director should be appointed to
coordinate and supervise the medical team. A medical doctor should most likely serve as the medical director for a race.
He or she should be knowledgeable in exercise physiology and specific medical concerns of runners. The medical
director must work closely with the race director to coordinate adequate medical support. He or she will be responsible
for all medical questions that may arise regarding the participants in the race.
Depending on the number of participants and the distance of the race, a medical operations manager or coordinator
should be designated by the medical director. The medical operations manager should assist the medical director in
securing volunteers and providing logistical help in covering the event. The medical operations manager should
preferably be an emergency medicine technician (EMT), triage nurse, or a sports medicine professional [certified athletic
trainer (ATC) or physical therapist (PT)]. He or she should have knowledge in the appropriate personnel, as well as the
equipment and supplies needed for the race.
A medical organizing committee should be formed for each race event. The committee should consist of the medical
director, race director, medical operations manager (if applicable), representatives from the local emergency medical
service, representatives from the police force, and a medical communications coordinator. The committee should meet
before the event to discuss important issues such as the race date and time, recruitment of medical personnel,
recruitment of supplies, runner education programs, and racecourse coordination. A reasonable time limit should be
designated for the racecourse (6 hours for a marathon).
The medical organizing committee should carefully consider the time and date of the event. Local weather history should
be used to avoid unacceptable levels of environmental extremes. Races should avoid the hottest summer months and the
hottest part of the day. The American College of Sports Medicine ( 97) recommends that “all summer events should be
scheduled for the early morning, ideally before 8:00 am, or in the evening after 6:00 pm, to minimize solar radiation.”
However, caution also should be taken in early fall and late spring races because great variations in local temperatures
may occur.
Team Personnel
Medical personnel should include medical doctors with an expertise in emergency medicine, sports medicine,
orthopedics, or primary care. Nursing personnel, especially trauma and surgical nurses, are required. Podiatrists should
be included to handle foot and ankle concerns. Certified athletic trainers (ATCs) and physical therapists (PTs) with
experience in working with injured runners should also serve on the medical team. Massage therapists, primarily those
skilled in sports massage, may be included. Additional volunteers serving as recorders for the medical team are useful on
race day. The recorders should be responsible for the documentation of all runners' injuries treated at the event, as
instructed by the members of the medical team.
To secure needed volunteers, members of the medical organizing committee should contact local hospitals and local
medical organizations. In addition, mailing lists of various professionals can be obtained from local and state allied health
organizations. Recruitment letters can be a successful way to enlist potential volunteers. Volunteer recruitment forms
should include needed demographic information, expertise and experience, and desired location and assignment for the
race day. It also may be beneficial to know which volunteers are capable of starting an intravenous line. Medical
volunteers should be questioned on their individual professional liability insurance. Liability insurance that is provided for
sanctioned events does not cover medical personnel. At present, there has been no reported litigation brought on by a
competitor regarding the medical care rendered at a road race. However, professional liability should always be
considered as an important issue. Each medical volunteer should inform his or her professional liability insurance carrier
or employer of his or her intent to serve as a medical volunteer at a road race.
All medical volunteers should be clearly instructed that they are under the direction of the medical director. Specific job
responsibilities and guidelines should be provided to each medical volunteer before race day. If possible, an orientation
program should be provided for the medical volunteers. This program should include aid station reporting, aid station
closing times, racecourse opening and closing times, overviews of the medical support for the race, proper injury
management/documentation, and a review of the current Occupational Safety and Health Administration (OSHA)
standards of universal precautions for the handling of blood and body fluids ( 98). All volunteers should be given some
type of credential that clearly identifies them as members of the race medical team. In addition, clearly marked medical
volunteer T-shirts and hats can be used for easy identification.
The Athletics Congress/USA (TAC), now called USA Track and Field, has published a manual that provides an overview
of medical care for long-distance road races ( 99). The TAC manual recommends 5 to 10 professional and 5 to 10
nonprofessional volunteers per 1,000 runners, depending on the race distance and type of course. Fewer volunteers are
recommended for a 10-K or an out-and-back course. For the Pittsburgh Marathon, which averages 3,500 runners, the
medical team will number between 80 and 100 volunteers. These figures include both medical personnel and nonmedical
personnel.
The level of care provided by the medical team should include basic cardiopulmonary resuscitation (CPR), advanced life
support (ALS), treatment of environmental injuries, first aid treatment for orthopedic and podiatric problems, general
medical considerations associated with road racing, and facilities for physically challenged competitors, if appropriate
(99).
Communications
A medical communications system should be coordinated by the medical organizing committee. The principal function of
the medical communications system is to relay information regarding runners who require immediate medical attention.
The communications system should also function to relay necessary information such as weather conditions to the
medical director. This system can be used to track runners who have received medical attention at an aid station or who
are on a dropped-out runner vehicle after dropping out of the race.
The use of amateur (ham) radio operators or vehicles equipped with citizen band (CB) radios is recommended. The radio
operators should be placed every 1 to 2 miles on the racecourse. Ideally, a radio operator should be positioned at the
start of the race, at each medical aid station on the racecourse, and at the finish line. A radio operator should also be
placed in all dropped-out runner vehicles. Cellular phones or long-range pagers can be used by the medical organizing
team on race day to facilitate communications.
The communications system should interface with race operations, local emergency medical services, and the local
police force. All communications should be coordinated through a centralized command center, which should be located
at the finish line ( Fig. 36.24). If possible, mobile radio operators should shadow the members of the medical organizing
committee so important communications between those parties can be expedited. This setup should provide the medical
communications manager with immediate access to the medical director. Any additional radio operators can serve as
medical spotters at various locations on the racecourse.
FIGURE 36.24. Ham radio operators in communications command center at finish line. (Courtesy of the University of
Pittsburgh Medical Center.)
The medical communications manager should notify all local hospital emergency rooms of the date and time of the race.
This will prepare the hospital staffs for any seriously injured runners who may be brought into their facilities. In addition,
this will facilitate communication with emergency rooms when verifying the status of any injured runners that are treated.
Aid Stations
Medical aid stations should be located at the start and finish lines for all road races. The finish line medical area should
be large enough to accommodate many runners as well as spectators. For a 10-K race, there should also be at least two
aid stations on the racecourse. For races longer than 10-K, additional aid stations should be located at least every 2
miles. At the Pittsburgh Marathon, aid stations are located every 2 miles for the first 10 miles of the racecourse and then
approximately every 1 mile until the finish line ( Fig. 36.25).
FIGURE 36.25. Medical aid station on a marathon racecourse. Courtesy of the University of Pittsburgh Medical Center.
Aid stations should be clearly marked with appropriate signs. The aid station signs should be positioned on posts above
eye level so that they can be viewed easily. To assist runners needing medical attention at the aid stations, warning
signs that say “Aid 100 Yards Ahead” can be placed on the racecourse ( Fig. 36.26).
FIGURE 36.26. Sign to notify runners of upcoming medical aid and fluid stations. Courtesy of the University of Pittsburgh
Medical Center.
Noble and Bachman (100) recommend a team of at least three medical personnel consisting of physicians, podiatrists,
nurses, or EMTs at each medical aid station per 1,000 runners. In addition, each aid station may include an orthopedist
or podiatrist, or both. At least two physical therapists or athletic trainers should be present at each medical aid station to
assist with minor musculoskeletal problems.
The personnel requirements for the Pittsburgh Marathon also take into account the injury data that demonstrates a
significant increase in the number of runners treated on the racecourse after mile 15. As a result, the personnel
requirements for medical aid stations after mile 15 are approximately twice the number recommended by Noble and
Bachman.
The finish line medical area should have one triage officer for races with more than 1,000 participants. The finish line
medical area should also have a team consisting of at least four to six primary care or emergency room physicians,
nurses, or EMTs for every 1000 runners. At least 20 physical therapists or athletic trainers should be needed at the finish
line medical area.
At the Pittsburgh Marathon, the finish line area consists of a 40 by 100—foot tent that houses three medical areas: acute,
general, and sports medicine. Three triage physicians evaluate each runner as he or she enters the medical tent. On the
results of the evaluation, the runners are moved to the appropriate medical area ( Fig. 36.27).
FIGURE 36.27. Finish line medical area at the Pittsburgh Marathon. Courtesy of the University of Pittsburgh Medical
Center.
Medical escorts should also be placed in the finish line chutes. These escorts should be medically trained personnel able
to properly triage the runners ( Fig. 36.28). Parallel chutes between the runners' chutes should be planned so that the
medical escorts have access to the runners. Approximately 10 to 15 medical escorts are needed per 1,000 runners. To
prevent exercise-associated collapse, it is imperative that the escorts encourage runners to continue to move through the
chute system. The chutes should be extended far enough so that the runners can move quickly and have access to the
finish line medical area. At the Pittsburgh Marathon, the finish line chute area is supervised by an emergency medicine
physician and staffed by athletic trainers. Emergency medical personnel with stretchers should be stationed in close
proximity to the chute area for downed runners needing assistance.
FIGURE 36.28. Medical personnel escorting runners through finish line chutes. Courtesy of the University of Pittsburgh
Medical Center.
Nonmedical personnel are also needed at the finish line medical area. Security personnel should be placed at all
entrances to the finish line medical area to ensure the privacy of the runners who are treated. A “Family Reunion/Lost
Runner” area should be positioned outside the finish line medical area. The radio operators at the various aid station
locations on the course should report periodically to the communications center with the entry number of those
participants who were treated at their respective stations. In addition, the operators of the dropped-out runner vehicles
should report periodically on the runners they are transporting. These reports should be sent from the communications
center to the Lost Runner area. The personnel at the Lost Runner area can provide the status of a runner to a family
member or friend who is waiting at the finish line. However, family members are requested to use the services of the Lost
Runner area only if they have been waiting longer than 1 hour past the runner's predicted finish time.
Depending on the number of runners, at least two ambulances should be placed at the finish line. There should also be
at least two ambulances on the course for the first 1,000 runners, and a single ambulance for each additional 1000
runners. For the Pittsburgh Marathon, volunteer ambulance services from the county assisted the city's emergency
medical services to allow for one ambulance at each medical aid station.
In addition to the emergency vehicles, there should be at least one dropped-out runner vehicle for a 10-K race and one
vehicle per 1,000 runners for a marathon. These vehicles are responsible for transporting runners who have dropped out
of the race for nonmedical reasons or for those runners who have been treated and released from a medical aid station
and will not be returning to the race. One vehicle should serve as a sweep vehicle trailing along the course to pick up
runners at the projected time limit per mile (e.g., for a marathon it is 13 to 14 minutes per mile). A radio operator should
be placed in each vehicle so he or she can communicate with the command center.
Equipment and Supplies
The TAC manual suggests equipment and supplies needed per 1,000 runners for aid stations and for the finish line
medical area (99). As a result of experience with the Pittsburgh Marathon, the author has modified the lists to include
intravenous setups at aid stations as well as at the finish line. The modified equipment and supplies takes into account
the expected increase in the number of runners treated after the midpoint of the marathon. This list of supplies is
presented in Table 36.2 and Table 36.3.
TABLE 36.2. THE PITTSBURGH MARATHON MEDICAL TEAM'S RECOMMENDED EQUIPMENT FOR ALL AID
STATIONS (PER 1,000 RUNNERS)
TABLE 36.3. PITTSBURGH MARATHON MEDICAL TEAM'S RECOMMENDED EQUIPMENT FOR FINISH LINE
MEDICAL AREA (PER 1,000 RUNNERS)
Fluid Stations
Adequate fluid stations should be placed throughout the entire racecourse, including the start and finish lines. The TAC
guidelines for the starting line are one 8-oz. cup of water per runner for races less than 10 miles and two 8-oz. cups of
water for races longer than 10 miles (99). For aid stations, the TAC manual recommends 6 to 8 ounces of water or diluted
electrolyte replacement drink totaling 1.25 times the number of runners ( 99). The finish line area should have at least two
8-ounce cups of water and diluted electrolyte replacement drinks per runner. Plans should include having additional
fluids and ice available for warmer days.
Appropriate signs should be positioned at each fluid station. The signs should be posted above eye level. Signs should
also be posted before the fluid stations to alert runners of their location. If possible, the runners should be made aware of
the brand of electrolyte drink that will be available on race day.
Environmental Considerations
The American College of Sports Medicine (ACSM) recommends the use of a wet bulb globe temperature (WBGT) for
measuring environmental conditions ( 97). The WBGT measures ambient temperature, humidity, and radiant heat. The
following formula is recommended: WBGT=(0.7 Twb)+(0.2 Tg)+(0.1 Tdb), in which Twb is temperature, wet bulb
thermometer; Tg is temperature, black globe thermometer; and Tdb is temperature, dry bulb thermometer. Instruments
used to measure WBGT are available commercially. To ensure accuracy, the weather readings should be measured at a
location on the racecourse.
The ACSM recommends the use of the color-coded flag system to indicate the risk of environmental stress ( 97) (Table
36.4). A set of each of the five flags should be included in the supplies and equipment for all aid stations. Weather
readings should be taken every 30 minutes and medical communications should contact all aid stations to indicate the
appropriate flag to display. Each aid station should place the appropriate flag at a level easily visible to the runners as
they proceed along the course.
TABLE 36.4. ACSM COLOR-CODED FLAG SYSTEM
Runner Education
Prerace seminars can be extremely useful in educating potential participants, especially novice runners. Seminar topics
should include medical screening before running a race, guidelines for training, environmental considerations, fluid and
electrolyte replacement, and the prevention and management of common running injuries. A seminar on the day before
the race should include an overview of the racecourse and the medical support available, final race preparations,
expected weather conditions, and techniques to recover quickly from the race.
Medical information can be supplied to the runners in their prerace packets. For the Pittsburgh Marathon, runners
received a medical information brochure that detailed tips on what they should do from the night before the race through
the days following the race. In addition, the participants were asked to provide demographic information and medical
histories. This information was printed on the back of the entry numbers they wore on their shirts during the race.
At least 15 minutes before and immediately before the start of the race, the medical director should make pre-race
announcements by loud speaker to the runners. This announcement should include the current and expected weather
conditions for the race, reviews of the ACSM color-coded flag system, locations of the aid stations, locations of the fluid
stations, and any other pertinent information.
Conclusions
Providing for the safety of participants in a road race includes a well-coordinated medical team. Proper planning is
essential in providing effective medical support during a road race. The medical organizing team should be prepared for
all potential medical problems. Appropriate personnel and equipment are needed to provide the optimal medical support
for the event. A thorough medical communication system assists in the effectiveness and efficiency of the medical
support. In addition to the medical support for the race, runners should be educated on proper training methods and
injury prevention.
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37 Scuba Diving
37
SCUBA DIVING
KEVIN O'TOOLE
History of Diving
The Underwater Environment
Definitions
Gases Used in Diving
Gas Laws
Heat and Heat Transfer
Diving Equipment
Open-Circuit Scuba
Buoyancy Compensator
Face Mask
Weight Belt and Weights
Swim Fins
Submersible Timer and Depth Gauge
Knife
Protective Clothing
Diving-Related Injury Statistics
Medical Problems
Nitrogen Narcosis
Barotrauma
Pulmonary Overinflation Syndrome
Ear Barotrauma
Sinus Barotrauma
Face Mask Squeeze
Ear Canal Squeeze
Dental Barotrauma
Decompression Sickness
Prevention of Injuries
Nitrogen Narcosis
Pulmonary Overpressurization Accidents
Middle Ear Barotrauma
Sinus Barotrauma
Face Mask Squeeze
Ear Canal Squeeze
Sport-Specific Treatment
Chapter References
The sport of scuba (self-contained underwater breathing apparatus) diving has had phenomenal growth over the last 25
years. It has gone from an activity that was limited to a relatively few physically fit individuals to one that has many
millions of participants, many of whom are not in peak condition. In the United States, it is estimated that there are 3
million active divers. The incident rate for injuries is surprisingly low at 0.04%, which places it at the same level as
bowling. However, the types of injuries that occur in scuba diving can be serious, even fatal. In 1997, there were 82
recreational scuba diving deaths involving U.S. citizens. This number has been as low as 66 (1988) and as high as 147
(1976). The fatality rate for scuba diving has declined from 8.6 per 100,000 in 1976 to 3.7 per 100,000 in 1990 ( 1). This
decline in death rate in the face of a large increase in the number of divers may very well be the result of rigorous
standards for training recreational divers. It is a tribute to the training organizations involved that there are few deaths in
a sport that can be extremely dangerous to its participants. This chapter is intended to allow the physician to recognize
injuries and illnesses unique to scuba diving and to initiate treatment. It also is intended to be a guide for the practitioner
as to when to refer the patient for specialty care.
HISTORY OF DIVING
Scuba diving as an entity is a relatively new activity. Diving, however, goes back many centuries. Breath-hold diving is
the earliest form of diving known to humankind. It has been shown to have been practiced around 4,500 bc. These divers
were diving for food and for treasures ( 2). In early times, the divers also were used for military purposes, as they are
today. Free diving continues to be a popular method of diving today. Examples include pearl divers and recreational
snorkeling.
The next innovation in diving was the diving bell. This allowed for a longer time underwater because there was an air
supply for the diver. It is recorded that Alexander the Great descended in a diving bell in 330 bc. to view the recovery of a
ship (2). The continued problem with a diving bell is that it limited the mobility of the diver. Until the 17th century, the
diving bell was state of the art in diving.
The development of surface-supplied diving apparatus in the 17th and 18th centuries dramatically increased the mobility
and capabilities of divers. Now a diver was free to move about and not have to worry about returning to the diving bell for
the next breath of air. This allowed the diver to do a significantly greater amount of work. This hard-hat diving is still used
today by the military and in the underwater construction fields.
The development of a self-contained breathing apparatus was the next evolutionary step in diving. From the middle
1800s, various individuals attempted to create such a device. It was not until 1943, when Emile Gagnan and Captain
Jacques-Yves Cousteau unveiled their so-called aqua lung, that the development of the modern scuba gear occurred ( 2).
It is because of the work of these two individuals that we have the sport of recreational scuba diving. It was no longer
necessary to be tethered to a surface-supplied air source while wearing a heavy and cumbersome diving suit. This
opened the door to ordinary citizens being able to enjoy the underwater environment. All of today's scuba gear is a
refinement on this initial apparatus.
THE UNDERWATER ENVIRONMENT
The world of the scuba diver, if looked at objectively, is an extremely hostile one. The surrounding “atmosphere” is one
that cannot support a diver's oxygen needs without special equipment. This atmosphere is continually changing its
ambient pressure with every change in the diver's depth. It is this change in pressure that leads to many of the medical
problems that develop in divers. A diver cannot see well if he or she is not wearing a mask. Even with a mask, objects are
distorted by appearing closer and larger than they truly are. The surrounding water tends to drain the heat from a diver
and expose him or her to the risks of hypothermia. The diver can visit this world for only a limited time, because the air
supply is finite and because of the risks of decompression sickness. As can be seen, there are many factors that work
against a diver. They are not, however, insurmountable, as evidenced by the popularity of the sport. It is important for the
diver, as well as his or her physician, to understand the physics of the underwater environment. A diver learns this while
undergoing training. For the physician, to understand the pathophysiology of diving injuries requires a basic
understanding of underwater physics. As will be shown, most of the common and serious injuries unique to scuba diving
occur because of the effects of pressure on gases in the body.
Definitions
Several terms will need to be defined to understand the gas laws that are discussed below. Pressure is defined as an
amount of force acting on a unit area. In diving, pressure is usually expressed as pounds per square inch (psi).
Mathematically, it can be expressed as pressure=force/area, or p=F/A.
The amount of pressure that is exerted on a body by the earth's atmosphere is defined as 1 atm. When measured at sea
level, it is equal to 14.7 psi. At higher elevations, it is less. Atmospheric pressure acts in all directions at any specific
point equally. For this reason, its effects are usually neutralized. In diving, pressures also are expressed in atmospheres.
For example, a pressure of 147 psi is 10 atm (10 × 14.7 psi).
Hydrostatic pressure is the pressure produced by the weight of fluid acting on a body submerged in the fluid. It is equal in
all directions at any particular depth. In sea water, for every 1 foot a diver descends, the hydrostatic pressure increases
0.445 psi. This number is 0.432 psi for fresh water. For sea water, the pressure at 33 feet is equivalent to 1 atm. For
fresh water, every 34 feet is the same as 1 atm, or 14.7 psi.
The definition of absolute pressure is the sum of the atmospheric and hydrostatic pressures exerted on a submerged
body. Its units of measure are pounds per square inch absolute (psia) or atmospheres absolute (ata). The term ambient
pressure is defined as the pressure surrounding a submerged body (atmospheric + hydrostatic) and is usually stated in
absolute pressure terms.
Gauge pressure is defined as the difference between the pressure being measured and the atmospheric pressure. Most
gauges used in scuba diving are calibrated to read zero at normal atmospheric pressures. Gauge pressure is what is
measured on a diver's depth gauge. To convert gauge pressure to absolute pressure, one needs only to add 14.7 psi to
the gauge pressure.
The final pressure that needs to be defined is partial pressure. In a mixture of gases, the proportion of the total pressure
contributed by a single gas in the mixture is called the partial pressure. This partial pressure is directly proportional to the
percentage of the total volume of the mixture that the individual gas occupies. The partial pressure of a gas determines
how much of the gas will be dissolved in the tissues and blood. The concentration of gases in tissues plays an important
role in the development of specific diving illnesses such as nitrogen narcosis and decompression sickness.
Gases Used in Diving
There are a number of important gases that are encountered in recreational scuba diving. Air, in a compressed form, is
the mixture of gases that are used in sport diving. It is composed of 78% nitrogen, 21% oxygen, 0.9% argon, 0.03%
carbon dioxide, and a mixture of other rare gases (0.003%).
Oxygen, as is well known, is essential to life. It is the only gas that is used metabolically by the diver. All other gases in
air serve only to dilute the oxygen concentration. In high enough concentrations, oxygen is toxic to the pulmonary and
central nervous systems (3). Until recently, sport diving did not include the use of oxygen-enriched gas mixtures for this
reason.
Nitrogen is the most abundant gas in air. It is an inert gas and does not support life. Nitrogen is involved in a number of
the illnesses associated with diving. Its anesthetic effects at high partial pressure is the cause of nitrogen narcosis, also
known as the rapture of the deep ( 4). The formation of nitrogen bubbles in tissues and blood is the cause of
decompression sickness, or the bends ( 5,6,7,8 and 9). Nitrogen does serve a useful purpose for the sport diver,
however. It dilutes the oxygen so that the diver is not at risk for oxygen toxicity, which would develop at higher partial
pressures of oxygen.
Carbon dioxide is normally found in minute amounts in air. Normally, it is not of any concern to the diver. However, if the
diver would happen to get a tank of air contaminated with carbon dioxide, the results could be disastrous. Carbon dioxide
in high concentrations (>10%) is toxic to humans and can lead to seizures and death ( 2,3,10). Having a reputable
supplier of compressed air is the principal way to prevent this potential disaster.
Carbon monoxide is produced by the incomplete combustion of hydrocarbons in internal combustion engines. It is an
extremely poisonous substance that must be excluded from the diver's air supply at all costs. The most common cause of
carbon monoxide contamination of a diver's air supply is the intake of an air compressor being near an exhaust system of
an internal combustion engine ( 2). Again, prevention of this disorder can be accomplished by obtaining compressed air
only from reputable dealers.
Gas Laws
To understand fully how changes in pressure can lead to the common ailments that are seen in scuba diving, it is
important to understand some common gas laws. The effects of change in pressure on liquids is negligible. For this
reason, most of the body, which is made up of liquids, has no direct effects from the pressure. It is the air-filled body
cavities—the middle ears, sinuses, lungs, and gastrointestinal tract—that are most affected by pressure changes. To
understand what changes occur and why they occur, it is essential to discuss several gas laws. The behavior of all gases
can be explained by three factors: the pressure, volume, and temperature of that gas. The interrelationships between
these factors has been explained by the gas laws. There are four of these laws that are applicable to the diver: Boyle
law; Charles law; Dalton law; and Henry law.
Boyle's law can be stated as follows: At a constant temperature, the volume of a gas varies inversely with absolute
pressure, whereas the density of a gas varies directly with absolute pressure. For any gas at a constant temperature,
Boyle law can be written as follows:
where p=absolute pressure, V=volume, and K=constant. This law is vital to the scuba diver in that it describes what
happens to an air-filled cavity in the body if it cannot be equalized with the ambient pressure. An example would be
barotrauma to the middle ear caused by eustachian tube dysfunction.
Charles law is stated as follows: At a constant pressure, the volume of a gas varies directly with absolute temperature.
For any gases at a constant volume, the pressure of a gas varies directly with absolute temperature. This law can be
expressed mathematically as follows:
where p=absolute pressure, V=volume, T=absolute temperature, and R=universal constant for all gases. This law comes
in to play when dealing with the compressed air tanks that divers use as their air supply. If a tank is left in direct sunlight,
it can be seen from the formula given earlier that either the pressure or volume must increase. Because the air tank is
rigid, making the volume constant, the pressure in the tank will increase. This can lead to an overpressurization of the
tank and possible tank or valve rupture.
The definition of Dalton law is as follows: The total pressure that is exerted by a mixture of gases is equal to the sum of
the partial pressures of each of the gases if it alone were present in the same volume. The mathematical formula for this
law is written as follows:
where ptotal=total pressure of that gas, pp1=partial pressure of gas 1, pp2=partial pressure of gas 2, ppn=partial
pressure of other gas. Dalton law is important when one is discussing contaminated air supplies, nitrogen narcosis, and
decompression sickness.
Henry law deals with the solubility of gases in a liquid. It can be stated as follows: The amount of any given gas that will
dissolve in a liquid at a given temperature is a function of the partial pressure of the gas that is in contact with the liquid
and the solubility coefficient of the gas in the particular liquid. To put it simply, in a diver, the amount of gas that will
dissolve in blood and tissues will increase with increasing depth until the point of tissue saturation takes place. The
formula is as follows:
where VG= volume of gas dissolved at standard temperature and pressure (STP), VL = volume of the liquid, ;Va. =
Benson solubility coefficient at specified temperature, p1 = partial pressure in atmosphere of that gas above the liquid.
Henry's law is the basis for the development of decompression sickness and is explained later in this chapter.
HEAT AND HEAT TRANSFER
No matter where a person is diving, be it in the tropics or the cold waters of the Great Lakes, heat loss from the diver's
body occurs. Because the human body requires a relatively narrow temperature range to function normally, this loss of
heat energy can have significant effects on diver performance and health. There are several mechanisms by which a
diver loses body heat: radiation, convection, evaporation, and conduction.
Radiation heat loss by the diver is not significant compared with conduction and convection. Radiation heat loss from the
body is in the form of infrared waves. The head, neck, and hands, if left exposed, are areas of the body where radiation
heat loss can occur in cold water.
Conduction is the transfer of heat energy by direct contact. This is the most significant cause of heat loss in divers. Water
conducts heat much better than air, and a diver that is unprotected loses a great deal of heat by direct contact with the
water. The purpose of a diver's wet suit is to prevent the conductive heat loss.
Convection is the transmission of heat energy by the movement of currents. In a diver, even sitting perfectly still, little
currents are formed by the rising of water heated by conduction and its replacement by cooler water. This leads to the
loss of heat by convective currents.
Evaporation of water vapor from the lungs is another method of heat loss in a diver. The compressed air in a scuba tank
has essentially no water vapor present. Each time a diver takes a breath, this air enters the lungs, where large amounts
of water vapor and thus heat are transferred to it. This heat is lost with each exhalation.
All of the above-mentioned mechanisms can, in the appropriate setting, combine to cause hypothermia in a diver, leading
to physical problems.
DIVING EQUIPMENT
To understand the diver and the sport better, it is important to know what kinds of equipment and tools are required.
Divers frequently carry 50, 60, or more pounds of equipment with them on each dive. Each piece of equipment has a
specific and important function. Some equipment failures can be life-threatening and some knowledge by the physician of
their purpose is helpful in caring for the diver. The minimum amount of equipment a sport diver uses includes the
following:
1. Open-circuit scuba
2. Buoyancy compensator (BC)
3. Facemask
4. Weight belt and weights
5. Fins
6. Submersible timer and depth gauge
7. Knife
8. Protective clothing
Each of these essential pieces of equipment will be discussed briefly.
Open-Circuit Scuba
Open-circuit scuba is what makes scuba diving possible. It consists of the compressed air tank or tanks, a demand
regulator, and a backpack to hold the tanks. The air tanks are constructed from steel or aluminum and are filled to a
pressure of 2,000 to 3,000 psi. Tanks require an internal visual inspection yearly and hydrostatic testing every 5 years as
mandated by federal law. The average tank holds approximately 70 cubic feet of air. This is enough air to fill the
average-size phone booth.
The scuba regulator is the key to scuba diving. It is a two-stage apparatus that allows the diver to breath air at whatever
ambient pressure he or she is at. It is a demand valve so that air is released only when the diver takes a breath. This
allows for conservation of an already small air supply. Modern-day scuba regulators are dependable if the diver cares for
it properly. Rarely is a diving accident caused by a faulty regulator.
The backpack that holds the tank is usually part of the buoyancy compensator. It consists of one or two straps that hold
the tank in place.
Buoyancy Compensator
The buoyancy compensator (BC) has two functions. First it allows the diver to adjust his or her buoyancy underwater
while changing depth. The second function is to act as a life preserver in the event of an emergency. The BC is a vestlike
device with air bladders within it. The diver is able to inflate the BC using either a low pressure inflator connected to the
regulator or an oral inflation valve. The same inflation valve is used to allow air to escape. By adding or emptying air, the
diver is able to make himself or herself neutrally buoyant and, therefore, stay at a particular depth effortlessly. Inability to
master the use of the BC is a common problem among new divers and can lead to serious medical problems. If a diver
inflates the vest too vigorously and shoots to the surface, there is a significant possibility that the diver may suffer an
arterial gas embolis. Proper instruction is the key to the correct use of this piece of equipment.
Face Mask
The main purpose of the face mask is to allow the diver to see in the aquatic environment. An air pocket is required to be
present between the eye and the water so the eye can focus correctly. This air pocket is provided by the face mask.
There are many different styles of masks, and one offers no distinct advantage over another. Divers who require
corrective lenses can have them inserted directly into the mask glass. Glasses should not be worn under the mask.
Contacts have been used successfully but can be washed out of the eye if the diver's mask becomes flooded.
Weight Belt and Weights
Because most divers are positively buoyant (i.e., they float) when fully equipped, they require the use of weights. The
weights are worn on a belt around the waist. It has a quick-release clasp that allows for rapid removal of the weights in
case an emergency ascent is required. The amount of weight a diver needs is highly individual, with more obese
individuals requiring more added weight than an individual of similar body weight but who is more fit. The most common
mistake divers make with weights is to overweight themselves, thus making their buoyancy control more difficult and
increasing the work of diving. Experimenting with different amounts of weight will eventually lead to the optimum amount
for each particular diver.
Swim Fins
The use of fins allows divers to propel themselves with much less effort than if they were swimming barefoot. They allow
divers to swim faster and farther with less effort. There are many different styles and sizes on the market. Larger fins
sometimes cause cramping and exhaustion in divers who do not have strong enough legs to use them. As with the
amount of weight a diver should use, the selection of a style and size of fin is best done after trying several different
types.
Submersible Timer and Depth Gauge
These are two very important instruments. They are necessary to keep track of the length of time the diver has been
submerged and to document the deepest depth of the dive. The timer can be a simple water-resistant watch or a timer
that automatically turns itself on when the diver enters the water. The depth gauge is usually part of a console that
contains a compass and a pressure gauge that keeps track of the remaining air supply. The information obtained from
these instruments is used to calculate when a dive may require decompression stops as well as for future dive planning.
As is shown later, the length and depth of a dive are important in the development of decompression sickness.
A relatively new piece of equipment that sport divers are using more is the diving computer. This instrument continually
monitors the diver's depth and calculates how much longer the diver can stay at that depth. It has become a popular
piece of equipment because it allows divers to stay underwater longer compared with the standard decompression
tables. It remains to be seen if these dive computers are leading to more cases of decompression sickness. One
interesting feature of most of these computers is that they keep in their memory a record of the diver's dives. This
becomes important if a diver is believed to have decompression sickness. It is then relatively easy to obtain the pertinent
information about the depth and duration of the dives that may have led to the problem.
Knife
Most divers carry one of several styles of knife with them while diving. Contrary to popular belief, the knife is not for
defense against marine life. Its main role is to free a diver who has become entangled in fishing line, kelp, and other
items. The knife is usually worn in a sheath attached to the leg for easy access.
Protective Clothing
The type of protective clothing worn by the diver is determined by the diving conditions. A dive in the tropics may require
nothing more than a bathing suit. In contrast, an ice diving trip require sat the minimum a 0.25-inch neoprene wet suit.
Many divers use a dry suit in these conditions. This is an outfit that keeps the diver's body dry by having waterproof
zippers and connections at the neck, wrists, and ankles. The diver's environment dictates what type of protective clothing
will be needed for the dive. It is when the protection is inadequate that the potential for hypothermia is present.
DIVING-RELATED INJURY STATISTICS
As stated earlier, diving has a relatively low injury rate compared with other sports. However, diving is a potentially
dangerous and deadly sport in which participation must not be taken lightly. The Divers Alert Network (DAN), which is
based at Duke University, keeps yearly statistics on diving deaths, as well as the most serious diving injuries. The
organization's hard work and dedication to diving medicine has led to a better understanding of what causes deaths in
scuba diving. DAN has reported that scuba deaths are the result of multiple factors, leading to a final event that is usually
drowning. A look at the 1997 data on contributing factors for drowning deaths shows multiple factors ( 1). Insufficient air,
entrapment, cardiovascular medical problems, and alcohol and drugs lead the list. Remaining factors include air
embolism, nitrogen narcosis, boat accident, diabetes mellitus, panic state, head injury, carbon monoxide, and seizure
disorder. A review of the list shows that a number of these contributing factors are completely preventable. Running out
of air should never occur to a properly trained and motivated diver. Alcohol and drugs are under the control of the diver,
who has been taught by his or her instructor that diving and drugs do not mix. Careful and conservative divers should be
able to lower their risk of death while diving just by following their training procedures.
In addition to tracking diving deaths, DAN also keeps records on serious diving injuries such as arterial gas embolism
and decompression sickness. In 1997, DAN received reports of 830 cases of decompression sickness and 68 cases of
arterial gas embolism (AGE) (1). Since 1986, the number of cases have increased each year except for 1988. A full
report of each year's statistics can be obtained from the DAN organization.
MEDICAL PROBLEMS
The type of medical problems that the scuba diver may encounter are quite varied. Any medical problem that affects the
general population can affect a diver. However, there are a number of unique medical conditions that affect divers. Each
is described, and the appropriate immediate treatment as well as definitive treatment is discussed. Also,
recommendations on when to obtain specialty consultation are made.
Nitrogen Narcosis
Nitrogen narcosis may be better known as the rapture of the deep. As the partial pressure of nitrogen increases with
increasing depth, the nitrogen begins to have an anesthetic effect ( 11). Symptoms usually are not observed until a diver
exceeds 100 feet, but there is a wide variation among different divers and even within a single person on different dives.
Signs and symptoms are similar to those of ethanol intoxication ( 12,13). Initial symptoms may include a feeling of
excitement and exhilaration. The diver may notice tingling or numbness in the lips and extremities. He or she may
become overconfident at this point. Mental activity becomes increasingly slowed as depth increases. The ability to make
rapid and potentially life-saving decisions is impaired. In new divers, there may not be euphoria but more of a feeling of
terror. This intoxication leaves the diver more susceptible to having an accident while at the same time less capable of
responding appropriately. The only treatment for this disorder is to ascend to a shallower depth. Once this is done, the
effects dissipate rapidly. The diver should not attempt to return to the deeper depth on the same dive that he or she
developed nitrogen narcosis.
Barotrauma
Barotrauma is a general term used to describe any injury that has been caused by pressure, specifically pressure
changes. Any of the air-filled body cavities are susceptible to barotrauma. The trauma occurs when the pressure is
unable to be equalized because of air trapping. This is quite common in the middle ear and can be quite deadly in the
lungs. Each specific area is addressed with emphasis placed on prevention of the barotrauma.
Pulmonary Overinflation Syndrome
Pulmonary overinflation syndrome includes several different possible injuries. The one common underlying mechanism of
injury is air trapping within the lung. There are two main reasons that this occurs. The first is that the diver holds his or
her breath while ascending. The most common reason for this is that the diver has an underwater emergency and must
make an emergency ascent. Divers are taught during their training to exhale continually during ascent. Unfortunately,
during an emergency, many divers, especially inexperienced ones, panic and forget to do this extremely important step.
During the ascent with a closed glottis, the air within the lungs continues to expand. If the glottis remains closed, the
alveoli will rupture, with air entering the pleural space, subcutaneous tissues, or into the pulmonary veins. Depending on
where the air goes, the development of the various components of pulmonary overpressurization will occur.
The second cause of air trapping is the result of underlying lung disease. Individuals with asthma, emphysema, or
chronic bronchitis can have areas of the lung that are susceptible to air trapping ( 14,15,16 and 17). Also individuals who
have had thoracic surgery or spontaneous pneumothorax can have areas of lung that are abnormal and more prone to air
trapping. It is for this reason that individuals with the above-mentioned illnesses are advised not to scuba dive. No matter
what the cause of air trapping, any of the individual illnesses of pulmonary overpressurization can occur. Each of these
diseases is discussed in detail.
Arterial gas embolism (AGE) is perhaps the most feared complication of scuba diving, and with good reason. Many diving
experts believe that it is the leading cause of scuba diving fatalities. Many of the diving fatalities that are reported as
drowning are more than likely deaths due to AGE. Because the diagnosis of AGE requires a very specific autopsy, many
of these deaths go undetected and are simply listed as drowning.
The cause of AGE is the entry of air into the arterial system, which then embolizes to the various organs of the body.
With alveolar rupture, air enters the pulmonary veins. It is then carried back to the left side of the heart, where it then
travels to the brain, heart, and other organs. The air bubbles then occlude the vascular supply to these vital organs,
leading to organ dysfunction ( 9,12). As the ambient pressure decreases further as the diver ascends, the air bubbles will
increase in size, further obstructing blood flow.
The onset of symptoms in AGE are usually immediate and occur not more than 10 minutes from surfacing
(1,8,9,12,13,18,19,20 and 21). The diver may surface unconscious or in full cardiac arrest. Those that surface in arrest
usually cannot be resuscitated unless they are immediately placed in a recompression chamber. The signs and
symptoms of AGE can include any of the following: headache, shock, unconsciousness, weakness, parasthesias, ataxia,
visual disturbances, nausea and vomiting, chest pain, shortness of breath, bloody sputum, and confusion. Almost any
neurologic symptom or sign can occur with AGE, depending on where the air emboli is lodged. Any diver who within 10
minutes of surfacing develops any of the above-mentioned symptoms should be considered to have an AGE until proven
otherwise.
The appropriate treatment for AGE is recompression therapy at the earliest possible time. Initially, the airway must be
secured and adequate oxygenation maintained. The patient should be placed on 100% oxygen as soon as possible. The
use of a simple face mask is not adequate because 100% oxygen is not obtainable. One needs to use a nonrebreather
mask or endotracheal intubation to obtain as close to 100% as possible. An intravenous line should be started and
cardiac monitoring initiated. In the past, much was made of placing the patient in the Trendelenburg position with the left
side down. The thinking was that this would trap remaining air bubbles in the apex of the heart and thus prevent further
embolization. Recent work in dogs has shown this not to be true. There is no trapping of air at the apex of the heart,
because the blood flow through the heart is a strong force and will move any air in the heart out into the systemic
circulation. Also, the Trendelenburg position can worsen cerebral edema that can develop with central nervous system
(CNS) insults from AGE. Another reason not to place the patient in Trendelenburg position is that this can compromise
the patient's pulmonary function as a result of the abdominal organs pushing on the diaphragm, thereby decreasing total
lung volume. For these reasons, it is advised to lie the patient flat on his or her back (or side, if vomiting and aspiration
are a concern).
As stated earlier, recompression is the only definitive treatment for AGE. Arrangements should be made early for
recompression therapy. Tests such as computed tomography (CT) and magnetic resonance imaging (MRI) have no place
in the acute management of AGE. The diagnosis is made clinically and any delay to recompression therapy to obtain
these tests is unwarranted. The success of recompression is directly related to how soon the patient receives the
treatment. If there is no hyperbaric chamber at the facility, make arrangements early for transfer to a hospital with a
hyperbaric chamber. These arrangements can be facilitated by contacting DAN at Duke University. This organization can
help with patient management, as well as helping to arrange transfer of the patient to the nearest appropriate hyperbaric
chamber. It must be remembered that the earlier the patient receives recompression therapy, the greater the chance that
he or she can make a complete recovery.
The second type of pulmonary overpressurization accident is that of pneumothorax. The mechanism is the same as in
AGE, that is, rupture of alveoli secondary to air trapping; however, instead of air entering into the pulmonary circulation, it
enters into the pleural space. It should be remembered that pneumothorax also may be present in patients with AGE. A
diver is not limited to just one of the overpressurization accidents at a time. As the diver ascends farther, the air in the
pleural cavity expands. This can lead to collapse of the involved lung and even the development of a tension
pneumothorax. This condition can lead to cardiovascular collapse and death if it is not treated appropriately.
The signs and symptoms of pneumothorax include shortness of breath which began acutely, dyspnea, pleuritic chest
pain, sudden onset of cough, tachycardia, cyanosis, shock, distended neck veins, and decreased breath sounds on the
involved side along with increased tympany on the involved side. If the tension pneumothorax is severe, one may notice
a shifted trachea away from the involved side. One may notice the patient bending the chest toward the involved side
(8,18,20,21 and 22).
Treatment of pneumothorax begins with the recognition of the problem. A scuba diver who develops shortness of breath
or pleuritic chest pain immediately after a dive should have the diagnosis of pneumothorax entertained. The patient
should be put on 100% oxygen and an intravenous (IV) line placed. If the patient is stable, a chest x-ray study should be
obtained. If, however, the patient is in extremis, treatment should proceed before an x-ray study. Based on the physical
examination, a 12-gauge IV catheter should be inserted into the involved hemithorax. The location of the catheter should
be the second intercostal space in the midclavicular line. If the patient does have a tension pneumothorax, a rush of air
should be heard when the catheter is inserted. Leave the catheter in place so that air does not reaccumulate before the
insertion of the chest tube. After the chest x-ray study in the stable patient and after the catheter decompression in the
unstable patient, a chest tube should be inserted into the involved side. This should be connected to an underwater seal
and a post-chest tube x-ray study obtained to confirm lung reinflation and proper tube placement. Most of these patients
have an uncomplicated course and require no further treatment other than the chest tube.
A third component of overpressurization accidents is mediastinal emphysema. The cause is the same as the previous two
injuries and develops when air enters the mediastinum after tracking along the larger airways. Signs and symptoms
include retrosternal chest pain that may be described as pressure or a dull ache. This pain is made worse with deep
breathes or coughing. Swallowing also can make the pain worse. Radiation of the pain occurs to the shoulders, back,
and neck. There also may be dyspnea, cyanosis, cough, and in severe cases, shock ( 8,10,19,20 and 21).
This disease by itself is usually not life-threatening. What it does signify is that an overpressurization accident of the lung
has occurred and that the possibility of an AGE or pneumothorax exists. Unless AGE is present, the patient does not
need hyperbaric treatment. Placing the patient on 100% oxygen may hasten the resolution of the mediastinal emphysema
and improve the patient's symptoms.
The last component of overpressurization accidents is subcutaneous emphysema. This results from the movement of air
out of the mediastinum to the subcutaneous tissues of the chest and neck. Although patients with this disease may look
terrible, this is usually not a serious illness. The patient may notice a fullness in the neck and crepitus with palpation.
Because of involvement of the vocal cords, a change in voice may be noted. Some patients also develop a cough, but
shortness of breath is not a component of subcutaneous emphysema alone ( 10,19,20 and 21).
Again, unless AGE is present as well, recompression therapy is not needed. Placing the patient on 100% oxygen may be
helpful. Reassurance of the patient that he or she is not seriously ill is probably the most important intervention the
physician can make.
Ear Barotrauma
There is probably not an active scuba diver alive who has not experienced at least once a middle ear barotrauma, or
squeeze. This is the most common barotrauma experienced by divers ( 8,9,13,23,24). This disorder is the result of the
inability to equalize the pressure between the middle ear and the environment. It is during the first 10 to 15 feet of a dive
that the greatest pressure changes occur. It is in this depth range that the problem of middle-ear squeeze is common.
The most common cause of this inability to equalize is eustachian tube dysfunction ( 8,9,12), which can be the result of
upper respiratory infections, allergic rhinitis, or smoking. Any process that causes edema and mucous production in the
eustachian tube will make the individual more susceptible to middle ear squeeze.
Most cases of middle ear squeeze occur on descent, but a minority of cases can occur on ascent ( 9,11,12). The initial
symptom is a sense of fullness in the ear. If the diver continues to descend without equalizing the pressure, pain will
develop. The diver will notice a decrease in hearing in the involved ear. This is secondary to the hemorrhage that has
occurred within and behind the tympanic membrane. Tinnitus and vertigo can also develop with middle ear squeeze. If
the diver continues to descend despite these symptoms, tympanic membrane rupture can occur. This may lead to severe
vertigo and vomiting secondary to the caloric stimulation that will occur with the entrance of water into the middle ear
(8,9,11,12 and 13,23,24). This event can be life-threatening if the diver vomits into the regulator. Another complication of
continued descent is that of round or oval window rupture ( 11,12 and 13). If this problem occurs, by either the squeeze
itself or forceful attempts at clearing the ears, severe long-lasting complications may develop, including hearing loss,
tinnitus, and vertigo.
If a diver develops an ear squeeze, further diving should be avoided and the ear should be checked by a physician.
Otoscopic examination of the ear may reveal an injected tympanic membrane, hemorrhage within or behind the eardrum,
or a rupture of the tympanic membrane. If the drum is not ruptured, decongestants, both spray and oral, along with
appropriate pain medication should be given. If the eardrum is ruptured, oral antibiotics can be started. Avoid any
medications being placed directly into the ear canal. The rupture usually heals on its own. Have the patient return in
several weeks for a recheck of the ear drum rupture. There should be no further diving until the rupture has healed
completely. Ear, nose, and throat (ENT) referral should be made if there is a persistent rupture and the patient wishes to
dive again.
Any diver who surfaces with significant acute hearing loss, vertigo, tinnitus, or gait disturbance may have suffered a
round or oval window rupture (11,12 and 13). These patients should be referred immediately to an ENT specialist
because this is considered a serious and emergent condition. These patients may require immediate surgery to prevent
permanent damage to the inner ear. Absolutely no further diving should be attempted until the activity is cleared by the
ENT surgeon.
Sinus Barotrauma
Sinus squeeze occurs when the ostia to the sinuses become obstructed and, therefore, do not allow equalization of
pressure while descending ( 9,11,13,19,24). Causes of the ostia obstruction are the same as in ear squeeze, namely
upper respiratory infections and allergies. Individuals with chronic sinus problems are particularly susceptible to this
disorder. One also can develop sinus squeeze on ascent. This tends to happen when a sinus polyp acts as a one-way
valve and obstructs the ostia. The unequal pressures in the sinuses lead to exudate and hemorrhage within the sinuses.
The diver first notices a full feeling in the forehead, between the eyes or in the upper teeth. The location depends on
which sinuses are involved. This fullness can progress into severe pain and actual numbness. With hemorrhage into the
sinus, the diver may develop epistaxis because some blood escapes from the sinus.
Treatment with nasal decongestant drops and oral decongestants is usually all that is needed. If the diver develops
worsening pain or a purulent nasal discharge, secondary sinus infection should be suspected and appropriate antibiotics
started. All diving should be avoided until the symptoms have cleared. Referral to an ENT specialist is advisable if the
symptoms become prolonged (longer than 2 weeks) or worsen. Most patients will have an uncomplicated course and
should be able to return to diving without any long-term sequelae.
Face Mask Squeeze
An interesting but usually benign condition called face mask squeeze develops when the diver fails to equalize the
pressure in the mask (20,22,24). The diver is able to do this simply by exhaling occasionally into the mask. The soft
tissues of the face, especially the eye and surrounding tissues, can be injured. The diver may notice a suction sensation
on the face that can then become pain as the pressure difference increases. When the diver surfaces, the face is noted
to be edematous within the region covered by the mask. There may be petechia and subconjunctival hemorrhage as well
(20,22,24). There have been reports of optic nerve damage and blindness in severe cases, but this is usually a
self-limiting disorder. Ice and analgesia can be prescribed for symptomatic relief.
Ear Canal Squeeze
Ear canal squeeze occurs in divers who wear tight-fitting hoods while diving ( 11,19,20,22). If the hood is tight enough to
prevent water from entering the external ear canal, an air cavity develops that cannot equalize pressure. Symptoms
include fullness or pain, or both, over the external ear region, blood or fluid drainage after surfacing, or a ruptured
eardrum. Treatment includes pain medications and, if the eardrum is ruptured, the same treatment as with middle ear
squeeze and rupture of the eardrum.
Dental Barotrauma
Although the condition is relatively rare, dental barotrauma, or aerodontalgia, can be quite painful. It develops in teeth
that have gas spaces from either carious teeth or improperly filled teeth ( 20,22,25). During descent, these air spaces
become filled with blood or surrounding soft tissue, leading to pain. The pain may become so severe that further descent
is impossible. Treatment consists of the immediate administration of analgesia, with dental repair of the involved teeth.
Further diving should not be attempted until the patient has been evaluated and treated by a dentist.
Decompression sickness (DCS), also known as the bends or caisson disease, is a disorder that occurs after inadequate
decompression after being exposed to increased pressures. It consists of a constellation of signs and symptoms that can
occur after a reduction in barometric pressure leads to the formation of bubbles within the tissues and bloodstream of the
body (8,9,11,13,19,20,22,26,27 and 28).
During the time a diver is underwater, there is a continual loading of nitrogen gas into the blood and tissues of the body.
The amount of nitrogen dissolved depends on a number of factors but the two most important are depth (pressure) and
time. The longer and deeper a dive, the more nitrogen that is forced into solution within the body. There are numerous
dive tables that have been devised that take this into account and list safe limits. However, these limits are not absolute
and numerous instances of decompression sickness have occurred well within these tables. If a diver returns to the
surface too quickly or without making the necessary stops, the blood and tissues become supersaturated from the
reduction in ambient pressure, and nitrogen comes out of solution in the form of bubbles. It is the nitrogen bubbles that
lead to the disorder known as DCS.
Nitrogen bubbles can cause problems by several different mechanisms ( 8,11,13,19,26). Intracellular bubbles can
physically disrupt cells. Intravascular bubbles lead to obstruction of vessels, which causes tissue ischemia. Extravascular
bubbles can cause extrinsic compression and stretching of nerves and blood vessels. Finally, the bubble-blood interface
activates the early phases of blood coagulation and causes the release of vasoactive substances.
There are a number of predisposing factors that can lead to the development of DCS ( 11,19,20,27,29):
1. Pushing the dive tables. This means going out to the extreme limits on the published diving tables. Most of these
tables are based on work conducted by the U.S. Navy. These limits were calculated using fit, young navy divers.
The vast majority of recreational scuba divers would not fit into this category of fitness. So a diver, for example, who
stays 60 minutes at 60 feet is theoretically within the limits of the table but is placing himself or herself at risk for
2. Missed decompression stops. All of the major diving training organizations recommend a stop at between 10 and 20
feet for several minutes at the end of a dive. This approach is believed to give the body time to rid itself of some of
the nitrogen load. Many divers do not follow this advise and may be making themselves more susceptible to
developing the bends.
3. Fatigue. Divers who are not well rested are more likely to get “bent.”
4. Vigorous physical activity. Activity both during and immediately after the dive has been shown to be a risk factor.
5. Hypothermia. A cold diver is at greater risk for DCS.
6. Alcohol use before a dive. Not only is it unwise to drink because of the effects on cognitive functions, but it also
appears to make the bends more likely.
7. Obesity. Adipose tissue has a great affinity for nitrogen.
8. Age. All other factors being the same, the older the individual, the more likely he or she is to develop
9. Poor physical condition. Those who are out of shape are more at risk.
10. Dehydration. Increasing the blood viscosity by dehydration further complicates DCS.
11. Tissues with previous injury. Any area of the body that may have an underlying injury for which the blood supply is
decreased is at increased risk for DCS.
12. Flying too soon after diving. It is advisable to wait at least 24 hours after multiple days of diving. The further
decrease in barometric pressure on the aircraft may be just enough to cause bubble formation.
13. Patent foramen ovale. Recent studies have shown that a large percentage of patients who have had documented
DCS also have a probe patent foramen ovale. It is postulated that bubbles that would normally be safely filtered out
by the lungs are crossing through the foramen ovale and manifesting as DCS. This may occur in certain situations
such as a Valsalva maneuver. Further study is needed before any recommendations can be firmly made regarding
diving and a patent foramen ovale ( 30,31,32).
If DCS is being considered as a diagnosis, asking the patient some specific questions about his or her dives can be
helpful. The following questions can be useful in determining whether or not decompression sickness is likely to have
occurred:
1. Was the diver using compressed air or another gas mixture?

2. Any preceding alcohol or drug use? Evidence for dehydration?
3. Did the patient take an airplane flight less than 24 hours after the last dive?
4. How many dives were done on this dive trip?
5. How many dives were done a day on average?
6. How deep were the dives, and how long did they last (bottom time)?
7. Were deep dives done first or last? Doing deep dives later increases the nitrogen loading.
8. Were there any missed safety stops?
9. How soon after the last dive did the symptoms start?
The answers to these questions will allow the diving medicine specialist to determine the patient's risk of having DCS.
Ask to see the diver's log book to help you obtain the above-mentioned information.
Clinically, decompression sickness is arbitrarily divided into types 1 and type 2. These divisions are helpful in
determining the severity and treatment of the DCS, but there is overlap. A certain number of the less severe DCS type 1
cases are eventually be determined to be DCS type 2. It is important to realize this, because the treatment and outcome
can be quite different for DCS type 2.
DCS type 1 is also known as pain-only DCS (8,9,11,13,19,20,22,26,27 and 28). This group includes musculoskeletal
symptoms and symptoms involving the skin or lymphatics. The symptoms usually begin within several hours of the dive,
with the vast majority occurring before 24 hours. However, there have been cases that have begun several days after the
last dive. Symptoms within this class include musculoskeletal pain, itching, skin marbling, and lymphatic involvement.
The mildest cases of DCS type 1 are those that involve the skin. Rashes and itching are quite common after diving and
are usually transient, requiring no specific therapy. Marbling or mottling of the skin is a form of DCS and may require
recompression therapy.
Lymphatic involvement of DCS is unusual and manifests as a painless swelling. This swelling is believed to be caused by
obstruction of lymphatic flow by the bubbles. There may be pain in the involved lymph nodes in addition to the edema.
Recompression therapy alleviates the pain, but the edema may remain for some time after treatment.
In addition to the above-mentioned symptoms, excessive fatigue and anorexia are included in DCS type 1. A diver may
have a general feeling of “something is not right.” There may be no specific complaints that the diver has other than
fatigue out of proportion to the amount of physical activity performed. A trial of treatment as outlined below for DCS type
1 may be warranted in these particular patients.
The most common symptom of DCS type 1 is pain, which is usually localized to a joint. The joints of the arms are affected
more than those of the legs. The onset is gradual and early in the course may be missed or ignored by the diver. The
pain is described as dull and throbbing deep in the joint and surrounding tissues. The pain may or may not be increased
by movement of the affected joint. The pain may be severe enough that the patient may be unable to use the limb. Rest
does not relieve the pain. Physical examination of the involved area is usually unremarkable. There is no edema or
discoloration. The area is not tender to palpation. By definition, the neurologic examination of the affected extremity is
normal. If there are any neurologic findings, the diagnosis of DCS type 2 must be made. There are no laboratory tests or
radiographic procedures that are helpful in making the diagnosis of DCS type 1. The diagnosis is made by history and
physical examination and a high index of suspicion.
The treatment of DCS type 1 should begin with the application of 100% oxygen. This may be all that is needed to resolve
the symptoms. Even if symptoms resolve, the patient should be observed for several hours as recurrences can happen
after initial resolution. Look for progression to the more serious DCS type 2. If there is any doubt as to the severity of the
DCS, the patient should undergo recompression therapy. Contact DAN for consultation with a diving medicine specialist.
This physician will be of assistance in arranging transportation to an appropriate hyperbaric facility.
DCS type 2, also known as neurologic bends, is the more severe form of DCS. This class of DCS includes any cases
involving the following: respiratory symptoms, shock, or CNS or peripheral nervous system involvement
(8,9,11,13,19,20,22,26,27 and 28).
The signs of symptoms of DCS type 2 can be quite varied and multiple in nature. The spinal cord is the most commonly
involved organ in recreational scuba divers. Signs and symptoms often do not follow typical nerve distributions and may
vary and shift early in the course of the disease. Spinal cord DCS may present with paralysis, sensory loss, paresis, loss
of sphincter control, and a girdle-like distribution of pain in the trunk.
Patients with cerebral DCS can have any of the following: headache, visual disturbances, dizziness, tunnel vision,
confusion, disorientation, concentration difficulties, psychotic features, and loss of consciousness. DCS involving the
labyrinthine apparatus presents with nausea, vomiting, vertigo, and nystagmus. It is also called the “staggers.”
Pulmonary DCS is relatively rare, occurring in about 2% of DCS cases. It can be deadly if it is not recognized and treated
appropriately. Symptoms include substernal chest pain worsening with inspiration, coughing, and severe shortness of
breath.
In all of the various cases of DCS type 2, symptoms usually begin within several hours of the dive. They can begin
several days out, but this is not common. Treatment before arriving at the hospital should involve the administration of
100% oxygen as soon as possible. This measure may reduce or even relieve the symptoms. Because dehydration plays
a factor in the development of DCS, either oral or IV can commence in the prehospital setting. Overhydration should be
avoided so as not to complicate the cerebral or spinal cord edema further that can develop with DCS. Rapid transport to
the hospital should be carried out so that early recompression therapy can begin.
In the hospital, arrangements should be made for the rapid recompression of the patient, because this is the only
definitive treatment for DCS type 2. If there is not a hyperbaric chamber available at your hospital, make arrangements to
transfer the patient with the help of DAN. The rationale for the use of hyperbaric oxygen in the treatment of DCS is as
follows:
1. It decreases the volume and thus the diameter of the gas bubbles. This approach will allow the bubble to pass more
distally and, it is hoped, allow the return of blood flow to ischemic tissues.
2. It improves the diffusion gradient of the nitrogen out of the bubble, thus causing the rapid absorption of the bubble.
3. It improves oxygen delivery to ischemic tissues by increasing the amount of oxygen dissolved in the blood to
superphysiologic levels.
While waiting for the patient to undergo recompression therapy, several other interventions can be carried. Hydration
should be continued with isotonic solutions to maintain a urine output of 1 to 2 cm 3 per kg per hour. For any neurologic
involvement, steroids have classically been given. They have never been shown to improve outcome in DCS but are still
widely used. If it is decided to use them, hydrocortisone, 1 g, or Decadron, 10 to 20 mg, can be given intravenously.
Aspirin, 500 to 1000 mg, should be given by mouth for its antiplatelet activity. Lidocaine may be useful for any cardiac
arrhythmias, and it has been shown experimentally to improve neurologic outcome. However, its routine use for this
purpose cannot be advised until further studies are done.
Remember, there are no diagnostic laboratory or radiographic procedures for DCS. Delaying recompression therapy to
obtain a CT or MRI is unjustified. Patients have the best chance for complete recovery when they undergo early
recompression therapy. Even a patient who will not have symptoms for several days should be given the benefit of a trial
of recompression therapy. The advantages of the treatment far outweigh the possible complications of the therapy. There
have been many reports of patients getting excellent results approximately a week before the start of their DCS.
PREVENTION OF INJURIES
Scuba diving is an exiting and popular sport. Many millions in the United States alone are enjoying this sport. However, it
is a sport that requires a certain level of physical conditioning and health to remain safe. There are numerous situations
in the underwater environment in which good physical conditioning will be the difference between a tragedy and a good
outcome. Although being an excellent swimmer is not a prerequisite for diving, being in good physical condition without
major medical conditions is necessary for safe diving. Table 37.1 shows the medical conditions that are contraindicated
for diving. Many of these conditions are placed in the table for theoretical reasons and have not been well studied. They
appear in the table because they could lead to the death or severe disability of the diver. Some would argue that the
decision to dive should be left to the individuals themselves. Others would argue that the individual is placing others at
risk as well if he or she should become ill. This includes the dive partners and anyone else with the diver. For many of
these illnesses, there is no clear-cut answer. Each decision about diving must be made individually. Referral to a diving
medicine specialist can be helpful in instances for which there is some question about contraindication to diving. DAN
maintains a list of physicians throughout the country who have this particular expertise. Table 37.1 shows the absolute
and relative contraindications to recreational scuba diving, divided by organ system ( 22,32,33,34,35,36,37 and 38). Listed
below are factors that can be modified by the diver in an attempt to prevent diving injuries and illnesses.
TABLE 37.1. ABSOLUTE AND RELATIVE CONTRAINDICATIONS TO RECREATIONAL SCUBA DIVING
Nitrogen Narcosis
Factors that can contribute to the development of nitrogen narcosis include fatigue, drug and alcohol use, anxiety, cold,
and the use of concurrent sedating medications such as antihistamines and sedatives. By eliminating as many of these
factors as possible, a diver will decrease the risk of nitrogen narcosis on future dives.
Pulmonary Overpressurization Accidents
Prevention of these diseases is the best form of therapy. Vigorous training of individuals learning to dive is and should
continue to be the mainstay of prevention. Making potential divers aware of this deadly risk and how to avoid it is the key
to lowering the numbers of AGE. Also, until it can be proven otherwise, individuals with asthma, emphysema, and chronic
bronchitis should be told that their participation in scuba diving is ill advised and can be life-threatening. Some dive
physicians have relaxed their prohibition on diving for certain subsets of patients. As a general rule, however, any patient
with the above-mentioned pulmonary diseases who wish to dive should be referred to a diving physician for evaluation as
this is an area in continued flux.
Middle Ear Barotrauma
Treatment of middle ear squeeze begins with prevention. Any diver with an upper respiratory infection or active seasonal
allergies should delay diving until illness has passed. Many divers refuse this option and request an alternative. Nasal
decongestant sprays and oral decongestants have been recommended and may be useful in some divers. Frequent
equalization of the ears during descent, for example, every foot with the modified Valsalva or the Frenzel maneuver,
frequently prevents middle ear squeeze. Descending in the head-up position also makes equalizing easier and the
descent more controlled. Advise the patient that if he or she encounters difficulty clearing, ascend a few feet and try
again. If the diver is still unsuccessful, the dive should be aborted and the diver should go to the surface. Yawning or
swallowing has also proven useful for some divers in clearing their ears.
Sinus Barotrauma
Treatment of sinus squeeze again begins with prevention. Diving should not be attempted if one has cold or allergy
symptoms. If during descent, the fullness or pain develops, the dive should be aborted and the diver should return to the
surface.
Face Mask Squeeze
Prevention by occasionally exhaling into the mask is the best course of action.
Ear Canal Squeeze
The disorder can be prevented by allowing water to enter the ear canal by holding the hood away from the head while
underwater. Once water has entered the canal, the hood can remain tight without causing a squeeze.
As seen in the section on DCS, there are a number of factors that come into play in making one more susceptible to the
condition. A number of these factors can be controlled or modified by the diver. Being in good physical condition,
avoiding alcohol and drugs while diving, and being well rested will decrease the chance of developing DCS. Diving
conservatively, staying well hydrated, and waiting the appropriate time period before flying will also help prevent DCS.
Sport-Specific Treatment
Unlike many other sports, scuba diving injuries are not as amenable to treatment that allows immediate return to the
activity. After any injury, improving one's general physical condition is beneficial to any of the injuries.
The trauma that occurs with barotrauma causes edema and bleeding into the middle ear and sinus cavities. This worsens
the underlying pathology involved in barotrauma and can lead to more severe damage if diving is attempted. Many weeks
may be required before the ear or sinus is healed and capable of tolerating more diving. This becomes a problem for
participants who are on an expensive vacation. Many may wish to attempt diving soon after a squeeze. A number of
divers use both oral and topical decongestants as well as antihistamines in an attempt to hasten eustachian tube or sinus
ostia function. Many of these divers will report improved function but no appropriate studies have been performed that
show that this practice is safe. These drugs, especially the antihistamines, can have a negative effect on the diver's
mental alertness. The author is involved in the first known study that will examine the neuropsychiatric effects of these
drugs on divers at depth. Until more information is available on the effects of these drugs on diver performance, no
recommendation can be made for their use.
Divers who have had a pulmonary overinflation injury have suffered an insult to the lung parenchyma. They must undergo
a thorough evaluation by an appropriate diving physician. They should not dive until cleared to do so. It must be
determined if this was a so-called deserved hit or not. A deserved hit would mean that the diver held his breath while
surfacing, thereby leading to the overinflation. If not deserved, an underlying risk factor must be found. This will usually
lead to a pulmonary evaluation. If it is determined that there is bronchospasm involved, the participant should be advised
not to dive again. Also, if any underlying lung pathology is found, the patient should be advised not to dive. Any diver left
with a residual deficit after an overinflation accident, whether deserved or not, should not dive again.
Recovery from decompression sickness is varied. Resolution of DCS type I is hastened by the use of 100% oxygen or
hyperbaric oxygen. Once the patient is symptom free, he or she should wait 1 week before returning to diving. DCS type
2 may require multiple treatments with hyperbaric oxygen before the patient is free of symptoms. A number of patients
are left with permanent findings and should not return to diving. Someone who has completely recovered from DCS
should be cleared to dive by a diving physician. Recommendations vary from 6 weeks to 6 months before diving should
resume. When the participant does resume diving, it should be done under more conservative conditions, i.e., less
underwater time and less depth. Divers who have suffered DCS should be informed that they are now at increased risk
over the general diving population for another DCS episode.
CHAPTER REFERENCES
1. Divers Alert Network. Report on 1997 diving accidents. Durham, NC: Duke University Medical Center, 1999.
2. NOAA. Diving manual. Washington, DC: U.S. Department of Commerce, 1991.
3. Thom SR, Clark, JM. The toxicity of oxygen, carbon monoxide and carbon dioxide. In: Bove AA, Davis JC, eds. Diving medicine.
Philadelphia: WB Saunders, 1990:82–94.
4. Bennett PB. Inert gas narcosis and HPNS. In: Bove AA, Davis JC, eds. Diving medicine. Philadelphia: WB Saunders, 1990:69–81.
5. Kindwell EP. A short history of diving and diving medicine. In: Bove AA, Davis JC, eds. Diving medicine. Philadelphia: WB Saunders,
1990:1–8.
6. Sanford JP. Medical aspects of recreational skin diving. Ann Rev Med 1974;25:401–410.
7. Betts J. Sports medicine (2). Common medical problems in subaqua sport. Practitioner 1981;225:1169–1174.
8. Smith DJ. Diagnosis and management of diving accidents. Med Sci Sports Exerc 1996;28:587–590.
9. Hardy KR. Diving-related emergencies. Emerg Med Clin North Am 1997;15:223–401.
10. U.S. Navy. Diving manual, Vol. 1. Air. 2nd rev. Washington, DC: Department of the Navy, 1988.
11. Arthur DC, Margulies RA. A short course in diving medicine. Ann Emerg Med 1987;16:689–701.
12. Kizer KW. Diving medicine. Emerg Med Clin North Am 1984;2:513–530.
13. Melamed Y, Shupak A, Bitterman H. Medical problems associated with underwater diving. N Engl J Med 1992;326:3–35.
14. Wolf SL, Twarog F, Weiler JM, et al. Discussion of risk of scuba diving in individuals with allergic and respiratory diseases: SCUBA
Subcommittee [Editorial]. J Allergy Clin Immunol 1995;96:871–873.
15. Neuman TS, Bove AA, O'Connor RD, et al. Asthma and diving. Ann Allergy 1994;73:344–350.
16. Schanker HM, Spector SL. Scuba diving in individuals with asthma. Allergy Asthma Proc 1996;17:311–313.
17. Wallace JM, Stein S, Au J. Special problems of the asthmatic patient. Current Opinion in Pulmonary Medicine 1997;3:72–79.
18. Strauss RH. Diving medicine. Am Rev Respir Dis 1979;119:1001–1023.
19. Neuman TS. Diving medicine. Clin Sports Med 1987;6:647–661.
20. Dickey LS. Diving injuries. J Emerg Med 1984;1:249–262.
21. Bradley ME. Pulmonary barotrauma. In: Bove AA, Davis JC, eds. Diving medicine. Philadelphia: WB Saunders, 1990:188–191.
22. Edmonds C, Lowry C, Pennefather J. Diving and subaquatic medicine, 3rd ed. Oxford, UK: Butterworth-Heinemann, 1992.
23. Replogle WH, Sanders SD, Keeton JE, et al. Scuba diving injuries. Am Fam Phys 1988;37:135–142.
24. Juss JH. Medical aspects of skin and scuba diving. J School Health 1972;42:238–242.
25. Kieser J, Holborow D. The prevention and management of oral barotrauma. N Z Dent J 1997;93:114–116.
26. Francis TJR, Dutka AJ, Hollenbeck JM. Pathophysiology of decompression sickness. In: Bove AA, Davis JC, eds. Diving medicine.
27. Strauss RH. Medical concerns in underwater sports. Pediatr Clin North Am 1982;29:1431–1440.
28. Good RF. Diagnosis and treatment of decompression sickness. A general survey. In: Shilling CW, Carlston CB, Mathias RA, eds. The
physician's guide to diving medicine. New York: Plenum Press, 1984:283–312.
29. Vann RD. Mechanisms and risks of decompression. In: Bove AA, Davis JC, eds. Diving medicine. Philadelphia: WB Saunders,
1990:29–49.
30. Moon RE, Camporesi EM, Kisslo JA. Patent foramen ovale and decompression sickness in divers. Lancet 1989;51:513–514.
31. Wilmshurst PT, Byrne JC, Webb-Peploe MM. Relation between interartrial shunts and decompression sickness in divers. Lancet
1989;2:1302–1306.
32. Bove AA. Medical aspects of sport diving. Med Sci Sports Exerc 1996;28:591–595.
33. Anonymous. Appendix 2. In: Bove AA, Davis JC, eds. Diving medicine. Philadelphia: WB Saunders, 1990:314.
34. Linaweaver, PG. Physical and psychological examination for diving. In: Shilling CW, Carlston CB, Mathias RA, eds. The physician's guide
to diving medicine. New York; Plenum Press, 1984:489–520.
35. Millington JT. Physical standards for scuba divers. J Am Board Fam Pract 1988;1:194–200.
36. Dembert ML. Physical examination of scuba divers. Am Fam Phys 1979;20:91–93.
37. Becker GD, Parell GJ. Medical examination of the sport scuba diver. Otolaryngol Head Neck Surg 1983;91:246–250.
38. Dembert ML, Keith JF III. Evaluating the potential pediatric scuba diver. Am J Dis Child 1986;140:1135–1141.
38 Soccer
38
SOCCER
JOHN H. LOHNES
WILLIAM E. GARRETT, JR.
RAYMOND R. MONTO
The Game of Soccer

Biomechanics of Soccer
Kicking
Heading
Physiology and Conditioning
Nutrition and Fluid Needs
Epidemiology
Incidence, Treatment, and Prevention
Head and Neck
Upper Extremities
Back, Trunk, and Pelvis
Lower Extremities
Contusions
Chronic Compartment Syndrome
Muscle Strain Injuries
Knee Injuries
Tibial Fractures
Ankle Injuries
Foot Injuries
Special Concerns
Indoor Soccer
Women's Soccer
Youth Soccer
Chapter References
Soccer is the world's most popular team sport. Soccer's governing body, the Federation International de Football
Association (FIFA), had 203 member associations in 1998, representing over 200 million active members ( 1). In the
United States, soccer receives less attention as a spectator sport; nevertheless, soccer is the third most popular team
sport among children ages 12 to 18 years, and ranks second in participation among children ages 6 to 11. In 1995, there
were almost 3 million players registered with the three major national youth soccer organizations, and the number of high
school players has increased 150% since 1980. Although three out of four soccer players in the United States are
younger than age 18, adult participation is also increasing rapidly. Registration with the U.S. Amateur Soccer Association
(adults over 19) has doubled in the last 20 years ( 2). The NCAA listed 694 men's and 696 women's varsity college soccer
programs in 1997 (3).
Although it is similar in many ways to other team field sports, soccer is unique in the use of the head and feet to advance
the ball, creating injury patterns and problems particular to this sport. The advent of indoor soccer and the rapid growth of
women's soccer in the last two decades have added new dimensions to this previously male-dominated outdoor game.
This chapter describes the physical demands of soccer; reviews the epidemiology of soccer injuries; and discusses the
mechanisms, pathology, and treatment of common soccer-related injuries and medical disorders.
THE GAME OF SOCCER
Modern soccer involves two teams of 11 players opposing each other on a field measuring approximately 75 m wide by
110 m long. The game is played in two 45-minute periods with a 15-minute half-time. Periods are often reduced to
30-minutes in youth soccer matches. International rules allow only two substitutions during the course of a match,
although unlimited substitution is allowed in U.S. interscholastic and intercollegiate soccer.
Field players are allowed to advance the ball with any portion of their bodies except their arms or hands, although the
ball is thrown in to restart play when the ball goes out of bounds on the sidelines. Goalkeepers may use their arms or
hands but only within the designated “penalty area” around the goal. The ball may be advanced by heading (striking with
the head), passing (kicking the ball to another player using any portion of the foot), or dribbling (running while controlling
the ball with the feet). The ball also may be controlled with the chest or thighs.
Soccer is a moderate-contact sport in which the basic rules are few and open to interpretation by the referee. This can
lead to rough play and increased exposure to injury. Recent trends in the style of play have been away from strict
position orientation and tactics to the concept of total soccer by which all 11 players are involved with every phase of
attack and defense.
BIOMECHANICS OF SOCCER
Biomechanical factors relevant to soccer include the technical performance of soccer skills, the equipment used, and the
causative mechanisms of specific soccer injuries ( 4). Technical skills unique to soccer include kicking and heading. Ball
size and construction, shoewear, protective equipment, and playing surface conditions are all mechanical factors that can
be potentially modified if implicated in injuries. Individual playing styles and techniques are less easily controlled.
Kicking
The ball may be struck with any portion of the foot. The medial and lateral sides of the foot are generally used for making
short, accurate passes. However, the instep kick is the primary method for advancing the ball powerfully over a long
distance.
The standard soccer ball weighs 400 to 450 g and is made of molded plastic or stitched plastic-coated leather. The
plastic prevents the ball from becoming saturated with water. The standard size 5 ball has a circumference of 68.5 to 71
cm and should be inflated to a pressure of between 8.5 and 15.6 pounds per square inch (psi). Smaller sized 3 or 4 balls
are used by young children.
A strong instep kick can accelerate a soccer ball to speeds in excess of 120 km per hour ( 5). The typical instep soccer
kick consists of three main phases: approach, ball strike, and follow-through. Biomechanical analyses of the soccer kick
by Gainor et al. ( 6) have demonstrated that the usual instep kick generates a varus torque on the proximal tibia greater
than 200 Newton-meter (N-m) during approach and ball strike. This is followed by an equally large valgus torque on the
tibia during follow-through. There are even higher amounts of extension torque on the proximal tibia during approach,
ball strike (280 N-m), and follow-through (230 N-m). By comparison, the standard North American football toe kick exerts
similar extension-flexion torque on the knee but does not exhibit varus-valgus torque.
The majority of this torque is generated by the hip flexors that act concentrically with the knee extensors as agonists
during the kicking motion (Fig. 38.1). In addition to the dramatic forces on the thigh and abdominal musculature during a
kick, the soccer player's knee joint must withstand large translational and rotational stresses. This may help to explain the
frequent occurrence of knee injuries during unchallenged kicks.
FIGURE 38.1. The long soccer volley just before ball strike, demonstrating forceful contraction of hip flexors and
abdominal musculature.
The maximum kinetic energy generated by a soccer kick has been estimated at 2000 N-m ( 5). This force is of sufficient
magnitude to fracture a femur. Because only 15% of this kinetic energy is actually transferred to the ball, the remaining
amount must be absorbed by the kicking leg. The majority of this force is dissipated by the hamstrings as they fire
eccentrically to decelerate the kicking leg during follow-through. Because of this, the leg is quite vulnerable to injury
during this stage of the kick. Any incidental contact with the ground or the leg of a defender creates additional impact
loads and retards force dissipation in a leg already functioning at the limits of force toleration. This can lead to fracture
or, more often, ligamentous disruption.
Because of these high energies, the kicking leg can itself become a dangerous projectile during follow-through. The
hazard to the player challenging the kicker is increased because the transferred force cannot be efficiently dissipated.
Heading
One of the unique facets of soccer is the use of the head to advance the ball. A soccer player heads the ball an average
of six times during a match (7). Given the large impact energies that are generated at ball contact, the skull, cervical
spine, and neck musculature are subjected to high stresses. Several recent biomechanical studies have documented the
extent of these stresses and their potential for acute and chronic injury.
Schneider and Zernicke (8) used a dynamic head-neck model to study the biomechanics of the interaction. In a series of
studies, they compared frontal and lateral head impacts in adults and children, using various mass ratio–impact velocity
combinations. By comparing measurements of linear and angular acceleration velocities with standard industrial head
injury tolerance criteria, the relative risks of head trauma were obtained.
They concluded that the injury risk from angular head accelerations is greater than that from linear head accelerations.
Lateral head impacts have greater angular accelerations than linear accelerations compared with frontal impacts and are
considered more dangerous. This is because the moment of inertia of the head for rotations about the sagittal axis is less
than for those about the coronal axis. Linear accelerations are also higher during frontal impacts because of increased
axial mobility of the head. The study concluded that at the low mass ratios present when children use a standard soccer
ball (size 5), angular accelerations exceeded head injury tolerance levels for frontal impact at ball velocities faster than 9
m per second and for lateral impacts faster than 7.5 m per second. These represent relatively slow ball speeds for a
soccer match. Linear accelerations were better tolerated but still eclipsed safe levels at ball speeds greater than 21 m
per second.
For the higher mass ratios in the range commonly seen in adult soccer, angular accelerations were found to result in
significant injury risk for frontal impacts at velocities more than 19.5 m per second and for lateral impacts higher than 13
m per second. Unlike the lower mass ratio data found in children, linear accelerations were found to be within safe levels
for frontal and lateral impacts at all ball velocities. Based on these data, it is recommended that mass ratios be
maximized by using smaller, lighter balls in youth soccer and prohibiting the use of adult-size balls by children younger
than age 12. Hazardous lateral head impacts should also be minimized by emphasizing proper heading techniques.
These conclusions were echoed in a mathematical study by Townend ( 9) that documented a linear relationship between
impact force and ball mass. Impact forces were also higher when lighter (i.e., younger) players headed balls of equal
size.
Townend calculated the impulsive force absorbed by the head at ball impact to vary between 669 and 689 N. Other
experimental measurements at ball velocities of 18 m per second have found peak impact forces of 851 N for molded
soccer balls and 912 N for stitched balls ( 10). Despite this higher force profile, stitched balls may be safer because they
take nearly 28% longer to reach their maximal force at impact than do molded balls. This increased rise time allows more
time for force dissipation by the head and neck.
Although the impact forces during soccer heading may be an order of magnitude lower than the 6300 N that a
heavyweight boxer can deliver with a punch to the head, there is a growing body of evidence to suggest that they may
still lie in the hazardous range. The average duration of ball impact in soccer heading is 13 to 18 msec ( 8,11). Impact
forces of only 670 to 1100 N can cause zygoma fractures in cadavers ( 8). In contrast, the forehead requires much higher
impact forces (1700 to 4000 N) for fracture production, again emphasizing the importance of proper heading techniques
to avoid injury. Burslem and Lees ( 11) have demonstrated that, unlike unskilled players, skilled players decelerate their
heads to produce head-neck-torso rigidity at ball impact. This lowers the risk of injury by decreasing rotational
accelerations of the head at contact and thus minimizing the magnitude of the impact force. With the rigidity afforded by
good techniques, these impact forces also are dissipated through a longer kinetic chain. Because the impact forces
involved in soccer heading normally lie at the upper limits of safety, significant injury can result from any combination of
poor techniques, accidental contact, or ball-to-head weight mismatch.
The incidence of head and neck injuries and clinical evidence of the long-term effects of repetitive soccer heading are
discussed later in this chapter.
PHYSIOLOGY AND CONDITIONING
Soccer requires frequent bursts of high-intensity anaerobic activity within longer periods of aerobic exercise. Rapid
changes in speed or direction, fast reaction time, and a high level of psychomotor coordination and agility are all key
requirements of the sport. Time-motion analyses of soccer players have found that the typical adult competitive field
player covers approximately 10 km during a match (12). This distance is covered by a combination of jogging (40%),
walking (25%), cruising (15%), sprinting (10%), and backing (10%) ( 13). Midfielders typically cover 10% greater distance
on average than forwards and defenders. Interestingly, the average length of time an individual player actually has
possession of the ball during a match is no more than 2 min ( 14).
The physical demands of a soccer match can be extreme. Aerobic metabolism is frequently stressed to 80% or more of
maximum, heart rate may increase to 150 per minute, and venous lactate levels reach up to 12 mmol per L ( 15).
Likewise, the distance covered does not reflect the amount of energy expended due to the rapid directional and speed
changes (16). Muscle glycogen stores have been found to be completely diminished in top-level players following a
game, with corresponding decreases in speed and distances traveled as the match progresses. In hot weather,
approximately 5 kg of fluid loss has been observed ( 17).
Despite the intense physical demands of a match, the physiologic training effects of soccer tend to be midway between
those of a pure endurance sport such as distance running and an anaerobic sport such as sprinting. Vo 2max
measurements of soccer players have been found to range widely between 50 and 70 mL per kg per minute, depending
on player position, level of play, and type of training ( 15). Increased heart size, decreased resting heart rate, and
increased forced expiratory volume and flow have been observed as training effects of soccer ( 17). Muscle fiber number
and size, muscle capillary density, and muscular power have also been found to be increased in soccer players
compared with nonathletes of the same age (18). The small-sided version of soccer (four or five players to a side) tends
to result in a greater physiologic work rate than the normal game and may be a useful training method for improving
overall fitness levels ( 19).
Unlike some other sports, body size and mass are less important determinants of success in soccer than they are in
certain other team sports such as American football or basketball. However, several researchers have observed that
postadolescent and adult soccer players tend toward mesomorphy or mesoectomorphy ( 20,21). The trend toward leaner,
taller, and heavier players has been observed in many other sports and may simply be reflective of the general trends in
the population ( 22). It is unlikely that somatotype is an important predictor of individual soccer skill or of team success.
When compared with other athletes, both male and female soccer players tend to fall in the midranges of various
measures of fitness, including aerobic endurance, anaerobic power, and strength ( 13,23,24 and 25). This reflects the
hybrid physical demands of the sport. As with other sports, the level of fitness increases with the level of play, with
national team and professional players exhibiting the highest fitness levels ( 24,26,27). Differences in fitness levels
between different player positions have been observed, with midfielders tending to exhibit greater levels of strength and
endurance than other players ( 28,29).
Various physical tests to measure soccer fitness have been devised, but no single test has been found to be an accurate
predictor of soccer success. Other less easily measured factors such as psychomotor coordination and agility, tactical
skill, and even personality type are equally important determiners of soccer ability. Thus, conditioning for soccer players
consists ideally of a mixture of endurance, strength, and technical skill training, plus instruction in tactical strategies.
NUTRITION AND FLUID NEEDS
A field player may use up to 90% of muscle glycogen reserves during a strenuous match or practice ( 17,30,31). Because
of the frequency of training and competition during a typical season, soccer players need to pay close attention to the
timing, quality, and quantity of carbohydrate consumption.
A competitive adult soccer player requires about 8 g of carbohydrate per kilogram of body weight (3 to 4 g per pound).
Carbohydrate loading as practiced by endurance athletes is probably not particularly helpful for soccer players before a
match under most circumstances and may be impractical given the frequency of games. However, a diet consisting of
about 60% complex carbohydrates should be maintained through the competitive season. The pregame meal should be
eaten 3 to 4 hours before competition to allow adequate time for gastric emptying. Meat and fried foods should be
avoided and liquids encouraged.
When a series of matches are to be played within a short span of time, as in tournament competition, particular attention
should be paid to replenishing glycogen reserves. It may take up to 48 hours to replenish muscle glycogen after
exhaustive exercise. However, studies indicate that muscle is most avid for glycogen during the first 4 hours after
competition; therefore, carbohydrate consumption should be particularly encouraged during this time. The use of glucose
polymer drinks has been shown to aid glycogen replacement. In limited quantities, they may also be useful immediately
pregame and perhaps at half-time. However, because these drinks may also slow fluid absorption, they are not
recommended for use during games in hot weather but are reserved for immediate postgame consumption.
Endurance training can influence the rate of muscle glycogen depletion by sparing glycogen in favor of fatty acids as a
source of energy. Endurance training will be of particular benefit to midfielders who tend to run greater distances during a
match.
Soccer players, like most competitive athletes, require between 1 and 1.5 g of protein per kg of body weight. Most people
typically consume more than this amount daily, so protein supplements are unnecessary, particularly because excess
protein is not stored in the body. Likewise, vitamin and mineral supplements are usually unnecessary if the player is
consuming a well-balanced diet.
Plenty of plain, cool water should be consumed during matches and heavy practice sessions. During extreme conditions
of heat and humidity a player may lose 2 to 3 kg of fluid. To avoid dehydration and heat exhaustion a player should drink
150 mL every 15 min. Weighing before and after exercise can help gauge the amount of fluid lost, with each pound of
body weight being equivalent to about 2 cups of water.
Elias et al. ( 32) established guidelines for tournament play in severe heat conditions based on experience with a large
youth soccer tournament. In an effort to avoid morbidity caused by dehydration and heat exhaustion, modification in
game timing and structure were recommended based on the wet bulb globe temperature (WBGT), which accounts for
both relative humidity and ambient temperature. For WBGT greater than 82°F (28°C), they suggested the following
modifications to the game: unrestricted substitutions, shorter game time, fluid breaks during play, quarter breaks, and
rescheduling to a later or earlier time of day.
EPIDEMIOLOGY
Given the popularity of the sport, it is surprising that there have been few well-controlled, long-term prospective studies of
soccer injuries. Most of the reports available are limited in either time or scope or have been retrospective in nature.
Therefore, it is difficult to state accurately either the incidence or prevalence of injuries in soccer.
There are many cohort studies available that examine injuries occurring during a league or club season
(33,34,35,36,37,38,39,40,41,42,43,44,45,46,47 and 48). The ages and numbers of participants, the level of competition,
and the methods of injury reporting tend to be quite variable in these studies; nevertheless, some consistent general
trends regarding injury patterns can be observed. The best of these studies are of professional European teams.
Although these studies typically involve relatively small numbers of elite players, the subjects can be observed more
closely with consistent follow-up and reporting methods.
Several prospective studies exist of injuries occurring over a series of days or weeks in tournament events or camps
(49,50,51,52 and 53). The populations in these studies are typically large and the conditions well controlled, with
improved reporting of injury by having medical care available on site. The incidences of injury reported in these studies
tend to be higher than those observed in other studies, perhaps because even minor injuries are recorded, not just those
that result in lost playing time.
Other studies (54,55,56,57,58,59,60,61,62 and 63) have looked retrospectively at soccer injuries presenting to hospitals or
clinics or reported to insurance companies. The population sizes in these studies are usually large; however, there is
reporting bias inherent in such studies because only the players who seek medical care are recorded. Therefore, the
incidence or prevalence may be underestimated. Nevertheless, they do provide percentages of the types and locations of
injuries.
The only large ongoing prospective record of adult soccer injuries in the United States is conducted by the Injury
Surveillance System of the National Collegiate Athletic Association (NCAA) ( 3). This project has compiled sports injury
statistics on a sample of Divisions I, II, and III college teams since 1982. Men's and women's soccer has been included
annually since the 1986–1987 season, making it possible to view injury trends over several years. A total of 105 men's
teams and 97 women's teams contributed to this project in 1998–1999. Injury incidences have tended to remain fairly
constant through the seasons examined and will likely become more accurate as the number of participating schools
increases. At present, these data are probably the most reliable figures available for adult soccer injuries in the United
States. Injury incidence or rate is reported per 1,000 “athlete exposures” (AE) rather than as a percentage of total
numbers injured. An athlete exposure is one athlete participating in one practice or game in which he or she is exposed
to the possibility of injury. This reporting method more accurately describes the risk associated with participation rather
than simply providing total numbers. A reportable injury is defined as one that causes the loss of at least one day of
participation. The mean total injury rates for men's and women's teams during the period from 1986–1998 are
summarized in Table 38.1. For both men and women, only about 25% of all injuries resulted in more than 6 days missed
from participation.
TABLE 38.1. AVERAGE INJURY RATES IN NCAA COLLEGE SOCCER (1986–1998) PER 1,000 ATHLETE
EXPOSURES
It is impossible to compare directly the results of the various epidemiologic studies reviewed because of differences in
population size and demographics, levels of play, and the definition and reporting of injuries. However, some general
trends can be observed in all studies.
The incidence and severity of injuries increases with increasing age, level of play, and frequency of competition.
The incidence of injury varies widely in reported studies, from 2 to 40 per 1,000 exposure hours but with an average
of about 12 per 1,000 hours.
The rate of injury in games is greater than that in practice.
Injuries in youth players, especially those younger than the age of 12 years, are uncommon and typically do not
result in significant lost playing time.
For reasons not yet explained, girls appear more likely than boys to be injured in the younger age groups. This
difference typically disappears after puberty, with the notable exception that knee injuries are about twice as
common in women players than men of the same age and playing level.
Center forwards and midfielders have the highest injury rates, although goalkeepers are the most likely to sustain
upper extremity injuries.
Injuries to the lower extremities account for between 50% and 66% of all injuries.
Contusions, ligament sprains (especially ankle sprains), and muscle strains account for about 75% of all injuries.
Serious, permanently disabling injuries are, fortunately, rare, accounting for less than 0.1% of injuries at all levels.
Knee injuries usually result in the most time lost from participation.
INCIDENCE, TREATMENT, AND PREVENTION
Head and Neck
Acute Injuries
Injuries to the head, face, and neck account for between 5% and 15% of all injuries. Typically, these injuries are minor
lacerations, abrasions, or contusions. Skull fractures, concussions, and cervical spine trauma occur infrequently despite
the absence of protective headgear and the sometimes large forces sustained by heading the soccer ball. A recent
prospective study of collegiate players found the incidence of concussion to be 0.4 per 1,000 AE in women and 0.5 per
1,000 AE in men (64). The NCAA Injury Surveillance System data suggest even higher rates in game situations. The
majority (72%) of these concussions were grade I, usually the result of collision with other players, the ground, or the
goalpost, not from intentional heading of the ball.
Sane and Ylipaavalniemi ( 65) reported on dental injuries sustained in soccer. They reviewed 8,640 soccer injuries
occurring in players ages 8 to 47 years and found that 6.4% affected the teeth, alveolar processes, or lower or middle
third of the facial skeleton. Only 4.3% of the injuries occurred in players younger than age 15 years. These findings are
similar to those seen by Nysether ( 66). Both authors recommended the use of protective mouthpieces or dental guards.
Burke et al. (67) reviewed 12 soccer ball–induced eye injuries in youth players (ages 6 to 21). Hyphema and retinal
edema were present in all injuries. Vitreous and retinal hemorrhage, corneal abrasion, traumatic iritis, and retinal tear
also were observed, although in no case was there any permanent impairment. Similar findings were reported by Orlando
(68).
There is some controversy regarding the benefits of protective headgear—helmets, eye protectors, and dental
guards—in soccer, especially for children. Serious eye injuries are very rare in soccer, and it may be argued that the use
of eye protectors actually increases the risk of facial lacerations and contusions. Dental guards, however, can reduce
dental injuries and are especially recommended for goalkeepers and for players with orthodontic devices, caps, or other
dental work. The risk of dental injuries for other field players is relatively low and mandatory use of protective mouth
guards may be unwarranted. Nevertheless, their use should be encouraged.
The most important preventive measure for avoiding acute head and neck injuries from the ball is to establish proper
heading techniques, using the head actively to counteract the force of the oncoming ball with the forehead rather than
passively absorbing the shock with the top of the head. As mentioned earlier, the use of smaller balls for youth players
also can significantly reduce the risks inherent in heading the ball.
As in all sports, any injured player who loses consciousness should be sent to a medical facility for further evaluation and
observation, regardless of his or her symptoms on regaining consciousness. Likewise, any player who complains of neck
pain, radicular pain, numbness, tingling, or weakness in the extremities following acute injury should be assumed to have
a cervical spine fracture until proven otherwise. These players should be immobilized on the field and transferred to a
medical facility for radiographs and evaluation.
Chronic Effects of Heading
The possible chronic effect of repetitive soccer heading has been a subject of some controversy. Reports of impaired
cognitive function, cerebral atrophy, and brain wave abnormalities have been reported as well as accelerated
degenerative changes of the cervical and lumbar spine. Tysvaer et al. ( 69,70) conducted a series of studies to investigate
the neurologic effects of heading. One study of 69 Division I Norwegian players (mean age 25 years) demonstrated a
higher incidence of electroencephalographic (EEG) disturbances in soccer players compared with a control group. A total
of 54% had a history of significant head injury while playing soccer and 55% complained of intermittent headaches
associated with playing. Another four players had had concussions, and 12% gave a history of protracted symptoms
related to their head injuries. Although only one of these players had an abnormal neurologic clinical examination, 35%
displayed abnormal EEG tracings compared with only 13% in the control group. Abnormal EEGs were seen with more
frequency in the younger players: 44% of the 15- to 24-year-olds compared with 26% of the 24- to 34-year-olds. Across
(71,72) found similar EEG changes.
Sortland and Tysvaer (73) performed computerized tomography (CT) scans of the brains of 33 former elite soccer players
with an average age of 49 years and compared them with normal standards of cerebral architecture. They found that 27%
had central cerebral atrophy with widening of the lateral ventricles. Cortical atrophy was seen in 18%, and 6% had a
septum pellucidum cyst. Only 1.5% of normal adults have these type of cysts. Large cysts of the septum pellucidum are
classically seen in boxers who have sustained repeated subconcussive blows to the head.
In an attempt to provide clinical correlation for these findings, Tysvaer et al. ( 70) performed an extensive battery of
psychological tests on these former players. Of 37 players examined, 81% exhibited mild to severe deficits in
psychological tests of attention, concentration, memory, and judgment. These results were attributed to neuronal damage
caused by repeated minor head trauma. Similar findings were reported by Matser et al. ( 74). The effects of repeated
concussions is likely more of a factor in possible long-term problems than is routine heading of the soccer ball.
Another study by Tysvaer et al. ( 75) examined the possible chronic effects of heading on the cervical spine. Radiologic
and clinical examinations were performed on a group of 43 former Norwegian national soccer team players and
compared the results with age-matched controls. A total of 21% of the former players had chronic neck pain or stiffness,
and 58% had decreased range of neck motion. Five of these players (8%) had evidence of healed compression fractures
of the lateral masses, and the majority demonstrated accelerated degenerative arthrosis at all cervical levels compared
with the control group.
Further studies are needed to determine the significance of these findings and to make possible recommendations for
prevention. However, players with a history of protracted headaches, nausea, dizziness, visual field disturbances, neck
pain, or radicular upper extremity symptoms after heading should be restricted from heading. These players should be
further evaluated for subtle brain or cervical spine pathology with EEG, CT, or magnetic resonance imaging (MRI) scans,
or cervical spine radiographs.
Upper Extremities
Although injuries to the upper extremities (shoulder, elbow, arm, and hand) are commonly encountered in soccer, they
seldom result in extensive lost playing time for most field players and are not discussed in detail here. More detailed
descriptions of the evaluation and treatment of upper extremity injuries can be found elsewhere in this text.
Upper extremity injuries account for between 5% and 15% of all soccer injuries and are far more common in goalkeepers
than in field players. In the NCAA, the incidences of injuries to the upper extremities (shoulder, arm, and hand) typically
range between 1 and 1.5 per 1,000 AE ( 3).
Curtin and Kay (76) reviewed 52 soccer-related hand injuries. Approximately 33% occurred in goalkeepers, mainly the
result of contact with the ball. Other players usually injured the hand through contact with the ground or another player.
Phalangeal fractures were most common—17 out of 47—and usually involved the dominant hand. For goalkeepers,
finger injuries are typically sustained by catching the ball on the end of the finger, with fractures to the distal or middle
phalanges or the interphalangeal joints. Despite the advent of padded gloves, there has been little change in the
incidence of hand injuries in goalkeepers.
Forearm fractures and wrist fractures or sprains may also occur as the goalkeeper attempts to stop the oncoming shot
(Fig. 38.2). Fractures of the scaphoid are of particular concern due to the risk of nonunion ( 77). Shoulder
acromioclavicular separations are not infrequent in field players. They are caused by falls on the shoulder or outstretched
arm.
FIGURE 38.2. Humerus fracture in goalkeeper.
Back, Trunk, and Pelvis
Injuries above the waist to the back or thorax are uncommon in soccer. Injuries below the waist to the pelvis, hips, and
groin are slightly more common, but combined injuries to the back, thorax, abdomen, pelvis, and groin generally account
for less than 10% of all injuries resulting in lost playing time. Complaints of lower-back pain are most often the result of
muscle strains or ligament sprains and usually respond well to conservative management. However, persistent or
recurrent back pain or radicular symptoms should warrant a further diagnostic evaluation. Congenital spondylolisthesis is
not an uncommon source of lumbar pain in young soccer players and is often aggravated by playing on hard or artificial
surfaces. Spondylolysis or fractures of the pars interarticularis may also occur in goalkeepers because of the repetitive
lumbar hyperextension required in diving saves. Degenerative disk disease and disk herniation are much less common,
but both are known to occur at a younger age in the athlete than in the general population.
Injuries to the lower trunk, pelvis, or upper leg are common in soccer, although the actual incidence of these injuries is
difficult to determine. The true location of the injury may be obscure and the pathology may be recorded differently in
different epidemiologic studies. Martens et al. ( 78) in Belgium treated 109 athletes with either adductor tendinitis or
rectus abdominus tendopathy; of these, 95 (87%) were soccer players. The iliopsoas is also a frequently injured muscle
in soccer players (79).
Chronic Groin Pain
Soccer places repetitive stresses on the hip, inner thigh, and lower abdominal musculature, making both acute and
chronic injuries to these areas quite common. Recurrent adductor and abdominal strains, tendinitis, osteitis pubis, and
osteoarthritis are all frequent sources of chronic groin pain in the athlete ( 80). Inguinal hernias and genitourinary and
visceral pathology should also be considered.
One notable condition common in soccer players involves pain related to a weakness in the pelvic floor musculature
between the inguinal canal and the rectus abdominus insertion ( 81,82). Known variously as “athletic pubalgia,” “Gilmore
groin,” or “sportsman's hernia” in the literature, the problem often eludes easy diagnosis and is notoriously unresponsive
to conservative management.
The exact cause of pain in this condition is poorly understood but mimics a direct hernia in presentation. The internal
oblique begins lateral to the cord and traverses proximally and medially, with a few fibers looping back down behind the
cord to attach onto the inguinal ligament along the pectineal eminence. These fibers conjoin with the transversalis tendon
and often are quite weak in men, and indeed there may be no contribution of the internal oblique to this conjoined
tendon. Repetitive overloading at this site may cause recurrent inflammation and pain. Concurrent tightness of
lower-back, hamstring, gluteus, and other posterior pelvic musculature is also thought to be a contributing factor ( 83).
Osteitis pubis and sacroiliac abnormalities may coexist with this condition, and several authors believe these problems
are related ( 84).
Sometimes, there may be an acute groin strain that initiates the pain. However, frequently the onset is insidious,
presenting as progressive pain while running and often lasting several hours or days afterward. It is aggravated by
activity and usually relieved by rest but usually returns quickly even after prolonged periods of rest. The pain is primarily
felt in the inguinal area but frequently radiates posteriorly to the ischium or superiorly to the lower abdomen and may be
difficult for the player to clearly localize. There may be point tenderness in the inguinal area, especially at the anterior
pelvic tubercle near the rectus abdominus insertion. Rarely is an actual hernia or defect palpable. Active hip flexion,
adduction, and internal rotation usually reproduce sharp pain. Sit-ups may also be painful. Diagnostic studies such as
radiographs, bone scans, CT, and MRI are frequently negative, although MRI may demonstrate abnormal signal in the
superior pubic ramus (85).
Nonsteroidal antiinflammatory drugs (NSAIDs), cortisone injections, and standard physical therapy usually provide little
or only temporary relief of athletic pubalgia. In some cases, physiotherapy that combines deep tissue massage and
stretching of the lower back and posterior pelvic musculature with progressive strengthening of adductor and abdominal
muscles has proved successful. Unfortunately, conservative treatment frequently fails to relieve symptoms in many
players. In a study by Martens et al. ( 86), 70% of the patients treated conservatively did not improve and eventually
underwent surgical procedures. A variety of surgical techniques have been recommended for athletic pubalgia. Most of
these involve reinforcing the pelvic floor musculature or tenotomy of the adductor longus. A modified Bassini-type
herniorrhaphy has proved highly successful. In this procedure, the transversus abdominus aponeurotic arch is sutured to
the lacunar-inguinal ligament and the conjoined tendon is reinforced near its insertion along the pectineal eminence.
Adductor longus tenotomy is also recommended when there is clear tenderness at the tendon origin.
LOWER EXTREMITIES
Lower-extremity injuries account for approximately 60% or more of all soccer injuries. Contusions to the lower extremities,
muscle strains of the thigh (adductors, hamstrings, and quadriceps), and ankle sprains are the most common acute
injuries. Stress fractures and a variety of overuse injuries involving the leg, ankle, and foot in adult soccer are overuse
injuries frequently encountered by soccer players. In the NCAA Injury Surveillance System record, the ankle has
consistently been the most frequently injured body part, with the upper leg and knee generally following second and third
(3).
Contusions
Contusions to the thigh and calf are common but rarely result in much lost playing time. The use of shin guards greatly
reduces the frequency of leg contusions and is now required in many leagues. Deep muscle contusions, however, can be
quite disabling and may lead to complications such as acute muscle compartment syndrome or myositis ossificans.
Acute Compartment Syndrome. A compartment syndrome is the result of increased pressure within an enclosed fascial
space, causing local tissue hypoxia with secondary ischemic muscle and nerve damage. Acute compartment syndrome
occurs when local capillary flow is compromised following blunt trauma or fracture when local tissue pressure reaches
within 40 mm Hg of the mean arterial pressure. As intracompartmental pressures continue to rise, progressively more
severe neuromuscular damage ensues. The duration of compromise is particularly critical. At 30 minutes, tissue
compromise is fully reversible. Although capillary damage occurs at 3 hours, full clinical recovery is still possible after 4
hours of elevated compartment pressures. After 6 hours, tissue damage is only partially reversible and recovery is
incomplete. A delay of 8 hours or more leads to permanent cell death and a poor prognosis for functional recovery. As
pressures increase, less time is available for diagnosis and effective surgical relief.
Diagnosis of acute compartment syndrome relies on clinical suspicion and invasive documentation of intracompartmental
pressures with Wick catheter measurements. Pain is usually the primary symptom and is aggravated by passive motion
of the joints adjacent to the involved compartment. Any player with persistent pain and swelling in the calf after sustaining
a direct blow should be monitored closely for the next several hours. The presence of pulses can be misleading, because
local intracompartmental tissue pressures do not usually exceed arterial blood pressure in even the most severe cases.
Numbness and paraesthesias, however, are a disturbing sign of local tissue compromise and possible compartment
syndrome. The presence of an open wound does not exclude a concomitant diagnosis of acute compartment syndrome.
Acute compartment syndrome is a surgical emergency. Documentation with Wick catheter measurements of all four
compartments (anterior, lateral, posterior, and deep posterior) of the lower leg should be made both before and after
surgical release. The limb should not be elevated, because this only serves to aggravate the condition by decreasing the
local arteriovenous pressure gradient. Ice should also be avoided because of its capillary constrictive effects, which
could exacerbate local tissue ischemia.
Myositis Ossificans. Myositis ossificans is another possible complication of deep muscle contusions, especially to the
anterior thigh. As Walton and Rothwell ( 87) suggest, the development of myositis ossificans following blunt trauma may
be caused by inefficient force transfer in the deeper muscle layers. Clinical examination reveals a tender, erythematous,
firm mass in a previously traumatized muscle group. Radiographs demonstrate a fluffy opacity with increased peripheral
density. Histologic studies are frequently misleading and can imply a tumor. For this reason, biopsy of a suspected
myositis ossificans lesion should be discouraged.
Treatment of a deep thigh contusion is symptomatic at first with rest, ice, and NSAIDs. Massage should definitely be
avoided. Some authors have recommended immobilizing the knee in flexion for the first 24 hours to tamponade the
bleeding and avoid the development of a hematoma. Later, passive range-of-motion and whirlpool helps to maintain
mobility, although crutches may be required for several days.
Players who do develop myositis ossificans can generally be treated conservatively with NSAIDs. Surgical removal can
be difficult and should be reserved only for symptomatic patients with lesions at least 6 months old. This approach allows
the zone of injury to mature and decreases the chance of recurrence ( 88). Players who develop recurrent or multiple
myositis ossificans lesions should have their blood clotting status evaluated with a coagulation profile.
Chronic Compartment Syndrome
Chronic exertional compartment syndrome is frequently seen in soccer players and represents a real diagnostic and
therapeutic challenge for the physician. The usual location of chronic exertional compartment syndrome is the anterior
compartment of the leg, although it can involve the lateral or deep posterior compartments as well ( 89). The differential
diagnosis includes tibial stress fracture, venous thrombosis, local nerve compressions, and periostitis. In the older player,
intermittent claudication should also be considered. Frequently the condition is perceived as shin splints, with pain
increasing with the intensity of exercise and improving with rest.
Muscle bulk increases up to 20% during exercise and this may contribute to a transient elevation in intracompartmental
pressure. As the pressure rises, the blood flow to muscle during the relaxation phase decreases, resulting in a cramping
leg pain. The symptoms are frequently bilateral and sometimes are accompanied by swelling or numbness extending to
the dorsum of the foot.
Some key diagnostic clues in the history are that the symptoms tend to resolve quickly, usually within 1 hour after
stopping exercise, and are not present with normal daily activities. Furthermore, players with a chronic compartment
syndrome cannot play through the pain. This is unusual for the soccer player who is accustomed to frequent
lower-extremity injuries and typically has some chronic leg or foot problem.
Diagnosis of chronic compartment syndrome can be confirmed with Wick catheter measurements of preexercise and
postexercise intracompartmental pressures. Resting pressures may be slightly higher than normal subjects but frequently
are not greater than 15 mm Hg. However, postexercise pressures that remain greater than 15 mm Hg for more than 15
minutes are considered abnormal.
Chronic compartment syndrome may be treated effectively with elective surgical release of the involved muscle
compartment. This may be accomplished on an outpatient basis through small incisions. Total rehabilitation varies from 6
to 12 weeks, with deep compartment involvement leading to a longer recovery period.
Muscle Strain Injuries
Although frequently overlooked as minor injuries, muscle strains can nevertheless become chronic, recurrent, and
refractory to therapy. Strains of the hamstrings, adductors, and quadriceps are extremely common in soccer players and
result in extended periods of limited or lost playing time. Recent advances in the understanding of the basic pathology
and healing of muscle strains have helped in both the treatment and prevention of these troublesome injuries.
Pathophysiology and Healing
Muscle strains typically occur in eccentrically loaded muscles which span two joints (e.g., quadriceps, hamstrings, and
gastrocnemius). A high percentage of strain injuries occur in type II muscle fibers, with the tear occurring at the
muscle–tendon junction. The syncytial nature of muscle fibers is thought to ensure fiber viability even though the terminal
portions of the fibers are disrupted ( 90). The cellular response following strain injury follows a characteristic sequence.
Hemorrhage occurs initially around the ruptured fiber ends followed by fiber necrosis and inflammation during the first 24
hour (Fig. 38.3). By 48 hours after injury, there is a proliferation of inflammatory cells and fibroblastic activity at the
myotendinous junction with complete breakdown of muscle fibers. After 7 days, hemorrhage, edema, and inflammation
are seen to resolve and muscle regeneration becomes evident with fibrosis and myotube formation ( 91).
FIGURE 38.3. MRI scan demonstrating increased signal (edema and hemorrhage) in the left adductor longus following
strain injury in 25-year-old professional soccer player.
The treatment of grade I and II muscle strain injuries should be accomplished with the above-mentioned pathophysiology
in mind as well as the anatomy and kinematics of the particular muscle involved. Ice, compression, and elevation during
the first 24 hours will help limit bleeding and edema. NSAIDs have been shown to be effective in controlling the pain
associated with the inflammatory response, but it remains unclear whether they significantly alter the course of healing
(92).
Immobilization of muscle strains is generally not recommended, because it results in muscle atrophy, diminished ability to
produce force, and shortening of the muscle–tendon unit. Gentle, passive range-of-motion exercises should be started
soon after strain injury, followed by active motion and strengthening as tolerated.
Occasionally, complete rupture (grade III) muscle tears do occur and may require surgical repair. However, even some
grade III tears result in no functional disability because other muscles in the group hypertrophy and compensate.
Complete rupture of the rectus femoris is a common example of this in soccer players ( Fig. 38.4).
FIGURE 38.4. Clinical appearance (A) and CT scan of a rectus femoris rupture (B).
Prevention
Warmup and stretching have been assumed to prevent or limit the severity of muscle strain injuries and are routine in
most training programs. However, the amount and type of warmup and stretching varies widely. Experimental studies in
animal models have demonstrated that activated (contracted) muscle can absorb more energy before tearing than
unactivated muscle (93). Likewise, warming of the muscle also increases the load required for failure.
Passive stretching does decrease the stress on a muscle at a given length owing to the viscoelastic properties of the
muscle fibers (94). In experimental studies only three or four repetitions of a stretch are required to improve muscle
elasticity and decrease the risk of strain injury.
Knee Injuries
Acute Knee Injuries
Knee injuries in soccer are less frequent than may be expected but are of great concern because they result in
substantial physical disability, financial cost, and lost playing time, and may end a career. Knee injuries are the most
common reason for surgeries in soccer. Engstrom et al. (95) investigated the incidence and effects of serious knee
injuries in a group of 64 elite professional male players. Of these, 12 players sustained major knee injuries that resulted
in 80 to 348 days of missed playing time. Of these, seven were to the anterior cruciate ligament (ACL) or medial cruciate
ligament (MCL). The authors concluded that of all the injuries observed in the course of their study, knee injuries
accounted for the most time lost.
Meniscal tears and ligament injuries in soccer typically result from pivoting or sudden deceleration stresses rather than
from direct contact as in American football or rugby. The role of neuromotor control and proprioception in causing ACL
injuries is under investigation, and there is some evidence that the incidence of these injuries in soccer may be reduced
through greater emphasis on proprioceptive training ( 96). Articular cartilage or osteochondral injuries are also not
infrequent and may result from the hyperextension loading of the strong shot or kick. Such lesions typically occur in the
femoral condyle and should be strongly suspected when a persistent effusion develops in the absence of discrete point
tenderness or instability ( 97) (Fig. 38.5). An MRI scan can be extremely helpful in confirming this diagnosis. Osseous or
osteochondral injuries should always be suspected in association with ACL or MCL tears. Isolated posterior cruciate
ligament tears can occur if the player is struck directly against the anterior tibia as the femur and upper body continue
forward.
FIGURE 38.5. Articular cartilage defect of medial femoral condyle in 27-year-old female soccer player.
Tears of the ACL are generally the most disabling of knee injuries for the soccer player and accounted for the majority of
time lost due to knee injuries in most of the studies reviewed. For unknown reasons, the rate of ACL tears in women is at
least twice that seen in men at similar levels ( 98). Few soccer players are able to remain competitive with an
ACL-deficient knee despite strengthening and bracing, and surgical reconstruction should be recommended for all
patients who wish to continue the sport. Successful return to a highly competitive level is possible following surgery and
rehabilitation, although two recent reports from Europe showed that a high percentage of players studied eventually gave
up soccer because of poor knee function or fear of new injury, regardless of the type of treatment ( 99,100). Elite
professional players were more likely to return to the game. The pathophysiology, natural history, and surgical treatment
of ACL tears are discussed in more detail elsewhere in this volume.
Overuse Syndromes of the Knee
Iliotibial band friction syndrome, popliteus tendonitis, patellar tendonitis (jumper's knee), pes anserine bursitis, and
irritation of synovial plicae are common overuse syndromes observed about the knee in soccer players. Iliotibial friction
syndrome (or ITB bursitis) presents as lateral knee pain that progressively worsens during running after a pain-free start.
A tight iliotibial band over the lateral femoral condyle can result in an inflamed bursa with heavy training. Players with
varus knees and an oversupinated gait may be more prone to this condition. The treatment is generally conservative with
ITB stretching, NSAIDs, and occasional cortisone injection in the bursa. However, chronic cases in elite players may
require surgery. Surgery involves excision of the inflamed bursa and excision of a posteriorly based triangular portion of
the iliotibial tract at the level of the lateral femoral condyle.
Patellar tendonitis results from cyclic overloading of the extensor mechanism during jumping and kicking. Pain and
tenderness are localized to the patellar tendon and can become chronic if not treated early with rest, NSAIDs, and
eccentric quadriceps strengthening exercises. Chronic tendonitis may result in a thickened tendon with focal
degenerative areas. Steroid injections should be avoided for this reason. Chronic, severe cases may respond well to
surgical excision of the nodular degenerative areas.
The chronic effects of playing soccer on the knee were investigated by Chantraine ( 101). He found that radiologic signs
of knee osteoarthritis in veteran soccer players increase with age at a much greater percentage than in a random
population of the same age. Of the 81 players examined (ages 40 to 74 years), 56% of the knees had radiologic signs of
osteoarthritis. A total of 26% knees had had prior meniscectomies and all of these showed degenerative changes. The
author concluded that in the remainder, soccer playing alone had contributed to the degenerative joint changes
observed. However, only 30% of the knees with radiologic changes were clinically symptomatic.
Tibial Fractures
Direct kicks to the anterior leg are quite common in soccer and may result in tibia fractures despite the use of shin guards
(Fig. 38.6 and Fig. 38.7). Experimental studies by Van Laack (102) have shown that shin guards decrease the magnitude
of these forces by increasing the amount of contact time. The best results were seen when forces were less than 3000 N.
Although the force reduction due to shin guards is substantial enough to prevent some tibial fractures, they were more
effective at decreasing the amount of soft tissue damage sustained at impact. Shin guards also decrease the magnitude
of the contact forces by dissipating them over a larger area. Nevertheless, the forces generated by a direct kick to the
tibia can still be sufficient to cause fractures, and a fracture should be strongly suspected if an injured player is unable to
bear weight due to pain in the shin. Suspected tibia fractures should be referred acutely for radiographs and further
treatment by an orthopedist.
FIGURE 38.6. Mechanism of injury for tibial fracture.
FIGURE 38.7. Nondisplaced midshaft tibial fracture.
Nondisplaced midshaft tibia fractures may not require casting if the bone is stable and may often be treated successfully
with a removable brace and crutches. The advantages to maintaining mobility and muscular strength during the healing
phase are obvious for the active player. Comminuted or displaced tibial shaft fractures are preferably treated by
unreamed intramedullary rodding. This method of fixation offers minimal surgical exposure and early functional return to
sport. Its disadvantages are that it does not allow for postoperative adjustments in alignment and at least temporarily
disrupts local intramedullary blood flow to the fracture site. Fractures in the proximal and distal shaft can be difficult to
stabilize with an intramedullary rod, and a circular external fixation device such as the Ilizarov and Monticelli-Spinelli
systems can provide an excellent treatment alternative.
Jacchia et al. (103) reviewed 4,683 tibia fractures seen at an orthopedic clinic in Florence, Italy, from 1962 to 1988. Of
these, 126 (2.7%) were in soccer players. They observed that the development of internal fixation devices and more
recently the Ilizarov apparatus significantly reduced the long- and short-term disabilities these fractures cause for soccer
players. Despite these advances, a recent study in England showed the return to sport following tibial fracture averaged
7 to 8 months (104).
Stress fractures of the tibial shaft may become a recurrent problem for some players. Custom-molded orthoses to correct
excessive varus or valgus deformities and to increase shock absorption limit recurrent tibial stress fractures. However,
chronic or recurrent tibial stress fractures may progress to complete fractures and require immobilization or even surgical
fixation.
Ankle Injuries
Ankle Sprains
Ankle sprains are certainly the most common injuries accounting for lost playing time at all age levels and levels of
competition in soccer. Ekstrand and Tropp ( 105) found the incidence of ankle sprains in male adult players to vary
between 1.7 and 2.0 per 1,000 hours of exposure. Between 17% and 20% of all injuries were ankle sprains. They also
found a 50% chance of reinjury in players with histories of previous ankle sprains. Ankle sprains are the most common
injury resulting in lost playing time in the NCAA ( 3). An observed decrease in the flexibility of soccer players' ankles may
contribute to recurrent sprains ( 106).
As in other sports, the typical ankle injury involves an inversion and plantarflexion stress with injury to the lateral
ligaments. In severe injuries with an audible pop and significant pain, swelling, or bleeding, a fracture should always be
suspected and radiographs obtained.
A “high” sprain involving an eversion and external rotation stress may tear the anteroinferior tibiofibular ligament (AITFL),
the posteroinferior tibiofibular ligament (PITL), the inferior transverse ligament, or the syndesmotic (interosseus)
ligament—the strongest of the group. This sprain is distinguished from the inversion and plantarflexion injury by
tenderness along the lateral aspect of the distal tibia. These sprains typically involve much longer recovery times.
The basic tenets of ice, elevation, and compression apply acutely to most ankle sprains, and a splint and crutches may
be required for several days. However, the trend has been away from strict immobilization, even following severe sprains,
and toward allowing the patient to begin weight bearing as tolerated and early range of motion. It is not unusual for a
player to experience persistent pain and swelling for many months following a severe ankle sprain, and it is important
that rehabilitation continues during this time. As pain and swelling subside, progressive strengthening and proprioceptive
exercises are particularly important components of the rehabilitation process for soccer players, because ball control
depends heavily on ankle and foot coordination.
Ekstrand and Gillquist ( 36) have demonstrated that the incidence of ankle sprains can be significantly reduced through
proper preventive measures and rehabilitation following injury. Prophylactic taping is expensive and time-consuming, and
has not been shown to reduce the incidence of sprains in a previously uninjured player. However, for players with a
history of repeated ankle sprains and residual joint laxity, taping or bracing can be effective. Soccer players typically do
not tolerate extensive restrictions on their ability to plantarflex the ankle, because this movement is crucial to controlling,
passing, and shooting the ball. Therefore, taping or bracing should emphasize limiting inversion primarily. Players with
chronic, recurrent ankle sprains and extreme instability should be referred for possible surgical reconstruction of the
lateral ligaments.
Peroneal Tendon Subluxation or Dislocation
Subluxation or dislocation of the peroneal tendon can be one cause of chronic lateral ankle pain. It can occur with
forceful ankle plantarflexion and inversion as the peroneal tendon sheath is torn ( 107). This allows the peroneus brevis to
dislocate anteriorly to the lateral malleolus. Despite being the most common tendon dislocation in the foot and ankle, it is
still frequently mistaken for a lateral ankle sprain. A split in the tendon also can occur and result in recurrent episodes of
peroneal subluxation. A good test to detect these “snapping” peroneal tendons is to have the player roll his or her foot in
circles. Another test to elicit subluxation is to perform resisted eversion and dorsiflexion of the ankle.
Radiographs are usually normal but may reveal a small wafer of bone in the event of a severe sheath or peroneus brevis
avulsion. Acute cases can be treated with 3 weeks of immobilization but chronic cases require surgical debridement and
reconstruction of the tendon sheath ( 107).
Ankle Fractures
Although ankle fractures are not the career-threatening injuries they once were, their frequency and severity make them
problematic for soccer players. Because precise anatomic restoration is necessary to maximize function and minimize
osteoarthritis, surgery is usually recommended for competitive players. The biomechanical tolerances of the ankle are so
demanding that even a malalignment of 2 mm can lead to disability. Accurate classification of the fracture based on the
mechanism of injury and the radiographic appearance will help to guide surgical treatment. The Lauge-Hansen system
and the AO system of classifying ankle fractures are the two most commonly used.
Achilles Tendonopathy and Rupture
The ankle is unique in that all of its tendons cross at least two joints. Therefore, it is particularly susceptible to overuse
syndromes. These problems can be exacerbated by poor anatomic alignment, surface conditions, or footwear. Conditions
can range from mild inflammation and microscopic breakdown to partial or complete tendon rupture. A recent article by
Kaanus and Jozsa (108) disclosed preexistent degenerative changes in 97% of Achilles tendons that sustained
spontaneous rupture. Changes included tendolipomatoses and calcifying tendinopathy. Despite this, spontaneous
rupture occurs in 66% of cases without prodromal symptoms.
In Achilles tendonosis, players present with reports of calf or heel pain that often track diffusely along the heel cord. It is
worsened during kicking or passive ankle plantarflexion. Overuse leads to microscopic disorganization of the tendon's
collagen bundles. It should be distinguished on physical examination from discrete tendon tears or bursitis. Inspection
may disclose diffuse swelling, erythema, and tenderness. Thompson “squeeze” test of the calf is negative. Hindfoot varus
is sometimes an associated finding.
Radiographic examination is usually negative, but occasional Hagland exostoses are seen at the calcaneal insertion of
the heel cord. MRI scanning or ultrasound also can help differentiate tendinosis from partial tendon rupture.
Treatment should begin with a temporary heel lift, NSAIDs, and a gentle stretching program. If this approach fails, local
excision of the microscopic nests of interstitial degeneration with their central necrotic cores can be performed. Steroid
injection in and around the Achilles tendon is to be avoided, because this is a relatively avascular area and the risk of
heel cord rupture is increased.
Propagation of local tissue necrosis can result in eventual partial or complete attritional rupture of the tendon. Patients
with chronic partial Achilles tendon ruptures do poorly, with approximately 75% unable to return to strenuous activity
(109). Chronic partial tears should be explored and repaired early for best results ( 110).
Acute partial and complete ruptures of the Achilles tendon are seen in the older soccer player and can sometimes be
missed. Diagnosis is confirmed by clinical evidence of a positive Thompson squeeze test of the calf. A palpable defect in
the tendon's contour is not always evident. Active plantarflexion of the foot can be misleading because of intact long
flexor tendon function.
Open surgical repair of Achilles tendon ruptures in soccer players offers the most reliable and predictable results. Closed
treatment of these lesions has a recurrence rate nearly twice that of surgical repair ( 111,112 and 113).
Ankle Impingement Syndromes
Impingement syndromes of the foot and ankle are extremely common in soccer players but remain a diagnostic and
therapeutic challenge to the clinician. First described by Morris ( 114) in 1943, and later termed footballer's ankle by
McMurray (115) in 1950, tibiotalar osteophytes are frequently observed on routine ankle radiographs of soccer players
(Fig. 38.8). Higher than normal incidences of tibiotalar spurs and posterior osteophytes were noted by Massada ( 116).
Although the young player may initially be asymptomatic, continued anterior and posterior tibiotalar capsular traction and
impingement over a career may lead to chronic ankle pain ( Fig. 38.9). In its most severe form, surgical resection of
calcified capsular tissue may be necessary if a trial of conservative treatment is unsuccessful.
FIGURE 38.8. Anterior ankle tibial osteophyte (arrow).
FIGURE 38.9. Mechanism of anterior traction and posterior impingement of the ankle during the soccer kick.
The os trigonum syndrome is primarily seen in soccer players, ballet dancers, and javelin throwers ( 117). It presents as
vague posterior ankle pain worsened by kicking or passive ankle dorsiflexion. Retrocalcaneal tenderness is noted on
physical examination, and the differential diagnosis includes Achilles tendonitis, retrocalcaneal bursitis, flexor hallucis
peritendonosis, and local stress fractures.
Radiographic evidence of an os trigonum is necessary for the diagnosis but not specific for it. Ossa trigona represents a
persistent osseous remnant of the posterior calcaneal synchondrosis that normally fuses by age 11. Chronic posterior
impingement of the talocalcaneal joint during instep kicking may result in failure of the synchondrosis to ossify or lead to
a stress fracture of the posterior talar process.
Symptomatic ossa trigona should be treated conservatively with rest, ice, and short-course NSAIDs. Persistent discomfort
may require surgical resection of the bony fragments and inspection of the flexor hallucis longus tendon to rule out
peritendonosis or synovitis ( 117).
Other Tendonitis About the Ankle
Peroneal tendinitis is frequently encountered in soccer players and presents as diffuse lateral retromalleolar pain. It is
usually associated with slight heel valgus or tibial varus. Routine radiographs occasionally disclose calcifications in the
region of the peroneal tendon sheath but are often negative. Acute cases can be treated successfully with a lateral heel
wedge insert and a brief course of NSAIDs. In refractory or chronic cases, surgical exploration and debridement of
degenerative tissue should be considered before an attritional rupture or partial split occurs ( 107). MRI may be useful in
localizing such degenerative changes in the tendon and facilitate surgical planning.
Posterior tibial tendonitis is more common in soccer than other sports because the foot is repetitively forced into
hyperpronation during the kick. Symptoms include arch and medial retromalleolar pain. The differential diagnosis
includes medial ankle sprain, accessory navicular syndrome, flexor hallucis longus tendonitis, and tarsal tunnel
syndrome. Initial treatment should include a medial heel wedge insert and NSAIDs. As in peroneal tendonitis, MRI
scanning may disclose discrete areas of degeneration within the tendon. Treatment in these situations should be
aggressive because of the potential for tendon disruption. Inability to perform a routine single-legged heel rise on the
involved side should raise suspicion of an attritional rupture (so-called acquired flatfoot).
Tendonitis of the flexor hallucis longus (FHL) tendon can also present as medial retromalleolar ankle pain. It can be seen
alone or in combination with posterior ankle impingement ( 117). It results from repetitive hyperplantar flexion of the ankle
during kicking. The FHL tendon is particularly vulnerable to irritation because of its passage through a fibro-osseous
canal, extending from the posterior talus to the sustentaculum tali, and its pully-like mechanism of action. Once it is
established, FHL tendonitis is difficult to treat in soccer players because the flexibility of the toe box and the low-cut
design of the shoe accentuate the normal excursion of the FHL tendon. Irritation and thickening of the FHL tendon
causes it to catch within its fibroosseous canal and begins a cycle of spiraling inflammation and eventual degenerative
damage.
A local injection of 1% lidocaine should eliminate pain with forced plantarflexion and confirms the diagnosis. This test
should help differentiate FHL tendonitis from retrocalcaneal bursitis—another common problem in soccer players, which
results from the ankle rubbing against the stiff heel counter of the shoe. Early treatment of FHL tendonitis should include
early restrictive taping of the ankle and first metatarsophalangeal joint. If this fails, immobilization may be required. In
refractory cases, local debridement may safely be performed through a medial retromalleolar approach with isolation of
the neurovascular bundle.
Foot Injuries
Midfoot Sprains
Tarsometatarsal junction injury can occur when the foot is hyperextended and overloaded during a tackle. Repetitive
microtrauma and macrotrauma in the midfoot can cause osteophytes in this region. Acute tarsometatarsal dislocation
(i.e., Lisfranc injury) is uncommon in soccer players, but chronic stresses can lead to indolent chronic midfoot pain
secondary to ligamentous attrition. The presence of dorsal osteophytes in this zone on radiographs may be adaptive
rather than pathologic, so plain films are only diagnostic if subtle evidence of dissociation is seen with bilateral
comparative weight-bearing studies.
Plantar Fasciitis
The plantar fascia spans from its origin on the calcaneal tubercle to its insertions at the bases of the proximal phalanges.
During phalangeal dorsiflexion at push-off, the plantar fascia tightens by a windlass action and the longitudinal arch is
elevated. Repetitive microtrauma during bursts of sprinting can lead to significant damage to the plantar fascia in soccer
players and cause arch or heel pain. Microscopic tears at the medial calcaneal origin of the plantar fascia are most
commonly seen.
Symptoms are aggravated by the flexible toe box of soccer shoes, which allow excessive dorsiflexion and exaggerate the
windlass effect on the plantar fascia. Heel or plantar arch pain can be reproduced in the affected player by passively
dorsiflexing the phalanges of the involved foot. Radiographs sometimes demonstrate a calcaneal traction spur secondary
to chronic inflammation. Additional clinical findings of mild foot cavus, pes planus, or Achilles tendon contracture may be
present.
Primary treatment should consist of arch supports to unload the tension on the plantar fascia with weight bearing.
Progressive stretching of the heel cord is also sometimes helpful. Oral antiinflammatory medications and ice can also
afford some relief. Heel cups and cushions are rarely effective. Almost all cases resolve eventually with conservative
management and steroid injections and surgery are rarely necessary.
Fifth Metatarsal Fractures
Acute fractures of the fifth metatarsal occur primarily in two forms: diaphyseal and avulsion. Diaphyseal fractures are
similar to the classic description of “dancer's fractures” provided by Sir Robert Jones in 1902. It results from forced foot
inversion with the heel elevated—a common position for soccer players during tackling. The strong ligamentous
attachments between the fifth metatarsal base and the cuboid and fourth metatarsal result in fracture of the diaphysis
before dislocation ( Fig. 38.10). This fracture is difficult to treat conservatively in the competitive soccer player and may
require intramedullary screw fixation for good clinical results.
FIGURE 38.10. Fracture of base of fifth metatarsal.
Avulsion fracture of the base of the fifth metatarsal was once thought to be due to the pull of the peroneus brevis muscle,
but is now more correctly acknowledged to be a result of the tough fascial attachments of the plantar aponeurosis and
abductor digiti minimi. It may be treated effectively with a short-leg walking cast and rarely results in long-term disability.
Sesamoiditis and Sesamoid Fractures
Pathology of the complex sesamoid-metatarsal-phalangeal joint of the great toe is extremely common among soccer
players (118,119). The sesamoids are under constant tensile loading cycles because they are buried in the substance of
the flexor hallucis brevis tendon. Because of this, they tend to fracture transversely and have a high nonunion rate.
Repetitive microtrauma during loading cycles at the hallucal sesamoids during soccer may lead to stress fractures or
avascular necrosis from local ischemic insult. Fracture through a previous synchondrosis of a partite sesamoid also can
occur and causes pain. The presence of a metal stud or cleat directly beneath the hallucal metatarsophalangeal joint on
nearly all soccer shoes may aggravate the problem by increasing local stresses during push-off. This may lead to an
increase in local ischemia and subsequent avascular necrosis with fragmentation.
The diagnosis of sesamoid fracture or fragmentation can be confirmed by comparing clinical findings of localized point
tenderness over the sesamoid with an increase in pain on passive dorsiflexion of the toe. Axial radiographs are useful,
and a bone scan or MRI may provide further diagnostic help ( Fig. 38.11). It is difficult to distinguish a discrete sesamoid
fracture from sesamoiditis of a congenitally partite sesamoid. Local lidocaine injection can provide pain relief in either
case. In the absence of a discrete partite sesamoid with a positive bone scan, the diagnosis of sesamoiditis is more
secure.
FIGURE 38.11. Medial sesamoid fracture.
In either case, treatment is symptomatic with initial rest, ice, and NSAIDs. A custom-molded foot orthosis, incorporating a
support proximal to the first metatarsal head, can be extremely effective in relieving pain. Cast immobilization may be
necessary in both sesamoiditis and stress fractures. If pain becomes refractory, surgical removal of all or part of the
involved sesamoid has been recommended ( 119). Complete removal of a sesamoid has potential to result in an
imbalanced “cock-up” toe deformity. Return to soccer should be possible even if surgical removal of the fragmented
sesamoid is necessary. More typically, the vast majority remain as painless (or tolerably painful) nonunions and respond
well to orthotic treatment.
Digital Fractures
Contusions to the toes are so common in soccer players that digital, or phalangeal, fractures may go unrecognized.
Osseous damage can easily result from direct trauma during ball strike because of the soft, supple nature of the soccer
shoe's toe box. Discrete tenderness of the involved phalanx should alert the physician of a possible fracture, and plain
radiographs should be obtained. Nondisplaced phalangeal shaft fractures and those that involve less than 30% of the
articular surface may be treated conservatively with buddy taping and toe box shoe reinforcement. Displaced fractures
require closed reduction, and more severe fractures (i.e., associated with joint subluxation) may necessitate open
reduction and internal fixation for a good result. Because of the nature of the sport, toe fractures in soccer players should
be treated with the same aggressiveness and expertise that finger fractures would be given in the general athletic
population. Protective rigid shoe inserts may be used during the rehabilitation process to hasten healing and return to
effective play.
Stress Fractures
Stress fractures of the foot and ankle in soccer are most typically seen in elite or professional players with heavy daily
training and game schedules. Stress fractures in the fore foot usually involve the second and third metatarsals, perhaps
due to their decreased motion in relation to the midfoot, which results in less contact force distribution and increased
local stresses during running. This situation is aggravated by local muscular fatigue and the poor cushioning and support
of most soccer shoes. These fractures are usually diaphyseal, whereas stress fractures of the first metatarsal involve the
base, because of load transfer to an area with increased cancellous bone content. Stress fractures of the fourth and fifth
metatarsals are less common but do occur (120).
Physical examination discloses fusiform swelling, localized tenderness, and pain on passive motion of the involved ray.
Radiographs exhibit a periosteal reaction in diaphysial stress fractures, but can be negative. Basilar stress fractures of
the first metatarsal instead display a pattern of basilar sclerosis that may be easily missed. In a case in which clinical
suspicion is high in a player with persistent discomfort but negative radiographs, bone scan can be diagnostic ( Fig.
38.12). Although a bone scan is the sensitive means of diagnosing stress fractures, it is less specific than other methods
such as CT scan. The role of MRI scanning remains unclear, because it may confuse the diagnosis by disclosing
subclinical metabolic changes in the bone ( 120,121).
FIGURE 38.12. Bone scan of 23-year-old soccer player, demonstrating stress fractures of the fifth metatarsal.
Stress fractures of the metatarsals are often already in the healing phase at the time of their diagnosis. Treatment
consists of relative rest, that is, avoiding pain-producing activity. Immobilization is rarely necessary. Players can be
returned to sport earlier when fitted with a custom-molded rigid orthosis. Refractory cases or those involving the fifth
metatarsal diaphysis may require casting or surgical fixation.
In contrast to metatarsal stress fractures, stress fractures of the calcaneus, talus, navicular, or malleoli can be quite
difficult to diagnose and treat effectively. Players frequently complain of diffuse ankle and midfoot pain during running
and shooting that is hard to localize. Tarsal-navicular stress fractures are frequently occult on plain radiographs because
of routine underpenetration ( 122). Fatigue fractures in this region are located in the central third of the navicular and are
linear in orientation. They tend to begin as incomplete fractures dorsally and propagate to complete fractures if they are
left untreated. Bone scan, plain tomography, or CT scanning confirms the diagnosis.
Initial treatment should include 6 to 8 weeks of cast immobilization. Radiographic evidence of a nonunion does not
necessarily preclude a good clinical result, but persistent symptoms may necessitate eventual bone grafting and internal
fixation.
Calcaneal stress fractures are infrequent but remain part of the differential diagnosis of heel pain in the soccer player.
Symptoms can lead to its delayed diagnosis and confusion with plantar fasciitis, retrocalcaneal bursitis, os trigonum
syndrome, and Achilles peritendonosis, which are all common problems in soccer players. Because the calcaneus is
primarily composed of cancellus bone, stress fractures appear as dense sclerotic lines on plain radiographs oriented
parallel to the line of pull of the Achilles tendon. The diagnosis can be confirmed by bone scan, plain lateral tomography,
or CT scanning.
Stress fractures of the talus, cuboid, or cuneiforms are uncommon. However, the possibility of avascular necrosis of the
dome of the talus should be considered in complaints of persistent ankle pain.
Malleolar stress fractures can occur in soccer players complaining of persistent pain, especially in the setting of recurrent
ankle sprains. Plain radiographs should be inspected carefully for subtle fracture lines oriented perpendicularly to the
plafond. Because they are potentially unstable fractures, internal fixation of medial malleolar fractures should be
performed. Lateral malleolar stress fractures have a lower potential for nonunion and can be effectively treated with
closed methods.
In general, persistent foot and ankle pain in a soccer player should lead to a thorough diagnostic workup to rule out the
presence of a stress fracture. Early recognition and treatment of these injuries may obviate the need for later surgical
management because of displacement or nonunion.
Turf-Toe
Turf-toe is an injury to the plantar capsule of the metatarsophalangeal (MTP) joint of the great toe. It was first described
in American football players following the introduction of artificial turf in the mid-1960s ( 123). A partial tear of the plantar
capsule of the hallucal MTP joint occurs from repetitive forced hyperdorsiflexion and overload caused by flexibility of the
standard turf shoe and the increased traction of the surface. Capsular damage in this zone is aggravated by increased
shear stresses across the hallucal MTP joint during cutting and push-off. Microruptures in the flexor hallucis brevis
muscle and collateral ligaments also may be associated and sesamoidal fractures or fragmentations can be seen with
this painful condition.
The diagnosis is made by clinical findings of a tender, swollen hallucal MTP joint with increased tenderness on passive
dorsiflexion. Initial treatment should include rest, ice, a brief course of NSAIDs, and protective taping to limit MTP
dorsiflexion. More severe cases may warrant the use of orthoses or a wooden healing shoe until symptoms resolve.
Surgery is only beneficial in cases for which dorsal subluxation of the joint is present or severe osteoarthrosis
necessitates arthrodesis of the joint.
Reverse Turf-Toe (Soccer Toe)
First described in ballet dancers, reverse turf-toe condition refers to acute and chronic capsular damage to the dorsal
aspect of the hallucal MTP joint (124). It results from repetitive forced hyperplantar flexion of the joint, especially during
instep ball strike because of the supple nature of the shoe toe box.
The diagnosis is confirmed by physical examination, with swelling and tenderness of the hallucal MTP joint. Pain is
exacerbated by passive plantarflexion of the joint. This condition is somewhat less refractory in soccer than turf-toe and
generally responds well to conservative treatment with taping to prevent MTP dorsiflexion. Orthoses are rarely needed.
However, chronic involvement can lead to hallux rigidus.
Hallux Rigidis
Hallux rigidus represents posttraumatic arthrosis of the hallucal MTP joint secondary to previous fracture,
osteochondritis, avascular necrosis, turf-toe, or soccer toe. Dorsal osteophytes form at the hallucal MTP joint, with
subsequent pain and stiffness while cutting or pushing off.
Diagnosis is made by the presence of a chronically stiff and tender hallucal MTP joint with a painful, decreased range of
motion. Radiographs generally demonstrate evidence of dorsal osteophyte impingement. A diagnostic intraarticular
injection with 1% lidocaine provides temporary pain relief and aids in the diagnosis.
Treatment options include rest, NSAIDs, and protective taping or shoe orthosis. However these treatments are often
unsatisfactory, and more aggressive therapy is generally required. Intraarticular steroid injection is unpredictable but can
help early in the disease. Surgical options include cheilectomy, which requires removal of approximately 30% of the
dorsal metatarsal head; a dorsally based wedge osteotomy of the proximal phalanx; MTP arthrodesis; and metatarsal
head resection. Hallucal MTP arthrodesis is recommended for advanced disease in soccer players because of the need
for a strong push off during running. Still, younger players with less severe disease may do well with an osteotomy.
Subungual Hematomas of the Toes
Most soccer players will sustain numerous subungual hematomas of the toes during their career. These injuries generally
occur to the great toe as the result of a direct crush by the foot of another player or from the shear stresses of sudden
stops and starts as the toe impacts against the close-fitting toe box of the soccer cleat. For many players, the toenail
becomes dystrophic as the result of repeated damage to the nailbed. Although seldom a serious problem, it can become
so troublesome that some professional players have been known to have the toenail of their great toe permanently
removed just to prevent its recurrence.
An acute subungual hematoma can be quite painful and the initial treatment should involve releasing the pressure of the
blood collected beneath the nail. This can be accomplished with a special drill designed specifically for this purpose; a
more convenient technique involves heating the end of a paper clip wire and burning a hole through the nail.
Generally, the nail should be left intact even if it is detached from the nailbed. It should be taped in place if necessary to
protect the nailbed as the new nail grows out.
SPECIAL CONCERNS
Indoor Soccer
Indoor soccer is played with only five players on a side on an artificial turf the size of an ice hockey rink. The goal is
smaller and the ball may be played off the side walls. It tends to be a much quicker game with more sudden stops and
starts and changes in direction. Hoff and Martin ( 43) found the incidence of injuries in indoor youth soccer to be 4.5 times
higher than that observed in outdoor soccer. However, the reporting methods were quite variable and based on survey
responses rather than a prospective analysis; therefore, the numbers may be imprecise. Differences in field size and
surface, game speed, officiating, and player numbers were all possible causes cited for the increased incidence of injury
observed in the indoor game. Other studies have generally found no greater incidence of injuries among adults in the
indoor game (125,126).
Artificial Surfaces
Ekstrand and Nigg (126) reviewed surface-related injuries in soccer and found that most authors reported no significant
increases in injury frequencies or changes in injury patterns on artificial turf. This conclusion is also supported by annual
data from the NCAA (3). However, there is some evidence that players who alternate frequently between grass and
artificial surfaces may be at higher risk for injury and a period of adaptation in proper shoewear would reduce the risk ( 4).
As more and more facilities adopt artificial turf because of its ease of maintenance, there will be more opportunities to
observe any possible differences in injury patterns.
Women's Soccer
The number of women playing soccer has increased rapidly in the past two decades, most notably in the United States
and Scandinavia. In a survey conducted by the Soccer Industry Council of America, 40% of women surveyed in the
United States reported having played soccer at least once during 1996 ( 2). Most of these women (74%) were under age
18. It was estimated that over 7 million women and girls in the United States participate in soccer at some level.
As mentioned previously, girls under age 12 seem about twice as likely to be injured as boys in soccer. The reasons for
this are obscure and have been variously ascribed to differences in physical development, psychomotor coordination,
and behavioral patterns. The common practice of mixing boys and girls on the same team at young ages may also be a
contributing factor.
At collegiate and adult levels, overall injury rates for men and women appear to be comparable, but few studies of elite
female players have been done. Engstrom et al. ( 41) reported a significantly higher injury incidence in a study of 41 elite
female players in Sweden. The overall incidence of injury was 12 per 1,000 AE, with a rate of 24 per 1,000 AE for games
and 7 per 1,000 AE for practices. This compared with an overall injury incidence of 5 per 1,000 AE for men at the same
level. They observed that the mean training time for the female players was half that of the male players and posited this
may have been a factor in the higher injury rate among the women. In the NCAA, in which training times are similar for
men and women, the overall injury incidence for women is almost identical to men, and in fact is slightly less in regular
season game competition (Table 38.1) (3).
In both of these series, women were observed to have a greater incidence of knee injuries than their male counterparts.
Engstrom et al. found that 23% of all injuries involved the knee, with 17% of players sustaining major injuries involving
ligament or meniscus tears. NCAA statistics reveal the incidence of ACL injuries among women to be twice as high as
that occurring in the men (98). This finding mirrors that for other pivoting sports such as basketball. The reason for the
high incidence of knee injuries in female soccer players, particularly injuries to the ACL, is unknown. Differences in
strength, flexibility, knee anatomy and biomechanics, personality types, and playing styles have all been suggested but
no studies have proved any single factor as the cause.
Moller-Nielsen and Hammer (127) found a significantly higher incidence of injuries in women during the premenstrual and
menstrual period compared with other times of the menstrual cycle. This was attributed to both the physiologic and
psychological symptoms that occur during this time, such as increased irritability and breast and abdominal pain and
cramping.
The physical training and nutritional requirements of female soccer players do not differ significantly from those of men.
Douglas (128) examined the hematologic status of 30 collegiate women soccer players through a competitive season and
found no evidence that strenuous physical training caused iron-deficiency anemia. However, coaches, trainers, and
clinicians should be alert for what has been called the “female athlete triad”: amenorrhea, osteoporosis, and disordered
eating. Exercise-induced oligomenorrhea or amenorrhea (less than three menstrual periods per year) result from a
complex combination of nutritional deficiency, hypoestrogenemia, low body weight, stress, and increased training
intensity (especially when the girl is premenarchal). Eating disorders such as bulimia and anorexia nervosa and the
abuse of diuretics, laxatives, and diet pills has been found in a disturbingly high percentage of competitive female college
athletes (129). The combination of these two disorders may result in bone demineralization or osteoporosis and resultant
stress fractures of the lower extremities. Female players with unusual weight loss or suspected eating disorders should
be referred for nutritional or psychiatric counseling.
Youth Soccer
Injury patterns are different in children and may involve problems that are not common in adult players. Children are less
likely to sustain serious injuries. Contusions and abrasions are the most common injuries and most of these do not result
in lost playing time. Most studies of youth soccer have found a slightly higher incidence of upper extremity injuries
compared with adult levels. This may be the result of more frequent falls, illegal ball contact, decreased technical
expertise, and greater fragility of upper extremity epiphyses.
In the lower extremities, epiphyseal and avulsion fractures, slipped capital femoral epiphysis, and subcapital compression
fractures should always be considered when evaluating children's soccer injuries. Apophysitis of the iliac crest, tibial
tuberosity (Osgood-Schlatter disease), calcaneus (Sever disease), and fifth metatarsal should be suspected in youth
players presenting with chronic focal pain at these sites.
The effects of soccer training programs on prepubescent children have been examined. Berg et al. ( 130) found no
significant changes in cardiorespiratory fitness, peak knee torque, or flexibility in a group of 11-year-old boys following a
12-week soccer conditioning program. Mosher et al. ( 131), however, did find significant increases in aerobic fitness in
this same age group following a similar 12-week training program. Although slight gains in aerobic capacity can be
achieved through endurance training, the emphasis in youth soccer is probably better aimed at developing basic
individual skills and concepts of team play.
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39 Surfing
39
SURFING
RONALD A. NAVARRO
Evolution of Surfing
The Sport and Lifestyle
Wave Characteristics
Board Surfing
Body Surfing
Epidemiology of Surfing Injuries
The Surf Doc
Specific Surfing Injuries
Minor Lacerations
Soft Tissue Sprains and Dislocations
Bone Injuries
Life-Threatening Injuries
Ear
Eye Injuries
Skin Injuries
Idiosyncratic Injuries
Ocean Hazards
Prevention of Surfing Injuries
Surfer's Medical Association
Acknowledgments
Chapter References
The use of the ocean's waves for board surfing or surfcraft riding has blossomed in popularity since the early 1960s. A
surfer is generally defined as any person who rides a wave on a board. Traditionally, only those who stand on boards
would be included, but for the sake of this chapter, it also includes those who ride boards seated (surf skiers and surf
kayakers), on their knees (knee boarders), on their belly (foam, belly, body or boogie boarders), with a sail (windsurfers),
and those who just use flippers or nothing at all (bodysurfers). Surfing, a sport that was once only associated with
Australia, California, and Hawaii, now has been embraced by enthusiasts on every part of the globe. Its growth has been
fueled by a billion-dollar surfing-related clothing industry, which markets the cultural idiosyncrasies of surfing to the
nonsurfer with great success. With the advent of water theme parks and wave pools that simulate real surf, more
landlocked populations will be able to learn to surf. Owing to the combination of the speed obtained during wave riding
and the fact that the board can become a weapon of injury, there exists a risk of potentially serious injury, especially for
the novice.
EVOLUTION OF SURFING
For hundreds of years Hawaiian royalty rode heavy koa wood surfboards on waves, unseen by foreigners. After Captain
Cook landed on the island chain, reports describing the sport began to emerge from the islands ( 1). After Hawaiian surfer
George Freeth surfed in Redondo Beach, California, in 1907 to promote real estate, the sport spread throughout the
mainland. Olympic swimming champion Duke Kahanamoko became surfing's ambassador to the world. A central fin or
skeg was added to the bottom of the board for greater stability in the early 1900s. Balsa wood blanks were enhanced with
Fiberglas in the 1950s, but the boards were still up to 12 feet long. Polyurethane foams were introduced in the 1960s
and, when combined with Fiberglas, created lightweight controllable boards. An array of different board lengths, numbers
of skegs or fins, and tail shapes and noses have been combined to create the best functioning board. The advent of the
leash essentially eliminated swimming after lost boards ( Fig. 39.1). Shorter boards became the rage in the early 1980s,
and with the addition of multiple fins in different locations on the board, untold numbers of new surfers were attracted to
the sport. Extreme crowding has become a major problem and “localism” (i.e., territorial attitudes of surfers, leading to
malicious acts) has brought notoriety to the sport. Nonetheless, surfing remains popular owing to the exhilarating
experience wave riders enjoy. Surfers describe their sport as one in which the ocean's energy is harnessed and then
released without damage to the environment. Because most surfers would describe it more as a lifestyle, there is no
sport comparable to surfing.
FIGURE 39.1. The ankle leash keeps the board in the vicinity of the surfer in the setting of a wipeout but can also lead
the board to recoil and endanger the surfer.
THE SPORT AND LIFESTYLE
Surfers are itinerent, independent sorts who enjoy the sport mainly for mood achieved during the wave riding sequence
(Fig. 39.2). For most surfers, the only competition is internal, between rider and environment. In the past, there seemed
to be an anecdotal relationship between surfers and drug and alcohol use. Now multiple generations in the same family
surf, with more women in the water than ever before. Many surfers arrange the rest of their activities around surfing, and
many travel to find the best waves. This obsession for the sense of well-being derived from the sport can make surfers
override medical advice when it involves losing “water time.”
FIGURE 39.2. The individualistic qualities of surfers can often be evidenced in the illustrations airbrushed on their
boards.
WAVE CHARACTERISTICS
To understand the mechanisms of surfing injuries, the characteristics of how waves are created should be understood.
Waves may be created by the wind of storms, changes in the atmospheric pressure, passage of the moon, earthquakes,
and landslides. Velocity, duration, and direction of the wind are important factors. When the initial influence of the inciting
event dissipates, the energy is transformed into smooth, long swells that can travel thousands of miles, losing little
energy. The wave finally breaks when the swell meets the resistance of the rising ocean bottom. The contour of the
ocean bottom determines the intensity of the break. The swells hit the Hawaiian islands with such intensity because,
unlike the U.S. mainland, there is no continental shelf to dissipate the energy. The top of the swell is pushed upward and
it becomes a steep wall of water, with a face and a crest. When the top of the swell falls down the face of it, the wave is
breaking.
Surfers are vulnerable to injury, largely because of the inherent power of an ocean wave. For example, a 4 foot high
wave delivers approximately 300 ft-lb of energy per foot of wave crest, whereas a 12 foot wave delivers 300 ft-tons. In the
impact zone (whitewater area), the downward and turbulent forces can easily turn the buoyant surfboard into a missile or
hold a surfer under water for prolonged periods of time (more than 2 minutes in large surf) ( 2).
BOARD SURFING
In order to reach the “line-up” or area where the wave can be caught, a surfer must paddle out to this area. Most surfers
lay prone on the surface of the board and use a swimmers crawl type of motion to propel themselves forward. On long
boards, the surfer can occasionally kneel and simultaneously scoop the ocean with both arms. Paddling can be a
rigorous task and is a part of surfing ignored by those unknown to the sport. In fact it is an integral component and often
separates surfers from one another. If one is more adept at paddling he or she will engage more waves and subsequently
become more skilled. Paddling requires savvy to read the breaks and time entry into the ocean or to pick paddling
channels which avoid impact zones. The best surfers develop stamina to doggedly paddle into the correct position.
Once a surfer is beyond the impact zone, he or she waits facing out to sea, usually while sitting or straddling the board.
When a surfer sees a potentially rideable wave he or she must turn the board toward shore lay prone and begin paddling
to attain a speed that will allow transfer to the wave as the source of power, which will now propel the board. The surfer
takes off and stands as the swell is being pushed up and attempts to ride the face of the wave, avoiding the area where
the wave is breaking. When the top of the swell (white foam) falls down the face of the swell, the wave turns into a
moving wall of water. When conditions are favorably smooth (as in the morning before the wind begins to blow), a tube is
actually formed by the moving concave vertical wall and the water of the crest pitching forward. The surfer on the
surfboard slices down on the face of the wave, right into the tube, and glides out of the tube and out of the area where all
of the water is going to fall at the last moment.
Because of the speed that can be obtained during the act of surfing, injuries can occur if the surfer is thrown from the
board. The power of the surf can potentiate or multiply the possible injurious situations. “Wiping out” in shallow water with
submerged obstacles (packed sand, coral, and rocks) and or being “pounded” by the surf with the anxiety-provoking
sensation of being held under by strong surf are situations any surfer must be aware of. The board itself can become a
weapon during the scramble after a wipe out. The fins and nose have produced lacerations as well as puncture wounds,
some resulting in devastating eye injuries with resultant loss of vision ( Fig. 39.3). The board can also produce blunt
injuries to the head, torso, and extremities during a wipe out.
FIGURE 39.3. Application of rubberized nose caps or nose guards can blunt the effect of the sharp tip which has
otherwise lead to devastating injuries.
In addition to “the wave,” the surfer must contend with other surfers (both body and board surfers); and other objects in
the water such as surfboards (with their points, tails, and fins), air mattresses, Boogie boards, canoes, kayaks, and
catamarans. Some of these items are directly dangerous on contact, whereas others can be distracting or physically
upsetting, causing the surfer to lose control, which could be dangerous.
BODY SURFING (3)
Body surfing is one of the most challenging and stimulating individual sports enjoyed by many. The Hawaiian Islands
(mainly Oahu), southern California, Florida, and Australia top the areas where this sport is popular. It may be thought of
as a one-on-one competition: the body surfer versus the wave, one's body lying on and within a curving wall of rapidly
moving water.
The body surfer need only wear a swimsuit and use one necessary accessory, a pair of fins or flippers (occasionally a
single fin). The body surfer must be a strong swimmer, because he or she may be carried out beyond the surfline. Foot
fins help speed and endurance as well as one's ability to cover longer distances if necessary. The initial cost is low, but
the cost of injury can be horrendous—permanent paralysis secondary to spinal cord injury or death caused by drowning.
Knowledgeable body surfers first study the surf from the beach. The inexperienced body surfer may be injured by just
entering unfamiliar waters. If the newcomer should choose to run and dive into the surf, he or she may hit the head,
usually the vertex, on the uneven sand or coral bottom, on a projecting hidden rock, or on the head of an oncoming body
surfer. The body surfer may walk into the water because he or she sees many others in the surf, but standing only knee
or waist deep, the body surfer may be almost immediately pounded downward or thrown backward by a huge wall of
water that crashes violently to the ocean bottom. Concussion; near drowning; fractured cervical, thoracic, or lumbar
vertebrae; arm and shoulder dislocations; hip dislocations; lacerations; and severe sand abrasions can occur.
If body surfing at a lifeguarded beach, there is a good chance of rescue, resuscitation, stabilization, and expeditious
transfer to an acute care hospital, all too familiar with the receipt and care of such an injured surfer. Not all body surfing
beaches have lifeguards.
An experienced body surfer enters the water, put on his or her fins, treads water (or stands in water about chest deep),
and faces out to sea, watching each wave as it approaches. When a surfer believes he or she is in a correct position and
capable of riding the oncoming wave (usually 2 to 6 feet high) and has analyzed the direction of the break of the wave
(left to right, right to left, or straight ahead), he or she then decides whether to “take it” or not. If the body surfer decides
not to take the wave, he or she dives under and through the base of the wave and comes up on the other side in front of
the next wave. It may be necessary to do this several times in a row, thus requiring stamina and good breath-holding
abilities. If the body surfer decides to take the wave, he or she turns and faces the shore; and when the nearly breaking
wave is several feet behind the body surfer, he or she begins to swim rapidly with several short, strong strokes and kicks
to gain momentum so that as the wave catches the body surfer, he or she can ride it. Once caught by the wave, the surfer
should be in front of the wave with the upper body, with the remainder of the body encased in the mass of moving water.
The body surfer extends an arm straight in the direction of the angled body (right arm extended when going to the right
on a left to right breaking wave) and rides the wave. It may crash in just a few feet or roll for several yards and even
“tube” such that the surfer exits far down the tube from where he or she entered, having been completely surrounded by
a tunnel of moving water for several ecstatic moments.
Once the ride is almost over, the surfer must safely terminate it before the wave crashes. The proper and safest way is to
“curl under” (cut out, kick out) and come out behind the wave, heading out to sea to face the next one. This end of the
ride is the most dangerous part, and it is here that even the experienced body surfer can become injured. It is the timing
of this critical move that has cost lives as a result of head injury with loss of consciousness, spinal cord injury with
paralysis, and drowning. It is here that the head and neck-flexed surfer can be driven head first into the beach bottom,
sustaining a neck injury. The surfer may escape with only a cervical vertebral body compression fracture or perhaps only
a spinous process fracture, or he or she may sustain a fracture-dislocation with resultant, usually immediate, spinal cord
injury. The experienced body surfer may also be injured by collision with other surfers (body or board) or objects, but the
most serious remains a collision with the ocean bottom.
Body surfing can now include riding on an air-filled beach mattress, Boogie board (a soft, light, preformed Styrofoam
board about 3 feet long), and short, thin, hard plywood boards. These add a new risk for the rider, because they are
frequently ridden directly into shore and can cause an over-the-falls-type of injury, with the rider being thrown forward by
his or her own momentum as the wave stops abruptly and crashes down. The surfer may land with neck flexed into the
water ahead of the wave (now only inches to perhaps 1 foot deep) or in a head-neck extended position, each causing its
own particular type of cervical spine injury.
No swimmer or surfer should be in the water alone, and the beginner or novice body surfer must have respect for all
waves. Prevention of injury is the only way to enjoy body surfing. One should surf only at a lifeguarded sand beach, be
an accomplished swimmer, and choose waves that break slowly and smoothly and are not too high (1 to 2 feet as seen
from the front).
Beach areas that allow board surfing, boat launching and landing, and sail boarding should be avoided. There are
beaches that are restricted in use for the appropriate water sport. When a red flag is posted at a guarded beach, the surf
is considered dangerous even for the expert!
EPIDEMIOLOGY OF SURFING INJURIES
A variety of reports have led to estimations of surf injury incidence. Incidence of injury in surfing has been estimated to be
1 injury per 17,500 surfer days ( 4). A rate of four moderate to severe injuries per 1,000 surfing days (3.5 hours of
surf/day) has been estimated (5). It has also been estimated that the average surfer surfs 2.7 days per week and 4 hours
per day (6). Lacerations occur in 41% of all surfing injuries, with the surfer's own board responsible for most ( 6). Sprains
and strains have been seen in 35% and fractures in 15% ( 7). Eye and ear injuries are common. Fortunately, catastrophic
head and spinal injuries, as well as drowning events are uncommon. Alcohol and drug use has been variously associated
with injuries during surfing. Less experienced surfers have increased risk of injury ( 3).
An ongoing epidemiologic study is under way at the Brown University School of Medicine. The study can be accessed at
www.surfstudy.sitehosting.net (8) and was active at the time this manuscript went to press. The study hopes to evaluate
the types, causes, and frequencies of surfing-related injuries and deaths. The questionnaire is divided into four parts and
contains 12 to 34 questions. It takes approximately 5 minutes to complete the survey. The site states that the results of
this survey will be published on the web page or in a surfing magazine at some time in the future.
THE SURF DOC
Any health care professional who cares for surfers must understand the stereotypical psyche of the surfer to help combat
the cavalier health-related attitudes they sometimes display. Surfers' pursuit of the exhilaration of the ride occasionally
supersedes surfing safely. Overcoming fear is inherent in the sport (taking off on large waves), so excessive risk taking
amongst this population has been seen. In the future, physicians can help lead the fight for nose and fin protection, surf
schools to promote preventative health in the water, and helmet guidelines in appropriate events ( 9).
Surfers take many trips in search of waves and some destinations include foreign travel. The prepared surf doc will be
able to advise surfers about the key issues involved in travel medicine. The major health risks in facing serious surf
travelers include malaria, cholera, dengue fever, hepatitis A and B, Japanese encephalitis, and accidents (leading cause
of death to travelers) ( 9). Be sure the surf traveler's routine health matters are up to date (tetanus and measles boosters,
tuberculosis screening, and sexually transmitted disease awareness).
An online dialogue with a surf doc is available through www.surfermag.com (10), at their “Ask the Surf Doc” forum. All
previously answered surfing medicine questions are listed. A sample surf doc bag for the prepared traveling surf doc is
listed in Table 39.1.
TABLE 39.1. SURF DOC BAG
SPECIFIC SURFING INJURIES
Minor Lacerations
Surfers are susceptible to lacerations ( Fig. 39.4). The etiologic agents involved include surfboards (self-inflicted and
other surfer's boards) and submerged rocks and coral. The skull, chin, foot, leg, and eyebrow most commonly require
sutures. Lacerations have occurred even in settings where the wetsuit remained intact ( 2). Excess sewage outfalls are
near many surf breaks, so thorough irrigation and debridement of wounds before closure is required to avoid chronic
suppurative infections ( 11). Some advocate delayed closure if the wound incurred prolonged exposure to aquatic
environs before definitive irrigation. Lacerations have a higher propensity to develop into infected or chronic ulcers
because many surfers attempt to get back into the water before adequate epithelialization can occur.
FIGURE 39.4. The fins or skegs on a board help to steady the board during wave riding but can also be a source of
potential injury as they can lacerate soft tissue easily.
Soft Tissue Sprains and Dislocations
The most common muscle sprains reported involve the low back and cervical spine. The knee and ankle are frequently
involved as well. Overuse and stress from vigorous surfing maneuvers are the leading causes of injury. The shoulder is
frequently injured, and it is thought that rotator cuff impingement during the act of prone paddling (excessive
hyperextension and internal rotation) leads to a “surfer's shoulder” syndrome ( 12) (Fig. 39.5). Acromioclavicular,
glenohumeral, and knee dislocations have been reported. Surfer's elbow has been described as a form of lateral
epicondylitis ( 13). Rest, functional rehabilitation, and antiinflammatory medications usually adequately treat most of these
injuries. Stretching and warm-up activities before surfing are emphasized to reduce the incidence of injury.
FIGURE 39.5. The constant paddling required in surfing can lead to overuse injuries of the shoulder.
Bone Injuries
Fractures are relatively uncommon and affect the nose, arms, hands, tibiae, feet, and teeth. Rib fractures can occur with
particular surfing maneuvers ( 14), and glenohumeral dislocations ( 15) as well as acromioclavicular separations ( 16) are
documented in the literature. An exacerbation of spondylolisthesis has been described, as have wrist and humerus
fractures in body surfers (2). A talar osteochondral lesion has been described due to the penetrating effects of the skeg
(2). Basic splinting techniques are employed before the surfer obtains definitive fracture care.
Life-Threatening Injuries
Fortunately, life-threatening injuries are rare in surfing. Severe trauma that would result in extended hospitalization has
been estimated at 1 incident per 175,000 days surfed ( 17). Closed head injury, cervical spine injuries, thoracolumbar
spine fractures, splenic rupture, drowning, and axillary artery injury have been described ( 3). The most devastating of the
injuries remains the spinal column injury, usually cervical, often resulting in permanent quadriparesis or quadriplegia.
The mechanism is usually a head-first fall with impact and leads to either vertical compression, hyperextension, or
compression. If a surfer presents with this mechanism and has neck pain, the cervical spine should be immobilized until
cleared by neuroimaging studies ( 2). If neurologic impairment occurs in the ocean, immediate ocean rescue and
resuscitation is mandatory. Quadriplegia may be accompanied by neurogenic shock, manifested by hypotension,
bradycardia, and possibly hypothemia ( 2). The incidence of catastrophic injury is increased in the most experienced
surfers due to their choice of most difficult surf conditions. Knowledge of cervical spine precautions and cardiac life
support is recommended of any health care provider who intends to cover surfing competitions.
Ear
Surfer's ear is the presence of exostoses in the external ear canal ( Fig. 39.6) in response to the irritation of water and
wind (11,18,19). Symptomatic surfer's ear can be treated with antibiotic drops with cortisone to reduce inflammation. Use
3 to 4 drops per ear, three to four times per day for 1 week. Rupture of the tympanic membrane can occur if the ear
suffers impact with waves. Antibiotic ear suspension and avoidance of the ocean is required. Occasionally, surgical
myringoplasty may be required to close a large perforation ( 11,18,19).
FIGURE 39.6. This severe case of external exostoses or surfer's ear was seen in a surfer who had been exposed to
many years of wind and ocean water.
Eye Injuries
Pingueculae and pterygia are hyaline nodules of the conjunctiva, usually found on the nasal side of the cornea. They are
thought to be caused by irritation of sun, water, and wind ( 11). Although pingueculae can be treated symptomatically,
pterygia can encroach on the pupillary area and interfere with vision. Those that do can be removed with a simple
operative procedure. Ocular burn should be prevented with appropriate protection. Eyewear that eliminates ultraviolet
light while on the beach and brims or visors while in the water afford excellent shading for the eyes. Unfortunately, most
surfers do not wear the eye protection in the water ( 11). Blunt trauma to the eye has decreased with the introduction of
padded nose guards that eliminate the sharp point of surf boards ( Fig. 39.3).
Skin Injuries
Nipple and axilla rashes are less common now with the advent of rash guard shirts. These nylon shirts protect the surfers'
nipples from a tender rash that occurs a result of friction from the surfboard and wax, when surfing during the spring and
summer. They are worn with seams on the outside so that irritation, which occurs from paddling in wetsuits about the
axilla, is lessened. Protection from the damaging effects of the sun is afforded with sunscreens and block. Older surfers
should be screened for any malignant or premalignant lesions because many older surfers predate the awareness of skin
cancer and its prevention ( 11). High-risk, seldom-examined areas such as the tops of the ears, the back, and the back of
the leg should be evaluated. New moles and previously badly sunburned areas should be especially scrutinized with
referral to a specialist if the area is in question.
Idiosyncratic Injuries
Surfer's sinus is a chronic rhinitis and sudden sinus fluid release seen commonly in individuals who frequent the ocean.
“Surfer's chest knots” are innocuous subcutaneous masses over the lower rib cage many veteran surfers have developed
(20). “Surfer's rib” is an isolated first rib fracture secondary to performing a layback maneuver, in which the surfer is in a
limbo-like position. “Surfer's neuropathy” is a peroneal nerve compression as a result of sitting on a surfboard ( 11).
“Surfer's knots or knobbies” ( 21) are overgrowths of connective tissue at the tibial tubercle and dorsal foot seen in surfers
who paddle long boards in the kneeling position.
Ocean Hazards
Surfers are at risk for stings from various sea organisms, most of which are benign. Sharks, needle fish, sea urchins,
sting rays, blow fish, and Portuguese men-of-war have caused injuries to the body surfer, with Portuguese men-of-war
being the most common. Shark attacks have been reported but are highly infrequent. Coral cuts and deep sand
abrasions also need medical attention.
PREVENTION OF SURFING INJURIES (22)
Precautions for surfers that can increase safety in the ocean include (a) properly fitted wet suits to prevent hypothermia;
(b) surfboards without sharp points and edges; (c) use of a leash to protect other surfers from stray boards and as a
flotation device in cases of severe injury; (d) use of sunscreens to protect from the ultraviolet light; (e) contact lenses in
the water if vision correction is required on land; (f) specific knowledge of the surf, the bottom, and the tides; g) surfing
with a companion; (h) avoidance of the path of oncoming surfers when paddling out; i) avoidance of shore breaks; (j)
caution of your board or other surfers when coming to the water surface after a wipe-out; (k) avoidance of alcohol and
drugs when surfing (23); and (l) preparedness for medical emergencies when planning extended surf trips to remote
regions (i.e., first aid, water rescue, CPR). Learning to fall or wipeout safely is covered in Table 39.2.
TABLE 39.2. WIPEOUT TECHNIQUES
SURFER'S MEDICAL ASSOCIATION
The Surfer's Medical Association ( 24) is an international organization of surfers committed to helping all surfers be
healthier. The organization consists of surfing physicians and other health professionals, scientists, and barefoot doctors
(surfers interested in the health and medical aspects of surfing). Every surfer is welcome to join.
The goals and objectives of this organization are (a) to educate surfers so they can spend minimal time hassling with
doctors and maximal time surfing, (b) to conduct and support research and educational activities on surfing and health,
(c) to represent the sport of surfing in the fields of medicine and science, (d) to teach physicians about the unique health
problems of surfers and how to care better for surfers, (f) to create a network of barefoot doctors and surfing health
professionals around the world, and (g) to protect and preserve the surfers' natural environment—the waves, the ocean,
and our beaches.
To obtain more information regarding this association write to Surfer's Medical Association, P.O. Box 1210, Aptos,
California 95001-1210 or log on to the web site at www.damoon.net/sma/index.
ACKNOWLEDGMENTS
Acknowledgment is made to Mark Renneker, M.D., and the Surfer's Medical Association, who have mobilized all of those
interested in Surfing Medicine into one collective for all of the best reasons.
CHAPTER REFERENCES
1. Renneker M. Surfing: The sport and the life-style. Phys Sportsmed 1987;15:156–162.
2. Bergschneider M, Navarro RA. Surfing. In: Safran MR, McKeag D and Van Camp S, eds. Manual of Sports Medicine. Philadelphia:
Lippincott-Raven, 1998;606–608.
3. Taniguchi RM, Blattau J, Hammon WM. Surfing. In: Schneider RC, Kennedy JC, Plant ML, eds. Sports Injuries—Mechanisms, Prevention,
and Treatment. Baltimore: Williams & Wilkins, 1985.
4. Allen RJ, Eiseman B, Strackly CJ, et al. Surfing injuries at Waikiki. JAMA 1977;237:668–670.
5. Lowdon BJ, Pitman AJ, Pateman NA, et al. Injuries to international competitive surfboard riders. J Sports Med 1987;27:57–63.
6. Lowdon BJ, Pateman NA, Pitman AJ. Surfboard riding injuries. Med J Aust 1983;2:613–616.
7. Stone DA. Surfing. In: Fu FH, Stone DA, eds. Sports Injuries—Mechanisms, Prevention, and Treatment. Baltimore: Williams & Wilkins,
1994;625–632.
8. www.surfstudy.sitehosting.net. Brown University School of Medicine, 1999.
9. Renneker M, Starr K, Booth G, eds. Sick surfers—ask the surf docs and Dr. Geoff. Palo Alto: Bull Publishing, 1993.
10. Ask the Surf Doc at www.surfermag.com, 1999.
11. Renneker M. Medical aspects of surfing. Phys Sportsmed 1987;15:96–105.
12. Lowdon BJ. Surfing injuries: immediate and long term problems and prevention. Athletic Training 1984;19:105–108.
13. Mc Danal CE, Anderson B. Surfer's elbow. Hawaii Med J 1977;36:108–109.
14. Bailey P. Surfer's rib: isolated first rib fracture secondary to indirect trauma. Ann Emerg Med 1985;14:246–349.
15. Kahn ML, Bade HA, Stein I. Body surfing as a cause of luxatio erecta: a report of four cases. Orthop Rev 1987;16:729–733.
16. Sage J. Recurrent inferior dislocation of the clavicle at the acromioclavicular joint: a case report. Am J Sports Med 1985;10:145–146.
17. Kennedy M, Vanderfield G, Huntley R. Surfcraft injuries. Aust J Sports Med 1975;3:53–54.
18. Seftel DM. Ear canal hyperostosis—surfer's ear. Arch Otolaryngol 1977;103:58–60.
19. Umeda Y, Nakajima M, Yoshioka H. Surfer's ear in Japan. Larygoscope 1989;99:639–641.
20. Burdick CO. Surfer's knots [Letter to the Editor]. JAMA 1981;245:823.
21. Erickson JG, Gemmingen GR. Surfer's nodules and other complications of surfboarding. JAMA 1967;201:134–136.
22. Ryan M. Making your surf board safer. The Surfer 1983;23:26.
23. Mackie I. Alcohol and aquatic disasters. Med J Aust 1978;1:652–653.
24. Surfer's Medical Association, www.damoon.net/sma/index. 1999.
25. Renneker M. The surfer's medical kit. Surfing Medicine 1999;18:7–10.
40 Swimming
40
SWIMMING
PETER J. FOWLER
Swimming Strokes
Injury
The Shoulder
Tendinopathy (Swimmer's Shoulder)
Evaluation of Swimmers for Tendinopathy
Shoulder Instability
Knee
Prevention and Treatment
Foot and Ankle
Elbow
Back
Chapter References
Swimming at all levels is enjoyed by an estimated 100 million participants. Generally, swimmers begin to compete in
early childhood, and for many, this activity continues into their senior years. The increasing popularity of masters
swimming and triathlons have contributed to the sport's continued growth. Because swimming is virtually a no-impact
activity, there are relatively few inherent risks. Its intensely repetitive nature, however, frequently leads to overuse
problems. Although these problems involve the shoulder primarily, injuries of the elbow, lower limb and back can occur
as well.
SWIMMING STROKES
The front crawl, the backstroke, the breaststroke, and the butterfly stroke are the four competitive strokes that are swum
in various distances alone or in combination. Table 40.1 summarizes the action of each. The four phases common to all
the competitive strokes, the reach, catch, pull, and recovery, are described in Table 40.2. The main power (75%) of
propulsion is provided by arm action during the pull phase in all strokes except the breaststroke, which is unique in both
upper and lower extremity motion. In front crawl, backstroke, and butterfly stroke, the motion of the arm through the water
starts with hand entry and proceeds with continual adduction and internal rotation of the glenohumeral joint. In the
out-of-water phase, the arm is in abduction and internal rotation, so that it is again positioned for hand entry and
repetition of the cycle.
TABLE 40.1. MAIN COMPONENTS OF THE COMPETITIVE SWIMMING STROKES
TABLE 40.2. COMPONENTS OF THE FOUR PHASES
INJURY
The Shoulder
Anatomy
The shoulder joint is the most mobile joint in the human body and has little bony support or protection. It relies on its
capsule, surrounding ligaments, and rotator cuff muscles, as well as larger muscles such as the pectoralis major and the
serratus anterior, for the stability that allows the arm to function with power and precision throughout its range of motion.
The four rotator cuff muscles work in a force couple combination with the deltoid and the long head of the biceps to
contain the humeral head in the glenoid fossa. The supraspinatus muscle inserts on the uppermost facet of greater
tuberosity. It acts as a fulcrum for the deltoid during abduction and is active throughout that movement. It also assists the
other rotator cuff muscles to resist any upward displacement of the humeral head in other arm actions. The infraspinatus
and the teres minor are external rotators. In the horizontal plane, the infraspinatus muscle also works in combination with
the supraspinatus and the subscapularis to depress the humeral head.
A primary internal rotator of the shoulder is the subscapularis. It stabilizes the humeral head by resisting anterior or
inferior displacement in the glenoid fossa and exerts a depressive force on the humeral head in combination with the
supraspinatus and the infraspinatus.
The long head of the biceps has a role in both forward flexion and stabilization of the humeral head. Its function should
not be overlooked in shoulder mechanics.
The scapular muscles, serratus anterior, rhomboids, and trapezius work constantly in swimming arm action. If these and
particularly the serratus anterior fatigue, the scapula may have a relative downward tilt that will alter the mechanics of the
glenohumeral joint. This, in turn, may increase subacromial stress during forward flexion of the arm.
Tendinopathy (Swimmer's Shoulder)
Injury to the shoulder is the most common problem facing the competitive swimmer regardless of age. The repeated
demands made on the shoulder stress its muscles and tendons far in excess of their normal usage and design. Anatomic
features, biomechanical forces, and intense training schedules combine to cause “swimmers shoulder.” This term was
first used by Kennedy and Hawkins in 1974 and refers to tendinopathy of the supraspinatus or biceps tendon ( 1). They
cited a 3% incidence of shoulder pain in a group of competitive swimmers surveyed. Current literature reports rates
ranging from 15% to 80% (2).
Causal Factors
Training
In today's training programs, a swimmer of national caliber typically practices in the water in 2-hour sessions twice daily
for a minimum of 5 days a week. A normal range is 4,000 to 8,000 meters during each practice session. Time in the
water, which improves both conditioning and technique, is augmented by dry-land training to build strength and
endurance. With these rigorous schedules, overuse injuries are inevitable.
Overwork
Because it is the least stable joint, the shoulder is the most vulnerable to injury when it is in the overhead position. To
keep up with the continuous, repeated demands of swimming, the muscles of the rotator cuff are required to work
excessively to contain and stabilize the humeral head. This work load may overfatigue the muscles and provoke a
chronic condition. Superior migration of the humeral head and increased subacromial loading may occur with a
subsequent onset of tendinopathy. Along with rotator cuff fatigue, scapular muscle fatigue will alter the mechanics of the
entire shoulder complex.
Hypovascularity
The functional relationship between arm position and blood supply to the supraspinatus and the biceps tendon was
studied by Rathbun and Macnab (3). In adduction and neutral rotation, the tendons are stretched tightly over the head of
the humerus, compromising their blood supply. In abduction, the vessels fill and circulation is restored. This repeated
hypovascularity, known as a “wringing out” mechanism, occurs in the area of the tendon most vulnerable to impingement.
By compounding the potential for damage by repetitive stress, this mechanism may contribute to early degenerative
changes.
Impingement (Soft Tissue Factors)
The supraspinatus and biceps tendons are particularly susceptible to impingement. Their tendons insert on or across the
humerus directly below the coracoacromial arch formed by the coracoid process, the coracoacromial ligament, and the
anterior acromion. When the arm is in abduction, forward flexion, and internal rotation (a position assumed in the catch
phase of all competitive strokes), the humeral head moves under the arch where the tendons may be repeatedly
impinged. A mechanical irritation, which further compromises the space under the coracoacromial arch, may result, and if
the problem is left untreated, it will go on to include the subacromial bursa and the acromioclavicular ligament.
Impingement (Osseous Factors)
The relationship between acromial shape and rotator cuff pathology has been described. Bigliani et al. found in a 1986
cadaver study that full-thickness rotator cuff tears were associated with changes in acromial shape ( 4). They described
three acromial types—type I, flat; type II, curved; and type III, hooked—and found a higher incidence of tears in type III,
in acromions with anterior spurs and acromions with a greater angle of anterior slope. Morrison and Bigliani later found
that there was a close correlation between their anatomic study and the incidence of acromial types in a clinical
population of 200 patients (5). Seventy percent of patients with full-thickness rotator cuffs had type III acromions. Also
there was a higher incidence of tears with acromions of a greater anterior slope angle. This is supported by the results of
a 1995 study by Tuite et al. that correlated acromial angle on x-ray studies with impingement and rotator cuff tears in a
group of patients who had undergone shoulder arthroscopy. They found a significant correlation between increasing
severity of rotator cuff disease and increasing acromial angle. Forty-three percent of patients with a full-thickness cuff
tear had an acromial angle of 30 degrees or greater. An angle of 25 degrees or more was measured in 63% of patients
with impingement and an intact cuff (6). These studies and others suggest that type III acromions or ones with an
increased anterior angle may be anatomic factors in refractory tendinopathy that does not respond to treatment. A
competitive swimmer with an acromial arch of decreased dimensions may be predisposed to impingement and more
easily develop a tendinopathy that will be resistant to treatment.
On the other hand, Ogata and Uhthoff have suggested that pathologic changes within the rotator cuff substance are the
result of a primary tendinopathy, and that acromial changes occur as a secondary phenomenon ( 7). They also suggest
that the changes seen within the rotator cuff occur initially on the humeral surface of the tendon near the enthesis, as
opposed to the bursal side, where one would expect to see lesions resulting from mechanical impingement from the
acromion and concluded that rotator cuff tears are unlikely to be caused by impingement but result from a degenerative
tendinopathy. Internal impingement, a recently described mechanism of injury in the overhead athlete, has not been
reported in swimming.
Impingement Positions in Swimming Strokes
At entry and the first half of the pull phase, the shoulder is in forward flexion, abduction, and internal rotation. This forces
the head of the humerus under the acromion and the coracoacromial ligament, and may impinge the supraspinatus and
biceps tendons, particularly in the fatigue situation.
Lateral impingement can be associated with the recovery phase of freestyle and butterfly strokes. The arm must abduct
to return to the entry position. If there is associated internal rotation or horizontal abduction, or both, the head of the
humerus comes up against the lateral border of the acromion.
During the end of the pull phase, the shoulder is in adduction and internal rotation, a position corresponding to the
wringing-out mechanism.
An analysis by Webster appeared to correlate the freestyle arm position at the time swimmers experienced pain with the
biomechanical factors implicated in tendinopathy. In almost one half of the swimmers with shoulder pain, it occurred
during entry or the first half of the pull phase; 14% experienced pain during the second half of the pull phase; 23%
reported pain during the recovery; the remaining 17.8% had pain during the entire pull or the recovery phase. Some of
this latter group had pain throughout the entire stroke ( 8).
Increased Laxity
Increased laxity should be ruled out as a contributing factor in the athlete with a resistant tendinopathy. The effects of
overwork have been described. However, in a swimmer with loose or lax shoulders, the rotator cuff may already be
working excessively hard just to contain the humeral head. The added rigor of training makes additional demands on
already fatigued or fatiguing muscles.
The association between rotator cuff tendinopathy and shoulder laxity was described by Fowler and Webster ( 9). A
comparison of 188 competitive swimmers and 50 recreational athletes without shoulder pain revealed a history of
shoulder pain in 50% of the swimmers, and some degree of posterior laxity in 55% of the swimmers and 52% of the
control group. This suggests that swimming does not predispose an athlete to increased posterior laxity. In 25% of the
swimmers, there was a history of tendinopathy and increased posterior laxity in the same shoulder.
Shoulder Strength Imbalance
At manual testing performed on these same swimmers there was external rotator cuff weakness in one or both shoulders
in 40 (of 188), with 33 having both weakness and a history of tendinopathy in the same shoulder. A second study was
undertaken to measure rotation strength about the shoulder. This revealed a significant difference in the rotation torque
ratio between swimmers and controls in the neutral and 90-degree abduction positions ( 10). This was attributed to the
greater strength of the internal rotators in swimmers. Because the pull-through phase, which involves adduction and
internal rotation at the glenohumeral joint, is the power portion of the stroke, most swimmers selectively train their internal
rotators. The resulting imbalance between the internal and external rotators may be a contributing factor in the onset of
rotator cuff tendinopathy ( Fig. 40.1). It is reasonable that a strong muscle will resist stress better than an unconditioned
one. There was no significant difference in external rotation strength between the two groups.
FIGURE 40.1. This algorithm outlines the many pathologic entities that can culminate in rotator cuff tendinopathy.
Evaluation of Swimmers for Tendinopathy
Palpation of the supraspinatus tendon medial to its insertion on the greater tuberosity will elicit tenderness if there is
tendinopathy. If the long head of biceps is involved, there will be tenderness over the bicipital groove.
Those with tendinopathy of the supraspinatus tendon often demonstrate a painful arc in the coronal plane at 60 to 100
degrees of active abduction. Symptoms of biceps tendinopathy can be reproduced by resisting forward flexion of the
straight arm while the forearm is supinated. This can be indicative of refractory supraspinatus tendinopathy.
Various tests reproduce pain by placing the shoulder in the impingement aggravated position. In the one described by
Neer, pain is elicited when the examiner forcibly elevates the forward flexed arm, a maneuver that drives the humerus
against the anteroinferior border of the acromion ( 11). In an appropriate test for swimmers, the shoulder is flexed forward
90 degrees, the elbow is flexed 90 degrees, and the arm is internally rotated by the examiner, pushing the humeral head
against the coracoacromial ligament reproducing pain ( Fig. 40.2).
FIGURE 40.2. A clinical test for impingement. Here, the tendons are impinged under the coracoacromial arch. Because
minimal pressure causes pain, care must be taken when using this test.
Muscle weakness, particularly in the external rotators, should be ruled out. With the patient's arm in adduction, external
rotation, and with the elbow flexed 90 degrees, the examiner applies an internal rotation force that the patient is asked to
resist. Gross muscle weakness will be readily apparent. This test is often accompanied by pain.
Generalized laxity is documented, particularly as it relates to the shoulder. Increased laxity or frank instability contributes
to the progression of tendinopathy or may be the cause of the pain. The apprehension-relocation test is used to assess
anterior instability. The arm is stressed in external rotation and 90 degrees of abduction. The test is positive if the patient
exhibits a feeling of anxiety, often with pain, or will not allow further external rotation. This apprehension is alleviated by
applying posterior pressure on the upper arm to contain the humeral head, allowing more external rotation ( Fig. 40.3A
and Fig. 40.3B).
FIGURE 40.3. A: The arm is abducted and externally rotated, and the humeral head is levered anteriorly. With anterior
glenohumeral instability, the athlete will experience apprehension or discomfort, or both. B: Relocating the humeral head
in the glenoid fossa will relieve the symptoms and allow more external rotation.
Posterior glenohumeral translation can be assessed in both the sitting and supine positions ( Fig. 40.4A and Fig. 40.4B).
Movement of the humeral head by 50% of the glenoid width is considered normal and motion greater than this, although
not necessarily abnormal, would influence shoulder mechanics by creating an increased workload for the rotator cuff. If
the shoulder is unstable, applying an axial load may reproduce the symptoms experienced while swimming. In this
instance, the cause of pain would be instability.
FIGURE 40.4. A: Posterior glenohumeral translation is assessed in the sitting position. One hand stabilizes the shoulder
girdle, and the opposite hand grasps the humeral head between the thumb and index finger and a posterior stress
applied. B: In the supine position, posterior laxity the arm is held at 20 degrees abduction and forward flexion and in
neutral rotation, and a posterior stress applied to the humeral head. The abducted position imitates arm position in a
variety of activities.
The presence of a sulcus with inferior traction indicates instability in this direction.
Clinical Presentation
The progression of tendinopathy is insidious. Pain becomes generalized about the shoulder and is often present at night
or at rest. The athlete avoids painful positions and those that aggravate the symptoms. To minimize pain during
swimming, subtle changes in stroke mechanics are developed. The athlete will modify all aggravating positions during
other activities as well. A gradual loss of shoulder range of motion and muscle weakness may occur, and supraspinatus
and infraspinatus wasting may become apparent. In the mature athlete, this may be an indication of degeneration or
partial tears of the rotator cuff tendon. However, this is seldom seen in age-group swimmers and is rare in athletes
younger than 25 years of age.
The clinical classification of tendinopathy is based on Blazina's categories for jumper's knee ( 12). In grade I, the athlete
has pain following the activity; in grade II, there is pain during and after the sport, but it is not disabling; in grade III, there
is disabling pain both during and after the activity; and grade in IV, there is pain with activities of daily living.
Prevention of Tendinopathy
Overuse syndromes about the shoulder are easier to prevent than to treat. Table 40.3 summarizes a basic preventive
program. This includes balanced muscle strengthening, flexibility, technique modification, and avoidance of overwork, all
of which should be incorporated into a training schedule from the outset. Ongoing stroke analyses will allow the coach to
guide the swimmer away from stroke errors that contribute to tendinopathy.
TABLE 40.3. PREVENTION OF SWIMMER'S SHOULDER
Avoidance of Overwork
Again, overwork is one of the primary causes of tendinopathy and is frequently the result of increased training intensity.
Training progressions should occur gradually as the season progresses. Rigorous training sets before the athlete is
ready or exceedingly difficult practices early in the training schedule can trigger the onset of tendinopathy. Practice
sessions should be organized so that the difficult segment of the workout is completed before the swimmer begins to
overtire. After the difficult work has been completed, the workout can continue, with emphasis on stroke drills, alternating
stroke and leg work, and start and turn techniques. With proper instruction, swimmers can become aware of how fatigue
is influencing their stroke mechanics and make appropriate adjustments.
Balanced Muscle Strengthening
As previously mentioned, in competitive swimming, both pool and dry-land training emphasizes strengthening the internal
rotators and extensors to optimize propulsion. It is important not to ignore strengthening the antagonists as well, because
they play a significant role in containment of the shoulder. An exercise program that includes strengthening the external
rotators as well as the biceps and scapular muscles will help prevent an external and internal rotator imbalance. Surgical
tubing, pulleys, dental dam, and free weights can be used in isotonic and eccentric drills performed in neutral, 90
degrees of abduction, and 90 degrees of flexion to mimic arm positions in swimming ( Fig. 40.5A and Fig. 40.5B). This
approach improves power and control in both prime mover and antagonist muscle functions.
FIGURE 40.5. External rotators are strengthened in neutral (A) and 90 degrees of abduction (B).
Biceps strengthening exercises should incorporate the functions of the biceps as elbow flexor and forearm supinator and
be performed in several positions of shoulder range of motion. During weight training, painful subacromial loading
positions should be avoided. Paddles must be used with caution because the increased leverage may overload the
rotator cuff muscles.
Flexibility
A 1985 study by Griep determined that regardless of the swimmer's sex or the stroke most frequently used, those
swimmers with restricted flexibility were more likely to develop a tendinopathy than those who had enhanced their
flexibility with a stretching program ( 13). Stretching should be included in the daily training warmup routine. Pairs
stretching is appropriate for swimmers older than 15 years of age, because this age group should be sufficiently mature
to understand that over stretching the soft tissues can irritate the rotator cuff tendons and must be avoided. These
techniques are either passive or proprioceptive neuromuscular facilitated (PNF). In the passive techniques, the partner
very slowly and gently stretches the swimmer to a pain-free limit and then holds the position. In PNF stretching, the
swimmer to be stretched moves to the limit of range. The partner maintains that position while the swimmer contracts
against the partner's resistance. These stretches are repeated a variable number of times. Younger swimmers should
stretch individually.
Technique Modification
Poor technique not only slows a swimmer down but can also cause injury. Again, prevention of overwork and fatigue of
the rotator cuff should be foremost in a coach's mind as training programs are planned and the athlete progresses.
Ongoing stroke analysis to pinpoint breakdowns in stroke mechanics should be routine so that the swimmer can adjust
technique to limit impingement stress. This is particularly important during fatigue. Insufficient body roll in freestyle or
backstroke can contribute to lateral shoulder impingement. In freestyle, the high elbow position during recovery should
be achieved with body roll rather than muscle activity. Attempting to force the elbow into a higher position with muscle
activity can induce subacromial impingement.
In the catch phase of all strokes, one is preparing for maximum propulsion. Overreach with excessive internal rotation
may cause undue subacromial loading and excessive activity for the cuff muscles to contain the humeral head. Also,
excessive internal rotation may intensify the wringing-out phenomenon. Changes to body roll, reach, and the degree of
shoulder rotation can reduce the frequency and the length of time that the shoulder is in a precarious position. Evidence
of the effect of breathing patterns on the incidence of tendinopathy is contradictory ( 8). Breathing to alternate sides
keeps the swimmer from leaning constantly on the same shoulder.
Treatment of Tendinopathy
Grade I
Conservative management of a grade I tendinopathy includes increases in both warmup and warmdown times, particular
attention to prepractice stretching, icing, correction of external rotation weakness, decrease in workload, and temporary
elimination of painful strokes. It is important that practice strokes be pain free. Stretching to increase blood flow, restore
range of motion, and decrease potential for impingement should involve all the shoulder structures, including the anterior
ones.
The in-the-pool warmup should be prolonged, slow-paced, and use only pain-free strokes. Additional arm warmup
exercises can follow kicking sets and the training session completed with a warmdown period in the pool.
Icing the shoulder with ice cups for a maximum of 15 minutes after practice is effective. Strengthening the external
rotators is important in controlling the glenohumeral joint and increasing muscle work efficiency. The external rotators are
worked in adduction progressing to varying degrees of abduction. If only one stroke causes pain, it should be
discontinued until the pain subsides and then gradually reintroduced. Faulty mechanics must be corrected.
Grade II
Management of grade II tendinopathy incorporates the programs described earlier with relative rest, physiotherapy, and
medication. Relative rest allows the swimmer to use strokes that do not cause pain and to emphasize leg work. Kick
boards place the shoulder in pain-provoking positions and should not be used. Running and cycling can augment limited
swimming workouts. In addition antiinflammatory medication will help provide symptomatic relief.
At this stage, physiotherapy is indicated. A rehabilitation program will be planned by the therapist following an
assessment to determine the intensity and duration of pain, range-of-motion limitations, and strength loss in arm and
shoulder girdle muscles. Effective modalities are ultrasound and electrotherapy, which includes transcutaneous nerve
stimulation, interferential, muscle stimulation, and microcurrent. Loss in range of motion is treated with passive
mobilization techniques and range-of-motion exercises.
If there is an imbalance in muscle strength or a significant weakness in any muscle group, the therapist will plan an
appropriate strengthening program. Depending on the nature and presentation of the pain, joint range of motion, and
weakness, the exercises will be isometric, isotonic, or where possible, isokinetic. As in prevention, an effective treatment
program can be developed using free weights or rubber tubing. It is important that the exercises do not reproduce pain.
Often, the pain is felt in certain positions and the exercises can be done around these. If, however, exercises are painful
throughout the entire range of motion, they should be discontinued or the number of repetitions decreased to a level that
is pain-free.
Control of movement is an area of growing importance in the treatment of shoulder problems. In a joint with the mobility of
the glenohumeral joint, the ability to control the joint and its stabilizers through full range of motion and maintain strength
and power requirements is essential. This introduces the concept of proprioception of the shoulder girdle. Glenohumeral
kinesthesia or proprioception has recently been given some attention but is difficult to assess objectively. However,
providing the patient with controlled tasks may identify specific difficulties. Ease of performance, comparison to the other
side, and reproduction of joint position (eyes closed) can be subjectively assessed. Challenging positions, such as
overhead or abduction with external rotation, would be a progression. As with the lower extremity, it is important to
perturb stability and force a controlled reaction of the musculature. This can be done using physioballs, a Bodyblade,
tubing, water exercises, balance boards, and Profitters ( Fig. 40.6). Once the concept has been defined and understood,
the exercises are limited only by the imagination of the therapist. Proprioceptive exercises should be progressed through
gradations of difficulty of speed, position, and type of contraction required. They should also be progressed to include a
functional component that is individualized according to each patient's needs. In swimmers, ball exercises performed
overhead against a wall are appropriate ( Fig. 40.7).
FIGURE 40.6. Demonstrates functional proprioceptive training with a Bodyblade.

FIGURE 40.7. Here, a proprioceptive ball exercise in a functional position for swimmers is shown.
The use of water as a medium for exercise and retraining is very valuable and underused. Buoyancy allows the therapist
to devise a variety of exercises and activities to enhance range of motion, strength, and proprioception. In water,
resistance is not isolated to one plane, and no muscle can act independently without sufficient trunk stability. The
neuromuscular reeducation that occurs when these exercises are performed correctly can effectively accelerate the
rehabilitation process. These exercises can be progressed using paddles, water wings, air mattresses, or pool noodles
(Fig. 40.8). Unfortunately, the availability of this medium in the clinic setting can be limited. But with adequate instruction
and demonstration on land, compliant patients can benefit from unsupervised pool activities.
FIGURE 40.8. This figure demonstrates the use of hydrotherapy to train for strength and control of the glenohumeral joint
(abduction and adduction), with a pool noodle providing resistance.
A successful treatment program will allow a gradual return to a full training schedule. It is advised that the therapy
continue until the preinjury level of activity is attained.
A steroid injection into the subacromial space should be considered if there is no response to treatment and if
impingement aggravated tests still elicit pain. The swimmer's load should be decreased following injection. Return to
previous levels of activity should occur over a 4- to 6-week period. Steroid injections should never be used routinely.
Grade III
If the tendinopathy progresses to grade III and becomes refractory in spite of the measures outlined earlier, the options
available to the athlete include a change of sport or surgery. Unless there is potential for a high-caliber career at the
national or international level, most young swimmers choose to participate in another sport. In most instances, this is to
be encouraged.
If surgery is planned, the swimmer must understand that a serious commitment to a rehabilitation program is mandatory
and that the success of the procedure will depend on compliance. This would include progressive exercises to restore
range of motion and balanced muscle strength. Return to the pool should begin with slow swimming that advances to
interval training and guided stroke modification.
Grade IV
Grade IV tendinopathy is most often seen in the mature athlete and may indicate a torn rotator cuff. Imaging techniques
such as athrography, ultrasonography, and magnetic resonance imaging may confirm the clinical diagnosis. Lesions such
as partial-thickness tears and thickened subacromial bursa can be identified by shoulder arthroscopy. Anterior and
posterior superior quadrant labral tears that cause pain in the swimmer can be treated successfully with arthroscopic
excision (14). These are not a frequent cause of pain in the younger swimmer.
Bursectomy alone followed by appropriate rehabilitation can provide relief in this group. However, a more radical
decompression, which includes resection of the anteroinferior acromion and a portion of the coracoacromial ligament, is
usually recommended. The athlete should understand that return to preinjury level of participation is unlikely.
Postoperatively, range of motion is often limited. Also, muscle strength, endurance, and power deteriorate, particularly in
the abductors and external rotators. Physiotherapy to rehabilitate all the muscle groups about the shoulder girdle plays a
significant postoperative role.
Shoulder Instability
Anterior Instability: Prevention and Treatment
Compared with throwing activities, the arm is seldom in the provocative position during swimming strokes. Therefore,
anterior instability is not often the cause of pain in this group and is usually secondary to a traumatic incident in another
sport. Primary conservative treatment of anterior instability is stroke modification and balancing-strengthening exercises.
If symptoms do not subside, examination under anesthesia or arthroscopy will assist in diagnosing intraarticular lesions
such as a Bankart or Hill-Sachs. An anterior stabilizing procedure can provide relief, and athletes can return to preinjury
levels if their motion and strength are regained.
Posterior and Multidirectional Instability: Prevention and Treatment
Swimmers with frank posterior instability may have pain from dislocating their shoulders during the swimming stroke
cycle. The at-risk position of forward flexion and internal rotation occurs in all strokes. Pain in swimmers with congenital
or acquired multidirectional instability must be differentiated from that experienced by those suffering from painful
tendinopathy who have concomitant increased laxity.
In swimmers with prolonged periods of instability, persistence with a nonoperative program is recommended. In most
cases, stroke modification, correction of strength deficits, and modification of training programs to minimize the
magnitude and incidence of abnormal motion can be successful. Surgical intervention such as an inferior capsular shift, a
reefing procedure to the posterior cuff and capsule, or glenoid osteotomy should be considered only when all
nonoperative treatments have been exhausted. These procedures, although providing symptomatic relief from pain for
daily activities and for recreational participation in swimming and other sports, will, because of restricted motion,
terminate a competitive swimming career.
KNEE
In a survey of 2,496 swimmers, Kennedy and Hawkins found that 90% of 261 individuals with orthopedic complaints had
shoulder, calf, or foot problems ( 15). Eighty-five calf and foot problems were divided almost evenly among the four
competitive swimming strokes. All 70 knee problems were caused by the whip kick during the breaststroke. The whip kick
is considered the superior breaststroke kick in terms of speed and propulsion. However, it subjects the knee to unnatural
motion, and because of the intensity and number of repetitions performed, even proper execution does not protect the
breaststroker from injury. Knee pain in the swimmer is usually caused by medial collateral ligament (MCL) stress
syndrome, patellofemoral syndrome, medial synovitis with or without a pathologic medial synovial shelf.
Medial collateral stress syndrome, a common cause of pain in the elite breaststroker, affects the superficial fibers of the
MCL that arise from the adductor tubercle of the femur and extend downward and forward to their insertion 4 to 5 cm
distal to the knee joint on the anteromedial surface of the tibia. In a study of the pathomechanics of this problem by
Kennedy et al. (16), it was found that tension on these fibers increased as the knee moved from flexion to extension,
increased further with a valgus stress, and increased dramatically when external rotation forces were applied to the knee.
Point tenderness along the course of the ligament is suggestive of medial collateral stress syndrome. Tenderness is
often located at the origin of the MCL at the adductor tubercle and also where the superficial fibers cross the upper tibial
margin. Pain may be reproduced when a valgus external force is applied to the knee flexed at 20 to 30 degrees.
Patellofemoral syndrome is an abnormal alignment of the lower extremity as well as hypermobility or frank instability of
the patellofemoral joint, which may be associated with patella alta. Palpation of the patellar facets or femoral condyles
will elicit tenderness. Carrying out a patellar compression test or laterally deviating the patella may reproduce the
symptoms. The fact that more severe patellofemoral syndromes occur in club swimmers may be due to the improper
execution of the kick. However, those with inherent instability of the patellofemoral articulations may be precluded from
reaching elite levels of breaststroke swimming by the forces generated by the whip kick.
Medial synovitis was confirmed by Keskinen et al. at arthroscopy in seven out of nine breaststrokers with knee pain ( 17).
This was attributed to a combination of high angular velocities and excessive outward rotation. In a review of 36
breaststrokers with knee pain, Rovere and Nichols found a significant relationship between frequency of knee pain,
increased age, increased years in competition, increased training distance, and decreased warmup distance ( 18). They
also found that the medial aspect was the most common site of knee pain. Of the subjects examined, 47% had a tender,
thickened medial plica. This implicated medial synovial plica syndrome. Both the extension phase of the breaststroke kick
and plica palpation produce similar pain. During repeated knee flexion and extension, the fold or plica snaps across the
medial femoral condyle, producing friction that results in pain and inflammation of the plica. This synovitis may be the
same type noted by Keskinen. Diagnosis is made by eliciting local tenderness and palpating the thickened synovium as it
crosses the medial femoral condyle.
Because the etiology of many knee problems in swimmers may be multifactorial, pathologies such as chronic
ligamentous instability, torn medial meniscus (although uncommon in the stable knee), and osteochondritis dissecans
must be ruled out.
PREVENTION AND TREATMENT
A proper warmup period of a minimum of 1,000 to 1,500 yards before beginning hard breaststroke training along with
gradual increases in training distances is recommended by Rovere and Nichols ( 18). Altering training programs so that
the majority of workout time is devoted to other strokes and at least 2 months per year of total rest from swimming is
recommended. In addition, the breaststroker with knee pain can continue training by swimming with the arms only.
Once pain occurs early diagnosis is important. A knowledgeable coach will identify mechanical reasons, such as faulty
whip kick technique, which is known to be a correctable cause of knee pain ( 19). Communication among coach,
physician, therapist, and swimmer is essential. Knee pain in the elite breaststroker is often more easily controlled than
severe shoulder pain in swimmers. Anatomic factors such as significant patellofemoral or ligament instability may be
incompatible with the stress inherent in the whip kick. A prolonged treatment program in athletes with these conditions
may be doomed to failure.
Therapeutic measures depend on the diagnosis and include antiinflammatory medication for inflammation of the medial
collateral ligament or medial synovial plica and ice and ultrasound to control acute symptoms. For athletes with
patellofemoral pain, it is important to teach strengthening exercises to overcome muscle deficiencies and stretching
exercises for lower extremity musculature. These exercises should be performed on an ongoing basis. Steroid injections
should play only a minor role and, when used, should be directed into the pathologic synovial tissue and not
intraarticularly. Rovere and Nichols have noted the effectiveness of these in treating the inflamed medial synovial plica
(18). Once the acute phase of the injury has subsided, prevention and treatment should continue. The reintroduction of
the breaststroke should be gradual and closely monitored to prevent recurrence.
Foot and Ankle
The extensor tendons of the ankle and foot are firmly bound over the dorsum of the ankle by the extensor retinaculum.
Tendinopathy of these tendons, which are enclosed in sheaths and susceptible to irritation, is the most common cause of
pain, regardless of the stroke performed. The foot and ankle are carried into extreme plantarflexion and then back to
neutral in both the flutter and dolphin kicks. This repetitive work causes inflammation and edema, which are not well
tolerated under the tight retinaculum. In most instances, the diagnosis is obvious because crepitus is both felt and heard
when the foot is passively brought from plantarflexion to dorsiflexion. Again, prevention should be stressed with routine
extensor tendons stretching before practice. Local therapy modalities include ice and ultrasound. Wrapping the foot and
ankle and administering antiinflammatory medication are often effective. Swimming can generally be continued with less
or no kicking. The return to normal kicking should be gradual ( 12,20).
Elbow
Stress syndromes about the elbow are caused by the arm pull in the butterfly and breaststroke and less frequently in the
freestyle. The elbow-up pull, in which the elbow is bent and held higher than the hand throughout the first part of the pull,
is used by most competitive swimmers (19). This position allows the swimmer to push the water backward at the most
efficient angle with a maximum backward thrust of the hand. The elbow then bends about 100 degrees as the arm is
pulled under the body with the upper arm medially rotated and the forearm pronated. The butterfly stroke is very
dependent on this arm pull, and the mechanics are similar to those of the freestyle. The early component of the
breaststroke is also comparable to the butterfly and freestyle strokes. In a high elbow position, the swimmer has the
sensation of reaching over a barrel ( 19). Lateral epicondylitis referred to as tennis elbow and described by Nirschl and
Petrone can ensue (21,22). With this disorder, the extensor carpi radialis brevis and extensor communis aponeurosis at
the lateral epicondyle of the humerus become inflamed. The overwhelming moments of force, along with repetition, result
in a combination of extrinsic overload and excessive muscle contractions that appear to be the prime etiologic factors.
Dropping the elbow, which produces a less efficient angle, hence requiring more force from the common extensor
muscles, is recognized as a frequent fault in the swimmer's stroke pattern.
Lateral epicondylitis in the swimmer is treated with ice, the discerning use of antiinflammatory medication, and physical
therapy modalities such as ultrasound to relieve acute and chronic inflammation. Forearm extensor power, flexibility, and
endurance are increased by applying eccentric loads. Stroke alteration may decrease the moments of force placed on
the elbow. In most cases, stroke alteration is essential for management over the long term. Steroid injection to the
localized area is appropriate in resistant cases. Because there is evidence of associated collagen disorganization and
weakening for approximately a 6-week period, steroids be used judiciously and infrequently ( 23). In refractory cases,
surgical treatment may include exposure and excision of the degenerative lesion, as described by Nirschl ( 22). This must
be followed by a slow and methodical return to training.
Back
Many breaststroke swimmers pull from the glide position with extended arms using earlier elbow flexion and arm
abduction. This maneuver prolongs the elbow-up position and propels the torso above the water, which aggravates the
already lordotic attitude of the lower back. This may cause a variety of low back problems, including stress fractures of
the pars interarticularis or even frank spondylolisthesis. More often, however, accentuation of a mildly symptomatic
spondylolisthesis or a mechanical low back pain from posterior facet irritation occurs, limiting the competitive
breaststroker's training. In the butterfly stroke, inefficient and incorrect mechanics are frequently the cause of these back
problems, which are primarily pain with some radiation into the buttocks. Hamstring tightness may direct the physician
toward a diagnosis of spondylolisthesis. Positive findings often include a step deformity at the spine of L-5 that can be
palpated, and an abnormal gait with a backward pelvic tilt. The diagnosis is confirmed radiographically. In the presence
of normal x-ray studies, a bone scan will aid in the diagnosis of a pars stress fracture. A stress fracture of recent origin
requires, first and foremost, a prolonged period of rest. Treatment of spondylolisthesis is symptomatic depending on the
severity of the complaints. Return to training must be carefully planned and monitored with hamstring stretching and
abdominal strengthening playing a particularly important ongoing role. If the low-back pain is mechanical, a similar
program is beneficial. Prolonged treatment that includes other modalities such as transcutaneous nerve stimulations or
repeated mobilizations to the affected area may be required in more resistant cases. A steroid injection into the inflamed
facet may be necessary for relief as well.
The term adolescent swimmer's back was coined by Wilson and Lindseth ( 24) to describe three adolescent swimmers
with backache aggravated by the butterfly stroke. These patients were all diagnosed with Scheuermann kyphosis. The
authors did not determine whether vertebral abnormalities were caused by the forceful contraction of the chest and
abdominal musculature or whether these were aggravating factors. Two of three experienced dramatic relief by stopping
the butterfly stroke. Patients such as these should be encouraged to continue with their swimming program but to limit
their swimming to the backstroke and freestyle.
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17. Keskinen K, Eriksson E, Komi P. Breast stroke swimmer's knee. Am J Sports Med 1980;8:228.
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1985;13:164.
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41 Track and Field
41
TRACK AND FIELD

JEROME V. CIULLO
JEREMY R. CIULLO
Exogenous Factors
Running Shoes and Orthotics
Blood Doping
Diet
Drugs
Field Conditions
Stretching and Weight Training
Running Events
Sprints
Relays
Hurdles
Middle Distance
Distance, Marathon, and Cross-Country
Race Walking
Jumping Events
Long Jump
Triple Jump
High Jump
Pole-Vault
Throwing Events
Shot Put
Hammer Throw
Discus
Javelin
Combined Events
Conclusions
Chapter References
Track and field events afford the athlete the opportunity to demonstrate his or her capability in the most basic forms of
physical prowess. Running, throwing, and jumping skills are individually emphasized, as compared with other sports in
which such skills are used in various combinations and for various goals. These events enjoy a rich heritage, tracing their
origins to ancient times, as documented in records of the ancient Olympic games.
The Greeks stressed athletics for two reasons. First, their religious beliefs revolved around the whole man concept, in
which integration and development of body, mind, and soul was necessary in order to achieve one's potential. Second,
athletic competition supplied physically fit soldiers ( 1). Running and jumping events prepared the soldier for offensive
and defensive maneuvers. Throwing sports, such as javelin and discus, emphasized both strength and accuracy and
closely paralleled activities of war ( 2). Athletic competition allowed proof of the best soldiers and military might without
loss of life.
The events comprising modern track and field competition fall into two groups, those that have basic explosive power
requirements and those that emphasize endurance. Track and field events can result in sport-specific injury patterns. An
epidemiologic analysis of sports injuries at the 1985 Junior Olympics reported that 35% of track participants required
medical treatment related to their performance ( 3). In an analysis of 257 high school track and field athletes over one
season, one injury occurred for every 5.8 men and 7.5 women, with the average injury resulting in 8.1 days missed
practice. Sprinting events caused 46% of injury ( 4). Another 1-year study demonstrated an injury exposure rate of 3.9 per
1,000 training hours. Most injuries involved the lower extremities, primarily being stress fractures (21%) and hamstring
strains (14%). Middle-distance and distance runners had more overuse injuries, whereas sprinters, hurdlers, jumpers,
and multievent athletes had more acute injuries. Higher age, increased flexibility, and menstrual disturbance were
associated with greater likelihood of injury ( 5). In competitive athletes aged 17 to 26, another epidemiologic study found
incidence of 0.7 stress fractures per 1,000 hours of training ( 6). The number of supervised training sessions has also
been positively correlated with injury ( 7). Special Olympic athletes with Down's syndrome were 3.2 times as likely to
encounter a medical problem during participation than their counterparts ( 8). It has been suggested that individuals with
sickle cell trait have a selective advantage for the brief and explosive throw and jump events ( 9). Power athletes have
been found with higher lumbar bone mass than sprinters ( 10).
Analysis of Olympic track and field competitors over the past 100 years has shown that the age at which peak
performance is achieved has remained remarkably consistent ( 11). For both men and women, the age of peak
performance increases with the length of the foot race, with women generally achieving peak performance at younger
ages. In the 100-meter dash, the mean age of gold medal winners in the last 100 years is 22.85 years for men and 21.42
years for women. This contrasts with longer distance events. For men, the average age of 10,000-meter winners was
27.53 years. In field events, the mean age for male long jump champions was 23.05 years compared with 24.44 years for
women. High jump gold medallists averaged 23.15 years for men and 22.75 years for women, and shot put gold
medallists averaged 24.00 years for men and 26.11 years for women. In master athletes, the 400-meter run and the long
jump events were most affected by advancing age in both male and female participants ( 12). One hundred and fourteen
elite Swedish track and field athletes were followed at age 50 to 80, and compared to the general population. Arthrosis of
the hip was increased threefold in the athletic group, arthrosis of the knee also increased, but neck and shoulder
problems decreased (13). In follow-up of 983 Italian track and field athletes, comparison with the general population
mortality tables demonstrated increased life expectancy, with an observed to expected ratio of 0.73 for males and 0.48
for females (14).
Track athletes with abnormal gait patterns and posture have an increased incidence of stress injuries with performance.
A simple preparticipation screen includes assessment of flexibility of all major joints, responsiveness of primary postural
muscles, posture, balance, and gait. In addition to a thorough cardiorespiratory evaluation, this basic motor screen is
valuable in predicting which athletes are more susceptible to stress injuries.
EXOGENOUS FACTORS
Running Shoes and Orthotics
There is no single ideal running shoe. Athletes must find a shoe that is comfortable and suits their style of running.
Runners compete in spikes, but such shoes are not suitable for either distance or early season training, for which “flats”
or commercial running shoes demonstrate superior shock-absorbing capacity. Some shoes are cut narrow, whereas
others are cut wide; the sole may be curved or straight.
The toe of a running shoe is usually box shaped and provides enough clearance for slight toe motion. This motion is
imperative to prevent blisters, calluses, corns, cracked nails, and hematoma under the nail itself. The runner's foot bends
at the ball; therefore, this is the place the shoe should also bend. If it is not flexible for the forefoot, the athlete is forced to
“run over” the shoe, which causes a muscular imbalance and stress, so that Achilles tendinitis, shin splints, or strains can
occur. If shoes are too stiff, scoring the undersurface at the forefoot with a knife will increase flexibility. The entire sole of
the shoe must be well padded but not too soft. Padding can reduce the incidence of bone bruising of the heel, calcaneal
fat pad contusion, midfoot sprains, and spurring at the ball of the foot. The midfoot should be supported with a slight
wedge. In addition, the external stripes or “lazy S” pattern of the outside of the shoe also serves to brace and stabilize
the foot. The back of the shoe must not irritate the back of the heel. A wider or so-called wheelbarrow heel may be of
some benefit in distance running, in which repetitive shock is distributed. Similarly, heel height can decrease strain on
the Achilles tendon by slight elevation. Again, this is a matter of preference, because some well-trained athletes are used
to walking normally in countersunk or negative heels and may in fact find a lower heel more comfortable. This is in
contrast to the high jump, in which maximum sole height is regulated.
Inserts or orthotics may be an occasional tool used in treating an injury such as posterior tibialis strain. They have not
been documented in injury prevention. With excess pronation of the foot, the lower leg compensation may result in a
diffuse pain along the patella, which on occasion responds to orthotics.
Hard orthotics are occasionally helpful to recreational athletes, but competitive athletes find them difficult to wear. The
musculotendinous unit takes a long time to adapt, and if orthotics are used, they must be adapted to also. Runners find
soft orthotics more comfortable. Distance runners may need two pairs of orthotics, the first, a hard pair for distance
training, and a second softer pair for competition.
In a large series of long-distance runners who had used orthotic shoe inserts for symptomatic relief of lower extremity
complaints, it was found that these devices are most effective in the treatment of symptoms arising from biomechanical
abnormalities such as excessive pronation or leg length discrepancies ( 15). Other diagnoses in which orthotics were
used included excessive pronation, leg-length discrepancy, patellofemoral disorders, plantar fasciitis, Achilles tendinitis,
and shin splints. The results of treatment with the orthotic shoe inserts were independent of the diagnosis or the runner's
level of participation.
In a longitudinal, double-blind study, the effects of sock fiber composition on the frequency and size of blistering events
in long-distance runners were examined ( 16). It was found that socks composed of 100% acrylic fiber were associated
with fewer and smaller blisters when directly compared to socks composed of 100% cotton fiber.
Blood Doping
Some Scandinavian and European distance runners have used a method of storing 1 to 2 units of their own blood 2 to 8
weeks before their event, and retransfusing it just before competition. The added blood volume is thought to allow
increased performance by increasing oxygen transfer capability and increasing cardiac contractility (stroke volume) for
distribution of the blood. This may be effective in acclimatizing to higher altitude where the air is thinner, thus avoiding
the need to train and adapt at that altitude. Otherwise, advantageous effects in training and competition at similar
altitudes are highly controversial.
Diet
Athletes may try to alter their performance by dietary intake. Carbohydrate loading has become popular for the
endurance-type athlete but not for the sprinter or thrower. This is largely due to the muscle fiber type used in specific
events. Sprinters and throwers concentrate on development of type II or fast-twitch fibers. These bulky-type, muscled
individuals have fibers that are activated specifically for short bursts. In contrast, endurance runners have developed
their slow-twitch, type I, dark, or endurance-type fibers. These are lean muscles that respond to endurance training by
increasing capillary supply to deliver oxygen and mitochondrial content to resynthesize adenosine triphosphate (ATP)
and, therefore, are well suited for postural and endurance activity.
In contrast, the fast-twitch fibers used in strength events like weight lifting, shot putting, and discus throwing do not
respond as well to training in producing mitochondria or increasing capillary supply. Therefore, they have a relatively low
capacity to resynthesize ATP through oxidative phosphorylation, and they fatigue quickly.
Muscles store glycogen to use as fuel in endurance-type activity. When not enough oxygen is available to convert this
fuel into energy, the fuel is only partially metabolized, and lactic acid is the result. Lactic acid within the muscles or
exhaustion of stored fuel quickly causes fatigue. The distance runner will call this “hitting the wall.” In the well-trained
athlete, this occurs after 1½ to 2 hours of prolonged activity. In order to avoid this calorie depletion, some athletes have
used a system called carbohydrate loading.
A well-trained athlete uses carbohydrate loading following an exhaustive training period during which muscle glycogen is
depleted. This is followed by a 3-day period in which carbohydrate intake is kept extremely low. Three days before the
competitive event, a high-carbohydrate diet is initiated. The depleted muscles soak up carbohydrates like a sponge and
become supersaturated with glycogen. It is estimated that an untrained individual has approximately 13 g of glycogen per
kg of muscle, and with training, this can increase to 32 g after carbohydrate loading. In a well trained individual, storage
can increase up to 35 or 40 g.
Many athletes avoid carbohydrate loading because it is considered to be a major shift from their routine diet. The body
meets periods of carbohydrate avoidance with burning fat, and the end result is ketosis. This chemical shift can lead to
irritability and an electrolyte imbalance resulting in irregularity of the heartbeat. Because 3 g of water are stored with
each gram of glycogen, a “loaded” distance runner may gain 3 to 5 pounds of weight, leading to a feeling of tightness and
heaviness.
Drugs
Drugs have been used by athletes and warriors for more than 3,000 years to protect them from evil, increase power, and
improve performance. Among the agents that have been found in athletic drug use are mushrooms, caffeine, alcohol,
nitroglycerin, ether, strychnine, cocaine, opium, camphor, ephedrine, glycerine, gelatin, iron, oxygen, aspartic acid,
amphetamines, tranquilizers, vitamins, steroids, and red blood cells. Polypharmacy, or the abuse of multiple drugs at the
same time, is not uncommon, particularly by the strength event athletes. Vitamins are among the most overused drugs.
The use of multiple vitamins is overrated. A young healthy adult, athletic or otherwise, has no need for vitamins or
supplements if a normal diet is eaten. Many vitamins are quickly eliminated from the body after ingestion. Nevertheless,
some fat-soluble vitamins like A, D, E, and K are stored within the body and have the potential to achieve toxic
proportions.
In strength events, B-complex vitamins are used to augment a positive nitrogen balance. They are believed to be useful
in increasing the heme component of both hemoglobin and myoglobin, and thus to increase utilization and transfer of
oxygen needed for metabolism. The body absorbs only a small portion of ingested B-complex vitamins, and the rest are
excreted. Their actual need or value is controversial.
Vitamin C compounds may be of more benefit in the athlete. As collagen turns over in the process of remodeling and
adapting to increased stress and in the healing phase encountered with the microtrauma of training, ascorbic acid or
vitamin C is a necessary cofactor in sulfur cross-linking and strengthening of the collagen fibrils. Therefore, vitamin C
may be useful in coping with the stress of vigorous athletic training. Nevertheless, only approximately 500 mg of vitamin
C can be absorbed daily, and megadoses have the potential to lead to crystalline deposits in the kidneys. Ascorbic acid
also acts as a cofactor to increase the absorption of B-complex vitamins by the gastric mucosa.
Many athletes involved in strength field sports believe that protein supplements are essential to establish the positive
nitrogen balance needed to obtain maximal benefit from anabolic steroids and training. Nevertheless, with megadoses of
protein, uric acid levels within the blood increase and microdamage of the kidneys and joints may be the result. Protein is
not normally used in athletic performance, because the body usually burns protein only in starvation.
The use of anabolic steroids remains controversial. Physicians and the general public tend to view these drugs as
dehumanizing, possibly allowing an unfair advantage to the athletes using them, and definitely tainting the spirit of fair
play. A report on doping from the health organization of the League of Nations in 1939 was the first official statement to
suggest that the use of male sex hormones could theoretically enhance athlete performance ( 17). The official ban on and
testing for anabolic steroids by the International Olympic Committee have reinforced in the athlete's mind that such drugs
can indeed enhance performance, and that, in not using drugs, they would be operating at a definite disadvantage. The
use of these drugs and possible advantages were discovered at the university level and even down to the junior high
level in the early 1970s. The medical community banded together to condemn anabolic steroids ( 18). Physicians cited
known side effects of steroid use such as renal disease, testicular atrophy, and adrenal suppression known to have
occurred in diseased individuals. At the same time, they implied that these same side effects could be expected in a
healthy athlete. They also cited poorly designed clinical studies in which untrained individuals were used, or in which
anabolic steroid dosage was very small, in order to demonstrate that use of these drugs was not only dangerous but
ineffective. To tell young athletes that such drugs were of no advantage and, in fact, had side effects such as decreasing
libido has cost the sports medicine community much of its credibility; many track and field athletes have gone elsewhere
with their sports-related problems because of this. Track and field athletes have indeed demonstrated enhanced
performance, in spite of warnings of adverse side effects. Most notably, Ben Johnson of Canada won the 100-meter dash
in the 1988 Olympics but was subsequently disqualified for steroid use. The basic science of steroids is discussed in
Chapter 9 on Ergogenic Drug Use in Sports. It is estimated that between 1 and 3 million male and female U.S. athletes
have used anabolic steroids; some researchers have considered the incidence of serious health risks to be overstated
(19).
The U.S. Food and Drug Administration does not regulate nutritional supplements. Creatine and androstenedione are
examples that have been popularized by their use by Mark McGuire in his establishment of a new home run baseball
benchmark. Creatine (methylguanido acid) is normally produced in small levels in the liver. In the muscle cell, conversion
to creatine phosphate (CP) occurs. Two grams are metabolized by the body daily, the same amount that is produced; this
maintains a creatine balance. CP is stored in the cell until it is used to produce ATP. It is claimed that producing a
positive creatine state will retain water in cells to create a pumped-up look, provide more energy to increase exercise
endurance, and lower recovery time. None of this is proven. The long-term effect on the kidney, liver, and cardiovascular
structures is not yet known, and therefore, caution must be advised. Androstenedione is only two carbon fragments away
from being testosterone; though liver metabolism, immediate conversion is accomplished. This supplement must be
banned in young track and field athletes because in addition to mood swings and steroid acne, premature growth plate
fusion may occur.
Caffeine is now considered to be one of the most abused drugs in high-performance athletes. Normally, muscles are
dependent on stored glycogen. Caffeine from tablets, coffee, or cola drinks releases fats from tissue into the
bloodstream, making them available to muscle. The muscles then burn these fats in preference to stored glycogen and,
therefore, are able to work longer and to avoid fatigue. Three hundred milligrams of caffeine, or about the amount found
in two cups of coffee, have been found to be enough to produce this effect in the trained athlete ( 20). In fact, any amount
above this level can lead to caffeine overdose or fine muscle tremors that decrease athletic performance.
Field Conditions
Important to track and field construction is accessibility of dressing quarters for the athletes and proximity to parking
spaces for the spectators. Nevertheless, the surface itself is most important to athletes. Athletes have invested so much
time and energy in the training process that they deserve a safe and proper surface on which to compete. Although
proper methods of track construction are suggested in the literature, certain errors that can affect performance must be
emphasized (2).
Running tracks are essentially oval in shape, with the inner oval length measured at ¼ mile (440 yards), or 400 meters,
depending on when construction occurred. Adequate drainage is essential so that the runners need not run in mud.
Curving or canting can also help in this drainage effect. A water supply may be needed to sprinkle the surface to make it
soft enough for competition, as well as to provide a drinking water supply. Most high schools use a cinder-type surface
on the track. Clay is commonly used because of cost, but if it is used, it must be watered regularly; otherwise, it will seal
and actually prevent seepage of water. If the clay-cinder track is allowed to dry, it becomes brittle and actually flakes
under the impact of running shoes.
It is a common error to use 3- to 5-ton street maintenance rollers when leveling cinders. These are used as a matter of
convenience, because such equipment is readily available. Nevertheless, this can decrease the resiliency and shock
absorption qualities of the track; a ½-ton roller should be used instead.
The alternative to frequent maintenance is the all-weather track, which is becoming more of the norm. The most popular
synthetic track is the one popularized in the 1968 Mexico City and the 1972 Munich Olympic Games. With such a surface
in conjunction with a good drainage system, little, if any, maintenance is necessary, and lanes and start and finish lines
can be permanently marked. In the high school, setting the track surrounds the football field. Football cleats can cause
damage to the track in walking to the field. Nevertheless, energy storage within muscle and subsequent muscle
contraction has been enhanced on this synthetic polyurethane surface. With proper engineering, shock to the
musculotendinous unit can be minimized, while energy storage and subsequent release are maximized.
Unfortunately, two medical conditions have developed because of these surfaces. The synthetic turf syndrome has been
described as painful aching in the ankle joint, thigh musculature, tibia, and patella, and has been found in athletes who
compete on these synthetic surfaces. It has been suggested that it be related to shock vibrations in these synthetic
surfaces that have not found with conventional cinder tracks. Vibration, damping, and elasticity of the track surface as
well as ground contact time and step length can be altered by variance of the track stiffness. These need to be adjusted
for the individual events to be performed on these surfaces. Rebound variation must be in synchrony with reciprocating
eccentric and concentric contraction for energy absorption and release to be maximized. Otherwise, energy handled out
of phase will lead to tissue stress and injury.
The second problem encountered with these synthetic polyurethane tracks is abrasion. Synthetic granules, when
embedded within the skin surface, lead to a long-lasting weeping reaction. Abrasions encountered with contact with
synthetic surfaces must be treated aggressively, that is, with scrubbing and antibiotic solutions, in order to avoid a
potentially long-lasting and annoying problem.
In the jumping events, rubberized synthetic surfaces can be used for approach ramps and aprons. In the long jump, triple
jump, and pole-vault, many schools have limited the width of the approach strip to 2 feet rather than the standard 4 feet in
order to save money. A misstep from this narrow strip can lead to ankle sprains, twisting of the knee, ligament injuries, or
falls and associated contusions. Therefore, the temptation to use narrower approach strips, as cost-containing measures,
should be avoided for the sake of the athlete. Otherwise, the same drainage and building materials can be used for the
runways and aprons as is used for track construction itself. The same measures used in maintenance of the track must
be carried out in maintenance of the runways. The athlete must police the runway himself or herself before utilization in
order to make sure that no holes or obstacles are evident that will cause injury or decrease performance. Takeoff boards
at the end of the runway for the broad jump and hop, skip, and jump may need frequent replacement, due to contact with
spikes and internal breakdown related to use.
The landing pits used for jumping events should extend from a point 10 feet in front of the takeoff board for 20 or more
feet beyond. They should be filled with builder's sand and be kept slightly moist. They should be turned daily in order to
decrease jarring encountered at the time of contact. At least 12 to 18 inches of builders' sand or foam is necessary to
lessen the shock.
The pole-vault is a very specific activity, necessitating runways on both sides of the pit to help compensate for wind
conditions. Sawdust or sand must be available to place in the planting box to lessen the shock of pole planting if the
athlete believes that it is necessary. Standards used in the pole-vault and high jump should be well machined and
weighted to fall away from the individual at contact to avoid athletic injury. The landing pits should be made of foam
rubber and should be properly constructed to extend around the planting box, or slightly under the high jump bar,
because the athletes frequently do not clear the bar and fall directly downward; therefore, they must be shielded from
injury. The crossbar used in both pole-vault and high jump should be made of fiberglass. Although the metal crossbars
may be cheaper, they can cause more injury if the athlete falls on them.
The weight circles for discus and hammer must consider the athlete's action of pivoting on the feet so that the texture of
the surface and the shoes used correspond. It is imperative that the surface be as smooth as possible because of the
pivoting so that ankle sprains and stress on the knees can be minimized. Proper construction detail is readily available
(21). The ramp for the javelin throw should be constructed in a manner similar to those of the long jump and pole-vault.
Stretching and Weight Training
Slow, steady stretching is important prior to track and field participation. Such eccentric warmup increases circulation by
wasted heat. Contractility is thus increased by enzymatic induction. This effect lasts for up to ½ hour following a single
stretch, which can be a significant factor during competition. Stretching after muscular activity, such as a light jog
following athletic performance, helps clear metabolites, so that stiffness leading to fatigue will not be a problem in future
performance. Stretching following athletic activity also helps overcome biologic creep, viscoelastic contraction of
myofibrils and collagen, increasing the limits of flexion and extension somewhat; if muscular hypertrophy develops in
proportion to increased range of motion, more effective storage and utilization of contractile energy may be possible.
There is a danger of overstretching, however, and it is important to realize that the musculotendinous unit performs
optimally at a basal length that is a product of muscle hypertrophy, elasticity, and flexibility.
Weight training is particularly beneficial in increasing myofibril hypertrophy and capillary ingrowth, both of which can
increase contractility and decrease fatigue. Nevertheless, if fibers are cold, weakened by previous injury,
undernourished, overstretched, or fatigued, chronic strain or tendinitis may develop. Repetitive microtrauma may lead to
a major disruption or rupture.
Stretching must become a routine to prevent overload of the musculotendinous unit related to training excess or error.
Before a race, athletes must warm up to increase the efficiency of the muscles and thereby reduce the incidence of
strain. This also decreases the mental fatigue that leads to strain or sprain injury. Proper warmup can significantly
decrease and even eliminate the initial period used to attain the “second wind” level of performance. Middle- and
long-distance runners need more time than sprinters to warm up circulation-dependent type I endurance fibers. A period
of easy running and light flexibility exercises, working up a slight perspiration, followed by a short series of warm-up
sprints and easy jogging, striding, and rest before race time can be carried out, followed by a 5-minute period of rest to
get breathing back to normal. After completing the distance event, athletes must continue to jog for a lap or two in order
to encourage circulation and help clear metabolic waste products from muscle so that fatigue and stiffness do not set in
during the next few days. Going through a light jog and stretching routine the day following competition helps work out
tightness and encourage circulation.
RUNNING EVENTS
Sprints
Sprinting events are those in which the contestant runs at full speed over the entire distance; these include 100-, 200-,
and 400-meter events (formally 100-, 220-, and 440-yard dashes), and are limited by the limits of anaerobic metabolism.
Running was part of original Olympic competition, first wearing a loin cloth, then competing naked. There was a starting
gate device or hysplex, to make sure that no one started early. There were three original events: the stade (the length of
the stadium, about 200 meters), the diaulos (two stade lengths), and the dolichos (ranging from 7 to 24 stades). The early
100-yard dash was run on a cinder track starting from a standing position. In 1887, U.S. athlete Charles Sherrill
developed a major change in technique, by kicking small foot holes in the track and using them for a crouch start. In
1928, U.S. coaches Tuttle and Breshnahan introduced starting blocks for more reliable starts, and to protect the track.
Electrically recorded time became the standard for world record measurement in 1977.
Forward human locomotion is measured within a gait cycle. A normal walking cycle is measured from heel strike to heel
strike of the same foot. In sprinting, this changes to analysis from toe strike to toe strike. Motion has been analyzed in
terms of a stance or support phase in which the foot strikes the ground, attains some support, and then takes off. This is
followed by a swing, or recovery phase, where there is follow-through, forward swing, and foot descent. In walking, one
foot is always on the ground. As speed of gait increases, the stance phase is eliminated such that neither lower extremity
is in contact with the supporting surface. The double support phase, when both feet simultaneously contact the ground, is
eliminated by establishment of a double float phase, when neither foot contacts the ground ( 22). As the speed of gait
increases, the need for forward propulsion and acceleration leads to increased ground reaction force ( 23).
Sprinters reach top-running speed quickly, and they do this by maximizing initial acceleration. It had been noted that by
keeping the center of gravity low, leaning forward, and pushing off with a strong quadriceps, acceleration could be
achieved quickly. As mentioned earlier, sprinters learned that kicking holes in the track could be used to some advantage
in pushing off. Such practices, nevertheless, left the track in poor condition, so that in 1927 removable and adjustable
starting blocks were allowed, and finally sanctioned by the International Amateur Athletic Federation in 1937.
It is said that sprinters are born rather than developed ( 24). A sprinter has a short reflex time and a quick reaction time.
Sprinters need a full range of motion for all extremities because they start from a low position to mobilize the body's
center of gravity, then move slowly to a more upright position. Initial acceleration necessitates the generation of power.
This generation of power starts with preloading the muscles by lowering in the starting blocks, and it is aided and
amplified by synchronization of upper and lower extremity motion. The hands are thus held tight to generate lower
extremity push-off (Fig. 41.1). Sprinters do not burst out of the block but learn to run out of the blocks. By clinching the
fists and swinging the arms strongly, sprinters are able to amplify crossed-extensor reciprocal eccentric and concentric
energy utilization.
FIGURE 41.1. Block start. A crouched position is used in the start to generate the most effective power by raising the
center of gravity slowly. Here, efficient use of energy, preloaded by lowering oneself into the blocks, is maximized.
The starting blocks must be reset for each athlete. Although the setting is somewhat dependent on the athlete's size,
flexibility, muscle strength, and stride length are all important factors that necessitate that each athlete find his or her own
ideal setting. The sprinter must be quite flexible and capable of reciprocal flexion and extension of the extremities to
maximize musculotendinous performance. When the reciprocal pumping action of the arms and legs do not work
together, strained muscles are the result. This is due to either overstretch or muscular imbalance overloading
antagonistic muscles in the eccentric phase ( 25).
Because of the need to maintain forward propulsion while the center of gravity is forward of the planted foot and because
sprinting is a process of pushing with that extended leg, quadriceps strength is emphasized. In weight work, an emphasis
must be made to maintain hamstring strength at approximately 80% of that of quadriceps strength to maintain proper
balance. The hamstrings and posterior tibialis muscles must be stretched and strengthened to help prevent injury. In
eccentric contraction, the reverse extended leg at the time of the start is capable of generating a tremendous hamstring
response. If the muscle is not flexible, or has not been warmed up, a hamstring “pull” or strain results, and in fact, this is
the most common injury in sprinters.
It is important in the evaluation of hamstring injuries to examine the entire musculotendinous complex unit. Avulsion
injuries can occur from the ischial tuberosity. These injuries are most often treated nonoperatively, but in cases of
considerable displacement, operative treatment can be considered in elite athletes. More commonly, however, these
injuries occur within the substance of the muscle belly or at the musculotendinous junction. Stretching and strengthening
can help this problem. It is important that the coach allow adequate time for adaptation and rest of the hamstrings.
Avoiding block drills too early in the season or on two subsequent days during the season are helpful preventive
techniques.
The rehabilitation of hamstring injuries consists of a gradually increasing program of mobilization, strengthening, and
activity. These injuries frequently heal slowly and can often recur, following premature return to competition. Therefore,
return to sport should only be allowed when full muscle strength, endurance, and flexibility have been regained.
Because the sprinter runs on the toes, he or she is prone to injury of the posterior tibialis, flexor digitorum longus, and
flexor hallucis longus musculotendinous units. Most of these injuries consist of tendinitis and can be treated with
orthotics, ice, rest, and antiinflammatory medication. Rupture of the posterior tibialis tendon is diagnosed by tenderness
at the bony insertion, as well as by loss of the longitudinal arch medially. In addition, when viewed from behind, the
patient exhibits the “too many toes” sign, in where more toes are seen laterally on the affected side as compared with the
unaffected side. Complete tendon ruptures are treated surgically. Stretching is of great importance in avoiding symptoms
of tendinitis.
Because greater contact force is generated at higher speed, and because sprinters run on their toes, Achilles tendinitis,
or inflammation of the common tendon of the gastrocnemius and soleus muscles, is a frequent problem. Localization of
the area of maximal tenderness is usually approximately 2 cm proximal to the insertion of the Achilles tendon on the
calcaneus. Nodularity, palpable within the tendon, is indicative of partial tendon injury with subsequent mucinous
degeneration of tendon substance. Achilles tendinitis is treated conservatively with stretching, antiinflammatory
medication, and heel lifts. Surgery is only performed in recalcitrant cases. Achilles tendon rupture is most commonly seen
between the ages of 30 to 40 years. Best results are obtained with surgical approximation of torn tendon ends in elite
athletes. Symptoms of Achilles tendinitis are worsened when the sole of the shoe is so rigid that athletes are made to run
over it, decreasing their push-off ability and contact time of the ball of the foot. Rigid orthotics may also accentuate the
problem. Calf muscle strengthening and heel cord stretching are the keystones of prevention of Achilles tendinitis.
The gastrocnemius-soleus muscle group must be kept strong to allow running on the sprinter's toes. Otherwise, the heel
may drop back too far and the stretch placed on the sole of the foot can lead to plantar fasciitis or a secondary heel spur,
or both. In contrast, running on the toes without proper flexibility can also lead to metatarsalgia. Plantar fasciitis and
metatarsalgia are difficult problems to treat; maintaining proper flexibility and shock-absorbing muscle tone of all groups
of lower-extremity musculature best avoid them.
Quadriceps contracture, tight hamstrings, weak vastus medialis, high-riding patella, or excess pronation of the foot can
lead to a lateral patellar compression syndrome, leading to chondromalacia or roughening of the weight-bearing surface
of the underside of the patella. Such roughening increases the coefficient of friction, which will lead to further articular
damage, shedding of articular fragments, synovitis and associated effusion of the knee, and early arthritis. Such
problems are minimized or avoided by stretching and strengthening the vastus medialis obliquus. Extension exercises
are performed in the final 30 degrees of terminal extension to isolate this musculature. Occasionally, because of
anatomic variation, a surgical release of the lateral patella retinaculum may be necessary to correct extensor mechanism
malalignment.
Stress fractures are usually a product of training error. Fibular and tibial fractures are characteristic of the sprinter and
are seen early in the season when the musculotendinous unit has not perfected its shock-absorbing properties, and
again late in the season from simple overuse. Highly concentrated muscle force acting across a specific bone because of
demands imposed by particular repetitive tasks enhance the loading that occurs merely from direct weight bearing on the
affected part (26). Once localized tenderness is elicited on physical examination, x-ray evaluation is mandatory. Stress
fractures, however, may take 10 to 14 days to be demonstrable radiographically; they can be diagnosed earlier with
technetium scintigraphy. Treatment is by immobilization with weight bearing, depending on the individual fracture.
Avoiding the use of spikes too early in the season and initiating training on soft surfaces, allowing gradual adaptation to
occur, can minimize such complaints.
The ankle is most secure due to talar dome configuration when locked in a dorsiflexed position. Thus, the athlete is
subject to ankle sprain with a misstep or by turning a plantarflexed ankle on a wet surface. It is, therefore, the athlete's
responsibility to inspect the entire lane for wet spots, holes, or debris before an event. Because the longer sprinting
events must incorporate curves, it may mean that using one of the outside lanes may be safer than an uneven or poorly
drained inner lane.
Ankle injuries most commonly occur on uneven surfaces and as the sprinter turns. Although ligamentous sprains are by
far the most commonly occurring injuries, chondral and osteochondral lesions of the talar dome, and less commonly, of
the tibial plafond can occur. These injuries present in a clinically similar manner to ligamentous injuries but fail to
progress in their healing and rehabilitation. Diagnosis is rarely made by plain x-ray studies but can be seen more
accurately with computerized axial tomography and magnetic resonance imaging. Treatment is dependent on the size
and location of the lesion. Loose or unstable chondral or osteochondral fragments are best excised arthroscopically.
Stress injuries have also been described in the posterior aspect of the talus. These injuries can involve either the os
trigonum just posterior to the talus or the posterior process of the talus. These injuries if recalcitrant to conservative
treatment are best diagnosed with technetium scintigraphy. Although most injuries to the os trigonum heal after a period
of immobilization, recalcitrant cases may require local injection of corticosteroids. Rarely, these injuries require surgical
excision of the symptomatic ossicle.
It is customary to run events around the track in a counterclockwise fashion. This causes supinating forces on the left
foot and pronating forces on the right foot, leading to torquing and potential incoordination ( Fig. 41.2). The pronated
outer right foot flattens, and the leg externally rotates to increase the ability to push off and further accelerate around the
curve. Torque on the right knee leads to medial symptoms. Voshell's bursa, between the superficial and deep portions of
the medial collateral ligament, may become inflamed at the medial collateral ligament just below the joint line. With the
internal rotation of the lower leg induced by forced pronation, the outer leg sustains stress in the posterior lateral aspect,
which can lead to symptoms of popliteal tendinitis. Point tenderness along the course of the popliteus, particularly
posteriorly at the musculotendinous junction or at its femoral insertion just anterior to the fibular collateral ligament, will
help make the diagnosis.
FIGURE 41.2. The muscular stresses and counter stresses are shown as the runner takes the curve.
The inner left leg being forced into heel supination with corresponding arch elevation and external rotation of the lower
leg places stress on the medial hamstrings, which are involved in acceleration around the curve. A strain of the medial
collateral ligament is commonly confused with a medial meniscal tear, and in spite of joint tenderness at the joint line,
lack of effusion within the joint may be used to lead to proper diagnosis. Maximizing the shock-absorbing properties of
the musculotendinous unit by strengthening and stretching in an effort to avoid injury best minimize the above three
conditions.
The shorter length and increased banking of indoor surfaces can lead to iliotibial band friction syndrome near the lateral
knee or hip in athletes with tight structures. It is mandatory to undergo vigorous iliotibial band stretching exercises,
particularly if such conditions are anticipated. In running curves indoors, the athlete retains a slight lean to the inside
when facing into the turn. The outside arm swings across the body, and the pelvis rotates to potentiate momentum. The
athlete should run as close to the inside lane as possible; because of this, short-legged athletes may have an advantage
in indoor competition. Because a great deal of energy is expended to maintain angular velocity, the athlete attempts to
increase acceleration about the curve to accelerate out of it. In doing so, tremendous torque is generated through the
knees and hips.
Although Olympic-class outdoor running tracks have an overall lap length of 400 meters, turn radii are not specified, thus
giving rise to an assortment of tracks with varying aspect ratios. The maximal speed attainable while running on a finite
radius turn is considerably less than that running along a straight line. The value of speed reduction to the runner
depends on the effective radius of the turn and the runner's top speed. This is secondary to an increase in the foot
contact time necessary to maintain constant vertical impulse to compensate for the vectorial decrease of available
vertical force as the individual's heel turns over into the turn. The increased foot contact time causes a corresponding
decrease in the ballistic air time. As a result, there is a discrepancy in the maximal speed attainable when running
different lengths on an oval track. In fact, the outer lanes in a conventional oval racetrack have a speed advantage over
the inner most lanes. This discrepancy is greatest when one considers tracks with tight turns, as is the case with many
indoor facilities ( 27).
Relays
The New York Athletic Club introduced relay races in the 1880s, being modeled after the New York Fire Department's
charity event, in which a red pennant was relayed every 300 yards. A relay race is an event in which, originally, two and
now four runners run a specified distance, each relieving the previous runner at designated points within fixed zones.
The first Olympic relay in 1908 had four legs: 200 meters, 200 meters, 400 meters, and 800 meters. In 1912 this was
changed to two events: 4×100 meters and 4×400 meters. These remain as the standard for both male and female
athletes.
The first runner is allowed to start from blocks, and all subsequent runners start in an upright position, passing a 1-foot
baton (first wooden, then metal) within a 20-meter passing zone, although modification in 1963 allowed 10 meters in front
of the passing zone to build up momentum for the pass. Initially, the relief runner would start his or her leg of the relay
after touching the hand of the oncoming contestant. This presented a problem in judging whether such hand contact had
actually taken place, so the baton was introduced, bringing an additional hazard to the relay. An attempt is made to
exchange the baton with full arm extension by both runners while at maximum speed. There is a right-to-left to right-to-left
hand sequence of exchange among the four runners, which must be well practiced. The curve runner holds the baton in
the right hand and the straightaway runner holds it in the left. An underhand pass technique is used in the sprint; the
outgoing runner extends an open hand downward into which the incoming partner slips the baton, a procedure
necessitating much practice. The baton missing the open hand can jam into the outgoing runners hip, can lead to
contusion or laceration, or result in a misstep or dropping baton.
The runner must establish beforehand which side of the lane to come in on and on which side of the lane the next runner
is to exit. Crossover passing, such as right hand to right hand, must be avoided, because there is a significant risk of
running over the partner's feet or heels, leading to a spiking injury, sprain, or contusion to the ankle or the calf area.
In the distance relay, the incoming runner will undoubtedly be fatigued, and therefore, it is necessary for the outgoing
runner to look backward and follow the baton visually during the exchange. Unlike the blind pass used in the sprint, this
must be a visual pass and must be well practiced to avoid the crossover stepping or misstepping that can lead to knee or
ankle injury. The baton must be exchanged within the prescribed distance, and, without proper practice, the lead runner
may be forced to decelerate to obtain the baton; and this may lead to a torquing anterior cruciate ligament injury.
Baton exchange introduces the factor of hand trauma. Lacerations and jammed fingers are an occasional occurrence.
Dislocated phalanges must not be taken lightly, because fracture or collateral ligament damage may be associated.
Therefore, x-ray evaluation is mandatory with these injuries. Ulnar collateral ligament sprain of the thumb can be related
to poor passing technique. Obviously these injuries can be minimized by synchronized baton exchange, which can only
be accomplished through practice. Walking and jogging through the exchange is mandatory before attempting it at full
speed.
Hurdles
Although spectators erroneously consider hurdling a jumping event, in fact, it is a sprinting event in which the participant
must clear obstacles at various heights, and because these are sprinting events, the distance is limited to about 400
meters. These events originated in England in the 1830s, when the 100-yard dash was run over fixed wooden barrels. At
Oxford, in 1864, this became a ten-obstacle 120-yard race. The French added 28 cm in 1888, initiating the 110-meter
event, which has remained the men's classic since that time. Women first competed in 1926 in an 80-meter event, and it
became an Olympic event in 1932. The 100-meter distance was sanctioned by the International Amateur Athletic
Federation as the new women's standard in 1969, and became an Olympic event in 1972. Inverted T-shaped knock-over
hurdles were introduced for safety in 1895, finally replaced by counterbalanced L-shaped hurdles in 1935. The 440-yard
hurdles were introduced in England in 1860, with 12 heavy wooden embedded barriers. This was changed to 400 meters
with 10 barriers in the 1900 Olympics, and has remained the standard since. The first hurdle remains 45 meters from the
start, and the tenth placed 40 meters from the finish line. Women first competed at this distance in 1971; it was
sanctioned in 1974, and became an Olympic event in 1984.
As a sprint event, participants use blocks and stay within their lanes. Early hurdlers merely tucked their legs under their
bodies to accommodate the barriers. Kraenzlein of the United States created the technique of straddling the hurdle and
taking three steps in between. Although hurdlers are used to attaining some height to clear obstacles, they must avoid
rising up too quickly in their start so that they can both cut down in time and avoid strain to the low back, which can result
in either paraspinous muscle spasm or transverse process fracture. To avoid rising too quickly as well as to maintain
correct body lean, hurdlers must look toward the ground at least until their fifth stride, by which time they have elevated
their centers of mass sufficiently to accommodate the first hurdle. Hurdlers approach each obstacle with maximum speed
so that they run over the hurdle and do not jump over it. This is important because they decelerate in the jumping process
and can only obtain speed by running on the ground.
Hurdlers must drive the knee of the leading leg forward to obtain sufficient spring with the push-off foot to clear the
hurdle. The moment they become airborne, they lean forward in order to get the leading leg back on the ground as soon
as possible so that they can continue their sprint. If they lean forward too quickly, they will run into the hurdle, and by
waiting too long, the center of gravity will land behind the leading leg and they will fall backward. In this way, they drive
up with the knee, straighten the leg, and as they are just above the hurdle, they snap their leg down over it. Beginners
may want to throw their foot up rather than drive up with the knee. In doing so, they will throw their center of gravity
backward and will have a difficult time clearing the hurdle ( Fig. 41.3).
FIGURE 41.3. Hurdling technique. As the back leg pushes, the leading leg quickly extends helping the back leg to flex in
order to clear the bar reciprocally. The front leg then dips over the bar to make ground contact quickly; since acceleration
is only gained on the ground. The center of gravity also remains in a nearly perfect straight line, thus aiding in
acceleration.
Hurdlers keep their arms out in front of the body when accommodating the hurdle. This not only centralizes the center of
gravity but also allows enough clearance to raise the trailing leg so that it can avoid contact with the hurdle. The trailing
leg must be brought up into a flexed position and should not be whipped around, because this can lead to an imbalance
that is accommodated by straightening the arms out to the side. This slows forward momentum so that the trailing leg and
the ankle are at risk of contacting the top of the hurdle.
Hurdlers must lean forward as they come off the hurdle so that the center of gravity is forward, allowing them to sprint
toward the next hurdle. They must also know how to clear a hurdle with either leg. Although they may have an ideal
number of strides between each hurdle, as the race progresses, they may fatigue; the adaptation is a shorter stride
length, with more strides between each hurdle. If they do not know how to clear the hurdle with either foot, they may have
to slow their pace to add an increased stride in order to use a favored leg. To do so, they must decelerate. This not only
lessens the chance of winning the race; it also can lead to an anterior cruciate ligament sprain in the knee.
As the lead leg snaps down toward the ground, hurdlers must land on the balls of their feet. If they come down too
flatfooted or on a heel, they will suffer a heel bruise, which is usually one of two entities. The most common is fat pad
contusion, in which the infracalcaneal fat pad sustains an element of hemorrhage. The fat may break down, undergoing
the process of saponification. Clinically, there is point tenderness under the heel. The spongy bone of the calcaneus may
also be subject to a microfracture or stress fracture that may take weeks before it can be demonstrated on standard x-ray
study. A bone scan may be helpful in delineating the problem sooner, but it is best to avoid the problem with proper
technique, because heel injuries commonly take months to clear up.
With the amount of stretch needed to clear the hurdle in both the lead leg and the trail leg, hamstring strain or frank
muscle rupture, groin pull, and pelvic avulsion fracture have historically been extremely common. Because of this,
hurdlers have religiously done stretching exercises, including the traditional hurdler's stretch, so that in fact, the number
of such injuries are probably less common than actually found in sprinters. The importance of stretching for the
prevention of strain cannot be overemphasized. Nor can emphasis on proper coaching technique, because a misstep can
lead to ligament sprain, muscle strain, or repetitive contusion and myositis ossificans.
Hurdlers must make sure that their lane is clear of foreign objects or obstructions, and that the hurdles are square within
it. When running, their eyes must be kept forward at all times. If they look back either to see where opponents are or in
response to the sound of an opponent hitting an obstacle, they shorten their stride, decrease their momentum, and
interfere with their technique enough that they are at risk of injury.
If hurdlers work hard on one day, they will need a recovery day of gentle stretching, muscle adaptation, and healing.
Warmup takes at least half an hour a day and begins with jogging half a mile or jumping rope. In the off-season, they may
be involved with indoor track, but if not, they work on endurance. Because there are so many factors in hurdling
techniques, the coach must not confuse the athletes with too many variables at once and must refrain from trying to
change technique on the day of the event. This day is for competition, not for training. The technique of lining up a
number of hurdles and having athletes run over them in one direction and run back in an opposite direction is extremely
dangerous. A hurdle is designed to tip over forward with an 8-pound counterbalance; the athlete risks a broken leg or
other injury by running over it from the wrong direction.
Hurdling technique is not easy to learn. Training must start on grass to decrease the number of abrasions and injuries.
Soft-top hurdles and sponge rubber protectors of the heel, ankle, and knee of the takeoff leg, as well as the knee of the
trailing leg, are mandatory in training and should be eliminated only as the athlete gains proficiency. Heel cups are
needed throughout the training season to help prevent heel bruising. The old style hurdling shoe had a stiff counter with
six spikes in the front and two in the back. This encouraged athletes to land on their heels or flatfootedly, and heel
bruising and plantar fasciitis were common. The newer hurdling shoes have spikes in the front and none on the heel; in
fact, they have a higher back to encourage athletes to land on their toes and the shoes provide cushioning if they
inadvertently land on their heel as they fatigue.
Another injury, which is common in hurdlers, is medial synovial plica syndrome. With repetitive contusions on the medial
aspect of the knee of the trailing leg, a synovial plica may become fibrotic. With subsequent sprinting and hurdling
techniques, the irritation of the plica rubbing across the medial femoral condyle may become quite severe. Although
icing, quadriceps and hamstring stretching and strengthening, or a patella brace are somewhat effective in treatment,
arthroscopic resection of the plica may become necessary.
Middle Distance
Standard middle distances today are 800-meter (previous a half-mile/880 yard equivalent) and 1,500-meter (1-mile
equivalent) events. The 800-meter athletes are the swing runners; that is, some may be asked to run in the longer
distance sprints such as the 400-meter, whereas others may be asked to run in the 1,500- or 5,000-meter events if the
need arises. This places a particular burden on the middle distance runner, and therefore, some must train as sprinter
800-meter athletes and others as endurance 800-meter athletes. Ideal middle distance runners should have the speed of
sprinters and the endurance of distance runners. They should have good balance of both types I and type II muscle
fibers, and should work hard at interval training to build up both endurance and speed. Interval training, running 200,
300, and 400 meters at a slow pace with short jogging segments in between. By varying the distance, the speed of the
run, repetitions, and the recovery interval, speed and endurance are enhanced. Fartlek training (Swedish: to run or play)
combines interval and cross-country training. The athlete runs until he or she tires, will then jog until he or she tires, and
then walk up to 50 meters, and then start to run again.
The stride of middle-distance runners is shorter than that of sprinters, and longer than that of distance runners. They
make contact with the surface with the balls their feet and roll back onto their heels. As they become more fatigued, they
run more flatfooted. Without a proper forward lean, they will land on their heels and may develop heel bruises or
calcaneal stress fractures. Like sprinters who accommodate by turning a counterclockwise rotation around the track, they
are subject to supinating forces in the left lower extremity and pronating forces in the right. Too much of a body lean
around the curves adds torque and increases risk of injury. Therefore sprinter–middle distance runners are subject to the
same injuries as sprinters, whereas endurance–middle distance runners are subject to the type of injury that is discussed
with distance runners.
Lead runners have a definite advantage in that they set the pace for the race. In order to avoid injuries, runners must
learn to run on the outside shoulder of the runner in front in an attempt to avoid being boxed in. If they are boxed in,
runners can sustain a strain injury by a misstep associated with being knocked off the track; they can sustain a sprain or
a spike injury in an attempt to change position from the cluster. The sprinter distance runner often has a close finish
similar to that of the sprinter ( Fig. 41.4).
FIGURE 41.4. Middle distance spring. A: The leading runner on the inside is barely ahead of her outside competitor. She
swings her left arm forward, reaching for the tape. B: This maneuver breaks her stride as she lunges forward. With a
burst of speed, the outer competitor hits the tape as the inner runner hits the track (C) and rolls across the finish line in a
frustrated second place finish (D). (From Steve Powell. Sports Illustrated 1983;August 22:16–17, with permission.)
In the off-season, middle distance runners train as distance runners, and as they get into the season, training varies
according to their anticipated swing position. In the off-season, they may participate in cross-country for stamina and
endurance. This is also the time for experimentation in running form, such as degree of trunk lean or length of running
stride. Athletes must be careful not to mimic the stride length of a teammate, because this stride may not be ideal for
them (28). Too long a stride will overstress musculotendinous units and too short a stride will overtax endurance level,
leading to fatigue, stiffness, and strain.
Distance, Marathon, and Cross-Country

Long distance events evolved from 3-mile (now officially a 5,000-meter event) and 6-mile (10,000-meter equivalent)
races, and now include a 3,000-meter steeplechase. The steeplechase developed over a wager by Oxford students in
1850, imitating a 2-mile equestrian event, crossing obstacles and streams. This was adopted into English track
championships in 1879, and as 2,500-meter and 4,000-meter Olympic events in 1900. In 1954, the rules were
standardized for a 400-meter track with obstacles consisting of 3-foot hurdles and a 3.66-meter wide 0.7-meter deep
water jump spaced at 78 meters apart. Competitive distances are 2,000 and 3,000 meters, with the latter being the
Olympic standard for men. Women have competed in the United States and the former Soviet Russia, but this is not yet
internationally recognized women's event.
Cross-country courses have varied from approximately 2-mile, 3-mile (5-K), 4-mile, or 6-mile (10-K) lengths for a sport in
which approximately seven team participants work together in order to enable their top five members score lower than
opponents. The marathon is an individual event devised in the first revived Olympics (1896) to follow the legendary
40-km route between Marathon and Athens in 490 B.C. The distance was changed to 42 km, 195 m, the distance between
London's White City Stadium and Windsor Castle, in 1908. Cross-country racing is considered off-season training for the
distance runner, whereas marathon and the triathlon are considered the ultimate individual tests of endurance.
Technique does not vary much with the different distance events. In 1952, Zatopek won the 5.000-meter and
10.000-meter Olympic events. He then ran his first marathon in the same Olympics and won, having never trained for the
event.
In distance running, the trunk angle is straighter. It is inclined from 5 to 9 degrees, depending on stride length and state
of fatigue, as compared with 15 degrees in a middle distance runner, and 25 degrees in the sprinter. Sprinting depends
on type II fiber, speed, and strength; whereas distance running depends on type I myofibril and associated capillary
hypertrophy for stamina. Distance runners must be able to estimate pace so that they can speed up at the proper time in
the race and fall back to a normal pace when appropriate. They can only develop this ability with practice, and they tend
to practice mainly at race pace. They must learn to train without straining, because in overuse, their biologic substances
break down faster than they adapt. Whereas overstressing the musculotendinous unit in an attempt to accelerate
typically injures the sprinter, the distance runner typically injures the musculotendinous unit merely by overuse in training.
Distance runners must run relaxed and with a specific cadence in order to develop an efficient stride. This even cadence
is the key to success. Distance runners use short strides, low knee lifts, and relaxed arm action. They merely swing their
arms and do not pump them. They land on the balls of their feet, drop to their heels, and push off with their toes. They
need full flexion and extension of the joints of the lower extremities and have a slight forward body lean. If their stride is
too long, if their foot lands in front of the center of gravity, they decelerate and constantly work against themselves;
patellar tendinitis and cruciate sprain can result. Ideally, foot plant should always be underneath the center of gravity so
that toeing off will produce propulsion. Nevertheless, there is no ideal running style, merely tendencies that seem to be
found in successful distance runners. This may be a process of natural selection because efficiency results from practice,
training, and integrating biomechanical characteristics. This is measured as running economy, or the oxygen cost of
running at a given velocity ( 29).
In changing pace, runners place strain on their well-tuned and conditioned biologic mechanism. Sudden acceleration will
increase the energy storage within eccentrically contracting muscle, leading to strain injury. Once fatigue sets in, runners
may become unbalanced or attempt to change stride length and also stress the musculotendinous unit. Increasing stride
length increases strain during eccentric contraction; decreasing stride length decreases optimal utilization of the energy
storage system so that fatigue sets in, and again injury may be the consequence ( 28).
It is important to train and not to strain, because the body can take only so much pounding; if an athlete is faltering, it is
the coach's responsibility to slow down training somewhat. In this way, training programs for distance runners are highly
individualized. They should run long runs at less than race pace, distances shorter than the race distance at the race
pace, and even shorter distances at faster than race pace. Interval training and work on hills is particularly valuable in
developing cardiovascular fitness.
The marathon is the ultimate in distance training and is often used as an off-season test for endurance in the distance
runner. Here again, it is important to run an even pace. This becomes immediately apparent to the well-trained athlete
who at the finish of the marathon may feel that he or she could run much farther at the same pace but not really much
faster over the marathon distance. Runners usually need 6 to 12 months of training to achieve marathon conditioning.
This is achieved by mixing long runs of 12 to 20 miles with multiple light runs. They may break up training to two periods
daily to decrease lactic acid buildup, fatigue, and the effects of repetitive stress, in order to minimize the chance of injury.
The steeplechase is a particularly difficult 3,000-meter event, consisting of seven laps over four fixed hurdles 3-feet-high,
and 1 water jump, with 35 barriers in all. Two different techniques are used to accommodate the barriers. The athlete can
either hurdle over the barriers or step over them. The standard hurdling technique must be used in attempts to hurdle the
barrier. Again, heel bruising and calcaneal stress fractures are common, particularly after fatigue sets in. If athletes land
behind their center of gravity, they may fall backward, suffering either a head contusion from contact with the stationary
hurdle or a decelerating knee ligament injury. Some runners prefer to “run the barriers,” that is, to step over them, as
opposed to hurdling them. This increases risk of loss of balance or contact deceleration; energy dissipation may result in
ankle, knee, or leg injury. The water jump is 12 feet in length on the other side of a barrier. It is impossible to clear with a
hurdle, so here, stepping over the barrier is the preferred method. Unlike hurdling, in this technique, the lead leg does not
become the contact leg. In fact, after contact is made on top of the hurdle, the opposite leg swings forward in a
pendulum-like action in an attempt to generate horizontal momentum to clear the water. There is much strain and torque
placed on ligaments and joints in this event. Athletes should not compete on a course like this more than once a month.
Here athletes concentrate on both endurance training and hurdling techniques. Without adequate ability in both, they are
certainly at risk of injury.
Important equipment in endurance training is the running shoe with its padding to absorb the shock of repetitive contact.
It also has a heel lift to enhance some forward lean as well as supports at the midfoot to give some strength and to aid
the midfoot in locking into position; it also has some flexibility at the ball to allow push-off. The wheelbarrow heel and
doughnut or waffle iron bottom seems to distribute stress well and decrease stress reactions. If the shoe is not broken in
slowly or fits improperly, blisters or subcutaneous bursitis (so-called pump bump) are known to occur. Most
distance-related injuries are due to training error, commonly due to overtraining. In overtraining, athletes fatigue. In an
effort to accelerate themselves further, they run flatfooted, which leads to increased pronation of the heel.
The ideal running uniform is loose fitting and comfortable. It allows adequate ventilation. It should not bind or prevent free
easy movement. A thin coat of petroleum jelly and an adhesive strip bandage covering in those particularly susceptible
can prevent nipple abrasion. Thigh chaffing is a particular problem in endurance training, and many athletes will wear a
shorter pair of pants over a slightly longer pair to absorb friction; commercially available polypropylene long leg girdle
devices are available for this purpose. A thin layer of petroleum jelly or talcum powder helps diminish symptoms while
healing and training progress.
Distance training is monotonous and is rarely done around a track. Sometime during the season, athletes may
demonstrate loss of appetite, worry, excessive fatigue, sleepiness, weight loss, change in attitude toward an event, or
illness. These are signs of staleness. Athletes may feel as if they have reached a plateau and are not improving. They
will begin to perform at a level much lower than their ability. The psychological and physical fatigue associated with this
condition leads to injury if the coach is unable to find the origin of the problem and remove the athlete from it. It is most
likely due to the athlete's having settled into a certain pattern of training. Changing this pattern can increase the athlete's
feeling of well-being and performance. Varying the method of practice is preventive. Stress-related injuries may occur
from overtraining as the body fails from repetitive abuse. Training programs must allow for gradual increases in applied
load to biologic tissues. Nevertheless, training is important. Analysis of participants of the 1994 New York City Marathon
demonstrated corns, calluses, blisters, muscle cramps, acute knee and ankle injuries, plantar fasciitis, and metatarsalgia
to be common complaints. Adaptation was effective in that an inverse relationship was found between the number of
miles trained per week, and the incidence of injury ( 30).
Endurance runners are subject to what they call second wind. They start off at a slow pace, gradually building up speed
while increasing respiratory rate, but eventually, they reach a point where, when stride is shortened slightly, they run
comfortably and breathe easily. At this point, athletes have achieved their second wind, which means that the
musculotendinous units have finally warmed up, falling into a cadence or pattern of efficient reciprocal eccentric
preloading and concentric contraction. Over time, with proper training and avoidance of injury, this pace will quicken.
Occasionally, the novice will develop a pain in the side and label this a second wind. This is a different phenomenon
resulting from fatigue of the diaphragm muscles or venous congestion of the spleen and liver circulatory system that
becomes active in mobilizing glycogen for endurance work. This is usually a sign of lack of training or of an attempt to
perform above the athlete's level of training; decreasing the pace allows circulation to catch up to metabolic demand.
Endurance training is not usually done around a track, because this practice would become very boring and the surface
is usually too hard for continuous training. Therefore, golf courses, cross-country courses, schoolyards, or local
roadways become the training environment. The surface should be relatively even to avoid sprains and strains. Running
through the woods may be cooler during summer training and provide a soft surface, but trails must be policed well so
those obstacles do not lead to misstep, tripping, or injury. Hill training must be minimized because pronation and related
internal leg rotation needed to accelerate uphill leads to knee torque. This may develop symptoms of lateral pain related
to stretching of the iliotibial band or lateral patellofemoral compression, or medial pain related to a symptomatic plica or
strain of the semimembranosus. Meniscal problems rarely result from track and field activities, but with preexisting injury,
symptoms may be accentuated with running hills.
Repetitive downhill running also presents a hazard. Although an increase in stride length with the assistance of gravity
can increase speed, acceleration is limited by the need for balance. In deceleration to gain control, runners keep the
center of gravity behind the landing foot, which slaps down in a plantarflexed position; they tighten calf muscles and
eccentrically contract the extensor mechanism. This leads to corresponding stretch in the posterior aspect of the knee,
the musculotendinous junction of calf muscles, the Achilles tendon, and the extensor mechanism itself ( 31). Extensor
mechanism complaints are due to “jamming on the brakes,” that is, driving the patella into the femoral trochlear groove
while the quadriceps tightens in an effort to decelerate downhill. Lateral retinacular pain and popliteal tenosynovitis
frequently result. Medial retinacular pain is occasionally seen. Lateral quadriceps tendon pain occurs, as does
chondromalacia and tenderness along either the origin or insertion of the patella tendon. Foot slap associated with
downhill running may also aggravate symptoms of plantar fasciitis. The treatment of these conditions consists of
decrease and avoidance of inciting factors and temporary change in the contact stress points to help heal damage that
has occurred on a microscopic level. This can be done with taping, bracing, or banding to decrease relative tension on
the tendons. Stretching of the iliotibial tract and hip abductors is beneficial in the prevention of iliotibial friction syndrome
(32).
Hyperpronation of the foot in running downhill may lead to popliteal tendinitis due to torque placed in the posterior lateral
aspect of the knee. This is similar to the torque the leg sustained while running on a banked track or the banked surface
of the gutter of a typical paved street. Posterior pain of the popliteal muscle or tenderness in the popliteal tendon just
anterior to the fibular collateral ligament on the femur will indicate the diagnosis. Alleviating the training error is the
solution to the problem.
A word of caution must be given to distance training in an urban environment. First of all, carbon monoxide from exhaust
fumes may permanently bind to hemoglobin to decrease oxygen-carrying capacity and relative performance. The time of
day for training may need to avoid times of heavy traffic or smog. Overuse problems in training in such an environment
are perhaps the more clinically relevant problems. The athlete should attempt to train on a soft grass surface before
turning to the streets. If a smooth dirt surface such as the shoulder of a road or a maintenance road along a viaduct is
available, this should be the next phase, followed by running along an asphalt surface. Running on concrete should be
avoided if at all possible, but frequently avoidance is impossible. Training on paved roads may introduce other training
errors.
If the runner always runs either with traffic or facing traffic (in some areas this is mandated by local law), one leg
becomes the “up leg,” while the other becomes the “down leg.” This is because most roads are designed with drainage in
mind and not the runner. There is a crown at the top and a bank on either side. Running along this bank means that the
down leg, or lower leg, does most of the work; that is, it must extend and push off to help the runner thrust over the upper
leg, which is used more or less for balance. The lower foot supinates, and the leg externally rotates, causing stress along
the medial joint posteriorly, which can produce semimembranosus strain, medial retinacular stretch, medial collateral
ligament strain, medial plateau stress fractures, and accentuation of preexisting medial meniscal problems. More
common is the development of symptoms in preexisting lateral meniscal problems. Suprapatellar lateral knee pain in
distance runners may be due to a thickened fibrotic suprapatellar plica. Failure to respond to nonoperative management
is an indication for arthroscopic resection of this tissue. Occasionally, other symptoms such as lateral retinacular pain
may result.
Because of inclement weather, many northern high schools encourage indoor training before the beginning of track
season. The cement floors of the schools may have fewer shock-absorbing properties than the pavement in the
neighborhood streets. The fact that these athletes are relatively unconditioned means that they have decreased
shock-absorbing ability of the musculotendinous unit and lack osseous hypertrophy; stress will lead to breakdown. This,
in turn, can lead to shin splints ( 33), a sign of training error. Pain in the shin may be related to overuse or stress of the
muscles within the extensor or flexor groups, stress fracture, or induced ischemia within muscular compartments, leading
to compartment syndrome. Physical examination of the patient with shin splints demonstrates diffuse tenderness along
the posteromedial cortex of the tibia along the tibialis posterior muscle. When the tenderness is localized to one
particular area on the tibia, consideration is given to a possible stress fracture. These injuries can be differentiated with
x-ray studies and bone scanning. Stressing the musculotendinous unit by maintaining stress across the ankle, toe, or foot
will increase pain related to a tear within that unit. If weight bearing or longitudinal compression accentuates the constant
pain, a stress fracture is suspected. Fatigue fractures occur if the system is continually overloaded. They can occur on
more than one level ( Fig. 41.5A, Fig. 41.5B and Fig. 41.5C) and may not be visualized by standard x-ray studies until the
healing process is established ( 34). Such reactions can occur on any level in the novice, but in the well-trained individual,
common posterior medial tibial cortical stress fracture is characteristically tender about 13 cm above the medial malleolus
at the posterior medial margin of the tibia ( Fig. 41.6).
FIGURE 41.5. Stress fracture. Stress reaction to overtraining or abuse may actually lead to breakdown of bone. A: The
microfracture process may not be obvious at first but eventually will show a periosteal reaction, as seen on the posterior
cortex of the tibial midshaft. B: The runner may learn to train with pain, so that multiple stress reactions may develop. C:
Early in the process, occasionally a fracture cannot be identified by x-ray, and a bone scan is useful. Here an
unsuspected stress fracture was found in the opposite tibia.
FIGURE 41.6. Shin splints. Repetitive microtrauma and overuse in running will lead to soft tissue and even bony
breakdown; a process commonly called “shin splints.” Muscle overpull can lead to periostitis, strain, or trabecular
breakdown. The area approximately 13 cm proximal to the tip of the medial malleolus along the posterior tibial cortex
appears to be maximally at risk.
Early in the season, as rapid remodeling of bone and tendon collagen turnover occurs in adaptation to increased
workload, these structures are found to be particularly at risk. Abuse or overuse may supersede within the adaptation
process, leading to stress fracture or strain while in this weakened state. Later in the season, as the adaptation has
progressed, abuse from overtraining will still lead to breakdown when adequate recovery time is not allowed. Athletes
must have enough common sense and, in fact be encouraged, to discuss their injuries with their trainer and coach so that
treatment can begin quickly and loss of performance can be minimized. To play “hurt” is to risk further injury ( Fig. 41.7).
In distance running, common stress fractures include distal fibula, proximal and distal tibial shaft, second and third
metatarsal shaft, and femoral neck and shaft. Although most of these injuries heal with time, displacement of a fracture,
particularly of the femoral neck, can be a devastating injury.
FIGURE 41.7. “Playing hurt.” This 14-year-old female runner had developed pain in the proximal tibia running indoors in
gym shoes in preseason practice. She was encouraged to run through her pain. At midseason, in initiating her sprint to
the 1-mile finish, she felt something snap in the area of her previous pain. Although rare, displacement through a stress
fracture can occur, and emphasizes that when playing while hurt, the athlete invites further and more significant injury.
Muscle units in the lower leg are in enclosed compartments defined by surrounding fascial envelopes. With hemorrhage
and edema due to contusion or strain, circulation to the muscles and nerves within a compartment may be compromised.
Strenuous exercise can initiate compartment syndrome by swelling associated with metabolic waste product buildup.
Muscle swelling due to restricted venous or lymphatic outflow may be related either to acute swelling of the muscle due
to overuse or to a transient swelling related to congenital fascial thickening. Most often, findings are transient and related
to muscular exertion; symptoms disappear when the inciting activity is stopped only to reappear during a subsequent
period of exercise. An acute compartment syndrome may develop primarily or as the result of transient ischemia.
Immediate fasciotomy is mandatory to prevent muscle ischemic necrosis. With numbness and pain related to activity,
prophylactic fasciotomy is often the treatment of choice in the athlete who wishes to remain active. Although such
complications are rare, the physician dealing with track and field athletes must be aware of the potential problems.
Serial biopsies taken from marathon runners at different intervals after competition have shown ultrastructural changes in
skeletal muscle (35). In biopsies obtained 1 to 2 days after an event, findings have included focal fiber injury and repair,
intracellular and extracellular edema with endothelial injury, myofibrillar lysis, dilation and disruption of the T tubular
system, and focal mitochondrial degeneration without inflammatory infiltrate. The mitochondrial and myofibrillar damage
showed progressive repair by 3 to 4 weeks. At 8 to 12 weeks, biopsies have demonstrated central nuclei and satellite
cells characteristic of the regenerative response. Veteran runners have also been noted to have intracellular collagen
deposition suggestive of a fibrotic response to repetitive injury.
Back pain is rare in experienced distance runners. If they are executing technique properly by slight forward body lean
and placing center of gravity just above the planting foot, locomotion becomes relatively effortless. If, however, they
attempt to stand too upright, the center of gravity is shifted behind the planting foot, and they must make an effort to vault
over it; the center of gravity moves up and down. In effect, the energy stored in eccentric preloading is wasted in
production of a vertical vector of propulsion rather than an efficient horizontal vector. Energy used to propel the body
upright over a planted foot will produce a bounding-type gait in which the head bobs up and down. This leads to quick
fatigue and symptoms of stress manifested by heel pain from landing on the heel, plantar fasciitis from rolling over the
flatly planted foot, or back pain developed from the jarring effect of repetitive falling due to inefficient vertical lifting.
Although the generation of heat within the musculotendinous unit is beneficial and increases contractility and pliability of
muscle in distance running, it may also have adverse effects. Heat cramping, heat fatigue, and heat stroke are a
continuum of maladies discussed in Chapter 4. Acute renal failure is a multifactorial event that is rarely seen in marathon
runners (36). The condition is secondary to the combined effects of rhabdomyolysis, dehydration, hypotension,
nonsteroidal antiinflammatory drugs, and hyperuricemia. Prevention is achieved by correcting potential dehydration and
by minimizing the use of nonsteroidal antiinflammatory drugs.
The maintenance of adequate serum electrolyte concentrations is essential in long distance running ( 37). In a study of
ultramarathon runners racing in a 100-mile race, it was found that with ingestion of sufficient quantities of carbohydrate
electrolyte solution, normal metabolic parameters could be maintained. These runners each ingested up to 22.4 L of fluid
during the race.
Stretching must become routine to prevent overload of the musculotendinous unit that is related to training excess or
error. Before a race, athletes must warm up to increase efficiency of muscles and thereby reduce the incidence of strain.
This also decreases the mental fatigue that leads to strain or sprain injury. Proper warmup can significantly decrease and
even eliminate the initial period used to attain the “second wind” level of performance. Middle and long distance runners
need a longer period than sprinters to warmup circulation-dependent type I endurance fibers. A period of easy running
and light flexibility exercises working up a slight perspiration, followed by a short series of warmup sprints and easy
jogging, striding, and rest before race time can be carried out, followed by a 5-minute period of rest to get breathing back
to normal. After completing the distance event, athletes must continue to jog for a lap or two in order to encourage
circulation and help clear metabolic waste products from muscle, so that fatigue does not set in during the next few days.
Going through a light jog and stretching routine the day following competition helps work out tightness and encourage
circulation.
Race Walking
Race walking has recently gained public attention and is included in many track and field distance events. The event is
often criticized because it “looks funny.” This is a walking event; there is no airborne phase as there is in running. The
rules clearly state that there must be unbroken contact with the ground and that the advancing foot of the walker must
contact the ground before the rear foot leaves the ground. During the period of each step while the foot is on the ground,
the leg must be straightened and not bent at the knee for at least one moment ( Fig. 41.8).
FIGURE 41.8. Race walking. Proper form necessitated by the rules of race walking place tremendous strain on every
muscle of the body. Since the advancing foot must contact the ground before the rear foot leaves the ground, strain in
eccentric loading is common. Proper strength training and flexibility and adherence to form are necessary here as in
every event to prevent injury.
In order to ambulate with an erect posture and no forward lean, the strain against eccentrically loaded muscle is severe,
so that stretching of upper and lower extremities becomes mandatory ( 38). Rigid orthoses are definitely contraindicated,
because athletes would lose stride in vaulting over them. The forefoot of the shoe must be extremely flexible in this
event. The upper body is used to amplify lower body motion; most race walkers race with clenched fists. Therefore, race
walkers demonstrate the qualities of upper extremity amplification and increased stride length similar to a sprinter, but
without forward lean or an airborne phase. To centralize the center of gravity in forward momentum, new, accentuated
motions are introduced to allow a narrowing of stride width. This is done by a small burst of hip adductor muscle activity
at the end of the swing phase.
Increased ankle dorsiflexion is needed because of lack of an airborne phase, so that pretibial muscles may not overwork
and develop symptoms of shin splints. Because erect position due to lack of forward lean is associated with increased
trunk rotation, erector spinae and paraspinous muscle strain is extremely common. If the competitor is not flexible,
increased stride length will lead to posterior knee pain, heel cord strain, and extensor mechanism complaints.
Hyperextension forces of the knee during race walking will put stress on the posterior structures of the knee so those
popliteal symptoms commonly occur, which hamstring strengthening and quadriceps stretching can prevent. Achilles
stretching exercises can avoid heel cord strain; but if strain does develop, heel lifts may aid in limiting symptoms. With
increased trunk rotation, strain of the external oblique, transverse abdominus, and rectus abdominus muscles commonly
occur. Strain of the abdominal muscles may lead to pain radiating down the inguinal canal, which is particularly
bothersome and best avoided. Athletes participating in this sport must use an aggressive program of rotational,
abdominal, and paraspinous muscle stretching and strengthening exercises.
JUMPING EVENTS
Long Jump
The running broad jump, or long jump, is one of the five original events of the ancient Olympic games. It was a
component of the Pentathlon in 708 B.C ., not a single event. The ancient jumper would gain acceleration by swinging
hand held weights (39). It was reintroduced in American track and field when the New York Athletic Club was founded in
1868, with a takeoff board into a sandpit. Hand weights were not used, and have not been since. The Amateur Athletic
Union adapted it as a standard event in 1876, and it was adopted for high school use at the University of Pennsylvania
High School Relays in 1895. It was formalized as a university level event at the University of Chicago in 1901. Female
Olympic competition initiated in 1948.
The long jump can be divided into four consecutive parts: approach, takeoff, flight, and landing. The approach occurs
from the moment the athlete starts walking or running toward the board until, but not including, the instant the takeoff foot
strikes the ground for the last time before takeoff. This is the most important phase in that major adjustments are made in
the first few strides, and fine-tuning occurs in the last four strides before takeoff ( 40). The second phase is the takeoff,
which consists of touch down until the instant at which the takeoff foot breaks contact with the ground. Third is the flight,
which is from the instant of take off until the instant the athlete first makes contact with the sand in the landing pit. And
last, the landing, which occurs from the instant of landing until the athlete's center of gravity passes forward of the feet or
comes to rest. Available data suggest that elite long jumpers attain approach speeds of 95% to 99% of their maximum
sprinting speed before takeoff.
In the approach, a runoff is used that varies from 120 to 150 meters in college, less in high school. The object of the
approach is to develop maximal speed. There is a short period of half speed, a short period of three-quarter speed, and a
long period to adjust to full speed. The jumper sets checkmarks at the side of the runway to signal change of cadence. At
the end of the run, eccentrically stored potential energy is released as kinetic energy in production of forward momentum.
The number of strides needed to attain full speed comfortably will vary for each competitor. The fewer strides a jumper
takes, the easier to keep the checkmarks accurate.
The takeoff distance for the fourth-to-last stride, the landing distance for the last stride, and the height for the center of
gravity at takeoff into the jump are significantly correlated with the distance of the jump ( 41). These three position
variables are significantly related to the distance of the jump through their relationships with the velocity of the approach
and through the vertical velocity of the center of gravity at takeoff into the jump.
If jumpers miss the mark, they must learn to run over the board and into the pit. They must not suddenly decelerate; to do
so risks eccentrically loaded muscle strain or knee or ankle ligament injury. The heel hits the board first and goes through
a standard heel, ball, toe motion for takeoff. The opposite knee is driven forward into flexion to drive the center of gravity
forward and to amplify the push of the extended takeoff leg. As the center of gravity moves forward, clenched hands,
which have been moving in a normal sprinting fashion, drive forward and upward to maintain balance. In the flight or
airborne phase, jumpers must maintain balance and must also position the body for an effective landing; long jumpers
originally used a hang technique, tucking their legs under the body during takeoff, extended them, then drew them in
again for landing. In 1922, Hubbard introduced the hitch kick motion of running in air during the airborne phase. In either
case, motion must be timed so that landing can occur with both knees partially bent so they can eccentrically absorb
contact energy to be used in the forward spring and to prevent falling backward ( Fig. 41.9A). Falling backward onto
extended hands can result in injuries to the shoulder. This reverse extension combined with contraction of the biceps
muscle can cause an injury to the superior aspect of the glenohumeral joint, resulting in the so-called SLAP lesion. This
is an avulsion of the biceps insertion at the superior labrum in an anterior-to-posterior direction. Nonoperative
management consisting of nonsteroidal antiinflammatory medications and physical therapy that emphasize rotator cuff
strengthening is stressed initially. Failure of nonoperative management is an indication for operative intervention. These
lesions can be debrided or repaired arthroscopically, or they may require open surgical superior mechanism
reconstruction.
FIGURE 41.9. Long jump. A: As the planting foot makes contact with the board, this leg extends, propelling the jumper
forward. The athlete may either attempt to walk through the air, amplifying crossed-extensor reflex patterns, or may
merely tuck his knees in preparation for landing. It is this presetting of muscles that allows the jumper to eccentrically
absorb energy at landing for forward propulsion. B: Triple jump. The biologic basis of the triple jump is progressive
increase of height and distance made by effective storage of kinetic and contact energy with amplification through reflex
integration. The takeoff foot lands in the step. Both feet make contact in the jump. Amplification of energy storage is
provided by arm motion, and presetting of muscles allows eccentric energy storage at impact to help propel the body
forward.
In the early phase of training, hard jumping must be avoided. Throughout training, the pit must be either turned daily if
made of builders' sand, or kept dry if the foam rubber-type practice pit is used. Improper acceleration, that is, reaching
maximal stride either too early or too late, will lead to strain injury. Inaccurate placement of checkmarks leads to uneven
strides, which leads to strain of eccentrically loaded muscles. Contacting the board with the knee too straight settles the
center of gravity too far posterior, and induced deceleration detracts from an effective jump or causes knee sprain. Arm
action must parallel leg action; when the left knee comes forward, the right arm must also come forward, as it does in
sprinting and walking. Any attempt to circumvent the body's natural motion can lead to injury. It is the responsibility of the
athlete and the coach to examine the takeoff board. If it is loose, uneven, or excessively worn, its use invites injury.
Triple Jump
The original Greek triple jump was a series of three consecutive simple jumps. The Celts practiced a continuous series of
three jumps. This was regulated as a hop-hop-jump event and was modified in the United States as the hop-step-jump
event in 1900. Women competed in the United States in 1889 but not on an international level until 1993.
The triple jump uses the same runway as the long jump. With the hop, athletes land on the same foot that had been
placed on the takeoff board ( Fig. 41.9B). They then enter the step phase, in which they take off on the foot from which
they had landed to land on the opposite foot to jump. Essentially, this is a normal long jumping action in which the
athletes develop further forward momentum.
Triple jumpers must concentrate on technique in order to maximize forward momentum. A misstep will decrease distance
and risk injury. If they concentrate too much on height, they lose distance. This is individualized, because there is no
optimal vertical height to horizontal velocity phase ratio for all jumpers ( 42). Pretensing the hopping leg allows storage of
eccentric energy from the landing impact for use in the next step. Although the heel comes down first on the landing leg,
there is a quick roll, so that landing is essentially flatfooted. If it is not, calcaneal fat pad bruising and stress fracture will
result; or the braking motion caused by the center of gravity being behind the planted foot may cause a knee ligament
injury through deceleration. To absorb the shock of impact, the landing foot is pulled back quickly and preset; otherwise
hamstring, quadriceps, or gastrocnemius strains commonly results. After planting the foot, it is important to drive the
opposite knee up in order to develop forward momentum through crossed-extensor amplification. In evaluation of
lower-extremity muscle strain involving the hamstrings, quadriceps, or gastrocnemius, the examiner must delineate the
areas of maximal tenderness. Occasionally, the examiner can feel bunched-up areas of muscle within the muscle bellies
that are indicative of actual muscle pull. It is important to examine the entire length of the muscle to rule out bony
avulsion injuries from the pelvis. With simple muscle strains occurring in the substance of the muscle belly or near the
musculotendinous junction, treatment is focused on retaining strength and mobility before return to sport.
In the second jump, or the step, athletes again preset their lower extremity and swing both arms behind the body so that
at impact they can swing them forward to drive the body's center of gravity forward in the jump. Driving the upper
extremities forward and backward can cause a rhomboid, pectoralis, levator scapulae, or serratus anterior strain,
particularly if athletes are off balance. Flexibility and strength help reduce the incidence of strain injury.
In the third phase of the jump, athletes must make an effort to attain maximal height and distance, and do so by throwing
their hips forward; without proper flexibility and strength, gluteus or paraspinous muscle strain can develop ( 31). Because
horizontal speed is diminished greatly, proper technique is necessary to maximize use of energy stored within muscle;
foot contact must be perfect, and double arm swing use must potentiate energy on push-off. Ending the jump, the athlete
lands in a near-sitting position ( Fig.41.9B).
Many characteristics of the kinematics of the triple jump have been found to correlate highly with total jump distance ( 43).
The horizontal position of the center of gravity of the body in relation to the support foot at takeoff correlates highly with
the total distance of the jump, as does the distance of the hop phase. The vertical velocity into the hop and step phases
correlates highly with the respective distance of each phase, and there is an inverse correlation between the maximum
height of the center of gravity during flight phase of the step and the total distance.
For optimal distance, the triple jumper must gain great run-up velocity and exert forces during each supporting phase that
are 3.6 to 4.4 times the body weight, resulting in a force vector angle of about 101 degrees at each takeoff.
The greatest potential for injury is related to the landing phase. The foot lands in plantarflexion and inversion so that
internal rotation injury of the ankle is common; lateral sprain and actual tibial and fibular fractures may be seen.
Off-balanced landing in ankle dorsiflexion encourages medial ankle sprain and calcaneal fracture. When evaluating foot
and ankle injuries occurring during the landing of the triple jump or the long jump, the examiner must clearly define the
areas of maximal tenderness and swelling. If actual bony tenderness over the medial or lateral malleoli or over the
calcaneus is found, the examiner must be suspicious of possible fracture and obtain appropriate x-ray studies. More
commonly, however, ligamentous injury occurs in the area of maximal tenderness and coincides with that of the anterior
talofibular and calcaneofibular ligaments. Less commonly, deltoid ligament injuries can occur medially. Because the
landing is so important in these jumping events, the rehabilitation of these ankle sprains must concentrate on retaining
muscle strength and full range of motion of the ankle without pain. Taping is used as necessary. Knee ligament injury and
meniscal injury may occur due to compressive and rotatory forces sustained by the knee in an unbalanced impact. If
there is not enough spring in the runway contact board, or if the athlete tends to decelerate at impact with the board,
“jumper's knee” patellar tendinitis or peroneal subluxation can develop, as is discussed in the next section.
High Jump
The running high jump may have been introduced as an athletic event in one of the ancient Olympiads, but it was
definitely practiced by the Celts. The first English competition took place in 1840. It was introduced into American track
and field in 1868 with the founding of the New York Athletic Club, and was recognized by the amateur athletic union in
1876. Women first competed in the United States in 1895 and on an Olympic level in 1928.
The original technique consisted of a running start with a feet-first jump. William Page of the United States introduced the
scissors kick to clear the bar in 1874 ( Fig. 41.10A), and the technique was then modified as an eastern style ( Fig.
41.10B). In the early 1900s, the western roll developed on the Pacific coast. These forms are no longer used on a
collegiate level, because they are rarely effective above 6 ½ feet. They are still used at the high school level. Until 1936,
the crossbar had to be crossed feet first. Steers developed the head first style in 1941.
FIGURE 41.10. Older high jump technique. The outer leg was used to propel the body over the bar with the scissors
technique (A) and eastern technique (B). C: In the western technique, the inner leg was used in high school, where
groin, hamstring, and paraspinous muscle flexibility must be emphasized to prevent injury. D: Straddle technique. E:
Newer high-jump technique. In the Fosbury flop form, the jumper crosses on his or her back. Paraspinous strain and
vertebral fracture plague this technique.
Fosbury introduced what has been labeled the Fosbury flop in the 1968 Olympic Games. This has become the most
popular form in attaining a height greater than 7 feet. Like the original technique called the scissors jump, takeoff is from
the outside foot but then turns into a back dive over the bar ( Fig. 41.10E). The jumper is able to obtain full speed on the
approach and can convert this momentum into vertical lift. The J-pattern approach is used, using a straight line for the
first five steps, converting to a semicircular path, maximizing lift with the effects of acceleration in pulling out of centrifugal
force. Such an approach is extremely hard on the ankles and leads to frequent ankle sprains. Softer landing pits made
the flop a feasible technique by limiting the danger of spinal trauma associated with landing on one's neck and back.
In the 1940s, the straddle form developed (Fig. 41.10D). Still used today, it is sometimes called the modified western or
belly roll. Clearance of the crossbar is done by straddling the bar while facing down. The approach is very similar to the
western form (Fig. 41.10C), The last stride is lengthened and the rock-up on the toe is from a flatfooted or heelball
landing of the takeoff foot. The jumper strikes the ground hard with the takeoff foot to obtain a rebound. The opposite leg
is swung high toward the bar, not fully straightened, and continues to move while slightly bent. Both arms are thrown
upward with emphasis on the arm contralateral to the upswing leg. The center of gravity is over the plant leg, which fully
extends at the knee in push-off. In rocking up on the toe and swinging the opposite leg, the jumper leaves the ground.
The lead leg swings over the bar, and the chief concern becomes getting the previous plant leg over the bar without
touching. This is often accomplished with a sharp kick in the air, which must be precisely timed. The twisting motion
involved leads to a high incidence of abdominal and back strains.
In straddle, western, and belly roll forms, sand or foam pits necessitate falling on both arms and at least one leg, and
broken bones in both upper and lower extremities were common. Practice of indoor gymnasium mat falling techniques
has been useful in preventing injuries, because rolling at the time of impact was found to reduce the jar and minimize
danger of injury. Introduction of foam pits enhanced safety and decreased overall numbers of injury.
Proper foot plant is mandatory; otherwise, the jumper loses control and, in attempting to clear the bar, will strain muscles
in the abdomen or lower back.
Because of acceleration of the horizontal approach and translation into vertical lift, braking action is required in
conversion of linear motion. Braking is accomplished through quadriceps muscle tension, and extensor mechanism
problems may result. These problems may range from quadriceps tendon superior, medial or lateral strain,
chondromalacia of the patella, and patellar tendinitis. Actual rupture of the patellar tendon is more common here than in
any other event. Patella tendinitis, or jumper's knee, is the most common pathologic entity known in high jumpers. The
jumper complains of sharp anterior knee pain, which on physical examination, is found localized to the insertion of the
patellar tendon at the inferior pole of the patella ( 44). In evaluation of the extensor mechanism of the knee, the examiner
must palpate for areas of maximal tenderness and carefully feel for any defects either in the quadriceps tendon insertion
at the superior pole of the patella or at the patellar tendon origin at the inferior pole. Both quadriceps and patellar tendon
ruptures are treated surgically. More commonly, however, these extensor mechanism injuries are tendinitis at both the
quadriceps and the patellar tendon insertions on the patella, as well as irritation of the chondral surface of the patella.
There may be infrapatellar fat pad hypertrophy and occasionally intraarticular effusion related to associated
chondromalacia of the patella. Resisted knee flexion and weighted squat exercises may reproduce symptoms. The
pathologic origin of the jumper's knee consists of microscopic disruption of the insertional fibers of the patella tendon at
the inferior pole of the patella. Prevention of this condition is accomplished by keeping the quadriceps and hamstring
muscles strong and flexible so that their shock-absorbing properties are maximized. This is only useful in conjunction with
execution of proper technique. Symptoms range from pain following activity, to pain with and following activity, and
finally, to pain interfering with performance. Icing, antiinflammatory medication, stretching, and patella tendon bracing or
strapping may be useful in limiting progression of the disease.
Improper landing technique can result in acute or chronic traumatic injuries to the cervical spine ( 45). In such cases,
repetitive flexion injuries can cause late instability and neurologic damage. They are often not seen on routine lateral
radiographs. The presence of slight anterior subluxation, simple compression fractures, or subtle kyphotic angulation at
one cervical level should alert the physician to this diagnosis. Flexion and extension views are useful to demonstrate this
instability.
In spite of fewer severe injuries due to softer landing areas, the flop technique has introduced more significant injuries.
With fatigue and inflexibility, energy used in the vaulting technique commonly leads to paraspinous muscle spasm or
transverse process fracture. Because jumpers vault over the bar and land on their backs, it is important that they know
proper landing techniques. Both arms should shoot out and drive into the mat at contact in order to soften the contact of
the back and help limit vertebral compression fractures of the cervical, thoracic, and lumbar spine. Nevertheless, such
injury may be unavoidable ( Fig. 41.11). A backboard and sandbags must be available in high jump and pole-vaulting
areas because of the potential severity of spine injury.
FIGURE 41.11. Vertebral injury. With the modern techniques incorporating a back landing in the high jump and
pole-vault, vertebral injury is more common. Proper landing technique must be emphasized. Here, a 20-year-old college
high jumper who uses the “flop” style is found with wedge and compression fractures as well as Schmorl nodes during
evaluation for his back pain.
Energy transfer following foot plant for both eccentric loading and subsequent contracture leaves the hamstring and
low-back muscles particularly at risk. Strains are common, and their incidence can only be reduced with adequate
warmup and stretching. Approach, planting, energy transfer, torquing over the bar, and landing are all difficult
techniques, and only one aspect can be coached at a time. Asking the athlete to concentrate on multiple points will lead
to confusion. Practice of difficult techniques requires repetition to make such technique habit. The “straddle” form is often
used in the lower qualifying heights and the “flop” technique in higher jumps. This conserves energy and lessens the
chance of severe injury. Hamstring stretching is mandatory for the first form, whereas landing technique must be well
rehearsed in the second.
Pole-Vault
Pole-vaulting has prehistoric origins. Ancient humans found that by adding the lift of a pole to a running broad jump,
barriers such as small streams and gullies could be crossed. The Cretans and Greeks would use poles to vault over
bulls. German gymnastic competitions in 1775 used a pole to accomplish a vertical jump. In 1850, a running pole leap
allowing the athlete to climb a rigid pole was introduced. The concept of competition for height evolved, and in that form,
it was introduced in America in 1877. Vaulters from Northern Britain soon became the early champions, but they were
pole climbers and not pole-vaulters ( 46). Movement of the hands along the pole was banned in the United States in 1889,
and the technique of crossing the bar stomach down was introduced. The pole receiving box was introduced in 1900, as
was the bamboo pole that was used until 1942. Aluminum, steel, and finally, fiberglass poles increased height obtainable
(47), and a landing pad improved safety. The first sanctioned international women's championship was in 1996.
A pole-vaulter is essentially a sprinter with a pole. The fiberglass pole, introduced in 1960, allows speed comparable to
that of a sprinter. There are four traditional means of pole carrying; high-point carry, elevating the tip approximately 45
degrees; intermediate carry, elevating the tip 25 degree; horizontal carry, with the pole parallel to the ground; and a
low-point carry, with the tip below horizontal. An effective plant of the pole tip is the most important technique the vaulter
must master. If a vaulter misses a plant, the pole tip may lodge in the substance of the foam pit, and sudden jarring will
lead to shoulder subluxation or acromioclavicular (AC) joint sprain. An attempt to decelerate rapidly at the end of a long
sprint on the gripping surface of modern synthetic runways while accommodating a heavy pole may lead to anterior
cruciate ligament disruption. The vaulter must be taught to slowly decelerate and let the pole slide through the hand if he
or she misses the marks.
The classic technique in the pole-vault consisted of an approach of less than full speed, moving the hands closer
together, planting the pole, stomping the dominant leg (which is the opposite of the dominant arm due to the
crossed-extensor reflex), and propelling one's self upward, making one's body parallel to the bar to maximally use
centrifugal force, turning the body, using the scissors kick to clear the bar, and giving attention to landing to avoid
fracture, strain, or sprain ( Fig. 41.12A). This technique was used effectively with a metal pole due to pole stiffness. The
same technique will lead to imbalance and injury if used with a fiberglass pole. Unfortunately, many high schools still use
metal poles for monetary reasons, and if athletes try to remain competitive, they are most likely to find it impossible to
switch techniques if proper equipment become available.
FIGURE 41.12. Pole-vault form. A: With the metal pole, the vaulter must maximize forward momentum in order to propel
him over the bar; thus, he must run through his approach. B: With the fiberglass pole, approach speed can be increased
because energy is stored within the pole, which helps catapult the vaulter over the bar; he jackknifes to clear the bar and
lands on his back.
Fiberglass poles are slightly longer than metal poles, being up to 18 feet. The pole tip is held above head level, at about
a 15- to 20-degree angle with a grip wider than shoulder width; both factors allow use of slightly heavier poles. Vaulters
are taught that they are sprinters with poles; they are to approach the pit at full speed. Because of this, they must have
practiced effective planting techniques and an even stride; otherwise, they tend to plant the pole late and decelerate
momentum. In the new technique, at the last stride, the pole is held over the head, arms are separated, and with a
circular motion, the pole will be planted down into the box. The top hand pulls down while the bottom hand pushes up,
making use of their separated positions to store further energy in the pole, effectively using it as a bow and arrow. As the
feet continue propelling forward, the pole bends backward, largely encouraged by the separated hand position; the
energy of the sprint approach is transferred to the fiberglass pole until rebound release catapults the vaulter over the bar.
When the pole is directly vertical, vaulters are thrust upward so they are effectively allowed to do a gymnastic handstand
to clear a standard, which is, in fact, higher than the pole they use. Abdominal and hip muscles then come into play to
help the athletes jackknife over the crossbar and continue the fall to land on their backs. Faulty technique leads to
abdominal, hip, or paraspinous muscle strain, cervical sprain, vertebral or skull fracture, or spinal cord injury ( Fig.
41.12B). The U.S. National High School Federation in 1995 banned long “mushy” poles, used with a raised grip. A high
handhold on a soft pole will not allow to pole to unbend. This decreases effectiveness of the vault, breaks the pole, and
injures the vaulter. The shorter “stiffer” poles have lead to a decreased injury incidence. Recent digitalization motion
analysis has been found effective in analysis of training error ( 48).
Knowledge and mastery of technique is mandatory in this event. If vaulters have not achieved sufficient speed, the pole
will not advance to a full vertical position, and they will fall backward into the box or runway. If they fail to store energy by
bending the pole at takeoff, the pole will advance past the standard, and they may even be thrown past the padded pit
area. If the plant is not correct, they may be thrown off to the side and into a standard, where a laceration or a contusion
injury is common.
Vaulters must practice planting technique for 5 or 6 weeks before attempting a vault. Their checkmark adjustment and
stride length must be accurate, because stepping beyond the ideal takeoff point will lead to shoulder subluxation, and
falling short of the ideal takeoff point will lead to decreased momentum so that they will fall back on the runway. They
must be taught to run through their plant by relaxing their grip on the pole if they miss their marks. If not, supraspinatus
sprain, shoulder subluxation, AC joint sprain, or anterior cruciate ligament disruption will commonly occur.
Examination of the injured shoulder from pole-vaulting initially focuses on areas of maximal tenderness. AC joint injury
will result in tenderness both over the AC joint and, often, just cephalad to the coracoid in the area of the coracoclavicular
ligaments, which are also often injured. X-ray examination is mandatory to evaluate AC joint injuries and possible
fractures of the distal clavicle. Rotator cuff injuries are best diagnosed by weakness of the supraspinatus in isolation.
This is tested by having the patient extend the arms in front of the body, slightly to the outside of straight forward
position, with the thumbs pointing down. The examiner then attempts to push downward on the outstretched hands. If
pain and weakness are elicited, a supraspinatus strain is likely. A positive apprehension sign is the best indicator of
anterior shoulder subluxation. This sign is elicited with the arm abducted and in external rotation at the shoulder. The
athlete notes pain and symptoms of feeling as if the shoulder will pop out of joint. Treatment of these injuries is specific to
the injury involved. AC joint injuries are most commonly treated nonoperatively. This, however, depends on the degree
and severity of ligamentous injury. Full-thickness rotator cuff tears are quite uncommon in the younger athletic age group,
and most supraspinatus strains will recover with time and rehabilitation, thus avoiding surgical intervention. Shoulder
subluxation, if recurrent, may require surgical treatment, and the recent advent of arthroscopic thermal tightening may
make it possible to allow the athlete to return to competition within a short period of time ( 49).
Pole-vaulters must have proper flexibility to arch their backs in crossing the bar while keeping their arms down. This
maneuver facilitates pushing the pole backward with the thumb and prevents the athlete from throwing the arms up in the
air, which would force the chest and body into the bar and cause imbalance, thus leading to cervical, paraspinous,
abdominal, hip, quadriceps, and gastric strain. The athlete must concentrate on landing as soon as he or she clears the
bar so that the athlete can land relaxed near the middle of the foam pit ( 50). The proper technique is to tuck up one's
knees while clearing the bar and rolling back for landing. On landing on the back, the jumper should slap the mat firmly
with the arms at a 45-degree angle to the body to help dissipate energy and decrease the chance of spinous injury.
THROWING EVENTS
Shot Put
Putting a 14-pound stone with rounded edges was a game recorded in Ireland and Scotland as early as 632 B.C. When
the Amateur Athletic Union (AAU) used a 16-pound iron ball with the modern reintroduction of this event in 1876, the
rules were essentially the same. A square with 7-foot sides was used in 1860. A 7-foot circular platform was utilized in St.
Louis in the 1904 Olympics, and made official in 1906. Women competed with a 4-kg shot in France in 1917 but did not
compete in the Olympics until 1948.
The metal sphere now used is 16 pounds in college, AAU, and Olympic competition; 12 pounds in high school; and 8
pounds for grade school. The spheres are made of iron, bronze, or brass with a lead center. Shot putting is a power
event; the missile is pushed rather than thrown. The thrower must be familiar with the rules of his event ( 51).
The restrictions of the 7-foot circle have necessitated developing techniques that are effective in producing momentum
within a small distance. A side-step action was developed in the United States in 1876. In the 1950s, O'Brien in the
United States modified the long-used straight explosive style. He replaced this with a low-set rotational style in which the
center of gravity started low (from a backward-facing position at the back of the circle), and would rise with rotation along
a straight line, rotating 180 degrees to gain momentum for release at the front of the circle. Emphasis on weight training
helped develop explosiveness for crossed-extensor amplification at release of the shot. In 1976, the Russian
Barychnikov introduced a discus style spin that greatly increased the momentum produced within the limits of the circle
and will perhaps be the new dominant form.
Speed must be controlled in order to keep the athlete's balance and rigid attention to form, and practice is the only
means to increase speed effectively without injury. Rotational motion in the newer techniques produces tremendous
torque. To prevent strain injury, flexibility is necessary. The elbow and throwing shoulder remain behind the shot and hips
to produce an effective final push. The newest discus-throwing technique of spinning in the arc, consisting of 540
degrees of rotation while attempting to accommodate a 16-pound iron weight, is difficult. In this technique, the weight is
kept behind the center of gravity to increase centrifugal force in rotation, producing the effect of an extra burst of energy
similar to the effective use of the sprinter's blocks ( Fig. 41.13).
FIGURE 41.13. Shot put. A whirling discus style has recently been introduced in competition and may eventually prove to
be more effective.
Warmup must not be too vigorous, because four quick preliminary trials are necessary before qualification for semifinal
or final events. However, shot-putters must warm up quickly to maximize quick type II myofibril bursting activity. They
must stretch and bend all muscle groups involved in the event, particularly concentrating on the leg, back, and shoulders.
The optimal release angle is about 41 degrees, so athletes practice this with a rubberized or indoor shot against set
positions on a wall to get the feeling for proper angle. Sprinting, jogging, and agility drills are important in developing
speed and coordination. Torquing techniques are particularly hard on the knees, back, and shoulders, so that in
midseason, the shot-putter rarely throws the shot in practice more than six repetitions twice a week.
Injury is commonly due to error in technique. Owing to torque and generation of momentum, paraspinous muscles spasm
at any point along the spine can occur. Sacroiliac stress reaction has been reported ( 52). In combination with hip thrust in
the final push, gluteus strain or hip capsular strain will occur if athletes are slightly off-balance. External oblique or
transverse abdominus sprain is also common. Athletes commonly plant their nondominant foot under the toe bar at the
end of the movement to stop momentum, gain balance, and avoid fouling. This is an extremely dangerous technique,
which must be avoided, because continuation of momentum leading to internal rotation on the planted lower leg easily
causes anterior cruciate ligament disruption, and future pivoting on this leg for performance of athletic technique may
become impossible.
The shot is released with a final push resulting from stored energy produced through a complex technique. With the
elbow and shot held behind the center of gravity and propelled forward, the push must be straight. A bent arm throw was
banned early in the history of this event, and if done by mistake can lead to humeral shaft fracture ( 53). If there is slight
imbalance, the weight and the push against a shot on the extended fingertips commonly produce lateral epicondylitis, or
inflammation of the tendinous origin of the extensor muscles in the forearm. Finding tenderness with palpation over the
lateral epicondyle and pain on resisted wrist extension makes the diagnosis of shot-put/tennis elbow. The lesion has
been found to be consistently located within the origin of the extensor carpi radialis brevis. Epicondylitis is treated with
nonsteroidal antiinflammatory medications in mild cases, local cortisone injection or iontophoresis in moderate cases,
and cortisone injection with concomitant deep friction massage in recalcitrant cases. On cessation of pain, therapeutic
exercises are beneficial to strengthen the musculature before the resumption of throwing. Surgery is performed after
exhausting all nonoperative management. Although a tennis elbow strap may help decrease symptoms, pain in the final
push will decrease competitive performance. Strict adherence to technique is implicated in injury prevention. Athletes
may benefit from wall and standard fingertip push-ups to help coordinate balance and must also choose a shot that feels
balanced to hold.
Early in the season, athletes propel the shot forward from the hand. As the season progresses and they gain balance,
they both hold and propel the shot from the fingertips. Early in the season, wrist sprain is extremely common and may be
prevented by wrist strengthening exercises, avoidance of hyperextension in technique, and taping. Athletes must not
progress to fingertip push-off too early; otherwise, volar plate sprain, collateral ligament sprain, or interosseous and
lumbrical muscle strain may commonly occur. Performance of proper technique is only possible through proper
progression and attention to form. Athletes must not attempt complex advanced maneuvers until they have been coached
properly and are well prepared.
Hammer Throw
Hammer throwing originated in Ireland about 500 B.C. In the 1860s, throwing a 16-pound shot on an oak handle from
behind a line while on the run was introduced into American collegiate sports; the wooden handle was replaced in 1887
by a 1.2-m wire attached to a grip. After 1880, a 7-foot throwing circle was used. With the introduction of the circle, a form
developed in which two circular winds within it preceded delivery of the hammer. Three turns were introduced in the
1900s. Offsetting the center of balance to traverse a straight line and develop momentum demands exacting technique,
so that technique rather than speed is emphasized. In maximizing centrifugal force, the hammer actually leads the
athlete, and by pivoting on one's toes, quick turns and maximal acceleration become possible. The hammer may be
placed outside the throwing circle at the beginning of the throw ( 50).
Hammer throwers keep their bodies crossed. This means that the hips are locked into position ahead of the shoulders,
which are also locked into position. The athlete generates torque through an almost seated position. In the mid-1960s,
the Europeans perfected techniques capable of generating four turns within the 7-foot circle.
Hammer throwers must be quick, well coordinated, and have extremely strong legs and backs. They must be flexible.
Rather than worry about rotational speed, technique must be perfect so that extended arms and perfect positioning of the
center of gravity will help propel the 16-pound shot forward at the end of the chain.
Throwers learn to lead the hammer and not drag it. The idea is to transfer the energy from powerful leg muscles and the
back through the hips, shoulders, and arms ahead of the hammer. In order to keep the hammer in a solid position;
throwers must be flexible and strong. They must not allow the hammer to get ahead of them, or the tremendous torque
generated will lead to subluxation of the shoulder.
The technique of throwing demands smooth flowing continuous action, so that each turn is faster than the previous one.
There are no pauses between different turns, so athletes learn to turn on their toes, and momentum progressively
increases. Although athletes must remain in the circle, the hammer does not need to do so; there is, however, no ideal
starting position for the hammer.
Athletes start by facing the back of the circle with knees flexed 30 degrees. They start low, generating momentum forward
and upward progressively with a smooth lifting motion. As they generate torque, they sit back on their hips, extend their
arms and shoulders fully, thus increasing the radius of leverage and achieving a mechanical advantage. Because
acceleration can only progress with both feet on the ground, they learn to turn quickly on the ball of the foot. They must
emphasize keeping the outer leg close to the body against centrifugal force to prevent imbalance. The back must be
locked into position. Without the proper flexibility, paraspinous muscle strain and associated transverse process fracture
is extremely common. In sitting back with the arms extended, leverage is increased, using the pelvis to balance the pull of
the hammer. Hip capsular sprain, pubic symphysitis, or iliotibial tract friction syndrome commonly occurs with slight
misstep. To keep control of the hammer, athletes must strive for quick tight turns, attempting to keep the hammer
wire-tight through the entire motion. Extreme strength and polished technique are needed.
The speed of the hammer increases progressively with every turn. The hips always lead the shoulders in order to control
centrifugal force. Counterbalance of the hips is accomplished by leaning opposite to the direction of the hammer. The
torque generated by such training not only stresses the back muscles, but places extreme strain on abdominal muscles,
so that the abdominal oblique, transversalis, and rectus muscles can be strained with slight imbalance ( Fig. 41.14).
FIGURE 41.14. Hammer throw. This event is all technique in that the center of gravity and leverage must be perfectly
balanced in order to generate momentum and energy. Using abdominal and back muscles to lock the upper body in
position over the lower body, energy is stored and amplified by reciprocating crossed-extensor reflex during rotation.
The arms must be kept locked and extended in an X-position behind the center of gravity, and therefore the pivoting hips.
If this position is not maintained, torque on the elbows will lead to medial or lateral epicondylitis. To prevent this problem,
the swing must first be practiced without a hammer. The swing must be even because disruption of rhythm will lead to
jerky motion of the hammer, and strains of the hips, back, shoulder, and neck commonly result. Effort must be made to
sustain upward and progressive drive, gradually elevating the center of gravity in production of momentum; otherwise, a
last-minute backward lean to produce elevation will lead to rhomboid, levator scapulae, or a rotator cuff
musculotendinous strain. In elevating too quickly at the end of this technique, lateral collateral knee ligament strain is
common.
Athletes must take special care of their equipment and pay strict attention to their competitive area. They must watch out
for frayed wires, which may break and cause a fall backward if the weight is released during a turn. The hammerhead
must revolve freely on its spindle, and if it does not, it should be stored vertically on a hook to prevent the wire from
kinking, which leads to wire failure.
Athletes may want to wear a leather glove or tape their fingers to increase grip and decrease friction. They must make
sure that the surface is even to help prevent incidence of sprain injury. It is sometimes best to practice with two hammers
so that energy can be conserved and not wasted in retrieval. Most important, they must pay attention to other athletes on
the field to make sure that no one is subject to injury when the hammer is thrown.
Discus
In Homer's epic poetry, the discus was mentioned as an athletic event occurring as early as 1300 B.C. It was originally
made of stone, then of iron, lead, then bronze. The discus was one of the original five events in the Pentathlon when it
was instituted in 708 B.C., and thrown from an almost stationary position. The Greek discus was heavier than the present
discus. When reintroduced into the 1896 Olympics, it was thrown from a pedestal, which severely limited background
momentum. The Swedes threw the discus from a 2.5-meter square. A 7-foot diameter throwing circle was introduced in
1897 in the United States, but it was increased to 2.5 meters in 1908. The original static throw was changed to a Nordic
swing. In 1926, a turning and skipping style was developed by Houser in the United States. The advent of the concrete
throwing circle in 1954 allowed increased speed of rotation. Women competed in the United States in 1914 with a
1.25-kg discus, but the standard has been changes to 1-kg since the 1928 Olympics.
In 1907, the modern discus was standardized to weigh 2 kg and had a diameter of 22 cm. The high school discus is
scaled down to 3 pounds, 9 ounces. For practice purposes, the discus may be made of rubber, significantly decreasing
contact injury. Standard running or track shoes may be used, but many athletes remove most spikes, particularly in the
left shoe, in order to allow pivoting. Small rubberized spikes may be useful on the new synthetic surfaces. The most
frequent injury in discus throwing is blistering or laceration of the fingers. Physical examination of deep finger lacerations
concentrates on possible injuries to digital nerves and arteries, as well as to flexor tendons. Isolated distal
interphalangeal joint flexion is tested to rule out flexor digitorum profundus injury. Tendon lacerations are treated
surgically. More commonly, however, lacerations involve only the skin and subcutaneous tissues, which can be treated
with thorough irrigation and primary wound closure. Small spurs that develop on the metallic surface of the discus must
be filled immediately, and the use of a compound such as tincture of benzoin or resins are allowed to secure grip,
particularly in wet weather.
In the original technique, while standing in a fixed position on a pedestal, the athlete was merely allowed to swing back
and forth repetitively to develop momentum ( Fig. 41.15A). With the institution of a 2.5-meter throwing circle in 1910,
allowing generation of momentum in a one-and-a-half turn pattern ( Fig. 41.15B) potentiated the momentum of the early
swing. In the 1930s, a hop was added to the previous style of one-and-three-quarters turn, which added considerable
momentum. The addition of weight training, anabolic steroids, and strict attention to technique have significantly
increased the distances generated since the 1950s.
FIGURE 41.15. Discus. A: Originally, the discus was thrown from a pedestal. B: Additional momentum was gained with
the institution of a throwing circle, which allowed a pivot rotation energy amplification process. C: A linear rotation pattern
has since developed that further amplifies momentum.
Preliminary swings are used to establish proper balance, reassurance, and generation of momentum. From this point,
momentum can be either amplified by the crossed-extensor mechanism in rotation or increased by incorporation of a
jump. Athletes must be well tuned to their technique; otherwise, too much speed works against them. They become
unbalanced and commonly suffer knee injuries, ankle sprains, shoulder strains, or subluxation. If the knee is not bent
enough during rotation, athletes lose considerable drive. Conversely, if the knee is bent too much, the arm does its work
prematurely, so that the discus will be hurled before maximum generation of energy ( Fig. 41.15C).
The feet must be kept close to the body in an effort to consciously counteract centrifugal force. Only while the feet are in
contact with the ground can acceleration develop. In the initial swing, throwers are able to preload energy, much like the
sprinters lowering into the blocks. The lower body generates energy, and the upper body acts as a sling. The upper body
is held rigidly through the back in order to maximize the sling effect, therefore torquing strain to the lumbar, thoracic, and
cervical spine muscles is extremely common. If the arm lags too far behind the pivoting motion of the lower extremities,
sprain of the anterior capsule of the shoulder, subluxation of the shoulder, or strain to the trapezius or scapular muscles
may develop. Athletes start in a crouched position and slowly raise the center of gravity during rotation in order to
generate a power snap at the wrist. Wrist sprain is common, as is de Quervain tenosynovitis, when wrist snap is
overemphasized. Pain over the first dorsal compartment of the wrist and pain on resisted extension of the thumb are the
hallmarks of de Quervain tenosynovitis. Treatment of mild cases includes nonsteroidal antiinflammatory medications,
local cortisone injections, and splinting. In recalcitrant cases, surgical release of the stenotic tunnel in the first dorsal
compartment provides excellent relief of symptoms.
Blistering injury is common, and aids to increase surface friction are necessary. Holding the discus in the initial swing
may also present a problem. If the discus is held in a position too horizontal to the ground, tension is placed on the
pectoralis major and conjoined tendons so that strain of these muscles may occur. To eliminate strain, a more
perpendicular holding technique is used, which, in fact, allows the athlete to turn more in the windup. Unfortunately,
changing the plane of the discus from perpendicular to horizontal is not easy and may lead to shoulder, wrist, or elbow
strain.
In practice, a strapped discus may be useful in that multiple consecutive turns can be allowed with minimal risk while
developing a sense of balance. Balance is also obtained by keeping the knees and trunk bent so that the hips travel
through a wider arc in order to develop greater momentum. The center of gravity must be kept ahead of the feet so that
the upper body and hips lead into the turn. Nevertheless, the discus throw is a continuous movement. Halting technique
will place tension on ankles, hips, knees, back, and shoulders, and strains will result. Athletes must police the throwing
circle for debris that could lead to an ankle sprain. They must follow through on their technique at the completion of the
throw so that sudden deceleration will not result in a knee ligament sprain.
Javelin
The javelin was the first field event in the first ancient Olympic Games and consisted of two forms: throwing at a fixed
target from horseback, or throwing for distance. It originally consisted of a spear made of wood with a metal point for a
target, or a weighted blunt end for distance. It also had the qualification of having the foremost point no greater than 110
cm from the center of gravity, or less than 90 cm. A central whipcord near the center of gravity was mandatory for the
distance form, being 16 cm in length. Initially, the overall length of the shaft was approximately 240 cm, and the weight
was 400 g. The Scandinavians changed the standard in 1780 to the present 2.6 meters and 800 grams; the whipcord is
no longer used, nor is the horse. The throw line became an arc in 1952. Erausquin of Spain introduced a rotational
throwing method in 1966, which has since been banned as too dangerous. Women first competed in 1916, in Finland.
The weight was originally 800 g, but this has been dropped to a standard of 600 g. Women's javelin became an Olympic
event in 1948.
A system has been developed to measure initial conditions in the javelin throw rapidly enough to be used by the thrower
for feedback in performance improvement (54). This is achieved with digital high-speed video recording with subsequent
graphic presentation to the thrower of release conditions and a simulation of the subsequent flight, together with optimal
conditions and flight for javelin release. This system allows instant feedback to javelin throwers and is expected to
provide greater control and consistency of throwing variables by these athletes.
High-speed cinematography has demonstrated that in order to attain maximal throwing distance, the javelin thrower
should achieve positive acceleration during the running approach, effective thrusting with the right leg on the penultimate
stride, and carry the javelin during the last strides at an optimal angle for release between 32 and 36 degrees ( 55).
Athletes use full acceleration and a sudden stop in order to generate tremendous force in throwing the javelin. They hold
the javelin above their heads, with the elbow forming about a 90-degree angle in their approach. As they generate speed,
the throwing arm begins to extend with the hand slightly lower than the shoulder and the palm turned out. The crossover
step is used in which the body is kept well in front of the javelin to maximize forward momentum while developing a
strong delivery position. The shoulders are kept in line with the direction of the throw. As the arm extends, the body
rotates and the javelin is pulled quickly over the body near the ear. The head leans to the opposite side as the javelin is
brought through the center of gravity. The arm must remain flexible to maximize “whip” in the throw. As the javelin is
thrown over the contralateral hip and planted foot, the abdominal muscles are activated to pull the chest around and
maximize power. The knee ipsilateral to the throwing arm is brought through flexed and high so that it can quickly follow
through and block forward momentum just short of the scratch line. This action should square off the body in the direction
of the throw so that a sidearm throw, which generates supraspinatus and teres minor shoulder strain, is less likely to
occur.
The elbow must lead the hand in the throw. If the arm is too extended, torque is generated through the elbow. Medial
epicondylitis at the elbow is the most common javelin injury and can be prevented by flexibility and proper technique.
Physical examination of this injury demonstrates tenderness over the medial epicondyle and common flexor wad at the
elbow, and pain elicited on resisted palmar flexion of the wrist. Treatment includes nonsteroidal antiinflammatory
medication, epicondylitis straps, and, if symptoms continue, local cortisone injection or iontophoresis. Surgery is
performed only in recalcitrant cases.
There are two popular styles in approach, a smooth, fast Finnish style ( Fig. 41.16A), and a more hopping American style
(Fig. 41.16B). In the Finnish style, cross-stepping is low, and a front facing position is generated in the throw by strong
abdominal muscles. The throw is made over a rigid and fully extended contralaterally planted foot. While approaching the
final steps, a series of rapid crossover steps are utilized, turning the feet slightly to the side of the throwing arm and
obtaining a strong throwing position. This hinged-type approach allows progressive and steady acceleration.
FIGURE 41.16. Javelin. A: Low cross-stepping Finnish style uses abdominal muscles in the throw. B: The American
approach uses a high cross-step style and a throw in which the shoulders are perpendicular to the direction of throw; this
can lead to shoulder impingement and elbow medial capsular injury.
American athletes, used to throwing a baseball from center field, have developed a cross-step style of throw. In this
crossover step, the shoulders are in line with the direction of the throw, and the head and feet are turned approximately
45 degrees to the throwing side while the upper body is turned 90 degrees. This style is less energy efficient than the
Finnish style and leads to more shoulder injuries because of the torque generated to the upper extremity.
The speed of the approach is related to the athlete's mastery of technique. Too quick an approach will not allow
coordination of arm and leg motions so that misstep and related injury occur. If the approach is too slow, power
generation is significantly decreased. Nevertheless, the speed of approach is optimally related to the style used.
The angle of release of the javelin is optimal at 35 degrees. In elevating the tip of the spear while producing acceleration,
tremendous stress is placed on the AC joint. If technique is not properly executed or if there has been some prior injury to
the shoulder or elbow joint, stress to the AC joint is increased, and a sprain of its capsule or disk is common.
Throwing motion must be well rehearsed. It occurs in four stages, and most important in preparing for the throw, there
appears to be a sequential activation pattern of muscular activity. The deltoid fibers fire first, followed by supraspinatus,
infraspinatus, teres minor, and finally culminating with subscapularis activity ( 56). If a throw is not made near the center
of gravity, an imbalance will occur, and strain to any of these muscles can develop, depending on which phase of activity
is stressed. A late release can pull on and detach the biceps base, causing a SLAP lesion ( 57). With imbalance of the
rotator cuff muscles, scapular strain or subscapular bursitis can occur. Any sporadic motion in the throw may lead to a
glenoid labrum tear (58). Without proper warmup, a strain of back muscles and triceps is extremely common in the javelin
thrower because of torque on these muscles. Insufficient warmup also leads to impingement and elbow injury.
The most common shoulder injury in javelin throwers is impingement (59). Chronic impingement syndrome of the
shoulder, from repetitive javelin throwing, results in the development of bursitis and supraspinatus tendonitis.
Impingement syndrome is described in detail in Chapter 53. Treatment focuses on avoiding this provocative maneuver,
strengthening the rotator cuff musculature to enhance depression of the humeral head, and the administration of
antiinflammatory medications. Nonsteroidal antiinflammatory medications are most commonly used. Cortisone injections
are used in more severe cases. Continuance of rotator cuff irritation with the development of bursitis and tendonitis can
eventually lead to full-thickness rotator cuff tearing. This is diagnosed by loss of strength with pain on resistive
maneuvers of the supraspinatus. Full-thickness rotator cuff tears are treated surgically. The bursa is also swollen initially
and later becomes fibrotic, in either case, interfering with its normal gliding and lubricating function ( 60). Maintaining cuff
strength, elbow and shoulder flexibility, and using proper technique will decrease incidence of this injury.
Stress fractures involving the olecranon have been reported in javelin throwers (61). These injuries are due to a forceful
avulsion force applied by the triceps during the throwing mechanism. These fractures have been treated operatively and
nonoperatively. There is, however, a high risk of delayed union and nonunion with this injury, and some authors
recommend open reduction and internal fixation of these fractures.
Fingertip lacerations are common because of abrasion against the normal rotation of the grip cord at release. Limiting the
number of practice throws so that fatigue does not set in minimizes such injury. Fatigue-accentuated erratic motions
result in injury. In sudden deceleration at the end of the run, athletes must strive for control. In attempting to decelerate
momentum while turning inward on a planted and slightly flexed knee, anterior cruciate ligament sprain can occur.
COMBINED EVENTS
The Pentathlon was first staged during the 18th Olympiad in 708 B.C. , and consisted of five events: jumping, discus,
javelin, running, and wrestling. The first three events were only held as part of the pentathlon, while running and wrestling
were also individual events. In 1851, the men's Pentathlon, consisting of the high jump, long jump, 36-pound shot put,
880-yard run, and 55-foot rope climb, was introduced into the modern Olympics. This was changed to the Decathlon in
1904 with four running events, three jumping events, and three throwing events occurring over 2 days. Day one consists
of the 100-meter dash, long jump, shot put, high jump, and 400-meter dash. Day two consists of 110 meter high hurdles,
discus, pole-vault, javelin, and 1,500-meter run. The first women's combined event was held in Germany in 1928 and was
also called the Pentathlon. It was held over 2 days and became an Olympic event in 1964. The International Amateur
Athletic Federation changed this women's event to the Heptathlon in 1981, which entered Olympic competition in 1984.
The first day of this event includes 100-meter hurdles, shot put, high jump, and the 200-meter dash. Day two consists of
long jump, javelin, and 800-meter run. A High School Decathlon has been devised for boy's track in various forms. Some
have reduced events to six or eight; others have decreased distance by 25%. The events have included modifications
such as using 39-inch hurdles, a lighter discus, a 12-pound shot, a 1,200-meter run, and a football throw.
No one is quite sure how the ancient events were scored. The modern combined events are scored by a complex system,
introduced in Germany. Each component of the combined event is worth between one and 1,000 points, with the
1000-point level being the world record for that event. The significance of Bruce Jenner being the first to break the 8,500
mark, scoring 8,538 points in the 1976 U.S. Olympic track and field trials, cannot be overstated.
The combined events require skill, speed, strength, stamina, and determination. Mental staleness must be avoided.
Different coaching theories have evolved as to whether the athlete should emphasize his or her strongest or weakest
events during training. There are no unique injuries in these combined events, because the athlete is susceptible to any
injury that commonly occurs in each of the individual components. The increased number of events leads to increased
incidence of injury. Attention to detail, toning many different reflex patterns, is the key to success. In addition to practice
of the actual events, weight work is required: high repetition and light weight for sprinting, and low repetition and heavy
weight for the power events. Thirty to forty hours of overall training per week may be required. An hour of stretching, light
jogging, and setting markers for the jumping events must be used before competition. The ability to perform depends on
the athlete's perception of how burnt out he or she feels following competition. Some may be effective once a month;
others may be limited to four competitions per year.
CONCLUSIONS
Effective track and field techniques are seen to be dependent on proper form. Each facet of form must be individually
emphasized and individually developed to maximize efficiency. Performance hinges on practice and perseverance.
Without attention to detail, injury is common.
Proper form maximizes efficiency of energy use. Through technique, use of the body's own energy-amplifying system can
be maximized. Crossed-extensor amplification of energy stored in eccentric contraction becomes the basis of competitive
performance. Maximal efficiency is only possible by keeping the musculotendinous unit healthy. Injuries heal with
scarring, and scar tissue lacks contractility and energy storage potential. Therefore, to maximize performance, injury must
be minimized.
In speed technique, injury is commonly related to avulsion or disruption of cold or fatigued fibers. Injury in track and field
is more commonly due to training error. Breakdown of tissue related to repetitive microtrauma leads to a decrease of
performance ability but can be minimized by proper training technique. To train while injured invites further injury.
The musculotendinous unit is particularly at risk in athletic performance. Individual fibrils, if fatigued or cold, will become
brittle and easily break down. Keeping fibers warm by stretch and warm-up prior to activity will decrease incidence of
breakdown. Strength and flexibility further maximize performance and proper technique while decreasing incidence of
injury.
The athlete, coach, trainer, and physician must work together to treat the injury early and aggressively to minimize
sequelae. Training errors must be identified early and eliminated, if possible. The use of proper equipment and
maintenance of that equipment is necessary to help avoid injury, as is policing the area where athletic competition occurs
to prevent misstep, strain, and sprain injury. Training must be approached gradually and seriously to avoid injury and to
maximize performance.
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42 Triathlon
42
TRIATHLON
MARY L. O'TOOLE
THOMAS K. MILLER
W. DOUGLAS B. HILLER
Injuries
Incidence of Injury
Anatomic Location
Type and Severity of Injury
Injury Prevention
Technique
Conditioning
Training and Racing Schedules
Treatment of Injuries
Tendinitis and Tendinosis
Stress Fractures
Inflammatory Pain Syndromes
Back Pain
Summary and Conclusions
Chapter References
The triathlon is an endurance competition made up of three events done sequentially with little or no rest between race
segments. By definition of the International Triathlon Union, the world governing body for the sport of triathlon, the sport
consists of an open water swim, a bicycle race on roads, and a run on roads ( 1). Race distances vary and finish times
range from approximately 30 minutes to several days ( Table 42.1). Although the Ironman distance race is perhaps the
most well-known, races of Olympic distance or shorter are by far the most popular, representing 97% of racing
opportunities.
TABLE 42.1. STANDARD DISTANCES FOR TRIATHLON COMPETITIONS (MILES)
Since the first modern triathlon competition (San Diego, USA, 1974), interest in the sport has steadily risen so that
currently there is worldwide participation by millions of amateurs in thousands of events annually ( 2). The sport continues
to show remarkable growth. In 1998, the number of individuals participating in at least one triathlon sanctioned by USA
Triathlon (national governing body in the United States) increased by 20% over the previous year. There is also
high-level competition by professionals in world championship events, including the 2000 Olympic Games.
This chapter examines the types of injuries seen in triathletes, their incidence and causative mechanisms, strategies for
prevention, and treatment plans to minimize recovery time for the triathlete. The medical consequences of multisport
training and competition are examined for the primary care physician.
INJURIES
Triathletes sustain both traumatic and nontraumatic overuse injuries. The latter account for 80% to 85% of
musculoskeletal injuries to triathletes, with the overwhelming majority (more than 75%) of these occurring during training
(3). Although many athletes and medical personnel believe that training in multisport activities (e.g., triathlon) reduces
the chance of injury because of a more even distribution of loads on individual musculoskeletal structures, this theory has
not been borne out in training-injury studies. The incidence of injury among triathletes during any given training period
appears to be high.
Incidence of Injury
The exact incidence of injury is difficult to ascertain. Information on injury has typically been gathered from triathletes who
volunteer to answer training and injury questionnaires. When large groups have been given the opportunity to participate,
the rate of return of questionnaires has varied from 29% to 78%. Therefore, it is difficult to make comparisons across
studies or to know whether samples were biased by a higher rate of return from those who had sustained injuries than
from those who had not. Other problems inherent in self-report surveys of injuries include different definitions of what
constitutes an injury (e.g., reducing training, stopping training, needing medical attention), differences in grading the
severity of injury, potential inaccuracies from diagnostic categorizations of injury made by nonmedical personnel, and
different time frames for the surveys.
Of the 14 studies found in the literature reporting on injuries to triathletes, only one ( 6) was a prospective study. In this
study, the incidence of training injury for 155 triathletes was 37% during only 8 weeks of training. The other 13 studies
were retrospective, self-report questionnaire surveys ( Table 42.2). The reported incidence of injury ranged from 49% to
91%. The largest study (n = 2,438 triathletes) reported incidences of specific injuries, but not an overall incidence of
injury (W.D.B. Hiller, M.L. O'Toole, and P.S. Douglas, unpublished data, 1989). Seventy-nine percent of the participants
in that study reported having at least one injury to the lower extremity below the knee. Therefore, the overall incidence of
injury was probably greater than 79%. Levy et al. ( 7) compared the incidence of injury of triathletes with that of swimmers,
cyclists, and runners. Their data suggest that triathletes are injured more frequently per training hour than either
swimmers or cyclists, but not as often as runners. Amid these high injury reports is an encouraging statistic from Williams
et al. (8), who reported that 68% of the triathletes they surveyed believed that previously incurred injuries improved
during their involvement with triathlon training. Although triathletes in these surveys were heterogeneous with respect to
triathlon experience, skill levels, training distances, and competitive distances, no clear association was evident between
any of these factors and injury. Similarly, no relationship between gender and overall incidence of injury was reported.
Some specific injuries, however, were more common in men or in women (see later discussion).
TABLE 42.2. SUMMARY OF THE RESULTS OF STUDIES REPORTING ON INJURIES TO TRIATHLETES
Anatomic Location
Just as an accurate incidence of injury is difficult to determine, it is also difficult to accurately identify the anatomic sites
most frequently injured. Different methods of defining and grouping injuries make comparison among studies difficult. For
example, knee injuries are reported as a separate category, but also in combination with thigh injuries, lower leg injuries,
or lower extremity injuries. Another problem is that, although most studies asked participants for any triathlon-related
injuries, others asked for only the triathlete's worst injuries ( 9,10).
Nonetheless, it is possible from the available information to develop a general picture of anatomic sites likely to be
injured. Structures in the lower extremity appear to be involved as much as 85% of the time ( 9,10). The knee was
identified as the most commonly injured site by several studies ( 10,11 and 12), but none of these reported percentages of
knee injuries. Other studies reported that anywhere from 14% to 52% of the injuries were to the knee ( 13,14). The back,
however, accounted for 7% to 72% of the injuries in various groups of triathletes ( 9,15). The foot and ankle were reported
to be involved 4% to 61% of the time (15,16). Other anatomic sites mentioned in the surveys were the shoulder (3% to
14%), hamstrings (4% to 26%), quadriceps (3% to 13%), Achilles tendon (3% to 21%), hip or groin (5% to 11%), and
neck (4% to 6%). In two of the studies, 23% of the injuries did not fit into well-defined anatomic site categories and were
classified as miscellaneous ( 9,10).
The most common pattern was for athletes to report having sustained multiple training injuries (1.5 to 3.5 injuries per
athlete) (6,10,14,15). However, this information is also difficult to interpret because time frames for the surveys varied
from 8 weeks to a lifetime of triathlon training. Additionally, no information is available about the potential relationship of
one injury to another. From the survey information, there is no way to know whether each injury was an independent
event or whether initial injuries contributed to subsequent injuries. Although it is difficult to identify a particular structure
most at risk for triathlon training injury, it seems clear that any of the musculoskeletal structures involved in swimming,
cycling, or running are potential sites of overuse injury. There does seem to be general agreement that the lower
extremity and the back are most susceptible to cycling and running injuries, respectively, and that the shoulder is the
most common site of injury during swimming.
Type and Severity of Injury
The types of injuries seen in triathletes are similar to those seen in swimmers, cyclists, and runners. The severity of the
injuries varies from nuisance to significant. Ireland and Micheli ( 9) reported that the average training time lost because of
injury was 3 weeks, while O'Toole et al. ( 12) reported the average time lost to be 2 months. In some cases, injury was
dealt with by altering rather that stopping training. Approximately 75% of the injured triathletes studied by Ireland and
Micheli (9) and by Wilk et al. ( 17) reported changing their training regimen because of the injury. Only 20% of those
studied by Williams et al. ( 8) indicated that their injuries were severe enough to stop training or withdraw from a race.
This disparity may be the result of varying definitions of injury, or it may be that there is wide variation in how individual
athletes deal with their injuries. Vleck and Garbutt ( 14) reported that training time lost depended on which of the triathlon
disciplines the injury was attributed to; run injuries resulted in the most days lost to training, and swim injuries the least. In
their prospective study, Korkia et al. ( 6) reported that 78% of injured triathletes had to temporarily stop running, while
37% and 21% of those injured had to stop cycling and swimming, respectively. During the short period studied (8 weeks),
16% of those injured had to temporarily stop all triathlon training. Vleck and Garbutt ( 14) reported that club triathletes lost
more training time to injury than did either developmental or elite triathletes. Ireland and Micheli ( 9) reported that 51% of
the worst injuries recurred within a 1-year period, so the interpretation of data on training time lost may be as
straightforward as it seems. It would appear that getting triathletes to allow injuries to heal thoroughly before returning to
full training is the largest challenge facing the physician.
The following sections detail the expected incidence and natural history (with unspecified treatment) of injuries that
commonly occur in triathletes. Unless otherwise referenced, the information is from a large (n = 2,438) sample of Olympic
distance triathletes surveyed by Hiller, O'Toole, and Douglas ( unpublished data, 1989).
Tendinitis is a commonly reported problem, accounting for 15% to 21% of triathlete injuries ( 6,9,10). Achilles tendinitis
was reported by 21% of triathletes, with men being more susceptible than women. Vleck and Garbutt ( 14) reported that
the average number of days lost to training as a result of Achilles tendinitis was 54 days. Because their survey covered a
5-year training period, it is difficult to know whether this figure represents days lost because of one bout of Achilles
tendinitis or cumulative time out of training as a result of recurrent episodes over the 5-year period. Knee tendinitis (both
patellar and popliteal) was reported by 19% of triathletes. Although 80% of these recovered in 3 months, 12% progressed
to a chronic problem. Knee tendinitis appears to be more common in women. Tendinitis in the foot (7% incidence) can be
expected to get better in 86% of those injured within 3 months; 9%, however, may have lingering problems. The
incidence of ankle tendinitis is similar (6%), but it takes longer to heal (82% recover in 6 months) and more triathletes
continue to have problems (chronic problems in 15%). Although supraspinatus tendinitis has been reported to be
common in swimmers (18), Migliorini ( 13) reported that the incidence in triathletes was 3%. No information could be found
on its natural history in triathletes.
Stress Fractures
Some 24% of female and 17% of male triathletes can expect to sustain a stress fracture. The most common sites are the
foot and ankle complex (10%) and the lower leg (7%). Although stress fractures of the hip, pelvis, and spine were
reported, they were uncommon (less than 1%). The reasons for the high prevalence of stress fractures in triathletes are
unknown.
The knee is the site of two common inflammatory problems: patellofemoral dysfunction and iliotibial band (ITB)
syndrome. The former affects 14% of triathletes and may be difficult to treat successfully. Sixty-eight percent of the
triathletes reporting patellofemoral syndrome recovered in 3 months, but for 20% this became a chronic, nagging injury.
ITB syndrome affected 10% of triathletes responding to the survey, 80% of whom recovered within 3 months. The
condition was chronic in 12%, some of whom required surgery to resolve the problem. Both of these knee syndromes
were significantly more common in women than in men.
Shin splints (medial tibial stress syndrome) was reported by almost half (43%) of the 2,438 triathletes surveyed. Most of
these (93%) also reported that they had recovered in 3 months. Shin splints developed into a chronic condition in 4%.
Plantar fasciitis can be expected to occur in approximately 15% of triathletes. This can be a nagging problem, with only
73% of those affected reporting complete recovery in 3 months, and 9% continuing to have chronic problems.
Back Injury
Low back pain appeared to be as ubiquitous in triathletes (62%) as it is in the general population. However, 73% of the
low back pain injuries reported were mild and had a minimal effect on training. Fourteen percent reported their back pain
to be severe, but not severe enough to completely stop them from training, although training was modified until back pain
resolved. Ninety-six percent of those with low back pain reported that swim training either had no effect on the back pain
or improved it. Thirty-two percent reported that run training made it worse, as did cycling for 20%. Fifteen percent of the
triathletes sampled reported having sciatica with or without back pain. As with low back pain alone, 98% reported that
swimming either did not affect the sciatica or made it better. Thirty-seven percent reported that running made it worse,
and the relationship of cycling training to sciatica was unclear. Nine percent reported back pain that was severe enough
to interrupt training, and 3% required hospitalization.
Traumatic injuries to triathletes are almost always the result of falls during cycling or running. The shared mechanism for
traumatic injuries is the application of a force that exceeds the inherent tensile strength of a tissue, usually bone or
ligament. The cause of many overuse syndromes is far less clear: although the shared mechanism for this
heterogeneous group of injuries to triathletes is repeated microtrauma, exact causes are hard to identify. The most
common exercise-related causes of microtrauma are repeated impact on bone and excessive eccentric loading of the
musculotendinous unit. This frequently manifests as local tissue destruction followed by an inflammatory response, pain,
dysfunction, and ultimately an overuse syndrome. Intrinsic factors such as body malalignment or poor biomechanics may
contribute to the development of injury, as may extrinsic factors such as training errors or use of improper equipment.
The development of an overuse syndrome usually occurs over an extended period, but it may also result from a single
inappropriate training session. Although the term “training error” is commonly used, it is difficult to define. Practices that
may be appropriate for one athlete may be an “error” for another. Training practices commonly associated with injury
include abrupt changes in training (e.g., increasing mileage too quickly) and excessive amounts of a particular type of
training (e.g., too much speed work or hill training). Swim practices by triathletes that have been implicated in the
development of overuse injuries include too much distance or pace and being too aggressive with leg kicking. Common
cycling errors include excessive distance, speed, or hill riding. Gradual increases in distance, speed, and amount of hill
training can minimize the incidence of overuse injuries resulting from these factors. Inappropriate gearing (pedaling in
gears that are too high) is another cycling error. Riding in too high a gear causes very high forces to be transmitted
through the patella, with resultant compression of the articular cartilage and subchondral (patellofemoral) bone pain
(4,19).
Run training errors by triathletes are similar to those of single-sport runners and include excessive distance, pace, hills,
and inadequate stretching, particularly of the posterior calf muscle and hip flexors. In their prospective study, Korkia et al.
(6) found no association between time spent running on hard versus soft surfaces and incidence of running injury. As
with cycling injuries, increasing mileage, speed, or hill training too rapidly is frequently sited as the precipitating factor in
the development of overuse injuries associated with run training. Korkia et al. ( 6), however, found no evidence of an
association between injury and increases in training load, even though training loads were increased by approximately
37% during a 6-week period. The reason for this finding is unknown, and it might have been reversed if the triathletes
had been observed for longer than 8 weeks. Migliorini ( 13) suggested that former swimmers and cyclists may be at
greatest risk for development of running injuries during triathlon training because they “lack running experience and
sufficient muscle elasticity.” No data are available to confirm or refute this hypothesis.
Cipriani et al. ( 4) suggested that in addition to the usual mechanisms of injury seen in single-sport runners, triathletes
may be at risk for cumulative stress injuries. For example, when posterior calf muscles and the Achilles tendon are
stressed by excessive plantar flexion during swimming and by repeated force production during cycling, it may take far
less stress during running to cause an overuse injury in a triathlete than in an athlete who trains only in running. In
support of this theory are the data of Massimino et al. ( 10), which show a greater incidence of foot, ankle, and Achilles
tendon injuries among triathletes who do not routinely stretch before cycling or running or after swimming. This
cumulative stress theory deserves more investigation.
Improper biomechanics may also put the triathlete at risk for an overuse syndrome. In swimming, improper stroke
mechanics, particularly in relation to trunk and head movement (body roll) have been implicated ( 20). Common errors in
swim stroke technique of triathletes include having the arm enter the water too far across the midline and having a pulling
action that is too deep ( 19). In the former case, subscapularis bursitis is likely to occur; in the latter, supraspinatus
tendinitis is often the outcome ( 19). Proper setup of the bicycle is critical to maintaining appropriate biomechanics during
cycling. Factors that should be considered include saddle height and position, stem height and position, angle and
inclination of handle (aero) bars, pedal position, and angle of saddle inclination ( 4). Improper positioning, such as having
the foot in a “heel-in” or “heel-out” position or having the seat too high or too low, may predispose the triathlete to an
overuse injury by changing the forces across the knee joint. A heel-in position may result in ITB syndrome, and a heel-out
position may cause patellofemoral pain ( 19). Low back pain or neck pain may result from improper seat position. A seat
that is too high may cause bilateral facet joint dysfunction, while one that is too low may result in muscular dysfunction, a
reflection of the riding position's being too cramped ( 19). Manninen and Kallinen ( 16) suggested several reasons why an
aerodynamic cycling position might contribute to the development of low back pain, but their data do not support their
speculations with a significant association ( p = .065) between positioning and low back pain. Poor run biomechanics,
including heel contact, amount of forward lean, symmetry of arm swing, pelvic motion, and step length, may contribute to
the development of running-related injuries in triathletes ( 4). Additionally, abnormal sole, heel counter, and midsole wear
of running shoes may contribute to the development of overuse injury. Achilles, ankle, foot, or patellofemoral tendinitis;
ITB syndrome; or stress fractures may result from poor running biomechanics or footwear ( 19).
INJURY PREVENTION
Prevention of triathlon training injuries should not be different from that in other sports. The hallmarks of prevention are
proper technique, proper conditioning, and appropriate training and racing schedules. The unique aspect of triathlon
training, however, is that a triathlete must consider each of the component activities (swim, cycle, run) not only as
separate entities, but also as cumulative tasks.
Technique
Attention to swimming and cycling technique, particularly at the beginning of triathlon training, is essential for subsequent
injury prevention. Because approximately 20% of triathletes come to the sport of triathlon with a swimming background
and only 10% with a cycling background, proper techniques need to be developed in these activities. Toussaint ( 21)
reported that triathletes were far less efficient during swimming than competitive swimmers, suggesting that stroke
mechanics were poorer and could perhaps contribute to the development of overuse injuries. A triathlete who does not
have a swimming background would be well advised to join a master's swim club or otherwise enlist the aid of a swim
coach to develop proper swimming technique before worrying about training distance and pace.
Similarly, triathletes who are unfamiliar with competitive cycling should enlist the aid of a qualified bike shop to help with
the proper setup of the bicycle. In most cases, poor biomechanics that may predispose a triathlete to overuse injury can
be avoided simply by correcting the cyclist's position on the bicycle ( 19). Educating the inexperienced triathlete to use a
practice of spinning in light gears rather than using heavy gears is another effective preventive technique ( 4).
Technicians at a good bike shop can also educate the triathlete about bicycle safety, which is important in the prevention
of traumatic injuries (4). For example, proper technique in gluing tires to the rim is essential to avoid having the tire roll
off around sharp corners. A good bike shop can also advise the triathlete about proper tire inflation; for example, in wet
conditions tires should be underinflated to give the athlete more control on the road ( 19). Wearing an approved hard shell
helmet is an obvious but sometimes overlooked practice that is crucial for prevention of serious cycling injuries.
Changing the mechanics of running is more difficult. Careful attention to choosing appropriate running shoes is essential
to prevent running-induced overuse injuries. Shoes should fit properly at the toe box and at the heel counter. Semicurved
lasts are recommended for individuals with a rigid foot, while a straight last is better for an overpronating foot ( 22).
Taunton et al. ( 22), whose research showed that 60% of a shoe's shock absorption is lost after 250 to 500 miles,
recommended that runners replace their shoes within that interval. There is no reason to believe that triathletes should
not do this as well.
Conditioning
The specific physiologic demands of triathlon vary with the length of competition and are reflected by some variations in
training practices (Table 42.3). The actual amount of training done by an individual triathlete is based on athletic
background and current training status. For optimal triathlon performance, both central (mainly cardiovascular) and
peripheral (mainly musculoskeletal) conditioning and adaptations are necessary. The central adaptations result from
nonspecific endurance conditioning, occur as long as the load on the heart is adequate, and are not likely to cause
overuse injury (23). Because the peripheral musculoskeletal effects of training are specific to the training mode,
triathletes must swim, bike, and run in amounts appropriate to the anticipated competitive distances. Migliorini ( 13)
suggested that to prevent injury the triathlete should aim to improve muscle elasticity through plyometric training and a
focused stretching program. Others ( 4,9,10,16) have also advocated stretching to prevent injury. However, because of
the retrospective nature of the survey data available on training practices and injury, it is not possible to determine
whether a stretching program is indeed important for injury prevention. Prospective studies should be done to investigate
this question.
TABLE 42.3. AVERAGE WEEKLY TRAINING PRACTICES (MEAN ± S.D.)
During a triathlon season, individual triathletes rarely maintain a static training schedule. Most attempt to increase
training distance or pace, or both, during the course of a season. Some evidence suggests that these increases in
training can be a more important precursor to overuse injury than the actual distance or pace ( 4). According to triathletes'
perceptions, the majority of injuries result from an increase in training mileage, rather than from the actual mileage. A rule
of thumb that has been suggested for training progression is that no aspect of training should increase by more than 10%
at a time. That is, if distance is increased, pace should be kept the same or increased only slightly to keep within the
overall 10% limit. Although 10% is an arbitrary value that has not been subjected to scientific appraisal, it appears to be a
useful measure. The triathlete, however, should consider not only the increment within a given activity but also the
cumulative effect. For example, both Cipriani et al. ( 4) and Massimino et al. (10) suggested that a cumulative effect of
stress on particular structures (e.g., Achilles tendon) may predispose the triathlete to overuse injury. So, although it
would intuitively seem to be acceptable to increase swim and run training concurrently, this may not be the case;
likewise, and perhaps easier to understand, concurrent increases in run and bike training would not be acceptable. There
are no studies addressing this important issue or offering scientifically based guidelines.
Training and Racing Schedules
Little information is available regarding the influence of training or racing schedules on the development of overuse
injuries. Because triathletes train concurrently in swimming, cycling, and running, identifying a training schedule or
pattern associated with injury is difficult. In fact, because the onset of overuse injury is often insidious, tying an injury to a
particular training incident or even to a particular sport can be difficult. Most studies have failed to find a close
relationship between training practices and incidence of injury. Therefore, it is difficult to suggest training or racing
schedules that will minimize the chance of injury.
However, there are a few factors that should be considered when setting up a training schedule. Not all triathletes,
particularly novices, should perform multiple workouts each day. As with other sports training, triathletes should strive to
find a balance between hard workouts and lighter workouts in each discipline and overall. Ireland and Micheli ( 9) noted
that athletes who sustained three or more injuries tended to train over longer distances in cycling and running. The
triathlete would be well advised to periodize training so that a shifting emphasis allows relatively easy workouts in one of
these disciplines while increased emphasis is placed on the other. Because of the increased stress on bones, joints,
muscles, and tendons immediately after the transition from cycling to running, Migliorini ( 13), along with many triathletes,
believed that transition training from cycling to running should not be done more often than once a week. There is no
scientific evidence available regarding the effects of transition training on injury. In one study that examined the
relationship between a triathlete's racing schedule and overuse injuries, Korkia et al. ( 6) reported that incidence of injury
was not associated with time spent in competition. Common sense, however, dictates that the triathlete allow enough
recovery time between races to decrease not only susceptibility to overuse injury but also development of the
overtraining syndrome. What that means for the specific racing schedule of an individual triathlete is unknown.
TREATMENT OF INJURIES
Basic treatment of triathlon injuries is not different from that of comparable injuries from other sports. However, there may
be additional considerations that are specific to the triathlete in terms of protecting the injury from worsening or speeding
the recovery so that the triathlete can return to training and competition. One advantage the triathlete may have is the
ability to continue to train with musculature not involved in the injury, thereby preserving some of the training adaptations.
The following methods have been found to be effective in the treatment of common triathlon training injuries.
Management of inflammatory problems involving the muscle-tendon unit and its attachment to bone require
understanding of the pathologic process involved and the fact that a continuum of damage may be present. Repetitive or
excessive (usually eccentric) load to the tendon and sheath may cause an inflammatory response in or around the
tendon. With chronic inflammation, this may proceed to scarring and cystic degeneration of the tendon. On rare
occasions, tendon rupture may be seen. When these injuries manifest as acute inflammation of the tendon or sheath they
are referred to as tendinitis or tenosynovitis; those involving degeneration of the tendon are better referred to as
tendinosis. Between these extremes is a spectrum of inflammation, microtearing, and scarring of the tendon. In all cases,
initial management requires control of the inflammatory process, reduction of load (absolute or repetition), correction of
any biomechanical abnormalities (those native to the athlete and those imposed by equipment or training) that lead to
overload of the tendon, and, finally, restoration of flexibility and strength to the muscle-tendon unit. If symptoms resolve,
load (training) can be gradually resumed. Significant scarring about the tendon or intrinsic damage to the tendon may not
respond to such measures and may require operative intervention.
Achilles Tendinitis
The classic presentation of Achilles tendinitis is “heelcord” stiffness or pain localized 4 to 5 cm above the tendon
insertion that is present at the beginning of a run, resolves or at least diminishes during activity, recurs after rest or
cooldown, and then is present on a waxing or waning basis with daily activity. It usually is not problematic during cycling
(except for hard out-of-saddle climbing in severe cases). With chronicity, discomfort increases, may not resolve with
activity, and intrudes further into nonathletic activities. Morning stiffness and pain are often present (diminishing with
stretching or daily activities). A history of uphill running (repeats) or running on very soft surfaces can often be obtained;
usually, hills are avoided in subsequent workouts. Speed training or competition in racing flats (after most prior work has
been done in training-type shoes) is not uncommon as a precipitating event. The most common contributing factors cited
are “overtraining,” functional hyperpronation, and diminished gastrosoleus flexibility ( 24).
With acute presentation, swelling and crepitus about the tendon may be seen. With chronicity, tenderness of the tendon
may be seen at the “watershed zone,” 4 to 5 cm above the tendon insertion ( 25,26). Over time, more generalized
tenderness (toward the insertion) may occur. In severe, chronic cases, narrowing of the tendon secondary to peritenon
scarring or nodular swelling of the tendon (caused by intrasubstance degeneration) is present. Passive dorsiflexion of the
foot is less than on the unaffected side, and hyperpronation is not uncommon.
In all cases, initial management involves control of inflammation by use of ice and nonsteroidal antiinflammatory drugs
(NSAIDs). Injection of corticosteroids into or about the tendon is contraindicated. Running should continue only if pain is
minimal on starting and resolves completely within a very short distance. Intrusive pain or stiffness after a workout or the
next day requires further reduction in running or cessation until no symptoms are present with activities of daily living.
Hills and interval work must be avoided until symptoms resolve completely. Cycling is usually well tolerated and may
even be used to assist in restoration of flexibility. Pool running assisted by use of a flotation vest can be substituted for
aerobic activity. Although swimming itself is not problematic (except for push-off from the wall in cases of extreme
inflammation), the chronically plantar-flexed foot posture seen during swimming and exacerbated by the use of swim fins
may contribute to compromise in the restoration of heelcord flexibility. The cornerstone of long-term management is
restoration of gastrosoleus flexibility through a stretching program ( 25,27). Use of a heel lift and, on occasion, an orthotic
device to control hyperpronation may be needed to reduce tendon load. Operative intervention is reserved for those
situations in which all conservative measures have failed and is directed to the pathology anticipated or found. Most
typically this requires release of the tendon sheath and adhesions or excision of degenerated tendon and cyst with
tendon repair (28,29). Return to competition may take up to 6 months after surgical intervention.
Patellar Tendinitis
Patellar tendinitis usually manifests with pain originating at the attachment of the tendon to the inferior pole of the patella.
It is seen secondary to excessive load in cycling, preseason weight lifting, or eccentric load in running. Cyclists usually
complain of pain related to “pushing a big gear” while climbing in a seated position. This is a common problem early in
the season, when the athlete returns to the road after a winter of indoor training. Although the cyclist may be able to
“spin,” some strength may have been lost in the off-season, and the tendon may not tolerate the same load that it could
at the end of the previous race season. Attempting to train at the same level of load or intensity without gradual
adaptation results in inflammation at the tendon origin. Use of off-season weight training to avoid this problem may itself
cause difficulties if excessive loads are used in squatting-type closed chain training. Runners complain of pain when
running downhill. This is often seen when long or steep downhills are part of training or racing (especially at the end of
long runs). In addition to pain with cycling or running, it is not uncommon to hear of pain with stair training, especially
walking down (i.e., eccentric load).
On examination, pain and crepitation at the distal pole of the patella (patellar tendon origin) is a classic finding.
Discomfort may also be elicited with squatting or the extremes of passive knee flexion. Hamstring inflexibility is an
associated finding.
Management involves reduction of inflammation (as with other tendinopathies) as a first step. Reduction of excessive or
eccentric load is subsport specific. In cycling, load can be reduced by concentration on spinning (cadence of 80 to 100
rpm) when possible or out-of-saddle climbing if necessary. Training to spin can be assisted by use of a cadence monitor
cycling computer; the ability to spin may require use of a smaller front chain ring or larger rear gear cluster. Running
requires avoidance of eccentric load (elimination of downhill running). Pool running allows “active rest” of the tendon
during the acute inflammatory phase. Complete cessation of activities usually is not required. “Brick” workouts (cycling
followed immediately by running) should be avoided and certainly should not consist of hill running. Weight training
should concentrate on lower load and increased repetitions; a short period of open-chain short-arc quadriceps exercises
may need to be substituted for squats, but eccentric quadriceps exercises at lower load are eventually necessary for
return to cycling or running ( 30). Strengthening of ankle dorsiflexors has also been reported to be of benefit ( 31).
Improvement in hamstring flexibility is essential to allow healing and prevent recurrence.
Popliteal Tendinitis
Popliteus tendinitis usually manifests as the fairly precipitous onset of posterolateral knee pain during a run with
significant (length or steepness) downhill running. The pain may be so severe on presentation that running activity must
cease with its onset. Patients complain of “deep” pain in the “back corner” of the knee. When runners are carefully
questioned, they usually report that pain is felt during early “swing-through” in the gait cycle or with weight bearing on a
partially flexed knee. Running on a banked surface or track may also precipitate symptoms. Excessive saddle height or
malaligned cleat (excessive toe-in) positioning on cycling shoes may also contribute to this problem.
Examination reveals pain along the pathway of the popliteus to its attachment on the lateral femoral condyle. Patients
often have pain only immediately after running or with long-standing inflammation. Cleat alignment on the cycling shoe,
cleat wear from walking in cycling shoes, and degree of knee extension and position over the pedal should also be
reviewed.
After control of inflammation, management involves avoidance of downhill running (uphill running is often tolerated) and
of runs on severely cambered roads. Cleat realignment and a change in saddle position to decrease tendon load should
be considered. One adjustment should be tried first, followed by the other, in small increments to reduce secondary
problems that may occur with drastic changes in bike position. Although swimming is well tolerated, use of swim fins
(especially if used to increase lower-extremity load) or long “kick” sessions may exacerbate symptoms. Recalcitrant
cases may benefit from peritendinous injection of corticosteroids. Complete cessation of running until symptoms resolve
may rarely be required. In these cases, the possibility of additional intraarticular pathology (e.g., lateral meniscus tear,
anterior cruciate ligament tear, synovitis of the posterolateral corner of the knee) must be considered.
Supraspinatus Tendinitis
In the course of evaluation and management of triathletes with shoulder complaints, a curious mix of old and new may be
seen. Because most triathletes come to the sport with a primary background in running, the shoulder injuries seen are
often those associated with training errors of enthusiasm or poor technique. A smaller group of athletes come from a
swimming background and often bring with them a history of tendinitis or bursitis that recurs with the resumption of
swimming. A number of triathletes, by the nature of the cycling component of the sport, have been involved in accidents
resulting in upper-extremity injuries (e.g., acromioclavicular separation, clavicle fracture). The contribution of the injury,
alteration of strength and flexibility after injury, and alteration of swim mechanics during recovery must be taken into
account in any evaluation and management plan.
The mere repetitive action of the swim stroke does not, in and of itself, mandate rotator cuff problems. To repeat this
action in a volume adequate to allow for competitive training does, however, require a delicate balance between
glenohumeral stability, muscle (cuff) strength, scapular mechanics, and bony anatomy. Any compromise of this balance
can lead to compression and or abrasion of the tendons (usually supraspinatus) during the swim stroke. Unlike cuff
dysfunction seen in throwing athletes (i.e., repetitive tensile load to the tendon with microtearing), swimmers often
develop true impingement of the rotator cuff.
The function of the rotator cuff is to depress and center the humeral head on the glenoid surface, in balance with stability
provided by the joint capsule. In swimming, this occurs during the recovery phase ( 32) to “set up” for arm entry (into
water) and pull-through. During the propulsion phase, the cuff, in conjunction with inherent joint stability, helps maintain
the humeral head location during load across the joint and with rotation of the proximal humerus beneath the
coracoacromial arch.
Rotator cuff problems usually appear as training load (intensity or volume) increases. Athletes complain of symptoms
associated with long workouts or repeat interval sets. Complaints are initially of a vague shoulder stiffness that resolves
with swim workout and slowly recurs. Pain is a complaint as tendon irritation worsens. There may be pain at the end of
the recovery phase of the stroke (just before progressing to hand entry) and pain during pull-through (located at the
leading edge of the acromion or biceps groove). In severe cases there may be night pain and significant stiffness. That
this occurs can be explained by the balance concept just presented. With time, a relative imbalance between internal
rotators (propulsion) end external rotators (cuff) develops. This can be exacerbated if weight training focuses only on
propulsion musculature. During a long swim workout, this imbalance becomes evident as the cuff fatigues and cannot
maintain the humeral head in appropriate position. This allows anterior translation of the humeral head, with increased
contact, load, and abrasion of the cuff under the coracoacromial arch. Any degree of anterior instability exacerbates this
anterior translation. Finally, compromise of the anterior arch (bony or functional) increases cuff abrasion. During a long
workout or with repeat intervals, scapular stability is compromised with fatigue of the serratus muscles ( 33). This allows a
“tilt” of the scapula and closure anteriorly. Bony spurring or beaking of the anterior acromion (as documented on an
“outlet” radiograph of the shoulder) may also place the cuff at risk for compression because of a compromised
subacromial outlet.
Treatment relies on relief of rotator cuff irritation, restoration of glenohumeral flexibility, improvement in rotator cuff
strength, and attention to scapular stability (particularly serratus strength). Training modifications include reduction in
absolute swim distance, decrease in repeat intervals, increase in recovery time between sets, or a combination of these
measures. Attention to swim mechanics should focus on appropriate hand entry, avoidance of crossing over the midline
with reach and entry (both of which minimize the impingement position), and learning bilateral breathing. In rare
circumstances (severe acute symptoms or very persistent cases), injection of the subacromial space is needed to control
inflammation.
Specific to triathlon, these athletes spend a large amount of their cycling time using aerodynamic handlebars. These
systems rely on an arm position of shoulder adduction, forward elevation, and internal rotation. This can lead to
increased load to the shoulder girdle (particularly the rotator cuff beneath the acromion). This additional load may
exacerbate minimal impingement symptoms. Modification of hand position, arm rotation, stem length, elbow pad position,
or the amount of time spent in the aero position (to reduce impingement loading) may be necessary to reduce symptoms.
Stress Fractures
Stress fractures occur when loads applied repeatedly to bone over a long period are such that the bone is unable to
adapt and remodel to tolerate such loads. Any stress applied to bone stimulates a process of remodeling (resorption
followed by bone formation); during training, cardiac and muscular adaptation occur sooner than the bony adaptation. If
training continues without allowance for bony remodeling to “catch up” to training loads, microfractures can occur; the
aggregate of these is a stress fracture. If bony microfailure without adequate bone formation is allowed to continue, these
injuries may progress to a “true” fracture. Any process that compromises bone quality can increase the risk for these
fractures. Female endurance athletes may be at increased risk of fracture secondary to the triad of eating disorders,
amenorrhea, and osteoporosis; there is a higher incidence of stress fractures reported among female versus male
triathletes. The high incidence of stress fractures in triathletes brings into question the protective value of cross-training.
This may be explained if the training volume in a component sport (running), although coupled to the demands of two
other disciplines, approaches that usually seen for the same individual sport.
Athletes with stress fractures usually complain of a dull pain at the stress site. This is often seen after a sudden change
in training (distance increase or addition of interval or speed work); it may be seen in the weeks after a long race or if
racing is attempted on multiple consecutive weekends. Most athletes present with a history of trying to “train through”
pain. Those with femoral shaft fractures may complain of nonspecific thigh pain; navicular fractures may involve midfoot
or low ankle pain; metatarsal fractures may be associated only with forefoot swelling. Any endurance athlete (especially a
woman) with complaints of groin or medial thigh pain should be considered for the possibility of a stress fracture of the
femoral neck. Symptoms are usually worse with load activities and diminish with rest; over time even daily activities may
be associated with pain. On examination, subcutaneous bones may be painful to pressure (fibula, midshaft tibia,
metatarsal); there may be swelling and bruising, and load across bone (femoral shaft) may cause discomfort. Any athlete
with a history or examination consistent with a stress fracture requires radiographic assessment. Initial radiographs may
be negative in early presentation, because bony remodeling (lucent areas or new bone) may not yet be seen. After 4 to 6
weeks of symptoms, most radiographs will show bony changes. If plain films are negative in the face of a strong history,
bone scans may pick up early changes. Magnetic resonance imaging may better assess those areas at great risk (e.g.,
femoral neck, tarsal navicular), especially in the acute setting.
The cornerstone of treatment of these injuries is reduction of impact activities. Low-load or nonload activities may
continue. A rule of thumb in recovery is “pain free plus 6 weeks” to resume training. Return to training should be
progressive, with scheduled periods of reduced training to allow for bony adaptation. Biomechanical abnormalities (e.g.,
hyperpronation, leg length inequality) should be addressed; this is usually done by use of an orthotic device. Muscle
imbalance, weakness, and flexibility can be corrected during this “rest” time. At-risk athletes require nutritional
assessment, may be considered for counseling if there is a question of an eating disorder, and may benefit from bone
density assessment (especially if there has been more than one such fracture). Femoral neck stress fractures carry a
high risk of complications. Tension side lesions are particularly prone to displacement and require protection by drastic
reduction of weight bearing, careful monitoring, and possibly aggressive management with internal fixation. Tarsal
navicular lesions are notoriously slow to heal and should be immobilized, followed by delayed return to weight-bearing
training. One advantage for the practitioner treating the triathlete is that this athletic population is somewhat more
receptive to alternative training modes.
Patellofemoral Dysfunction and Medial Shelf Plica Syndrome
Retropatellar and peripatellar pain is fairly common and is related to both cycling and running. A complaint of “noise” with
extensor mechanism load is not itself worrisome, but it becomes a concern when it is associated with pain, swelling, or
mechanical complaints. Athletes with patellofemoral dysfunction complain of a “deep” pain or pain behind the kneecap.
This may be associated with grinding or the sense of catching with load, especially during stair training (down), standing
from a squat, some quadriceps strengthening exercises, cycling (especially climbing hills or pushing a big gear), or
running downhill. Patients with plica symptoms have similar complaints but when carefully questioned admit or recognize
that their pain is medial peripatellar in its location. Either group may complain of swelling, popping, and the sensation of
the knee's “giving out” or occasionally being unreliable. Pain or stiffness after sitting is very common. Questions about
training (cycling terrain, run course), “brick” workouts, bike setup (gearing, saddle height and degree of knee extension,
use of clipless pedals, cleat rotation and float) must be part of history taking.
With isolated patellofemoral problems, patellar compression or extension against resistance may elicit pain. A “clunk” on
passive mobilization may be noted. Patellar instability or maltracking is often present, as is relative quadriceps weakness
and hamstring inflexibility. A symptomatic plica often can be palpated as a painful band over the femoral condylar ridge.
In addition to quadriceps weakness, atrophy of the vastus medialis is often present.
Management requires attention to muscle and flexibility imbalances, control of biomechanical problems, and attention to
training and equipment errors. Relative quadriceps weakness must be addressed but in a manner that does not further
aggravate or damage the patellar or femoral articular cartilage; vastus medialis weakness must be corrected. Hamstring
inflexibility must be restored. The goal is a quadriceps mechanism that can absorb load, allow normal (or improved)
patellar tracking, and decrease anterior compressive forces. Training should be changed to minimize anterior load and
medial knee tension. Avoidance of climbing and concentration on spinning (i.e., trying to not push big gears) are key.
Long or steep downhills should be avoided, especially at the end of long runs. If road camber results in increased medial
tension, alternate run courses should be considered; track workouts (based on direction) may also increase medial
tension, and their role in training should be reviewed. Brick workouts (cycling followed immediately by running) may need
to be at shorter total distances, especially the run distance. Weight training should be done through a painless arc of
motion with reduced load. Raising the bike saddle in 2- to 3-mm increments can decrease anterior load (knee extension
at the bottom of the pedal stroke usually has 20 to 30 degrees of residual flexion). Repositioning bike cleats to a slight
toe-in position can decrease medial (plica) load. Use of an orthotic device to reduce pronation or a medial wedge under
the cycling cleat may minimize plica irritation.
Iliotibial Band Syndrome
ITB syndrome is caused by repeated abrasion of the ITB over the lateral femoral condyle. Triathletes with this problem
complain of lateral knee pain that is fairly well localized to the lateral condyle (approximately 3 cm above the joint line)
and is made worse with downhill running or during the pedal stroke near or at terminal extension. On occasion there is
associated proximal (greater trochanter) pain. Intrinsic causes of ITB irritation are ITB inflexibility, leg length inequality,
and varus knee posture. Extrinsic causes are bike setup (e.g., saddle height too high, saddle too far back, toe-in position
secondary to cleat alignment, cleat wear causing varus posture), road camber (down side leg), and shoe wear (excessive
lateral wear).
Physical examination shows tenderness over the later femoral condyle ( 34), sometimes proximal pain at the ITB origin, a
positive Ober test, and occasionally a varus knee alignment.
Management, after control of inflammation, is directed toward reduction of ITB load. Lowering saddle height (small
increments over time), moving the saddle forward, use of a cleat spacer to correct leg length inequality, use of cleats with
rotational freedom or float, cleat realignment toward a relative toe-out position, and use of a lateral cleat wedge can be
considered. Avoidance of steeply cambered roads and downhills may also be of benefit. Physical therapy directed toward
improving ITB flexibility (proximal and distal) and use of therapeutic modalities (including iontophoresis or
phonophoresis) should be included in the treatment plan. Corticosteroid injection along the ITB or its bursa may be
attempted in persistent cases. Surgical release is sometimes used if all conservative measures fail.
Medial Tibial Stress Syndrome
Medial tibial stress syndrome, also known as shin splints, posterior tibial tendinitis, or tibial periostitis, refers to
running-related midshaft medial tibia pain. The condition usually manifests after a change in training volume, although
terrain change or use of racing flats may be implicated. The differential diagnosis in runners presenting with tibial pain
includes tibial stress fracture and exertional compartment syndrome.
Physical examination reveals tenderness to palpation along the posteromedial border of the tibia at the junction of the
middle and distal third. Hyperpronation may be but is not always present. Relative weakness (absolute strength or ability
to perform repetitions) of the anterior tibialis may be seen. Limitation of dorsiflexion secondary to gastrosoleus tightness
is present. Radiographs are usually unrevealing, although thin line of periosteal new bone along the length of the medial
midtibia may be present. A three-phase bone scan showing diffuse uptake along the length of the tibia, as opposed to a
focal area of intense uptake seen with a stress fracture, may help in the differential diagnosis ( 35). By anatomic
dissection, the site of this increased uptake is the medial origin of the soleus muscle rather than the posterior tibialis ( 36).
After ruling out the primary differential diagnoses, management consists of NSAIDs, relative rest (cycling and swimming
are not restricted), heelcord flexibility, dorsiflexion strengthening, and the use of an orthotic to reduce hyperpronation, if
present.
Plantar Fasciitis
Plantar fasciitis is usually attributed to repetitive load to the plantar aponeurosis near its attachment at the medial
tuberosity of the calcaneus that results in microtears with attempted (incomplete) repair and chronic inflammation ( 37).
The classic presentation is that of a runner with complaints of morning pain on first weight bearing, progressive decrease
in pain with ambulation (but a persistent dull ache in the heel, often described as a “stone bruise”), and recurrence of
pain on ambulation after rest or sedentary activities. Central or medial heel pain after rest is the hallmark of this problem.
Physical examination may reveal pain at the medial calcaneal tuberosity or deep in the central portion of the heel.
Side-to-side compression (squeeze test) of the heel should be performed to assess for the possibility of a calcaneal
stress fracture. Heelcord tightness ( 38,39), hyperpronation, or excessive heel varus may be noted (although the
syndrome may also be seen with a cavus foot posture). The calcaneal fat pad status should be assessed for thinning,
especially if prior treatment attempts have included multiple injections of the heel. Radiographs of the heel may show a
spur, but in and of itself this is not diagnostic of plantar fasciitis. Alterations of the bony trabeculae or medial density on a
45-degree oblique view of the heel may be seen with stress fractures ( 40).
If the athlete presents within 6 weeks after the onset of symptoms, the condition can usually be managed by restriction of
impact activities, NSAIDs, ice massage of the fascial origin, heelcord stretching, peroneal and posterior tibialis
strengthening, and cushioning of the heel. Cycling, in-water running, and swimming (so long as additional attention is
paid to heelcord flexibility after a swim) are well tolerated. The use of semirigid orthotics to support the arch and unload
any area of tenderness may help with initial return to running. Use of such a protective device should be considered for
daily shoe wear in addition to running shoes. Significant biomechanical abnormalities may require long-term orthotic use
in running shoes, and on rare occasions in cycling shoes also. In more recalcitrant or recurrent cases, symptoms may
benefit from use of a 5-degree dorsiflexion night splint ( 41) or, in some cases, a 4-week trial of casting followed by
management as for acute onset. Injection of an area of localized tenderness with an anesthetic and steroid of choice may
be considered; repetitive injection should not be a part of long-term management. Most patients become asymptomatic
but over a protracted time frame. The 5% who do not respond to conservative measures and who do not have another
cause for failure to improve (e.g., seronegative arthropathy, nerve entrapment, stress fracture) should be considered
candidates for release of the medial fascial origin ( 37,42).
Back Pain
Triathletes presenting with back pain complain of discomfort that is directly related to cycling or that presents with the
transition between cycling and running. It is rare to hear of low back pain related to swimming. In addition to muscle
spasm, physical examination should assess hamstring flexibility and leg lengths and include a careful neurologic
examination. A number of causes or contributing factors have been postulated to explain the frequent occurrence of
these problems. On the bike, an overly short top tube may result in a flexed posture and increased intradiskal pressure.
An overextended position from a long tube or very low stem may increase lumbar lordosis, result in hip flexor tightness
with training or in increased hamstring tension. Long periods spent in this position may cause difficulty with the initial
phase of running because of stiffness and poor shock absorption. Excessive saddle height may cause “rocking” during
the pedal stroke, resulting in facet or sacroiliac irritation. The bike itself may contribute. Stiff, deep-section aero rims,
high-pressure tires, and stiff frames used to maximize power transmission translate to increased shock transmission to
the rider.
Management includes proper bike fit and use of more forgiving components in training (e.g., traditional training rims,
wider tires with lower pressure). “Beam,” with their ability to absorb shock, may have a role for those with long-standing
problems. Saddle height should be appropriate to allow a smooth pedaling motion. Rehabilitation should address
hamstring inflexibility and abdominal strength. Any athlete with complaints of persistent neurogenic pain should be
evaluated for nerve compression. Lumbar stress fractures, although rare, merit radiographic evaluation (possibly
including a bone scan).
SUMMARY AND CONCLUSIONS
Diversity of training is undoubtedly a principal reason for the popularity of the sport of triathlon. The athlete must train
concurrently in three activities to be successful. Many individuals believe that with such variable training the chance for
injury is minimized, compared with single-sport training. Available evidence suggests that this may not be true and that
the incidence of injury to triathletes is relatively high. However, the majority of injuries to triathletes are nontraumatic
overuse injuries that heal with few long-term consequences to the athlete. This chapter has reviewed the types of injuries
seen in triathletes, their incidences and causative mechanisms, and strategies for prevention and treatment.
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43 Volleyball
43
VOLLEYBALL
KATHLEEN A. SWANIK
STACEY C. INGLIS
Position Requirements
Training
Shoulder Injuries
Glenohumeral Joint Injuries
Rotator Cuff Tears
Tendonitis
Nerve Pathology
Bursitis
Treatment and Prevention
Wrist Injuries
Hand Injuries
Lumbar Spine Injuries
Hip Injuries
Knee Injuries
Acute Knee Injuries
Patellofemoral Overuse Injuries
Ankle Injuries
Chapter References
Volleyball is a sport that attracts participants of all ages, with multiple levels of athleticism. Because of the specific
demands of each position, year-round conditioning programs, and various types of playing surfaces, injuries related to
volleyball can encompass a broad spectrum, ranging from acute lower leg pathologies to overuse syndromes in the upper
extremity. Acute injuries are more prevalent close to the net, sustained while performing blocking, hitting, or setting
maneuvers; chronic injuries result from faulty technique, amount of repetition, or type of playing surface. The harder
playing surfaces (wood, concrete, or synthetic floors) contribute to injuries in the upper extremity when diving for a ball,
whereas the softer surfaces (sand or grass) may predispose the athlete to lower-extremity injuries.
POSITION REQUIREMENTS
Volleyball, like any sport, has specific technical skills and conditioning requirements for each position, but all players
must be proficient at both offense and defense. The offensive positions include the setter and hitters, located in the front
row, while the defensive component of the game is the primarily responsibility of the back row. The setter is responsible
for “calling the play.” This position is the most demanding mentally and often requires additional training and coaching
instruction on volleyball strategy ( Fig. 43.1). Setters spend a significant amount of time with their arms overhead while
using the intrinsic muscles of their hands to appropriately guide the ball to a hitter or over the net. All front row players
must also block the ball at the net, often performing this maneuver in pairs. Blocking is a defensive skill that requires
quick reactive movements involving a vertical jump with the arms in full extension and fingers spread apart ( Fig. 43.2).
One back row player is responsible for initiating the defensive plays and is referred to as the defensive specialist. This
athlete dives, passes, and digs for the ball to initiate the upcoming offensive play.
FIGURE 43.1. The setter, positioned close to the net, “sets” the ball for the upcoming offensive play.
FIGURE 43.2. Blocking involves a quick vertical jump at the net.
There are additional skills specific to volleyball that all athletes must be proficient in performing. The volleyball serve
dictates the beginning of play and is performed at the perimeter of the court. It usually involves a forceful overhead hit to
achieve maximum ball speed, or the ball can be hit in such a fashion that it “floats” over the net ( Fig. 43.3) Diving is an
explosive defensive movement that requires the athlete to fully extend the body while falling to the floor to intercept and
pass the ball ( Fig. 43.4). Passing the ball is another defensive maneuver that occurs in response to the opponent's serve
or hit of the ball and is performed to set up the offensive play. This technique is usually executed in a standing or
squatting position with the athlete's arms extended and the palmar surfaces of the wrists touching. This technique is
performed in a controlled manner, directing the ball to the setter by rebounding it off the forearms ( Fig. 43.5). Digging is a
defensive technique that is similar to passing but much quicker and more explosive. The athlete is often in a squat
position, leaning forward or rotated laterally to make contact with the ball near the ground. Hitting or “attacking” the ball is
often performed in combination with a vertical jump. Because hitting is a unilateral maneuver, back hyperextension and
torso rotation occur to obtain maximum velocity on the ball ( Fig. 43.6). All of these positions require explosive,
coordinated movements, and therefore technique is crucial for both successful execution of the task and as injury
prevention.
FIGURE 43.3. The overhand serve initiates offensive play and is performed at the perimeter of the court.
FIGURE 43.4. Diving is an explosive defensive maneuver performed to keep the ball in play.
FIGURE 43.5. Passing is a controlled defensive maneuver typically performed to set up the defensive play.
FIGURE 43.6. Hitting is an offensive technique performed unilaterally with a vertical jump to return the ball over the net.
TRAINING
Physical conditioning is a year-round complement to the rehearsal of technical skills in the highly competitive volleyball
athlete. Several components are incorporated into the training regimen, including both aerobic and anaerobic
conditioning for the development of strength, power, flexibility, and endurance. In-season aerobic conditioning is
important and is typically accomplished by executing high repetitions of volleyball drills or technical activities that closely
mimic the demands of competition. In the off-season, traditional endurance training activities (e.g., running, biking,
swimming) are incorporated to maintain cardiovascular fitness. Because volleyball also requires quick, explosive
movements, anaerobic training is also crucial. This type of training often entails short sprint drills that are performed
within the boundaries of the court. Agility skills can be integrated into anaerobic conditioning, and each task is designed
to improve coordination, timing, and sport-specific muscle firing sequences.
Strength training is another component of physical conditioning that varies throughout the year. Preseason and
postseason training emphasize low repetitions with high resistance. In-season, the focus of strength training shifts to
sport-specific tasks and includes performing more repetitions with lower resistance at high velocities (explosive). Strength
training should include all muscle groups, with emphasis on isolating those muscles required for performing volleyball
maneuvers. For example, the gluteals, quadriceps, hamstrings, and calf musculature are all necessary for jumping and
explosive movements. Therefore, exercises such as the power clean, squat, and plyometric activities are often included
in the training program.
Strength training for the upper extremity varies. Competitive volleyball athletes, especially women, often present with
anterior capsular laxity in the shoulder. For this reason, proper technique and appropriate strength exercises are
necessary for the prevention of overuse injuries in the upper extremity. Traditional upper-extremity exercises may also
predispose the athlete to injury. For example, exercises such as the “lat pull-down” can be executed by pulling the bar
from the overhead position either behind the neck or in front, to the chest. Performing this exercise behind the neck
places unnecessary stress on the anterior shoulder capsule and therefore is not an advised exercise for volleyball
training. However, pulling the bar to the chest offers adequate strength training to the latissimus dorsi without placing
undue stress on the capsule. Exercises that use a straight bar also subject the shoulder to high shearing forces,
particularly if there is laxity or impingement. For this reason, dumbbell exercises should be substituted for the straight
bar, especially during the competitive season. Strength training in functional positions is also important and is often
omitted from traditional programs. Elastic tubing exercises can be implemented to condition muscle groups in
sport-specific or functional positions. These exercises can replicate hitting or serving motions while incorporating
strength and endurance training.
Power is a component of training that is emphasized in volleyball and is critical for developing explosive moves such as
the vertical jump or the overhand swing. Again, high repetitions of jump training or hitting are used. Furthermore, power
training must include the torso for optimal performance and injury prevention.
Plyometrics, or stretch-shortening exercises, are synonymous with jump training. These activities can be performed at
various levels of intensity and are very effective in improving muscle efficiency for the explosive movements that are
required in competitive volleyball. The most common plyometric exercises for the lower extremity involve multiple
repetitions of jumping on and off boxes from different heights. Resistance can be added to these tasks, making them
more challenging. Plyometrics for the upper extremity is often neglected but should also be incorporated into the
conditioning regimen to improve muscle-firing sequences of the structures that surround the shoulder. Upper-extremity
plyometric activities include variations of throwing and catching weighted balls and are progressed by increasing the
number of repetitions or the amount of weight. However, the strength and ballistic requirements associated with
plyometric training may predispose athletes to overuse injuries. Therefore, it is critical to emphasize proper technique,
slow progression, and adequate recovery if plyometric activities are to be implemented successfully as a training tool.
Flexibility training is also important for performance enhancement and injury prevention and should be incorporated into
the daily practice regimen. Static stretching should be performed both before and after practice. For optimal results, each
stretch should include two or three repetitions, and each should be held for at least 15 to 30 seconds. Lack of flexibility
has been blamed for several overuse injuries discussed later in this chapter.
SHOULDER INJURIES
The demands that volleyball place on the shoulder can be compared with those of the pitching motion; both sports
require powerful, precise, and coordinated movements performed at high velocities through the extreme ranges of motion
(1,2). For this reason, the shoulder is the joint most vulnerable to injury in the competitive volleyball athlete. Although the
shoulder girdle comprises several articulations, the acromioclavicular (AC) and glenohumeral (GH) joints are particularly
susceptible to injury.
A force that separates the scapula from the clavicle characterizes injuries to the AC joint and can be the result of acute
trauma or repetitive overuse. Acute AC injuries usually occur from the impact of a fall on a hard surface while diving for
the ball. AC contusions are common, particularly in defensive specialists. AC sprains have been classified into six stages
according to the severity of damage to the soft tissue and the amount of laxity ( 3). Accurate diagnosis of chronic AC
sprains is critical because the symptoms are similar to those of rotator cuff tendonitis. Chronic injuries to this joint result
from degeneration of the articulating surfaces and are more prevalent among older competitive athletes. Radiographs are
necessary to distinguish between an injury isolated to the AC ligament and one that also includes the coracoclavicular
ligament.
The treatment of AC sprains is determined by the severity of the injury. Typically grade I and II sprains are best treated
with rest, antiinflammatory medication, and immobilization. It is unlikely that an AC sprain above a grade II will occur as a
result of a volleyball injury. Rotator cuff strengthening exercises should be performed at 0 degrees and increased to 90
degrees of shoulder abduction. Slow progression back to overhead hitting is warranted to prevent chronic AC
degeneration.
Glenohumeral Joint Injuries
The GH joint offers little inherent bony stability and relies heavily on the ligaments and muscles that surround the
shoulder to maintain congruency of the articulating structures. The sudden impacts and repetitive loads to the GH joint
that occur in volleyball predispose these stabilizing structures to injury involvement. There are several injuries associated
with the GH joint, ranging from acute dislocations to overuse injuries such as impingement or tendonitis.
Traumatic dislocations in volleyball are usually anterior in direction because of the extreme external rotation needed to
hit or serve the ball. However, posterior dislocations can occur, particularly in defensive specialists who frequently dive to
the floor on an outstretched arm (see Fig. 43.4). Radiographic imaging should be performed to rule out detachment or
tears to the labrum as well as Bankhart or Hill-Sachs lesions. These athletes are immobilized for up to 4 weeks and
prescribed a rehabilitation program that emphasizes external or internal rotation to protect against excessive anterior or
posterior translation, respectively. If rehabilitation fails, surgical options should be considered.
Labral fraying or tears can occur in the volleyball athlete because of the acceleration and deceleration demands placed
on the shoulder; they may be acute or may result from chronic overuse. The likelihood of labral pathology increases with
excessive GH translation, instability or overloading of the biceps ( 4,5). Labral tears are often found in the anterosuperior
portion of the labrum; this is referred to as a SLAP lesion (6).
Labral tears result in pain during overhead activities. In volleyball, serving and hitting increase these symptoms. These
athletes may also present with anterior laxity. A positive Speed's test may be indicative of a SLAP lesion, but magnetic
resonance imaging (MRI) or an MRI arthrogram is recommended to confirm these findings ( 4). Conservative management
should be attempted, but surgical repair is a consideration for the competitive volleyball athlete.
Rotator Cuff Tears
Rotator cuff tears are typically the result of blocking, serving, or diving activities and can be acute or chronic due to the
progressive deterioration of the tendons. Full-thickness tears usually occur in older athletes who have had chronic
impingement symptoms. The repetitive demands placed on the shoulder can also predispose the young, highly
competitive athlete to partial or full-thickness tears ( 5,7). These tears seem to be isolated to the supraspinatus or
infraspinatus muscles as a result of the eccentric loads that obtain during the follow-through phase of hitting.
Occasionally, subscapularis tears occur when there is a strong hit or delivery of a late block while at the net.
Isolated rotator cuff tears are a challenge to diagnose accurately because they often resemble the later stages of
impingement syndrome and pain is not an accurate indicator of a tear ( 5,7). Atrophy of the surrounding musculature and
weakness during external rotation are consistent findings. MRI can be used to confirm the clinical examination. Partial
tears are initially treated with conservative management, but arthroscopic evaluation and surgery are warranted if
treatment fails. When full-thickness tears are discovered, surgical intervention is necessary for the volleyball athlete.
Instability is defined by the amount of GH translation that occurs relative to the glenoid fossa; it develops as a result of
repetitive demands placed on the capsule. Over time, volleyball athletes are particularly susceptible to acquiring anterior
GH instability. The repetitive stress from hitting or serving can cause microscopic tears to the capsule, elongating the
capsular restraints and eventually leading to anterior subluxation. Posterior instability can occur in the highly competitive
volleyball athlete because of repetitive diving to the floor.
Athletes with instability complain of pain in positions that stretch the capsuloligamentous structures involved. Anterior
instability results in pain with horizontal abduction and external rotation. Athletes with posterior instability usually have
pain while diving for the ball. Athletes with instability also complain of “dead arm syndrome” or fatigue ( 8,9). It is
important to consider that most competitive volleyball athletes, particularly women, have anterior asymptomatic laxity or
functional instability. These athletes are more susceptible to symptomatic overuse injuries as well as multidirectional
instability. They should be prescribed a preventative strength program to enhance dynamic stabilization.
Impingement syndrome is one of the most common injuries in volleyball athletes, particularly in the older athlete. It is a
result of the repetitive demands required to successfully hit, serve, and block the ball with a specific emphasis on the
eccentric loading of the rotator cuff musculature. Hitting and serving require the arm to be at maximum external rotation
and approximately 140 degrees of shoulder abduction. Contact with the ball requires immediate internal rotation and
adduction of the shoulder. This activity places high demands on the stabilizing structures of the shoulder to control the
humeral head in the glenoid fossa, particularly during the follow-through phase of hitting. Blocking the volleyball also
requires the shoulder to be in a compromising position, approximately 150 degrees of shoulder flexion with slight internal
rotation. The onset and symptoms of impingement may be exacerbated by poor biomechanics during arm swing.
There are three “progressive” stages of impingement. Stage I is defined as edema and hemorrhage, stage II as fibrosis
and tendonitis, and stage III as tendon degeneration and calcification ( 7,10). It is important to consider the
coracoacromial arch and the anatomic structures that pass through the arch while performing the evaluation. Thickening
of the coracoacromial ligament or rotator cuff tendons can result in further narrowing within this space, ultimately
compromising the efficiency of the rotator cuff and humeral head depression during shoulder abduction. This decrease in
subacromial space also reduces the amount of blood flow through the coracoacromial arch, limiting tissue healing and
further complicating impingement syndrome.
Athletes complain of pain while performing overhead activities, particularly when the arm is at or beyond 90 degrees of
abduction. Often, pain causes them to alter the mechanics of their arm swing, predisposing the joint to further injury.
Range-of-motion testing should be performed in functional positions for an accurate diagnosis. Positive tests reveal pain
in abduction, horizontal adduction, and flexion at or beyond 90 degrees. Weakness of the posterior cuff may be evident,
although athletes with significant deficits in strength should also be evaluated for rotator cuff tears.
Tendonitis
Tendonitis and impingement typically occur simultaneously in volleyball athletes. Rotator cuff tendonitis results from
chronic eccentric loading of the rotator cuff musculature during shoulder acceleration and deceleration. Injury to the static
structures also increases the demand placed on the rotator cuff as a dynamic restraint, compromising both of these
structures as GH stabilizers. Furthermore, improper positioning of the scapula and function of the surrounding muscles
often contributes to rotator cuff pathologies. Eventually, this activity combined with the demands already placed on the
cuff during the overhead positions causes fatigue and inflammation leading to tendonitis ( 5).
Repeated overhead hitting has also been blamed for a change in the delicate strength ratio between the external and
internal rotators of the shoulder. High repetitions of hitting and serving have a tendency to increase the strength of the
internal rotators while maintaining the strength of the external rotators, thereby affecting the strength ratio of the rotator
cuff. Loss of the 2:3 strength ratio between the rotators places greater strain on the posterior cuff as it attempts to
decelerate the humerus during the follow-through phase of hitting.
Tendonitis in the volleyball athlete may be related to this strength imbalance within the rotator cuff and most often affects
the supraspinatus, infraspinatus, and biceps brachii. Weakness leads to early fatigue and, ultimately, damage to the
muscle and tendinous structures. Improper mechanics, fatigue, or both can result in superior migration of the humeral
head, causing a decrease in the subacromial space, inflammation, and pain.
The role of the biceps in overhead motions is also critical to humeral head stability if any degree of instability is evident.
Bicipital involvement is the result of instability or weakness in the shoulder. The role of the biceps is minimal during an
overhead activity in the athlete with a healthy shoulder, compared to one diagnosed with anterior shoulder laxity ( 11).
Tendonitis most often affects the long head of the biceps and results from involuntary attempts to control the humeral
head during the acceleration and follow-through phases of the arm swing ( 11). If a volleyball athlete presents with
isolated bicipital tendonitis, further evaluation for instability, rotator cuff weakness, or scapular involvement must be
considered.
Athletes with tendonitis complain of pain localized to the affected muscles. These symptoms increase during performance
of overhead activities. Examination reveals weakness with external rotation as well as limitations in range-of-motion
testing due to pain. Traditional special tests such as the Speed's test and the Empty Can test assist in making an
accurate diagnosis. Treatment should include strengthening of the affected musculature in addition to a reduction in
hitting and serving activities until symptoms subside.
Nerve Pathology
The incidence of suprascapular nerve entrapment is high in competitive volleyball, compared with other overhead sports
that require similar demands on the shoulder. It has been estimated that 20% of elite volleyball athletes demonstrate
atrophy of the infraspinatus muscle because of suprascapular nerve entrapment ( 12,13). This neuropathy has been
linked to a specific skill, “the floating serve.” The object of this serve is to hit the ball with more “trajectory.” This requires
the athlete to retract the arm immediately after hitting the ball ( 12,13). The sudden deceleration force used in an attempt
to “brake” the arm places extremely high demands on the external rotators, specifically the infraspinatus muscle, and
results in stretching of the suprascapular nerve.
The neuropathies that occur in volleyball athletes have been attributed to the functional anatomy of the scapula during
shoulder movement. The suprascapular nerve is “slack” while the shoulder is at rest. With abduction the nerve becomes
taut, sliding onto the bony surface of the scapula, and external rotation causes it to be pulled medially, predisposing to
impingement against the spine of the scapula ( 13,14). Subsequent atrophy of the infraspinatus muscle decreases the
efficiency of the rotator cuff in controlling the humeral head and could result in further injury if nerve entrapment remains
undetected or untreated. Therefore, proper diagnosis is necessary. Evidence of atrophy of the infraspinatus muscle,
compared with the uninvolved side, with no difference in the supraspinatus, is a consistent finding for this pathology
(13,15). Atrophy results in strength deficits to external rotation. Ferretti found a 25% deficit in strength, when tested
isokinetically, in those athletes with posterior suprascapular nerve entrapment, compared with the uninvolved side ( 13).
Pain is not an effective indicator of suprascapular nerve pathology, but entrapment of this nerve may cause pain in the
posterior and lateral area of the shoulder. Referred pain in the arm or neck has also been described ( 13,16).
Range-of-motion testing reveals pain in all motions that stretch the nerve. Pain with horizontal adduction across the body
and in forward flexion could be indicative of nerve entrapment. Point tenderness over the spinoglenoid notch may also
elicit pain ( 17,13). Diagnostic testing should include an electromyographic analysis demonstrating denervation of the
infraspinatus muscle. These athletes may present with normal radiographic findings, but MRI has been successful for
detecting infraspinatus atrophy in this athletic population ( 18).
Conservative treatment involves positioning and strengthening the shoulder without stretching the nerve. This includes
eliminating overhead motions. Strengthening should be focused on the external rotators with special attention to isolation
of the infraspinatus muscle. Surgical intervention is rare but is indicated if a painful neuropathy is present.
Bursitis
Acute subacromial bursitis can occur during diving activities when the humeral head is forced onto the acromion. In these
instances, hemorrhage is usually present. It is recommended in the younger athlete to treat acute bursitis conservatively
but first to rule out rotator cuff tears, subluxation, and dislocation ( 10). Chronic bursitis is often the result of repetitive
humeral head migration and has been associated with impingement syndrome.
Treatment and Prevention
Methods for conservative treatment and prevention of shoulder injuries are similar. Rehabilitation should include
flexibility, strength, proprioceptive, and endurance training. Athletes who present with overuse symptoms often have
limited internal rotation and exaggerated external rotation. Therefore, a disciplined flexibility program should be initiated
that emphasizes internal rotation to resolve this deficit. Several studies have established a concentric strength ratio of
2:3 for external to internal rotation ( 19,20,21,22 and 23). Eccentric strength has revealed weakness in external rotation
and has been attributed to intramuscular connective tissue tearing and chronic inflammation due to repetitive eccentric
loading. Alterations to this ratio can offset the delicate balance of the musculature controlling the humeral head, placing
unnecessary strain on the GH ligaments and leading to injury of the static or dynamic restraints, or both ( 19,24). These
findings are important in the rehabilitation and prevention of overuse injuries in volleyball. Strengthening should focus on
only those muscles that showed weakness on physical examination in order to reestablish the 2:3 strength ratio. This
usually involves the posterior rotator cuff musculature. Both concentric and eccentric exercises should be incorporated
into the rehabilitation program. Strengthening of the external rotators begins with the shoulder in 0 degrees of abduction.
The rehabilitation specialist should remember to place a block between the body and the shoulder while the arm in is this
position, to allow adequate blood flow through the arch. Slow progression of rotator cuff exercises should include
functional positions of 45 and 90 degrees of shoulder abduction. Exercises that require muscle-firing sequences should
also be integrated, along with activities that mimic the overhead hitting activity. Plyometrics (stretch-shortening) are
commonly used in the later stages of rehabilitation and have been successful if used appropriately.
These athletes often present with some level of anterior laxity, so it is important to incorporate proprioceptive activities
into the rehabilitation program in order to reestablish joint position sense. The demands of this sport on the shoulder also
require an emphasis on endurance for the upper extremity, performing high repetitions (25 to 50) using light resistance or
elastic tubing. Lastly, overuse injuries may cause changes in the mechanics of the overhead swing due to pain.
Therefore, appropriate progression to overhead activities and evaluation of the biomechanics of these movements is
necessary.
WRIST INJURIES
Acute injuries to the wrist occur when an athlete dives onto the floor and falls on an outstretched hand. In these
instances, radiographs should be obtained immediately to rule out a fracture, particularly of the scaphoid. If there is
tenderness over the anatomic snuffbox and the films are negative, the injury should be treated as a fracture, with
splinting of the thumb and wrist for at least 2 weeks. Radiographs should then be repeated to rule out evidence of a
fracture. If the athlete is pain free and the films are negative, exercises should begin, emphasizing ulnar and radial
deviation of the wrist as well as the intrinsic muscles of the thumb. A rigid splint should be made to protect the wrist and
thumb during practice and competition. Slow progression back to serving and diving to the floor is emphasized to avoid
reinjury.
Because of the position requirements of setters, they are prone to overuse injuries in the wrist. Setting requires a
substantial amount of strength and endurance in the forearm, wrist, and intrinsic muscles of the hand, particularly in the
highly competitive athlete. The setting motion involves extreme hyperextension and radial deviation followed by a quick
movement to wrist flexion and ulnar deviation. The fingers control the ball and assist with its release; small, quick
movements from flexion into extension are used. These motions are performed with the athlete's arm in the overhead
position (see Fig. 43.1). Furthermore, setters require additional technical training for ball control, predisposing them to
overuse syndromes such as carpal tunnel syndrome or tendonitis.
Carpal tunnel syndrome is an overuse injury that results in compression of the median nerve as it passes through the
carpal tunnel of the wrist. Setters are subject to this syndrome both because of their position and repetitions required,
causing fibrosis and tenosynovitis of the flexor tendons ( 25). Repetitive diving to the floor on the wrist can also
predispose to this injury; however, this usually occurs in the older competitive athlete (see Fig. 43.4).
Athletes complain of paresthesia and pain over the palmar surface of the wrist, hand, and fingers. Depending on the
duration of symptoms and age of the athlete, the palmar aspect of the wrist may appear to be thickened. Range of motion
is limited owing to paresthesia or is limited in full flexion and extension, or both. Splinting the wrist in a neutral position
can reduce these symptoms. Prevention of the extreme ranges of wrist flexion and extension with athletic tape has also
been successful at controlling the symptoms.
Tendonitis can occur as a result of the high repetitions of hyperextension and radial deviation of the wrist. Again, setters
are more prone to this injury. These athletes complain of pain and stiffness while setting the ball. If the injury is detected
early, symptoms can be controlled with antiinflammatory medication and ice. However, athletes usually wait until
symptoms cannot be tolerated before seeking medical attention. They complain of stiffness in the morning and increased
pain after practice and in the evening. Splinting and taping should be used to limit the range of motion at the wrist,
allowing time for healing.
Treatment for these injuries begins with pain management and limitations in training. When developing a rehabilitation
program, the demands on the wrist during practice need careful consideration. These athletes usually present with tight
wrist extensors and weak wrist flexors. Therefore, strengthening of the flexor group and flexibility of the wrist extensors
should be emphasized. Finally, to achieve full recovery from these injuries, rehabilitation programs should also include
endurance and functional activities into the later stages.
HAND INJURIES
Injuries to the hand are usually traumatic and occur from blocking or hitting the ball at the net. Blocking the volleyball at
the net requires timing and appropriate hand placement. Jumping late to block the ball puts the fingers below the ball,
predisposing them to dislocations, phalangeal sprains, or “mallet finger.” The first and fifth phalanx seem to be most
vulnerable to dislocation. However, blocking also requires the fingers to be spread apart, making all the digits vulnerable
to injury (see Fig. 43.2).
Close physical examination of the collateral ligaments and radiographic assessment should be performed to rule out the
chance of a fracture. Pain often dictates when the athlete can return to competition. If the injury is isolated to the soft
tissue, the athlete's return is usually immediate, provided splinting and/or taping is used to protect the joint. It is important
not splint the third and fourth fingers together, because this predisposes the second and fifth digits to injury. The
demands of handling the volleyball necessitate both strengthening and endurance training for the intrinsic muscles of the
hand; this training should begin as soon as the joint is “stable.”
LUMBAR SPINE INJURIES
Low back injuries are prevalent at all levels of competitive volleyball and are usually related to the technical requirements
of the sport. Hitting involves quick lumbar movements of hyperextension, immediately followed by forced flexion ( Fig.
43.7) (26). If the ball and the attacker are not aligned, trunk rotation is also added to these movements, resulting in a
compromised position for the low back. The position of the defensive specialist is also demanding on the lumbar spine,
because the athlete is required to begin each play in a squat position with the arms in full extension in front (see Fig.
43.5). Explosive movements, such as diving for a ball, begin in this position, placing tremendous demands on the lumbar
area. Furthermore, high repetitions of hitting, attacking, or diving during practice and competition may also predispose
these athletes to lumbar spine injuries.
FIGURE 43.7. Hitting is often performed with back hyperextension to increase force production to the ball.
Spondylolysis refers to a defect in the pars interarticularis of the articular process of the vertebrae ( 27). It is most often
attributed to congenital weakness but may be caused by microtrauma associated with repetitive hyperextension ( 27).
Spondylolysis typically begins unilaterally, although bilateral stress fractures can cause slipping of a vertebra on the one
below, resulting in spondylolisthesis. The technical requirement to hyperextend the back while hitting the ball
predisposes the volleyball athlete to this condition. Athletes complain of sharp, localized pain over the affected vertebral
segments. Symptoms of irritation and stiffness are more prevalent after exercise. Athletes may also experience radiating
pain bilaterally to the gluteal regions if horizontal translation of the vertebra is significant enough to cause impingement
on the spinal nerves. Spondylolisthesis or spondylolysis is commonly found between the L-4 and S-1 junctions in
volleyball athletes, and may be revealed on an oblique radiograph, computed tomographic scan, or MRI ( 27). A single
photon emission computed tomographic (SPECT) scan is typically used to diagnose this condition.
Faulty mechanics or trauma to the back and its supporting structures can lead to a herniated disk and nerve root
compression (26,28). Pressure within the intervertebral disks varies with position. Although constant at standing, the
pressure increases by 33% with slight trunk flexion and by 52% as the flexion angle increases while in the standing
position (29). For this reason, the forward flexion and trunk rotation used in defensive diving and digging for the volleyball
can result in a herniated disk. Disk pathology includes central pain that radiates unilaterally to the buttocks or down the
leg, following a dermatome pattern. Forward bending increases pain, while extension diminishes it. The Cross
straight-leg test and muscle weaknesses are also indicative of a herniated disk ( 30). MRI can confirm these clinical
findings.
The sacroiliac joints are the largest articular joints in the body. Landing after a block or attack transmits forces through
the lower extremities up to the pelvis and lumbar spine. If the pelvic stabilizing muscles are unbalanced in strength or
fatigued, sacroiliac joint stability may be compromised. The constant low position required while playing defense can
cause nagging low back pain and stress to the sacroiliac joints. Pain is usually located in the posterior superior iliac
spine region and occasionally radiates into the buttocks. Sacroiliac joint pathology may be related to malalignment of the
pelvis and is common in volleyball due to the constant diving and rolling on the floor or from landing unilaterally after
hitting the ball. For this reason, it is important to check levels of the posterior and anterior superior iliac crests as well as
for leg length discrepancies. The strength and range of motion of muscles should be examined, paying close attention to
the hip flexors, hamstrings, piriformis, paraspinal, and lower abdominal muscles. Often, inflexibility of the hip flexors and
extensors affects the function of the sacroiliac joints. There are several special tests (e.g., Long Sit Test, FABER Test,
Sacroiliac Compression and Distraction Test) that can also help distinguish disk pathology from sciatic nerve irritation or
sacroiliac joint dysfunction ( 31).
Sciatic nerve pain can mimic the signs and symptoms of lumbar disk and sacroiliac joint pathology. Nerve pain resulting
from irritation or inflammation is not a pathology but rather a symptom of an underlying problem. Decreases in muscle
flexibility, particularly in the hamstrings or piriformis muscles, can put pressure on the sciatic nerve, causing irritation.
Muscle imbalances and pelvic instability can also be contributing factors to sciatic nerve pain. Athletes with sciatica
should be closely evaluated to determine an accurate diagnosis and an appropriate course of treatment.
Management of overuse injuries in the lumbar spine includes the use of therapeutic modalities (e.g., cryotherapy) for pain
and inflammation, electrical stimulation, and antiinflammatory medications. Gentle stretching and an exercise program
must correspond to the findings in the evaluation. Pelvic stabilization exercises should be emphasized in the
rehabilitation program. Strengthening and flexibility exercises vary but often include muscle groups such as hip flexors,
lateral rotators, hamstrings, abdominals, and lumbar extensors. Because of the repetitive demands required for
competitive volleyball, an endurance component for the pelvic stabilizing musculature must also be incorporated into the
rehabilitation program. Progression to low-impact activities should not be introduced until the athlete is pain free and has
reestablished strength in the affected muscle groups. Hitting, blocking, and explosive defensive movements should not
be permitted until the last stage in the recovery process. Braces that prevent extreme ranges of hyperextension or that
apply compression are sometimes helpful to reduce symptoms.
HIP INJURIES
Hip injuries are uncommon among volleyball athletes, but defensive maneuvers, including diving and rolling, can result in
hip pathology such as hip pointers and trochanteric bursitis (see Fig. 43.4). Athletes who fall directly on the anterior iliac
crest or anterior superior iliac spine while diving to dig a ball can develop a hip pointer. This contusion can produce
immediate pain, spasms, and transitory paralysis, resulting in difficulty with hip flexion and trunk rotation. Radiographs
should be obtained to rule out possible fractures. Diving on the floor and landing on the greater trochanter can inflame
the trochanteric bursa, resulting in acute bursitis. Irritation of the bursa can cause palpable pain over the lateral
trochanter and occasionally pain radiating down the leg. Care for these injuries includes pain management,
range-of-motion and strengthening exercises for the hip abductors, flexors, and external rotators as indicated. It is
suggested that the area be padded for practice and competition to prevent reinjury.
Strains to the hip musculature are prevalent at all levels of volleyball. Sharp cutting movements and explosive jumps
increase the likelihood of injury. Strains to the rectus femoris can occur while performing activities that require sudden
contractions of this muscle, such as blocking and hitting. If the rectus femoris is weak or inflexible, it is predisposed to
tears. Quick lateral movements in direction are common in both offensive and defensive players. Changes in direction
involve abrupt rotary movements at the hip, causing strains to this musculature. In our experience, the adductor longus
seem to be the hip muscle most commonly injured while playing volleyball. The athlete complains of feeling a “pull” or
“twinge” followed by pain, point tenderness, and loss of function. Deep muscle tears are more painful than peripheral
tears and result in point tenderness, spasm, and loss of function. Passive and resistive range-of-motion testing helps to
distinguish which muscle is affected by the injury.
Management of acute strains to the hip begins with ice, compression, rest, and antiinflammatory medications. If the strain
occurs in the deep muscle tissue, the athlete usually presents with an altered gait due to pain. Crutches should be used
until the symptoms subside. As pain diminishes, progressive resistive exercises and mild stretching can be introduced,
followed by low-impact activities. Straight-ahead running and sprinting drills, progressing to explosive jumping and cutting
activities, should be pain free before the return to full participation. A neoprene or elastic wrap can provide additional
support and warmth as the athlete returns to practice.
KNEE INJURIES
Acute Knee Injuries
Acute knee injuries to the ligaments or meniscus can cause significant loss of playing time ( 26,28,32). The most frequent
mechanism of injury is a rotational force to the knee when landing from an attack ( Fig. 43.8) (32). If the body and ball are
not aligned, athletes are forced to reach for the ball, landing on one leg or off balance, making them susceptible to acute
knee injuries. Acute injuries can also occur while blocking the ball. The longer the ball is in play, the more frequently the
body must pivot, resulting in fatigue and loss of balance, with an increased likelihood of injury to the knee. Passing and
digging for the ball can also subject the knee to ligamentous injuries owing to the potential for rotational forces to occur
while trying to make contact with the ball.
FIGURE 43.8. Landing patterns are often unilateral, predisposing the athlete to lower-extremity injuries.
The collateral ligaments are important components of knee stability. Sprains of the collateral ligaments in volleyball
athletes usually occur while blocking or hitting or as a result of landing off balance, on the foot of another athlete, or on
one leg (see Fig. 43.6). Sharp, sudden cutting movements performed while passing and digging could result in sprains to
the collateral ligaments. Medial collateral ligament (MCL) sprains are more prevalent than sprains of the lateral collateral
ligament (LCL). Sharp changes in direction, as seen with cutting and pivoting, cause internal femoral rotation, imposing
valgus forces on the knee and increasing the risk of injury to the MCL. Varus forces are rare and may occur only in the
event of a collision between two athletes. Symptoms include point tenderness over the ligament and slight swelling. A
varus stress test to the LCL or a valgus stress test to the MCL can be used to assess the integrity of these ligaments.
These tests reproduce symptoms and can determine the severity of damage to the ligament by the amount of joint laxity.
The anterior cruciate ligament (ACL) is important for knee stability and function, particularly in the highly competitive
athlete, and damage to the ACL is often a season-ending injury. External rotation of the tibia while the body is internally
rotated and hyperextension of the knee are common mechanisms of injury for the ACL ( 26,28,32). Blockers are
particularly susceptible to this injury because they often land on one leg, off balance, or while transitioning from blocking
to immediately attacking the ball. Defensive players can also sustain an injury while cutting sharply or diving for a ball.
Athletes who tear the ACL usually hear or feel a “pop” or “tearing” sensation followed by immediate disability. Rapid
effusion along the joint line is evident. A positive Lachman sign, anterior drawer sign, pivot shift, and jerk test are
indicative of an ACL tear (33). This injury is often accompanied by other tissue damage, for this reason an evaluation of
the posterior cruciate ligament, collateral ligaments, and menisci should also be performed. Diagnostic testing should
include an MRI to confirm the injury and to rule out additional damage to the joint. Although conservative treatment has
been successful, surgery should strongly be considered if the athlete intends to return to volleyball.
Injuries to the menisci are often difficult to definitively diagnosis. The most common mechanism of injury is a rotary force
while extending or flexing the knee during weight-bearing activities. A defensive move to dig a ball or an unbalanced
landing from a block or attack could subject the meniscus to injury. Meniscal injuries are also seen accompanying MCL
injuries and ACL damage. The MCL and coronary ligaments have attachments to the medial meniscus that anchor it to
the tibia, making it more prone to valgus or torsion injuries. The LCL is more mobile and therefore less susceptible to
injury. Athletes with a meniscal injury may complain of pain along the joint line, intermittent locking or “giving way,” pain
with squatting, and a gradual development of joint effusion. Evaluation may also reveal a positive McMurray click test.
MRI may confirm the clinical diagnosis.
Treatments for acute knee ligament and meniscal injuries begin with ice, compression, pain modulation modalities,
antiinflammatory medication, and crutches if weight bearing is painful. Unlocking the knee is necessary if the meniscus is
caught in the joint line. Conservative treatment begins with exercises that focus on the muscles providing dynamic
stability to the joint and should be performed in pain-free ranges of motion. Examples of such exercises include
isometrics and straight-leg raises. The regimen is then progressed to closed kinetic chain activities such as the mini
squat and leg kicks to increase strength. Terminal knee extension and closed-chain squats between 60 and 90 degrees
should be avoided in those athletes with ACL pathology, because these movements cause anterior translation of the
tibia, thus stressing the ligament ( 34). Proprioception and kinesthetic activities can also be initiated to improve position
sense and balance (35). Strength and flexibility of the muscles surrounding the knee are essential in providing joint
stability and include the quadriceps, hamstrings, hip adductors, hip abductors, and gastrocnemius muscles. Protective
bracing may offer some stability and decrease stress on the injured ligament when beginning weight-bearing activities,
and is suggested. The severity of the injury often dictates the progression of functional exercises. However, before full
participation, these athletes must be proficient in cutting, jumping, and digging maneuvers.
Patellofemoral Overuse Injuries
The knee is subject to overuse injuries in volleyball athletes ( 26,28,36). Jumping, landing, and deep knee squatting are
fundamental actions of the sport. Emphasis on jump training and plyometrics is evident at all levels of competitive
volleyball, because gains in vertical height improve setting, hitting, and blocking skills. These actions put stress on both
the quadriceps tendon and the patellofemoral joint. The technical requirements and repetition of passing, diving, and
digging also predispose these athletes to overuse injuries in the knee.
The most common overuse injury reported in volleyball athletes is patellar tendinitis or “jumper's knee” ( 28). Jumping to
hit or block the ball requires a high rate of force development in extension and external tibial rotation, stressing the
patellofemoral joint and tendon ( 37). Furthermore, eccentric loading of the quadriceps during landing can also
compromise these tissues. Repetition of these mechanical stresses can cause microtears, irritation, and inflammation,
resulting in symptoms of pain and swelling localized to the lower pole of the patella, followed less frequently by pain at
the upper pole or tibial tuberosity ( 38). Occasionally, weakness in the quadriceps muscle may be present. Pain seems to
increase after exercise; however, as the condition advances, pain becomes constant throughout practice. Athletes with
jumper's knee often present with deficits at full knee flexion or extension.
Patellofemoral syndrome is also common in volleyball athletes. Abnormal tracking of the patella within the femoral groove
can cause irritation of the articular surface of the patella and inflammation in the femoral groove itself. Repeated forced
extension of the knee, as seen in hitters and blockers, or the demands placed on the knees of defensive specialists can
stress on the patellofemoral joint, particularly if the patella is not aligned appropriately within the femoral groove. The
etiology behind patellar malalignment varies. An increased Q angle may result in lateral tracking of the patella and can
be further complicated by several anatomic variants such as genu valgum, genu recurvatum, patella alta, pronated feet,
wide pelvis, and external tibial torsion ( 39,40). Inflexibility of the iliotibial band and lateral retinaculum tightness or,
conversely, laxity in the medial capsular retinaculum or a weakness in the oblique portion of the vastus medialis can all
result in lateral tracking of the patella. The vastus medialis obliquus muscle seems to be most affected of the quadriceps
muscles and is subject to atrophy with knee injuries. This may occur because of inhibition or poor recruitment of muscle
fibers resulting from joint effusion ( 41). Altered timing of muscle contractions between the vastus medialis and vastus
lateralis may also cause lateral drifting of the patella ( 42). Close attention should be given to female athletes, because
they are more susceptible to these tracking abnormalities. Athletes who have patellofemoral symptoms experience pain
with jumping and squatting. Stair climbing or sitting for long periods also increases knee pain. Tightness in the
hamstrings and quadriceps groups and swelling due to patellar irritation often results in a pain-related decrease in knee
range of motion. Crepitus and a positive patellar grind test are indicative of patellofemoral stress syndrome.
Management of overuse patellofemoral injuries begins with ice and antiinflammatory medication. Close attention to
patellar tracking is necessary to rule out any anatomic abnormalities, especially in the female athlete. Exercises and
biofeedback techniques to strengthen and improve recruitment of the vastus medialis obliquus are used to improve
medial patellar stability. Patellar mobilization techniques, iliotibial band stretching, and orthotics to correct hyperpronation
are designed to reestablish lateral patellar mobility. Hamstring and quadriceps flexibility and strengthening exercises
should also be initiated. Superficial heat, whirlpools, ultrasound, and friction massage are methods frequently used to
treat patellofemoral symptoms. McConnell taping, patellar stabilizing braces, and patellar straps can also be helpful in
reduction of pain (43).
Straight-leg raises and resistance exercises in pain-free ranges of motion are initiated and are progressed to close
kinetic chain activities such as partial squatting and lunges. Eccentric strength of the quadriceps should also be
incorporated but slowly progressed into the rehabilitation program. Low-impact exercises that provide an eccentric
component include wall slides and backward stair climbing. If participation in these activities is pain free, exercises can
be advanced to explosive drills and tasks that mimic the demands of volleyball. Endurance and balance training activities
are also warranted in the rehabilitation process. If conservative treatment to reduce symptoms is unsuccessful, surgical
options should be considered.
Ankle Injuries
The most common acute injury occurring in volleyball is the inversion or lateral ankle sprain ( 26,28,36). Studies have
shown that ankle sprains account for 15% to 60% of recorded injuries in volleyball athletes ( 26,28,44). A thin line
separates players on opposing teams, and often their feet become entangled after jumping for the ball, leading to a high
incidence of ankle sprains. These injuries frequently occur when players block and land on the foot of an opponent or
teammate, particularly when blocking is performed with two front row players (see Fig. 43.2) (26,28,45). Lateral ankle
sprains have also been attributed to attacking. This maneuver involves a forward jump that, during landing, often
positions the athlete close to or over the line of scrimmage, in order to make contact with the ball.
The initial treatment for ankle sprains involves ice, compression, and elevation. The application of a horseshoe pad,
compression wrap, or support stirrup is effective to control hemorrhaging ( 46). Athletes should be kept from weight
bearing if their gait is altered due to pain, then slowly progressed to full weight-bearing activities, allowing for appropriate
tissue healing to occur. Range-of-motion and isometric exercises should immediately begin after the injury. Slow but
aggressive progression of strengthening and proprioception exercises are integrated in pain-free ranges of motion.
Functional exercises should begin with low-impact activities and advance to cutting and jumping activities. A semirigid
brace is strongly suggested when the athlete returns to competition. This brace should allow plantar flexion and
dorsiflexion but limit ankle inversion and eversion. However, tape, ankle orthoses, or high-topped shoes can also be
used to provide stability to the ankle and prevent further injury or repetitive sprains ( 28,47,48). These devices offer
stability to the ankle during weight-bearing activities while continuing to allow for functional ranges of motion; therefore,
they reduce the amount of muscular atrophy or proprioception deficit that occurs with complete immobilization. If
instability after a grade II or III ankle sprain persists after a conservative treatment protocol, surgical intervention may be
required.
Plantar fascitis is common in volleyball athletes because of the repetitive jumping requirements of the sport. The surface
and type of shoe can also contribute to this condition. Athletes who practice on hard surfaces without adequate arch
support are predisposed to plantar fascitis. Other contributing factors include a tight gastrocnemius-soleus complex, a
tight longitudinal arch, and excessive subtalar pronation.
Athletes experience pain in the anterior medial heel region. Pain is exacerbated in the morning and during jumping or
running activities. Passive dorsiflexion easily reproduces this pain. Treatment is similar to that in other sports, but with
the emphasis on jumping, these symptoms are difficult to manage in some cases.
Achilles tendonitis is another common overuse injury associated with volleyball athletes. The repetitive eccentric loads of
jumping, particularly on hard surfaces, can cause microtears within the tendon. Tight hamstrings, tibial varus, pes cavus,
and tight gastrocnemius-soleus complex may also predispose these athletes to tendonitis. Athletes complain of pain
while jumping or running that increases over time. Tenderness, localized swelling, thickening, and crepitus are indicated
on palpation. Strength testing may reveal weakness in plantar flexion. Treatment should include a reduction in jumping
activities, stretching of the gastrocnemius-soleus complex, ultrasound, and taping to reduce dorsiflexion. Strengthening is
initiated if weakness is presented on examination. A 10- to 15-mm heel lift for each shoe also reduces stress on the
tendon. As symptoms subside and flexibility increases, a slow progression back to jumping activities is indicated.
However, it is suggested to keep the heel lift in the shoes for the first 7 to 14 days of practice to offer some shock
absorption and protection to the Achilles tendon.
Rupture of the Achilles tendon can occur while playing any position in volleyball. Chronic Achilles tendonitis and constant
tightness in the gastrocnemius-soleus complex can predispose the older competitive athlete to this injury. Athletes often
hear a loud snap and experience a quick burst of pain. This usually happens during the push-off phase or while the knee
is in full extension during jumping or sprinting activities. The inability to perform a standing heel raise and a positive
Thompson test are indicative of a tear. Although conservative treatment is an option, surgical repair is recommended for
the volleyball athlete.
Peroneal tendonitis is common in volleyball athletes with a pes cavus foot. Frequent dorsiflexion and eversion
movements while setting and playing defense are the usual causes. Excessive pronation and supination could also
predispose the athlete to this condition. For this reason, gait analysis should be performed. Tenderness, inflammation,
and crepitus may be palpable along the peroneal tendons. Range-of-motion testing in dorsiflexion and eversion may
reproduce symptoms of pain. Treatment includes ice, compression, elevation, and antiinflammatory drugs for pain
management. Exercises should be initiated to strengthen the peroneal musculature. Warmup and stretching before and
after competition is also important. Arch taping, orthotics, and foot wedges can be used to aid in correcting
biomechanical abnormalities.
A peroneal retinacular tear can be debilitating to the volleyball athlete because of the amount of lateral movement
required in this sport. Tearing of the retinaculum occurs when a dorsiflexed and everted foot moves into plantar flexion
causing the peroneal tendon to sublux or dislocate. This injury is often misdiagnosed as an ankle sprain. Tenderness,
swelling, discoloration, and crepitus may be present over the peroneal tendons and lateral ankle. As the acute symptoms
subside and athletes are progressed back to activity, they complain of a snapping or popping sensation on the lateral
side of the ankle just below the malleolus while running or jumping. Resisted eversion and dorsiflexion replicate these
symptoms. Treatment should include ice, compression, elevation, and antiinflammatory medication. A horseshoe- or
J-shaped pad can be placed around the lateral malleolus in an attempt to compress the tendon and prevent it from
subluxing from its groove. Range-of-motion exercises followed by progressive resistive exercises and balance training
are implemented at 5 to 6 weeks. If conservative treatment fails, surgery may be warranted to repair the retinaculum.
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44 Water Skiing
44
WATER SKIING
ROBERT L. WALTRIP
NOELLE GRACE
Evolution of Competitive Water Skiing/Arenas of Competition

Specifics of Traditional Three-Event Competition
National and International Profile
Injuries, Mechanisms, and Epidemiology
Recreational Versus Competitive Water Skiing
Incidence of Injury
Safety, Prevention, and Conditioning
Obligations of Skier, Driver, and Observer
Equipment
Environmental Hazards
Safety Standards and Recommendations
Fitness Training and Conditioning
Specific Management of Injuries
Unconscious Skier
Near-Drowning
Hypothermia
Spine Injury
Concussion
Bleeding
Propeller Injuries and Lacerations
Fractures and Dislocations
Muscle and Ligament Strains, Sprains, and Tears
Douche and Enema Injuries
Ruptured Tympanic Membrane
Otitis Externa
Heel Contusions
Hand Callouses
Summary
Acknowledgments
Chapter References
Water skiing is an increasingly popular sport with over 30 million recreational and competitive athletes worldwide. The
sport has evolved tremendously since its beginnings as aquaplaning in the early 1900s. Ralph Samuelson has been
commonly credited with inventing water skiing in 1922 as he made the transition from the single, rectangular wooden
board called an aquaplane to a pair of self-designed independent wooden skis. After an initial trial using the curved
wooden planks from barrel staves, he ultimately fashioned his own skis from two 8 feet by 9 inch boards. Using his
mother's copper kettle, he boiled and bent the tips of the boards upward. He then secured leather straps to the boards to
hold his feet. An iron ring attached to a rope and held by the skier replaced the previous towing method of securing the
rope to the aquaplane. The day before his 19th birthday, Ralph Samuelson successfully skied across Lake Pepin in
Minnesota to become the first “water skier.”
EVOLUTION OF COMPETITIVE WATER SKIING/ARENAS OF COMPETITION
Since Samuelson's first journey, water skiing has experienced rapid growth, closely paralleling the development of leisure
boating. Most are familiar with recreational water skiing. Although competitive skiing has been practiced for decades, it is
only recently gaining greater attention. Competition water skiing officially began in 1939 with the establishment of the
American Water Ski Association (AWSA) and subsequently the first National Water Skiing Championships in Long
Island, New York. The popularity of water skiing was further increased by water skiing exhibitions in the form of show
skiing. The first water ski show was organized in 1942 at Cypress Gardens in Florida. Water skiing then gained an
international presence upon becoming an exhibition sport in the Olympics in 1972.
Over the years, several subdivisions and modifications of water ski competition have led to increased interest in the
sport. Organized tournaments in water skiing exist for classic three-event skiing, show skiing, and ski racing.
Subcategories of three-event competition exist for both collegiate and disabled skiers. Related arenas that have been
spinoffs of water skiing include barefooting, kneeboarding, and wakeboarding ( Table 44.1).
TABLE 44.1. ARENAS OF COMPETITION
SPECIFICS OF TRADITIONAL THREE-EVENT COMPETITION
Since the first national water ski tournament, the three classic events of water ski competition have included slalom, trick,
and jump skiing. Slalom skiing competition involves the participant skiing around a series of six buoys in a zig-zag
fashion at progressively increasing boat speeds and decreasing rope lengths ( Fig. 44.1). After the skier completes a pass
of six buoys at a fixed length of rope, the boat speed increases by 2 mph to a maximum speed based upon the
participant's age category. Maximum boat speeds are usually 34 or 36 mph, and skiers may achieve speeds in excess of
60 mph as they pull across the wakes. Once all six buoys are negotiated at the maximum speed, the rope is shortened by
a predetermined amount with each successive pass. Each shortening of the rope increases the difficulty by requiring
greater acceleration and more attention to technique. The winner is the skier who rounds the largest number of buoys
without a miss or a fall.
FIGURE 44.1. A slalom skier rounding the buoy on the slalom course prepares for the sudden acceleration across the
wakes to the next buoy.
Competitive trick skiing involves awarding points for completed maneuvers based on their predetermined level of
difficulty. The skier is usually given two twenty-second passes in which to complete as many tricks as possible. Boat
speeds are selected by the participant and usually range from 15 to 20 mph. If the skier performs any “toe tricks,” in
which the foot is placed in a strap to hold the rope, an assistant rides in the boat to pull a release for the rope in case of a
fall (Fig. 44.2). These toe tricks and wake flips are some of the more difficult tricks.
FIGURE 44.2. A trick skier in the toehold is susceptible to injury with improper release of the rope in the event of a fall.
Traditional competitive ski jumping ranks participants solely on distance ( Fig. 44.3). The skier selects the speed of the
boat to a usual maximum of 32 or 35 mph, depending on the age division and the level of the skier. The skier uses
special long jump skis that have a low profile fin. Ramps are usually wet, wax-coated fiberglass surfaces 5 to 6 feet high.
A skier's distance will be based on the speed of the boat, the speed of the skier upon reaching the ramp, and individual
technique. The top jump skiers approach the ramp at over 60 mph as they “crack the whip” behind the boat to fly
distances of over 200 feet.
FIGURE 44.3. Jump skiing requires precise timing and controlled technique to avoid injury.
NATIONAL AND INTERNATIONAL PROFILE
There are currently between 15 and 20 million recreational and competitive water skiers in the United States. Athletes
participate in over 500 local water ski clubs nationwide. USA Water Ski, formerly known as the AWSA, acts as the
national governing body and sanctions over 750 tournaments annually throughout the country.
Internationally, there are over 75 countries with formal water ski organizations. The International Water Ski Federation
(IWSF) acts as the world governing body and sponsors the World Championships on a biennial basis. Currently, efforts
are being focused toward including water skiing as an official Olympic event.
INJURIES, MECHANISMS, AND EPIDEMIOLOGY
Recreational Versus Competitive Water Skiing
When discussing injuries associated with water skiing, one must recognize the difference between the two classes of
water skiers, those who ski on a recreational basis and those who compete. The recreational water skier generally has
no formal technical instruction on either driving or skiing safety. In contrast, the competitor has detailed knowledge of the
sport, its challenges, and risks; therefore, he is more apt to be disciplined and careful. The importance of this factor is
relayed in a study by Radford et al. ( 1) who studied 145 water skier injuries and noted that 45% were associated with
lack of experience or poor judgment. A second important difference, competition water skiers usually ski in a more
controlled, familiar, and less congested environment. In addition, competitive skiers usually prepare physically and have
individually adapted or customized equipment.
The spectrum of injury types differs between the recreational and the competitive athlete. Recreational athletes are more
apt to sustain injuries resulting from improper boating or propeller mishaps ( 2,3,4,5,6,7,8,9 and 10). Additionally, they are
more likely to sustain douche and enema injuries as they drag through the water during takeoff or loss of balance,
especially while learning to ski ( 11,12,13,14,15,16,17,18,19,20,21 and 22).
Injuries sustained in competitive skiers are best evaluated by examining the safety reports of the AWSA. These reports
are completed at all sanctioned events and include descriptions of all injuries sustained, mechanisms, and external
factors contributing to the injury. The ability level of the skier is also included. One unpublished study by Carder, Garrick,
and Requa reviewed three years of AWSA safety reports and demonstrated that competition skiing has a low rate of both
overall and severe injury. Knee and minor back and neck strains were found to be the most commonly reported injuries.
Knee and shoulder injuries, followed by lower extremity fractures, were the most frequent “severe” injuries requiring
treatment beyond first aid. The authors concluded that the majority of injuries in competition were sustained by the most
novice and the most elite competitors. Apart from statistics compiled by the AWSA, only a few studies exist detailing
injuries sustained by competitive water ski athletes ( 23,24 and 25). Some studies suggest that competition water skiers
are more likely to sustain knee injuries, low back pain, and minor injuries such as sprains or pulled muscles ( 24,26,27).
It is helpful to categorize water ski injuries according to their mechanism for the purposes of both study and prevention
(Table 44.2). In considering the mechanism, one must realize that water ski safety involves not only the skier, but also a
close interplay of the driver and the observer. Apart from human factors, the towboat, skier equipment, and environmental
conditions are additional important factors that may relate to skier injury.
TABLE 44.2. MECHANISMS OF INJURY
Skier Falls
The most common falls by the water skier are into obstacle-free water. The skier is subject to both the impact upon the
water itself and large torsional forces related to the long lever arm of the ski and the skier's speed. Frequent injuries
include contusions, muscle sprains, and torn ligaments with fractures and dislocations occurring less commonly. The
knee and shoulder sustain the majority of injuries. Ankle injuries are less likely to occur with the use of higher profile ski
bindings that better support and protect the ankle. Though rare, spiral fractures of the tibia and fibula can occur as
torsional stresses are concentrated at the superior aspect of the binding. In addition to musculoskeletal injuries, falls
have been reported to cause douche injuries to the vagina ( Fig. 44.4) (11,12,14,15,18,19,21,28), rectum (13,17,20,29,30),
and tympanic membrane (1,15,24,31,32 and 33).
FIGURE 44.4. In a crouched position with the buttocks hitting the water at increasing speeds, there is a risk of injury to
the genitalia or rectum. A vaginal douche or rectal enema injury may be sustained during takeoff or during loss of
balance.
Skier Versus Solid Objects or Shoreline
Collision with solid objects may take several forms. Occasionally, and more commonly with the recreational skier who
may not be familiar with the skiing environment, the skier may strike submerged objects while skiing. Paterson ( 24)
reported a 25-year-old male who hit a submerged sand bank and sustained a C5-6 dislocation causing immediate
quadriplegia. More frequently though are falls into known objects while attempting to land, such as falls into docks or the
shoreline. Attempts by the recreational skier to “spray” persons on the dock or shore with water by turning abruptly often
cause collision injuries. Any misjudgment of speed or angle can result in an impact of considerable force. Poor lighting,
due to bad weather or the dull light of dusk, aggravates this risk.
In competitive jumping, the skier may also sustain collision injuries. In order to obtain maximum speed, the competitive
skier approaches the ramp from the opposite side of the wake at an acute angle. Improper timing or misjudging the angle
may lead to severe injuries if the skier impacts the ramp surface or side curtain ( Fig. 44.5). Most commonly, injuries occur
to the knee ligaments, particularly the anterior cruciate ligament (ACL). Though less frequent, the skier may also sustain
fractures, dislocations, and head and neck injuries.
FIGURE 44.5. Timing is extremely important in the jump event. The skier shown above misjudged his speed and position
on his approach and struck the side of the ramp.
Boat and Propeller Injuries
According to U.S. Coast Guard (USCG) statistics, boat collisions are by far the most common cause of injuries sustained
by the recreational boater. Accordingly, collisions involving towboats account for a substantial number of the injuries and
fatalities associated with water skiing. Unfortunately, there is little or no marine traffic control in most areas and a safety
certificate or permit is usually not required to drive a boat. In addition, many states still have no minimum age
requirement for boat operators. The majority of accidents have been attributed to operator inattention and inexperience
(34). Specifically, in water skiing, driver inattention to other boats may be caused by watching the skier rather than relying
on the observer for notification when the skier has fallen. Another important factor in boating accidents is alcohol use.
USCG data for 1996 demonstrates alcohol involvement in 10% of all reported boating accidents and 27% of all fatalities
(34).
One of the most devastating injuries with a high rate of morbidity and mortality occurs when a moving propeller strikes a
person. These injuries may occur to the fallen water skier or a boat occupant upon falling from the boat. May and Piliero
(35) have described the “water-skier seer syndrome” that commonly occurs with inexperienced drivers. In this situation, a
front-seated observer falls from the boat after the boat strikes a large wave. The driver sees the victim fall overboard and
steers the boat away from the fallen passenger, thus bringing the boat's stern and propeller directly over the person ( Fig.
44.6).
FIGURE 44.6. A: Incorrect method of turning the bow away from the fallen passenger brings the stern and thus the
propeller directly over the victim. B: The correct method for the boat driver to avoid a fallen passenger directs the stern of
the boat away from the fallen person.
Propeller injuries have been described to cause massive tissue destruction, severe lacerations, open fractures,
amputations, and death (3,5,6,7,8,9 and 10,24,36). USCG data reported 674 injuries and 38 deaths from persons struck
by a boat or propeller for the 5-year period from 1992 to 1996 ( 34). However, the true magnitude of propeller injuries is
likely to be much greater since accidents without fatalities often are not reported to the USCG. This fact is highlighted in
a report by Price and Moorefield ( 7) of a mail survey of approximately half the members of the Florida Orthopaedic
Society. Survey participants could identify 195 propeller injuries in a 5-year period from 1979 to 1983. For the same time
period, only 30 such injuries were reported to the USCG.
Propeller injuries usually resemble a series of deep, parallel lacerations caused by the blade rotating and moving along
the victim's body (Fig. 44.7). Transection of major vessels and nerves, as well as amputations, contribute to the high
morbidity and mortality of these injuries. In addition, severe soft tissue trauma and open fractures are often complicated
by subsequent infection despite irrigation, debridement, and antibiotic coverage. Increased vigilance by the driver and
the use of propeller guards have been suggested as possible methods to prevent these injuries.
FIGURE 44.7. The typical propeller injury consists of multiple parallel lacerations and severe soft tissue injury. (From
Mendez-Fernandez MA. Motorboat propeller injuries. Ann Plast Surg 1998;41:113–118, with permission.)
Skier Versus Skier
Occasionally, recreational skiers will ski together behind the same boat on multiple towropes. Collisions between skiers
may occur and can cause significant injuries as the two persons impact each other and their equipment. Many collisions
and resultant injuries occur when recreational skiers are attempting stunts such as crossing each other behind the boat
or spraying water upon each other. When multiple skiers are being towed, both skiers should be experienced enough to
maintain a safe distance from one another. In addition, the rope lengths should be identical.
Towline Injuries
Towline injuries take several forms and may cause injury to the skier, observer, or driver. Injuries to the beginning skier
often occur at takeoff. A characteristic rope burn injury to the thighs has been described. After a failed takeoff attempt,
the novice skier falls backwards and releases the rope late. The highly tensioned rope springs forward and strikes the
thighs of the skier with considerable force leaving an erythematous or ecchymotic impression on the anterior thighs ( 37).
In addition to rope abrasions or contusions, the towline may cause entanglement injuries. In a report by Banta ( 3), a ski
instructor's leg became entangled in the rope upon takeoff and caused a fracture-dislocation of the ankle. Other potential
injuries include soft tissue avulsions and amputations. Though extremely rare, these entanglement injuries may even
cause drowning and death (4).
Towrope-related injuries commonly occur when excess slack is quickly taken up after the skier turns suddenly. Most
frequently, these injuries involve minor shoulder sprains. Greater forces, however, may rarely cause tears of the rotator
cuff (23) or dislocations of the shoulder. A superior labral injury may also occur when the skier falls with his arm forward
flexed and abducted as in turning around a buoy during slalom competition ( Fig. 44.8). Romano et al. (33) described
another shoulder injury in which a skier sustained a traction brachial plexus injury by a similar mechanism.
FIGURE 44.8. An arthroscopic view of a superior labral anterior-posterior “SLAP” lesion sustained in an elite competition
water skier upon falling while rounding a buoy on the slalom course. H, humerus; G, glenoid; L, labral tear; B, biceps
tendon. (Photograph courtesy of John King, M.D.)
Competition trick skiing has the potential for towrope injuries to the skier. Most injuries are related to “toehold turns,” in
which the skier straps one of his feet into the trick harness to hold the rope (see Fig. 44.2). A release mechanism
activated by the observer is utilized to drop the rope should the skier fall with his foot in the toehold. This system requires
the careful attention of the observer to release the rope at the proper time. The most common injuries from improper
release include adductor strains and ligamentous injuries to the knee and ankle as the skier is dragged through the
water. Apart from toehold-related injuries, the potential for entanglement also exists as the competitive trick skier
frequently wraps the rope around the body in preparation for turns.
Towropes may cause injuries to both the driver and the observer. These injuries occur when the skier has fallen and
releases a highly taut rope late after falling. The rope then recoils back toward the boat and the handle may strike boat
occupants. Though this injury mechanism is well-known to competitive skiers, only a couple of reports in the medical
literature document specifics of these injuries. In a report by Pearl et al. ( 38), a boat driver pulling a barefoot water skier
turned around, was struck in the face, and sustained a ruptured globe and multiple orbital fractures. In another report by
Navon (39), the boat observer was similarly struck in the face by a recoiled handle causing a ruptured globe, multiple
orbital and maxillary fractures, and permanent blindness. Towrope recoil injuries have been well-recognized by the
AWSA, and this organization has been instrumental in promoting the use of “shock tubes” in competitive skiing. These
foam tubes through which the rope passes are usually approximately 4 feet in length and attach to the pylon of a
competition ski boat. Since their use in AWSA-sanctioned tournaments began, the incidence of recoil injuries has
dramatically decreased. Shock tubes are now mandatory for all AWSA-sanctioned slalom events and are recommended
for jump competition. Other methods to prevent these injuries have included safety netting in the boat and rope designs
to lessen the rope's inherent elasticity.
Incidence of Injury
The overall incidence of water ski injuries has not been well-described and is difficult to ascertain. The USCG has stated
that “only a small fraction of all non-fatal boating accidents occurring in the United States are reported to the Coast
Guard, state, or local law enforcement agencies” ( 34). Nevertheless, the number of USCG-reported injuries related to
skier mishaps for the 5-year period between 1992 and 1996 totals 1568. The number of water ski-related fatalities over
this period, which is more likely to accurately reflect total numbers, is reported as 35. Importantly, the USCG suggests
that approximately 80% of all reported accidents involve operator controllable factors, including inattention, carelessness,
and inexperience ( 34).
In organized competitive water skiing, a controlled environment with experienced skiers, drivers, and observers provides
for a safe sport with relatively few injuries. Considering the high speeds, intensity of impacts, and leverage imposed by
the skis themselves, the potential for injury is high. However, reports from AWSA-sanctioned tournaments demonstrate a
remarkable safety record. According to an AWSA statistical summary of safety reports from 1990 to 1996 ( 40), the overall
incidence of injury has been estimated to average 220 per 100,000 skier exposures. This time period includes 4,359
tournaments with 240,913 skiers and 543,497 estimated skier exposures. The unpublished study by Carder, Garrick, and
Requa, which examined three years of AWSA safety reports, further subcategorized injuries into minor and severe
groups. Severe injuries were those which required more than simple first aid, suturing, splinting, or casting. In the
evaluation of 1,402 tournaments between 1991 and 1993, the incidence of severe injury was only 32.6 per 100,000
rounds. Furthermore, since organized competition began, no fatalities have ever occurred in traditional water skiing
events in AWSA-sanctioned competition.
SAFETY, PREVENTION, AND CONDITIONING

Obligations of Skier, Driver, and Observer
There are three individuals involved in the water skiing team: the skier, the boat driver, and an observer, each with his or
her own responsibilities. Importantly, all members of the team should be familiar with the universal water skiing hand
signals (Fig. 44.9). In addition, all should be well-rested as fatigue may cloud judgment, dull responses, and lengthen
reaction time. Likewise, for obvious reasons, drugs and alcohol have no place in the sport of water skiing for any of the
participants.
FIGURE 44.9. The universal hand signals in water skiing.
Skier Responsibilities
A water skier should be at least a comfortable swimmer, able to swim 50 m and stay afloat (i.e., tread water) for a
minimum of 5 minutes. He should be familiar with the skiing area and alert to any physical hazards. The skier should ski
within his ability and avoid risky behavior such as landing on docks or the shore or attempting to spray water on persons
or objects. The skier is responsible for his equipment, including an approved flotation device. Even the most
accomplished swimmer who sustains a major head injury or loses consciousness is at risk without a life jacket. Beginners
and jumpers should wear protective pants to prevent douche-type injuries. The skier should note proper position of the
rope between himself and the boat prior to takeoff to prevent entanglement injuries. After a fall, the uninjured skier should
signal “ok” with the appropriate hand signal. The skier may also hold a ski out of the water to enable better visualization
by other boat drivers. Pregnant women should avoid water skiing after the first trimester due to the risks of preterm labor
or abruption initiated by a fall with blunt trauma to the abdomen.
Driver Responsibilities
Driving safety includes many variables. The driver must take his responsibility seriously and should familiarize himself
with the skiing area before taking off. The driver is primarily responsible for keeping track of the marine environment,
including the positions of other boats. The driver should not drive within 100 feet of any fixed or moving objects, such as
the shore, docks or other boats or skiers. Additionally, it is the driver's responsibility to confirm the stability and safety of
the towboat. This includes insistence on having an observer as well as proper weighting and balancing of the boat for
maximum maneuverability. Sharp turns must be avoided.
When pulling skiers, starts should be gradual for water takeoffs and should have sudden acceleration just before the
towrope is taut for dry or dock starts. Dry and dock starts should only be attempted by experienced drivers and skiers.
The towrope should be seen to be disentangled from the skier prior to takeoff. The driver should not begin until he has
received confirmation of skier readiness by a previously agreed upon verbal signal, such as the commonly used “hit it!”
The driver must then carefully adjust speed according to the skier's skills and needs. After a fall, the driver must safely
and quickly bring the towrope back to the skier ( Fig. 44.10). In approaching a fallen skier, the driver should position the
boat with the skier on the driver's side and in the driver's sight at all times. Care should be taken to avoid swinging the
boat into the skier, and wind and current conditions should be appreciated.
FIGURE 44.10. In the “keyhole method” of skier retrieval, the boat driver must always maneuver the boat with the fallen
skier on the driver's side. The boat should always remain a safe distance from the skier though close enough to return
the rope. Care is taken to avoid abrupt turns which could bring the stern of the boat toward the skier.
Observer Responsibilities
A competent observer facing the rear of the boat has the chief responsibility of watching the skier and informing the
driver of the skier's progress. This includes notifying the driver of the skier's hand signals, informing the driver of a skier
fall, and making the driver aware of potential safety hazards. The observer should relay information regarding any boat
traffic approaching from the stern. In most areas, there is a legal requirement for an observer to be present in the boat
while a water skier is being towed. The observer should wear a flotation device and be prepared to assist the skier in the
water in the event of an injury.
Equipment
Skis and Bindings
Skis and bindings often affect injuries sustained in water skiing. Skis differ in their design for the different water ski
events. There are also differences between the skis and bindings used by recreational and competitive skiers.
Furthermore, technologic advancements in ski design have changed the materials, structure, and performance of modern
water skis. Newer competitive slalom skis are composed of stiff, lightweight carbon-graphite fiber for increased
acceleration and improved handling. Skis used for jumping have increased in length over the last decade with some
modern jump skis over 80 inches in length. The general need for ski safety is recognized by International Water Ski
Federation (IWSF) rules which state, “There must be no unnecessary sharp or abrasive (to the touch) metal, wood, or
other attachments to the ski which could, in the opinion of the Safety Director, inflict injury to the skier should he come in
contact with the ski in a fall” ( 41). As another important safety measure, all screws should be checked for tightness prior
to ski use.
Bindings are variable, with recreational skiers often using adjustable bindings. This contrasts with the customized
high-wrap bindings worn by many competitors. Stanisavljevic et al. ( 42) previously noted the problems with torsional
injuries that may occur when novice skiers wear bindings that are higher profile and may not release as easily. Some
newer hard plastic designs called “hard shells” more closely resemble snow ski boots than the traditional rubber water ski
bindings. Advocates for hard shell bindings tout their customized fit, improved edge control, and efficiency in energy
transfer to the ski. Though these bindings might better support the ankle and prevent ankle injuries, they will not release
the skier's foot and may concentrate stresses above the binding. The potential for knee ligamentous injuries may be
heightened when the ski remains attached to the skier after a fall. Many designers are currently evaluating systems to
release the binding from the ski to lessen this risk.
A significant related problem occurs commonly with recreational slalom skiers when they use stiff, high-wrap bindings for
their front foot and a toe strap for their back foot. The rear foot easily releases during a fall, but the front foot may stay
attached to the ski and subject the skier to extreme torsional stresses in the front leg. To reduce the chance of injury,
recreational skiers should use a softer, low-wrap binding with a back toe strap to allow both feet to more easily release
during a fall. More advanced skiers may use the stiffer, high-wrap rubber or hard shell bindings for both the front and rear
foot.
Towropes, Handles, and Pylons
The rope, handle, and pylon must withstand tremendous forces, especially with the strong pull and resistance of a slalom
skier on the course. Specifications for the towrope and handle have been set by both the AWSA and the IWSF for size,
tensile strength, load to failure, and elasticity. They must float and be free of knots and irregularities such as fraying.
Pylons must also follow certain guidelines. The most effective pylons are located centrally in the boat rather than at the
stern to minimize the horizontal pull of the boat produced by a powerful slalom skier.
Power Boats
The towing craft must be strong, stable, and maneuverable to be safe. Inboard or outboard motors should have at least
enough horsepower to enable the skier to easily plane above the water from a water start. Boats used for water skiing
should have a speedometer, rearview mirror, and seating allowing the observer to face toward the rear. Basic safe
boating accessories, including USCG-approved life jackets for each passenger and a fire extinguisher, are imperative.
Propeller guards are an optional safety addition that may reduce the incidence of propeller injuries.
Flotation Devices
USCG-approved flotation ski jackets should be worn by water skiers at all times. Old belt type devices are unsafe
because they are easily dislodged and ineffective for both the skier and the boat occupant. Thinner neoprene vests that
allow greater mobility are often used by the competitive skier. However, the skier should take care in selecting one of
these jackets, because many provide less flotation and are not USCG-approved. Requirements are more strict for
competitive ski racers. Life jackets for ski racers must have two leg straps and must be certified every three years.
Safety Devices
Special safety equipment is required in certain competitive events. For example, in competition jumping, helmets are
mandatory at both AWSA-sanctioned and IWSF tournaments. It is recommended that helmets are constructed of
high-impact material, have a three-point chin strap, be non-bucketing, and fit well. In ski racing, specially designed
helmets are required for the driver, observer, and skier. Another special safety device is the towrope release used in trick
competition. This device releases the rope should the skier fall while he is engaged in a toe hold maneuver. Safety
issues also led to the requirement for shock tubes in all slalom competition.
ENVIRONMENTAL HAZARDS
Many environmental conditions can be hazardous to the water skier. First, the skier should never ski at night or in
conditions of poor visibility, such as fog or steady rain. Stormy weather should likewise be avoided. Second, high wind
conditions produce turbulent water and cause difficult driving and skiing conditions. The skier will fatigue rapidly and
have a greater risk of injury. Third, hypothermia from cold water exposure may occur in certain climates. Wet suits and
dry suits should be used accordingly. Fourth, the area for skiing must meet certain safety criteria. In addition to allowing
100 feet on each side of the boat free from obstacles, a minimum depth of 5 to 6 feet of water is recommended. Length of
the ski area should be at least several thousand feet. The entire skiing area should be surveyed by the team prior to
skiing in order to identify any potential hazards or warning buoys.
Safety Standards and Recommendations
Safety is a major priority of both USA Water Ski and the International Water Ski Federation. In addition to educational
programs and information dissemination, the organizations provide safety training programs. Technical rule books and
safety manuals include sections on specific safety issues ( 41,43,44). All competitions are required to have a trained
Safety Director who oversees all safety concerns, including equipment, facilities, and operation of the tournament. The
rule books and safety manuals delineate specific safety equipment requirements, such as flotation devices, shock tubes,
and helmets. These requirements vary with the specific event. Safety personnel trained in first aid, emergency
resuscitation, and water rescue techniques are required to be present in boats or along the shore for all competitions.
Safety boats must carry specific equipment, including a back board, a cervical immobilization device, tools to cut through
towlines or straps, a two-way radio to allow communication with the Safety Director, a basic first aid kit, an extra flotation
device, and a fire extinguisher ( 44). Medical officers and medical stations are mandatory at all international tournaments.
Fitness Training and Conditioning
Physical fitness is important in water skiing to maximize performance and prevent injuries. During the ski season and in
the off-season, stretching, weight training, and cardiovascular exercises are important to maintain top conditioning.
Stretching should be performed regularly, including both before and after each skiing session. Flexibility is especially
important for the trick skier. Important muscles to emphasize for skiing include the lower back, abdominal muscles,
pectoral muscles, quadriceps, hamstrings, deltoids, and biceps. Grip strengthening exercises may also benefit the
competitive skier. Furthermore, cardiovascular exercise will help to reduce injury rates by decreasing fatigue factors.
SPECIFIC MANAGEMENT OF INJURIES
Unconscious Skier
As with the medical evaluation of any unconscious patient, the unconscious skier must have an adequate airway. If the
victim is not breathing, artificial respiration must be started, even in the water. While flotation devices keep the skier
afloat, the neck must be kept in neutral and immobilized either manually or with a collar. The airway must be kept clear
and open as the cervical spine is immobilized. The unconscious skier should never be passively hoisted into a boat but
should be pulled to shore with the head and neck under control where he or she can be floated or lifted onto a backboard
to safety. Helmets should not be removed, except by experienced medical personnel. Ski racing helmets may require
removal of a face-piece for access to the airway.
Near-Drowning
The term “near-drowning” refers to survival after a temporary period of asphyxia by submersion in water ( 45). As with the
unconscious skier, initial treatment efforts should be directed toward ensuring an adequate airway, breathing, and
circulation. The importance of immediate administration of cardiopulmonary resuscitation (CPR) cannot be
overemphasized. However, though artificial respiration may be started in the water, external chest compressions require
a hard surface to be effective and are not generally useful until the victim has been removed from the water. The skier
should be given high concentration supplemental oxygen as soon as it becomes available.
All patients should be evaluated at a medical center where attention should be focused on pulmonary and cardiac
function. Arterial blood gas measurements are important in determining oxygenation status. Often, these patients require
intubation and use of positive end-expiratory pressure to reverse severe hypoxemia. A combined respiratory and
metabolic acidosis frequently necessitates optimizing ventilation and administering sodium bicarbonate. From the
cardiovascular standpoint, many near-drowning victims have ventricular dysrhythmias or asystole. Standard advanced
cardiac life support (ACLS) protocols should be followed. Volume resuscitation is often necessary and may be guided by
the use of central venous pressure catheters or pulmonary artery catheters.
Hypothermia
Hypothermia, though infrequent, may occur in skiers with prolonged water exposure in cold climates. Importantly, the rate
of loss of body heat in cold water is approximately 25 times the rate of loss of heat in air ( 46). The rate of heat loss also
varies inversely with the water temperature. Skiers who experience minor symptoms of hypothermia may only exhibit
shivering. More severe hypothermia may cause altered mental status or cardiac dysrhythmias, including bradycardia,
atrial and ventricular fibrillation, and asystole.
Treatment of minor hypothermia consists of drying the patient and wrapping him with warm towels or blankets. Rescuers
of persons with advanced hypothermia should remember to be gentle with the victim because rough handling may
precipitate ventricular fibrillation ( 47). Patients with more severe hypothermia should be gradually rewarmed and receive
CPR and ACLS as necessary. One should always remember that CPR efforts should always be continued in the
hypothermic patient until the body temperature has normalized.
Spine Injury
The majority of injuries to the spine are minor sprains and strains, with fractures or serious spinal cord injuries occurring
only rarely. When fractures or cord injuries do occur, they are most frequently located in the cervical spine. Rechtine and
Reed (48) have attributed the cause of most spinal injuries to the sudden transient deceleration forces that occur with
falls during high-speed slalom, barefoot, and jump skiing.
When approaching the skier with a presumed spine injury, standard principles of management should be followed. First,
the spine should be immobilized to prevent further injury. The cervical spine may be held in position either manually or
with a collar while the skier remains in the water. The skier is then carefully positioned as a unit on a backboard. Helmets
and flotation vests should be left in place and removed only by trained medical personnel.
In addition to acute spine injuries, chronic spine deformities have been reported to occur with water ski jumping in young
or adolescent patients. A study by Horne et al. ( 27) demonstrated a high prevalence of Scheuermann's disease and
vertebral body wedging in adolescent ski jumpers. The percentage of affected skiers increased with increasing time of
participation in the sport. The clinical significance of these abnormalities is, however, undetermined.
Concussion
Concussion is defined as a trauma-induced alteration of mental status that may or may not be associated with a loss of
consciousness (49). The mechanism for concussion in water skiing is similar to that of other sports with injuries usually
caused by a fall or a collision. Most commonly, the skier will have a low-grade concussion and will experience a brief
period of posttraumatic amnesia and confusion. He may appear dazed and disoriented, have slurred speech, and be
unable to concentrate. Boat personnel should be aware that a confused skier may thrash about in the water with his arms
above his head in such a way that this could be mistaken for an “OK” signal. Occasionally, the skier will require
neurosurgical evaluation if he has prolonged or worsening symptoms, a period of unconsciousness, or an abnormal
neurologic examination.
The skier who experiences a concussion should be assisted out of the water immediately. He should then be evaluated
routinely for any signs of serious head injury. Mental status testing and a neurologic examination should be performed.
Importantly, the athlete should not return to water skiing or other sports until all postconcussive symptoms have
completely resolved. Even a minor injury after a low-grade primary concussion has been noted to precipitate the
“second-impact syndrome” (50,51,52,53,54,55 and 56). This syndrome, which involves a cascade of events leading to
severe cerebral edema, has a high mortality rate even with appropriate medical treatment ( 52,55,57).
Bleeding
Most bleeding can be stopped with direct firm and constant pressure over the site. A bandage can be applied over the
area, even if immersed. Importantly, water washes away clots and may prolong the bleeding. Bandages should not be
removed once applied, but should rather be reinforced as necessary. Major lacerations must be repaired at a hospital,
where intravenous fluids and blood may be given to patients in hypovolemic shock.
Propeller Injuries and Lacerations
Propeller injuries and lacerations may be severe and should be managed promptly according to emergency principles
regarding airway, breathing, and circulation priorities. Bleeding should be controlled by firm direct pressure at the site. All
wounds must be considered contaminated and strict surgical wound care principles should be followed. Banta ( 3) has
stated that the treatment of propeller injuries should be “comparable to the treatment of massive battle wounds, with
adequate debridement and secondary closure techniques in addition to appropriate antibiotic therapy.”
Antibiotic regimens must be wide-spectrum to cover marine-specific organisms. Several bacterial species have been
found to cause water-associated wound infections. In particular, Aeromonas hydrophila has been described as a virulent
fresh water pathogen that may infect soft tissue wounds and open fractures and may cause septicemia
(9,58,59,60,61,62,63 and 64). Sanger et al. (63) describes a water ski injury in which the skier sustained a soft tissue
forearm avulsion by the towrope. The wound subsequently became infected with Aeromonas and required extensive
repeat debridements. In addition to Aeromonas species, Mann, in his reports on propeller injuries ( 6,36), has noted that
water is often contaminated by Pseudomonas species.
Other particularly virulent pathogens that may cause severe local infections and septicemia are the Vibrio species.
Specifically, Vibrio vulnificus from inland brackish waters has been noted to cause extremity wound infections. The
infections may vary in appearance but most often are erythematous, ecchymotic areas with bullae, vesicles, and necrotic
ulcers (65,66,67,68,69 and 70). These infections may be life-threatening and can progress rapidly. Therefore, prompt
irrigation and debridement with administration of appropriate intravenous antibiotics is mandatory.
Another pathogen that may be associated with the aquatic environment is Mycobacterium marinum (9,71). This infection
differs with the aforementioned bacterial infections because of its chronic presentation. Infections appear initially as small
papules which enlarge, suppurate, and eventually ulcerate. Associated swelling along tendon sheaths and around joints
may cause pain and stiffness.
In addition to tetanus prophylaxis and aggressive irrigation and debridement, wide-spectrum prophylactic antibiotics
should be given for significant marine-acquired wounds. The regimen should cover routine gram-positive organisms as
well as gram-negative organisms, including Aeromonas and Pseudomonas. Morris et al. (72) has suggested that the best
antibiotic for Vibrio organisms is tetracycline, though this organism is usually also susceptible to chloramphenicol and
aminoglycosides. Chronic infections caused by Mycobacterium marinum should be treated with rifampin and ethambutol.
Less significant M. marinum wounds may alternatively be treated with tetracycline or trimethoprim-sulfamethoxazole ( 71).
Suspected fractures should be splinted in the water, preferably with available splints or, alternatively, by taping the
injured leg snugly to the opposite leg. An injured arm can be anchored to the chest or supported in a sling. Boat cushions
or ski jackets can be used as temporary emergency splints.
Dislocations should be evaluated by competent medical personnel. They should be reduced promptly, especially if
complicated by neurovascular compromise. Early reduction of the acute dislocation is often easier before significant
muscle spasm has ensued. This may be accomplished in most instances with longitudinal traction and gentle rotational
movements.
Muscle and Ligament Strains, Sprains, and Tears
Muscle strains and sprains are common in both the recreational and the competitive water skier. Most commonly, these
injuries involve the knee, shoulder, lower back, and neck. Strains of the forearm muscles are also frequent in competition
slalom skiers. These injuries should be treated with the standard protocol of rest, ice, and elevation if an extremity is
involved. Nonsteroidal antiinflammatory medications may be taken by persons without contraindications. Many of these
injuries are related to fatigue and may therefore be prevented by appropriate conditioning and avoiding skiing when
fatigued. Stretching may also help prevent muscle strains and sprains.
Hamstring injuries are relatively frequent in both recreational and competitive water skiers ( 25,73,74). Sallay et al. (25)
has described a series of 12 patients who sustained hamstring injuries while water skiing. Most sustained their injuries
either at takeoff or upon submerging the ski tips while crossing the boat wake. The mechanism of injury involves knee
extension and hyperflexion of the hips. As described by Sallay et al. ( 25), injuries commonly occur in the novice upon
takeoff with an incorrect body position. The skier tends to straighten his legs prematurely causing the ski tips to
submerge. Extreme hip flexion then stresses the proximal hamstrings as the skier is pulled forward. In a separate case
report by Blasier and Morawa (73), a skier sustained a complete proximal hamstring avulsion upon submerging his skis
while crossing a wake. A similar mechanism has been reported for the jump skier who lands with his center of gravity
shifted forward causing the ski tips to catch the water first ( 25). The skis then suddenly decelerate and the forward
momentum of the skier causes rapid hyperflexion of the hips ( Fig. 44.11). Additionally, the elite trick skier may sustain a
hamstring injury while attempting flips if he has the incorrect amount of rotation and the tip of the ski first enters the water.
FIGURE 44.11. The jump skier who lands “out the front” with the tips of the skis first in the water is susceptible to
hamstring injury. As the skis decelerate, forward momentum hyperflexes the hips and stresses the proximal hamstring
origin.
In addition to minor muscle strains and sprains, more severe complete tears of muscles may occur. In a report by Dragoni
et al. (23), a 33-year-old competitive water skier sustained an isolated partial tear of the subscapularis muscle. While
rounding a buoy with an outstretched arm, the skier injured his shoulder as he quickly changed from a position of
maximum abduction and external rotation to a position of adduction and internal rotation. In another case report by
DiChristina and Lustig ( 75), a 19-year-old skier sustained a rupture of the short head of the biceps through the muscle
belly. In both cases above, the injuries were repaired surgically and the skiers returned to activity four months later with
good results. A further muscle injury noted by Romano et al. ( 33) is tear of the adductor muscles. The adductor injuries
are usually caused by the inexperienced skier doing the “splits” on a pair of skis.
Ligamentous injuries are among the most common injuries sustained by both recreational and competitive skiers. The
knee is the most commonly affected area with the majority of injuries occurring to the collateral and anterior cruciate
ligaments. The magnitude of injury, concomitant injuries, and patient goals will determine treatment. ACL reconstruction
is favored for the competitive skier who sustains a complete intrasubstance ligament tear.
Douche and Enema Injuries
Douche and enema injuries often present with bleeding and pain. Any rectal or vaginal bleeding must be evaluated
quickly and thoroughly, hence the advantage of having good medical facilities at hand. Treatment includes controlling
bleeding, treating hemorrhagic shock as necessary, and surgical repair of the vaginal or rectal wall. These wounds
should be evaluated in the operating room as laparoscopy and sigmoidoscopy or colonoscopy may be necessary to rule
out further injury (14,17,20). Associated injuries to the vulva, bladder, cervix, and urethra may occur ( 11,16,18,22). As with
other lacerations, appropriate prophylactic antibiotics should be administered. Most importantly, the majority of these
injuries could be prevented if all beginners and jump skiers would wear protective rubber pants or a wetsuit.
Ruptured Tympanic Membrane
Another “douche” type of injury that is relatively common in water skiing occurs to the external auditory canal causing
perforation of the tympanic membrane (15,24,32,76). This injury may occur when the skier falls directly on the side of his
head during a slalom turn or upon catching the edge of the ski in trick or jump skiing. The skier will present with pain,
bloody or purulent otorrhea, and occasionally hearing loss. Predisposing risk factors may include prior otitis media, an
atrophic tympanic membrane, or poor eustachian tube function ( 32,76). Though most perforations are small and heal
spontaneously, all persons should be referred to an otolaryngologist for full evaluation.
In a multistudy review by Kristensen et al. ( 77) including over 500 tympanic membrane perforations, 88% of traumatic
ruptures (excluding battlefield blast injuries) healed without surgical intervention. In another study by Griffin ( 78), 20% of
the tympanic membrane perforations specifically associated with water skiing injuries failed to heal. He further noted that
contamination and resultant infection decreased the chance for spontaneous healing. The importance of prophylactic
antibiotics and preventing infection after tympanic membrane rupture has been stressed ( 77,79).
In general, the water skier sustaining a ruptured tympanic membrane should refrain from further water sports until healing
occurs. Entry of water through a perforation may cause otitis media, mastoiditis, and potentially meningitis or permanent
hearing loss (77,79). Though some authors have stated that swimming after tympanic membrane perforation is possible
with the use of waterproof plugs ( 79,80), we would not recommend these plugs for the water skier because of their
potential to be dislodged during a fall.
Otitis Externa
Otitis externa may be manifested in the water skier by pain, tenderness, itching, discharge, and even hearing loss.
Pseudomonas aeruginosa and Staphylococcus aureus are the usual pathogens involved. Treatment generally consists of
topical antibiotic ear drops, though more advanced infections may require systemic therapy. A malignant form of otitis
externa may cause severe infection and necrosis in the diabetic or immunocompromised patient. Skiers prone to
developing external otitis may prophylactically irrigate their ears after skiing with a solution of 80% rubbing alcohol. This
solution will act as both a dessicant and a bactericidal agent.
Heel Contusions
Heel pain is frequent in the competitive water ski jumper. In a reference to unpublished data in a review by Roberts and
Roberts (26), calculated and measured forces by the water ski jumper upon striking the jump and landing are stated to be
5 to 9g. Contusions to the heels can cause significant pain even with normal ambulation. Treatment should include rest
and antiinflammatory medications for discomfort. Attention should be directed toward prevention of these injuries by
frequently changing heel pads in skis and attempting to absorb the shock upon landing by bending one's knees.
Hand Callouses
Callouses are often seen early in the season; they are exacerbated by switching from cold to warm water environments.
Most commonly they occur on the palmar aspect of the metacarpophalangeal joints and the distal palmar crease. Padded
gloves designed for water skiing may help to prevent or alleviate callous formation. In addition, some skiers use
Kevlar-reinforced gloves or glove liners as further resistance against abrasive forces.
SUMMARY
As the popularity of both recreational and competition water skiing continues to increase, attention should be directed
toward prevention of common water ski-related injuries. Though this exciting sport is relatively safe, certain hazards will
remain. Added to the usual risks associated with falls in other sports are the powerful motor boats, various marine
obstacles, and the fact that the injured must be rescued from the water. The incidence of injuries can be minimized by
careful attention to safe driving practices, use of safety equipment and protective devices, and controlled skiing within the
limits of the skier's ability.
ACKNOWLEDGMENTS
The authors thank USA Water Ski and the United States Coast Guard for their assistance. Illustrations drawn by Sophie
Zaworski.
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45 Wrestling
45
WRESTLING
MARK C. MYSNYK
Incidence of Injury
Mechanism of Injury
Direct Blows
Friction Injuries
Twisting and Indirect Force
Unknown Mechanisms
Prevention
Treatment
First Aid and Emergency Treatment
Subacute Treatment
Weight Loss and Making Weight in Wrestlers
Pros and Cons
What Weight Class?
Safe Weight-Cutting Guidelines
Conclusions
Chapter References
Wrestling is one of the oldest competitive sports, and it is practiced in one form or another in all countries. The Olympic
Games and other international competitions involve one of two styles of wrestling. Freestyle is directly descended from
ancient forms of wrestling as depicted in Greek and Egyptian art. Greco-Roman wrestling is a more modern form
developed in Europe in the late 19th century. Both styles emphasize takedowns and pinning with very little mat wrestling.
In both freestyle and Greco-Roman competitions, a wrestler has 10 to 20 seconds after getting a takedown to turn an
opponent to his back for additional points or a pin. If this cannot be done, both wrestlers start on their feet again to
attempt a takedown. Greco-Roman style differs from freestyle in that no holds can be applied to an opponent below the
waist, and the legs cannot be used to trip or hold the opponent.
High school and American collegiate wrestling, called “folkstyle,” was developed from the British Lancashire style. The
takedown maneuvers are much the same as in freestyle wrestling, but in addition there is “mat” wrestling, which involves
the top man trying to maintain control or pin his opponent and the other man trying to get an escape or reversal.
Wrestling is very popular in the United States, with more than 216,000 high school participants in the 1997–1998 season,
the sixth most popular high school sport in terms of number of participants ( 1). Its popularity is based in part on the fact
that multiple weight classes allow competitors of all sizes to participate. It has also been a popular college sport, but
because of Title IX and other factors the number of college programs has been steadily decreasing.
INCIDENCE OF INJURY
Wrestling is associated with a high injury rate. Injuries in preadolescence have not been extensively studied, but in one
study of 7- to 12-year-old wrestlers at a single folkstyle tournament, the conclusion was that “wrestling may be
considered a relatively safe contact sport for preadolescent boys” ( 2). In contrast, another study grouped the injury data
from three tournaments (two freestyle tournaments and one Greco-Roman tournament) for boys age 6 to 16 years. The
overall injury rate was 12.7%, with 4.6% of the participants suffering injuries severe enough to require them to withdraw.
Both injury rate and severity of the injuries correlated with increasing age. It was concluded, “There is still a substantial
risk for injury [in preadolescent wrestlers]” ( 3).
Most injury surveillance studies rank wrestling second only to football in injury risk ( 4,5). Depending on how injuries are
defined, the injury rate in high school is between 23% and 75% ( 5,6 and 7), while in college more than 50% of
participants sustain an injury severe enough to see a trainer or physician ( 8,9 and 10). Looked at another way, collegiate
wrestlers sustain an average total of 0.7 to 2.4 injuries per wrestler.
The risk of injury is further emphasized by the National Collegiate Athletic Association (NCAA) Injury Surveillance
System, which has tracked injuries in various sports from representative schools since 1985. In the 11 years between
1985 season and the 1995–1996 season, wrestling was second only to football in overall injury rate (practice and game)
at 9.6 injuries per 1,000 athlete exposures, third in practice injury rate (7.2 per 1,000 exposures), third in number of
injuries resulting in 7 or more days' time lost (3.7 per 1,000), and third in rate of injuries requiring surgery (0.58 per
1,000). It was concluded that spring football, wrestling, and women's gymnastics are the riskiest sports ( 11). Although the
injury rate is high, catastrophic injuries have been quite rare in wrestling, with one exception. In the fall of 1997 there
were three deaths related to weight loss, which are discussed later in this chapter.
The anatomic area of greatest concern is the knee. It accounts for the most injuries, the most serious injuries, the most
surgeries, and the most long-term problems (8,9,10,11 and 12). Incomplete ligament sprains and strains are the most
common knee injury, followed by meniscal tears and prepatellar bursitis ( 11). The shoulder and ankle are the second and
third most commonly injured regions, followed by the head and neck ( 11). In addition, although many studies do not
include skin disorders in their list of injuries, those that do clearly indicate that skin infections are a major area of
concern. (8,9). In the NCAA surveillance data from the 1997–1998 and 1998–1999 seasons, infection was second only to
ligament sprains in frequency ( 13).* At least at the college level, the most frequent infection is herpes simplex, followed
by ringworm and impetigo/bacterial infection ( 13). Infection rates cannot be calculated from the published NCAA data
(i.e., there may have been more than one infection per wrestler), but these three types accounted for a total of 192
infections among 984 wrestlers surveyed in the 1997–1998 and 1998–1999 seasons ( 13). In an older article, the
prevalence and incidence among college wrestlers of herpes alone were reported to be 18.8% and 7.6%, respectively,
and there was a 2.6% incidence among high school wrestlers ( 14).
More injuries occur in practice than during competition, but this is due solely to the fact that much more time is spent in
practice than in matches. The actual rate of injuries per match is much greater than the rate of injuries per practice; in the
11 years of NCAA surveillance, the match rate was four times greater ( 11). When expressed as injury rate per exposure
time, rather than per exposure, wrestlers were 40 times more likely to be hurt in a match than in practice ( 10). Takedowns
are the highest-risk activity; more specifically, most injuries occur to the wrestler being taken down. The bottom position
on the mat is the next riskiest position, and the top position on the mat is the safest ( 11).
MECHANISM OF INJURY
Direct Blows
This type of injury is caused by direct contact with the mat or the opponent. The rules do not allow slams, and, at least in
high school and collegiate competition, most dangerous throws and moves have been made illegal. However, a typically
safe move can become dangerous if not done properly or is “partially” countered, as demonstrated in Figure 45.1.
FIGURE 45.1. Fireman's carry. A: There is a direct blow to the top of the head, resulting in a possible compression injury.
B: The same move is shown causing a possible brachial plexus stretch injury.
Direct blows to the head resulting in compression or stretch injuries to the neck (or brachial plexus), or to the shoulder
resulting in acromioclavicular sprains, are the most frequent injuries from throws.
Neck injuries can also be caused by hyperextension. This can occur when a wrestler's head hits the opponent's thigh as
he is penetrating for a takedown ( Fig. 45.2).
FIGURE 45.2. A cervical spine hyperextension injury can occur as the wrestler “shoots” or penetrates during a takedown
attempt.
The knee frequently hits the mat during a “shot” or takedown attempt ( Fig. 45.3). Prepatellar bursitis can result from
either a single blow or repetitive trauma, causing a bloody or serous effusion.
FIGURE 45.3. The knee is subject to repeated blows. In this case, the attacking wrestler's right knee has hit the mat
during a routine single-leg takedown attempt.
The most frequent injury caused by contact with the opponent is a nosebleed. Broken noses are much less common.
Concussions and facial lacerations result from direct head-to-head collisions, as when both wrestlers attempt a takedown
at the same time. Also relatively frequent are auricular hematomas, or “cauliflower ear” ( Fig. 45.4). As a result of sheer
forces on the ear, a hematoma forms between the perichondrium and underlying cartilage. Whereas it represents a
permanent scar in our culture, it is a source of pride for European and Asian wrestlers, who rarely use headgear.
FIGURE 45.4. Chronic cauliflower ear. This can be prevented by proper treatment of acute episodes.
Friction Injuries
These injuries probably account for most of the infections seen in wrestlers. Herpes simplex, or “herpes gladiatorum” as it
has been colorfully labeled ( Fig. 45.5), can spread through an entire team. A review of an outbreak at a Minnesota
wrestling camp in which 60 (34%) of 175 wrestlers contacted herpes supported the belief that the spread of herpes was
primarily from skin-to-skin contact (15). This was also the presumed primary cause for the spread of ringworm and
impetigo, but other probable agents included contaminated mats, towels, and clothes ( 16).
FIGURE 45.5. Stages of herpes gladiatorum on a wrestler's forehead. A vesiculopapular rash (A) progresses (B and C)
to a crusted lesion.
One other infection endemic to wrestlers is septic prepatellar bursitis. Some cases are thought to be bloodborne from a
distant infected source, but most apparently result from direct penetration of the offending organism, even though a break
in the skin is rarely detected. Staphylococcus aureus is the organism most often responsible (17).
Twisting and Indirect Force
This is a common injury mechanism, especially for knee injuries. Figure 45.6 shows a common mechanism during a
takedown that results in valgus stress to the knee. Forces such as these can produce muscle pulls, ligament sprains, and
meniscal tears. Meniscal tears account for the most surgeries. Whereas in other sports and in the general population,
medial meniscal tears are approximately four to five times more common than lateral tears ( 18) (when the meniscal tear
is not associated with a cruciate ligament injury), in wrestlers the incidence is approximately the same. The ankle,
shoulders, and fingers are also all susceptible to twisting injuries.
FIGURE 45.6. As the offensive wrestler is driving into his opponent, significant valgus stress to the knee can result.
Unknown Mechanisms
In part because of the intensity of the sport, but also possibly because of the accumulation of multiple, relatively mild
stresses that finally produce a significant injury, the wrestler frequently is unable to identify exactly when he got hurt. This
is especially true for meniscal tears, which may insidiously start to ache or may lock for the first time after a trivial stress.
In a Workers' Compensation case, a similar history may create some question as to the seriousness of the problem, but
when dealing with wrestlers the treating physician should be aware that a significant injury may be present.
PREVENTION
The most important factor in the prevention of wrestling injuries is the coach. The techniques wrestlers use reflect the
coach's teaching, and their attitudes toward the sport reflect his philosophy. The coach is in complete charge of the
wrestling room, and absolute discipline is essential. The responsibilities of the coach include wrestlers' personal hygiene,
proper care of the mats, and ensuring that team members wear their headgear at all times.
Proper equipment is a necessary part of injury prevention. High school and collegiate rules require the use of headgear
in matches, but it is up to the coaches to make sure they are used in practice. Although auricular hematomas can occur
even when a wrestler is using headgear, such injuries are infrequent, and headgear should be worn at all times.
However, use of headgear is currently illegal in international competition, and although it is allowed in both American
Freestyle and Greco-Roman competitions, must be removed if the opponent so requests. Hopefully these rules will be
changed. Once a hematoma occurs, it may help to build up the circumference of the headgear with Plastizote to provide
further protection (Fig. 45.7).
FIGURE 45.7. Headgear modified with a piece of Plastizote added to the circumferential cushion to provide additional
protection for a wrestler recovering from a cauliflower ear.
Mouth guards are not mandatory, but their use should be encouraged, and they should be mandatory for wrestlers with
braces (for both their own and their opponents' protection). Likewise, although not all wrestlers need kneepads, they
probably decrease the risk of prepatellar bursitis. In a wrestler who is recovering from or has “fully” recovered from an
episode of bursitis, the bursa is likely to be thickened and more prone to recurrence. These wrestlers should wear a
kneepad at all times.
Wrestling mats must be of proper resiliency to cushion falls. Because they lose resiliency with time, they should be
periodically reconditioned (or replaced). If a school is fortunate enough to have two mats, they should be placed one on
top of other in the practice room to provide extra protection (rather than rolling one of them up and storing it). A wrestling
room must be of proper size to accommodate many wrestling pairs. It has been estimated that 50 square feet per
participant is the minimum space needed to conduct practices and minimize collisions between pairs of wrestlers ( 19).
In any sport fatigue is an added factor that increases the risk of injury, and conditioning is important in the prevention of
injuries. It has been reported that the injury rate is highest early in the wrestling season, and this is thought to be due in
part to inadequate conditioning ( 10). Wrestlers who want to both maximize their performance and decrease their risk of
injury need to begin a cardiovascular conditioning program at least 6 weeks before the start of the season, and
year-round conditioning is even better. Both endurance and strengthening exercises are important, but the former is more
critical for both injury prevention and success on the mat. Neck conditioning and strengthening exercises are especially
important and should be part of the off-season, preseason, and in-season conditioning program. Likewise, flexibility and
stretching exercises are of vital importance, and coaches should see that these are done year-round.
An additional component of preventing “injuries” applies to skin infections. Prevention and early recognition are the major
components in controlling this problem. A protocol of preventive or early intervention steps is presented in Table 45.1,
compiled from my own experience and other various sources (20; J.W. Hand and R.R. Wroble, Prevention of tinea
corporis in collegiate wrestlers, unpublished data; C.S. Kimmel, A guide to infectious skin diseases in wrestlers,
unpublished data, 1997).
TABLE 45.1. SKIN INFECTIONS PREVENTION PROTOCOL
A final component of prevention, especially in regard to reinjury, is compliance. Wrestlers as a group are notoriously
noncompliant, and this definitely increases the risk of reinjury. Anything that can be done to increase compliance is
obviously important. As an example, if a knee absolutely must be immobilized, a cast may be necessary rather than a
removable immobilizer. Secondly, the wrestler, his parents, and the coach should be carefully advised of the nature of
injury and the treatment plan. The treating physician cannot assume that the wrestler is relaying all the details to his
parents and coach.
Even if these precautions are followed, however, many wrestlers will still be noncompliant. One wrestler we treated was
placed in a cylinder cast after excision of a recurrent prepatellar bursitis, and the day after his hospital discharge he ran 3
miles with the cast on!
Because most wrestlers are compulsive and seek out physical activity, it is best to specifically prescribe an activity rather
than telling them to do nothing. For example, if the patient has an upper-extremity injury—let him continue to run, ride an
exercise bicycle, lift weights with the legs, and so on. Although it varies for each specific injury, a general ranking of
lower- to higher-risk activities, which can be used to gradually return injured wrestlers to full participation, is listed in
Table 45.2.
TABLE 45.2. RELATIVE INJURY RISK OF WRESTLING ACTIVITIESA
Finally, a physician should be present at all wrestling matches. This may have no effect in preventing injuries, but, as in
any sport, proper initial treatment may prevent minor injuries from becoming more severe, and severe injuries from
becoming catastrophic. In addition the physician can aid the referee or coach in deciding whether an injured wrestler can
safely continue. A compilation of rules that may be helpful for a match or tournament physician to know is provided in
Table 45.3 (21).
TABLE 45.3. INJURY RULES MEDICAL PERSONNEL SHOULD KNOW
TREATMENT
First Aid and Emergency Treatment
High school and collegiate rules allow a competitor 90 seconds of injury time. This is cumulative time for both treatment
of and recovery from injuries. The rules also state that in cases of unconsciousness or serious injury to the head, neck, or
spinal column, the contestant is not allowed to continue without the approval of a physician. In cases when the referee
questions the ability of the competitor to continue, the examination does not need to be hurried, because, if the injury
time runs out, an official timeout can be declared to allow completion of the examination. Once an official timeout is in
effect, only an examination, not any treatment, can be done. If a wrestler is unable to continue because of an injury, the
opponent is awarded the bout by default unless the injury occurred as a result of an illegal move on the part of the
opponent, in which case the injured athlete is awarded the decision by default ( 21).
Nosebleeds are one of the most frequent injuries during matches. Bleeding may be marked but can in almost all cases be
stopped by laying the wrestler down and plugging the nostril with cotton.
Lacerations require pressure to stop the bleeding, followed by butterfly or Steri-Strip closure of the wound and further
protection with an elastic wrap. Once the match is completed, if the laceration is severe enough it should be sutured,
then protected with a sterile dressing, and the wrestler is allowed to continue competition. Using a surgical stapler is an
emergency option during a match to control significant bleeding that cannot be controlled by simpler means.
A wrestler frequently can continue to wrestle with a finger sprain by simply buddy-taping the injured digit to an adjacent
one. If an actual fracture is present, treatment must be individualized. Some phalangeal and metacarpal fractures are
unstable and need extended cast immobilization or even surgery. Others (especially some metacarpal fractures) are
stable, and the treatment is symptomatic. However, the rules do not allow bandages, dressing, or casts of any materials
that “do not allow normal movement of the joint” ( 21).
Probably the most demanding injury to evaluate at mat side is the cervical injury. Although most cervical injuries are
strains, the wrestler must be questioned and examined concerning any radicular symptoms. These can be caused either
by a stretch injury of the brachial plexus or by compression of a nerve root. If a wrestler suffers only transient radicular
pain or burning into one or both arms that resolves completely within 1 to 2 minutes and there is no neurologic weakness
or deficit, he may return to competition immediately. Also, if there were never any neurologic symptoms but only neck
pain and stiffness, the wrestler may continue to wrestle if his neck motion is functional (not necessarily completely
normal, but nearly so). In contrast, if any weakness or neurologic deficit remains, the wrestler should not be allowed to
continue. Competition may resume after the neurologic symptoms and deficits resolve and neck strength and motion are
normal.
Subacute Treatment
Knee Injuries
As previously mentioned, the knee accounts for most injuries. Although most knee injuries are minor, a knee effusion
should alert the treating physician that there may be a serious intraarticular injury. Injuries to the anterior cruciate
ligament are much less common in wrestlers than in other athletes, and in a wrestler an effusion usually indicates a
meniscal tear (although tears frequently occur without an effusion).
Sprains of the collateral ligaments are the most common type of knee injury. The wrestler with a first-degree sprain can
return to play as soon as pain allows. Second- and third-degree sprains can be treated as in other sports. The
conservative option is with restriction from wrestling, work on early motion and strengthening, and use of an immobilizer
at all other times. As the ligament laxity tightens, the wrestler can gradually get back into competition. Alternatively, the
more aggressive treatment involves the use of a padded, hinged functional knee brace, and the wrestler is allowed to
return to competition as soon as he has near-normal motion and strength. Several factors, such as time of the season
(early- or late-tournament time), age and ability of the wrestler, and presence of other associated injuries, must obviously
be considered.
Because prepatellar bursitis is common in wrestlers, it is important to consider this entity when evaluating a swollen
knee. One simply needs to determine whether the swelling is superficial to the patella or patellar tendon or deep to them.
Aggressive initial treatment is essential to decrease morbidity and time lost.
An important component of this aggressive but appropriate treatment is aspiration of every acute case of bursitis.
Although prepatellar bursitis is usually not very painful, and if the patient absolutely had to wrestle he could, it is
important to rule out infection and to get the acute episode under control. If only a few milliliters of fluid is present, the
wrestler usually can return to practice the next day (with a good kneepad in place). If more than 20 mL is present, the
knee should be wrapped, immobilized, and examined (and reaspirated if necessary) daily or every other day until the
bursitis has resolved. If the wrestler returns to play too soon and the bursa is traumatized again, the bursal wall can
become thickened, resulting in recurrences after minimal trauma (chronic bursitis). Although surgery is rarely required for
prepatellar bursitis in the general population, it is often necessary in wrestlers if a chronic bursitis is established.
However, surgical treatment usually can wait until the off-season.
In addition to optimizing the chance that an acute traumatic bursitis will resolve, a second reason for aspirating all cases
of bursitis is to rule out infection. Unlike septic arthritis, septic bursitis is commonly missed clinically (e.g., it was
unsuspected in more than half of the cases in one report [ 17]), because the wrestler is usually afebrile, has little or no
pain, and has minimal or no erythema or warmth. The aspirate must be sent for culture, because the appearance of the
fluid and the results of Gram staining are normal in more than half of the cases, and the white blood cell count is rarely
greater than 30,000 cells per cubic millimeter ( 17).
If the infection is diagnosed early, oral antibiotics and frequent aspirations (daily or every other day) may control it. If the
infection is unresponsive, parenteral antibiotics and bursotomy are indicated. Bursotomy consists of making a 1- to
1.5-cm incision on the medial or lateral aspect of the bursa, inserting a sterile hemostat to break up any adhesions or
loculations, and then wicking the wound. If the bursitis does not respond to this further treatment, surgery (bursectomy) is
necessary.
Osgood-Schlatter disease is not caused by wrestling, but because participants must be on their knees, wrestling may
aggravate the condition. If the pain is tolerable, no treatment is necessary. If it becomes more severe, the initial treatment
is the use of kneepads and adjustments in the practice regimen or techniques so that not as much time is spent on the
knees. If the condition does not respond, the wrestler needs to refrain from wrestling until the pain is tolerable.
Shoulder Injuries
The most frequent shoulder injury in wrestlers is an acromioclavicular sprain. Treatment for a first-degree sprain (no
displacement) is symptomatic. Although the injury is caused by a fall on the shoulder, surprising relief can usually be
achieved with a donut-type pad of firm foam rubber or felt taped over the joint. If there is a stepoff (a second- or
third-degree sprain), the wrestler usually needs to stop wrestling until normal range of motion and at least 90% of
strength return, which typically is at least a couple of weeks.
Auricular Hematomas
Numerous treatments have been suggested for auricular hematomas. The goal is to aspirate the hematoma and then
apply compression to prevent recurrence. The traditional treatment is aspiration with an 18-gauge needle and application
of a cotton dressing soaked in collodion ( 22). However, even if the wrestler wears headgear, it is difficult to get back to
practice because the dressing frequently falls off. If the treatment is to be effective, the wrestler should probably be held
out for at least a few days. Variations include incorporating a swimmer's nose clip within the collodion ( 23), substituting
felt (White Wool) or Webril for the cotton ( 24), using a plaster (25) or a silicone splint ( 26,27), suturing buttons (28) or
cotton bolsters (dental rolls) in place ( 29), incising the hematoma and leaving a Penrose ( 30) or continuous vacuum drain
in place (31), and using open drainage with excision of the fibroneocartilage ( 32).
When evaluating the alternatives, the following must be considered: effectiveness, invasiveness, cost, complications, and
return to wrestling. Given these factors, aspirating or incising if necessary to totally drain the hematoma and securing
anterior and posterior cotton bolsters ( 29) or silicone splints ( 27) with through-and-through suture ( 29) is probably the
best choice. (Readers are referred to the cited references for details concerning technique.) This procedure can be done
in the office, allows immediate return to wrestling, and is highly effective. Because there is a risk of infection, 4 to 7 days
of prophylactic oral antibiotics and daily application of an antibiotic ointment on the suture line should be used. The
bolsters are left in place for 14 days. Wrestlers with recurrences should be referred to an otolaryngologist or plastic
surgeon.
Skin Infections
Although some would not consider them injuries, skin infections are a major problem in wrestlers. Physicians who treat
wrestlers must be able to recognize and treat the more common infections. Following the prevention and early
intervention steps outlined in Table 45.1 is the key to controlling this problem.
It is estimated that 80% to 90% of the general population harbor the virus herpes simplex type 1. The incubation period
for primary infections is 2 to 14 days ( 33). There typically are no systemic manifestations, although infection may be
associated with fever (25%), chills (27%), sore throat (40%), or headache (22%) ( 15). The lesions, most commonly
located on the right side of the wrestler's face, neck, and arm (the primary sites of skin-to-skin contact) ( 15), first appear
as clusters of vesicles on an erythematous base. They are contagious until they progress to the crusted stage (see Fig.
45.5C).
Herpes simplex cannot be cured, but the early use of acyclovir (200 mg given three times daily for 10 days), may reduce
the communicable period by half (16) and the course of the disease from 2 weeks to 2 days (20). Valacyclovir
hydrochloride (famciclovir) may also be effective. Because the virus is heat sensitive, the use of a hair dryer on a low
setting and 10% Benzoyl peroxide applied two times each day may help the lesions dry faster ( 34). For wrestlers with
recurrent herpes, suppression for the remainder of the season with acyclovir 200 mg twice daily or valacyclovir 500 mg
daily should be considered.
Ringworm (tinea corporis) is a fungal infection that can occur on any part of the body. The lesions are typically
well-demarcated, circular lesions with raised borders and central clearing that produces rings, which give rise to the
name. There is a long incubation period, and it is uncertain how long therapy must be continued until the patient is not
contagious. In addition to following the prevention protocol (see Table 45.1), the basis of treatment is the use of a topical
antifungal, such as clotrimazole, miconazole nitrate, or ketoconazole. For disseminated lesions or hair involvement, oral
ketoconazole is recommended. Likewise, for wrestlers with multiple or chronic lesions, or when a team is faced with a
widespread outbreak, “pulse therapy” with a 7-day course of oral ketoconazole has been recommended for the whole
team (33).
The last common skin infection is impetigo. This is usually caused by S. aureus or by Streptococcus species. It typically
first appears as a rash with small pimples or blisters that burn and itch. The blisters usually break open and form a
honey-colored crusting with surrounding redness. Treatment is with oral antibiotics, such as dicloxacillin or a
first-generation cephalosporin.
WEIGHT LOSS AND MAKING WEIGHT IN WRESTLERS
Before the 1997–1998 season, weight-cutting issues centered primarily on the competitive pros and cons and the
potential short- and long-term health risks. However, the potential risks became very real when, within 5 weeks at the end
of 1997, three collegiate wrestlers in three different states died while attempting to lose weight. In the 4 days before their
deaths, the wrestlers lost, respectively, 13 pounds (6.2%), 12 pounds (7.2%), and 15.3 pounds (9.0%) of their body
weight. The total difference between the three wrestlers' preseason weight and planned competitive weight averaged 30
pounds (range, 25 to 38 pounds) ( 35). Each wrestler was attempting to make weight for a weigh-in on the day before a
competition; with potentially more than 12 hours of recovery time before he would have to wrestle. These are the first
known weight loss–related deaths among high school or collegiate wrestlers.
At the college level, the NCAA instituted rule changes that essentially made this degree of weight loss impossible. The
weight classes themselves were altered, eliminating the lightest weight class. Minimal weight classes are to be
determined early in the season using fat percentage determinations, and the wrestler is not allowed to wrestle below this
weight (with or without a physician's approval). Measures were also put in place to make it unlikely that a wrestler can
lose too much weight too fast to get to a certified weight class. The use of rubber sweatsuits and saunas to dehydrate
was made illegal. The time between weigh-in and the start of a dual meets or tournament was dramatically shortened. In
the past, there had been 5 to 24 hours between weigh-in and competition, and there was a single weigh-in for multiday
tournaments. Although both of these rules were designed to decrease the focus on making weight, they both probably
encouraged wrestlers to lose even more weight, since they had a longer time to recover. Now weigh-ins are done 1 hour
before competition, and multiday tournaments have weigh-ins on each day of competition. These changes have indeed
changed weight loss practices in college wrestlers. In the 1997–1998 season, before the new rules were instituted, 46%
of wrestlers lost more than 11 pounds from their preseason weight to their competitive weight; in the 1998–1999 season,
with the new rules in place, only 19% did so ( 13).
At the high school level, many states already had weigh-ins 1 hour before competition, but starting with the 1999–2000
season, this practice was made mandatory for all states. Similarly, many already had minimal weight rules before the
three deaths, and now all must have them (36). The minimal weight plans vary among states, in terms of both the fat
percentage used to calculate minimal weight and the appeal process (if any) for wrestling at a lower weight. Most states
that allow an appeal process require a physician's written approval for the wrestler to compete in a lower weight class.
Issues the physician must face include the following: If a wrestler requests you to sign his appeal, should you? What are
safe weight-cutting guidelines? What is the accuracy of the fat percentage calculations? What is the risk of another
weight cutting–related death? What other short- and long-term risks are involved in making weight? Is there any actual
competitive advantage to losing weight? Whether the wrestler is appealing his minimal weight class or not, if he requests
“professional” advice on weight loss practices, what should your response be? Whether the wrestler is losing weight or
not, what advice should you give regarding proper nutrition? These issues are covered in the following sections.
In an attempt to reach a lower weight class and at least theoretically gain a competitive advantage, wrestlers lose weight
through a combination of caloric restriction (dieting), exercise, and short-term dehydration. The dehydration may be from
exercise alone, exercise wearing a rubber sweatsuit, or the use of a sauna (the latter two have been illegal in high school
for years but were legal in college until the middle of the 1997–1998 season). The use of diuretics, laxatives, and
self-induced vomiting has been reported but is not thought to be a major problem ( 37) and is illegal.
As stated earlier, new collegiate rules have altered weight loss practices, but before these changes the reported weight
losses from preseason to competitive weight class, which involved both dieting and short-term dehydration, averaged
7.5% (38) to 7. 3% (39) for college wrestlers and 5.7% for high school wrestlers ( 38). Weekly weight loss (which in most
cases was a result of short-term dehydration) averaged 3.1% in high school wrestlers and 4.4% in college wrestlers ( 38).
Or, expressed as the amount lost, 49% of high school wrestlers lost 3 to 5 pounds and 23% lost 6 to 10 pounds weekly.
In college wrestlers, 44% reported losing 6 to 10 pounds and 41% stated that they lost 10 to 20 pounds weekly ( 37).
In 1967 the American Medical Association's committee on medical aspects of sports published a “physician stand on
weight control in wrestling,” repeating their previous “unqualified objection on both ethical and physiologic grounds, to the
indefensible practices of “making weight”' ( 40). They have not given an updated statement. In 1976 the American College
of Sports Medicine (ACSM) issued a similar condemnation of weight-cutting, stating that it hurt performance and caused
numerous adverse physiologic responses ( 41). Both of these statements either overlooked or misinterpreted much of the
literature available at the time and obviously could not have taken into consideration the research that has been done
since they were released. The ACSM issued a revised position statement in 1996, which was aimed more at encouraging
smart weight-cutting practices (42). The latest ACSM position stand is a good general review of the weight-making
process but does not provide the details necessary to answer the questions posed at the beginning of this section.
Pros and Cons
The only possible “pro” of weight-cutting, whether from dieting or dehydration, is a competitive advantage. The “cons,” on
the other hand, are numerous (Table 45.4) and can be divided into possible health risks and performance concerns.
Each one of these will be dealt with separately.
TABLE 45.4. CONCERNS OF WEIGHT CUTTING IN WRESTLERS
Cardiovascular or Heart Disturbances
Although elimination of the use of rubber sweatsuits and saunas to make weight has reduced the amount of acute
dehydration in wrestlers, the intensity at practices is such that it is not unusual for a wrestler to lose 5% of his weight in a
typical practice. When wrestlers undergo a short-term dehydration, they do not fully rehydrate if they have 5 hours or less
between weigh-in and competition, and therefore they compete in a dehydrated state ( 43,44,45,46 and 47). If dehydration
is significant, it can cause a decrease in plasma volume, which in turn decreases stroke volume ( 48,49).
Several studies showed no significant change in exercise heart rate after a short-term weight loss (primarily through
dehydration) of 1% to 11.8% ( 50,51,52 and 53). Other studies showed an increased submaximal exercise heart rate that
is reversible after a short period of rehydration. After a weight loss of 3.8% to 6.8%, the initial exercise heart rate was
increased, but it was restored to normal after a partial rehydration period lasting 1 to 5 hours ( 54,55,56 and 57). One
study concluded that ad libitum fluid replacement after a 48-hour weight-loss regimen (as typically practiced by wrestlers)
“can effectively restore cardiovascular dynamics within one hour” ( 54). However, other researchers demonstrated a
persistently increased exercise heart rate ( 49,58). The consensus seems to be that short-term dehydration of less than
5% poses no significant load on the heart and no adverse effect on performance.
Heat Illness
Within these limits of a 5% short term dehydration weight loss the decreased plasma volume poses no significant cardiac
risk; however, it can impair sweat production ( 48) and theoretically predispose the athlete to heat illness. There are four
disorders commonly referred to as heat illness: heat cramps, heat syncope, heat exhaustion, and heat stroke. The last of
these can be fatal. They are a potential risk for any athlete or any individual who works on a hot day or in a hot
environment and sweats. There were 54 heat-related deaths in football players between 1964 and 1983 ( 59).
The three weight loss–related deaths described previously were the first known cases among high school or college
wrestlers. They all happened within 5 weeks of the beginning of the 1997–1998 season. Although these athletes were all
attempting to lose much more weight in a short time than any informed authority would recommend, thousands of
wrestlers have lost the same amount of weight without any deaths occurring. In fact, based on historical weight-cutting
information, the odds of any three wrestlers' dying in the same season when the only factor is the amount of weight lost
were calculated to be between 1 in 4,100,000 and 1 in 4,100,000,000,000 ( 60).
Although weight loss is certainly the biggest factor, there almost certainly must be another factor, although one has not
been identified. The Centers for Disease Control and Prevention concluded that use of the supplement creatine was not
a significant factor (61), but there are several reasons why it may be a contributing factor. Excess creatine must be
excreted by the kidneys, and the urinary creatine excretion rate increases as much as 90 times after a loading dose of
creatine (62). There is a documented increased muscle mass with creatine supplementation, but it is unknown whether
this is caused by increased water within the muscle cells or by some other mechanism. An intracellular water shift could
accentuate dehydration from any other cause (e.g., making weight). There have been at least two documented cases of
renal dysfunction in individuals taking creatine ( 62). In addition, in one of the three wrestling deaths, rhabdomyolysis was
the final cause of death, and the altered muscle structure could predispose to muscle breakdown at a lower threshold, or
to a greater degree once it starts, or both. Finally, if there is an additional factor besides weight loss that contributed to
the deaths, it most likely would be something that became popular just before 1997, which is the case with creatine.
Although this discussion is speculative, it is included to emphasize that there almost certainly were other factors than the
weight loss alone that contributed to the wrestlers' deaths, and to suggest that, given the opportunity, any medical
authority should counsel against the use of creatine in anyone who may deliberately dehydrate to make weight. In fact,
the manufacturers of creatine suggest taking large amounts of water with their product. In any case, the implementation
of weigh-ins 1 hour before competition and the elimination of the use of rubber sweatsuits and saunas has almost
certainly eliminated the risk of death in an otherwise healthy wrestler.
Impaired Renal Function
Blood and urine chemistries panels of high school and college wrestlers at weigh-ins revealed changes consistent with
dehydration (39,43). It has been speculated that this dehydration can cause acute renal ischemia and perhaps produce
renal problems when these wrestlers reach middle age ( 63). It is well documented that exercise alone is associated with
proteinuria, decreased renal blood flow, decreased glomerular filtration rate, decreased urinary water excretion, changes
in electrolyte excretion, hemoglobinuria, and myoglobinuria ( 64,65). These changes are associated with any form of
exercise, are related to the intensity of exercise, and can be exacerbated by dehydration. Wrestling certainly combines
intense exercise with dehydration, and therefore all of these changes can occur in wrestlers. However, all of them are
acute changes that are reversible and cause no known long-term problems.
To evaluate for possible long-term effects of wrestling on renal function, the renal function of 320 former wrestlers was
compared with that of 220 control subjects who had never wrestled. All subjects were between the ages of 30 and 84
years. Blood samples were used to estimate creatine clearance, and urine specimens were analyzed to calculate a urine
protein/creatinine ratio as an estimate of proteinuria. It was concluded that “the reported acute changes in renal function
associated with exercise and accentuated by dehydration have no long-term adverse effects on renal functions” ( 38).
Supporting this finding is a survey of former college wrestlers that found no increased incidence of renal disease
compared with nonwrestling control subjects ( 66).
Hypertension
There is no evidence that wrestlers, as a group, are hypertensive ( 63), but it has been suggested that renal damage
could cause hypertension later in life ( 43). As just explained, there is no evidence of any long-term renal damage in
former wrestlers. In addition, as part of the same study on renal function ( 38), the blood pressure of all subjects was
recorded. There were no significant differences between the former wrestlers and controls.
Growth
Because wrestlers typically diet in addition to dehydrating to make weight, it is thought that the process may impede
normal growth and development (41). There are anecdotal reports of individuals who wrestled being several inches
shorter than their nonwrestling brothers ( 67), and one investigator stated that his studies, “crude and limited as they
are—imply that a reduction in growth will result from chronic weight-cutting” ( 68). No evidence was presented to support
this hypothesis, however.
It would take a longitudinal study of the growth curves of individuals who did and did not participate in wrestling, starting
before they began wrestling and continuing until they reached skeletal maturity, to determine whether wrestling has an
effect on height. However, there is evidence to suggest that it does not. Among adolescents, it has been shown that
chronic caloric deficiency can retard normal growth ( 70,71). Whether the deficiency is corrected ( 69,70) or not (71),
skeletal growth and maturation can be slowed and the growth spurt delayed, but the growth period is prolonged and
normal adult height is eventually achieved.
It would seem that if there is this much resiliency to growth despite several years of uncorrected caloric deficiency, no
adverse effects would be expected in wrestlers who at worst have repeated short-term episodes of caloric deficiency
interspersed with normal eating during a 3- to 4-month season.
Supporting this idea is a study that compared the height of skeletally mature former wrestlers with that of controls who
never wrestled. Both absolute height and heights relative to the height of the subject's father were compared. Although
former wrestlers were shorter than nonwrestlers, there was no correlation between the amount of weight lost during their
wrestling career and their height relative to their father's height. It was concluded that wrestlers were not short because
they wrestled but that they became wrestlers because they were short (i.e., a selection phenomenon) ( 72).
Decreased Metabolic Rate
A group of wrestlers classified as “weight cyclers” (those who lost more than 4.5 kg at least 10 times a season) were
found to have a lower resting metabolic rate than noncyclers (those who lost less than 1.4 kg weekly). It was concluded
that weight cycling produced a lower resting metabolic rate and that in adult life this could cause weight control problems
(73). In contrast, a longitudinal study that evaluated the resting metabolic rate in preseason, midseason, and postseason
showed that, although the rate decreased during the season, the postseason value was similar to the preseason value.
The authors concluded that weight cycling did not produce a lasting decreased resting metabolic rate ( 74). Furthermore,
no significant differences were found in amount of weight gained after graduation when former collegiate wrestlers were
compared with former nonwrestling athletes (66).
Testosterone Levels
It has been demonstrated that testosterone levels in wrestlers decrease in midseason and that serum testosterone levels
correlate with low body fat. The levels returned to normal after the season was over ( 75,76). This effect is not unique to
wrestlers: in any endurance athlete the serum testosterone level tends to be low ( 77,78). In contrast, short-term exercise
generally causes a transient rise in serum testosterone ( 77).
Eating Disorders
If a wrestler diets and exercises to make weight an average of two times per week for 3 months (the season being 4
months), is overconcerned about his weight (which could be expected at each weigh-in), and eats a large amount after
making weight, he has met a liberal interpretation of four of the five criteria listed by the Diagnostic and Statistical Manual
of Mental Disorders (3rd ed., revised) for bulimia. If during the weigh-in meal, because of extreme thirst or hunger or for
any other reason, he feels a lack of control, he has met all five criteria. Obviously, this practice is not bulimia, but an
evaluation of college wrestlers suggested that wrestlers may be at risk for the development of sports-induced eating
disorders, although no definite abnormalities were found ( 79). The authors emphasized that “caution must be invoked in
interpreting the results of these questionnaires as measuring symptoms of psychopathy associated with eating.”
Performance
There are both proponents and opponents of weight-cutting when performance is discussed. The theoretic reason for
losing weight, experimental findings, and epidemiologic findings are discussed here.
Theory
The theoretic reason for losing weight is to gain a competitive edge in physical size and strength. This can be illustrated
with the example of two wrestlers of equal ability, both at 14% body fat 2 months before the season begins. One weighs
135 pounds and decides he is not going to lose any weight and will wrestle at 135. The other weighs 150 pounds and
begins his diet 2 months before the season starts. He gradually loses fat weight and gets down to 135 pounds at 5%
body fat. If both of these athletes weighed in at 135 pounds, the wrestler who dieted should have more muscle mass and
therefore should be stronger than the wrestler with higher body fat. If that same wrestler had a short-term dehydration of
5 pounds, he could compete in the 130-pound weight class, which would give him even a greater potential strength
advantage. However, the theoretic argument against this is that the weight-cutting process will weaken and fatigue the
wrestler who lost weight and thereby place him at a competitive disadvantage.
Experimental Findings
Many experimental studies have been done to assess the effects of weight loss (through various combinations of
exercise, dehydration, and calorie restriction) on strength, endurance, exercise heart rate, cardiovascular conditioning
(maximal oxygen uptake), and work capacity. Conflicting results are found in the literature, largely because of variations
in experimental design. It is known that there may be different physiologic effects according to whether the weight is lost
by use of diuretics, dehydration in a sauna, or exercise ( 80). The environment in which the tests are conducted
(comfortable, hot-wet, or hot-dry) (48,81); the subjects' diet (high or low carbohydrate content) ( 82,83); whether the
subjects are heat acclimatized (the heart rate increases less after dehydration with heat acclimatization) ( 46,84); the
conditioning of the subjects (49,85); whether a period of recovery and/or rehydration is allowed ( 55,56,86,87), and the
time frame for the weight loss can all affect the results.
One final factor that can drastically affect performance in experiments or in actual wrestling competition after weight loss
is the psychological response to that weight loss. This can vary dramatically with individuals. Since it is impossible to
control for this effect, it must also be considered when looking at and comparing the results of the studies. Given these
variables, a brief review of the literature follows.
Maximal oxygen uptake. There are at least four studies showing no significant decrease in maximal oxygen uptake after
a short-tem weight loss (49,52,83,88), although one of these did show a “trend” in that direction ( 52).
Strength. From Table 45.5 it can be seen that the majority of studies showed no decrease in strength with a weight loss
of 8% or even more. Those few studies showing a negative effect on strength demonstrated it in only a small minority of
the muscles tested.
TABLE 45.5. EFFECTS OF WEIGHT LOSS ON STRENGTH
Endurance and Work Capacity. It has been suggested that weight-cutting may impair performance by various means:
exercise-related depletion of glycogen stores, increased muscle temperatures, or a decreased plasma volume and
electrolyte shifts ( 89). The effects of these changes are hard to separate experimentally, and in addition the
psychological effect of weight loss, mentioned earlier, must be considered. It therefore is not surprising that the
experimental effects of weight loss on muscular endurance and work capacity are quite variable.
No effect on endurance was shown in three studies involving weight losses of 4% ( 90), 3.7% to 9.5% (88), and 5% (46).
In contrast, an evaluation of subjects tested in euhydrated, dehydrated, and partially rehydrated states concluded that
“both isotonic and isometric endurance...decreased significantly” ( 91). However, an analysis of the data showed that, of
the four muscle groups tested, two were not significantly affected isometrically or isotonically by dehydration, and in the
rehydrated state (which would parallel a wrestling situation) three of the muscle groups tested isometrically were
increased over the euhydrated levels. Another study showed a 10% decrease in work capacity and a 12% decrease in
run time to exhaustion, but the subjects were allowed no food or water in the 12 to 16 hours before testing, which is not
realistic for wrestlers ( 92).
Three experiments compared work performance in the euhydrated versus dehydrated state with no rehydration allowed.
In a 6-minute arm-crank test, wrestlers who lost approximately 6.2% of their weight over 4 days by diet restriction,
exercise, and dehydration and had been on a low-carbohydrate diet during the 4 days demonstrated a 7.9% decrease in
total work. With the same weight loss but a high-carbohydrate diet, the decrease was significantly less, and some
wrestlers actually improved their performance ( 82). After a 3.6% to 4% weight loss in nonwrestlers with “marked
differences in fitness,” work time on a bicycle ergometer was significantly decreased. Well-trained subjects showed a
smaller decreased work time than those in poorer shape ( 49). In contrast, after a 5% dehydration weight loss wrestlers
showed no significant decrease in average or peak power nor in work time on a bicycle ergometer anaerobic test. In fact
the wrestlers' total and peak power per kilogram of weight increased with the weight loss, suggesting a benefit of
weight-cutting (93).
In a situation similar to what a college wrestler would have experienced before the 1-hour weigh-in rule, three studies had
present or former wrestlers lose 5% ( 84,85), 3.7% to 9.5% (88), or 8% (94) of their weight and then allowed them to eat
and rehydrate over 3 to 5 hours. In two of these studies, a decreased performance was measured when the subjects
were tested within 1 hour of making weight, but all four studies showed a return to normal after 5 hours. Because there
may have been an effect at 1 hour and the weigh-in rules have now changed, these studies need to be repeated to match
the current situation. One of these studies included muscle biopsies to assess glycogen levels ( 94). During the 96 hours
of weight reduction, muscle glycogen levels decreased 46%; they recovered only 14% during the 3-hour rehydration
period. Nevertheless, neither performance, strength, nor maximal oxygen uptake was significantly decreased.
In summary, as would be expected, some physiologic changes do occur with weight losses of 3% to 12%. There is no
universal effect on all muscle groups. In addition, significant recovery occurs when 5 hours of rehydration is allowed
before testing. In addition, it appears that if the subjects are regularly consuming a high-carbohydrate diet and are well
conditioned, the changes that do occur will be lesser. Although there may be exceptions, if a rehydration period of at
least 5 hours is possible, significant detrimental effects on exercise heart rate, maximal oxygen uptake, muscle strength,
endurance, and performance are unlikely after short-term weight losses of 5% or even more. With only 1 hour of
rehydration allowed, there may be changes, and the wrestler and coach should analyze performance measurements for
such changes.
Epidemiologic Findings
Table 45.6 shows the fat percentages of various wrestlers. Heavyweights, who do not have to lose any weight, naturally
have the highest fat percentage, and in general the lowest weight classes have the smallest fat percentage. Most
successful wrestlers have less than 7% body fat, and some have less than 5%. It could be argued that these same
individuals would have been at least as successful at a higher fat percentage. However, as can be seen in Table 45.7, in
the only three studies comparing the fat percentages or skinfold totals with the wrestling success, in each case the more
successful wrestlers were leaner.
TABLE 45.6. DOCUMENTED FAT PERCENTAGE OF WRESTLERS

TABLE 45.7. STUDIES COMPARING FAT PERCENTAGES OF SKINFOLD TOTALS WITH LEVEL OF SUCCESS
In a high school tournament when the wrestlers were allowed to weigh in the night before competition, weight difference
the next day (immediately before competition) was directly related to success on the mat. That is, the wrestlers who
gained the most weight in the approximately 12 hours between weigh-in and competition, and therefore had presumably
lost the most weight to “make weight,” were the most successful ( 95). (These results may not apply since the institution of
the 1-hour weigh-in rule.) A similar study in college wrestlers showed no correlation between weight gain and success
(96).
In summary, a reduction to 5% body fat and a short-term dehydration of up to 5% have not been shown to have
detrimental effects on health or performance. Within the parameters discussed, there is in fact theoretic, experimental,
and epidemiologic evidence that performance may be enhanced. However, many of the studies allowed at least 5 hours
of rehydration time, and the results may not be applicable with only 1 hour of rehydration time, as is now in effect.
What Weight Class?
Most current recommendations condemn any dehydration and suggest 7% as the minimum fat percent in high school
wrestlers (96). The most recent ACSM position stand on weight loss in wrestlers suggests a minimum fat percentage of
7% in those age 16 years and younger and 5% in those older than 16 years of age ( 42). The policy of not allowing a
wrestler to compete below 7% body fat must be questioned, however, because most successful wrestlers in the past
have been below 7% and some even below 5% (see Table 45.6). Whether any dehydration is used to make weight
should be based on performance (discussed later) and should take place only within certain limits: that is, it should be
short term (less than 12 hours) and should equal no more than 5% of the wrestler's weight.
Because individual wrestlers react differently, both physiologically and psychologically, to dieting and dehydration, there
is probably no one ideal fat percentage that can be applied to every wrestler. Except for the heaviest weight classes, 5%
to 7% body fat can be used as a guide, but some wrestlers can more effectively compete at a lower and some at a higher
fat percentage.
Another reason why everyone should not be encouraged to conform to one “ideal” fat percentage is that the methods
used to determine fat percentage are not accurate enough. Hydrostatic weighing (densitometry), anthropometry
(measurement of skinfolds or body dimensions), and bioelectrical impedance analysis have been used to estimate fat
percentage. Although the prediction of mean values for a large population is relatively good, prediction of individual body
fat percentages is not (97), and “it is clear that, regardless of the methods used, determination of minimal wrestling
weights is a process which is inherently subject to relatively broad margins of error” ( 98).
Underwater weighing is considered the gold standard, but the calculated fat percentage is accurate only within ±2% to
4% (99). Skinfold measurements have been used most frequently for wrestlers for reasons of convenience and cost. The
various equations have a 3% to 9% margin of error ( 100). Even the best skinfold equations with experienced testers have
only a 68% confidence level, which spans at least 4.88 kg (10.75 pounds) ( 101). This standard deviation covers more
than two high school wrestling weight classes, and in one of three cases the error will be even greater! Although some
gifted individuals can wrestle successfully at any of two or three weight classes, there are many more examples of
wrestlers who could win, and win safely, a state or NCAA title at one weight class but not even place at two or even one
heavier weight class. With the inaccuracies of minimal weight predictions, they should not be used as more than a rough
guide to the proper weight class.
What should determine the proper weight class? Performance! Wrestlers, parents, and coaches should be educated on
proper weight-cutting and nutrition, and then the three parties together should decide on the proper weight class based
on performance—not just on the mat but also in school and at home. If a wrestler is so preoccupied with making weight
that family relations are strained or school work suffers, he is either cutting too much weight or losing it incorrectly. If the
wrestler is not performing well on the mat and seems to be getting tired near the end of the match, he could be cutting too
much weight, or be cutting it wrong, eating incorrectly, be out of shape, or not getting enough sleep. There are many
possible explanations for poor performance besides cutting too much weight, and each must be examined.
It is important that a wrestler not mistake water loss for fat loss. In the example given previously of the 150-pound
wrestler with 14% body fat, he could get down to 135 pounds by gradually reducing to 5% body fat without any
dehydration at all. As outlined previously, these would be safe parameters. However, it would not be prudent for that
wrestler to dehydrate 9% to get down to 135 pounds. If he gets to his “target” weight by means of excessive dehydration,
it will probably affect his performance and pose a health risk. As mentioned earlier, it is not unusual for a well-hydrated
wrestler to lose 5 pounds of water weight during an intense workout. For a wrestler to lose more than this, or for a
dehydrated wrestler to lose even this much, would typically require the use of rubber sweatsuits or a sauna, both of which
are now illegal. Conversely, if a wrestler seems to be getting beat because he is getting outmuscled, and if the fat
percentage estimate indicates that he has fat to lose, it can be suggested that he try a lower weight class. No wrestler
should ever be forced to go down to a lower weight, however, because that can be the quickest way to make a wrestler
lose interest in the sport.
Safe Weight-Cutting Guidelines
There are few absolutes concerning proper weight-cutting, but one is that not everyone needs to “cut” weight. Target
figures for most weight classes are 5% to 7% body fat. Heavyweights and those in the upper weight classes may have a
much higher percentage. Successful wrestlers may be found above and below this range. Furthermore, it must be
remembered that, even with the “gold standard” of underwater weighing, a wrestler told that he has 10% body fat may
actually have 8% to 12% body fat—and with skinfold determinations the range is even larger.
Another absolute concerning proper weight-cutting is that there is no place for diuretics, laxatives, or self-induced
vomiting!
If a wrestler is going to lose weight, he should start his diet early (at least 1 month before the season starts) and plan to
lose 1 to 2 pounds per week. More-rapid weight loss from dieting could result in loss of lean muscle mass rather than fat.
A 1-pound loss is equal to a 3,500-calorie deficit, so either input has to be decreased or output has to be increased, or
both. Running 1 mile uses approximately 125 calories, and an intense 30-minute workout uses 500 calories. The wrestler
should consume a minimum of 1,500 to 2,500 calories per day (depending on his size) both preseason and in-season.
The goal is to lose the fat weight by the start of the competitive season. If he so desires (not everyone needs to), the
wrestler can safely dehydrate up to 5% in the short term (less than 12 hours) to make weight. Dehydration over a longer
period could interfere with concentration in school or with the conditioning and technical aspects of wrestling practice and
may pose a health risk.
The wrestler should regularly consume a balanced diet of 50% to 60% carbohydrates, 25% to 30% fats, and 10% to 20%
proteins. Athletes that are regularly consuming a balanced diet with enough calories do not require a vitamin supplement.
However, in the case of wrestlers, a supplement is a good idea. A simple multivitamin should suffice (there's no need for
expensive supplements). Common sense dieting tips include counting calories (using a food content and calorie book),
eliminating junk food and fluid-retaining (salty) foods, consuming low-calorie or calorie-free fluids, substituting white meat
for red meat, and avoiding frying in food preparation.
Because a hard workout and an overnight fast can deplete muscle and liver glycogen stores, wrestlers should ideally
have their weight under good enough control so that they can have a good meal (one high in carbohydrates) the night
before a match. It is at that time that they should change to fluids with calories. Wrestlers “drift” or lose 0.5 to 2 pounds
overnight, and each wrestler should know precisely how much he drifts and take this into account when he plans how
much to eat or drink the night before. If a workout is needed on the day of the match it should be a light one to avoid
further glycogen depletion.
The precompetition meal is best consumed 5 hours or more before competition. However, with the new weigh-in times,
this usually is not possible. If there is less than 2 hours between weigh-in and competition, any “meal” should consist of a
liquid supplement. If there are 5 hours between weigh-in and competition, the meal should be very high in carbohydrates,
since fats slow absorption and excessive protein may worsen dehydration due to an obligatory water excretion with
excess nitrogen (102).
Regardless of the time interval between weigh-in and competition, if any dehydration was used to make weight, fluid
replacement should begin immediately after the weigh-in. A 6% to 10% carbohydrate drink should be consumed; such
liquids are absorbed as quickly as water and, in addition, supply needed carbohydrates and calories ( 103). Caffeine
should be avoided because it may have a diuretic effect and therefore promote water loss.
During a tournament, wrestlers may wrestle several times in a single day. They therefore should replenish fluids and
carbohydrates throughout the day. Although it is convenient for coaches, the entire team should not wait for a break
between matches to go eat. The wrestlers in lighter weight classes will finish (and subsequently start) at least 2 hours
before the heavyweights and should therefore begin to eat and drink soon after they finish their last match of the session,
to allow as much time possible for rehydration and glycogen replenishment.
Getting back to the question posed at the start of this section, if a wrestler asks you as the physician to approve his
competing in a weight class lower than his certified weight, should it be approved? My personal opinion is as follows:
whether he is losing 1 or 20 pounds, I would want to make sure that the athlete, his coaches, and hopefully his parents
understand the basics of safe weight loss and proper nutrition as outlined in this chapter. If this is the case and there is
only 5 pounds difference between his desired weight and his certified weight (which is most commonly the case), I would
almost always approve it. If the difference is greater than 5% of their weight, I think the decision needs to be
individualized based on the wrestler's age, growth history, competitive weight the previous season, experience, the
coaches' experience (in terms of managing safe weight loss practices), willingness of the parents to help, and the
wrestler's own grasp of proper weight-cutting guidelines as presented here.
CONCLUSIONS
Wrestlers as a group pose a definite challenge to their treating physicians. Wrestling is arguably the most intense and
physically demanding sport and carries a relatively high injury rate. As a group, wrestlers are noncompliant. And weight
cutting, a process inherent to wrestling, involves complex health and performance issues about which physicians are
expected to be knowledgeable. In order to optimally treat wrestlers, the attending physician should be familiar with the
principles discussed in this chapter.
* Conclusions drawn from or recommendations based on the data provided by the NCAA are those of the author, based on my own analyses and
evaluations, and do not represent the views of the officers, staff, or membership of the NCAA.
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46 Soft Tissue Athletic Injury
46
SOFT TISSUE ATHLETIC INJURY

WAYNE B. LEADBETTER
Epidemiology
Spectrum of Injuries: Definition of Terms
Composition and Function of Injured Tissues
Cellular Elements of Connective Tissue
Extracellular Matrix Components
Seven Basic Mechanisms of Sports Injury
Tissue Response to Physical Injury
Acute Macrotraumatic Tissue Response
Chronic Microtraumatic Injury Response
Acute Versus Chronic Clinical Injury Profile
Adaptation Versus Injury
Epigenetic and Genetic Effects on Soft Tissue Healing
Aging
Vascularity
Hormonal Influence
Rest
Genetic Influences
Structural Variability
The Principle of Transition
Injury Response Patterns in Specific Tissues
Muscle Injury
Tendon Injury
Ligament Injury
Synovial Injury
Sources of Pain in Soft Tissue Injury
Therapeutic Management of Soft Tissue Sports Injury
General Principles
Basic Elements of Diagnosis
Specific Treatment Alternatives
Medical Modifiers
Physical Modalities
Rehabilitative Therapeutic Exercise
Surgical Indications in Soft Tissue Injury
Returning the Athlete to Sports Participation
Conclusions
Chapter References
Soft tissue athletic injuries are the most challenging and controversial problems encountered in sports medicine. As the
most frequent disability associated with athletic competition and recreational athletics, injury to the dense connective
tissue of ligament, tendon, and associated muscle is as difficult to qualify as to quantify. Representing the largest tissue
component of the body, these “connecting tissues” include a diverse histologic family comprising not only muscle,
tendon, and ligament but also joint capsule, fascia, meniscus, articular cartilage, synovium, intervertebral disk, and
adipose tissue. Although sports differ in risk because of the quantitative differences in stresses to different anatomic
areas, soft tissue injuries still make up the majority of complaints in all sports and at all levels of competition. It is
estimated that 30% to 50% of all sports injuries are caused by soft tissue overuse ( 1). Although many of these complaints
create symptoms of inflammation, a variety of tissue responses may take place when a sports injury occurs. Some of
these responses are predictable, but others are unanticipated. The predictability of wound healing and repair forms the
basis of present-day therapy, but those who treat injured athletes soon become aware of the vast number of variables
that defeat textbook application of such logic to any single case. In addition, there is growing evidence for basic
pathohistologic and pathophysiologic differences between the acute and chronic (overuse) forms of soft tissue sports
injuries (2,3 and 4).
The goal of sports medicine therapy is to minimize the adverse effect of traumatic inflammatory responses while
promoting tissue repair, thereby expediting a safe return to performance. To accomplish this goal, the sports medicine
clinician must be familiar with human tissue biologic capabilities and limitations. This chapter provides an overview of the
basic cellular and molecular events in wound healing, the initiation and treatment of inflammation, repair and
degeneration, and the sources of sports-induced athletic pain. Considering injury within the greater context of cell-matrix
adaptation and tissue maintenance, additional attention is called to the role of transition as an important injury cofactor.
The specific injury responses and management of the most commonly injured soft—tissues muscle, tendon, and
ligament—are discussed. Several hypothetic models are offered to assist in the understanding of these clinically
observed patterns of sports injury.
EPIDEMIOLOGY
The epidemiology of sports-induced soft tissue injuries has been analyzed with respect to site of injury, gender, age,
choice of sport, and level of participation.
The site of injury varies according to the sport. Garrick and Requa pointed out that most sports injuries involve the lower
extremities, reflecting the strenuous running, jumping, and cutting maneuvers common to the most popular sports ( 5). As
many as 90% of sports injuries are sustained by the hip, thigh, knee, leg, ankle, and foot. These injuries run the gamut
from contusions to sprains and strains. Shoulder and upper extremity complaints predominate for the overhead athlete in
racquet, throwing, and swimming sports. DeHaven and Lintner ( 6) found that 48.1% of baseball injuries involve the
shoulder and upper extremity and that 57% of world class swimmers have experienced shoulder pain. Ligament sprains,
the most common injuries to joints in general and to the knee in particular, account for 25% to 40% of all knee injuries in
most studies. Whitman et al. (7), in a review of 1,280 urban sports medicine patients with an average age of 30.2 years,
found the most frequently injured areas to be the knee (45.5%), the ankle (9.8%), and the shoulder (7.7%). Of these
injuries, 53.9% involved soft tissue.
Gender studies point to a difference in the severity and types of injury in male and female athletes. Chandy and Grana
(8), in a 3-year study of seven paired sports in 130 Oklahoma secondary schools involving 24,485 boys and 18,289 girls,
found a significant difference in rate of injury only in basketball, in which the girls had significantly more injuries and more
severe injuries. Overall, the girls had more sprains and dislocations, whereas the boys had more strains and fractures.
There was a significant variance in site of injuries—boys had significantly more shoulder complaints, and girls had more
knee injuries. DeHaven and Lintner ( 6) found patellofemoral pain to be more prevalent in women (19.6%, compared with
7.4% in men). Sprains and strains occurred in 33.4% of men and in 28.7% of women. They also confirmed the higher rate
of knee injuries among injured female athletes (20.7% versus 8.5%). In a study of four Seattle high schools, Garrick and
Requa (5) found that the average injury rate for all athletes in 10 sports was 5.2%. The rate for girls was 3.5%, and the
adjusted rate (excluding football and wrestling) for boys was 3.0%. Again, although the injury rate for all girls' sports was
lower, a higher percentage of the girls' injuries required a loss of 5 days or longer (52%, compared with 44% for boys).
These studies point to a difference in the severity and types of injuries in male and female athletes, but they do not
resolve the effects of such variables as level of conditioning, performance technique, anatomic predisposition, and
coaching.
Age is associated with a changing spectrum of sports soft tissue injury. Of all children participating in sports programs in
the United States, 3% to 11% are injured annually ( 9). In a survey of Irish school children between the ages of 10 and 18
years, the overall incidence was found to be 2.94 injuries per 100 children per calendar year. More than half of these
were sprains, strains, and contusions (10). The rare occurrences of tendinitis or inflammatory changes at the
musculotendinous junction in children have been attributed to the transfer of forces to the tendon apophysis. Hoffman
and Lyman (11), assessing sideline injuries in high school football, found that contusions (26.6%), sprains (21.6%), and
strains (8.6%) accounted for 56.8% of all injuries. The knee (14.4%), the lower leg (13.7%), and the ankle (11.5%) were
the most common sites of injury.
With aging, the injury spectrum shifts toward degenerative processes and aggravation of previously acquired injury.
Comparatively speaking, the aging athlete may actually have a higher rate of injury. Keller et al. ( 12) found 15 to 30 times
as many soccer injuries among senior and professional athletes than among youths. Hip and thigh injuries were also
more common in the senior and professional athletes. Notable exceptions were knee and ligament sprains, which
accounted for one third of the soccer injuries regardless of age. Contusions were more often significant in youths. These
differences can be explained in part by the intensity of the game. Menard and Stanish ( 13) noted that masters athletes
are often “the victim of two sets of injuries: those that are incurred in their youth and those that result from their current
training regimen.” Inflammatory problems such as tendinitis or bursitis gradually increase in importance. Grossman and
Nicholas (14) called attention to the changing pattern of knee injuries with age. Chondromalacia patellae, patellar tendon
rupture, and degenerative arthritis are common knee injuries in aging athletes.
Both collision and endurance sports are characterized by the predominance of soft tissue injury. DeHaven and Lintner ( 6)
found 12 times as many injuries in football as in the next highest sport, basketball. Football accounted for 63.9% of all
injuries as well as 60% of all the knee injuries, which were primarily internal derangement and medial collateral ligament
(MCL) injuries. The total injury rate among high school football players ranged from 25% to 65%, depending on the
definition of injury and the method of data collection. Rates of significant injury ranged from 15% to 18%. Sprains and
strains were the most common injuries. Requa and Garrick (5) found wrestling to be second only to football in the
incidence of knee injuries requiring surgery. Rovere et al. ( 15) studied soft tissue inflammation in theatrical dance
students. Hip tendinitis produced an average loss of participation of 6.9 days. For ankle sprains, the average loss was
2.1 days. Soccer caused two to five times fewer injuries in young athletes than did American football. Sprains, strains,
contusions, and tendinitis dominated the injury patterns. In a collision-prone recreational sport such as downhill skiing,
soft tissue injury still predominates. In an analysis of 2,596 skiing injuries, Johnson and Pope ( 16) found that soft tissue
injuries accounted for 53.4% of the total. The five most frequent diagnoses were knee sprains (20.9%), thumb sprains
(10.2%), leg contusions (8.7%), lacerations (7.8%), and ankle sprains (5.8%).
Endurance sports include jogging, running, swimming, cycling, rowing, and race-walking. The incidence of running
injuries has ranged from 46.6% to an estimated 70% (17,18 and 19). Inflammatory disorders of soft tissue accounted for
five of the six most common problems in the series of James et al. (17). Musculotendinous injuries predominated in track
and field. Knee pain, representing a broad spectrum of overuse soft tissue complaints, occurred in 23% to 40% of all
runners (20). Clement et al. (21) noted a decrease in the prevalence of Achilles peritenonitis—from 11% of all injuries, as
reported by James et al. (17), to 6%—possibly owing to changes in training and shoewear; historically, however, Achilles
tendinopathy has been a difficult lesion for runners. Welsh and Clodman ( 22) reported in 1980 that 16% of those affected
had abandoned running, and 54% still participated despite discomfort. The prevalence of injury in running is directly
proportional to the load exposure. Mann ( 23) calculated that the ground-reaction force at midstance in running is equal to
two to three times body weight. A 70-kg runner, at 1,175 steps per mile, absorbs at least 220 tons of force per mile.
Swimming is another endurance sport characterized by excessive cumulative load. Competitive swimmers swim 8,000 to
20,000 yards per day, 5 to 7 days per week. This distance is equivalent to running up to 11.4 miles daily. It is estimated
that during a 10-month swimming season, a male swimmer performs 400,000 strokes and a female swimmer performs
660,000 strokes (24). Glenohumeral instability, secondary subacromial tendon impingement, muscle fatigue, and
tendinosis are typical causes of “swimmers shoulder” ( 24). Incorrect mechanics in the whip kick and breast stroke has
been cited as a primary cause of soft tissue overuse in the medial aspect of the knee, and even inflammation of extensor
tendons of the dorsum of the foot has been reported in swimmers (25).
Regardless of the level of play, the factors that contribute to soft tissue injury are frequency, intensity, and duration.
Keller et al. (12), in a study of soccer injuries, concluded that professionals sustained a higher rate of injury because of
their greater intensity of play. Leach's ( 26) description of the Major League baseball pitcher's typical throwing rotation is
another example of the different levels of intensity within a sport between amateurs and professionals. A Major League
baseball pitcher usually pitches every 4 days and throws 110 to 130 pitches in the course of a regular game. The next
day the pitcher's arm typically is so sore that it is difficult to raise it. The second day is characterized by recovery and
easy throwing, and the third day by a normal workout. The pitcher returns to starting on either the fourth or fifth day. An
injury analysis of the Olympic Games from 1968 to 1972 revealed that sprains, strains, and contusions were the most
common soft tissue injuries treated, accounting for 61% to 96% of soft tissue problems ( 27).
SPECTRUM OF INJURIES: DEFINITION OF TERMS
Sports-induced soft tissue injuries are characterized by a spectrum of interrelated cell-matrix responses or by the
processes of inflammation, repair, and degeneration ( 2,3 and 4). It is helpful to define these terms in order to more fully
understand the observed clinical problems.
Trauma implies an injury from a mechanical force that is applied externally to the involved tissue, causing structural
stress or strain that results in a cellular or tissue response. Load is a measure of external mechanical force. Use implies
the accumulation of load over time (i.e., a rate). Such repetition is seen in endurance sports in the form of cyclic loading
and overuse. The effect of load on tissue is described by the terms “strain” and “stress.” Strain is the deformation of a
structure in response to external load, whereas stress is its internal resistance to such deformation ( Fig. 46.1). Sports
trauma may be thought of as the mechanism by which injury occurs.
FIGURE 46.1. Strain-stress. Strain represents a tissue deformation; stress is the internal tissue resistance to
deformation. Both may affect cell matrix biology.
Sports injury (from the Latin injure, meaning “to make unjust, not right”) is the loss of cells or extracellular matrix resulting
from sports-induced trauma (28). As in other wounds, an athletic wound is a disruption of normal anatomic structure and
function. All wounds result from pathologic processes beginning internally or externally to the involved part ( 29). Acute
wounds are characterized by the generation of an orderly and timely reparative process that results in the sustained
restoration of anatomic and functional integrity. Chronic wounds are those that have failed to proceed through such an
orderly and timely process or have proceeded through the repair process without establishing a sustained anatomic and
functional result. Injuries are also divided into acute and chronic types, according to the rate of onset and the mechanism
of the injury. Chronic injury often represents a failure of cell-matrix adaptation to load exposure ( 29).
The mechanism of injury has much to do with the subsequent pathohistologic pattern. “Overuse” and “overload” may not
be synonymous terms, because injury can result from excessive and rapid change in use without significant change in
resistance—hence, the origin of the term “failed cumulative trauma disorder,” or preferably, “failed cumulative cell-matrix
adaptive response.” Synovial structures, such as the tendon sheath and the peritenon structures, are prone to this form
of stress response (2). Injuries can further be divided into acute and chronic patterns according to rate of onset. Acute
injuries are typified by a sudden crisis followed by a fairly predictable, although often lengthy, resolution. Acute
disruptions of structures accompanied by bleeding provide the best model for adherence to the classic acute phase
inflammatory reaction seen in other forms of human postnatal wounding. In tendon, an acute injury often consists of
midsubstance ruptures occurring either through aberrant tissue or as the result of high strain rates ( 30,31). Chronic injury
is characterized by slow, insidious onset, implying an antecedent subthreshold spectrum of structural damage. Eventually
this leads to a crisis episode that is often heralded by pain or signs of inflammation, or both. Chronic injury may last
months or even years and is distinguished by a persistence of symptoms without resolution. Synovitis, bursitis,
peritenonitis, and tendinitis are typical of such complaints. It is now known that perturbation of in vivo or in vitro cell
populations induces the release of chemical mediators and initiates cascades of inflammatory products ( 32,33 and 34).
How these events lead to further change in matrix integrity of connective tissue is only now becoming understood.
Furthermore, it is not clear whether microdamage caused by tensile overload and formed element separation with tissue
fatigue is the initiating event or whether some overwhelming effect on cell metabolism occurs first, with resulting loss of
the cell's capacity to maintain tissue integrity through increasing its synthesis. It is likely that both processes occur under
different circumstances. There appears to be some overlap between acute and chronic injuries, with the bridging stage at
4 to 6 weeks termed the subacute stage of injury. Another perspective on the acute versus chronic process would define
a chronic injury as an acute injury that occurs in association with some impairment to healing (T.K. Hunt, personal
communication, 1993). In the athlete, there are both intrinsic and extrinsic factors that can impair recovery ( 35).
It is difficult to define sports injury clinically. From the athlete's point of view, an athletic injury is any painful problem that
prevents or hampers usual sports performance. Furthermore, athletic soft tissue injury complaints are often defined solely
by the amount of pain or the inability to perform. Attention has been directed to the inadequacy of this definition of injury
and the importance of determining the exact anatomic extent in occurrence of tissue injury ( 36). Epidemiologic research
uses such variables as duration of disability, need for medical attention, and degree of structural tissue damage to define
injury (36). Proper therapy often depends on defining the exact anatomic extent and occurrence of tissue injury ( 36,37).
Classic signs of inflammation after injury are not always present or identifiable as a reliable guide. This is typically true of
deeply located muscle injury. A complaint is not so much identified with a specific structure as within an anatomic area. It
is a “painful shoulder,” not a painful biceps tendon; it is a “painful knee,” not a painful patella tendon. And although the
immediate onus on the examiner is to be competent and accurate in making the physical diagnosis, the elicitation of pain
does not necessarily shed light on the exact pathology or mechanism of injury. For instance, tendon injury relating to
occult joint instability or dynamic tendon stress overload, as may be present with a hyperpronating foot, may be revealed
only by further dynamic analysis. Of all the clinical signs, it is loss of function (functio laesa) that provides the necessity
for treatment of soft tissue injuries, and indeed of all sports injuries.
Rovere's (15) attempt to define tendinitis in a study of theatrical dance students exemplifies this difficulty. He defined
tendinitis as “a syndrome of pain and tenderness localized over a tendon, usually aggravated by activities that bring the
particular muscle tendon unit into play, usually against resistance.... The syndrome is inclusive of tenosynovitis and
tenovaginitis as well as actual inflammation of the tendon substance itself.”
Sports-induced inflammation (from the Latin inflammare, “to set on fire”) is a localized tissue response initiated by injury
or destruction of vascularized tissues exposed to excessive mechanical load or use ( 2,4,38). It is a time-dependent,
evolving process characterized by vascular, chemical, and cellular events leading to tissue repair, regeneration, or scar
formation. Clinically observed pathways of sports-induced soft tissue inflammation include spontaneous resolution,
fibroproductive healing, regeneration, or chronic inflammatory response ( 4) (Fig. 46.2). Not all sports injuries produce a
classic inflammatory pattern of response, nor are all tissues capable of generating such a response ( 4,28,39,40). The four
cardinal signs of acute inflammation were defined by Celsus (a.d. 14 to 37) in the often-quoted phrase, “rubor et tumor
cum calore et dolore” (redness and swelling with heat and pain) ( Table 46.1). It is important to note that this was most
likely a description of an empyema and fistula of the chest ( 41). Based on such an historical tradition, pain has assumed
a disproportionate importance in the definition of inflammation, such that any painful structure is immediately presumed to
be inflamed. It has taken the advent of more accurate noninvasive assessment modalities (e.g., magnetic resonance
imaging) and the accumulation of surgical biopsy evidence to correct what may be an improper clinical emphasis. As
discussed later, the source of connective tissue pain is now known to be multifactorial ( 42).
FIGURE 46.2. Schema of the theoretic pathways of sports-induced inflammatory response. (From Leadbetter WB. An
introduction to sports-induced inflammation. In: Leadbetter WB, Buckwalter JA, Gordon SL, eds. Sports-induced
inflammation: clinical and basic science concepts. Park Ridge, IL: American Academy of Orthopaedic Surgeons, 1990;2,
with permission.)
TABLE 46.1. RECOGNITION OF THE “CARDINAL SIGNS” OF INFLAMMATION
Repair of soft tissue injury has been defined as replacement of damaged or lost cells and extracellular matrices with new
cells and matrices (28). Regeneration is a form of repair that produces new tissue that is structurally and functionally
identical to normal tissue ( 28,43,44 and 45). Repair by scar is the postnatal mammalian response to injury; in contrast,
the fetal wound is capable of healing without exuberant scar formation ( 46). Acutely injured tissues such as tendon or
ligament accomplish repair by scar deposition that never exactly replicates the histologic or biomechanical properties of
the original structures ( 28,47). Regeneration is often seen as the ideal wound healing response; however, depending on
the athlete's demands, the response in soft tissue healing may result in either an adequate or an inadequate response.
Healing is a complex dynamic process that results in the restoration of anatomic continuity through an orderly biologic
repair process (29). Qualities of wound healing have been defined as ideal, acceptable, minimal, and failed ( Table 46.2).
An ideally healed wound is one that has returned to normal anatomic structure, function, and appearance. An acceptably
healed wound is characterized by restoration of sustained function and anatomic continuity ( 29). A minimally healed
wound is characterized by the restoration of anatomic continuity but without a sustained functional result; hence, the
injury may recur. In failed wound healing, no anatomic restoration or sustained function is achieved. In the treatment of
soft tissue injury, ideal wound healing is rarely if ever obtained, while acceptably healed wounds are common. It is the
challenge of the treating clinician to avoid returning an athlete to play with a minimally healed condition.
TABLE 46.2. ADEQUACY OF WOUND HEALING
Degeneration describes a change in tissue from a higher to a lower or less functionally active form ( 4). Such weakened
structures are then more vulnerable to sudden dynamic overload or cyclic overloading, leading to mechanical fatigue and
failure. A prominent source of degeneration is cell atrophy, which is the decrease in size and/or function of a cell that
occurs in response to the presence (or lack of presence) of an environmental signal ( 48). Such downregulation involves
decreased protein synthesis and a decrease in such activities as energy production, replication, storage, and
contractility. In sports injuries, immobilization is a prominent cause of cell atrophy in connective tissues ( 28). Additional
causes include decreased nutrition, diminished endocrine hormonal influence, persistent inflammation, aging, and
denervation (4). Reversal of the degenerative process is not a typical feature in degenerative conditions beyond an
undefined cell-matrix limit. Ultimately, degeneration represents a profound imbalance in cell-matrix homeostasis ( Fig.
46.3).
FIGURE 46.3. Cell matrix response to change in functional level. In this model, tendinosis results from a failed cell-matrix
adaptation to excessive changes in load use. Such failure is modified by both intrinsic and extrinsic factors. It is likely that
all connective tissues demonstrate some type of change in response to functional level. (From Leadbetter WB. An
introduction to sports-induced inflammation. In: Leadbetter WB, Buckwalter JA, Gordon SL, eds. Sports-induced
inflammation: clinical and basic science concepts. Park Ridge, IL: American Academy of Orthopaedic Surgeons, 1990;2,
with permission.)
Necrosis is that structural change that occurs in cells after their death in a living organism ( 49,50 and 51). This is a focal
process that results both from the presence of extracellular enzymes and from the release within the cell of
self-degrading lysosomal hydrolytic enzymes in response to the rising acid pH of a hypoxic or anoxic metabolism, a
process known as autolysis (41). The process of this enzymatic degradation of cell membrane, lipids, and intracellular
organelles, along with the breakdown of tissue macromolecules, provides the prime stimulus for the mobilization of
inflammatory cells from blood and nonnecrotic tissues surrounding an area of necrotic injury ( 48,49). As Robbins and
Cotran (50) noted, “Necrotic cells are dead cells, but dead cells are not necessarily necrotic.” This refers to the fact that
cell necrosis, by definition, cannot occur suddenly; hence, viable cells that are placed in a tissue fixative (e.g., formalin)
do not demonstrate necrosis but do undergo cell death. Furthermore, although initiation of inflammation does not require
necrosis (for example, in the immune response), necrosis always stimulates inflammation if there is adequate tissue
vascularity (48). The severity of sports injury depends on the extent of cell death. Apoptosis is a genetically mediated
form of cell necrosis also known as programmed cell death or cell suicide. Dysregulation of apoptosis is associated with
a wide variety of triggering events (e.g., hypoxia). Hypogenesis of many diseases involve this mechanism of cell death;
this may account for the histopathologic finding in tendinopathy (see Fig. 46.14).
FIGURE 46.14. Hypothetic scheme for the relationships between ion deregulation and the progression of cell injury
resulting from ischemia leading to cell death (apoptosis). Decreased adenosine triphosphate (ATP) production leads to
cessation of Ca2+ and Na+/K+-ATPases accompanied by increases in cytosolic H + , Na+, and Ca 2+. The increased Ca 2+ is
detrimental, particularly through activation of proteases, endonucleases, and phospholipases. (From Trump BF,
Berrezesky IK, Smith MW, et al. The role of ionized cytosolic calcium (Ca 2+) in injury and recovery from anoxia and
ischemia. Md Med J 1992;41:505–508, with permission; and Hetts SW. To die or not to die–and overview of apoptosis
and its role in disease. JAMA 1998;279:300–307.)
The pathology of cell injury represents a spectrum of stress responses to the altered environment—from the undetectable
and totally reversible, to the terminally irreversible event of cell death ( 51,52). A critical point beyond which cell metabolic
function cannot be revived is referred to as “the point of no return” ( 52). This point remains ill-defined because the exact
critical functions that must be compromised before cell death ensues remain controversial. Cell injury or death can be
initiated by such factors as ischemia, postischemic reperfusion, inflammation, chemical toxicity, or ionizing radiation ( 48).
The hypovascularized, dense connective tissues of the athlete are vulnerable to irreversible cell damage both during
tissue deformation and during use ( 2). Mitochondria are extremely sensitive to this ischemic stress. Mitochondrial
swelling with the collapse of the cytochrome oxidase and electron transport enzyme systems results in the release of
intracellular calcium stores. Increased intracellular calcium ion is a prominent signal mechanism for increased
phospholipase and calcium-dependent protease enzyme activity ( 52). Phospholipid degeneration with a loss of
cell-membrane integrity resulting from lipid peroxidation is another common pathway of cell injury and is one of the
theoretic pathways for all of aging ( 48). Under such conditions as postischemic reperfusion or inflammation, unstable
molecular species resulting from the incomplete reduction of oxygen (O 2 to H2O) may be produced. A free radical is any
molecule that has an odd number of electrons. These oxyradicals can react either as electron receptors (i.e., oxidants) or
as electron donors (i.e., reductants). Free radicals are extremely reactive, chemically unstable, and therefore short-lived,
and they usually occur in low concentrations ( 48). They may chemically attack the phospholipid structure of cell
membranes by the process of lipid peroxidation, forming unstable lipid peroxide radicals that break down into smaller
molecules, leading eventually to the dissolution of the cell wall. Phagocytic cells, such as the neutrophil, generate high
volumes of oxygen free radicals during inflammatory and repair process ( 53) (Fig. 46.4). This accounts in part for the
additional tissue injury that becomes the focus of acute athletic treatment. Although acute cell injury and cell necrosis
always stimulate inflammation (48), in theory, under conditions of microtraumatic sports injury, such factors as tissue
hypoxia and cell-matrix deformation may alter cell metabolic activity, possibly increasing harmful metabolic products such
as free radicals and thereby leading to lipid peroxidation. Such theory may provide an additional explanation for
observed degenerative pathology ( 2,48,54).
FIGURE 46.4. Pathway for the production of various activated oxygen species. (From Wahl SM, Wahl LM. Inflammation.
In: Cohen JK, Diegelmann RF, Lindblad WY, eds. Wound healing. Philadelphia: WB Saunders Co, 1992;40, with
permission.)
Chronic inflammation involves the replacement of leukocytes by macrophages, plasma cells, and lymphocytes in a highly
vascularized and innervated loose connective-tissue milieu at the site of injury ( 48). Although findings of chronic
inflammation are typical in sites such as lateral epicondylar lesions of the elbow ( 55), such responses are not found in all
chronic sport injuries ( 56,57). The mechanism that converts an acute inflammation to a chronic inflammatory process is
not known; continued abusive load and irritation may stimulate the local release of cytokines, resulting in modulation of
further cell activity through both autocrine (cell self-stimulation) and paracrine (stimulation of adjacent cells) mechanisms
(32,43,58).
Inflammation, degeneration, and repair form a functional spectrum of cell-matrix responses. The predominance of any
one response depends on the type of injury, the homeostatic balance of the tissue, and the timing of the observation.
COMPOSITION AND FUNCTION OF INJURED TISSUES
The individual cell holds the key to the regulation of the body's trauma response. Sports medicine therapy is increasingly
challenged to understand and anticipate these cellular responses in predicting recovery from injury or justifying the value
of any therapeutic measure. In this context, the clinician must “think like a cell” and come to appreciate that the body's
cellular response to sports trauma takes place in the context of a changing biochemical environment, constantly
influenced by such factors as oxygen tension, nutrition, genetic endowment, and aging and modified by physical forces
that initiate communication to and between cells. One of the most important results of the integration of these variables is
the maintenance of structural integrity during use and of tissue renewal after injury.
Connective tissues are composed of two basic elements: cells and extracellular matrix ( 39). However, there is great
variation in the relative composition and structural characteristics of these two elements in normal connective tissue.
Reparative response in connective tissue is essentially a cellular event, the success of which hinges on the ability of a
tissue to increase its rate of synthesis of DNA and macromolecules ( 40). Once considered an inert amorphous ground
substance, the matrix is now known to be a vital, responsive, biochemical saline gel that contains many important types
of macromolecules, including collagen, proteoglycans, hyaluronic acid, elastin, and fibronectin ( 4,40). There is growing
evidence that the matrix may be the modulating medium that prompts cells to change their patterns of protein synthesis in
response to load or use. For example, cartilage cells remain in a differentiated state only so long as they are in contact
with type II collagen and cartilage-specific proteoglycans in the surrounding matrix ( 40,59). In muscle injury, the removal
of muscle fiber cytoplasm may provide a stimulatory role for myogenesis and repair ( 60). After forced muscle lengthening
of the rat soleus, Fritz and Stauber found an interdependence between myofibers and extracellular matrix proteoglycans
(61). This implies both scaffolding functions by matrix components, to guide myogenesis and myofiber orientations, and
activation and inhibition effects on cellular repair ( 61).
Cellular Elements of Connective Tissue
The embryonic mesenchymal cell is the ancestor of most of the indigenous cells of adult dense connective tissues,
including the fibroblast, the tenocyte, and the myoblast or muscle satellite cell ( 62). These cells make up the resident cell
populations of the respective connective tissues. The macrophage and mast cells, which originate from bone marrow
stem cells and migrate to their connective tissue site, together with in situ endothelial cells, can arbitrarily be classified as
additional resident cells. The immigrant cell population in connective tissue consists mainly of inflammatory cells such as
monocytes (tissue macrophages), neutrophils, lymphocytes, plasma cells, and additional endothelial cells present as a
result of chemotaxis and wound repair activation. If an injury results in sufficient damage to create a wound gap or tissue
necrosis, new cells must be supplied to reconstruct the connective tissue fabric ( 44,45). After an injury, such new cells
are derived from one of three sources: migration of cell populations, replication of resident cells, or modulation of cells
present at the injury site ( 40). Added variables in sports trauma healing are the differing capacities of resident cell
populations to modulate their reparative behavior and of new cells to access the injury site. In most cases, this access is
directly the result of adequate vascular supply. Avascular tissue does not heal in vivo (43,44). The resident cell
populations are primarily responsible for tissue matrix maintenance, remodeling, and adaptive change ( 40,62).
Resident Cell Populations
The term fibroblast refers to cells with differing functions but similar morphologies ( 45,63,64). The fibroblast is a
spindle-shaped cell that is characterized in conventional histologic section by tapering eosinophilic cytoplasmic
extensions. It is the workhorse of most connective tissue injury repair ( 62). This cell possesses a well-developed, rough
endoplasmic reticulum on which the precursor polypeptides of collagen, elastin, proteoglycans, and glycoproteins are
synthesized (62). Not only do tendon fibroblasts have functions and properties different from those of skeletal muscle or
liver fibroblast, for example, but fibroblasts within the same tendon also demonstrate different potentialities ( 33,65). For
instance, the epitenocytes function as modified fibroblasts with an aggressive capability to repair tendon laceration or
crush damage. However, the tendon endotenocytes appear to have more limited potential to increase their reparative
function (33,65). The term fibroblast is best understood as indicating a generic cell phenotype that may refer to
connective tissue cells, stem cells, phagocytic cells (histiocytes), protein-secreting cells (fibrocytes), or contractile cells
(myofibroblasts) (45). In mature animals, fibroblasts continue to synthesize and maintain elements of the connective
tissue matrix (e.g., collagens, fibronectin, fibroglycans, other proteins). The matrix is constantly turned over and
remodeled by fibroblasts and the degraded enzymes that they secrete (e.g., collagenases, proteoglycanases,
glycosaminoglycanases, other proteases) ( 64). By light microscopy, inactive fibroblasts in granulation tissue are oval and
show indistinct cytoplasm with an elongated nucleus. Cells with this appearance include at least three functionally distinct
mesenchymal cell types: stem cells of connective tissues, cells with Fc receptors and phagocytic capabilities (histocytes),
and fibrocytes (64). Fibrocytes are those connective tissue cells differentiated by electron microscopy that appear within
days at the site of wound repair. They exhibit active synthesis of extracellular matrix components such as collagens,
fibronectins, and proteoglycans. Fibroblasts in vivo adhere to and grow in a complex extracellular matrix that is difficult to
reliably produce in vitro. The cellular processes or pseudopodia of fibroblasts are attached to substrates at sites known
as adhesion plaques, which are characterized by the presence of increased actin filaments and by a specific
actin-binding protein called vinculin ( 64). Fibroblasts are capable of considerable modulation in response to lymphokines,
monokines, and cytokines; these provide chemotactic signals for direct migration of fibroblasts from neighboring
connective tissue to the site of injury and for proliferation or a mitogenic response ( 66). This mitogenic response consists
of two phases: competence, which occurs in the early G 1 phase of the cell cycle and renders the cell competent to
replicate its DNA (but does not result in DNA synthesis or the S phase), and progression, which results in DNA synthesis
and occurs only in competent fibroblasts. This scheme of cell activation and modulation is typical of cellular reparative
cascades in all connective tissues ( 45). Myofibroblasts are characterized by an abundance of contractile elements
(actin-myosin filaments) in the peripheral cytoplasm, a concentration of synthetic organelles (rough endoplasmic
reticulum and Golgi apparatus) in the perinuclear region, and an indented nucleus ( 45). These modified fibroblasts are
thought to be responsible for wound contraction and are prominent in the wound site 3 to 10 days after injury ( 45,48).
Myoblast is the proper term for a myogenic cell that is withdrawn from the cell cycle, implying a nonproliferating, highly
differentiated condition ( 60). A highly specialized member of the connective tissue family, it is a skeletal muscle cell that
may derive from embryonic mesoderm. Skeletal muscle cells are permanent cells with no proliferative capacity; the
reparative cell in muscle is the satellite tissue cell ( 45,60). The muscle satellite cell is a mononucleated cell that lies
between a muscle fiber and its surrounding basal lamina. Satellite cells may represent myoblasts that do not fuse into
multinucleated muscle fibers during embryonic myogenesis ( 60). Muscle is formed from the cooperative interplay
between cells of two unique and separate developmental lineages, one associated with the formation of individual muscle
cells and the other accounting for connective tissue “packaging” of individual muscles ( 60). This mesenchymal cell
lineage provides capacity through differentiation to form bone and cartilage after trauma, as exemplified in myositis
ossificans as well as scar (45,67). The myogenic cell injury response is ultimately related to the innervation pattern and
the connective tissue milieu ( 60,66). In the face of necrotic muscle degeneration with cell death in vivo, spindle-shaped
reserve myogenic cells, with macrophage mediation, are capable of proliferation and limited regeneration ( 60). More
commonly, muscles are prone to form scar after macrotrauma (45,47,66,68).
Endothelial cells are resident within the vascular structures of connective tissue, and they also represent a cell population
that is capable of dramatic migration and tissue immigration during the process of angiogenesis in wound repair
(43,45,48). Endothelial cells are capable of a wide variety of metabolic responses to specific stimuli, including
immigration, proliferation, and differentiation ( 43). At the onset of posttraumatic inflammation, stimulation of endothelial
cells by vasoactive mediators initiates a complex series of biochemical events, causing cell contraction, loss of tight
junctions, and gap formation with extravasation of intravascular fluids ( 48). Endothelial cells can be induced by cytokines
secreted by activated macrophages and lymphocytes to express a distinct set of glycoproteins that promote inflammatory
cell adherence and localization to sites of inflammation ( 47,48). IL-1 and tumor necrosis factor stimulate the adhesive
capacity of endothelial cells for monocytes, a factor critical to the recruitment of circulating cells to sites of tissue injury.
Under ischemic conditions, endothelial cells are a source of xanthine oxide and may generate oxygen free radicals
(47,48).
Immigrant Cell Populations
The immigrant cell populations are involved primarily with connective tissue inflammation, injury repair, and healing.
Included in this group are tissue macrophages or histiocytes, neutrophils, lymphocytes, plasma cells, mast cells, and
platelets.
Tissue macrophages function as the “starships” of wound healing. They are pluripotential cells capable of generating
almost any known mediator (38,43). These cells are intimately responsible for matrix degradation, remodeling, and
regulation (43). Primarily derived from circulating monocytes and, to a lesser degree, from proliferation of local
macrophages, the activated macrophage becomes the dominant wound phagocyte on decline of the neutrophil
population, regulating lymphocytic responses to antigen and cueing the proliferation and functionality of fibroblast,
muscle, and endothelial cells ( 45). Although it is possible for wound healing to progress without neutrophils, in the
macrophage-depleted animal there is a marked delay not only in tissue debridement but also in fibroblast proliferation
and wound fibrosis (43). Macrophages and fibroblasts probably function interchangeably at times in repair ( 45). Activated
macrophages differentiate into multinucleated giant cells and long-lived tissue macrophages, which together with
lymphocytes and plasma cells are the hallmark of chronic inflammation ( 45,48,53).
Polymorphonuclear leukocytes are highly specialized phagocytic cells that are capable of both chemotactic response to
protein ligands (i.e., any molecule capable of interacting with a cell receptor) and activation by vasodilating agents such
as serotonin, histamine, bradykinins, arachidonic acid metabolites, kallikrein, plasminogen activator, the factors involved
in coagulation and fibrinolysis, platelet derived growth factor (PDGF), and platelet factor 4 ( 53,69). The activated
neutrophil releases lysosomal enzymes and metalloenzymes (collagenase, gelatinase) and displays marked activation of
the nicotinamide adenine dinucleotide (NADPH) oxidase system in the cell membrane. This so-called “respiratory burst”
represents a dramatic increase in oxygen consumption and is accompanied by the generation of various activated
oxygen free radical species, including superoxide, the anion (O 2–), hydrogen peroxide, (H 2O2), and hypochlorous acid
(HOCl) (53,54) (see Fig. 46.4). These potent products of oxidation are not only bactericidal but also toxic to the neutrophil
and surrounding cells and tissues. Under ordinary conditions, endogenous and exogenous antioxidants, so-called
molecular scavengers (e.g., vitamin E, glutathione, superoxide dismutase enzyme), provide normal cells with protection
against injury caused by free radicals ( 54). Together with the release of other catabolic enzymes, oxygen free radicals
contribute to the initiation of a zone of secondary injury ( 54,68). During the inflammatory process, there is a balance
between tissue injury and host defense that depends in part on the total number of neutrophils. This “neutrophil load” is
proportional to neutrophil influx and disposal ( 43). Reducing the disability of iatrogenic neutrophil injury and the
secondary edema and pain that occur after injury is a prime therapeutic target of sports medicine ( 2,54). Reactive oxygen
metabolites and lysosomal enzymes are synergistic in producing tissue injury. Proteins and glycosaminoglycans exposed
to oxidants are rendered more susceptible to degradation by proteases and acid hydrolases, respectively ( 48).
Polymorphonuclear leukocytes, although characteristic of acute inflammation, may also be observed at sites of chronic
inflammation, demonstrating the continuum of morphologic features between the acute and chronic inflammatory
responses.
The lymphocyte is a primary cellular component of chronic inflammation and is represented by two subtypes. The first is
the B lymphocyte (referring to its bursal or bone marrow derivation). It is the only cell that is capable of producing
antibodies; hence, it is characterized by a prominent rough endoplasmic reticulum. This cell often differentiates into a
specialized form called the plasma cell. The second is the T lymphocyte (derived from the thymus), which makes up the
cytotoxic lymphocytic population ( 47,48,70). In response to antigenic stimulation, a subset of T cells, the helper cells,
secrete protein hormones called cytokines whose function is to promote the proliferation and differentiation of the T cells
and of other cells including B cells and macrophages ( 70). Cytolytic T cells are a second subset of T cells. They lyse
cells producing foreign proteins; in addition, they participate in allograft rejection ( 70). Natural killer cells, also called
large granular lymphocytes, are circulating cells derived mainly from the spleen ( 70). They attack tissue cells and have
been implicated in chronic muscle injury ( 61,66,71,72). Lymphocytes and derived plasma cells are important in both
humeral and cell-mediated immune responses (48,53).
The tissue mast cell and the related circulating basophil play an important role in the regulation of posttraumatic vascular
permeability and smooth muscle tone as well as allergic hypersensitivity reactions ( 48,69). Characterized by
electron-dense storage granules, this cell is the primary source of histamine, acid mucopolysaccharides (including
heparin), and chemotactic mediators for neutrophils and eosinophils ( 69). By releasing arachidonic metabolites, including
slow-reacting substances of anaphylaxis (SRS-As) —leukotrienes C 4 (LTC4), LTD4, and LTE4—and platelet-activating
factor (PAF), these cells contribute to increased vascular permeability and edema in the acute phase reaction of
inflammation and repair ( 69). Mast cells enhance the effect of xanthine oxidase and oxygen radical production ( 54). Mast
cells also appear prominently in the early phases of eccentric muscle injury response ( 61,71) and delayed-onset muscle
soreness (73).
The platelet is a “cell” without a nucleus. One of the earliest effects of soft tissue injury is the release of granule
constituents from activated platelets on the site of vascular disruption. Platelets possess three distinct granules: (a)
dense granules rich in serotonin, histamine, Ca 2+, and adenosine diphosphate; (b) alpha granules containing fibrinogen,
coagulation proteins, PDGF, transforming growth factor-b (TGF-b), and other peptides and proteins; and (c) lysosomes
containing acid hydrolases ( 48). Degranulation is associated with the release of serotonin and histamine, inducing
changes in vascular permeability. In addition, thromboxane A 2 is produced to aid further platelet aggregation. Platelets
are a major source for growth factors, including PDGF, insulin-like growth factor I (IGF-I), and, particularly, TGF-b, all
three of which have profound paracrine effects on macrophages and tissue mesenchymal cells ( 46,69,74).
Extracellular Matrix Components
Cell regulation, including migration, differentiation, proliferation, and synthesis, is now recognized to be an important
function of cellular interaction with the extracellular matrix components ( 39,59). It is the matrix that best defines the
structural nature of soft tissue. Matrix components that are found to have influence on inflammatory reactions and
associated tissue repair processes modulate cell activity both by direct continuous effect and through the byproducts of
degradation at sites of tissue injury. For instance, type I collagen in alpha I, alpha II and alpha I CB5 peptides and types
II, III, and IV collagen are able to induce platelet aggregation in vitro (67). Collagen degradation products have been
recognized as chemotactic agents for circulating monocytes and connective tissue fibroblasts at sites of injury and
inflammation in vivo, based on observations of bacterial-degradated collagens on blood monocytes and dermal
fibroblasts (72). The collagens form a family of stiff helical and soluble macromolecules that provides the scaffold for
tensile strength in dense, regular connective tissue ( 39). Of the dry weight of the ligament and tendon, 70% to 90% is
collagen (39). A function of the fibroblast collagen synthesis begins inside the cell and leads to the secretion of a
three-peptide chain procollagen molecule. Enzymatic cleavage of the low-molecular-weight procollagen molecule
produces the tropocollagen form, which self-assembles extracellularly into the collagen fibril (fibrillogenesis) ( Fig. 46.5).
Of the various types of collagen, type II is the principal collagen of articular cartilage, and types I and III are important in
dense musculoskeletal tissues.
FIGURE 46.5. Collagen biosynthesis: intracellular events and secretion. (From Gamble JG. The musculoskeletal system:
physiological basics.) New York: Raven Press, 1988;63, with permission.)
Type I collagen, the normal fabric of tendon, ligament, and muscle as well as bone, derives its strength from two or three
covalent intramolecular bonds, or cross-linkings, found in each collagen molecule ( 39). This cross-linking is tissue
specific, with strong trivalent bonding associated with high tensile demands, such as that found in Achilles tendon or
anterior cruciate ligament (ACL) ( 75). Under increasing load, these cross-links give way, leading to fibril failure and
eventual tendon rupture. Failure begins at 8% to 10% strain (i.e. change in length divided by length) ( 76).
Type III collagen has smaller fibrils and fewer cross-links. During repair increased quantities of type III collagen are often
deposited, resulting in long-term structural weakening and delayed recovery ( 75). This initial inadequacy of repair is
partially compensated by an increased volume of matrix deposition and collagen synthesis ( 27). Type III collagen is
gradually replaced by type I collagen, but this process may take several years ( 39,75).
Proteoglycans, the other principal group of matrix molecules, possess great water-binding capacity ( 39). Proteoglycans
vary in composition according to tissue type and change composition with age ( 13,77). The proteoglycan aggregate of
connective tissues consists of a glycosaminoglycan side chain attached to a core protein, linked to a hyaluronic acid
backbone. These molecular aggregates possess an enormous molecular domain and act as electrostatic sponges to
provide viscoelastic properties to such soft tissues as tendon, ligament, and cartilage ( 28) (Fig. 46.6). Hyaluronic acid is
a constituent of the wound extracellular matrix that appears in the early phases of healing to interact with fibrin, creating
a matrix that facilitates inflammatory and reparative cell migration. The presence of hyaluronic acid appears to affect cell
aggregations and chemotaxis during the inflammatory response ( 43). Subsequent degradation products derived from
both fibrin and hyaluronic acid serve as important regulatory molecules to control cellular functions involved in the
inflammatory process, as well as wound angiogenesis ( 43,46). With respect to the role of extracellular matrix
macromolecules in the regulation of connective tissue metabolism, there are several excellent reviews ( 43,59,77,78).
FIGURE 46.6. Molecular structure of a typical proteoglycan aggregate. (Courtesy of Dr. Lawrence Rosenberg.) (From
Salter RB. Continuous passive motion (CPM): a biological concept for healing and regenerations of articular cartilage,
ligaments, and tendons from origination to research to clinical applications. Baltimore: Williams & Wilkins, 1993, with
permission.)
Fibronectins are noncollagenous glycoproteins with the ability to promote the attachment, spreading, and proliferation of
fibroblasts and phagocytosis by cells (particularly of the endothelial system), thus facilitating repair of damaged
connective tissue (45).
Integrins are a group of cell-surface proteins containing two polypeptide chains, alpha and beta. These molecules span
the extracellular intramembranous and intracellular compartments. As such, they may play an important role in cell-matrix
communication (45). Interaction of the integrins with the subplasmalemmal protein talin itself connected to cytoplasmic
filaments, results in intracellular and extracellular information exchange. Integrins are extracellular matrix binding
proteins with specific cell-surface receptors. These heterodymic, small-molecular-weight polypeptides (Da 140,000)
provide a mechanism for cell regulation of tissue adaptation resulting from mechanical load and use ( 79), along with
cytoskeletal deformation ( 79,80).
SEVEN BASIC MECHANISMS OF SPORTS INJURY
There are seven basic mechanisms by which the athlete may sustain injury: contact or impact, dynamic overload,
overuse, structural vulnerability, inflexibility, muscle imbalance, and growth ( Table 46.3). These mechanisms may occur
singularly, as in acute tissue damage resulting from contact or collision, but more commonly they occur in combinations,
especially in the endurance athlete.
TABLE 46.3. SEVEN BASIC MECHANISMS OF SPORTS INJURY
Contact is the most obvious source of acute macrotraumatic injury. It generally results in a classic inflammatory wound
repair reaction initiated by the onset of a bleeding hematoma and clot formation ( 2,68). Direct muscle contusions and
severe ligament sprains with possible traumatic joint dislocations are typical examples of soft tissue contact injury. The
corollary of contact is impact. This often-underrated mechanism of injury is exemplified by the cumulative microtrauma
experienced by tissues exposed to repetitive load ( 23). For example, the ground reactive force at midstance in running is
250% to 300% of body weight. A 70-kg runner at 1,175 steps per mile absorbs at least 220 tons of force per mile ( 1).
Although contact may produce more notorious injuries, it is the cumulative damage of impact that produces the more
common spectrum of overuse injuries.
Dynamic overload describes the tissue failure that results from sudden intolerable strain deformation. An acute tendon
rupture or intramuscular strain is often caused by dynamic overloading during jumping, sprinting, or kicking. Tendons are
particularly at risk during the eccentric loading that may occur when landing. Overuse or overload represents failed
cumulative cell-matrix adaptive responses as seen in the context of the repetitive use of an anatomic part. Of the 30% to
50% of all sports injuries that are related to overuse, an estimated 70% are caused by training errors ( 1). In the presence
of other mechanisms, overuse often is proximal cause of an injury crisis. Structural vulnerability may contribute to fatigue
and eventual tissue failure secondary to focal overload and excessive strain or stress. Hyperpronation of the foot during
running, pathologic laxity of the ligamentous support of a joint, and malalignment such as that seen with excessive
persistent femoral anteversion in the lower extremity constitute structural vulnerabilities capable of contributing to the
onset of injury during sports play ( 21). Inflexibility and muscle imbalance are interrelated mechanisms relating primarily to
muscle conditioning and usage. Repetitive patterns of muscle use during athletic activity promote muscular imbalances
and resultant joint inflexibility. Muscular fatigue often underlies the promotion of muscular imbalance ( 81). A fatigued
muscle is more prone to strain (82,83). Joint inflexibility may lead to biases in articular contact, thereby initiating a cycle
of degeneration. By definition, growth is a mechanism seen in the growing or child athlete. “Overgrowth syndrome” and
“growing pains” are terms emphasizing the muscular imbalances and inflexibilities coinciding with changing skeletal
proportions during maturation ( 84) that create potential dynamic overload of soft tissue structures. Acquired inflexibilities
and muscular imbalances during periods of growth often persist for inordinate periods and even into adulthood in the
absence of appropriate rehabilitation and conditioning.
It is important to recognize these common mechanisms of sports injury in order to prescribe useful modifications in
behavior, conditioning, rehabilitation, or structural support. In the absence of such intervention, a sports clinician is often
left with the alternative of treating the symptoms of tissue injury and inflammation without ever stemming the contributing
cause. Such an approach inevitably leads to persistence of the pain-injury cycle and represents the typical failure of
nonsports medicine–oriented care.
TISSUE RESPONSE TO PHYSICAL INJURY
All sports-related connective tissue injury responses occur in the context of two interrelated categories: macrotraumatic
(acute tissue destruction) and microtraumatic (chronic abusive load or use).
Acute Macrotraumatic Tissue Response
Acute tissue loss or damage may result from sudden compression, laceration, extreme tensile load, or shear. The
moment of tissue injury is defined by the onset of vascular disruption and the initiation of the clotting mechanism with
platelet activation. A cascade of overlapping processes that has been described as “predictable” then follows:
inflammation, cell replication, angiogenesis, matrix deposition, collagen protein formation, contraction (e.g., remodeling),
and, in the case of exposed wounds, epithelialization. These highly interdependent events are summarized in Table 46.4
and Fig. 46.7 as phases 1, 2, and 3 of the acute injury tissue response. With respect to time, there is great disparity
between the phases. Although phase 1 subsides in a few days, phase 3 may extend indefinitely. Severe muscle strains,
spontaneous Achilles tendon ruptures, and surgical wounds typically generate this type of response ( Fig. 46.8). In reality,
this represents an ideal sequence of events that is influenced not only by the type of insult but also by such factors as
age, vascularity, nutrition, genetics, hormonal changes, innervation, and activity level. The literature contains many
excellent and exhaustive reviews of the vascular, cellular, and biochemical events in this process ( 2,28,43,44 and
45,53,68,69,78,85). What follows is a pertinent summary of some of this literature regarding the acute connective tissue
injury response and its three phases.
TABLE 46.4. PHASES OF ACUTE INJURY TISSUE RESPONSE
FIGURE 46.7. Ideal wound healing model, originally derived from the study of skin lacerations; a variety of factors may
distort the actual healing sequence in the tendon. Although this diagram is an accurate portrayal of cell-matrix
wound-healing events, note that the temporal relationship among the various phases is such that the duration of phase 1
is measured in hours or a few days, but phase 3 may extend indefinitely. Normal tendon is not regenerated, however.
PMN, polymorphonuclear cell. (Adapted from Gamble JG. The musculoskeletal system: physiological basics. In:
Hunter-Griffin L, ed. Athletic training and sports medicine. New York, Raven Press, 1988;105, with permission.)
FIGURE 46.8. Achilles tendon rupture. Hemorrhage, clot, and tissue disruption provide a strong stimulus for an acute
injury response.
Phase One: Acute Vascular–Inflammatory Response
After wounding, the first reparative “cells” to appear in most vascularized wounds are platelets, which are a prominent
source of cell mediators such as PDGF, platelet factor 4, IGF-I, TGF-b1 and -b2, and an uncharacterized
chemoattractant to endothelial cells ( 46). Activation of the coagulation cascade and formation of a fibrin clot containing
fibronectin with cross-linking to collagen and hyaluronic acid is vital to facilitate reparative cell activity ( 43). Also known
as the reaction phase, this first phase is characterized by inflammatory cell mobilization aided by an acute vascular
response that begins within moments after injury and lasts from a few minutes to several days. Alterations in the anatomy
and function of the microvasculature are among the earliest responses to injury. An acute vasoconstriction lasts a few
minutes and is followed by vasodilatation, primarily of precapillary arterioles that bring increased blood flow to the injured
area, causing swelling. Blood from the disrupted vessels collects locally; with cellular debris and early necrotic tissue, it
then forms a hematoma. The extent of the initial hematoma in the area of devitalized tissue defines the zone of primary
injury (68). A humoral response occurs almost coincident with the neurovascular events and centers on activation of
Hagman factor (clotting factor 12) in the plasma, resulting in four subsystems of mediator production that have the
following functions:
1. The coagulation systems reduce blood loss by local clot formation, a process activated in part by collagen exposed
in the walls of damaged blood vessels.
2. Fibrinolysis discourages widespread blood clotting by fibrin degradation.
3. Kallikrein produces the strong vasodilator bradykinin, which increases capillary permeability and edema.
4. Complement activation produces anaphylatoxin, which activates chemotaxis—the attractant of inflammatory cells in
the activation of phagocytosis in wound debridement ( 85).
Stimulated by the complement system, mast cells and basophils release histamine. Platelets, in addition to providing clot
formation, are primary sources of serotonin. Histamine and serotonin work to increase vascular permeability ( 69).
Fibronectins are a class of noncartilaginous glycoproteins that act as adhesive molecules, integrating the extracellular
matrix (45). Hyaluronic acid, a high-molecular-weight matrix glycosaminoglycan, interacts with fibronectin to create a
scaffold for cell migration; later, its degradation by neutrophil hyaluronidases to a smaller molecular form stimulates the
angiogenesis that supports fibroblast activity ( 43).
There are three major consequences of the inflammatory phase: first, some initial wound strength is provided by the
cross-linking of fibronectin and collagen; second, damaged tissue from the initial trauma is removed; and third,
endothelial cells and fibroblasts are recruited and stimulated to divide ( 46). During this phase, release of complement
activates polymorphonuclear cell migration into the extravascular space, providing for the removal of cellular debris and
initiating chemotaxis of additional inflammatory cells, including tissue macrophages. Granules within leukocytes release
hydrolytic enzymes that hydrolyze cell membrane phospholipids and result in the production of arachidonic acid
metabolites, cytokines, proteases, and oxidants ( 69). The resulting arachidonic acid cascade is an enzymatically driven
sequence leading to markedly increased production of prostaglandins, thromboxanes, leukotrienes, eicosanoids, and
slow-reacting substance of anaphylaxis (SRS-A) ( 69) (Fig. 46.9). Collectively, these polypeptide proteins activate further
inflammatory cellular behavior. For this reason, they are the targets of modern antiinflammatory drug therapy. The
intense chemical activity and exudation of this phase produce the initial clinical signs of inflammation, edema, and
hypoxia and create the zone of secondary injury ( 68) (Fig. 46.10). This cascade is the primary chemical event producing
the cardinal signs of inflammation. Initiated in minutes, this phase lasts essentially as long as the body requires and is
the igniting step for subsequent repair. Assuming no coincident infection or repetitive disturbance to the wound, this
usually is a matter of 3 to 5 days ( 46).
FIGURE 46.9. Generation of arachidonic acid metabolites. HETEs, hydroxyeicosatetraenoic acids; HPETEs,
hydroperoxyeicosatetraenoic acid compounds; LT, leukotriene. (From Fantone JC. Basic concepts in inflammation. In:
Leadbetter WB, Buckwalter JA, Gordon SL, eds. Sports-induced inflammation: clinical and basic science concepts. Park
Ridge, IL: American Academy of Orthopaedic Surgeons, 1990, with permission.)
FIGURE 46.10. Mediators of the inflammatory response. (From Fantone JC. Basic concepts in inflammation. In:
Leadbetter WB, Buckwalter JA, Gordon SL, eds. Sports-induced inflammation: clinical and basic science concepts. Park
Ridge, IL: American Academy of Orthopaedic Surgeons, 1990, with permission.)
Phase Two: Repair–Regeneration
Beginning at 48 hours and lasting up to 6 to 8 weeks, this phase is characterized by the presence of the tissue
macrophage, formally a circulating monocyte. This pluripotential cell is essentially capable of directing the complete
sequence of events in this proliferative phase ( 43,46). The macrophage is characteristically mobile, capable of releasing
a wide menu of growth factors, chemoattractants, and proteolytic enzymes when appropriate or necessary for the
activation of fibroblasts and wound repair. The reparative connective tissue cell, in this phase, is the modified fibroblast,
chondroblast, or myofibroblast. This cell is the source of collagen production, protein mediators of repair, and matrix
proteoglycans. The fibroblast cell populations of dense connective tissue are typically classified as stable cells, meaning
that fewer than 1.5% are mitotically active at any one time ( 45). The cells have a characteristic low respiratory quotient
and a low rate of collagen turnover ( 86,87). Found normally within a dense linear-oriented collagenous matrix, these cells
take on a distinct activated behavior and a fibroproductive phenotypic expression that can be further altered by
deformation or changes in cell shape. Initially, in acute wounding, type III collagen in a woven pattern is rapidly deposited
(30). (Type III collagen is characterized by a small fibril that is deficient in cross-linking.) The remainder of the repair
process is characterized by a shift to the deposition of type I collagen that continues for an indeterminate period in the
final maturation phase (2).
The critical driving force in this stage of the wounding response is a relative hypoxia in the wound microenvironment and
a rising lactate level contributed in part by the release of large amounts of lactate by the tissue macrophage ( 46). At the
same time, a process of vascular proliferation and ingrowth (angiogenesis) occurs; tiny blood vessels grow and
anastomose with each other to form a new capillary bed. Granulation tissue is the visible evidence of this process ( 43).
Various growth factors that promote this activity are prevalent in the wound ( 43,45,69).
Phase Three: Remodeling–Maturation
This phase is characterized by a trend toward decreased cellularity and an accompanying decrease in synthetic activity,
increased organization of extracellular matrix, and a more normal biochemical profile ( 88). Collagen maturation and
functional linear realignment are usually seen by 2 months after injury in ligament and tendon ( 28,89). In the lacerated
flexor tendon, by approximately 4 months after injury, there appears to be complete maturation of the repair site and the
fibroblasts revert to quiescent tenocytes. However, final biomechanical properties can be reduced by as much as 30%
despite this remodeling effort ( 65). The endpoint at which remodeling ceases in soft tissue injury response has not been
determined (65,90). Biochemical differences in collagen type and arrangement, water content, DNA content, and
glycosaminoglycan content persist indefinitely, and the material properties of these scars never equal those of the intact
tissue (30,89).
Clinically, it should be appreciated that the human inflammatory repair response to acute injury is not so much purposeful
as it is simply an example of the way things work. The factors that initiate healing, control its rate, and eventually signal
its completeness are not fully understood ( 44). Whatever relative benefit there may be in the expediency with which initial
healing takes place must be balanced against the costs of early loss of function (due primarily to inflammatory pain) and
late functional deficit (due to scar). If the “purpose” of inflammation is healing ( 73), then the body's “good intentions” pave
the way to pain and performance loss. Although the system works well enough for survival, for the injured athlete with an
urgent competitive goal, well enough is seldom soon enough. A summary of the events associated with the acute injury
tissue response is presented in Fig. 46.11.
FIGURE 46.11. Summary of events in macrotraumatic wound response. (From Martinez-Hernandez A. Basic concepts in
wound healing. In: Leadbetter WB, Buckwalter JA, Gordon SL, eds. Sports-induced inflammation: clinical and basic
science concepts. Park Ridge, IL: American Academy of Orthopaedic Surgeons, 1990;78, with permission.)
Chronic Microtraumatic Injury Response
Microtraumatic soft tissue injury, as typically occurs in tendons, is distinguished by the observation that degenerative
changes are a prominent histologic feature, especially in cases of spontaneous tendon rupture ( 2,56,57). This
degenerative tendinopathy is thought to be the result of a hypoxic degenerative process involving both tenocyte and
matrix components. Inflammatory cell infiltration and an orderly, phased wound repair, as seen in macrotrauma, seem to
be absent or aborted in microtrauma. Much of the histologic evidence for degenerative tendinopathy has been derived
from the treatment of spontaneous tendon rupture. Kannus and Jozsa ( 56) studied the histopathologic changes
preceding spontaneous rupture of tendon in 891 patients (397 Achilles tendons, 302 biceps brachii tendons, 40 extensor
pollicis longus tendons, 82 quadriceps tendons and patellar ligaments, and 70 other tendons) and found that 97%
showed prior pathologic change. The mean patient age was 49 years. Similar pathologic changes were found in 34% of
the otherwise asymptomatic control population.
The microtraumatic response to load and use is best understood within the context of a failed adaptation to physical load
and use (2). The histologic picture includes a range from synovial inflammation to tissue degeneration. Leadbetter
reported similar findings in adult athletes with overuse tendon injury requiring surgical treatment before rupture ( 2,3).
Specimens included Achilles tendon, posterior tibial tendon, digital flexor tendon, lateral elbow extensor, medial elbow
flexor tendon, patellar tendon, and triceps tendon. All specimens displayed varying degrees of the following conditions
(Fig. 46.12 and Fig. 46.13):
FIGURE 46.12. Normal tendon. Note relative hypocellularity and regular collagen fiber orientations with subtle crimp
pattern.
FIGURE 46.13. Tendinosis: gross appearance of lesion in patellar tendon. Note dull, abnormal intratendinous
degeneration (arrow). B Tendinosis (microscopic appearance). Chronic inflammatory granulation tissue is characterized
by abortive scar repair, scattered macrophage-like inflammatory cells, fibroblasts rich in cell mediators, and increased
microvasculature with accompanying nociceptor innervations (hematoxylin and eosin stain) (original magnification, ×
162.5).
1. Tenocyte hyperplasia
2. Blast-like change in morphology from normal resting tenocyte appearance
3. Prominent small vessel ingrowth with accompanying mesenchymal cells
4. Perivascular collections of histiocytic or macrophage-like cells
5. Endothelial hyperplasia and microvascular thrombosis
6. Collagen fiber disorganization with mixed reparation and degenerative change
7. Microtears in collagen fiber separations
Statistically, these findings have a strong correlation with aging and with sedentary tissue disuse ( 88). In theory, epigenic
factors compromise connective tissue cell adaptability to the point at which tissue homeostasis and maintenance fail ( 2).
Evidence based on other models of sublethal cell stress response (e.g., cardiac ischemia) suggests that fluxes in
intracellular calcium ion concentration may play an important role in the signaling of synthesis behavior and may be
associated with tissue degeneration ( 51,91) (Fig. 46.14). The generation of oxygen free radical species (as a result of
either the inflammatory process or a hypoxic stress response), leading to cell lipid membrane peroxidation and cell death,
is another prominent theoretic model for the observed pathobiology in microtraumatic soft tissue injury ( 54).
The synovial sheath and peritenon are also involved in microtraumatic injury, especially as a result of friction with
excitation of the synovial cells. The synovial A cell, in particular, is an immunologically competent cell with potential for
pronounced cytokine production ( 92). Kvist et al. studied 16 athletes presenting with peritenonitis ( 93). Increased enzyme
activities were found mainly in the fibroblast, inflammatory cells, and vascular walls in the peritenon. The results indicated
that marked metabolic changes occur, with an increased catabolism, lowered pH, and decreased oxygenation of the
inflamed areas. Typical findings included fibroexudation with deposition to fibronectin and fibrinogen, proliferation of
blood vessels, and, in some cases, marked endothelial hyperplasia with obliteration of microarterial vessels ( 93,94).
Growth factors have been substantiated to modulate this process. Badalmente et al. in studying the biopsied tissues of
typical cumulative trauma disorders (including trigger-finger deQuervain disease and carpal tunnel syndrome), identified
fibrocartilaginous metaplasia in the trigger-finger deQuervain condition, but not synovitis ( 34). A chondroid metaplasia
response appeared to be present. Leadbetter found both chondroid metaplasia in the pulley A1 tissue and synovitis in
the tenosynovium (3). In carpal tunnel syndrome, a proliferation of type B synovial cells in the tendon sheath was found
(34). Almekinders et al. demonstrated an in vitro capacity of the human tendon tenofibroblast to produce inflammatory
mediators, including prostaglandin E 2 (PGE 2) and LTB4, in response to repetitive motion (32).
In flat tendons, such as the extensor carpi radialis brevis of the lateral elbow, there are findings of intratendinous
degeneration, with a dull, immature, edematous gross appearance and peritendinous granulation tissue ( 3,55) (Fig.
46.15). This tissue has essentially the same appearance as chronic granulation tissue seen in various tendon sites
throughout the body in response to microtraumatic injury. It characteristically has many small fibrosensory nerves and,
presumably, a high concentration of nociceptor-stimulating substances. The term “angiofibroblastic hyperplasia” ( 55)
coined to describe these findings, does not merit recognition as a distinct pathologic entity.
FIGURE 46.15. Chronic inflammatory granulation tissue characterized by abortive scar repair, scattered macrophage-like
inflammatory cells, fibroblasts, and neovasculature (hematoxylin and eosin stain) (original magnification, ×162.5).
The electron microscopic appearance of microtraumatic injury response is typified in tendons by degenerative findings,
as reflected in alterations in the size and shape of mitochondria and in the nuclei of the internal fibroblast or tenocyte.
Intracytoplasmic or mitochondrial calcification may be seen. Dystrophic calcium pyrophosphate salts precipitate in
degenerative connective tissues as a result of mitochondrial injury. The resulting calcification is deposited in the collagen
matrix as chalky-appearing hydroxyapatite crystals, the “tombstones” of tendon injury ( Fig. 46.16). Cytoplasmic vacuoles,
lipid deposition, and cell necrosis changes are thought to result from relative tissue hypoxia ( 2) (Fig. 46.17). However,
similar changes have been documented in reparative cells after tendon laceration, presumably as a result of the hypoxic
wound microenvironment (65). Changes in the collagen fibers at sites of microtrauma in tendons include longitudinal
splitting, disintegration, angulation with a unique bent-fiber appearance (knicking), and abnormal variation in fiber
diameter (57).
FIGURE 46.16. A: Typical intratendinous dystrophic calcification of Achilles tendon and calcaneal plantar fascia spur.
Occurring at sites of degeneration, these reactions are the “tombstones” of tendon injury. B: Intratendinous calcification
with prominent surrounding inflammatory response (hematoxylin and eosin stain).
FIGURE 46.17. Tendinosis: electron microscopic appearance. Note lipid deposition, swollen mitochondria, and
disorganized cell organelles, which imply a hypoxic stress response (original magnification, × 10,750).
These observations reinforce the concept of chronic injury as being that pattern observed when the acute injury repair
response is impaired.
Acute Versus Chronic Clinical Injury Profile
In addition to the histopathologic pattern of injury and repair, Leadbetter distinguished acute and chronic injuries
according to their clinical injury “profiles” ( 2). The acute injury profile is characterized by a defined time of onset, with the
trauma episode generally observed as a sudden catastrophic occurrence (e.g., collision or contact injury) or, in the case
of a tendon, as a spontaneous midsubstance disruption. At the moment of injury, pain is likely to be severe. This is
typically followed by a period of gradually decreasing pain as inflammation is treated intensively. Pain eventually falls
below an arbitrary threshold after which the patient feels well. When pain is no longer inhibiting, the athlete usually
requests a return to activity; however, when the biologic curve of wound healing is plotted against the subjective pain
response over time, a potential period of reinjury vulnerability appears. The duration of this period of vulnerability is
proportional to the original severity of the structural damage, the rate of healing of the given individual (which is likely to
be slower with age), the nature of the target tissue that is injured, and the expected demand or load exposure on return to
sports. The period of vulnerability after an acute injury would in theory be lengthened by any raising of the arbitrary pain
threshold of the athlete or by any rapid removal of the subjective pain (e.g., with aggressive antiinflammatory treatment or
analgesic treatment). It would be lengthened by the adverse effects of any inappropriate immobilization, but it would be
shortened by functional rehabilitation or protective bracing that expedites fibrogenesis or decreases tensile load on a
tendon. Because research has suggested that an injured connective tissue may attain only 70% to 80% of its original
structural and biomechanical integrity after as much as 12 months, the period of vulnerability can be lengthy, implying a
need for protected activity despite the absence of pain and for an ongoing rehabilitation program to recruit muscular
support (Fig. 46.18).
FIGURE 46.18. Hypothetic profile of acute macrotraumatic tissue injury. This profile is typical of an acute partial tendon
strain or the pattern of healing in other acutely injured connective tissues (e.g., lateral collateral ligament sprain in the
ankle). The curved dashed line indicates pain, and the curved solid line indicates tissue healing. (From Leadbetter WB.
Cell-matrix response in tendon injury. Clin Sports Med 1992;11:553–557, with permission.)
Chronic soft tissue injuries differ from acute injuries in several important ways. The moment of injury, in the athlete's
perception, may be a moment of noxious pain. This often occurs after overexertion (e.g., a long-distance run, intense
throwing), resulting in pain that becomes insidiously inhibiting over a period of time or explosively disabling hours or days
after the event. Muscle, tendon, and synovial structures typically evidence this type of stress response to sports activity.
The examiner's inquiries about preinjury training patterns and cumulative load exposures are critical to understanding
why this type of tissue response has been triggered. For instance, a careful history in a marathon distance runner might
reveal that an inadequate amount of time was spent in prerace preparation and that several weeks of mild, but not
inhibiting, pain symptoms had been generated by abusive training before the actual moment of injury. This is the
transitional injury pattern. In theory, subclinical injury and dysfunction (e.g., microtrauma) precede the moment of
conscious injury. The implication is that damage has been accumulating for a long time before the first opportunity for
medical treatment. This is distinct from acute injury, in which the onset of injury and initial treatment often closely
coincide. The accumulation of repetitive scar adhesions, degenerative changes, and other adverse effects in chronic
microtrauma imply that recovery will be slower. Again, a period of vulnerability to reinjury results, which is increased
when conventional antiinflammatory measures and pain reduction techniques are applied without regard for the lack of
adequate structural integrity. In chronic inflammatory injury, it is the history that provides a proper recommendation and
adjustment of activity (Fig. 46.19).
FIGURE 46.19. Profile of chronic microtraumatic soft tissue injury. This profile is typical of overuse tendon injury. The
solid line indicates percentage of tissue damage. (From Leadbetter WB: Cell matrix response in tendon injury. Clin
Sports Med 1992;11:533–557, with permission.)
ADAPTATION VERSUS INJURY
Adaptation may be defined as the process by which an advantageous change is achieved in the function or the
constitution of an organ or tissue to meet new conditions ( 95). A maladaptation is a disadvantageous change in an organ
or tissue. In pathology, examples of cell adaptation include cell hypertrophy, hyperplasia, metaplasia, protein or lipid
storage, dysplasias, increased DNA synthesis, and even changes in cell receptor properties ( 48). Such adaptations may
prove disadvantageous to the athlete.
The process by which connective tissues renew their cell populations and their matrix contents is known as morphostasis
(45). The continual turnover of collagen in dense connective tissue is an example of such tissue maintenance ( 75).
Although it is difficult to quantify, collagen turnover is most rapid in bone and relatively slower in connective tissue and
articular cartilage ( 75). Mediators are protein hormone messengers (e.g., cytokines, growth factors) that represent the
most prevalent and universal method of cell-to-cell and cell-to-matrix regulation throughout the body ( 59,96). There are
several subcategories of cytokines: monokines, so named for their derivation from mononuclear phagocytes;
lymphokines, produced by activated T lymphocytes; colony-simulating factors, produced by both lymphocytes and
mononuclear phagocytes; interleukins, principally synthesized by leukocytes; and growth factors such as TGF-b, PDGF,
fibroblast growth factor (FGF), and epidermal growth factor (EGF), which are produced from a variety of sources
including platelets, fibroblasts, and tissue macrophages ( 97,98).
Such biologic response modifiers are not limited to cell-synthesized protein molecules. For example, the degradation
products of such structures as cell wall lipoproteins (e.g., prostaglandins) or traumatically induced fragments of
proteoglycan molecules (e.g., from muscle or cartilage) act as potent cell stimuli in tissue trauma responses. All of the
molecules interact like letters of the alphabet to create words, sentences, and whole messages. Taken out of context, the
meaning of any one component is often lost. After injury or during exercise-induced adaptations, it is often the relative
concentration and timing of appearance of these messengers that dictate the final tissue response ( 96,97 and 98).
Furthermore, many of these molecules are a normal requirement for tissue or organ functions. For example, PGE 2 is
normally an important factor inhibiting gastric hyperactivity. Likewise, proper hepatic, uterine, and renal functions depend
on the presence of prostaglandins; hence, oversuppression of prostaglandin synthesis by nonsteroidal antiinflammatory
medications (NSAIDs) has both advantages (e.g., decreased inflammation) and risks (e.g., peptic ulceration, renal
failure). Taken as a whole, mediators influence virtually all tissue cell activity after load, use, or injury in the body,
including cell recruitment, migration, differentiation, proliferation, and protein synthesis.
Castor (59) noted that “connective tissue cells function as a community of diverse interacting cell types exerting a high
degree of mutual local control over neighboring cells. In perturbed states, as in injury, those metabolic phenomena with
survival value stand out in their major thrust as repair. Metabolic functions of cells during the repair process are
genetically programmed activities largely regulated by autacoid mediators (cell self-stimulation), feedback control
mechanisms, and environmental factors converging on the cell to yield an appropriate metabolic response.”
Although there may not exist a central control mechanism at the tissue level for such metabolic activity as previously
mentioned, variations in load and use would appear to play a dominant role in the clinically observed maintenance
adaptations in response in sports-injured tissues ( 28). Cells may be seen as the transducers of load in this process ( 80).
Cells respond to load by changing shape or composition, protein synthesis, growth rate, mitochondrial density, and
collagen turnover rate ( 80). Extremes of overload or immobilization increase their synthesis of matrix degradation
enzymes, a condition clinically known as tissue breakdown. In theory, a physiologic “window of stress” response defines
a synthetic homeostatic and degradative cell behavior for any of a given athlete's tissues ( 2,28,31,89) (Fig. 46.20).
FIGURE 46.20. Principle of transition: the more rapid the transition, the greater the risk. (From Leadbetter WB. The
physiology of tissue repair. In: Hunter E, ed. Athletic training and sports medicine, 2nd ed. Park Ridge, IL: American
Academy of Orthopaedic Surgeons, 1991;96, with permission.)
The effect of load on tissues is described by the terms strain and stress. Research suggests that both strain and stress
promote cellular or matrix biologic responses ( 28). For example, tendon structures are subject not only to tensile load but
also to high compressive forces ( 28,89). Such compression occurs extrinsically at sites of pulleys and bony prominences.
Intrinsic compression is the result of a cyclic torque load seen secondary to pronation of the foot in the Achilles tendon, in
the ACL during rotatory movement of the knee, and in the rotator cuff during torque about the shoulder ( 2). An
accumulation of large-molecular-weight proteoglycans has been demonstrated in regions of human posterior tibial tendon
posterior to the medial malleolus, implying a synthetic stress response as a physiologic adaptation to compressive forces
(99). Similar findings were noted in the ACL tissue, and in bovine flexor tendons, where fibrocartilaginous matrix
metaplasia is a common finding. Woo and Buckwalter, in analyzing the mechanical properties of tendon ligaments,
theorized an ideal homeostatic level of stress and strain duration to maintain mechanical properties and tendon mass
(28). The cells, collagen, and matrix in tensile and pressure zones of different tendons may differ. Whether these effects
are mediated by cytoskeletal deformation or are caused by such factors as local piezoelectric effects of matrix on cells is
unknown (80). Based on such observations, a theoretic model has been suggested for Wolf's law of soft tissue ( 30) (Fig.
46.21).
FIGURE 46.21. Theoretical schema for Wolf's law of soft tissue. (From Amadio PC. Tendon and ligament. In: Cohen IK,
Diegelmann RF, Lindblad WJ, eds. Wound healing: biochemical and clinical aspects. Philadelphia: WB Saunders Co,
EPIGENETIC AND GENETIC EFFECTS ON SOFT TISSUE HEALING
There are both epigenetic and genetic influences on connective tissue healing. Epigenetic factors are defined as those
factors that can influence the phenotypic expression (i.e., protein production) of the cell without altering the genome.
Vascularity, hormonal influence, and rest may exert epigenetic influence on tissue injury healing. Genetic factors are
intrinsic to the individual but may be variably expressed. In theory, such poorly understood phenomena as the “quality” of
collagen synthesis, the rate of healing, the propensity to inflame after injury, and the rate of recovery are to some degree
under genetic control. Aging may be considered to have both an epigenetic and a genetic role in injury response.
Aging
Aging is best characterized by a failure to maintain homeostasis under conditions of physiologic stress. The salient
characteristic of aging is not so much a decrease in basal functional capacity as it is a reduced ability to adapt to
environmental stress (48). The aging process is universal, decremental, progressive, and intrinsic to the athlete's tissues
(13). Generally, tissue aging parallels overall trends in cellular senescence ( 63).
There is evidence to suggest that the tendon collagen fiber possesses all of the cross-linkages it will ever have shortly
after its synthesis (13). During maturation, reducible cross-linkages gradually stabilize. This results in a less compliant
collagen fiber subject to shear-stress injury. Aging results in a significant decrease in tendon and ligament
glycosaminoglycan concentration ( 30). There are extensive data on the aging of cells in vitro (100). Collagen synthesis
has long been thought to decrease with age; however, this decrease is not an intrinsic incapability, because collagen
synthesis can be stimulated in the presence of ascorbic acid ( 78). Generally, aging results in changes in matrix integrity
and in the rate of wound healing, although aging does not prevent adequate clinical wound healing, which can be
stimulated by physical training.
There are documented morphologic, immunologic, and biochemical changes associated with aging ( 101). With aging,
collagen fibers increase in diameter and vary more in thickness; in addition, there may be an overall increase in insoluble
collagen (13). These morphologic changes correspond to biochemical changes that include a decrease in proteoglycans
and a decrease in water content. Parallel changes in elastic fibers also occur ( 101). With age, adaptation requires a
longer interval of rest and recovery ( 48). This is presumably related to the documented downregulation in cellular biology
of the older athlete. Injured tendons display biochemical and morphologic tissue changes ( 2,28,30,86). In comparing an
area of tendon degeneration in a 25-year-old adult with spontaneous Achilles tendon rupture with the Achilles tendon of a
normal 24-year-old, Ippolito et al. noted that, in the area of tendinosis, there was a 34% loss of collagen and a more than
100% increase in proteoglycans, with a significant increase in water and glycoprotein content ( 102). Similar histologic
evidence of this type of tissue response in the very young athlete has not been documented.
Vascularity
Vascularity has long been thought to play a prominent role in tendon degeneration, especially in the supraspinatus
portion of the rotator cuff, in the Achilles tendon, and at sites of extrinsic bone pressure ( 103). Since the injection studies
of Rathbun and McNab, a watershed area in the distal supraspinatus tendon has been offered for an explanation of
rotator cuff degeneration (104). However, there is evidence that the vascularity in the critical zone of the supraspinatus
tendon is actually hypervascular secondary to a low-grade inflammatory incitation with neovascularization after
mechanical irritation (105). Brooks et al. likewise came to the conclusion that no significant difference existed between
the vascularity of the impinged supraspinatus portion and other portions of the rotator cuff. It was concluded that factors
other than vascularity were important in the pathogenesis of supraspinatus tendon rupture ( 106). These assertions tend
to shed a different light on the theory of hypoxic intratendinous degeneration and the etiology of tendinosis. Focal load
influences on cell-matrix metabolism may play as great a role as any proposed diminished vascularity. Wilson and
Goodship measured a core temperature increase of 5° to 9°C secondary to hysteresis energy losses in the equine
superficial digital flexor tendon during exercise. This radiant energy was equal to 10% of the lost elastic energy on
unloading and was theorized to be potentially cytotoxic ( 107). There seems to be a preponderance of support for a
diminished microvascular debt in the central core of a round tendon, such as the distal third of the Achilles tendon ( 108).
Further research is needed to resolve this question.
Hormonal Influence
Hormonal influence on tendon biology relates primarily to estrogen and insulin. It has been suggested that diminished
estrogen levels, premature menopause, and premenopausal hysterectomy may be associated tendinosis in women; no
other data are available to support this contention ( 109). In addition, diabetics are known to heal with some difficulty
(110).
Rest
Rest has long been clinically recognized to aid the patient with a soft tissue injury. Yet the beneficial role of rest as a
therapeutic intervention in the inflammation repair process remains empiric and undefined. Although it may be said that
rest does not heal ( 37), theoretically, cell reparative efforts may catch up in the face of rest. The effects of rest are
probably multifactorial and may include improved vascularity in the tendon at rest or an improved morphostatic balance
between matrix degradation and production. Different forms of rest include total abstinence, protected activity, and
altered activity (35). Such classifications imply an attempt to control both cell-matrix load signal and recovery from cell
loading. There is evidence that repetitive motion and variation of frequency (i.e., cycles) may create a positive reparative
signal after injury (65). Absolute rest or abstinence does not de facto increase the athlete's potential to tolerate renewed
load during participation ( 2,35,37). Modified load rehabilitative prescription has been shown to be important to any
successful return to sports performance (76,111).
Genetic Influences
Genetic influences are implicated in the modulation of soft tissue cell-matrix response based primarily on clinical
observations. The mesenchymal syndrome may be a genetically determined cause of failed healing ( 109). Tendinosis
appears in multiple sites in approximately 15% of such patients and in sites not necessarily subjected to obvious overuse
(109). An association among lateral epicondyle extensor carpi radialis brevis tendinosis, rotator cuff degeneration, carpal
tunnel syndrome, cervical and lumbar disk degeneration, plantar fasciosis, deQuervain syndrome, and trigger-finger
tendinosis has been observed ( 2,55). Blood type O has been statistically related to tendon rupture ( 112). Achilles tendon
rupture in children is uncommon and has been encountered only in children whose parents have themselves experienced
tendon rupture (113). Young adult herniated disk syndrome is often seen in the presence of a familial history
(unpublished observation). An underlying collagen diathesis can be theorized. The clinical significance of the
mesenchymal theory lies in early recognition of patients who present with frequent tendon complaints disproportionate to
their level of activity. Systemic disease must be ruled out; in addition, these patients are unusually vulnerable and must
be counseled about proper participation and moderation in their activity.
Structural Variability
Structural variability in connective tissues may explain alterations in response to injury and adaptive capability that are
observed both in animal models and clinically ( 28). Lyon et al. called attention to the inherent differences between MCL
and ACL structures that superficially appear similar but biologically behave differently with respect to healing ( 114).
These differences include alterations in basic crimp pattern, a more cartiloid and plumper cellular appearance to the
fibroblast in the ACL, a more spindle-shaped linear cellular phenotype of the fibroblast in the MCL, and differences in the
cytoplasmic processes between these two structures. Chandrasekharam et al., in characterizing the intrinsic properties of
ACL and MCL cells, revealed in an in vivo cell culture that the ACL cells had a slower rate of proliferation, a spread-out
phenotypic appearance (compared with an elongated appearance of MCL cells), relatively more stress fibers and a
higher actin content (implying possible earlier senescence), and a lesser tendency toward confluence in cell culture
(implying a lowered proliferation and migration potential), compared with MCL cells ( 115). The authors concluded that
these factors may contribute to the differential healing potentials of these ligaments seen in vivo (115).
The observed structural and biochemical differences among ligaments and tendons are probably caused by different
mechanical demands and different levels of local nutritional supply ( 28). Furthermore, ligaments are nonuniform
structures. For instance, differences have been found in thickness, collagen content, hexosamine, and percentage of
total water in different areas of the same rabbit MCL ( 116). In the past, ligaments and tendons were thought to be
structurally distinct, with ligaments composed of densely packed collagen bundles arranged in a less linear orientation,
compared with tendons (117). However, cadaver studies of rotator cuff tendons revealed a complex interwoven
multilayered orientation combining microscopic features of both ligament and tendon ( 118). These characteristics directly
affect the potential evolution of injury as well as the location of initial degenerative lesions in such injured tissues.
Muscle structure also displays great variability. There are fusiform, parallel, unipennate, bipennate, and multipennate
muscle forms. Because of the larger number of their parallel fibers, pennate muscles are more powerful, whereas
fusiform muscles allow for greater range of motion (ROM) (119). Muscles and ligaments display differing failure patterns.
Muscles injuries occur primarily at the myotendinous junction or at bony attachment sites ( 60,119). Ligaments vary in
failure pattern, from osseous detachment to intrasubstance disruption, depending on strain rate ( 31).
Therefore, it is clear that all connective tissues are not the same. Not only do dissimilar structures possess different
biomechanical and biologic properties, but similar structures also differ. It is likely that no two ligaments are the same,
and that any one ligament may vary from day-to-day and even from site-to-site within its structure. Based on such
findings, it is necessary to temper generalizations regarding the adequacy and predictability of the connective tissue
healing response, unless the wounding mechanism, the biologic nature of the involved tissue, and the environmental
conditions are carefully defined.
The factors contributing to potential failed healing response in soft tissues are both intrinsic and extrinsic ( 35) as shown
in Table 46.5.
TABLE 46.5. FACTORS LEADING TO FAILED SOFT TISSUE HEALING
THE PRINCIPLE OF TRANSITION
The principle of transition states that sports injury is most likely to occur when the athlete experiences any change in
mode or use of the involved part ( 4). Transitional injury is rate dependent: sudden, ill-timed activity changes are more
injurious. Whether in training or during injury recovery, the result is an undesired breakdown response that may outstrip
tissue morphostatic efforts by imposing overload or overuse demands on the cell-matrix environment. There is growing
evidence for a cellular disuse transitional response, as well as an overuse breakdown response ( 120). The factors that
correlated with the incidence of jumper's knee were a hard playing surface and an increased frequency of training
sessions (121). A relationship between complete rupture of the Achilles tendon and a sedentary lifestyle has been noted;
although the issue is not specifically addressed in the report, it is likely that many of these injuries occurred during the
transition from inactivity to activity ( 88). A study on Achilles tendinitis and peritendinitis identified a training error as the
primary etiologic factor in more than 75% of all cases, the majority representing a sudden increase in mileage ( 21). Too
rapid a return to activity was also noted as a prime cause of reinjury ( 21). Illizarov, in an attempt to determine the
influence of rate and frequency of osseous distraction on cellular behavior, was able to identify a window representing a
tolerable distraction rate of 1 mm per day with as many as 60 incremental lengthenings, thereby creating a gradual
transition stress response. He found the rate effects to be proportional to the growth of the fascial fibroblast and capillary
ingrowth (122). Examples of transitional risks include any attempt to increase performance level; any change in position
played; improper training methods; changes in equipment or environment (e.g., a new playing surface, a different training
altitude); alterations in frequency, intensity, or duration of training; attempts to master new techniques; return to sport too
soon after injury; and even body growth itself. Transition theory correlates with current recommendations on periodization
in athletic training ( 123,124) (see Fig. 46.20).
INJURY RESPONSE PATTERNS IN SPECIFIC TISSUES
Muscle Injury
A strain is an injury to the musculotendinous unit. Muscle injuries are classified as either (a) acute muscular strains and
avulsions, (b) contusions, or (c) exercise-induced muscle injury or delayed-onset muscle soreness (DOMS) ( 4,120,125).
Muscle injuries can be caused by strain or by a direct blow ( Fig. 46.22). Muscle strain may be generated by passive
overstretching or by sudden voluntary eccentric or concentric contraction ( 119) (Fig. 46.23). Such sudden overloads
define the dynamic overload mechanism of injury ( 18). Fatigue contributes to the risk of injury by decreasing the
load-to-failure capacity and the absorption of energy to failure of muscle ( 83). Muscle tissue is well vascularized and is
capable both of generating an acute phase inflammatory response to disruption of its ultrastructure and of displaying a
variety of metabolic disturbances in muscle homeostasis ( 60,78,80,126,127).
FIGURE 46.22. A: Mechanism of muscle and ligament injury: The sprains are tension injuries, whereas the contusion
results from compression. B Computed tomographic scan of severe intramuscular hematoma, right quadriceps (arrows),
occurring after a direct blow. The injury was self-treated with immediate application of heat; markedly increased
compartment pressure led to emergency fasciotomy of the thigh. (From Ciullo JV, Jackson DW. Track and field. In:
Schneider RC, Kennedy JC, Plant ML, eds. Sports injuries: mechanisms, prevention and treatment. Baltimore: Williams &
Wilkins, 1985;214, with permission; and Leadbetter WB, unpublished case.)
FIGURE 46.23. Severe hamstring muscle strain. Note pronounced hemorrhage and swelling 72 hours after injury.
Forced lengthening of muscles was noted by Stauber and colleagues to induce both a cellular infiltrative response in
muscle tissue and alterations in proteoglycans in the surrounding matrix ( 61,71). Tissue macrophages and mast cells
predominated in the early phase; this was followed by a second wave of lymphoid cells, thought to be cytotoxic and
capable of producing both pain and continued elevation of serum enzymes, with possible continued muscle damage by a
cell-mediated response not related directly to initial mechanical damage. There was a prominent degradation in heparan
sulfate proteoglycan in the surrounding myofiber matrix. Heparan sulfate proteoglycan is thought to be involved in the
regulation of myofibroblast proliferation ( 61).
The severity of muscle strains is categorized similar to ligament injuries: first-degree (mild) strains are defined by minimal
structural damage, minimal hemorrhage, and early resolution; a second-degree (moderate) strain is defined as a partial
tear, most often at the myotendinous junction, accompanied by pain, significant hemorrhage, inflammatory pain, and
functional loss; and third-degree (severe) strains are accompanied by obvious hemorrhage, swelling, and, often,
complete and palpable muscle tissue disruption. As with all soft tissue injury, the inherent difficulty with such a
classification is in differentiating moderate from severe muscle strain. Clinical errors, of both undertreatment and
overtreatment, may result.
Although muscle cells are permanent cells and have no proliferative capacity, reserve cells that lie in the basement
membrane of the muscle fiber are able to proliferate and differentiate, forming new skeletal muscle. Therefore, the
regeneration of muscle fibers in even complete muscle tears is theoretically possible ( 60). However, when muscle tissue
is completely disrupted, it is more common for scar tissue to form ( 128). Scar tissue prevents the muscle from
regenerating and creates adhesions that restrict contractile and adjacent joint function. Initially, injured muscle can lose
up to 30% to 50% of its strength ( 60,128), primarily due to inflammatory pain (128). Nikolaou et al. showed that recovery
of strength begins as soon as 48 hours after injury, but that there is significant permanent loss of contractile ability (10%
to 20%) (60,128). What causes this residual weakness is not fully known, but its possible causes include intramuscular or
intermuscular restrictive adhesions, change in resting length, and coincident or innervation injury.
DOMS appears 12 to 48 hours after an exercise session and represents the clinical syndrome of exertional muscle injury
response. DOMS is characterized by tenderness on palpation, by increased muscle stiffness, and by restriction in ROM
(73,129). Although the exact mechanism remains unresolved, there is considerable evidence for both inflammatory and
metabolic dysfunction secondary to muscle damage (73). In support of the inflammatory model, Smith noted the following
similarities between DOMS and the classic acute inflammatory response ( 73):
1. Pain, swelling, and loss of function are observed.

2. Cellular infiltrates are noted, particularly macrophages.
3. Fibroblasts have been seen in association with both events.
4. Increased lysosomal activity occurs during both events.
5. The progression and size of the lesion occur in both instances in about 48 hours.
6. Increased levels of IL-1 and acute phase proteins occur in both events.
7. Signs of healing are observed at approximately 72 hours.
Structural abnormalities after eccentric exercise have been identified ( 130,131) and include primary and secondary
sarcolemmal disruption, swelling or disruption of the sarcotubular system, distortion of the myofibril contractile elements,
cytoskeletal damage, and extracellular myofiber matrix abnormalities.
Exertional rhabdomyolysis has been associated with increased plasma levels of intramuscular proteins such as
creatinine kinase, lactic dehydrogenase, and myoglobin ( 127). The cytokine IL-1 has been called the “endogenous
pyrogen” and has been shown to stimulate muscle proteolysis in vitro. IL-1 in vivo is a prominent stimulator of PGE 2,
which is known to increase muscle lysosome function ( 127). As in other sublethal cell stress responses ( 52) (see Fig.
46.14), increased intracellular Ca 2+ ion levels may evolve from structural damage to the sarcolemma, especially during
eccentric muscular actions ( 127,130). This initial calcium overload phase of intracellular accumulation then may
precipitate an autolytic phase, in which proteases and phospholipases increase in activity, resulting in myofibrillar and
membrane degradation. A regenerative or repair phase then follows ( 127,130).
A muscle contusion results from an external force that is sufficient to cause muscle damage (see Fig. 46.22). Contusions
may be graded in severity according to the restriction in ROM of the subtended joints. A mild contusion causes a loss of
less than one third of the normal ROM of the adjacent joint, whereas severe contusions limit motion to less than one third
of normal excursion. Contusions result in vascular disruption, producing two types of injury: intermuscular hematoma (a
hemorrhage occurring along large intermuscular septa or fascial sheaths) and intramuscular hematoma (a hemorrhage
occurring within muscle substance). Intermuscular hematomas are more likely to disperse and be reflected by distal
ecchymosis and diffusion of degradating blood components. Intramuscular hematomas are more difficult to resolve and
are associated with scar contraction or myositis ossificans ( 125). In severe cases, rapid bleeding may cause acute
compartment syndrome and require urgent surgical fasciotomy (see Fig. 46.22B). In the case of contusions of the
quadriceps muscles, the Jackson-Feagin classification has proved useful in assessing prognosis and rate of recovery
(132). Contusions were classified as mild (localized tenderness, ROM greater than 90 degrees, normal gait, and the
ability to do a knee bend); moderate (swollen and tender muscle mass, ROM less than 90 degrees, antalgic gait, and
inability to climb stairs or arise from a chair without pain); or severe (marked tenderness and swelling, ROM less than 45
degrees, severe limp requiring crutches for ambulation, and pain in the ipsilateral knee) ( 132,133). Myositis ossificans
developed in 13 of 18 patients with grade 2 or 3 contusions, but in none of the 47 athletes with grade 1 contusions ( 132).
Myositis ossificans traumatica is a condition of heterotopic ossification response usually confined to a single muscle or
muscle group; it occurs in almost all cases after a prior episode of trauma, whether single or repetitive ( 132) (Fig. 46.24).
The pathologic course is that of a benign, self-limited process characterized by both dystrophic calcification (e.g., calcium
phosphate precipitation in damaged tissue) and bone formation in areas of preexisting hematoma and injured tissue
caused by severe contusion, strain, or repeated trauma ( 134). Clinically, myositis ossificans can be a source of
considerable and lengthy disability to the athlete because of inflammatory pain and contracture ( 60,67,119). Parosteal
and intramuscular locations are more common than periosteal; this distinction is sometimes helpful in the radiologic
differentiation of this lesion from osteosarcoma ( 133).
FIGURE 46.24. Myositis ossificans: magnetic resonance image of vastus lateralis. Note parosteal location and peripheral
calcification pattern.
The most common clinical findings of myositis ossificans are a soft tissue mass with restriction of joint motion ( Fig.
46.25). In patients with myositis ossificans the pain and the size of the mass decrease as the lesion matures, whereas in
those with osteosarcoma the mass and the pain are known to increase with time (133). The quadriceps, femoris, and
biceps brachii are most often involved, reflecting their exposure to direct trauma. Although the exact mechanism of onset
remains unknown, experimental evidence suggests that extensive cell necrosis stimulates connective tissue cell
metaplasia (60,67). The pathologic process of ossification begins with the initial injury to muscle and connective tissue
associated with muscle fiber disruption and hemorrhage. The pathophysiologic sequence may be muscle trauma,
inflammation, cellular proliferation, concentration of growth factors, induction of bone forming cells, and, finally,
ossification. NSAIDs have been shown to prevent heterotopic ossification, implying that prosta-glandins may play a role
in the inflammatory generation of myositis ossificans ( 134). Increased exercise, stress, and younger age have been
thought to be associated with heterotopic bone deposition ( 133). Myositis ossificans is most common in the second and
third decades of life for unknown reasons; contributing factors are thought to include a high activity level, coupled with
rapid growth resulting in increasing muscle length, and larger muscle volume ( 133). The onset of myositis ossificans has
been related to the severity of contusion. Jackson and Feagin found that 72% of athletes afflicted by moderate or severe
contusions developed heterotopic ossification ( 135). Reinjury of a contused quadriceps was associated with 100%
subsequent development of myositis ossificans. A presentation of pain, a palpable mass, and an associated flexion
contracture after muscle injury strongly suggests the possibility of early myositis ossificans ( 133,135). The clinician may
note localized warmth and local tenderness. Radiologic evidence of intramuscular calcification usually is delayed until 6
to 8 weeks after onset, with gradual evolution to mature bone over a period of subsequent months ( 67,133,135).
FIGURE 46.25. Quadriceps contracture secondary to myositis ossificans after contusion injury. Prone examination, often
best, demonstrates loss of knee flexion by eliminating compensating hip flexion.
The most important differential diagnosis of myositis ossificans is malignancy (i.e., osteosarcoma). There are some
helpful differentiating characteristics between these characteristics. Myositis is characterized by a pattern of decreasing
pain and size of the mass over time, a diaphyseal location, a lack of associated bone destruction, the presence of a
radiolucent line of separation of the lesion from adjacent diaphyseal bone, and characteristic zones of radiodense mature
bone at the periphery of the lesion with a more lucent center correlating with the known histologic zonal maturation
pattern of this lesion. In contrast, tumors tend to develop more dense calcification centrally ( 133) (see Fig. 46.24). None
of these radiologic features is without exception, and attention has been called to the wide variety of appearances on all
imaging modalities, especially magnetic resonance imaging (MRI), which can be correlated with different stages of lesion
maturation (136). Forty percent of patients with osteosarcoma have a history of trauma in the involved limb ( 133). Serial
plain radiologic observation is mandatory in all cases and usually suffices to resolve the diagnosis. Surgical biopsy is
discouraged owing to the confusing, callus-like pseudomalignant histology of benign myositis ossificans, the propensity
for local recurrence of the lesion, and the tendency for spontaneous resorption ( 67,134). In rare cases, surgical removal
of a symptomatic lesion is indicated for persistent pain—usually no sooner than 1 year after onset.
Myofascial pain syndrome is a painful musculoskeletal response that can occur after muscle trauma. Myofascial trigger
points are small, chord-like or nodular sites that are associated with local muscle spasms and are acutely painful ( 137).
Fibrositis is a diffuse, multisite complaint that is not associated with muscle spasm or weakness and that most often
affects women between the ages of 30 and 60 years. It is not caused by trauma and is associated with emotional
disturbances (138). One of its symptoms is generalized muscle soreness and deep tenderness to palpation. Orsen has
provided an excellent review of myofascial pain ( 139). Both myofascial pain syndrome and fibrositis are theorized to have
a possible neurogenic origin at the central or spinal cord level. Neither condition is known to be inflammatory.
Tendon Injury
Because of their prevalence in sports, injuries to tendons and tendon insertions have received considerable attention.
There are many types of tendon and fascial injuries. Enthesopathy is an injury in which tendon fibers are either microtorn
or inflamed at their bony insertion ( 95); it is a term more often reserved for rheumatologic conditions. The tendinosis
lesion is an initially asymptomatic tendon degeneration caused either by aging or by cumulative microtrauma without
histologic evidence of acute inflammation ( 2,57,95) (Fig. 46.26). Peritenonitis is an inflammation of the tendon sheath and
is heralded by pain, swelling, and, occasionally, local crepitus ( 2) (Fig. 46.27).
FIGURE 46.26. Gross appearance of Achilles tendinosis lesion. Note fusiform tendon swelling and hyperemic
tenovagium with incidental intact plantar tendon.
FIGURE 46.27. A: Typical appearance of Achilles peritenonitis. B: Peritenonitis: microscopic appearance. Note
prominent inflammatory cells with synovial hyperplasia.
In tendinitis there is injury to the tendon tissue proper, and, if partial or complete tearing is involved, capillary damage,
vascular injury, and intratendinous inflammation are present. Depending on the specific tendon, complete tendon tears
may require surgical repair (e.g., long head of the biceps, Achilles, pectoralis major, extrinsic tendons of the hand,
patellar tendon). Normal tendon has a tensile strength that measures 45 to 98 N per millimeter, but tendon begins to fail
at 8% to 10% strain (76). The stage at which this failure causes pain and the mechanism involved in healing of this type
of injury are matters of conjecture. It is not clear whether inflammation precedes degeneration or is incited by gradual
mechanical failure. Available evidence from surgical biopsy suggests that inflammation occurs after a tendon tear. The
pathology of microtraumatic tendon injury was discussed previously. The current classification of tendon injury
emphasizes the distinction between peritenon or synovial inflammation and direct involvement of the tendon substance,
reflecting the variable stress responses of tendon structure ( Table 46.6).
TABLE 46.6. TERMINOLOGY OF TENDON INJURY
Ligament Injury
A sprain is an injury to a ligament. The nomenclature of ligament injury varies in different schemes ( Table 46.7). Healing
of sprained ligament tissue is analogous to healing in other vascularized tissues. Disruption of ligament is followed by
hematoma and soft tissue inflammatory repair. Full recovery may take more than 1 year, and the ultimate tensile strength
may be reduced by 30% to 50% (89). This seems to be a result of the differing qualities of scar and matrix in healing
ligament (28,89). An increased amount of ligament scar helps to counteract mechanical weakness, but other
biomechanical properties (e.g., bending stiffness) are not improved ( 89). Therefore, once a ligament is damaged,
“normal” ligament tissue is not restored ( 31,89). Cell structure, rate of maturation, and metabolic activity may differ from
ligament to ligament (89,114).
TABLE 46.7. SCHEMES FOR ASSESSING LIGAMENT INJURY
Tendons and ligaments share the structural property of crimp, a regular wavy undulation of cells and matrix that is seen
under a microscope (76). This crimp acts as a buffer or shock absorber that allows the ligament to avoid damage during
elongation. Under load, the crimp pattern slowly straightens out. Collagen fibers straighten completely at about 4%
elongation ( 89). Beyond this limit, tropocollagen molecular stress occurs. Ligaments display viscoelastic behavior (i.e., a
nonlinear deformation with respect to load). This biomechanical characteristic is both rate and history dependent: the
more rapidly a ligament is loaded, the more strain resistance develops. This observation underlines the importance of
slow static stretching of both tendon and ligament. A previously deformed ligament remembers “being stretched” by
responding slightly differently to each stretch in a series and being able to return to its prestretch length ( 89). The
mechanism for this response is thought to reside at the molecular level of the matrix, and it provides the additional
adaptive advantage of adjusting joint load under a variety of loading conditions while preventing failure ( 125). A failure to
adapt results in injury.
Synovial Injury
The synovial membrane is a thin layer of cells loosely classified as a specialized form of connective tissue. Synovitis is a
frequently associated complaint of tendon and ligament sports-induced injury and therefore deserves some special
consideration.
Synovial cells consist of three basic types. The macrophage like synovial type A cells make up 20% to 30% of the
synovial lining. Most of the remaining 70% to 80% of normal synovial lining cells (type B) have fibroblast-like
characteristics, including prominent, rough endoplasmic reticulum, and are associated with collagen and scar production.
Type AB cells have also been described; they show a combination of characteristics. Synovium functions to regulate the
peritendinous environment, much as it does the articular cartilage environment in joints ( 140). Synovial type A cells are
active in phagocytosis and the degradation of particulate matter from the cavities they surround; they demonstrate
pronounced immunologic and inflammatory potential.
Synoviocytes produce a variety of cytokines, including IL-1, FGF, TGF-b, b 2-microglobulin, amyloid A, and other
unidentified factors (141). Such cytokines are intensely inflammatory and may incite stenosing fibrosynovial response.
Bursitis and tenosynovitis are accurate descriptions of the underlying histopathology ( Fig. 46.28). Vascular endothelial
cells in the synovium maintain nutrition and also participate in inflammatory reactions to trauma. Afferent neurons in the
synovium and in the joint capsule contain substance P, a neuropeptide that is a primary source of pain after injury. Both
connective tissue fibroblasts and macrophages appear to assume the structure and function of synovial lining cells under
conditions that are yet to be precisely defined. A special synovial cell has been identified to interdigitate with the immune
T lymphocytes, a cell known to mediate chronic inflammatory processes ( 141).
FIGURE 46.28. Arthroscopic view of synovitis of the knee. The highly vascularized hypertrophic appearance typifies the
inflammatory pathology seen in tenosynovium or bursa.
The synovial membrane contains freely available unsaturated phospholipids, a ready source of prostaglandin and
prostacyclin production through the arachidonic acid cascade. When in excess, both molecules are potent pain
stimulators. Synovial lining cells have been noted to bind antigen-antibody complex, present antigen to T lymphocytes,
produce cytokines that promote the activation and proliferation of T lymphocytes, and respond to signals from
mononuclear cells (141). Explosive swelling, such as that seen in the olecranon bursa of the dart thrower or in the
prepatellar bursa of the wrestler, and the marked peritendinous reactions brought on by overuse seem to be triggered by
conditions of use as well as frictional shear. It is theorized that wear fragments of matrix molecules may promote this
inflammation (142). The type A cell is a secretor of hyaluronic acid, which serves as a synovial lubricating factor to
counteract frictional irritation ( 141). Trauma to a bursa or joint with vascular injury and bleeding (hemobursa) rapidly
triggers an inflammatory process mediated by the prevalent source of cytokines found in platelets as well as in synovial
cells. Lysosomal enzymes released into the bursal or peritenon space may damage exposed tendon surfaces with loss of
matrix proteoglycans (140). Medications such as corticosteroid injections or NSAIDs reduce synovial inflammation
through direct suppression of the arachidonic acid cascade (see Fig. 46.28).
SOURCES OF PAIN IN SOFT TISSUE INJURY
The origins of soft tissue pain are multifactorial and include both inflammatory and biomechanical sources ( 42) (Fig.
46.29). Synovial sites are capable of secreting a wide variety of inflammatory mediators, in particular IL-1 and PGE 2, and
provide a ready source of nociceptor stimulation in synovial-lined joints, bursa, and peritenon. The internal tendon
fibroblast is capable of producing inflammatory mediator proteins under repetitive stress ( 32). Elongation of a tendon or
ligament beyond its elastic limit may trigger nociceptors as well as myotendinous reflexes ( 143). Direct injury to small
connective tissue nerves may be a source of retinacular pain in the knee ( 144). Substance P is a peptide
neurostimulating substance found in high concentrations at sites of soft tissue pain and inflammation ( 42) (Fig. 46.30).
FIGURE 46.29. Possible mechanisms of musculoskeletal pain. (From White AA III. The 1980 symposium and beyond. In:
Frymoyer JW, Gordon SW, eds. New perspectives in low back pain. Park Ridge, IL: American Academy of Orthopaedic
Surgeons, 1989;3–17, with permission.)
FIGURE 46.30. Schema of the positive-feedback relationship that develops during the course of inflammation secondary
to sports-related injuries. (From Hargreaves KM, Troullos ES, Dionne RA. Pharmacologic rationale for the treatment of
acute pain. Dent Clin North Am 1987;31:675–694, with permission.)
There would appear to be a distinction between the pathobiology of pain caused by inflammation and that caused by
degeneration. Pain due to inflammation evolves when excessive loading results in immediate tissue damage and
necrosis, producing the onset of an acute inflammatory cascade, as seen in typical macrotrauma, with resulting chemical
nociceptor stimulation. Degenerative pain may evolve when excessive cyclic microloading results in matrix molecular
alterations, loss of tissue strength, resultant increased strain deformation with loading, and subsequent stimulation of
pain mechanoceptors. Resulting cell deformations and damage may contribute to biochemical cascades that further
stimulate nociceptor response. Systems for grading the severity of sports-induced soft tissue inflammation and the
progress of healing are used to recognize the severity of injury, to judge its resolution, and to make recommendations on
level of activity and return to competition ( 145). Such staging concepts for sports trauma, which have been applied to
both acute and chronic injuries, attempt to describe subjective or qualitative symptoms or behaviors in quantitative terms.
An early example, the traditional American Medical Association classification of ligament injury, set up three grades:
grade 1, mild stretching; grade 2, partial tear; and grade 3, severe complete tear. These grading systems are based on
the following assumptions (145):
1. There is a measurable response to soft tissue injury.

2. The duration and subjective appreciation of severity and type of pain correlate directly with the degree of tissue
injury.
3. A given level of pain correlates with a specific quality of tissue pathology.
The scheme for identifying ligament injury severity in the prototypical example is shown in Table 46.7.
Although these assumptions have been substantiated in selected cases, they usually cannot be scientifically documented
by such parameters as histologic biopsy. Therefore, in the individual athlete there are exceptions to the arbitrary
application of these grading systems. In the traditional scheme of defining three grades of injury, the grade 2 injury is the
“gray zone,” for it often shares signs and symptoms of both lesser and higher grades of injury. The resolution of this
question is no small point. The clinician is at liberty to allow return to play with fairly minimal concern for a grade 1 injury,
aside from preventing recurrence and identifying the initial contributing causes. Grade 1 injuries, by definition, produce
only localized pain and tenderness without any significant disability or lengthy interruption of play and may resolve fairly
spontaneously. With experience, the clinician will not find it difficult to identify the grade 3 injury, because soft tissue
signs and symptoms are pronounced and the disability is prohibitively severe. The distinguishing features between grade
2 and grade 3 injuries are often best determined by stress assessment of the injured part. Palpable loss of muscle
continuity or a stress radiograph that reveals instability of a joint defines a grade 3 injury. Grade 3 injuries require
prohibition from play. Grade 2 injuries remain the challenge in both diagnosis and recommended intervention. It is often
possible, with additional brace and support protection, to allow limited participation in athletic competition. For example, if
an athlete presents with a swollen lateral ligament injury of the ankle and stress radiographs of the ankle mortise reveal a
stable mortise, intensive treatment of the acute phase inflammation, followed by dynamic ankle support with a playing
brace or taping, may allow for an earlier return to competition without prohibitive risk.
The decision on when to allow athletic competition after soft tissue athletic injury is determined not only by the initial
assessment of the grade or severity of injury but also by the progression or trend in the recovery from that injury. In this
respect, grading systems have been useful because they allow a consistent, albeit subjective, means of quantifying and
qualifying the healing progress of the athlete. The clinician can often improve on the grading concept by having the
athlete create a log, noting the level of activity and including such variables as frequency, intensity, and duration, along
with the symptom severity and whether pain or a physical manifestation such as swelling is present, using a scale of 1 to
10. Such a log can be surprisingly helpful in revealing what levels of activity and what forms of activity precipitate or what
patterns of rest facilitate recovery.
These staging systems do not accurately distinguish between the symptom of pain and the real presence of inflammation.
To the degree that there are multiple pathways for the origin of pain, as well as modifications of its appreciation at the
cerebral level, attention is again called to possible mechanically and biochemically mediated effects on cell and matrix
(42). A cautionary word must also be mentioned regarding the symptom of night pain. Although night pain is not
uncommon for the patient with a chronic tendon injury (e.g., to the rotator cuff), pain that awakens the patient at night
may be the harbinger of a more serious coincident lesion, notably neoplasms. So-called sports tumors often present with
night pain; the clinician should be alert to reassess the diagnosis and to repeat, if necessary, appropriate imaging in the
face of this persistent symptom (146). A summary grading scheme is shown in Table 46.8.
TABLE 46.8. CLINICAL GRADING OF SPORTS-INDUCED SOFT TISSUE INFLAMMATIONS
THERAPEUTIC MANAGEMENT OF SOFT TISSUE SPORTS INJURY
The therapeutic management of soft tissue athletic injury requires, first, establishing an accurate diagnosis; second,
understanding the mechanism contributing to the injury; and third, providing an intervention that ensures the most benefit
for the least risk to the athlete. Ultimately, successful management is the sum of diagnosis, treatment, and preventative
rehabilitation. Depending on the type of injury, treatment decisions may be readily apparent, or they may be arrived at
only through a trial of therapy. The traditional approach has been to view athletic soft tissue injuries as either acute or
chronic. This oversimplification often breaks down, because previous or recurrent acute injuries may contribute to an
evolving chronic pattern. The following discussion emphasizes the principles and rationales underlying current sports
medicine diagnostic and therapeutic practice.
General Principles
The key steps in the management of soft tissue athletic injury have been defined as follows ( 147):
1. To establish an accurate and complete diagnosis of all the anatomic and functional deficits resulting from the injury
2. To minimize the deleterious local effects of the acute injury
3. To allow anatomic healing of the injury
4. To maintain other components of athletic fitness
5. To regain previous athletic function
Both acute and chronic injury may lead to functional effects and inflammatory symptoms ( Fig. 46.31). The first objective
in acute injury treatment is to control hemorrhage and initial excessive inflammatory pain (acute phase response effects)
and to limit subsequent necrosis and tissue edema (zone of secondary injury). These principles are summarized in the
mnemonic RICE'M: Rest, Ice, Compression, Elevation, and Mobilization ( Fig. 46.32 and Fig. 46.33).
FIGURE 46.31. Injury-pain cycle. The promotion of healing and performance depends on accurate diagnosis of excessive
inflammatory response and adequate rehabilitation.
FIGURE 46.32. Severe acute ankle sprain. Hemorrhage and edema contribute to the zone of secondary injury. Note the
“antalgic posture” with early Achilles contracture and plantar flexion of foot and ankle. Immobilization and splinting in a
position of function are essential early treatments.
FIGURE 46.33. Ankle sprain: cryotherapy. Immediate controlled compression and cooling is expedited by a cryocuff.
The initial objective in the treatment of chronic overuse injury is to recognize the problem in the greater context of
inadequate or abusive training. This shift in emphasis is summarized in the mnemonic REST'M: Rest and rehabilitation;
Education; Support of the injured part; Training and technique; Modification of activity, modalities, and medication ( 35).
Regardless of the type of injury, the rule is, first, do no harm. In prescribing treatment, it is wise to remember that every
treatment has its cost as well as its proposed benefit. An NSAID drug may add cost and side-effect risks without
significantly improving soft tissue healing. Improper or lengthy immobilization that results in atrophy or contracture can
delay functional recovery even though it provides immediate pain relief. No cure should be worse than the problem it
addresses. Although acute injuries are often accompanied by obvious physical findings, the diagnosis of most overuse
injuries requires familiarity with a good history, physical examination techniques, and proper radiographic imaging ( 37).
Plain radiographs may reveal unsuspected arthritis, tumors, or stress reactions, and they should always be done. With
the exception of dystrophic calcification, plain radiographs may only confirm negative findings in true soft tissue injury;
however, the triphase technetium bone scan, the MRI, and the ultrasound scan have proved useful in the identification of
persistent, chronic structural soft tissue injury ( 148) (Fig. 46.34).
FIGURE 46.34. Achilles tendinosis: typical appearance on magnetic resonance imaging. Note bright intratendinous
signal implying matrix degeneration or injury.
The focus of the therapeutic program may vary, depending on the soft tissue structures involved. The primary
consequence of muscle injuries is loss of strength, mobility, and potentially adverse cosmetic effects (e.g., rupture of the
pectoralis major muscle in a body builder). Tendon injuries result in persistent pain and loss of movement. The disability
of ligament injuries is instability. Diagnosis and treatment should proceed on a need-to-know basis, which is established
by the nature of the structure injured, the competitive level of the athlete, and the specific sport. Establishing what the
athlete can do and cannot do, as well as what the athlete wishes to do, helps in determining the extent of the diagnostic
evaluation. The clinician must “know the sport” with respect to the techniques and dosing demands of musculoskeletal
load and use if a successful sports-specific solution is to be prescribed. When encountering the injured athlete, one must
be prepared to Listen, Look, and then Locate the problem.
Basic Elements of Diagnosis
History and Physical
It is helpful to establish a consistent mental approach to the diagnosis of athletic soft tissue injury. It can be useful for the
examiner to keep in mind the seven basic mechanisms of injury: by a process of elimination, the most likely contributing
causes to the athlete's pain can be singled out. The differentiation of acute from chronic injuries is made easier by simply
asking the athlete, “Did this problem begin by your hurting it, or did it begin hurting you?” It is the absence of a contact or
single sudden injury that often defines the overuse mechanism. Basic fact-finding should include asking when the injury
began, what the exact activity was at the time of injury, what the athlete felt at the time he or she became “injured,” and
whether there was a previous injury. If a previous injury did occur, it is mandatory to spend time defining exactly what
occurred at that time. Often the injured athlete glosses over such occurrences, not recognizing a causal relationship with
the current complaint. A statement such as, “I twisted my knee 2 years ago skiing” may reveal the onset of an
incompletely evaluated ligamentous instability; stating that there was a prior fracture of an ankle requiring cast
immobilization may provide the clue for a persistent atrophy or proprioceptive deficit. Such disabilities may exist for years
without the benefit of diagnosis or complete rehabilitation. The pattern of pain may be helpful. A history of immediate
disability after injury or the loss of ability to play sports from an injury is a more ominous symptom implying significant
structural damage. Any persistent dysfunction such as a limp requires full evaluation.
Although the history is helpful in acute injury assessment (e.g., the acknowledgement of a “pop” on twisting of knee
implies an ACL injury), it is invaluable in assessing the chronic complaint. Overuse injury is a diagnosis by deduction.
Questions concerning training load, athletic technique, rest patterns, competitive schedule, playing position, equipment
changes, nutrition, and hydration patterns may contribute to the diagnosis. The history should seek to identify any
change or transition in athletic performance that would imply a legacy of abusive overuse (i.e., improper training) and
new adaptive demand. This can best summarized by the so-called Rule of Too's—too often, too hard, too soon, too
much, too little, too late, and so on ( 35). Work exposures also contribute to adaptive demands. The weekend tennis
player who happens to carry a briefcase or perform extensive labor with the affected arm during the week may
accumulate more adverse effects than would be apparent from his or her sports participation alone. If a fitness jogger
with a painful Achilles tendon must, in addition to jogging, repeatedly climb stairs or use a ladder while working,
improvement from conventional treatment may be frustrated. The onset of pain immediately on activity implies a structural
deficit; pain that is absent at onset and increases during the activity implies an underlying mechanical deficiency with
fatigue or chronic inflammation. In the face of a subsequent benign physical examination with no initial traumatic episode
by history, the examiner may be confronting an overuse injury. However, there are also spontaneous afflictions that can
produce synovial inflammation, a mass, unrelenting pain, or prominent limb dysfunction. Neoplasms, systemic or
rheumatologic disease, and primary muscle disease may manifest as athletic injury ( Fig. 46.35). A brief medical history
should disclose allergies and drug intolerances, important coincident illnesses (e.g., peptic ulcer), and a current list of
medications. It is important to know what previous therapeutic measures were prescribed, whether there was proper
compliance by the athlete, and the relative effect. Did the problem improve, stay the same, or become worse, and what
contributed to these trends? Pain diagrams and analogue scales have been useful in aiding such description.
FIGURE 46.35. Severe scapular winging associated with scapulo-facial-humeral dystrophy. Patient presented de novo
with a complaint of weakness.
The physical examination of athletic soft tissue injury requires familiarity with a variety of evocative tests and maneuvers.
Competence with these techniques allows the examiner to more accurately differentiate specific structural injuries in the
same anatomic area. For example, differentiation of chondromalacia patella from patella tendinitis, dysfunction of the
scapula-stabilizing muscles from glenohumeral instability, or attenuation of the posterior tibial tendon from a flexor
hallucis longus tendinitis hinges on the examiner's familiarity with both anatomy and examination techniques. In this
respect, the physical assessment of athletic soft tissue injury is a lifelong learning experience. Specific methods for
physical assessment are further described throughout this text.
The examiner should strive to develop a precise and organized approach. Remember to compare and to first examine the
uninjured limb; this helps to reduce the athlete's anxiety and establishes the range of normal individual variation.
Because most chronic injuries do not occur as an isolated event but represent a failure in a complex kinetic chain ( 37,81),
the physical examination provides an opportunity to identify intrinsic alignment abnormalities and soft tissue (muscular,
tendinous, and ligamentous) insufficiencies ( 37,81). The overhead athlete complaining of shoulder pain may require
assessment of more proximal scapula-stabilizing musculature or even lumbar pathomechanics; a runner with a knee
complaint may clearly demonstrate persistent femoral anteversion with increased torque on the patellofemoral joint or
excessive pronation as structural vulnerabilities that can be supported and palliated by an orthotic device. Although the
physical examination provides ample opportunity for static assessment, dynamic contributions to athletic soft tissue injury
are often overlooked. Whenever possible, the athlete should be provided the opportunity to imitate the sports motions
during which pain is experienced. Examples of such techniques include providing a racquet in the clinic, a ball for making
short tosses, a treadmill or an even larger space for sprinting or jogging, or a simple stair-step to assess patellofemoral
confidence.
SPECIFIC TREATMENT ALTERNATIVES
The treatment of athletic soft tissue injury may target both the cellular and the functional level of the injury, the former in
an attempt to influence the resolution of inflammation, and the latter in an effort to increase the rate of repair and repel
cumulative adverse injury effects on various body tissues and systems. Changing the inflammatory repair process in
connective tissues implies controlling a cellular and/or matrix tissue response ( 2).
In clinical medicine, such attempts are common and involve the prescription of a modifier. Potential modifiers include
antiinflammatory medications (which may be oral, injectable, or topical) and physical techniques such as thermotherapy,
cryotherapy, electrical field induction, ultrasound, and rehabilitative exercise. At the cellular level, modifiers are intended
to reduce extracellular edema, improve oxygenation, improve blood flow, correct pH imbalance, and generally improve
the cell-matrix environment. At the tissue level, such modifiers are intended to decrease pain, reduce immobilization
effects, improve neuromuscular coordination, avoid adhesions and adjacent joint stiffness, and decrease pain, thereby
allowing compliance with a rehabilitation protocol.
The effectiveness of these interventions depends in large part on where in the spectrum of tissue injury between
inflammation-dominant and degenerative tissue–dominant conditions the particular athletic injury lies ( Fig. 46.36). It
should be emphasized that significant promotion of healing has been poorly documented for all forms of intervention, with
the exception of therapeutic rehabilitation. Use of these other forms remains largely adjunctive to the normal,
time-dependent healing process of the body. Whatever the treatment program selected, it must adhere to the following
principles (1,37,147,149,150):
FIGURE 46.36. Spectrum of soft tissue injury response.
1. Protection of the early phases of tissue healing, while “normalizing” as much as possible all remaining limb function
2. Avoidance of excessive immobilization
3. Restoration of total limb function by emphasizing the timely application of therapeutic and rehabilitation techniques
4. Retraining and establishment of appropriate criteria for return to play
5. Elimination of faulty or abusive technique
Medical Modifiers
Nonsteroidal Antiinflammatory Drugs
NSAIDs block the cyclooxygenase enzyme breakdown of arachidonic acid to prostaglandins and derivatives ( 48). The
toxicity of NSAIDs is related to their capacity to inhibit normal prostaglandin function in such organs as the liver, lining of
the stomach, and kidney (150). Because the initiation of the arachidonic acid cascade is a critical step in igniting the
further steps in acute injury repair, NSAIDs could seriously inhibit injury repair. Unlike the derivatives, NSAIDs have not
been shown to significantly slow the normal healing process, a reflection of their more selective site of action in the
arachidonic acid metabolism ( Fig. 46.37). Paradoxically, the suppression of prostaglandin synthesis by NSAIDs has been
shown to unmask other mediators, in particular leukotrienes and thromboxanes (see Fig. 46.9), and, in a complex
fashion, to result in potentially increased damage from inflammation ( 149,151). The effectiveness of NSAIDs in the
treatment of acute and chronic soft tissue injury remains controversial.
FIGURE 46.37. Scheme for arachidonic acid metabolism showing differing sites of action of traditional nonsteroid
antiinflammatory drugs and corticosteroids versus COX-2 inhibitor drugs. The cyclooxygenase (COX) enzyme exists as
two isoforms: COX-1 and COX-2. COX-1 is constitutively expressed and performs a “housekeeping” function by
synthesizing prostanoids (prostaglandins and thromboxane) that regulate normal cell activity, notably in the gastic
mucosa, kidney, vascular endothelial cells and platelets. In contrast, COX-2 expression is dramatically induced by
cytokines during inflammation. The differing spectrum of these classes of antiinflammatory drugs is largely explained on
this basis. (Adapted from DuBois RN, Abramson SB, Crofford L, et al. Cyclooxygenase in biology and disease. FASEB J
1998;12:1063–1073.)
Using a prophylactic dosage of ibuprofen, given either prophylactically or 24 hours after the onset of eccentric exercise of
the knee, Hasson et al. found improvement in perceived muscle soreness, knee extensor torque decline, and less decline
in vastus lateralis electromyographic magnitude ( 152). The group of patients treated prophylactically displayed 40% to
50% less muscle soreness and significantly less decline in isometric, concentric, and eccentric torque at 24 hours. There
was no difference between treated and untreated groups with respect to measured muscle damage as determined by
creatinine kinase levels. The effect of piroxicam on healing of an experimental injury to the MCL in the rat demonstrated
increased early strength in the treated ligament when the dosage was administered shortly after injury but did not
improve the ultimate strength when healing was complete (153). Other experimental evidence suggested a delay in
muscle regeneration after strain injury treated with piroxicam ( 154).
Weiler, in an exhaustive review of the literature, could find only 11 studies that were double-blinded, randomized, and
placebo-controlled for the efficacy of NSAIDs in sports-related injury ( 151). Of these, eight reported positive results and
three reported negative results. It was also noted that topical applications of NSAIDs seemed to fare better than placebos
in the treatment of acute injury, without subjecting the athlete to the myriad of adverse events associated with oral
administration of NSAIDs. Weiler further concluded that despite the benefits seen in the treated patients, such as slightly
more rapid healing and decreased inflammation, the use of NSAIDs could neither be condemned nor strongly
recommended (151).
In general, about half of those patients who receive NSAIDs have an adverse event associated with the use of these
medications, and 1% to 2% of these reactions are serious ( 151). The toxic effects of aspirin may be enhanced when a
nonaspirin, nonsteroidal, or corticosteroid drug is used concurrently ( 155). The risks of NSAIDs may be minimized by
prescribing short-term treatment (7 to 10 days) for acute injury and by careful monitoring in the chronically treated
patient. The advent of new generations of antiinflammatory pharmacologies promises to reduce these morbidities (see
Fig. 46.37). However, so-called COX-2 selective drugs have not been shown to significantly improve athletic injury
recovery.
Corticosteroids
Corticosteroids may be administered either orally or by injection. Oral corticosteroids have generally been avoided in the
treatment of sports-related injury. Claims that short-burst, low-dose prednisone, in the form of a Dose-pak, may be helpful
for neuritis, peritenonitis, and bursal inflammation remain empiric, but in my experience they appear to be helpful. By
contrast, corticosteroid injection therapy continues to be widely employed, although the mechanism of its alleged
therapeutic effect has not been documented in the human. In animal models, corticosteroid tendon injection has resulted
in early collagen disarray and degenerative effects, followed over a period of weeks by a trend of reparative healing
(156). The functional significance of these improvements is not known. Likewise, spontaneous tendon rupture occurring
after corticosteroid injection remains a controversial phenomenon. The argument centers on whether tendon
degeneration precedes the injection effect, making the tendon rupture inevitable, or whether repeated damage from
tendon injection directly precipitates a spontaneous rupture ( 156). Alternatively, corticosteroid injection anabolic effects
may further potentiate sports-induced cell-matrix failure.
To date, efforts to resolve these questions have been frustrated by the lack of adequate animal models. Bachman et al.
described a rabbit model for chronic Achilles peritenonitis with tendinosis ( 157). However, the consistency and
reproducibility of such a model has not been validated; therefore, either normal tendons have been injected, or
inflammatory injury has been artificially induced by acute wounding ( 156). In addition, such animals may not react to
these substances in the same way as humans would (158). Because there remains controversy regarding the
suppression of collagen synthesis during the repair phases of healing, current clinical practice avoids injection of steroid
preparations directly into tendons. The best indication for steroid injection remains a localized inflammatory site such as
a synovial cavity, bursa, or tendon synovial sheath ( 156). Side effects observed after corticosteroid injection can be
problematic, and the athlete should be warned of the risk of local skin depigmentation ( Fig. 46.38), subcutaneous atrophy
with hypersensitivity, spontaneous tendon rupture, and possible chemical irritation from intratendinous or intrabursal
precipitate ( 156). A common adverse systemic effect of local injection in the diabetic is a sudden transient elevation of
the serum glucose level. I have documented serum rises of 300 to 400 mg per mL in a 24-hour period. Although this
effect is usually controllable, it could cause clinical symptoms. Patients should be appropriately cautioned as to their
diabetic control.
FIGURE 46.38. A: Complications of steroid injection. Subcutaneous atrophy, most often seen at the elbow epicondyle.
Note loss of subcutaneous fat; the skin becomes hypersensitive. B Complications of steroid injection. Cutaneous
depigmentation after wrist peritendinous injection.
Factors contributing to lack of response to injection therapy may be either athlete related (e.g., persistent overuse, faulty
technique, evidence of advanced tissue trauma) or physician related (e.g., improper diagnosis, inadequate injection
technique) (156). It is my impression that there is indeed a “tissue responder” who seems uniquely predisposed to
inflammatory reaction in the face of soft tissue sports microtrauma and whose inflammatory cycle can be mollified by the
proper timing of corticosteroid injection. Because surgical options are often considered after a trial of nonoperative care
that includes injection, corticosteroid injection should not be the first treatment alternative, nor should it be the last used
in aiding the athlete. Efforts should be made to dispel the false sense of security in the athlete that the symptomatic relief
resulting from steroid injection may produce, because it could lead to self-abuse and more serious reinjury. Sports
participation after injection adjacent to a major tendon should be delayed for a minimum of 3 weeks ( 37,156).
Recommendations for injection of acute muscular strains or ligamentous sprains to reduce the acute inflammatory phase
after injury have not been substantiated by controlled studies. Guidelines for the appropriate clinical use of corticosteroid
injection have been defined ( Table 46.9).
TABLE 46.9. USE AND ABUSE OF CORTICOSTEROID INJECTION
Anabolic Steroids
Anabolic steroids have gained attention as possible modifiers of healing and repair because of the observed increases in
strength and muscle size that anabolic steroid regimens produce in the intensively strength-training athlete ( 159,160).
Regardless of the documented adverse side effects of anabolic steroids (which include an increased risk of coronary
artery disease, impaired glucose tolerance, dysfunction of the liver, hepatic cancer, reproductive alterations,
psychological changes, and premature epiphyseal closure), anabolic steroids have documented catabolic as well as
anabolic effects on connective soft tissue ( 159). Miles et al. found that, in the rat, anabolic steroid treatment produced a
stiffer tendon that absorbed less energy to failure. Alterations in the size of collagen fibrils was noted on electron
microscopy (161). In a study of anabolic steroid effects on collagen synthesis in rat skeletal muscle and tendon, a
transient decrease was noted in collagen biosynthesis, implying another underlying rationale for spontaneous rupture
(162). The mechanisms and physiologic effects of anabolic steroids in resolution of soft tissue inflammation and repair
remain unsubstantiated (160).
Dimethyl Sulfoxide
Dimethyl sulfoxide (DMSO) is a commercial, chemical byproduct of the wood pulp industry; it is a powerful solvent and a
medium for other chemical reactions ( 163). It lowers the freezing point of biologic fluids, a quality useful in
cryopreservation of animal and human tissues and cells. Since the early 1960s, DMSO has gained notoriety, especially
among athletes, as a black market therapy for the treatment of injury. Claims of reduction in pain and swelling and more
rapid return to sports play led to a series of clinical studies. Percy and Carson reported on the use of DMSO in tennis
elbow and rotator cuff tendinitis; no therapeutic effect could be demonstrated ( 164). In a study of DMSO effects on mice
Achilles tendon, a decrease in mean separation force of up to 20% after a 7-day treatment was found ( 163). Myrer et al.
applied DMSO topically to traumatized muscle in adult male rats and found that significantly fewer healing cells were
present in the experimental group than in controls during the early period of inflammation. This was construed to imply
that some antiinflammatory effect might be rendered. However, no improved healing response was noted during the
course of the experiment (165). Complications of DMSO use have included local rash, burn, blisters, itchiness, hives,
scaling, dryness of the skin, foul breath, and potential teratogenic effects ( 153). The role of DMSO in the treatment of
athletic injury remains unsubstantiated, and it is not recommended.
Antioxidants
Antioxidants are chemical scavenger molecules that buffer excessive production of oxygen free radicals, themselves
byproducts of oxidative damage and exercise-induced lipid peroxidation of cell membranes ( 54,166). Antioxidants are
normally present in the body to help reduce the activity of these radical-induced reactions. As previously mentioned, such
reactions commonly occur due to the lysosomal activity of neutrophils in the acute phase response after injury. Oxidative
distress is also a byproduct of intensive exercise ( 167). Normal tissue sources of antioxidant defense include the enzyme
superoxide dismutase, catalase, glutathione peroxidase, and the antioxidant vitamins ( 54). Vitamin E (a-tocopherol) and
vitamin C (ascorbate) are powerful antioxidants implicated in the treatment of cancer, aging, and arthritis, as well as
exercise-induced oxidative stress ( 166). In athletics, the role of vitamin E has been studied in a number of endurance
sports. There is conflicting evidence of improved performance ( 166,168). Because evidence of muscle damage after
exercise has been widely reported, the question arises whether lipid peroxidation is a cause or a consequence of tissue
damage. Although oral antioxidant therapy is relatively safe, a significant effect on tissue repair and injury recovery has
not been demonstrated.
Physical Modalities
Physical modalities are frequently prescribed to promote healing and recovery after injury ( 125,149,150,169). There is
much claimed and much more unknown about the various physical techniques, their indications, efficacy, and potential to
modify the inflammation repair cycle, yet it is safe to say that the role of physical modalities remains largely experiential
and theoretical.
Cryotherapy
Cryotherapy remains a mainstay in the physical treatment of sports injury ( 169). External application of cold has been
demonstrated to result in decreased regional blood flow, decreased and more rapid resolution of edema, decreased local
hemorrhage, and improved analgesia (149,169). A primary goal of cryotherapy is to reduce the zone of secondary injury
in acute macrotrauma (169) (Fig. 46.39). Ice therapy has the additional advantages of being adaptable, available, cheap,
and relatively safe. However, there have been reports regarding cryogenic superficial nerve injury as well as the risk of
frostbite from inappropriate application ( 170). The risk of such injury can be diminished by limiting ice application to 20
minutes or less, avoiding excessive compression, and protecting the underlying skin from direct contact ( 170).
Cryotherapy has been attempted synergistically with other modalities. In a study combining transcutaneous electrical
nerve stimulation (TENS) and cold application, a significant decrease in perceived pain, an increase in elbow ROM, but
no significant improvements in muscle strength were shown (171). In my experience, cooling may be used after acute
injury until signs of swelling and hemorrhage have completely abated. This can take many days.
FIGURE 46.39. Typical surgical technique in tendinosis of patellar tendon. Excision of degenerated tissue or calcific
deposit is formed by reparative scar response.
Thermotherapy
Thermotherapy (heat application) produces physiologic effects as a result of vasodilatation, increased nutrition, and
increased enzymatic activity ( 172). There is evidence that collagen synthesis increases with the application of exogenous
heat (59,149). Tissue extensibility and metabolism are enhanced, and muscle spasm is decreased ( 149,172).
Thermotherapy is usually applied in the range of 102° to 110°F (39° to 43°C) ( 125). The amount of permanent elongation
resulting from a given amount of stretching increases in a thermal environment of 103°F (39.5°C) or greater. At 104°F
(40°C) and above, there is a thermal transition in the microstructure of collagen that significantly enhances the
viscoelasticity of collagen tissues, allowing for greater deformation without excessive strain. This observed phenomenon
is thought to be caused by changes in molecular creep and increased viscoelastic properties ( 125). Structural weakening
produced by loading varies inversely with temperature. In addition, tissues that are stretched under heated conditions
and then allowed to cool while under tension maintain a greater proportion of their plastic deformation than structures
allowed to cool in an unloaded state. The mechanisms for these observations remain controversial, but it is presumed
that an alteration occurs in the collagenous microstructure ( 125).
These observations provide a rationale for the application of therapeutic modalities in the treatment of connective soft
tissue injury. Guidelines for the safe application of heat after injury remain argumentative. Although some would apply
heat to aid in the resolution of inflammation and ultrasound or diathermy in an effort to encourage the resolution of a
thigh contusion (125), other opinions oppose any use of heat under these conditions ( 150). The premature use of heat
after acute injury runs the risk of encouraging intracompartmental hemorrhage (see Fig. 46.22). In my opinion, heat
application should be reserved for chronic conditions and to warm up indolent tissue damage before rehabilitative
exercise.
Therapeutic Ultrasound
Therapeutic ultrasound is another energy source that results in the heating of deep tissues. Conflicting reports exist as to
its effectiveness. Pulsed ultrasound appears to have greater therapeutic effectiveness ( 173). Various studies have
suggested that wound healing is improved by ultrasound application, as for venous stasis ulcers or in an animal wound
model (173). Such studies suffer from a lack of direct application to athletes in that the form of wounding, the
environmental stressors, and the biologic system vary from those seen in sports medicine. In a study of acute wound
healing of rat Achilles tendon, Frieder et al. found a therapeutic effect only after nine treatments over a 3-week period
(174). However, in a similar study, collagen synthesis was increased 5 days after injury, with evidence of increased
collagen synthesis ( 175).
Diathermy is a high-frequency current, short-duration impulse form of electromagnetic radiation that is used as another
vehicle for delivering heat to an injury area. Its general physiologic actions are unknown ( 173).
High-Voltage Pulse Galvanic Stimulation
High-voltage pulse galvanic stimulation (HVPGS) is currently advocated for treatment of both acute and chronic athletic
soft tissue injuries. HVPGS is an electrical stimulation unit with an output of more than 100 to 150 V and a pulsatile
monophasic wave form, often twin peaked, from 5 to 100 microseconds in duration ( 176). The short pulse and the high
voltage dramatically reduce skin resistance to current flow, allowing potentially unlimited depth of penetration. HVPGS
applications include temporary relaxation of muscle spasm, prevention or retardation of disuse atrophy, increased local
blood circulation, reeducation of muscles atrophied from disuse, and biofeedback control of trigger-point pain. Alterations
in ion, free amino acid, and protein flow (cataphoresis) by this imposed electrical current are thought to account for the
observed therapeutic effects (176). Used in conjunction with cryotherapy, HVPGS may reduce edema by reducing
microvascular permeability to plasma proteins ( 176).
There is still much to be learned regarding the ultimate cell-matrix effects, dosage, timing, and synergistic or additive
effects of modalities. In a comparative study of ice massage, ultrasound, iontophoresis (transcutaneous electrically driven
corticosteroid application), and phonophoresis (corticosteroid applied transcutaneously in conjunction with continuous
ultrasound) for shin splint syndrome, Smith et al. found no treatment modality to be superior to another, yet all were
clearly superior to a control treatment program ( 177). The controversies underlying modality use in athletic injury were
underlined in an exhaustive review by LaBelle et al. regarding the lack of scientific evidence for the treatment of
epicondylitis of the elbow ( 178). Of 185 articles published since 1966, only 18 were randomized, controlled studies. The
remaining papers were reviewed with respect to therapy used: ultrasound, iontophoresis, oral NSAIDs, and steroid
injection. These studies were found to be characterized by poor methodologic design, prominent placebo effect, small
sample size, and/or the finding that significant improvements from baseline were present in all trials, confirming either
that all treatments had a therapeutic effect or that the condition improved spontaneously with time. The authors
concluded that there was not enough scientific evidence to favor any particular treatment for acute lateral epicondylitis
(178).
In a review of the effective use of physical modalities, Polikoff made the following statement, with which I agree: “When
using physical therapy modalities, it is important to avoid implanting the thought of permanent disability and invalidism.
The patient should be encouraged to go through an orderly program and encouraged to progress. As soon as possible
the patient should be discontinued from attendance at specific sessions with a therapist since this may perpetuate
modality dependency. There is no objection to placing the patient on a home program reinforcing responsibility for self
help, and emphasizing that the patient is in a mending state rather than in a continued state of physical disability” ( 179).
Rehabilitative Therapeutic Exercise
Rehabilitative therapeutic exercise has the strongest rationale for use in the treatment of sports-induced soft tissue
athletic injury (37,80,81,125,147,149,180). Cellular and biomechanical responses to exercise documented in tendon,
ligament, and muscle include changes in collagen turnover rate; changes in collagen cross-linking at the intramolecular
and intermolecular level; alteration in tissue water and electrolyte content; and changes in the arrangement, number, and
thickness of collagen fibrils ( 28,150). Both tissue stress and strain may play a role in modifying changes in cell-matrix
synthesis (28). Exercise counteracts the hazards of prolonged immobilization after injury ( 181,182) (Table 46.10). Goals
of a rehabilitative prescription include the following ( 27,37,38,147,150):
TABLE 46.10. ADVERSE EFFECTS OF IMMOBILIZATION
1. Prevention of further contractural loss of motion and tissue atrophy

2. Promotion of resolution of the acute phase response to injury
3. Promotion of the reparative phase of collagen synthesis
4. Reclamation of performance attributes such as strength, endurance, power, agility, speed, ROM, and
sports-specific technique
It is important to emphasize what the athlete can do, as well as the functional limitations, during recovery. Beyond
physiologic limits, rest and antiinflammatory medications do not heal ( 37). A rest program allows for decreased
sensitivity, early initiation of healing, and decreased pain disability, but only rehabilitation restores performance ability. In
addition to rehabilitation of the injury site, a total-body fitness program emphasizing aerobic conditioning as well as
maintenance of general body performance reduces the risk of reinjury on return to sport ( 147). O'Connor et al. identified
the advantages of such a program (37):
1. Increasing regional perfusion through central and peripheral aerobics

2. Providing neurologic stimulus to the injured tissue through neurophysiologic synergy and overflow
3. Minimizing weakness of adjacent uninjured tissue (decreasing or eliminating a destructive domino effect in the
kinetic chain)
4. Minimizing negative psychological effects
5. Controlling unwanted fat and accumulated weight
Surgical Indications in Soft Tissue Injury
Surgery may be indicated in both acute and chronic forms of athletic injury. It is less appropriate to speak of
“conservative” versus “aggressive” alternatives than to consider all treatment in terms of nonoperative and operative
solutions. In the case of a severe rotator cuff tear, an acute rupture of the Achilles tendon, or a patellar tendon or biceps
tendon disruption, timely surgical intervention may be appropriate and, indeed, conservative. In general, grade 3 injuries
of either ligament and tendon often require surgical repair, the notable exception being ankle sprains and MCL injuries of
the knee. Because of the technical difficulty of suturing muscle tissue and the extensive scar reaction, direct repair of
muscle tissue disruption is not commonly advocated. Repair attempts are usually preceded by protection and followed by
aggressive rehabilitation of the remaining intact fibers.
The surgical treatment of overuse injury is indicated only after failure to respond to a rigorous nonoperative program. The
athlete must qualify for surgery. Lack of compliance and inadequate rehabilitation most often lead to inappropriate
surgery and a poor result. An analysis of currently recommended surgical procedures in chronic overuse tendon injury
revealed a variety of surgical goals ( 35) (Fig. 46.40, Table 46.11):
FIGURE 46.40. Typical surgical technique in tendinosis of patellar tendon. Excision of degenerated tissue or calcific
deposit is formed by reparative scar response.
TABLE 46.11. COMMON SURGICAL TECHNIQUES IN THE TREATMENT OF OVERUSE TENDON INJURY
1. To alter the tissue structure and restore strength by inducing reparative scar
2. To remove a nidus of offending adherent scar (e.g., chronic granulation tissue, degenerative tendon, hypertrophic
synovium, calcific deposit)
3. To encourage revascularization of tendon tissue
4. To relieve extrinsic pressure, either bony or soft tissue
5. To relieve tensile overload
6. To discover and repair gross interstitial tendon rupture
7. To repair or augment injure tendon structure (e.g., transverse grafts)
Indications for such soft tissue surgery include: (a) a failed monitored rehabilitative program of at least 3 to 6 months'
duration; (b) altered quality of life; (c) persistent pain with or without activities or sports play; (d) night pain (grade 4); (e)
objective signs of radiologically confirmed lesion (plain radiograph, arthrogram, MRI, sonogram, bone scan); and (f)
persistent weakness, atrophy, and dysfunction ( 35,37). The perioperative considerations and preoperative management
of chronic overuse injury are depicted in Figure 46.41.
FIGURE 46.41. Algorithm for the treatment of overuse tendon injury. Surgical treatment is only one alternative in an
extensive therapeutic plan.
Surgical treatment of tendinitis and chronic overuse injuries induces a change in the tendon cell-matrix environment by
promoting a renewed wound repair cycle and by removal of aberrant tissue ( 35). However, the end result is not
regenerated tendon or ligament or muscle, but remodeled connective tissue and scar repair, which is indeed different.
With so many variables surrounding postoperative management, including extended rest, immobilization, and
rehabilitation, it should be emphasized that the factors responsible for clinical improvement postoperatively are not well
established.
Insidious onset, an inherent nonoperative nature, and the lack of opportunity for tissue assessment postoperatively have
slowed surgical insight. The primary reason to employ operative treatment in athletic soft tissue injury remains the
empiric observation that improvement can be achieved in selective cases. The main argument against surgical treatment
remains the fact that the improperly selected patient may do poorly and that the majority of chronic overuse complaints
do not require such intervention for improvement ( 35). Although a well-timed surgical incision may be a powerful stimulus
to initiate the local tissue release of biologic cell mediators for repair, the factors that contributed to the chronicity of the
injury (e.g., genetic predisposition, aging, biomechanical deficiencies) may not be altered. It is simplistic to claim that
“bad scar” is replaced by “good scar” as a result of surgical intervention. More often, structurally inadequate or
excessively inflamed tissue is replaced by an initially immature and disorganized collagen fabric that may evolve into
adequate tissue but not into normal tissue. Placed under the repetitive demands of sports performance, such tissue may
be very sensitive to transitional stress and of vulnerable durability.
Returning the Athlete to Sports Participation
Guidelines for return to activity should be provided to the athlete to allow a safe progressive return to competition.
Blazina et al. first developed the phasing concept of overuse injury with their description of “jumper's knee syndrome” or
patellar tendinitis ( 183). Since that initial description, guidelines have come into common usage
(18,38,76,145,147,150,180); they are summarized in Table 46.8. In counseling return to activity, it is the progression in
the pattern of pain that dictates success. Participation is usually prohibited if the athlete has any pain on daily activities.
Pain should be assessed as to intensity, duration, and length of recovery time needed after activity. Keeping a log may
help the athlete to quantify the subjective experience. With respect to the physical findings, local swelling, tenderness,
and loss of motion should be monitored. It is important to point out that the rate of tissue healing is roughly proportional
to the visible resolution of hematoma or the progressive healing of a cutaneous postoperative scar. In addition, objective
standards of strength, endurance, power, agility, speed, and ROM must be assessed. Such testing should not rely merely
on manual judgments, but on mechanical measurement, in order to provide a comparative record of performance.
Although sports drills may begin at about 80% of normal strength and endurance, unrestricted play is not allowed until
90% or better comparative functional return. The well-equipped sports medicine rehabilitative center can provide some
methodology for such testing to be carried out. Functional testing (e.g., jumping, sprinting, carioca drills, sports-imitative
skill exercises) provides another opportunity to observe and counsel the athlete on readiness for competition. A pattern
of increasing pain or physical findings such as swelling or warmth should be viewed with caution and should initiate
readjustment of the training schedule. The variables affecting athletic performance after injury are the same as those of
all fitness attainment—namely frequency, intensity, and duration. It is appropriate to initiate an alternate-day participation
program and to allow increases in intensity only after frequency and duration of exercise are significantly improved. A
typical example of a progressive return to play is Brody's plan for a return to running activity after injury ( 184) (Table
46.12). Ultimately, the athlete should not be allowed full athletic competition until after all clinical symptoms and
biomechanical deficits have resolved and are no longer causing subclinical maladaptations ( 147).
TABLE 46.12. RETURN TO RUNNING AFTER INJURY
Finally, attention must be given to faulty technique and abusive play, which may often have initiated the current injury.
The sports medicine clinician is obligated to educate the patient about the potential risks of inappropriate training and to
make suggestions regarding improved equipment and technique. It is often appropriate to prescribe professional
teaching and fitness training for the highly competitive athlete. In grade 1 and 2 soft tissue injuries, as well as in the
return-to-sports phase, performance may be empowered by a variety of supportive devices. These include taping,
neoprene sleeves, force-sparing braces, and constraining functional braces. In the case of the ankle or elbow, such
braces have been shown to be of value in improving performance, possibly through subtle neuromuscular feedback
(185). Potential adverse effects and impairments of limb function have also been identified, emphasizing the importance
of comprehensive rehabilitation and patient education ( 186).
CONCLUSIONS
Athletic soft tissue injuries present an intriguing problem to the sports medicine clinician. As Bowerman ( 187) aptly
stated, “It is the circumstances of the injury, the risk taking involved, and the continued exposure to risk, that produce
interesting characteristics of the injury in sport.” In this respect, the clinical predictability of soft tissue healing in
sports-induced trauma must always be qualified by the imposed demand. All connective tissues are not the same.
Intrinsic differences in the biologic nature of connective tissues have yet to be fully understood in regard to their impact
on the quality of healing. There are basic differences between the acute trauma response and the overuse trauma tissue
response, both of which are processes that are time and cell matrix dependent. Transition plays an important role in the
determination of these processes. The success of treatment often depends on its timing and the relative balance of
inflammation and degeneration that is present at the site of injury. What distinguishes the “fast healer” from the “slow
healer” remains obscure. Reliance on rest and on medical and physical modalities should not be a substitute for a
comprehensive therapeutic program. Physical rehabilitation remains a singularly important solution to sports-induced
inflammation, scar, or degeneration, and the resultant biomechanical dysfunction.
Hippocrates (188) noted that “Healing is a matter of time but is sometimes also a matter of opportunity.” In this age, when
sports medicine has been an art earnestly seeking its science, the modern sports medicine clinician must be increasingly
aware of the biologic events and reparative capabilities of human tissues. For while the art of sports medicine may be
extended through experience, the future therapeutic opportunities of sports medicine will be extended only by its
scientific basis.
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47 Dermatology
47
DERMATOLOGY
ARLENE S. ROGACHEFSKY
WILMA F. BERGFELD
JAMES S. TAYLOR
Anatomy
Radiologic Evaluation
Treatment of Specific Injuries
Mechanical Trauma
Cutaneous Infections
Contact Dermatitis
Physical and Environmental Factors
Return to Play
Conclusion
Acknowledgment
Chapter References
Athletes are at risk for a vast number of common skin disorders which may be specific to themselves or unique to a
particular sport. Dermatologic problems of athletes are caused by mechanical trauma, cutaneous infections, contact
dermatitis, and physical and environmental factors.
ANATOMY
The skin has three layers: the epidermis, dermis, and subcutaneous fat. The epidermis functions as a barrier against the
environment and is thickest in areas of maximum friction, such as the palms and soles. In the epidermis, keratinocytes
produce keratin, which contributes to the physical barrier of the skin; melanocytes protect the skin from ultraviolet
radiation; and Langerhans cells play an immunologic function in skin disorders such as contact dermatitis. The dermis is
a support structure containing collagen and elastic fibers, ground substance, blood vessels, nerves, hair follicles, and
eccrine, apocrine, and sebaceous glands. Blood vessels and eccrine sweat glands function in temperature regulation;
apocrine glands are responsible for body odor; and nerves help detect the sensations of touch, temperature, and pain.
The third and deepest layer, the subcutaneous fat, provides a caloric residue and insulation from cold and trauma.
PHYSICAL EXAMINATION
In evaluating the athlete, it is crucial to do a complete skin examination. Sites of predilection of sports-related skin
diseases are noted in Table 47.1.
TABLE 47.1. SPORTS-RELATED SKIN DISEASES BY SITE OF PREDILECTION
RADIOLOGIC EVALUATION
Radiologic evaluation is valuable in the workup of specific athletic skin injuries and dermatoses. X-rays should be used to
assess deep lacerations. Additional indications include corns, turf toe, and frostbite.
TREATMENT OF SPECIFIC INJURIES
Mechanical Trauma
Mechanical trauma accounts for a myriad of sports-related skin conditions. Most are caused by acute trauma, and the
rest by repeated mechanical trauma (e.g., calluses and corns). Although these skin injuries are very frequent, most are
minor and many are preventable.
Abrasions occur most commonly from generalized trauma or friction of skin against equipment, mats, or turf. More
abrasions occur with artificial than with natural turf because of its enhanced surface friction and harder quality ( 1).
Clinically, the abrasion appears as a localized crusted or weeping erosion.
Lacerations consist of cut or torn skin and may extend through one or all three layers. A 4-year prospective review of a
Division I intercollegiate ice hockey team found that mandatory use of facemasks resulted in a reduction in facial
lacerations (2).
Prevention of abrasions and lacerations includes wearing recommended protective gear and ensuring tetanus
immunization. Immediate treatment should consist of flushing and debriding of the wound, oral and/or topical antibiotics
and, in some cases, sutures.
Friction blisters occur when repeated shearing forces in the face of moisture and heat cause a split in the epidermis ( 3).
The resulting blister manifests as a tender vesicle or bulla, most commonly on the foot of an athlete wearing ill-fitting
shoes or socks (4). Blisters also occur on the hands of racquet-sport players and rowers and on the fingers of baseball
players and fencers (5).
Although there are conflicting studies regarding the advantages of acrylic versus cotton socks in preventing friction
blisters (6,7), one review supported the use of acrylic socks because of the fabric's lower compressibility and lower
tendency to absorb and retain moisture ( 3). Other preventive recommendations include wearing properly fitting shoes
and double socks ( 8), particularly with a polyester inner sock ( 9). Treatment comprises prompt drainage, leaving the
blister roof intact, and application of topical antibiotics and the traditional multilayer, cotton gauze dry dressing or a
synthetic occlusive dressing such as Duoderm or Op-site ( 10).
The advantages of occlusive dressings include associated shorter healing time, lower frequency of infections, less
associated pain, enhanced reepithelialization and dermal repair, simpler wound care, and greater compliance ( 11). The
classification, indications, advantages, and disadvantages of the five basic types of occlusive dressings are summarized
in Table 47.2.
TABLE 47.2. OCCLUSIVE DRESSINGS
Calluses are hyperkeratotic plaques, usually localized to bony prominences of the feet and hands. They represent the
skin's attempt to compensate for friction by producing a more resilient barrier at points of continuous contact. Unlike
friction blisters and corns, calluses are rarely painful and are considered a competitive advantage in gymnasts, archers,
dancers, runners, and basketball and football players ( 12). Chronic thenar pads, calluses on the distal palmar aspects of
thumbs, occur in weightlifters who use the “hooking” technique ( 13).
Corns develop because of extreme pressure associated with bony deformities, poor foot mechanics, or improper
footwear. Frequently painful and sometimes located within calluses, these compact collections of keratin are typically
located below the metatarsal heads or on the dorsum of the interphalangeal joints of the toes.
Prevention of calluses and corns focuses on identifying rare predisposing correctable biomechanical problems and
wearing cushioned pads to redistribute pressure. Calluses can be treated early with topical salicylic acid. Corns and
advanced calluses should be pared after hydration with warm water. Surgical removal of underlying bony protuberances,
which may be required, poses a particular challenge for the athlete because of lost time.
“Black heel,” consisting of punctate petechiae over the lateral surface of the heel, represents posttraumatic punctate
hemorrhage of the skin. Synonyms include “talon noir,” “calcaneal petechiae,” and, when located on the palm, “black
palm” (5). The sudden appearance of a painless black spot on the heel or palm of an athlete helps to differentiate this
entity from malignant melanoma and benign melanocytic nevus. If necessary, paring and/or biopsy of the lesion will
establish the diagnosis. No treatment is required. Prevention may be accomplished by minimizing shearing stress to the
hands and feet with appropriate padding socks or gloves.
Subungual hemorrhages are typified by their sudden onset and bilateral occurrence; they are occasionally painful and
secondary to chronic trauma. Also called “tennis toe,” “jogger's toe,” or “skier's toe,” the disorder classically occurs
secondary to cramming of the distal nails into the athlete's shoes. In tennis players, the first or second toe is most
commonly affected, whichever is longer. In runners, the third, fourth, or fifth toe is usually affected ( 14). Fingernail
subungual hemorrhages, called “frisbee nail” and “golfer's nails,” have also been reported ( 15).
Because subungual hemorrhages in athletes are secondary to trauma, the discoloration usually appears at the distal nail
plate. However, when discoloration is located in the middle third of the nail plate, it is more likely to be related to
subacute bacterial endocarditis. Malignant melanoma must also be differentiated. Trimming the distal toenails, wearing
properly fitting shoes, and padding susceptible fingers and toes are helpful preventive measures. Conservative treatment
includes rest and warm soaks. For painful hemorrhages, incisional drainage with a hot wire is indicated.
Turf toe, traumatic injury to the metatarsophalangeal joint of the great toe as a result of severe dorsiflexion, occurs with
high incidence in football players. The great toe presents as a tender, red, dorsally swollen joint. The increased incidence
of turf toe since 1970 has been attributed to the introduction of artificial turf and the wearing of flexible shoewear ( 16,17).
Early treatment should include rest, ice, compression, and elevation (RICE). Long-term morbidity rates are high,
approximately 50% after 5 years (18).
Piezogenic pedal papules (Fig. 47.1) occur rarely. They are painful, fleshy papules located on lateral surfaces of the heel.
Because they result from pressure-induced fat herniation through defects in the dermis and often disappear with rest,
obesity and athletic activity have been implicated ( 19). Smaller, nonpainful piezogenic papules have also been described
(20). There is no definite treatment, and permanent disability may occur.
FIGURE 47.1. Piezogenic pedal papules. These pressure-induced fat herniations are usually seen on lateral surfaces of
the heel but can occur medially
The term athlete's nodules refers to collagenomas—benign, often asymptomatic connective tissue nevi—located at sites
of friction or recurrent blunt trauma ( 21). These firm intradermal nodules tend to occur on the knuckles of boxers ( 22) and
marble players and on the knees and dorsal feet of football players and surfers ( 21). For an extensive differential
diagnosis, see Cohen et al. ( 23). Topical or intradermal corticosteroids or surgical excision is the recommended
treatment (23).
Acne vulgaris (Fig. 47.2) and its variants—pseudofolliculitis barbae, dissecting cellulitis of the scalp, and acne keloidalis
nuchae—may be worsened in athletes. Those taking anabolic steroids are at particularly high risk. New-onset acne
keloidalis has been attributed to wearing a football helmet ( 24). Acne mechanica results from pressure, occlusion,
friction, and heat and is most likely to affect football and hockey players ( 25). Sites of involvement include the chin-strap
area of football players, under the headgear of hockey players, under the leotards of exercisers, on the lower lateral back
of golfers carrying bags, and on the back of weightlifters having continuous contact with weight benches ( 25). Prevention
requires minimizing the four precipitating factors. Athletes should wear cotton T-shirts under their uniforms and
equipment and should cleanse themselves after all events.
FIGURE 47.2. Acne vulgaris is a disorder of the hair follicle and sebaceous gland that is worsened by heat, humidity,
friction, occlusion, and pressure.
Acne treatment is guided by whether the acne is mild (comedonal), moderate (papules, pustules), or severe (nodules,
cysts). Topical agents are used to treat mild acne. Examples include benzoyl peroxide, retinoids such as tretinoin
(Retin-A), and topical antibiotics such as clindamycin or erythromycin. For moderate acne, topical medications should be
continued and supplemented by oral antibiotics such as tetracycline or minocycline. Severe acne usually requires a
5-month course of isotretinoin (Accutane). Athletes should not be prescribed oral isotretinoin during the season because
of the potential side effects of myalgias, arthralgias, benign intracranial hypertension, diffuse skeletal hyperostosis, and
decreased wound healing.
Striae distensae most commonly affect the shoulders, upper outer arms, chest, lower back, and thighs of athletes who
take part in weight-training or use anabolic steroids. In one review, 4% to 12% of high school senior athletes and 2% to
20% of intercollegiate athletes reported using anabolic steroids ( 26). Striae have been estimated to occur in up to 70% of
adolescent girls and at least 40% of adolescent boys ( 27). The 585-nm pulsed dye laser has been used to treat striae
(28,29).
Alopecia, especially androgenetic alopecia, may occur in athletes who self-administer anabolic androgenic steroids ( 30).
Friction alopecia secondary to break dancing and traction alopecia secondary to jogging while wearing a heavy
headphone have been reported (31).
Miscellaneous dermatoses are listed in Table 47.3.
TABLE 47.3. MISCELLANEOUS DERMATOSES IN ATHLETES SECONDARY TO MECHANICAL TRAUMA
Cutaneous Infections
A number of common and rare bacterial, viral, fungal, and parasitic infections occur in athletes. Perspiration, elevated
body temperature, occlusive clothing and sports equipment, close interpersonal contact, and trauma to the skin are
predisposing factors. Both athletic trainers and physicians must be aware of the temporarily disqualifying infections and
infestations. These include impetigo, furunculosis, generalized folliculitis, hidradenitis suppurativa, secondary syphilis,
herpes simplex, herpes zoster, varicella, molluscum contagiosum, verrucae, tinea capitis, tinea corporis gladiatorum ( 32),
and moderate-extensive tinea corporis ( 12). Prompt diagnosis and disqualification of athletes with infectious conditions
along with proper prevention, education, and more aggressive treatment, will significantly decrease the transmission rate
and occurrence of epidemics ( 33).
Bacteria
Preventive and therapeutic recommendations for sports-related cutaneous bacterial infections are presented in Table
47.4.
TABLE 47.4. SPORTS-RELATED DERMATOLOGIC BACTERIAL INFECTIONS: PREVENTION AND TREATMENT
Impetigo (Fig. 47.3) is usually caused by group A b-hemolytic streptococci or Staphylococcus aureus, or both. Wrestlers,
swimmers, and gymnasts are particularly susceptible (34). A study of college and high school wrestling teams nationwide
found that approximately half of all trainers sampled during the 1984–1985 season had team members with impetigo, the
incidence being second only to that of fungal infection ( 35). Outbreaks of group A b-hemolytic streptococci transmitted by
person-to-person spread from football and rugby players have been reported ( 36). Because active lesions are highly
contagious, athletic participation should be temporarily prohibited.
FIGURE 47.3. Impetigo. The characteristic honey-colored crusts commonly occur on the face or other exposed areas of
athletes, especially wrestlers, swimmers, and gymnasts.
Furuncles, or “boils,” are most commonly caused by S. aureus. After an outbreak among football and basketball players,
skin injury and direct contact with furuncles were identified as the two greatest risk factors ( 37). Fomites play a minimal
role in disease transmission ( 37,38 and 39). Because virulent staphylococcal strains can cause epidemic furunculosis,
infected athletes should avoid swimming and contact sports.
Folliculitis is most commonly caused by S. aureus. Occlusion by clothing or protective equipment predisposes to its
development on the chest, back, arms, and legs. As with impetigo and furunculosis, staphylococcal nasal carriers are
prone to recurrences.
Hot tub folliculitis is typically a gram-negative self-limited folliculitis caused by Pseudomonas aeruginosa. Follicular
papules and pustules on intertriginous areas and skin underneath the bathing suit usually appear within 2 days after
exposure to a hot tub, whirlpool, Jacuzzi, or swimming pool ( 40). The eruption may be accompanied by low-grade fever,
malaise, nausea, vomiting, headache, pharyngitis, and external otitis. Lacour et al. ( 41) reported diving suit dermatitis
caused by P. aeruginosa, differentiating it from standard pseudomonal folliculitis by its disseminated nonfollicular
papulopustules, its origin from bacteria proliferating in the humid environment of the suit or the water used to clean it, and
its serotypes (O:10 and O:6), different from those serotypes (O:11) causing typical folliculitis.
Dermatitis palaestrae limosae, the rare dermatitis of mud wrestling, is a gram-negative folliculitis caused by
Enterobacteriaceae, specifically Enterobacter cloacae and Citrobacter species (42). These gram-negative organisms
have been implicated because of their prevalence in soil, the abrasive nature of mud wrestling causing trauma to the
skin, and the three cases documented by skin culture ( 42). The natural history and recommended treatment have not
been determined.
Erythrasma, caused by Corynebacterium minutissimum, presents as well-demarcated, reddish-brown patches in

intertriginous areas demonstrating characteristic coral red fluorescence under a Wood light.
Pitted keratolysis, termed “toxic-sock syndrome,” is a superficial infection of the plantar skin of feet also caused by C.
minutissimum. Malodorous feet with 1- to 3-mm pits on weight-bearing surfaces are typically noted. Because of their
occlusive footwear and hyperhidrotic environment, basketball players, tennis players, and runners are most commonly
affected (43).
Viruses
Herpes simplex virus (HSV) infections, type 1 and type 2, are prevalent in the general population and are extremely
contagious. In a review of 38 sports-related infectious disease outbreaks over 30 years, of the 24 agents that were
transmitted by person-to-person spread, HSV was most common, accounting for 50% of cases. All herpes epidemics
were related to either wrestling (n = 8) or rugby (n = 4) ( 36).
Herpes gladiatorum refers to the unique clinical presentation of herpetic vesicles on extramucosal sites of wrestlers and
rugby players. It most commonly occurs on the forehead of rugby players ( 44) and on the face and arms of wrestlers due
to the “locking-up position” at the beginning of the match ( 35). Prior infection with HSV type 1 may offer protection against
herpes gladiatorum (45).
Skiers are particularly susceptible to recurrent herpes labialis from exposure to ultraviolet (UV) radiation at high altitude
and reflection off the snow. UV light is a potent stimulus for reactivation of latent infection ( 46,47), and prospective
studies of patients with herpes labialis have implicated sunburn as a precipitating event in 13% to 22% of recurrences
(48,49). This may be attributed to the statistically significantly elevated UV-B susceptibility trait among patients with
recurrent herpes labialis compared with controls ( 50). Studies of the efficacy of sunscreens in preventing recurrences in
skiers have shown either no benefit ( 51) or likely benefit ( 47).
Antiviral treatment for herpes simplex ( 52,53), listed in Table 47.5, should accompany disqualification of the athlete.
Famciclovir and valacyclovir demonstrate superior pharmacokinetics compared with acyclovir and allow for less-frequent
daily dosing with higher achievable serum drug concentrations, but they are more costly. Topical acyclovir has little
efficacy and no role in the management of HSV infections ( 54). However, topical drying agents such as witch hazel are
helpful. Oral acyclovir, 400 mg twice daily, is effective in suppressing herpes labialis in immunocompetent adults with
frequently recurrent infection (six or more episodes per year or two or more episodes in 4 months). Suppressive acyclovir
dosing has been shown to reduce the number of clinical recurrences, viral shedding, and time to healing ( 55) and is safe
and well tolerated (56).
TABLE 47.5. STANDARD TREATMENT OF HERPES SIMPLEXa
Vasily and Foley from Lehigh University ( unpublished data, 1999) found that HSV cultures from under crusts ( 57) were
routinely negative by day 3 of therapy with valacyclovir and by day 5 with acyclovir. Therefore, at Lehigh University, all
wrestlers with herpes gladiatorum or first-episode herpes labialis are treated with an extended 7-day course of
valacyclovir 1,000 mg twice daily. Recurrent herpes labialis is treated with 500 mg twice daily for 5 days. Valacyclovir at
prophylactic doses of 500 mg per day has also been found to be very effective in preventing recurrences in wrestlers,
with the 1,000 mg daily dose reserved for wrestlers with breakthrough on 500 mg daily (Vasily and Foley, unpublished
data, 1999).
Plantar warts are frequently seen among athletes and swimming pool users ( 58). Some studies have questioned
transmission linked to swimming-pool or locker-room usage. The strongest association is with shower-room usage
(59,60), and crucial preventive measures include wearing sandals in gyms and showers and having a personal bath mat.
Treatment must be tailored to include keratolytic agents such as salicylic acid and to avoid destructive methods that
could hamper performance and cause scarring. Periungual warts ( Fig. 47.4) are particularly resistant to treatment.
Disqualification may be necessary.
FIGURE 47.4. Periungual warts. Warts, or verrucae, result from infection of epithelial cells by human papillomavirus
(HPV).
The differential diagnosis includes callus, foreign body, and stress fracture. The observation of pinpoint bleeding during
paring favors wart over callus. Stress fractures, most frequently encountered by runners, ballet dancers, and gymnasts,
typically manifest without recall of specific injury as insidious onset of forefoot pain during activity, which disappears at
rest. Point tenderness over the affected metatarsal is helpful in differentiating stress fracture from wart ( 61).
Molluscum contagiosum (Fig. 47.5) most commonly affects school-aged children and involves high school athletes more
often than college athletes ( 35). Two other affected populations are sexually active adults and immunocompromised
individuals. Transmission is via person-to-person contact, contaminated objects, and autoinoculation ( 62).
FIGURE 47.5. Molluscum contagiosum. Typical flesh-colored or translucent dome-shaped papules with central
umbilication.
Epidermal injury facilitates inoculation, but infection through intact skin may also occur ( 63). The sharing of clothing,
towels, and equipment has been implicated in transmission. Molluscum has been prevalent in runners ( 64), wrestlers
(65), and swimmers (66,67). A study of 19,492 elementary school children from a small city in Japan showed that
swimmers had an incidence twice that of nonswimmers (7.5% versus 3.6%) (66). Athletes with molluscum should be
disqualified until the lesions have been treated.
Transmission of human immunodeficiency virus (HIV) and hepatitis B may occur during sports activities. Although
hepatitis B has a much higher transmission rate than HIV, only one episode of documented hepatitis B transmission
during athletic activity has been reported; this was an outbreak among sumo wrestlers in Japan ( 68). There has been one
report of presumed HIV seroconversion after a head-to-head collision in a soccer game between an HIV-positive
intravenous drug user and a seronegative player ( 69). There are also two reports of HIV transmission during bloody
fistfights, not formally sports related ( 70,71).
Currently, there is no evidence documenting the transmission of HIV from sweat or saliva ( 72). The overall risk of HIV
transmission in professional football, a sport with a high level of contact, has been estimated at 1 per 85 million game
contacts (73). The principal risks for athletes acquiring HIV are related to “off-the-field” activity, including increased
numbers of sexual partners and episodes of sexually transmitted diseases, inconsistent contraceptive use, and high rates
of intramuscular injections of anabolic steroids ( 26). Many practical approaches to prevent transmission of bloodborne
pathogens have been devised ( 74,75).
Fungi
Dermatophyte superficial fungal infections are the most common dermatologic infections in athletes ( 10). The most
common dermatophyte implicated in tinea pedis is Trichophyton rubrum, followed by Trichophyton mentagrophytes and
Epidermophyton floccosum (76). In a study of 150 swimmers, 15% presented with tinea pedis, two thirds with obvious
lesions and one third without lesions. The high percentage of asymptomatic infections contributes to disease propagation
(77). Preventive measures include wearing shower shoes, inspecting the feet in athletes with hand dermatitis because of
the id reaction, and treatment with topical and/or oral antifungals.
Tinea cruris, predominantly caused by T. rubrum and E. floccosum, typically occurs in male athletes and spares the
scrotum (Fig. 47.6). If scrotal involvement is present, candidiasis or erythrasma would be more likely.
FIGURE 47.6. Tinea cruris affects the groin, the proximal and medial thighs, and sometimes the buttocks. It produces
sharply marginated, erythematous or dusky plaques, with scale that is most prominent at the periphery. A potassium
hydroxide (KOH) preparation of the scale shows typical, branching hyphae.
Although tinea corporis less commonly affects athletes than tinea pedis or cruris does, numerous epidemics have
occurred among wrestlers. The first documented outbreak of tinea corporis gladiatorum was caused by Trichophyton
verrucosum during the 1966 Swedish wrestling epidemic ( 78). In 1992, three more epidemics among wrestlers were
noted, all caused by Trichophyton tonsurans (79). In 1994, Beller and Gessner urged that tinea corporis gladiatorum be
added to the list of temporarily disqualifying skin disorders ( 32).
Standard antifungal therapy for dermatophytoses of the skin, hair, and nails is listed in practical form in Table 47.6.
Length of therapy should be prolonged for the athlete. The topical imidazoles have a broad spectrum of activity against
dermatophytes, yeasts, and Malassezia furfur. In the athlete, allylamines are preferable to the imidazoles because of
their faster onset of action and shorter time to mycologic cure due to their presumed fungicidal action ( 80,81). An
excellent review of topical antifungal therapy has been published ( 82).
TABLE 47.6. ANTIFUNGAL THERAPY FOR SKIN, HAIR, AND NAILSa
For treatment of tinea capitis and extensive tinea corporis, the only oral allylamine available is terbinafine (Lamisil). For
the general population, the recommended length of therapy for tinea corporis is 1 to 2 weeks ( 83,84). The athlete's
course should be extended to 2 to 4 weeks. Prophylactic itraconazole (Sporanox) pulse therapy has been proposed for
prophylaxis and treatment of tinea corporis in wrestlers ( 85). Although itraconazole is effective in theory, it has not been
clinically effective in wrestlers (Vasily and Foley, unpublished data, 1999).
Tinea capitis has classically been treated with griseofulvin, which is one of the best oral agents against Microsporum
canis. Terbinafine and itraconazole are more effective against T. tonsurans in vitro and may become the standard agents
in the future ( 86,87).
Because terbinafine and itraconazole are rising in popularity, awareness of drug interactions and recommended
laboratory monitoring are crucial. Drug interactions to terbinafine are limited to cimetidine and rifampin ( 88). Itraconazole
inhibits the cytochrome P-450 enzyme system and therefore should not be taken with drugs such as cisapride,
terfenadine, astemizole, midazolam, and lovastatin ( 89). The Physician's Desk Reference or a dermatologist should be
consulted for data on specific laboratory monitoring requirements.
Other fungal infections, such as tinea versicolor and candidiasis, also occur frequently in athletes. These should be
expediently diagnosed and treated with topical agents such as selenium sulfide 2.5% lotion (for tinea versicolor) and
nystatin or imidazole creams (for candidiasis).
Parasitic Infections
Seabather's eruption is a benign, self-limited syndrome that begins with a pruritic papulopustular dermatosis occurring
underneath bathing suits of ocean swimmers 4 to 24 hours after sea bathing. It is caused by larvae of the thimble
jellyfish, Linuche unguiculata, along the southern Atlantic coast ( 90) and of the sea anemone, Edwardsiella lineata, along
the North Atlantic coast (91). Larvae become trapped in the swimmer's bathing suit and inject toxin into the skin.
Confirmation has been made by means of serologic studies (enzyme-linked immunosorbent assay) and measurement of
specific immunoglobulin G antibodies against the thimble jellyfish ( 92). Preventive measures include wearing sunscreen
(93) and avoiding constrictive clothing while swimming in highly inhabited seawater.
Cercarial dermatitis, or “swimmer's itch,” is caused by cercariae of blood flukes that infect animals, usually birds, rodents,
or ungulates. It manifests as an intensely pruritic, self-limited, maculopapular eruption that lasts approximately 1 to 2
weeks (94). In contrast to seabather's eruption, cercarial dermatitis has no characteristic distribution, and, although it
occurs in salt water, it typically is associated with contaminated lakes. Prevention involves avoidance of contaminated
waters and application of the topical molluscicide, niclosamide, to bathing areas of the skin ( 94).
Cutaneous larva migrans, or “creeping eruption,” is caused by the dog and cat hookworms, Ancylostoma caninum and
Ancylostoma braziliense, respectively. The slightly raised, serpiginous, pruritic burrow usually occurs on the ankles of
recreational swimmers or children who have played in sand containing dog or cat feces contaminated with larvae.
Stings and Infestations
Cnidarians are a group of marine animals with stinging structures called nematocysts. Examples include jellyfish,
anemones, hydroids, Portuguese man-of-war, and corals ( 95). They contribute to the myriad of aquatic dermatoses
affecting athletes and recreational sports participants.
Scabies and pubic lice (Fig. 47.7) are the two most common infestations encountered by athletes. Because both
conditions are highly contagious, they are considered disqualifying skin disorders in athletes. Immediate treatment with
topical permethrin (preferred) or lindane should be initiated ( 96).
FIGURE 47.7. The pubic louse, Pthirus pubis, is one of the most common infestations of athletes.
Contact Dermatitis
Contact dermatitis typically manifests as an acute vesicular or chronic scaling inflammatory disorder of the skin. The two
main types are irritant and allergic. Irritant contact dermatitis is the nonallergic type; it arises from mechanically or
chemically irritating substances. Allergic contact dermatitis results from acquired delayed hypersensitivity to a specific
allergen applied to the skin with chemical penetration and then reexposure. In order to make a proper diagnosis,
sleuth-like history-taking and noting the arrangement and distribution of the rash are essential. The gold standard for
diagnosis of allergic contact dermatitis is patch testing.
Irritant contact dermatitis is caused by mechanical friction from headbands or wristbands in runners, helmets in football
players, gloves and Fiberglas equipment in hockey players, and adhesive tape in basketball players ( 5,12). Irritation may
also occur after application of medicaments, antiseptics, insect repellants, cosmetics, oily sunscreens, or leakage of
“cold-pack” chemicals (5,12).
Allergic contact dermatitis is caused most commonly by nickel-containing objects; rubber, adhesives, or dyes in athletic
tape, gear, or running shoes; topical medicaments; and plants (e.g., Rhus). Reactions are induced or elicited by the
athlete's perspiration, which leaches the chemical allergens from the gear ( 97). Table 47.7 lists common contact
allergens and their sources in the athlete.
TABLE 47.7. IDENTIFYING ALLERGIC CONTACT DERMATITIS IN ATHLETES
Athletic tape, especially that which is rubber-based, has been identified as the most common contact allergen among
athletes (1). Rubber-based tape is now frequently replaced with tape made of cloth and other adhesives, such as
p-tertbutylphenol formaldehyde resin (PTBP-FR) and acrylics, because of their durable, flexible, and rapidly adherent
qualities (98).
Nickel is the most frequently identified allergen of patients undergoing patch testing. Athletes are probably predisposed
to nickel allergy, and the most significant factor in its development is not the nickel concentration in the object or coating
but the amount released onto the skin during exposure to human sweat ( 99). Dermatitis appears at contact sites of metal
tag chains, whistles, buckles, clasps, and other gold-plated items first coated with nickel. Using the commercially
available dimethylglyoxine spot test to identify sources of nickel exposure is an effective means of prevention ( 99).
Running shoes and athletic gear contain rubber accelerators, antioxidants, and other rubber additives that are common
causes of contact allergy. Among the potential allergens are thioureas, thiurams, carbamates, N-isopropyl-N-phenyl-p
-phenylenediamine (IPPD), and mercaptobenzothiazole (MBT) ( 100,101).
Despite the high prevalence of shoe allergy, causative agents of athletic shoe dermatitis are rarely identified ( 102,103).
Confirmed allergens include ethylbutylthiourea ( 104) as well as MBT and dibenzothiazyl disulfide, both identified by
extraction from shoe material and chromatographic separation ( 103). Allergen alternatives include shoes made mostly of
polyurethane ( 104) and those with components that are patch-test negative.
Swimmers and divers are exposed to numerous rubber-containing articles such as masks, mouthpieces, goggles, diving
suits, bathing caps, nose clips, ear plugs, fins, and fin straps ( 101). Scuba-diver mask facial dermatitis, called “mask
burn,” spares the central face and may be caused by IPPD (105) and thiuram (106). p-Phenylenediamine black rubber
antioxidants in a snorkel were reported to cause edema of the tongue and dyspnea ( 107). MBT is also a sensitizer in
masks and mouthpieces; allergen alternatives are masks and mouthpieces made of silicone rubber ( 101).
Allergic contact dermatitis to goggles can present as a bilateral eyelid eczema or a raccoon-like periorbital leukoderma
(108,109). We identified diethylthiourea and ethylbutylthiourea as allergens in swim goggles ( 109). Special nonthiourea
black neoprene or polyvinylchloride goggles are allergen alternatives.
In wetsuits, rubber accelerators are the most important allergens, specifically the substituted thiourea compounds,
ethylbutylthiourea ( 110), diethylthiourea (111), and diphenylthiourea ( 112). Of these chemicals, diphenylthiourea was
identified as having the highest overall sensitization potential ( 113). Allergic contact dermatitis has also been reported to
IPPD, thiuram (106), and PTBR-FR (100) in a diving suit. For thiourea-sensitive individuals, Rubatex Corporation
manufactures a grade of closed-cell neoprene without thiourea (material #G-231-N). Because thiourea is also used as an
adhesive for bonding the nylon stretch fabric to the rubber sheet, a truly thiourea-free suit of G-231-N has no nylon on
the inside ( 101).
Natural rubber latex allergy is an important immediate contact reaction (type I IgE-mediated) that should not be
overlooked because of its life-threatening potential. It may be more frequently seen in atopic athletes, in those with spina
bifida (wheelchair sports), and in part-time athletes in health care professions ( 104).
Resins, especially those containing epoxy, colophony, and PTBP-FR, are used as adhesives and glues in sports
equipment. Reports of contact allergy include facial dermatitis from epoxy resin glue inside a helmet ( 114), erythematous
facial dermatitis from colophony in a bowlsgrip ( 115), and a well-demarcated linear erythematous vesicular patch on the
back of a leg from PTBP-FR and/or phenol-formaldehyde resin in a knee guard ( 116).
Medications, particularly topical agents, are responsible for localized or generalized allergic eczema. Almost any topical
antibiotic can produce contact allergy; neomycin and bacitracin are among the most common ( 117,118). Topical acyclovir
(119) and imidazole antifungal agents are also potential allergens ( 120).
Topical anesthetics (e.g., benzocaine) and topical antihistamines (e.g., diphenhydramine, doxepin) may cause allergic
contact dermatitis (Fig. 47.8), and diphenhydramine is an occasional photosensitizer ( 121,122). Povidone-iodine is used
in sports for its antiseptic and adherent qualities, and allergic reactions ( Fig. 47.9) are rare (123,124). Methylsalicylate, a
topical analgesic, causes irritant or allergic dermatitis in athletes and, in one case, caused systemic contact allergy after
rechallenge with oral aspirin ( 125). Athletes who are allergic to sunscreens containing p-aminobenzoic acid (PABA) may
have a cross-reaction with benzocaine, p-aminosalicylic acid, sulfonylurea antidiabetic agents, procainamide, or thiazide
diuretics. The reader should consult standard contact dermatitis texts for lists of numerous other topical medicament
allergens.
FIGURE 47.8. Patch testing reveals allergic contact dermatitis (3+ reaction) to caine mix (benzocaine). Benzocaine is a
local anesthetic used primarily in nonprescription topical medications to ease pain and pruritus.
FIGURE 47.9. Allergic contact dermatitis to povidone-iodine. The presence of bullae indicates an acute contact
dermatitis.
Oral medications taken by athletes may also be allergenic, particularly the nonsteroidal agents (especially piroxicam) and
antibiotics (ciprofloxacin, nalidixic acid, sulfonamides, tetracyclines), which are photosensitizers ( 126). Prior sensitization
to thiuram rubber accelerators makes athletes susceptible to systemic eczematous dermatitis if Antabuse (disulfiram, a
thiuram derivative) is given orally ( 127).
The Rhus plants, which include poison ivy, oak, and sumac and contain the allergen urushiol, are the most common
cause of allergic contact dermatitis in North America, affecting 50% or more of the population ( 10,128). A vast array of
plants, including primrose and Compositae, cause contact dermatitis, airborne dermatitis, contact urticaria, and
phytodermatitis. They are a potential threat to athletes participating in outdoor sports.
Plant extracts are now popular in topical medicaments and cosmetics, and athletes using these “natural remedies” are
particularly susceptible to the development of contact allergy ( 128). There are reports of allergic contact dermatitis to
witch hazel, which has been used as an antipruritic in eye gel ( 129); to tea tree oil, a eucalyptol-containing antiacne
treatment (130); and to chamomile, an essential oil with presumed sedative and antiinflammatory effects that contains
sesquiterpene alcohol, bisabolol, and an oxidation product as possible allergens ( 131).
Aquatic contact allergies include Red Sea coral contact dermatitis, a presumed allergic contact dermatitis to the animal
tissue of the coralline Alcyonidium hirsutum (132). Swimmers and coral collectors in the shallow waters of the eastern
coastline of the Red Sea, particularly those with seafood allergies, are susceptible to the resulting acute urticarial or
eczematous dermatitis and chronic lichen planus–like eruption. Pseudophytodermatitis occurred in a nickel-sensitive
individual after contact with Ludwig repens, an aquatic plant with a high concentration of nickel ( 133).
Treatment of contact dermatitis requires limiting exposure to the irritant or allergen. Topical steroids are the mainstay of
treatment. For more extensive involvement, oral antihistamines or systemic corticosteroids, or both, may be necessary.
There are five types of topical corticosteroid formulations: ointments, gels, creams, lotions, and solutions. Ointments are
the most efficacious, but creams have greater cosmetic appeal; lotions, gels, and solutions are preferred for hair-bearing
areas of the body. Topical corticosteroid preparations vary greatly in potency and are categorized into seven groups,
group I being superpotent and group VII having the lowest potency. Examples of commonly used steroids include
clobetasol propionate (Temovate cream 0.05%) from group I, triamcinolone acetonide (Kenalog cream 0.1%) from group
IV (medium potency), and hydrocortisone (Hytone cream 1%) from group VII. Medium-potency and superpotent topical
corticosteroids should not be applied to the face or body folds for longer than 2 weeks.
Physical and Environmental Factors
Various physical stimuli affect athletes, including cold, heat, physical exertion, and UV light. These factors can create
new skin disorders or aggravate preexisting ones. Urticaria (hives), for example, can be induced by cold, heat, exertion,
or UV light. Physical urticaria must be differentiated from other causes of hives, such as drugs, foods, infections, and
natural rubber latex.
Cold
Skiers, ice-skaters, joggers, mountain climbers, and outdoor enthusiasts are prone to cold-related skin injuries ( 134). In
athletes, frostnip, or superficial frostbite, is the most common cold-induced skin disorder. Frostnip manifests as white
patches, typically over the nose, cheeks, chin, ears, and anterior neck; the anterior neck is the most vulnerable area ( 25).
Rapid rewarming is the recommended treatment. Prevention encompasses covering all possible areas of exposed skin,
applying sunscreens and/or emollients to vulnerable sites, and postponing face-washing and shaving, which remove the
skin's naturally protective sebum ( 25).
Frostbite is a deeper injury that sometimes damages the subcutaneous muscle, tendon, and even bone. With the body's
attempt to increase core temperature, circulation to the extremities is decreased and the skin turns waxy white. Hands,
feet, extremities, ears, and nose are the most commonly affected sites. Associated burning and pain may predispose to
complete numbness. Blisters may appear 24 to 36 hours later. Treatment of choice is rapid rewarming in a water bath at
38° to 44°C and oral analgesics ( 25). Rewarming should not be undertaken if there is further risk of freezing. Permanent
sequelae from severe frostbite include cold intolerance, hyperhidrosis, dystrophic nails, osteoporosis, and fibrosis with
decreased mobility.
Pernio (chilblains) is a chronic, recurrent, painful skin condition that typically occurs in women several hours after cold
exposure and lasts for 1 to 2 weeks. It is an abnormal reaction to cold temperatures above freezing combined with high
humidity. Red-purple plaques with associated swelling and pruritus are usually symmetrically distributed over the dorsal
fingers and plantar aspects of the toes. Preventive measures include wearing warm, dry clothing and avoiding
constrictive clothing. Nifedipine, a vasodilating calcium-channel blocker, has proved to be an effective therapy and
prophylaxis for pernio (135).
Equestrian cold panniculitis is a type of perniosis that occurs in young horsewomen who wear tight-fitting, uninsulated
breeches (136,137). Bright-red or violaceous, itchy, painful nodules occur on the lateral aspects of the thighs, particularly
in athletes with thicker layers of adipose tissue. Tobogganer's thighs were also reported in a 16-year-old boy who wore
tight jeans and developed ulcerated chilblains on the inner aspect of both thighs after tobogganing ( 138). These two
unusual sports-related pernioses share three predisposing factors: (a) exposure to cold, producing vasoconstriction; (b)
obesity, with a thicker layer of subcutaneous fat insulating blood vessels; and (c) constrictive clothing, which further
decreases blood supply to the skin.
“Pulling boat hands” is an unusual blistering hand dermatitis caused by a combination of the vascular effects of
nonfreezing cold injury and the mechanical trauma of rowing ( 139). It causes painful and pruritic macules, plaques, and
vesicles of the hands. Eight of nine women affected had Raynaud's phenomenon. One differentiating factor between
“pulling boat hands” and pernio is the presence of subepidermal vesicles in the former ( 139).
Bicyclist's nipples are classified as a thermal rather than a mechanical injury ( 140). This painful dermatosis results from
prolonged cycling during cool or cold weather while wearing perspiration-moistened underclothing.
Heat
Heat-induced intertrigo occurs commonly among heavy athletes. Weight reduction, loose-fitting underclothing, and
optimal hygiene are helpful preventive measures.
Athletes may develop miliaria crystallina, miliaria rubra, or miliaria profunda; the latter is the least common type.
Predisposing factors include temperature extremes and occlusive clothing. Football players practicing during summer
months are particularly susceptible ( 10).
Erythema ab igne can occur in athletes at the sites of chronically used hot packs or heating pads and produces an
endogenous tattoo (melanin and/or hemosiderin). Typical sites include the lower back ( Fig. 47.10) and anterior legs.
Erythema ab igne may progress to squamous cell carcinoma (141). There is no effective treatment, and it generally fades
in time.
FIGURE 47.10. Erythema ab igne. Reticular hyperpigmentation in an area exposed to chronic heat exposure, such as a
heating pad used for back pain.
Other Factors
The myriad effects of UV radiation are beyond the scope of this chapter. The outdoor athlete is at greatest risk of acute
sunburn. Exposure to photosensitizing drugs or psoralens (present in perfumes, limes, and celery) increases the risk.
Malignant melanoma in adults may be caused by intermittent intense sun exposures as a youth ( 142). Outdoor swimmers
younger than 15 years of age were reported to have an increased risk of melanoma; in this case-controlled study, the
effects of sunlight versus swimming per se (i.e., chlorine in water) could not be separated ( 143). Squamous and basal
cell cancers and photoaging are other potential long-term effects of UV light exposure.
Physical exertion is well known for causing acute urticaria and angioedema ( 144). Prolonged exercise can also result in
leukocytoclastic vasculitis through altered cutaneous microcirculation with extracellular deposition of eosinophil granule
proteins (145), complement activation, increased circulating immune complexes, and altered immune function ( 146,147).
Other environmental factors produce nitrogen rash and green hair. Scuba divers may develop nitrogen rash from
dissolution of nitrogen in subcutaneous tissue at atmospheric pressure greater than 1 atm. It manifests as a self-limited,
tender, pruritic eruption of the elbows and flanks ( 148). Green hair has traditionally been seen in blondes after exposure
to pool or tap water containing copper from corroded pipes or algaecides. Predisposing factors include prior hair
damage, frequent contact with chlorinated water, and use of alkaline shampoos ( 149). Green hair is not specific to
swimmers; it has been described in cobalt, chromium, and nickel workers ( 150,151) and in users of selenium sulfide,
yellow-mercuric oxide, and tar- or copper-containing shampoos ( 149,152). Treatment most commonly involves regular
shampooing (153), use of d-penicillamine or edetic acid–containing shampoos ( 154), or immersion of the hair into 3%
hydrogen peroxide for 2 to 3 hours ( 153).
Physical or environmental factors frequently exacerbate preexisting dermatoses. For example, heat, perspiration, and
frequent bathing intensify atopic eczema. Localized pressure and trauma exacerbate psoriasis, lichen planus, and
vitiligo, through the Koebner phenomenon. UV light may trigger flares of lupus erythematosus, polymorphous light
eruption, or other photosensitizing disorders.
RETURN TO PLAY
For athletes with mechanical trauma, nondisqualifying cutaneous infections, contact dermatitis, or physical or
environmental dermatoses, return to play should take place after appropriate treatment has been initiated and/or medical
clearance has been obtained.
With regard to disqualifying infections, the medical literature often fails to provide the minimal duration or optimal
treatment to ensure noninfectiousness. The most rational return to play recommendations have been devised with the
help of medical research and practical experience. These guidelines for coaches and athletes to follow are summarized
in Table 47.8. Supplemental data to the return-to-play guidelines are provided here.
TABLE 47.8. DISQUALIFYING SKIN DISEASES AND RETURN TO PLAY GUIDELINESa
Most studies of the treatment of impetigo have used endpoints such as subjective improvement or elimination of signs
and symptoms rather than microbiologic cure. One study examining microbiologic cure showed that 100% of
Staphylococcus aureus and Streptococcus pyogenes organisms were eradicated with an average treatment duration of
8.2 days with mupirocin ointment, versus 7.7 days with erythromycin ( 155). A subsequent prospective, double-blind study
(156) comparing oral erythromycin, cephalexin, and penicillin V found that cephalexin was the most effective treatment,
erythromycin was almost as effective, and penicillin V was inadequate for treatment of impetigo. Topical mupirocin was
then compared with oral cephalexin and was found to be equally as effective for treatment of localized impetigo ( 157).
Recommendations for treatment of impetigo in the athlete and for subsequent return to play are provided in Table 47.4
and Table 47.8, respectively.
Primary syphilis (158) has been more closely examined than secondary syphilis ( 159) with regard to infectivity before and
after treatment. The Centers for Disease Control and Prevention does not address the issue of when it is safe to resume
activities such as sexual intercourse after treatment of secondary syphilis. It is implicit that treated individuals should wait
until lesions are completely healed before engaging in sexual intercourse or athletic activities.
The polymerase chain reaction (PCR) has detected HSV ( 57,160) and varicella-zoster virus ( 57) from crusts; whether
these are live or dead virions is unknown. PCR has proved to be more sensitive than enzyme immunoassay in the
diagnosis of recurrent HSV infection ( 160). Appropriate control measures for herpes infections, including the presence of
firm adherent crusts, are listed in Table 47.8.
With molluscum contagiosum, a lesion-free period of 4 months after successful treatment has been suggested before the
patient can be regarded as cured ( 161). Disqualifying affected athletes or covering all treatment sites for the 4-month
period is impractical. The general consensus for return to play is that treatment is sufficient.
For localized tinea corporis, Evans et al. conducted a double-blind study comparing a single application of terbinafine 1%
cream with 3, 5, and 7 days' once-daily therapy and found no significant difference between groups ( 162). One-day
therapy may be sufficient for nonathletes, but a minimum of 3 days is recommended for athletes.
In the future, the varicella live vaccine may be recommended to all immunocompetent athletes who have not had varicella
to reduce its severity and associated morbidity and the incidence of herpes zoster ( 163,164). The HSV vaccine, shown to
effectively treat recurrent genital herpes, may also be an option for athletes ( 165).
CONCLUSION
In athletes, mechanical trauma evokes innumerable minor dermatoses, infections propagate disqualifying epidemics,
contact dermatitis is the great mimicker, and physical and environmental factors are ubiquitous. Recognition, treatment,
and prevention of sports-related skin diseases, along with adherence to proper disqualification and return-to-play
recommendations, will maximize the athlete's performance and general well-being.
ACKNOWLEDGMENT
This chapter was modified and updated from Rogachefsky AS and Taylor JS. Skin disorders in athletes. In: Kanerva L,
Elsner P, Wahlberg J, Maibach H, eds. Handbook of occupational dermatology. Heidelberg: Springer Verlag; 2000, pp.
1072–1083.
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48 Sports Neurology
48
SPORTS NEUROLOGY
STEVEN GOLDSTEIN
LAWRENCE R. WECHSLER
NEIL A. BUSIS
Headache
Migraine Headache
Posttraumatic Headache
Headache with Exertion
Treatment
Prognosis
Seizures
Classification
Etiology
Sports and Seizures
Treatment
Stroke
Carotid Dissection
Vertebral Artery Dissection
Cardiac Arrhythmias
Paradoxic Embolus
Drug Abuse
Peripheral Nerve Injuries
Overview
Cervical Radiculopathy and Brachial Plexopathy
Specific Nerve Injuries
Spinal Accessory Nerve
Supraclavicular Nerve
Suprascapular Nerve
Long Thoracic Nerve
Axillary Nerve
Musculocutaneous Nerve
Radial Nerve
Median Nerve
Ulnar Nerve
Digital Nerves in the Upper Extremities
Pudendal Nerve
Sciatic Nerve
Posterior Cutaneous Nerve
Femoral Nerve
Saphenous Nerve
Obturator Nerve
Lateral Femoral Cutaneous Nerve
Peroneal Nerve
Posterior Tibial Nerve
Sural Nerve
Digital Nerves in the Lower Extremities
Supraorbital Nerve
Conclusions
Chapter References
Sports-related neurologic syndromes are being increasingly recognized and can affect the central or peripheral nervous
systems. Some syndromes are directly related to athletic endeavors. Others are common in the general population and
occur in nonathletes as well as athletes. Some athletes may have preexisting conditions (e.g., hereditary liability to
pressure palsies) that predispose them to specific sports-related neurologic injuries ( 1). This chapter reviews several
topics in sports neurology: headache, seizures, stroke, and peripheral nerve injuries. A monograph on the topic is also
available ( 2).
HEADACHE
Migraine Headache
Headache is one of most frequent complaints in clinical practice. The most common etiologies include tension or muscle
contraction headache and migraine ( Table 48.1). Although muscle injuries occurring during exercise cause head or
posterior neck pain, they seldom result in diagnostic confusion. Migraine headaches with or without neurologic
accompaniments present a more dramatic picture that alarms both athletes and trainers.
TABLE 48.1. CAUSES OF HEADACHE IN ATHLETES
Estimates of migraine prevalence vary from 5% to 30% of the population ( 3). The term common migraine refers to
unilateral throbbing headaches accompanied by nausea, vomiting, and photophobia without aura or neurologic
accompaniments. Similar headaches preceded by visual disturbances or other neurologic symptoms are called classic
migraines. These visual symptoms are often characterized by scintillating scotomata or fortification spectra, which
typically occur 15 to 30 minutes before onset of headache. In complicated migraine, neurologic accompaniments may
occur with headache or with only minor headache, often raising concerns about cerebrovascular disease or other
neurologic conditions. Sensory, motor, speech, and/or language dysfunction may accompany headache in complicated
migraine. However, complicated migraine is a diagnosis of exclusion and should prompt an immediate evaluation for
possible ischemic stroke, intracranial hemorrhage, or mass lesion. Migrainous visual or sensory disturbances
characteristically evolve over 15 to 30 minutes before reaching maximal intensity. This slow buildup or spread is unusual
with transient ischemic attacks or focal seizures and helps identify the process as migraine. Headache usually follows
resolution of the neurologic symptoms by minutes to hours.
Posttraumatic Headache
Headaches with characteristics of common or classic migraine may be precipitated by minor head trauma encountered
during athletic activities. In some cases, there is a background of similar spontaneous headaches; in others, the
headache occurs for the first time during sports participation. Matthews ( 4) described headaches that occurred after
repeated heading maneuvers in soccer players, using the term footballer's migraine. Neurologic symptoms similar to the
aura of classic migraine sometimes preceded the headaches. Repeated head blows in boxing can cause similar
headaches. The trauma is usually minor, not resulting in loss of consciousness or significant memory loss. In some
cases, headaches recur with repeated injuries in a stereotyped fashion. This type of headache occurs most frequently in
children or adolescents but occasionally occurs in adults.
The pathogenesis of headache associated with minor head trauma is uncertain. Vasospasm induced by “jarring” of
arteries and spreading depression have been suggested as causes of the neurologic accompaniments associated with
posttraumatic migraine (5). Dynamic isotope brain scans obtained within 3 days in eight patients with classic migraine
related to head trauma were normal (5). In a few cases, investigations with angiography demonstrated vascular
occlusions (6,7) in cerebral branch vessels, suggestive of arterial embolization. This is not a likely mechanism for most
cases, because permanent neurologic sequelae would be expected. It is possible that individuals with headache or
neurologic accompaniments after minor head trauma have a predisposition to migraine, with trauma serving as a
triggering mechanism, similar to certain foods or stress.
Treatment is problematic because not every head blow precipitates headache. Ergotamine prevented attacks in a soccer
player with recurrent headaches ( 4). Ergots can cause nausea and vomiting and are contraindicated in patients with
hepatic or renal dysfunction. Preventive therapy with b-blockers or calcium blockers is indicated only if headaches occur
frequently without exercise.
Headache with Exertion
Exertion associated with weight lifting, running, or swimming has been reported to cause headache. Headaches
associated with weight lifting were found to begin abruptly and were usually brief ( 8,9). An interval of a few minutes to
several hours occurred between exertion and onset of headache. Pain recurred with repeated attempts to lift weights,
and in some cases orgasmic migraines or onset with other types of exertion also occurred. Headaches often resolved
within 6 months, and full activity levels could resume without further events. Rooke ( 10) monitored patients with exertional
headaches and found that 70% became headache free after 10 years. Often case reports of exertional headaches are
incomplete and computed tomography (CT) scans or lumbar punctures are not performed to clearly exclude other causes
for headache. Subarachnoid hemorrhage from a cerebral aneurysm may be preceded by one or several “warning leaks.”
These are brief, severe headaches with abrupt onset, sometimes accompanied by neck stiffness. CT findings may be
negative but lumbar puncture usually reveals blood or xanthochromia. These headaches may resolve within hours,
mimicking a migraine. Exertion, particularly activities such as weight lifting, may trigger small leaks and must be
distinguished from weight lifter's cephalgia. After a first such event, a CT and lumbar puncture should be performed if
there is clinical suspicion of a warning leak.
Weight lifters are subject to neck strain, which can also lead to headaches ( 9). These headaches are typically occipital,
although there may be radiation to the frontal region. Headaches have been associated with tight-fitting goggles in
swimmers (“goggle migraine”) (11). Other athletic activities and equipment also are likely to precipitate migraine in
susceptible individuals, and adjustment of an exercise regimen or equipment should be considered when repeated
headaches occur.
The mechanism of migraine induced by exercise remains speculative. Hyperventilation and hypocapnia associated with
exercise possibly lead to vasoconstriction of the basal cerebral arteries and migrainous auras ( 12). Vasodilation follows,
causing headache by stretching of pain-sensitive fibers in the walls of these vessels ( 13). Distention of venous sinuses
during exercise, particularly straining during weight lifting, has also been proposed as a mechanism ( 8). As more is
learned about migraine, the role of exercise in inducing such headaches will be clarified.
Unless headaches occur frequently, it is not usually necessary to institute preventive treatment. Indocin has prevented
headaches in some cases (14), but no large clinical studies have been reported. Other causes of headaches should be
considered before it is concluded that headaches induced by exercise represent migraine. Examination for signs of
raised intracranial pressure or focal neurologic signs should be performed. Sinus problems or temporal mandibular joint
dysfunction can occasionally mimic migraine. If there is any suspicion of an intracranial process, a CT scan of the head
should be obtained. Migraine should be diagnosed when symptoms are typical and all other potential sources of
headaches are excluded.
Treatment
Great advancements have been made in the treatment of acute migraine headache. Selective serotonin receptor
agonists are now available for subcutaneous, oral, and intranasal use. Sumatriptan, the first serotonin receptor agonist
available for clinical use, reduced headache in 63% of patients within 30 minutes when given by subcutaneous injection
(15). When given in oral form, sumatriptan demonstrated a similar response rate within 4 hours after administration ( 16).
At the 4-hour mark, a response rate of 77% was achieved for both a 50-mg and a 100-mg oral dose of sumatriptan ( 17).
In patients with severe nausea and vomiting, intranasal sumatriptan may be particularly useful, with a 62% to 63%
response rate at the 20-mg dose. Onset of relief can begin as early as 15 minutes after administration ( 18). A response
rate of up to 75% rate was demonstrated for zolmitriptan within 4 hours after an oral dose of 2.5 mg ( 19). Naratriptan, a
third serotonergic agent available for clinical use, may be especially useful in patients with rebound headache because of
its longer half-life and greater bioavailability ( 20).
The use of ergot derivatives for migraine headache has been extremely useful for many years. Dihydroergotamine is
available for intravenous, intramuscular, and, most recently, intranasal use in patients with acute migraine
headache(21,22). The use of serotonergic agents or ergot derivatives in patients with complicated migraine, severe
cardiovascular disease, poorly controlled hypertension, or cerebrovascular disease is contraindicated.
Prophylactic treatment of migraine headache involves the use of several different classifications of pharmacologic
agents. b-Adrenergic blockers, antidepressants, calcium channel blockers, serotonin antagonists, anticonvulsants, and
nonsteroidal antiinflammatory drugs (NSAIDs) have all been used with varying degrees of success as prophylactic
therapy (23,24).
Prognosis
Return to exercise for patients with migraine is limited primarily by the pain induced by specific activity. In migraine
headache, once the headaches spontaneously remit or respond to medication, previous levels of exercise can resume.
Headaches that occur after minor head injury must be approached more cautiously. Relatively minor head trauma during
sports rarely results in rapid development of coma and death from cerebral edema ( 25); a previous recent concussion
may predispose to this complication ( 26). Complete resolution of headache and any postconcussion symptoms such as
dizziness, confusion, or headache should be required before the patient returns to sports play. If symptoms persist, a CT
scan of the head should be performed. Headaches occurring after even a minor head injury occasionally signify
intracranial hemorrhage or a vascular injury such as dissection of an intracranial or extracranial artery. Examination by an
experienced physician is mandatory whenever symptoms become persistent or are out of proportion to the perceived
injury.
SEIZURES
Epilepsy refers to a pattern of recurrent seizures. A single seizure does not necessarily imply a seizure disorder. Most
issues in sports concern the safety of individuals with seizure disorders during participation in athletic activities. Children
with seizures are often unnecessarily encouraged not to participate. If seizures are well controlled and easily identified,
most sports can be enjoyed with minimal risk.
Classification
Seizures are divided into partial and generalized seizures ( Table 48.2). Partial seizures include focal discharges within
the brain, which cause localized motor or sensory phenomena without loss of consciousness. Generalized seizures
include grand mal seizures, complex partial or temporal lobe seizures, and petit mal seizures; loss of consciousness
occurs in all generalized seizures. Partial seizures occasionally become secondarily generalized (e.g., Jacksonian
seizures, in which focal motor activity spreads to become a generalized motor seizure).
TABLE 48.2. CLASSIFICATION OF SEIZURES
Grand mal or generalized motor seizures usually begin with a tonic stage with rigidity of all muscles, which at times
results in transient respiratory paralysis and cyanosis. This may be followed by clonic jerking movements of the
extremities with return of respirations. Incontinence occurs when motor activity ceases. Consciousness returns, initially
with confusion and agitation that gradually clears. There is typically amnesia for events that occurred during or
immediately after the seizure. Muscle aches, headache, tongue soreness, and sleepiness are frequent sequelae.
Seizures are occasionally preceded by an aura consisting of odd smells, sensations, or experiences.
Complex partial seizures also include loss of consciousness but without the generalized motor activity characteristic of
grand mal seizures. Lip smacking, repetitive hand movements, or other automatic motor activities are the hallmarks of
this seizure type. Again there is amnesia for events during the seizure. Confusion and sleepiness also frequently follow
complex partial seizures.
Petit mal or absence seizures occur mostly in children and are characterized by brief staring spells with immediate return
of full awareness. A sentence may be interrupted by a seizure, with continuation of the sentence at the point of
interruption when the seizure ends.
Several seizure types may occur in a single individual, and a careful history is essential to proper diagnosis and
assessment of response to therapy.
Etiology
The most frequent cause of seizures varies with age. Idiopathic seizure disorders usually begin before 30 years of age.
Brain tumors, head trauma, and infections predominate between ages 30 and 60 years. Cerebrovascular disease
becomes the most common etiology after age 60. Alcohol or barbiturate withdrawal may cause a single seizure or a
series of seizures. Sleep deprivation, stress, or medications can precipitate seizures in susceptible individuals.
Sports and Seizures
Many physicians advise patients with seizures against participation in sports. Transient loss of consciousness may lead
to injury, particularly in contact sports such as football or boxing. Sports in which driving is necessary pose an obvious
hazard. Exercise decreases absorption of many drugs and reduces both hepatic and renal clearance ( 27), potentially
altering anticonvulsant levels. No data are available concerning the effects of exercise on the pharmacokinetics of
anticonvulsants, so the clinical significance of these changes is unknown.
Another concern is whether overexertion or injury during sports causes seizures with or without an underlying seizure
disorder. Several cases of seizures occurring during strenuous exercise have been reported. Korczyn ( 28) described five
patients with seizures during a variety of athletic activities. Seizures recurred later under similar circumstances in some
patients and occasionally were unrelated to exertion. A total of 90 other epileptic patients were surveyed, but none
suffered seizures during sports, suggesting that this is an infrequent phenomenon. Ogunyemi et al. ( 29) described three
patients with seizures related to exertion. Electroencephalographic (EEG) recordings made while the patient was riding a
stationary bike demonstrated epileptiform discharges not seen at rest or during hyperventilation ( 29). In a similar study,
Goetze et al. (30) recorded EEG signals from 30 patients with epilepsy while they were performing deep knee bends.
Seizure discharges diminished during exercise, in contrast to the finding in the previous study, suggesting an increase in
seizure threshold during exercise and a decrease in the likelihood of clinical seizure activity. No information regarding
the relationship of seizures to physical activity was included for these patients. Animal models also suggest that exercise
might reduce the probability of seizures. Stress lowers seizure thresholds, possibly by release of endogenous
epinephrine (31). Stress factors were associated with seizures in only 37 of 1,250 patients surveyed by Friis and Lund
(32). The most common factors were sleep deprivation and emotional stress, although overexertion was reported in 16
patients. In most cases there were multiple stressful influences.
Data regarding the effects of exercise on seizure threshold are conflicting. Seizure thresholds may increase or decrease
in different individuals. Clinical data indicate that seizures precipitated by physical activity rarely occur, and it would seem
unfair to prohibit all patients with seizures from participation in sports. Accident rates during physical activity are no
different for epileptics than for nonepileptics ( 33), and minor head injuries likely to be encountered during sports play do
not increase the likelihood of seizures in susceptible individuals ( 34). Epilepsy often accompanies physical and cognitive
deficits that preclude most athletic endeavors. Those patients with well-controlled seizures and the ability and desire to
engage in sports should be encouraged to participate.
Treatment
Anticonvulsant therapy should be administered whenever recurrent seizures occur. Treatment of a single, unprovoked
seizure is controversial. Some physicians advocate observation rather than immediate treatment, because seizures recur
in only 20% to 70% of patients (35,36). The decision to treat can be further complicated by the desire to participate in
athletics. Sports predisposing to minor head trauma (e.g., football) or activities with potential danger should a seizure
occur (e.g., swimming) might favor treatment to avoid the risk of recurrent seizures in those settings. Phenytoin (Dilantin)
or carbamazepine (Tegretol) is usually the initial choice for anticonvulsant treatment. Both potentially cause sedation or
cognitive impairment when given in therapeutic doses. Careful gum hygiene is important when taking Dilantin, because of
the possibility of gum hypertrophy, particularly in children. Valproic acid and ethosuximide are both used as a first-line
agents to control petit mal seizures; however, because of its effectiveness against convulsive seizures, valproic acid is
the drug of choice. A host of newer antiepileptic drugs is now available ( 37,38), including gabapentin, lamotrigine,
tiagabine, topiramate, vigabatrin, and felbamate. Lamotrigine has been demonstrated to be effective as monotherapy in
patients with newly diagnosed epilepsy ( 39) and in patients with partial complex epilepsy ( 40). Gabapentin has also been
shown to be effective as monotherapy in patients with newly diagnosed partial seizures ( 41). The use of felbamate has
been restricted because of its rare but definite association with aplastic anemia. In most cases, a single drug adequately
controls seizures, regardless of type. If there is any question that seizures are continuing despite treatment, contact
sports, swimming, and other activities in which brief loss of consciousness could lead to injury should be avoided.
STROKE
Only 3% of strokes occur before the age of 40 years. The incidence of stroke in the young adult population has been
estimated at 25 per 100,000 persons annually. Even fewer occur in otherwise healthy individuals engaging in vigorous
sports. Atherosclerosis occurs less frequently in this age group but accounts for 20% of all strokes ( 42). Embolism,
primarily from cardiac sources, and hypercoagulable states cause much of the remainder. Arterial disorders, including
vasculitis and dissection, are rare causes, but they are important because specific therapy is required.
Most strokes in young individuals are unrelated to physical activity. A sedentary lifestyle predisposes to stroke, and
physical stress has not been identified as a risk factor. However, physical activity occasionally triggers a cardiac or
vascular process that results in cerebral ischemia. Because these strokes are rare in comparison with more common
stroke types, a statistical association would not be identified. Dissection of the major cerebral vessels, cardiac
arrhythmias, and paradoxic embolism may be precipitated by vigorous physical activity and should be considered when a
stroke occurs in this setting.
Carotid Dissection
Dissection of the cerebral vessels results from blunt trauma to the neck but also occurs with minor or seemingly
insignificant trauma. In some cases, no definite injury is identified. Carotid artery dissection has been reported in
association with a variety of sports, including jogging ( 43), football, tennis, basketball, volleyball, skiing, and bowling ( 44).
The extracranial carotid artery becomes compressed against the transverse process of the cervical vertebra with neck
extension and rotation, possibly tearing the wall of the vessel ( 44). Underlying vascular pathology such as fibromuscular
dysplasia or cystic medial necrosis predisposes to dissection with minor trauma. Dissection into the adventitia or media
creates a false lumen and expands the size of the vessel. Subintimal dissection narrows the true lumen and may lead to
carotid occlusion. Although expansion of the artery with compression of adjacent structures causes a variety of
symptoms, the most serious consequence of dissection is vascular occlusion. Reduction of perfusion in the ipsilateral
hemisphere may lead to stroke when collateral vessels are inadequate. In addition, thrombus forming at the site of recent
occlusion may fragment and result in embolic occlusion in the intracranial vessels. In one population-based study of
young adults, dissection accounted for 4% of all strokes ( 42).
The most common symptoms of carotid dissection are ipsilateral headache or neck pain, Horner syndrome, visual
scintillations, self-audible bruit, and dysgeusia ( 45). Head pain typically occurs around the eye or in the temple ipsilateral
to the dissection (45). Angiography demonstrates narrowing of the vessel, extending from several centimeters beyond the
carotid bifurcation to the base of the skull ( 46)—in contrast to the typical site of atherosclerotic narrowing, within the first
3 cm of the internal carotid artery. The other common site of carotid dissection is in the upper cervical region at the level
of C1-2. Bilateral or multiple dissections occur occasionally and are usually associated with fibromuscular dysplasia ( 47).
Symptoms of head or neck pain typically follow a sudden twist or extension of the neck. Examination reveals signs of a
Horner syndrome, including ptosis and meiosis. The hypoglossal nerve may be compressed, causing ipsilateral tongue
weakness (48). Amaurosis fugax or sudden stroke often follows the injury by one or several days. Recognition of the
early signs of dissection is critical, because institution of appropriate therapy may prevent subsequent stroke.
Noninvasive diagnosis is now available through the use of magnetic resonance imaging (MRI) techniques ( 49). With the
development of helical CT scanners, CT angiography has emerged as a useful technique to aid in the noninvasive
diagnosis of dissection ( 50).
Anticoagulation with heparin is usually administered initially, and warfarin (Coumadin) is given for long-term treatment.
Although worsening of dissection with anticoagulation seems plausible, this has not been observed in practice. The
optimal duration of treatment for dissection has not been established, but in some cases the stenotic vessel recanalizes,
eliminating the need for continuing anticoagulation. In serial ultrasound studies, the median time to recanalization was
found to be 6 weeks, and most arteries recovered by 3 months. Arteries that fail to recanalize by 6 months are not likely
to improve thereafter (51). Surgical intervention to remove occluding thrombus may be considered within the first few
hours after dissection, but it is unclear whether the risk of this procedure is warranted or whether outcome is improved
compared with medical management.
Athletic activities may be resumed after recanalization of dissection or after an occluded vessel has been allowed
sufficient time to ensure organization of intravascular thrombus. Our usual practice is to treat with Coumadin for 3 months
and to repeat CT angiography or MR angiography at that time. If complete recanalization has occurred, Coumadin is
discontinued and aspirin treatment is instituted. The same procedure is repeated at 6 months if the 3-month study fails to
demonstrate recanalization. If angiography demonstrates evidence of fibromuscular dysplasia or other vascular
anomalies predisposing to additional dissections, strenuous sports, particularly those involving sudden head and neck
movements, should be avoided.
Vertebral Artery Dissection
Dissection also occurs in the vertebral and basilar arteries. The cervical or intracranial segment of the vertebral artery
may be involved. Adventitial dissection in the intracranial segment causes subarachnoid hemorrhage in addition to the
typical symptoms of dissection. Pain from vertebral artery dissection most frequently localizes in the posterior neck or
behind the ear. Vertigo, diplopia, and other symptoms of vertebral-basilar ischemia may occur at the onset of dissection
or within the next several days. Basilar artery dissection is rare. Pain is usually suboccipital, and clinical syndromes
correspond to the distribution of ischemia in the basilar artery territory. This often occurs in young individuals, and in
boys more frequently than in girls ( 52).
Chiropractic manipulation has been associated with vertebral dissection ( 53), but other types of neck manipulation can
also cause vessel injury. Vertebral artery dissection has been reported with yoga ( 54), gymnastics (55), archery (56), and
swimming (57). Other sports that involve sudden turning of the neck could also potentially lead to dissection.
Fibromuscular dysplasia or cystic medial necrosis is found in some but not all patients. Sudden neck rotation causes
stretching of the vertebral artery and sometimes mechanical injury. The most common site of dissection is between C1
and C2 (58). The mechanism of intracranial vertebral or basilar artery dissection is unknown.
Anticoagulation is usually begun if the vessel is severely stenotic or occluded to prevent extension of thrombus or distal
embolization. Subarachnoid hemorrhage must be excluded in cases of intracranial vertebral artery dissection before
anticoagulation is initiated.
Cardiac Arrhythmias
In a large stroke data bank study, cardioembolic stroke accounted for approximately 19% of all ischemic strokes ( 59).
Atrial fibrillation is an important risk factor for stroke, and 15% of all strokes are associated with atrial fibrillation ( 60).
Stroke occurs with increased frequency in patients with atrial fibrillation regardless of etiology ( 61). However, young
patients with atrial fibrillation and no clinical heart disease may represent a subgroup with low stroke risk ( 62,63). Atrial
fibrillation is occasionally found in otherwise healthy athletes ( 64). Whether transient fibrillation in a healthy individual
without heart disease explains some cases of cerebral embolization associated with exercise is unknown. The published
data in the Stroke Prevention in Atrial Fibrillation Studies ( 65,66) suggest that Coumadin may be more effective than
aspirin for the prevention of ischemic stroke in patients with atrial fibrillation. However, in younger patients with
nonvalvular atrial fibrillation and without evidence of congestive heart failure, left ventricular dysfunction, hypertension, or
previous thromboembolism, the risk of embolic stroke is lower and treatment with aspirin alone may be considered.
Paradoxic Embolus
Atrial or ventricular septal defects predispose to right-to-left shunts and possible paradoxic emboli causing stroke.
Contrast echocardiography in one study demonstrated a potentially patent foramen ovale in 40% of patients with stroke
of unclear origin ( 67). In addition to a communication between the right and left sides of the heart, right-sided heart
pressures must be elevated before a paradoxic embolus can occur. There also must be a source of venous thrombus,
such as deep vein thrombosis. Pulmonary hypertension or multiple pulmonary emboli increase right-sided heart
pressures, but this would not be likely to occur in an individual who is well enough to participate in sports. The Valsalva
maneuver acutely raises right-sided heart pressures and may transiently open a potentially patent foramen ovale,
allowing right-to-left shunting. Exercise or exertion involving the Valsalva maneuver in predisposed individuals creates
circumstances favoring paradoxic embolization and possibly stroke. The frequency of such events is unknown, but in
most patients who have stroke associated with exercise contrast echocardiography is not performed. This mechanism
should be considered and investigated whenever stroke occurs at the time of strenuous physical activity.
Treatment decisions regarding patients with cryptogenic thromboembolic disease in the setting of a patent foramen ovale
remain controversial. Options include antiplatelet agents, anticoagulation, surgical closure, and transcatheter techniques.
There are conflicting reports regarding the effectiveness of surgical closure in the literature based on reports with
relatively small sample sizes ( 68,69 and 70). Until all therapeutic options are evaluated by large clinical trials, treatment
decisions will be driven by the risk of thromboembolism ( 71) and individual patient considerations.
Drug Abuse
Substance abuse has become increasingly frequent among athletes. Some agents (e.g., steroids) may lead to a
hypercoagulable state ( 72) and predispose to stroke. Amphetamines cause subarachnoid and intracerebral
hemorrhages. Angiography and pathologic studies often show evidence of cerebral vasculitis ( 73). Although some
reports have emphasized intravenous administration as the major risk for stroke, many cases are associated with oral
amphetamines (74). Cocaine has been associated with stroke, although a definite cause-and-effect relation has not been
convincingly established ( 74). A careful history of drug use should be elicited in any young patient with stroke, including
those occurring during sports participation.
PERIPHERAL NERVE INJURIES
Overview
The peripheral nerves of athletes can sustain several types of injury. Trauma can be macroscopic or microscopic, with
remodeling of connective tissues near the nerve or direct nerve damage caused by repetitive stresses ( 75). Pressure,
stretch, angulation, and friction all play a role. Nerves can be exposed to brief periods of high pressure or chronically to
lower pressures. Nerves and their blood supply can be compressed in tight fibrous or fibro-osseous passageways, by
anomalous or hypertrophied muscle, soft tissue swelling, scar tissue, tumor, or orthopedic deformity. Stretch can result
from anatomic deformity such as occurs in displaced fractures. The nerve axon, myelin sheath, connective tissue sheath,
or various combinations of these tissues can be damaged. Nerve injuries can be classified according to the type of
anatomic structures that are involved ( 76,77).
Neurapraxia is focal demyelination without axonal damage. It is the result of relatively blunt trauma or compression.
Demyelination leads to segmental conduction block, which leads to weakness and sensory loss. A lesser degree of
demyelination leads to segmental conduction slowing, which is useful diagnostically on neurophysiologic studies but may
not be clinically significant. Recovery occurs after remyelination, a process that takes several weeks to a few months.
Axonotmesis is axonal interruption with preservation of the connective tissue sheath around the peripheral nerve. The
distal nerve stump undergoes Wallerian degeneration over the first 3 to 5 days after the injury, and then the proximal
axonal stump attempts to regenerate. Axons can regenerate at a rate of about 1 mm per day or 1 inch per month. The
preserved connective tissue sheath acts as a guide for axonal regeneration and reinnervation. However, recovery is not
always predictable. Neurotmesis is interruption of axons and the endoneurial connective tissue sheath. More severe
types of neurotmesis are associated with interruption of perineurium or perineurium and epineurium (transection of the
nerve trunk). Reanastomosis of the connective tissue sheath is necessary if regeneration is to occur. Traumatic
neuromas can form at the proximal stump; they can impede further axonal growth and can become spontaneously
electrically active, causing pain. Aberrant regeneration can occur, causing synkinetic movements.
Peripheral nerves are subdivided into fascicles, each containing many individual axons. In many nerve injuries, different
fascicles sustain different degrees of damage to axons, myelin, and connective tissue sheaths. Recovery from these
mixed nerve injuries is biphasic, with the early phase of recovery caused by remyelination and the later phase the result
of axonal regrowth. Diagnosis of focal sports-related neuropathies depends on an accurate history, physical examination,
and often on electromyography (EMG) and nerve conduction studies and imaging procedures.
Injuries to nerve roots, plexuses, and individual nerves or their branches cause specific patterns of motor and sensory
alteration, pain, reflex change, and sometimes autonomic dysfunction. Motor and sensory symptoms can be caused by
overactivity or underactivity of motor and sensory axons. These symptoms are termed positive and negative, respectively.
Positive motor symptoms are cramps, fasciculations, and other types of abnormal motor activity. Negative motor
symptoms are weakness and wasting. Positive sensory symptoms are paresthesias such as “pins and needles,” tingling
feelings, or pain. “Tinel sign” refers to the paresthetic feeling elicited by tapping over the site of an injured nerve.
Negative sensory symptoms are sensory loss to one or more modalities.
EMG and nerve conduction studies are often of critical importance in diagnosing peripheral nerve injuries in athletes ( 78).
These studies may confirm the clinical diagnosis and determine its pathophysiology, its severity, and perhaps its
prognosis. At times a neurologic problem different from that initially suspected is revealed, and at other times a negative
examination helps diagnose a soft tissue injury without neurologic involvement.
There are certain limitations to EMG and nerve conduction studies that must be recognized to interpret the results
correctly. These studies can potentially distinguish between nerve injuries caused by segmental demyelination and those
caused by axonal interruption, but timing of the studies is crucial. As discussed earlier, Wallerian degeneration of axons
takes at least 3 to 5 days to occur. Denervated muscles first develop fibrillation potentials and positive sharp waves (the
EMG hallmarks of denervation) at 10 to 14 days. Usually, the full range of pathologic findings is present only if the EMG
and nerve conduction studies are performed 3 to 5 weeks after the injury. Timing of EMG and nerve conduction studies is
less critical in the diagnosis of a chronic process. Only surgical exploration of the nerve can determine the integrity of the
connective tissue sheath.
Nerve conduction studies primarily measure the number and conduction velocity of the large-diameter, fastest-conducting
sensory and motor fibers. Syndromes in which the symptoms are predominantly the result of positive phenomena (e.g.,
pain); in which the symptoms are caused by intermittent, reversible impingement of nerve fibers (especially those with
mainly sensory involvement); or in which small-diameter fibers are preferentially affected may be associated with normal
findings on nerve conduction studies. EMG and nerve conduction studies are most likely to be abnormal in cases of
subacute syndromes (3 weeks to 6 months) in which weakness is present.
In neurapractic lesions, the demyelinated segment may be quite short. Focal conduction slowing, an electrodiagnostic
hallmark of neurapractic lesions, may not be detected if only long segments of the affected nerve are studied. Sometimes
only the “inching technique,” in which 1- to 2-cm long segments of a given nerve are studied serially, reveals the
conduction slowing.
Although a majority of focal sports-related nerve injuries involve the shoulder girdle, routine median and ulnar motor and
sensory nerve conduction studies do not adequately assess the cervical roots and brachial plexus. Additional, less
commonly studied nerves should be assessed if the examination is to be maximally helpful. Furthermore, many of the
important shoulder girdle muscles are difficult to study because they overlie one another, and it is difficult to activate
them selectively.
The presence of a severe peripheral nerve lesion may mask another, more proximal, one. For example, a patient with a
severe brachial plexopathy may also have coexistent cervical radiculopathy that would not necessarily be detectable
electrophysiologically.
There are relatively few data on the usefulness of preoperative EMG and nerve conduction studies in predicting
prognosis after surgery, and there is often poor correlation between the degree of clinical recovery after surgery and
electrophysiologic findings. In particular, there can be persistence of EMG and nerve conduction abnormalities
postoperatively, even when there has been marked clinical improvement. This observation complicates the interpretation
of abnormal EMG and nerve conduction results in a patient for whom surgery (e.g., carpal tunnel release) did not lead to
the expected improvement.
Treatment options for focal neuropathies include both nonsurgical and surgical approaches. In general, conservative
nonsurgical measures such as rest, splinting, recognition, amelioration of provocative factors, and use of NSAIDs are
tried first. Local anesthetic or steroid injections can be useful in certain situations. If symptoms and signs persist and are
severe, surgical treatment may be indicated. Surgical approaches usually involve decompression of the nerve by removal
of those anatomic structures thought to be responsible for the entrapment. Sometimes the nerve itself is moved to
another location. Because scarring of the nerve trunk itself can cause persistent entrapment, epineurectomy or
epineurotomy is sometimes indicated. The utility of extensive internal neurolysis, in which individual nerve fascicles are
decompressed, is more controversial.
Well-defined and easily diagnosed disorders such as carpal tunnel syndrome are often treated successfully by
nonsurgical or surgical approaches, depending on the severity of the lesion. Less well-defined or controversial
syndromes, such as resistant radial tunnel syndrome, carry a less optimistic prognosis. A detailed discussion of the
treatment of each of the focal neuropathies reviewed here is beyond the scope of this chapter.
Excellent reviews of the causes, clinical presentation, evaluation, differential diagnosis, and treatment of entrapment
neuropathies have been published ( 79,80). Much of the material presented in this chapter is discussed in greater detail in
these publications.
Specific sports-related peripheral nerve injuries are discussed in the following sections and have also been reviewed
elsewhere (2). Much of the evidence comes from individual case reports, several of which are not detailed. Some of the
“focal neuropathies” in the sports neurology literature may really represent other entities. For example, some of the
reported mononeuropathies about the shoulder girdle may actually be the result of idiopathic brachial plexus neuropathy,
a well-described condition in the general population ( 81).
Cervical Radiculopathy and Brachial Plexopathy
The “stinger” or “burner” is a common syndrome affecting football players ( 82). After a tackle or similar hard jolt in which
the ipsilateral shoulder is depressed or the head is deviated back or toward the contralateral shoulder, the player
develops stinging or burning pain in the arm, which can radiate from shoulder to hand, and arm weakness. Usually, the
pain subsides in seconds and the weakness resolves in minutes. Repeated episodes may lead to more prolonged
weakness. In the majority of cases, the arm weakness is nonsegmental; if it persists, shoulder abductors and external
rotators and forearm flexors usually are involved. Sensory dysfunction also is not usually dermatomal. Lateral flexion of
the neck to the painful side is usually limited and may reproduce the sensory symptoms.
The site of pathology underlying the stinger is not certain. EMG and nerve conduction studies have variable results.
Some have suggested cervical radiculopathy ( 82), others brachial plexopathy ( 83,84). Some patients with the syndrome
underwent cervical laminectomy and had scarred C5 and C6 nerve roots at the points where they emerged from the
vertebrae (85).
Recurrences may result from chronic instability caused by ligamentous or facet laxity in the cervical spine or fibrosis with
edema around the nerve roots. The patient should forego athletic participation until symptoms and signs have resolved.
Preventive measures include a cervical collar, possibly raising the shoulder pads, and neck-strengthening exercises.
Acute trauma can cause severe brachial plexopathy in football; in bicycle and dirt bike accidents; and in snow-related,
equestrian, and water-related sports. Some patients may require operative intervention ( 86). Brachial plexopathy as a
late complication of clavicular fracture in a football player has been reported; the condition was caused by callus
formation (87). However, brachial plexopathy manifests acutely, without specific inciting trauma or long after acute
trauma, is probably acute brachial plexus neuropathy, as mentioned previously ( 81).
Cervical radiculopathies must be distinguished from brachial plexus injuries. Although there can be differences in history
and examination findings in these entities, neuroimaging studies and EMG and nerve conduction studies ( 88) are often
crucial for differentiation.
SPECIFIC NERVE INJURIES
Spinal Accessory Nerve
The spinal accessory nerve may be injured by local trauma in stick-handling sports such as hockey and lacrosse, or by
stretch of the supraclavicular area during exercise ( 89). Symptoms consist of shoulder aching and difficulty lifting the
arm. On examination, there is scapular winging when the arm is abducted to the side and there is weakness of shoulder
shrugging or abduction. EMG and nerve conduction studies can confirm the diagnosis and provide prognostic information
by quantitating axonal loss and continuity ( 90). Conservative therapy consists of analgesia and physical therapy. Surgical
exploration should be considered for a persistent deficit.
Supraclavicular Nerve
A patient who had midclavicular pain and tenderness, with associated sensory loss over the anterior shoulder and under
the midportion of the clavicle, was found to have entrapment of the supraclavicular nerve as it passed through a canal in
the clavicle. Pain was relieved, but numbness persisted ( 91).
Suprascapular Nerve
There are several potential sites of entrapment for the subscapular nerve, including the suprascapular notch, the superior
transverse scapular ligament, the inferior transverse scapular ligament ( 92), and the spinoglenoid notch at the lateral
border of the spine of the scapula. Repetitive shoulder movements in baseball pitchers ( 93), fencers (94), weight lifters
(95), and volleyball players ( 96) can injure the nerve. Blows to the suprascapular region or anterior dislocation of the
shoulder can also cause the syndrome ( 97,98,99 and 100). The primary symptom is pain in the posterolateral shoulder
that can be increased by flexing the shoulder. Shoulder weakness may be noted. Examination reveals weakness or
atrophy of the supraspinatus and infraspinatus muscles or just of the infraspinatus muscle. Pain can be reproduced or
aggravated by scapular abduction maneuvers or neck rotation toward the asymptomatic shoulder. Tenderness at the site
of entrapment may be noted. EMG and nerve conduction studies may differentiate between suprascapular nerve injury,
cervical radiculopathy, and brachial plexus palsy. Surgical exploration is indicated for signs and symptoms that persist
despite conservative therapy or in cases of acute onset without obvious cause ( 101).
Long Thoracic Nerve
The long thoracic nerve can be injured by heavy backpacks or in the course of weight training ( 102), swimming the
backstroke (103), tennis, bowling, golf, soccer, hockey, gymnastics ( 104,105), or volleyball ( 106). Many “injuries” may
actually be formes frustes of idiopathic brachial plexus neuropathy ( 81). Symptoms include dull, aching shoulder pain
and shoulder weakness. Examination reveals a sagging, weak shoulder. With arms extended forward, the scapula wings.
In one series, patients required an average of 9 months before full recovery. Traumatic etiologies are associated with a
relatively poor prognosis ( 107).
Axillary Nerve
Most axillary mononeuropathies are caused by overt trauma such as shoulder dislocation, humeral head fracture, traction
injury, or a direct blow to the shoulder ( 108,109). Symptoms consist of shoulder weakness. On examination there is
deltoid weakness and there may be deltoid atrophy and sensory loss over the lateral shoulder. Conservative treatment
includes splinting of the shoulder in partial abduction. If there is no significant improvement in 3 months, then the nerve
should be explored.
The axillary nerve can be entrapped in the quadrilateral space by abnormal fibrous strands or muscle hypertrophy ( 110);
this has been described in baseball pitchers ( 111,112), in football players, and in a rower. Symptoms include pain in the
anterior shoulder that is worsened by abduction and external rotation of the humerus. Shoulder and upper arm
paresthesias may be present. Subclavian arteriography can confirm the diagnosis, demonstrating occlusion of the
posterior humeral circumflex artery with the arm in abduction and external rotation. Surgical correction is possible ( 113).
Musculocutaneous Nerve
The musculocutaneous nerve may be injured by strenuous exercise—in which case the entrapment may be the result of
a hypertrophic coracobrachialis muscle ( 114)—or in contact sports such as football ( 115), hockey, and rugby. Symptoms
consist of elbow flexion weakness. Examination reveals painless weakness of biceps and brachialis muscles and can
show sensory loss over the lateral forearm. EMG and nerve conduction studies can confirm the diagnosis and assess
axonal continuity. Treatment consists of a sling and physical therapy. Surgery is rarely indicated.
The lateral antebrachial cutaneous nerve, the sensory termination of the musculocutaneous nerve, may be entrapped by
the biceps aponeurosis and tendon at the antecubital fossa ( 116). This injury may be caused by repetitive forceful
forearm pronation with elbow extension, direct trauma, or muscular hypertrophy and has been reported in swimmers,
weight lifters, racquetball players, and athletes in throwing sports. Symptoms include pain in the proximal forearm and
elbow, worsened with elbow extension or repeated pronation and supination of the forearm, and dysesthesias and
numbness over the anterolateral forearm. On examination, there is tenderness over the nerve at the antecubital fossa
and sensory loss over the anterolateral forearm. If conservative therapy fails, surgical decompression is indicated.
Radial Nerve
Radial nerve injuries at several levels have been reported in swimming, tennis, golf, weight lifting, and throwing sports
(117). Mechanisms include direct trauma or stretch and compression by either the lateral head of the triceps muscle or a
fibrous arch coming from this muscle ( 118,119).
High radial nerve injuries are defined as those lesions proximal to the bifurcation of the nerve into the posterior
interosseous nerve and the sensory branch. In such lesions, triceps function may or may not be affected, depending on
the level of injury. There can be pain, paresthesias, and numbness along the superficial radial nerve distribution (dorsal
radial area of the hand), as well as wrist and finger drop. There may be tenderness and a Tinel sign at the site of
entrapment.
Compression of the posterior interosseous nerve may occur at the arcade of Frohse. Symptoms are wrist and finger
weakness. Pain is not prominent in the classic syndrome; it is noted in only half of the cases and is usually brief. On
examination, there is prominent finger extensor weakness. Wrist extension may be weak, but only partially so, because
innervation to extensor carpi radialis longus and brevis is proximal to the lesion. Tenderness may be present over the
nerve in the extensor muscle mass just distal to the elbow.
EMG and nerve conduction studies are useful in confirming these two classic syndromes of radial neuropathy and can
quantitate the deficit, assisting management.
The classic symptom of tennis elbow is pain over the lateral epicondyle, although pain in the medial elbow has also been
reported. Although one potential source of the pain is muscle or tendon damage ( 120,121 and 122), it is possible that
some patients actually have entrapment of the posterior interosseous nerve by the extensor carpi radialis brevis, the
arcade of Frohse, or the supinator muscle ( 123,124). This syndrome is called “resistant tennis elbow” or “radial tunnel
syndrome.” In these patients, forceful supination or wrist or middle finger extension produces pain, and there is
tenderness over the radial nerve and not the lateral epicondyle. EMG and nerve conduction studies sometimes reveal
pathognomonic abnormalities (125). Surgical decompression of the posterior interosseus nerve has led to improvement
in a number of patients (126,127).
The superficial branch of the radial nerve can be entrapped in the distal forearm. Repetitive pronation, supination, and
ulnar flexion may produce stretch injury in the nerve, presumably at the site where it exits from under the brachioradialis
to assume a subcutaneous position, because it is relatively fixed there. The nerve also can be directly compressed by
tight wrist bands or direct trauma. Symptoms include pain and paresthesias over the dorsoradial aspect of the hand.
Examination reveals radial distribution sensory loss and a Tinel sign at the site of entrapment. Pain is worsened with
ulnar deviation and flexion of the wrist ( 128,129). EMG and nerve conduction studies can confirm the diagnosis and rule
out more proximal radial nerve pathology and cervical radiculopathy or brachial plexopathy.
Median Nerve
The median nerve may be entrapped at the ligament of Struthers in the distal humerus, the proximal forearm (pronator
teres syndrome), the midforearm (anterior interosseous syndrome), or the wrist (carpal tunnel syndrome) as a result of
repetitive upper-extremity exertion or direct trauma.
About 5 cm proximal to the medial epicondyle, some patients have a bony spur, a supracondylar process. The ligament
of Struthers runs from this spur to the medial epicondyle. Symptoms and signs in this syndrome are poorly defined but
may consist of varying degrees of pain above the elbow; tenderness over the ligament; weakness of pronation, wrist and
finger flexion, and thumb abduction; and median distribution sensory loss. The diagnosis can be supported by
radiographic demonstration of the supracondylar process, although the ligament can be present in some patients without
this bony protuberance. Surgical exploration is sometimes indicated.
In the pronator teres syndrome, the median nerve is entrapped within the pronator teres muscle itself by hypertrophy or a
fibrous band, in a tight fibrous arch of the flexor digitorum superficialis, or in a thickened lacertus fibrosus ( 130). This
syndrome has been reported in sports requiring forceful repetitive forearm pronation or gripping, such as baseball
(131,132), racquet sports, weight lifting, and gymnastics, as well as in contact sports, after acute trauma to the proximal
forearm. Symptoms include anterior forearm pain on exertion with or without clumsiness, loss of dexterity, hand
weakness, and paresthesias. Accentuation of symptoms by forceful forearm pronation or repetitive elbow motion supports
the diagnosis. On examination, pain or median-distribution paresthesias may be produced by forceful compression of the
pronator muscle mass. A Tinel sign may be present. Median motor deficits are sometimes present but are variable.
Sensory findings are usually poorly defined. Although EMG and nerve conduction studies are rarely abnormal, in some
patients the studies clearly demonstrate a median nerve lesion proximal to the wrist. EMG and nerve conduction studies
may also rule out other conditions in the differential diagnosis such as carpal tunnel syndrome and cervical
radiculopathy. If conservative therapy is unsuccessful, surgical decompression is indicated.
The anterior interosseus nerve can be compressed at the tendinous origins of the deep head of the pronator teres
muscle or flexor digitorum superficialis to the long finger or by several types of accessory muscles, tendons, and blood
vessels (133). Acute trauma or chronic trauma, with a preexisting anatomic disposition, can cause anterior interosseus
entrapment. Settings include weight lifting and activities requiring repetitive elbow flexion and pronation. Symptoms
include pain in the proximal forearm or arm, loss of dexterity, and loss of the ability to pinch. On examination there is
weakness of flexion of the interphalangeal joint of the thumb (flexor pollicis longus) and of the distal interphalangeal joint
of the index finger (flexor digitorum profundus of the index finger). In addition, there is weakness of forearm pronation
when the elbow is flexed (pronator quadratus). There can be tenderness over the pronator muscle mass and increased
pain on resisted pronation. A Tinel sign can be present. There is no sensory loss. EMG and nerve conduction studies
may show denervation in the involved muscles or prolonged distal motor latency to the pronator quadratus. If a prolonged
trial of conservative therapy fails, surgical exploration is indicated.
Median nerve entrapment at the wrist (carpal tunnel syndrome) can occur from bicycling, excessive forceful gripping,
excessive throwing of a curve ball (baseball pitchers), repetitive wrist flexion-extension movements (various racquet
sports) (134), or direct trauma to the volar surface of the wrist ( 135), including fracture-dislocation and crush injuries.
Symptoms include pain and paresthesias in the wrist and hand, which are often worse at night or with use of the hands.
The pain can spread all the way to the shoulder in some patients, although the paresthesias are present only in the
fingers. Hand clumsiness or weakness may also be noted. On examination, sensory loss can be found in the
median-innervated digits (thumb, index finger, middle finger, and lateral border of ring finger). There can be weakness of
the abductor pollicis brevis muscle and atrophy of the thenar eminence. A Tinel sign or Phalen sign may be present,
although they are sometimes present in the absence of carpal tunnel syndrome.
Conservative treatment consists of immobilization of the wrist with a splint, worn at night, and use of NSAIDs. Injection of
corticosteroids into the carpal tunnel is sometimes helpful. Failure of conservative treatment and a severe median nerve
lesion are indications for surgical treatment.
Ulnar Nerve
Ulnar nerve entrapment at the elbow (condylar groove or cubital tunnel) can be caused by repetitive elbow flexion, an
inflamed or calcified collateral ligament, loose bodies in the cubital tunnel, osteoarthritis, a severe valgus deformity, an
anomalous muscle (136), or hypermobility of the nerve caused by lax or ruptured ligaments ( 137). Inflammation or a
constricting band that entraps the nerve at the entrance to the cubital tunnel, the origin of the flexor carpi ulnaris, may be
present. Entrapment has been reported in baseball pitchers ( 138,139,140,141 and 142) and weight lifters, as well as
racquetball players and other stick-handling athletes ( 143).
Symptoms consist of elbow pain, intermittent paresthesias in the fourth and fifth digits, and sensory alteration in the
fourth and fifth digits and ulnar border of the hand. A sensory deficit over the medial dorsal aspect of the hand
(distribution of the dorsal cutaneous branch of the ulnar nerve) implies that the lesion is proximal to the wrist. Weakness,
if present, can range from mild clumsiness to definite weakness associated with intrinsic hand muscle atrophy. On
examination, there can be ulnar distribution sensory loss (palmar and dorsal surfaces of medial hand, entire fifth digit,
medial half of fourth digit); weakness of the flexor carpi ulnaris, flexor digitorum profundus of fourth and fifth digits, and
abductor digiti minimi; and first dorsal interosseous weakness. Partial deficits are more common than complete ones,
probably because of unequal involvement of the different ulnar fascicles. A Tinel sign or tenderness over the nerve at the
elbow may be present. EMG and nerve conduction studies can often confirm the diagnosis but do not always
demonstrate focal slowing or conduction block across the elbow, probably because of the fascicular nature of the injury in
many patients.
If definite bone or joint deformities are absent, conservative treatment of ulnar neuropathy at the elbow, with splinting and
protection of the elbow with a soft pad and a short course of NSAIDs, is tried first. If conservative measures fail, then
surgical intervention is indicated. Surgical treatment includes decompression of the nerve at the cubital tunnel or anterior
transposition of the ulnar nerve. The results of surgical decompression are variable.
Ulnar nerve entrapment at the wrist may result from chronic or repeated trauma; from hamate or pisiform bone fractures;
or, rarely, from ganglia, arthritis, anomalous muscle, lipomas or other tumors, arteriovenous fistulas, aneurysms, or
thrombosis of the ulnar artery at or near Guyon's canal ( 144). Bicyclists (“handlebar palsy”) ( 145,146), baseball catchers,
weight lifters, gymnasts, martial arts practitioners, racquetball players, golfers, video game enthusiasts ( 147), and a man
who did a lot of push-ups on a hard floor ( 148) have been reported with this injury.
Depending on the site of the lesion, four different syndromes of ulnar nerve entrapment at the wrist have been described.
Compression of the nerve just proximal to or within Guyon's canal causes weakness of all ulnar-innervated hand muscles
and sensory loss over the palmar aspect of digit five and the medial aspect of digit four. Entrapment of the most proximal
deep terminal branch results in pure weakness but no sensory loss. Compression of the deep terminal branch distal to
the innervation of the hypothenar eminence results in weakness of ulnar-innervated hand muscles, except those of the
hypothenar eminence. Compression of the superficial terminal branch in or just distal to Guyon's canal results in pure
sensory loss involving the distal palmar hypothenar area and the palmar aspects of the ulnar-innervated digits. There
may be pain and local tenderness; in cases caused by repetitive trauma, a callus over the base of the palm may be
present. Diagnostic tests include radiographs of the wrist with a carpal tunnel view to look for fractures and EMG and
nerve conduction studies.
Initially, conservative treatment of ulnar neuropathy at the wrist is recommended. Avoidance of external pressure, the use
of protective padding, and NSAID therapy are usually adequate. In cyclists, preventative measures include well-padded
gloves and handlebars, correct bicycle frame size and distance from seat to stem, and frequent changing of hand
positions on the handlebars ( 149). If conservative measures fail or if a mass is present at Guyon's canal, surgical
exploration at Guyon's canal and distally may be indicated ( 150).
Digital Nerves in the Upper Extremities
Bowler's thumb is a digital neuropathy of the thumb ( 151). A cheerleader who did a lot of clapping and cartwheels
developed a median palmar digital neuropathy ( 152). Digital neuropathies have also been described in catchers and
batters (153). Symptoms consist of pain over the nerve and paresthesia and hypesthesia in the distribution of the
involved nerve. A Tinel sign may be present, as may skin atrophy and callus formation. For digital neuropathies, surgical
correction may be indicated if conservative measures fail.
Pudendal Nerve
The pudendal nerve may be damaged along with a pelvic fracture caused by a fall from a bicycle or motorcycle.
Numbness of the shaft of the penis (154) and impotence (155) have been reported after prolonged bicycle riding. The
symptoms presumably resulted from compression of the pudendal nerves between the bicycle seat and the pubic
symphysis.
Sciatic Nerve
Sciatic nerve entrapment can occur in the gluteal region around the sciatic notch and gluteal fold or in the thigh ( 156).
The most common cause of sciatic nerve injury is trauma (e.g., fracture-dislocation of the hip) or severe traction injury, as
seen in motorcycle racing accidents. Transient sciatic neuropathy in cyclists has been reported and presumably was the
result of pressure on the nerve in the perineal area ( 157) or at the sciatic notch from the bicycle seat ( 158).
The sciatic nerve can also be injured in the thigh. Complete sciatic nerve laceration caused by a closed femoral shaft
fracture in a motorcyclist has been reported ( 159). Traumatic hematomas of the thigh and myositis ossificans in the
biceps femoris muscles (reported in a cricket and soccer player) can also cause sciatic entrapment ( 160,161 and 162).
Hamstring entrapment of the sciatic nerve was reported ( 163), but no EMG or nerve conduction studies were done to
support the diagnosis.
A complete sciatic nerve lesion results in paralysis of the hamstrings and all muscles below the knee, sensory loss in all
areas below the knee except for the medial calf, and an absent ankle jerk reflex. Most sciatic nerve lesions are
incomplete, however. The lateral (peroneal) trunk is more vulnerable than the medial (posterior tibial) trunk, so that in
some patients with sciatic neuropathy the clinical findings are similar to those expected for a lesion of the common
peroneal nerve at the fibular head ( 164). EMG and nerve conduction studies, including evaluation of the short head of
the biceps femoris (the only muscle innervated by the lateral trunk proximal to the fibular head) can establish the
diagnosis. Imaging studies to look for fractures and pelvic masses are also useful.
Compression of the sciatic nerve in the piriformis muscle is a controversial entity ( 165). No patients reported to have this
syndrome had significant neurologic deficits, although EMG evidence of sciatic distribution denervation was noted in one.
Some authors state that lack of a neurologic deficit is an essential diagnostic criterion. Symptoms have been relieved by
surgical exploration and division of the piriformis muscle in some patients ( 166).
Posterior Cutaneous Nerve
A bicyclist developed a neuropathy of the posterior cutaneous nerve of the thigh ( 167). Symptoms of this entrapment
include paresthesias over the lower buttock or posterior thigh, or both.
Femoral Nerve
Femoral neuropathy has been reported in gymnasts (168), judo practitioners, parachute jumpers, dancers performing
exercises in which their hips are hyperextended ( 169), and athletes doing repeated somersaults. Sudden flexion or
extension, stretching of the nerve during hyperextension of the hip for a long period, and compression of the nerve under
the inguinal ligament may be etiologic factors.
Symptoms and signs of femoral neuropathies include weakness and atrophy of the quadriceps muscle, reduction or
absence of the knee jerk reflex, and sensory loss over the anteromedial thigh and along the medial aspect of the lower
leg. Little or no sensory loss can be seen in partial nerve lesions. Iliopsoas or thigh adductor weakness rules out pure
femoral nerve involvement. Iliopsoas muscle weakness can be seen in an upper lumbar plexopathy or L2-3
radiculopathy. Thigh adductor weakness can be seen in obturator neuropathy, lumbar plexopathy, or L2-3 radiculopathy.
EMG of the lumbar paraspinal muscles, iliopsoas, thigh adductors, and quadriceps can assist in the differential
diagnosis. Imaging studies of the lumbar spine and pelvis (which may reveal a hematoma or mass) are also useful ( 170).
Conservative treatment includes analgesics and physical therapy. Bracing may be necessary. Surgical exploration may
be indicated if the lesion is severe or if laceration of the nerve is suspected.
Saphenous Nerve
Surfers can develop a saphenous neuropathy caused by pressure on the nerve when the medial aspects of knees are
pressed against the surfboard ( 171). Symptoms consist of dysesthesia over the anteromedial aspect of the leg below the
knee. Examination revealed sensory loss in the saphenous distribution.
Obturator Nerve
The obturator nerve is most often injured by trauma, such as a pelvic fracture. Symptoms and signs include weakness of
hip adduction, sensory loss, pain and/or paresthesias in the medial thigh, and sometimes groin pain. Quadriceps strength
and the knee jerk reflex are normal. In most cases of obturator nerve involvement, a lesion of the femoral nerve also is
present. EMG and nerve conduction studies are useful in the diagnosis, as are imaging studies of lumbar spine and
pelvis. Treatment depends on the cause of the neuropathy.
Lateral Femoral Cutaneous Nerve
Lateral femoral cutaneous nerve entrapment is termed meralgia paresthetica (172). The lateral femoral cutaneous nerve
enters the thigh by passing through a tunnel in the lateral attachment of the inguinal ligament to the anterosuperior iliac
spine and supplies sensation to the anterolateral aspect of the thigh. Meralgia paresthetica has been reported in weight
lifters who wear tight corsets, belts, or trusses (perhaps as a result of direct compression of the nerve at its point of exit
from the pelvis), in gymnasts (perhaps due to the impact of the thighs on the uneven parallel bars or to repetitive flexion
and extension of the hip in rope jumping) ( 173), and in a jogger. Symptoms and signs include pain, paresthesias, and
sensory loss in the anterolateral thigh. A Tinel sign or tenderness at the anterosuperior iliac spine may be present.
Symptoms often increase during standing or walking. EMG and nerve conduction studies are valuable in excluding
lumbar radiculopathy, lumbar plexopathy, and femoral neuropathy, but nerve conduction studies of the lateral femoral
cutaneous nerve are unreliable in most hands. Conservative treatment consists of analgesics and avoidance of
precipitating factors such as certain exercises or tight corsets, belts, or trusses. Nerve blocks or local steroid injections
may help. If conservative therapy fails, surgery may be indicated. The nerve can be released at a level of exit from the
inguinal ligament. Nerve section carries the risk of producing unpleasant paresthesias due to neuroma formation.
Peroneal Nerve
The peroneal nerve is injured most frequently at the head and neck of the fibula. Acute adduction of the knee joint with
rupture of the lateral ligaments, twisting of the ankle, or sudden stretching may lead to a severe traction injury of the
nerve (174). Peroneal nerve entrapment at the fibular head has been reported in tennis and racquetball players ( 175), in
runners (176,177), and in a skier who had distal fractures of the tibia and fibula caused by severe ankle inversion injuries
(178). An athlete with exertional knee pain had entrapment of the peroneal nerve in the popliteal space by a fibrous band
(179). Symptoms and signs include foot drop with weakness or paralysis of the ankle and toe dorsiflexors and weakness
of ankle evertors. Sensory loss involving the anterolateral aspect of the lower leg and dorsum of the foot can be present.
Variable patterns of motor and sensory deficit can be seen, depending on the relative involvement of the superficial and
deep peroneal branches. A Tinel sign may be present at the fibular head. Persistent pain implies a true entrapment in the
fibular tunnel or compression by tumors or cysts. EMG and nerve conduction studies can help confirm the diagnosis and
can help rule out lumbar radiculopathy, lumbar plexopathy, and sciatic neuropathy. Imaging studies of the knee can also
be useful. Conservative treatment consists of bracing with a plastic orthosis molded to the posterior calf of the foot, to
provide stability while walking, and avoidance of extrinsic pressure at the fibular head (e.g., by avoiding crossing the legs
at the knees). Surgical therapy is indicated for patients with persistent pain and progressive motor and sensory loss.
The deep peroneal nerve can be entrapped in runners, soccer players, and skiers. The most common site of entrapment
is the anterior tarsal tunnel (inferior extensor retinaculum), although other nearby entrapment sites have been described.
Recurrent ankle sprains or trauma may be contributory. Symptoms include pain in the dorsum of the foot with radiation to
the first web space, worsened by running. Examination reveals decreased sensation in the first web space, and there
may be extensor digitorum brevis weakness and atrophy. Pain can be provoked by dorsiflexion or plantar flexion of the
foot, depending on the site of entrapment.
Entrapment of the superficial peroneal nerve can occur in runners as well as soccer, hockey, tennis, and racquetball
players. The usual point of entrapment is at the exit point from the deep fascia, 10.5 to 12.5 cm proximal to the lateral
malleolus. About 25% of patients have a history of previous trauma, most commonly an ankle sprain. Injuries to the
superficial peroneal nerves may also result from wearing tight ski boots or roller skates ( 180). Fascial defects with muscle
herniation may be present (181). Symptoms include pain over the outer border of the distal calf and the dorsum of the
foot and ankle. There may be sensory loss in the same distribution. The pain is worse with exertion. On examination,
there may be point tenderness where the nerve exits the deep fascia. A Tinel sign may be present. Sensory loss may be
noted, as may a palpable fascial defect.
Injuries to the deep and superficial peroneal nerves leading to pain and numbness on the dorsolateral foot may result
from ankle sprains, blunt trauma, or rupture of the peroneus longus muscle ( 182).
Posterior Tibial Nerve
An athlete with exertional knee pain had entrapment of the tibial nerve in the popliteal space by fibers of the medial
gastrocnemius muscle (179). The distal tibial nerve or its major distal branches can be entrapped at the ankle or foot
(183).
The posterior tibial nerve can be entrapped in the tarsal tunnel in runners and other athletes. In some cases there are
abnormalities of the fibro-osseus tunnel or its contents. Extrinsic pressure may also be involved. Tight golf shoes caused
the syndrome in one of our patients. About 33% of cases are related to trauma. Symptoms consist of burning, sharp pain,
and paresthesias that radiate into the sole of the foot. Standing, walking, or running exacerbates the symptoms.
Numbness and nocturnal pain are less common. On examination, there may be a Tinel sign over the tarsal tunnel.
Sensory loss in the medial and/or lateral sole may be noted. Intrinsic foot muscle weakness may be present.
Entrapment of the medial plantar nerve occurs in joggers in the region of the master knot of Henry. Patients often run with
excessive pronation of the feet or excessive heel valgus. Arch supports may compress the nerve. Symptoms include pain
in the medial aspect of the arch that is worsened with running or the use of a new orthosis. On examination, there is
tenderness near the navicular tuberosity. A Tinel sign may be present. Decreased sensation on the medial sole may be
present after running.
The first branch of the lateral planar nerve can be entrapped (usually in runners) between the deep fascia of the abductor
hallucis muscle and the medial caudal margin of the quadratus plantae muscle, over the plantar side of the long plantar
ligament, or in the osteomuscular canal between the calcaneus and the flexor digitorum brevis. Symptoms consist of
chronic heel pain worsened with walking or running. On examination, there is tenderness over the nerve deep to the
abductor hallucis muscle. A Tinel sign is sometimes present over the nerve.
Entrapment of the calcaneal nerve branch has been reported in athletes with chronic heel pain that was unrelieved by
conservative therapy (184). This neuropathy occurred in long-distance runners and in a badminton player.
Therapy for these disorders is primarily conservative. Tight shoes, straps, and taping are to be avoided. Alteration in
technique or playing surface, appropriate exercises, NSAIDs, rest, ice or heat, massage, and injections may be helpful.
Surgery may be needed if conservative measures result in no improvement.
Sural Nerve
The sural nerve may be injured by avulsion fracture of the base of the fifth metatarsal bone in runners ( 185), a tight-fitting
ski boot, fibrosis secondary to recurrent ankle sprains, ganglions, or myositis ossificans at the musculotendinous junction
of the Achilles tendon. Symptoms include pain and paresthesias in a sural distribution. Examination may reveal
tenderness over the nerve, a Tinel sign, and sensory loss.
Digital Nerves in the Lower Extremities
Measurable differences in vibratory sensation threshold and in lower-extremity nerve conduction were found in
long-distance runners compared with controls, perhaps because of multiple small injuries to the toes and feet ( 186).
However, none of the runners had clinical symptoms or signs of neuropathy.
Interdigital neuroma (Morton neuroma) is not uncommon in runners ( 187). Plantar digital nerves are subjected to
repetitive microtrauma against the distal edge of the intermetatarsal ligament. Usually, the third web space is involved.
Symptoms include plantar or forefoot pain associated with running. Numbness or tingling of affected toes is sometimes
present. On examination, there is point tenderness on the plantar aspect between the metatarsal heads at the affected
web space.
Supraorbital Nerve
Supraorbital neuropathy was reported in a swimmer; it was presumably caused by pressure on the nerve from tight
swimming goggles. Symptoms consisted of ipsilateral headaches and supraorbital ridge pain. A Tinel sign was present at
the supraorbital notch ( 188).
CONCLUSIONS
Awareness of sports-related neurologic syndromes should lead to more rapid and precise diagnosis and should improve
the development and institution of preventative measures.
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49 Head Injuries
49
HEAD INJURIES
DONALD W. MARION
Epidemiology
Anatomy and Pathology: Radiologic Evaluation
Closed Head Injuries
Primary Versus Secondary Injury
Treatment
Prehospital Treatment
Emergency Department Management
Intensive Care
Mild Head Injuries
Neuropsychological Testing After Mild Head Injury
Return to Play
Summary
Acknowledgment
Chapter References
In the United States, sports and recreational activities cause far fewer head injuries than do motor vehicle accidents,
falls, or assaults. Because the brain is so intolerant of trauma, however, head injuries that do occur in sports are often
more debilitating to the athlete than injuries involving most other areas of the body. Moreover, rehabilitation of the
damaged brain is not nearly as successful as rehabilitation of a damaged limb. Although the treatment of head trauma
has made great strides, those who suffer a severe injury and are rendered comatose for a prolonged period still are
unlikely to recover fully from all neurologic or cognitive impairment.
The team sports that most commonly cause head injuries are the contact sports, primarily football, boxing, rugby, and ice
hockey. Other sports associated with a high risk are gymnastics, diving, horseback riding, bicycling, and skiing. Although
these activities do not often result in injuries severe enough to cause prolonged coma, mild head injuries are quite
common in contact sports, and there now is a large amount of data indicating that these injuries can lead to substantial
and, at times, incapacitating behavioral and cognitive deficiencies. Persistent dizziness, headaches, inattentiveness, or
memory problems can impair an athlete's performance significantly and preclude return to play. In addition, studies have
found that sustaining one mild head injury increases the vulnerability to future injury ( 1).
The best treatment for head injury is prevention. The use of protective head gear in most contact sports significantly
limits the severity of injury from a cranial impact. Yet protective helmets still are not worn in many situations that pose a
significant risk of injury, such as bicycle riding. In some sports, the best preventive measure would be modifications that
eliminate particularly dangerous practices, such as high sticking in ice hockey.
After a review of the epidemiology of sports-related traumatic brain injury, this chapter describes the anatomic and
physiologic characteristics of the various types of head injury and their treatment and prognosis. Finally, the cognitive
sequelae of minor head injury and return-to-play issues are discussed.
EPIDEMIOLOGY
Because most severe head injuries occur between 14 and 30 years of age, they account for more potential years of life
lost than do cancer and cardiovascular disease combined. In 1984, an estimated 500,000 hospital admissions or deaths
in the United States resulted from traumatic brain injury ( 2). Between 3% and 10% of these were caused by sports or
recreational activities. Of the 43,000 outpatient emergency department visits for head injuries in the state of Pennsylvania
in 1988, 13% were caused by a sports-related injury ( 3). Table 49.1 shows the incidence of head injuries in various
sports considered to be particularly hazardous.
TABLE 49.1. INCIDENCE OF HEAD INJURIES/CONCUSSIONS IN SELECTED SERIES OF SEVERAL OF THE

HIGHEST RISK SPORTSa
Published statistics are not available for minor head injuries—that is, those that lead to a brief period of confusion but
allow the player to return to competition within minutes. Even in those sports with the highest incidence of head trauma,
however, the great majority of injuries are minor and do not require hospitalization. A 10-year survey of football injuries in
the United States determined that the yearly incidence of severe head injuries causing intracranial hemorrhage was no
more than 4 per 100,000 players among college athletes and less than 2 per 100,000 among high school students ( 4).
The study also found that only 1 of 100,000 football players in college and half as many in high school died each year of
a head injury. During the 1975–1984 seasons, a total of 69 deaths resulted from head injuries in organized football at all
levels of play; 87% of these were caused by a subdural hematoma ( 5).
Minor head injuries are not necessarily innocuous, however. They not only can cause immediate confusion and
alterations of consciousness but also can lead to prolonged headaches, dizziness, memory difficulties, and irritability.
These symptoms are a part of the postconcussion syndrome and can be so severe that they limit the athlete's ability to
function in the sport, at work, or in school. In soccer, a sport in which players frequently use their heads to hit the ball, a
study revealed that 16.4% of players complained of some constellation of postconcussive symptoms ( 6).
The risk of head injury from bicycling accidents is low, compared with most other sports. Nonetheless, bicycle riding is an
increasingly popular activity that causes an estimated 1,300 deaths each year, and in 70% to 80% of all bicycling
fatalities the cause of death is attributed to head trauma ( 7). The estimated chance that a fall from a bicycle will cause a
head injury is 50%, and a fall from a bicycle traveling 20 mph can be fatal if the unprotected head strikes a hard object
(8).
As the typical age of bicycle riders has increased, so has the age of those suffering severe head injuries. In the 1960s,
most victims of fatal bicycling accidents were younger than 15 years of age, but by 1985, two thirds of bicycling fatalities
occurred in those older than 15. Thompson et al. found that the use of an approved bicycle helmet reduced the risk of
brain injury by 88% (9). Despite these facts, it is estimated that fewer than 1% of bicycle riders wear an approved helmet.
Helmet use also has been shown to reduce the frequency of head trauma in football and ice hockey ( 10,11). In football,
the number of head injury–related fatalities that occurred between 1975 and 1984 was dramatically lower than in the
previous 10 years (69 versus 162 deaths) ( 5). This sharp decline was attributed partially to the first national safety
standards for football helmets, which went into effect for college football in 1978 and for high school football in 1980.
Although few well-designed studies have been conducted to establish the safety factors for these helmets, most experts
agree that the best helmets are those with a hard shell and a polystyrene liner ( 12). Under impact conditions that emulate
contact sports, such helmets have proved far superior to the once-popular suspension helmets, which no longer are
recommended for use (13). The thickness of the liner, and not the rigidity of the shell, has been correlated most closely
with protection from severe head injury. Because impact distorts the liner, causing it to lose some of its thickness, either
the helmet or the liner should be replaced after each severe impact.
Changes in the rules of play have also been instituted to reduce the number and severity of head injuries in particular
high-risk sports such as football, ice hockey, and boxing. In 1976, the National Collegiate Athletic Association and the
National Federation of State High School Athletic Associations implemented severe penalties for intentionally striking a
runner with the crown of a helmet and for spearing. Such rule changes share the credit with helmet improvements for the
reduction in fatal head injuries in this sport. For boxing, most states now impose mandatory suspensions for boxers who
suffer even minor head injuries. In ice hockey, however, the current penalty system seems ineffective in reducing head
injuries. Pforringer and Smasal reviewed the causes of head injury in 246 ice hockey players and concluded that 76% of
the injuries were caused by violence that was not a necessary part of the game: 45% from a blow with a hockey stick
(high sticking), 20% from a deliberate push, and 11% from a fistfight ( 14). Fewer than 20% of the head injuries were
caused by mechanisms of injury traditionally associated with hockey, such as checking, sliding into the boards, or being
hit by a hockey puck. Therefore, more stringent rules appear to be necessary in this sport.
ANATOMY AND PATHOLOGY: RADIOLOGIC EVALUATION
The management and prognosis of head injuries are related not only to the severity of the injury but also to the cause.
There are important differences in the treatment required for various types of brain injury and in their neurologic
prognoses, depending to a large extent on the mechanism of injury. It is useful to consider a head injury as either a
closed or a penetrating wound, because each has certain unique characteristics. Closed head injuries are those in which
the entire head undergoes translational or rotational acceleration, and this motion damages the enclosed brain or its
covering. In penetrating head injuries, a missile or missile fragments actually pierce the skull and brain.
Closed Head Injuries
Most sports-related head injuries result from rapid acceleration or deceleration of the brain within the skull after a blunt
force has been applied to the head. The victim usually is not permanently disabled and may only lose consciousness or
experience amnesia briefly after the impact. The incidence of severe injury causing prolonged loss of consciousness or
requiring surgical intervention is very low, and sports injuries rank far behind motor vehicle accidents and falls as causes
of fatal head injuries.
Mild closed head injuries commonly are referred to as concussions, and traditionally this term has excluded anatomic
disruption of brain tissue. Rather, there is a transient, physiologic disruption leading to a brief loss of consciousness or
amnesia surrounding the traumatic event. However, studies have demonstrated that even these mild injuries can cause
profound long-term behavioral or cognitive deficits that severely limit the victim's ability to perform in sports, in school, or
at work (15).
More severe trauma can cause injuries of various types to the soft tissues surrounding the skull, fractures of the skull,
blood clots between the skull and the brain, or damage to the brain itself. The types of injuries sustained depend on the
mechanism of injury and, in the case of low-velocity injuries, on the location of the impact on the skull. Therefore,
knowledge of the mechanism and location of the injury can help the physician to anticipate the type and severity of
damage that might follow the accident.
Hematomas and focal contusions that produce a mass effect and require immediate surgical intervention are much more
common after low-velocity blunt trauma to the head, such as occurs with falls or assaults. In contrast, head injuries
caused by motor vehicle accidents are more likely to involve diffuse injury to the brain with brain swelling but often do not
cause hematomas or other focal mass lesions requiring surgery. With high-speed motor vehicle accidents in particular,
the injury often has a prominent rotational component. Because the cortex of the brain is more dense than the underlying
white matter, severe rotational forces cause disproportionate acceleration of these two layers, leading to shear injuries at
the gray-white interface. This kind of injury leads to diffuse brain swelling and is often neurologically devastating, but it
usually does not lead to large hematomas that require emergency surgery.
Blunt trauma can cause a contusion, abrasion, or laceration of the scalp. The scalp is composed of five layers: the skin,
subcutaneous fibrous tissues, the galea aponeurotica, loose areolar tissue underlying the galea, and the pericranium
attached to the outer table of the skull ( Fig. 49.1). A blunt injury of the scalp can rupture the small vessels within it, and
the blood from these vessels tends to dissect into the plane of least resistance, the loose areolar tissue under the galea.
Therefore, a soft, sometimes boggy area of the scalp found after blunt trauma usually represents a subgaleal hematoma.
In the frontal scalp regions, blood can dissect this plane down to the periorbital soft tissues and cause periorbital
ecchymoses. Patients with large frontal subgaleal hematomas should be forewarned that they can expect to have “black
eyes” in several days.
FIGURE 49.1. Layers of the scalp and meninges.
Trauma to the scalp should raise the suspicion of an underlying skull fracture, which should be investigated
radiographically. Skull fractures can occur either over the convexity of the skull or through the skull base. Low-velocity
blunt trauma is more likely to cause convexity fractures, whereas basilar skull fractures usually are caused by
high-velocity acceleration injuries. Blunt trauma to the surface of the head can cause a linear fracture, the edges of which
may or may not be separated. Separation of the fracture edges is referred to as diastasis. When inspecting radiographic
films of the skull for the presence of linear skull fractures, confusion often arises as to which linear markings on the film
represent fracture lines and which are normal sutures of the skull. The coronal sutures frequently are mistaken for skull
fractures. True skull fractures have smooth, sharp edges and not the serrated edges of sutures ( Fig. 49.2). Knowledge of
the normal location of the major sutures also helps in distinguishing them from fractures. As might be expected, linear
skull fractures are most common in the thinnest areas, which include the squamous portion of the temporal bones (lateral
surfaces of the skull).
FIGURE 49.2. Lateral skull radiograph of a linear skull fracture (solid arrow). The sharp edges of the fracture contrast
with the serrated edges of the coronal suture (arrowhead) and the meandering, blurred appearance of normal vascular
markings (open arrow).
The single most important feature of a linear skull fracture is its location relative to major venous sinuses or arteries that
lie adjacent to the inner table of the skull. Convexity fractures that cross the midline at the vertex of the skull and
fractures that extend posteriorly and cross the occipital protuberance or nuchal line can disrupt the underlying superior
sagittal sinus or transverse sinuses and thereby cause an intracranial hemorrhage ( Fig. 49.3). Fractures through the
temporal bones anterior to the ear can lacerate the middle meningeal artery or one of its branches, causing a massive
hemorrhage into the space between the inner table of the skull and the dura mater (epidural hematoma) ( Fig. 49.4).
Linear skull fractures per se usually are not significant problems and rarely require surgical repair, but they do indicate a
certain severity of injury. Their presence therefore should raise concern about underlying injuries such as intracranial
hematomas or cerebral contusions.
FIGURE 49.3. Axial computed tomographic image of right frontal and occipital comminuted skull fractures. The occipital
fracture is particularly ominous because it lies over the superior sagittal sinus and may have lacerated it, causing an
intracranial hematoma.
FIGURE 49.4. Typical appearance of an epidural hematoma on an axial computed tomographic image.
Blunt impact to the head also can cause fracture and depression of a skull fragment (depressed skull fracture) ( Fig. 49.5).
If the depressed fragment of bone extends beyond the inner table of the skull, it is likely that the underlying dura has
been torn and that the surface of the brain is contused. Depending on the location of the depressed skull fracture, injury
to the underlying brain tissue can cause neurologic deficits as well as seizures. The depressed fragment often maintains
some continuity with the skull on one side and therefore may maintain some of its blood supply.
FIGURE 49.5. A lateral skull radiograph demonstrating a depressed skull fracture.
Open depressed skull fractures can result from severe blunt head injuries, such as when the head is struck by a hockey
puck or baseball bat. By definition, an open depressed skull fracture involves a depression of the skull with a laceration
of the scalp overlying the depression. An edge of the depressed fragment of skull may lacerate the meninges of the brain
and the brain tissue. Therefore, risks are present for neurologic dysfunction, depending on the area of the brain that is
damaged, and for seizures, because the cerebral cortex has been disrupted. In addition, the scalp laceration opens a
direct route from the contaminated scalp and hair to the depressed bone fragment and cerebrospinal fluid (CSF). As a
result, bone-fragment infection, meningitis, or cerebritis can develop. Patients with open depressed skull fractures require
careful observation and antibiotic treatment to help reduce the risk of serious central nervous system (CNS) infections.
Rapid acceleration or deceleration injuries and some forms of blunt impact can cause fractures through the base of the
skull. The most common basilar skull fractures are those through the cribriform plates of the anterior cranial fossa. These
fractures often are accompanied by laceration of the underlying dura and, if so, result in a CSF communication between
the subarachnoid space and the nasal cavities or paranasal sinuses. Because both of these areas normally harbor
bacteria, this passage is another potential route of CNS infection. In addition, air can enter the cranial cavity through
such a fistula and become trapped, leading to pneumocephalus and producing a mass effect on the brain (tension
pneumocephalus). Fractures through the floor of the anterior cranial fossa frequently extend through the orbital rim ( Fig.
49.6), rupturing small vessels in the overlying soft tissues or causing bleeding from the bone itself. The resultant
bleeding leads to periorbital ecchymoses, commonly called the raccoon sign; this sign is a physical indication of a
possible basilar skull fracture. Other important signs of a basilar skull fracture are CSF leakage from the nose (CSF
rhinorrhea) and profuse bleeding from the nose after blunt head trauma. Fractures through the floor of the anterior cranial
fossa also can extend posteriorly and involve the optic canals, damaging the optic nerves. Most anterior basilar skull
fractures severe enough to cause CSF rhinorrhea also disrupt the olfactory nerves and cause a loss of the sense of
smell.
FIGURE 49.6. Axial computed tomographic image showing multiple fractures through the orbital rims, extending into the
floor of the anterior fossa.
Basilar skull fractures through the petrous bone are less common than those through the anterior cranial fossa, but they
can cause CSF leakage from the ear and a CNS infection. Longitudinal fractures of the petrous bone often continue into
the mastoid eminence, and associated bleeding results in ecchymosis over this prominence (Battle sign). If the fracture
extends into the middle ear (Fig. 49.7), bleeding can cause a hemotympanum, and if the tympanic membrane is
disrupted, a CSF leak through the external auditory canal can develop (CSF otorrhea). In either case, a conductive
hearing loss is common but usually transient. Fractures that traverse the internal auditory canal often damage the
seventh and eighth cranial nerves. Consequently, facial paresis and sensorineural hearing loss may develop, and deficits
thus caused usually are permanent. All patients with a suspected posterior basilar skull fracture based on radiographic
evidence or on the presence of CSF or on blood leaking from the ear should undergo thorough testing of hearing and
facial nerve function.
FIGURE 49.7. A basilar skull fracture involving the petrous bone is seen on an axial computed tomographic image (solid
arrow). The fracture extends into the middle ear (open arrow) and could cause a conductive hearing loss by disrupting
the tympanic membrane or the ossicles of the middle ear. Such a fracture also could cause hemorrhage into the middle
ear cavity, resulting in hearing loss.
In short, the real danger from a skull fracture is not the fracture itself, but rather the risk of a CNS infection with open
depressed or basilar skull fractures and, with any skull fracture, the potential for intracranial hemorrhage or cerebral
contusion. Contusions and hemorrhage are not always apparent on the initial computed tomographic (CT) scan and may
take 24 to 48 hours to develop (Fig. 49.8). It has been estimated that intracranial hemorrhage is 20 times more likely to
occur after a head injury if there is a skull fracture than if not ( 16). Chan et al. studied 418 patients, 11- to 15-year-olds,
who were admitted to their hospital with closed head injuries ( 17). Twenty-six had skull fractures, and an intracranial
hematoma developed in 13 of them, even though at admission 10 of these 26 patients had a Glasgow Coma Scale (GCS)
score of 15 (alert, oriented, following commands). In contrast, no patient without a skull fracture had an intracranial
hematoma. Multivariate analysis of the study population showed that skull fracture was the only significant independent
risk factor predictive of intracranial hematoma in adolescents.
FIGURE 49.8. Intracranial hemorrhage or cerebral contusion is not always apparent on computed tomographic (CT)
images obtained immediately after the injury. These axial CT images were obtained from a patient with a left-sided open
depressed skull fracture at 3 hours (A) and 36 hours (B) after the injury. Note the appearance of a hemorrhagic contusion
underlying the fracture on the later scan.
Posttraumatic hemorrhage inside the skull can occur in several intracranial compartments, which are separated by the
membranes covering the brain, or within the brain substance itself. Between the inner table of the skull and the surface of
the brain are three membranes and three potential or real spaces: the epidural potential space, the dura mater, the
subdural (potential) space, the arachnoid membrane, the subarachnoid space, and the pia mater (see Fig. 49.1). These
membranes and spaces are invested with an abundance of arteries and veins. Rapid acceleration or deceleration, blunt
trauma, or skull fracture can lacerate or rupture these vessels, causing them to bleed into any of the three spaces.
Intracranial hematomas that develop after a severe head injury are described according to their location, either within
these spaces that surround the brain or within the brain or its ventricles. The most common location for posttraumatic
intracranial hemorrhage is the subarachnoid space. A subarachnoid hemorrhage usually can be detected on CT images
of the brain (Fig. 49.9). The most likely cause of subarachnoid hemorrhage is rupture or tearing of bridging vessels in the
subarachnoid space. Posttraumatic subarachnoid hemorrhage usually does not cause permanent neurologic morbidity,
although evidence suggests that there is a risk of vasospasm ( 18,19). Bleeding into the subarachnoid space can cause
headaches and neck pain in the first few weeks after a head injury.
FIGURE 49.9. Axial computed tomographic image demonstrating an acute subdural hematoma (sdh) on the right side,
with herniation of the medial temporal lobe into the tentorial notch (arrowhead). The midbrain is outlined by subarachnoid
hemorrhage in the perimesencephalic cistern (arrows). bs, brainstem.
The most common intracranial hematoma of surgical consequence is the subdural hematoma. These blood clots most
often are seen after relatively low-velocity trauma such as that caused by a fall or an assault. They result from tearing of
larger veins on the surface of the brain or from laceration of the cortical surface after a blow to the head. Subdural
hematomas therefore tend to develop slowly and usually do not cause rapid neurologic deterioration. Often, however,
they cause a mass effect that shifts the intracranial contents to the opposite side. When the shift seems out of proportion
to the size of the subdural hematoma, there may be diffuse swelling of the ipsilateral hemisphere ( Fig. 49.10), and the
injury may be more complicated than just a clot. In such cases, surgery to evacuate the clot is treacherous, because
swollen brain tissue can herniate through the craniotomy site.
FIGURE 49.10. Typical appearance of an acute subdural hematoma (open arrows) on an axial computed tomographic
image. The degree of shift of the midline structures (arrowhead) is greater than the thickness of the subdural hematoma,
suggesting significant parenchymal injury to the hemisphere in addition to the hematoma.
Epidural hematomas occur in the potential space between the dura mater and the inner table of the skull. They usually
are the result of a tear in the middle meningeal artery caused by a skull fracture in the adjacent temporal bone. In the
squamous (lateral) portion of the temporal bone, this artery lies within a groove in the bone ( Fig. 49.11). The artery is
trapped or tethered at this point, and fractures through the temporal bone can easily tear it, leading to an epidural
hematoma. These lesions extend by stripping of the dura mater from the inner table of the skull and form clots that have
a classic lenticular shape on CT images ( Fig. 49.4). Because of their arterial source, epidural hematomas rapidly enlarge
and can cause abrupt neurologic deterioration. However, these hematomas rarely cause damage to the underlying brain,
and their early evacuation often leads to an excellent recovery.
FIGURE 49.11. The middle meningeal artery is tethered in a groove in the temporal bone and is easily lacerated by
fractures through this bone. Hemorrhage from the middle meningeal artery causes an epidural hematoma.
Severe head trauma can disrupt or contuse the brain parenchyma and vessels within the substance of the brain, leading
to intracerebral hematomas or hemorrhagic contusions. The most common sites for these lesions are the anterior
portions of the temporal lobes and the inferior portions of the frontal lobes ( Fig. 49.12). At these locations, the brain
comes in contact with irregular surfaces of the skull ( Fig. 49.13), so that rapid shifts of the intracranial contents more
easily can cause contusions. However, low-velocity blunt force also can cause focal contusions in other areas of the
brain. Depending on the mechanism of the injury, the focal contusion may occur adjacent to the point of impact (coup
contusion) or contralateral to the point of impact (contrecoup contusion). If the head is in motion before impact with a
stationary object, as in a fall, contrecoup damage is usually much more extensive than coup damage. Conversely, if the
head is stationary and sustains a severe blow, contrecoup damage is rare and coup damage severe ( 20).
FIGURE 49.12. Axial computed tomographic image demonstrating hemorrhagic contusions of the inferior frontal lobes (F)
and left temporal lobe (T). The left-sided temporal hemorrhagic contusion also contains air (arrowhead), which was
entrained through an overlying scalp laceration, skull fracture, and dural laceration.
FIGURE 49.13. The floors of the anterior (A) and middle (M) cranial fossae are very irregular, and acceleration of the
inferior frontal and temporal lobes against these surfaces often causes contusions of these lobes.
After very severe injuries, intracerebral hematomas can develop quickly. More often, the hematoma does not appear until
12 to 24 hours after the injury, because the source of the hematoma is located in slowly-oozing small vessels. Large
intracerebral hematomas can cause damage by compressing surrounding tissues or by rupturing into the ventricles of the
brain (intraventricular hemorrhage). In most cases, however, posttraumatic intracerebral hematomas are secondary to
very severe cerebral contusions, which are the immediate cause of the brain damage.
Both intracranial hematomas and severe brain swelling can lead to neurologic deterioration by causing a mass effect and
shifting of the brain. The intracranial contents are divided into three compartments by two semirigid dural
membranes—the falx cerebri and the tentorium cerebelli ( Fig. 49.14). The tentorium cerebelli separates the posterior
cranial fossa from the middle and anterior fossae. A curvilinear notch, Kernohan's notch, provides an opening between
the two compartments, through which the brainstem passes. The midbrain lies within the notch. A second important
dividing structure is the falx cerebri, a dural membrane that separates the two hemispheres of the cerebrum. This
membrane also is incomplete, and a central opening allows passage of the corpus callosum and the third ventricle. The
inferior border of the falx is at the level of the cingulate gyri, which lie just above the corpus callosum.
FIGURE 49.14. Location of the falx cerebri and tentorium cerebelli within the skull.
When a lateral vector of force is produced by a large mass, such as a blood clot or focal brain swelling, there is a
potential for herniation of the brain tissue that is adjacent to the openings in these dural partitions. Masses in the
temporal or inferior parietal lobe can push the medial temporal lobe (the uncus) into the tentorial notch (transtentorial
herniation) (see Fig. 49.9). Such herniation can compress the brainstem and cause unconsciousness, because the
reticular activating system (responsible for consciousness) is located largely in the midbrain. In addition, transtentorial
herniation often causes torsion of the midbrain, from which the third cranial nerve (the oculomotor nerve) emerges,
together with its parasympathetic fibers, which provide pupillary constrictor tone. Midbrain torsion can stretch the third
cranial nerve, causing a third nerve palsy, manifest by a fixed and dilated pupil. Very severe herniation can affect the
third nerve of both sides, whereas moderate herniation affects the nerve only ipsilateral to the herniation. In patients with
a head injury, transtentorial herniation most often results from an acute subdural hematoma, but it also can be caused by
an epidural hematoma or by intracerebral hematomas or severe brain contusion and swelling in the temporal or parietal
lobes. Less commonly, diffuse brain swelling involving large portions of both cerebral hemispheres also can cause a
rostral-caudal vector of force, leading to transtentorial herniation.
Subfalcine herniation—that is, herniation of the cingulate gyri under the inferior border of the falx cerebri—frequently
accompanies acute subdural hematomas or unilateral cerebral swelling. Although the patient usually has no focal
neurologic deficit directly attributable to this type of herniation, it can cause compression of the distal branches of the
anterior cerebral artery.
Herniation of the cerebellar tonsils into the foramen magnum and compression of the medulla oblongata can result from
posttraumatic cerebellar hematomas (Fig. 49.15). Because central control of breathing resides in the medulla oblongata,
this type of herniation can cause apnea. Cerebellar tonsillar herniation also can cause lower cranial nerve dysfunction,
leading to swallowing and speech difficulties. Severe cerebellar injuries are rare after trauma, however; they occur in
fewer than 5% of patients with severe head injuries.
FIGURE 49.15. Axial computed tomographic images demonstrating a hemorrhagic contusion of the right cerebellar
hemisphere (A) associated with a fracture through the floor of the posterior fossa on the right side (B).
Primary Versus Secondary Injury
Trauma to the head causes mechanical deformation of the brain, which can result in various degrees of physiologic and
anatomic disruption of brain tissue, depending on the severity of the impact. Disruption of brain tissue that occurs at the
time of the impact is called primary brain injury. If it is severe enough, the patient can die within minutes or hours after the
injury. Although most patients who are comatose after head trauma do not have severe primary brain injury, many still
succumb within days or weeks after the incident. Often, brain swelling and ischemia develop, followed by brain death.
Brain injury that occurs after the traumatic event is referred to as secondary brain injury. Whereas severe primary brain
injury generally is considered irreversible, secondary brain injury may be treatable and reversible. The existence of
secondary brain injury and the potential for effective intervention are supported by several lines of evidence. Povlishock
demonstrated that some types of structural brain damage previously thought to result from the impact, such as diffuse
axonal injury, actually do not appear until 24 to 48 hours after impact and probably are caused by potentially reversible
metabolic consequences of secondary brain injury ( 21). In addition, many patients with a severe head injury have a
relatively lucid period before neurologic deterioration sets in, suggesting that much of the brain injury does not occur at
the time of impact but is the result of later events occurring in the brain.
Local or regional ischemia is the most likely cause of secondary brain injury. Graham et al. found ischemic cell changes
to be common in patients who died after a severe head injury ( 22). Moreover, my colleagues and I have documented
abnormally low cerebral blood flow in patients during the first 4 to 6 hours after a severe head injury ( 23), and studies of
cerebral oxygen extraction and lactate production indicate that such low blood flow reflects ischemia ( 24). Ischemic cell
damage, at least in part, represents an excitotoxic lesion caused by enhanced release and/or diminished uptake of
glutamate or related excitatory amino acids. Normally, glutamate is cleared rapidly from the synapse after its release, but
during ischemia the glutamate concentration at the synapses surrounding the focal ischemic lesion can be increased for
sustained periods. The toxic action of this and related excitatory amino acids is caused mainly by enhanced calcium
influx into the cell. High intracellular levels of calcium initiate several biochemical reactions that ultimately lead to the
production of free radicals. Ionized intracellular calcium is a catalyst for the arachidonic acid cascade and lipid
peroxidation and interrupts normal oxidative phosphorylation. The metabolic byproducts of these reactions are free
radicals. Free radicals are toxic to cell membranes and cause their disruption ( Fig. 49.16). They also may disable
autoregulatory mechanisms of the cerebral vessels, leading to vasodilation and cerebral hyperemia. The end result is
brain swelling, which can cause increased intracranial pressure, compromised cerebral blood flow, and further brain
damage or brain death.
FIGURE 49.16. The progression of major neurochemical and physiologic events thought to be responsible for secondary
brain injury.
The discovery and characterization of these biochemical events that occur within the first few hours after injury and
leading to brain swelling have provided a number of opportunities for therapeutic intervention. A clinical study
demonstrated that administration of high doses of methylprednisolone, a free radical scavenger, in the first 24 hours after
CNS (spinal cord) trauma led to an improved neurologic outcome ( 25). Ongoing clinical studies are evaluating other free
radical scavengers, such as 21-aminosteroids and superoxide dismutase. Clinical investigators also are studying the
efficacy of treatment to reduce the extracellular concentration of excitatory amino acids (moderate hypothermia), the
blockade of the membrane-bound receptors mediating calcium entry into the cell (MK-801, naloxone), and the blockade
of the arachidonic acid cascade with nonsteroidal antiinflammatory agents. Results of this research should be available
within the next 2 to 3 years. Rather than any individual measure, however, the optimal treatment for secondary brain
injury probably will be some combination of these therapies. It also is anticipated that various types of brain injuries will
respond better to different combinations of therapies.
TREATMENT
Prehospital Treatment
The initial treatment of patients with head injuries depends largely on the severity of the injury. Nevertheless, several
principles apply regardless of severity. The most important of these is that attention must be focused on the entire
individual, and not just the CNS. In most sports-related head injuries, victims have only a brief loss of consciousness from
which they recover rapidly. Persons who have no neck or back pain and no major injury elsewhere may be allowed to
walk. To estimate the duration of pretraumatic and posttraumatic amnesia, injury victims should be asked about the
incident, with special attention given to their recollection of the events immediately before and immediately after it
occurred. They also should be asked several questions to determine their level of orientation and attention span (e.g.,
their name and address, the date, where they are) and their short- and long-term memory (e.g., the names of the
president and vice-president, a description of a recent event). In addition, calculation abilities should be tested by asking
the victim to subtract 7 from 100 and then to continue subtracting 7 from each subsequent answer. Finally, abstract
thinking should be tested, for example by asking what the patient would do if he or she were in a crowded theater and
smelled smoke. Many of these questions, particularly the serial 7s, provide information about attention span as well as
calculation and other abilities.
Responses to these questions also provide a quick estimate of the victim's response time, ability to function
independently, and general ability to perform on the playing field. Problems in responding to these questions suggest that
the patient may not be able to function well and should not be allowed to return to play until the sensorium has cleared. In
many cases, this occurs within 10 to 15 minutes and activity may be resumed.
Those who are unresponsive for longer than 5 minutes have a more severe head injury; their evaluation and treatment
must proceed rapidly and systematically. The first priority is to establish and maintain adequate breathing, including
intubation if necessary. Intubation of an unresponsive patient with a head injury can be difficult and should be performed
only by someone experienced in the necessary technique. The presence of a cervical spine fracture should be
presumed; therefore, the patient's neck must not be hyperextended to facilitate intubation.
Blind nasotracheal intubation usually is the safest intubation technique when cervical spine instability is suspected, but
orotracheal intubation occasionally can be accomplished without extending the neck. If the first responders are not
comfortable with these intubation techniques, the patient with respiratory distress is often best treated by bag-valve-mask
ventilatory assistance until more experienced personnel arrive or the patient has been transported to an emergency
department. Portable pulse oximetry equipment is becoming widely available and provides immediate information about
the adequacy of ventilation.
While emergency resuscitation is underway, the cervical spine should be immobilized by a second person, who applies
gentle axial traction to the head. Angular movement of the neck must be avoided in the patient who is comatose or
complains of neck pain. If the athlete is wearing a helmet, the helmet should be left in place until arrival at an emergency
care facility. A facemask, if present, may need to be removed to provide adequate access to the airway. If this cannot be
done without removing the helmet from a patient who is in respiratory distress, the helmet can be removed if one person
supports the patient's neck and applies gentle axial traction while another person manually distracts the sides of the
helmet and slides it off. Bolt cutters, if available, should be used on the facemask.
The next priority is the patient's blood pressure. Venous access always should be established as soon as possible for
obtunded patients, preferably by inserting a large-bore (14- to 16-gauge) catheter in a large arm vein. Measurement of
the blood pressure or assessment of skin color and capillary refill time provides vital information. If the patient is
hypotensive (systolic blood pressure less than 90 mm Hg), 500-mL boluses of isotonic saline should be given as rapidly
as possible. Pressure dressings should be applied to any site of active bleeding. Posttraumatic hypotension never is
caused by an intracranial hemorrhage and most commonly is caused by intraabdominal hemorrhage.
These basic principles of hemodynamic and pulmonary resuscitation are included in this chapter on head injuries
because hypotension and hypoxia occurring immediately after the injury are important causes of permanent brain
damage and can undermine any neurosurgical attempts to treat patients with severe head injuries. Because the injured
brain is particularly vulnerable to ischemia, permanent neurologic deficits often can be avoided if adequate cerebral
perfusion and oxygenation are restored soon after a head injury.
After the airway and blood pressure have been attended to and the spine has been immobilized, the patient's neurologic
status can be assessed and scored according to the GCS ( 26,27). This score can be obtained quickly and provides
important information about the patient's neurologic status in a convenient shorthand that can be transmitted to
neurosurgeons and emergency medicine physicians at the receiving hospital. The overall GCS score ranges from 3 to 15
and is composed of points assigned as follows: motor response, 1 to 6; verbal response, 1 to 5; and eye-opening
response, 1 to 4 (Table 49.2). The highest scores in each category are assigned when the patient can comprehend and
respond appropriately to verbal requests; the lowest scores, when there is no response even to painful stimuli. Testing is
an active process: the tester must provide verbal stimuli and, if the patient does not respond, must apply painful stimuli in
the form of a sternal rub or supraorbital pressure. When there is asymmetry of right and left eye opening or of motor
scores, the side with the best scores is used for calculating the GCS.
TABLE 49.2. GLASGOW COMA SCALEa

The size and reactivity of the patient's pupils also should be observed. Normally, pupils are 3 to 7 mm in diameter,
depending on the ambient light, and they constrict briskly in response to direct light. A pupil that does not respond to light
or is larger than 8 mm in diameter may indicate transtentorial herniation of the medial temporal lobes caused by an
intracranial blood clot or cerebral contusion. However, 20% of the population may normally appear to have asymmetric
pupils, and 5% have measurable differences of 1 to 2 mm ( 28). Therefore, if the patient is alert and awake, the finding of
asymmetric pupils after a minor head injury usually does not indicate significant intracranial injury.
If a patient has a GCS score of 9 to 15, the brain injury usually is not severe and is unlikely to require surgery. For those
with a GCS score of 8 or less, the probability of a surgical intracranial mass lesion is much higher. This group of severely
injured patients almost always benefits from early endotracheal intubation. If the patient's neurologic status remains
stable, the ventilatory rate should be approximately 12 breaths per minute. Those who deteriorate during transport should
receive ventilatory assistance at a rate of 20 to 25 breaths per minute to help reduce intracranial pressure. Elevated
intracranial pressure, often from a mass lesion such as a hematoma, is a common cause for progressive neurologic
deterioration after a head injury, and hyperventilation is a rapid and effective technique for reducing intracranial pressure.
However, because ischemia is so common immediately after a head injury and hyperventilation (more than 12 breaths
per minute) exacerbates cerebral ischemia by causing cerebral vasoconstriction, its use is not recommended for
neurologically stable patients.
Patients who have severe head injuries causing prolonged loss of consciousness should be transported as quickly as
possible to the emergency department of the nearest trauma center. Trauma centers are those hospitals that are capable
of dealing with all aspects of trauma care and have a surgeon in house at all times. Such hospitals also should have
neurosurgical and orthopedic support available within 10 to 15 minutes after the patient arrives. Many states in the
United States have established mechanisms for systematic evaluation and designation of trauma centers, and patients
with severe head injuries are best served by rapid transport to such centers. Stopping at a nearby emergency department
not equipped to deal with trauma is usually appropriate only if the patient does not have a severe head injury or if airway
or hemodynamic instability persists despite field resuscitation efforts.
Specific indications for transport to a trauma center include either the loss of consciousness or retrograde amnesia
lasting longer than 5 minutes. Both of these are associated with a significant risk of intracranial hematomas. A victim of a
head injury who has any of the following signs or symptoms also should be taken to an emergency room: neck or back
pain; disorientation or confusion lasting longer than 15 minutes; an intense headache; blurred vision or diplopia; a focal
neurologic deficit (weakness, numbness); a scalp laceration; or discharge of CSF or blood from the nose or ears. Those
who have neck or back pain should be kept immobile during transport. Paramedical personnel should be involved as
quickly as possible; such personnel should be skilled in providing intravenous access, administering sedative
medications, and intubating patients. Those with neck or back pain who are agitated must be sedated to be adequately
immobilized. Occasionally, this requires intubation. If protective head gear is present, it should be left in place until the
patient is evaluated in an emergency department, unless it significantly compromises the airway or causes difficulties in
protecting the airway or intubating the patient.
Steroids have not been found to be beneficial for patients with head injuries and are not recommended. Many
investigators have reported finding no improvement in the rate of good recovery with the use of steroids ( 29,30 and 31).
Although steroids reduced the mortality rate in some studies, careful analysis of those studies suggests that the only
additional survivors were patients in a persistent vegetative state who otherwise would have died.
Emergency Department Management
Once the victim of a head injury has arrived at the emergency department, the advanced trauma life support protocol for
initial assessment and stabilization ( 32) is recommended. The primary survey includes airway assessment and
stabilization, assessment of breathing with treatment of respiratory distress, and stabilization of the blood pressure.
Sources of internal or external hemorrhage are sought and controlled rapidly. The spine remains immobilized until these
immediate, life-threatening problems have been addressed adequately. The secondary survey involves a more detailed
clinical and radiographic assessment of the patient, including a neurologic examination and a CT scan of the head. Once
the patient's neurologic status has been evaluated thoroughly, a systemic neuromuscular-paralyzing agent often is given
to calm an agitated but seriously injured patient so that good-quality imaging studies can be obtained. When patients with
unstable spine fractures are agitated, such medication also can prevent them from seriously injuring themselves. If the
CT scan reveals a surgical intracranial mass lesion such as a subdural or epidural hematoma, the patient is taken
immediately to the operating room to undergo a craniotomy and evacuation of the mass. Not infrequently, neurosurgeons
and general surgeons operate simultaneously on a patient who has serious cranial and abdominal or thoracic injuries.
The need to elevate depressed skull fractures depends somewhat on the severity of the depression. If the depressed
bone does not extend beyond the inner table of the skull, there is no evidence that elevation of the fracture reduces the
risk of seizures or of a permanent neurologic deficit. If there is an overlying scalp laceration (open depressed skull
fracture), reports suggest that elevation of the depressed fragment also does not reduce the risk of infection, provided
that the scalp wound had been debrided, thoroughly irrigated, and closed ( 33,34).
For patients who have severe open depressed skull fractures in which bone fragments penetrate the meninges and/or the
brain, operative debridement and elevation of the bone fragments are advocated. However, the purpose of these
measures is not to reduce the risk of seizures or neurologic deficits; the risk of these complications is determined by the
severity of the underlying brain injury and is not increased by the presence of the depressed bone fragment. Rather,
when bone fragments are depressed through the meninges and into the brain, the risk of infection is increased and
cannot adequately be prevented with scalp debridement and antibiotics.
In all cases of open depressed skull fracture, I advocate the prophylactic use of antibiotics (a cephalosporin and an
aminoglycoside) for 10 to 15 days and anticonvulsants (carbamazepine or phenytoin) for 6 months.
The next priority is to identify spinal injuries. Anteroposterior and lateral radiographs are obtained of the entire spine if
the patient is comatose or of the spinal areas where there is pain in the awake patient. In addition, an open-mouth
odontoid view of the cervical spine is obtained. Because the cervical spine is injured in 5% to 10% of all patients who
suffer a severe head injury, the obtunded patient must be assumed to have an unstable spine until spinal injury is
radiographically disproved. Cervical spine injuries account for 50% of all traumatic spine injuries, and manipulation of an
unstable cervical spine can lead quickly to irreversible quadriplegia. Therefore, every effort must be made to identify
cervical spine fractures as soon as the patient is stable.
Evidence supports the following protocol for radiographically clearing the cervical spine ( 35). Three cervical spine views
are obtained: lateral, anteroposterior, and open-mouth odontoid views. The lateral view must reveal the entire cervical
spine from the occiput to the upper border of the T-1 vertebra. Axial CT scans are obtained through any areas where the
plain films indicate a possible fracture. Patients who have a short neck or large body habitus that precludes obtaining
radiographs of the lower cervical spine should undergo axial CT scanning of the lower cervical spine instead. If the
patient is awake and complains of severe neck pain but findings on all of the previous radiographs and CT scans are
normal, flexion and extension lateral cervical spine radiographs also should be obtained. If no abnormalities are found on
these films, the cervical spine can be considered stable. When a patient has a neurologic deficit referable to the cervical
spine and radiographs do not show a dislocation of the vertebrae, further evaluation with magnetic resonance imaging
(MRI) or myelography must proceed immediately to exclude the possibility that there is soft tissue compression of the
spinal cord. Such soft tissue compression may be caused by a herniated disc or an epidural hematoma, and immediate
surgical removal of such lesions may prevent permanent neurologic deficits in patients with incomplete spinal cord
injuries.
Intensive Care
Once the life-threatening issues have been addressed and emergency surgery has been completed, patients with severe
head injuries should be admitted to an intensive care unit capable of comprehensive physiologic monitoring. The nursing
staff should be experienced in identifying subtle signs of neurologic deterioration and should perform a neurologic
assessment at least every 60 minutes for the first several days after the injury. The detailed medical treatment of the
patient with a severe head injury is outside the scope of this chapter, but its primary goal is to prevent secondary brain
injury. Because regional cerebral ischemia is the most likely cause of secondary brain injury, every effort is made to keep
the cerebral perfusion pressure higher than 60 to 70 mm Hg. Cerebral perfusion pressure is defined as the difference
between mean arterial pressure and intracranial pressure; it is important to maintain an intracranial pressure lower than
15 to 20 mm Hg and a mean arterial pressure greater than 90 mm Hg.
Hyperventilation traditionally has been used to help reduce intracranial pressure, but evidence suggests that it often can
exacerbate the problem of regional cerebral ischemia. The reduction in the partial pressure of carbon dioxide caused by
hyperventilation results in vasoconstriction and a reduction in cerebral blood flow. If the brain already has critically
reduced blood flow, this further reduction could lead to ischemia or infarction. Therefore, hyperventilation should not be
used prophylactically for patients with severe head injuries and that it be used only when absolutely necessary to control
intracranial pressure, and then only for brief periods.
The injured brain also is very sensitive to hypoxia, hypotension, hyperthermia, and hyperglycemia. Every attempt should
be made to maintain an arterial oxygen partial pressure value greater than 96 mm Hg, a mean arterial pressure greater
than 90 mm Hg, and a core body temperature lower than 38°C. Glucose-containing intravenous solutions should not be
used during the first 24 to 48 hours after injury, and the serum glucose level should be maintained at less than 200 mg
per dL, with insulin administration if necessary.
MILD HEAD INJURIES
The most common head injuries encountered in athletic competition are collisions that cause a concussion. These
injuries do not cause prolonged loss of consciousness, and the victims usually can function normally soon after the
impact. Ommaya and Gennarelli observed that the level of consciousness and the presence and extent of pretraumatic
and posttraumatic amnesia were associated with the likelihood of subsequent disability. They devised a grading system
for the severity of concussion which, with modifications from Cantu and Kelly, is widely accepted by major athletic
organizations ( 36,37,38 and 39) (Table 49.3). A grade I concussion is defined as mild, temporary confusion after impact
with no loss of consciousness and 5 to 15 minutes of posttraumatic amnesia. The patient may have a dazed look and
some unsteadiness of gait, but all symptoms subside within 15 minutes after the injury. If the athlete has posttraumatic
amnesia lasting 30 minutes or longer but no or only a very brief period of loss of consciousness, the concussion is
considered grade II. A grade III concussion is characterized by loss of consciousness for longer than 5 minutes and
posttraumatic amnesia lasting for longer than 1 hour. The higher the grade of the concussion, the greater the likelihood
that the victim will not be able to function normally, either in the game or otherwise, for an extended period after the
injury. More importantly, those with a grade III concussion are at increased risk for a surgical intracranial mass lesion.
TABLE 49.3. GRADES OF CONCUSSION
The more severe grades of concussion also carry the greatest likelihood of postconcussion syndrome, although at least
one study found no clear relationship between the duration of posttraumatic unconsciousness or amnesia and the onset
of postconcussive symptoms (40). Postconcussion syndrome is characterized by a constellation of symptoms that
includes headaches, inattentiveness, vertigo, gait unsteadiness, emotional lability, sleep disturbances, intermittent
blurring of vision, and irritability. Not all of these symptoms are apparent in every patient, and symptoms may not emerge
until several weeks after a mild head injury. They can last for several months or even several years in some instances,
but they are rarely permanent. In one study, 90% of 114 adults with minor head injuries experienced one or more of the
described symptoms after their injury, but the symptoms lasted an average of only 2 weeks ( 41). This study also
suggested that hospitalization may have prolonged the symptoms and did not reduce their incidence or severity. Patients
with postconcussion syndrome often are suspected of feigning their symptoms for purposes of secondary gain, but in
most cases the symptoms do not subside even after compensatory damages have been awarded to the victim ( 40).
The etiology of postconcussion syndrome is poorly understood. The symptoms are particularly difficult to treat and can
be quite disabling, not infrequently precluding the return to school or work. A minority of patients benefit from treatment
with tricyclic antidepressants or b-adrenergic blocking agents. The best approach in particularly severe cases of
postconcussion syndrome is to enroll the patient in a multidisciplinary treatment program that includes physiatrists,
physical therapists, psychotherapists, and pain specialists. Such programs usually are available through local
rehabilitation hospitals.
There is increasing evidence that even mild head injuries can lead to both measurable deterioration of subtle cognitive
functioning and electrophysiologic abnormalities. In addition, structural disruption of brain tissue has been detected on
MRI studies performed days or even months after such injuries. In most cases, particularly with the less severe injuries,
these abnormalities are reversible. However, after relatively severe injuries, especially those that involve prolonged loss
of consciousness, subtle alterations in attention, memory, and the speed of processing information may last for 10 to 20
years and endure long after the level of intelligence has normalized (as measured by conventional psychometric tests
such as the Wechsler intelligence scales) ( 42). One of the most extensive studies of psychological deficits caused by
mild head injury was reported by Gronwall and Wrightson in 1974 ( 43). They studied patients aged 17 to 25 years who
had suffered a mild closed head injury and had had no previous concussion. Compared with age-matched, uninjured
control subjects, psychological testing revealed that trauma victims had a slower rate of information processing and an
increased central processing time but were not significantly more distractible. Most patients, especially those with the
least severe injuries, recovered normal function after 4 weeks. Subsequent studies have shown that both attentional and
information processing deficiencies are common after mild closed head injuries. Reaction time typically is slowed, an
impairment that is most prominent under complex conditions and during the first month after the injury ( 44). Pretraumatic
abilities usually return within 3 months after the injury ( 45). Long-term recovery from cognitive deficiencies has been most
closely correlated with the severity of impairment during the first few days after the injury ( 46).
Several studies have demonstrated abnormalities in cerebral electrical conduction after minor head injuries. Tysvaer and
Storli studied 69 soccer players, a group of athletes who often use their head to hit the ball as a routine part of the game.
They found a significantly higher incidence of electroencephalographic abnormalities in this group than in age-matched
control subjects, the greatest incidence occurring in the youngest players ( 47). Gorke and Schmidt performed
visual-evoked potentials in 50 children who had had mild head injuries. Although none had lost consciousness from the
injury, 36% had significantly prolonged latencies, which usually returned to normal within 2 to 3 months ( 48). Abd al-Hady
and coworkers studied brainstem auditory-evoked potentials in 40 adults with mild head trauma and found
high-frequency conductive and sensorineural hearing losses in 20% ( 49). They also found a significant increase in the
absolute wave V latency and in wave III–V interpeak latency in these patients. Among 15 adults with mild head injuries,
Podoshin et al., demonstrated that such abnormalities were usually temporary and that brainstem conduction latencies
had returned to normal 2 months after the injury ( 50). They concluded that the reversibility of the evoked potential
abnormalities supported the hypothesis that transient ischemia rather than structural or axonal damage cause the
symptomatic abnormalities associated with a mild head injury.
MRI provides much more sensitive imaging capabilities than does CT scanning. Yokota et al. compared MRI and CT
findings for 134 victims of mild head trauma (initial GCS scores, 13 to 15) ( 51). Almost half of the patients were studied
within 6 hours after their injury, and all within 3 days. Parenchymal lesions of the brain were detected in 34 of the 134
patients by MRI but in only 9 patients by CT. Most of the lesions demonstrated by MRI but not by CT were in the cerebral
cortex. The significance of such lesions is unclear, however. In my experience most of the lesions detected on acute MRI
studies of patients with mild head injury no longer are visible on MRI scans obtained 3 months later. Because MRI is
particularly sensitive to edema (52), the lesions seen on MRI and not on CT images during the first few days after injury
probably represent very small contusions magnified by the presence of surrounding edema. Any structural or permanent
damage is probably minimal in such cases.
Neuropsychological Testing After Mild Head Injury
The most common neuropsychological deficits caused by mild head injury include impaired attention and concentration,
distractibility, memory loss, problems with executive functioning, posttraumatic amnesia, and posttraumatic stress
disorder. Of these impairments, short-term memory loss is one of the most common complaints of victims of mild
traumatic brain injury: as many as 60% of these patients have short-term memory problems at some point after their injury
(53,54).
Numerous tests are available for defining general neuropsychological impairment (e.g., Halsted-Reitan
Neuropsychological Battery, Luria-Nebraska Neuropsychological Battery) and specific cognitive deficits ( 55). One of the
most common tests used to assess the degree of posttraumatic amnesia is the Galveston Orientation and Amnesia Test
(56). This test can be administered within 10 minutes by nursing staff and has been shown to have excellent interrater
reliability. Many of the other neuropsychological tests take much longer and must be administered by a skilled
neuropsychology technician.
A common difficulty with the application and interpretation of neuropsychological tests in athletes is the lack of
information about their premorbid capabilities. In some cases, it cannot be determined whether cognitive deficits
observed after injury were caused by the recent injury, by past head injuries, or by other factors. Many tests depend, to
some extent, on the patient's premorbid intellectual abilities. In high school athletics, gauging preinjury mental status is
less problematic since the intellectual capabilities of those students tend to be relatively similar. Among college and
professional athletes, however, premorbid intellectual capabilities are far more heterogeneous. Several clinicians have
developed and used a brief neuropsychological evaluation for preseason neuropsychological testing of all professional
and college athletes. Results of these tests can be placed in the athletes' personal files and can be used to determine the
extent of any new injury caused by concussions during the season and the extent of recovery from those concussions.
Return to Play
Familiarity with the pathophysiology of mild head injuries can help to determine when a player should be allowed to
return to the game. The degree of neurologic impairment within the first few hours after the injury is one of the best
predictors of cognitive function several months later. Impaired cognition is manifested primarily as a slowing of both
information processing and reaction time, the latter being particularly severe in complex situations. Therefore, it is not
surprising that the likelihood of a second injury is increased by returning the player to the game too soon after an initial
mild head impact. A mild head injury, particularly for athletes, increases the risk of sustaining future head injuries. One
study of high school football players found a fourfold risk of head injury among those who had suffered a previous mild
head injury (1). Moreover, neuropsychological deficits after a second mild head injury have been shown to last longer
and to be more severe than those caused by the first ( 57).
The risk of a second injury if an athlete resumes play too soon after an initial head injury, and the risk of prolonged or
permanent neurologic impairment with multiple mild head injuries during a single season, have led several groups to
develop practical guidelines for when an athlete might be allowed to return to play ( 37,39) (Table 49.4). These guidelines
arbitrarily prescribe a period of time during which athletes should be kept out of competition, the duration of which varies
depending on the severity of the initial injury and the presence of single versus multiple injuries. The guidelines account
for the fact that those with more severe grades of concussion and those who have more than one concussion during a
single season should be kept out of competition for longer periods. They are relatively conservative and are intended to
aid coaches, trainers, and physicians in developing their own policies. Each athlete must be considered individually, and
these guidelines may not apply in specific cases. They should not be considered standards, because they have not been
subjected to a prospective clinical trial.
TABLE 49.4. GUIDELINES FOR RETURNING TO PLAY
It is emphasized that no athlete should be allowed to return to competition until he or she is completely neurologically
asymptomatic and without headache. All players should undergo a thorough neurologic evaluation immediately after their
injury and again immediately before being allowed to resume play. Mental status testing should include tests of
orientation, concentration, and memory. Commonly used tests of concentration include asking the athlete to repeat lists
of numbers in reverse order or to name the months of the year in reverse order. In addition, external provocative tests are
recommended. They might include having the athlete do a series of push-ups or sit-ups or run a 40-yard sprint, and then
retesting for cognitive deficits ( 58). In some instances, the changes in catecholamines or cerebral blood flow caused by
such provocative tests evoke neurologic symptoms that were not present when the athlete was sitting or lying down but
might recur when the athlete is in competition.
SUMMARY
Although sports and recreational activities cause far fewer head injuries than do motor vehicle accidents, those that do
occur are often more debilitating than injuries elsewhere in the body. The prevention of head injuries must be a concern
of all those involved in sports, including players, coaching staff, and trainers. It is recommended that, during particularly
high-risk sports such as football and boxing, protective headgear should be worn at all times. It is also recommended that
authorities in schools, professional athletic organizations, and communities regularly monitor the incidence of head
injuries in the various sports, updating rules and regulations as needed. At the present time, these recommendations
seem particularly urgent for activities such as bicycle riding and ice hockey.
Preparations should be made in advance of organized athletic competition for rapid evaluation and triage in the event of
a head injury. The coach, team trainer, or team physician must be well versed in the principles of advanced trauma life
support and immediately available to direct the proper care of the athlete from the moment of injury. In the field, emphasis
should be placed on establishing or maintaining hemodynamic and respiratory stability and on immobilizing the cervical
spine if the injured party is rendered unconscious or is complaining of neck pain. All victims of head injury who remain
unconscious, confused, or disoriented should be taken to the emergency department of the nearest trauma center as
soon as possible. The same recommendation applies to those who have persistent headaches, nausea, vomiting, or
focal neurologic deficits.
Most sports-related head injuries do not cause prolonged unconsciousness. Players who experience only brief confusion
or who are temporarily dazed may be allowed to resume play 10 to 15 minutes after the injury, but only after the coach or
team trainer has carefully assessed the player's mental status and has determined that the player is completely alert and
oriented in all spheres. Both those supervising and those participating in sports should be aware that the speed of
information processing typically is slowed after a minor head injury and that the likelihood of further injury is increased by
a first injury. The possibility of posttraumatic symptoms such as prolonged headaches, dizziness, memory loss, and
emotional lability also must be considered. However, such symptoms never should be ascribed to posttraumatic
syndrome until the patient has had a thorough neurologic evaluation, usually including a CT or MRI scan of the head.
Neuropsychological testing may be very helpful in documenting the severity of subtle cognitive deficits caused by a minor
head injury. Such testing also can be used to guide the determination of when to allow the athlete to return to play. The
role of MRI in this regard is not yet clear. Although MRI is more sensitive than CT in detecting small parenchymal brain
injuries, as yet there is no documented correlation between these small injuries and subsequent neurologic capabilities.
ACKNOWLEDGMENT
The author gratefully acknowledges the editorial assistance of Helene Marion in the preparation of the manuscript.
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50 Treatment of Sports Eye Injuries
50
TREATMENT OF SPORTS EYE INJURIES

ROBERT G. DEVENYI
ROBERT C. PASHBY
THOMAS J. PASHBY
Assessing an Eye Injury

Minimum Equipment Needed by Team Physicians and Trainers
Examining the Injured Eye
Types of Eye Injuries and their Management
Soft Tissue Injuries
Foreign Bodies on the Surface of the Eye
Hyphema
Choroidal Injuries
Macular Injuries
Retinal Injuries
Rupture and Avulsion of the Optic Nerve
Corneal Injuries
Injuries to the Lens
Traumatic Glaucoma
Orbital Fractures
Ruptured Globe
Contact Lenses
Common Eye Infections
Infections of the Eyelids
Conjunctivitis
Conclusion
Chapter References
The eye accounts for only 0.002% of the body's surface area and 0.10% of the erect frontal silhouette, yet it is the victim
of 1% of sports-related injuries ( 1,2). In 1985, there were an estimated 32,433 sports and recreational product–related
eye injuries treated in emergency rooms. By 1994, the estimate had grown to 43,659. These estimates do not include
athletes treated in training rooms or physicians offices ( 3).
It has been estimated that the actual number of sports and recreational ocular injuries could be two or more times greater
when including all medically attended games ( 4).
The incidence of eye injuries varies with the country and sport. In the United States, baseball is responsible for the most
eye injuries in children younger than 15 years old. Basketball and football are the sports most commonly associated with
injury in the 15- to 24-year-age range, and racquet sports in the population over 24 years. However, in Canada and
Sweden, ice hockey is the most dangerous sport. In Ireland, it is hurling. In England, Australia, and New Zealand, it is
racquet sports (5).
Injured eyes require immediate assessment and early treatment. Ideally, every eye injury deserves treatment by an
ophthalmologist or a medical doctor who is familiar with using the ophthalmoscope and able to interpret the finding of an
intraocular examination.
However, the optimum treatment is not always immediately available. Often, the athletic trainer or team physician must
deal with the injured player. Therefore, it is extremely important that these people understand the anatomy and
physiology of the eye, the means of testing and assessing central and peripheral vision, and the equipment required to
examine and treat minor eye injuries.
This chapter presents guidelines to enable trainers and team physicians to examine the eye and recognize minor ocular
injuries they can handle, injuries that require ophthalmologic care, and injuries that demand immediate, on-the-spot
treatment before the person is sent for specialist care.
In addition to familiarizing themselves with the present material, athletic trainers and medical personnel should be aware
of more detailed texts (6) and should avail themselves of management courses that include study of the eye. The need
for physicians who practice sports medicine to serve as instructors in such courses is obvious.
ASSESSING AN EYE INJURY
Minimum Equipment Needed by Team Physicians and Trainers
Probably the minimum equipment (Fig. 50.1) necessary to perform an eye examination is as follows:
Vision card
Penlight
Sterile fluorescein strips
Sterile eye pads
Eye shields
Tape
Sterile cotton-tipped swabs
Sterile irrigating solution
FIGURE 50.1. This display shows probably the minimal equipment necessary to examine the injured eye in an
emergency.
Examining the Injured Eye
A routine ocular examination is necessary to determine the seriousness of an eye injury. A penlight is used to obtain an
oblique illumination of the eye that may indicate damage to the conjunctiva, cornea, anterior chamber (the area bounded
by the cornea and the iris-lens diaphragm), pupil, iris, and lens ( Fig. 50.2 and Fig. 50.3). The following procedure is used:
FIGURE 50.2. The eye is shown in sagittal section.
FIGURE 50.3. This view demonstrates the eye in relationship to its surrounding structures.
1. Inspect the lids and brow for lacerations, bruising, and hematoma.
2. Inspect the conjunctival sac for hemorrhage, laceration, and foreign bodies. Eversion of the upper eyelid often
shows a foreign body that can easily be brushed away. Displaced contact lenses are often found by this means.
3. Examine the cornea for any foreign body, abrasions, or lacerations. Abrasions are well outlined by fluorescein dye,
which is applied by pulling the lower lid downward and then dipping a sterile fluorescein strip into the pool of tears
in the lower fornix.
4. Assess the clarity and depth of the anterior chamber and compare with the other eye.
5. Compare the size, shape, and light reaction of the pupil in the injured eye with the other eye.
6. Compare the iris colors of each eye.
7. Test visual acuity using a reading card or newspaper and compare with the uninjured eye. It is useful to know the
patient's vision in each eye with glasses or contact lenses before injury. Vision less than 20/40 should be referred.
8. Test peripheral vision (confrontation perimetry) by having the patient fix on the examiner's nose and, after occluding
the other eye, having patient identify the number of fingers held up in all fields of gaze ( Fig. 50.4). A normal minimal
visual field extends 85° temporally, 65° downward, 60° nasally, and 45° upward. Any person with a loss of visual
field must be referred for specialist care.
FIGURE 50.4. Peripheral vision is being tested by confrontation perimetry.
9. Assess ocular movements by asking the patient to look to the right, then upward, then downward, similarly to the
left, up and down (the six cardinal positions of gaze). With both eyes moving together, there should be no diplopia
(double vision) when a light is held in the primary position and the six cardinal positions of gaze. Any double vision
must be referred for specialist care.
10. Compare the eyes to determine whether the injured eye is sunken, making the palpebral aperture narrower, or
proptosed, in which case the aperture would be enlarged. A fracture of the orbital floor results in enophthalmos (a
sunken eye), while a retrobulbar hemorrhage causes proptosis (a pushing forward of the eye).
If a medical doctor is available, an intraocular examination should be performed with an ophthalmoscope to identify
damage to the lens, vitreous, and retina.
After the eye examination is completed, a decision must be made regarding management. Always err on the side of
caution. If there is any doubt about the seriousness of the injury, make sure the patient is seen by an ophthalmologist as
soon as possible.
Turrif and Gerali have suggested that referral to ophthalmology should be automatic after a blow to the eye if any of the
following signs or symptoms are noted:
1. Blurred vision that persists after blinking

2. Symptoms of retinal detachment, that is, flashing lights, partial or complete loss of the visual field in conjunction
with floaters or flashing lights
3. Pain that is sharply stabbing or deeply throbbing
4. Signs and symptoms of possible structural damage to the orbit or eye muscle entrapment such as double vision or
one eye moving less than the other
5. A visible foreign body in the eye or sensation of a foreign body
6. Damage to the eyelid with abnormal function including a cut or tear
7. Cuts, scratches, or punctures
8. Swelling of an eye
9. Abnormal shape or size of a pupil
10. A hyphema
11. Subconjunctival hemorrhage (7)
Filipe et al. ( 8) in a prospective study on 84 consecutive patients with sports-related eye injuries noted that the severity of
the anterior segment injury was not a good predictor of posterior segment damage. Of 45 patients presenting with a
hyphema, 24 were found to have a vitreous or retina lesion. However of the 39 patients without a hyphema, 13 still had a
vitreous or retinal injury. It was their opinion that even a black eye should be evaluated by an ophthalmologist.
Forcing the Injured Eye Open
To examine an injured eye, it is necessary to have the eye open. However, the injured person may have an obviously
lacerated eyelid or present with pain, lacrimation, and blepharospasm that make opening the eye and its examination
difficult. If these symptoms are severe, it is better not to force the lids open, because this could cause further damage.
Such patients should have a sterile eye pad applied and be transported to hospital for ophthalmologic care.
The reverse is the case with chemical burns (Fig. 50.5), as for example, from lime on the playing field. Such injuries
demand immediate treatment by forcibly opening the eye, removing any solid particles with a cotton-tipped swab, and
irrigating the opened eye with copious amounts of water (at the very minimum a quart and for at least 5 minutes). If water
is not available, soda pop or Gatorade can be used. While this is being done, another person should notify the nearest
emergency facility, describing the type of injury and giving the patient's name. The patient must be transported to hospital
with the eye uncovered. A chemical burn is an emergency and must be treated at once.
FIGURE 50.5. Lime burns occasionally result from the chemical contact on the playing field.
TYPES OF EYE INJURIES AND THEIR MANAGEMENT
In personal experience of over 3,800 eye injuries associated with sports ( 9,10,11 and 12), the incidence of the various
types of eye injuries was as follows: soft tissue injuries, 34%; hyphemas, 27%; other intraocular injuries, 23%; corneal
injuries, 9%; orbital fractures, 4%; ruptured globes, 3%. Approximately 11% of these injuries rendered the eye legally
blind (20/200 or less).
Orbital Hemorrhage
Orbital hemorrhage (black eye) ( Fig. 50.6) may occur after blunt trauma to the orbital region. Proptosis of the affected
eye, associated with hemorrhage into the lids and beneath the conjunctiva, and restriction of ocular movement may
occur. If the hemorrhage is severe, the vascular supply to the optic nerve and retina may be shut off, causing visual loss.
It is urgent that ophthalmologic consultation be sought immediately. During transport, an ice pack should be applied and
the head kept elevated.
FIGURE 50.6. The left eye has sustained a contusion and an orbital hemorrhage.
Any soft tissue lid injury should be assessed before extreme swelling ensues, which would preclude a proper examination
of the globe. Such an examination includes visual acuity and fields; pupillary size, shape, and reaction; iris color; and
tests for diplopia. Any foreign body in the eye must be identified and recorded.
Lid Lacerations
Lid lacerations ( Fig. 50.7) may be caused by sharp objects, blunt trauma, or objects that catch the lid and actually tear it.
Bleeding is controlled by direct pressure, allowing the extent of the laceration to be assessed. Lacerations through the lid
margin require meticulous surgical repair for proper cosmetic results and the prevention of subsequent tearing.
Lacerations or punctures of the upper or lower lid should be repaired by an ophthalmologist, who will clean the wound
thoroughly, explore for foreign material, and make anatomic closure of muscle and skin layers. Lid tissues that may
appear to be irreparably jeopardized, with respect to blood supply, should not be discarded but repaired. A sterile eye
pad is applied before transport to control bleeding and prevent infection.
FIGURE 50.7. Such a lower lid laceration (arrow) may occur from a hockey stick blow.
Lacerations of the Lacrimal Apparatus
Medial lacerations of the upper or lower lid usually involve the lacrimal drainage system ( Fig. 50.8). The canalicular
laceration is best repaired by an ophthalmologist using a microscope. Do not repair the lid laceration but refer the person
for canalicular repair immediately.
FIGURE 50.8. The right lower lid laceration involves the lacrimal system.
In case of severe eyelid trauma, the eyelids may become disinserted from their attachments of the medial or lateral
orbital margins. Reattachment of the ligaments to the bone is necessary for good functional and cosmetic results.
With lid lacerations, as with any wound, general considerations must be remembered, namely control of bleeding with
sterile gauze, assessment of globe damage, application of a sterile eye pad, and general tetanus prophylaxis. The
importance of examining the globe cannot be stressed enough, and for this reason, any significant injury in the region of
the eye should be assessed by an ophthalmologist. Remember, it is much easier to examine the globe before lid swelling
occurs.
A record must be kept of visual acuity, visual fields, the presence or absence of diplopia, and intraocular findings.
Conjunctival Injuries
In minor lacerations of the conjunctiva, suturing is not necessary. A search for and removal of any dirt particles or other
foreign material must be carried out. An eye pad is applied for 24 hours, and a follow-up examination is made at that
time.
Foreign bodies often lodge just under the margin of the upper eyelid ( Fig. 50.9). Eversion of the eyelid will reveal their
presence, and removal is usually achieved by wiping with a moist cotton-tipped swab. The team physician should be
familiar with the procedure of everting the upper eyelid ( Fig. 50.10).
FIGURE 50.9. The patient is told to look down while the examiner grasps the upper lid lashes, pulling them away from the
eye while at the same time exerting counter pressure backward with a cotton swab at the upper border of the tarsus. The
upper lid is then readily everted.
FIGURE 50.10. Eversion of the upper lid of the right eye has exposed the foreign body.
Foreign Bodies on the Surface of the Eye
Foreign bodies on the ocular surface are a common problem on the playing field. They are commonly lodged under the
upper eyelid ( Fig. 50.10).
To examine the area, the upper eyelid must be everted by having the patient look down with both eyes open; then, the
upper lid lashes are grasped and the lid is pulled away from the eyeball. Counterpressure on the upper lid with a
cotton-tipped applicator will evert the lid (the lashes are rolled over the cotton-tipped swab) ( Fig. 50.9). The foreign body
can often be wiped away with a moist cotton swab. It helps to have inserted a drop or two of local anesthetic solution into
the eye beforehand [tetracaine (Pontocaine) or proparacaine (Ophthetic)].
Hyphema
Hyphema is a collection of free blood in the anterior chamber of the eye. It is the most common intraocular injury
associated with sports, occurring in 27% of injured eyes in the authors' series. This percentage may seem high; however,
all reported injuries required ophthalmologic care. The person rendering initial treatment must be familiar with its
appearance.
At the time of injury, a hyphema appears as a haze in the anterior chamber. The iris looks somewhat muddy in color
compared with the fellow eye, and the pupil is usually irregular in shape and sluggish in reaction to light. Vision is
somewhat blurred. With rest, the blood settles to form a level in the anterior chamber ( Fig. 50.11), unless bleeding
continues; in which case, blood fills the chamber to create an “eight ball” eye. Most hyphemas clear in a few days, but in
about 15% of cases, a secondary hemorrhage occurs, usually between 2 and 5 days after the initial injury. The reason for
such recurrent hemorrhage is thought to be retraction of the original clot, causing additional bleeding of the vessels
injured at the time of the initial injury. The bleeding typically comes from torn vessels within the “angle” of the eye.
Secondary bleeding is typically much more severe than initial bleeding.
FIGURE 50.11. This hyphema or blood in the anterior chamber resulted from a contusion to the eye ball.
All hyphemas require ophthalmologic care. They must be recognized and must be referred. Treatment, although
controversial, usually entails hospitalization with limited ambulation to promote rest, avoidance of aspirin containing
products, as well as eyedrops to reduce inflammation (steroids) and to prevent dilatation and constriction of the pupil,
which could cause secondary bleeding (cycloplegics). In most cases, the blood settles down and forms a level in the
anterior chamber, which absorbs in a matter of 4 or 5 days, depending on the amount of blood. The use of tranexamic
acid and aminocaproic acid, agents that reduce the risk of recurrent hemorrhage, have become routine ( 13).
These patients need lifelong follow-up for the possible development of glaucoma and retinal detachment. Acute
glaucoma occurs in up to 25% of patients ( 14). Late glaucoma occurs in association with postcontusion deformity of the
angle in approximately 10% of patients ( 15).
A player with a hyphema should refrain from exercise for approximately 2 weeks, during which time he or she needs to be
under the regular supervision of an ophthalmologist.
Choroidal Injuries
Choroidal injuries result from a blunt, compressive blow to the front of the eye. A split occurs in the choroid, and if this
split involves the central macula (the “fovea”), central visual acuity is typically permanently lost ( Fig. 50.12).
FIGURE 50.12. This choroidal tear resulted from a blow to the eye such as occurs in racquetball players.
Such injuries occur because as the eye is compressed, from an anterior to posterior direction, the choroidal vessels are
stretched and, as a result, torn. The result, acutely, is hemorrhaging beneath the retina, with a central blind spot, and
central visual acuity loss. Over time, typically 3 to 5 weeks, as the hemorrhage is absorbed, central acuity slowly returns,
if the actual rupture in the choroid does not pass through the central fovea.
Such injuries need to be followed by an ophthalmologist. The injured player cannot return to action until the central acuity
returns.
Macular Injuries
Macular edema (Berlin edema or commotio retinae) can occur as a result of a severe concussive injury to the globe and
an anteroposterior force. Central vision is seriously affected. Often, this edema resolves over several weeks, with return
of vision. However, the macular swelling may result in the formation of a macular cyst that may rupture, causing a
macular hole (Fig. 50.13). Such holes can often now be repaired with modern vitreoretinal surgical techniques (e.g., pars
plana vitrectomy with membrane peeling and air–fluid exchange). However, glaucoma may occur in up to one third of the
eyes that have had vitrectomy–lens extraction. ( 6).
FIGURE 50.13. Trauma caused this hole in the retina at the site of the macula.
Retinal Injuries
Intraretinal hemorrhages are common with blunt injury to the eye ( Fig. 50.14). They are typically not of visual
significance, unless they involve the central macular region. With such injuries, however, one needs to be concerned that
a retinal tear has occurred. Retinal tears can lead to retinal detachment ( Fig. 50.15), with associated sudden and severe
visual loss. Trauma can also cause a disinsertion of the anterior most aspect of the retina (“retinal dialysis”), which can
also lead to retinal detachment.
FIGURE 50.14. Such a retinal hemorrhage may result from a blow to the eye by an opponent's elbow in a basketball
game.
FIGURE 50.15. This pathologic lesion of retinal detachment is not too uncommon in boxers.
Early recognition and treatment (e.g., with laser or cryotherapy) of retinal tears and dialyses is essential, because such
treatment can usually prevent retinal detachment ( 16). For this reason, eye injuries associated with any direct impact to
the globe need to be referred to a qualified ophthalmologist, for a detailed, dilated retinal examination, with scleral
depression. If a player complains of “flashing lights” interfering with his or her vision, this is very suggestive of traction by
the vitreous on the retina and the need to be promptly examined for the possibility of retinal tears. If a player complains of
a “dark curtain” in the visual field, this is very suggestive of a retinal detachment and the need to be promptly referred to
a vitreoretinal surgeon.
Retinal detachments require immediate surgery ( 17). Any sudden, painless loss of vision, accompanied by a loss of
visual field suggests a retinal detachment. When the retina is detached, the retina is separated from the majority of its
blood supply, and therefore, the nerve cells within the retina degenerate. Therefore, it is necessary to diagnose and
surgically correct a retinal detachment as soon as possible to minimize the degree of damage to the nerve cells of the
retina. The sooner such surgery can be performed, the more likely is the person to regain better vision in the eye.
Rupture and Avulsion of the Optic Nerve
A severe, direct blunt injury to the eye may rupture the optic nerve where it enters the eye. One injury, which was
personally seen by the author, resulted in immediate blindness to an eye kicked by a boot. This is an unusual but very
severe injury for which there is no chance of visual recovery.
Corneal Injuries
Corneal injuries cause lacrimation, photophobia, and blepharospasm. There is sudden onset of sharp pain.
Foreign bodies ( Fig. 50.16), if they are superficial, can either be brushed off using a moist, sterile cotton-tipped swab or
irrigated off using a sterile irrigating solution. If they are not easily removed, a sterile eye pad may be applied, and the
person taken to the hospital for removal, using the slit lamp and a sterile needle or spud. After removal, a firm eye pad is
applied for 24 hours, at which time, a follow-up examination is carried out.
FIGURE 50.16. While sliding into second base, a baseball player occasionally gets a corneal foreign body in his eye.
Corneal abrasions produce similar symptoms ( Fig. 50.17) and can be outlined with fluorescein, which stains the denuded
area green. After determining that no other eye problem exists, a sterile eye pad is applied for 24 hours, and then a
follow-up examination is conducted.
FIGURE 50.17. Corneal abrasions occur in contact sports as the elbow or padded thighs brush against the player's eye.
Corneal lacerations are accompanied by severe pain with tearing, photophobia, and blepharospasm ( Fig. 50.18). If the
eye can be opened easily, the pupil will be seen to be irregular, the anterior chamber shallow, and the iris adherent to or
prolapsed outside the wound ( Fig. 50.19). Do not forcibly open the lids because this will cause further damage.
Immediate ophthalmologic treatment is necessary. A sterile eye pad and shield should be taped in place ( Fig. 50.20) and
the patient transported to hospital for repair.
FIGURE 50.18. A blow to the cornea may cause more than an abrasion with a true tear or laceration of the cornea.
FIGURE 50.19. With more severe trauma of the eye, there may be an iris prolapse.
FIGURE 50.20. After examination and first aid, the eye may be covered with the pad and eye shield in place.
In case of corneal injury or any other ocular injury, a record must be kept of visual acuity, fields of vision, and diplopia (if
present) as well as intraocular findings, if possible.
Injuries to the Lens
The lens can be injured by blunt trauma causing concussion that results in cataract formation. This may occur
immediately or after a few days, weeks, or even months. In mild cases, the iris, driven forcibly against the anterior lens
capsule, leaves a circular mark like that of a rubber stamp on the anterior lens capsule. This is readily seen as the pupil
dilates. As a rule, this type of blow does not lead to cataract formation.
More severe blows can cause a rupture of the lens capsule allowing aqueous (the clear fluid in the anterior chamber of
the eye) to enter, causing the lens to become cataractous. Localized cataracts may develop after a blow without capsular
rupture. Such opacities often take the form of a rosette in the subscapsular areas of the lens ( Fig. 50.21).
FIGURE 50.21. A severe blow has caused a localized cataract, resulting in a rosette effect.
Blunt injury may cause the lens zonule to rupture so that the lens loses its moorings. If the entire zonule ruptures, the
lens becomes dislocated and may disappear into the vitreous or even migrate forward to appear in the anterior chamber.
If only part of the zonule ruptures, subluxation occurs, and the lens will shift away from the zone of zonular rupture ( Fig.
50.22).
FIGURE 50.22. This lens has been dislocated by a direct blow to the eye.
Treatment of cataracts entails removal of the cataractous lens and restoration of visual function using a contact lens.
Some professional athletes have continued their careers under these circumstances. Direct injury to the lens, after
penetrating wounds of the cornea, is common. The lens material is removed at the time of corneal repair. Injuries to the
lens must be recognized by the person performing the initial evaluation and referred for ophthalmological care.
Traumatic Glaucoma
Following blunt injury to the eye, the intraocular pressure may rise and fall, swinging between hypertension and
hypotension for a few days, before settling back to normal. In such cases, there is usually no permanent structural
damage within the eye. However, blunt injury may damage the anterior chamber angle, resulting in a split of the ciliary
body with deepening of the angle and interference with aqueous outflow.
Glaucoma develops in 10% of cases of split angle: It may occur soon after injury or even many years later. Problems of
this type should be followed by an ophthalmologist, who can monitor intraocular tensions, because the development of
glaucoma is usually insidious, causing damage to the optic nerve without the patient being aware of anything happening.
Any loss of peripheral vision (field loss) resulting from glaucoma cannot be restored. A dislocated lens is another cause
of secondary glaucoma; in this case, it is necessary to remove the lens for control of intraocular pressure.
Secondary glaucoma is common with hyphema, especially with secondary hemorrhages. Irrigation of the anterior
chamber and removal of the blood clot are indicated. Should the intraocular pressure remain high with blood in the
anterior chamber, not only is the optic nerve in danger but blood staining of the cornea may occur ( Fig. 50.23). Even
when the intraocular pressure is controlled, the blood staining remains, taking years to absorb.
FIGURE 50.23. Such blood staining of the cornea may be slowly absorbed.
Orbital Fractures
Orbital fractures are usually sustained by blunt trauma. The most frequent is a fracture of the orbital floor caused by blunt
trauma to the eye. This forces the eye back into the orbit, thereby increasing the orbital pressure and causing a “blow
out” of the thin, weak orbital floor. One may see limitation of ocular movement, especially on elevation ( Fig. 50.24),
because of entrapment of the inferior ocular muscles in the fracture. Enophthalmos ( Fig. 50.25), owing to orbital tissue
herniation into the maxillary sinus, is usually evident. Diplopia is also commonly present, being more marked on upward
and downward gaze.
FIGURE 50.24. A blunt orbital floor trauma resulted in a fracture and left inferior rectus muscle entrapment with double
vision.
FIGURE 50.25. Note the narrowing of the left orbital fissure due to escape of orbital contents through the orbital floor
fracture into the maxillary sinus.
Ophthalmologic examination of the globe and investigation of the fracture with x-ray studies are mandatory but not an
absolute emergency. At times, the entrapped muscle can be freed by forcibly elevating the eye with forceps after topical
anesthesia. If this is not possible, surgical exploration may be necessary, as may the insertion of a Teflon support along
the orbital floor to cover the fracture.
Additional orbital fractures may occur in the maxilla or other portions of the orbital rim. These injuries often can be
diagnosed by direct palpation and must have appropriate x-ray and clinical evaluation. Fractures of the roof necessitate
neurosurgical assessment, with the ophthalmologist being a consultant.
Fracture into one of the sinuses often allows air to leak into the orbital cavity, which produces crepitus (a crackling
sound) when finger pressure is applied on the swollen area. The air and fracture are readily demonstrated on x-ray study.
Resolution without surgical intervention is usual ( Fig. 50.26), but prophylactic antibiotic treatment is a good idea.
Williams et al. ( 19) retrospectively reviewed the incidence and outcome of fractures about the orbit in the National
Football League. They identified 41 facial fractures in 41 players from 1980 through 1997. The most common signs and
symptoms were decreased visual acuity (74%) and decreased eye movement (42%). The most common mechanism—a
digital poke (74%). Fifteen athletes underwent surgery. Ultimately, 16 players were able to return to full football activity
(19).
FIGURE 50.26. There has been resolution of the fracture into one of the sinuses without surgical intervention.
Ruptured Globe
Ruptured globes (Fig. 50.27) usually result from contact with a hockey stick or puck, a golf ball or club, a ski tip, a squash
ball or racquet, a tennis ball, or a baseball. They are usually caused by high-velocity, low-mass missiles. Rupture can
also occur when a slower moving, high-mass object, such as a fist or large ball, strikes the eye with a glancing blow. This
type of rupture usually occurs near the limbus, where the sclera is thinnest. Most of these injuries result in enucleation
(9).
FIGURE 50.27. A severe glancing or direct blow to this right eye has resulted in a rupture globe.
A direct blow on the front of the cornea by an object larger than the orbital opening is more likely to produce a blow-out
fracture. When ruptured, the globe will appear soft or collapsed and sunken in the orbit. Such an eye must be gently
covered with a sterile eye pad and shield, and the patient must be transported directly to the hospital for ophthalmologic
repair.
Contact Lenses
In the 1940s, scleral contact lenses were custom made for a National Hockey League player. These lenses cleared the
cornea and rested on the sclera. The corneal cup was filled with a balanced salt solution before insertion. However, this
solution tended to cloud during play, and fresh solution was required between periods of the hockey game. These lenses
were difficult to make and somewhat uncomfortable.
Late in the decade, hard corneal lenses became available. They were easier to fit and insert but also more easily
displaced after a blow. They might also migrate down into the lower fornix or more commonly up under the upper lid ( Fig.
50.28A). The displaced lens could either be removed by irrigating with sterile eye solution or lifted off by applying a small
suction cup.
FIGURE 50.28. A: The contact lens has been displaced upward and laterally by a blow to the eye. B:Traumatic hockey
injury resulted in this split of the hard contact lens.
A hard contact lens has been known to split in two halves from a blow in a hockey game ( Fig. 50.28B) with resultant
corneal abrasion but no permanent visual defect. At times, small foreign bodies could become trapped under these hard
contacts, scratching the cornea, causing much pain and preventing continuation of play.
In the 1960s, soft contact lenses became available. They were more comfortable but more fragile and required nightly
disinfection and cleaning to prevent bacterial and fungal growth. They did not dislocate easily from the cornea and they
sealed out foreign bodies because of their larger size and snugly fitting edge. There was no spectacle blur on switching
to regular glasses as had commonly been the case with hard contacts. Soft contacts were usually replaced every 6 to 12
months because of the buildup of tear deposits.
A wide range of soft hydrophilic lens materials became available with higher water content and greater oxygen
permeability. The very thin, high water content lenses were approved for extended wear, but experience showed that this
regimen led to a substantial increase in ocular infections.
Recently, disposable soft contact lenses have become available and can be recommended. They are available in powers
up to 9 diopters of myopia and will compensate for up to 2 diopters of astigmatism. The Canadian cost is approximately
$12.00 per pair. They are discarded after 1 week of wear. Because of their high water content, they are very comfortable,
and because they are discarded after 1 week of wear, there is no problem with protein deposits on the lens. They are
easy to insert and remove.
The advantages of contact lenses over regular glasses include improved peripheral field of vision and less tendency to
be displaced; in addition, they do not fog. It must be stressed, however, that they provide no protection against injury.
Safety glasses or other types of eye protection must be worn when risk of a direct blow to the eye is increased.
COMMON EYE INFECTIONS
Bacterial and viral infections of the external eyes and lids are frequently contagious and can be passed from one
individual to others. Individual wash cloths and towels should be used to prevent spread of the infection. Warm
compresses four times daily, followed by sulfacetamide or broad-spectrum antibiotic drops, are needed for 5 to 7 days
until the infection clears.
Contact lenses must not be worn while an eye infection is present.
Infections of the Eyelids
Blepharitis is a low-grade chronic infection of the eyelid margins usually due to Staphylococcus aureus. The eyelids are
red and often scaly and sticky, particularly on awakening. Scrubbing the eyelid margins with a clean moist face cloth or
with baby shampoo–soaked cotton-tipped swabs and then applying an antibiotic ointment at bedtime is indicated.
Hordeolum, or styes, are infections in the eyelash follicles causing redness, swelling, and pain. Warm compresses and
antibiotic drops are indicated. Staphylococci are the usual cause.
Chalazions occur with a blockage of the meibomian glands of the eyelid, forming a granuloma. Swelling, redness, and
pain in the lid proper is the rule. The chalazion may point toward the skin but usually points backward toward the eye
causing a foreign body sensation. It is better seen by everting the lid, unless too painful. Warm compresses and
antibiotic drops are indicated, plus the addition of systemic antibiotics, if severe or with involvement of the preauricular
gland. When they are persistent, surgical incision and curettage are indicated.
Conjunctivitis
Conjunctivitis of bacterial or viral origin is contagious. The eye is red (called pinkeye), often photophobic, and sticky
discharge is present. Warm compresses four times daily, followed by the instillation of antibiotic drops is indicated for 5
to 7 days, or until the infection subsides.
Allergic conjunctivitis causes swelling, redness and itching. Tearing is present but without sticky discharge. Treatment
with systemic antihistamine tablets and antiallergy eyedrops afford relief. ( Table 50.1 lists commonly used eyedrops.)
TABLE 50.1. COMMONLY USED EYEDROPS
CONCLUSION
In conclusion, it may be noted that eye injuries incurred during sports participation have been recorded over the past 20
years by Canadian ophthalmologists, with 4,136 sports eye injuries recorded to date (October 1993), including 456 blind
eyes (Table 50.2). It is estimated that 90% of these injuries could have been prevented had the participants worn
available certified eye protection.
TABLE 50.2. EYE INJURIES IN CANADIAN SPORTS
CHAPTER REFERENCES
1. Hornblass A. Eye injuries in the military. Int Ophthalmol Clin 1981;21(4):121–138.

2. Tolpin HG, Vinger PF, Tolpin DW. Ocular sports injuries. Economic considerations. Int Ophthalmol Clin 1981;21(4):179–201.
3. Jeffers JB. Sports related eye injuries. Pennsylvania Medicine 1996;(Suppl):76–83.
4. National Society to Prevent Blindness. 1993 eye injuries associated with sports and recreational products F509. Schaumberg, IL:1993.
5. Napier SM, Baker RS, Sanford DG. Public health and the eye. Surv Ophthal 1996;41:229–244.
6. Newell FN. Ophthalmology: principles and concepts, 8th ed. St. Louis, MO: Mosby, 1996.
7. Turrif TW, Gerali PS. Don't play games with your eyes. J Ophthal Nurs Tech 1991;10:82–83.
8. Capao Filipe JA, Battos H, Castro-Correia J. Sports related ocular injuries: a three-year follow-up study. Ophthalmology
1997;104:313–318.
9. Pashby TJ. Eye injuries in Canadian hockey. Phase III: older players now at most risk. Can Med Assoc J 1979;121:643.
10. Pashby TJ. Eye injuries in Canadian hockey. Phase II. Can Med Assoc J 1977;117:671.
11. Pashby TJ, Bishop PJ, Easterbrook WM. Eye injuries in Canadian racquet sports. Can Fam Physician 1982;28:967.
12. Pashby TJ, Pashby RC, Chisholm LDJ, et al. Eye injuries in Canadian hockey. Can Med Assoc J 1975;113:663–674.
13. McGetrick JJ, Jampol LM, Goldberg MF. Aminocaproic acid decreases secondary hemorrhage after traumatic hyphema. Arch Ophthalmol
1983;101:1031–1033.
14. Read J and Goldberg MF. Comparison of medical treatment for traumatic hyphema. Trans Acad Ophthalmol Otolaryngol 1974;78:799.
15. Wilson FM. Traumatic hyphema, pathogenesis and management. Ophthalmology 1994;87:910.
16. Antaki S, Labelle P, Dumas J. Retinal detachment following hockey injury. Can Med Assoc J 1977;117:245.
17. Haynie GD, D'Amico DJ. Scleral bucking surgery. In: Albert DM, Jakoviec FA: Principles and practice of ophthalmology, Vol. 2.
Philadelphia: W.B. Saunders, 1994:1092–1110.
18. Diamond GR, Quinn GE, Pashby TJ, et al. Ophthalmologic injuries. Clin Sports Med 1982;1:469.
19. Williams RJ, Marx RO, O'Brien SJ, et al. Incidence and outcome of fractures about the orbit in Professional American Football Players.
Abstract AOSSM 25th Annual Meeting, Traverse City, MI, June 22, 1999:407.
51 Cervical Spine and Spinal Cord Injuries
51
CERVICAL SPINE AND SPINAL CORD INJURIES

ROBERT G. WATKINS
ROBERT G. WATKINS IV
Clinical Anatomy, Signs, and Symptoms

C-3 to C-4 Level
C-4 to C-5 Level
C-5 to C-6 Level
C-6 to C-7 Level
C-7 to T-L Level and Below
Prevention of Burners
Treatment of Burners
Decision Making in Neck Injuries in Athletes
On-Field Discussion
Transportation and Immobilization
Facemask Removal
Helmet Removal
Equipment
Locker Room Decisions
Radiographic Evaluation
When to Do In-depth Studies
Continued Play Decision: Risk Categories
Congenital Abnormalities
Rehabilitation of Neck Injuries
Cervical Stenosis
Types of Stenosis
Measurement of Cervical Stenosis
Factors in Decision Making in Transient Quadraparesis and Spinal Canal Stenosis
Other Factors in Any Continued-Play Decision
Chapter References
In many of today's sports, particularly in contact sports, the neck is at risk for injury because of an inability to pad, brace,
or protect the cervical spine and allow it to maintain its function. The flexibility and motion of the cervical spine must
deliver the head and eyes to the right place at the right time. The function of the spine also includes being a conduit for
the central nervous system, with the spinal cord and the cervical nerve roots passing through, making injury to the neck a
potentially catastrophic event. The incidence of sports-related injuries to the spinal cord in football has been reported by
Clark (1) to be 54% of all spinal cord injuries in school and college athletics. Torg ( 2) has reported on the findings of the
National Football Head and Neck Injury Registry, which was established to document the incidence and nature of severe
intracranial and cervical spine injuries resulting from tackle football. The criteria for inclusion in the Registry are injuries
that require hospitalization for at least 72 hours, injuries of the neck involving fracture subluxation or dislocation, injuries
involving intracranial hemorrhage, or injuries with associated quadriplegia or death. A recent update on the Registry ( 2)
has shown that between 1971 and 1984, there were 1,412 cervical spine injuries meeting these criteria.
The prevention of cervical spine and spinal cord injuries is of paramount importance. The responsibility for educating
athletes in methods to prevent neck injury is most important in those sports in which the risk of trauma to the cervical
spine is the highest. Contact sports, such as football, rugby, and wrestling, have been identified as being particularly
high-risk activities for cervical trauma ( 2). The use of the head as an offensive weapon to block and tackle makes football
a significant source of cervical injuries. Even noncontact sports, such as diving, water skiing, surfing, water polo, and
body surfing, can be responsible for traumatic spinal injuries ( 3). The prevention of neck injuries in athletes involves the
education of players, trainers, and physicians. Prevention of these injuries must incorporate appropriate rule changes for
those sports that are at highest risk. After research by Joseph Torg ( 2) and others proved the role of head contact in
catastrophic injuries of the head and neck in football players in the mid-1970s, the National Collegiate Athletic
Association (NCAA) made rule changes that condemned the use of the head in tackling and effectively outlawed the
technique of blocking and tackling known as spearing. These rule changes have been noted to have had significant
impact on the instance of traumatic cervical spine and spinal cord injuries in football players from the high school through
the collegiate level and up to the professional level ( 2). Also, modification of protective gear to incorporate newly
developed modern materials and equipment into properly fitting shoulder pads and neck pad modifications has
contributed, it is hoped, to decrease incidence of neck injuries in athletes. The treatment of the athlete with neck, cervical
spine, or spinal cord trauma remains one of the most medically challenging of all aspects in sports medicine. There have
been no “miraculous” medical breakthroughs that have made a significant impact on the catastrophic consequences of a
young, active athlete suffering a complete spinal cord injury.
Recently, Braacken et al. ( 4), published their findings of a study of high-dose intravenous corticosteroids administered
immediately after spinal cord injury and its effectiveness on the subsequent neurologic outcome of those patients. They
showed that a 24-hour course of corticosteroids administered within 6 to 8 hours after cervical spinal cord injury may be
associated with an improved prognosis for cervical nerve root sparing and may lead to the cervical spinal cord–injury
patient recovering one to two more cervical nerve root levels. However, even this ray of hope in the treatment of spinal
cord injury is not enough to allow for complacency in the continual goal of the sports medicine community to decrease
further the incidence of cervical spine and spinal cord injuries in athletes.
Football players are at greater risk for cervical injury than are the average adult in the United States. The nature of the
game of football requires violent contact between the head and shoulders of a player and the body of his opponent or the
hard surface of the playing field. Besides protective equipment and educational techniques to enhance the football
player's awareness of the potential for neck injury, several other protective factors can be maximized to decrease the risk
of cervical spinal cord injury in these athletes. Neck-strengthening exercises can build muscle bulk and increase the
protective capability of the thick sleeve of neck and shoulder muscles that surround the cervical spine. The
biomechanical advantage afforded by powerful and bulky neck flexors, extensors, and rotators, as well as massive
trapezius and shoulder girdle musculature, is evidenced in the modern professional football player. This is particularly
true when it is understood that many of the professional football athletes playing today may have narrowed cervical
spinal canals secondary to degenerative changes in the cervical disks and cervical facet joints with hypertrophic bony
encroachment of the spinal canal. Yet, the incidence of catastrophic cervical spinal cord injuries in professional football
players is exceedingly low. By increasing the level of conditioning of the athlete and improvements in balance,
coordination, and skill, the natural and acquired protective actions of the cervical musculature and shoulder musculature
are increased. The likelihood of fatigue causing a diminution of these protective mechanisms is decreased.
The responsibility for teaching and enforcing proper tackling techniques must fall to the football coaches and referees.
Safe tackling techniques must become second nature to the player and must be enforced. Safe blocking and tackling
avoid the use of the head in initial contact. Spearing and the use of the head as an offensive weapon increase the risk of
cervical spine fractures and quadriplegia. Because the rule changes banning the use of the head as a battering ram, the
incidence of quadriplegia in football players has dropped dramatically ( 2). The biomechanics of cervical spine fracture
illustrates that direct head compression, with axial loading and flexion, is a major mechanism of injury fracture or
dislocation of the cervical spine in football players. To resist the loading impact, attacking players straighten out their
cervical spine to a neutral position. The loading on the crown of the athlete's head plus the velocity of body weight
compress the cervical spine. Just as one would buckle a simple soda straw by squeezing the ends between the fingers,
the spine buckles in the middle, and produces an axial loading flexion rotation injury. There is an accordion effect of bone
and ligamentous failure of the cervical column ( 2). This is exactly the injury pattern that may occur to the cervical spine
when the player uses the head as a battering ram, particularly when that player is fatigued, is wearing inadequate
protective equipment, does not have adequate neck strength and muscle bulk, and does not have adequate levels of
overall conditioning.
CLINICAL ANATOMY, SIGNS, AND SYMPTOMS
The cervical spinal cord is housed in the neck by the rigid intercalated spinal motion units. Rigid bony protection against
direct blows as well as protection against axial loading, flexion, extension, and torsional injuries is afforded by the lamina,
spinous processes, facet joints, and vertebral bodies of the cervical spine. However, with axial loading and bending that
surpasses the bony element's biomechanical capability and strength, there may be the resultant fracture, dislocations, or
both. This failure of the bony elements of the spine may cause injury to the spinal cord or cervical nerve roots. The same
may occur when the mechanical limits of the ligamentous and muscular support of the neck are exceeded in traumatic
situations. The spinal cord begins at the cervical medullary junction and extends through the cervical and thoracic spine
to terminate caudally at the L-l to L-2 junction as the conus medullaris. From the conus medullaris, the lumbosacral nerve
roots emanate like a horse's tail, hence the name cauda equina. The lumbar and sacral nerve roots exit the spinal cord
through the corresponding neural foramina. In the neck, the cervical spinal cord produces the cervical nerve roots, which
exit above the named cervical vertebra through the neural foramina. For example, the sixth cervical nerve roots exit the
cervical spinal canal through the neural foraminal formed by the fifth cervical vertebra, cephalad, and the sixth cervical
vertebra, caudally. This relationship between spinal level and root level has important diagnostic and prognostic
implication when an athlete sustains a spinal cord injury. From a surgical viewpoint, the precise anatomic level
corresponding to nerve tissue damage is critical in ensuring that surgical intervention, if warranted, is performed at the
correct level. Prognostically, the potential for functional independence in a quadriplegic patient increases dramatically
with each functioning root level below the fourth cervical nerve root. Clinically, the difference between a C-5–level
quadriplegic and a C-7–level quadriplegic is dramatic. In fact, the recovery of a single additional cervical nerve root level
in a quadriplegic patient can mean the difference between a completely dependent existence and a completely
independent and functional life.
Cervical spine or spinal cord injury has a more favorable prognosis when identification of the injury is made before any
further movement of the injured patient. An unstable fracture or dislocation without neurologic injury has catastrophic
sequelae if improper transportation techniques are used, even if they are performed by well-meaning and concerned
individuals. The player with an unstable cervical spine injury may not be aware of the magnitude of the injury because of
the minimal amount of pain felt by the player at the time of injury. During a game, it is not unusual for the player to shrug
off even the most serious neck injuries as minor because of the minimal symptoms present on the playing field. However,
once the problem is identified as a spinal cord injury, the level of cord injury can be quickly assessed by simple pinprick
sensation testing along the cervical dermatomes and by manual muscle strength testing. The fifth cervical nerve root
supplies sensation to the deltoid region in lateral brachium distally to the elbow. The sixth cervical nerve root supplies the
skin sensation to the lateral forearm from the elbow distally to include the thumb and index finger. The seventh cervical
nerve root supplies the sensation to the upper extremity and the dermatomal pattern that includes the midpalm as well as
the long finger. The eighth cervical nerve root supplies the dermatomal pattern that includes the ulnar border of the
forearm as well as the ring and small fingers. The first thoracic nerve root supplies the dermatomal region medially at the
elbow and proximally up toward the middle part of the arm. It is not unusual for there to be some overlap of adjacent
dermatomes in individuals.
The motor deficits identifiable in cervical spinal cord injury are categorized according to which motor groups are spared.
Remember, the third cervical root exits at the level of the second and third cervical disks. Schneider ( 5) has summarized
the injury levels.
C-3 TO C-4 LEVEL
Injury at the C-3 to C-4 level may result in complete paralysis of the trunk and extremities, with a complete loss of all
normal unassisted respirations due to a paralysis of the diaphragm as well as of the thoracic musculature. A loss of
sensation of pain to pinprick, to a point just below the clavicle, including the upper extremities, may be evidenced.
C-4 TO C-5 LEVEL
Athletes can only shrug their shoulders, indicating trapezius innervation via the second and third cervical nerve roots to
the motor branch of the spinal accessory nerve. The arms, the lower extremities, and trunk will be without movement, with
the toes pointed outward. These patients exhibit only abdominal breathing. The progression of spinal cord swelling or
hemorrhage may occur, particularly if inappropriate immobilization techniques are used, even if only one more segments
toward the head, and may mean the cessation of spontaneous respirations. The motor fibers to the diaphragm through
the phrenic nerve, from the C-3 and C-4 nerve cell bodies, exit from the spinal cord with the upper portion of the C-5 root.
The absence of pain sensation is present to the level of the outer border of the upper extremity between the shoulder and
elbow.
C-5 TO C-6 LEVEL
At this level, players are able to bend their arms at the elbows and they tend to remain flexed in that position unless they
fall downward with gravity. Attempted movements of the hands result in hyperextension at the wrists, with inability to
close the fingers voluntarily. Extension of the arms is markedly impaired. There may be a loss of pain on pinprick over the
region of the thumb and index finger of the hand.
C-6 TO C-7 LEVEL
With injury at this level, athletes are able to close their hands very weakly and grasp with the fingers. The arms can be
flexed and extended weakly at the elbows. They may be unable to spread the fingers apart strongly because of loss of
the intrinsic musculature innervation to the hands. Pinprick sensation is intact over the thumb and index finger, but will
usually be lost over the middle and radial half of the ring finger.
C-7 TO T-L LEVEL AND BELOW
Injuries occurring at the C-7 to T-l junction and below can result in complete sparing of the muscle function of the upper
extremities, with only lower extremity paraplegia resulting. Trunk control, including the control of the rectus abdominis,
internal and external oblique muscles, and the spinal extensor muscles is, however, affected by the level of the thoracic
spinal injury. With a more caudal level of thoracic spinal cord injury, there is an increased ability of the patient to adapt to
activities requiring controlled and coordinated trunk musculature activity. Pinprick sensation is impaired from the
dermatomal level corresponding to the level of injury. Fracture dislocations of the thoracic or lumbar spine are much less
common in the athlete, in part, because of the benefit of protective equipment, such as shoulder pads covering the area.
Also, the thoracic rib cage imparts significant structural support to the thoracic spine. The lumbar spine is more protected
than the neck because of the increasing size and strength of the vertebra and of the surrounding trunk musculature.
Schneider (6) has stressed that these are rather simple tests that are far from a complete neurologic examination and are
meant only as a quick method of determining the level of neurologic injury in a player that is, for example, laying on the
playing field. A very high degree of suspicion must be maintained when examining players injured on the field if there are
indications that a neck injury has occurred. When there are questionable findings or when the examining coach, trainer,
or physician believes that a neck injury has occurred, but the player's complaints include only some vague neck stiffness
or neck pain, or when there are minimal objective findings to support concern, these players should be treated as if they
have a true injury until it can be proven otherwise.
Much more common than complete or incomplete spinal cord injury are the lesions known as burners and stingers. The
characteristic motor and sensory manifestations are thought to be quite common among football players. At least 50% of
college players have experienced a burner ( 7). Cervical nerve root or brachial plexus neuropraxia is considered to be the
etiology of stingers and burners. Such lesions are identified by intense burning pain, accompanied by numbness,
paresthesias, and transient weakness in the arm. The symptoms usually last from a few seconds to 15 minutes. The
symptoms start immediately after head and shoulder contact, usually with the opponent but sometimes after striking the
playing surface. The pain typically involves the entire arm from the fingertips up to the neck and shoulder. Commonly, the
last symptoms to resolve are that of the C-5 or C-6 dermatomal pattern. Players may complain of recurrent stingers and
burners throughout the season and in the off-season. Almost always, when the symptoms are recurrent, the same
dermatomal pattern, the same motor deficit, and the same biomechanical mechanism of injury are present in the
subsequent episodes. However, it is not unusual for a multiroot pattern to be found. Repeated episodes over a season
may result in significant weakness of the deltoid and biceps ( 8). A residual neurologic deficit may persist for days to
months following more severe episodes. Stingers are a very common occurrence in football and other sports. A thorough
understanding of the pathomechanics of the stinger, comprehensive clinical assessment and diagnosis, and a thorough
familiarity with rehabilitation techniques are the key to managing stingers and burners properly.
The mechanism of injury most often seen in professional football players is an off-center axial load that is applied to the
head, with the head uncontrollably forced both into extension and lateral flexion. This forces the head toward the
ipsilateral side of the resultant burner and stinger. Biomechanically, the spinal cord, nerves, and canal respond in a
predictable manner. Extension of the spine produces a slackening of the cord and spinal nerves; whereas flexion
increases nerve tension. Extension decreases the size of the spinal canal and foraminae, and flexion increases the size
of the canal and foraminae. With extension and bending of the cervical spine toward the involved shoulder and arm, the
neural foramina are abruptly narrowed, allowing for the bony walls of the neural foramina, or for an intervertebral disk or
osteophytes to pinch the nerve root and its dorsal ganglion as it exits the spinal canal. The mechanism of injury is
equivalent to the Spurling maneuver ( 9), which is a diagnostic sign that can be elicited in the clinical examination in the
office setting of patients with cervical radiculopathy. The Spurling maneuver consists of extension of the head lateral
bending and rotation of the head and neck toward the painful side. When these maneuvers are performed together, a
positive Spurling sign is identified by pain that is reproduced in the patient's shoulder and arm, identical to the pain that is
the patient's presenting clinical complaint. A positive Spurling test indicates cervical foraminal stenosis due to either soft
disk herniation or osteophytes encroachment of the neural foramina. The ipsilateral rotation and axial loading mechanism
of injury seen with burners implies that the pathomechanics involve multilevel root contusion from narrowing the canal
and foramina. It may be possible to detect a subtle foraminal narrowing at one or more levels on a contrast CT scan.
Other cases may demonstrate profound central canal and foraminal narrowing. There are certainly cases, however, when
complete diagnostic evaluation including magnetic resonance imaging, computed tomography (CT), and
electromyographic (EMG) and nerve conduction studies fail to reveal the source of pathology.
The other possible mechanism of injury in the production of burners and stingers involves an abrupt stretching of the
existing cervical nerve roots or the adjacent brachial plexus. The head is forced away or to the opposite side of the
depressed shoulder and symptomatic arm. There is an increased tautness to the brachial plexus with this mechanism.
Although this mechanism of injury is also associated with transient signs and symptoms, the potential for long-term
neurologic deficit is present, as it is with the pinching mechanism previously described.
Two distinct and useful classification systems of burners and stingers have been described by Seddon ( 9), and Clancy et
al. (10). In Seddon's classification system, neurapraxia is the mildest lesion that has identifiable histologic findings and
corresponds to demyelinization of the axon sheath without intrinsic axonal disruption. Recovery of neural functioning
generally occurs within 3 weeks. Axonotmesis includes disruption of the axon and the myelin sheath with preservation of
the fibrous epineurium. The epineurium serves as a conduit for the regenerating axon in axonotmesis. In most healthy
adults, the rate of recovery in axonotmesis can be expected to be approximately 1 mm per day, with an initial 7-day delay
from the time of injury. This expected rate of recovery is measured from the site of injury to the motor endplate to which
the nerve supplies motor impulses. Neurotmesis corresponds to complete nerve transaction. In neurotmesis, there is
generally no possibility of distal nerve regeneration without surgical repair and reapproximation of the nerve sheath.
Clancy et al. (10) used Seddon's classification system for definition of the burner syndrome from brachial plexus injury.
Grade I injuries had an initial recovery of motor and sensory function generally within several minutes of injury, with a
complete recovery noticed by 2 weeks. These injuries correspond to Seddon's definition of neurapraxic lesions. Grade II
injuries can result in motor loss to the deltoid, biceps, intraspinatus, and supraspinatus muscles. Weakness can last from
weeks to months and corresponds to axonotmesis. Grade III lesions would be quite rare and are more typically seen in
trauma patients who have suffered from penetrating injury to the neck or shoulder region from a motor vehicle accident,
knife fight, gunshot wound, or shrapnel injury from an explosion. Additionally, falling in this classification of injuries would
be the scapulothoracic dissociation injury that is associated with high-energy trauma and results in evaluation and
separation of the shoulder girdle from the thorax. Scapulothoracic dissociation is additionally associated with significant
trauma to the traversing major blood vessels, neurologic structures, and muscular structures. EMG studies show
abnormalities in type II and type III lesions. Generally, patients with grade I neurapraxia do not show EMG or nerve
conduction velocity abnormalities.
The long-term EMG findings have been studied in a group of 20 athletes with burners by Bergfeld et al. ( 11). They
selected a group of players with clinical findings of severe neurologic involvement after athletic injuries that caused
burners or stingers. In the study by Bergfeld et al. ( 11), the EMG findings generally localized to the upper trunk of the
brachial plexus, as well as cervical nerve root and peripheral nerve root levels. This study demonstrated that the EMG
abnormalities lagged behind the motor strength recovery of the individual as the injury resolved. They demonstrated that
utilizing the EMG as a criterion for return to play after a burner or stinger is an inaccurate and ineffective prognostic
measure. We routinely use a precise history of symptoms, a detailed neurologic examination, along with provocative
testing such as the Spurling maneuver to decide on a player's timing for return to play after a burner or a stinger.
Certainly, an appropriate diagnostic imaging workup is included in the evaluation of patients with burners or stingers so
that the underlying pathology can be identified. Especially in the older athlete, a severe first-time burner may be the
symptom of a cervical disk herniation. Under these circumstances, restricting play until the chance of a disc herniation is
eliminated by magnetic resonance imaging (MRI) is a safe procedure.
Examination of the player on the sidelines usually reveals the mechanism of injury by careful questioning and head
range-of-motion testing. Spurling maneuver reproduces the symptoms. The shoulder abduction test, in which the hand is
placed palm down on the top of the head, may alleviate the symptoms somewhat (7). Davidson et al. (12) have observed
a series of patients with cervical myeloradiculopathies due to extradural compressive disease in whom clinical signs
included relief of radicular pain with abduction of the shoulder. The mechanism by which shoulder abduction may relieve
pain from cervical root impingement at the level of the neural foramen was thought to be due to the shorter distance that
the nerve root must traverse and is, thus, under less tension when the shoulder is abducted. The study by Davidson et al.
included two patients who had myelographically proven extradural impingement of the cervical root. Of the patients in the
study by Davidson et al., 68% noted relief of pain with abduction of the affected shoulder. On the field, players with
burners or stingers classically hold themselves with the head forward and flexed posture, and they report a stiff neck. The
arm is too weak to elevate. Attempts to elicit the Spurling sign are generally met with pain. Occasionally, head
compression reproduces the symptoms. Persistent neck pain with head compression may be considered a fracture or
disk herniation until proven otherwise.
Garfin and associates ( 13) have studied the question of whether compressive neuropathy of spinal nerve roots is a
mechanical or a biologic problem. They believe that, pathophysiologically, nerve root pain production is a complex issue.
They have identified clinical and basic science data that suggest that mechanical compression, per se, may not always
be the sole cause of radicular pain and dysfunction. Specifically, they have identified that acute compression of a normal
cervical nerve usually does not cause pain but rather causes numbness, paresthesias, motor weakness, and related
signs and symptoms. They also identified mechanical compression of a normal spinal nerve root, which also seems to
induce similar sensory and motor impairment without associated pain. However, the compression of inflamed nerve roots
and mechanical deformation of inflamed and irritated nerve roots causes pain. This has been proven in neurophysiologic
studies in which the experimental response to the manipulation of normal versus irritated nerve roots has been
dramatically different, indicating that, for consistent reproduction of pain in a nerve root distribution, there is generally an
underlying degree of inflammation and nerve root irritation suggestive of repetitive mechanical deformation of the nerve.
The sources of inflammation, acute nerve compression, and the symptoms of a burner or a stinger are difficult to
correlate. Animal and in vitro studies may fail to simulate the true clinical situation seen in football players.
PREVENTION OF BURNERS
The primary preventive rule for burners is wearing properly fitting shoulder pads. Shoulder pads should accomplish four
basic functions: (a) absorb shock, (b) protect the shoulders, (c) fit the chest, and (d) fix the midcervical spine to the trunk.
The typical shoulder pad ( Fig. 51.1), worn by a professional defensive lineman, is a very soft thin-padded material that
has questionable shock-absorbing properties and fits the chest in a semiarc type of configuration. The fixation to the
chest is less than ideal and allows sliding of the shoulder pads on the shoulder during contact. In order to fit the chest
properly, the pads should be more of an A-frame type, with very rigid, long anterior and posterior panels. The shoulder
pads should fit well to the subxiphoid portion of the chest and fit snugly around the chest. A proper shoulder pad should
encompass many of the characteristics of proper cervicothoracic orthosis. Immobilization of the cervical spine in any type
of cervical orthosis requires rigid fixation to the chest. All studies evaluating fixation methods that include only the neck,
such as a hard or soft cervical collar, demonstrate poor fixation and limitation of cervical spine motion. It is only when the
base is extended and fixed firmly to the chest, as in a proper cervicothoracic orthosis, that there is any restriction of
cervical spine motion. Although there are limitations on the ability to fix the head to the chest in football players because
they must have full range of motion of the cervical spine, it is possible to fix the chest rigidly to the base of the neck, and
the shoulder pads should accomplish this.
FIGURE 51.1. The typical shoulder pad worn by a professional, defensive lineman is a soft arc of very thin padded
material that has questionable shock-absorbing properties and fits the chest in a semiarc type of configuration.
The majority of neck rolls that are attached to the top of the shoulder pads rotate away from the neck at the moment of
contact (Fig. 51.2). This rolling back of the shoulder pads adds to a lack of protection for the cervical spine in resisting
compression. This axial compression mechanism of injury is commonly seen in serious neck injuries and plays a big role
in burners. As a shoulder pad rolls back, the head coils into the hole in the shoulder pad. There is no protection against
head compression in injuries and the extension, compression, and rotation mechanism of the burner. It is very difficult to
get a collar roll on the back of the shoulder pads that can block extension during contact. One professional veteran used
a stiff cervical collar that was tied tightly around his neck posteriorly and attached to the shoulder pads by strings to the
laces on the front of the pads. This was an attempt to prevent the failure to block extension seen with collar rolls ( Fig.
51.3). Important characteristics of a proper shoulder pad include a modified A-frame shape to the shoulder pad that fits
the chest and prevents shoulder pad roll during contact. Firm circumferential fixation to the chest is important. After fixing
the chest, fix the neck to the chest by the fit of the shoulder pad at the base of the neck. Thick, comfortable, stiff pads at
the base of the neck are the key. It is this support laterally at the base of the neck that offers fixation to the cervical spine.
Some posterior support could be helpful but is very difficult to obtain. Higher, thicker lateral pads inside the shoulder pad
that are tighter at the base of the neck can improve fixation of the cervical spine, especially when the pad fits the chest
and shoulders well. The lateral pad seen in the Donzis shoulder pad is a good example of a proper pad.
FIGURE 51.2. A well-constructed shoulder pad.

FIGURE 51.3. Lifters provide additional neck support.
A common method of adapting pads is to add lifters (Fig. 51.4). The lifters provide a pad at the base of the neck that
supplements the typical shoulder pad. Often, a combination of lifters, the preexisting pad, and the neck roll add to an
improved fit of the pad laterally at the base of the neck. Because most of the rotation in the cervical spine occurs at C-1
to C-2, it is believed that this support should not limit the player's visibility and should provide some added support in the
middle and lower portion of the cervical spine.
FIGURE 51.4. This illustration shows shoulder pads after they have been modified.
Regarding the shock-absorbing capability of the shoulder pad, proper fit to the chest is important in distributing the shock
to the shoulders evenly, over the pad and to the thorax. Better resistive padding and better plastics in the outer shell of
the pad absorb shock and allow the use of the shoulder in proper blocking and tackling techniques. Better shoulder
protection should allow one to deemphasize the use of the head as a blocking and tackling instrument.
TREATMENT OF BURNERS
In addition to prevention, treatment is critically important. Once the symptoms occur, we emphasize the chest-out
posturing and thoracic outlet obstruction exercises. Chest-out posturing produces three effects.
1. It opens the intervertebral foramina to its maximum size. Sticking the chest out brings the head back over the body
and produces a strengthening or less extension in the cervical spine. Flexion in the cervical spine, while tightening
the nerve roots slightly, does increase the size of the intervertebral foramina. Extension closes the foramina and
decreases the central canal's diameter.
2. It reduces the effect of the weight of the head. The lever arm effect of the weight of the head on the cervical spine is
eliminated as the head is brought back over the body with the chest-out posturing. This is important in relieving
neck strain and decreasing the force exerted on the spine by the weight of the head.
3. It opens the thoracic outlet. By changing the alignment of the scalene muscles and the clavicle relative to the neck,
the thoracic outlet is opened with a chest-out posturing. A stoop-shoulder, head-forward posture adds to thoracic
outlet obstruction and causes the symptoms of brachial plexus irritation to persist. Many heavily muscled athletes
have adopted a round-shoulder, head-forward posture. When they sustain an injury to a nerve root or brachial
plexus, symptoms persist because of an inability to produce proper chest and head alignment. All strengthening of
weak muscles owing to a brachial plexus and or nerve root injury should be conducted while emphasizing a
chest-out posture.
We frequently use a basic group of preventive and therapeutic exercises designed for neck and shoulder problems. The
key to these exercises is emphasizing the chest-out posture. By emphasizing the chest-out posture during
upper-extremity, shoulder, and neck exercises, proper head and neck alignment is enhanced. A general exercise
program could include the shoulder and rotator cuff exercises, as well as dorsal glides, midline neck isometrics, shoulder
shrugs, arm rolls, and a weight program. The athlete should stick the chest out and not attempt to hold the shoulders
back or forcefully tuck the chin. The chest, abdomen, and buttock muscles should be used. The important factor is the
chest-out posture.
Neck strengthening is also important. Neck and radicular pain causes muscle weakness and dysfunction in the muscles
that support the head. The same emphasis that is used on quadriceps strengthening for knee injuries should be used for
neck muscles in neck injuries, but the exercises must be performed carefully. Resistive neck exercises are begun very
slowly so that the compressive load on the cervical spine does not produce pain. Neck isometrics should be performed
with the head in the midline only, and resisting forces should be applied perpendicularly to the head from every direction.
Very slowly, the head can be taken out of the midline after no pain is present whatsoever with strengthening in the
midline, but extremes of head flexion, anteriorly, posteriorly, or laterally against resistance, are seldom indicated for
adequate neck strengthening. Our emphasis has been on midline isometric strengthening.
Stretching exercises are critically important to allow for the protective flexibility and range of motion for the cervical spine.
Cervical stiffness is produced by nerve, ligament, or disk injury. The reactive stiffness can produce chronic contractures
and a loss of range of motion if the condition is not corrected. Chronic contractures are a great enemy of a pain-free neck
so that if a contracture exists, sudden motion at a moment of contact through that restricted range of motion reproduces
the injury and severe pain. Relieve the contractures and restore a protective range of motion with a program of cervical
active range of motion exercises. Use motion into the painless areas initially, then slowly move into the painful areas.
Extension is usually the most painful motion, but it cannot be neglected. Dorsal slides and passive neck stretches are
important. Remember that chest-out posturing should be used during the exercises. Aggressive stretching and motion
exercises should be performed with extreme caution, because it is the most common cause of flare-ups in therapy.
Decision Making in Neck Injuries in Athletes
Decision making in managing neck injuries in athletes often centers on whether or not a player is cleared to return to
play. It involves a more complex decision centered around what risks are involved in returning to play either on that day
or later. The decision that allows a player to resume football play depends on the diagnosis, prognosis, and risk factors
for future injury. Crucial to the decision-making process is a physician who is trained in evaluating, diagnosing, and
treating neck injuries, and who also has a thorough understanding of the game. When dealing with football players, it is
important that the physician has an understanding of the mechanics involved in football as well as the effects of the
stress of the game on the particular injury that the player has received. For the physician to make a reasonable
recommendation for return to play, factors such as the mechanism of the player's injury, any prior history of neck injury,
the findings on the initial physical examination of the player immediately after injury, and the diagnostic studies that have
been obtained must be assessed. Factors to be avoided in this decision-making process are contract provisions,
disability contracts, the player's desire to play, and the desires of others (girlfriends, wives, coaches, team owners, and
parents) . Everyone, regardless of what is said, is looking to the team physician for medical advice only. The physician
should review only the medical facts of the case and provide the same information to all concerned about the known risk
factors. To help in our decision making, we have developed a system for classifying the risk of continued play or return to
play, based on the radiographic findings after a specific type of neck injury, coupled with the patient's current signs and
symptoms, as well as the patient's detailed prior history of neck injury. The history of prior neck injury must include the
frequency of occurrence of such incidents as burners, stingers, transient neuropraxia, and neck stiffness, as well as the
length of duration of these episodes of neurologic embarrassment or neck injury. The type of treatments that the player
has received, as well as the player's response to these treatments, is important in assessing the readiness of the player
for return to play. The classification system that has been developed combines the published clinical and scientific
information related to specific neck injuries, as well as our experience in diagnosing and treating neck injuries in football
players. We use radiographic component studies and many other factors in the final outcome of such a decision-making
process. We categorize the player's case into risk categories. The risk categories are both the risk of permanent injury
and the risk of recurrent symptoms.
On-Field Discussion
Decision making begins with the player that has been injured in the game and is down on the field. The only diagnostic
capabilities are the physician's history, physical examination, and knowledge of the mechanics of the injury. The key
decision to make is whether to move the player (whether he has a spinal cord injury or not). The first issue is whether a
player has radiating arm pain and loss of function, such as paresthesias and weakness, or more global paresthesias and
weakness indicative of a transient neuropraxia of the cervical spine. Radiating arm pain and neurologic deficit can be
indicators of a more serious problem, such as spinal instability, that can lead to a permanent neurologic deficit from
further cord or nerve root injury. Additionally, some players may be neurologically intact but may have a stiff, painful
neck. Neck stiffness and loss of cervical range of motion may indicate a cervical fracture.
Initial muscle spasm that occurs after a cervical spine injury can mask an underlying unstable cervical spine lesion. The
patient's pain perception may be altered by the emotion of the game, as well as by the player's dedication to the coach
and the team. A controlled head compression test that produces radicular symptoms may indicate a cervical fracture.
Players with new pain and residual loss of neck range of motion and neck stiffness should not be allowed to return to
play until further diagnostic evaluation is performed.
Spinal cord neuropraxia, with four-extremity involvement, including, possibly, loss of consciousness, temporary
quadriplegia or quadriparesis, or burning dysesthesias of the arms and legs indicates a significant but temporary injury to
the spinal cord. Often, players who have transient neuraraxia of the spinal cord that lasts for less than 10 to 15 seconds
may arise from the playing field and exit the field on their own power, and only then, when the player is at the sideline, is
the trainer or team physician made aware of the symptoms. Examination of these players on the sideline or on the field
involves evaluation for motor weakness, sensory deficits, and signs of myelopathy. It is important that all players with the
possibility of cervical spine injury and acute neurologic deficit are treated with cervical spine immobilization and
appropriate transportation and diagnostic studies.
Transportation and Immobilization
Guidelines for transportation and immobilization are being developed. An outline of these proposed guidelines is shown
in the following list:
Any athlete suspected of having a spinal injury should not be moved and should be managed as though a spinal
injury exists.
The athlete's airway, breathing and circulation, neurologic status, and level of consciousness should be assessed.
The athlete should not be moved unless absolutely essential to maintain airway, breathing, and circulation.
If the athlete must be moved to maintain airway, breathing, and circulation, the athlete should be placed in a supine
position while maintaining spinal immobilization.
When moving a suspected spine injured athlete, the head and trunk should be moved as a unit. One accepted
technique is to manually splint the head to the trunk.
The Emergency Medical Services system should be activated.
Facemask Removal
The facemask should be removed prior to transportation, regardless of current respiratory status.
Those involved in the prehospital care of injured football players should have the tools for facemask removal readily
available.
The athletic helmet and chin strap should only be removed
If the helmet and chin strap do not hold the head securely, such that immobilization of the helmet does not also
immobilize the head.
If the design of the helmet and chin strap is such that even after removal of the facemask, the airway cannot be
controlled or ventilation be provided.
If the facemask can not be removed after a reasonable period of time.
If the helmet prevents immobilization for transportation in an appropriate position.
Helmet Removal
Spinal immobilization must be maintained while removing the helmet.
Helmet removal should be practiced frequently under proper supervision.

Specific guidelines for helmet removal need to be developed.
In most circumstances, it may be helpful to remove cheek padding or deflate air padding prior to helmet removal.
Equipment
Appropriate spinal alignment must be maintained.
It must be realized that the helmet and shoulder pads elevate an athlete's trunk when he or she is in the supine
position.
Should either be removed, or if only one is present, appropriate spinal alignment must be maintained.
The front of the shoulder pads can be opened to allow access for cardiopulmonary resuscitation (CPR) and
defibrillation.
When confronted with an individual on the playing field who complains of symptoms of neck pain or stiffness, or any
upper- or lower-extremity neurologic manifestations, the initial response of the trainer or team physician is to ensure
prompt and adequate immobilization of the cervical spine and establish an airway. Transportation techniques are vital to
avoid increasing neurologic injury in any spinal cord injured–patient. Stabilization of the cervical spine in an injured
player does not require routine prehospital removal of the helmet and shoulder pad before transport. No morbidity has
been documented because of not removing the helmet and shoulder pads. In a player with neck injury and respiratory
compromise, either the mask must be able to be removed or large bolt cutters or other tools capable of transecting the
face mask must be available. The removability of facemasks should be continually checked and properly monitored so
that in an emergency, the face mask should be removed easily. If the provision of an adequate airway is necessary, then
the bolt cutters should be used to transect the metal stays attaching the facemask to the helmet. If the player is
unconscious and exhibiting inadequate respiratory effort, then the airway may be opened by grasping the angle of the
mandible with both hands and thrusting the jaw forward. Hyperextension of the head to obtain an open airway is usually
not necessary when cervical spine injury is considered a possibility. It is only after cervical spine immobilization has been
provided that the individual may be transported to the sidelines, the locker room, or the emergency room. When there is
doubt concerning the necessity for neck immobilization and transportation of a player with neck injury, proper instruction
of the coach and trainer by the team physician, as well as practice in the transportation techniques by those involved in
the provision of the transportation, is required ( Fig. 51.5 and Fig. 51.6). The team trainer, as well as the fire rescue
personnel in attendance at the game, must be provided with and comfortable with the use of standard cervical
immobilization collars. The most common collars in use include the Nec-loc and the Philadelphia collar. When
appropriate, these collars can be applied to the player before transportation.
FIGURE 51.5. Immobilization of the head to the trunk. The person in charge holds the trapezius-clavicle-scapula area
with his hands and holds the head between his forearms.
FIGURE 51.6. A: Hand position for helmet removal. B: Helmet removal, side view. C: Helmet removal, the assistant pulls
out on the helmet and slips it off.
The transport technique should be standardized and practiced by the trainer, coach, and team physician before the start
of the playing season. The procedure requires five to six people to move the player safely. Trying to transport the patient
with only three people is inappropriate. A frequent error in transport is not having enough people available who know how
to transport a player with a potentially unstable cervical spine injury ( Fig. 51.7). The most important key to the technique
is to have one person controlling the head and shoulders, not just the head. Holding the head only and trying to visually
match the head to the body is impossible. The individual holding the head and neck is in charge of the timing of
transportation. This person should grab the trapezial, clavicle, and scapular area with his or her hands while cradling the
helmeted head of the player between the forearms. The person in charge should not be responsible for any of the weight
of the transfer. The additional members of the transportation team include one individual holding the player's shoulders
and upper torso. The third and fourth persons holding the player's trunk and upper thighs on each side of the player. The
fifth and sixth members of the turning team are responsible for lifting and turning the legs.
FIGURE 51.7. The transport technique should be standardized and practiced, and it requires five or six people to move
the player safely. This figure illustrates the multiman carry. The “chief” immobilizes the head, neck, and shoulder and
calls the signals. Three men on each side of the body (the three on the near side are not pictured) join hands and lift the
player on the “chief's” command. The spine board is brought underneath the player.
The person holding the head is responsible for announcing each move in the transportation process. At no time should
the person in charge hold only the head and not the shoulders. When practicing these maneuvers, try having the person
in charge hold only the head in an awake, uninjured volunteer, and proceed through the turning maneuvers. Then ask the
awake volunteer how much he felt his neck move during the turning procedure. Generally, a significant amount of neck
motion can be felt, thus reinforcing the need for the person in charge to maintain a firm grasp connecting the shoulders to
the head, thus ensuring adequate immobilization of a potentially unstable cervical spine. It is possible for the person in
charge to grasp both the trapezius inside and a shoulder pad outside, but this is not quite as stable as the prior
recommended method. Another person may be used to squeeze the forearms of the person in charge to the head, thus
further increasing the stability of the grasp on the player's shoulders and head. Once all individuals are in place, the team
members on each side of the body then join hands in a weaved grip, with the palm placed against the forearm of the
individual directly across from them, underneath the player. When the team chief calls the signal, the assistants gently
elevate the player off the ground while a rigid backboard is slid directly under the player.
If the player is face down on the field, the chief rotates the player's arms and grasps his head and shoulders in a similar
fashion. In this situation, it is mandatory that an assistant grasp the chief's arms and squeeze them together to increase
the hold on the player's shoulders and head. Safely turning the prone player to the supine position requires multiple
assistants to roll the player over gently while the team chief maintains the alignment of the head with the shoulders
during the turn. Once the player is turned, then the standard transportation protocol is used ( Fig. 51.8).
FIGURE 51.8. If the player is face down on the field (A), the chief rotates his arms and grasps the player's head and
shoulders in a similar fashion (B). C: In this situation, it is mandatory that an assistant grasp the chief's arms and
squeezes them together to increase the hold on the player's shoulders and head. D: Safely turning the prone player to
the supine position requires multiple assistants to roll the player over gently while the team chief maintains the alignment
of the head with the shoulders during the turn. E: Once the player is turned, then the standard transportation protocol is
utilized.
Once the player is on the backboard, then the player can be safely transported off the field to the appropriate health care
facility, while the team chief maintains the grasp on the player's shoulders and head. Once the player is on the
backboard, if an appropriate cervical orthosis is available, such as a Philadelphia collar, then the team chief may safely
relinquish his hold on the neck at the same time applying the cervical orthosis. If the cervical orthosis cannot be applied
because of the helmet or the shoulder pads, then the team chief must maintain his grasp on the individual until
transportation to the locker room or emergency room is completed. It may be necessary to use a backboard that has
built-in neck and head supports or use the sandbags taped into place rather than the original grasp of the person in
charge.
Locker Room Decisions
Our decision-making process involves evaluating players for return to play who have had either significant, persistent, or
severe enough symptoms to warrant transportation to a medical facility or to a locker room where radiographic equipment
is available.
Once x-ray studies are available, it is mandatory to obtain adequate visualization of the cervicothoracic junction at C-7 to
T-1, as well as an adequate-quality x-ray study that can be safely interpreted. Generally, the lateral x-ray study is
obtained first (Fig. 51.9) and should be interpreted and evaluated before proceeding with the remainder of the
radiographic evaluation. Thomas ( 14) has reported that the appropriate sequence of x-ray studies that should be
obtained in the neck-injured player should include the anteroposterior (AP) projection, the lateral x-ray study and the
neutral position, the open mouth view of the atlantoaxial articulation, and each oblique position. It is not until the initial
sequence of cervical spine films has been reviewed and evaluated for any potential instability, fracture, or dislocation that
subsequent flexion-extension x-ray studies should be considered. If such instability, fracture, or dislocation is identified,
then the next appropriate step is to continue cervical spine immobilization and proceed with definitive treatment or further
diagnostic studies including CT or MRI as indicated by the nature of the lesion. When the basic radiographic evaluation
indicates spinal instability, fracture, or dislocation, then the lateral flexion-extension films may be contraindicated and
unsafe.
FIGURE 51.9. A typical lateral x-ray study of a football player.
The radiographs should be evaluated for obvious vertebral body fracture or malalignment; also, the anterior
retropharyngeal space should be evaluated. At the anterior aspect of the body of C-3, there should be no more than 4
mm of space between the posterior pharynx and the anterior vertebral body. An increase in the retropharyngeal space
indicates soft tissue swelling and may be indicative of cervical spine injury. The posterior margins of the vertebral bodies
and the spinal laminar lines should be evaluated for a symmetric and smooth contour. The facet joints should be
evaluated for symmetry and congruity. Changes in the rotational position of the spinal column from one motion segment
to the next may be indicative of facet subluxation or dislocation. The criteria of White and Panjabi ( 15), including
subluxation of 3.5 mm or more and kyphotic angulation of the injured level that is 11 degrees or greater than an adjacent
level, is generally considered as cervical spine instability. These criteria pertain to any lateral cervical spine view
including the flexion view.
The evaluation of C-l through T-l is imperative and can be facilitated by the use of traction on the player's hand in a
downward fashion by an assistant during the radiograph or by the use of the Boger straps. We prefer the Boger straps,
which are passive-action Velcro straps that are connected to the wrists and passed around the bottoms of the feet. They
are tightened with the knees flexed. As the knees are straightened out by pushing down on the knees, the straps tighten
and pull the arms down. A sandbag can be placed on the knees in an unconscious patient, thereby maintaining traction
on the arms. We have never had a patient in which C-7 was not visualized using the Boger straps. Occasionally, traction
on an arm with cervical radiculopathy produces too much pain to pull for a long time. If Boger straps are not available,
then the “swimmer's view,” a special radiographic view obtained by centering the beam on the lateral projection at C-7,
can be used. The patient's arm closest to the source of the radiographic beam is left at the patient's side, while the
opposite arm that is adjacent to the radiographic plate is fully abducted over the patient's head. If adequate visualization
of the cervicothoracic junction remains a problem after the swimmer's view is obtained, then the next step in radiographic
evaluation is a CT scan to include that region. We will not clear a patient's cervical spine film unless the full cervical
spine is visualized. Also important on the lateral view is the atlantodens interval. An atlantodens interval of greater than 2
to 3 mm may be considered indicative of cervical spine instability at the atlantoaxial articulation, particularly if this
atlantodens interval markedly increases on flexion films.
One difficult aspect of the radiographic evaluation is to determine if there is an acute injury, an old injury, or an
asymptomatic finding. One complicating factor is the presence of a hypermobile segment over a stiff, arthritic segment.
Many athletes who do neck strengthening exercises on a regular and consistent basis, especially those starting at a
young age, have relative osteoarthritic changes in the lower cervical spine region. The biomechanical stiffness of these
levels may produce a relative increase in mobility through a compensatory mechanism at the levels just above these less
mobile lower segments. To find an asymptomatic never-injured level that exceeds the White-Punjabi criteria would be
rare (15).
The adequate identification of an area of ligamentous instability may be particularly difficult in the acute situations
secondary to the associated muscle spasm from the injury.
Compression fracture noted in the lateral film must be interpreted with caution. What may be interpreted as a simple
compression fracture may, in fact, include an injury with associated cervical spine instability. A review of 27 patients with
cervical compression fractures revealed that six of these injuries were later noted to have associated spine instability
(16). When doubt continues as to the stability of a cervical spine injury, such as when there is too much spasm to obtain
flexion-extension views, continued immobilization with a cervical orthosis is expected until additional radiographic
evaluation in subsequent days with flexion-extension views at that time is obtained. Once a fracture has been identified
on plain film or CT scan, it should be classified into the standard classification system used today, depending upon the
level of the spine affected and the fracture configuration.
Often important in the radiologic evaluation is the determination of whether a radiographic finding is an acute injury, on
old injury, or an asymptomatic degenerative change. Boden et al. ( 17) have identified the incidence of asymptomatic
degenerative changes occurring in the cervical spine in a group of volunteers who underwent MRI of the cervical spine
while being asymptomatic for problems related to the neck. They were able to identify a 14% to 35% incidence of
herniated cervical disk, osteophytes, and degenerative disk disease in these completely asymptomatic individuals. They
underscored the importance of the clinical correlation among the radiographic findings and the history and physical
examination findings and individuals being evaluated for cervical injuries.
Once in a controlled environment, removing the player's helmet should be accomplished in a safe fashion. First, remove
the facemask. The appropriate hand position of the team chief for helmet removal includes having that team chief grasp
the base of the occiput and the base of the neck with open palms and fingers. An assistant may first spread the sides of
the helmet, then gently slide the helmet in a cephalad direction and off the player while neck control is maintained by the
team chief. Absolutely no cervical flexion should be allowed during this maneuver. If the shoulder pads do not allow for
adequate cervical spine examination and radiograph, then they should be removed at this time. They should be removed
in a similar fashion, while maintaining cervical immobilization and not allowing cervical and head flexion.
When to Do In-depth Studies
The logical answer to this question is when they are needed to make the diagnosis when the results would change your
treatment. As a practical measure, studies are obtained on players with severe, persistent, or recurring problems. For a
stiff, painful neck due to recent injury, a bone scan may identify an acute fracture. MRI and plain CT scans are helpful,
and a contrast CT scan will help identify disk herniations and fractures. An EMG with a nerve conduction study is helpful
in distinguishing a peripheral nerve problem from a cervical nerve root problem but not as helpful in following a case for
progression. Liberal use should be made of whatever tests are taken to diagnose the problem properly.
Continued Play Decision: Risk Categories
The spinal consultant or the team physician is often called on, in the preseason, to examine players and evaluate their
risk for play during the upcoming season. Guidelines for participation after injury involve a number of different factors,
including age, experience, the individual's level of participation, position played, and the spinal condition itself with its
resulting symptoms. Obtaining informed consent for all concerned is probably the most important obligation of the
physician evaluator. The team physician must be able to give a clear-cut “yes” or “no” answer to the team's management
and to the player himself, or the player's parents. It is often the spinal consultant who is asked to make that decision in
players who have had documented neck injury and are thought to be at some risk for further play. A comprehensive
diagnostic workup involving myelography, contrast CT scan, and MRI are necessary before excluding someone from play
after the onset of neurologic symptoms resulting from stenosis. As consultants, the radiographic data are combined with
the history and physical examination of the player to develop a risk category into which that particular player can be
placed in regard to his chance for permanent damage to the neck, spinal cord injury, permanent nerve root injury with
paralysis and pain, or death. Also, risks may be categorized in terms of percentage of chance of recurrence of symptoms
that would hinder future play. An important factor in this decision is the level of play at which the player participates. In a
high school player, of course, the parents' opinion is very important. If there is a suggestion of structural damage and
even a minimally increased risk to a high school player, the decision is often for the athlete to discontinue playing
football. In professional football, the players themselves need to be advised of the approximate level of risk so that they
may give an informed consent as to their future level of play and an appropriate decision can be made by the player and
all concerned.
Although no published data can precisely dictate the individual player risk for return to play, a system that incorporates
clinical experience in dealing with football players and the published literature related to cervical spine injuries is used.
The criteria for return to play has been analyzed by a number of different sources. Each individual injury has its
characteristics that have led investigators to estimating the risks involved in return to play after incurring specific types of
injuries or symptoms (5). A minimal risk is the term used to suggest that there is very little increased risk, as compared
with playing the game as it is normally done. Moderate risk means that there is a reasonably high chance that the patient
will have a recurrence of symptoms and a reasonable chance that he will run some risk of permanent damage. Extreme
risk means that the patient runs a very high risk of permanent damage and recurrence of symptoms. It is critical that all
factors related to the player's symptom, history of injury, radiographic findings, results of any special studies needed, and
expectations be included in the ultimate recommendations made to the player in regard to his likelihood of injury if he
returns to the sport of football. When considering other sports that involve bodily contact, similar recommendations can
be made.
Extreme-Risk Category
Fractures of the first cervical vertebra (Jefferson fractures) generally represent an axial loading injury often resulting from
head-on collision by the player with the opponent or the ground. The Jefferson fracture is disruption of the ring of the first
cervical vertebra and may be identified on the open mouth AP view as eccentric or excessive overhang of the lateral
mass of the first cervical vertebra on the second cervical vertebra. A CT scan precisely identifies the configuration of a
C-l fracture. At the level of the atlas, there is considerable room for the spinal cord secondary to the large central spinal
canal at that level. As such, neurologic injury secondary to Jefferson fracture is unusual. The mechanism of injury
involves axial loading that forces the occipital condyles into the lateral mass of the atlas, resulting in failure of the ring of
the atlas, often at the thinner region just medial to the trough that lies at the level of the vertebral artery. Certainly, return
to play after a recent Jefferson fracture is contraindicated. It is only after bony healing has occurred and appropriate tests
for ligamentous stability can be obtained that a recommendation as to return to play can be made. If the bone completely
heals, a full, normal range of motion is present, and no residual instability is noted on flexion-extension views, then return
to play is possible. Certainly, if there is any residual instability or if there is residual neck stiffness or discomfort, then the
recommendation for return to play would include placing that player in an extreme-risk category. Occasionally, C-l ring
fractures heal with a fibrous union, as evidenced on CT scan, and in these players with no residual neck stiffness or pain,
then a moderate, significant risk category for return to play would be offered. Figure 51.10 illustrates a Jefferson-type
fracture with 7 mm of overhang resulting from head-on collision; the player is a college senior defensive back. Projected
as a first-round draft choice in the National Football League, this injury certainly placed the player in a high-risk category.
FIGURE 51.10. A: This flexion fracture resulted from a head-first tackle. The key measurement is the amount of lateral
overhang. An amount over 7 mm may indicate a ruptured transverse ligament. B: CT scan shows a fracture with
separation.
Transverse ligament ruptures result from high-velocity axial loading injuries. Transverse ligament injuries are quite rare
and occur in only 3% of all cervical spine injuries ( 18). The odontoid is held snugly against the back of the atlas by the
strong fibers of the transverse ligament. These fibers arise from the lateral masses of the atlas, just behind the origin of
the accessory ligament. Rupture of the transverse ligament is identified by abnormal motion between the atlas and the
odontoid on the flexion-extension views or by an atlantodens interval greater than 5 mm on the neutral lateral film. Partial
tears of the transverse ligament may be identified by an atlantodens interval of 2 to 5 mm. We have treated a player who
had a partial tear of the transverse ligament; he was a starting professional defensive tackle who had suffered a
high-velocity injury with residual stiffness and pain in his neck. This player was thought to be in an extreme-risk category
for further play. We have also treated a 17-year-old high school football player who presented after a significant neck
injury that resulted in upper cervical spine stiffness and pain. He presented with a V-shaped atlantodens interval. The
diagnosis for this youngster was the partial transverse ligament tear, even though there have been references made to
this entity being an incidental finding. Our recommendation to this child and his parents was that he would be at an
increased risk of neurologic injury from continued participation in football.
The open-mouth view is used to identify odontoid fractures and can be classified according to the system of Anderson
and Alonzo (19) into either type I fractures, which include the tip of the odontoid and are thought to be stable fracture
configurations. A type II fracture runs through the base of the odontoid and is the least stable and most likely to lead to
nonunion. Type III odontoid fractures, which involve variable components of the vertebral body of C-2, are likely to lead
to early union. Odontoid fractures that heal completely, without deformity and with free, unrestricted, painless neck
motion are considered to place that player at a mild risk of secondary injury from continued play. However, any residual
deformity or the suggestion of a fibrous union between the odontoid and the body of C-2 is considered a potentially
unstable situation, and this finding would place a player in an extreme-risk category because a football player can be
expected to place significant biomechanical stress on that fracture.
A fracture of the pedicles of C-2 is termed a hangman's fracture because of its association with the sudden
hyperextension provided by the hangman's noose. Hangman's fractures have been classified according to the system of
Effendi (20) and modified by the system proposed by Levine and Edwards ( 21). Type I injuries are considered to be
stable and are fractures through the pars interarticularis, with less than 1to 2 mm of displacement at that fracture site.
Type II injuries often have some degree of displacement and occur through the isthmus. In these fractures, there may
also have been some rebound flexion with associated disruption of the posterior ligamentous structures or the C-2 to C-3
disks, resulting in residual angulation and subluxation.
Type IIA fractures have been introduced by Levine and Edwards ( 21) and include fractures that have less displacement
but more angulation than the type II injury described by Effendi et al. ( 20). These fractures may have been associated
with primary flexion force and are particularly prone to increased angulation and displacement when traction is applied.
Type III fractures are generally secondary to flexion injury and may be associated with facet capsule disruption between
C-2 and C-3. This allows for fracture through the pars interarticularis. If the hangman's fracture heals completely, with no
fibrous union, and there is satisfactory reestablishment of the posterior arch of C-2, then this is thought to signal only a
mild risk for subsequent injury in that player. However, any suggestion of fibrous union or significant residual deformity
after bony union would increase the chance of injury and would be considered an extreme-risk category. Often, the soft
tissue injury involves both the posterior and middle column, and occasionally, the anterior column as well and is an
extreme risk.
The hidden flexion injury of McSweeney can be identified as a subtle subluxation presenting on the flexion view that is
actually a total ligamentous disruption. This diagnosis is made on the lateral or flexion film ( 22). The x-ray findings may
include a gapping of the spinous processes, a localized endplate deformity, or a subtle avulsion fracture of the anterior
edge of the vertebral body. The findings may be quite subtle, and the radiographic findings may take several weeks to
become apparent secondary to the residual stiffness and spasm present immediately after the accident. Failure to
diagnose this residual ligamentous stability and allowing these players to return to play would be extremely dangerous.
This type of residual ligamentous instability certainly places these players at extreme risk. Herkowitz et al. ( 23) have
documented this particular ligamentous and radiographic finding after cervical spine trauma. Delay in the diagnosis and
treatment of this injury can also lead to a fixed kyphotic deformity, placing the patient or player permanently in the
extreme-risk category.
Fractures of the vertebral bodies C-3 to C-7 can be associated with compression and flexion forces as well as torsional
forces that may leave the player with a significant cervical spine instability. Vertebral burst fractures may include
significant spinal cord injury and are occasionally associated with facet dislocations that place the player at significant
risk for complete neurologic injury. Certainly, there is not always a good correlation between the degree of spinal cord
injury and the amount of bony injury or dislocation on the plain films. The prognosis for return to play after vertebral burst
fractures, which may or may not have included subluxation or dislocation in the cervical spine, depends on the neurologic
injury and the residual deformity present after complete healing. Certainly, if there is no residual neck pain or stiffness, no
residual neurologic deficit, no residual associated cervical instability, and no residual deformity or canal narrowing, then
players having suffered cervical spine compression or burst fractures may be allowed to return to play but still are at
some mild risk.
Both bilateral and unilateral facet dislocations, can occur with head compression and flexion-rotation injury. The facet
dislocation that reduces completely and heals with no residual deformity or instability would place that player in a
moderate-risk category because of the damage to ligamentous support for that segment. Facet dislocations that heal with
any residual deformity or instability would certainly place the player at an extreme risk of further injury.
Moderate-Risk Category
Fractures of the cervical facet or pillar fractures through the lateral mass may present like a facet dislocation because of
the frequently seen anterior subluxation of one vertebral body on another. For these fractures, the ultimate
recommendation as to return to play depends most significantly on any residual deformity that persists after healing has
occurred, as well as any residual instability or cervical stiffness that is manifested after appropriate treatment has been
completed.
Herniated cervical disks are reasonably common in adult football players. Most of the herniated cervical disks that we
identify in athletes have a lingering or persistent radiculopathy in those players with a first-time severe burner at the
professional or college level. Because the incidence of disk bulges and herniations in asymptomatic people and players
is significantly high, the finding of a herniated cervical disk in a football player who was completely asymptomatic for
signs and symptoms of cervical myelopathy or radiculopathy related to that herniation would not be considered to place
that player at an increased risk of injury. However, players who have evidence of radiculopathy are placed in a
moderate-risk category. There is often a great deal of difficulty in determining whether a disk herniation is acute, chronic,
hard as in a cervical osteophyte, soft, whether it is a free fragment, or simply a contained disk bulge. It is very important
in evaluating these players that any radiographic diagnostic imaging abnormalities be closely correlated with the physical
findings. It is important that the physical findings match the herniation for an accurate prognosis to be made. The
treatment for herniated, extruded cervical disks is an anterior cervical discectomy and fusion. After such treatment, we
often place the player in a mild-risk category, secondary to the biomechanical alterations that must necessarily occur
above and below the fused cervical motion segment. It is for this reason that, if given the appropriate clinical indications,
we might recommend a microscopic cervical foraminotomy for the treatment of monoradiculopathy secondary to foraminal
stenosis in an athlete involved in contact sports. For the athlete with significant intermittent radiculopathy, a positive
Spurling hyperextension test, and foraminal stenosis, a posterolateral foraminotomy is a reasonable approach. The
technique of this operation is adopted from Robert Warren Williams ( 24) and includes a minimal resection of the
posterior wall of the foramina only until nerve root pulsations are clearly present. A significant facet resection would
contraindicate the player's return to football.
Minor-Risk Category
Undisplaced fractures that heal without any residual deformity indicate a low risk for return to play. Clay-shoveler
fractures are avulsion fractures of the tip of the spinous process of C-7 caused by strong muscular contractions of the
trapezius and shoulder. They present with point tenderness, otherwise negative studies, and dual rigidity. Lateral mass
fractures always heal but may have a slight subluxation of one vertebra on another. The degree of risk depends on the
degree of subluxation. There is rarely ligamentous damage with this injury. Laminar fractures that heal without deformity
are a minor risk condition. Disk herniations that have become asymptomatic over many months or years are not of
significance except as to how they have left the central canal narrowed. Foraminal stenosis is important when it is
symptomatic, but because of the high incidence of asymptomatic foraminal stenosis, we would not consider a nerve root
to be in danger just because radiographic foraminal stenosis is present.
CONGENITAL ABNORMALITIES
Congenital abnormalities of the cervical spine may or may not place the player at an increased risk for neurologic
damage, depending on the precise morphology of the congenital abnormality present. Os odontoideum, which has been
documented in the literature as most likely secondary to a traumatic lesion is a potentially significant unstable situation in
which the risk of injury places the player in an extreme-risk category ( Fig. 51.11). Frequently, os odontoideum presents in
the younger player as an asymptomatic and incidental finding and, as such, can be a particularly difficult problem to
explain in the otherwise young, healthy, high-caliber athlete. Multiple levels of failure of segmentation, as found in the
Klippel-Feil syndrome, place the adjoining spinal motion units at an increased biomechanical disadvantage secondary to
the compensatory increased motion that occurs adjacent to the fused levels. In general, we would list this constellation of
segmentation defects as a moderate to extreme risk that would depend somewhat on the findings on flexion-extension
films, as well as on the distribution of the fused segments. Sprengel deformity in association with Klippel-Feil syndrome is
not unusual and is an extreme risk. Some examples in the high-risk category are given in the following list:
1. Os odontoideum
2. Ruptured transverse ligament at C-1 to C-2
3. Occipitocervical dislocation
4. Odontoid fracture
5. Total ligamentous disruption of a neuromotor segment of the lower cervical spine
6. An unstable fracture dislocation
7. Unstable Jefferson's fracture
8. Cervical cord anomaly
9. Acute large central disc herniation
FIGURE 51.11. A: AP x-ray study revealing an unstable os odontonium in a 20-year-old college freshman athlete who
suffered pain in his neck for the first time from an automobile accident. B: Lateral view.
Examples in the moderate-risk category are presented in the following list:
1. Facet fractures
2. Lateral mass fractures
3. Nondisplaced healed odontoid fractures
4. Nondisplaced healed ring of C-l fractures
5. Acute lateral disk herniations
6. Cervical radiculopathy due to a foraminal spur
Examples in the minimal risk category include the following:
1. Asymptomatic bone spurs

2. Certain healed facet fractures
3. Burners
4. Stingers
5. Healed disc herniation
6. Healed lamina fracture
7. Fractured tip of the spinous process
8. Asymptomatic foraminal stenosis
In conclusion, the decision-making process that each team physician uses when approaching the cervical spine–injured
football player must rely on the medical facts and the current medical knowledge. Attention to detail, with structured
preplanning and a practiced on-the-field routine are critical to ensuring that no additional damage is done to the injured
player after the accident. Counseling the player and other concerned individuals must be uniform and should only include
the medical facts. It is important to remember that the team physician's role is only to convey the medical information as
well as to instruct and to train the players, coaches, and trainers in techniques that will be useful to prevent player injury
and to prevent further injury once a player is down on the field. There are no strict guidelines that have been published
that are considered the standard of care. The ultimate recommendation of the team physician must be based on the
medical facts as he or she finds them. Familiarity with the game of football or the particular athletic event for which the
team physician is covering and the particular needs and desires for those athletes helps shape a more appropriate
decision-making process. An understanding of the relative risk of a spine disorder or a spine injury to an individual player
both at the time of injury and for recommending return to play must come from advanced training in sports-related spine
injuries or from clinical experience that comes from active participation in the care of athletes on a regular basis.
REHABILITATION OF NECK INJURIES
Certainly, for the athlete who is expecting to return to contact sports, it is imperative that the individual regains a full,
pain-free range of motion of the cervical spine before being allowed to return to the sport. In football, in particular, the
interrelationship among the head, neck, and shoulders in the development of a synchronous flow of movement is
imperative to minimize the risk of recurrent injury. As such, the rehabilitative protocol must concentrate on strength, bulk,
and coordination in the rehabilitation of the spinal flexors, extensors, and the shoulder girdle musculature. Once the
acute phase of the injury has subsided and the player is regaining the less painful range of motion of the neck, then
progressive isometric strengthening of the neck musculature is begun. As symptoms further diminish, the player is
progressively allowed to resume a normal weight-training schedule in the attempt to regain any lost muscle strength and
to regain the muscle bulk that is necessary to protect the underlying skeletal structures. Correction of posture is the key
to neck rehabilitation.
We recommend a progressive isometric trunk-strengthening exercise program aimed at placing the neck in a
biomechanically sound position with the shoulders, back, and chest in a posturally correct position. This exercise
program concentrates on trunk strengthening and trunk mobility. Throughout the program, the patient is instructed in
postural modifications that place the patient in a chest-out posture, which effectively normalizes the lumbar lordosis while
bringing the shoulders backward and bringing the head and neck back over the shoulders. This is quite similar to the
military position of attention and, in that position, the cervical lordosis is normalized while the neural foramina are
opened. Athletes involved in the use of the upper extremities require a rigid cylinder of strength in their torso to transfer
torque from their legs to their upper extremities. Trunk and leg strength generate the strength of the upper extremity
activity, while the arms and hands generally provide the fine control. Fatigue in the trunk or legs can reduce the fine
control in the upper extremities available for overhead activities, such as in racquet and throwing sports. When there is
loss of the rigid trunk cylinder strength, there is a resultant loss of synchrony between the arms and legs. There is a
similar linkage among the legs, trunk, neck, and head in regard to the fine control available for blocking and tackling
techniques that must be utilized precisely and reproducibly throughout a game. Loss of synchrony between the arms and
legs can cause a resultant loss of coordination between the trunk and neck as well as a loss of precise coordination
between the trunk and upper extremities. As the trunk flexors and abdominal musculature weaken due to fatigue, the
lumbar lordosis increases and low back pain may result. Asymmetric, asynchronous upper-extremity athletic activities
can result in neck pain, neck strain, and cervical spine injury. Interscapular pain can be directly related to bad posture,
round-shoulder and head-forward posture, and asynchronic muscle activity. A weak trunk produces undue arm and
shoulder strain because the upper extremity must compensate for the weak trunk, and arm muscles are used for strength
instead of fine control. The joints, cervical spine, shoulder, and elbow are not under undue strain. Nowhere is this better
demonstrated than in athletes who throw as part of their sport.
Throwers require a rigid cylinder of strength to transfer torque from their legs to their throwing arms. Trunk and leg
strength generate the velocity of the throw and the arm provides the fine control strength. Fatigue reduces the control of
the pitching motion and ball location. A major factor in ball control is a loss of tone and strength in the trunk caused by
trunk muscle fatigue. A loss of the rigid trunk cylinder produces a loss of synchrony between the legs and arms. This
causes a change in the pitching motion. As the trunk flexors and abdominal musculature weaken because of fatigue,
lumbar lordosis increases and the back arches. The subtle change of a few degrees puts the arm behind in the pitching
motion, promoting earlier ball release, and the pitch comes up. Arm strain increases as the trunk musculature fatigues.
Attempts to compensate for loss of trunk strength and a slow arm increase the use of the arm musculature and
predisposes the shoulder to injury. Attempts to compensate for loss of trunk strength may involve the use of blocking and
tackling techniques that are more dangerous, placing the player at an increased risk for cervical spine injury. As such,
our trunk conditioning program is aimed at developing power in the torsional strength of the trunk musculature including
the trapezius muscles, the spinal erector musculature, the latissimus dorsi, the internal and external obliques as well as
the transversus abdominus, the rectus abdominus sheath of muscle, the gluteal musculature as well as the hip flexors,
extensors, abductors, adductors, and the thigh musculature. Trunk-strengthening exercises are designed not only to
enhance performance but also to prevent subsequent injury to the back, the neck, and the arms.
We have recognized that attempts to increase the strength of the trunk or neck musculature by exercising the neck and
back through a full range of motion may be counterproductive to the ultimate goal of relieving neck and back pain.
Rather, we stress an isometric set of exercises that can accomplish adequate trunk and neck strengthening to diminish or
relieve symptoms of neck or back pain. However, most important to recognize is that the isometric trunk-strengthening
program that we have designed is easily taught to athletes without back or neck pain. When an individual trainer or
physician is treating an athlete with neck or back pain after an injury, then the full clinical details of that patient must be
incorporated into the development of a rehabilitation and exercise protocol that is designed specifically for that individual
and for that individual's injuries. However, we have found that our isometric trunk-conditioning program is effective at
preventing back injuries and is useful in many individuals with active neck or back pain. Although treatment plans for
symptomatic back and neck pain patients as well as patients who have suffered cervical spine and spinal cord injury may
include similar exercises, each of the treatment plans should be designed to match the examination and the symptoms.
Any trunk-strengthening and trunk-conditioning program necessarily places a biomechanical strain on the spine and can
exacerbate any underlying inflammatory or degenerative condition that is symptomatic. Therefore, the implementation of
this isometric trunk-strengthening and trunk-conditioning program requires a safe and controlled program that proceeds
progressively from less vigorous activity to more vigorous activity as the patient's symptoms diminish. The key to safe
strengthening of the back and neck is the ability to maintain the spine in a safe, neutral position during the strengthening
exercises. For upper-body strengthening, the spine must be well aligned with a chest-out posture. Isometric trunk
exercises and upper-body exercises that emphasize this chest-out posture also strengthen the supporting structures for
the cervical spine and the postural muscles necessary for maintaining proper body alignment; ultimately, these exercises
are useful preventive measures for neck pain during athletic activity. In individuals other than football players, we do not
recommend specific neck-strengthening exercises except for modest isometric exercises that can be performed manually
only. There are certainly exceptions in sports, such as wrestling, rugby, and other contact sports; the individual
neck-strengthening exercises must be tailored appropriately.
The establishment of a finely coordinated set of muscles that transfer the torque from the lower extremities up through
the trunk, chest, and back musculature to the arms and neck requires a practiced and controlled sequence of exercises
aimed at increasing the coordination among these interlinked musculoskeletal elements. Establishing finely coordinated
control through a series of exercises that enhance the coordination between these muscle groups is the theory behind
this isometric trunk-conditioning program. The key to the trunk stability exercises is learning to maintain and control a
neutral, pain-free position of the trunk. Every exercise in this program could be done by any reasonably conditioned
athlete with no training whatsoever, but the key is doing the exercises correctly. The program initially starts with the
athlete learning to obtain and maintain a neutral, pain-free position for the trunk and being able to hold the trunk muscles
including the buttocks, the paraspinous musculature, the abdominal oblique musculature, the rectus abdominus
musculature, and the thigh musculature in a tight, rigidly controlled trunk position. One objective of the trunk-stabilization
program is to retrain the trunk muscles to fire to protect the spine when the person is using his or her arms and legs.
Another objective is for these muscles to work and function in a coordinated fashion during activities in which the
individual does not have time to think and activate consciously the trunk musculature in the sequence of firing that is
necessary to perform the particular activity. This exercise program retrains trunk muscles through a balancing and
coordinating group of exercises. These exercises teach a balanced and coordinated muscle-firing sequence of adequate
strength to protect the spine during the sport activity. The ability to do 5,000 sit-ups may protect the back while doing the
sit-up but not while throwing a football, throwing a baseball, or tackling another player. The key to the exercises is the
first step—being able to isolate trunk musculature, provide a tight contraction, and hold the spine in a neutral, pain-free
position. The therapist and trainer initially assist the individual in learning where the neutral, pain-free position is and how
to use the muscles to maintain that position.
We have found this particular program of exercises helpful in the postoperative recovery of patients after neck and back
surgery. After neck surgery, an appropriate period of spinal immobilization with an orthotic device is required. Then, the
patient may initiate this series of exercises with the assistance of the physical therapist.
Generally, within 3 to 6 weeks after neck or back surgery that does not require bony healing or bony fusion to take place,
we will initiate our isometric trunk-stabilization program. If the wound is well healed, the patient is able to take part safely
in a water rehabilitation program. We will allow patients to enter into a gentle water rehabilitative program at 3 weeks,
doing exercises in the swimming pool, with the individual running in the water while using the wet vest. By 6 weeks
postoperatively, the patient has been able to advance to dry-land exercises that have included progressive walking for
aerobic conditioning. Once well into the healing process, the individual can progress to the Swedish ball exercises, which
use a large beach ball that is able to support the weight of the individual. A whole host of exercises is then performed on
the beach ball, progressing from crunches to wall slides, all the way through full sit-ups, as well as rotational sit-ups and
resistive exercises on the ball.
Isoband exercises use a flexible rubber stretch band and are useful in all aspects of rehabilitative programs including
upper-extremity and lower-extremity strengthening, and in particular, for hip extensor and hip adductor strengthening.
Aerobic conditioning includes skipping rope, exercise bicycle, climbers (Versa Climber), ski machines (Nordic Trac) and
stair machines (Stairmaster). We have been particularly pleased with water running, which includes the performance of
running in place while wearing a flotation-type wet vest. A buoyancy vest or life jacket from a boat can also be useful for
these individuals. As the individual progresses in aerobic conditioning, he or she may even assume the use of old tennis
shoes to increase the weight and resistance on the legs and, thus, increase the aerobic capacity. Water running is
particularly useful in postoperative lumbar spine patients because the non–weight-bearing activity significantly limits the
amount of low back pain present. In fact, it is extremely unusual for even the most severely affected postlaminectomy
syndrome patient to be unable to adapt progressively to a water running program. We recommend a Water Workout
Recovery Program (25) as a source of useful techniques for treating patients in the weight-free environment of the
swimming pool.
CERVICAL STENOSIS
Cervical spinal stenosis and its associated transient neuropraxia of the cervical spinal cord is a source of great
controversy as to recommendations for continued play. Grant ( 26) first described the clinical entity of cervical spinal cord
neuropraxia with transient quadriplegia. Torg describes the clinical picture as an acute transient neurologic episode of
cervical cord origin with sensory changes that may be associated with motor paresis involving either both arms, both
legs, or all four extremities, following forced hyperextension, hyperflexion, or axial loading of the cervical spine ( 27). The
sensory changes include burning pain, numbness, tingling, or loss of sensation, and motor changes consist of weakness
or complete paralysis. Congenital cervical spinal stenosis is associated with a decreased AP diameter of the cervical
spinal canal as measured from the posterior vertebral body to the anterior spinal laminar line on the lateral radiograph.
Acquired spinal stenosis is more likely to occur in the professional level football player with multiple levels of
degenerative disk disease, multiple levels of osteophyte formation, disk bulging, disk herniation, hypertrophy of
ligamentum flavum, and hypertrophy of the facet joints. This combination of degenerative and hypertrophic changes in
the professional football player are not unusual. The absolute minimum sagittal diameter of the cervical spinal canal that
can accommodate the spinal cord without cord compression is somewhere between 11 and 13 mm, depending upon the
relative diameter of the spinal cord. The classic work of Penning ( 28) documented that if the sagittal diameter is less than
11 mm in extension, there is a strong suspicion of spinal cord compression. It was Penning who illustrated the “pincer's
mechanism,” in which the spinal cord is pinched between posterior vertebral osteophytes off of the lip of the vertebral
endplate and the posterior lamina. Certainly, this mechanism of injury is commonly responsible for the production of the
central cord syndrome in individuals with preexisting degenerative disk disease and osteophyte formation who suffer a
hyperextension injury of the head and neck. However, there is ample clinical experience in dealing with professional
football players with sagittal cervical spinal canal diameters of less than 11 mm who have no signs or symptoms of spinal
cord compression. Therefore, as with all radiographic findings, precise clinical correlation of the radiographic findings
with the patient's and physical examination, as well as a basic understanding of the mechanical considerations of the
patient's sport must be considered before making a judgment as to the individual player's risk category. Torg has
concluded that patients in whom an acute transient neurologic episode resulted from forced hyperextension, hyperflexion,
or axial loading of the cervical spine, clearly those individuals with developmental spinal stenosis are not predisposed to
more severe injuries with associated permanent neurologic sequelae.
Torg's assessment of the relationship of cervical stenosis to transitory neuropraxia led to the conclusion that
developmental narrowing of the cervical canal in a stable spine does not predispose an individual to a permanent
catastrophic neurologic injury and, therefore, should not preclude an athlete from participating in contact sports.
However, he believed that athletes who have developmental spinal stenosis as well as demonstrable cervical spine
instability, or acute or chronic intervertebral disk disease should not be allowed further participation in contact sports
(29). We believe there are many factors that must be considered before making such a determination.
Types of Stenosis
There are three basic types of cervical stenosis:
1. Congenital stenosis—which is typified by the short pedicles and funneling shape to the basic bony structure of the
spinal canal, observable on the lateral x-ray
2. Developmental stenosis—which occurs during life and may be the result of thickening of the bone due to increased
stress. For example, upper-body weight lifters, strengtheners, and people who do upper-body and
neck-strengthening exercises produce a larger cervical spine bone, just as they produce larger muscles in the neck
and upper extremity, and as a result, the spinal canal may narrow as the bone increases in size.
3. Acquired cervical stenosis—which is due to cervical spondylosis with bone spurs, disk bulges, bulges of
ligamentum flavum occurring with disk space narrowing, and osteophytes on the facet joints, all contributing to the
cervical stenosis. Of course, there may be more than one type of cervical stenosis present in any patient.
Measurement of Cervical Stenosis
There are different techniques for measuring the size of the spinal canal in order to assess the presence and degree of
cervical stenosis. Torg and Pavlov ( 27) described a ratio of the central canal sagittal diameter to the vertebral body
sagittal diameter measured on the lateral x-ray study in order to remove the x-ray magnification that is always a
consideration in direct measurements. The determination of what is a normal Pavlov ratio in certain population groups is
still somewhat unclear. A Pavlov ratio of 0.8 or less has been used to indicate cervical stenosis, but the ratio was based
on symptoms of transient cord neuropraxia in people with 0.8 or less and a lack of symptoms in people with ratios higher
than that and was scientifically correlated to stenosis. In a group of myelopathic and radiculopathic nonfootball patients,
Schnebel et al. ( 30) compared the ratio to CT scan central canal diameters and found the 0.8 ratio to be an extremely
sensitive but not specific measurement. Every patient who had 10 mm or less of central canal diameter had a 0.8 ratio or
less. The excellent study by Herzog et al. ( 31) that used CT scans and plain x-ray studies of football players provided the
key factors concerning the Torg ratio. He showed that 78% of the football players with an abnormal Torg ratio had a
normal-sized spinal canal. The football players had larger vertebral bodies, therefore distorting the ratio and rendering it
useless in identifying players with cervical stenosis. The report also showed that standardized distance lateral x-ray
studies—with calculations done to eliminate magnification—do correctly identify bony spinal stenosis.
The contribution made by Joseph Torg cannot be underestimated. The 20 years of acquiring records concerning injuries
to football players provided great insight into the overall problem of cervical paralysis in football players. Although many
cases show distinct differences and have characteristics of a number of different injuries, it was Torg's impression and
understanding that there were no instances of permanent quadriplegia in football players that resulted from disk
herniations or spinal stenosis only ( 2). Certainly, there are cases of fracture dislocations that may have had
characteristics of stenosis or a disk herniation, but as isolated entities, there are no records of football players having
been totally paralyzed with these two entities. The 0.8 ratio should not be used as a screening tool because whether
there is a 0.8 ratio or not has no correlation to permanent neurologic deficit. If there is an episode of transient
quadriparesis, then there is a 90% chance there will be a ratio of 0.8 or less, but because the incidence of the transient
quadriparesis has been estimated to be 7 in 10,000 ball players, then whether there is a 0.8 ratio or not cannot be
statistically correlated with any increased chance of transient neuropraxia or permanent deficit. The Torg ratio is of little
value for screening and should not be used for continued play decisions. Because 17+5 mm is the normal sagittal
diameter (32), 10 mm is considered by most to be abnormal stenosis. The contrast CT scan is the definitive technique for
measuring central canal diameter. The contrast CT scan allows one to measure not only the central canal diameter but
also a functional central canal diameter. The functional central canal diameter in the sagittal plane can be defined as the
amount of canal available for the dural sac and spinal cord. The trefoil-shaped canal or the canal with the small, peaked
empty space, exactly in the midline, are canal shapes that do not allow full expansion of the dural sac and cord
throughout its central diameter. When measuring the central canal diameter, including a small, peaked area of space that
could account for 2 mm of measurement yet will not accommodate the dural sac gives a measurement that is of little
consequence to cord function. This is seen also in the lumbar spine, where lateral recess stenosis very commonly
produces a major compression on the entire sac, leaving an empty dorsal portion of the spinal canal.
Matsuura et al. (33), at Rancho Los Amigos Hospital, found a strong coordination between the shape of the spinal canal
and the extent of neurologic injury with fractures and dislocations. They used the ratio of sagittal-to-transverse diameter
and found a strong positive correlation between this ratio and spinal cord injury when compared with controls. Although
the transverse diameter was inversely proportional and the sagittal diameter was directly proportional to the spinal cord
injury, the area of the spinal canal was not. The exact mean ratio varied at different levels but was best correlated at the
three most important levels, C-4, C-S, and C-6. The control mean was approximately 0.6 and the spinal cord injury mean
was 0.5. In this report, the Torg ratio was stated to be not as powerful a discriminator as the sagittal diameter. Ogino et
al. (34) used the sagittal-to-transverse compression' ratio as an indicator of cord damage in myelopathy patients. This
study, performed on cadaveric specimens, shows a relationship between compression ratio and the degree of cord
damage in people with cervical stenosis and myelopathy. The area of the canal as related to the area of the cord has
been found to be important in radiculopathy and myelopathy ( 35) (Fig. 51.12). Measuring the surface area of the dural
sac versus the canal presents some difficulties in determining the surface area of canal available for the sac. The lateral
portions of the canal and the area of the nerve root sleeves, which will not accommodate much cord expansion, should
not be included in the area available for cord expansion.
FIGURE 51.12. X-ray study of a professional football player who persisted with a C6 radiculopathy. The symptoms began
with a forearm blow to the head. Although no myelopathy was present, there was a significant distortion of the cord and
dural sac.
There are cases with a larger spinal cord or a smaller cord-to-sac ratio. Measuring exact cord shapes is dependent on
exact radiologic technique. The presence of a large volume of dye circumferentially around the cord is a good sign, and
the obliteration of dye volarly can be an important sign of volar compression. As seen in cases with a poor compression
ratio, a flat spinal cord is a bad sign.
The amount of motion in the cervical spine is probably proportional to the risk from stenosis. Dynamic MRI has been
used to demonstrate the narrowing of the cervical canal that occurs with extension ( 36). It is well known that that the
cervical spinal canal can narrow up to 2 mm in full extension as compared with the neutral or flexion position. Neurologic
tissue in the spine becomes slack and loose in extension, taut in flexion, and the spinal canal narrows in extension and
opens in flexion ( 37). Numerous clinical syndromes are dependent on these dynamic factors affecting spinal cord and
nerve root function in addition to exact central canal measurements and ratios. The biomechanics of the spinal column
and neurologic tissue motion must be considered in continued play decisions in cases of cervical stenosis.
Bohlman (38) has pointed out the importance not only of canal diameter but also of blood flow to the cord and cervical
motion as three important factors in the determination of symptoms of cervical myeloradiculopathy. Exact quantification of
vascularity to the cervical cord is difficult clinically, but there are vascular abnormalities and insufficient areas of flow that
can certainly predispose an individual patient to neurologic injury.
A fixed kyphotic cervical spine does not respond to axial loading normally and may present a volar cord compression,
with the cord tethered over volar osteophytes. Batzdorf and Batzdorf ( 39) showed that patients with a kyphotic cervical
spine had more neck pain and responded less well to laminectomy for cervical myelopathy than did patients with a
lordotic cervical spine.
FACTORS IN DECISION MAKING IN TRANSIENT QUADRAPARESIS AND SPINAL CANAL

STENOSIS
There are numerous decision-making factors in these cases. Among these factors are severity of the episode, extent of
neurologic deficit, severity of the symptoms, age, player position, and neck size. The numerous methods of assessing
cervical canal size bear consideration. Regardless of the canal diameter, it is more dangerous for someone who suffers a
greater neurologic injury with the episode to return to play. The severity of the episode is important. A person who had
symptoms of myelopathy lasting more than 6 months is obviously at greater risk for return of those symptoms than
someone who had the episodes for 5 seconds. Each case is a variation of severity of symptoms, type of neurologic
deficit, extent of neurologic deficit, and longevity of the symptoms. The important things are the history and physical
examination. One must document very carefully exactly what happened through the history and physical examination.
The neurologic examination must be immaculate to identify and to quantify the deficit present.
We have found the rating system shown in Table 51.1 to be helpful in assessing the severity of the episode. However,
every factor in a case may be considered in its entirety.
TABLE 51.1. RATING SYSTEM TO ASSESS SEVERITYa
In terms of the three major risk factors in Table 51.1, adding in the canal diameter rating to the time and extent of deficit
scale, we use a general rating of 6 or below as a mild risk factor, 6 to 10 as a moderate risk factor, and 10 to 15 as a
severe risk factor. It must be emphasized, however, that each case is very individualized. For example, a player with a
brief episode with a 4-mm canal or 6 months of myelopathy with a 15-mm canal may be precluded from play forever. The
rating scale is only a guideline. Clinically, we use the rating scale, extenuating factors such as the level of play and the
risk vs. benefit to the patient. The risk-versus-benefit ratio is often an unquantifiable factor. An informed consent
concerning continued play with cervical stenosis and a prior episode of transient quadraparesis should include an
accurate assessment of as many known facts as possible. The incidence of permanent paralysis in professional football
players is rare. Permanent paralysis in any football player is most related to blocking and tackling techniques. An episode
of transient quadraplegia does not necessarily precede an incident of permanent neurologic loss. Cantu ( 40) reports
three cases in which this occurred but did not have such a case in the Registry. Just because one has stenosis does not
mean he will tackle someone head-on, get a fracture dislocation, and be a permanent quadriplegic. Indeed, it may have
no specific relation to such a future incident.
A good example of a consent would be to inform those concerned that there is no direct predisposition between having
stenosis and getting the fracture dislocation that typically paralyzes football players. Give advice concerning what we do
know about nonfootball players. There are several facts known about cervical stenosis in nonfootball players. The report
by Eismont's et al. (41) demonstrates that the greater degree of cervical stenosis with a specific cervical spine injury, the
greater the neurologic deficit. Matsuura et al. ( 33), as stated previously, found that it is not just the central canal diameter
but the shape of the canal that is important. The greater the compression ratio, the greater the degree of neurologic
deficit with a spine injury. Edwards et al. ( 42) demonstrated that an individual with a cervical canal stenosis is more likely
to require surgery with a cervical disk herniation and less likely to be able to recover nonoperatively ( 42,43). Radicular
pain is more common in smaller canals ( 44). In the Epstein study (45), there were 20 patients of 200 admissions to an
acute spinal cord injury unit who had no fracture or dislocation but had complete neurologic deficit. Among these cases
were various diagnoses of cervical spondylosis, congenital stenosis, and others, but the study indicates that permanent
neurologic deficit can occur with spinal stenosis ( 17). The incidence of permanent tetraplegia in spinal column injury has
varied from 4% to 70% of pediatric neck injuries, depending on the sample studied. Others have hypothesized on the
etiology of quadriplegia without fracture dislocation to be a combination of injury to microvascular blood supply,
longitudinal traction on the cord, acute disk prolapse, or compromise of the vertebral spinal arterial system ( 46,47,48,49
and 50). A common pathology in these cases is a central cord infarct ( 51). As for the recurrence of symptoms, multiple
episodes do occur but can potentially be prevented through proper equipment, conditioning, and technique.
OTHER FACTORS IN ANY CONTINUED-PLAY DECISION
Although every position on the football field is subject to head trauma, the worst are the impact positions of defensive
back and linebacker. Blocking and tackling techniques can rarely be changed at the professional level. If the player is a
head hitter, he usually stays a head hitter. Education for proper blocking and tackling by using the shoulders, not the
head, must be aimed at athletes at younger ages, starting with those in grade school and continuing through college.
What are the chances of recurrent injury once a player has been injured? Albright et al. ( 52) have offered some excellent
insight into this situation. At the high school level, the reinjury rate, after all neck injuries, one third of which had extremity
or neurologic symptoms, was 17.2%. The twice-injured players at all levels of play had an 87% chance of future injury or
significant history of past injury. After an injury for which time in the game is lost, the recurrent injury rate was 42%; 62%
in the next season; and 67% in future seasons ( 37). Therefore, the recurrent injury rate is significant regardless of the
type of injury received and is higher with the time-lost neck injury.
What can be done to prevent this recurrence? Conditioning can prevent injury. A preconditioned response to predicted
head stresses can allow an increased protective muscle reflex response to ward off even relatively unexpected blows
(53). Neck strengthening can help protect the player from neck injury ( 54). Probably the greatest testament to
conditioning is the ability of professional football players to deliver or receive high-impact blows without injury.
Using the head for contact produces dangerous mechanisms for cervical injury ( 55). Protective wear is limited to good
shoulder pads with a high neck roll that is built up on the lateral neck. The posterior rolls are not as helpful as the side
rolls because the shoulder pads are more likely posterior at contact and the neck straight. The spine straightens with
slight flexion to deliver the axial loading blow with the top of the head ( 53). Although the mechanism of pure extension
has been implicated as a source of serious injury, others believe that it is not a significant source of major cervical injury
in football. The lateral pads can help with lateral flexion and rotation toward the painful arm so common in burners and
stingers. The majority of stingers and burners are root injuries, not a brachial plexus traction injury, and C-6 is the most
common root involved. The most effective method of preventing the high risk of recurrent neck injury is to allow total
recovery of pain, relief from tenderness, and restoration of a normal range of motion as well as maximum strength before
returning to action. Normal clinical muscle function is more important than changes, for example. Good nonoperative
cervical care, such as may be used with a herniated cervical disk, can improve symptoms from neck injuries in football
players. A mainstay of our exercise rehabilitation program is a chest-out posturing exercise program, which concentrates
on entire trunk strength as well as neck and upper extremity strength.
Responsibility is always a consideration, and it is important to emphasize that the doctor who performs the players'
physical examinations and clears them to play bears a certain responsibility to the patient. Through proper informed
consent, the patient and family are also responsible. The team, as an employer, in any worker's compensation situation,
is naturally responsible for the health of its employees as well as for fielding an effective team. Earlier, reference was
made to risk versus benefit to the patient. The benefit of continued play to the patient is well known to the patient, family,
agent, team, and others. The risk to the patient can be very difficult to define as a reality. Proven facts are science, and
predictions are basically educated guesses. Nevertheless the physician must present the risks to the patient as clearly as
possible. It is hoped that this chapter provides some guidelines for decision making in situations in which football players
have injured their necks and want to return to football. Obviously, there are many factors to consider in a decision that is
of great importance to those involved.
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52 Lumbar Spine Injuries in Athletes
52
LUMBAR SPINE INJURIES IN ATHLETES

ROBERT G. WATKINS
LYTTON A. WILLIAMS
Anatomy
Diagnosis
Biomechanics
History and Physical Examination
Nonoperative Care
Trunk Stretching and Strengthening Program
Operative Care
Individual Sports
Gymnastics
Ballet
Water Sports
Pole Vaulting
Weight Lifting
Football
Rotational and Torsional Sports
Golf
Baseball
Tennis
Chapter References
Low back pain has been a significant factor in many different types of athletic activity. The severity and extent of back
pain often determine the actual ability to compete and are a worry to all concerned from the athlete, the family, coaches,
and trainers to those responsible for paying the bills. Essentially, treatment of the athlete with a lumbar spine injury
involves an understanding of basic anatomy, biomechanical function of the spine, the diagnosis of conditions affecting
the lumbar spine, proper use of diagnostic studies, and a systematized all-inclusive history and physical examination. We
must understand some factors that are important in predisposing the athlete to lumbar spine problems, as well as training
and therapeutic techniques to prevent lumbar spine problems in athletes. Among the predisposing factors to back pain in
athletes are increased trunk length and stiff lower extremities ( 1). Occulta spina bifida is found in a higher incidence of
patients who develop lower lumbar spondolytic defects ( 2). The exact relation of exercise and back pain in athletics,
when compared with the average population, does not demonstrate an increased incidence in back pain in athletes
participating in organized sports as opposed to regular students. Fairbank et al. ( 1) found that back pain was more
common in students who avoided sports than those who participated. In 1984, Fisk et al. ( 3) found that prolonged sitting
was the important factor in the pathogenesis of Scheuermann's disease as opposed to athletes lifting weights,
undergoing compressive stresses, or doing heavy lifting and part-time work. This study showed that 56% of men and
30% of women had some x-ray evidence of changes similar to Scheuermann's disease in one review of 500 17- and
18-year-old students ( 3).
In an interesting review of back injuries, Keene et al. ( 4) found that 80% of back injuries occurred during practice, 6%
during competition, 14% during preseason conditioning. Eight percent were men and 6% women, which was of no
statistical significance. The nature of the injury was usually an acute injury in 59%, overuse injury was found in 12%, and
aggravation of a preexisting condition was found in 29%.
ANATOMY
The vertebral column is a series of linked intervertebral joints. The joint is made up of the intervertebral disk; its two facet
joints; and concomitant ligaments, vessels, and nerves, and is referred to as a neuromotion segment. A neuromotion
segment is considered as one of the basic units of spine anatomy and function. The lumbar spine has a lordotic curve,
which plays an important role in the biomechanics of the lumbar spine. The spine is broken down into two basic columns.
The anterior column consists of the disk and vertebral bodies and the accompanying longitudinal ligaments, the anterior
longitudinal ligament, and the posterior longitudinal ligament. The posterior column consists of the facet joints, lamina,
spinous process, ligamentum flavum, and pars interarticularis. The disk itself may be described as a circular,
multilaminated ligament that connects the two vertebrae together. The nucleus pulposus is the central, more gelatinous
portion of the disk; the annulus is the multilayered woven basket with fibers at precise angles to resist torsional and
compression forces. The annulus is firmly anchored to the endplate of the vertebrae. The annulus, nucleus, and the
accompanying endplates are excellent at resisting compressive forces, but they do not resist torsional forces as well. The
orientation of the facet joint is different at every level of the spine. In the lumbar spine, the facet joints are oriented in a
more transitional phase from parasagittal in the upper lumbar spine to often a more coronal orientation in the lower
lumbar spine. This parasagittal orientation allows good motion in flexion and extension, and less motion in lateral flexion.
The parasagittal orientation of the facet joints would naturally resist rotation, but produces victims of high torsional forces
that overcome the strength of the joint, tearing the annulus and injuring the facet joints. When considering the anatomy of
the spine, one must consider the important role of the entire cylinder of the trunk and its supporting muscles. The static
ligamentous structures of the spine provide considerable resistance to injury, but this resistance in itself would be
insufficient to produce proper spine strength without the additional support provided the spine through the trunk
musculature and lumbodorsal fascia. Muscle control of the lumbodorsal fascia allows a much higher resistance to
bending and loading stresses. The lumbodorsal fascia and the muscles attaching to it must be considered of equal
importance to the more specialized function of the intervertebral disk and facet joints.
DIAGNOSIS
It cannot be emphasized enough that obtaining a proper diagnosis in the athlete presenting with low back pain is crucial.
It is the key to initiating an appropriately aggressive diagnostic and therapeutic plan ( 5,6). Especially in the adolescent
and younger athlete, a high index of suspicion must be maintained to diagnose conditions such as stress fractures and
spondylotic defects accurately ( 7). A great variety of pathologic conditions can be diagnosed on plain x-ray study, and
their relationship to the athlete and his sport can be more specifically addressed ( 8). The bone scan is a vital part of the
diagnostic armamentarium of the physician caring for lumbar spine problems in athletes. An adolescent athlete with
significant back pain persisting longer than 3 weeks should undergo x-ray studies and a bone scan. Unusual conditions
range from osteoid osteoma, infections, and stress fractures of the sacroiliac (SI) joint to the more routine spondylotic
defects. The incidence of spondylotic defects seen on x-ray study is approximately 30% to 38%, and 35% of young
athletes presenting with significant lumbar pain have a positive bone scan ( 7,9).
In diagnosing the exact etiology of the lumbar spine pain in athletes, age is an important factor. Young athletes are
certainly more likely to have stress fractures and to have congenital predispositions to stress fractures. Diseases that
affect growing cartilage are more common in young athletes, such as Scheuermann disease. In the mature athlete, often
the radiologic assessment involves distinguishing between age-related, asymptomatic changes and symptomatic recent
trauma. Is the L-5 to S-1 disk degeneration the symptomatic level in a 30-year-old athlete, or is it an asymptomatic
finding? The diagnostic plan must use an organized system of diagnosing the most common conditions as well as
retaining the ability to diagnose the rare conditions such as a herniation of the inferior lumbar space ( 10) or osteoid
osteoma.
One of the most important diagnoses to make in the athlete with back and leg pain is that of peripheral nerve injury and
peripheral nerve entrapment. There is a great variety of peripheral nerve problems ranging from a generalized peripheral
neuropathy to carpal tunnel syndrome, piriformis syndrome, perineal nerve injury, femoral neuropathy, and interdigital
neuroma. The chief reason for obtaining an electromyogram (EMG) and nerve conduction study of the lower extremities
is to diagnose a peripheral nerve problem. The nerve conduction study combined with a careful physical examination can
at least raise the distinct possibility of a peripheral nerve problem and heighten the diagnostician's skepticism concerning
small, potentially asymptomatic spinal lesions in the role of the patient's extremity nerve pain.
SPONDYLOLYSIS AND SPONDYLOLISTHESIS
Age is important in the natural history of spondylolysis and spondylolisthesis. There is a 4.4% incidence at age 6 years,
increasing to 6% by adulthood. It is unusual for children to present with spondylolysis before the age of 5 and unusual for
young children to present with severe spondylolisthesis, which is defined as grade III or IV. Most symptoms appear in
adolescence, but luckily, the risk of progression after adolescence is low, being approximately 15%. Symptoms cannot be
correlated with the degree of slip. A high degree of slips may present with deformity and very little pain. Many times, it is
the pain of an injury that leads to the identification of spondylolisthesis that may not be originating in the spondylolisthetic
segment.
Isthmic spondylolisthesis develops as a stress fracture. It is believed that there is a hereditary predisposition to
developing the stress fracture, and there is certainly the predisposition in conditions in which the bone of the pars
interarticularis is not sufficient to withstand normal stresses. Also, certain mechanical activities that expose the patient to
repeated biomechanical challenge, increasing stress concentration on the pars interarticularis, have a higher incidence
of spondylolisthesis. The concept of repeated microtrauma with concentration of these stresses in the pars interarticularis
has become increasingly recognized in adolescent athletes participating in certain sports such as gymnastics and weight
lifting.
The most common site for spondylolysis and spondylolisthesis is L-5 to S-1. The slippage in spondylolisthesis results
from the lack of support of the posterior elements produced by the stress fracture of the pars interarticularis. The
spectrum of neurologic involvement runs from rare to more common with higher degree slips. The majority of neurologic
deficits are an L-5 radiculopathy with an L-5 to S-1 spondylolisthesis. Cauda equina symptoms are more likely in grade III
or IV slips. Cauda equina neurologic loss is rare.
The diagnostic and therapeutic plan for spondylolisthesis begins with a high degree of diagnostic suspicion in the
adolescent athlete with low back pain. Approximately one third of adolescent athletes presenting with low back pain have
a positive bone scan for a stress fracture. Certainly, a patient with low back pain that is not resolved within 3 weeks
should have a bone scan. If the bone scan is positive, the patient should have a computed tomography (CT) scan to
determine whether there is a demonstrable stress fracture or if the bone is hot due to impending fracture. If the bone
scan is negative and the lumbosacral pain persists, a magnetic resonance imaging (MRI) scan is indicated. A
combination of an MRI, a bone scan, and a CT used in this manner should indicate the diagnosis of most significant
pathologic conditions in the lumbar spine.
The treatment plan for spondylolisthesis is basically rest or restriction of enough activity to relieve the symptoms. This
may vary from simply removing the athlete from the sport until the pain has significantly improved; to immobilization in a
lumbosacral corset, Boston brace, or TLSO; or bed rest and casting.
In summary, stop the pain through whatever amount of inactivity it takes. In a patient with a hot bone scan, we routinely
brace the patient and restrict that activity for a minimum period of 3 months. Repeat the bone scan, and if it is negative,
sufficient healing has taken place to allow beginning a rehabilitation program. If the bone scan is still positive, and the
athlete is asymptomatic, it is a very difficult decision at times whether to begin the athlete in a rehabilitation program or
continue further restriction. We usually continue restrictions another 3 months. Injuries that are found on unilateral hot
bone scans with or without fracture have a reasonably high incidence of healing, and adolescent athletes in general
should be treated with the idea in mind of healing the defect. Bilateral stress fractures are less likely to heal despite
comprehensive nonoperative therapy.
If the bone scan is cold and there is a spondylitic defect present, we treat these patients as we would any patient with
mechanical low back pain. This approach usually involves a progressively vigorous trunk stability rehabilitation program.
We put no permanent restrictions on athletes with spondylolysis or spondylolisthesis. It should be obvious that patients
with grades III to IV spondylolisthesis are less likely to be able to participate in vigorous sports activities without pain and
discomfort. They should probably avoid the heavy strength sports such as football and weightlifting.
There is a high incidence of spondylolysis and grades I and II spondylolisthesis in sports. As a long-term factor, this
condition is not considered to be significant enough to impair an athlete's ability to play or not.
BIOMECHANICS
The understanding of the basic biomechanics of the lumbar spine begin with an understanding of the forces and stresses
applied to the spine as related to the normal curvatures of the spine. Because of the lordotic shape of the spine, the
results of vectorial force on the spine are usually made up of a vertical axial loading compressive force perpendicular to
the surface of the disk and one horizontal to the disk, producing a shear strain. The combination of these two forces
produces both tensile stress in the annulus fibrosis and a shear force on the neural arch. The center of gravity of body
weight is anterior to the spine. This weight times the distance back to the spine produces a lever arm effect of the weight
of the body. This is resisted by the erector spinae muscles and the lumbodorsal fascia. When there are abnormal
stresses applied to this equation, it may result in annular tears of the intervertebral disks or stress fractures on the neural
arch due to this excessive resistive force. The most common place for stress fractures, of course, is the pars
interarticularis.
The basic mechanism of injury produces a combined vector of force that may be difficult to analyze in a force diagram.
The three basic mechanisms of injury to consider are
1. Compression or weight loading to the spine.

2. Torque or rotation. This may result in various shear forces in a more horizontal plane.
3. Tensile stress produced through excessive motion on the spine.
The compressive type of stress is more common in sports that require high body weight and massive strengthening such
as football and weight lifting. Torsional stresses occur in athletes throwing the javelin, baseball players, and golfers.
Motion sports that put tremendous tensile stresses on the spine include gymnastics, ballet and other forms of dance, pole
vault, and high jump.
Sprains and strains result from direct blows. Certainly in sports like football, there can be muscle contusions, muscle
stretches, tears of fascia, ligaments, and occasionally, muscle.
Lumbar fractures can occur from direct blows to the back with fracture of the spinous process or twisting injuries that
avulse the transverse process. Vertebral body endplate fractures from axial compression load on the disk is a relatively
common source of compressive disk injury, whereas the annulus is more likely injured in rotation. The endplate is more
vulnerable to compression than the annulus. Flexion rotation fracture dislocations of the cervical and lumbar spine are
certainly possible. Axial loading compression injuries can result from jarring injuries in motor sports or boating. In any
sport in which one athlete falls on another, the mechanism is similar to that of the coal face injury, with the rock falling on
the coal miner while he is on all fours. An athlete can suffer an asymmetric loading, rotational injury to his thoracolumbar
spine.
The intervertebral disk is injured predominantly through rotation and shear. Producing circumferential tears and radial
tears. Initially, the layers may actually separate or the inner layers may break. As the inner layers weaken and are torn,
there is added stress on the outer layers. This can produce a radial tear of the intervertebral disk. With the outer layers
torn, the inner layers of annulus break off and, with portions of the nucleus, are forced with axial loading to the place of
least resistance, the weak area in the annulus. The outer areas of annulus are richly innervated, producing tremendous
pain and reflex spasm when the annulus tears. The spasm and pain are mediated through the sinu-vertebral nerve with
anastomosis through the spinal nerve to the posterior primary ramus. As the herniated material extrudes and produces
pain from the transversing or exiting nerve root itself, the patient may develop sciatica or radiculopathy. Intradiskal
infiltration of the granulation tissue adds increased potential for painful sensation in the annulus. With time, the annulus
can heal, although the healing annulus will not retain the same biomechanical function capability as the original
intervertebral disk.
Biomechanical functioning of the spinal column and its relationship to the biomechanics of nerve tissue involves several
basic concepts:
1. In the spine, flexion of the lumbar spine increases the size of the intervertebral canal and the intervertebral
foramina (11).
2. Extension decreases the size of the intervertebral canal and the intervertebral foramina ( 11).
3. Flexion increases dural sac and nerve root tension ( 12).
4. Extension decreases dural sac and nerve root tension ( 12).
5. Front flexion, axial loading, flexion, and upright posture increase intradiscal pressure.
6. With flexion, the annulus bulges anteriorly ( 13).
7. With extension, the annulus bulges posteriorly ( 13).
8. Nuclear shift in an injured disk is poorly documented but probably corresponds with annular bulge ( 11).
9. Rotation and torsion produces annular tears and disk herniations ( 14).
It can be concluded from these facts that motion does have an effect on the nerves and the neuromotion segments of an
injured area. For example, if there is a spinal obstructive problem, such as spinal stenosis, extension exercises can
further compress the neurologic structures and make them worse; or if there is a nerve root tension problem, such as disk
herniation, then flexion can produce increased tension in an already tense nerve and increase symptoms.
HISTORY AND PHYSICAL EXAMINATION
The key to a proper history and physical examination is to have it standardized because that practice accomplishes the
needed specific objectives.
1. Quantitate the morbidity. Use a scale value of pain, function, and occupation to understand how sick the patient is.
Converse in detail with the patient to hear the inflections and manner of pain description. Detail the time of disability and
the time of origin of the pain.
2. Delineate the psychosocial factors. Know what psychological effect the pain has had on the patient. Know the social,
economic, and legal results of the patient's disability. Understand what can be gained by his or her being sick or well.
Derive an understanding of what role these factors are playing in the patient's complaints.
3. Eliminate the possibility of tumors, infections, and neurologic crisis—these conditions have a certain urgency that
requires immediate attention and a diagnostic and therapeutic regimen that is very different from those required for disk
disease.
4. Diagnose the clinical syndrome:
a. Nonmechanical back or leg pain. Inflammatory, constant pain, minimally affected by activity, usually worse at night
or early morning.
b. Mechanical back or leg pain. Made worse by activity and Valsalva maneuver; relieved by rest.
c. Sciatica. Predominantly radicular pain and positive stretch signs, with or without neurologic deficit.
d. Neurogenic claudication. Radiating leg pain or calf pain, worse with ambulation and spine extension, negative
stretch signs, relief with flexion.
Pinpoint the pathophysiology causing the syndrome. Three important determinations are the following:
1. What level? Which neuromotion segment?

2. What nerve?
3. What pathology: What is the exact structure or disease process in that neuromotion segment that is causing the
pain?
The history and physical examination are the first steps in determining the clinical syndrome. Some key factors are:
1. The time of day during which the pain is worse.

2. A comparison of pain levels during walking, sitting, and standing.
3. The effects of the Valsalva maneuver, coughing, and sneezing on pain.
4. The type of injury and duration of the problem.
5. A percentage of back versus leg pain. We insist on getting an accurate estimate of the amount of discomfort in back
and legs. There must be two numbers that add up to 100%.
The physical examination should address:
1. The presentation of sciatic stretch signs.

2. The neurologic deficit.
3. Back and lower extremity stiffness and loss of range of motion.
4. The exact location of tenderness and radiation of pain or paresthesias.
5. Maneuvers during the examination that reproduce the pain.
The history determines whether it is an axial (back pain) or extremity (leg pain) problem. What is the exact percentage of
back versus leg pain? Is the pain made worse by the mechanical activity or is it a constant resting pain? Is the pain
worsened by maneuvers that increase intradiscal or intraspinal pressure? Is there significant night pain?
Classic radiculopathy causes radicular pain radiating into a specific dermatomal pattern, with paresis, loss of sensation,
and reflex loss. The radicular pattern of the pain and neurologic examination determines the nerve involved.
The classic history for radiculopathy resulting from a disk herniation is back pain that progresses to predominantly leg
pain. It is made worse by increases in intraspinal pressure such as coughing, sneezing, and sitting. Leg pain
predominates over back pain, and mechanical factors increase the pain. Physical examination shows positive nerve
stretch signs. A dermatomal distribution leg pain that is made worse by straight leg raising, sitting or supine, leg-straight
foot dorsal flexion, neck flexion, jugular compression, and direct palpation of the popliteal nerve or sciatic notch is
characteristic of radiculopathy. A source of radicular pain not found in this description is that caused by spinal stenosis.
Spinal stenosis usually lacks positive nerve stretch signs but has the characteristic history of neurogenic claudication
(i.e., leg and calf pain produced by ambulation). Pain that does not go away immediately on stopping is made worse with
spinal extension and is relieved by flexion. The pain progresses from proximal to distal.
The pain drawing is a major help in accomplishing the objectives of the physical examination. Each patient completes the
pain drawing using a rating system, which distinguishes organic from psychological pain fairly well. It also helps localize
the symptoms for future reference with pain reproduction studies such as with discography and postoperative
evaluations.
The initial history and physical evaluation determine the aggressiveness of the diagnostic and therapeutic regimens. The
morbidity rating and the time the patient has had the problem are important parts of the history and physical examination
that help determine the aggressiveness and invasiveness of the diagnostic plan. The leg pain versus back pain ratio is
an important factor in determining which diagnostic tests are indicated. Leg pain leads to tests for nerve function and
obstructive pathology in EMG/NC, myelogram, contrast CT scan and MRI. Evaluation of back pain includes, at times,
bone scan, MRIs, and discograms. The clinical syndrome should be distinguished as predominantly mechanical pain,
axial pain, and leg pain. An appropriate treatment program can begin, based on the initial evaluation.
Most athletic injuries to the lumbar spine fall under the category of mechanical, axial, back, or leg pain. Within this
category a number of different syndromes exist:
1. Annular tear of the intervertebral disk—usually a loaded compressive rotatory injury to the lumbar spine producing
severe, disabling back spasm and pain. The pain is usually worse in flexion with coughing, sneezing, straining, upright
posture, sitting, and with any other situations that increase intradiscal pressure. There may be referred leg pain, low back
pain with straight leg raising, and anterior spinal tenderness. Annular tears can be produced with as little as 3 degrees of
high-torque rotation ( 15). Facet joint alignment that protects the disk from rotatory forces may lead to facet joint injuries
as the annulus fails in rotation.
2. Facet joint syndrome—more typically occurring in extension with rotation, reproduced with extension rotation during
the examination. May present with a pain on rising from flexion, with a lateral shift in the extension motion. Point
tenderness in the paraspinous area over the facet joint and may be associated with referred leg pain.
3. Tears of the lumbodorsal fascia and muscle injuries and contusions present with muscle spasm, stiffness, and many of
the characteristics of facet joint syndrome in annular tears.
4. Sacroiliac joint pain and pain in the posterior superior iliac spine. The most common referred pain area for pain from
the annulus in the intervertebral disk, and the neuromotion segment of the spine is across the posterior surface of the
ilium, which includes the posterior superior iliac spine and SI joint. Sciatic pain can hurt in the sciatic joint area as well as
the sciatic notch and buttocks. Although injuries can occur to the SI joint, the vast majority of syndromes presenting with
SI joint pain are believed to be the result of referred pain from a neuromotion segment in the spine.
The most important thing to be accomplished during the physical examination of the athlete is to demonstrate what types
of motions reproduce the patient's pain. Where exactly is the tenderness? What deformity is present in the spine? If there
is a lateral shift, in which direction? The chief advantage that physical therapists and athletic trainers have in the
treatment of the athlete with lumbar spine pain is the hands-on approach directed specifically to motions and activities
that produce and relieve the pain. Local modalities can be directed specifically to localized areas of inflammation and
pain. Treatment of referred pain areas through localized treatment in the area of the referred pain plays a major role in
the relief of symptoms and return to performance. Therefore, techniques of treatment of referred pain should be
understood and used. This may vary from injections of local anesthetic, cortisone injections, transcutaneous electrical
nerve stimulator (TENS) units, ultrasound, and ice.
Another important diagnostic category in these patients is to identify areas of contracture and weakness on the physical
examination. The physician and therapist can make the diagnosis by carefully examining the patient for areas of muscle
atrophy and loss of range of motion. Some very sophisticated testing and dynamic EMG function has identified localized
areas of weakness in the shoulders as well as in the abdominal musculature of baseball pitchers ( 16). There is a great
deal of skill involved in the physician being able to recognize these deficiencies in the physical examination and design a
rehab program to correct them.
NONOPERATIVE CARE
The nonoperative treatment plan begins with several basic rules.
1. Stop the inflammation

2. Restore strength.
3. Restore flexibility.
4. Restore aerobic conditioning.
5. Return the patient to full function.
To stop the inflammation of the spine in an injured athlete often requires rest and immobilization. We try to limit the rest
and immobilization to the minimum. Bed rest produces stiffness and weakness, and in turn, stiffness and weakness
causes the pain to persist. Stiffness and weakness are the antithesis of the body functions necessary for athletic
performance. Every day of rest and immobilization may increase the of rehabilitation before the athlete is able to return to
performance. As in motion treatment of lower-extremity injuries, that is, fracture bracing and postoperative continuous
motion machines, rapid rehabilitation of lumbar injuries in athletes requires effective means of mobilizing the patient. Bed
rest for longer than 3 to 5 days is not of any benefit in the natural history of the disease. Rapid mobilization requires
strong antiinflammatory medications, ranging from epidural steroids, oral methylprednisolone (Medrol Dose Pak), or
indomethacin (Indocin SR) to other nonsteroidal antiinflammatory agents and aspirin, ice, a TENS unit, and mobilization
with casts, corsets, and braces. Corsets and braces are used for only limited periods of time, and strengthening
techniques are started when the brace is applied in order to remove braces as soon as possible. Braces in themselves
can cause a significant amount of stiffness and weakness. Exact timetables are difficult. The amount of time the brace is
left on should be based on the individual patient's history and physical examination. As a general rule, we treat acute
disk herniations with 3 to 5 days of bed rest; physical therapy within seven days; a corset for no longer than 10 to 14
days; indomethacin (Indocin), occasionally methylprednisolone (Medrol), and less commonly, epidural injections. The
therapist begins the neutral position, isometric trunk strengthening program, and depending on the response of the
patient, evolves into resistive strengthening, motion, and aerobic conditioning as tolerated.
Part of the key to being able to initiate early therapy is understanding, based on the physical examination, what creates
the symptoms. Nonoperative care should be the basis of any therapeutic approach to athletes with lumbar spine injuries.
With the exception of cauda equina injuries, this should also be true in the athlete with a neurologic deficit. The key to
effective nonoperative care is to have a well thought-out, balanced biomechanical approach. Common questions asked
are whether to do extension exercises, flexion exercises, or twisting exercises; what type of aerobic exercising should be
done; when can someone lift weights; what role do Nautilus beautification exercises have in rehabilitation of the athlete;
and also, what type of nonoperative rehabilitation is best for the individual athlete's sport?
All physicians are concerned about the risk of increasing neurologic deficit and the risk of producing a neurologic deficit
through nonoperative care. So often, nonoperative care, in the face of a neurologic deficit, consists of no care. Bed rest
is the usual, initial stage of the athlete with a lumbar spine injury and neurologic deficit. It is believed that bed rest best
protects the patient from increasing injury to the spine and, therefore, increasing neurologic deficit. Unfortunately, bed
rest also produces profound weakness, loss of biomechanical function, and actually increasing risk of injury owing to the
weakness and stiffness produced by bed rest. If the purpose of bed rest is to decrease inflammation, the logical
substitute would be aggressive antiinflammatory medication. If the objective of bed rest is to prevent motion, braces and
casts can be substituted. If the objective of bed rest is to prevent abnormal motion that could injure the spine, it is with the
understanding that certain mechanical functions have to take place. Patients get on and off of bed pans, and they get up
to go to the bathroom. They roll over in bed. They cough, sneeze, and eventually have to walk. It seems logical that if we
could design an exercise system that would prevent abnormal motion while restoring strength and flexibility in a
biomechanically sound fashion, then the spine could be protected from the abnormal motion that produces injury, and
healing potentially can be enhanced. This enhancement takes place through normal biomechanical motion in the injured
part through increasing strength and flexibility in the adjacent portions of the body that can absorb the stress potentially
directed to the injured part and in preventing the atrophy, weakness, and stiffness caused by inactivity.
Lumbar spine injuries in athletes is a category that often demands prevention of atrophy and stiffness, as well as
restoration to maximum function as early as possible. Also, it follows that if this restoration can be achieved in athletes, it
can function just as effectively in steelworkers, secretaries, weekend athletes, and housewives. Obviously, the key to the
program lies in safety and effectiveness. If you could summarize an overall basis to our preferred rehabilitation program,
it would lie in the concept of neutral position isometric strengthening for the spine. This program is derived from work by
Jeff Saal, Arthur White and others, including Celeste Randall, Ann Robinson, and Clive Brewster.
TRUNK STRETCHING AND STRENGTHENING PROGRAM
This exercise program concentrates on trunk strength and trunk mobility, balance, coordination, and aerobic conditioning.
A practical application of the use of trunk strengthening is in back treatment, injury prevention, and improved
performance in throwers.
It certainly appears that the place to begin the rehabilitation program in an injured lumbar spine, with or without
neurologic deficit, should be with neutral position isometric strengthening. The basis of the trunk stability program is to
have the patient find a neutral, pain-free position, lying supine on the ground with the knees flexed and feet on the
ground. This is the least traumatic approach to rehabilitation. Also, it forms the basis of an important concept not only in
athletic function but in activities of daily living for everyone. We retrain muscles to work to support the spine while the
patient is using the arms and legs. It is not only theoretically ideal but is practically possible. Teaching muscle control
with tight, rigid contraction of the muscles and controlling the spine through the lumbodorsal fascia, with the gluteus
maximus, oblique abdominals, latissimus dorsi, not only produces protection of the lumbar spine but also improves
athletic performance. The power and strength of any throwing athlete comes from the trunk. Lifting weights requires
functioning of the lumbodorsal fascia.
Trunk strength also prevents back injuries and is an important treatment method for back pain. Although treatment plans
for symptomatic back pain patients may include similar exercises, each of the treatment plans should be designed to
match the examination and the symptoms. Any trunk-strengthening plan puts strain on the spine and can produce back
pain due to overload. Therefore, it should be conducted in a controlled, progressive manner.
The key to safe strengthening is the ability to maintain the spine in a safe, neutral position during the strengthening
exercises. For upper-body strengthening, the spine must be well aligned with the chest-out/chin-tucked posture. Doing
isometric trunk exercises and upper-body exercises emphasizing this chest-out/chin-tucked posture will strengthen the
support for the cervical spine, strengthen the postural muscles necessary for maintaining proper body alignment, and
prevent neck pain due to athletic activity.
For the lower body, trunk control plays a vital role in the ability to rotate and transfer torque safely. Trunk-strengthening
exercises such as sit-ups and spine extensions produce strength. Flexibility produces a protective range of motion, but
often, the key is providing trunk strength and control at the proper moment during the athletic activity. For example, a
baseball hitter goes from flexion through rotation to extension. If his trunk musculature does not maintain rigid control,
despite these changes in the axis of alignment, he may lose power or get a back injury. Therefore, you can have strong
muscles, but if they do not fire in sequence at the proper time, they will not protect the athlete from injury and certainly
will not enhance performance. A key to producing a safe range of motion is to begin trunk control in the safe, neutral
position; establish muscle control in that position; and maintain it through the necessary range of motion to perform the
athletic activity.
We begin our identification of the neutral spine position with the dead-bug exercises. Dead-bug exercises are performed
supine with the knees flexed and feet on the floor ( Fig. 52.1). With the assistance of the trainer or therapist, the player
pushes his lumbar spine toward the mat until he exerts a moderate amount of force on the examiner's hand. This is not
exaggerated, back flattening, extreme force, but a moderate amount of painless force on the examiner's hand. The player
is then taught to maintain this same amount of force through abdominal contraction while
FIGURE 52.1. Identification of the neutral position begins with the dead-bug exercises.
1. Raising one foot.

2. Raising the other foot.
3. Raising one arm.
4. Raising the other arm.
5. Raising one leg.
6. Raising the other leg.
7. Doing a leg flexion and extension with one foot.
8. Doing a leg flexion and extension with the other foot.
These same exercises can be performed with weights on arms or legs.
The next stage for torque transfer athletes is resistance to rotation, first supine, then sitting, and then standing, in which
the player maintains the neutral spine control position while resisting rotation of the upper body on the lower body. The
player resists the rotational activity exerted by the therapist or trainer.
In the next stage, the player maintains trunk control while actively rotating through a short range of motion against the
trainer's resistance. This is done in numerous positions to teach trunk control regardless of the positions of the patient
(Fig. 52.2).
FIGURE 52.2. The athlete learns trunk control regardless of his or her position.
An additional benefit can be beach ball exercises. A ball 4 feet in diameter can be used to do partial sit-ups while
maintaining control of the ball with the trunk in neutral position. The sit-ups and resistive sit-ups are done on the ball ( Fig.
52.3 and Fig. 52.4).
FIGURE 52.3. The athlete performs partial sit-ups on an exercise ball while maintaining control of ball and keeping the
trunk in the neutral position.
FIGURE 52.4. The athlete performs extension exercises on an exercise ball while maintaining control of the ball and
keeping the trunk in the neutral position.
Lower-extremity, trunk, and upper-extremity strengthening must be performed with concentration on maintaining the
neutral trunk control position. It must be taught away from the sport, without a bat or ball, on the training table or floor. A
routine is established for the player, who is told to focus on trunk control, neutral position, and tense contractions. Trunk
control is incorporated into throwing or batting. This will ultimately produce a more efficient transfer of torque from the
lower to the upper extremities, that is, better bat control for a hitter and better endurance and ball control for a pitcher. An
additional valuable benefit can be prevention of spine injuries and spinal pain due to the athletic activity.
After establishing neutral-position isometric control of the spine, extremity strengthening can begin. Probably the most
important muscles needed to protect the spine itself is the quadriceps. The ability to return to work after a back injury has
been directly related to quadriceps strength. Yet, quadriceps strengthening should not be done in the standard, sitting,
full-knee extension position in a patient with severe lower back pain. Quadriceps strengthening should be done without
aggravating lumbar spine mechanical pain. Also, the ability to move a weight from 90 degrees to zero may not relate as
specifically to lumbar spine function as quadriceps strength obtained through functional strengthening. Functional
strengthening is done initially through wall slides, sliding down the wall, holding the position for 10 seconds, and
returning to full-knee extension using varying depths. We begin this routine immediately after surgery in our patients.
Throwing the medicine ball in a flexed-knee position. Sports such as a versi-climber, stationary cycle, and other
techniques are used to teach quadriceps function while maintaining trunk control and during sports-related activity.
Gluteal and hip extensor strengthening is important, but the exercises must be done without inadvertently hyperextending
the lumbar spine. Exercise bands that provide resistance to hip extension without a lot of spine extension are important,
as is spine motion while producing isometric extensor strength. The key to the use of Nautilus machine, which can be
very important, is a safe, protected range of motion for extremity strengthening. The key to use of these machines is good
isometric trunk control in a pain-free neutral position before use of the machines. If you can establish trunk control first,
then a safe protected range of motion is a good position for the spine. Therefore, military presses, lats, and arm and
lower-extremity leg strengthening with machines can be of benefit while protecting the spine. Spine-strength testing
machines have been shown to be of benefit in predicting return to work. The ability to perform flexion and extension
exercises or resistance rotational exercises on a machine may not translate to functional spine activity during athletics.
We have not recommended those machines for treatment of lumbar injuries.
Stretching exercises are an important part of any rehabilitation program. The more flexible the legs, arms, and upper
body are, the more likely there will be a proportional decrease of motion stress on the injured lumbar spine. If some
muscle control is established first, through the strengthening program, then the spine can be held in a stable position
while stretching of the extremities takes place. It is important to note that hamstring stretching too often is taken to the
extent that produces abnormal lumbar spine motion. Stretching the leg past the point of pelvic motion only strains the
spine and does not increase hamstring looseness. Too often, lumbar spine conditions are irritated because of excessive
lumbar motion during hamstring stretching. The spine should be neutralized, held in a neutral, stable position when doing
hamstring stretching exercises. Lumbar spine motion, although important, is not the initial stage of the rehabilitation
program. Lumbar spine motion is begun with good muscle control of the spine during the motion exercises. The most
common initial stage of motion is the cat/cow exercise. In this exercise, control can be most easily maintained when the
spine is in the arched position.
Stretching exercises are a critical component of the program. They increase the functional range of motion of the trunk
and legs. Increasing the functional range of motion decreases the likelihood of lumbar spine injury during the
strengthening program during play.
Most low back injuries occur when the player exceeds the strength of the spine and its range of motion. The stretching
program provides a greater area of pain-free and injury-free function. For example, if a player who is stiff, having 10
degrees of spine extension and 20 degrees of spine rotation, suddenly reaches for a ball, producing 25 degrees of
extension and 40 degrees of rotation, injury to his back can occur through tearing stiff tissue. If the mobility exercises
produce a functional range of motion of 40 degrees of extension and 50 degrees of rotation, injury is less likely to occur.
This is a protective range of motion.
The chief finding in our ball players with back pain is loss of spine extension, loss of rotation (usually more in one
direction), poor mechanics in rotation, and weak abdominal muscles. Once back pain begins, the weakness and
contractions increase. But, this program is designed for performance enhancement and injury prevention, not treatment
of back pain.
AEROBIC CONDITIONING
There are numerous methods available for aerobic conditioning. Often, we see athletes who prefer a specific technique
such as running but have developed pain and problems directly related to running.
Cross-training is critically important in recovering from aerobic exercise–induced injury. Not only does the runner with an
injured back have to do the stretching and strengthening rehabilitation program, but he or she must learn cross-training
for aerobic exercise. Water running, swimming, cycling, Nordic Trac, versi-climber, and rowing machines can produce the
needed aerobic conditioning outside of the injurious sport. The benefit of swimming and water running program ( 17)
should be obvious. The complete removal of weight from the spine in water removes many of the compressive loads and
allows good physical activity without the tremendous pounding and straining of running. The Nordic Trac builds
tremendous conditioning with strong use of the arms and increasing cardiac output without the pounding of running. The
versi-climber and stationary cycle have several things in common. First, the back can be positioned in a very beneficial
position for back protection while still obtaining good aerobic conditioning. The cycle is slightly bent forward, which of
course, helps the stenotic spine. The versi-climber is erect, which removes as much nerve root tension as possible. Both
have the same potential hazard in that the pelvis should not tilt laterally during cycling or use of the versi-climber. For the
versi-climber, short steps should be taken to prevent a lot of pelvic tilting with the motion, and in cycling, the legs should
not become fully extended with the effect of reaching for the peddles that allows the pelvis to tilt down. Keep the pelvis
and spine in a firm, neutral position with good isometric control during the aerobic conditioning. Running stairs or
stair-walking machines produce good leg strength and good hip extensor strength. Rowing machines obviously can injure
the back, but if the machines are used properly with rigid muscle control of the spine in a neutral, pain-free position, the
benefit from the upper-extremity and lower-extremity function, the benefit of quadriceps strengthening can produce good
aerobic conditioning without stress on the spine. The better aerobic condition the athlete is in, the less likely he or she
will sustain injury, and that includes lumbar spine injury. Therefore, aerobic conditioning is an important part of every
spine rehabilitation program.
The summary of an effective nonoperative treatment program for lumbar spine injuries is as follows:
1. Stop the inflammation. We prefer to use antiinflammatory medications, Indocin SR being our most standard
medication. Patients should be advised of potential complications of any antiinflammatory medications. Medrol
Dose Pack may be used in increasingly difficult clinical situations, as well as in epidural steroid injections.
2. Restricted activity. This may vary from 24 to 72 hours of bed rest to immediate immobilization in a lumbosacral
corset and restriction of painful activities.
3. Spine stability rehabilitation program. We began this rehabilitation program as soon as practically possible. It may
vary from in bed, in the hospital, at 24 hours, to the first available outpatient appointment in physical therapy.
In conclusion, in reference to some of the questions asked earlier:
1. Do you start flexion or extension exercises? The answer is you start neither. You start neutral isometric control
exercises.
2. Do you do twisting exercises? Twisting exercises can be the most injurious exercises in any rehabilitation program;
however, torsional rotation is an important part of many sports. The answer lies in producing tight, rigid trunk control that
controls the spine during rotational activities, with the motion occurring predominantly in shoulders, hips, and legs. The
athlete is able to produce a parallelism between his shoulders and pelvis during rotation, especially during the contact
portion of the rotational sport. A twisting exercise that allows loss of muscle control of the spine during exercise can be
injurious and may not be of benefit. Rotational strengthening can be important but has to be started with close
observation and control. We twist many times in an average day, and twisting is a part of many sports. Having a pain-free
rotational range of motion is important; therefore, proper, slow active stretching in rotation is important. Part of the key is
do not twist; learn to rotate your whole body.
3. What type of aerobic conditioning should be done? The athlete should perform the type of aerobic conditioning that
holds the spine in its most advantageous position and best removes injurious compressive loads from the spine. The
athlete should cross-train, using a variety of aerobic conditioning techniques.
4. When can someone lift weights? The athlete can lift weights when he or she can do it safely, meaning that the person
has tight, rigid trunk control. The athlete can protect the spine while strengthening his or her extremities. The person can
lift weights when he or she can understand the role of balance, speed, and proper mechanical advantage in weight lifting.
The key to functional weight lifting for the athlete is not to lift the weight at the greatest mechanical disadvantage, but to
simulate positioning used in his or her sport. The focus should be on isometric trunk control and position protection first,
then resistive weight lifting.
5. What role do weight machine exercises have? Weight machines can be a distinctly advantageous, controlled situation
for resistive weight lifting. All machines that strengthen the extremities require proper spine control first. We have not
used trunk-strengthening machines such as the flexion, extension, or rotation machines in patients with back problems.
Questions still linger as to their benefit. I am sure the key probably lies in proper use of the equipment and combining the
equipment with a functional isometric control-type system such as the trunk stability rehabilitation program.
6. What type of nonoperative rehabilitation is best for the individual athlete's sport? It depends on the sport and its
demands as related to rotational activity, compressive load, and tensile extremes of range of motion.
7. When can a professional athlete return to his or her sport after spine surgery or a serious injury that has been treated
nonoperatively?
The athlete can return when he or she can:
a. Complete Level 5 of our trunk-stabilization program.

b. Complete a course of sport-specific exercises for his or her sport.
c. Attain an appropriate level of aerobic conditioning for the sport.
d. Practice the sport fully.
e. Return slowly to the sport with some limit on minutes played.
f. Continue to do the Level 5 stabilization exercises after return to play.
OPERATIVE CARE
The chief indications for surgery in the athlete are the same as those in any patient. The basic principles are still of major
importance in the athlete:
1. Sufficient morbidity to warrant surgery.

2. Failure of conservative care.
3. An anatomic lesion that can be corrected with a safe, effective operation.
4. A proper, fully developed postoperative rehabilitation program. Not enough emphasis can be placed on a proper
postoperative rehabilitation program. To fail to have the patient participate in postoperative spinal rehabilitation
would be similar to a failure to do postoperative knee strengthening after reconstruction of the knee or a failure to
do postoperative strengthening and range-of-motion exercises after surgery on a shoulder. The patient wants
restoration of function. The surgeon should be able to guide the patient through this restoration. The morbidity of
the patient, amount of pain, loss of function, and occupation are the critical factors.
Spinal operations to enhance performance rather than relieve disabling pain are a part of managing the care of athletes,
a part that requires a great deal of experience not only in spinal surgery but also in dealing with athletes.
There are numerous factors to consider. One must always keep in mind the full longevity of the patient. Young players
can take off for a year after a significant spinal surgery and still return to play. Older players are less likely to return to
play after a major spinal reconstructive operation.
What kind of function the player will have after his career—the condition of his spine at that time—should be of major
importance in the decision making early in the player's career.
A major factor is calculating the risk if the operation is successful. In many sports, after a spinal fusion, for example, or a
major resection of a supporting structure in a decompression, the percentage chance of return may be no greater after
the operation than without the operation.
A surgeon must carefully question his advice concerning surgery if he does not have a proper alternative to the surgery
and good, effective nonoperative care. Frankly, if all one knows is the surgical technique and if one does not have a
proper understanding of and delivery system for a nonoperative care program, then, that person should not advise
surgery for the athlete. An appropriate team approach among specialists in nonoperative care and specialists in
operative care can be worked out so that the decision for surgery is well founded. However, the surgeon must understand
and participate in that portion of the decision making process, namely, has the patient had a sufficient nonoperative
treatment plan?
The anatomic lesion is critically important. A simply extruded disk herniation, of course, can be very amenable to a
one-level microscopic lumbar discectomy, but an annular tear of the intervertebral disk with mild nerve root irritation will
not be made better by a decompressive laminectomy and usually will be made worse because of abnormal motion in the
injured disk and segmental instability with a nerve root scarred to the back of the annulus. In spondylolisthesis, the
obvious solution may be, as it is in the majority of the patients facing surgery, a spinal fusion. Some athletes can return to
their sport after a successful spinal fusion, and some may not. Part of the danger is in curing the x-ray study and not the
patient. Another possibility is curing the patient with a successful operation and leaving the player without a job. As with
everyone, an absolute indication for surgery and lumbar disk disease is progressive cauda equina syndrome or
progressive neurologic deficit. Strong, relative indications are static significant neurologic deficit, unrelenting pain at
night, and major loss of functional capability. Mild relative indications for surgery falls more under the category of
performance enhancement and return to play. There will always be patients who could live the way they are but cannot
perform the way they are. This is a relative indication for surgery, but it must be a frequent consideration in lumbar spine
injuries in athletes.
INDIVIDUAL SPORTS
The lumbar spine is a highly vulnerable area for injury and a number of different sports. The incidence varies from 27%
(18) to 7% (4) to 13% (6). It appears that although the incidence and time lost are significant, probably the most important
problems lie in fear of spinal injuries and the necessity of a therapeutic plan. Lumbar pain is a big part of many sports,
but an organized diagnostic and therapeutic plan can prevent permanent injury, and allow full function and maximum
performance.
Gymnastics
With reference to lumbar spine injuries, gymnastics is probably the most commonly mentioned sport. The motions and
activities of gymnastics produce tremendous strains on the lumbar spine. The hyperlordotic position used with certain
maneuvers such as the back walkovers exerts tremendous forces on the posterior elements and requires a great deal of
flexibility. The amount of lumbar flexion and extension used during flips and vaulting dismounts require a great deal of
strength to support the spine during these extremes of flexibility. In 1976, Jackson et al. ( 2) pointed out that female
gymnasts have an incidence of spondylolysis of 11%. Spondylolysis is a fatigue fracture of the neural arch, and it is
believed that the vigorous lumbar motion in hyperextension in gymnastics produces the fatigue fracture. It is also
interesting to note that Jackson found spina bifida occulta in 9 of the 11 gymnasts with pars interarticularis defects. It is
known that there is a hereditary predisposition to the stress fracture of the spondylolysis, and the findings of occult spina
bifida may point out a weakness of the dorsal arch in certain of these gymnasts. But certainly the role of the sport itself
plays a tremendous role in a much higher incidence of spondylolysis and a much higher incidence of back pain in
general. Garrick et al. ( 19) pointed out a very high incidence of low back pain in female gymnasts and recommended the
vigorous trunk-strengthening exercises that are used today to properly prepare gymnasts for their sport.
Ballet
Many of the motions used in ballet are similar to those in gymnastics. The classic maneuver that produces back pain
problems is the arabesque position. This position requires extension and rotation of the lumbar spine. Performing a
proper arabesque maneuver is the key to preventing lumbar strain. Several points have been emphasized, keep the
pelvis stable, keep the extension of the spine symmetric over all the levels of the spine, and obtain good extension
through the hip joints ( 20).
Ballet involves the lifting of dancers, especially lifting in awkward positions. The outstretched hand produces tremendous
level-arm stresses across the spine of the lifting partner. Off-balance bending and lifting is a hallmark of back problems in
industrial workers, and yet, ballet, although balanced, is designed often to produce some of the most difficult lifts. The
male dancers follow the body weight of their female partners very closely.
Spondylolysis and spondylolisthesis play a critical role in dancers and may often produce severe mechanical back
dysfunction.
Water Sports
In addition to injuries to the wrist and cervical spine in diving, the lumbar spine is subjected to added strain due not only
to rapid flexion and extension changes but also to the severe arching of the swimmer's back after he or she enters the
water. Although swimming and water exercises are a major part of any back rehabilitation program, certain kicks, such as
the butterfly kick, produce a lot of vigorous flexion and extension of the lumbar spine, especially in young swimmers. The
swimmer must learn good abdominal tone and strength in order to protect the back during a vigorous kicking motion.
Thoracic pain and round back deformities in young female breast-strokers can be a problem because of the repeated
round-shoulder type of stroke motion.
Pole Vaulting
Pole vaulting is another sport that involves a maximum flexion and extension and muscle contraction during the sport.
The range of motion of the lumbar spine has been documented with high-speed photography from 40 degrees of
extension to 130 degrees of flexion in 65 seconds. One can imagine the tremendous forces generated across the spine
with these functional demands (21).
Weight Lifting
As we move from the motion sports, meaning those sports that require tremendous amounts of flexibility in addition to
strength and involve large degrees of changes in range of motion, we go to the heavier sports. The sports that require
strength, lifting, and high body weight. Of course, the most common would be weight lifting. The incidence of lower back
pain and problems in weight lifters is estimated to be 40% ( 22). The tremendous forces exerted on the lumbar spine by
lifting weights over the head produce tremendous lever-arm effects and compressive injury to the spine. The three most
important things in performing weight lifting are “technique, technique, technique.” Squats and dead lifts can be done, but
the technique must be perfect in order to decrease the risk of a disk injury. For example, a dead lift requires erect
posture, lumbar lordosis, and balancing the weight on the heels. Most lifts are begun with the spine in tight, rigid muscle
control. There is tremendous extension force at the hips and knees, with the spine held in a rigidly stable position.
Success in this portion of the lift requires the body to generate tremendous rigid immobilization of the spine in the power
position of slight flexion. To do a forward bent motion with the spine out of this position can be quite dangerous, resulting
in tremendous shear forces across the spine. Lifting weights with the spine flexed at 90 degrees, whether they are lighter
arm weights or weights across the upper back, generate tremendous lever-arm effect forces. The weight times the
distance back to the spine results in tremendous shear forces across the lumbar spine, especially if weight is to be
moved in this position. One cannot imagine muscles that must be strengthened in this dangerous and mechanically
disadvantageous position. A dangerous time for weight lifters is the shift from spinal flexion to extension that occurs with
lifting the weight over the head as in the clean jerk maneuver or the “snatch.” Making the transition from flexion to
extension must be done with rigid, tight muscle control. Inexperienced lifters, especially, have no muscle control as the
spine shifts from flexion to extension. A trained lifter, again, controls that shift with rigid muscle control of the lumbodorsal
fascia. The position of holding weight over the head invariably draws increased lumbar lordosis. These tremendous
extension forces of the lumbar spine naturally lead to a discussion of spondylolysis and spondylolisthesis. The incidence
of spondylolysis in weight lifters has been estimated at 30% and the incidence of spondylolisthesis at 37% ( 23). Many
newer training techniques in weight lifting emphasize the role of general body conditioning, flexibility, aerobic
conditioning, speed, cross-training, and the ability to lift weight.
Football
Football players lift weights. It is part of the sport. The upper body forces and leg strength necessary to play football for
most of the athletes involved in the sport require tremendous strength. Some football players, of course, rely on great
agility and jumping ability, throwing ability, and eye-hand contact, but strength is the backbone of football. Every year,
every pro team needs heavier, stronger athletes. It is difficult to prepare an athlete in the off-season for the tremendous,
rapid back extension against weight necessary for blocking in the offensive line. Extension jamming of the spine
produces facet joint pain, spondylolysis, and spondylolisthesis. It is similar to position of lifting weight over the head in
weight lifting except that it must be generated with forward leg motion and off-balance resistance to the weight while
trying to carry out specific maneuvers such as blocking a man in a specific directions. Lumbar spine problems in these
athletes require specific training in back strengthening exercises in order to prevent the injuries ( 24,25).
Safety in weight lifting is an important part of football. To have a promising football player injured in the weight room is
not an uncommon occurrence. It has been estimated that more injuries may actually occur in training rather than during
competition (26). This problem can be avoided through proper weight lifting techniques. In addition to these extension
and lifting type of forces, football involves sudden off-balance rotation. This rotation may produce transverse process
fractures, torsional disk injuries, and tears in the lumbodorsal fascia. Sudden off-balance twisting is part of the game and
may be caused by tremendous loads or in a loose, unloaded position. Football has the added dimension of receiving
unexpected, severe blows to the lumbar spine that may produce contusion or fracture. A helmet in the ribs produces rib
fractures, and a helmet in the flank can produce renal contusion, retroperitoneal hemorrhage, and transverse process
and spinous process fractures. Many aerobatic receivers and runners suffer spondylotic defects for the same reasons as
gymnasts and ballet dancers, but the most common incidence of problems is in the weight lifting. The role of the strength
coach in teaching proper weight lifting techniques and designing training schedules that prepare the lumbar spine for
what is expected with football is important to prevent lumbar spine injuries in football players.
In addition to weight lifting, another sport that produces stiffness is running. Distance runners must cross-train with
flexibility in order to prevent injury. Running involves maintenance of a specific posture with tremendous muscle exertion
over a long period of time. Low back pain as well as intrascapular and shoulder and neck pain are very commonly
reported in runners. We cure the vast majority of runners who have mechanical low back pain with stretching exercises.
There is also the natural tendency in runners to develop isolated abdominal weakness. Running does not naturally
involve constriction of abdominal and spine-stabilizing musculature. Frequently, there is a significant imbalance between
flexors and extensors, not only in the legs but also in the trunk. Intrascapular back pain also results from abnormal
posture during running. The key to posture not only in running, but in every patient, is good isometric trunk strength that
holds the body in an upright chest out position. Runners with low back pain should be treated with:
1. A vigorous stretching program that stretches trunk as well as the lower extremities.
2. Cross-training and muscle-strengthening techniques that strengthen the antagonist muscle such as hip extensors
and knee extensors.
3. Abdominal strengthening and isometric trunk stability exercises to enhance abdominal control.
4. Chest-out strengthening exercises. The program begins with abdominal strengthening, and adds upper-body
shoulder shrugs and arms behind the back exercises to emphasize chest-out posturing and tight abdominal control.
The basis of back pain treatment in runners is stretching exercises.
5. Proper footwear for cushioning and enhancement of foot function.
Rotational and Torsional Sports
Rotational and torsional sports have certain characteristics in common despite the exact sport itself. Baseball, golf, and
the javelin all require rotation and have distinctly different demands on the spine. The javelin requires a tremendous
amount of force to be generated in going from a hyperextended to a full flexion forward position. You do not throw a
javelin 200 feet with your arm. Although shoulder and arm injuries are common in javelin throwers, the key is rigid
abdominal strength that produces the torque necessary to throw the javelin. Attempting to throw with the arm only will
produce arm injury and in no way can generate any type of distance. Every arm injury in a javelin thrower has to be
treated with trunk exercises and trunk strengthening. A rotatory lumbar spine injury in a javelin thrower is a completely
debilitating injury that requires tremendous care and correction before the athlete can return to the sport.
Golf
Golfers notoriously have the highest incidence of back injury of any professional athlete. In one review by Paul Callaway
and Frank Jobe of injuries on the PGA tour 1985–1986 of 300 professional golfers, 230 of the 300 were injured for an
incidence of 77%. Of the total injuries, 43.8% were spine related; 42.4% were lumbosacral. Lumbar spine pain in golfers
results in torsional stress on the lumbar spine, and the key to prevention of the lumbar spine pain in golfers is to minimize
the torsion stress by absorbing the rotation in the hips, knees, shoulders and spreading the rotational stresses on the
spine out over the entire spine. Maintaining rigid, tight control through the power portion of the swing is critical. Proper
technique in golf begins when addressing the ball. The knee flexion of the address position tenses the abdominal
musculature. This abdominal tension initiates the trunk control necessary for a properly placed swing. The majority of the
emphasis is on maintenance of parallel shoulders and pelvis though the majority of the swing. This requires rigid
abdominal control and rotation between shoulders and hips, and loss of this rigid parallelization of the shoulders and
pelvis can generate rotational strain on the lumbar spine. Rotation occurs between the hips and shoulders in the
backswing, and the amount of backswing is not as important to the power of the swing as the ability of the golfer to regain
tight muscle control as he or she proceeds from maximum backswing down through the power portion of the swing. It is
the ability to obtain tight control and parallelism and maintain it that produces the power and protection for the lumbar
spine. The most important advice for any recreational golfer with back pain is to cut down the backswing and the
follow-through. Concentrate on the power portion of the swing. Concentrate on tight abdominal control during the power
portion and minimize the excesses of rotation with backswing and follow-through. It is important also that the golf swing
be symmetric. The same amount of extension on backswing and follow through is important. Lateral bending should be
avoided, especially in the follow-through. There is a tendency to bend to the left side, or use an off-balance lateral
bending position and load the spine asymmetrically, producing injury. Golf is usually restricted according to the patient's
symptoms.
There is no condition of the lumbar spine for which we specifically restrict golf. Many people with spondylolisthesis,
through superb conditioning and care, can play relatively pain free. Premature, symptomatic degenerative disk disease is
common among golfers who play a great deal, especially among professionals who not only play but practice long hours.
People can return to golf after decompressive lumbar surgery or spinal fusions. There are significant questions about the
effect of a spinal fusion on an adult professional golfer. The effect on adjacent segments and on overall spine function
may not allow any better function. Under these circumstances, a fusion procedure should be a last resort.
Basic Mechanics of the Golf
The essence of a mechanically sound golf swing is strength, balance, proper posture, and flexibility. For many years, it
was believed that strength in the arms and shoulders generated the power and speed in the golf swing; actually,
however, the trunk generates the power, and the hip and trunk muscles transmit this power and speed. This is not to say
that the shoulders (rotator cuff muscles) and arm muscles do not play integral roles. The rotator cuff muscles are
responsible for providing a coordinated and harmonious movement to protect the glenohumeral complex.
The purpose of trunk stabilization exercises is to retrain the musculature to control, coordinate, and optimize
function—especially that of the spine—in sport-specific movements. Again, these exercises not only assist in the
rehabilitation of the player's spinal injuries but also enhance a golfer's ability to perform an “athletic golf swing.” An
athletic golf swing is a swing that uses the large trunk muscles to provide the needed power and speed while supporting
the lumbar spine in a relatively constant neutral position throughout the swing. This is believed to be the safest way to
swing. For many years, golfers were taught a swing in which the hips slid (rather than rotated) from side to side, with the
lumbar spine finishing in extreme hyperextension or a reverse C. However, the reverse C swing is not only harmful but
also inefficient because the off-balance golfer loses the power generated by the trunk and hip muscles.
In contrast, the athletic swing is a golf swing in which the larger muscles of the trunk dictate the golf swing. David
Leadbetter, world-renowned golf teacher, describes the athletic swing as “the efficient coiling and uncoiling of one's torso
in a rotary or circular motion which maximizes centrifugal force. Centrifugal force is the force created away from the
center of one's swing, transmitting from your body (trunk and hips) out through your arms and hands. This creates club
head speed and maintains the club on a steady orbit or arc.” This is an important concept in the rehabilitation of the
golfer's spine, because if the neutral position of the lumbar spine is lost (excessive lumbar flexion or extension) during
the golf swing, power and speed also will be lost, and more important, the steady arc of the club head will be disrupted as
it travels on an incorrect plane.
The athletic golf swing not only maximizes the power generated but also causes less stress on the lower back.
Furthermore, the athletic swing can be imitated by an amateur or a patient with a spinal injury, because it does not
require excessive flexibility in the trunk and hip region. The finish in an athletic golf swing is much more upright (although
the lumbar spine is still neutral) than the reverse C swing.
The five basic phases of the athletic golf swing are as follows:
Setup/address—Posture of the golfer, ready position
Take-away/move-away—From ball address to the top of the backswing
Transition—From the end of the backswing until the arms return to horizontal
Acceleration—From the arms horizontal to ball contact
Follow-through—From ball contact to the end of the golf swing
Phase 1: Setup/Address
In phase 1, balance and posture are the most important factors in preparing and allowing the body to make a powerful
and safe swing. Theoretically, if a perpendicular line were dropped from the shoulder, it would intersect the patella. The
golfer should be in a ready and balanced position. Many golfers rock forward and then backward to find middle, or
balanced, position on the balls of their feet.
Phase 2: Take-Away/Move-Away
Phase 2 covers the period from ball address to the top of the backswing. Here, proper coiling in the backswing is
mandatory for maximum power (3). Many golfers believe that they are coiling when they turn their hips, shoulders, and
chest the same amount during the backswing. They are certainly turning, but they are not coiling, and therefore, they lose
a lot of power. Ideally, a golfer needs a 2:1 ration (shoulder turn to hip turn). This coiling is needed to put the trunk
muscles (lumbar rotators, abdominal obliques) in an optimal stretch position to achieve maximal firing of those muscles.
For example, if two ends of a rubber band are moved in the same direction and one end is let loose, there will be little, if
any, recoil from the rubber band. On the other hand, if one end is taken farther away from the other end, there will be a
considerable recoil once the one end of the rubber band is released. This example holds true for the trunk muscles.
Phase 3: Transition
Phase 3 covers the period from the end of the backswing until the arms are horizontal. A smooth transition from
backswing to downswing depends on the movement in the lower portion of the body, specifically the legs ( 27). The hips
begin the swing as the left leg pulls and the right leg pushes the pelvis forward. In the right leg, the gluteus, biceps,
femoris, and semimembranosus muscles push the pelvis forward for power (14). Tightness in the hip flexor muscles can
hinder the amount of this hip extension. Therefore, it is imperative that the hip flexors be loosened (e.g., by stretching,
massage, myofascial release) on a regular basis. In the left leg, the adductor magnus is most active as it pulls the pelvis
forward. This pushing and pulling results in pelvis rotation ( 14).
NOTE: Research at the Centinela Fitness Institute, Inglewood, California, revealed that, of the golfers on the PGA Tour
who were tested, the internal rotators of the left hip of the average right-handed PGA player were stronger than those of
the right, and the external rotators of the right hip were stronger than those of the left. A possible explanation of these
findings is that a highly repetitive, reproducible pattern develops strong right hip external rotators and left hip internal
rotators during the transitional and acceleration phases.
Phase 4: Acceleration
Phase 4 covers the period from when the arms are horizontal to the moment of ball impact. There is continued power
transmission from the trunk and hip region, with controlled weight shifting from the right to the left side. At impact, the
angle of the lumbar spine should be a neutral.
Phase 5: Follow-Through
Phase 5 covers the period from ball contact to the end of the golf swing. Just after impact, the golfer should feel the left
side “firm up” because the hip muscles are used to stabilize the hip and pelvis as the weight and torque are transferred to
the left side. Weakness in the left hip region increases the risk of injury to the left sacroiliac joint and lumbar spine
because there is no control or support as the body rotates through the swing. If the player uses the lower body to support
the hip and pelvis, the upper body will be able to rotate through the ball.
Many times golfers report “not being able to stay down on the ball” or having a “hard time getting through the ball.” This is
sometimes due to problems in the hips. Some patients with hip problems (e.g., restrictive capsule, muscle tightness) may
find it easier to swing by turning the left foot outward (externally rotating) to allow for more freedom and less stress on the
hips during the follow-through phase.
Aerobic Conditioning for Golf
Because golf is not an aerobic sport, aerobic conditioning should be included in any effective lower-back rehabilitation
program. Nutter (1) showed that higher aerobic fitness shows a strong negative correlation with the incidence of both
lower-back pain and disk herniation. Exercise results in increased aerobic metabolism in the outer annulus and the
central portion of the nucleus pulposus, bringing about reduction of lactate concentration ( 24).
Also, aerobic conditioning plays a significant role in muscle coordination during periods of fatigue. Fatigue can produce
abnormal muscle function and overcompensation, and thus, resultant injury. Fatigue obviously can affect performance
through a lack of proper balance and coordination as a result of inappropriately, selective, weak muscles.
Unfortunately, some patients cannot tolerate certain types of aerobic conditioning that have high levels of loading to the
spine, such as jogging. However, several types of aerobic conditioning exercises are highly effective without loading the
spine [e.g., water exercises ( 21) and the stair climber].
Evaluation, Treatment, and Rehabilitation for Golf
Because structure governs function, similarly, abnormal structure governs dysfunction ( 24,26). Thus, a thorough
evaluation must be undertaken before strengthening and stretching exercises are begun. The examination is completed
by use of x-ray films, magnetic resonance imaging, computed tomography scanning, muscle testing, range of motion,
segmental testing of vertebrae for hypomobility and hypermobility, postural evaluation, palpation, and various other
methods or tests.
Once the dysfunction is identified, appropriate treatment techniques must be used to correct the structural abnormality.
This will allow for enhanced function and, therefore, improve the rehabilitation process in which trunk strength, muscle
coordination, and balance are stressed. Trunk strength involves the muscles of the thighs, hips, and trunk. The trunk
muscles include the rectus abdominis, oblique abdominis, paraspinal musculature, latissimus dorsi, and further up the
spine, the scapular stabilizers. The muscles that insert into the lumbodorsal fascia play a key role in providing adequate
balance and strength for the lumbar spine and the trunk during the golf swing. Trunk strength provides a synchrony of
motion between the upper and lower extremities in that there is a controlled unwinding of the upper body relative to the
trunk. The power of the golf swing is transferred from the strong leg and hip musculature through the trunk and out to the
end of the club head.
Trunk fatigue produces a loss of this synchrony between the upper and lower extremities. This reduction in muscle
strength prevents a proper transfer of force and leads to compensations by the body. Thus, the improvement of muscle
strength, coordination, the firing sequence of muscles, and body balance underlies the entire rehabilitation process and
facilitates the golfer's achieving a consistent, reproducible, effective swing.
An injury to the spine can cause pain, which produces weakness and a loss of muscle control. This loss of muscle
control, which can lead to further injury because the joint is now unsupported, is similar to quadriceps weakness and its
cause-and-effect relationship to a knee injury. As soon as referred pain begins, muscles in the area of referred pain
become weak. Any attempt to reproduce a proper golf swing under these circumstances can be difficult and can lead to
continued pain, poor swing mechanics, and subsequently poor performance. Obviously, just as in a knee injury, the
solution to this problem is to first correct the structural or damaged area and then strengthen that area by use of
golf-specific exercises.
Baseball
Torsional problems develop in both baseball pitchers and baseball hitters. Hitters are required to initiate a violent lumbar
rotation based on instantaneous ocular information, and the role of the lumbar spine in a baseball hitter begins with
visualization of the ball. If a hitter is not seeing the ball properly, the mechanics of the swing will be disturbed. The most
common problem is the delayed recognition of the ball, producing a rotation with the hips in front of the shoulders, a loss
of parallelism of the shoulders and hips, and increased torsional strain of the lumbar spine. The most important point is to
see the ball properly and initiate a symmetric swing. The trunk should move quickly as a solid unit, through the baseball
swing.
Hitting
Hitters, who make up another interesting group of players, include any player who has to swing a bat. Hitters who take a
lot of batting practice, swing with great velocity, and swing with a heavy bat are subject to lumbar spine injury. However,
an infrequent hitter, such as a pitcher, who does not have good hitting mechanics is also vulnerable to injury. Lumbar
spine problems in hitters begin with their eyes; that is, the ability to see the ball is a critical factor in swing mechanics.
Abnormal swing mechanics involve a loss of control between the hips and shoulders, essentially a loss of body
synchrony. Irregular and uncoordinated motion of the upper extremity and upper torso puts undue rotational strain on the
lumbar spine. Injury of the lumbar spine in someone required to engage in this type of torsional activity further
compounds the problem by producing stiffness, weakness, and asymmetry that add to the pain and prevent satisfactory
healing. The biomechanics of hitting can be considered an ocular-muscular reflex, a reference to the fact that the
triggering of the bat mechanics (the triggering of the muscles) is a split-second response to what the hitter is able to see.
A hitter who is not picking up the ball well tends to open the hips too early. With the bat and upper torso lagging behind,
there is a sudden torsional stress to catch the shoulders and the bat up with the rest of the body. Poor visualization of the
ball produces delays in hand and arm responses.
Hitting Mechanics
To diagnose and treat lumbar spine problems in the hitter, the physician should understand that hitting mechanics
require power in the legs and trunk; a rigid, solid cylinder of torque transfer; and fine muscle control of the arms and
wrists.
Test Design. For a scientific look at hitting mechanics, EMG studies of trunk musculature in hitters were performed in our
laboratory and included 18 professional baseball players at the Los Angeles Dodgers' instructional training camp in
Phoenix, Arizona. Among the batters, 13 were right-hand dominant and 5 were left-hand dominant. Ages ranged from 19
to 44, averaging 22 years.
The Basmajian technique (27) was employed to insert fine-wire electrodes into the muscles of the supraspinatus, triceps
(lateral head), posterior deltoid, and middle serratus anterior (sixth rib) of each subject's lead (forward) arm, as well the
lower gluteus maximus of his trail (back) leg. Surface electrodes monitored muscles of the right and left erector spinae,
abdominal obliques, vastus medialis obliques (VMO), semimembranosus, and biceps femoris (long head) of the trail leg.
A lightweight belt pack allowed transmission of the EMG signals through frequency modulation (FM) telemetry to a
recording console. Resting and maximum manual muscle test (MMT) recordings were made for each muscle.
Each subject was allowed to warm up until comfortable and then hit six pitched fast balls (approximately 75 miles per
hour). Simultaneous high-speed motion picture photography using 16-mm film at 400 frames per second captured each
swing. An electronic pulse marked the film and EMG record, which facilitated film synchronization with the recorded EMG
data.
The film was examined and divided into four discrete phases ( Fig. 52.5), as follows:
FIGURE 52.5. Diagram demonstrating the phases of a batter's swing.
Phase I—The windup began as the lead heel left the ground and ended as the lead toe reestablished ground contact.
Phase II—The preswing began as the lead forefoot struck the ground and ended as the swing began.
Phase III—The swing was subdivided into early, middle, and late, as determined by the bat position.
a. Early swing began as the bat moved forward until it was perpendicular to the ground.
b. Middle swing continued until the bat was parallel with the ground.
c. Late swing continued until ball contact.
Phase IV—The follow-through began with ball contact and ended as the lead shoulder reached maximum abduction and
external rotation.
The EMG data were then converted from analogue to digital data by sampling 2,500 times per second and were
integrated by averaging groups of 200 samples per second. By means of resting signal as baseline and a peak 1-second
MMT as the 100% level, these records were then processed by computer to yield a relative activation figure. Activity
patterns were assessed every 5 msec and expressed as a percentage of the activity recorded during the MMT. The mean
percentage of MMT and standard deviations were obtained for each muscle throughout the swing. An analysis of
variance (ANOVA) (p < .5) was performed to determine statistically significant differences between phases for each
muscle and between specific muscle groups. When the ANOVA revealed such differences, a posthoc sequential Tukey
multiple comparison test was completed.
Test Results
Lower extremities. Hamstring activity (biceps femoris and semimembranosus muscles) was below 50% MMT in the
windup. During the preswing, however, activity increased significantly to 154% and 157% MMT, respectively. Activity
decreased significantly in the early swing to 100% and 90% MMT, respectively, and continued declining throughout the
remainder of the swing to its lowest level (<4% MMT) in the follow-through.
Lower gluteus maximus activity was lowest during the windup (25% MMT) and increased significantly during the preswing
to 132% MMT. Activity remained high in the early swing (125% MMT), decreased thereafter in the middle swing (65%
MMT), and decreased again in the last swing (45% MMT). Activity decreased in the follow-through to a low of 26% MMT.
VMO activity increased significantly from the windup (26% MMT) to the preswing (63% MMT) and again from the
preswing to the middle swing, during which it peaked at 107% MMT. It diminished thereafter through the late swing (97%
MMT) and follow-through (78% MMT).
Trunk. During the windup, activity in both erector spinae was low (24% MMT) but increased significantly to more than
90% MMT throughout the preswing, early swing, and middle swing. Activity then decreased in the late swing (98% MMT
lead, 85% MMT trail) to significantly lower levels during the follow-through (58% MMT, 68% MMT). There was no
significant difference in activity between the lead and trail erector spinae during any phase.
As in the erector spinae, both abdominal oblique muscles demonstrated relatively low levels of activity during the windup
(<30% MMT). Activity jumped significantly to greater than 100% MMT in the preswing and remained elevated throughout
the remainder of the phase. No significant differences in activity were found between lead and trail oblique muscles.
Comparison of the abdominal oblique and erector spinae muscles revealed a statistically significant difference in activity
level only during the follow-through phase, during which the abdominal oblique activity remained high (101% MMT, 134%
MMT) relative to the decreasing erector spinae level (58% MMT, 68% MMT).
Upper extremities. Posterior deltoid activity increased significantly from a low in the windup phase (17% MMT) to a high
in the preswing (101% MMT). Signal intensity subsequently decreased throughout the remainder of the swing, and this
decrease was significant between the late swing (76% MMT) and follow-through (25% MMT).
The triceps demonstrated low activity in the windup (25% MMT), which increased significantly in the early (92% MMT)
and middle swing (73% MMT). Activity then declined significantly between the middle swing and follow-through (23%
MMT).
Supraspinatus muscle activity remained relatively low (32% MMT) throughout the swing. The lowest activity occurred
during the windup (13% MMT), which revealed significantly less activity than during the preswing, midswing, or late swing
(32% MMT each).
Middle serratus muscle activity remained low throughout the swing (<40% MMT), particularly during the windup (18%
MMT), which showed significantly less activity than either the middle or late swing (39% MMT each).
Test Evaluation
Windup. Activity levels during the windup were relatively low except in the trail leg hamstrings. During this period of
single-leg stance, hamstring activity maintained hip extension as a weight shifted to the trail leg in preparation for the
swing.
Preswing. The high level of activity in the hamstrings and lower gluteus maximus muscles during the preswing indicated
their role in hip stabilization and initiation of power. Both lead and trail erector spinae and abdominal oblique muscles
were also quite active at this time for trunk stabilization and power transmission. As the body was lowered during the
preswing and early swing, posterior deltoid and triceps activity increased markedly to maintain lead shoulder elevation.
Swing. During the preswing and early swing, there was increased activity in the VMO, which prevented collapse of the
increasingly flexed trail leg and promoted push-off to facilitate force transfer. When weight was transferred to the lead
leg, hamstring and gluteus maximus activity in the trail leg declined. Trunk activity in both erector spinae and oblique
muscles remained high throughout the swing, with erector spinae activity declining just before the ball contact. This
demonstrated the importance of the trunk in power transmission as the body uncoils.
Swing progression yielded decreasing, albeit relatively high, activity in the posterior deltoid and triceps muscles,
suggesting their likely positional role. Although they may contribute to power generation, their consistently decreasing
levels throughout the swing suggest they are not the main “drivers.” The trunk muscles (erector spinae and obliques) play
an important role not just in power transmission but also in coordinating upper-extremity to lower-extremity muscle
function.
Follow-Through. Activity levels in the lower and upper extremities were low during the follow-through except for the
VMO, which maintained an extension force on the flexed trail knee. Back and abdominal oblique muscle activity levels
remained high, maintaining trunk rotation and stabilization.
Overall Assessment. In summary, a distinct pattern of muscle activity was observed during the batting swing. Lower
extremity groups appear important in early pelvic stabilization and power generation. The hamstrings maintain hip
stabilization in addition to contributing to the “thrust” provided to initiate rotation (uncoiling mechanism). VMO activity
increased throughout swing as the lower extremity pushed against the ground and through the bent knee to contribute
the forward thrust of the pelvis and trunk.
The erector spinae and abdominal oblique muscles were extremely active in trunk stabilization and rotation for smooth
power transfer. The lack of discernible activity differences between lead and trail spinal or oblique muscle muscles
suggest their premier importance in torso stabilization and rotation, rather than power generation per se. However, it is
also possible that our use of surface electrodes for the oblique muscles recorded information from both the internal and
the external oblique muscles inasmuch as these are relatively thin adjacent muscles. This may preclude the ability to
discern a “coupling force” between the internal and external fibers and thus the lead and trail sides as well. Differences
between the lead and trail erector spinae muscles may have been similarly masked because of their proximity.
The posterior deltoid and triceps muscles appeared to be more important in positioning than in power generation. The
middle serratus anterior and supraspinatus muscles did not significantly contribute to the swing.
The uncoiling of the wound-up pelvis, trunk, and upper extremities on a stable base provides the power of the baseball
batting swing. Of the muscles tested, there appears to be a sequence of activity, from the lower extremities (most active
group in preswing) through the trunk (highest in early swing) to the upper extremity muscle groups. This sequence
appears nearly identical to that observed in the golf swing, in which initiation of the swing begins in the hip ( 25). As in
batting analysis, EMG studies of the golf swing show the importance of the trunk in stabilization and power transfer ( 2). In
the golf swing, the serratus anterior and supraspinatus muscles were more active than during the batting swing, and the
posterior deltoid was less active ( 5,28). This is most likely due to the higher position of the golf club, which requires
scapular protraction and humeral abduction. The baseball bat is held in a position of more horizontal abduction and thus
initiates relatively more activity in the posterior deltoid. The pectoralis major and latissimus dorsi muscles in the golf
swing may contribute to the power by internally rotating and abducting the humerus. This position places the arm in a
stable position to transmit the power to the ball. However, this study did not monitor activity in these muscles. Future
studies of additional upper extremity muscle groups will be of great interest in furthering our present understanding.
The following conclusions were drawn:
1. Hamstring and lower gluteus maximus activity contribute significantly to the stable base and the
“power-or-the-thrust” form that the torso “uncoils” during the swing.
2. Skilled baseball batting relies on a coordinated transfer of muscle activity from the lower extremities to the trunk
and finally to the upper extremity.
3. The high level of activity in the erector spinae and abdominal oblique muscles throughout the swing suggests the
importance of emphasizing abdominal and back exercises in a comprehensive exercise and conditioning program
for baseball batters.
4. Unlike previous study conclusions, the triceps and other muscles of the upper extremity studies appear most
important in positioning the swing. Contribution of other upper-extremity muscles to power generation remains an
area for future study.
5. This study provides a baseline on which further investigation of the baseball batting swing can be performed.
Prevention and rehabilitation of batting injuries can be more specifically focused, given an understanding of the
biomechanics of the batting swing.
Evaluation from the Athlete's Perspective. For a more practical understanding of hitting, we turned to a hitting coach
and a skilled batter (15,29).
The swing starts with the stance, which relies on balance. Every player uses a slightly different approach: open or closed,
feet further apart, feet closer together. The ideal is probably placement of the feet at shoulder width, but the key is
balance. The batter can fashion a hole for the back foot to use in pushing off, changing the stance slightly from closed to
opposite-field open for an inside pitch. No matter where the player is and what he is doing before initiating the hitting
motion, control is based on balance in the stance and proceeds to the forward stride. As a pitcher begins the windup and
approach to the plate, the hitter coils up. This coiling maneuver brings the bat to the position necessary to initiate the
swing. Again, regardless of the amount of motion activity, most bats come to a relatively standard position in relation to
the strike zone just before the forward stride is initiated.
The hitter assumes the correct body position: the coiled hips and head are approximately parallel to the ground, and the
knees are slightly bent. There is some flexion of the lumbar spine, the shoulders are level, and the head is turned as the
hitter looks directly at the pitch, chin against the shoulder. Hand position varies slightly according to each player. A
reasonable amount is 4 to 8 inches from the body, letters high to shoulder high. In the coiled position, the hitter holds the
bat at approximately 45 degrees, with the elbow parallel to the ground and out from the body. Hands that are held too far
from the body may reduce power, whereas if they are too close to the body or too low, the bat speed is reduced. In most
missed pitches, especially the fast ball, the hitter swings below the ball. Holding the hands too low not only reduces the
bat speed, but except in exceptional cases, may reduce the contact zone. In the coiled position, the hitter begins moving
with the forward arm motion of the pitcher, picking up the ball from the pitcher's hand and beginning to time his stride
forward and swing.
Obviously, the most important key to hitting is vision. The hitter who does not see the ball can only guess and will not be
able to make contact. Not only is visual acuity a critical factor but eye control and eye function are of equal importance.
The hitter must have clear binocular focus to be able to visualize the ball and to predict its location. The speed of the ball
makes it virtually impossible to completely follow the ball to the bat. The ideal is to follow the ball as far as possible and
then make a prediction as to its line of projection. Without visualization, concentration, and focus, the hitter will fail to
project the arrival point of the ball, and inadequate ball contact is the consequence. In addition, balance and control are
determined by eye focus, as in any coordinated muscle activity. If the eyes and head are locked and focused on a point,
the body has a much greater chance of reproducing a coordinated, balanced motion than if the eyes are closed or poorly
focused.
Thus, the key in the stance and coil position is balance, eye focus, and body readiness to start the stride. What happens
before this coiling mechanism is not of great importance, but body and head position in the coiled portion of the swing
should at least place the bat in a position that will facilitate the stride.
Batting coaches indicate that there are five basic aspects of the swing starting with the stride, as follows:
1. Back foot rotation, in which the heel is rotated out and the body pivots on the ball of the back foot
2. Forward stride with the left foot
3. Rapid hip and trunk rotation that takes the navel from a position parallel with the pitch to being perpendicular to the
pitch
4. Triangulation of the arms and extension of the arms
5. Lateral flexion of the wrist
Stride. Efficiency of motion is essential to the hitter ( 29). The hitter must avoid needless motion. Motion must be
balanced and coordinated in the forward stride. The backward motion in the coiling position precedes the forward motion.
The front leg internally rotates, and the coil position will externally rotate in the stride. The stride should be directly
toward the pitcher. The weight shift in a hitter is very important. With the forward stride, the weight stays back on the
back foot as the forward foot strides forward lightly on the ball of the foot. The front leg now rotates externally, and the
knee goes into extension. The ability to lock the knee of the front leg, providing firm rigid resistance to body motion, is
important in keeping the axis of rotation of the body centered. If the knee flexes, the body weight shifts forward, and the
proper axis of rotation is lost. As the foot lands evenly, it may be slightly open. The knee, of course, is initially slightly
flexed as the foot lands and then locks in extension as the hips come through. This rotation around a center axis is
important.
The midsection is the core of the swing action from which the hitter generates power ( 29). Maintaining a center axis of
motion and balance plays a critical role in maintaining head position. Too much head motion equals loss of both
coordination and visualization of the ball. Locking the head to the center of axis of rotation is a key to the stride and
swing positions. The bat in the coiled position is approximately at a 45-degree angle. As it comes through, there is a
relative leveling of the bat, usually with less than 10 degrees of angulation. The pitch starts high because the pitcher is
on the mound and throwing downward, whereas the bat comes through level. There will be a difference of a certain
number of degrees of angulation between the ball and the bat. The bat comes down as the ball comes down.
Rotation. The forward stride of the legs and the rotation of the hips are reasonably standard in speed and approach.
Large muscles of this type cannot be controlled quickly enough to allow the hitter to adjust to the speed at which a pitch
is thrown. Therefore the stride, at a fairly standard distance, with standard open or closed length, allows compensation.
One of the important parts of batting-training technique is a rapid, sudden hip twist in which the navel goes from 90
degrees to the pitch to directly parallel to the pitch. A rapid, swift twist of the hips is what, in many ways, determines the
bat speed and allows the hitter to be in a prime position to adjust to the speed and type of pitch. Therefore, stride length
and hip rotation, with the navel toward the pitcher, are the same in virtually every pitch and must be a standardized,
balanced, well-coordinated motion.
After this sudden hip rotation occurs, adjustments to various speed pitches and pitch locations become crucial. As in golf,
there is a ratio of derotation of the body as it leaves the coil position to the point of contact. In hitting, there is an
adjustable ratio of derotation. With the power generated through hip and belly rotation, the fine control comes with the
speed of the upper body uncoiling ( 22), elbow extension (24), and wrist lateral flexion ( 8). Location of the pitch, of course,
varies tremendously, and the fine adjustment takes place in these latter three components. Therefore, the upper body
trails behind the derotation of the hips. Trailing behind does not imply a helter-skelter, uncoordinated motion. Because
the ratio of derotation of upper body to lower body must vary with the pitch, it requires even more muscular trunk control
to allow the proper rotation to take place, depending on the pitch. Therefore, the hitter must visualize the ball and, in less
than a second, determine the ratio of derotation of the upper body, as well as the position of the head, elbows, and hands
for the point of contact with the ball. This maneuver requires excellent muscle control, balance, and coordination. Proper
hitting depends on retraining muscles to fire and respond to changes in balance and coordination, and retraining trunk
muscles to maintain a tight and rigid but mobile control between the upper and lower body. Lumbar pain that prevents
proper rotation or that causes muscles to stop, to work improperly, or to work in an uncoordinated fashion can have a
devastating effect on the player's ability to deliver the bat to the ball.
After hip rotation, with the upper body trailing behind slightly under maximum muscle control at a specific ratio of
derotation determined by the pitch, the upper body rotates through to the point of ball contact. The head is level, going
down with the pitch while the eyes focus on the ball. The chin of the right-handed batter, which is against the left
shoulder in the coiling position, will end up against the right shoulder after ball contact. (The opposite, of course, is true
for the left-handed hitter.) Again, head motion equals poor efficiency. At this point, with the bat coming through the strike
zone, the shift is to the shoulder and upper arms, with triangulation of the arms: the chest as the base and the two arms
parallel as they extend out. Locking the lead shoulder is of critical importance. Stabilization of the lead shoulder allows
extension of the lead elbow and proper generation of bat speed. The bottom hand pulls and anchors the bat: the top
hand pushes and guides the bat. As the arms and elbows extend, the bat is still trailing behind, with the wrists still in the
cocked position.
Obviously, proper technique—including the weight shift from the back foot to the forward foot and the position of the
elbows, hands, wrists, and the bat—allows the hitter to delay the final commitment of bat position as long as possible. It
provides longer visualization of the ball and a better prediction of the point of contact—all taking place at the same time
the body is generating tremendous torsional force. Therefore, the reproducible bat swing must generate the power and
force necessary for the swing while delaying final commitment of bat position, allowing the wrists and hands to provide
fine bat control and bat position at the point of contact. It is certainly possible to make contact with the ball with neither
trunk rotation nor power but without sufficient results on the field. The follow-through after ball contact is not of major
consequence. Weight is shifted to the front foot, and the left knee is locked. Adequate control of quadriceps function of
the front leg is imperative. The arms are extended; the top hand should roll over at an appropriate time and should not be
rushed too early. Follow-through is a natural part of the swing and not of major consequence.
In summary, stance, balance, control, head in proper position, stride, standardized lower body stride and position, and
uncoiling of the upper body require maximum trunk control and balance to produce the correct ratio of derotation that will
allow the bat to arrive at the appropriate place. The locked lead shoulder provides a rigid upper arm for proper elbow
extension. Tight wrist control is obtained with proper lateral flexion of the wrist. The head rotates from the lead shoulder
in the coiled position to the trailing shoulder in the follow-through.
Pitching
Some of the most difficult cases of lumbar spine problems are seen in baseball pitchers. It is extremely common in spring
training to see throwers, especially baseball pitchers, having pain in the opposite-side SI joint. This is due to
unaccustomed torsional strain, probably in the lower facet joints, after the winter break. There is a high incidence of back
stiffness in throwers as they start to regain peak mechanical functioning and begin throwing again. A common occurrence
is referred discogenic or facet joint pain in the typical pattern (i.e., through the facet joint, across the posterior superior
iliac spine, SI joint, posterior ilium, and into the area of the greater trochanter). A concomitant problem is the
development of secondary contractures, weakness, bursitis, tendinitis, and inflammations in the referred pain area. Often,
a pitcher will have greater trochanteric bursitis or SI joint pain that produces its own secondary effects.
A key aspect of a pitcher's rehabilitation is not only the resolution of the back problem; the secondary inflammatory
effects of referred pain can produce the same biomechanical abnormalities in the pitching motion, thus leading to further
injury. The pain itself may prevent proper pitching and performance, and thus cause additional injury. True sciatica and
muscle weakness in a leg result in a critically important dysfunction in a pitcher: severe abnormalities of pitching motion
that place the arm, shoulder, and elbow in jeopardy. Sciatica, especially with associated pain of increasing intradiscal
and intraabdominal pressure, can result in severe dysfunction during the throwing motion. Trunk stability is critical to a
pitcher's throw, and any pain that produces weakness and stiffness can lead to a potentially catastrophic injury.
Dynamic Electromyographic Analysis of Torque Transfer
EMG evaluation of trunk muscle activity during participation in sports is a well-recognized technique that provides insight
into performance and injury. In an effort to study better the role of trunk musculature and lumbar injury in the professional
baseball pitcher—who engages in one of the most demandingly precise high-speed torsional activities in sports—we
turned to EMG evaluation of trunk musculature in the Centinela Hospital gait laboratory.
With help from Harry Farfan and from professional pitchers, coaches, and trainers, we initially postulated that trunk
fatigue produces increased lordosis of the lumbar spine and, therefore, places the shoulder and arm behind in the
throwing motion. This leads to a high release point, and the ball rises in the strike zone and becomes easier to hit. Also,
arm strain can result from using the arm muscles to try to catch the arm up to the trunk.
In an attempt to evaluate this phenomenon of the so-called slow arm secondary to timing changes, we had to understand
the normal patterns. First, 20 nonprofessional athletes underwent EMG analysis of trunk musculature while pitching. This
evaluation indicated a basic pattern of firing sequences needed for the pitching motion. The contrasting patterns
indicated a sequence necessary for skilled performance. Fifteen professional baseball pitchers from the Dodgers' staff
volunteered to be tested. The objective of this study was to document the firing sequence and intensity of contraction of
the trunk musculature during the baseball pitch in the professional pitcher. Our goal was to provide a foundation for the
analysis of pitching biomechanics, trunk conditioning, and rehabilitation that could be used to improve the efficiency of
the athlete and decrease the incidence of injuries.
The 15 volunteers underwent EMG activity amplitude evaluation through surface electrode telemetry of their trunk
musculature, including the abdominal obliques, rectus abdominis, lumbar paraspinous, and gluteus maximus bilaterally.
These activity levels were collected during the pitching sequences, with the players using proper biomechanics at
approximately 60% to 70% of maximum velocity, as measured by radar gun. After an evaluation by a physical therapist,
with the aid of computerized telemetry and ensured proper electrode placement, all the players warmed up before the
study pitches.
Then each player was asked to do four runs consisting of 40 pitches; adequate telemetry recording of each muscle group
was obtained with the use of high-speed film (450 frames per second) and a speed gun. Two separate series of runs
were conducted, as delineated by the individual muscle groups tested.
The signals from the leads were transmitted by means of an FM-FM telemetry system capable of transmitting data from
four muscles simultaneously. Correct electrode placement was confirmed through MMT specific to the tested muscle, as
documented on an oscilloscope. Each subject wore a battery-operated FM transmitter belt pack designed to prevent
restriction in bodily movement. Muscle activity patterns were synchronized with high-speed film (450 frames per second)
to obtain muscle activity values at each phase of the pitching motion. The film was then synchronized for computer
analysis in terms of the following phase of pitching:
1. Trunk movement to hands apart

2. Hands apart to foot touch (leading leg)
3. Foot touch to maximum external rotation (dominant shoulder)
4. Maximum external rotation to ball release
5. Ball release to end of follow-through
Results. The key factor in evaluating even a homogeneous group of subjects is determining the consistency of trends
and reproducible changes. Even with exclusively professional pitchers, we found wide variety of delivery styles, physical
characteristics, and techniques, which produced a wide range of absolute values but consistent and predictable trends in
muscle activity.
The nondominant rectus abdominis, lumbar paraspinous, and abdominal oblique muscles all showed consistent and
significant increases in activity over their dominant-side partners at predictable phases. The glutei demonstrated bilateral
increases consistent with the phases of pitching.
The nondominant rectus exhibited individual increases into the active phase of fivefold to 20-fold, with sustained
increases throughout the active phase as high as 10-fold. The mean increase over the active phase through ball release
for the nondominant rectus abdominis was 40% higher than that of the dominant side. In the actual cocking phase (foot
touch to maximum external rotation), individual activity levels increased from 5 to 100 and from 12 to 114 (2,000% and
950% increases, respectively) from the prior phase on the nondominant side. At this same point, the dominant side was
35.5 and 11.5 (compared with 100 and 114, respectively).
Four players demonstrated slight dominant-side predominance in cocking, two were reversed or balanced in delivery,
and all pitchers were in nondominant-side control at the time of ball release and follow-through.
The nondominant lumbar paraspinous demonstrated individual increases of 100% to 400% during the active phases, with
an occasional subject showing dominant-side increases as well. During the maximum cocking phase, through and
including ball release, this nondominant muscle demonstrated a mean of 50% increase in activity over the dominant side.
The dominant lumbar paraspinous was much more active than the rectus abdominis counterparts at an earlier phase.
However, in every subject, during each of the active phases through ball release, the nondominant side demonstrated
increased activity. In the cocking phase, the mean increase was 51%, whereas in the delivery phase the mean was only
16%, with generalized increases overall on both sides and individual increases on the nondominant side from 6% to
250%.
The abdominal oblique muscles demonstrated consistent increases in the nondominant side as opposed to the dominant
side during the active phases. Increases of 300% to 500% activity were seen in 9 of 16 pitches in the active phases, with
increases in all pitchers on the nondominant side over the dominant side. Mean increases of 85% in the nondominant
abdominal oblique muscles of all subjects and all runs occurred in the final three phases, a greater increase than in any
other muscle or pair of muscles—nondominant versus dominant—in any phase.
The glutei are firing bilaterally in an expected pattern, as seen by stance phases of the pitching motion. The dominant
side bears all the weight initially as rotation begins, and as the stride begins during the cocking and acceleration phases,
the nondominant side becomes equally active and must balance as the dominant side pushes through hip extension in
the controlled falling of delivery. The nondominant side remains flexed at the hip, the gluteus stabilizing the pelvis as the
trunk derotates, and delivery and ball release follow.
Evaluation. The concept of trunk strengthening and control is not a new one. Over the years, however, most of the data
have been collected in regard to the failed back, discogenic disease, and spondylolisthesis ( 28) as opposed to athletic
performance. Most EMG data have focused on posture, loading, and muscle effects on ligamentous and bony structures.
Until recently, no reliable, accepted measurement of trunk strength and coordination has been available. We hoped the
results of our study would lead to multiple applications. Our first objective was to document the firing sequence and
activity levels of the trunk musculature in pitching at the professional level. These baseline data provide trends and
patterns that can be used to evaluate faulty biomechanics and thus to develop a successful rehabilitation tool. With
continued refinement and growth of the database, we hope to be able to evaluate effectively prospective athletes and
potential professionals.
A phase of coiling or rotational loading immediately before the cocking phase is one of the most important load
components in the pitching motion. This phase loads the body so that the arm can both load and release with maximum
power and efficiency. During this phase, the dominant gluteus maximus muscle is the key factor, first working in neutral
and slight extension for balance to allow maximum coiling as a stabilizer of the pelvis and trunk and, immediately
following, as a powerful extensor to provide maximum power transmitted through the leg. During these cocking and
acceleration phases, which take less than 0.3 second ( 26), the player goes through the phenomenon of controlled falling
(20). This controlled falling sequence is a combination of deceleration and derotation of the trunk during maximum
cocking and subsequent acceleration of the pitching arm to ball release and follow-through. These oppositional forces
cause an imbalance and result in the pitcher's falling toward the dominant side. This action must be resisted to maintain
body position for both power and accuracy, and to prevent injury in the trunk and arm.
It is during this transition that the nondominant-side trunk muscles become most important. The predominance of
contralateral muscles to control rotation is a well-documented concept ( 3,22). These paraspinal muscles act as
stabilizers, while the oblique muscles act to initiate further flexion or rotation ( 3). In other posture and loading studies of
EMG back muscle activity using asymmetric loading on an increased angle at a fixed point, higher activity was found on
the contralateral side in the lumbar region ( 22).
In this situation of controlled falling, both rotational forces and gravity must be resisted. Asmussen ( 24) and Asmussen
and Klaussen (8) documented the counteraction of gravity to be maintained (primarily by one set of back muscles). The
abdominal muscles affect posture only 20% to 25% of the time ( 8). Previous data support our findings in applying this
concept of trunk support and the rotational component involved. Donisich and Basmajian's work ( 14) also documented
this paradoxic activity of increased lumbar contralateral EMG function in axial rotation. All of the previous work based on
a form of external load have been lifting studies, studies of resisted movements, or studies of static postures ( 22). To
evaluate trunk muscle function during active motion, the subject is measured in various postures and in transition,
resisting his own acceleration and deceleration and generating power through the trunk as in lifting. Previous studies
have shown that during rotation or transition, the contralateral rotations and trunk stabilizers have been most active
(3,8,14,22,24).
In analyzing the pitching data, we find the same patterns of muscle activity, and therefore power, that is seen in simple
postural loading activities. Thus, it should be possible to apply the concept of trunk strengthening to improved function
and decreased injury. Chaffin and Moulis ( 1) proposed that strengthening the deep back muscles relieves pressure on
the intervertebral disks and, therefore, should decrease injury during loading. Parnianpour et al. ( 19) documented the
effect of fatigue on both the motion output and the patterns of trunk movements, showing that fatigued muscles are
slower and subsequently take longer to respond to change in loads. This demonstrated the phenomenon of
compensation by secondary muscle groups causing loading in some injury-prone patients. Nordin et al. ( 21) have shown
that after discectomy, male patients have a loss of 55% to 71% of isometric strength in flexion and extension,
respectively. These data applied to athletic injury show that it is crucial for a pitcher to have maximum strength to
maintain his level of performance and avoid injury. Thus, maintaining a strong trunk helps avoid stressing the shoulder
and elbow by protecting them from the overuse and abnormal motion seen with poor trunk mechanics.
One might question the importance of demonstrating a mean firing sequence of trunk musculature ( 22) and the
differences in firing sequence among a top-level pitcher, a strong outfielder, and a rookie pitcher ( 24). In our short study,
all three athletes are strong and have good musculature. The point is that trunk muscle coordination is as important as
trunk muscle strength in the ability to perform as a top-level baseball pitcher. When coordination and strength are
combined, the player is more effective and experiences less fatigue. Therefore, a logical conclusion is that a
trunk-strengthening program that incorporates balancing and coordination is more effective and provides a shorter route
to good training. On this basis, we have considered the possibility of using gait laboratory analysis in decision making as
a predictive indicator for success in terms of biomechanics and muscle activity. Obviously, there is a need for a larger
sampling of pitchers, with particular emphasis on those who have had continued success over time and the fewest
injuries. It is our hope that gait analysis will be added to the current methods of pitcher evaluation. The most important
practical application is to aid the athlete through use of the complete data package, muscle activity levels, firing patterns,
with their trends and timing, and the aforementioned high-speed photographic techniques. By means of careful laboratory
analysis, coupled with evaluation by coaches and trainers, we can aid in the detection of biomechanical changes and,
through rehabilitation or changes in technique, improve the athlete's efficiency.
The use of gait analysis for the injured athlete in need of rehabilitation is an important concept. The significant
association of the injured shoulder or elbow with the weak or injured lumbar spine needs further documentation.
Unfortunately, under laboratory conditions, we could not replicate a pitcher's fatigue and study the resultant interaction of
the arm and spine. It is an accepted concept in baseball that fatigue causes an early release point in the throwing motion,
which, in turn, causes the ball to rise at the batter, making it easier to hit. This fatigue originates in a weak trunk and
increased lumbar lordosis that places the arm behind the body, causing the arm to work harder and predisposing it to
injury. By using laboratory evaluation, we hope to aid in rehabilitation programs by emphasizing the role of trunk strength
in shoulder rehabilitation.
Implications. The documentation of trunk activity in the dynamic stage of baseball pitching clearly demonstrates a
reproducible pattern of muscle function based on strength combined with coordination. This pattern directly affects the
biomechanics of the throwing arm by controlling the stability and loading characteristics responsible for maximum power
and control. The implication of such a pattern is that the play of athletes can objectively be analyzed to maintain peak
technique or to improve biomechanics.
In conclusion, throwers require a rigid cylinder of strength in order to transfer torque from their legs to their throwing arm.
Trunk and leg strength generate the velocity of the throw, and the arm provides the fine control strength. Fatigue reduces
the control of the pitching motion and ball location. A major factor in ball control is a loss of tone and strength in the trunk
due to trunk muscle fatigue. There is a loss of the rigid trunk cylinder that produces a loss of synchrony between the legs
and arms. This causes a change in the pitching motion. As the trunk flexors and abdominal musculature weaken due to
fatigue, lumbar lordosis increases and the back arches. The subtle change of a few degrees puts the arm behind in the
pitching motion, promoting earlier ball release and the pitch comes up. Arm strain increases as the trunk musculature
fatigues. Attempts to compensate for loss of trunk strength and a “slow arm” increase the use of the arm musculature and
predispose the shoulder to injury. Developing power in torsion depends on trunk strength, that is, strengthening
abdominal, back, buttock, and thigh muscles. Trunk strengthening exercises are designed not only to enhance the
performance, but also to prevent arm injury. Trunk strength is superseded only by balance and coordination. The firing
sequence of trunk muscles in a professional baseball player follows a consistent median pattern. An alteration in that
pattern produces an inconsistent, uncoordinated pattern, leading to arm strain and back injury ( 16).
Tennis
In terms racquet sports in general, Chard and Lachmann ( 27) when reporting on racquet sport injuries, separated the
incidence into squash, 59%; tennis, 21%; and badminton, 20%. Thirty-eight of professional tennis players have missed
tournaments due to back pain. Trunk strengthening should be a major part of the tennis player's regimen ( 30).
Tennis as a sport involves speed, rotation, extreme flexion, lateral bending, and extension. It involves the power aspects
of the overhead serve and the effect of trunk strength on shoulder function, which are many of the aspects brought out in
the other sports. The one most consistent, important factor in protecting the spine in tennis is to bend the knees. Leg
strength, quadricep strength, the ability to play in a bent knee, hip flexed position while protecting the back is the key to
prevention of back pain. In the serve, trunk strength in proceeding from the back extended to the follow-through position
requires strong abdominal control. Gluteal latissimus dorsi, abdominal obliques, and rectus abdominus strength control
the lumbodorsal fascia and deliver the power necessary through the legs up into the arm.
In summary, the keys to proper management of lumbar spine problems in athletes include
1. Comprehensive diagnosis
2. Aggressive, effective nonoperative care
3. Pinpoint operations that do as little damage as possible to normal tissue but correct the pathologic lesion
FIGURE 52.6. A–C: A 34-year-old professional golfer with L-5 to S-1 spondylolisthesis and L-4 to L-5 and L-5 to S-1 disk
degeneration. Discography reproduced the patient's L-5 radiculopathy from the L-5 to S-1 disc. The contrast CT scan
demonstrates the closed proximity of the bone spur and the caudal facet of the pseudarthrosis, which is in proximity to
the L-5 nerve root. A two-level fusion would be the most definitive solution to the problem. A limited decompression may
play a role in relief of the radicular symptoms, and a postoperative rehabilitation program may produce sufficient stability
to avoid the fusion.
FIGURE 52.7. A and B: This 30-year-old professional golfer has an L-5 to S-1 spondylolisthesis and severe two-level
degenerative disk disease with a large pseudodisc at L-5 to S-1. He responded to a trunk stability rehabilitation program.
Because he did his exercises, he has been able to perform effectively and remain relatively asymptomatic.
FIGURE 52.8. A and B: The MRI of a 34-year-old starting American League third baseman. This patient suffered multiple
episodes of mechanical back dysfunction without significant radicular symptoms.
FIGURE 52.9. This 21-year-old infielder had an S-1 radiculopathy. Recommended treatment was a one-level microscopic
lumbar discectomy and postoperative rehabilitation. It can be seen that the patient suffers from two-level degenerative
disk disease and has significant degenerative changes in the L-5 to S-1 disk space. It is predicted that the patient will
need significant postoperative rehabilitation to return effectively to his sport.
FIGURE 52.10. This 22-year-old American League baseball pitcher had bilateral spondylotic defects. T2-weighted MRI
revealed normal water content. The patient reproduced his pain, and it was blocked by injection of the spondylotic
defects. He failed to respond after 1 year of nonoperative rehabilitation and underwent a posterolateral fusion, and
returned to pitch with minimal lumbar spine symptoms.
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1987;6:767–783.
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Roentgenol 1985;145:1039–1044.
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53 Shoulder Injuries
53
SHOULDER INJURIES
JOHN J. PERRY
LAURENCE D. HIGGINS
Functional Anatomy
Biomechanics
History and Physical Examination of the Shoulder
Provocative Tests
Glenohumeral Instability and Labral Tests
Rotator Cuff Tests
Biceps Tendinitis Tests
Injuries to the Athletic Shoulder
Instability
Rotator Cuff Problems, Impingement, and Biceps Tendinitis
Biceps Labral Complex Injuries
Injuries to the Acromioclavicular Joint
Dislocation of the Sternoclavicular Joint
Fractures
Neurovascular Injuries
Chapter References
The shoulder is a frequent site of injury in competitive athletes. Shoulder injuries comprise between 8% and 13% of all
athletic injuries ( 1). These injuries may result from repetitive overhead activities (in swimmers, baseball pitchers, tennis
players, and javelin throwers) or direct trauma (in football and rugby players). Table 53.1 lists the incidence of typical
injuries seen in specific sports ( 1,2,3,4,5,6,7,8,9,10 and 11). Within a given sport, most shoulder injuries are position
specific. In baseball, shoulder injuries are more common among pitchers. In swimming, shoulder injuries are most
common in those who compete in butterfly, freestyle, and backstroke events. In addition to the nature of the sport and the
position played, shoulder injuries in the athlete depend on the anatomic variants specific to each athlete, their age,
conditioning, level of play, level of overhead activity, techniques used, and the length of participation in their respective
sport.
TABLE 53.1. INCIDENCE OF SPORT-SPECIFIC SHOULDER INJURIES
An increased understanding of shoulder abnormalities and the existence of newer diagnostic modalities such as
ultrasound, magnetic resonance imaging (MRI), magnetic resonance arthrography (MRA), and shoulder arthroscopy
have led to an increased awareness of problems specific to the athlete's shoulder and to more successful treatments of
pathologic conditions. In this chapter, the more common shoulder problems seen in athletes are discussed. The
emphasis is on the relevant biomechanics and pathophysiology, with special attention given to diagnosis and treatment.
The discussion begins with a section on functional shoulder anatomy and biomechanics. Then physical examination,
diagnostic imaging of the shoulder, and finally specific shoulder injuries and problems are discussed.
FUNCTIONAL ANATOMY
An understanding of normal shoulder anatomy is essential to diagnosing and treating shoulder injuries. Normal shoulder
motion is actually a combination of motions of four joints: (a) the glenohumeral joint, (b) the scapulothoracic joint, (c) the
sternoclavicular joint, and (d) the acromioclavicular (AC) joint. The glenohumeral joint contributes approximately 120 of
the 180 degrees of upward motion of the arm. The remaining 60 degrees is the result of scapulothoracic motion. Virtually
all rotation of the upper arm occurs at the glenohumeral joint. The glenohumeral joint's capsule is by necessity loose and
redundant to accommodate the large range of motion of the shoulder. The joint capsule is reinforced by thickenings that
form three ligaments: the superior, middle, and inferior glenohumeral ligaments ( Fig. 53.1). The superior glenohumeral
ligament arises from the glenoid labrum anterior to the biceps tendon and inserts into the humeral neck in the region of
the bicipital groove of the lesser tuberosity. The glenoid labrum is a fibrocartilage ring that attaches to the relatively small
bony glenoid fossa. It serves as an attachment for the inferior glenohumeral ligament and effectively deepens the socket
to contain the much larger humeral head as the shoulder moves through a range of motion ( 12,13). The superior
glenohumeral ligament helps control inferior translation when the shoulder is adducted and posterior translocation when
the shoulder is adducted, flexed, and internally rotated ( 14). The middle glenohumeral ligament acts as a secondary
restraint to inferior translation when the shoulder is in the position of adduction and external rotation ( 14). The inferior
glenohumeral complex is a hammock-like support for the glenohumeral joint and is a primary restraint to anteroposterior
(AP) and inferior translation in the abducted shoulder ( 15) (Fig. 53.2). The capsule and glenohumeral ligaments are richly
innervated with sensory nerve endings: Ruffini organs, pacinian corpuscles, and Golgi-tendon organs, which detect
motion, acceleration, tension, and speed ( 16). These sensory features aid the muscles with important feedback during
the highly coordinated demands placed on the shoulder during athletics.
FIGURE 53.1. Diagram of the Bankart lesion. A, anterior; IGHL, inferior glenohumeral ligamen; MGHL, middle
glenohumeral ligament; P, posterior; SGHL, superior glenohumeral ligament.
FIGURE 53.2. “Hammock-like” inferior glenohumeral ligament complex with anterior and posterior capsular thickenings
showing tensioning with internal and external rotation of the abducted humerus.
The scapula with its glenoid, acromion, and coracoid processes rests on the chest wall and is stabilized by the clavicle,
levator scapulae, trapezius, serratus anterior, and rhomboid muscles. These muscles are jointly referred to as the
scapular stabilizers. The clavicle functions as a strut and provides lateral offset of the shoulder on the thorax. It is the
only bony connection between the shoulder and the chest wall. Without this strut, the scapular stabilizers would not have
a stable fulcrum on which to move the scapula about the chest wall. The rest of the connections of the shoulder to the
chest wall are muscular and function to stabilize the scapula, while the prime movers of the glenohumeral joint contract.
Attached to the coracoid process are the coracoacromial ligaments, the coracoclavicular ligaments (the conoid and the
trapezoid ligaments), the pectoralis minor muscle, the conjoined tendon of the coracobrachialis, and the biceps brachii
muscle (Fig. 53.3).
FIGURE 53.3. Shoulder specimen dissection showing attachments to coracoid (start). BP, brachial plexus; CA,
coracoacromial ligament; CC, coracoclavicular ligaments; CL, clavicle; HH, humeral head. The pectoralis minor
attachment has been removed.
The primary muscles around the glenohumeral joint consist of two layers. The outer layer, the deltoid muscle, and the
inner layer consisting of the rotator cuff muscles: the supraspinatus; the infraspinatus; the teres minor; and the
subscapularis. The deltoid muscle (axillary nerve), along with the pectoralis major (medial and lateral pectoral nerves)
and the latissimus dorsi (thoracodorsal nerve), supplies most of the power for shoulder motion. The rotator cuff muscles
act primarily to control the humeral head within the glenoid fossa. The supraspinatus (suprascapular nerve) originates on
the medial three quarters of the supraspinatus fossa of the scapula and inserts into the greater tuberosity of the humerus.
This muscle passes under the coracoacromial ligament and is primarily responsible for initiating shoulder abduction and
containing the humeral head in the glenoid during abduction. The teres minor (axillary nerve) and infraspinatus
(suprascapular nerve) act as external rotators of the humerus. The teres minor originates on the axillary border of the
scapula, while the infraspinatus originates in the medial three quarters of the scapula in the infraspinatus fossa. Both
muscles insert on the greater tuberosity and are supplied by the suprascapular nerve. The subscapularis muscle
originates on the medial four fifths of the anterior surface of the scapula and inserts into the lesser tuberosity of the
humerus. This muscle is innervated by the upper and lower subscapular nerves and acts as an internal rotator of the
humerus. The long head of the biceps passes through the interval between the subscapularis and supraspinatus.
BIOMECHANICS
Injuries to the shoulder are commonly seen in athletes who are throwers or swimmers. To understand the nature of these
injuries, it is necessary to understand the biomechanics of shoulder motion during throwing and swimming. Forces on the
shoulder generated during the acceleration and deceleration phases of throwing are explosive. The acceleration phase
of a pitcher's throw generates 14,000 in.-lbs of internal humeral torque with an angular velocity of 6,100 degrees per
second (17,18). Although each throwing sport has specific mechanistic patterns, there are similarities between the sports
(19). Because of these mechanistic similarities in the patterns of throwing and most of the current understanding of
sport-specific biomechanics comes from examination of pitchers, the discussion of throwing biomechanics is based on
the baseball pitch.
The baseball pitch involves five stages ( 20,21) and is discussed in detail elsewhere in this book. Pitching involves a
coordinated motion of the entire body to generate momentum for the throw. The muscles of the shoulder alone cannot
generate the kinetic energy required to throw a baseball at high velocities, nor can these muscles alone adequately
dissipate the energy once the throw is completed. Injuries can, therefore, occur when the shoulder muscles generate or
dissipate energies beyond their capabilities. Studies have shown that professional pitchers are able to use the
subscapularis muscle exclusively, while the remaining rotator cuff muscles remain silent during the acceleration phase of
pitching. Amateur pitchers, on the other hand, tend to use all the rotator cuff muscles as well as the biceps muscle ( 18).
Therefore, overuse injuries may occur often and earlier in those pitchers who use the rotator cuff muscles unnecessarily.
Proper throwing mechanics are essential to the prevention of overuse injuries of the shoulder.
The swimming stroke basically consists of a pull-through and a recovery phase ( 22). During the recovery phase, the
supraspinatus, infraspinatus, and middle deltoid are primarily active. They function to rotate externally and abduct the
arm in preparation for a new pull-through phase. The recovery phase is similar to the cocking phase seen in throwing. It
is in this position that subacromial impingement may occur ( 23). The serratus anterior allows the acromion to rotate clear
of the abducting humerus and provides a stable glenoid platform for rotation of the arm, thereby decreasing the risk for
impingement or instability. The biceps, as in pitching, functions primarily at the elbow. The latissimus dorsi and pectoralis
major are the major propulsive muscles during the swimming stroke, and their actions are similar to the acceleration
phase seen in throwing. Therefore, baseball pitching and swimming can be thought of as highly complex, repetitive,
coordinated efforts of the muscles about the shoulder. It can then be appreciated that any abnormality in biomechanics or
technique can be greatly magnified as the result of the repetitive increased stress during swimming or pitching. These
increased stresses can lead to shoulder injury.
HISTORY AND PHYSICAL EXAMINATION OF THE SHOULDER
A thorough examination of the athlete's shoulder involves a careful history and physical examination that includes
specific provocative tests. The history should include present symptoms, a detailed discussion of the nature of the
symptoms, and the response to medication and therapy. The history of the present symptoms should include a
description of events surrounding the current report of pain and a prior history of shoulder problems. The physician
should establish whether or not trauma was involved, the mechanism of injury, length of symptoms, and specific
symptomatic activities and arm positions. For example, swimmers may complain of shoulder pain only during one type of
stroke or baseball pitchers may complain of pain only during a certain portion of the throwing motion. Symptoms may not
involve only pain, but the athlete may complain of stiffness, weakness, catching, or a feeling that his or her shoulder is
“giving out.” Rowe initially described the “dead arm” sensation patients with anterior instability may report after overhead
exertion. It is also important to inquire about associated neurovascular symptoms in the arm and hand and pain in the
neck. The physician should also establish whether or not the athlete has been treated with medication, pain modalities,
or formal physical therapy and what response, if any, there has been to treatment. Finally, the physician should
determine whether or not the patient has any previous diagnostic studies.
Following a complete history, a careful physical examination should be performed. The cervical spine should be
examined for range of motion and reproduction of symptoms. The arm should also be examined for neurologic or
vascular pathology. The shoulder can be thought of as four separate joints: the sternoclavicular, the AC, the
glenohumeral, and the scapulothoracic joint. A careful examination includes each of these joints and proceeds by
inspection, palpation, range of motion testing, strength testing, and provocative tests.
The physical examination begins with the patient seated and relaxed, with both shoulders exposed. Men should be
undressed above the waist and women should wear a halter top or have the gown positioned above the breast with the
straps tied in back. Both shoulders must be free for comparison. Inspection of the sternoclavicular joint involves looking
for prominences, depressions, or asymmetry. As is discussed later, this joint can be involved in sprains, subluxations,
dislocations, fractures, or degenerative arthritis. The sternoclavicular joint may be palpated while standing behind the
patient. The physician should palpate the medial end of the clavicle and determine whether gentle pressure over the
articulation elicits pain. Pain without a palpable deformity is consistent with a sprain or arthritis, whereas a palpable
deformity is consistent with a subluxation or dislocation. In an anterior subluxation or dislocation, the sternal end will be
prominent and may be mobile in the superior or inferior direction. With a posterior dislocation, clavicular depression is
palpable. Because a posterior dislocation can be associated with acute neurovascular compromise, the athlete's
peripheral pulses and airway must be assessed. Adduction of the arm across the chest compresses the joint and may
cause pain in cases of degenerative arthritis or trauma.
Following examination of the sternoclavicular joint, the AC joint should be evaluated. The most common disorders of this
joint are acute ligamentous injuries and arthritis. The lateral aspect of the clavicle should be inspected bilaterally for
prominence relative to the acromion. The clavicles should be palpated beginning medially and progressing laterally
toward the AC joint. Tenderness or deformity along the clavicle should be noted. Tenderness over the coracoid may
represent fracture or more commonly injury to the coracoclavicular ligaments as seen in AC joint separations. Direct
pressure over the AC joint will elicit pain in the setting of an acute injury or arthritis. The glenohumeral joint and its
surrounding bony and soft tissue structures allow for a complex balance of mobility and stability. Examination of the
glenohumeral joint begins with careful observation. The physician should observe the shoulders from the front and back,
looking for any asymmetry. This asymmetry may take the form of muscle atrophy or abnormal prominences. The deltoid,
infraspinatus, and supraspinatus should be examined for atrophy ( Fig. 53.4). The biceps should be inspected for
evidence of distal enlargement, which may be consistent with an intraarticular rupture of the long head. An anterior
prominence of the humeral head is suggestive of an anterior dislocation, whereas a posterior dislocation may present as
a prominence of the coracoid process. Most important, the symptomatic side must be compared with the asymptomatic
side for evidence of subtle atrophy or abnormal prominences.
FIGURE 53.4. Example of infraspinatus wasting secondary to suprascapular nerve entrapment.
Following inspection, the bony prominences surrounding the glenohumeral joint are palpated. With the physician
standing behind the patient, the coracoid process, acromion, and greater tuberosity of the humerus can be palpated.
Anterior and medial to the greater tuberosity lays the bicipital groove, which is bordered medially by the lesser tuberosity
and laterally by the greater tuberosity. Inflammation of the biceps or its synovial lining may result in pain with palpation.
Deep palpation of the biceps tendon in a normal shoulder can result in considerable discomfort. The spine of the scapula
with the surrounding infraspinatus and supraspinatus muscles should also be palpated. A depression at the site of the
supraspinatus or infraspinatus may indicate a muscle tear or supraspinatus nerve injury. Following gentle palpation of the
shoulder girdle, the glenohumeral joint should next be evaluated for passive and active motion. The shoulder has motion
in every plane, and to access initial function and to follow progress, both passive and active motion must be documented
accurately. Passive and active motion should be measured and recorded separately because active motion can be
altered by pain and may be a less accurate assessment of progress. Motion of the opposite shoulder should always be
measured and recorded for comparison. The passive motion of forward elevation, internal rotation, external rotation, and
rotation in abduction should be measured and recorded. Passive forward elevation is measured with the patient supine.
Neer (24) advocates measuring elevation in the scapular plane because there is less tightening of the glenohumeral
capsule and thus less restriction of motion than in either the coronal (abduction) or the sagittal (flexion) planes. The total
elevation is the combination of the scapular and glenohumeral motion ( Fig. 53.5). Passive external rotation also is
measured with the patient supine, which provides a reference point and eliminates trunk rotation and scapulothoracic
contribution. Rotation is remeasured with the arm at the side and the elbow flexed at 90 degrees. In this position, the
capsule and glenohumeral ligaments are relaxed. Active internal rotation is measured with the patient sitting and the
thumb is brought up the spine by the examiner. The highest level on the spine that the thumb reaches is recorded. It
should be noted that this measurement also reflects shoulder extension and elbow flexion, and a stiff elbow will affect this
measurement. Scapulothoracic motion and its contribution to total shoulder motion is best determined by viewing the
patient from the back. Any asymmetries of motion should be noted and may be seen with such conditions as adhesive
capsulitis and winging of the scapula. Internal and external rotation should also be measured and recorded with the arm
in 90 degrees of abduction. This position eliminates scapulothoracic motion and tests for pure glenohumeral motion.
Pain, instability, strength, motivation, and passive motion all affect active shoulder motion ( 24). Active and passive
motion should be recorded separately. Total active elevation is measured and recorded by having the sitting patient raise
his or her arm against gravity. Active internal and external rotation can also be tested with the patient seated. Any
differences recorded between active and passive motion should be noted and investigated. A patient with a nerve injury
or a rotator cuff tear, for example, may have full passive motion but lack some degree of active motion. After passive and
active motion of the glenohumeral joint has been evaluated, the shoulder muscle strengths should be measured. The
muscles that should be tested include the deltoid, external rotators, internal rotators, supraspinatus, trapezius, biceps,
triceps, and serratus anterior. According to the American Shoulder and Elbow Surgeons' examination form, the strengths
are graded from 0 to 5 as indicated below.
FIGURE 53.5. Total shoulder abduction is the result of combined glenohumeral-scapulothoracic motion in a ratio of about
2 to 1.
5. Normal—complete range of motion (ROM) against gravity with full resistance.

4. Good—complete ROM against gravity with some resistance.
3. Fair—complete ROM against gravity.
2. Poor—complete ROM with gravity eliminated
1. Trace—evidence of contractility
0. Paralysis—no contractility
The anterior, middle, and posterior divisions of the deltoid can be tested by resistive testing with the arm in slight flexion,
abduction, and posterior extension, respectively. The examiner attempts to push the arm into the neutral position while
the patient attempts to resist. Most tears or disruptions of the deltoid can be palpated during resisting testing. The
external rotators of the glenohumeral joint (infraspinatus and teres minor) are best tested with the arms at the side and
the elbows flexed to 90 degrees ( Fig. 53.6A). The examiner stands behind or in front of the patient and attempts to push
both hands together as the patient resists. Similarly, the internal rotators of the shoulder (subscapularis, pectoralis major,
latissimus dorsi, and teres major) can be evaluated ( Fig. 53.6B). With the arm at the patient's side and the elbow at 90
degrees, the patient is asked to resist an external rotation force placed by the examiner. The pectoralis major and
latissimus dorsi can be tested by placing the arm at 30 degrees of abduction and asking the patient to adduct and
internally to rotate the arm. The latissimus dorsi can be palpated to assess strength and integrity. The trapezius is
innervated by the spinal accessory nerve and is tested by asking the patient to shrug his or her shoulders while slowly
increasing downward resistance. Normally, the other scapular elevators will contribute significantly to the action of the
trapezius; therefore, differences between the sides should be noted. The serratus anterior is responsible for scapular
protraction and is innervated by the long thoracic nerve. Scapular winging is noted with paralysis of the long thoracic
nerve or weakness of the serratus anterior and is evident when the patient does a push-up or pushes against a wall ( Fig.
53.7). Winging of the scapula may also be noted in a patient with adhesive capsulitis who tries to compensate for
decreased motion at the glenohumeral joint by increasing scapulothoracic motion. The supraspinatus can be isolated by
having the patient hold his or her arms at 90 degrees of abduction, 30 degrees of forward flexion, and internal rotation
with the thumbs pointing downward (Fig. 53.8). The patient is then asked to resist the examiner's downward force. Pain or
weakness is indicative of supraspinatus pathology. Because the biceps acts as both a flexor and supinator of the elbow,
it can be tested by having the patient flex his or her arm against resistance and supinate against resistance. The triceps
is tested by having the patient extend the elbow against resistance.
FIGURE 53.6. A: Manual muscle testing of external rotators of shoulder. B: Manual muscle testing of internal rotators of
shoulder.
FIGURE 53.7. Scapular winging due to paralysis of the right long thoracic nerve.
FIGURE 53.8. The supraspinatus resistance test.
PROVOCATIVE TESTS
Often, the history alone will give the physician enough information to form a presumptive diagnosis. The general physical
examination of the shoulder then helps confirm that diagnosis. With a particular diagnosis in mind, there are a number of
provocative tests that the physician can perform to confirm or redefine the diagnosis. These specialized tests should be
part of the complete physician examination of the shoulder in any athlete with suspected glenohumeral instability,
impingement, rotator cuff tears, and bicipital tendinitis ( Table 53.2).
TABLE 53.2. PROVOCATIVE TESTS AND IMAGING STUDIES FOR SPECIFIC SHOULDER DISORDERS
Glenohumeral Instability and Labral Tests
Instability of the glenohumeral joint is defined as excessive symptomatic translation of the humeral head on the glenoid
during shoulder rotation. Because shoulder instability may be a manifestation of generalized ligamentous laxity, it is
necessary to examine the athlete for generalized ligamentous laxity by the criteria described by Steiner ( 25), Schwartz et
al. (26), and Beighton and Horam (27). These criteria include (a) abduction of the thumb to touch the forearm with the
wrist fully flexed, (b) hyperextension of the little finger metacarpophalangeal joint beyond 90 degrees, (c) elbow
hyperextension beyond 10 degrees, and (d) knee hyperextension beyond 10 degrees. If three of four of these criteria are
satisfied, then the patient is considered to have ligamentous laxity ( 27). Assessment of increased laxity in the
glenohumeral joint is determined by the following tests: (a) apprehension; (b) relocation, with glenohumeral translation;
and (d) sulcus sign. It is important to compare side to side differences with all of these tests.
Anterior glenohumeral instability is perhaps best demonstrated by the anterior apprehension sign. In patients who
subluxate or dislocate their shoulders anteriorly, the “provocative position” or position in which they feel most fearful that
the shoulder will “come out” is that of abduction and external rotation. The apprehension test is performed with the
examiner standing behind the seated patient. The examiner palpates the humeral head while gently placing the arm in
abduction and external rotation. The test also may be performed in the supine position with the patient's shoulder at the
edge of the table. A positive apprehension sign is one in which the patient reports pain or contracts their muscles or
arches the back to resist further external rotation of the arm due to fear that the shoulder may come out ( Fig. 53.9). Pain
alone should not be confused with true apprehension because pain alone is a poor predictor of instability ( 28).
FIGURE 53.9. The apprehension test for anterior shoulder instability.
If a positive apprehension sign is elicited, then the relocation test as described by Jobe and Bradley ( 29) can be
performed with the patient supine. For the relocation test, the examiner places the arm in abduction and external rotation
and places a gentle posteriorly directed force on the humerus with the thenar eminence of the opposite hand ( Fig. 53.10).
The test is considered positive if the patient's apprehension is diminished with this maneuver. The response can be
graded as mildly positive, positive, or negative. An abrupt release of the posteriorly directed force may elicit an
immediate feeling of apprehension. This test is sensitive but not necessarily specific for increased anterior laxity. Pain
reduction alone with relocation is a poor indicator of instability and should precipitate a thorough evaluation for other
pathology (28). Because other pathologic conditions, such as superior labrum anterior posterior (SLAP) lesions and
biceps tendinitis, may elicit a similar response, additional clinical and imaging studies may be necessary to confirm the
diagnosis.
FIGURE 53.10. A: With the patient lying supine, the apprehension test is performed by placing the arm in abduction,
external rotation, and extension. B: The relocation test is performed by applying a posteriorly directed force to the
humerus. A positive test is the reduction of apprehension or pain.
In addition to the anterior apprehension test, a posterior apprehension test should also be performed. The test is
performed with the patient seated and the arm held across the chest, with the elbow flexed to 90 degrees. As the arm is
brought across the chest, a posteriorly directed force is placed on the elbow, which places a posteriorly directed force
across the glenohumeral joint. If posterior instability exists, the humeral head will slip posteriorly and the patient will
experience pain or apprehension. However, some authors believe that apprehension related to posterior instability is not
a reliable sign and translation of the humeral head in the glenoid socket should be assessed.
In addition to reproducing a symptomatic apprehension or subluxation by stressing the glenohumeral joint, instability can
be assessed by documenting the amount of translation possible between the humeral head and glenoid fossa when
stressed by the examiner. An assessment of anterior and posterior translation of the humeral head on the glenoid socket
is often difficult to appreciate even for the experienced physician. A demonstrable difference in the amount of translation
between sides is considered abnormal, and the amount of translation can be graded ( 30). Grade 0 is normal or no
instability. Grade I is translation of up to 50% of the diameter of the humeral head. A feeling that the humeral head is
riding over the glenoid rim and spontaneously reducing is considered grade II. In grade III translation, the examiner
experiences the feeling that the humeral head rides over the glenoid rim but remains dislocated on release ( Fig.53.11).
This test is most sensitive when performed with a patient under general anesthesia.
FIGURE 53.11. The sulcus sign is demonstrated by pulling inferiorly on adducted arm.
Translation of the humeral head can be demonstrated by the load-and-shift test ( 31). With this test, it is first necessary to
ensure that the humeral head is reduced with the glenoid fossa and not translated anteriorly, posteriorly, or inferiorly. To
ensure this reduction, the humeral head is “loaded” by being grasped and pushed into the glenoid fossa. Once the head
is loaded, the examiner applies directional stresses. The athlete is initially seated, with the examiner standing behind and
to the side. The examiner places one hand on the shoulder and scapula, and the other hand grasps the humeral head.
The examiner applies anterior, posterior, and inferiorly directed forces and notes the amount of translation, as indicated
earlier. Next, with the athlete supine, the arm is grasped and positioned in 20 degrees of abduction and forward flexion.
With the humeral head loaded, an anteriorly, posteriorly, and inferiorly directed force is applied and the degree of
translation noted. Greater laxity than the other shoulder in the inferior direction when the “hammock” of the inferior
glenohumeral ligament is taught is indicative of a lax inferior complex. As noted by Hawkins and Bokor ( 31), the accuracy
of the load-and-shift test depends on the examiner's skill and the ability of the patient to relax. It is often necessary to
perform the examination under anesthesia to maximize the information obtained. Most normal shoulders translate up to a
grade II posteriorly and up to a grade I anteriorly ( 31). Therefore, correlation should always be made with the uninvolved
shoulder.
Significant inferior glenohumeral instability is the hallmark of multidirectional instability. The sulcus sign is indicative of
inferior instability and is demonstrated by applying an inferiorly directed longitudinal force in line with the humerus with
the patient's arm at the side. The appearance of a sulcus or depression greater than 1 cm in the subacromial region as
the humeral head translates inferiorly is the sulcus sign ( Fig. 53.12). The sulcus sign performed with the arm at the side
with 30 degrees of external rotation has been found to be suggestive of an incompetent rotator interval ( 32). Thus
apprehension and translational testing should be performed in all athletes suspected of having glenohumeral instability.
The examiner should be able to reproduce the instability pattern (anterior, posterior, inferior, or multidirectional) through
a thorough examination.
FIGURE 53.12. A: Anterior drawer demonstrates complete dislocation (grade III). B: Posterior drawer demonstrates
complete dislocation (grade III) in a patient with multidirectional instability.
Glenoid labral pathology is a more recently understood entity, and labral provocative tests should be performed on all
athletes' shoulders during a complete examination. Provocative tests for SLAP lesions have been described by both
O'Brien and Kibler ( 33,34). O'Brien's test is performed by asking the seated patient to forward flex the shoulder to 90
degrees and adduct it 15 degrees across the body. With the thumb pointed at the ground, the patient is asked to resist a
downward pressure from the examiner. If pain or weakness is elicited but remit with turning the palm up, the test is said to
be positive ( Fig. 53.13A, Fig. 53.13B). If the patient describes the pain as superficial, then this indicates AC joint
pathology, whereas deep pain is indicative of a SLAP lesion. The anterior slide test as described by Kibler is performed
by asking the sitting patient to put the hand on the waist with thumbs facing backward. The examiner then places one
hand on the acromion with the other hand on the elbow and applies an axial load up the humerus to compress the
humeral head in an anterior and superior direction while the patient resists ( Fig. 53.14). The test is positive if pain or a
click is detected anteriorly over the shoulder. The anterior slide test has a reported specificity of 92%; however, this test
is not as sensitive as the O'Brien's test is reported to be ( 34).
FIGURE 53.13. A: The O'Brien's test for SLAP pathology, the patient forward flexes the shoulder to 90 degrees and
adducts it 15 degrees across the body. With the thumb pointed at the ground, the patient is asked to resist a downward
pressure from the examiner. B: If pain or weakness are elicited with the thumb down but remits with turning the palm up,
the test is said to be positive.
FIGURE 53.14. The anterior slide test, the sitting patient puts his or her hands on his or her waist with thumbs facing
backward. The examiner then places one hand on the acromion and, with the other hand on the elbow, applies an axial
load up the humerus while the patient resists. The test is positive if pain or a click are detected anteriorly over the
shoulder.
Rotator Cuff Tests
Impingement is defined as encroachment of the rotator cuff on the coracohumeral arch (acromion and coracoacromial
ligament) with forward flexion of the humerus (35). Patients with impingement often have palpable crepitation and an arc
of pain. As the arm is raised from the side and lowered in various degrees of rotation, the patient may experience pain
within an arc of motion. The maximum joint reaction forces and rotator cuff tension occur as the arm passes between 70
and 120 degrees. Pain within this range is consistent with a positive arc of pain. Impingement lesions can be separated
from other causes of shoulder pain by the impingement sign and the impingement test ( 35). The humerus is forward
flexed as the scapula is stabilized with the opposite hand so that the greater tuberosity comes directly under the
coracoacromial arch (Fig.53.15). Although this maneuver is sensitive for impingement, it is not specific, because pain
may be elicited with other conditions, including frozen shoulder, glenoid labrum pathology, AC joint inflammation, and
biceps tendinitis. The impingement test is used to exclude these other conditions. With the impingement test, the range
of motion and strength of the shoulder is noted before and after the injection of 10 mL of 1% lidocaine into the
subacromial space (Fig. 53.16). The patient is asked to evaluate subjectively the degree of pain relief by rating from 0 to
10, with a 10 representing complete pain relief. If rotator cuff weakness persists and no pain is present, then a tear in the
rotator cuff may be present. If the pain relief is only partial and the AC joint is tender, an injection is made into the AC
joint. If only mild or no pain relief is obtained with a subacromial injection, other diagnoses may be considered.
FIGURE 53.15. A: The impingement sign of Neer. B: The modified impingement sign of Hawkins. C: The cross-chest
adduction test elicits pain from acromioclavicular pathology.
FIGURE 53.16. The impingement (injection) test.

The physical examination with a possible rotator cuff tear should include the drop arm test ( 36). With the patient standing,
he or she is asked to abduct the arm to 90 degrees. The patient is then asked to lower the arm slowly. If the patient has a
large tear of the rotator cuff, he or she may not be able smoothly and slowly to lower the arm to the side. The strength of
the rotator cuff muscles should be tested in athletes suspected of a rotator cuff tear. Manual muscle testing should
include external and internal rotation, and abduction against resistance. Any weaknesses should be noted, and testing
should be repeated following subacromial injection. Supraspinatus weakness in athletes with suspected rotator cuff tears
may be caused by pain. In this situation, relieving the pain by a subacromial injection can resolve the weakness on
manual testing.
In the majority of cases, the rotator cuff tear occurs in the supraspinatus insertion on the greater tuberosity. Although it is
difficult to determine the exact size of the rotator cuff tear by physical examination, it is often possible to estimate the size
by selective manual muscle testing. A small tear may only show weakness on isolated supraspinatus testing. A larger
tear, on the other hand, may extend into the external rotators and become evident on resisted external rotation. Only
patients with large or massive rotator cuff tears will have a positive drop arm sign. Rare cases of traumatic isolated
subscapularis tears have been noted. In these cases, the patient demonstrates a positive lift-off test. In this test, the
patient attempts to lift the dorsum of the hand off his or her lumbosacral spine ( Fig. 53.17A). A positive test is one in
which there is severe weakness, which indicates injury of the subscapularis muscle. A modification of the lift-off test is the
belly press test (Fig. 53.17B). For patients lacking internal rotation, the hand is placed on the belly, with the elbow
positioned anterior to the coronal axis of the body. If the patient is unable to maintain this position with the examiner
trying to pull the hand off the patient's belly or the elbow falls posterior to the coronal plane of his or her body as he or
she resists the examiner, then subscapularis deficiency may be present. Testing the strength of the internal rotators, on
the other hand, will not necessarily be effective because other muscles can substitute for the subscapularis (e.g., the
pectoralis major).
FIGURE 53.17. A: The lift-off test is positive when the patient is unable to keep the hand off the spine. B: The belly press
is positive if the patient is unable to keep his or her hand on their belly.
Biceps Tendinitis Tests
Biceps tendinitis rarely occurs as an isolated entity in the athlete and is usually secondary to impingement or instability.
The athlete with biceps tendinitis may complain of anterior shoulder pain that is less intense with rest. The pain of
tendinitis may be difficult to differentiate from pain secondary to impingement. Biceps subluxation or dislocation is rare
and typically occurs with a partial subscapularis or supraspinatus tear ( 37). Biceps instability can present with a pain
pattern similar to that of bicipital tendinitis, but the athlete may report a palpable snap or pop with shoulder motion.
Examination of the biceps tendon is typically difficult in the athlete owing to its deep location under the often large deltoid
and pectoralis. The athlete with biceps tendinitis may have point tenderness in the bicipital groove, which can be
localized with the patient's arm held in 10 degrees of internal rotation ( 38). The point of maximal tenderness is located
approximately 3 inches below the anterior ridge of the acromion and will move as the arm is rotated. This tenderness
motion sign is thought to indicate bicipital tendinitis. With de Anguin test ( 39), the examiner has his or her finger in the
bicipital groove. A positive test occurs when the patient feels pain as the tendon glides beneath the finger. It must be
emphasized that owing to the complex anatomy in the anterior shoulder and the deep intraarticular location of the biceps,
tenderness in this area alone may not be specific for biceps tendonitis; therefore, other diagnoses should be entertained.
More commonly described tests include Speed and Yerguson sign. Yerguson sign ( 40) for biceps tendinitis is elicited with
the elbow flexed at 90 degrees and the patient forcibly supinating against resistance. A positive test is one in which pain
is referred to the anterior aspect of the shoulder. In Speed test ( 41) (Fig. 53.18), with the elbow extended and the forearm
supinated and the shoulder held at 90 degrees of abduction in the scapular plane, the patient flexes the shoulder against
resistance. Pain localized to the bicipital groove constitutes a positive test. Bennett recently found Speed test to have
90% sensitivity but only 13.8% specificity for biceps and labral complex pathology when physical examination was
compared with arthroscopic findings (42). Because the biceps tendon is contiguous with the superior labrum, tests for
SLAP lesions should be included in examination. If instability of the biceps tendon is suspected, then tests for
subscapularis and supraspinatus continuity (i.e., lift-off and belly press) should be performed.
FIGURE 53.18. Speed test for biceps tendonitis.
RADIOGRAPHIC EVALUATION
Once a thorough history and complete physical examination of the shoulder are performed, the physician may then
obtain the appropriate adjuvant diagnostic studies. The studies requested depend on the presumptive diagnosis.
Although injuries to the sternoclavicular joint can often be diagnosed clinically, appropriate radiographs should be taken
to fully evaluate the injury and rule out associated fractures. The standard AP or posteroanterior (PA) chest x-ray study is
often useful to demonstrate asymmetry of the sternoclavicular joint. The 40-degree cephalic tilt view, as described by
Neer and Rockwood (43), is easy to obtain and useful in demonstrating anterior or posterior subluxations or dislocations
of the sternoclavicular joint. The view is taken with the patient supine, with a cassette placed behind the patient and the
beam angled 40 degrees from the vertical and aimed at the manubrium. Computed tomography (CT) scans offer the best
information for evaluating the sternoclavicular joint. For posterior sternoclavicular dislocations with possible vascular
compression, contrast CT studies are valuable. A bone scan can also be used to detect inflammatory or degenerative
changes of the sternoclavicular joint. Athletic injuries to the AC joint are readily evaluated by radiographs. Because the
AC joint is relatively more superficial than the glenohumeral joint, 50% less x-ray voltage is necessary to expose the AC
joint than is necessary to expose the glenohumeral joint. The best view of the distal clavicle and AC joint is the Zanca
view (44). This x-ray study is obtained with a 10-degree cephalic tilt. An AP view of the AC joints can be taken with the
patient sitting or standing. Both shoulders should be imaged on a single cassette to compare the AC joint and the
coracoacromial distance of the injured versus the uninjured shoulder. If the AP views are not conclusive for a complete
AC dislocation but there is clinical suspicion, stress x-ray studies should be obtained. An AP x-ray study of the AC joints
is taken with 10 to 20 pounds of weight strapped to the patient's wrists ( Fig. 53.19). If these x-ray studies reveal a less
than 25% difference in coracoclavicular distance between the injured and normal shoulder, then a complete separation
can be ruled out. A cross-body adduction ( 45) view has been recently described. An AP study of the shoulder is taken
with the patient holding his or her arm across the body ( Fig. 53.20). If the clavicle rides superior to the acromion, then
complete AC separation is suspected, with rupture of the AC capsule and coracoclavicular ligaments. The standard
axillary view taken with the x-ray beam placed inferior to the axilla and aimed at an x-ray cassette superior to the
shoulder with the arm held in 70 to 90 degrees of abduction should be obtained to demonstrate anterior or posterior
displacement. The degree of clavicular elevation combined with anterior and posterior displacement determines the
severity of the injury and the type of treatment necessary.
FIGURE 53.19. Acromioclavicular joint view with weights to rule out AC separation.
FIGURE 53.20. Cross-body adduction view.

Diagnostic imaging of the glenohumeral joint begins with the trauma series (AP and axillary or scapular lateral), as
advocated by several authors (43,46,47,48 and 49). A more complete series involves the AP and lateral views in the
scapular plane and the axillary view. The AP view in the scapular plane is obtained with the beam angled 45 degrees to
the patient so that the scapula is parallel to the x-ray cassette. With this view, the glenoid appears in profile and can be
seen separately from the humeral head. Any overlapping of the glenoid and humeral head indicates a glenohumeral
dislocation. The lateral view in the scapular plane is also called the transcapular or Y lateral view ( 50). This view is a true
lateral view of the scapula and is helpful in determining the anterior and posterior displacement of the humeral head
relative to the glenoid. The axillary lateral, or Velpeau lateral view when combined with the AP and lateral in the scapular
plane, maximizes the information available. The axillary view clearly delineates the relationship between the humeral
head and the glenoid and allows for identification of dislocations. If because of pain or muscle spasm a true axillary view
cannot be obtained, then a Velpeau axillary view should be obtained. This view, described by Bloom and Obata ( 51),
eliminates the need for shoulder abduction. The patient stands or sits at the end of the x-ray table and leans backward
over the table. The x-ray beam is aimed directly over the shoulder and passes through the shoulder joint toward the
cassette (Fig. 53.21).
FIGURE 53.21. The Velpeau axillary view.
Following the standard trauma series, special radiographic views and imaging techniques are available to assess specific
pathology. Anterior shoulder dislocation or subluxation may be accompanied by small fractures of the anteroinferior
aspect of the glenoid rim. If the fracture is anterior and inferior, it may not be seen on the routine axillary view. In this
case, the West Point axillary view provides more information than the axillary view. The West Point view is taken with the
patient prone, the x-ray cassette positioned against the superior aspect of the shoulder, and the x-ray beam angled 25
degrees downward and 25 degrees toward the midline ( Fig. 53.22). Fractures or calcification about the glenoid rim may
also be seen on CT scans or arthro-CT scans. The Hill-Sachs ( 52) lesion is a compression fracture of the posterolateral
humeral head, which is often the result of anterior shoulder dislocations. The Hill-Sachs lesion may occur following a
single anterior dislocation or be the result of recurrent anterior dislocations. Because this lesion is on the posterolateral
aspect of the humeral head, it can often be seen on the AP x-ray study of the shoulder with the arm held in full internal
rotation (Fig. 53.23). Perhaps the best view to see the Hill-Sachs lesion is the Stryker-Notch view ( 43,52,53). For this
view, the patient is positioned supine with the x-ray cassette behind the shoulder with the x-ray beam angled toward the
shoulder at 10 degrees. The patient touches the top of his or her head and holds the arm in approximately 120 degrees
of flexion (Fig. 53.24). In this position, the arm is in internal rotation. The presence of the defect on x-ray study confirms
that the shoulder has been dislocated. A CT scan is also useful in documenting the presence and size of the Hill-Sachs
lesion. The apical oblique radiograph of the shoulder, as described by Garth et al. ( 54), is very useful displaying a
coronal profile of the glenohumeral joint. This projection allows for concomitant evaluation of glenoid fractures and
Hill-Sachs lesions in association with dislocations ( Fig. 53.25). In addition to the standard trauma series and special
radiographs, fracture dislocations involving the glenohumeral joint can be further evaluated by CT scan.
FIGURE 53.22. The West Point axillary view.

FIGURE 53.23. Hill-Sachs lesion (arrows) is demonstrated on AP view with arm in internal rotation.
FIGURE 53.24. A: Positioning of the Stryker-Notch view. B: Example of the Hill-Sachs lesion on the Stryker-Notch view
(arrows).
FIGURE 53.25. Garth view.
Athletes with a history of shoulder dislocations may have soft tissue injury to the shoulder. Bankart ( 55) described an
avulsion of the anterior capsule and glenoid labrum of the glenoid rim ( Fig. 53.1). This lesion is known as the Bankart
lesion and is associated with anterior shoulder instability. These lesions can be seen on arthrogram ( 56),
pneumoarthocomputed tomography (57) and arthro-CT (58). Noncontrast MRI or MRA with intraarticular gadolinium may
be performed to delineate further labral lesions or capsular anatomy. MRA is believed to improve sensitivity and
specificity over nonconstrast MR when detecting labral pathology ( 59,60 and 61). Benefits of MRI over CT include
delineation of associated rotator cuff pathology while sparing the patient exposure to ionizing radiation.
Posterior shoulder instability is less common than anterior instability. Posterior glenohumeral dislocations are often
missed if an inadequate physical examination is performed or inadequate x-ray studies are obtained. The trauma series
should be adequate to reveal a posterior dislocation. Posterior glenohumeral instability may result in an avulsion of the
posterior glenoid labrum known as a reverse Bankart lesion and a fracture seen in the anteromedial surface in the
humeral head known as a reverse Hill-Sachs lesion. An isolated lesser tuberosity fracture should call the examiner's
attention to a posterior dislocation. Axillary x-ray studies and CT scans are useful for evaluating bony lesions of the
posterior glenoid rim.
Radiographic techniques are important in evaluating impingement and rotator cuff pathology. The x-ray evaluation of
impingement consists of the standard AP view, a 30-degree caudal tilt view, and the scapular outlet view. The standard
AP view of the shoulder can reveal superior migration of the humeral head under the acromion and narrowing of the
acromiohumeral interval. A more sensitive measurement of rotator cuff dysfunction is to take several AP views while the
shoulder is abducted and measure the position of the center of the humeral head relative to the equator of the glenoid.
Normally, the humeral head remains perfectly centered. In the case of a rotator cuff tear, the humeral head translates
superiorly (Fig. 53.26). The 30-degree caudal view is taken as the standard AP view, with the x-ray beam angled with a
30 degrees of caudal tilt. This view demonstrates acromial spurring or proliferation of the anteroinferior acromion that is
associated with impingement. The scapular outlet view is taken with the patient positioned for a lateral view in the
scapular plane, but the beam is angled 5 to 10 degrees in the caudal direction ( Fig. 53.27). Bigliani et al. (62) used this
view to identify three types of acromion, which they correlated with the incidence of rotator cuff disease. Arthrography is
considered the gold standard for identification of full-thickness rotator cuff tears because it has a sensitivity rate for
detecting full-thickness rotator cuff tears of between 95% and 100% ( 49). However, because of the invasiveness of
arthrography, other techniques for evaluating the rotator cuff have been studied. The sensitivity of the MRI for diagnosing
full-thickness rotator cuff tears is also estimated to be between 95% and 97% ( 63,64). MRI also is useful in identifying
partial-thickness tears and edema within the tendons. Real-time ultrasound also is used in some centers for identification
of rotator cuff pathology. The results appear to be user dependent, but an accuracy of between 82% and 100% ( 63,64,65
and 66) has been reported. Compared with other imaging studies, ultrasound is reported to be safe, rapid, noninvasive,
and inexpensive.
FIGURE 53.26. The center of the humeral head (asterisk) moves above the equator of the glenoid as this patient with a
rotator cuff tear attempts to raise the arm.
FIGURE 53.27. A: The supraspinatus outlet is formed by the coracoacromial arch. B: Narrowing of the supraspinatus
outlet by a larger anterior acromial osteophyte (arrow).
The radiographic evaluation of the athlete with tendinitis or biceps tendon subluxation involves the Fisk ( 67) view. In this
view, the x-ray beam is superior to the shoulder. The beam is angled perpendicular to the bicipital groove. The patient
holds the cassette while leaning over the table. Patients with primary bicipital tendinitis may have degenerative changes
in the walls of the groove, whereas patients with subluxation may have a relatively shallow groove. Dislocations of the
biceps tendons can be seen on arthrogram ( 68), and biceps tendon lesions can be seen on ultrasound imaging ( 69) and
MRI (61). Table 53.3 summarizes the provocative tests and imaging studies for glenohumeral instability, rotator cuff
tears, impingement, and biceps tendinitis.
TABLE 53.3. PROVOCATIVE TESTS AND IMAGING STUDIES FOR SPECIFIC SHOULDER DISORDERS
INJURIES TO THE ATHLETIC SHOULDER
Instability
The glenohumeral joint has a unique anatomic arrangement that balances mobility and stability. This unique balance
makes the shoulder susceptible to injury when it is subject to athletic demands and especially in sports that require
repetitive overhead maneuvers. These sports can stress both the dynamic (rotator cuff) and the static stabilizers
(ligaments) of the glenohumeral joint beyond their physiologic limits, eventually leading to breakdown of these stabilizers.
This breakdown can result in glenohumeral instability and later impingement. In addition to this repetitive, chronic pattern
of instability, instability may result from a single episode of stress or trauma. Furthermore, specific pathologic lesions
have been implicated as causes of, or have been associated with, glenohumeral instability that includes glenoid labrum
detachments (Bankart lesion), excessive capsular laxity, subscapularis insufficiency, posterior lateral humeral head
defect (Hill-Sachs lesion), abnormal humeral and glenoid version, rotator cuff tears, and lateral humeral capsular
avulsions.
Instability of the glenohumeral joint is defined as symptomatic excessive translation of the humeral head on the glenoid
during shoulder rotation. There is a spectrum of instability that represents increasing degrees of injury to the dynamic
and static stabilizers of the glenohumeral joint. Subluxation is defined as increased humeral head translation beyond that
permitted by normal tissue laxity without complete separation of the articular surfaces. Because normal shoulders have a
certain degree of play, clinical subluxation requires increased translation of the humeral head in association with
symptoms. These symptoms include pain, a feeling that the shoulder is “loose,” or a painful giving way of the shoulder
associated with neurologic symptoms known as the so-called dead-arm syndrome. This translation can occur in the
anterior, posterior, or superoinferior planes.
Glenohumeral instability can be categorized into five groups, depending on the mechanism of injury and the direction of
instability:
1. Posttraumatic anterior subluxation and dislocation

2. Posttraumatic posterior subluxation and dislocation
3. Atraumatic anterior subluxation and dislocation
4. Atraumatic posterior subluxation/dislocation
5. Multidirectional subluxation/dislocation
The stability of the glenohumeral joint is based on the interaction of the static and the dynamic constraints about the
shoulder. Although there is some overlap of the anatomic structures in each category, the static constraints primarily
include bony anatomy, the glenoid labrum, and the capsular ligaments (superior, middle, and inferior glenohumeral
ligaments). The dynamic constraints of the glenohumeral joint are the rotator cuff muscles and the biceps. These muscles
function dynamically to contain the humeral head in the glenoid by causing joint compression. They also act
synergistically by contracting in a coordinated fashion to steer the humeral head into the glenoid in different arm
positions, which leads to tightening of the static capsular ligamentous structures. A careful history should be obtained
from any athlete suspected of having glenohumeral instability. This historical evaluation should attempt to classify the
nature and degree of the instability, which will, in turn, affect the prognosis and treatment. The classification should
include the frequency or timing of the occurrences leading to the instability. For example, does the athlete describe an
acute presentation of a one-time event, or does he or she describe multiple episodes. The direction of the instability
should also be determined. By the description of the arm position when symptoms occur, the direction of the instability
(anterior, posterior, or multidirectional) can often be determined. The onset of the instability should be determined. It
should be noted whether the instability was traumatic or atraumatic in origin or was the result of overuse. The physician
should also ascertain whether the subluxation and dislocation is completely involuntary or if there is a voluntary
component. Some patients may be able willingly to demonstrate their instability and are considered voluntary dislocators.
Patients who demonstrate their instability through arm positioning alone are considered involuntary dislocators. The
degree of instability should be noted. It should also be determined whether the shoulder subluxated or completely
dislocated and either spontaneously reduced or had to be reduced on the field, in the training room, or in the emergency
room. Finally, a history of generalized laxity of other joints should be obtained. The hallmark of multidirectional instability
is a positive sulcus sign on physical examination. Patients with multidirectional instability may give a history of pain and
instability with activities such as lifting light objects. Neurologic symptoms such as transitory numbness of the hands or
arm are common in patients with inferior instability. It is important to consider the possibility of multidirectional instability
in all patients being evaluated for instability, because when standard treatments for recurrent unidirectional instability are
applied to patients with multidirectional instability, they often fail. Multidirectional instability can be the result of one or
more episodes of significant trauma (football or wrestling), repetitive minor injuries seen in overhead activities, or varying
degrees of inherent ligamentous laxity ( 70,71).
Despite a careful history and physical examination and in light of inconclusive or negative radiographic studies,
approximately 10% of patients with instability remain a diagnostic dilemma. These patients have usually undergone a trial
of nonoperative management without success. An examination under anesthesia and diagnostic arthroscopy may be
considered for such patients. With the patient free of pain and without muscle guarding, a detailed examination, including
translational testing of both shoulders, can be performed. Often, a surgical decision is made on the basis of this
examination. The arthroscope can be used to visualize the translation of the humeral head, stretching or attenuation of
the capsule, displacement of the inferior glenohumeral ligament complex, impaction fractures of the glenoid rim, loose
bodies, and labral damage ( 72). A careful history, a thorough examination, and adequate radiographs should all be used
to assess the mechanisms, degree, and direction of the glenohumeral instability, so that the pattern of instability can be
put into one of the five categories and a treatment plan can be formulated.
Traumatic anterior dislocations of the glenohumeral joint account for more than 98% of shoulder dislocations ( 73). Often,
excessive abduction and external rotation forces are responsible for levering the humeral head out of the glenoid fossa.
Anterior dislocations may also be the result of a direct blow from behind. The anterior capsule stabilizing structures are
usually tom with the dislocation. The athlete will report acute pain and have a severely decreased range of motion
secondary to guarding. Often, the diagnosis can be confirmed by the history and physical examination before obtaining
x-ray studies (Fig. 53.28). The physical examination should include a neurovascular assessment of the upper extremity,
with particular attention directed toward the sensory distributions of the axillary and musculocutaneous nerves. The
physician may be able to feel the humeral head displace anteriorly. An immediate reduction may be attempted on the
playing field. If this reduction is unsuccessful, another attempt can be made in the locker room before muscle spasm has
set in. Frequently, the shoulder can be reduced with the Stimson ( 73) maneuver, in which the athlete is placed prone on
the examination table with a 10-pound weight hanging from the wrist ( Fig. 53.29). This technique is potentially the least
traumatic; however, a variety of other techniques may be used as well. Any technique used should involve only gentle
traction and manipulation to avoid iatrogenic fracture or nerve injury ( Fig. 53.30). If reduction cannot be accomplished,
then the athlete should be taken to the hospital for x-ray studies and the administration of analgesics and sedatives to
allow for a gentle reduction. If possible, x-ray studies should be obtained both before reduction, to excluded fracture, and
after reduction, to confirm the reduction. A neurovascular examination should be performed as soon after reduction as
possible. If the athlete has no prior history of shoulder instability following reduction, a sling should be used to immobilize
the arm in internal rotation for 6 weeks ( 73). The arm should be taken out of the sling several times a day to allow for
active elbow, wrist, and hand motion to avoid stiffness. No study to date has been able to determine an optimal time for
immobilization or if immobilization alters the rate of recurrent dislocations. Following immobilization, rehabilitation
exercises are begun, consisting of shoulder strengthening with emphasis on the internal rotators. In athletes older than
40 years of age, there is a greater incidence of rotator cuff tears and adhesive capsulitis following traumatic anterior
dislocations or subluxations ( 74). Therefore, these athletes should be immobilized for only 7 to 10 days and then begin
range-of-motion and strengthening exercises. The incidence of recurrence depends primarily on the age of the patient at
the time of the initial dislocation. In a series by Rowe and Sakellarides ( 75), it was noted that patients younger than 20
years of age have a 90% or greater chance of recurrence; whereas patients older than 40 years have a 25% or less
chance of recurrence. It is extremely important that the shoulder be completely rehabilitated before the patient returns to
athletics. The criteria for returning to sports are based on a full range of motion and full strength.
FIGURE 53.28. A: In an anterior glenohumeral dislocation, the arm is held to side and patient leans toward affected side.
B: Example of a locked anterior (chronic) dislocation as seen on AP and axillary view.
FIGURE 53.29. Stimson reduction maneuver for anterior dislocation.
FIGURE 53.30. A: Reduction of anterior glenohumeral dislocation by traction-countertraction method. B: Reduction by

scapular manipulation method. C: Reduction by Rowe technique of traction and gentle forward flexion.
Posterior traumatic subluxation or dislocation is much less common than anterior subluxation or dislocation. An acute
traumatic posterior dislocation is usually the result of a direct blow to the anterior shoulder or the result of direct forces
with the arm held in flexion, adduction, and internal rotation. Posterior dislocation can also result from seizures or
electrical shock. The patient usually presents with the arm adducted and internally rotated with limitation of external
rotation. Most posterior dislocations spontaneously reduce ( 73). The axillary view is critical in making this diagnosis. As
with anterior dislocations, a careful neurovascular assessment is essential. Following reduction, the shoulder should be
immobilized in a position of external rotation to allow tightening of the posterior capsule. In the athlete who is younger
than 40 years old, immobilization is continued for 4 to 6 weeks, followed by an aggressive physical therapy program that
emphasizes strengthening of the external rotators of the shoulder. In athletes older than 40 years of age, immobilization
should be continued for only 2 to 3 weeks ( 76). There is little documentation regarding recurrences of posterior
dislocations, but as with anterior dislocations, the younger the patient, the higher the recurrence rate.
Athletes, especially those involved in repetitive overhead activities, can experience signs and symptoms of shoulder
instability without significant initial trauma. Symptomatic anterior subluxation in throwers is often manifested during the
acceleration phase of throwing, when the arm is maximally abducted and externally rotated. Swimmers may notice
symptoms during the backstroke or during turns. The pain associated with anterior subluxation may be posterior because
of the stresses placed on the posterior tissues during anterior humeral head translation. The initial treatment of
symptomatic anterior dislocation involves a sling and antiinflammatory medication until acute pain and inflammation
subside. After the initial pain and swelling has subsided, a vigorous physical therapy program should be initiated with
range-of-motion and strengthening exercises for the rotator cuff.
Unlike posterior dislocations, which are rare in athletes, anterior subluxation is relatively common. The athlete usually
complains of pain rather than instability. The pain may be either anterior or posterior. The pain generally occurs when the
posterior capsule is stressed. This pain occurs most notably with follow through in pitching, during the pull-through phase
in swimming, and during serving motions or backhand in tennis. The initial treatment is similar to that of anterior
subluxation, that is, with a sling and nonsteroidal antiinflammatory drugs (NSAIDs). Physical therapy is then initiated
when pain and swelling subside. The goal of therapy is to increase strength of the external rotators of the shoulder.
Multidirectional instability of the shoulder is defined as instability occurring in more than one plane. This may involve the
anteroinferior or posteroinferior areas, or instability in all three directions. Multidirectional instability may have atraumatic
origins in persons with extensive ligamentous laxity, especially in those athletes who perform repetitive overhead
activities, or it may be the result of a traumatic insult to the shoulder in a person with generalized ligamentous laxity. The
clinical findings depend on the predominant direction of the instability. The patient may have multiple apprehension signs
and a positive sulcus sign. As with anterior and posterior instability, the initial treatment is conservative involving NSAIDs
and physical therapy.
Physical therapy for patients with instability first involves a stretching program to restore full motion to the shoulder. Once
full motion has been achieved, strengthening can begin. The goal of strengthening is to eliminate imbalance in the
rotators due to a deficiency caused by the subluxation. With posterior subluxation, the external rotators are often
deficient and with anterior subluxation it is the internal rotators that are deficient. Generally, spring exercises or rubber
tubing is used to provide resistive strengthening. The athlete may return to activities at a low level during therapy, as long
as the specific activities that cause symptoms are avoided. The therapy varies with the patient's age, motivation of the
patient, and the degree of damage to the shoulder. Therapy should progress until the patient can return to activities
without symptoms.
In traumatic and posttraumatic anterior, posterior, and multidirectional instability of the shoulder, operative intervention
should be considered for those athletes who fail at an adequate trial of physical therapy. These athletes are those whose
pain and instability preclude adequate functioning of the involved shoulder. Many surgical procedures have been
described to address glenohumeral instability. The type of procedure depends on the direction of the instability and the
pathology involved. In general, athletes who have surgical treatment for instability may lose some range of motion of the
shoulder, especially internal or external rotation. In the athlete who performs repetitive overhead activities, this loss of
rotation may result in some diminution of performance in his or her sport.
Rotator Cuff Problems, Impingement, and Biceps Tendinitis
Subacromial impingement is one of the most common causes of shoulder pain in the athlete ( 68,77). Impingement is
defined as encroachment of the acromion, coracoacromial ligament, and the AC joint on the rotator cuff mechanism that
passes beneath them when the glenohumeral joint is moved. A close relationship of impingement to lesions of the rotator
cuff, biceps, subacromial bursa, and AC joint has been recognized. Impingement lesions can be classified as outlet
impingement and nonoutlet impingement. Outlet impingement is by far the most common type and is defined as
narrowing of the supraspinatus outlet ( 78). The impingement occurs against the anterior one third of the acromion and
the AC joint. Supraspinatus outlet narrowing can be caused by an anterior acromial spur at the attachment site of the
coracoacromial ligament. These spurs rarely occur in patients younger than 40 years of age ( 78). The shape of the
acromion, the slope of the acromion, and the prominence of the AC joint can result in outlet impingement. The shape of
the supraspinatus outlet can be radiographically evaluated by the outlet view.
Nonoutlet impingement occurs with a normal supraspinatus outlet. Causes of nonoutlet impingement include a prominent
greater tuberosity of the humerus, malunion of the greater tuberosity fracture or surgical neck fracture, lesions of the
acromion, thickening of the subacromial bursa, loss of humeral head depression, and loss of glenohumeral fulcrum ( 78).
When the deltoid contracts, the humeral head is displaced upward. The rotator cuff and biceps tendon act to depress the
humeral head as the deltoid contracts. Loss of the stabilizing function of the rotator cuff causes displacement of the
humeral head upward and results in impingement. Loss of these stabilizing factors can occur with rotator cuff tears or
tears of the long head of the biceps. An unstable head that subluxates anteriorly due to capsular laxity may displace
upward against the acromion. This creates two clinical problems that can coexist: instability and impingement ( 79,80).
Morrison reported successful treatment of 413 of 616 (67%) shoulders with impingement with NSAIDs and isotonic
exercises (81). Once the shoulder is sufficiently stabilized through either physical therapy or surgical intervention, the
impingement is usually eliminated.
Impingement that is caused by instability of the glenohumeral joint is referred to as secondary impingement ( 79,80).
Secondary impingement may be the most common type of impingement seen in young athletes. As already noted,
overhead activities in the athlete place tremendous stress on the dynamic and static stabilizers of their shoulders.
Repetitive stresses result in microtrauma to the glenohumeral ligaments and eventually may lead to attenuation of these
structures. Without these stabilizers, an instability pattern can develop that places increasing demands on the rotator
cuff. Fatigue of the rotator cuff allows the humeral head to translate anteriorly and results in secondary mechanical
impingement of the supraspinatus tendon on the coracohumeral arch. This overlap of impingement and instability was
recognized by Jobe et al. ( 80). They noted that athletes who had shoulder pain and were involved in overhead activities
could be divided into four groups based on their history, physical examination, and arthroscopic findings: (a) pure
impingement, (b) instability secondary to anterior impingement, (c) instability caused by hyperelastic capsular ligaments
and tissues with secondary impingement, and (d) pure anterior instability.
The first group consists of athletes with pain secondary to pure impingement. The diagnosis of impingement is made by
history and physical examination. A patient with impingement usually has a painful arc, that is, when the arm is raised
from the side and lowered from overhead at various positions, pain will occur. The arc through which this pain occurs is
called the arc of pain. The examiner might also notice crepitus as the front and back edges of the acromion are palpated
and the humerus is rotated. These athletes will have a positive impingement test. The impingement sign maneuver,
however, may elicit pain in several other conditions as well, including frozen shoulder, glenohumeral instability, anterior
AC joint arthritis, and calcium deposits in the rotator cuff (calcific tendonitis). Therefore, the impingement induction test is
used to exclude these other conditions. In athletes with pure impingement, the joint is stable on stress testing and has a
normal labrum and normal glenohumeral ligaments arthroscopically. These patients are usually older than 35 years of
age and should be placed on a 6-month program of strengthening and avoidance of offending activities. Most of the
patients have been found to have a tight posterior capsule, which increases superior translation and aggravates
impingement. Stretching of the posterior capsule is critical in treating these athletes. If nonoperative treatment fails,
surgical treatment usually consists of a open or arthroscopic subacromial decompression with resection of the
coracoacromial ligament.
The second group are athletes with impingement pain secondary to glenohumeral instability. These patients have pain
with the apprehension test, a positive relocation test, and the presence of the impingement sign. Arthroscopic
examination reveals either an anterior labral tear or deficient anteroinferior glenohumeral ligament. Most of these athletes
will improve with strengthening of the rotator cuff or scapular rotators. For those who do not improve with conservative
strengthening exercises, operative repair of the capsular labral complex is an alternative. Because these patients have
impingement secondary to instability, it is necessary to address their instability. An isolated anterior acromioplasty is
unlikely to relieve their symptoms.
The third group of athletes consists of those with impingement pain secondary to instability because of hyperlax capsular
ligaments. Like group 2 patients, these patients demonstrate the presence of the impingement sign, and they have
positive apprehension and relocation tests. These patients may have generalized ligamentous laxity, and an examination
under anesthesia reveals laxity of both shoulders, with the dominant one being most involved. Arthroscopic findings may
include redundancy of the anterior capsule and a lax inferior glenohumeral ligament with an easily manipulated humeral
head. Initial treatment involved strengthening of the rotator cuff and scapular rotators. If at the end of 6 months this
treatment fails to relieve symptoms, an operative procedure may be necessary.
The fourth group is pure instability without impingement. These patients do not demonstrate the impingement sign but
have pain with apprehension testing and relief of their pain with relocation. Arthroscopy in these patients may reveal
labral damage and possibly a Hill-Sachs lesion. There may also be evidence of a loose anterior capsule and a lax inferior
glenohumeral ligament complex. Treatment for this group consists of physical therapy. Again, if physical therapy fails to
relieve symptoms, operative capsular reconstruction is indicated.
Impingement of the subacromial space is intimately related to rotator cuff disease. The wear on the humeral side is
centered at the supraspinatus tendon. Neer ( 35) classified three progressive stages of outlet impingement leading to
rotator cuff disease. In stage 1, there is edema and hemorrhage secondary to repetitive overhead activities. This lesion is
typically seen in patients who are younger than 25 years old and is completely reversible with rest, oral antiinflammatory
agents, and a strengthening program. In stage 2 impingement leading to rotator cuff disease, there is fibrosis and
tendinitis from repeated mechanical insults. This type of impingement is usually seen in the 25- to 40-year-old age group.
In patients who fail to respond to the nonoperative treatment and whose disability has persisted for more than 6 months,
the author's approach is to remove the thickened fibrous subacromial bursa, divide the coracoacromial ligament, and
perform an anterior acromioplasty, which is usually possible with an arthroscopic technique. A stage 3 lesion is
categorized by complete impingement tears of the rotator cuff. These lesions are rare in patients who are younger than
40 years old. If full restoration of strength and function is desired, it is usually necessary to repair the torn tendons in
addition to decompressing the outlet with an open or arthroscopic acromioplasty ( Fig. 53.31).
FIGURE 53.31. Arthroscopic acromioplasty removing anterolateral edge of acromion.

Internal glenoid impingement has been more recently described ( 82,83,84 and 85). It presents in the overhead athlete
complaining of vague posterosuperior shoulder pain precipitated by throwing without a clear history of instability. The
pain usually resolves with cessation of overhead activity and rest then recurs with throwing. Cadaveric, arthroscopic, and
MRI studies have shown that with the abducted, externally rotated humerus in the late cocking phase of throwing, the
greater tuberosity and supraspinatus tendon of the rotator cuff contact the posterior superior glenoid labrum ( 84,85). This
contact has been described in normal shoulders. It is believed that hyperangulation of the humerus with associated
subclinical anterior glenohumeral instability causes the pathologic impingement and the ultimate undersurface tear of the
supraspinatus (Fig. 53.32). It is unclear whether the initial lesion is the detachment of the posterosuperior labrum leading
to increased anterior translation, pseudolaxity, or acquired anterior laxity from repetitive overhead activities leading to
increased hyperangulation and internal impingement ( 86). A painful apprehension test and diminution of pain with the
relocation test is believed to be the best indicator of internal impingement because the anterior translation and
impingement is reduced with anteriorly placed pressure of the relocation test.
FIGURE 53.32. MRI showing internal impingement of rotator cuff.
Rehabilitation for internal impingement should focus on reducing fatigue and anterior translation, which leads to the
increased humeral angulation. Physical therapy must address strengthening the periscapular and cuff muscles.
Stretching of the posterior capsule to help diminish anterior translation is important while overstretching of the anterior
capsule should be avoided. Most athletes respond to rehabilitation after 3 months. If conservative management fails and
pain with anterior instability persist, then operative intervention is indicated. Successful outcomes can be obtained after
arthroscopic cuff and posterior labral debridement and open versus arthroscopic anterior labral and capsular
reconstruction ( 83,87). Other authors favor repair of the posterosuperior labral detachment, which diminishes anterior
pseudolaxity (82,86).
In the young athletic patient, rotator cuff tears may result from a breakdown of fibers within the tendons as a result of a
repetitive microtrauma. This microtrauma is seen in activities that place unusual stresses on the shoulder and subject the
rotator cuff tendons to large compressive and tensile forces and eccentric loading such as pitching. Occasionally, cuff
disruption in athletes can occur as the result of a single traumatic event such as an anterior shoulder dislocation. This
mechanism is more common in the older athlete, and it is now recommended that any individual older than 40 years of
age who has had an anterior dislocation and complains of persistent pain and weakness following closed reduction
should be evaluated for a rotator cuff tear ( 88). Although impingement may precede rotator cuff tears, it is more likely in
the young athlete that repetitive high loads impinge the rotator cuff tendons during overhead activities and lead to
gradual failure. This mechanism may be the cause of rotator cuff tears in competitive throwers. Rotator cuff tendon
injuries are more rare in swimmers. Rotator cuff inflammation most often results from transient shoulder impingement.
Pain does not represent true impingement but rather is the result of repetitive traction and compression of the rotator cuff
during subluxation of the glenohumeral joint.
Many of the characteristics of rotator cuff tears seen in the elderly are not present in the young athletic patient. Although
the young usually primarily reports pain during and after activities, the older athlete may complain of weakness as well as
pain. The throwing athlete with a rotator cuff tear will report a decreased velocity ( 89). The differential diagnosis of rotator
cuff injuries in the throwing athlete includes glenohumeral subluxation, multidirectional instability, and nerve injury. On
physical examination, the size of the tear may be determined by the loss of strength. A significant loss of external rotation
strength usually indicates a large tear, involving the infraspinatus as well as the supraspinatus tendons. The treatment of
a partial-thickness rotator cuff tear in a young athlete is a rotator cuff–strengthening program. If tendinitis persists but
instability is absent, arthroscopic subacromial decompression may relieve pain, but the athlete may not be able to return
to his or her previous level of overhead activity ( 77,90). Operative repair usually gives excellent pain relief; however, the
athlete's functional performance with overhead activities is variable. Following rotator cuff repair and 6 months of
rehabilitation, throwing activities are begun gradually over the next several months. Swimmers may begin swimming the
breast stroke at approximately 6 months after surgery ( 77,91,92 and 93).
Biceps Labral Complex Injuries
Biceps tendinitis and subluxation are causes of anterior shoulder pain in athletes involved in overhead activities ( 94,95).
The biceps tendon runs in the bicipital groove between the greater and lesser tuberosities. It is surrounded by a synovial
sheath and is stabilized in the groove by the transverse humeral ligament. A recent study has shown that unlike the
glenohumeral capsule and ligaments, which are innervated by proprioceptive organs, the biceps tendon is predominantly
innervated by free nerve endings that detect noxious stimuli ( 16). The biceps tendon functions as a depressor of the
humeral head preventing upward migration into the acromion ( 96).
Biceps tendinitis can be classified as primary or secondary. Secondary biceps tendinitis is by far the more common
problem and can result from osteoarthritis, rheumatoid arthritis, or impingement syndrome. The impingement syndrome,
as previously noted, may be primary impingement or secondary to instability. With elevation and external rotation of the
arm, the biceps tendon becomes vulnerable to impingement between the head of the humerus, the acromion, and the
coracoacromial ligament. Biceps tendinitis is most commonly seen in athletes who participate in golf, tennis, swimming,
and throwing sports. The athlete usually reports anterior shoulder pain that is less intense with rest. One or more of the
previously mentioned provocative tests will be positive. The treatment of biceps tendinitis secondary to impingement
closely follows that of impingement alone. If impingement is caused by underlying glenohumeral instability, then the
instability should be addressed ( 38). If the tendinitis is secondary to impingement without underlying instability and the
athlete does not improve with conservative treatment, then an arthroscopic or open anterior acromioplasty should be
considered. If the biceps tendon is extremely frayed in association with stage 2 impingement, biceps tenodesis may be
indicated (97). Biceps instability is often related to degeneration and associated with a tear of the subscapularis tendon
(98). It is rare in the young athlete. Treatment involves repair of the rotator cuff, anterior acromioplasty, and fixation of the
biceps tendon (99).
SLAP lesions have been addressed ( 97) (Fig. 53.33). The SLAP lesion is a condition in which there is damage to the
superior labrum of the shoulder from anterior to posterior in the area beneath the biceps tendon. These lesions have
been associated with partial-thickness tears of the rotator cuff, compression injury to the superior humeral head, and
anterior shoulder instability. The lesion of the biceps and labrum may be associated with instability of the glenohumeral
joint (97). The most common cause appears to be the result of a compression injury from a fall onto the outstretched arm
(97). Morgan and Burkhart have described the peel-back mechanism for biceps labral detachment, in which tension on
the long head of the biceps as the humerus is abducted and externally rotated peels the superior labrum from the glenoid
(82).
FIGURE 53.33. Arthroscopic view of a SLAP lesion. Bi, biceps; SL, superior labrum; G, glenoid. The probe is underneath
the superior of the labral tear.
The clinical examination is consistent with tenderness with resisted biceps motion, as noted by Speed or O'Brien test.
Ultrasound, radiographs, arthrogram, CT scans, and noncontrast MRI are usually inconclusive. MRI arthrography with
intraarticular gadolinium may increase the sensitivity and specificity ( 61). The definitive diagnosis of these lesions is
typically made at the time of arthroscopy. Classification of SLAP lesions was described by Snyder ( 97) (Fig. 53.34). Type
I lesions involve fraying of the labrum with a stable biceps labral anchor. Type II lesions are labral detachments from the
glenoid that leave the anchor unstable. Type III lesions are bucket-handle flap tears that extend into the biceps tendon
but leave the anchor intact. Type IV lesions are anchor detachment, like a type II lesion, but with extension into the
tendon. Treatment is based on the clinical symptoms of the patient and the findings at arthroscopy. The treatment options
involve debridement or repair of the labrum and repair, resection, or tenodesis of the involved tendon ( 97). Type I and III
lesions respond to debridement alone. Type II lesions are amenable to arthroscopic repair. Type IV lesions are debrided
and the biceps tendon is tenodesed in the bicipital groove.
FIGURE 53.34. Superior labrum anterior to posterior (SLAP) types.
Injuries to the Acromioclavicular Joint

Problems involving the AC joint in athletes can be divided into two categories: acute traumatic injury and chronic
degeneration. Chronic degeneration is usually the result of repetitive microtrauma such as weight lifting or repetitive
overhead activities. The most common mechanism of injury to the AC joint is a direct fall or direct blow to the acromion
(43). The result of the shoulder being depressed is either a clavicular fracture or a tearing of the AC ligaments. The AC
ligaments are primarily responsible for horizontal stability of the AC joint. With progressively more severe trauma, the
coracoclavicular ligaments will tear. The coracoclavicular ligaments are primarily responsible for vertical stability ( 100). In
the most severe injuries involving the AC joint, the deltoid and trapezius can be torn from their attachments on the outer
end of the clavicle. Other less common mechanisms of injury include a fall onto the outstretched hand and an indirect
downward force that may result from severe distraction of the abducted arm (43).
The most commonly used classification of AC injuries is a six-grade classification ( 101,102). This classification system is
based on the degree of ligamentous damage and the direction of distal clavicular displacement. Type I AC separations
are those in which there is no disruption of the AC or coracoclavicular ligaments, but rather there is a stretch of the AC
ligament. With a type I injury, the athlete experiences pain and tenderness on palpation. There is usually minimal
displacement of the AC joint seen on x-ray study. A type II separation involves disruption of the AC ligament, but the
coracoclavicular ligaments remain intact, whereas in a type III injury, the coracoclavicular ligaments are disrupted as well.
In type II and III injuries, deformity of the joint is obvious, and there is exquisite tenderness over the joint. On x-ray study,
the distal clavicle in a type II injury is displaced up approximately one half the normal superior inferior height of the joint
III injury, this distance is greater than one half the normal superoinferior height ( Fig. 53.35). In certain cases, AP stress
views with 10 to 15 pounds of weight in each hand may be helpful for differentiation of a type II from a type III injury.
Rockwood and Young (103) suggested that a 3-mm or a 25% increase in the normal coracoclavicular distance of 1.1 to
1.3 cm compared with the other side is diagnostic of a complete disruption of the coracoclavicular ligaments. A
cross-body adduction view may also be helpful in determining a complete disruption as the scapula rotates
anteromedially around the chest wall and the distal tip of the clavicle tents the trapezius posteriorly ( Fig. 53.36). For this
to occur there must be complete disruption of the coracoacromial and AC ligaments ( 45). In a type IV injury, the distal
clavicle is displaced posteriorly and may be buttonholed through the trapezius muscle ( Fig. 53.37). A type V injury is
similar to a type III injury but more severe, with disruption of the deltoid and trapezius attachments to the clavicle ( Fig.
53.38). A type VI injury is rare and results from abduction forces. The distal clavicle is displaced underneath the acromion
or coracoid process and may be associated with a brachial plexus injury ( 103).
FIGURE 53.35. Patient with left shoulder type III AC separation.
FIGURE 53.36. A: Normal cross-body adduction x-ray. B: Abnormal cross-body adduction x-ray with posterosuperior
displacement of clavicle.
FIGURE 53.37. Patient with left shoulder type IV AC separation. Note the posterior displacement.
FIGURE 53.38. Type V AC separation. The distal clavicle is subcutaneous.
Type I injuries are treated with ice for 24 hours, and then a sling is worn for 4 to 7 days until pain subsides. Once full
range of motion has been achieved and pain has resolved, athletic activity can be resumed. The amount of time usually
required for this process is 1 week. Type II injuries are treated with ice for 24 hours and in a sling for 1 to 2 weeks,
followed by range-of-motion exercises. Athletic participation can usually be resumed in 3 to 4 weeks, although throwing
may require 6 weeks. There exists controversy concerning the treatment of type III injuries. The patient usually is not
clinically symptomatic following nonoperative treatment, but a cosmetic deformity will be present. Many studies have
confirmed the fact that there is no objective or subjective evidence to support the conclusion that operative treatment of
type III injuries is better than nonoperative treatments. Therefore, if the athlete accepts this deformity, the authors'
treatment consists of a sling, range-of-motion exercises beginning at 1 week, and strengthening begun during the second
week. The athlete can usually return to throwing as soon as 4 weeks. Posteriorly displaced type IV acute injuries are
treated by open reduction with coracoclavicular fixation or ligamentous reconstruction ( 103). Open reduction also is the
treatment of choice for types V and VI injuries ( 101,103).
Not all AC joint injuries can be attributed to a single, specific injury. When subjected to the repetitive stresses
experienced by baseball pitchers or when following a type I or type II dislocation, degenerative changes may occur.
These changes may be associated with severe pain. Often, there is narrowing of the joint with subchondral cyst and
osteophyte formation. Long-term pain relief can be achieved by resection of the distal clavicle, which allows for return to
competitive throwing (104).
Osteolysis of the distal clavicle may result from an acute injury or be the result of repeated stress on the shoulder (i.e., in
weight lifters) (105). Typical symptoms are those of a dull ache, which is exacerbated by overhead activities. A bone scan
or AC joint injection may help to confirm the diagnosis (classic x-ray changes include osteoporosis, osteolysis, tapering,
or osteophytes of the distal clavicle) ( Fig. 53.39). The symptoms are usually self-limited and resolve with reduction of
offending activities. If symptoms persist despite conservative treatment, distal clavicular resection is usually curative.
FIGURE 53.39. Distal clavicle osteolysis.
Dislocation of the Sternoclavicular Joint
Traumatic dislocation of the sternoclavicular joint is a rare injury, because of the strong surrounding ligamentous
structures and the tremendous forces required to dislocate the joint. The sternoclavicular joint may be injured by either
direct or indirect trauma. A growing athlete usually sustains an epiphyseal fracture rather than a ligamentous dislocation
following trauma owing to the late age this physis closes. Traumatic injury may be classified in the adult as a mild sprain,
if the ligaments remain intact and the joint is stable, and a moderate sprain, if there is anteroposterior subluxation of the
sternoclavicular joint. In the case of the moderate sprain, the ligaments are partially disrupted. A severe sprain is one
with complete disruption of the sternoclavicular ligaments. Sternoclavicular dislocation may be either anterior or posterior
and presents with pain that is increased with arm movement. With an anterior injury, the medial end of the clavicle will be
prominent anterior to the sternum. A posterior dislocation is more serious because of the possibility of the distal clavicle
causing occlusion or tearing of large vessels as well as dyspnea from tracheal compression. Radiographs of the
sternoclavicular joint are often difficult to interpret, but occasionally, an AP view of the chest will reveal asymmetry of the
sternoclavicular joints. As mentioned previously, tomograms or CT scans may be necessary to view the dislocation.
The treatment of those injuries without instability involves only symptomatic treatment using a sling, ice, and gradual
return to activities. A subluxation is usually treated with ice for 12 hours and then heat and a well-padded figure-of-eight
clavicular strap. If the strap does not provide pain relief, then a sling can be used for 7 to 14 days. The athlete gradually
increases arm motion until full motion is achieved. Most anterior dislocations are unstable. A reduction is carried out with
suitable anesthesia and lateral traction placed on the abducted arm and direct pressure over the medial clavicle. A
figure-of-eight bandage can be used to hold the reduction; however, reduction is difficult to maintain and may be lost. If
reduction is lost, a malreduction does not appear to interfere with normal shoulder function, and operative repair is
usually not necessary ( 103). If a posterior dislocation is present and there is evidence of compression of the great
vessels in the neck or difficulty breathing or swallowing consistent with pressure on the mediastinum, it should be
considered a medical emergency. The appropriate cardiothoracic specialist should be contacted, and closed reduction
should be performed as soon as possible. Because of the serious complications associated with an unreduced posterior
dislocation, an open reduction should be performed if closed reduction fails ( 103). Continued compression on retrosternal
anatomy can present with dysphagia, late tracheal laceration, tracheoesophageal fistula, erosion into the great vessels,
venous thrombosis, thoracic outlet syndrome, brachial plexus compression, and compression of vagus and phrenic
nerves, leading to pulmonary and cardiac compromise ( 106). Therefore, symptomatic chronic posterior dislocations of the
sternoclavicular joint should be treated with a proximal clavicle resection and reconstruction ( 103). Several reconstruction
methods have been described. Success depends on conserving the local soft tissue and reconstructing the
costoclavicular ligaments. Failure to reconstruct the ligaments has recently been shown to diminish success rates when a
resection was performed (107).
Spontaneous recurrent dislocations of the clavicle are rare but may be present in athletes who have repeated stresses
on the sternoclavicular joint like swimmers and tennis players. These dislocations are usually anterior. When symptoms
persist, surgery may be indicated to reduce and stabilize the sternoclavicular joint with techniques mentioned earlier.
Osteoarthritis secondary to trauma may develop and result in chronic pain. Chronic pain can usually be relieved by
resection of the medial end of the clavicle.
Fractures
Fractures of the proximal humerus in the athlete are rare and the result of considerable trauma. These fractures may also
be associated with glenohumeral dislocations. Fractures were classified according to Neer ( 47) by the number of major
segments involved. For a segment to be considered displaced, it must be displaced 1 cm or angled 45 degrees from its
original position. The four segments are the head, neck, greater tuberosity, and lesser tuberosity. A greater tuberosity
fracture can be associated with an anterior dislocation of the glenohumeral joint, and a lesser tuberosity fracture is most
often seen with a posterior dislocation. These fractures can be seen on the standard anteroposterior lateral views in the
scapular plane and axillary x-ray views. Some form of axillary view is mandatory to rule out the fracture dislocation that
can worsen the prognosis. Following glenohumeral reduction, displacement of the fracture fragments requires an open
reduction and internal fixation. Isolated lesser tuberosity fractures are typically associated with a posterior dislocation
and should be repaired if displaced greater than a centimeter ( 108). Isolated greater tuberosity fractures can be seen
with anterior dislocations and should be repaired if displaced greater than 0.5 cm to minimize the chance for nonoutlet
impingement, as previously discussed ( 108). Surgical neck fractures can typically be treated in a sling if the angulation is
no greater than 50 degrees or 50% displacement in the adult ( 108). Three part fractures typically require open reduction
and internal fixation. Four-part fractures are rarely seen in the athlete but more commonly in the elderly patient. Four-part
proximal humerus fractures typically require hemiarthroplasty owing to the risk subsequent osteonecrosis of the humeral
head and the diminished results with later hemiarthroplasty after previous open reduction and internal fixation attempts
(109,110). In the young athlete, all attempts should be made to spare the native humeral head. Gerber found that
patients who had osteonecrosis but an anatomic restoration of the humeral head after open reduction and internal
fixation had greater functional outcome than those who underwent an acute hemiarthroplasty ( 111). The relatively high
expectations but diminished longevity of present-day prosthetics and cementing techniques in the younger patient should
be considered when contemplating hemiarthroplasty. With secure internal fixation that is assessed at the time of
operative fixation, motion may be started immediately. Nondisplaced proximal humeral fractures may be treated with a
sling and swathe until comfortable, and gentle range-of-motion exercises are recommended.
Glenoid fractures in athletes are also rare. Approximately 20% of traumatic shoulder dislocations have an associated
glenoid rim fracture (35). These fragments are generally small and best seen on axillary x-ray studies or CT scans.
Fractures greater than 25% of the anterior glenoid or 30% of the posterior glenoid should undergo open reduction and
internal fixation to restore glenoid anatomy and stability. Glenoid rim fractures of less than 25% can be typically excised
and the capsule advanced into the defect restoring anterior stability. A large central depression fraction can occur by
violent central impact of the head of the humerus. These fractures may render the joint unstable and incongruous, and
may require surgical treatment. Occasionally, osteochondral prominences can be seen at the posterior inferior aspect of
the glenoid near the origin of the long head of the triceps. These prominences are known as Bennett lesions and are
typically seen in baseball pitchers. Bennett initially attributed them to violent triceps contracture during throwing ( 43).
Ferrari later found an association with posterior labral tears ( 112). Bennett lesions are treated symptomatically and rarely
require arthroscopic surgical resection of the labral pathology ( 87).
Fractures of the body and spine of the scapula are rare and are usually associated with high-energy direct trauma.
Associated rib, clavicle, humeral, and intrathoracic injuries should be sought. These injuries are usually treated by care
for the surrounding soft tissues. This care involves ice for 48 hours, followed by heat. The patient also is immobilized in a
sling until comfortable ( 43) .
Clavicular fractures can result from similar forces as those producing AC separations. It is still unclear why some patients
sustain clavicle fractures and others AC separations. Approximately 80% of clavicular fractures involve the middle third of
the clavicle, 15% involve the distal third, and 5% the proximal third ( 43). Fractures of the middle third usually can be
manipulated into alignment and held in a figure-eight sling or just a simple sling. Operative indications for midshaft
clavicle fractures include open fractures, associated vascular compromise, pending skin penetration, severe
comminution, displacement greater than 1.5 cm scapulothoracic dissociation, and associated glenoid neck fractures.
Midshaft clavicle fractures have a high healing rate, and open reduction and internal fixation, if pursued, should minimize
devascularization of the bony fragments while giving rigid fixation to withstand the high torsional loads the clavicle
tolerates. Failure to adhere to these tenants can result in nonunion and hardware failure. The vast majority of midshaft
clavicle fractures heal with a mild prominence and little residual dysfunction.
Fractures of the distal third have been divided into three types ( 113). Group 1 fractures, the most common type of distal
clavicle fracture, have minimal displacement, intact coracoclavicular ligaments, and require only a sling for treatment,
because the tendency for displacement and nonunion is low. In group II, the coracoclavicular ligaments are detached and
render the medial clavicular fragment unstable while the coracoclavicular ligaments remain with the lateral fragment,
stabilizing it. Because adequate reduction is difficult to maintain, open reduction and internal fixation are advocated for
group II fractures of the distal clavicle. Group III fractures into the AC joint can lead to symptomatic arthritic changes in
the AC joint. These fractures can be subtle and may be misdiagnosed as a grade I AC separation. High-quality
radiographs are necessary to detect these injuries. If x-ray studies are negative and there is a clinical suspicion, a CT
scan may be helpful. These fractures are difficult to fix and are typically managed conservatively. If chronic pain persists,
a simple distal clavicular resection is usually curative ( 113). Fractures of the inner third of the clavicle that do not involve
the SC joint are typically treated with a supportive sling.
Neurovascular Injuries
Neurovascular problems in the shoulder of athletes are rare but potentially serious. It is important to include a thorough
neurovascular examination in any athlete who reports shoulder pain. Perhaps the most serious arterial problem
recognized in the shoulder of a throwing athlete is an acute axillary artery thrombosis. Rohrer et al. ( 114) concluded that
repetitive overhead activities in throwers could cause intermittent compression and intimal contusion of the axillary artery
by the humeral head. These changes result in a decreased blood flow and increase the risk of axillary artery thrombosis.
Anterior instability potentially produces more compression of the artery and increases the potential for thrombosis. The
clinical presentation may vary from muscle ache, fatigue, intermittent paresthesia to loss of pulses, cyanosis, and
decreased skin temperature. When the diagnosis is suspected, an arteriogram is usually necessary for confirmation.
Acute treatment consists of thrombolytic therapy, with possible need for long-term anticoagulation.
Neurologic entrapment syndromes include suprascapular nerve entrapment, quadrilateral space syndrome, and thoracic
outlet syndrome. The suprascapular nerve is a motor nerve origination from the C-5 to C-6 nerve roots and passes to the
upper border of the scapula and through the scapular notch. The scapular notch is roofed by the transverse scapular
ligament. The nerve innervates the supraspinatus before passing along the neck of the scapular spine through the
spinoglenoid notch, ultimately innervating the infraspinatus. The cause of the suprascapular nerve dysfunction may be
from entrapment of the nerve as it passes throughout the suprascapular notch, a traction injury in the spinoglenoid area,
or vascular compromise to the nerve (115). Because the supraspinatus or infraspinatus are not functioning properly,
other problems may occur such as rotator cuff tendinitis and bicipital tendinitis. The athlete with suprascapular nerve
entrapment may report deep diffuse pain that is often localized to the posterior lateral aspect of the shoulder. It may
radiate down the arm or into the neck ( 115). On physical examination, the athlete may have pain with adduction of the
extended arm or tenderness to pressure over the suprascapular notch. There may also be significant wasting of the
infraspinatus alone or in combination with the supraspinatus, depending on the level of entrapment. The diagnosis may
be confirmed by electromyographic (EMG) studies. MRI may show edema early with fatty infiltration and atrophy
occurring after chronic nerve compression. Initial treatment includes rest, flexibility, and a strengthening program ( 116).
Chronic cases may require a surgical release of the nerve.
The quadrilateral space syndrome results from compression of the neurovascular structures that pass through the
quadrilateral space. The quadrilateral space is bordered laterally by the neck of the humerus, medially by the long head
of the biceps, superiorly by the teres minor, and inferiorly by the teres major. The axillary nerve and posterior humeral
circumflex vessels pass through this space. These structures can be compressed during throwing when the arm is
maximally abducted and externally rotated (117). The athlete may complain of pain or paresthesias with a particularly
hard throw or during the acceleration phase of throwing ( 118). The examination of the shoulder may be normal except for
tenderness over the quadrilateral space. EMG studies are usually normal, and the diagnosis is confirmed by subclavian
arteriogram, which reveals occlusion of the posterior humeral circumflex artery during humeral abduction and external
rotation. Surgical decompression may be necessary for athletes who remain symptomatic.
Thoracic outlet syndrome is a complex of symptoms resulting from neurovascular compression to the arm. The clinical
presentation may vary, depending on the structures involved. The athlete may have vague complaints and confusing
physical signs (119). The thoracic outlet is defined as the area in which the great vessels leave the chest to enter the arm
and the nerves exit the neck to joint them. The brachial plexus courses to the upper extremity through the interscalene
interval formed by the anterior scalene muscle anteriorly, the middle scalene posterolaterally, and the superior surface of
the first rib. Direct or indirect injury to the scalene muscles or muscular imbalance of the scapular stabilizers can
precipitate compression of the plexus or subclavian vessels ( 120). Two other potential sites of compression include
clavicular compression on the first rib with shoulder abduction and at the subacromial region where the insertion of the
pectoralis minor to the coracoid passes. The clinical presentation may vary and include pain in the shoulder and arm
paresthesia (usually along the ulnar aspect of the forearm) and weakness of the ulnar nerve innervated intrinsics. The
periodicity of symptoms and their relationship to the position of the arm and shoulder are crucial in the diagnosis ( 121).
Symptoms of venous occlusion include pain and swelling following activities. The physical examination should include
careful evaluation of shoulder girdle posture, the cervical spine, scapular stabilizers, and intrinsic musculature of the
hands.
The overhead exercise test is a provocative test performed by having the patient elevate the arms and rapidly flex and
extend the fingers. A positive test is one in which cramping and fatigue occurs within 20 seconds. Several other
provocative tests have been described, including Adson and Wright maneuvers. In Adson maneuver, the arm is placed at
the side and the neck is rotated to the ipsilateral side and hyperextended while the patient inspires ( Fig. 53.40). In Wright
maneuver, the arm is abducted and externally rotated with the neck rotated to the opposite side ( Fig. 53.41). The patient
then takes a deep breath in order to reproduce symptoms.
FIGURE 53.40. Adson maneuver.
FIGURE 53.41. Wright maneuver.
Radiographs should include the cervical spine and first rib. Nerve conduction studies are useful to rule out more
peripheral lesions, such as ulnar neuropathy at the wrist or elbow (carpal tunnel or cubital tunnel syndrome). Vascular
studies should be obtained in symptomatic patients. The differential diagnosis includes cervical spine abnormalities,
lesions at the lung apex, brachial neuritis, carpal tunnel syndrome, reflex sympathetic dystrophy, and shoulder pathology.
Most athletes respond to conservative therapy, including heat, ultrasound, massage, NSAIDs, and most important, a
postural and scapular stabilizing exercise program. The exercise program should emphasize correction of postural
abnormalities and strengthening of the muscles of the neck and shoulder girdle. In those athletes who do not respond to
conservative treatment in 2 to 3 months surgical intervention should be considered ( 121). Surgical intervention may
involve sub or extraperiosteal first rib resection and/or release of the anterior scalene muscles.
Burners and stingers are typically sustained by football players. Burners are typically self-limiting, lasting only seconds to
minutes. The exact etiology of neural disruption is unclear. Mechanisms of injury include compression of the shoulder
pads on the superiomedial border of scapula or a traction injury when the shoulder is acutely depressed with a
contralateral rotation of the neck. Chronic stingers lasting weeks have been reported. Despite the chronic nature of some
stingers, no abnormal MRI findings have been reported. Patients with recurrent stingers, like those with chronic stingers,
should undergo complete radiographic evaluation of the cervical spine including flexion or extension views to rule out
subclinical instability. MRI should also be obtained to rule out congenital cervical stenosis or cord injury. ( 122) found that
players with a Torg ratio of less than 0.8 have a threefold higher risk of experiencing stingers. The Torg ratio is
calculated by dividing the distance between the posterior vertebral body and the laminar line by the width measured on
the lateral cervical radiograph ( 123).
Players typically present after contact and walk off the field supporting the affected extremity with the other hand. They
report an acute onset of burning pain after a hit, with radiation into the shoulder and arm with subsequent weakness of
the deltoid and biceps which are innervated by the upper plexus. Evaluation should include complete cervical and
neuralgic evaluation. Return to play is allowed when there is complete resolution of pain and weakness.
Rehabilitation should focus on strengthening of cervical and shoulder girdle musculature.
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54 Elbow Injuries
54
ELBOW INJURIES
MARC R. SAFRAN
JAMES P. BRADLEY
Functional Anatomy and Biomechanics

Bony Anatomy
Range of Motion
Ligamentous Anatomy—Lateral
Ligamentous Anatomy—Medial
Biomechanical Forces
Elbow Stability
Anteroposterior Stability
Varus Stability
Valgus Stability
Pathophysiology and Pathomechanics of Elbow Injury
Elbow Dislocations
Coronoid Fractures
Posterolateral Rotatory Instability
Olecranon Fracture
Radial Head
Distal Humerus Fracture
Supracondylar Humerus Fracture
Medial Epicondyle Fracture
Treatment of Overuse Injuries
Anterior Elbow Pain
Climber's Elbow
Distal Biceps Tendinitis
Distal Biceps Tendon Rupture
Ectopic Bone
Pronator Syndrome
Annular Ligament Disruption
Medial Elbow Pain
Medial Epicondylar Physeal Injury
Medial Epicondylitis
Flexor-Pronator Muscle Group Disruption
Snapping Triceps
Ulnar Collateral Ligament Injury
Ulnar Nerve Injuries
Posterior Elbow Pain
Olecranon Apophysitis
Triceps Tendinitis
Triceps Tendon Rupture
Valgus Extension Overload Syndrome
Olecranon Stress Fracture
Olecranon Bursitis
Lateral Elbow Pain
Radial Neck Physeal Fracture
Radiocapitellar Degeneration
Lateral Epicondylitis
Extensor-Supinator Muscular Disruption
Radial Nerve Entrapment
Conclusion
Chapter References
The elbow facilitates the highly skilled functions of the forearm, wrist, and hand that are needed for athletic endeavors.
Athletic activities involving throwing, catching, hammering, pushing, pulling, and hitting with a racquet ( Table 54.1) (1)
produce significant stresses about the elbow joint that can result in acute and chronic injuries. Elbow injuries so
commonly result from athletic endeavors that many injuries have colloquial names associated with them ( Table 54.2) (2).
TABLE 54.1. SPORTS THAT COMMONLY PRODUCE ELBOW INJURIES
TABLE 54.2. COMMON NAMES FOR ELBOW PROBLEMS
Injuries to the elbow may involve the muscles, ligaments, tendons, capsule, bones, articular surfaces, or nerves and
subsequently impair elbow function. Elbow injuries, particularly chronic overuse injuries, occur most commonly in athletes
that participate in throwing or overhead activities and frequently are the result of valgus stress.
Our understanding and treatment of elbow injuries is becoming more sophisticated in conjunction with better noninvasive
[magnetic resonance imaging (MRI)] and invasive (arthroscopy) diagnostic techniques ( 2). Elbow injuries are becoming
more common as more people participate in sports that involve throwing and racquet sports. Between 1980 and 1985,
medically reported injuries in people older than 14-years-old participating in racquet sports increased 112% ( 3).
The purpose of this chapter is to (a) define the significance of elbow injuries in athletics, (b) review the anatomy and
biomechanics of the elbow, and (c) discuss the prevention and treatment of elbow injuries. Acute elbow injuries, including
fractures and dislocations, as well as chronic and overuse injuries, are reviewed. Current surgical options are discussed,
but surgical technique is beyond the scope of this chapter.
FUNCTIONAL ANATOMY AND BIOMECHANICS
Bony Anatomy
The bony anatomy of the elbow allows for two complex motions: flexion-extension and pronation-supination. The
ulnohumeral articulation of the elbow is almost a true hinge joint with its constant axis of rotation through the lateral
epicondyle and just anterior and inferior to the medial epicondyle ( 4,5). This well-fitted hinge joint allows for very little
excessive motion or toggle. The olecranon tip fits precisely within the olecranon fossa in full extension. The ulnohumeral
joint has 11 to 16 degrees of valgus ( 4) the radius articulates with the proximal ulna and rounded capitellum of the distal
humerus. This radiocapitellar joint allows for pronation-supination.
Range of Motion
The range of motion at these articulations are 140 degrees of flexion from full extension, and from 75 degrees of
pronation to 85 degrees of supination ( 6). However, functional range of motion that allows for normal activities of daily
living (ADLs) are from 30 to 130 degrees of flexion, and approximately 50 degrees each of pronation and supination ( 7).
In the athlete, however, these acceptable ranges of motions for ADLs are not necessarily applicable. Gymnasts that
perform handstands, or other events that require weight bearing on their arms, require full extension to lock their elbows,
whereas baseball pitchers quite frequently have an elbow flexion contracture of their dominant elbow of up to 20 degrees
that does not limit their effectiveness. The valgus at the elbow results in increased forces at the radiocapitellar joint with
compressive axial loads in a ratio that produces 60% of the force through the radiocapitellar joint ( 8).
Ligamentous Anatomy—Lateral
The ligaments of the elbow are divided to the radial and ulnar collateral ligament (UCL) complexes. The lateral or radial
collateral ligamentous complex provides varus stability. These ligaments are rarely stressed in the athlete. This complex
consists of the radial collateral ligament, the annular ligament, the accessory collateral ligament, the posterolateral
(lateral ulnar) collateral ligament, and the anconeus muscle ( Fig. 54.1). The annular ligament surrounds the radial head
and originates and inserts onto the anterior and posterior margins of the lesser sigmoid notch of the ulna. The radial
collateral ligament arises from the lateral epicondyle and inserts into the annular ligament. The accessory collateral
ligament arises from the inferior aspect of the annular ligament and inserts onto the crista supinatoris of the ulna. The
posterolateral collateral ligament is a small ligament originating from the lateral epicondyle and inserting onto the crista
supinatoris of the ulna. The anconeus muscle originates from a rather broad site on the posterior aspect of the lateral
epicondyle and inserts onto the lateral dorsal surface of the proximal ulna.
FIGURE 54.1. Lateral collateral ligament complex of the elbow. (From Safran MR. Elbow injuries in athletes. Clin Orthop
1995;310:257–277, with permission.)
Ligamentous Anatomy—Medial
The ulnar or medial collateral ligament (UCL) complex consists of three ligaments ( Fig. 54.2): the anterior oblique,
posterior oblique, and transverse ligaments. The anterior oblique ligament is a thick, discrete ligament with parallel fibers
arising from the medial epicondyle and inserting into the medial coronoid process and is the most important of the
ligaments. The fan-shaped posterior oblique ligament is a thickening of the capsule that is best defined with the elbow
flexed at 90 degrees. This ligament also originates from the medial epicondyle and inserts onto the medial margin of the
semilunar notch. The transverse ligament arises from the medial olecranon and inserts into the inferior medial coronoid
process.
FIGURE 54.2. Ulnar collateral ligament complex of the elbow. (From Safran MR. Elbow injuries in athletes. Clin Orthop
Biomechanical Forces
The amount of force transmitted across the elbow joint varies with specific factors that include (a) loading configuration
and (b) angular orientation of the joint. A magnitude three times body weight has been speculated in certain functions
(9,10). ADLs necessitate approximately 50% of body weight transmitted across the joint, with maximal loads noted at
about 90 degrees of flexion (11,12).
ELBOW STABILITY
Anteroposterior Stability
Elbow stability in the anteroposterior (AP) plane is derived from the ulnohumeral articulation, in addition to the pull of the
flexor and extensor muscles, especially during lifting. The anterior capsule of the joint provides little support except when
the elbow is in full extension.
Varus Stability
The lateral collateral ligament complex provides stability in response to varus stress. The radial collateral ligament is taut
throughout flexion and extension, whereas the accessory collateral ligament is taut only with varus stress, unrelated to
flexion and extension. The posterolateral collateral ligament, although small, provides some additional static support,
whereas the anconeus is a dynamic stabilizer. The radial head provides some resistance to varus stress, varying
between 15% and 30%, depending on the load configuration and orientation of the joint ( 13). Studies of force
transmission across the elbow have shown that forces across the radial head are greatest in the first 0 degrees to 30
degrees of flexion and decrease with further flexion ( 14,15). Varus stress applied during full extension is resisted by the
anterior capsule (30%), the articular surface (50%), and the radial collateral ligament complex (15%) ( 15). In flexion,
however, the joint surface supports 75% of the load and the radial collateral ligament complex supports only 10% ( 15).
Valgus Stability
The athlete is most often exposed to chronic severe valgus stresses. While bony articulation resists these stresses with
the elbow flexed less than 20 or greater than 120 degrees ( 16,17 and 18), valgus stress is offset predominantly by the
UCL complex. The anterior band of the anterior oblique ligament is taut (and therefore functioning as a checkrein) from
full extension to 85 degrees of flexion, whereas the posterior band of the anterior oblique ligament is taut with flexion
beyond 55 degrees. The posterior oblique ligament functions with the elbow flexed beyond 90 degrees ( 8,17,19). The
tightening of the medial collateral ligament complex with increasing flexion is due to the cam effect of the hinge joint. The
transverse ligament, because it has its origin and insertion on the same bone, has no apparent contribution to joint
stability. With the UCL cut, studies have shown the greatest instability of the elbow is at 70 degrees. The radiocapitellar
joint is a secondary stabilizer to valgus stress (30%) ( 20). The flexor-pronator muscle group has its common tendon of
origin at the medial epicondyle. This muscle group is an important dynamic stabilizer to the medial elbow. The flexor
carpi ulnaris lays directly over the UCL and is believed to be the primary dynamic contributor to valgus stability, while the
flexor digitorum superficialis may also support valgus stability in greater degrees of extension ( 21). Additionally, the
wedge shape of the olecranon central ridge within the trochlea provides some bony varus-valgus stability with joint
compression from muscular forces across the elbow (from all the muscles that cross the joint and are contracting during
activity).
PATHOPHYSIOLOGY AND PATHOMECHANICS OF ELBOW INJURY
Elbow injuries can be classified as acute or chronic. Acute injuries include dislocations and fractures of the radial head,
the olecranon, and distal humerus. These acute injuries are treated as one would treat the nonathlete and are discussed
in this chapter under fractures and dislocations. Acute ligament and muscle injuries are discussed under each specific
problem.
The majority of injuries to the elbow in the athlete are chronic, overuse injuries. These injuries are the result of repetitive
intrinsic or extrinsic overload, or both, resulting in microrupture of soft tissue such as ligament or tendon. Intrinsic
overload is the force from muscular contraction, concentric or eccentric, which can lead to tendinitis or muscular injury.
Extrinsic overload is a tensile overload caused by excessive joint torque forces stressing the soft tissue resulting in
stretching and eventual disruption. Extrinsic overload may also be due to compression of the soft tissues, causing
abrasion or impingement of the tissue. The microrupture of the soft tissue results in compromise of the soft tissue by an
imperfect healing process. In children, apophyses are susceptible to stress injuries as they undergo ossification, resulting
in local inflammation, disordered or irregular ossification patterns, overgrowth, and pain. This is important, because a
forceful acute injury in the milieu of weakness and disordered ossification from recurrent microtrauma may result in small
avulsion fractures at the apophyses.
Valgus stress, from throwing or axial compression, causes increased distraction forces to the medial elbow. The loads on
the elbow are repetitious and high-velocity and are seen most often in overhead sports (e.g., baseball pitch, tennis serve,
javelin throw, football pass, hockey slap shot, and volleyball spike). They often predispose the elbow to overuse
syndromes (22). Many of these overhead sports activities require similar movements: rapid forceful extension of the
elbow, frequently accompanied by valgus stress and pronation of the forearm. The normal valgus angle of the elbow in
extension may particularly bias the medial aspect of the elbow to overuse injuries. The velocity, power, and
repetitiousness of the throwing motion all contribute to the ensuing microtrauma, particularly during the late cocking and
acceleration phases of the throwing cycle ( 22). It is estimated that elbow medial shear force exceeds 300 newtons during
throwing, and elbow extension occurs at up to 2,500 degrees per second ( 22).
As noted earlier, the primary dynamic stabilizer to valgus stress is the flexor-pronator muscle mass, particularly the flexor
carpi ulnaris and flexor digitorum superficialis ( 21). With repetitive throwing, this muscle mass may fatigue, imparting the
stress to the UCL. The UCL is the most important static stabilizer to valgus stress to the elbow between 30 degrees and
120 degrees of elbow flexion (16). Imperfect healing after the microtrauma results in attenuation of the ligament and
compression of the radiocapitellar joint. The result is increased forearm valgus resulting from ligamentous incompetency
and an elbow flexion contracture from attempts at repair and stabilization ( 23). With repetitive valgus stress, patients may
develop chondromalacia, loose bodies in the posterior or lateral compartments, injury to the UCL, myotendinous injury to
the flexor-pronator muscle group, osteochondritis dissecans (OCD), or ulnar neuritis (due to traction or inflammation).
Thus, the forces at the elbow due to repetitive valgus stress result in (a) traction of the medial side structures, (b)
compression of the lateral elbow, and (c) medial shear posteriorly ( Fig. 54.3).
FIGURE 54.3. The effects of valgus elbow forces during throwing.
The pathoanatomy and kinematics of hyperextension injuries to the elbow has recently been elucidated. Hyperextension
loads produce four lesions: (1) anterior capsule rupture, (2) L-shaped rupture of flexor-pronator origin with elongation of
the anterior part of the UCL, (3) occasional incomplete rupture of the lateral collateral ligament, and ( 4) small fragments
of cartilage near the posterior edge of the ulna ( 24).
Pain about the elbow may result from pathology remote to the elbow. The differential diagnosis includes cervical disk or
nerve root problems, thoracic outlet or brachial plexus pathology, primary nerve pathology, peripheral nerve entrapment
syndromes, Pancoast tumor, overuse injury of the neck, shoulder, or wrist, and diabetes mellitus.
FRACTURES AND DISLOCATIONS
Elbow Dislocations
The elbow is the most commonly injured joint in children, with dislocations accounting for 6% to 8% of elbow injuries
(25,26). The elbow is second only to the shoulder as the most commonly dislocated major joint in patients of all ages. It is
the most commonly dislocated major joint in children younger than 10 years of age ( 27). Approximately one half of all
elbow dislocations occur in patients younger than age of 20, and the peak incidence is reported to be between the ages
of 13 and 14 (28,29 and 30). In most series, sports injuries account for the largest group of etiologies. Typically, this
injury involves the nondominant extremity (28,29,30 and 31). A fall on the outstretched hand is far and away the most
common history given. Any sport with the potential of a fall, especially a violent fall, places the athlete at risk of an elbow
dislocation. Cycling, gymnastics, football, and wrestling have significant injury potential ( 32).
Dislocations are classified according to the displacement of the radius and ulna, which usually move together in elbow
dislocations. This includes posterior (straight, posterolateral, or posteromedial), anterior, medial, and lateral. Divergent
dislocations (in which the proximal radioulnar joint is disrupted) are divided into anterior, posterior, or mediolateral
(33,34,35 and 36). Posterior or posterolateral dislocations account for 80% to 90% of all dislocations of the elbow in the
series reported (28,29,30 and 31). Isolated radial head dislocations are extremely rare.
A fall on an outstretched hand is the typical history reported for posterior dislocations. There are two mechanisms
described: (a) The olecranon levers on the olecranon fossa as the elbow hyperextends until the coronoid process slips
posteriorly; a varus or valgus stress can create a posteromedial or posterolateral dislocation; or (b) the arm is slightly
flexed with the lateral sloping surface of the trochlea acting as a cam, converting the vertical force to lateral rotation and
valgus stress, which ruptures the medial collateral ligament or avulsing the medial epicondyle, allowing the ulna to slip
laterally and come to lie posteriorly or posterolaterally ( 32). Alternatively, a varus force can result in lateral collateral
ligament or lateral condyle or epicondyle avulsion injury.
Most cases of anterior elbow dislocations are reported to be caused by a direct blow to the olecranon posteriorly with the
elbow flexed.
There is a high incidence of associated fractures with elbow dislocations in children (up to 50%), especially fractures of
the radial head and neck, and the medial or lateral epicondyle ( 37). The soft tissue insult during posterior elbow
dislocations is significant. The anterior capsule is torn, usually from the ulna, and the posterior capsule may be stripped
off proximally along the distal humerus by the posteriorly driven radial head and olecranon.
The medial or lateral collateral ligaments are usually ruptured ( 38,39). Rather than a direct tear of the ligaments, the
medial epicondyle apophysis may be avulsed. The avulsed fragment can lie in an essentially nondisplaced position or
can even come to lie within the joint (see medial epicondylar fracture) ( Fig. 54.4 and Fig. 54.5).The incidence of medial
epicondyle fractures varies from 0 ( 31) to 30% (29) in the four major elbow dislocation series ( 28,29,30 and 31). The
lateral epicondyle fractures less frequently.
FIGURE 54.4. Incarceration of the medial epicondyle in the joint prevented closed reduction of this elbow dislocation.
(From Safran MR, Salyers S, Fu FH. Elbow dislocations. In: Reider B, ed. Sports medicine—the school age athlete, 2nd
ed. Philadelphia: WB Saunders, 1996:242, with permission.)
FIGURE 54.5. Schematic representation of medial epicondylar avulsion with displacement into the joint.
At the level of the joint, the brachialis is a large, fleshy muscle with a minimum of tendon compromising its thickness.
Extensive rupture of this muscle is often seen ( 38,40). An avulsion fracture of the coronoid may occur if the coronoid has
not completely ossified due to the pull of the brachialis. A fracture may occur in a completely ossified coronoid, and this
may be an avulsion injury or a shear injury as the coronoid impacts against the distal humerus ( 41). See below for more
information on coronoid fractures.
Damage to the wrist flexor or extensor origins also occurs to a varying degree. With a medial epicondyle fracture or
avulsion, the flexor origin remains attached to the fragment and acts as a displacing force. The radial head or neck can
be fractured by the force of this injury. This injury occurs in 5% to 10% of elbow dislocations ( 42).
The brachial artery can be torn. In certain situations, a tear in the brachial artery can be treated without surgery owing to
the excellent collateral flow about the elbow. However, as Louis et al. ( 43) have shown, the collaterals about the elbow
are consistently damaged with a dislocation, and brachial artery repair is strongly advocated. In Protzman's series of
patients, there were no brachial artery injuries, and this is consistent with what we have seen in athletic injuries ( 31).
The ulnar nerve can incur a traction injury during posterior or posteromedial dislocations. In children, entrapment of the
median nerve within the joint has been reported. There are three types of entrapment: (a) with the median nerve
displacing posteriorly to the humerus and passing through the joint, (b) bony entrapment between fracture surfaces, and
(c) a kinking nerve in the elbow joint ( 44). The incidence of these injuries is quite low, as seen in the West Point series, in
which there were no residual neurologic deficits ( 31).
When a posterior elbow dislocation is seen early, the diagnosis is easy ( 32). The extremity is held in flexion, with the
forearm appearing shortened. The olecranon is prominent posteriorly. The athlete is generally in severe pain. Palpitation
reveals the antecubital fossa to be full and the olecranon and the radial head prominent posteriorly. Above the olecranon,
a palpable indentation in the triceps is noted. Slight flexion and extension of the elbow while palpating for crepitus can
rule out a fracture with moderate certainty and can be performed if the clinician plans a reduction attempt on the field
prior to radiographic evaluation.
After the onset of swelling, difficulty occurs in differentiating this injury from a supracondylar fracture, lateral condylar
fracture, and in the young child, transcondylar fracture. Excessive manipulation to aid the diagnosis is unnecessary,
because radiographic confirmation is easy and reliable.
Before performing a radiographic evaluation, it is imperative to perform a careful neurovascular examination. This takes
only a few moments and can be performed without undue stress.
Standard AP and lateral radiographs should be obtained. Occasionally, special views or arthrography is indicated if your
clinical suspicions are not confirmed with routine radiographs ( 45). When an arterial injury is suspected, an arteriogram
or digital subtraction studies should be performed without hesitation.
Interpreting films of a posterior, posterolateral, or divergent dislocation is not difficult ( Fig. 54.6). The rare medial or
lateral dislocation can be overlooked on casual reading of the film, but the physical findings are not subtle. The hazards
of radiographic evaluation lie in identifying the associated fractures. The radial head and neck, coronoid, and medial and
lateral epicondyles must be carefully examined. All views are repeated and reevaluated after reduction.
FIGURE 54.6. A: A newspaper photographer caught this wrestler in the process of sustaining a posterior dislocation of
the elbow. B and C: A severely displaced posterior dislocation of the elbow of another wrestler. (From Safran MR,
Salyers S, Fu FH. Elbow dislocations. In: Reider B, ed. Sports medicine—the school age athlete, 2nd ed. Philadelphia:
WB Saunders, 1996:239, with permission.)
Spontaneous reduction of a dislocated elbow is common in children. The only evidence is a history of a fall and often a
swollen, boggy elbow with no obvious radiographic injury. Careful inspection of the radiographs may reveal signs of a
previous dislocation, including an avulsed coronoid fragment.
“All methods of reduction are directed toward sufficiently overcoming the muscle forces so that the coronoid process and
radial head can slip from posterior to anterior past the distal end of the humerus” ( 46). In order to achieve this, adequate
anesthesia is needed. This can be a general anesthetic, regional block, or sedation. If the diagnosis is reliably made at
the time of injury, a single attempt at gentle reduction can be tried on the playing field before muscle spasms become
pronounced. This can lead to disaster if the injury is a supracondylar fracture rather than an elbow dislocation, so caution
is advised. Nonetheless, reduction within 6 hours of the time of injury is preferred to reduce the edema and postreduction
stiffness.
Once adequate anesthesia is obtained, a closed reduction by gentle forces can nearly always be obtained. It is important
to correct medial or lateral displacements before reducing the posterior displacement. This may be performed in the
emergency room; however, if adequate relaxation cannot be performed there to afford proper elbow orientation, then
reduction under general anesthesia in the operating room may be necessary.
After reduction, it is absolutely critical to take the elbow through a full range of motion following reduction and test varus
and valgus stability. The degree of stability helps determine how aggressive the rehabilitation can be. There also should
be no grinding, mechanical block, or spongy feel with motion. If these problems occur, careful evaluation must rule out
intraarticular entrapment of the median nerve or the medial epicondyle.
Careful and compulsive repeat radiographic and neurovascular evaluations must be undertaken before applying a splint.
A long arm plaster splint with adequate padding is applied with the elbow flexed 90 degrees. If there is pronounced
swelling, a questionable vascular examination, concern about a compartment syndrome, or an unreliable patient,
hospitalization should be considered. Otherwise, instructing the parent how to observe the circulatory status is sufficient.
Ice and elevation are useful, as always. Aspiration of the joint is recommended to assist in resolving the hematoma,
improving joint motion after reduction, and decreasing pain.
Protzman's series at West Point contains a patient population most similar to that seen in a sports medicine practice ( 31).
He found that decreasing the period of immobilization leads to decreased loss of motion and a decreased period of
disability, as we have found in our clinical practices and other studies ( 47). With a simple posterior or posterolateral
dislocation without associated fractures, hand, wrist, and shoulder motion can begin the day of injury. Flexion from within
the splint can begin in 3 or 4 days, and the splint can be discarded in 7 to 10 days. After 1 week, the patient is fitted for a
hinged elbow brace and gentle active flexion and extension ranges of motions are encouraged under the supervision of a
physical therapist. Forced passive motion or manipulation has no place in elbow dislocation treatment owing to the risk of
loss of motion and increased heterotopic ossification. The risk for recurrent dislocation is very low with this protocol. At 3
weeks postreduction, the stability of the reduction will determine the course of therapy or bracing. Gentle strengthening
exercises usually can begin 3 to 5 weeks after the injury and progress as pain allows.
If there is an associated fracture or gross instability, treatment must be altered. A single axis elbow orthosis may allow
early motion in elbows that are believed to be unstable to varus or valgus stress ( Fig. 54.7).
FIGURE 54.7. Single-axis orthosis used for patients with elbow instability. (From Safran MR, Salyers S, Fu FH. Elbow
dislocations. In: Reider B, ed. Sports medicine—the school age athlete, 2nd ed. Philadelphia: WB Saunders, 1996:241,
with permission.)
The indications for open treatment of elbow dislocations are (a) open injury, (b) vascular injury, (c) fracture management,
(d) median nerve entrapment, and (e) inability to obtain reduction (a situation that is quite rare). One recent study noted
that closed reduction failed in 10% of traumatic elbow dislocations. In a prospective randomized study of surgical versus
nonsurgical management in 30 consecutive patients, Josefsson et al. ( 48) showed no advantage of operative treatment.
This is in direct contrast to Norwood et al. ( 49) and Durig et al. (50). DeLee (51) concluded that “the incidence of
recurrent dislocation is not sufficiently high nor the results of treatment by closed reduction sufficiently poor to warrant
primary operative repair in pure elbow dislocations.”
If an associated fracture of the radial head or neck is noted, it should be addressed in routine fashion. Coronoid fractures
should be managed as discussed later. Although not reported as an isolated problem, osteochondral fractures and
chondral flaps can occur ( 52). If the joint is opened for any reason, it should be inspected to rule out intraarticular
fragments, as may occur with osteochondral injuries associated with the dislocation or the reduction.
Joint stiffness, specifically loss of extension, is the most common complication. Patients should be counseled that 5 to 10
degrees of extension loss is to be expected but that this motion loss is associated with few symptoms. Early institution of
motion helps prevent this problem. Heterotopic ossification in the ligaments is a common radiographic finding associated
with few symptoms. This problem is less common in children. True myositis ossificans can lead to significant loss of
motion, but it is a rare complication. Furthermore, this complication occurs less frequently if the dislocation is not
associated with a fracture (30). If this problem occurs and limits the athlete's function, excision can be considered after
the inflammatory phase is complete and the ectopic bone is “mature.” This can be assessed by a “cold” technetium bone
scan. Following excision of the ectopic bone, prevention of recurrence using oral diphosphonates ( 53,54), irradiation
(55,56,57 and 58), or oral nonsteroidal antiinflammatory medications (NSAIDS) ( 59 and 60) is recommended.
Recurrent dislocation is also quite rare. Protzman observed no recurrent dislocations in an active population with a
minimum of postreduction immobilization (31). This is supported in other studies ( 28,29,30 and 31,38,47).
Josefsson et al. (38) reviewed 52 patients with elbow dislocation, with an average of 24 years postinjury. There were no
redislocations, persistent neurologic symptoms, or symptoms of instability. There were eight patients with signs of
abnormal valgus laxity, but these were asymptomatic.
Adult dislocators had an average loss of extension of 12 degrees, whereas childhood dislocators only lost an average of
4 degrees. There was essentially no loss of pronation, supination, or flexion. There were some mild radiographic findings
of osteoarthritis, but the only associated symptom was a mild increase in extension loss. Other large series reflect the
above-mentioned findings (28,29,30 and 31,38,42,47).
The student athlete can expect return to noncontact sports in 2 to 3 weeks ( 32). Contact sports require at least twice as
long for return, and the throwing athlete may not return for considerably longer. The long-term prognosis, however, is for
most of these athletes to return to their sport with little disability.
Coronoid Fractures
The coronoid process forms a significant portion of the articular surface of the proximal ulna and may influence stability
as an osseous buttress as well as an important attachment site for muscles and ligaments about the elbow. Associated
fractures of the coronoid may occur in approximately 2% to 15% of acute elbow dislocations ( 28,42,52). Un-united
coronoid fractures may result in chronic, recurrent elbow dislocations.
Regan and Morrey (61) in 1989 instituted a three-part classification system of coronoid fractures based on lateral
radiographs, CT scans or tomograms. They classified coronoid fractures as follows: type I—avulsion of the tip of the
coronoid process, type II—fracture involving less than 50% of the process, and type III—fracture involving greater than
50% of the process (Fig. 54.8). The fractures are also classified as to the degree of comminution and the presence of
associated dislocation of the elbow ( 61). Anatomic studies have revealed the pathoanatomy associated with these types
of coronoid fractures. Generally, the type I fragment (coronoid tip) is intraarticular without soft tissue attachment, the type
II fragment is attached only to the capsule, and type III fragments include the attachment of the brachialis, capsule, and
the anterior band of the MCL (62). Clinically, the radiographs describe only the bony injury. Although it is often difficult,
an attempt must be made at patient presentation to assess the extent of injury to the soft tissues.
FIGURE 54.8. Schematic representation of the classification of coronoid fractures. (From Regan WD, Morrey BF.
Fractures of the coronoid of the ulna. J Bone Joint Surg [Am] 1989;71:1348–1354, with permission.)
Several authors have implicated that the coronoid may play an important role in elbow stability ( 52,61,63,64,65,66 and
67). The incidence of acute elbow dislocation with associated coronoid fractures is reported to be 14% with type I
fractures, 56% with type II coronoid fractures, and 80% with type III ( 61). Thus, it appears that type III, and less commonly
type II, fractures of the coronoid ( 61) may be associated with instability of the elbow due to loss of at least half of the
anterior wall of the elbow joint.
Patients with elbow dislocations must be carefully examined and lateral radiographs must be performed to evaluate for
injuries to the UCL, radial head, and coronoid. The combination of injuries to these three structures has been termed the
terrible triad of elbow instability by Hotchkiss ( 68). The terrible triad reveals the significance of ligamentous and osseous
contributions to elbow stability.
Untreated, recurrent dislocations of the elbow due to nonunion of large coronoid fractures may result in destruction of the
distal humeral articular surface, chronic dislocation, arthritic pain, painful subluxation, weakness, and instability.
The key to this problem is prevention. Postreduction radiographs should be evaluated for the possibility of coronoid
fracture. Type I fractures are treated as one would treat a dislocation without fracture—early mobilization ( 69). Type II
fractures should be treated with early motion if the elbow is stable ( 69). If there is a type II fracture and the elbow is
unstable or a type III fracture, treatment should be with open reduction and internal fixation ( 69). If there is a comminuted
type III or unstable type II fracture, an elbow external fixation distraction device should be applied ( 69). If this is not done
or a fracture is missed, then a nonunion may occur resulting in chronic instability. One definitive indication for surgery
would be a displaced fragment that blocks full elbow motion, which would then require fixation or excision, depending on
the size and comminution of the fragment.
Nonoperative treatment includes triceps strengthening and a brace. Because the elbow is more stable in pronation, a
hinged elbow brace in pronation with an extension block may provide limited stability. Wearing a brace full time is often
not satisfactory to the patient. Furthermore, this treatment is unlikely to provide a satisfactory functional result as well.
Posterolateral Rotatory Instability
A recently described problem of the elbow is that of posterolateral rotatory instability (PLRI). This is a rotatory instability
pattern of the elbow due to injury to the lateral UCL. The mechanism, as described by O'Driscoll ( 71), is a combination of
axial compression, valgus stress, and supination that imparts a rotation force to the elbow and results in a spectrum of
soft tissue injury. The initial injury is to the ulnar portion of the lateral collateral ligament (LCL) complex and progresses to
capsular disruption, including the anterior and posterior capsule and even the medial complex if the injury is severe
(26,70,71 and 72).
The key to understanding PLRI is an appreciation of the pathomechanics. The instability results from a rotatory
subluxation of the combined radius and ulna relative to the humerus. Because the annular ligament is intact, the
radioulnar joint maintains its normal relationship and moves in a “coupled” motion. Osborne and Cotterill ( 39) were
probably the first investigators to appreciate fully the importance of the lateral ligamentous complex in recurrent
instability. Current biomechanical studies have demonstrated that the primary stabilizer to PLRI is the lateral ulnar
collateral ligament (LUCL) ( 26,70,71,72 and 73). The radial collateral ligament and anteroposterior capsule serve as
secondary restraints. It is the PLRI that most commonly manifests following LCL complex injury.
The diagnosis of PLRI is much more elusive and requires a careful history and physical examination. The physician must
maintain a high degree of suspicion in patients with vague reports of elbow discomfort. Patients with PLRI often report
painful clicking, snapping, clunking, locking, or giving way. The symptoms are often elicited when they extend their
elbow, with the forearm supinated (71).
The preliminary examination of strength, range of motion, and tenderness is often normal. The diagnosis requires a
provocative test of stability, termed the lateral pivot-shift test of the elbow ( Fig. 54.9 and Fig. 54.10A) (71). Briefly, the
test is performed with the patient supine and the examiner positioned above the patient's head. The involved extremity is
brought above the patient's head, and the shoulder is placed in full external rotation to stabilize the humerus for the test.
The patient's forearm is held is supination, with one hand grasping the wrist distally. A valgus force is applied with the
other hand of the examiner as the elbow slowly flexes from a starting point of full extension. The combination of
supination and valgus stress results in an axial compression of the joint, which produces a posterolateral rotatory
subluxation of the combined radius-ulna relative to the humerus. In an unanesthetized patient, this maneuver reproduces
the sensation of instability and elicits apprehension. The subluxation is maximized as the elbow reaches 40 degrees
flexion, and further flexion results in a sudden clunk as the joint reduces. Dimpling of the skin of the posterolateral elbow
can be seen with posterolateral rotatory instability ( Fig. 54.10B). This is the result of the displacement of the radial head
posteriorly. The reduction is generally only felt by the examiner in a patient under general anesthesia or occasionally
following an intraarticular injection of anesthetic. If a patient does display apprehension during the pivot-shift maneuver in
the office, then we recommend confirmation of posterolateral instability with an examination under anesthesia ( Fig.
54.10A). Lateral stress x-ray studies or fluoroscopy during the pivot maneuver demonstrates posterolateral dislocation of
the radial head with widening of the ulnohumeral joint (due to the subluxation of the ulna out of the trochlear groove) and
may be helpful for confirmation and documentation of the pathomechanics.
FIGURE 54.9. Schematic representation of the lateral pivot-shift test of the elbow for posterolateral rotatory instability.
(From O'Driscoll SW, Bell DF, Morrey BF. Posterolateral rotatory instability of the elbow. J Bone Joint Surg [Am]
FIGURE 54.10. Examination under anesthesia of a patient with posterolateral rotatory instability. A: Performing the
lateral pivot shift test. B: Demonstration of the posterolateral prominence of the radial head with dimpling of the skin,
consistent with posterolateral rotatory instability. (From Safran MR, Caldwell GL, Fu FH. Chronic instability of the elbow.
In: Peimer CA, ed. Surgery of the hand and upper extremity . New York: McGraw-Hill, 1996:478, with permission.)
Radiographs can often show the posterolateral subluxation. Lateral radiographs show that the ulna is rotated off the
distal humerus and the radial head is rotated with the ulna so that it rests posterior to the capitellum ( Fig. 54.11). The
normal radioulnar relationship differentiates this from radial head subluxation or dislocation in which the radial head is
displaced but the ulnohumeral joint is normal. MRI and arthrography have not been shown to be of benefit in aiding the
diagnosis, although stress radiographs may be of benefit. Stress radiographs of the posterolateral pivot shift may show
the above-noted findings (Fig. 54.11).
FIGURE 54.11. Lateral radiographs of a cadaver elbow after sectioning of the lateral ulnar collateral ligament. A: Without
stress at approximately 90 degrees of flexion. B: Radiograph with axial compression, valgus stress, and supination
(lateral pivot-shift test) at 45 degrees of elbow flexion resulting in posterolateral subluxation. Note that the ulnohumeral
articulation is not concentric, while the radial head is posteriorly subluxated in B. This is contrasted with isolated radial
head subluxation, in which the radial head is subluxated, yet the ulnohumeral articulation is normal. (From Safran MR,
Caldwell GL, Fu FH. Chronic instability of the elbow. In: Peimer CA, ed. Surgery of the hand and upper extremity. New
York: McGraw-Hill, 1996:479, with permission.)
No nonoperative treatment regimen has been provided in the reports that describe this entity. Morrey and O'Driscoll note
that in their experience, nonoperative treatment has not been successful, and this problem markedly interferes with the
patient's daily function ( 74). They do note that activity modification and a hinged brace with forearm pronation and an
extension block may help patients nonoperatively, although they note that few patients are content with this option.
Surgical treatment reattaches the avulsed LUCL ligament or reconstructs it with a free tendon graft to the lateral
epicondyle, similar to reconstruction of the medial UCL. Because the annular ligament is reported to be intact in these
patients, radioulnar dislocation does not occur, and surgery on this ligament is not indicated ( 74). If the condition is
diagnosed acutely, repair of the lateral UCL may be performed ( 75) (Fig. 54.12).
FIGURE 54.12. Radiograph of a snowboarder who fell on his outstretched hand. A: Acute posterolateral rotatory
instability was diagnosed, suggested radiographically by this lateral condyle avulsion fracture. B: The lateral ligament
complex was repaired acutely with suture anchors. This radiograph shows the elbow 6 months after primary repair for
posterolateral rotatory instability.
Olecranon Fracture
The olecranon is a final link in delivering force from the triceps mechanism to enable elbow extension. Fractures of this
process have some intraarticular component; therefore, the hallmark of olecranon fractures combines joint effusion and
loss of active elbow extension. Because ulnar neuropathy may accompany this injury, a good neurologic examination is
imperative. There is no accepted classification of these fractures that is considered useful to predict the outcome or
guide in the management of these injuries.
Nondisplaced fractures are treated with cast immobilization at 40 degrees of flexion for 2 weeks. These patients must be
able to demonstrate the ability to actively extend the elbow against gravity. Active motion may then begin, although full
flexion is discouraged until 6 weeks. Weekly radiographs are necessary for the first 4 weeks to confirm that the fracture
has not been displaced.
Noncomminuted fractures with more than 2 mm of articular displacement are treated surgically. Elbows that are stable to
ligament testing are usually fixed with the tension band wire technique, because this allows for early active range of
motion. Comminuted fractures with no elbow instability are usually treated with open reduction and internal fixation with
reconstruction plates and screws. Fractures associated with ligament instability are usually treated with open reduction
and internal fixation (tension band technique or plates and screws) with ligament repair or reconstruction. External
fixation is occasionally recommended in this situation as well.
Excision of the fracture fragment and reattachment of the triceps has been occasionally recommended in the treatment of
olecranon fractures (76). However, this option is usually not recommended in the athlete since An and Morrey have
shown that with serial excision of the olecranon (25%, 50%, 75%, 100%), there is a near-linear decrease in elbow
stability provided by the ulnohumeral joint in both 0 degrees and 90 degrees of flexion ( 8). See posterior elbow pain
section for discussion on olecranon apophyseal injuries.
Radial Head
Radial head fractures are common in athletes, especially in the adult population. They occur in 5% of all fractures and a
third of all elbow fractures ( 77,78). The typical mechanism of injury is a fall onto an outstretched hand, which transmits
force to the elbow. They can also occur concomitantly with elbow dislocations. Fractures of the radial head and neck may
be associated with injuries of the distal radioulnar joint, interosseous membrane, and nerve injuries. The Mason
classification of radial head fractures has proven helpful as a guideline for treatment ( 79). A type 1 fracture is a
nondisplaced fracture involving less than 25% of the radial head. Type 2 fractures are marginally displaced, including
angulation, impaction, or depression, although the degree of displacement is not defined. Type 3 fractures involve the
entire radial head and are comminuted. Type 4 fractures are any radial head fracture associated with ulnohumeral
dislocation.
Treatment of type 1 fractures is nonsurgical and includes splint support and early range-of-motion exercises. Joint
aspiration and instillation of a long-acting anesthetic may facilitate early motion. Simple sling immobilization, followed by
motion as tolerated by the patient, is the preferred mobilization regimen. Some degree of limitation of motion is to be
expected, with loss of extension of 10 degrees common ( 80).
Multiple options are reliable for management of Mason type 2 fractures, which include (a) splinting and early range of
motion, (b) open reduction and internal fixation, and (c) excision of the radial head. The final outcome for the
above-mentioned treatment methods are about the same. Surgery is necessary if displacement of more than 2 mm is
present; however, many surgeons treat these fractures nonoperatively because late resection of the radial head is equal
to early excision (81). To avoid complications of myositis ossificans, internal fixation should be carried out within the first
48 hours when possible, otherwise it is recommended to wait 3 to 4 weeks after injury before considering removal of the
radial head. Open reduction and internal fixation with either Herbert screws or cannulated interfragmentary screws is best
achieved when at least 50% of the radial head remains intact to provide a stable internal fixation platform. However, it
should be noted that open reduction and internal fixation are demanding procedures that require meticulous technique
and special instrumentation.
Mason type 3 fractures usually require excision of the radial head, although open reduction and internal fixation should
be undertaken, if possible. In the past, an anconeus approach was popular, but recently, a direct lateral approach to
spare the LUCL is favored.
A Mason type 4 fracture associated with an elbow dislocation is a complex problem, and controversy exists as to the best
treatment. If the radial head is comminuted, excision should be contemplated; however, if open reduction and internal
fixation is feasible, the radial head should be retained. Generally, the prognosis for return to sports at the same level of
activity with Mason type 4 injuries is poor ( 82).
If there is wrist pain or distal radioulnar joint pain in conjunction with a Mason type 2, 3, or 4 radial head fracture,
attempts should be made maintain the length of the radius during healing of the soft tissues, particularly the interosseous
membrane. Thus, internal fixation should be attempted when practical. If the bone does not heal or a malunion or arthritis
develops, the radial head may be excised later with satisfactory results. However, if open reduction and internal fixation
is not feasible, then temporary placement of a Silastic (Dow-Corning Wright, Arlington, TN) or metallic radial head
implant should be considered. Temporary placement of the prosthetic implant as a spacer while the interosseous
membrane heals may prevent long-term distal radioulnar joint dysfunction and pain. Removal of the Silastic implant after
2 to 3 months is recommended. Permanent Silastic implants may cause synovitis and possibly osteolysis, and thus are
not a good option for the athlete.
Any surgical treatment of radial head fractures may require additional procedures, including medial collateral or radial
collateral ligament repair and/or reduction of ulnohumeral dislocation.
Distal Humerus Fracture
Distal humerus fractures are severe injuries that, fortunately, are uncommon in athletes. These are usually high-energy
injuries that are due to a direct injury or fall on an outstretched hand. These fractures may be intraarticular or
extraarticular. Extraarticular and intraarticular fractures that are nondisplaced may be treated by nonoperative means.
Displaced intraarticular fractures are usually treated by open reduction and internal fixation with plates and screws. Other
alternative methods of treatment include traction, limited open reduction and internal fixation, external fixation, and
arthroplasty. There is a high incidence of elbow stiffness after this injury and any treatment, as well as the risks of fixation
failure, malunion, nonunion, infection, and ulnar nerve injury.
Supracondylar Humerus Fracture
Supracondylar fractures are the second most common fracture encountered in the pediatric age group ( 83). They are
basically classified into two types: extension and flexion. The extension types are usually produced by extension injuries
(i.e., fall onto outstretched hand) in which the distal fragment is pulled proximally and posteriorly by the pull of the triceps
(Fig. 54.13). The much less common flexion type is produced from a direct injury to the back of the elbow. Clinically, it is
important to distinguish supracondylar humerus fractures from pure elbow dislocations. In supracondylar fractures, the
normal triangular anatomic relationship between the medial and lateral epicondyle and the olecranon process does not
change, which is not the case in elbow dislocations.
FIGURE 54.13. Supracondylar humerus fracture—diagram showing muscular forces displacing the fracture.
Treatment of displaced supracondylar humerus fractures in the pediatric age group is fraught with potential problems.
Treatment is based on the neurovascular status of the distal extremity and the ability to maintain the alignment of the
fracture fragments. Generally, gentle closed reduction (using skin traction, gentle manipulation or skeletal traction
through the olecranon) followed by cast immobilization is adequate. However, if the reduction cannot be maintained or if
neurovascular compromise is present, percutaneous or open surgical treatment may be indicated. Risks include
compartment syndrome, brachial artery laceration or thrombosis, loss of motion, cubitus varus, and risks of surgery,
including pin tract infections and nerve injury.
Medial Epicondyle Fracture
This may be an acute injury or may be the result of a repetitive overuse injury. Skeletally immature overhead throwing
athletes may develop an injury to the medial epicondylar growth plate. The spectrum of growth plate injuries to the medial
epicondylar apophysis includes widening of the growth plate to frank fracture and separation of the apophysis from the
distal humerus. A full discussion of this spectrum of injury is included in the medial elbow pain section.
TREATMENT OF OVERUSE INJURIES
Treatment of overuse injuries should always start with prevention, which saves time, effort, money, and other resources.
Prevention should include education, overall flexibility, strengthening and endurance, proper warmup and stretching, and
avoidance of fatigue (84,85,86 and 87). To this end, adolescents are limited in the number of innings pitched and number
of pitches thrown, which has reduced the incidence of permanent disability. Proper mechanics and equipment are also
important. It has been shown that throwing an object with the shoulder at 90 degrees of abduction results in a greater
force on the medial elbow than throwing with the shoulder at 135 degrees ( 88). The harder one throws, the greater the
torque that develops because the forearm lags further behind the arm at ball release with greater resultant forces on the
medial elbow. Nirschl showed that proper equipment and technique are important factors in tennis elbow, as will be
elucidated later ( 89,90 and 91). Lastly, many sports medicine physicians advocate icing then stretching after throwing as
an important technique in prevention of injury ( 85).
Once an athlete develops an overuse injury, an aggressive nonoperative program is begun. The acronym PRICEMM
(Table 54.3) makes remembering it easy. First, protect the elbow from further injury. Rest the elbow from the offending
event, but allow the athlete to continue maintaining cardiovascular fitness. The elbow is iced, compressed with an elastic
bandage, and elevated. NSAIDs are quite successful at relieving the pain and inflammation. Several modalities such as
high-voltage galvanic electrical stimulation and iontophoresis have proven helpful as well ( 92).
TABLE 54.3. AGGRESSIVE NONOPERATIVE PROGRAM (PRICEMM)
A rehabilitation protocol should be instituted after the acute symptoms have resolved, and there should be a gradual
return to activity. Changes in technique are often required, especially in recurrent cases. When patients have not found
relief with a quality rehabilitation program, and have constant pain without activity, pain that affects activity, persistent
weakness, or atrophy or dysfunction, then surgery may be indicated. Many surgical techniques for the different chronic
tendinopathies have been described, but the common salient features include identification and excision of the
pathologic tissue and use of the adjacent normal tissue to close the defect, frequently after abrading underlying bone to
allow fresh scar to heal. This allows the body's healing response to close the defect with healthy scar tissue that can
withstand the repetitive stress that the weakened, abnormal tendon could not withstand. After the surgery, the tissue is
protected, and graded postoperative rehabilitation is performed before returning to sports to allow the scar tissue to
remodel and mature to resemble normal tendinous tissue architecture.
ANTERIOR ELBOW PAIN
The differential diagnosis of pain in the anterior elbow is extensive with only a few differing mechanisms ( Table 54.4).
Anterior elbow injury is usually due to stretch or tear of the anterior capsule, distal biceps, or brachialis tendons with or
without dislocation. This occurs from a fall on an extended elbow, pulling up or resisted elbow flexion, repetitive forceful
supination, hyperextension, or a direct blow.
TABLE 54.4. SITES AND SOURCES OF ELBOW PAIN
Climber's Elbow
Climber's elbow is defined as a strain of the brachialis tendon and can be confirmed by electromyography (EMG) ( 93).
However, some still believe that this is an injury to the anterior capsule or distal biceps tendon. This injury occurs in
association with repetitive pull-ups, hyperextension or repeated forceful supination, or occasionally from violent extension
against a forceful contraction (extrinsic overload). There often is pain with full elbow extension, resisted supination, and
elbow flexion, which may also limit flexion or supination strength. Treatment is based on the PRICEMM protocol, with rest
from throwing or climbing activities and an emphasis on early range of motion, especially extension. Slow steady
improvement is typical.
Distal Biceps Tendinitis
Tendinitis involving the distal biceps tendon is a rare entity. This injury occurs in association with repetitive pull-ups and
elbow flexion, hyperextension or repeated forceful supination, or occasionally, from violent extension against a forceful
contraction (extrinsic overload). Generally, however, this is considered an overuse syndrome. The bicipital tuberosity of
the radius may produce friction and inflammation of the biceps tendon, resulting in anterior elbow pain. Often, there is
pain with resisted supination or elbow flexion with reduced strength secondary to pain. Treatment is based on the
PRICEMM protocol, with rest from weight lifting, throwing, or climbing activities, and an emphasis on early range of
motion. Slow, steady improvement is typical, and surgical intervention is rarely warranted.
Distal Biceps Tendon Rupture
Distal biceps tendon rupture is a rare injury, representing only 3% of all biceps ruptures ( 94). It has been estimated that
the incidence of complete distal biceps tendon ruptures is 1.2 per 100,000 in the general population ( 95). The majority of
distal biceps tendon ruptures are complete, although partial tears have been reported ( 96,97 and 98). Untreated partial
tears may become complete ruptures (96). The mechanism is sudden, forceful overload, with the elbow near midflexion
(99,100). There is usually preexisting degenerative change within the tendon due to friction and erosion of the tendon
from repetitive rubbing against the bicipital tuberosity, although hypovascularity within areas of the distal portion of the
tendon may also be an etiologic factor ( 99,101). Despite the degenerative change within the tendon insertion, most
patients have no prior complaints related to the elbow or biceps tendon. The onset is sudden and usually there is no
history of prodromal symptoms (99). Localized pain and tenderness at the bicipital tuberosity, proximal displacement of
the distal biceps tendon with a bulge, and marked weakness of forearm supination and elbow flexion are usually present.
The pain and tenderness quickly subside, but a dull ache may persist for weeks. Ecchymosis is present in the antecubital
fossa 48 to 72 hours after the injury.
Treatment for partial ruptures usually begins with PRICEMM. Splinting or bracing may be used initially until pain and
inflammation subsides. This is followed by a stretching and strengthening program. If symptoms persist, surgical
exploration with debridement or reinsertion of the tendon into the radial tuberosity may be indicated ( 96,98).
Current treatment of complete ruptures is primary repair using the two-incision Boyd-Anderson technique ( 102,103). This
technique allows for reinsertion of the biceps tendon to restore power while reducing the risk of radial nerve injury. Some
authors recommend a single-incision surgical technique with suture anchors or endo button to help reduce the morbidity
of two incisions and hasten the surgical time, while reducing the risk of nerve injury ( 104). Recent biomechanical studies
suggest that transosseous sutures fail at a significantly higher load than suture anchors and that the anchors may
protrude from the bone (105). The anchor protrusion out of the tuberosity during cyclic loading may potentially result in a
gap at the repair site and interfere with forearm rotation ( 105). There are no published large series evaluating the results
of a single-incision technique using suture anchors, the recently discussed endo button ( 106), or comparing the results
with other surgical techniques in the treatment of distal biceps ruptures. Nonoperative treatment can be expected to yield
strength deficits of 30% in flexion and 40% in supination, whereas immediate repair results in near-normal strength ( 107).
Nonoperative treatment results in weakness, fatigue, pain, and disability, particularly with supination activities ( 100,108).
Subjective results of operative treatment have been reported to be good to excellent in up to 98% of patients ( 109). A
meta-analysis of treatment of distal biceps tendon ruptures revealed 90% good to excellent results with anatomic repair
and reinsertion at 3 years, as compared with only 60% good to excellent results at the same time period for nonanatomic
reinsertion, and only 14% for patients treated nonoperatively ( 110). Repair should be performed acutely, although
excellent results have been obtained after anatomic reinsertion 3 years after injury ( 110).
Ectopic Bone
Ectopic bone occurs after a traumatic blow to the anterior arm. It tends to occur within the brachialis muscle 3 weeks after
injury. Prevention with indomethacin and early range of motion is of paramount importance. Once the ossification begins,
indomethacin is of little benefit. Persistent symptoms that inhibit activity can be treated with excision after the ossification
has completed (technetium diphosphonate scan normalizes). See section on elbow dislocation earlier regarding the
treatment of this problem.
Pronator Syndrome
Anterior elbow pain may be a result of median nerve entrapment. The pronator teres syndrome results from median nerve
compression between the two heads of the pronator teres muscle with pronation, or under the lacertus fibrosis, ligament
of Struthers, or the fibrous arcade at the flexor digitorum superficialis (FDS) muscle. Patients with this syndrome usually
report radiating anterior forearm pain and occasionally numbness and tingling in the distribution of the median nerve. On
examination, these patients have increased pain with active pronation, passive supination, or resisted long finger flexion.
The Tinel sign may be present at the pronator muscle, and there may be weakness of the abductor pollicis brevis (APB)
and flexor pollicis longus (FPL) muscles (not seen with carpal tunnel syndrome). Decreased sensation in the distribution
of the median nerve may be present. Nerve conduction velocity testing frequently is positive. Treatment for this syndrome
is rest, NSAIDs, and therapy to strengthen the flexor-pronator muscle group and improve upper extremity range of
motion. If this is unsuccessful, surgical release may be necessary.
Annular Ligament Disruption
Disruption of the annular ligament is a rare cause of anterior elbow pain. This injury is often associated with radial head
subluxation or dislocation. The mechanism of this injury is usually forceful flexion against resistance. These athletes
report popping in their elbow with forceful flexion or supination. The diagnosis is made by radiographs or provocative
testing such as the posterolateral rotatory apprehension test (see below under lateral elbow pain ) (71). Treatment is
surgical fixation of the ligament back to bone.
MEDIAL ELBOW PAIN
A wide variety of problems cause medial elbow pain (Table 54.4). Because throwing imparts valgus stress to the elbow,
the medial elbow absorbs these tensile forces, causing injury to the soft tissues of the medial elbow and the bony tissues
of the lateral compartment (discussed earlier). The exception to this is the immature athlete—the physis is the weakest
link in the adolescent musculoskeletal system and thus is most susceptible to injury ( 111).
Medial Epicondylar Physeal Injury
Medial epicondylar physeal fracture can be a stress fracture or overt fracture due to repeated valgus stress, fall, or
repetitive violent forearm flexor muscle contraction in the skeletally immature athlete. Owing to repetitive valgus stress
from throwing, the medial epicondylar physis undergoes accelerated growth, followed by separation and eventual
fragmentation (Fig. 54.14) (112, 113). These children report pain with throwing, and their throwing effectiveness and
distance are reduced. Point tenderness can be elicited over the medial epicondyle. Frequently, these children have a
flexion contracture of more than 15 degrees based on muscular tightness and occasionally on capsular tightness as well,
although usually not as a consequence of bony impingement. Radiographically, the medial epicondylar physis appears
widened and occasionally fragmented when compared with the contralateral elbow ( Fig. 54.15). This finding may be
normal in throwing athletes ( 114). The treatment of the stress fracture or inflammation of the apophysis is rest from
throwing for 4 to 6 weeks, along with the application of ice (place a wet towel between the ice and the elbow to prevent
injury to the ulnar nerve) and the administration of NSAIDs to reduce the acute inflammation. After cessation of
symptoms, a strengthening rehabilitation program and gradual throwing program is instituted.
FIGURE 54.14. Medial epicondylar apophysitis and avulsion occur due to repeated stress from the ulnar collateral
ligament (arrow) and flexor-pronator muscle forces.
FIGURE 54.15. Thirteen-year-old baseball pitcher with medial elbow pain. A: Left (normal) elbow. B: Right, throwing
elbow showing widening of the medial epicondyle physis.
Progression of the apophysitis may result in a complete fracture or separation of the medial epicondyle. The avulsion
fracture of the medial epicondyle, however, may occur without prodromal symptoms of apophysitis due to a more severe
valgus force or violent muscle contraction. Fracture through the physeal plate can have two distinct patterns, as
described by Woods ( 115,116). A type 1 fracture occurs in the younger child and is characterized radiographically by a
large fragment, involving the entire epicondyle. This fragment is often displaced and rotated anteriorly and distally, and
may even become entrapped in the joint. Type 2 fractures occur in the adolescent and are radiographically notable for
medial epicondylar fragmentation with a small fracture fragment. The flexor-pronator muscle is essentially avulsed;
however, the anterior oblique ligament is usually intact ( 115,116). Treatment of this entity depends on elbow stability as
determined by the gravity stress test (Fig. 54.16). With the patient supine, the shoulder is brought into maximal external
rotation with the sagittal plane of the elbow parallel to the floor. With no support under the forearm, the weight of the
forearm is resisted only by the flexor-pronator muscle group and the UCL (particularly the anterior oblique ligament). A
standard radiograph is taken of the elbow. If the fragment of bone moves distally and the joint gaps open medially, the
elbow is defined as being unstable. Radiographs may show only minimal displacement without stress and thus may be
unreliable without stress views. Stable elbows and nondisplaced fractures are treated with rest for 2 to 3 weeks, with
return to throwing by 6 weeks after attaining full motion. Unstable elbows are treated by open reduction and internal
fixation with wires, pins, or screws. Furthermore, if the medial epicondyle is displaced greater than 1 cm, then it should be
pinned anatomically (Fig. 54.17) (117,118). Although selection of the distance of 1 cm is somewhat arbitrary, it is easy to
see how malunion of this fracture could lead to functional medial ligamentous laxity, which would be expected to be
symptomatic in a throwing athlete. Therefore, we recommend aggressive management to obtain adequate reduction. In
nonthrowing athletes or for the nondominant elbow, some authors recommend surgery only if displacement is 2 cm or
more.
FIGURE 54.16. Gravity stress test. Anteroposterior radiograph of the elbow taken in the supine position to allow the
weight of the arm to show ulnar collateral ligament insufficiency by increased distance in the radiocapitellar joint. (From
Safran MR. Elbow injuries in athletes. Clin Orthop 1995;310:257–277, with permission.)
FIGURE 54.17. Medial epicondylar avulsion fracture. A: Displaced medial epicondyle fracture. B: Fracture fixed with
internal fixation.
Occasionally the medial epicondyle fragment may become entrapped within the elbow joint with dislocation. Closed
manipulation with valgus stress and wrist extension can free the fragment and sometimes obviate the need to open the
elbow. Alternatively, an injection of air from the lateral joint may move the fragment out of the joint ( 117,119). Minimally
displaced medial epicondyle injuries can usually be managed closed. If surgery is required to manage this problem, UCL
evaluation is also performed and the ligament is repaired as needed.
Medial Epicondylitis
Medial epicondylitis is a tendinosis of the flexor-pronator muscle group. This entity primarily involves the pronator teres
and flexor carpi radialis (FCR) muscles, and occasionally the flexor carpi ulnaris (FCU) ( 120,121). These muscles are
susceptible to inflammation and injury due to repetitive valgus stress, resulting in overload from both extrinsic and
intrinsic forces. The flexor-pronator muscles are subjected to significant extrinsic forces. Because the muscles span two
joints, they are exposed to increased stretching associated with valgus forces at the elbow and intrinsic forces from
muscular contraction.
Medial epicondylitis is a much less common entity compared with lateral epicondylitis, occurring at a ratio of 1:7 to 1:20
(120,122). Medial epicondylitis, like lateral epicondylitis, seems to occur within the fourth and fifth decades of life
(120,121). Three of the more common types of athletes that develop medial epicondylitis are golfers, tennis players, and
baseball pitchers. In golfers, the trauma is induced by repeatedly hitting behind the ball (called hitting it fat), imparting
large amounts of stress to the medial structures. Conversely, it is noted in advanced tennis players who forcibly extend
their wrist while striking the ball on overheads and serves. The etiology in pitchers was discussed earlier in biomechanics
section. These patients occasionally note swelling of the medial elbow. The most consistent complaint is medial elbow
pain that is worse with throwing, serving, or hitting a forehand. These athletes are tender over the medial epicondyle and
have increased pain with resisted wrist flexion or pronation, as well as with passive wrist extension. Approximately 60%
of athletes with medial epicondylitis have associated ulnar nerve symptoms ( 88,121,123,124).
Treatment is conservative (PRICEMM). Recalcitrant cases may require a local injection with corticosteroids at the site of
maximal tenderness, which provides pain relief in the short term. ( 125). Care must be taken to not inject into the tendon
or ulnar nerve owing to the risk of tendon rupture or nerve damage. Once the symptoms have abated with relative rest,
ice, antiinflammatory medications and modalities, a systematic regimen of strengthening exercises are initiated. As
strength improves, a counterforce brace is applied and sports resumed. However, the patient is advised to seek
professional advice to improve the biomechanics of the desired sport. It is important to discuss with the athlete that the
treatment is the exercises, not an injection or medications. Most patients (85% to 90%) respond to nonoperative
management. (92,120,121,122 and 123,126). If symptoms persist after at least 10 weeks with the PRICEMM protocol,
surgical treatment may be necessary. Surgery entails release of the flexor origin with excision of granulation tissue,
roughening the bone at the medial epicondyle to stimulate bleeding, and reconstruction of the medial musculotendinous
unit, thus reinstating a good vascular bed to induce healing ( 121,127). Care must be taken to not damage the UCL during
surgery. Results with surgical treatment reveal 97% subjectively good to excellent results and 86% of patients without
limitation in elbow use at an average 7 years of follow-up ( 126). The results are not as good when there is associated
ulnar neuropathy (123). Results with just release of the muscles from the medial epicondyle are not as good. One report
of 38 patients found that there was only 69% good to excellent results for medial release when the injury was not
associated with ulnar nerve symptoms and much worse when associated with ulnar nerve symptoms and an ulnar nerve
release was performed (124). Exploration of the UCL at the time of surgery is indicated if the patient is a throwing athlete
and clinical examination is suggestive of elbow instability.
Flexor-Pronator Muscle Group Disruption
Disruption of the flexor-pronator muscle group is more common than that of the extensor muscle group, even though
epicondylitis is more common on the lateral side. This uncommon injury occurs during forceful extension of the elbow and
pronation of the forearm, although it may also occur with forceful valgus stress. Norwood found that the flexor-pronator
muscle group ruptured in all for of his patients with acute UCL tears, whereas Conway found a 13% incidence of
flexor-pronator muscle rupture near its origin on the medial epicondyle ( 49,128). The history usually reveals sudden
onset of pain along the medial epicondyle, although pain may be insidious with partial ruptures. Patients are tender at the
medial epicondylar origin of the muscle and have pain that is worse with wrist flexion. Complete rupture is associated
with weakness of wrist flexion. A palpable gap in the tendon may be felt, while a bulge may be felt in the proximal
forearm. Radiographs (including stress radiographs) are normal although some calcific deposits may be identified in the
tendon. Surgical reattachment is mandatory because the common flexor origin is an important stabilizer for the medial
elbow. However, repair is difficult and rarely restores competitive function.
Snapping Triceps
An unusual cause of elbow pain is the snapping elbow syndrome. This term is usually applied to the ulnar nerve
snapping out of the cubital tunnel. However, Dreyfuss has reported cases of the medial head of the triceps snapping over
the medial epicondyle ( 129). He reported two surgically proven cases of this problem in patients with ulnar nerve
irritation. The ulnar nerve irritation probably causes the symptoms (see later). Athletes with asymptomatic snapping are
observed because no known adverse sequelae have been identified. With chronic ulnar nerve irritation, detaching and
rerouting the offending portion of the triceps from the medial attachment under the triceps tendon to its lateral attachment
is recommended.
Ulnar Collateral Ligament Injury
Medial elbow pain may result from instability caused by acute or chronic UCL disruption or chronic attenuation of the
ligament. In 1946, Waris was the first to recognize and describe UCL tears, particularly isolated anterior oblique ligament
disruption, in 17 javelin throwers ( 130). Early reports suggested that this is a rare lesion; however, with better
understanding of the problem, it is clear that this is not uncommon in athletes. Patients with acute UCL ruptures report
sudden pain with or without a popping sensation that occurred with throwing, and they are unable to throw after the
injury. Symptoms of ulnar nerve irritation may also occur following acute UCL tears.
Patients with chronic instability from either complete disruption or attenuation of the UCL have pain or soreness along the
medial elbow with throwing. Overuse is the number one cause of UCL injuries in the throwing athlete ( 131). The athlete
may note repeated bouts of medial elbow pain during and after throwing that respond to conservative treatment. These
patients are unable to throw over 75% capacity owing to this pain ( 131). They may note, however, that there is a single
episode of “giving way” or sudden severe medial elbow pain, which is distinct and isolated and represents the final insult.
Many physicians consider injury to the UCL to have four stages: (a) edema and inflammation, (b) dissociation of
ligamentous fibers, (c) calcification, and (d) ossification in many chronic cases. The most common report is of pain at the
acceleration phase of throwing and second most commonly at ball release or point of impact in hitting the ball ( 128).
Owing to the chronic nature of the instability, they may have ulnar nerve irritation or symptoms of medial epicondylitis, or
symptoms of loose bodies.
On physical examination, these patients have point tenderness 2 cm distal to the medial epicondyle, and pain and
instability with valgus stress ( Fig. 54.18). The absence of increased pain with wrist flexion and the location of pain slightly
posterior to the common flexor muscle origin help differentiate this problem from flexor-pronator muscle rupture.
Ecchymosis frequently develops in the medial joint line and proximal forearm 2 to 3 days after an acute injury. With an
incompetent UCL, the medial joint opens with valgus stress and the nerve is stretched. Long-standing fixed flexion and
valgus deformities, as frequently seen in baseball pitchers and tennis players, are static deformities that predispose to
traction neuritis ( 23,132). Examination to determine the functional integrity of the UCL is performed with the humerus
stabilized and a valgus force applied to the elbow, which is flexed 30 degrees.
FIGURE 54.18. Valgus stress test of the elbow. Valgus stress applied to the elbow flexed 30 degrees, palpating the ulnar
collateral ligament for tenderness and opening of the medial joint line. (From Safran MR, Caldwell GL, Fu FH. Chronic
instability of the elbow. In: Peimer CA, ed. Surgery of the hand and upper extremity. New York: McGraw-Hill, 1996:471,
with permission.)
A recently described clinical test called the “milking maneuver” has been developed that produces a valgus stress to the
joint in flexion (Fig. 54.19) (133). The affected elbow is flexed beyond 90 degrees, and the opposite hand of the patient is
placed under the elbow to grasp the thumb of the affected hand, thereby exerting a valgus stress on the UCL of the
affected elbow. The UCL is palpated by the examiner for tenderness and joint line opening during this maneuver
(69,133). This technique of examination is believed to be more sensitive at 90 degrees of flexion based on the increased
valgus rotation of the elbow at 90 degrees compared with 30 degrees when using the normal elbow as the control ( 16).
FIGURE 54.19. Milking maneuver. The patient's contralateral extremity helps lock the shoulder of the elbow being
examined. While pulling down on the thumb of the elbow being examined, a valgus stress is imparted on the elbow and
the examiner palpates the medial joint line of gapping. (From Safran MR, Caldwell GL, Fu FH. Chronic instability of the
elbow. In: Peimer CA, ed. Surgery of the hand and upper extremity. New York: McGraw-Hill, 1996:471, with permission.)
Owing to the fact that the center of the varus-valgus axis is more medial than the midline, valgus stress testing of an
elbow with a disrupted UCL results in less medial joint gapping than if the LCL is injured. Medial joint gapping is usually
only a few millimeters with complete, isolated UCL injuries.
Radiographically, a small avulsion fracture fragment may be identified, confirming the diagnosis. Secondary findings on
plane radiographs suggestive of chronic UCL insufficiency include ossification within the ligament (18%) ( 134), loose
bodies in the posterior or lateral compartments, marginal osteophytes about the radiocapitellar or ulnohumeral
articulations, or olecranon and condylar hypertrophy. If there is no avulsion fragment, instability can be confirmed by
stress radiographs (Fig. 54.20). In the acute setting, however, this may require anesthesia due to patient guarding. A
commercially available stress device has become available to stress the UCL of the elbow at reproducible forces. This
device has been reported to be 94% sensitive and 100% specific in diagnosing UCL tears ( 135). It should be noted,
however, that there is increased laxity of the elbow to valgus stress (nearly 0.5 mm) in the uninjured, asymptomatic
dominant elbow of profession baseball pitchers when compared with their nondominant elbow ( 136). This is in
contradistinction to the lack of difference (up to 0.5 mm) in laxity between the elbows of a general population ( 137,138).
Thus, there may be a continuum of elbow laxity that may be asymptomatic to symptomatic instability when assessing
laxity by the relatively sensitive method. Because of the subtlety of this difference, these injuries may be underestimated
and misdiagnosed initially ( 139). Conway has presented his initial findings of stress radiographic findings in professional
baseball pitchers and found that 2 mm of relative increased laxity and 3 mm of absolute medial joint gapping were
consistent with an incompetent UCL (140).
FIGURE 54.20. Stress radiograph showing rupture of the ulnar collateral ligament complex with valgus instability.
The gravity stress test has been classically used to determine instability of the elbow ( 2,114). The gravity stress test is
performed with the patient supine and the shoulder is brought into maximal external rotation with the sagittal plane of the
elbow parallel to the floor ( Fig. 54.16). With no support under the forearm, the weight of the forearm is resisted only by
the flexor-pronator muscle group and the UCLs (particularly the anterior bundle). A standard radiograph is taken of the
elbow. If the fragment of bone moves distally or the joint gaps open medially, or both, the elbow is defined as being
unstable. An arthrogram may be useful in the acute injury; however, it is of little use in the chronic setting because dye
leakage from the ruptured medial capsule often is not seen in cases of chronic UCL insufficiency. The computed
tomographic (CT) arthrogram has been shown to be quite sensitive and specific for acute and chronic injuries to the UCL
in one study of 25 baseball players ( 141). Its one advantage is in visualizing an undersurface tear of the UCL, a newly
described pathologic entity of the UCL ( 141,142). The role of CT arthrography must still be confirmed and elucidated.
MRI has been of help in identifying torn UCL as well ( 141,143,144). However, more experience is necessary to determine
the true sensitivity and specificity of this tool in diagnosing this injury, and the possible role of intraarticular contrast.
Timmerman et al. have found that the most sensitive and specific way to diagnose UCL disruptions is to visualize the
medial compartment of the elbow arthroscopically while applying a valgus stress at 70 degrees. If the medial
compartment gaps open, UCL insufficiency exists (141). Field and Altchek confirmed that valgus stability of the elbow is
best assessed in 60 to 75 degrees of elbow flexion and was better noted in pronation ( 145). Rupture of the anterior
bundle only resulted in 1 to 2 mm of joint gapping, whereas complete release of the UCL resulted in 4 to 10 mm of medial
joint opening when evaluated arthroscopically ( 145). Thus, imaging studies may help confirm the diagnosis, but the
history and physical examination remain the mainstay for diagnosis.
Treatment consists of aggressive therapy with rest, anti-inflammatory measures, and physical therapy. With this
conservative regimen, Barnes found that 50% of his throwing athletes were able to return to throwing, whereas the other
50% required surgery (132). More recently, Rettig presented his results of nonoperative treatment of 31 UCL injuries in
throwing athletes (146). Nearly two thirds of the athletes were baseball pitchers. Forty-two percent of these athletes were
able to return to their previous level of competition at an average 24.5 weeks (13 to 54 weeks) of conservative
management (146). Jobe gives his athletic patients two cycles of 3 months of rest from throwing and rehabilitation, and if
pain occurs when throwing over 75% capacity, surgery is indicated, although the percentage of his patients succeeding
with rehabilitation is not reported ( 128,147). Rettig manages his patients with 2 or more months of rest from throwing,
upper-extremity strengthening, and bracing. When the athlete is pain free, a throwing program is initiated and advanced
over 1 to 2 months (146).
Surgical treatment for UCL tears has changed. Primary repair of the ligament for acute injuries had been advocated for
many years (49,114,132). Most avulsions were treated by reattaching the ligament to bone through drill holes, whereas
midsubstance tears were repaired primarily ( 49). However, more recently, Conway and Jobe published their data of 70
athletes with acute UCL disruptions and noted that 87% were midsubstance tears, 10% were avulsions from the ulna,
and only 3% were avulsions from the humerus (128). Their recommendation was to perform UCL reconstruction with free
tendon graft in the acute setting except in the few patients who have surgery soon after a proximal UCL tear, with no
ulnar nerve symptoms, and with the remainder of the ligament appearing normal ( 128,147,148). Most surgeons prefer to
perform ulnar ligament reconstruction for acute and chronic injuries as compared with primary repair ( 69). Ulnar nerve
transposition may be performed in conjunction with UCL reconstruction, although there is a significant number of
neurologic symptoms postoperatively (up to 21%) ( 128).
Ligament reconstruction is usually recommended for (a) acute ruptures in throwers; (b) significant chronic instability; (c)
after debridement for calcific tendinitis, if there is insufficient tissue to effect a primary repair in a throwing athlete; and (d)
multiple episodes of recurring pain (with subtle instability) with throwing after periods of conservative treatment.
Results of 56 UCL reconstructions using a palmaris longus free tendon graft reveals 80% good to excellent results at 2 to
5 years, with 68% of the athletes returning to their previous level of competition for more than 1 year ( 128). Though 21%
had postoperative ulnar neuropathies, 40% were transient (all but one patient returned to previous sports activity),
whereas 60% required a second operative procedure for the nerve (almost half returned to previous sports activity) ( 128).
This result has been confirmed by others ( 139). The results of reconstruction of the UCL were not as good when there
had been a previous operative procedure performed on the elbow. Revisions in technique to reduce complications, such
as not transferring the ulnar nerve and splitting the flexor carpi ulnaris muscle mass ( 149), elevating flexor-pronator
tendon without detaching it (139), and fixation of the graft with suture anchors onto bone as compared with tunnels ( 150),
are too recent to allow for critical review. Schwab recommended transfer of the anterior oblique ligament anteriorly and
superiorly when the UCL is present but attenuated ( 19). However, this treatment is not recommended in athletes because
the attenuated ligament is weaker due to microrupture, its position is not functionally isometric compared to its natural
position, and elbow extension tends to be limited by this procedure, which may not be acceptable in the high level
athlete. Synthetic ligament research is continuing, but it is too early to know if this will be successful.
Chronic UCL microtrauma occasionally heals with calcification. These calcifications are to be removed with
reconstruction. It is important to note, however, that these calcifications are within the ligament. Patients with medial
elbow pain and calcifications must be examined closely. These calcifications must not be mistaken for intraarticular loose
bodies. The calcifications are extraarticular, and removal of them without reconstruction of the UCL will render the elbow
unstable.
Ulnar Nerve Injuries
Ulnar neuritis is a common cause of medial elbow pain in athletes owing to its superficial location at the cubital tunnel
and its unfavorable response to valgus stresses. There are many possible causes for ulnar neuritis to which the athletic
population is susceptible. However, owing to the intensity of sporting activities and the biomechanics involved, the athlete
tends to develop ulnar nerve irritation from mechanical sources—compression, traction, and friction. Entrapment or
dislocation of the nerve is seen most often in throwing athletes and gymnasts. This population includes baseball players,
tennis players, javelin throwers, and football quarterbacks. Nordic skiing has also been implicated owing to the repetitive
elbow extension and forearm pronation motions (151).
Compression can occur proximal to the cubital tunnel owing to a tight intermuscular septum or hypertrophy of the medial
head of the triceps or anconeus epitrochlearis muscle ( 152,153 and 154). Compression can occur at the level of the
cubital tunnel due to osteophytic spurs, loose bodies, synovitis, or thickening of the arcuate ligament or chronically
inflamed UCL (152,155,156). It has been estimated that approximately 60% of patients with medial epicondylitis have an
associated compressive ulnar neuropathy (88,124). Biomechanically, during flexion, the ulnar nerve elongates an
average of 4.7 mm and can be pushed over 7 mm by the medial head of the triceps ( 155,157). As a result, with flexion
the cubital tunnel narrows 40% to 55%, resulting in compression ( 157,158). Distal to the cubital tunnel, compression can
occur between the two heads of the FCU muscle. This distal site is the most common area of compression of the ulnar
nerve. Traction neuritis can occur due to the valgus forces that occur with throwing. With an incompetent UCL, the medial
joint opens with valgus stress and the nerve is stretched. Long-standing fixed flexion and valgus deformities, as
frequently seen in baseball pitchers and tennis players, are static deformities that predispose the patient to traction
neuritis. Friction neuritis develops from subluxation or dislocation of the nerve owing to congenital or developmental
laxity of the soft tissue restraints that normally hold the ulnar nerve in its groove at the cubital tunnel. Recurrent
dislocation of the ulnar nerve at the elbow has been noted in 16% of the population ( 159). The nerve may become
tethered in an irregular ulnar groove from degenerative changes or old medial epicondylar separation, scar formation,
traction spurs, or calcific deposits in or around the UCL ( 160,161 and 162). It is very likely that in many athletes, the
cause of the ulnar neuritis is multifactorial. Pechan demonstrated elevation of pressures within the ulnar nerve three
times that of normal with the elbow flexed at 90 degrees and the wrist extended ( 158,163). This elevation of intraneural
pressure is believed to be due to the physiologic stretch of the nerve combined with compression by the FCU
aponeurosis (164). With further flexion of the elbow, extension of the wrist and abduction of the shoulder, as occurs with
throwing, this pressure can be elevated to as much as 6 times the resting intraneural pressure ( 163,165). The end result
is fibrosis from direct injury and possibly ischemia of the nerve due to prolonged or repeated elevation of pressures ( 164).
The athlete with ulnar neuritis may have symptoms similar to those in the general population with ulnar neuritis. In the
athlete, however, the earliest symptoms are often medial joint line pain or clumsiness or heaviness of the hand and
fingers associated with or exacerbated by throwing or overhead activity. The patient may report numbness and tingling in
the little and ring fingers, often at first only with overhead activity. Weakness of the FCU and flexor digitorum profundus
(FDP) is uncommon owing to the deep location of these nerve fibers in the tunnel ( 166). Medial elbow pain may radiate
down the ulnar side of the forearm to the hand. Reports of a painful snapping or popping sensation with rapid elbow
flexion and extension and sharp pains may predominate when their symptoms are due to recurrent nerve dislocation.
Symptoms improve or may disappear with rest but recur with increasing frequency with resumption of activity. On
examination, the nerve may feel thickened or doughy and can often be manually moved out of its groove ( 164). There
usually is tenderness when palpating the nerve within the cubital tunnel. The Tinel sign at the cubital tunnel is often
present, while the elbow flexion test may also be positive ( 167). Late physical findings, unusual to see in athletes
because their performance is affected much sooner, include sensory changes (hypoesthesia in the ulnar hand with or
without diminished two-point discrimination of the little and half of the ring finger) and/or motor weakness and atrophy
(interosseous wasting and loss of fine intrinsic muscle control). A complete series of elbow radiographs should be taken,
including the cubital tunnel view to rule out bony pathology ( 168). EMG is helpful, if positive, and correlates with severity
(160). When the diagnosis is in doubt, a dynamic EMG may be performed. Postoperative nerve conduction velocities are
helpful to follow recovery when compared with preoperative evaluation, if the findings are abnormal ( 169).
Treatment of acute cases of ulnar neuritis, in which symptoms are not yet severe and intrinsic atrophy is not present, may
respond well to conservative management (PRICEMM) (164). Rest and ice should be applied, along with immobilization
of the elbow in a splint for 2 to 3 weeks (particularly if the etiology of the neuritis is subluxation or dislocation).
Antiinflammatory medications are also useful. Steroid injection into the cubital tunnel is not recommended. Review of the
biomechanics of the event and correction of poor technique may help prevent recurrence. Indications for surgery for ulnar
neuritis include persistent ulnar nerve subluxation or dislocation, symptomatic tension neuropraxia, and intractable
hostile environment for the nerve. Surgical management of the problem may also be indicated when concomitant medial
elbow surgery is being performed for other problems that may or may not be related to the neuritis.
Surgical options for ulnar neuritis include simple decompression, medial epicondylectomy, anterior subcutaneous nerve
transposition, and anterior submuscular transposition. Simple decompression of the cubital tunnel has been advocated
because it leaves the nerve branches and vessels intact while relieving the compressive forces overlying the nerve.
However, the results of simple decompression are not as good as other procedures ( 124,153). The traction forces are not
eliminated in the overhead athlete, and the procedure may not address pathology within the cubital tunnel ( 158). Last,
this procedure may produce subluxation of the nerve in throwers, resulting in more symptoms ( 170). Medial
epicondylectomy is popular in the general population owing to the ease of the procedure; however, this procedure is not
recommended in athletes owing to the vulnerability of the origin of the UCL and the anatomic changes that take place
when reattaching the flexor-pronator muscle mass ( 171). This technique also allows for the nerve to sublux with throwing
(170). Anterior subcutaneous transposition is appealing because it avoids the morbidity of detaching and reattaching the
common flexor origin. Yet, the major disadvantage of this procedure is the vulnerability of nerve to direct trauma and
nerve instability due to its subcutaneous and unprotected location. A fascial sling is often recommended to prevent
subluxation into the nerve's previous location; however, the sling can be a site of compression or tethering. Anterior
submuscular transposition places the ulnar nerve deep to the flexor-pronator muscle mass. In this position, the nerve is
protected from both direct and indirect trauma during athletic activities and provides stable fixation preventing
redislocation ( 160), while providing a vascular bed with less scarring around the nerve ( 170). This approach also allows
for inspection of the UCL and possible arthrotomy for concomitant osseous problems such as loose bodies or
osteophytes when indicated. If the UCL is torn, repair or reconstruction is mandatory, otherwise surgical treatment of
ulnar neuritis will fail when the athlete returns to sports. Sixty-eight percent of throwing athletes returned to their previous
level of competition following isolated submuscular transposition of the ulnar nerve ( 170). The major disadvantage with
this procedure is the prolonged postoperative physical therapy necessary because the flexor-pronator group is detached
and reattached. Furthermore, there is a risk of medial epicondylitis developing because the flexor-pronator
musculotendinous unit must heal before throwing can begin.
The author's preference is to perform an anterior subcutaneous transposition for throwing athletes to avoid disrupting the
flexor-pronator origin and to perform an anterior submuscular transposition for athletes involved in contact sports.
Technical points of the transposition include (a) release proximally of the arcade of Struthers, (b) resection of a portion of
the intermuscular septum where the new course of the nerve lies, (c) preservation of the elbow articular branches of the
ulnar nerve, and (d) preservation of the motor branches to the flexor carpi ulnaris. If a subcutaneous nerve transposition
is performed, a fascial sling is made to prevent subluxation of the nerve. Postoperative management depends on the
method of ulnar nerve surgery performed.
POSTERIOR ELBOW PAIN

Fewer sources account for pain in the posterior part of the elbow ( Table 54.4). The triceps musculotendinous unit and the
olecranon are overloaded in activities that require repetitive forceful extension of the elbow. These activities include
racquet sports, baseball pitching, gymnastics, shot-putting, javelin throwing, and weight lifting. It is helpful to divide
posterior problems into musculotendinous unit overload (olecranon apophysitis, olecranon stress fracture, triceps
tendinitis and rupture) and bony problems (olecranon osteophytes and impingement, loose bodies combined with UCL
laxity, known as valgus extension overload syndrome), as well as the common olecranon bursitis.
Olecranon Apophysitis
In the skeletally immature individual, the physeal plate is the weakest link in the musculoskeletal system. Abnormal
stresses of the triceps attachment on the olecranon apophysis can result in a syndrome similar to Osgood-Schlatter
disease. This intrinsic overload can lead to separation of the olecranon secondary ossification center ( 172). This injury
may also occur as a result of valgus extension overload and has been reported in a baseball pitcher ( 173,174). These
adolescents complain of pain on resisted elbow extension and have tenderness over the olecranon. Radiographically,
this traction apophysitis of the olecranon may show widening of the physis.
Initial management of this problem, in which the physis is widened but not separated or avulsed, is rest from the
offending sport and throwing, in association with range-of-motion, flexibility, and eventually strengthening exercises. Ice
and antiinflammatory medications are also recommended if acute inflammation is present. In situations of severe pain, a
short period of immobilization may be necessary. If separation of the secondary growth center occurs or adolescents
have persistent pain from lack of fusion of the physis despite adequate conservative management, internal fixation is
recommended. If surgery is required, bone grafting is necessary due to the high incidence of fibrous union when bone
grafting is not used (175, 176). If the condition is left untreated, apophysitis of the olecranon may lead to an incompletely
fused olecranon physis, which has been reported to fracture with direct trauma in adults ( 173,174 and 175,177,178).
Unfused olecranon physis fractures in adults are treated with open reduction, internal fixation, and primary bone grafting
(175).
Triceps Tendinitis
Inflammation of the triceps insertion at the proximal olecranon is common in athletes who lift inordinate amounts of weight
or in explosive field events such as shot put, although it is also seen in throwing the javelin or baseball pitching. This
problem is due to intrinsic muscle overload of the triceps associated with the sudden snap of elbow extension. These
patients report pain at the tip of the olecranon that is aggravated by throwing. On examination, the point of maximal
tenderness is just proximal to the attachment of the triceps on the olecranon, or exactly at the triceps insertion. The pain
is accentuated by resisted active elbow extension or with complete passive flexion with shoulder flexion. This can be an
acute or a chronic problem. If this is a chronic problem, frequently radiographs will reveal calcific deposits within the
tendon. However, radiographs are usually normal. Treatment is conservative (PRICEMM). It is important not to inject
steroids into the tendon because of the risk of tendon rupture. If the symptoms do not respond to conservative treatment
and calcific deposits are present, surgery may be warranted to explore the tendon, to excise intratendinous and
extratendinous degeneration and granulation tissue, and to remove the calcification ( 179).
Triceps Tendon Rupture
Triceps tendon rupture is the least common of all tendon ruptures in the body and is a very uncommon cause of pain in
the posterior elbow ( 107). It is due to a decelerating counterforce during active extension of the elbow or a direct blow.
Systemic and local corticosteroid injections have been implicated as etiologic factors for triceps tendon rupture ( 180).
These patients cannot actively extend the elbow against gravity and have a palpable defect in the tendon. Radiographs
may show a fleck of bone in up to 80% of cases ( Fig. 54.21). This is usually an avulsion injury, although there are reports
of tears at the musculotendinous junction ( 107,181,182,183 and 184). These injuries should be treated as soon as
possible with a direct repair through drill holes in the olecranon, with or without fascial or tendon augmentation ( 107,185).
The results are universally good with repair.
FIGURE 54.21. Lateral radiograph of the elbow of a patient with an acute triceps rupture sustained while weight lifting.
The triceps tendon ruptured during eccentric contraction while bench pressing. The arrowheads point to two flecks of
bone, which is consistent with avulsion of the triceps tendon.
Valgus Extension Overload Syndrome
The valgus-extension overload syndrome is a common final pathway for posterior elbow problems that result from
excessive valgus forces (Fig. 54.3). Thus, this problem more commonly occurs in athletes who participate in racquet
sports, baseball, or throw javelin. In these sports, the olecranon is repeatedly and forcefully driven into the olecranon
fossa. In addition, there is typically a valgus stress that causes the olecranon to impinge against the medial wall of the
olecranon fossa. This situation is amplified when there is attenuation of the UCL. The tip of the olecranon, which is
intraarticular, causes local inflammation and, if it persists, eventually chondromalacia and osteophyte formation. With
continued impingement, these osteophytes break off and become loose bodies within the joint ( Fig. 54.22) (186). Loose
bodies may cause a mechanical block to flexion or extension or may produce a synovitis, resulting in an effusion and stiff
elbow. Professional baseball pitchers have been noted to have cubitus valgus and a narrowing of the olecranon fossa
due to bony hypertrophy. Such morphologic changes, in addition to the valgus elbow stress imposed on the elbow during
pitching (187), predispose pitchers to impingement of the olecranon process on the medial wall of the olecranon fossa
(23).
FIGURE 54.22. Radiograph demonstrating loose bodies in the posterior compartment (arrows) of the elbow in a baseball
pitcher who reported intermittent locking of the elbow.
Athletes with this syndrome report posterior elbow pain, sometimes with subjective clicking or grating. Furthermore, they
may complain that their pain occurs with full extension—either passive or active—that is accentuated with valgus stress.
When loose bodies develop, athletes may report catching or locking and that they need to manipulate the elbow to
release or unlock it. Examination uncovers tenderness posteriorly along the margins of the olecranon, although it is rare
to palpate loose bodies within the elbow. Radiographs reveal calcification at the tip of the olecranon, which can
frequently be confused with triceps tendinitis. An arthrogram or tomogram can be helpful in distinguishing between the
two conditions and may reveal the loose bodies. Radiographs may also show the offending osteophytes or enlargement
of the olecranon, or both ( Fig. 54.23). A modified cubital tunnel view may help reveal posteromedial olecranon
osteophytes.
FIGURE 5.23. Radiograph showing a posterior medial spur (arrow) associated with valgus extension overload.
Treatment for early phases of this syndrome, particularly if there are no loose bodies, include NSAIDs and strengthening
of the flexor-pronator muscle group to reduce inflammation and symptoms and to protect the joint. However, when
posteromedial osteophytes are present, physical therapy is usually not effective ( 186). Arthroscopy can be used to
determine whether osteophytes or loose bodies are present and can be used to shave down the osteophytes and remove
the loose bodies ( 188). Arthrotomy traditionally has been used with good results ( 132,186,187,190,191). Yet, current
results with the arthroscope in the elbow are quite good, with low complication rates ( 139,189,192,193 and 194), while
allowing for earlier and more aggressive rehabilitation and earlier return to sport, making this the preferred treatment for
loose bodies and osteophytes ( Fig. 54.24). However, elbow arthroscopy is a technically demanding procedure.
Furthermore, removal of the osteophytes and removal of the loose bodies do not treat a frequent underlying cause of the
loose bodies—attenuation of the UCL ( 139). As a result, there is a high reoperation rate (41%) if just removal of the loose
bodies or osteophyte is undertaken ( 139). Thus, the problem or symptoms may recur, but because it often takes years to
redevelop osteophytes and loose bodies, many authors consider this an acceptable treatment in face of the risks and
prolonged rehabilitation associated with reconstruction of the UCL.
FIGURE 54.24. Schematic representation of arthroscopic burring of olecranon osteophytes.
Olecranon Stress Fracture
Stress fracture of the olecranon is an uncommon source of elbow pain in the throwing athlete. Stress fractures of the
olecranon may occur through the physis or the persistence of the olecranon physis (discussed earlier). In skeletally
mature athletes, this fracture may occur at the tip or more commonly more distally and oblique ( 195,196 and 197). This
may be the result of intrinsic forces from the musculotendinous unit, or as a result of shear forces from valgus extension
overload. These patients may have pain at rest or during or after throwing. The pain is insidious in onset and increases
with an increased amount and intensity of throwing. It is due to the repetitive sudden snap of full extension. The healing
of the midolecranon stress fracture is slow with an associated high risk of nonunion ( 176). If symptoms do not resolve
with rest, NSAIDs, and modalities, treatment should consist of excising the tip fragment ( 195) or internally fixing the
olecranon if the fragment is large ( 176,196).
Olecranon Bursitis
Olecranon bursitis is an inflammation of the subcutaneous bursa of the olecranon. Olecranon bursitis is a common
finding in unpadded football linemen and rugby players, especially when playing on artificial turf ( 198). This can occur
after a single blow, after repeated injury, or as a result of an infection. The patient reports pain or tightness, or both, of
the posterior elbow as well as swelling of the elbow. The patient presents with an elbow that is quite distended but soft.
Unless it is acute or infected, there is usually no tenderness. However, if it is acute or infected it will be warm,
erythematous, and painful. Radiographs denote posterior soft tissue swelling, and sometimes calcification of the triceps
insertion on the olecranon ( Fig. 54.25). Once infection is ruled out, the treatment is rest, ice, and compression. Some
physicians treat recalcitrant cases in a hinged elbow brace that blocks full flexion. NSAIDs may be of some benefit. If an
infection is suspected, aspiration of the bursa with cultures and Gram stain, followed by appropriate antibiotic therapy
and immobilization, is necessary. If the bursitis affects range of motion, then aspiration may be indicated, although this
alone does not prevent fluid reaccumulation ( 198). Injection of corticosteroid into the bursa may be used for persistent
traumatic symptoms following aspiration, if infection is not present, to help prevent reaccumulation of fluid. This should be
combined with rest and immobilization. Bursal excision, either arthroscopic or open, is rarely necessary and is usually
reserved for chronic insistent bursitis or infectious bursitis ( 85,198).
FIGURE 54.25. Radiograph showing fluffy calcification at the triceps insertion.
LATERAL ELBOW PAIN
Pain in the lateral aspect of the elbow is the most common location of elbow pain in the general population. Although
there are many causes of lateral elbow pain ( Table 54.4), lateral epicondylitis (tennis elbow) is the most common.
OCD, another problem occasionally called Little Leaguer's elbow, is a focal lesion of the lateral elbow that occurs in
young throwers. Although OCD can occur in throwers and nonthrowers, in the dominant and nondominant elbows, and in
the capitellum, radial head, or both, it tends to occur in the capitellum of the dominant arm in throwers 10 to 15 years of
age (18,199,200,201,202,203 and 204). While the exact etiology of OCD remains a mystery, the current leading
hypothesis is that it is a lesion resulting from vascular insufficiency due to repetitive trauma or microfracture. Panner
showed the capitellar blood supply to be tenuous, with end-arterioles terminating at the subchondral plate ( 205). The
current popular theory proposes that compression at the radiocapitellar joint produces arterial injury and resultant bone
death (114). The radiocapitellar compression acts as a secondary restraint to the valgus stresses associated with
throwing (Fig. 54.3 and Fig. 54.27). This can be a disabling problem.
FIGURE 54.27. Schematic representation of radiocapitellar compression associated with valgus force and ulnar collateral
ligament laxity.
OCD must be differentiated from Panner's disease since the prognosis and treatment differ. The difference between the
two frequently confused entities focuses on age and degree of involvement of the capitellar secondary center of
ossification. Panner's disease is a focal, localized lesion of the subchondral bone and its overlying articular cartilage
(anterior central capitellum) in a young child, usually 7 to 12 years of age ( 205). OCD is a focal lesion in the capitellum
demarcated by a rarefied zone, with or without loose bodies in an older athlete, usually 13 to 16 years of age ( 114).
The athlete notes insidious lateral elbow pain and reduced throwing effectiveness and distance. He or she may also have
a flexion contracture of more than 15 degrees. Early x-ray films may be normal, although with time, islands of
subchondral bone demarcated by a rarified zone can be seen, and frequently loose bodies are present ( Fig. 54.26).
Tomography is often helpful in defining the extent of the lesion. Treatment of this problem is based on whether the
overlying cartilage is intact. The diagnosis is usually made by arthrotomogram, arthro-CT scan, or arthroscopy if plain
films do not show free fragments. MRI and ultrasound have also been found to be useful in detecting early OCD and to
assess the integrity of the overlying articular cartilage ( 206). If the overlying cartilage is intact, treatment is rest and
occasionally splinting. This is followed by range-of-motion and then strengthening exercises. Although the symptoms
subside with rest alone, throwing is contraindicated because the healing process is slow. The elbow is protected from
throwing and other heavy activities until there is radiographic evidence of healing. If pain and flexion contracture persist
for more than 6 weeks, Tullos notes that fragmentation is likely. If the cartilage is not intact at the time of surgery, Tullos
recommends excising the fragment regardless of size ( 114). He notes that although the patient will have a functional
elbow, he or she will not be able to throw or perform heavy labor ( 114). The current recommendation is to reattach large
fragments and internally fix them with screws, wires, or biodegradable pins after drilling the bed to enhance vascularity,
similar to the procedure described by Indelicato et al. ( 187), whereas smaller fragments are removed. If the large
fragment has been chronically detached, these fragments may be rounded and hypertrophied, and reattachment may not
be possible. In these cases, the bony fragment is removed and the crater is curetted or abraded of the fibrous tissue.
O'Driscoll and others report excellent short-term results of arthroscopy for removal of loose bodies due to OCD as well as
debridement of flaps of articular cartilage ( 194,207). Late sequelae of OCD after removal of loose bodies include residual
deformity of the capitellum and radial head, arthritis, loss of motion, pain, and often residual disability ( 208,209).
FIGURE 54.26. Osteochondritis dissecans of the capitellum (arrow).
Radial Neck Physeal Fracture
Valgus stresses at the elbow with attenuation or insufficiency of the UCL resulting in increased compressive forces to the
radiocapitellar joint may alternatively produce a fracture of the radial neck at the physis. This injury tends to be acute,
owing to sudden force to the radiocapitellar joint in an immature athlete. These children report radial head tenderness
and loss of supination and pronation, which are confirmed on physical examination. Radiographically, a fat pad sign is
present, and the fracture is identified if displaced or with stress films. Undisplaced fractures are treated with rest for 4 to 6
weeks until the fracture is healed. Displaced fractures are treated with closed versus open reduction based on the degree
of displacement.
Radiocapitellar Degeneration
In the adult, valgus stresses in the face of an incompetent UCL results in a radiocapitellar overload syndrome. The
repetitive increased forces to the radiocapitellar joint result in radial head abutment against the capitellum. This chronic,
repetitive radiocapitellar joint force produces chondromalacia, followed by cartilage and then bony degeneration ( Fig.
54.27). Continued radiocapitellar compressive forces eventually results in osteochondral fracture and loose bodies.
Patients report pain associated with catching, clicking, or locking of the elbow and occasionally complain that they must
shake or toggle their elbow arm to unlock it. These patients may have a palpable loose body and often have crepitus with
motion. Treatment is removal of the loose body, arthroscopically or open ( Fig. 54.28). However, the loose bodies will
recur if the athlete continues to perform the event that produced the valgus forces to begin with, especially if valgus laxity
persists. Most studies reveal that athletes (including professional baseball pitchers) return to their activity after removal of
the loose bodies. Bennett and Tullos ( 114) reviewed their experience with open removal of loose bodies and found that
the average professional pitcher continued to throw effectively 3 years after this procedure (range 2 to 11 years) ( 114).
However, as Tullos is quick to point out, loose bodies will recur in those athletes who return to throwing because pitching
is an inherently destructive process ( 114). Recent studies of arthroscopic removal of loose bodies confirm the usefulness
of this procedure with its low morbidity and possibly quicker return to activity as discussed earlier, especially if there is no
associated degenerative arthritis ( 194).
FIGURE 54.28. Schematic representation of arthroscopic removal of loose bodies.
Lateral Epicondylitis
Lateral epicondylitis is arguably the most common source of elbow pain in the general population. It occurs 7 to 20 times
more frequently than medial epicondylitis ( 120,122). It was first described over 100 years ago in a tennis player ( 210) but
since has been described in association with many other athletic and nonathletic endeavors. Lateral epicondylitis is a
chronic condition of the extensor muscles, primarily the extensor carpi radialis brevis (ECRB), due to overuse (from both
intensity and duration). It has been shown that there is no inflammatory tissue on pathologic specimens. The pathology
has been described as angiofibroblastic proliferation provoked by repetitive trauma ( 89).
It has been shown that 50% of club tennis players older than 30 years of age had experienced symptoms characteristic of
tennis elbow at one time or another ( 89). Half of these players noted minor symptoms with a duration of less than 6
months, whereas the other half had major symptoms lasting an average of 2.5 years. Lateral epicondylitis tended to occur
in recreational tennis players 35 to 50 years of age (average 41 years) playing three to four times per week, who are
inadequately conditioned and often use poor technique. Several factors are believed to help precipitate this problem:
heavier, stiffer, more tightly strung rackets; incorrect grip size, metal rackets; inexperienced players; and bad backhand
technique (89,91,211,212 and 213). Increased racquet vibration, typically initiated by off-center hitting (miss hits) that has
a direct correlation with poor mechanics, is another inciting factor. Advanced tennis players who warm up, use good
technique, and are well conditioned rarely suffer from this malady. Those who use a one-handed backhand technique are
at higher risk of developing lateral epicondylitis as compared with those who use two hands.
Lateral epicondylitis presents as a dull lateral elbow pain that has an insidious onset, beginning gradually after vigorous
activity and progressing to pain with activity. Frequently, the pain is present when turning a doorknob, lifting a milk
carton, or opening a jar. Night pain is not common but may appear in chronic cases. On examination there is pain with
passive wrist flexion and with active resisted wrist extension or resisted supination. There often is tenderness 1 to 2 cm
distal to the lateral epicondyle. Grasping or pinching with the wrist extended (the “coffee cup” test) usually reproduces
pain precisely at the point of tenderness ( 122). Radiographs are frequently normal, although 22% of patients have
evidence of a spur at the lateral epicondyle or calcification of the common extensor tendon ( 92). This calcification is
secondary to the chronic repetitive tension forces placed on the common extensor origin. Surgical pathology reveals that
the ECRB is the tendon implicated as the source of pathologic change and pain; however, the anterior extensor digitorum
communis (EDC), the underside of the extensor digitorum radialis longus (EDRL), and rarely, the origin of the extensor
carpi ulnaris (ECU) may be involved as well.
Initial treatment is conservative (PRICEMM) and is often quite successful. Wrist extension splints have also been
advocated to help rest the wrist extensor muscles as well during the acute and subacute phases. Care must be taken to
educate the patient that this is an overuse syndrome. Of additional importance is proper technique, reducing tension on
the strings of racquets, using a cushioned synthetic grip, conditioning, and the use of the counterforce brace.
Counterforce bracing has been found to be very useful in tennis elbow ( 214,215). Many theories have come about to
explain how the counterforce brace works (Table 54.5), but essentially the brace works by causing a change in the
sequence and direction of muscle contraction, which short circuits muscle forces by shortening the effective length of the
muscle. If the PRICEMM protocol is not effective, injection with lidocaine (Xylocaine) and corticosteroids just below the
ECRB is indicated and may be beneficial for short-term use ( 216,217,218,219 and 220). It is important to realize that
repeated steroid injections may lead to tendon compromise and complications. After the symptoms abate, a
comprehensive rehabilitation program is initiated, emphasizing strength and flexibility of the forearm flexors and
extensors. The patient should be instructed that the treatment, the exercises, and proper mechanics are important for
prevention of recurrence. The medications and injections are only temporizing factors to reduce the symptoms. The
patient should be encouraged to seek professional instruction to eliminate biomechanical errors in stroke production.
Typical errors include (a) improper weight transfer (hitting off the back foot), (b) hitting with the leading elbow during the
backhand, and (c) excessive pronation of the forearm during the serve or the overhead. In golf, lateral epicondylitis is
associated with “hooker's grip,” which is an attempt to close the club face by overpronating the hand.
TABLE 54.5. COUNTERFORCE BRACING
If conservative treatment fails to return the athlete to usual activities after 6 months, which occurs in 4% to 12%
(120,218,221,222), Nirschl recommends surgical intervention ( 92). Some authors recommend surgery for recurrence
following successful resolution by conservative means ( 129), although most would recommend another trial of
conservative treatment first. There have been many described surgical procedures at the elbow and wrist in the treatment
of lateral epicondylitis ( 92, 218,223,224,225,226,227 and 228). The authors prefer removal of the granulation tissue and
reconstruction of the lateral epicondyle ( 127). Basically, the common extensor hood is fastidiously elevated, and the
underlying granulation tissue is excised. The epicondyle is drilled or burred to bleeding bone to create a good vascular
bed, and the extensor hood is reconstructed ( 127). Care is taken to not injure the lateral ligamentous complex because
cases of posterolateral rotatory instability have been reported following surgery for lateral epicondylitis.
There have been reports of arthroscopic management of lateral epicondylitis. It has been noted that capsular rents or
holes have been identified in patients with this entity following arthroscopy ( 229). In one series, arthroscopic release from
the lateral epicondyle provided improvement in 93.3% of patients, with 71% having good to excellent results in patients
followed for at least 6 months (229). More series with greater follow-up are needed to confirm these results, and studies
need to be undertaken to compare arthroscopic with more standard techniques.
In one study of those who underwent open surgical treatment, 85% returned to full activities without pain, whereas 12%
improved but still had some pain with vigorous activities and 3% showed no improvement ( 218,222,230). Revision
surgery using the above-mentioned technique has also been found to be successful in 83% of patients ( 231). The most
common cause of failure of surgery was noted to be incomplete excision of degenerative tissue ( 231). As an alternative
to surgical treatment, multiple repeated steroid injections may be acceptable. Although several authors recommend no
more than three injections into this area per year ( 91), others believe that this is not a problem for lateral epicondylitis.
The consequence of more than three injections per year is degeneration of the tendon and subsequent rupture ( 232).
However, because this is, at least in part, the goal of current surgical therapy for this problem, the end result is the same
without the risk of surgery or the time away from sports. Such an approach does, however, put the normal surrounding
tissues at risk for degeneration from the steroids ( 233), and it is not the authors' recommended management.
Extensor-Supinator Muscular Disruption
Lateral muscular disruption due to athletic endeavors, without previous cortisone injection, is an uncommon injury ( 120).
Patients with this condition report severe acute pain, often associated with a pop or snap. Weakness of wrist extension
and forearm supination is present. If weakness persists after the pain subsides and if all or a major part of the extensor
tendon origin is ruptured, then primary surgical repair of the tendon to bone is indicated.
Radial Nerve Entrapment
Radial nerve entrapment at the elbow, also known as resistant tennis elbow, can occur by itself or in conjunction with
lateral epicondylitis in approximately 5% of cases ( 234,235). This syndrome occurs when the motor branch of the radial
nerve, the posterior interosseous nerve (PIN), becomes entrapped within the radial tunnel. The four possible sites of
entrapment are (a) at the arcade of Frohse, (b) under the midbelly of the supinator muscle, (c) as the nerve exits the
supinator muscle, and (d) the leash of Henry—the radial recurrent vessels lying beneath the brachioradialis and ECRL
muscles (236). These athletes report symptoms similar to lateral epicondylitis, often with an ache, frequently radiating
down the forearm. Because the PIN is a motor nerve, there are no sensory deficits. The use of counterforce bracing for
presumed lateral epicondylitis might aggravate the symptoms if the true etiology is radial nerve entrapment. There is
tenderness over the lateral epicondyle and anteriorly over the radial nerve as it passes through the supinator, although
occasionally, the pain is at the junction of the middle and proximal thirds of the forearm, where the nerve exits the
supinator. Pain is aggravated by active supination and passive pronation, as well as by resisted extension of the long
finger while the elbow is extended, depending on the site of entrapment. EMG is helpful only if positive, which it may be if
compression has been present for 7 to 9 months. Conservative treatment (PRICEMM) is first attempted, concentrating on
rest, NSAIDs, and rehabilitation, especially elbow motion and strengthening of the extensors and supinator. In
approximately 10% of patients, surgery is necessary to decompress the radial tunnel to cure this problem.
CONCLUSION
The elbow joint is a complex structure that allows for precision placement of the hand in space. In many sports, it must
withstand tremendous forces that are not often encountered in daily living. Thus, the elbow in athletes is subjected to
great stresses and, as a result, is subject to a wide variety of possible injuries. As the level of athletic ability continues to
climb with bigger, stronger, and faster athletes, the elbow will continue to be subjected to even greater stresses. As our
understanding of the elbow continues to expand, due in part to newer diagnostic techniques and research, our treatments
will continue to change and evolve.
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55 Hand and Wrist Injuries
55
HAND AND WRIST INJURIES

JAMES R. WILLIAMS
MATTHEW M. TOMAINO
Biomechanical Considerations
Epidemiology
Radial-Sided Wrist Pain
Distal Radius Fractures
Scaphoid Fractures
Rotatory Subluxation of the Scaphoid
Kienbock Disease
De Quervain Tenosynovitis
Intersection Syndrome
Wartenberg Syndrome
Ulnar Wrist Pain
Metacarpal Fractures
Metacarpophalangeal Joint Dislocations
Injuries of the Metacarpophalangeal Joint of the Thumb
Proximal Interphalangeal Joint Injuries
Collateral Ligament Injuries
Proximal Interphalangeal Joint Dislocation
Distal Interphalangeal Joint Injuries
Nerve Compression Syndromes
Carpal Tunnel Syndrome
Ulnar Nerve Compression
Bowler's Thumb
Conclusion
Chapter References
Diagnosis and treatment of hand and wrist injuries requires an understanding of normal anatomy and an appreciation of
its link with normal function. This allows successful restoration of function and, in the athlete, timely return to sport. This
chapter is a review of most common hand and wrist injuries encountered in treating athletes.
PHYSICAL EXAMINATION
Observation—view the patient as he or she enters the room; looking for any way in which they may be compensating for
their injury
Inspection—look for any signs of trauma; that is, abrasions, lacerations, swelling, ecchymosis, open fractures, bite marks
Palpation—assess for any areas of tenderness, that is, snuff box tenderness (scaphoid fracture)
Range of motion—active versus passive; that is to evaluate between a joint injury and a tendon injury
Neurovascular examination—evaluate ulnar and radial pulses and median, ulnar and radial nerve function
Radial-sided pain Symptom

De Quervain tenosynovitis Tenderness over first dorsal compartment: pain elicited by Finkelstein's test
Radial neuritis (Wartenberg Radicular, neuritic pain on radial side of wrist usually 6 to 8 cm proximal to radial
cheiralgia) styloid
Intersection syndrome Pain with flexion and extension of radial deviated wrist; usually 8 to 10 cm proximal to
radial styloid
Scaphoid fracture Tenderness in anatomical snuffbox
Scapholunate instability Tenderness at S-L interval; 1.5-2 cm distal to Lister's tubercle; Scaphoid shift test
Ulnar-sided pain Symptoms

Distal radioulnar joint Dynamic testing shows subluxation in either supination or pronation; piano key sign
instability
Ulnar impaction syndrome Pain with ulnar deviation and pronation of the forearm; due to impinge-ment of ulna and
lunate
Lunotriquetral instability Tenderness over lunotriquetral ligament; positive ballottment and compression test
Hook of hamate fractures Tenderness on palpation; pain with resisted flexion of the small and ring fingers
BIOMECHANICAL CONSIDERATIONS
Range of motion
Wrist NormalFunctional
Palmar flexion 65 5–10
Dorsiflexion 55 30–35
Radial deviation 15 10
Ulnar deviation 35 15
Hand Normal Stability

MCP joint 100 flexion Volar plate and collateral ligaments
PIP joint 110 flexion Joint congruity
DIP joint 80 flexion Joint congruity
Normal load: seen by the ulna/radius
Ulnar variance RadiusUlna

Neutral 80% 20%
2.5 mm negative 95% 5%
2.5 mm positive 60% 40%
EPIDEMIOLOGY
The incidence of hand, finger, and wrist injuries in sports is generally quoted as 3% to 9% ( 1,2 and 3). However the
incidence for any sport is variable from year to year and is higher in some sports than others ( 4). Retting et al. (1) found
that 30% of roller hockey injuries, but only 6% of judo injuries, involved the hand and wrist. In this study, the most
common injuries were hand and wrist sprains. Hand and wrist injuries in golfers affected 20% of all participants ( 5) in one
study, with the majority affecting the left wrist. The incidence of hand and wrist injuries in gymnasts is extremely high and
has been the focus of many studies (6,7,8,9 and 10).
RADIAL-SIDED WRIST PAIN
Distal Radius Fractures
Approximately one sixth of all patients seen in the emergency room are treated for an injury to the distal radius ( 4). Owing
to the large number of these injuries, considerable attention has been directed at the evaluation, classification, treatment,
and outcome following these fractures. The mechanism is usually a fall on an outstretched hand with hyperextension of
the wrist.
On initial examination, it is important to note the degree of soft tissue injury (i.e., swelling, ecchymosis, abrasions,
lacerations). All wounds should be examined to avoid missing an open fracture. A thorough neurovascular examination is
mandatory. Median nerve neuropathy is the most common associated problem. The neuropathy can be due to either
direct trauma from a fracture fragment or secondary to compression from hematoma. There is exquisite tenderness at the
fracture site. Distal radioulnar joint (DRUJ) instability must be ruled out because it often goes unrecognized despite being
present in approximately 50% of distal radius fractures.
After a thorough examinaton has been completed, the next step is to obtain appropriate radiographic studies. Initial
roentgenograms should include a posteroanterior (PA) and lateral view. From these initial views, it should be possible to
decide whether the fracture is extraarticular or intraarticular, or displaced or nondisplaced, and to determine whether
there is any comminution. If indeed there is displacement present, it should be determined how much displacement and
angulation exist because this will influence the stability of the fracture. Plain tomography or computed tomography (CT)
scan may be required to better assess articular incongruity. A high degree of suspicion must always exist for associated
injuries such as ulnar styloid fractures, DRUJ instability, and intercarpal ligament tears (i.e., S-L tears). Radiographic
parameters describing the normal anatomy of the distal radius are well documented ( 10). On the PA film, the normal
radial inclination of the wrist is 22 degrees and the radial length is 12 mm. The ulnar variance can also be determined on
this view. The lateral radiograph is useful in measuring the volar tilt, which is normally 12 degrees. Biomechanical studies
have shown that shortening of the distal radius by small amounts (2.5 mm) or the residual dorsal tilt of the distal articular
surface results in a significant increase in axial load transmission through the ulnocarpal joint ( 11,12). Biomechanical
studies have also shown that as the distal radius tilts dorsally, the contact area of the distal articular surface with the
scaphoid and the lunate decreases in size and shifts dorsally ( 13,14).
There have been many eponyms given in an attempt to describe distal radius fractures. A Colles fracture is a distal
radius fracture with dorsal comminution, dorsal angulation, dorsal displacement, and radial shortening ( 15). A Barton
fracture is a displaced, unstable articular fracture or subluxation of the distal radius with the displacement of the carpus
along with the articular fracture fragment ( 16). A Smith fracture is a fracture of the distal end of the radius 1/2 to 1 inch
from the articular surface, in which the distal fragment and the carpus are displaced anteriorly in relationship to the
forearm (17). Although they are commonly used, the shortcoming of all of the eponyms used to describe distal radius
fractures is their failure to describe the individual characteristics of each fracture.
In an attempt to improve communication between colleagues, many classifications systems have been developed. In
1967, Frykman developed a classification scheme that distinguished between extraarticular and intraarticular fractures
and the presence or absence of an ulnar styloid fracture ( 18). In 1984, Melone introduced a classification of distal radius
fractures that divided the distal radius into parts. This work underscored the importance of the “die-punch” fracture
fragment of the lunate facet of the distal radius ( 19). As the eponyms used before them, each classification system has
occasionally fallen short in guiding treatment.
The initial treatment of distal radius fractures has not changed much over time. If the fracture is displaced, an initial
closed reduction should be attempted, followed by appropriate immobilization. Following the reduction, postreduction
films should be obtained to assess the adequacy of the reduction. Also, at that time the neurovascular status of the
patient should be reexamined. The patient should usually have definitive care instituted within 7 to 10 days.
Treatment modalities include simple casting, pins and plaster, external fixation with or without pins, open reduction, and
internal fixation. The goals of treatment are to obtain an anatomic reduction ( Fig. 55.1A and Fig. 55.1B). If there is more
than 2 mm of articular incongruity present following the reduction, this should be addressed because 2 mm step-off has
been shown to lead to arthritic changes ( 20).
FIGURE 55.1. A: Intraarticular distal radius fracture with articular step-off. B: Anatomic reduction and fixation of distal
radius fracture.
Closed reduction and casting is a viable option for many patients if the fracture is either nondisplaced or an acceptable
reduction is obtained. These patients need to be followed very closely for loss of reduction as the swelling subsides and
the splint loosens. The usual course of treatment for these extraarticular, nondisplaced or minimally displaced fractures is
usually 3 weeks in a sugar tong splint, followed by 3 weeks in either a long or a short arm cast and then 3 weeks with a
removable splint. Neither the method of immobilization, the choice of short-arm versus long-arm cast, nor the position of
the forearm have been shown to have a significant influence on outcome ( 21), although the characteristics of each
fracture should be judged independently.
Some fractures are inherently unstable regardless of the adequacy of reduction due to either the amount of initial
displacement or the quality of bone. Lafontaine et al. studied 112 consecutive fractures treated conservatively and
suggested five factors that related to instability following reduction: ( 1) initial dorsal angulation greater than 20 degrees,
(2) dorsal metaphysical comminution, (3) intraarticular disruption, ( 4) associated ulnar fracture, and ( 5) patients over 60
years of age or massive osteoporosis (22). Others have found that the severity of initial shortening was the most reliable
indicator of instability ( 23). For these reasons, many have advocated alternative methods of fixation.
After the initial treatment, physical therapy should be started while the patient is still immobilized. Such therapy should
focus on the metacarpophalangeal (MCP), proximal interphalangeal (PIP), and distal interphalangeal (DIP) joint motion
and should aim to prevent further joint stiffness and potential reflex sympathetic dystrophy ( 24). After there is
radiographic and clinical evidence of union, a removable splint can be applied. At the same time, the patient is instructed
about active and active-assisted range-of-motion exercises of the wrist. The splint can be discarded in the following 2 to
3 weeks as the patient regains muscle strength and endurance.
In the pediatric patient with open physes and wrist pain, one must suspect a Salter physeal fracture. The pediatric patient
is at risk for fracture because the physeal cartilage is weaker than bone and is easily injured. When dealing with an injury
to the physeal plate, it must always be kept in mind that there is a risk of alteration of skeletal growth. At times, there are
subtle or no radiographic evidence of fracture. The usual treatment is casting for either 3 or 4 weeks. Following cast
removal, a series of gentle range-of-motion and stretching exercises can begin. Gradually the child can resume normal
activity.
SCAPHOID FRACTURES
The scaphoid is the most frequently fractured carpal bone, accounting for 60% to 70% of all carpal fractures ( 25), and the
most frequent wrist fracture in the athlete. Generally, the injury results from a fall on an outstretched hand or during
sports that subject the wrist to high-speed forces (such as hockey, football, boxing, and basketball) ( 26).
On initial examination, the patient reports pain in the region of the dorsal wrist and thenar eminence. There is usually
tenderness when the anatomic snuff box is palpated. The anatomic snuff box is the region on the dorsum of the wrist
between the extensor pollicis longus and the extensor pollicis brevis tendons, just distal to the radial styloid. The proper
radiographs include a PA ulnar deviation view, a lateral view, and two oblique views. Ulnar deviation results in scaphoid
extension, which allows visualization of the scaphoid without overlap by its tuberosity. The lateral view is helpful in
assessing carpal alignment, particularly lunate dorsiflexion. If injury to the scapholunate ligament is suspected, a
clenched fist anteroposterior (AP) view is taken. Power grip loads the wrist, and when scapholunate injury is subtle,
rotatory subluxation of the scaphoid may be provoked.
Occasionally, all roentgenographic studies are negative. When there is a high degree of suspicion for a scaphoid fracture
based on clinical examination, treatment should be instituted even in the absence of fracture. At this point, the patient
should either be brought back in 10 to 14 days for repeat radiographs, at which time resorption at the fracture will allow
identification of the fracture, or a bone scan or MRI can be ordered. In the athlete, this later approach is beneficial
because it avoids unnecessary casting and potential inactivity.
Optimal treatment of scaphoid fractures depends on making an early diagnosis as well as the proper identification of the
type of fracture. There are five locations where fractures of the scaphoid can occur: (a) tuberosity, (b) scaphotrapezial
joint osteochondral fracture, (c) proximal pole, (d) waist, and (e) the distal pole. The classification of scaphoid fractures is
important due to the high association of avascular necrosis and nonunion. Fractures of the proximal pole have a much
higher incidence of nonunion and avascular necrosis. This is due to the vascular anatomy of the scaphoid. The blood
supply for the scaphoid is from the radial artery and divides into a dorsal ridge and volar lateral branches that enter the
scaphoid distally. Thus, with a fracture of the proximal pole, the blood supply is cut off and healing may take 10 to12
weeks (27,28 and 29). Avascular necrosis may occur in 14% to 39% of fractures in this location ( 28,30,31). Other factors
that are significant when treating these fractures are (a) greater than 1 mm of displacement, (b) fracture orientation
(vertical oblique fractures being unstable), (c) degree of fracture comminution, and (d) associated injuries.
Historically, there have been three main areas of dispute in the nonoperative treatment of scaphoid fractures (a) wrist
position, (b) long versus short arm cast, and (c) the duration of immobilization. Numerous studies have shown that for
stable fractures, wrist position does not influence union rates. Similarly, unstable fractures usually require operative
treatment. The issue of using a long versus a short arm cast is still heavily debated. There are studies showing that as
long as there is thumb and wrist immobilization, forearm rotation does not influence intercarpal motion ( 32,33 and 34).
Dickson and Leslie (35) have shown a 95% union rate with short arm thumb spica casts. In contrast, Broome et al. ( 36)
and Gellman et al. ( 37) have shown a statistically significant reduction in healing time with long arm thumb spica cast
immobilization. For proximal pole fractures, our preferred treatment includes a long arm thumb spica cast for the initial 4
to 6 weeks, followed by a short arm thumb spica cast until clinical and radiographic evidence of union is present.
As defined by Cooney et al. (30), displaced or unstable fractures are those with greater than 1 mm of displacement, a
scapholunate angle greater than 45 degrees, or a radiolunate angle greater than 15 degrees. These fractures require
open reduction and internal fixation ( Fig. 55.2A, Fig. 55.2B, Fig. 55.2C and Fig. 55.2D). Cannulated screws allow precise
intrascaphoid central placement because a guide wire is first placed and imaged. Three frequently used devices include
the Herbert Whipple, Accufex, and AO screws.
FIGURE 55.2. A: AP view of scaphoid wrist fracture. B: Lateral view of scaphoid fracture. C and D: Operative fixation of
scaphoid fracture with Herbert screw.
The main issues of concern to the athlete and coaches are the restrictions and timing of return to play. There is no
cookbook answer for this determination, and each case must be decided individually between the athlete, parents,
coaches, and physician. Two certainties exist: (a) it is safe to return to play following union, and (b) a nonunion can be a
career-ending issue for the athlete. Some surgeons have allowed athletes with a stable fracture to return to play in a
short arm silicone cast as soon as pain permits ( 38,39). Others have treated nondisplaced fractures operatively in the
hope of returning the athlete to play more quickly. Although Herbert has recommended that contact sports be avoided for
3 months following operative fixation ( 40), we have allowed the athlete to return to play 2 weeks following surgery in a
padded thumb spica cast without complication.
Rotatory Subluxation of the Scaphoid
The term rotatory subluxation of the scaphoid actually encompasses a spectrum of injury and instability. Scapholunate
dissociation usually results from either a fall onto an outstretched hand or high-impact trauma to the extended wrist.
Pathomechanics involve wrist hyperextension, ulnar deviation, and intracarpal supination.
In 1980, Mayfield et al. (41,42) described the concept of progressive perilunar instability and divided it into four stages.
The initial and most common stage involves scapholunate ligament disruption leading to scapholunate instability.
Patients often report a trivial sprain of the wrist and present reporting progressive pain and weakness. Clinically, there is
usually tenderness over the dorsum of the wrist at the scapholunate interval. The scaphoid shift test, described by
Watson in 1988 ( 43), may also be positive. This provocative maneuver involves placing volar pressure on the scaphoid
tuberosity so that when the wrist is passively brought from ulnar to radial deviation by the examiner, the scaphoid is
unable to flex, resulting in a clunk as the proximal pole rides out of the scaphoid fossa because of scapholunate ligament
disruption or laxity.
Initial radiographic evaluation includes an AP grip view (supinated) and a true lateral view. The typical findings on the AP
view include a widened scapholunate gap greater that 2 mm, a foreshortened scaphoid leading to a distance of less than
7 mm (7 to 11 mm normal) from the cortical ring to the proximal pole, and a cortical ring sign which results from overlap of
the distal and proximal poles due to to scaphoid flexion. The lateral projection shows an increased scapholunate angle of
greater than 60 degrees (30 to 60 degrees is normal) owing to the combination of scaphoid flexion and lunate extension
(dorsiflexion intercalated segment instability).
Historically, treatment options revolve around the time at which the injury is diagnosed: (a) acute injuries—less than 3
weeks, (b) subacute—3 weeks to 3 months, and (c) chronic injuries—greater than 3 months. In acute injuries, most
recommend an open reduction and repair of the ligament, if possible ( 44). Chronic injuries may have some degenerative
changes present, and in most cases, quality ligament tissue is not available for repair. Treatment in such cases centers
around either full or partial wrist fusion, or proximal row carpectomy. Management of subacute injuries is more
controversial, but most hand surgeons would attempt open reduction with either ligament repair or capsulodesis ( 45).
Kienbock Disease
In 1910 Robert Kienbock (46) first described avascular necrosis of the lunate, and this disease continues to bear his
name. The etiology of Kienbock disease remains controversial, although it is thought to result from trauma and poor
blood supply. It is most commonly found in physically active individuals between 20 and 25 years of age and in patients
with negative ulnar variance. The incidence is unknown.
Clinical examination often demonstrates swelling on the dorsum of the wrist with tenderness in the area of the lunate.
There is often decreased range of motion and grip strength. Routine PA (neutral rotation) and lateral images should be
obtained. From these images, the ulnar variance as well as the stage of disease can be ascertained. Once appreciable
carpal collapse has occurred, rotatory subluxation of the scaphoid may also be present (stage IIIB).
Moberg accurately summarized the goals of treatment: “to retard or delay inevitable arthritic changes in the wrist” ( 47).
Current thinking is that in the ulna-minus wrist, a radial shortening procedure can be done, and in the ulna-positive and
or neutral wrist, many advocate a revascularization procedure, scaphotrapezio trapezoid (STT) fusion, or capitate
shortening. In the presence of any arthritic changes or carpal collapse, extraarticular procedures are less successful and
proximal row carpectomy or radiocarpal fusion may be required.
De Quervain Tenosynovitis
De Quervain tenosynovitis is the most common form of tenosynovitis reported in the athlete and is seen in racquet sports
most often. The etiology is thought to be due to activities associated with repetitive ulnar deviation, which leads to
inflammation of the tendons within the first dorsal compartment at the level of the radial styloid. The tendons involved
include the abductor pollicis longus and the extensor pollicis brevis.
Patients frequently report pain in the region of the first dorsal compartment, which they state is aggravated by use of the
thumb. Examination reveals swelling and tenderness along the tendons on the dorsoradial aspect of the wrist. A positive
Finkelstein test is diagnostic. This test involves ulnar deviation of the wrist with the thumb adducted in the palm. Most
patients can be successfully managed by conservative treatment alone, consisting of splinting and steroid injection. This
mode of treatment is successful 80% of the time ( 48). Recalcitrant cases need to undergo operative decompression. The
athlete can usually return to play immediately following removal of the sutures without restriction.
Intersection Syndrome
This is a condition in which the “outcroppers” (abductor pollicis longus and extensor pollicis brevis) are irritated at the
point where they cross over the second dorsal compartment (extensor carpi radialis longus and brevis). It is frequently
seen in sports that require repetitive wrist flexion and extension against resistance such as competitive rowing, weight
lifting, or gymnastics (49,50).
Nonoperative treatment is usually successful. Initial measures include nonsteroidal antiinflammatory medication,
avoidance of aggravating activities, and splint immobilization. When this has failed steroid injection is advocated into the
area of the abductor pollicis longus (APL) bursa. Following injection, immobilization is continued for 1 to 2 weeks. In
recalcitrant cases, surgical exploration and debridement of inflamed tenosynovium may be necessary. Postoperative
immobilization should be limited following surgery to allow range-of-motion exercises. When the patient has regained
range of motion and strength participation can be resumed.
Wartenberg Syndrome
This is a condition in which the superficial sensory branch of the radial nerve is irritated as it exits between the
brachioradialis and the extensor carpi radialis longus. Traction neuritis results when inflammation leads to adhesions and
fibrosis in this area.
Typically, patients present with complaints of pain and numbness and tingling over the dorsoradial aspect of the hand
and thumb. Examination often reveals a positive Tinel sign over the nerve and exacerbation of symptoms during wrist
flexion and ulnar deviation.
Nonoperative management is the mainstay of therapy and includes rest from aggravating activities until symptoms abate,
ice, and splinting in a cockup splint for 2 to 3 weeks. If an adequate trial of nonoperative treatment fails, then operative
management is recommended. Surgical decompression of the nerve is then carried out. It is important to ensure that the
nerve is released both proximally and distally so that there are no tethering bands remaining. Postoperatively, the patient
is placed in a soft dressing and encouraged to begin early motion to prevent early adhesions. Once full motion and
strength have returned, it is safe to resume training and competition.
ULNAR WRIST PAIN

Diagnosing the cause of ulnar-sided wrist pain can be difficult. The history and physical examination are often confusing.
The differential diagnosis includes triangular fibrocartilage complex (TFCC) tears, lunotriquetral sprain or instability,
hamate fractures, ulnar impaction syndrome, extensor carpi ulnaris (ECU) tendonitis, and pisotriquetral arthrosis.
Traumatic tears of the TFCC usually result from a fall on an outstretched, pronated hand. Patients may complain of
mechanical symptoms like popping, particularly with forearm rotation. Clinical examination may show painful forearm
rotation and wrist motion, tenderness over the TFCC dorsally, and a palpable or audible click with radioulnar deviation of
the wrist.
Radiographs include a PA view in neutral rotation as well as a true lateral. The PA view helps determine the ulnar
variance because many patients with TFCC tears are ulnar positive. Additional diagnostic studies include magnetic
resonance imaging (MRI) and arthrography. Arthroscopy is the most accurate means of making a diagnosis ( 51) and can
also be used in the treatment of the problem.
There are two types of tears as classified by Palmer ( 52): (a) traumatic and (b) degenerative. Each of these types is
further divided into subtypes based on the location. Of the traumatic tears, the most common in athletes are central tears.
As a general rule, the central area of the TFCC is avascular and thus has little healing potential. Thus, treatment of
central tears is usually debridement. On the other hand, peripheral tears are usually repaired, either open or
arthroscopically. As a rule, degenerative tears are usually associated with positive ulnar variance and occur because of
ulnocarpal impaction. In the face of impaction or evidence of lunate chondromalacia, the length of the distal ulna must be
addressed in order to restore neutral or slightly negative variance. The two most popular surgical alternatives are ulnar
shortening osteotomy and wafer excision.
Lunotriquetral instability, like scapholunate instability, results from a fall onto an outstretched hand. The mechanism is
that of dorsiflexion, ulnar deviation, and midcarpal supination, with the contact point being the hypothenar eminence.
Symptoms are typically intermittent and exaggerated by rotation and deviation of the wrist.
Clinical examination is likely to demonstrate limited range of motion and decreased endurance on grip strength. Usually,
there is also pain with ulnar deviation and rotation of the wrist. Three provocative tests have been described: (a) the
ulnar-sided compression test, (b) L-T ballottement test, and (c) the shear test. Radiographic studies should include PA
and lateral views. The most common finding on the PA view is disruption of the convex arc of the proximal row ( 53,54 and
55). A gap is not seen between the lunate and triquetrum as is seen with scapholunate ligament disruption. The lateral
view may show a volar intercalated segmental instability pattern.
Treatment for these injuries includes immobilization, debridement, ulnar shortening, and lunotriquetral fusion. These
decisions are based on the chronicity of the injury, degree of instability, and the presence of any associated injuries or
degenerative changes.
Fractures of the hook of the hamate usually occur from either a direct blow or a racquet type sport. Although these
fractures account for a small proportion of all carpal fractures, they can be very troublesome to the athlete. The
distribution of these fractures as shown in one study was: golf, 33%; baseball, 9.5%, tennis, 4.8%; weightlifting, 4.8%;
and diving, 4.8% (56).
Clinically, the most common symptom is pain in the hypothenar eminence aggravated by grasp. Loss of grip strength and
dorsal wrist pain are also frequent complaints, and ulnar nerve paresthesias may also develop. Tenderness is elicited on
palpation of the hamate. The proper radiographs include a PA, lateral, and carpal tunnel view ( Fig. 55.3A). Frequently,
the fracture may be difficult to identify on plain film and further imaging should be done with a CT scan.
FIGURE 55.3. Carpal tunnel view with fracture of hook of hamate.
Treatment is based on the time of diagnosis, as well as the amount of displacement. The rate of nonunion of these
fractures is significant. If the condition is diagnosed less than 2 weeks from injury, nondisplaced, and without neurologic
symptoms, a trial of cast immobilization is warranted. Return to sporting activity is recommended only when there is
evidence of fracture union.
Excision of the hook is advocated in the event that there is (a) nonunion, (b) diagnosis greater than 2 weeks from time of
injury, (c) displaced fracture, or (d) ulnar nerve symptoms. Following excision of the hook of the hamate, the athlete
should be allowed to resume sporting activities in 2 to 3 weeks or when scar tenderness has subsided ( 57).
Pisotriquetral arthritis is a condition frequently associated with activities that load the ulnar aspect of the wrist. This is
also known as racquet injury owing to its association with racquet-type sports. The diagnosis should be suspected with
tenderness on examination of the palmar ulnar side of the wrist. Also, in looking for this feature, one should extend, flex,
and ulnar deviate the wrist. Treatment involves rest and steroid injections and, with further symptoms, pisiform excision.
Metacarpal Fractures
Fractures of the metacarpals are the most common injury in the upper extremity (58) (Fig. 55.3A and Fig. 55.3B). These
fractures can be described by the bone of involvement, location within the bone, fracture pattern, displaced or
nondisplaced, stable or unstable, and closed or open.
Clinical evaluation shows local swelling, tenderness, and ecchymosis. It is imperative to do a careful neurologic
examination and assess flexor and extensor tendon function. There needs to be a careful inspection for any evidence of
bite marks in an individual involved in a fight. Often, a small, superficial puncture wound represents a large dorsal rent in
the extensor hood. These fractures must be treated as open fractures with aggressive irrigation and debridement. The
organism usually found is Eikinella corrodens. Rotational alignment and axial shortening must be assessed in every
metacarpal fracture. As a general rule, when flexed, all digits should point toward the volar distal tubercle of the
scaphoid, and the nails should lie roughly in the same plane.
Radiographic examination requires a PA, a lateral, and also two oblique views. The reason for the two oblique views is
that a standard lateral film will only be a true lateral of the long finger metacarpal. In order to get a true lateral of the
index metacarpal, an image needs to be taken in 30 degrees of supination. A lateral view of the small and ring
metacarpals requires an x-ray in 30 degrees of pronation. The classic posture of metacarpal neck and shaft fractures is
dorsal angulation owing to volar cortical comminution and the volar shortening forces of the intrinsic muscles and flexor
tendons (59).
Fractures involving the articular surface should be treated with the same principles as other fractures involving the joint
surface. The primary goal is an anatomic restoration of articular congruity. These fractures usually involve the index
metacarpal and are frequently the result of an axial load or direct trauma. The major complication encountered with these
fractures is stiffness. When these fractures occur in children, there should always be a high degree of concern for
epiphyseal growth arrest.
The most common metacarpal fractures involve the necks of the ring and small fingers. These boxer's fractures are most
often seen following a fight. A careful physical examination should be performed to make sure there are no signs of teeth
marks, and an assessment of length and rotation should be done. Radiographs can be used to judge the degree of
angulation and shortening. Owing to the increased mobility in the carpometacarpal joints of the ring and small fingers,
angulation up to 40 to 45 degrees can be tolerated in these digits. The index and long fingers can only tolerate 10 to 15
degrees of angulation. An attempt at closed reduction should be made in all of these fractures. Following the reduction, a
splint should be applied with the hand in the intrinsic plus position (MCP joints flexed to 70 to 90 degrees, and the PIP
and DIP joints extended). If an acceptable closed reduction is not obtained, the patient should undergo either an open or
a percutaneous fixation. Immobilization for 3 to 4 weeks is usually required for these fractures to achieve clinical union
before initiating range-of-motion exercises. Radiographic evidence of union lags behind clinical union by 2 to 3 weeks.
Shaft fractures are plagued by the same potential problems as neck fractures, including shortening, angulation, and
rotational deformity (Fig. 55.4A and Fig. 55.4B). These fractures can be transverse, spiral, oblique, or comminuted and
should be treated with initial closed reduction followed by open reduction and internal fixation if necessary. For the
athlete, an Orthoplast splint can often be used to allow early return to play. Approximately 20 degrees of angulation is
acceptable in the ring and small metacarpals, but no more than 10 degrees should be accepted in the index and long
(Fig. 55.5A and Fig. 55.5B).
FIGURE 55.4. A: AP view of comminuted fracture of ring finger metacarpal. B: AP view of restoration of length of
metacarpal with percutaneous fixation.
FIGURE 55.5. A: AP view of gunshot to index metacarpal. B: AP view of operative stabilization of index metacarpal.
Fractures involving the metacarpal bases are usually stable, and carpometacarpal dislocation or subluxation needs to be
ruled out. Proper radiographs, such as appropriate oblique views or CT scan, may be needed. More important, fractures
involving the base of the thumb and small metacarpal have a high risk of displacement, such as in Bennett and reverse
Bennett fractures.
Bennett and Rolando fractures are eponyms used to describe two types of intraarticular fractures of the base of the
thumb metacarpal. The mechanism is usually an axial load applied to a partially flexed metacarpal. The Bennett fracture
is really a fracture subluxation and the Bennett fragment is the ulnar or volar aspect of the metacarpal base. If the
fracture has a T or Y intraarticular pattern, then it is called a Rolando fracture and is a true fracture dislocation. The goals
when treating these fractures are to reduce the subluxation or dislocation at the carpometacarpal joint and to restore
articular congruity (60).
In summary, although there are many different types of metacarpal fractures, the tenets of treatment remain the same.
Restoration of articular incongruity, length, rotation, and prevention of joint stiffness are important to the functional
outcome. Most of these fractures can be treated closed, but do not hesitate to recommend surgery in the face of an
inadequate or lost reduction.
SOFT TISSUE INJURIES
Metacarpophalangeal Joint Dislocations
Injury to the MCP joints of the fingers are rare in athletics. This is due in part to the inherent stability provided by the
capsule, volar plate, collateral ligaments, deep transverse metacarpal ligament, and protected position at the base of the
fingers. Despite this elaborate intrinsic supporting structure, the MCP joint is vulnerable to dislocation and collateral
ligament injury by dorsally and ulnarly directed forces.
Dislocation of the MCP joints can be classified as dorsal and volar, and simple or complex ( 61). By definition, a simple
dislocation is reducible by closed reduction, but a complex dislocation is not. This distinction is due to the difference in
distortion of the normal anatomy created by each dislocation. In both types of dislocation, the volar plate remains
attached to the proximal phalanx distally. In a simple dislocation, by contrast, the proximal phalanx rests on the dorsum of
the metacarpal head and the proximal volar plate is not interposed. Complex dislocations allow the entire volar plate to
be drawn between the base of the proximal phalanx and the metacarpal head, owing to loss of contact between the
metacarpal head and the phalangeal base.
The reduction maneuver for simple dislocations should include wrist flexion, to relax the flexor tendons; hyperextension;
traction; and flexion of the proximal phalanges. This procedure slides the base of the proximal phalanx over the
metacarpal head into a reduced position ( 62). It is possible to convert a simple dislocation into a complex dislocation with
too aggressive traction and hyperextension. Following reduction, simple dislocations can be managed with extension
block splinting, with gradual resumption of active range of motion. After this, buddy taping is usually adequate treatment,
but risk of reinjury in the acute period warrants protective splinting once return to play occurs.
Patients with complex dislocations hold the finger in a slightly extended position and have no ability to flex the finger. The
distal joints are slightly flexed, and there is some deviation toward the adjacent, more central digit. Detailed examination
shows a prominence in the palm, which is the metacarpal head, and there may be some adjacent dimpling. Radiographs
reveal joint space widening, and a sesamoid may be identified in the joint space. This is pathognomonic of a complex
dislocation (61). The lateral image shows that the phalanx and metacarpal are parallel. A dorsal or volar surgical
approach can be used to afford reduction. The dorsal approach is advocated by many with less risk of neurovascular
injury. Others have insisted that the pathologic anatomy of the volar structures blocking reduction cannot be addressed
from a dorsal approach and advocate a volar approach. Following open reduction, extension block splinting is used to
prevent hyperextension. These metacarpophalangeal joints are usually immobilized in 30 degrees of flexion for 2 weeks
after which active range of motion is begun with blocking of the terminal 10 degrees of extension. At 4 weeks, a splint can
be used for protection. By 6 weeks the splint can be discarded.
Irreducible volar dislocations of the MCP joints have been described but occur rarely. The structures that impede
reduction include the dorsal capsule, which is pulled off the distal aspect of the metacarpal and interposed between the
proximal phalanx and the metacarpal head or the volar plate pulled off the base of the proximal phalanx distally. Given
adequate anesthesia, an attempt at closed reduction is warranted. Failure to obtain a closed reduction necessitates a
dorsal or combined volar and dorsal approach.
Collateral ligament injuries of the finger MCP joints most often involve the radial-sided ligament, and the ulnar three digits
are most commonly affected. The mechanism of injury involves an ulnar directed force on a flexed MCP joint. Unless
there is gross instability, initial treatment should consist of immobilization in 30 degrees of flexion for three weeks,
followed by 2 to 3 weeks of buddy taping to the adjacent radial digit. Pain may be present for up to 1 year following this
injury.
Injuries of the Metacarpophalangeal Joint of the Thumb
Injuries to the MCP joint of the thumb are frequently seen in skiers and ball-handling athletes (e.g., racquetball, football).
This joint has features of both a condyloid and ginglymus joint with motion in flexion and extension primarily and
secondarily in abduction and adduction, and pronation and supination. Range of motion of the MCP joint of the thumb
has been found to be the most variable of any joint in the human body and even differs from side to side in the same
individual ( 63).
The most common mechanism of injury is that of forced abduction (radial deviation) often resulting from a fall onto an
outstretched hand with the thumb abducted. Ulnar collateral ligament injuries occur 10 times more frequently than radial
collateral ligament tears ( 64). Often, there are associated injuries, and these include the dorsal capsule, ulnar portion of
the volar plate, and the adductor aponeurosis.
Examination reveals swelling, ecchymosis, and tenderness along the ulnar border of the metacarpophalangeal joint.
Treatment is based on differentiating between complete and partial tears. Clinical examination is critical to making this
diagnosis, although some use stress radiographs. The examination involves applying an abduction force to the proximal
phalanx while stabilizing the metacarpal. This should be done in extension as well as in 30 degrees of flexion. In a
complete injury there will be no endpoint and the joint can be abducted greater than 45 degrees. There may be some
laxity present in a partial tear, but there will still be an endpoint. Another indication is the ability to abduct the joint at least
15 degrees more than the contralateral thumb ( 65). It is mandatory to always test the uninjured side as a baseline. Some
patients have too much apprehension and guarding to allow an adequate examination of stability and may require an
initial digital nerve block.
Partial tears of the ulnar collateral ligament can be effectively treated by 4 weeks of immobilization in a thumb spica cast
or splint, followed by 2 weeks of splint immobilization, during which time active range-of-motion exercises can be begun.
Stress activity of the thumb should be avoided for 3 months. Football players may return to play with adequate
immobilization in 3 to 10 days. Volleyball and basketball players, however, require protective splinting for an entire
season because these sports cause frequent loading. Skiers can use gauntlet casts or commercially available gloves
with no time lost so long as pain does not restrict the ability to grip the pole.
The treatment of acute complete tears is not as straightforward as that of incomplete injuries. Owing to the regional
anatomy, the adductor aponeurosis is often interposed between the torn ligament and the phalanx. This is called a
Stener's lesion ( 66), and it will prevent healing of the ligament in an anatomic position. Owing to the significant
association of the Steners lesion and poor ligament healing, and the inability to determine whether one is present or not,
operative treatment has become the standard for all complete tears. The tear usually occurs distally at the insertion site
of the ligament on the proximal phalanx. The goal of treatment is to restore the ligament to its original anatomic position.
This can be done with either suture anchors or suture tied over a button. The tear is rarely in the midsubstance of the
ligament, in which case it would be amenable to primary repair.
If the condition is not recognized early, the patient may be left with a chronic gamekeeper's thumb and require ligament
reconstruction rather than anatomic repair of the native ligament. The reconstructive options available include tendon
transfer, tendon grafts, and fusion in the event that arthrosis is present.
Injuries of the radial collateral ligament of the thumb are less common and generally less debilitating because the thumb
is more subjected to abduction rather than adduction forces. The diagnostic and therapeutic approach is similar to that
for injuries of the ulnar collateral ligament.
Dislocations of the MCP joint of the thumb can occur either dorsally or volarly, with the dorsal type being more common.
Simple dorsal dislocations can be reduced with wrist flexion, interphalangeal joint flexion, and gentle volar pressure on
the proximal phalanx. Complex dislocations require open reduction. Generally, with a dorsal dislocation, the volar plate is
torn, but the collateral ligaments remain intact. For any of these dislocations, postreduction examination is mandatory to
assess joint stability. If the joint is unstable, the collateral ligaments must be examined and treated as previously
described.
Proximal Interphalangeal Joint Injuries
The spectrum of PIP joint injuries ranges from the athlete's mundane “jammed finger” to the potentially disabling
irreducible fracture dislocation. The PIP joint is a hinge joint with stability due to its bony architecture and periarticular
ligaments, and secondarily due to its adjacent tendon and retinacular structure ( 67). The ligamentous support is provided
by the volar plate, and primary and accessory collateral ligaments. In order for displacement to occur at the PIP joint, at
least two of the three sides of this complex must be disrupted. The normal range of motion is from 0 to 110 degrees of
flexion. The long lever arms of the proximal and middle phalanx predispose this joint to injury. These injuries need to be
treated expeditiously and aggressively to avoid late instability and stiffness.
Collateral Ligament Injuries
Collateral ligament injuries are quite common in most contact sports. Participants in football, wrestling, and baseball are
prone to such injuries, with the radial collateral ligament being the most common.
Clinical examination is paramount in determining the area of injury and should include an attempt at quantitating the
extent to which the joint opens and the proximal phalanx deviates with stress ( 68,69). The ultimate determinant of
treatment, however, is based on the stability of the joint with active motion. The patient should be asked to move his or
her finger through a complete range of motion. Adequate joint stability remains if there is no documented instability.
Redisplacement through the arc of motion indicates major ligament disruption. Then the PIP joint can be tested passively
to radial and ulnar stresses (in extension and 30 degrees of flexion) and dorsal and volar stresses. As with any joint
injury, the opposite side should always be used as a baseline. Studies have shown that greater than 20 degrees is
indicative of a complete ligamentous tear ( 68). Radiographs should include a true AP and lateral image of the digit to
make certain that there is no evidence of articular injury.
Incomplete tears should be immobilized with buddy tape to limit radial and ulnar deviation while allowing active flexion
and extension. This tape should be used for approximately 6 weeks during athletic participation. The treatment of
complete ligament injuries remains controversial. There are two camps. The patient can undergo closed treatment with
early motion and protective buddy taping, or primary repair. Nonoperative treatment leaves the patient with a swollen,
tender joint, that is potentially unstable and susceptible to reinjury. Although operative treatment may expedite the
athlete's return to sport ( Fig. 55.6A and Fig. 55.6B), the risks of operative intervention and subsequent stiffness must be
weighed against those of chronic instability. Reconstructive options exist to treat chronic instability, although these
procedures are difficult and results vary.
FIGURE 55.6. A: AP view of ulnar collateral ligament injury to long finger metacarpophalangeal joint. B: AP view of
restoration of ulnar collateral ligament of base of proximal phalanx.
Proximal Interphalangeal Joint Dislocation
PIP joint dislocations are most commonly seen in ball-handling sports, such as football, basketball, and baseball,
although they occur in many other sports and are commonly referred to as a “jammed finger.” The direction of dislocation
can be volar, lateral, or dorsal. There is often a tendency on the part of the athlete to minimize the injury, which can lead
to serious disability.
The mechanism of injury is one of hyperextension with some degree of axial loading of the PIP joint while it is in
extension. Often, these injuries are reduced on the playing field by a teammate or an athletic trainer. If no associated
collateral ligament injury or major fracture is noted, these injuries are amenable to volar splinting in 20 to 30 degrees of
flexion for 2 to 3 weeks. The athletes can be allowed to participate given adequate immobilization.
From a diagnostic standpoint, it is desirable to obtain AP and lateral images before reduction to determine whether there
are any fractures present. Postreduction radiographs are essential to document a congruous joint after reduction and to
be sure that there is no soft tissue interposition.
Dorsal dislocations of the PIP joint are the most common and result from a dorsal and axial applied load to an extended
PIP joint (Fig. 55.7A and Fig. 55.7B). In the vast majority of cases, dorsal dislocations are amenable to closed reduction
by gentle traction, mild hyperextension, and gradual flexion. These simple dislocations can then be treated with an
extension block splint for 3 weeks, thus allowing immediate motion and preventing instability. Following this period of
limited mobilization, buddy taping is encouraged for an additional 4 weeks. On rare occasions, the volar plate ruptures
proximally and can become interposed between the head of the proximal phalanx and the base of the middle phalanx
leading to an irreducible dislocation.
FIGURE 55.7. A: AP view of dislocation of proximal interphalangeal joint of index finger. B: Lateral view of dorsal
dislocation of proximal interphalangeal joint.
Distal Interphalangeal Joint Injuries
Distal Interphalangeal Joint Dislocation
Dislocation of the DIP joint usually results from a hyperextension type mechanism such as striking a helmet or trying to
catch a ball. Most of the time, these injuries are treated as trivial and reduced with longitudinal traction on the field by a
trainer or teammate. These injuries are usually stable following reduction but should be checked for associated injuries to
the collateral ligaments and or flexor or extensor tendons or fracture.
The direction of dislocation is dorsal in most cases. The DIP joint should be immobilized in extension excluding the PIP
joint for 6 to 7 weeks following the injury. At 3 weeks, the patient can begin flexion exercises, and protective splinting can
be worn for an additional 2 to 4 weeks during athletic participation until full range of motion is regained and no
tenderness is present.
Avulsion of the Flexor Digitorum Profundus
More commonly known as a jersey finger, this injury usually results when the actively contracting flexed fingers are
grabbing the jersey of an opponent, because the ring finger most commonly is extended.
The history is the key in making the diagnosis and should arouse a high degree of suspicion when evaluating the athlete.
Often, the athlete will present with pain and swelling in the finger, and the lack of DIP flexion will be dismissed as being
secondary to soft tissue edema and pain. Clinical examination often reveals a limitation of DIP motion and a diminished
grip strength. Radiographs are essential in the workup to rule out any associated fractures.
Leddy and Packer described three types of avulsions of the profundus tendon ( 70): (a) The first type involves avulsion of
the tendon with retraction into the palm. This injury must be treated expeditiously within 7 to 10 days, before tendon
degeneration and contraction. If this is not diagnosed acutely, a reconstructive option can be chosen. These options
include a free tendon graft, DIP joint fusion, or tenodesis. (b) The second type involves those injuries in which the tendon
is prevented from further retraction by the long vincula and is found at the level of the PIP joint. This injury can be treated
up to 6 weeks from the initial event because the vincular blood supply is preserved. Because a type 2 injury can convert
to a type 1 injury, it should probably be repaired in a timely fashion, as with type 1 avulsions. (c) The last group includes
tendons that are avulsed with a large fragment of bone and are held up by the A4 pulley at the level of the middle
phalanx. These injuries can be fixed by obtaining an anatomic reduction of the avulsed bony fragment.
Early recognition is key in dealing with these injuries in order to obtain a good result. Late symptoms include stiffness of
the DIP joint, decreased range of motion of the PIP joint, and possibly pain and a fullness in the palm.
Injury to the Extensor Tendon of the Distal Interphalangeal Joint
Often referred to as a mallet finger, these injuries are usually the result of a hyperflexion force on an already extended
DIP joint. These injuries are some of the most frequently seen and are especially common in the football receiver,
baseball catcher or fielder, and the basketball player ( 71,72).
Clinically, the patient presents with a finger in which the distal phalanx is held in a flexed posture and is swollen and
tender dorsally. The DIP joint can usually be extended passively. Early diagnosis is key in instituting treatment acutely
and preventing the development of a swan-neck deformity. This deformity classically occurs in the long-standing mallet
finger due to proximal retraction of the lateral bands in the presence of volar plate laxity. A mallet deformity can occur
from either complete disruption or attenuation of the tendon. Radiographs are important to rule out the presence of an
associated fracture fragment. On occasion, these injuries are the result of an avulsion-type mechanism and involve a
significant intraarticular component.
The acute injury can most often be treated with a conservative approach. This approach consists of immobilizing the DIP
joint in extension for 8 weeks continuously, followed by 2 to 4 weeks of nighttime wear. When placing the patient in the
splint, it is important to check the dorsal skin to be sure that there is adequate circulation and that the joint has not been
placed in hyperextension. If the joint is splinted improperly in hyperextension, blistering and loss of dorsal skin may result
(73). It is often debated whether a volar or dorsal splint is better, and a variety of splints are used. The athlete should be
instructed on the proper care of the digit, because the DIP joint must not be allowed to fall into flexion at anytime when
the splint is removed in order to clean the finger. If at any point during the 8-week period the DIP joint is allowed to fall
into flexion, some of the healing that has taken place can be disrupted, leading to failure of the treatment. The splint
should be worn for 2 months following treatment during athletic activities. Injuries up to 2 to 3 months after the initial
injury have been treated with this same protocol. In the presence of a painful arthritic mallet finger, arthrodesis in 5 to 10
degrees of flexion is the treatment of choice ( 74,75).
The treatment of the mallet finger with a significant intraarticular fragment remains controversial. Many advocate
attempting an initial closed reduction, followed by a lateral radiograph to evaluate joint congruency and restoration of the
articular surface. If closed reduction is successful, these injuries can be treated in a similar manner to soft tissue mallet
injuries. Follow-up needs to be conducted on a regular basis in order to repeat radiographs so that the joint can be
assessed. The results of surgical treatment are unpredictable even in the best of hands and should be restricted to those
individuals with significant joint pain, functional disability, cosmetic deformity, or swan-neck deformity resulting in altered
function (76). A splint should be used for 6 to 8 weeks, and for the next 2 months, the digit should be protected during
athletic participation with splinting or buddy taping. Surgical management for bony mallet fingers is mandatory if volar
subluxation of the distal fragment exists.
Fractures of the phalanges can occur in either the proximal, the middle, and or the distal phalanx of the hand, and are
some of the most common injuries seen in athletes. Many different treatment modalities are used for these fractures, from
splinting to open reduction and internal fixation. The decision to use operative versus nonoperative treatment is based on
the character of the fracture and the presence of significant intraarticular involvement. The therapeutic goals are to
maintain range of motion of the joint while avoiding any rotational or angulatory displacement, and or significant amount
of axial shortening.
Nondisplaced fractures of the phalanges can usually be treated nonoperatively regardless of location. The treatment
regimen usually involves a short course of splinting, followed by gentle active range-of-motion exercises. The therapy
should begin at 3 weeks, and the splint should be worn for 6 weeks during daily activities. Buddy taping to the adjacent
digit should be continued for 2 additional weeks during athletic competition.
Fractures involving the proximal phalanx usually develop apex volar angulation due to the pull of the intrinsics on the
proximal fragment and the pull of the extensor on the distal fragment. As long as the rotation and length of the fracture
can be controlled, these fractures can be treated conservatively. Intraarticular fractures are treated with the same
principles of articular restoration that apply to other joints. Fractures involving the condyles or those with rotational
problems need to be managed with open reduction and internal fixation, or closed reduction and percutaneous pinning.
Those fractures involving the middle phalanx can be either dorsally or volarly angulated depending on their location.
Extraarticular fractures can be managed conservatively with closed reduction and splinting, as long as there are no
associated rotational or length abnormalities. Fractures not amenable to closed techniques require operative
stabilization, as do displaced intraarticular fractures.
Distal phalanx fractures can also be treated with immobilization most of the time but must always be of concern when
there is involvement of the nail bed. The benign-appearing nail bed injury may mask an open fracture, which requires
irrigation and debridement to prevent acute infection, nonunion, and osteomyelitis.
These injuries can be rather debilitating to athletes involved in sports that require a lot of ball handling and should be
treated with adequate protection to allow an expedient and safe return to the particular sport.
Nerve Compression Syndromes
Although they are not as common as other injuries involving the hand and wrist, nerve compression syndromes are just
as disabling and troublesome to the athlete. These conditions more often are the result of repetitive activities and less
likely the result of an acute traumatic event. Like other aliments affecting the hand and wrist, an accurate diagnosis is
crucial in managing these syndromes. Conservative management is still the mainstay for any of these conditions in the
initial stages of treatment. When a thorough workup has been completed in the face of worsening symptoms, operative
management may be indicated.
Carpal Tunnel Syndrome
This is the most common, the best defined, and the most carefully studied entrapment neuropathy. It is usually found in
association with flexor tenosynovitis or lumbrical muscle hypertrophy, and it is usually seen in sports that involve
repetitive grasping activities.
The athlete typically presents with complaints of numbness and tingling in the radial three and one half digits, and it
usually occurs during activities. Occasionally, the patient gives a history of nocturnal awakening with pain and
paresthesias. On physical examination, the patient typically has a positive Tinel sign (high sensitivity), Phalen's test (high
specificity), and carpal tunnel compression test (most sensitive and specific). In chronic cases changes, in two-point
discrimination and thenar atrophy may be present. Electrodiagnostic studies are helpful, not only for confirming the
diagnosis but also in determining the severity of compression ( 77).
Initial management of the athlete with no signs of atrophy or sensory changes should include a program of extension
splinting to rest the wrist. A nonsteroidal antiinflammatory agent may be added if symptoms persist despite
immobilization. Another alternative is to administer a steroid injection in the carpal tunnel, which is both diagnostic and
therapeutic. Wood ( 78) has demonstrated a correlation between response to injection and results of surgical
decompression. When a patient has failed to improve, worsened, or has signs of chronic compression, surgical
decompression is warranted. Many different techniques are now available, although open decompression still remains
the gold standard. The athlete should be aware that it will be 3 to 4 months before grip strength returns to baseline.
Ulnar Nerve Compression
The ulnar nerve can be compressed at either the elbow or the wrist. Racquet-type sports and those that involve repetitive
trauma to the hypothenar area are risk factors for ulnar neuropathy at the wrist, although it is more common at the elbow.
Clinical examination is the key in documenting the anatomic site of compression. Cubital tunnel symptoms are usually
associated with elbow flexion, and symptoms are limited to paresthesias initially. Examination demonstrates a positive
Tinel sign at the elbow and a positive elbow flexion test. When the site of compression is at Guyon canal, the patient may
have a pure sensory, pure motor, or combined lesion. Advanced lesions can have associated intrinsic and hypothenar
wasting. Electrodiagnostic studies are valuable in confirming the diagnosis of distal compression, but are often normal in
cases of cubital tunnel syndrome. Treatment should initially include rest, immobilization, and antiinflammatory
medications. In advanced or unremitting cases, surgical decompression should be undertaken.
Ulnar nerve compression can also be due to other entities such as hook of hamate fractures, ulnar artery thrombosis, and
disorders of the pisiform. Cyclist's palsy is another cause of ulnar nerve symptoms and is usually due to repetitive
contusion at the wrist. Symptoms can be either pure sensory, motor, or both. Factors found to contribute to the frequent
development of this condition in cyclists include worn-out gloves, unpadded handlebars, vibration from rough roads,
riding a poorly fitted bicycle, and prolonged grasping of dropped handlebars ( 79,80). Management should include
cessation of activity that leads to continued pressure on the hypothenar eminence and splinting; nonsteroidal
antiinflammatory medications can be useful. If this measure fails to provide relief, then a decompression of the nerve at
Guyon canal is warranted. The athlete will be unable to return to activities for 6 weeks following surgery. Another cause
of ulnar nerve symptoms at the wrist is hypothenar hammer syndrome. Every patient with reports of ulnar nerve
symptoms at the wrist should undergo an Allen test to rule out ulnar artery thrombosis or aneurysm.
Bowler's Thumb
First described by Dobyns (81), bowler's thumb is thought to be due to chronic compression of the ulnar digital nerve of
the thumb secondary to irritation by the hole of the ball. Perineural fibrosis results in a spindle neuroma. Patients usually
present with complaints of distal paresthesias and alterations in sensation. Conservative treatment is usually satisfactory
to ameliorate the symptoms and consists of rest. Also, a padded glove can be used over the thumb to prevent further
irritation. Failure of conservative management requires neurolysis and possible transposition. Following surgery, the
patient should use a glove or padding over the thumb when bowling.
CONCLUSION
We have described the diagnosis and management of some of the more common athletic injuries to the hand and wrist.
In general, a good outcome is defined similarly in the athlete and nonathlete alike. In both situations, attention to detail
and compliance with postoperative therapy are critical to satisfactory return of function. In the athlete, quicker return to
activity may necessitate earlier surgical intervention at times, but if this is at the expense of the expected functional end
result, the patient needs to be fully aware of the ramifications.
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56 Knee Injuries
56
KNEE INJURIES
MARK B. SILBEY
FREDDIE H. FU
Anatomy
Joint Capsule
Extensor Mechanism
Medial Ligamentous Complex
Lateral Ligamentous Complex
Cruciate Ligaments
Menisci
Popliteal Fossa
Hamstrings
Neurovasculature
Biomechanics
Evaluation of Injuries
Disorders of the Extensor Mechanism
Evaluation
Radiographic Evaluation of the Patellofemoral Joint
Acute Patellar Dislocation
Patella Fracture
Ligamentous Injuries
Collateral Ligament Injury
Posterior Cruciate Ligament and Posterolateral Corner
Meniscal Injuries
Diagnosis
Treatment
Discoid Lateral Meniscus
Articular Cartilage Injuries
Anatomy
Physical Examination and Evaluation
Surgical Treatment of Articular Cartilage Injuries
Knee Dislocation
Evaluation
Management
Tibial Spine and Intercondylar Eminence Fractures
Signs and Symptoms
Treatment
Chapter References
ANATOMY
The knee is composed of a hinge joint between the femur and tibia, and an arthrodial joint between the femur and patella.
It is divided into three compartments: medial, between the medial femoral condyle and medial tibial plateau; lateral,
between the lateral femoral condyle and lateral tibial plateau; and patellofemoral, between the patella and the femur.
The femoral condyles form the rounded, articulating portion of the distal femur. The medial femoral condyle has a larger
anterior-to-posterior diameter and a more symmetric curve than the lateral femoral condyle. The lateral femoral condyle
is shorter than the medial femoral condyle and has a larger medial-to-lateral diameter. Between the two condyles is the
intercondylar notch, which is contiguous with the anterior surface along which the patella tracks, known as the trochlear
groove.
The proximal tibia is composed of the medial and lateral plateaus, the tibial spines, and the articular facet for the head of
the fibula. There is a 10-degree posterior slope. The medial plateau is larger and flatter than the lateral plateau, which is
concave. The medial and lateral tibial spines arise between the two plateaus.
The patella is a sesamoid bone located within the tendon of the quadriceps femoris muscle. It is divided by a ridge into a
larger lateral and smaller medial segment. These are then subdivided into thirds, plus a seventh or odd facet along the
medial border. With extreme flexion, only the odd facet is in direct contact with the trochlear groove.
The proximal tibiofibular joint is a diarthrodial joint composed of the head of the fibula and its tibial articulation just distal
to the lateral tibial articular surface. It allows for the slight up and down gliding motion and is stabilized by an articular
capsule, small anterior and posterior ligaments, and the interosseous membrane.
Joint Capsule
The articular capsule surrounds the knee joint and is lined by a synovial membrane. This membrane extends proximal to
the patella beneath the vastus muscles. It extends distally beneath the patellar tendon with the infrapatellar fat pad
separating the synovium from the tendon. The synovium is reflected anterior to the cruciate ligaments and inserts on the
tibia. The capsule joins with the menisci at their periphery, forming the meniscocapsular junctions. Also, medially and
laterally, synovial folds may converge in the joint cavity to form to plica on either side. Posterior to the lateral meniscus,
the capsule forms a sac between the meniscus and the popliteus tendon.
Extensor Mechanism
The extensor mechanism is composed of the quadriceps tendon, the patella, and the patellar tendon. The quadriceps
tendon is formed by the tendinous distal expanses of the rectus femoris, vastus medialis, and vastus lateralis muscles,
inserting on the proximal pole of the patella and forming a retinacular sheath over the patella. The vastus medialis
obliquus muscle has its own insertion at the proximal pole. The distal portion of the extensor mechanism is formed by the
patellar tendon (ligament), extending from the inferior pole of the patella to its insertion on the tibial tubercle. These
structures form the primary extensors of the knee, with the tensor fascia lata performing a secondary role.
Medial Ligamentous Complex
The medial and lateral sides of the knee are each composed of three layers (I, II, and III from superficial to deep), which
have been well described ( 1,2 and 3). On the medial side, the outer layer consists of the deep fascia that supports the
muscle bellies and neurovascular structures in the popliteal region. It contains the insertion of the sartorius muscle.
Separating layers I and II are the tendons of the gracilis and semitendinosus muscles. These tendons insert on the tibia
along with the sartorius muscle at the pes anserinus ( Fig. 56.1).
FIGURE 56.1. Anatomy of the medial aspect of the knee. (From Hoppenfeld S, deBoer P. Surgical exposures in
orthopaedics: the anatomic approach. Philadelphia: Lippincott, 1984:408, with permission.)
The medial or tibial collateral ligament extends from the medial epicondyle to the medial aspect of the medial tibial
plateau. It is composed of superficial and deep portions. The superficial medial collateral ligament (MCL) makes up layer
II. This structure, along with the tendon sheath of the semimembranous muscle, blends with layer III, the capsule of the
knee joint, at the posteromedial corner, forming the posterior oblique ligament ( Fig. 56.2). In addition, the oblique
popliteal ligament is formed by the fibers of the semimembranous tendon sheath that pass obliquely across the knee to
insert on the posterior aspect of the lateral femoral condyle ( Fig. 56.3). Also, the patellofemoral ligament is formed by a
band of fibers running from the anterior portion of the superficial medial collateral ligament to the lateral patella, deep to
the vastus medialis. It helps provide stability to the patellar-tracking mechanism. The deep portion of the MCL is formed
by a thickening of the capsular fibers of layer III and extends from the femur to the peripheral aspect of the meniscus and
tibia. The remainder of the capsule attaches the meniscus to the tibia, forming the meniscotibial or coronary ligament that
prevents excessive motion of the meniscus.
FIGURE 56.2. The posteromedial corner of the knee. Numbers correspond to the insertions of the semimembranosus
tendon and its sheath. (From Warren LF, Marshall JL. The supportive structures and layers on the medial side of the
knee. An anatomical analysis. J Bone Joint Surg 1979;61:56, with permission.)
FIGURE 56.3. The posterolateral corner of the knee. (From Seebacher JR, Inglis AE, Marshall JL, et al. The structure of
the posterolateral aspect of the knee. J Bone Joint Surg 1982;64:536, with permission.)
Lateral Ligamentous Complex
On the lateral side, the lateral or fibular collateral ligament extends from the posterior aspect of the lateral femoral
condyle to the lateral side of the head and styloid process of the fibula. The superficial layer of the lateral side, layer I, is
composed of two parts: the iliotibial tract anteriorly and the biceps femoris posteriorly ( 1). Just posterior to the biceps
tendon is the peroneal nerve. Layer II is formed anteriorly by the retinaculum of the quadriceps tendon. Posteriorly, it is
made up of two patellofemoral ligaments: one proximal and one distal. A patellomeniscal ligament is also present. Layer
III is the lateral joint capsule. A coronary ligament extends from capsule to meniscus, just as on the medial side. The
popliteus tendon passes through an opening to the coronary ligament, the popliteal hiatus. The capsule divides into two
laminae. The superficial lamina encompasses the lateral collateral ligament and forms the patellofibular ligament
posteriorly. The deeper lamina forms the arcuate and coronary ligaments. The arcuate and patellofibular ligaments insert
on the fibular styloid process and extend proximally to the lateral head of the gastrocnemius muscle. At this point, they
merge with the oblique popliteal ligament ( Fig 56.3).
Cruciate Ligaments
The two cruciate ligaments help check extension, lateral rotation, and motion of the tibia on the femur. The anterior
cruciate ligament (ACL) extends from the posterior aspect of the lateral femoral condyle anteriorly to the tibial eminence
and controls anterior motion of the tibia on the femur. The posterior cruciate ligament (PCL) extends from the lateral
aspect of the medial femoral condyle to the posterior aspect of the lateral meniscus and proximal tibia and controls
posterior motion of the tibia on the femur (Fig. 56.4). The ligaments are discussed in more detail later in this chapter.
FIGURE 56.4. A: Anterior view of anterior and posterior cruciate ligaments. B: Posterior view of anterior and posterior
cruciate ligaments. C: Lateral views of anterior and posterior cruciate ligaments.
Menisci
The menisci are cartilaginous structures that deepen their respective tibial articular surfaces. The medial meniscus is
crescent shaped and attaches to the tibia in front of the ACL and in the posterior intercondylar fossa. The lateral
meniscus is more circular and attaches to the tibia in front of the ACL and posteriorly behind the tibial eminence but
anterior to the medial meniscus. It also is attached to the medial femoral condyle through the anterior and posterior
meniscofemoral ligaments, known as the ligament of Humphry and the ligament of Wrisberg, respectively. The anterior
horns of the menisci are interconnected by the transverse ligament ( Fig. 56.5).
FIGURE 56.5. Tibial articular surface.
Popliteal Fossa
Posteriorly, the popliteal fossa is a diamond-shaped space. It is bounded by the biceps femoris muscle laterally and
above, the semimembranosus and semitendinosus medially and above, the lateral head of the gastrocnemius muscle
laterally and below, and the medial head of the gastrocnemius medially and below. The floor is formed by the femur,
oblique popliteal ligament, and popliteus muscle. The popliteal fossa contains the popliteal artery and vein, tibial and
common peroneal nerves, the termination of the small saphenous vein, the distal end of the femoral cutaneous nerve,
and articular branches of the obturator nerve ( Fig. 56.6).
FIGURE 56.6. Popliteal fossa.
Hamstrings
The semimembranosus and semitendinosus muscles (innervated by the tibial nerve), along with the sartorius and gracilis
muscles (innervated by the femoral and obturator nerves, respectively), make up the medial hamstring group. The biceps
femoris muscle makes up the lateral hamstring muscle and is composed of a long head (innervated by the tibial nerve)
and a short head (innervated by the common peroneal nerve). These act as the flexors of the knee joint along with the
popliteus, gastrocnemius, and plantaris muscles. As previously mentioned, the quadriceps femoris muscle (innervated by
the femoral nerve) and the tensor fascia lata (innervated by the superior gluteal nerve) are responsible for knee
extension. Medial rotation of the knee is achieved by the popliteus, semimembranosus, semitendinosus, sartorius, and
gracilis muscles. Lateral rotation is achieved by the action of the biceps femoris.
Neurovasculature
The arterial network about the knee arises from the popliteal artery as it emerges from the hiatus of the adductor magnus
muscle. The popliteal artery passes into the popliteal fossa, giving off superior medial, lateral and inferior medial, and
lateral geniculate branches. The popliteal vein is formed by the anterior and posterior tibial veins at the level of the
popliteus muscle insertion on the tibia. It continues proximally to form the femoral vein.
The sciatic nerve divides into tibial and common peroneal branches in the posterior thigh just proximal to the knee. The
tibial nerve passes deep to the biceps femoris and then crosses superficial to the vessels to reach the medial side. It then
continues distally as the posterior tibial nerve. The common peroneal nerve passes along the deep medial border of the
biceps femoris and distally around the fibular neck before dividing into the superficial and deep peroneal nerve branches
(4,5,6,7,8,9,10,11,12,13,14,15,16,17 and 18).
BIOMECHANICS
An understanding of the fundamental biomechanical principles of knee motion is crucial to the diagnosis and
management of sports injuries of the knee. As both a hinge joint and an arthrodial joint, the knee operates with six
degrees of freedom. There are three planes of translation and three planes of rotation. Translation occurs in the
anteroposterior plane (5 to 10 mm), the mediolateral plane (1 to 2 mm), and the compression-distraction plane (2 to 5
mm). Rotation occurs as flexion and extension, varus and valgus, and internal and external. The normal range of
extension is from 0 to 15 degrees of hyperextension. The normal range of flexion is from 130 to 150 degrees. Internal and
external rotation range from 20 to 30 degrees with the knee in full extension.
During the first 15 to 20 degrees of flexion, there is a pure rolling motion of the femoral condyles relative to the tibial
plateau. By 10 to 15 degrees of flexion on the medial side and 20 degrees on the lateral side, gliding of the femur
posteriorly on the tibia begins and becomes progressively more important as flexion continues. Subsequently, the
femoral condyles rest on the posterior horns of the menisci ( 4). In addition to the rolling and gliding motions, during
terminal extension, the tibia must externally rotate to accommodate the larger anteroposterior (AP) diameter of the medial
femoral condyle relative to the lateral femoral condyle. This is known as the “screw home mechanism” and is dictated by
the asymmetry of the condyles as well as the mechanical alignment of the knee and the integrity of the surrounding
capsular and ligamentous structures.
EVALUATION OF INJURIES
The sports medicine history and physical examination are critical to the accurate diagnosis and treatment of injuries.
Physical examination is discussed as it relates to specific injuries. However, a thorough history should be taken as part of
the examination and evaluation process. A basic history-taking format is followed, including chief complaint, history of
present illness, past medical history, and review of systems. History-taking and examination should not be confined to the
knee, because spine or hip problems, leg-length discrepancy, or other musculoskeletal pathology may result in symptoms
referable to the knee. In addition to basic history, a relevant sports history should include types of sports and level of
involvement, as well as prior injuries. A history of prior or concomitant injuries may be helpful in assessing compensatory
changes in the biomechanics of running, for instance, that may have produced the current symptoms. Similarly, changes
in the training regimen may have resulted in an overuse syndrome. The mechanism of injury plays a large role in
assessing the location of the pathology. Was the onset of pain sudden or gradual? Was this a repetitive stress situation
or was there an acute episode? If the episode was acute, was there a blow to the knee? If so, in what direction was the
blow struck? Was there a twisting injury? Was there an audible “pop?” Did the knee swell? Was the swelling gradual or
immediate? Does the knee lock or give way? When does the pain occur, while starting to run, after a few miles, or after
completing the run? Is there pain going up or down stairs ( 19,20)?
DISORDERS OF THE EXTENSOR MECHANISM
Extensor mechanism disorders may result from trauma but are often associated with intrinsic bone or soft tissue
abnormalities: Symptoms are related to alterations in patellar tracking in the trochlear groove and/or patellofemoral
contact forces (21). The patellofemoral joint is exposed to large forces, as reflected by the fact that the articular cartilage
on the posterior aspect of the patella that acts to transmit this force is the thickest cartilage in the human body. The force
is expressed as a load transmitted from the extensor mechanism to the trochlea by the patella. This load is directly
proportional to the force generated by the quadriceps mechanism and indirectly proportional to the angle of the knee
flexion. The patellofemoral joint reaction (contact) force varies from one-half times body weight with level walking to
seven times body weight with squatting or jogging ( 22,23,24,25 and 26).
The patella also serves to increase the effective power of the quadriceps muscle by increasing the distance of the
quadriceps mechanism from the axis of knee motion, thereby increasing the lever arm of the quadriceps mechanism.
Patellar tracking is affected by several factors. The quadriceps muscles and, in particular, the vastus medialis obliquus
muscle help maintain the patella within the trochlear groove throughout the full range of knee motion. Similarly, the
integrity of the medial and lateral retinaculum and patellofemoral ligaments help maintain proper tracking. Also, the
shape of the patellar and trochlear groove plays a role in patellar tracking. For instance, a flattened lateral femoral
condylar ridge may allow for lateral subluxation of the patella. The Q angle is defined as the angle formed by a line drawn
from the anterior superior iliac spine to the midpatella and a line drawn from the midpatella to the tibial tubercle ( Fig.
56.7). A normal Q angle is up to 10 degrees for men and up to 16 degrees for women ( 26). The Q angle may be
increased by external rotation of the tibia or a laterally positioned tibial tubercle, resulting in abnormal patellar tracking.
Similarly, rotational deformities of the hip or foot may alter the biomechanics of patellar tracking. Also, a high-riding
patella (patella alta) may be associated with tracking problems, whereas a low-riding patella (patella baja) results in
increased patellofemoral joint reaction force and subsequent arthrosis.
FIGURE 56.7. Q angle.
Evaluation
Extensor mechanism problems may be attributed to one of three subgroups: (a) problems of the patellofemoral
articulation; (b) problems of the supporting muscles, tendons, ligaments, and retinaculum; and (c) problems of
mechanical alignment, resulting in altered knee mechanics ( 27,28,29,30 and 31).
Examination of the function and integrity of the extensor mechanism includes evaluation of the entire lower extremity.
Initially, the patient's gait pattern is evaluated. Is the gait antalgic? Is there in-toeing or out-toeing that may reflect
excessive internal or external tibial torsion or femoral anteversion or retroversion? Next, a standing examination is
performed. Is there excessive genu valgum or varum? From the lateral view, is there genu recurvatum or flexion
contracture? This is followed by evaluation of the lower leg and foot alignment. In runners, in particular, it is important to
assess the position of the distal tibia relative to the floor. If the angle formed between the distal tibia and the floor
deviates laterally, then excessive subtalar joint pronation must occur to produce a plantigrade foot. This may occur with
tibia vara or genu varum and produce peripatellar pain ( 28).
The knee is next examined with the patient in the sitting position. The legs hang freely with the knees flexed 90 degrees.
First, patellofemoral crepitation may be tested by placing the examiner's fingertips on the patella and having the patient
actively flex and extend the knee. Crepitation may be graded as 1+, slight “scratching” sensation; 2+, more coarse
“sandpaper-like” scratching; 3+, palpable grinding; and 4+, palpable and audible grinding. This must be distinguished
from the more discrete synovial “pop” that may be normal and nonpathologic, and may reflect the presence of a plica
(synovial fold).
The position of the patella may also be evaluated from the sitting position. Normally, the patella rests in the trochlear
groove. When the knee is flexed 90 degrees, displacement is easily detected by palpating the position of the patella
relative to the femoral condyles. Proximal displacement is referred to as patella alta, and distal displacement is referred
to as patella baja. In addition, the position of the patella relative to the tibial tubercle is noted. Normally, with the knee
flexed 90 degrees, the midline of the patella lines up with the tibial tubercle. Deviation from this axis may contribute to
patellar tracking problems. As the patient extends the knee, the patella is noted to migrate proximally 5 to 7 cm. In the
case of abnormal lateral tracking, the patella is noted to sweep abruptly laterally as it exits the trochlear groove as the
knee reaches full extension.
The patient is next examined in the supine position on the examining table. Initially, the presence or absence of an
effusion is assessed. With the knee in the extended position, the distal thigh is cupped in the palm of the examiner's
hand and fluid from the suprapatellar pouch is gently milked distally ( Fig. 56.8). Using the opposite hand, the examiner
then palpates the peripatellar region for an accumulation of fluid. With the knee remaining extended, the medial and
lateral retinaculum are then palpated and any tenderness is noted. By gently moving the patella medially and laterally the
extent of patellar mobility may be assessed. Patellar gliding may be quantitated by dividing the patella longitudinally into
four quadrants and noting the amount of medial and lateral displacement. For example, gliding of the patella medially so
that two quadrants are displaced across the medial femoral condyle is denoted 2+ medial glide. Apprehension or
guarding on glide testing reflects a tendency toward patellar subluxation or dislocation ( Fig. 56.9). In conjunction,
tenderness along the medial retinaculum or the medial patellofemoral ligament or patellomeniscal ligament may reflect a
recent lateral subluxation or dislocation. This test may be performed more easily with the knee supported in a flexed
position at 30 degrees. Also, as the patella is moved medially and laterally, medial and lateral patellar facet tenderness
may be assessed by palpation of these regions.
FIGURE 56.8. Evaluation of a knee effusion.
FIGURE 56.9. Evaluation of patellar mobility.

Next, the patient is asked to perform a straight-leg raise by tightening the quadriceps muscle and elevating the leg. An
inability to elevate the leg reflects a disruption in the extensor mechanism (quadriceps tendon rupture, patellar tendon
rupture, or patellar fracture), and any soft tissue or bony defects should be palpated and noted. Occasionally, a patient is
unable to perform a straight-leg raise because of pain and accompanying effusion from other knee pathology. Under
such circumstances, the knee may be aspirated and injected with lidocaine. Such a procedure temporarily alleviates the
discomfort and allows for testing of the extensor mechanism. If this is done, the character and amount of the effusion
should be noted (yellow, blood-tinged, bloody, or cloudy) as well as the presence of any fat droplets, which are indicative
of fracture.
The functional quality of the quadriceps muscle is assessed by noting the size and tone of the musculature. In particular,
the degree of the development of the vastus medialis obliquus muscle is noted. If an effusion is not present, an objective
assessment of muscular development may be obtained by measuring the circumference of the distal thigh at a specific
point ( i.e.,10 cm proximal to the superior pole of the patella). In the case of unilateral involvement, a relative comparison
is made to the unaffected limb. The Q angle may be estimated by a line drawn from the anterior superior iliac spine to the
center of the patella and a line drawn from this point to the tibial tubercle.
Radiographic Evaluation of the Patellofemoral Joint
A standard knee x-ray series includes AP and lateral weight-bearing views and a tangential view of the patellofemoral
joint (Fig. 56.10). The AP and lateral views are useful in determining patella alta and baja. This can be done by a number
of methods. Insall and Salvati (32) described a ratio of length of the patellar tendon to the greater diagonal length of the
patella, as seen in the lateral view ( Fig. 56.11). The average value of the ratio is 1.02. This ratio should not deviate by
more than 20%. Therefore, a ratio of 0.80 or less represents patella baja and 1.20 or greater represents patella alta. This
is constant throughout the flexion range.
FIGURE 56.10. A: Standing AP radiograph. B: Standing lateral radiograph. C: Tangential view of the patella.
FIGURE 56.11. Insall and Salvati's method of evaluating patella alta and baja by ratio of patella tendon length ( A) and
greatest diagonal length of patella ( B).
A second method, described by Blumensaat (22), measures patella alta from a lateral view with the knee flexed 30
degrees. A line is drawn across the superior dome of the intercondylar notch. When this line is projected anteriorly, it
should intersect the inferior pole of the patella. If the patella is above this line, it represents patella alta. This
measurement is only applicable when the knee is flexed 30 degrees and may show variability based on the slope of the
dome of the intercondylar notch.
On the AP view, if the tip of the patella is more than 20 mm above a line drawn across the distal margin of the femoral
condyles, it is considered patella alta. AP views are also helpful in evaluating patellar fractures and bipartite patellae.
A tangential view is useful in evaluating the relationship of the patella to the trochlea. The most common methods of
obtaining tangential views were described by Hughston ( 33), Merchant (34), and Laurin ( 35,36). The techniques for
obtaining these views are illustrated in ( Fig. 56.12). The Hughston view is obtained with the knees flexed 55 degrees and
the patient prone. This position allows for assessment of lateral femoral condyle height and, therefore, bony restraint to
lateral subluxation. This is, theoretically, the position in which the greatest lateral force on the patella is created and,
therefore, is the most likely position to see lateral patellar subluxation ( 28,33).
FIGURE 56.12. Hughston, Merchant, and Laurin tangential views of the patellofemoral articulation.
The Laurin view is taken with the knee flexed 20 degrees. This view may be used to calculate the patellofemoral angle,
which is useful in assessing patellar tilt. Patellofemoral angle is measured by drawing a line tangent to the femoral
condyles and a second line along the lateral facet of the patella. The two lines should diverge laterally. Any deviation
from this is considered abnormal and may reflect a tight lateral retinaculum and a tendency toward lateral subluxation or
dislocation. A similar measurement may be made on the Merchant view.
Quadriceps Muscle Strain
In general, muscle strains occur due to a forceful contraction or stretch and affect the musculotendinous junction ( 38,39).
The athlete usually presents with anterior thigh pain. On physical examination, localized swelling and loss of knee flexion
may be noted. Because the rectus femoris muscle crosses the hip joint to act as a hip flexor as well as a knee extensor,
increased pain and decreased knee flexion with the hip in extension localizes the strain to this portion of the quadriceps
(40). Palpation usually reveals tenderness at the musculotendinous junction. Radiographs are usually normal, but a
magnetic resonance imaging (MRI) scan may elucidate the site and extent of injury.
Treatment of quadriceps muscle strains in the first 72 hours consists of rest, ice, compression, and elevation. The
benefits of nonsteroidal antiinflammatory agents has been debated, and may be used at the physicians discretion. A
program of stretching is begun early, followed by electrical stimulation and isometric exercises. This is followed by
isotonic and isokinetic exercises, and then a gradual return to sport-specific training. The rate of progression is
individualized based on the degree of injury and response to a staged treatment protocol ( 40). Return to sport is
permitted when the athlete has a pain-free, normal range of motion, with strength within 10% of the unaffected side ( 40).
Ruptures of the quadriceps muscles are rare and occur in the midthigh, usually within the belly of the rectus femoris or
vastus medialis muscle. This most commonly occurs with direct trauma to a maximally contracted muscle. Patients
usually present with a history of a direct blow to the thigh and complain of pain and swelling in the middle third of the
anterior thigh. A defect is often not palpable because of local hematoma formation. Treatment of quadriceps muscle
rupture is nonoperative. Only in the case of a large tear in a high-performance athlete should operative repair be
considered, and if so, it should be performed within 1 week of injury. Otherwise, early treatment may involve a brief
period of immobilization, crutches, and pain management. The same treatment and rehabilitation program can be
followed as is used for quadriceps muscle strains. Early motion is important in order to minimize stiffness and allow for
organization of the scar tissue.
Quadriceps Tendon Rupture
Quadriceps tendon ruptures occur when the quadriceps contracts with the knee held in a slightly flexed position; the
ruptures are found more commonly in patients older 40 years old ( 41,42). Ruptures may be confined to the tendon itself
or may extend to the distal aponeurosis of the vastus muscles. The majority of the tears are incomplete and involve the
rectus femoris tendon. The more extensive the tear, the more likely is the presence of a hematoma. There is mild to
moderate tenderness to palpation and pain in the suprapatellar region. A defect may or may not be palpable, depending
on the extent of the tear and the presence or absence of a hematoma. The patella may appear to lie more distally than
the uninvolved side. Most strikingly, the patient will be unable to extend the knee against gravity or maintain the leg in
extension. In the case of an incomplete rupture, the patient may be able to raise the leg from a supine position but not
from a flexed position. With active quadriceps contraction, a defect may become palpable and the patella will not migrate
proximally. Radiographs often reveal a patella baja or, occasionally, a bony avulsion fragment is seen off the superior
pole of the patella. Calcification may be seen at the site of quadriceps or patellar tendon insertion, representing areas of
previous microtrauma. MRI is often helpful in distinguishing partial and complete tendon rupture.
Partial tendon ruptures may be treated nonoperatively by immobilizing the knee in full extension for 4 to 6 weeks.
Complete tears require early surgical repair and may require augmentation with local tissue transfer, artificial material
(Dacron weave), or allograft. Early repair or reconstruction provides good functional results, while late reconstruction may
result in quadriceps weakness.
Patellar Tendon Rupture

Patellar tendon rupture occurs most commonly in patients younger than 40 years old who have had a history of patellar
tendinitis or jumper's knee. It results from a violent quadriceps muscle contraction against resistance in the extended
knee. Physical examination reveals a defect in the patellar tendon and an inability to extend the knee. The patella may
rest more proximally than the uninjured side and is seen to migrate proximally with active quadriceps contraction. Most
commonly, the tendon ruptures off the inferior pole of the patella and may be accompanied by a bony fragment that is
visible radiographically. X-ray studies also reveal the associated patella alta. MRI may be helpful in diagnosing a partial
tear. Less frequently, the tendon is ruptured at its insertion on the tibial tubercle. This is usually associated with prior
trauma, steroid injection, or Osgood-Schlatter disease. The tendon is rarely ruptured in the midsubstance, except when
associated with systemic disease. Patellar tendon rupture requires early surgical repair. If the tendon is normal, tendon
length can be restored and functional results are excellent ( 41).
Acute Patellar Dislocation
Patellar dislocation most often results from external rotation of the tibia relative to the femur, producing a lateral patellar
dislocation. It may also occur as the result of a direct lateral blow to the knee. The dislocation is usually reduced
manually by the patient or as the knee is brought into extension before being seen by the physician. Physical
examination is remarkable for a large hemarthrosis and tenderness along the medial retinaculum and patellofemoral or
meniscopatellar ligament. Radiographs may reveal an osteochondral fragment off of either the medial facet of the patella
or the lateral femoral condylar edge of the trochlear groove.
If the patella is dislocated on examination, it is reduced by bringing the leg into extension and applying gentle pressure to
the patella in a medial direction. If a significant osteochrondral fragment is present, it is repaired or excised. Avulsion of
the medial soft tissue also requires surgical repair. Otherwise, the majority of primary dislocations may be treated
nonoperatively with either an immobilizer, a brace, or a cylinder cast for 2 to 4 weeks. During this period, isometric
quadriceps exercises should be performed. Many of these patients have underlying malalignment problems that
predispose them to redislocation. They require continued quadriceps strengthening and rehabilitation, and possibly,
surgical intervention to correct an underlying condition ( 37,43,44).
Patella Fracture
Patella fractures occur in all age groups and result from either direct or indirect trauma. With the knee partially flexed, a
strong quadriceps contraction may generate enough force to produce a transverse fracture of the patella. In addition, the
location of the patella makes it susceptible to injury from a direct below, such as a fall or dashboard injury. Fractures
present with acute hemarthrosis, which is evident by inspection and palpation. The patient may or may not be able to
perform a straight-leg raise or extend the knee, depending on the extent of the fracture and integrity of the surrounding
retinaculum. AP and lateral radiographs usually reveal a fracture. However, one must be careful to distinguish a bipartite
patella from a fracture. A tangential view is helpful in determining any significant discontinuity of the fragments in the AP
plane.
Treatment options vary from operative to nonoperative, with the goal of restoring continuity of the extensor mechanism. If
the fracture is minimally displaced and the patient is able to perform a straight-leg raise or extend the knee (the extensor
retinaculum is intact), then the fracture may be treated nonoperatively. Nonoperative treatment involves immobilization of
the leg in full extension in a cylinder cast or brace for 4 to 6 weeks. During this time, the patient may ambulate with
crutches and be able to bear partial weight on the affected side. This is followed by an additional 4 to 6 weeks of
protected weight bearing and range-of-motion exercises. Isometric quadriceps exercises should be performed to help
prevent quadriceps muscle atrophy. Fractures that fail to meet the criteria for closed treatment and any open fracture
should be treated surgically.
LIGAMENTOUS INJURIES
Knee ligament injuries are common to athletics. The knee ligaments are composed of fibrous tissue that attaches to
adjacent bony structures. They are loaded in tension to provide both static and dynamic support to the knee. As noted
previously, the knee rotates about three axes, thereby providing six degrees of freedom. These motions are not limited to
a single degree of freedom and, as such, are coupled. For example, anterior displacement of the tibia on the femur is
coupled with internal rotation of the tibia. Similarly, posterior displacement is coupled with external rotation of the tibia.
The ligamentous structures are intimately associated with coupling of motion and the inherent stability of the knee. It is,
therefore, of utmost importance to be able to perform an accurate examination of the ligamentous structures.
An understanding of the process of ligament healing is fundamental to the treatment of these problems. As research
opens the doors to the understanding of ligament healing, the approach to the management of ligament injuries
continues to evolve. Warren ( 9) has stated that the ability of a ligament to heal depends on the blood supply, the
approximation of the tissue, the stress placed across the ligament, and the timing of the stress.
The collateral ligaments receive a relatively rich blood supply from the surrounding soft tissue. In contrast, the cruciate
ligaments receive a more sparse vasculature from the synovial sheath and infrapatellar fat pad arising from the branches
of the middle and inferior geniculate arteries ( 45). Neither the collateral nor the cruciate ligaments receive significant
vascular contributions from their bony attachment sites ( 45). The healing process is similar to that of other tissues. The
initial fibrin clot formation stimulates an inflammatory response. Within the first week after injury, there is penetration of
local vasculature and fibroblast proliferation. Collagen synthesis and degradation occur simultaneously, while overall
collagen content increases. By 2 weeks, the fibroblasts become organized into a parallel network, with good tensile
strength noted by 3 weeks. An essentially normal-appearing ligament is present by 8 weeks ( 45,46 and 47). In addition,
although it was originally thought that early motion was detrimental to ligament healing, more recent data suggest that
there is a beneficial effect of stress and strain on ligament healing. Animal models have shown that immobilization
decreases the strength and energy-absorbing capacity of the ligament–bone junction ( 46,47). It has also been shown that
MCL injuries recover well without surgery or immobilization. Secondary restraints to valgus motion provide sufficient
stability to allow for ligament healing. Surgical repair of MCL injuries, rest, and immobilization are being deemphasized in
favor of early controlled motion and functional rehabilitation.
However, in the last several years it has become evident that ligament injuries often represent damage to more than one
structure. Hughston et al. ( 48,49) described six forms of instability based on specific structural lesions or combinations of
lesions: anterolateral rotatory instability (ALRI); posterolateral rotatory instability (PLRI); combined ALRI and PLRI;
combined anteromedial rotatory instability (AMRI) and ALRI; combined ALRI, PLRI, and AMRI; and acute straight lateral
instability (SLI). Anterior rotational subluxation of the lateral tibial plateau relative to the lateral femoral condyle results in
ALRI. The tibia internally rotates on the axis of an intact PCL as the result of disruption of the ACL. AMRI results from
damage to the medial capsule and MCL (49,50 and 51). Posterolateral rotatory instability results from damage to the
arcuate complex (arcuate ligament, lateral collateral ligament, popliteus, lateral head of the gastrocnemius), producing
posterior rotatory subluxation of the lateral tibial plateau relative to the lateral femoral condyle with the tibia externally
rotating on the axis of an intact PCL ( 48,52,53 and 54). Straight lateral instability results from disruption of the lateral
collateral ligament and arcuate complex and PCL, and may be accompanied by an ACL injury. These instability patterns
are discussed later in this chapter.
Collateral Ligament Injury
Medial and lateral collateral ligament injuries are often referred to as sprains or strains. They may be further classified on
the basis of comparison with the normal (unaffected) side. A grade 1 injury produces pain along the course of the
ligament and may be accompanied by swelling. With varus or valgus stress testing, the joint line may open up to 5 mm
more than the unaffected side. A grade 2 injury produces 5 to 10 mm of joint line opening relative to the unaffected side.
The ligament may be stretched or partially torn; however, a firm endpoint is detectable with stress testing. A grade 3
injury produces more than 10 mm of opening relative to the unaffected side with no discernible endpoint. The ligament is
completely torn, and secondary capsular and ligamentous restraints are often disrupted. With any of these injuries, there
also may be associated ACL, PCL, or meniscal pathology.
The primary restraint to valgus stress is the MCL, with additional support afforded by the ACL, posterior oblique ligament,
and posteromedial capsule. Most commonly, the MCL is injured by a direct blow to the lateral side of the knee (valgus
blow) with the foot planted. An isolated MCL injury may produce localized swelling without a true knee effusion.
Localization of tenderness to the medial epicondyle as opposed to the medial joint line helps distinguish an MCL injury
from a medial meniscal tear. However, a medial capsular strain or midsubstance MCL injury may produce joint line
tenderness similar to a meniscal injury.
Clinical testing of medial laxity is performed with the patient in the supine position, allowing the thigh to rest on the
examining table. The leg is supported over the edge of the table by the examiner's hand, as depicted in Figure 54.12. A
valgus or abduction stress test is then performed with the knee in 30 degrees of flexion and in full extension, by placing
valgus stress on the knee with gentle abduction of the tibia. At 30 degrees of flexion, the cruciate ligaments and posterior
capsule are relaxed, and testing is more specific for the MCL. Laxity in full extension reflects a grade 3 injury with
disruption of the MCL, posteromedial capsule, posterior oblique ligament, often the PCL, and sometimes the ACL.
Most tears of the MCL can be treated nonoperatively. Grade 3 MCL injuries that are associated with anterior or PCL
injuries or repairable meniscal injuries are occasionally treated surgically ( 55,56). An acutely injured, painful knee may be
placed in a knee immobilizer for approximately 1 week, with the patient removing the immobilizer for range-of-motion
exercises several times per day. Patients are allowed to bear weight as tolerated, using crutches as needed. In the early
postinjury period, therapy includes patellar mobilization, active range of motion within pain-free limits, and isometric
quadriceps and hamstring exercises, along with modalities such as whirlpool and electrical stimulation. Grade 1 injuries
do not require bracing, while bracing of grade 2 injuries depends on the degree of stability, pain, swelling, and physician
preference. Grade 3 injuries should be protected with a hinged brace. In grade 3 injuries range of motion is limited to 30
degrees to 90 degrees of flexion for 2 weeks. Once the patient can walk without a limp and achieves flexion of more than
90 degrees, the brace can be discontinued. The same criteria can be used to begin a strengthening program, and use of
a stationary bicycle. Physical therapy includes leg presses, mini-squats, resisted knee flexion exercises, proprioceptive
training, and aquatic exercises. Straight-ahead jogging may begin when 60% of quadriceps strength compared with the
unaffected side is achieved. When 80% of quadriceps and hamstring strength is achieved a functional brace is used
while beginning a sport-specific training program. Return to sport varies from 2 to 8 weeks, depending on the grade of
injury and individual response. Once the athlete can complete an agility program appropriate for the sport, he or she may
return to competition. In grade 2 and 3 injuries, it is recommended that the athlete complete the season with use of a
functional brace, which should not be required for later participation.
Lateral Collateral Ligament
The lateral or fibular collateral ligament provides lateral restraint to varus stress, along with the arcuate ligament,
posterolateral capsule, lateral capsular ligament, popliteus tendon, iliotibial band, and lateral head of the gastrocnemius
(48). Most commonly, these structures are injured by a direct medial blow to the knee, with the foot planted and the knee
extended. These are often severe, high-impact injuries. Isolated injuries to the lateral collateral ligament are rare. These
lesions more commonly occur in association with damage to the other lateral restraints and to one or both cruciate
ligaments, resulting in PLRI or SLE ( 54).
Clinical evaluation of lateral knee injuries produces findings reflecting the severity of trauma. Palpation of the lateral bony
and ligamentous structures and lateral joint line is helpful in distinguishing the specific pathology. In addition, a joint
effusion may or may not be present. Varus or adduction stress testing is performed in the same position as for valgus
stress testing. With the examiner supporting the leg, a varus stress is produced as the tibia is adducted ( Fig. 56.13). With
the knee in 30 degrees of flexion, the posterior capsule and cruciate ligaments are relaxed, and the test is more specific
for the lateral collateral ligament (LCL). Grading is as noted earlier. Laxity with the knee in full extension reflects
additional injury to the posterolateral capsule, arcuate complex, and often the PCL. This constitutes a grade 3 injury. In
addition, with any LCL injury, it is important to evaluate the function of the common peroneal nerve. This nerve courses
from posterior to anterior, emerging from behind the biceps tendon to pass around the fibular neck. The nerve divides
distally into the superficial and deep peroneal nerves, providing motor function to the toe and foot dorsiflexors and foot
everters, and sensation to the lateral aspects of the lower leg and dorsum of the foot.
FIGURE 56.13. Testing for medial and lateral collateral ligament stability.
Mild SLI injuries (isolated LCL) are rare and may be detected with 1+ opening of the lateral joint line with varus stress
testing at 30 degrees of knee flexion. Severe SLI results in 2+ to 3+ opening to varus stress with the knee in full
extension. These injuries have a significant association with common peroneal nerve injuries ( 52).
PLRI usually results from a blow to the anteromedial aspect of the proximal tibia of an extended knee. In the acute
setting, there may be little or no effusion, mild posterolateral discomfort, and an anteromedial contusion ( 52,53 and
54,57). Specific tests for instability patterns are discussed later in this chapter.
Plain radiographs may reveal fibular head fracture, avulsion of Gerdy tubercle, or medial tibial plateau fracture in some
cases (58). Stress radiographs are helpful in assessing degree of instability but should be avoided in cases of severe SLI
to prevent further stress to the peroneal nerve. MRI scanning is frequently helpful in assessing the level of injury, and
associated pathology (59). In addition, examination under anesthesia and arthroscopic evaluation may be considered.
Mild SLI with incomplete injury to the lateral collateral ligament only is rare and may be treated nonoperatively. Similarly,
patients with minimal PLRI (isolated posterolateral corner injury with no more than 1+ laxity and less than 10 mm opening
on stress x-ray study) may be treated conservatively ( 54). More severe injuries of either type should be treated surgically.
The earliest description of the ACL dates back to Galen in a.d. 170. He described the anatomy of the “genu cruciate.”
Over the ensuing centuries, the function and anatomy of the ligaments of the knee were further delineated. It was not,
however, until 1850 that Stark recorded the first description of a rupture of the ACL. Reports of injuries and attempted
operative and nonoperative treatment of the ACL followed in the literature. In 1917, Hey-Groves ( 60) reported on an
attempt to reconstruct the ACL using a segment of fascia lata passed through a tibial tunnel. This formed the basis of
current concepts of intraarticular reconstruction. Numerous others contributed to the expanding literature on ACL injuries
and their management (61,62). O'Donoghue's (62,63,64,65 and 66) work in the 1950s and 1960s further defined the
concepts of ACL injuries and their surgical treatment. Since this landmark work, much has been accomplished in
understanding the structure and function of the ACL. It is critical that one understands the role of the ACL and its
biomechanical function before addressing its injury and treatment.
Anatomy
Hey-Groves (16), in 1920, was the first to describe the ACL's role as a stabilizer of the knee against anterior
displacement of the tibia on the femur. Subsequently, Butler et al. ( 67) and others (49,50,68,69,70,71 and 72) have shown
that the ACL acts as a primary restraint with the iliotibial band, MCL, and LCL, with the medial and lateral capsules acting
as secondary restraints. The secondary role of the ACL in the control of rotation and varus–valgus stability has also been
elucidated. These roles are directly related to the anatomy and orientation of the ACL.
As Arnoczky (45) has clearly described, the femoral attachment of the ACL is a semicircular region at the posterior
aspect of the lateral femoral condyle within the intercondylar notch. The ACL then courses anteromedially through the
notch beneath the transverse meniscal ligament to attach in a fossa slightly in front of and lateral to the anterior tibial
spine (Fig. 56.4).
The ACL is composed of a series of fascicles that spiral laterally as the ligament courses from femur to tibia. The
fascicles are divided into two major bundles: an anteromedial bundle and a posterolateral bundle. The anteromedial
bundle or band is tight in flexion and relatively lax in extension. The posterolateral band is tightest in extension and
relatively lax in flexion. The fascicles thus represent a continuum of fibers, some of which are taut throughout the entire
range of knee motion.
Both cruciate ligaments derive the majority of their blood supply from surrounding synovial vessels originating primarily
form the middle geniculate artery along with smaller contribution from terminal branches of the inferior geniculate
arteries. In addition, branches of the tibial nerve course with the synovial and periligamentous vessels, providing
mechanoreceptors and probably proprioceptive fibers to the ligament. Sensory nerve endings are limited within the ACL.
Biomechanics
The fundamental biomechanics and kinematics of knee motion have been described as a four-bar linkage system by
Kapandji et al. (4). Two rigid rods represent the anterior and PCLs. The length of the rods is proportional to the lengths of
the ACL and PCL. The rods are hinged at one end along a line that intersects a second line, representing the longitudinal
axis of the femur at a 40-degree angle that represents the slope of the intercondylar roof. The free ends of the rods are
attached to a coupler, representing the tibial plateau. As the coupler moves a series of lines are produced that form
tangents to a curve. The curve approximates the sagittal contour of the posterior half of the femoral condyles. The hinged
bars, then, represent the positions of the cruciate ligaments as the knee is brought through a range of motion. The model
also demonstrates the obligatory shifting of the bony contact points between femur and tibia as the knee changes
position. Therefore, as the knee is flexed, the femur glides posteriorly on the tibial plateau so that the femoral shaft does
not contact the posterior tibial plateau at terminal flexion. The ratio of rolling to gliding motion of the femoral condyle on
the tibial plateau is 1:2 in early flexion and 1:4 in late flexion ( 4). It is important to understand these concepts when
evaluating the function of the ACL and performing clinical diagnostic tests of ACL integrity.
History and Mechanism of Injury
The ACL is most commonly injured by a twisting force accompanied by varus, valgus, or hyperextension stresses on a
weight-bearing limb. ACL injuries are often accompanied by other structural injuries. In skiing, football, and soccer, the
most frequent mechanism of injury occurs with valgus and external rotation forces producing damage to both the ACL
and MCLs. In basketball, the most common mechanism of injury involves hyperextension with internal rotation of the tibia,
producing an ACL rupture as the player comes down from a rebound. Pure hyperextension may damage either the
anterior or the PCL or both. The ACL also may be damaged by hyperflexion, but this is rare.
In approximately 40% of cases, the patient will describe a “pop” that is heard or felt. This is caused by the release of
energy stored in the helicoid fibers of the ACL and is the single factor in the history that most reliably indicates an ACL
tear. The patient is usually unable to continue play and notes the gradual onset of an effusion over the ensuing 24 hours.
A more rapid onset of effusion should clue the examiner in to the possibility of an osteochondral fracture. Also, there is
minimal pain associated with a pure ACL rupture. This is because of the relative paucity of pain fibers within the ACL.
More severe pain may occur if associated injuries are present or over time as swelling produces joint distention.
General inspection of the knee, as described previously, is the first step in assessment of any knee injury. It is often
helpful to examine the unaffected knee first as a means of comparison as well as to relax the patient and allow him or her
to gain confidence in the examiner's ability to perform the appropriate tests gently. Muscle resistance to ligamentous
laxity testing not only makes testing difficult but also results in significant false-negative examinations.
Lachman Test
The Lachman test is the most sensitive test for ACL insufficiency and may be performed in the acute setting. The test is
performed with the knee in 20 to 30 degrees of knee flexion and the foot resting on the examination table. While the
femur is held posteriorly with one hand, the tibia is gently drawn forward with the opposite hand ( Fig. 56.14). The amount
of tibial translation is compared with the unaffected knee, and the degree of laxity is graded as previously described
(graded 1 to 3). A false-negative test may occur if a bucket handle tear of the meniscus blocks anterior excursion of the
tibia on the femur. If the limb is too large for adequate gripping, the test may be performed in the prone position. The leg
is supported with the knee in 20 to 30 degrees of flexion, and the tibia is gently drawn forward. In either case, the quality
of the end point (firm or soft) should also be noted.
FIGURE 56.14. The Lachman test.
Anterior Drawer Test
The anterior drawer test is less sensitive than the Lachman test for ACL insufficiency. The test is performed with the
patient lying supine, the hips flexed 45 degrees, and the knee flexed between 60 and 90 degrees. With both thumbs
placed on the joint line, the tibia is gently drawn forward, and excursion of the tibia is measured in comparison with the
unaffected side ( Fig. 56.15). Again, the quality of the end point should be noted. Grading is difficult and often depends on
the examiner's level of experience. However, even in the chronic setting, anterior drawer testing under the best of
circumstances still results in significant false-negatives results.
FIGURE 56.15. The anterior drawer test.
Anterior drawer testing may be helpful in assessing the integrity of secondary restraints. When the test is performed with
the foot in 15 degrees of external rotation, increased excursion of the tibia reflects damage to some or all of the
secondary medial restraints, which should be tight in this position. Similarly, when the test is performed with the foot in 30
degrees of internal rotation, the secondary lateral restraints should be tight. Increased excursion reflects damage to
some or all of these structures.
Flexion-Rotation-Drawer Test
The flexion-rotation-drawer test is performed by providing an anterior tibial stress while the knee is flexed and extended
(6,72). As the knee is extended in an ACL-deficient knee, the tibia subluxates anteriorly and the lateral femoral condyle is
observed to rotate externally as it falls off the convex slope of the lateral tibial plateau. Conversely, as the knee is flexed,
the iliotibial band pulls the lateral tibial plateau posteriorly, the knee returns to its anatomic alignment, and the lateral
femoral condyle is observed to rotate internally. Similar tests have been described by Hughston et al. ( 49) and Slocum at
al. (73,74), all of which are variations on testing for ALRI.
In some cases of chronic ACL insufficiency and resulting anterolateral instability, a patient may be able to exhibit an
active anterior drawer sign. With the patient either sitting up or lying down and the knee flexed 90 degrees with the foot
firmly planted, contraction of the gastrocnemius muscle may draw the tibia forward. In other patients, the same effect may
be demonstrated as the patient flexes and extends the knee with a slight valgus stress applied, while the leg bears partial
weight.
Pivot Shift
The pivot shift phenomenon describes the anterior subluxation of the lateral tibial plateau in extension in the
ACL-deficient knee. With the knee in extension, the action of the quadriceps muscles and iliotibial band draws the tibia
forward on the femur. As the knee is flexed, the axis of pull of the iliotibial band drops posteriorly and the tibia is pulled
posteriorly, back to its normal anatomic position ( Fig. 56.16). Numerous tests have been described to elicit this
phenomenon (69,70 and 71,75).
FIGURE 56.16. The pivot shift test. As the knee is brought into flexion, the iliotibial band reduces the tibia from its
anteriorly subluxated position. (Adapted from Insall JN. Examination of the knee. In: Insall JN, ed. Surgery of the knee.
New York: Churchill Livingstone, 1984).
MacIntosh Test
The MacIntosh test was described in 1972 ( 69,70 and 71). With the knee extended and the foot internally rotated, a
valgus stress is applied to the proximal tibia. The lateral tibial plateau is seen to subluxate anteriorly in the early phase of
flexion, the lateral tibial plateau reduces as a result of the action of the iliotibial band in flexion.
Losee Test
The Losee test is performed by grasping the foot of the affected leg with one hand. The thumb of the other hand is placed
behind the fibular head, with the fingers resting on the patella. The knee is flexed approximately 40 degrees and then
slowly extended. As the knee is extended, the foot is internally rotated and the thumb pushes forward on the fibular head.
As the knee reaches extension, the lateral tibial plateau is seen and felt to subluxate anteriorly ( 75,76).
Instrumented Testing
Because clinical testing is subject to variability between examiners, attempts have been made to develop mechanical
ligament testing devises. Three of the more commonly used devices are the KT-1000 arthrometer (Medmetric, San
Diego, CA), the Genucom (Faro Medical Technologies, Inc., Montreal, Canada), and the Stryker Knee Laxity Tester
(Stryker Co., Kalamazoo, MI). By producing an anterior displacement force on the tibia with the femur stabilized, maximal
tibial displacement may be quantified. Side-to-side measurement differences can be calculated between the injured and
noninjured knees to evaluate the degree of instability.
Treatment of Anterior Cruciate Ligament Injuries
Over the past several years, the advances in knowledge regarding structure, function, and physiology of the ACL have
allowed the treatment of ACL injuries to evolve. Numerous studies have suggested that progressive functional and
anatomic deterioration of the knee results from chronic ACL deficiency. Further studies have gone on to elucidate the
concepts of resulting meniscal damage, osteoarthritis, damage to secondary restraints, and overall decline of knee
function (77,78,79,80,81,82 and 83). Still, numerous articles in the past have advocated conservative management of ACL
injuries (84,85), primarily because the results of such management did not differ significantly from operative
management. More recent, research, however, has led to improved understanding of ACL biomechanics, anatomy, and
ligament healing and thus improved techniques for operative management and the recreation of a functional ligament.
Radiography
Plain radiographs often reveal only a joint effusion. In some cases, a lateral capsular sign (Segond sign) may be seen as
a bony avulsion of the lateral capsular attachment to the tibia. A lateral notch sign involving flattening of the superior
aspect of the lateral femoral condyle bordering on the intercondylar notch may also be observed ( 86). In the chronic
setting, “peaking” of the tibial spines may be evident. MRI scanning may be helpful in assessing both anterior and PCL
integrity, as well as any associated pathology of the menisci or collateral ligaments ( Fig. 56.17) (87,88 and 89). The
overall accuracy of MRI in detecting ACL injuries is approximately 95% ( 90). However, it is unnecessary to use MRI
routinely, because clinical examination and instrumented testing in experienced hands should yield similar accuracy
rates. As many as 80% of ACL-injured patients also show bone abnormalities (“bruises” or “contusions”) on MRI ( 91,92).
Although the long-term significance of these lesions has yet to be fully elucidated, it appears that these findings may
correlate with substantial damage to the articular cartilage and its homeostatic regulating system ( 91).
FIGURE 56.17. MRI scans. A: Demonstrates rupture of the anterior cruciate ligament. The area of relatively higher signal
intensity located between femur and tibia is normally occupied by a lower signal (dark) band, representing the anterior
cruciate ligament. B: Demonstrates the low signal band of an intact posterior cruciate ligament.
Indications for Treatment
Treatment decisions must be individualized. The physician must consider the patient's physiologic age, activity level,
ability and willingness to comply with a vigorous postoperative rehabilitation protocol, the additional anatomic
considerations of associated collateral ligament injuries and meniscal injuries, and the patient's overall degree of
generalized ligamentous laxity.
In general, a physiologically young person who remains active in sports that require jumping, cutting, and deceleration
and who does not wish to modify those activities is a candidate for surgical intervention. Surgery is further indicated in
those patients with risk factors for recurrent instability or coexisting progression of intraarticular damage. This would
include patients with associated grade 3 collateral ligament injuries, meniscal tears, and generalized ligamentous laxity.
Most authors agree that attempts to manage an ACL-deficient knee conservatively with associated grade 3 collateral
ligament injury will result in functional instability of the knee. In addition, when a meniscal tear accompanies an acute
ACL rupture, retear of the repaired meniscus or reinjury of the damaged meniscus is likely to occur if the ACL is not
reconstructed. Repair of the meniscus may be performed in a chronically ACL-deficient knee without performing ACL
reconstruction if the knee is functionally stable because of secondary restraints and the patient has a low-demand
lifestyle.
Conservative treatment is warranted in the physiologically older athlete who has a less-demanding physical regimen
(does not participate in cutting sports) or who is willing to modify his or her or her activity. This assumes that there is no
associated grade 3 collateral ligament damage or meniscal damage.
Partial Anterior Cruciate Ligament Injury
Partial ACL ruptures occur in 10% to 28% of all ACL injuries ( 7,85,93). It is unclear whether the degree of fiber disruption
can be correlated with the degree of instability and prognosis ( 93,94), because it is difficult to assess the amount and
effect of plastic deformation that likely occurs in the remaining ACL fibers. In these cases, one must assess the degree of
instability through clinical testing as well as patient's history, symptoms, and athletic demands. In some cases,
examination under anesthesia and diagnostic arthroscopy may be necessary to evaluate the situation fully. Warner et al.
(93) have suggested that a 25% tear of the ACL with a negative pivot shift may be treated conservatively; whereas a 25%
tear with a strongly positive pivot shift in an athletic individual should be treated with augmentation, using the
semitendinosus and gracilis tendons.
Nonoperative Management
The ultimate goal of nonoperative care of an ACL injury is functional stability. The knee is treated symptomatically over
the course of rehabilitation. A well-planned physical therapy regimen would include consideration of hamstring and
quadriceps strengthening as dynamic knee stabilizers, patellofemoral biomechanics, proprioceptive training, and overall
functional progression. The time needed to accomplish each step varies from patient to patient.
Early nonoperative management of an ACL injury includes measures to reduce pain and swelling and restore full range
of motion. Such measures include use of antiinflammatory agents, ice, and physical therapy modalities. Crutches and a
brace or knee immobilizer may be helpful in limiting discomfort but should be used for only a few days. Prolonged use
promotes muscle atrophy and adhesion formation, resulting in a stiff knee. With the exception of associated collateral
ligament injuries, braces or immobilizers are not necessary to protect the injured structures from daily activities involving
full weight bearing. Other early rehabilitation goals include gait training, patellar mobilization, the initiation of
neuromuscular activity, and patient education. Patients are counseled to avoid high-risk activities, at least until adequate
strength and training have been accomplished.
Intermediate rehabilitation goals include range of motion, gait training, strengthening, and proprioceptive training. Once
the effusion has dissipated and full range of motion has been attained, exercises such as swimming and bicycling are
begun, followed by light jogging (flat surface). The late phase of therapy should include functional training of the athlete.
The entire process may take 6 to 12 weeks before high-level activities can be resumed. This is reflected by muscle
strength testing, which demonstrates quadriceps and hamstring strength within 90% of the unaffected side, along with
completion of proprioceptive training and patient counseling. Bracing of the knee may provide a sense of reassurance to
the athlete and prevent tibial translation at low levels of activity. However, there is no evidence to suggest that functional
bracing can prevent tibial translation (pivot shifting) at higher demand levels. Therefore, bracing is not absolutely
indicated. It should be noted that nonoperative management does not mean that surgery is not indicated for associated
pathology. In cases of meniscal injury or when a portion of the remaining ACL stump impinges in the joint, surgery may
be necessary. Also, if nonoperative management is deemed unsuccessful by the patient and the physician because of
recurrent episodes of instability, then surgical reconstruction remains an option for treatment.
Operative Management
Over the years, there have been many accepted operative methods of treatment of an ACL-deficient knee. These include
primary repair, repair with augmentation, reconstruction using autogenous graft tissue, reconstruction using a prosthetic
ligament, reconstruction using both an autogenous graft and a prosthetic ligament, reconstruction with allograft tissue,
and extraarticular augmentation. Primary repair is best performed when the ACL is avulsed proximally from its femoral
attachment. This occurs uncommonly, and current recommendations are that repair should be performed in association
with intraarticular or extraarticular augmentation, preferably intraarticular using the semitendinosus and gracilis tendons
(93,95,96).
At present, the most common method of ACL reconstruction is autogenous graft reconstruction using the central one third
of the patellar tendon. Other structures that continue to be used include the hamstring tendons (gracilis and
semitendinous). Noyes et al. ( 97,98) documented the relative strengths of the various materials used for reconstruction.
These data showed that with the exception of the bone–patellar tendon–bone complex, all of the tissues were weaker
than the normal ACL. In contrast, the bone–patellar tendon–bone complex was 168% as strong as the normal ACL. In
addition to its strength, the use of the bone–patellar tendon–bone graft is preferable because of its availability and its
immediate strong fixation to bone with interference screws as well as the bone plugs' rapid healing into the femoral and
tibial bone tunnels in which they are fixed. The latter two of these allow for a more aggressive early rehabilitation
program. These factors seem to outweigh the disadvantages, which include damage to the extensor mechanism,
postoperative parapatellar pain, quadriceps weakness, and rare patellar fracture and rupture of the patellar tendon.
Thus, reconstruction using the central third patellar tendon has become the operation of choice for most knee surgeons.
Data have shown that more than 90% of patients are functionally stable, with excellent knee ligament rating scores
(99,100). Also, recent techniques of tissue looping and gracilis reinforcement appear to improve hamstring graft strength,
while new devices are providing better early fixation of the tissue to bone. Therefore, hamstring tendon for ACL
reconstruction is becoming more popular. Burger and Larson ( 101) reviewed the literature from 1981 to 1986 and showed
no significant difference in objective testing 2 years after surgery, regardless of autogenous tissue choice.
The use of prosthetic devices and allograft material for intraarticular ACL reconstruction has significant appeal. The
advantages include lower morbidity because harvesting of autogenous tissues is avoided. In the case of prosthetic
devices, there is immediate secure bone fixation, allowing for vigorous early rehabilitation. When used for augmentation,
they provide immediate strength and load sharing during the revascularizing and remodeling phases of healing of the
accompanying autogenous or allograft material. However, the current data on ligament augmentation devices have not
shown them to be better than autogenous grafts alone (96,102). At present, there is limited use of prosthetic ligaments in
the United States, but failure caused by fatigue, wear, and fretting has occurred at a high rate ( 96,102).
Allograft reconstruction of the ACL, using either the patellar tendon or the Achilles tendon, is gaining acceptance.
Allograft reconstruction provides the benefits of autogenous graft reconstruction while eliminating the morbidity of graft
harvesting. In addition, postoperative pain is diminished, cosmesis is improved because a smaller incision can be made,
and operative tourniquet time is decreased. With current screening and sterilization techniques, the incidence of HIV
transmission with allograft material is 1:1,677,00 ( 103).
Allografts may be particularly useful in patients (a) over 40 years of age, (b) with preexisting patellofemoral chondrosis or
extensor mechanism malalignment, (c) who require multiple ligament reconstruction (i.e., PCL and ACL), and (d) who
require revision ACL reconstruction. Overall, results of allograft ACL reconstruction appear to be comparable with
autograft reconstruction ( 104,105 and 106). In 33 patients followed at the University of Pittsburgh Center for Sports
Medicine and Rehabilitation over a 44-month period, 73% of patients returned to their preoperative activity level, a figure
comparable with most autograft studies.
Extraarticular reconstruction procedures (MacIntosh, Ellison, and Losee) are rarely used as isolated procedures for
treatment of the ACL-deficient knee. Initially, it was believed that by extraarticular tenodesis of the posterolateral aspect
of the knee, anterior translation of the tibia could be prevented. However, these tissues gradually stretch out with time
and, therefore, eventually fail to provide stability. Such procedures may still be helpful in augmenting intraarticular
repairs, particularly in the young athlete with open epiphyses, in whom the drilling of bone tunnels should be avoided.
Postoperative Rehabilitation
The postoperative rehabilitation process has evolved along with the changes in surgical techniques. As more is learned
about biomechanics and bone and soft tissue healing, these protocols will continue to change. However, protocols must
be modified according to the type of repair or reconstruction performed, associated ligamentous and meniscal surgery,
and the type of graft used. Rehabilitation has advanced from the long period of immobilization and non–weight bearing
once recommended. Current protocols allow for immediate full flexion and extension. Early motion limits disuse atrophy,
adhesion formation, and capsular contracture and promotes articular cartilage nutrition. The patient is allowed to bear
weight as tolerated with the aid of crutches. A postoperative brace is not necessary. Immediately postoperatively,
straight-leg raises and quadriceps setting is begun. Shelbourne et al. ( 107) have described an accelerated rehabilitation
program with basic objectives as follows: (a) Within the first 2 weeks after surgery, the patient should obtain full
extension and flexion to 90 degrees. Swelling is decreased, and quadriceps control is improved. (b) During postoperative
weeks 3 through 5, full range of motion should be established, and bicycling and closed chain exercises may begin. (c)
From 6 weeks on, closed-chain weight-bearing exercises are increased. Progression of the rehabilitation process must
be individualized. Athletes may begin agility training and sport-specific exercises when appropriate quadriceps and
hamstring strength parameters are met. Return to sports participation may range from 6 weeks to 6 months, with the
average being in the range of 4 to 6 months.
Posterior Cruciate Ligament and Posterolateral Corner
The primary function of the PCL is to act as a restraint to posterior tibial displacement. It also plays a role as a secondary
stabilizer to varus and valgus stress and to external rotation. The origin of the PCL is a broad region, approximately 32
mm in anteroposterior diameter, along the lateral side of the medial femoral condyle, with the distal fibers approximately
3 mm proximal to the articular margin of the condyle ( 14,108). The ligament averages 38 mm in length and 13 mm in
width (14,108), and courses posteriorly and distally to a broad insertion site (approximately 13 mm) ( 14,108) on the flat,
posterior surface of the proximal tibia, approximately 1 cm below the tibial articular surface. The PCL consists of
anterolateral and posteromedial components, as well as the meniscofemoral ligaments when tensioning patterns are
assessed (109,110). The meniscofemoral ligaments (ligaments of Humphry and Wrisberg) lie anterior and posterior to the
PCL.
PCL injuries are less common than ACL injuries, but the true incidence is undetermined because until recently, many
have gone undetected. As more has been learned about the anatomy and function of the posterior and posterolateral
structures of the knee, the diagnosis has been made more frequently. A broad spectrum of disability may be caused by
injuries to the PCL and posterolateral structures (e.g., arcuate complex, posterolateral capsule, biceps, and popliteus
tendon) of the knee, ranging from no functional disability to severe disability. Isolated PCL injury results in posterior
subluxation of the tibia on the femur, producing straight posterior instability. Injury to some or all of the posterolateral
structures in addition to the PCL produces PLRI, as the lateral tibial plateau subluxates posteriorly relative to the lateral
femoral condyle. The intact posteromedial structures act as a pivot point. It should be noted that these injuries occur
more commonly in conjunction with other knee ligament injuries, including ACL injury. PCL and posterolateral injuries
account for between 3% and 37% of all knee injuries depending on the population studied ( 111,112 and 113). Although
much has been learned about the basic science of the PCL, there is still considerable debate about surgical indications
and treatment.
Mechanism of Injury
The majority of PCL injuries occur in athletics and motor vehicle accidents, resulting from a direct blow to the flexed knee.
In sports, this may occur when the flexed knee strikes the ground with the foot plantarflexed. This concentrates the force
of the blow on the tibial tubercle, effectively creating a strong posterior drawer effect on the proximal tibia, thus rupturing
the PCL. Forced hyperflexion also may cause PCL rupture as the anterolateral fibers are stretched beyond their elastic
limit.
Hyperextension injury has been shown to produce ACL and PCL rupture in combination, whereas a varus or valgus blow
to the knee may produce a PCL rupture in association with collateral ligament injury. The posterolateral corner is most
commonly injured by the “valgus side-swipe,” which occurs when a blow is struck to the anteromedial aspect of the knee,
producing hyperextension and posterolaterally directed force ( 49,51,108). Less commonly, posterolateral injury may
occur with a severe external rotation force to the tibia.
History
As with other knee injuries, the history begins with a description of the mechanism of injury. In cases of chronic posterior
or posterolateral instability, pain is a predominant feature ( 51,57,71,108). The patient usually complains of posterolateral
pain, and in more chronic cases, patellofemoral symptoms may occur. Patients with chronic posterolateral instability often
report feelings of instability and that their knee gives way in extension or hyperextends. These patients exhibit a varus
and hyperextension deformity in the stance phase of gait ( 57,108).
These injuries have been commonly missed if a proper and thorough examination is not performed. The first key to
examination is observation. Posterolateral ecchymosis and swelling, along with anteromedial ecchymosis, swelling, or
abrasion are suggestive of the mechanism and location of injury. Of note, it is important to remember that significant force
is required to produce these injuries. Therefore, a thorough neurovascular examination should be part of the evaluation.
One must always consider the possibility of a knee dislocation (see “ Knee Dislocation,” below). Also, assessment of
peroneal nerve function is important because 10% to 30% of knees with lateral and posterolateral ligament damage have
associated peroneal nerve injury ( 49,108).
Posterior Drawer Test
The posterior drawer test is the most accurate way of assessing PCL competence. The test is performed in a similar
fashion to the anterior drawer test but with a posterior force directed on the tibia ( Fig. 56.18). The examiner must assess
the degree of posterior displacement and the quality of the endpoint (firm or soft). It is also helpful to palpate the medial
joint line. Normally, there is a 1-cm step-off between the anterior medial tibial plateau and the medial femoral condyle.
When the PCL is nonfunctional, the tibia sags posteriorly in the 90-degree flexed position and this step-off is eliminated.
Grade I injuries have a medial step-off that remains palpable but diminished. Grade II injuries have no step-off, but the
tibia cannot be translated further posteriorly. Grade III injuries have no palpable medial step-off, and the tibia can be
translated posteriorly beyond the anterior prominence of the medial femoral condyle, reflecting a complete PCL tear.
FIGURE 56.18. The posterior drawer test.
External Rotation Recurvatum Test
The external rotation recurvatum test was described by Hughston et al. ( 63,95,97) and is performed with the patient in the
supine position. The great toe is grasped, and the leg is elevated with the knee in full extension ( Fig. 56.19). External
rotation of the tibia and varus hyperextension (recurvatum) of the knee reflect injury to the arcuate ligament complex,
according to Hughston et al. However, it is now believed that pronounced hyperextension and external rotation are more
likely produced by arcuate complex injury accompanied by ACL and possibly PCL injury ( 108).
FIGURE 56.19. The external rotation recurvatum test.
Quadriceps Active Drawer Test
Daniel et al. ( 114) described the quadriceps active drawer test as a means of assessing the resting position of the tibia in
relationship to the femur. With the patient lying supine, the knee flexed 90 degrees, and the foot firmly planted, the
quadriceps muscle is actively contracted. In the PCL-deficient knee, the resting position of the tibia is posterior relative to
the femur and to its normal resting position. When the quadriceps muscle is contracted in the PCL-deficient knee, the
force vector is directed anteriorly, producing an anterior tibial translation that is visible to the examiner.
Tests for Posterolateral Instability
Varus–Valgus Stress Testing. Varus and valgus stress testing was described earlier; however, it should be noted that
injury to the posterolateral structures may produce varus instability when tested in 30 degrees of flexion and in full
extension. It should be remembered, however, that most of these are combined LCL and posterolateral injuries, and that
although PCL injury is not necessary to produce varus laxity in full extension, it is probably more commonly associated
with these injuries than not (108).
Posterolateral Drawer Test. The posterolateral drawer test is performed in a similar manner to the posterior drawer test
but with the foot externally rotated 15 degrees. As the tibia is pushed posteriorly, the lateral tibial plateau moves
posteriorly while the medial tibial plateau remains fixed. Evaluation of this test is somewhat subjective. Mild to moderate
posterior displacement of the lateral tibial plateau is indicative of damage to the posterolateral structures, whereas
marked posterior displacement is suggestive of combined injury, including PCL disruption.
Tibial External Rotation. Tibial external rotation evaluates the posterolateral structures by assessing external rotation of
the tibia on the femur. The patient is either prone or supine and the feet are grasped so that the test may be performed
on each knee for comparison. The test is performed at both 30 and 90 degrees of knee flexion by maximally externally
rotating the feet and comparing the relative amounts of external tibial rotation.
Reverse Pivot Shift. Jakob et al. (115) described the reverse pivot shift test, which is performed in a manner similar to
the pivot shift test for ACL injury. As the knee is brought from 90 degrees of flexion to full extension with a valgus stress
applied and the foot is externally rotated, the lateral tibial plateau is observed to move from a posteriorly subluxed
position to a reduced anatomic position. This is suggestive of posterolateral injury but is not an absolute finding. The
results of this test are most significant when there is asymmetry between the affected and the unaffected knee, because
there may be false-positive tests in individuals with ligamentous laxity.
Instrumented testing of PCL laxity, such as the KT-1000 used for ACL testing, has been attempted, but at present no
reproducible system has been perfected.
Evidence of PCL or posterolateral ligament complex injury is sometimes seen on routine plain radiographs. The lateral
radiograph commonly may show a posterior translation of the tibia relative to the femur or a bony avulsion at the tibial
insertion site of the PCL. In cases of lateral and posterolateral injury, bony avulsions may be seen off of the fibular head
or Gerdy tubercle. In the case of chronic PCL insufficiency, radiographs may reveal evidence of medial compartment or
patellofemoral arthritis. In addition, MRI can provide an excellent evaluation of PCL integrity and associated injuries,
allowing for appropriate treatment planning ( 116,117).
Classification and Treatment
Classification of PCL injuries depends on timing (acute versus chronic) and severity (isolated or combined injury). Both
variables affect treatment and prognosis ( 117).
Isolated acute PCL injuries rarely require surgery. Grade I and II instability (posterior drawer) likely represent partial
injury to the PCL. Partial PCL injuries are more common than partial ACL injuries. Treatment of this injury involves relief
of acute symptoms, protected weight bearing, and quadriceps muscle rehabilitation. Return to sports may occur within 4
weeks, when quadriceps and hamstring muscle strength is within 90% of the normal side ( 117,118). According to Harner
and Hoher (117), grade III injuries are treated with the knee braced in full extension for 2 to 4 weeks to minimize posterior
sag and the hamstring effect on posterior tibial translation. Partial weight bearing, quadriceps setting, and straight-leg
raising exercises are indicated. After 4 weeks, weight bearing may be progressed, along with active-assisted range of
motion. Quadriceps muscle strengthening is progressed, followed by functional exercises. Return to sport may vary
depending on the athlete and the sport but does not occur before 3 months. In addition, it is important to note that some
authors recommend surgical reconstruction of grade III injuries acutely ( 118). Chronic grade I and II PCL injuries usually
respond well to physical therapy, and do not require bracing.
Indications for surgery include (a) combined ligamentous injuries, (b) chronic PCL instability with posterior tibial
translation of more than 10 to 15 mm, (c) symptoms limiting daily activities despite conservative management, and (d)
early degenerative changes ( 108,119). Current surgical techniques involve primary repair or the use of autogenous
patellar tendon grafts and occasionally patellar tendon or Achilles' tendon allograft. The results of these procedures have
become increasingly more successful. As with the ACL, PCL reconstruction may now be performed arthroscopically or
with an arthroscopically assisted open technique. Acute combined injuries that require surgery are treated within 2 weeks
of injury (51,108,117), repairing or reconstructing all involved components.
Tibial PCL avulsion fractures producing small fragments and less than 10 mm posterior tibial translation at 90 degrees of
knee flexion may be treated nonoperatively, according to Veltri and Warren ( 118). Posterior translation of greater than 10
to 15 mm should be considered for operative PCL reconstruction or fixation.
Postoperatively, the knee is maintained in a brace locked in full extension for 2 to 4 weeks. The patient may bear partial
weight and begins quadriceps sets on the first postoperative day. The patient progresses to active knee extension from
90 to 0 degrees, along with straight-leg raising exercises. Knee flexion is gained slowly with passive flexion exercises
only, for 6 to 8 weeks (117,118). Five months after surgery the patient begins running, followed by sport-specific agility
drills at 6 to 7 months. The athlete may return to sports when quadriceps and hamstring strength are within 90% of the
uninjured side and sport-specific drills and exercises can be completed ( 118).
MENISCAL INJURIES
The menisci function in both load transmission and stability of the knee. In 1948, Fairbank ( 120) described the
radiographic appearance of knee joint changes after meniscectomy ( Fig. 56.20). He demonstrated squaring of the
contour of the femoral condyle, a medial ridge of the femoral condyle, and narrowing of the joint space. Since that time,
several investigators have shown that removal of the menisci will result in increased contact stresses on the underlying
cartilage and bone (121). This includes data that showed an increase in contact forces of greater than threefold with
removal of 16% to 34% of the meniscus (105,106,122,123 and 124). Further studies have demonstrated the increased
incidence of Fairbank's changes after meniscectomy in ACL-deficient knees ( 125,126,127 and 128). In addition, studies
by Markolf et al. (129) and Levy et al. (130) have illustrated the stabilizing effect of the medial meniscus. Therefore, it is
essential for the physician to be able to diagnose a meniscal injury and for the orthopedic surgeon to assess the type and
location of the tear to formulate an appropriate treatment plan.
FIGURE 56.20. Fairbank's radiographic changes of the knee joint after meniscectomy.
Diagnosis
Characteristically, meniscal injuries result from a twisting injury, with the foot planted. In the athletic population, a specific
incident can usually be cited, although with degenerative meniscal tears in the older population, this is often not the case.
The inciting episode is accompanied by joint line pain and the onset of swelling over the next few hours. Symptoms may
diminish over 1 to 2 weeks but usually recur when the patient resumes pivoting or cutting activities. Patients may
complain of swelling, episodes of locking or catching in which the knee may not fully straighten, and joint line pain ( 131).
Physical examination classically reveals an effusion, joint line tenderness, pain with squatting, and a positive McMurray
test. The McMurray test is performed with the patient in the supine position. The knee is gently maximally flexed with one
hand on the heel and the thumb of the other hand resting on the lateral joint line with the fingers across the medial joint
line (Fig. 56.21). With a valgus stress to the knee and external rotation of the foot, the knee is extended. A palpable or
audible click on the medial side is suggestive of a tear of the posterior horn of the medial meniscus. Similarly, extension
of the knee with varus and external rotation tests for a lateral meniscal tear. It should also be noted that the so-called
locked knee, which cannot reach full extension, may be caused by a “bucket handle” meniscal tear that has displaced
centrally into the joint, blocking a full range of motion. Acute isolated meniscal injuries rarely produce changes on plain
radiograph, whereas chronic meniscal pathology may produce the Fairbank's changes previously discussed. MRI
imaging is useful in cases of questionable meniscal damage ( Fig. 56.22).
FIGURE 56.21. The McMurray test.
FIGURE 56.22. Increased signal intensity within the wedge-shaped meniscus, which is indicative of a meniscal tear.
Treatment
Arthroscopic meniscal surgery was introduced by the Japanese in the 1960s and was further refined by O'Connor in the
1970s. The advent of arthroscopic surgery drastically changed the treatment of meniscal tears. Meniscal tears may be
resected or repaired arthroscopically. There are four basic patterns of meniscal tears: (a) longitudinal, (b) horizontal, (c)
oblique (flap), and (d) radial ( Fig. 56.23). Complex tears involve a combination of these injuries. These distinctions are
made at surgery and are important in the consideration of repair versus resection. Occasionally, however, meniscal tears
may be managed nonoperatively.
FIGURE 56.23. The four basic types of meniscal tear: I, longitudinal; II, horizontal; III, oblique; IV, radial. (Adapted from
Kalenak A, Hanks GA, et al. Arthroscopy of the knee. In: Evarts CM, ed. Surgery of the musculoskeletal system. New
York: Churchill Livingstone, 1990:3349, with permission.)
Nonoperative Management
Nonoperatively managed tears represent approximately 5% of all meniscal injuries ( 123). Most commonly, these cases
represent an incidental finding on physical examination of patients who report intermittent symptoms of pain but no
mechanical symptoms (e.g., locking, catching) and on physical examination have joint line tenderness but no effusion.
McMurray testing may or may not be positive. Generally, these represent partial-thickness or small, full-thickness
longitudinal tears that tend to be peripheral and, therefore, have blood supply to allow healing. These patients may be
treated symptomatically with rest, ice, and nonsteroidal antiinflammatory agents. If symptoms persist for longer than 4 to
6 weeks or become debilitating, surgical intervention remains an option.
Operative Management
The decision to perform a meniscus repair takes into consideration patient age and lifestyle, as well as biologic and
mechanical parameters. These include rim width, tear length, pattern of the tear, and knee stibiate. Patients younger than
the age of 50 are generally considered for meniscus repair if they meet the other criteria ( 132,133).
Arnoczky and Warren ( 134,135 and 136) have demonstrated the vascular anatomy of the meniscus. They showed that a
perimeniscal capillary plexus, first described by Policard, supplied branches that penetrated the peripheral 10% to 30%
of the menisci. The only exception is the posterolateral region of the lateral meniscus, immediately adjacent to the
popliteal tendon, which is devoid of vasculature. Tears confined to the peripheral regions, therefore, are amenable to
operative repair because of the potential for healing associated with vascularity, although the meniscus has been shown
to heal by fibrous scar formation, not by regeneration ( 135,136). Such tears are usually longitudinal in nature and may
include the classic bucket handle tear. Other indications for repair include peripheral detachments through the coronary
ligaments and selected peripheral, radial, and horizontal cleavage tears. Generally, tears within the peripheral 3 mm of
the meniscus are amenable to repair, with 90% to 95% success rate ( 137,138). The region from 3 to 5 mm remains a
gray zone in terms of repair, with data somewhat controversial regarding success of healing. However, some authors
have reported good results (137,139,140). Healing of menisci in regions greater than 5 or 6 mm from the periphery is
unlikely, but some success has been reported, particularly in cases of repair accompanied by ACL reconstruction, for
which results appear to be improved with all locations of meniscal tears ( 137).
It has also been noted that healing capacity is not directly affected by the age of the tear, but is proportional to the tear
length (132,133). Tear pattern is also important. Vertical longitudinal tears are ideal candidates for repair ( 141,142).
Radial tears may be reparable in the posterior horn. Flap tears and horizontal tears are generally not reparable.
There are three basic techniques for arthroscopic meniscal repair. The inside-out technique uses a cannula system to
pass sutures in a vertical mattress fashion across the tear and out through either a posteromedial or a posterolateral
incision (143). The outside-in method involves placement of needles percutaneously across the tear ( 137). Sutures are
then passed through the needles and retrieved from the joint through one of the arthroscopic portals. A knot is tied in the
end of the suture, which is then drawn back into the joint, pulling the ends of the tear into continuity. The all-inside
technique has been reserved for peripheral posterior horn tears ( 133), although recent technologic advances have made
the use of this method more popular for other reparable lesions. Fibrin clot may be used as an adjuvant to repair as a
means of promoting healing (144). The advantages of arthroscopic meniscal repair include the ability to repair more
central meniscal tears (2 to 6 mm) and posterolateral tears, which cannot be reached by open techniques. The risk of
neurovascular injury from needle passage is diminished in arthroscopic techniques by making a small posterolateral or
posteromedial incision for needle placement or retrieval.
Overall, arthroscopic meniscal repair is a successful procedure when performed by an experienced surgeon. Generally,
lateral meniscal repairs do better than medial meniscal repairs, and increasing size of the tear correlates with an
increasing failure rate ( 140,145,146).
Open Meniscal Repair
Tears within the peripheral 1 to 2 mm of the anterior third of the menisci are amenable to open repair. Tears in the middle
to posterior third require extensive exposure and, therefore, are better repaired arthroscopically. Open meniscal repair is
typically performed on vertical longitudinal tears of 5 mm or more in length. Although these tears may also be repaired
arthroscopically, some surgeons prefer the open technique, because it is believed that the repair bed may be better
prepared, it is easier to place the vertically oriented sutures, and there may be better anatomic orientation ( 145,147).
Postoperative rehabilitation is the same as for arthroscopic repair.
Rehabilitation After Arthroscopic Meniscal Repair
The specific timing of the meniscal healing process remains unclear. However, it is widely accepted that it is necessary to
protect the meniscal repair during the early healing phase, lasting for 4 to 6 weeks. The knee is protected from vigorous
activity for 6 months to allow for maturation of the healing collagen. Specifics of the rehabilitation protocol remain
somewhat controversial. Some authors immobilize the knee for 3 to 4 weeks and keep the patient non–weight bearing for
up to 4 weeks, whereas others allow immediate knee motion and weight bearing as tolerated. If an ACL repair has been
performed simultaneously, the basic ACL rehabilitation protocol is then followed. In isolated meniscal repairs isometric
quadriceps and hamstring exercises are begun immediately. At 6 weeks, closed kinetic chain exercises are instituted.
Progression varies with the individual, but once adequate strength is obtained along with full range of motion without pain
or effusion the patient may begin jogging and half-sped running, cycling, and swimming. This occurs at about 3 months.
By 6 months, the athlete is usually ready to return to full activities.
Arthroscopic Meniscectomy
Arthroscopic management of meniscal tears has replaced the historical open total meniscectomy. Arthroscopic partial
meniscectomy can be performed as an outpatient procedure, with minimal postoperative pain and morbidity and a rapid
return to activities. This procedure is indicated in symptomatic patients who have a nonreparable meniscal tear. At the
time of surgery, only the torn portion of the meniscus is removed, leaving behind a stable capsular rim to help maintain
joint stability. The remaining meniscal edge is smoothed and contoured to help prevent further meniscal injury. Numerous
authors have reported a high percentage of good to excellent results over a 5-year postoperative follow-up period ( 148).
The patient is allowed to bear weight as tolerated and begin full range of motion along with isometric quadriceps
exercises immediately postoperatively. These activities may be limited by pain and swelling, which can be treated with
ice and pain medication. Ice is used throughout the rehabilitation process to diminish any effusion. After 1 week, isotonic
and isokinetic exercises are begun, unless there is significant chondromalacia present, in which case these exercises are
avoided for 4 to 6 weeks. Usually, the patient regains a full range of motion within the first 2 weeks, by which time cycling,
walking, and swimming are begun. Once adequate strength is regained and there is no further pain and swelling, the
patient may resume full activities. This is usually 6 to 8 weeks after surgery. Nonsteroidal antiinflammatory agents may
be used for effusion or synovitis persisting for more than 2 to 3 weeks. Rarely is aspiration of an effusion indicated.
Meniscus Transplantation
Meniscus transplantation has been performed with limited success. The best results have been obtained in asymptomatic
individuals who have undergone recent total meniscectomy in an otherwise normal appearing knee. However, problems
of allograft sizing and preservation, immunogenicity, and disease transmission continue to be investigated.
Discoid Lateral Meniscus
Occasionally, meniscal problems in children may be caused by a discoid lateral meniscus (2.4% to 4.2%) ( 149,150).
Discoid medial meniscus is less common. The clinical syndrome associate with discoid menisci was described by Kroiss
in 1910 as a “snapping” or “clicking.” History is usually vague, because there is often no specific inciting episode.
Patients may complain of pain, swelling, locking, “snapping,” or limited motion, although the lesions may be
asymptomatic (151). Radiographs are helpful in ruling out other causes of the patient's symptoms. They are usually
normal in the case of a discoid meniscus, although there has been some association with flattened or hypoplastic lateral
femoral condyles, lateral joint space widening, hypoplasia of the lateral tibial spine, and elevation of the fibular head
(149,150,152).
Asymptomatic or occasionally “snapping” discoid menisci require no treatment. However, the symptomatic or torn discoid
meniscus poses a difficult surgical problem. Excision of the torn portion of discoid meniscus is technically challenging
(153). Once this is achieved, it is important to be certain that a stable meniscal rim remains behind. This can be difficult
in variants in which the meniscotibial ligament is congenitally absent. Postoperative management is the same as for
routine partial meniscectomy.
ARTICULAR CARTILAGE INJURIES
Anatomy
The primary function of articular cartilage is to distribute load and minimize stress on subchondral bone, while providing a
low friction articulating surface. Articular cartilage is composed primarily of type II collagen, proteoglycans, and
chondrocytes. Water makes up 60% to 80% of the wet weight. Collagen is a protein consisting of three amino acid chains
configured in a triple helix. Type II collagen accounts for 90% to 95% of the collagen in cartilage and forms a meshwork
that entraps large proteoglycans. Proteoglycans are composed of a protein core and glycosaminoglycan side chains
(hyaluronic acid, chondroitin sulfate, keratan sulfate, dermatan sulfate) ( Fig. 56.24). The chondrocytes reside in the
extracellular matrix, receiving nutrients through diffusion because there is no blood supply to the tissue. Articular
cartilage is arranged in four zones: superficial tangential, transitional, deep (radial), and calcified. The tidemark
separates the deep and calcified zones, whereas the subchondral bone underlies the calcified zone. Chondrocytes in
different zones differ in size, shape, and orientation to the articular surface, with each responding to loading in a different
manner. Mechanical, electrical, biochemical, and physicochemical events affecting the matrix play a role in stimulating
and suppressing chondrocyte function. Thus, proteoglycan synthesis is modulated and matrix composition is adjusted in
response to stress.
FIGURE 56.24. Normal articular cartilage structure. (Reprinted with permission from Nordin M, Frankel V. Basic
biomechanics of the musculoskeletal system, 2nd edition. Philadelphia: Lea & Febiger, 1989:31–57.)
The mechanical properties of articular cartilage reflect its viscoelastic nature. The collagen meshwork provides tensile
strength and resistance to shear. Proteoglycans and water provide stiffness and resilience when under compression. The
mechanical properties of articular cartilage change with disease (e.g., arthritides), age, and injury, resulting in decreased
strength and stiffness. This, in turn, increases the risk of further tissue damage. Injury may disrupt the collagen mesh,
causing chondrocytes to release degradative enzymes. This results in a relative decrease in proteoglycan content and
subsequent molecular changes that increase the matrix water content and decrease stiffness, which may then produce
further cartilage degeneration. Injury to articular cartilage is caused by repetitive overloading or a sudden impact, which
produces a high compressive and shear stress. Tissue response and healing depend on the type of injury and
involvement of subchondral bone.
Physical Examination and Evaluation

Cartilage lacks a nerve and blood supply. Therefore, injuries may not produce pain or inflammation. However, often
surrounding tissues with neurovascular input are injured simultaneously and pain, inflammation, and swelling may be
evident. The injured athlete may give a history of chronic, repetitive loading or of a single, acute event. Physical
examination requires a thorough evaluation of the structures of the knee, as has been previously described in this
chapter. Accompanying ligament or meniscal injuries are not uncommon. Buckwalter and Mow ( 154,155) have described
three general types of acute articular cartilage injuries based on the potential for repair. First, there may be damage
without visible tissue disruption. Such pathology may result from impact loads higher than those encountered in routine
daily activity but lower than those required to disrupt cartilage. Similar damage may occur with prolonged joint
immobilization and with synovial inflammation. Without associated injuries, symptoms and clinical findings may be
absent. Radiographs and MRI are within normal limits. If the collagen meshwork remains intact and viable chondrocytes
are present, the matrix may be restored. To maximize the possibility of healing, this individual should avoid impact
loading, prolonged joint immobilization, and inflammation.
Buckwalter's second category is mechanical disruption of articular cartilage alone. Blunt trauma or fracture may damage
the matrix and destroy chondrocytes. Often, there is associated swelling, synovitis, and mechanical symptoms. Lesions
are likely to be visible on MRI scan. Remaining chondrocytes may proliferate and increase synthesis of matrix
components at the site of injury. The amount of healing depends on size and location of the lesion, joint stability, and
alignment.
The third category is mechanical disruption of articular cartilage and subchondral bone. These are osteochondral injuries
that cause pain and hemorrhage owing to the penetration of the subchondral bone. As a result of the vascular input, a
cascade of healing events may occur. Fibrin clot may form, and an inflammatory and healing response may ensue.
Mesenchymal cells migrate to the area, proliferate, and synthesize a new matrix. Over a 6-month period, the subchondral
bone may be restored with bone and fibrous tissue. The articular cartilage defects may repair to a limited extent with
hyaline-like cartilage at the periphery and fibrous tissue filling a portion of the defect. In most of these cases, the fibrous
tissue gradually degrades, leaving a symptomatic area of exposed bone.
Surgical Treatment of Articular Cartilage Injuries
Analgesics, activity modification, and physical therapy may provide transient, limited symptomatic relief of articular
cartilage injuries. However, these lesions repair themselves infrequently and may result in progressive deterioration.
Therefore, a number of surgical treatment methods have been undertaken including shaving, abrasion arthroplasty,
drilling, and a variety of cartilage grafting procedures.
Arthroscopic shaving of fibrillated articular surfaces with debridement of loose cartilaginous debris may decrease
mechanical symptoms, whereas irrigation of the joint may reduce synovial inflammation and the presence of associated
degradative enzymes. However, the efficacy of this treatment for improving joint function and promoting healing appears
to be limited (154,156).
Arthroscopic abrasion arthroplasty involves disruption of a superficial layer of subchondral bone at the base of an
osteochondral defect. This disrupts the local blood vessels, resulting in hemorrhage and initiation of the healing and
repair cascade. Studies have shown that approximately 60% of patients will experience temporary symptomatic relief,
although the defect will fill to varying degrees with fibrocartilaginous tissue ( 154,157). Arthroscopic debridement and
drilling into the subchondral bone achieves a similar result, depending on the size and location of the lesion, as well as
patient age and activity level.
Because of the relatively limited clinical success of debridement, abrasion, and drilling procedures, various grafting
procedures have been and are currently under investigation. Periosteal and perichondrial grafts have been shown to fill
defects with tissue resembling articular cartilage, with the best results occurring in young patients. However, mechanical
durability remains an issue ( 155,156,158). Osteochondral allografts provide a source of viable chondrocytes without
donor site morbidity. The success of allograft treatment is dependent on lesion size, amount of bone transplanted with
the cartilage, freezing, and antigen matching. At present, this is only recommended for treatment of patients with severe
symptoms due to isolated posttraumatic lesions, osteochondritis dissecans, and avascular necrosis of the femoral
condyle (154,159).
Osteochondral autografts taken from a non–weight bearing area of the knee has also been shown, in a limited series, to
be an effective treatment in selected patients with isolated defects. However, donor site morbidity, contouring, and the
donor–recipient site interface continue to pose questions ( 160,161). In recent years, chondrocyte transplantation has
provided a new frontier in the treatment of articular cartilage injuries. In 1994, Brittberg et al. ( 162) presented data
showing promising results of treatment using autologous chondrocytes transplanted into defects in a staged procedure.
Autologous chondrocytes were grown in culture and reimplanted into the knee, producing a hyaline-like cartilage. Longer
term data are promising, but functional outcome remains to be assessed on a large scale.
On another front, the metabolic homeostasis of the articular cartilage meshwork is regulated by a number of polypeptide
growth factors. There is experimental evidence to suggest a potential therapeutic role for these agents in articular
cartilage healing and repair. Further research continues in this area, and in the development of synthetic matrices to
replace or aid in the reconstitution of damaged articular cartilage.
To date, none of these methods has provided an optimum solution to the problem of articular cartilage injury. In the
future, treatment will likely combine an evaluation of patient expectations with these concepts, along with mechanical
issues such as stability and alignment. This, along with appropriate physical therapy accounting for the biomechanical
issues of joint motion and loading, may provide a successful treatment algorithm.
KNEE DISLOCATION
Dislocation of the knee is a potentially devastating injury that occurs as a result of major trauma. These injuries produce
damage to multiple ligaments as well as to vascular structures in 30% to 50% of patients and nerve in up to 50% of
patients (11,163). As such, a knee dislocation is an orthopaedic emergency. Obvious knee dislocations must be
recognized and reduced quickly, and any knee with multiple ligament injuries including both cruciates should be
suspected of being a spontaneously reduced dislocation.
Classification of knee dislocations is based on the direction of tibial displacement relative to the femur. Anterior and
posterior dislocations are the most common types. Dislocations may also be medial, lateral, or rotatory. Rotatory
dislocations are further classified as anteromedial, anterolateral, posteromedial, and posterolateral.
Another dislocation is caused by hyperextension resulting from a direct anterior blow to the knee. Most often this occurs
in motor vehicle accidents, but it may also be produced by a football tackle when the helmet strikes the knee. Under such
circumstances, the PCL and often the ACL are torn, and the popliteal artery may be stretched or torn.
Posterior dislocation results from a direct blow to the anterior, proximal tibia, driving it posteriorly. Again, both the ACL
and PCL are disrupted. Also, the popliteal artery is stretched or torn as it is pushed posteriorly while tethered proximally
at the adductor hiatus. The risk of vascular and posterior dislocations.
Medial and lateral dislocations occur as a result of severe valgus or varus blows to the knee. These blows may produce
both cruciate and collateral ligament damage, along with possible neurovascular injuries. Similarly, angular blows to the
knee may produce rotatory instabilities, with motion hinged on the limited remaining intact structures.
Evaluation
Any knee with gross multiplanar instability should be considered as a frank or occult knee dislocation until proven
otherwise. A thorough history of the injury, the amount of trauma involved, deformity, and spontaneous or manual
reduction should be obtained in addition to performing a physical examination. The details of ligamentous examination of
the knee were discussed earlier.
Any patient with a suspected knee dislocation is at risk for arterial injury and, therefore, should have an immediate
arteriogram. In addition to complete rupture, arterial injuries may include intimal tears or intraluminal thrombus formation.
Therefore, signs and symptoms of arterial injury may not be present on the initial physical examination, despite an
underlying problem. As a result, the foot may be pink, warm, have good capillary refill, and a palpable pulse, despite
arterial damage. Signs and symptoms may manifest hours to days after the injury.
In the case of an arteriogram revealing popliteal artery occlusion or tear, repair or grafting of the vessel should be
completed within 6 to 8 hours of the injury to minimize the changes of ischemic damage to the limb and possible
amputation.
Common peroneal nerve injuries occur in approximately 35% of cases ( 11,163). These are most often associated with
posterolateral dislocations. The injuries range from neurapraxia to complete disruption. Treatment of nerve injuries
remains controversial. In general, if operative management of ligamentous injuries is pursued, the nerve may be
examined at that time. If the nerve is completely disrupted, then repair or grafting may be undertaken at that time.
Otherwise, observation and conservative management may be pursued.
Management
As already noted, initial management is directed toward the vascular status of the limb. A frankly dislocated knee should
be immediately reduced. In an occult dislocation, physical examination is performed, and the examiner should quickly
suspect a dislocation. In either case, an arteriogram is immediately obtained. Once the vascular assessment is
completed, emergency repair or reconstruction of the vessel is performed, if necessary. Ligamentous reconstruction may
be performed at the same operative sitting or within the ensuing 2 weeks. Operative techniques are the same as those
described elsewhere in this chapter. Sisto and Warren ( 164) reported that postoperative knee stiffness was more of a
problem than instability. However, with more recent advances in techniques of ligament reconstruction, allowing earlier
motion and producing a lower incidence of stiff knee, this is less likely to be a problem, and the authors advocate
operative stabilization. Nonoperative management involves bracing for 6 to 8 weeks, followed by physical therapy.
Postoperative treatment must be guided by the degree of associated arterial and neurologic injury and repair. Generally,
an early range of motion should be established. Postoperative rehabilitation protocols may then be adapted for the
specific complex of injuries sustained by each individual. The long-term prognosis for return of function depends primarily
on the neurovascular status of the limb. If adequate arterial flow and neurologic function are reestablished, then the
prognosis is good. The prognosis seems to be best for those limbs managed by surgical intervention. However, success
with nonoperative management has been reported.
TIBIAL SPINE AND INTERCONDYLAR EMINENCE FRACTURES
Tibial spine and intercondylar eminence fractures are often seen as isolated injuries and are associated with knee
instability. These fractures are most commonly caused by an athletic injury or motor vehicle accident. They result from
violent hyperextension or hyperflexion, varus or valgus stress, or twisting injury. Hyperextension or hyperflexion usually
causes an intercondylar eminence avulsion (with attached ACL), whereas twisting may produce a tibial fracture
(165,166).
Signs and Symptoms
The patient usually presents with reports of pain and swelling. Often, the knee does not reach full extension. This is
caused by a mechanical block because the intercondylar eminence is elevated into the intercondylar notch. The knee
may also be unstable as a result of ADL or collateral ligament injury. Fracture is usually evident on standard
anteroposterior and lateral views of the knee. However, CT scan or tomogram may be helpful in further evaluating the
extent of the fracture and amount of displacement.
Treatment
An isolated tibial spine fracture can usually be reduced by placing the knee in full extension. In this case, it can be
treated nonoperatively with a cast or brace in full extension for 4 to 6 weeks. However, if there is an associated ACL
injury in a young, active patient, this may need to be addressed surgically ( 167).
Similarly, a minimally to moderately elevated intercondylar eminence fracture can usually be reduced by placing the knee
in full extension. If this is the case, it may also be treated in full extension in a cast or brace for 4 to 6 weeks. However, if
the fracture cannot be anatomically reduced by a closed method, operative intervention is indicated. This may be done
arthroscopically, fixing the fragment with either a lag screw or a suture placed around the fragment and tied over the
anterior tibia.
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57 Foot and Ankle Injuries
57
FOOT AND ANKLE INJURIES

JOHN C. LINZ
STEPHEN F. CONTI
DAVID A. STONE
Epidemiology
Biomechanics of the Foot and Ankle
The Lower Leg
Exertional Leg Pain
Achilles Tendon Syndromes
The Ankle
Ankle Sprains
Anterior Impingement Syndrome
Posterior Impingement Syndrome
Peroneal Tendon Syndromes
Flexor Hallucis Longus Pathology
Osteochondral Lesions of the Talus
The Foot
Running Footwear
Fractures of the Foot
Stress Fracture of the Hallux Sesamoid
Other Sesamoid Problems
Plantar Heel Pain
Accessory Navicular Syndrome
Midfoot Sprains
Turf Toe
Other Tendon Problems
Nerve Injuries in the Athlete
Interdigital Neuroma
Tarsal Tunnel Syndrome
First Branch of the Lateral Plantar Nerve
Medial Plantar Nerve
Deep Peroneal Nerve
Superficial Peroneal Nerve
Sural Nerve
Chapter References
EPIDEMIOLOGY
Every sport predisposes the athlete to a particular subset of foot and ankle injuries ( 1,2,3 and 4). However, very little has
been written on the epidemiology of foot and ankle injuries in sports. Garrick and Requa ( 5) reviewed patient data from
the Sports Medicine Center at St. Francis Memorial Hospital over a 9-year period and found that 25.2% of 16,754 total
injuries were to the foot and ankle. Of the injuries, 9.7% were to the ankle and 15.5% to the foot. The sport with the
lowest incidence of ankle injuries was swimming, with only 0.5%. The sports with the highest were basketball and figure
skating, both at 21.1%. The sport with the lowest incidence of foot injuries was football at 2.0% and weight lifting at 2.1%.
The highest was hiking at 58%. Over half (50.4%) of the ankle injuries were sprains. By contrast, only 6% of the foot
injuries were sprains, with the majority of foot injuries characterized as “overuse” injuries. No data about the severity of
the injuries was provided. Knowledge of the demands of a given sport is important to prescribe safety gear and
recommend appropriate management when recovering from an injury. Some sports are associated with unique problems
caused by the use of special equipment or playing surfaces. For example, ice hockey is associated with a high
percentage of lacerations, including lacerations of the tibial tendons and vessels because of ice skates ( 6).
BIOMECHANICS OF THE FOOT AND ANKLE
Biomechanics, simply stated, is the application of mechanical laws to living structures. Understanding the biomechanics
of the foot and ankle is critical to the study of foot and ankle injuries ( 7).
Gait is a complex process that involves all major body segments. The foot and ankle must be viewed as just one
component of the system. Human gait is characteristically orthograde and bipedal with intraspecies variation ( 8). Ralston
(9) notes that human gait evolved to take individuals from one point to another with minimal expenditure of energy.
Energy is wasted with vertical displacement of an individual's center of gravity, a motion that serves no useful purpose.
One need only try to walk a short distance with a limp to try to realize that any major aberration of human gait causes a
major increase in energy expenditure. The key to understanding human gait lies in the realization that all body
movements responsible for gait are interrelated and serve to minimize energy expenditure ( 10). This applies not only to
the mechanisms of gait but the rate at which it occurs.
Gait is a cyclical process ( Fig. 57.1) that is divided into two phases: the stance phase, in which one limb is in contact with
the ground, and the swing phase, during which the same limb is propelled forward ( 8). For forward progression to occur,
four requirements must be satisfied. The limb must be stable in stance, and step length must be adequate. The foot must
be adequately prepositioned for ground contact and must clear the ground on swing. The stance phase is divided into
four points. Stance begins with initial contact, the point at which both limbs touch the floor. Initial contact evolves to a
loading response, when body weight and momentum is accepted. Midstance is a period of single support, at which time
the contralateral limb and body advance over the stationary foot. Terminal stance begins at heel rise and ends with
preswing, another period of double support. The swing phase is divided into three periods. Normally, the stance phase
accounts for 60% of the gait cycle (8).
FIGURE 57.1. The gait cycle is divided into the stance phase and the swing phase. The stance phase occupies 62% of
the gait cycle and is further divided into periods of single and double limb support.
Running is not understood to the same degree as walking. One main difference between running and walking is that one
limb is always in contact with the ground in walking. In running, the period of double support is replaced by an analogous
period of double “float,” when both feet are off the ground. The speed at which a person makes a transition between
running and walking is predictable. The equation that energy is a function of mass multiplied by distance traveled does
not hold true with the human machine. Running involves considerably more energy than walking ( 9,11).
The function of the foot may be divided into three general categories: accepting uneven terrain, providing a firm lever for
push-off, and absorbing shock. The ability to accept uneven terrain depends on the foot being pliable. The ability to
change from pliable to rigid is accomplished by altering the position of the hindfoot. In general, the hindfoot is rigid in
varus and pliable in valgus. Hindfoot valgus or varus is largely a result of subtalar movement. The subtalar joint is formed
by the undersurface of the talus and the dorsal surface of the calcaneus. It consists of three closely approximated
articulations or facets. The largest facet is the posterior facet. The anterior and middle facets differ from the posterior
facet by virtue of the fact that the posterior facet is concave on the calcaneal surface and convex on the talar surface.
The situation is opposite from the anterior and middle facets. The side-to-side motion of the subtalar joint can be likened
to the rocking of a boat ( 8).
The axis of the subtalar joint is actually at a 45-degree axis from the ground and at a 16-degree angle from the
longitudinal line drawn through the second metatarsal ( Fig. 57.2). This motion and the up-and-down motion of the foot at
the tibiotalar joint combine to form a “universal joint.” Movements through both of these joints position the foot. When the
hindfoot is supinated, the geometry of the tibia and calcaneus is such that the bones are immediately joined together and
the foot is stable. The hindfoot pronation unlocks this relationship, and a pliable foot is formed. In this way, the muscles
of the leg control the foot and its function in the gait cycle ( 8).
FIGURE 57.2. Motion about the subtalar joint occurs about an axis 45 degrees from the floor and 16 degrees medially
from the central axis of the second metatarsal.
The athlete must strive to maximize performance by conserving energy. This is accomplished by eliminating movements
or actions that do not serve a useful purpose. A seemingly insignificant foot injury may set up a pattern of compensatory
movements proximally that alter kinematics and increase disability. Treatment of injuries in an athlete must be predicated
on the fact that the foot and ankle unit is part of a larger and complex mechanism.
THE LOWER LEG
Exertional Leg Pain
Running athletes are predisposed to exercise-related lower leg pain of many etiologies. A proper diagnosis is the first
step in the treatment of this common problem. Exertional leg pain may be divided into three general categories: medial
tibial stress syndrome (shin splints), exertional compartment syndrome, and stress fracture.
The term shin splints is becoming outdated. The term medial tibial stress syndrome is preferred for leg pain and
tenderness that is characteristically localized to the medial border of the distal one third of the tibia without sensory,
motor, vascular, or radiographic abnormalities. Three-phase radionuclide bone scanning reveals increased linear uptake
along the posteromedial border of the tibia ( Fig. 57.3A and Fig. 57.3B). Magnetic resonance imaging (MRI) demonstrates
diffuse edema (Fig. 57.3C). This phenomenon is most likely the result of periosteal inflammation along the posteromedial
border of the tibia. The soleus or the posterior tibial muscles, or both, may contribute to symptoms. Resisted active
plantarflexion and inversion of the foot or resisted active plantar flexion alone reproduces pain. The distal one third of the
tibia is tender with palpation. Treatment consists of relative rest, cross-training to maintain cardiovascular endurance,
and muscle rehabilitation if obvious weakness or tightness is present. Surgery is performed in intractable cases (no
response over the course of 1 year) by stripping the periosteum from the posteromedial tibia.
FIGURE 57.3. A: This bone scan is consistent with posteromedial stress syndrome. The bone scan is “hot” along a broad
region of the central tibia. B: A stress fracture is “hot” at a markedly smaller region, consistent with the site of the stress
fracture itself. C: MRI demonstrates diffuse edema in the tibia of a patient with medial and tibial stress syndrome. ( A and
B from Mann R, Coughlin M. Surgery of the foot and ankle, 6th ed. St. Louis: Mosby–Year Book, 1993, with permission.)
Compartment syndromes are a result of increased pressure within a closed fibro-osseous space, causing local tissue
hypoxia with secondary ischemic muscle and nerve damage. Acute compartment syndrome occurs when local capillary
flow is compromised following blunt trauma or fracture. Local tissue pressure within 40 mm of mercury of the main arterial
pressure results in capillary collapse, and neuromuscular damage ensues. The duration of the compromise is critical. At
30 minutes, tissue damage is fully reversible. After 6 hours, tissue damage is only partially reversible and recovery is
incomplete. A delay of 8 hours or more leads to permanent cell death and a poor prognosis for functional recovery. As
pressures increase, less time is available for diagnosis and effective surgical relief. Diagnosis of acute compartment
syndrome relies on a high clinical suspicion and documentation of intracompartment pressures. Pain out of proportion to
the injury is usually the primary symptom and is aggravated by passive motion of the joints adjacent to the involved
compartment. Any athlete who sustains a direct blow to the lower leg who has persistent pain and swelling in the calf
should be monitored closely for several hours. Paresthesias, poikilothermia, paralysis, and pulselessness are also signs
that should be considered. The presence or absence of pulses can be misleading because local intracompartment
pressures do not usually exceed arterial blood pressure, even in the most severe cases. Intracompartment pressures that
are 20 mm of mercury below diastolic blood pressure or absolute measurements, of 30 to 45 mm of mercury are
indications for immediate release of the fascia and decompression of the involved compartments. An untreated acute
compartment syndrome of the lower leg can result in muscle atrophy, contracture, neurologic dysfunction, and even loss
of the limb.
A subtle but similar condition is the chronic exertional compartment syndrome. This syndrome characteristically involves
the anterolateral compartments and, occasionally, the superficial or deep posterior compartment of the leg ( Fig. 57.4)
(12). Mavor (13) was the first to describe chromic anterior compartment syndrome in 1956. In 1975, Reneman ( 14)
confirmed that the clinical manifestations were caused by increased compartment pressures. During exercise, there can
be a 20% increase in muscle volume, and as muscle volume increases, compartment pressures increase ( 15). A
compartment syndrome occurs in an athlete when the pressure within a compartment increases enough to compromise
tissues within the space. Patients usually complain of a dull ache without a history of trauma induced by activity that is
often consistently reproducible. This has led to the term third lap syndrome. Symptoms are bilateral 75% to 95% of the
time, although they are often worse in one leg than the other. Discomfort may persist for hours after activity, and some
patients have weakness, numbness, or paresthesias. Physical examination is rarely diagnostic unless symptoms are
unilateral. Increased tenderness and tension within the involved compartment may be noted if the patient has been
exercising before the examination. Pain with passive stretch of the involved musculature may be present. Fascial defects
resulting in symptomatic muscle herniations are noted in some patients but are not diagnostic.
FIGURE 57.4. Compartments of the leg. There are four compartments of the leg divided by fascial compartments. The
major nerves and vessels are consistenly present in their respective compartments.
Traditional anatomy books describe four compartments in the lower leg. Of these, the anterior compartment is the most
frequently involved, and the deep compartment is the second most commonly involved compartment. Some authors have
postulated that there are up to seven compartments in the lower leg, and the presence of an isolated compartment for the
posterior tibial muscle is debated. The authors do not routinely test for this when evaluating patients.
Diagnosis of chronic compartment syndrome is confirmed with intracompartment pressure measurements ( Fig. 57.5).
Although no consensus on the best technique for obtaining these measurements or which values constitute an absolute
diagnosis, the authors generally use Rorabeck's criteria ( Table 57.1).
FIGURE 57.5. Compartment pressure testing device with catheter taped in place.
TABLE 57.1. CRITERIA FOR CHRONIC EXERTIONAL COMPARTMENT SYNDROME
Nonsurgical management of chronic exertional compartment syndrome is successful only if the athlete is willing to give
up the activity that brings on the symptoms. Most athletes wish to continue with training and sports participation, and
surgical intervention is recommended. The choice of treatment is fasciotomy of all involved compartments. Care should
be taken to release completely the full extent of the fascial compartment, with meticulous attention to hemostasis.
Recurrences do occur and are often the result of inadequate release through minimal incisions, development of scar
tissue, iatrogenic neuroma formation, or development of a compartment syndrome in a previously asymptomatic
compartment (16,17,18 and 19).
The medial gastrocnemius strain was originally termed tennis leg in 1883 ( 20,21). It has also been called coup de fouet
(snap of the whip). The most common mechanism involves sudden dorsiflexion of the plantarflexed foot, such as landing
from jumping. The belief that the injury is really a rupture of the plantaris tendon, which recoils through the medial head of
the gastrocnemius, muscle was refuted by Arner and Lindhom (22), who performed surgical exploration of the injury and
demonstrated a tear of the medial head of the gastrocnemius at the musculotendinous junction. In all of their cases, the
plantaris tendon was intact at the time of surgery.
As with Achilles tendon ruptures, the patient often describes a prodromal period and reports a sharp pain associated with
a popping sound. It occurs more commonly in middle-aged men, and is seen most commonly in football, tennis, and
soccer players (23). Physical examination demonstrates swelling around the proximal calf, with localized tenderness in
the medial aspect of the midcalf. A defect in the medial head of the gastrocnemius is often palpable. Walking may be
quite difficult, and the pain is increased with attempts at toe walking or manually resisted plantarflexion. Thompson test is
negative. The differential diagnosis includes ruptures of the Achilles tendon and rupture of a Baker cyst. Diagnosis is
generally made on the basis of the history and physical examination. Plain radiographs are not helpful. MRI is the
diagnostic test of choice and demonstrates edema and disruption at the distal musculotendinous junction. Treatment is a
controlled rehabilitation program. Many physicians use short periods of immobilization for severe tears, but a controlled
trial of immobilization versus active aggressive rehabilitation has not been conducted. Immobilization of the foot in
dorsiflexion at the time of the injury may be effective but has not been studied.
Achilles Tendon Syndromes
The Achilles tendon is the largest and strongest tendon in the body but is frequently involved in overuse syndromes ( 24).
The biomechanical basis for Achilles tendon injury has been well studied ( 24,25 and 26). In individuals with forefoot
varus, compensatory pronation is used to achieve plantargrade positioning. This results in the tendon moving from
medial to lateral, producing a whipping action or bowstring effect with increased tension at the medial insertion. Torsional
forces before toe-off are thought to produce a “ringing out” of the relatively avascular area 2 to 6 cm above its insertion.
These forces produce a cumulative affect of the repetitive cycle of the running gait. Over time, it can lead to three types
of noninsertion Achilles tendon conditions: peritendinitis, which involves inflammation of only the paratenon;
peritendinitis, with tendinosis, which involves inflammation of the paratenon accompanied by degeneration of the tendon;
or tendinosis, which involves degeneration of the tendon without paratenon involvement ( Fig. 57.6) (27). In most cases,
the patient complains of gradual onset of pain and swelling 2 to 6 cm above the Achilles insertion. Symptoms occur after
activity but progress to pain during the activity. In cases of peritendinitis, swelling may be diffuse, but pain does not
change when the foot is moved from dorsiflexion to plantarflexion. Peritendinitis with tendinosis presents as a mass that
moves with ankle motion. The pain may not change substantially with ankle motion. Tendinosis pain changes with tendon
gliding as the foot moves from dorsiflexion to plantarflexion. All three conditions should initially be treated with a
nonoperative regimen of rehabilitation exercises, which emphasize eccentric strengthening of the gastrocnemius-soleus
complex, and the use of an orthosis to correct biomechanical abnormalities, if this is ineffective. Walking casts are rarely
necessary, and steroid injections cannot be recommended at the present time. Recalcitrant cases, which do not respond
to 6 months of nonsurgical intervention, are considered for surgical intervention. Chronic peritendinitis is treated with
stripping of the thickened paratenon and release of adhesions with early mobilization. Tendinosis is treated with open
debridement and repair or multiple percutaneous incisions ( 28). Surgery is followed by a variable period of immobilization
and a rehabilitation program to restore strength, flexibility, and endurance to the lower leg, followed by return to activity.
FIGURE 57.6. Achilles tendinosis. Note: Hypertrophic tendon replaced largely by scar.
Insertional Achilles tendinitis can occur alone as an attritional enthesopathy or in association with retrocalcaneal bursitis
or Haglund deformity. There is a continuum of disease beginning with retrocalcaneal bursitis, progressing to partial tear
of the Achilles tendon. Heterotopic ossification of the Achilles tendon is often associated with this condition. Symptoms
are similar to Achilles tendon problems that occur more proximally but are localized to the insertion. Patients may
complain of heel pain at night owing to direct pressure on the heel. Radiographs often show ossification within the tendon
or a Haglund deformity. MRI is not necessary, but can be helpful in determining the extent of Achilles tendon
involvement. Initial management should be nonoperative, again consisting of gastrocnemius-soleus stretching exercises,
judicious use of heel lifts and orthotics, and activity modifications. Rarely, a short leg walking cast is required. Again,
steroid injections are not recommended. Operative management is recommended for recalcitrant cases. Potential
procedures include retrocalcaneal bursectomy, excision of Haglund deformity (calcaneal spur excision), debridement and
repair with suture anchors, or tendon debridement with possible flexor hallucis longus transfer. For debridement alone,
early mobilization is possible while repair, reattachment, or reconstruction is treated with a period of immobilization
followed by rehabilitation.
Achilles tendon rupture is a serious cause of leg pain and dysfunction in the athlete ( 29). The Achilles tendon is the only
tendon crossing the ankle joint that is not encased in a synovial tendon sheath. It has a region of reduced blood supply
approximately 4 to 5 cm above its insertion into the calcaneus ( 29). A sedentary lifestyle accompanied by the sudden
initiation of strenuous sports in the middle-aged patient has produced an increasing incidence of Achilles tendon rupture.
Seventy-five percent of Achilles tendon ruptures occur during sporting activities in athletes between 30 and 40 years of
age (30,31). It is more common in men and with the type O blood group (32). Only 15% of patients have premorbid
Achilles symptoms (30,31,32,33 and 34). The mechanism of injury is usually eccentric loading of the foot into dorsiflexion.
The patients complain of a sudden sharp pain often associated with an audible snapping sensation. There is often a
palpable or visible defect in the tendon. The patient is unable to rise on the heel on the affected side and will have a
positive Thompson test (i.e., lack of plantarflexion when the calf is squeezed while the patient is prone) ( Fig. 57.7).
Radiographs help rule out a bony injury. Ultrasound or MRI can be helpful in evaluating the location and severity of
Achilles tears. Treatment of Achilles ruptures depends on the patient and his or her goals. The sedentary nonathletic
older patient may be treated with a short leg non–weight-bearing cast with the foot in equinus for 4 weeks, followed by 4
weeks in a short leg weight-bearing cast with the foot in the neutral position ( 35,36). For the athlete or active younger
individual, surgical repair is optimal ( 30,37,38,39 and 40). In comparison to nonoperative treatment, surgical repair is
associated with a lower rerupture rate, improved plantar flexion strength, and results in a higher resumption of sports
activity at the same level as before the injury ( 40). Recent studies looking at controlled early motion following repair or
following a short period of casting show promise as an alternative to longer casting regimens ( 41,42).
FIGURE 57.7. Thompson test is a reliable clinical test to identify the presence of a complete tear in the Achilles tendon.
When the Achilles tendon is torn, a positive test is elicited by squeezing the calf and seeing no plantar flexion of the foot.
A negative test occurs when the calf is squeezed and plantar flexion occurs in the foot.
THE ANKLE
Ankle Sprains
The ankle joint is responsible for plantarflexion and dorsiflexion of the foot, and is composed of the tibia, fibula, and talus.
The tibia and fibula form a mortise or notch distally for the body of the talus. This configuration is supported by three
strong sets of ligaments (Fig. 57.8). The anterior and posterior inferior tibiofibular ligaments or syndesmotic ligaments
join the distal tibia and fibula. A strong medial deltoid ligament is composed of a deep and superficial component. The
deep portion consists of the anterior tibiotalar and posterior tibiotalar parts. The superficial portion consists of the
tibionavicular, tibiocalcaneal, and posterior tibiotalar parts. The lateral ankle complex consists of four distinct ligaments:
the anterior and posterior talofibular, calcaneofibular, and the talocalcaneal ligaments. The body of the talus is widest
anteriorly. Therefore, the ankle is most stable in dorsiflexion when the anterior aspect of the talus articulates with the
mortise (8). Most inversion ankle injuries occur in plantarflexion, when the ankle is least stable. With the foot in this
position, the first ligament injured is the anterior talofibular ligament (ATFL). This ligament is actually a thickening in the
anterior ankle capsule and blends imperceptibly into it. Therefore, a torn ATFL is a capsular injury. The next ligament
injured is the calcaneofibular ligament (CFL). The ATFL need not necessarily be completely torn to allow damage to the
CFL. The CFL is part of the medial wall of the peroneal tendon sheath. The CFL may be injured without damage to the
ATFL in the uncommon situation of inversion stress applied across a dorsiflexed ankle. The posterior talofibular ligament
is rarely injured. An inversion injury may be likened to opening a book. The posterior talofibular ligament is located at the
binding and, therefore, is not generally torn ( 43).
FIGURE 57.8. The ankle joint consists of the tibia, fibula, talus, and the supporting ligamentous structures. It is usually
possible to identify which structures have been injured by careful palpation of the ankle joint because of the relative lack
of subcutaneous fat and muscle.
The ankle sprain is one of the most common injuries in sports ( 44). The incidence of inversion injuries has been
estimated as 1 per 10,000 persons per day ( 45,46). Many patients with ankle sprains do not seek medical attention but
prefer to treat themselves. Lack of or late diagnosis combined with inadequate treatment may lead to late sequelae in
30% to 40% of patients ( 47).
History and physical examination are the cornerstones for diagnosis of ankle sprains. The patient's description of the
mechanism of injury may not be accurate (48) but should be elicited as a starting point in making the diagnosis, and
helps guide the physical examination. Inability to bear weight immediately after injury may indicate a fracture because
even patients with severe sprains are able to bear weight for at least three steps after injury. Symptoms such as giving
way, swelling, and difficulty with cutting, jumping, and changing directions are frequent reports. Associated tenderness
over bony structures supports the possibility of fracture. Severe swelling, ecchymosis, and feelings of giving way during
gait are suggestive of severe ligament injuries. A lateral ankle sprain is a twisting injury to the ankle, causing damage to
the lateral ankle ligament complex. Inversion accounts for 85% of the ankle sprains that occur. The amount of force
causing the injury determines the degree of injury ( 49). The most commonly used grading system for ankle sprains is by
Leach (50). In this classification scheme, a first-degree sprain is defined as a partial tear of the ATFL. A second-degree
sprain is complete rupture of the ATFL and a partial tear of the CFL. A third-degree sprain is a complete tear of both
ligaments.
If the ankle is not examined soon after injury, edema and hemorrhage make determination of ligament tenderness
difficult. The ATFL may produce significant regional tenderness and make the diagnosis of a syndesmotic sprain difficult.
The CFL lies deep to the peroneal tendons and may also be difficult to evaluate. Serial examination may be needed to
determine the prognosis of an ankle sprain for this reason. The severity of ligament sprain is usually determined by the
use of the anterior drawer and talar tilt tests. The anterior drawer test ( Fig. 57.9) is similar the Lachman test used in the
knee joint to evaluate the anterior cruciate ligament. In the ankle, the test is performed by firmly grasping the heel with
one hand and gently moving the foot forward while securing the tibia with the other hand. Slight internal rotation is
applied to the foot hinging on the deltoid ligament. The test is done slowly with the patient relaxed. The foot is held in
slight plantarflexion ( 51). Results should always be compared to the contralateral side, because individual difference is
striking. The second test is the lateral talar tilt ( Fig. 57.10). The feeling of instability with talar tilt testing may be confused
with subtalar motion. This test is performed by gently applying an inversion stress across the tibiotalar ankle with the
ankle in the neutral position ( 51).
FIGURE 57.9. The anterior drawer test is performed by stabilizing the tibia and pulling the foot toward the examiner. A
positive test identifies the presence of a torn anterior talofibular ligament.
FIGURE 57.10. Talar tilt test is performed by inverting the foot and noting the amount of opening on the lateral side of the
ankle. It is useful in determining the presence of a torn calcaneofibular ligament and, in some cases, a torn anterior
talofibular ligament.
Stress x-ray studies can be used to provide a quantified measurement of the degree of anterior drawer or inversion talar
tilt by comparing the injured and uninjured sides. The test can be performed manually or by using an instrument (Telos).
This device offers the advantages of reproducibility and decreased exposure of ionizing radiation to the physician. When
using the Telos, Sauser et al. (52) found a talar tilt of 10 degrees or more to be associated with the lateral ligament injury
in 99% of cases. Normal values for talar tilt have reported to range from 5 degrees to 23 degrees ( 53). Chrisman and
Snook (54) noted when comparing both ankles that a difference of more than 10 degrees was significant when measuring
the ATFL and CFL. Gould et al. ( 55) thought that an increase of 4 mm was indicative of instability in the anterior drawer
test. However, Laurin et al. (56) believed that an increase greater than 9 mm was abnormal. Overall, values of up to 5
mm of separation between the talus and distal tibia are considered to be normal, whereas values between 5 and 10 mm
are probably abnormal. Values greater than 10 mm are grossly abnormal. Much controversy surrounds the use of
radiographic tests in evaluating ankle and subtalar instability. Because x-ray studies are a two-dimensional picture of a
three-dimensional structure that has a spectrum of rotatory instabilities, it is no wonder that a uniform opinion about the
clinical utility of stress x-ray studies has not been developed in the orthopedic literature.
More often than not, the x-ray study is used to rule out an accompanying fracture. The common fractures to consider
include osteochondral fractures of the talus, fractures of the medial and lateral malleoli, anterior process of the calcaneus
(Fig. 57.11), fracture of the base of the fifth metatarsal, and lateral process of the talus fractures. MRI often demonstrates
ligament disruption, tendon injury, osteochondral lesions, and occult fractures. It can often aid in making the decision to
use operative or nonoperative treatment or when planning appropriate operative intervention. Although it is very sensitive
in defining ligament structural abnormalities, MRI cannot assess soft tissue competency or instability. Formulating a
treatment plan based on history and physical examination, supplemented by specific radiologic tests, rather than an
emphasis on imaging studies, will lead to more rational diagnosis and treatment.
FIGURE 57.11. Anterior process of the calcaneus fracture. This injury must be distinguished from an ankle sprain. The
pain is distal and anterior to the ATF.
Medial ankle sprains result from eversion injuries ( 57). The medial ligament complex is collectively known as the deltoid
ligament because of its triangular shape. The apex of the triangle is the insertion on the medial malleolus of the tibia. The
deltoid ligament has a superficial and deep portion. The superficial portion consists of three ligaments: the tibionavicular
and the anterior and posterior tibiotalar ligaments. The deep portion consists of the anterior and posterior tibiotalar
ligaments. Medial instability resulting from a ligamentous eversion injury is distinctly uncommon. Commonly, the medial
malleolus fractures before rupture of the deltoid ligaments.
A syndesmotic or “high” ankle sprain occurs alone or in conjunction with a lateral ankle sprain. Syndesmotic sprains have
been estimated to occur in as many as 10% of all ankle injuries and are more commonly seen in collision sports such as
ice hockey, football, and soccer (Fig. 57.12). Syndesmotic sprains may involve any or all of the following structures: (a)
anterior inferior tibiofibular ligament, (b) posterior inferior tibiofibular ligament, and (c) interosseous membrane. Although
it is not entirely clear, the mechanism of injury appears to be primarily an external rotation injury, although
hyperdorsiflexion has been reported to lead to tears of the syndesmosis. Diagnosis is made by palpation directly over the
syndesmosis and more proximally along the interosseous membrane. The “squeeze test” is performed by compressing
the fibula to the tibia above the midpoint of the calf ( Fig. 57.13); the test is considered positive when proximal
compression produces distal pain in the area of the interosseous membrane and syndesmotic ligament ( 48). The external
rotation test (Fig. 57.14) is also useful in diagnosing syndesmotic ankle sprains and is performed by applying external
rotation stress to the foot and the ankle, with the knee held at 90 degrees of flexion and the ankle in neutral position ( 58).
A positive test produces pain over the anterior or posterior tibiofibular ligaments and over the interosseous membrane.
Radiographs can be helpful in indicating a syndesmotic injury. The presence of an avulsion fracture off the posterior
aspect of the distal tibia at the insertion of the posterior inferior tibiofibular ligament should prompt further evaluation.
Radiographic evidence of acute widening of the syndesmosis requires operative repair to restore the ankle mortise. Even
in the absence of radiographic changes, athletes with this injury will miss significantly more games and practices than
those with lateral ankle sprains alone. Complete recovery may take 4 to 12 weeks.
FIGURE 57.12. Syndesmotic ankle sprain. Calcification of syndesmosis in a professional football player.
FIGURE 57.13. The squeeze test is used to detect tears of the syndesmosis. It is positive when squeezing in the midcalf
produces pain in the distal interosseous membrane and syndesmosis.
FIGURE 57.14. The external rotation test is used to detect tears of the syndesmosis and is performed by stabilizing the
calf and externally rotating the foot.
A history and physical examination should always be obtained before ordering radiographic studies. The patient may
easily confuse ankle pain and foot pain, and a preliminary examination can localize the problem. The examination initially
begins with observation of the patient. A person's ambulatory status is the first clue to injury severity. Edema and
ecchymosis should be noted. The posterior tibial and dorsalis pedis pulses should be palpated, and sensation should be
tested. Palpation should then be carried out in an unhurried manner, taking care not to hurt the patient with excessive
force. The best starting point is the proximal fibula. Routine palpation enhances the diagnosis of Maisonneuve fracture, a
fracture produced by external rotation of the talus separating the fibula from the tibia and tearing the syndesmotic
ligament and interosseous membrane proximally to the level of the high fibular fracture ( 59). Tenderness at the proximal
fibula may indicate a fracture. Often, a patient will not relate lateral knee pain to an ankle injury. Missing the diagnosis
results in ankle arthritis secondary to altered weight bearing across the tibiofibular joint. The compartments of the lower
leg should also be palpated at this time. Acute compartment syndrome presents with firmness and pain of the various
compartments of the leg. Passive dorsiflexion and plantarflexion of the toes may also be helpful in making this diagnosis.
The examination should proceed with palpation of the lateral ligamentous complex, syndesmosis, sinus tarsi, and base of
the fifth metatarsal. The peroneal tendons, Achilles tendon, posterior tibial tendon, and tibialis anterior tendon should
also be palpated at this time. The peroneal tendons are often injured in conjunction with ankle inversion injuries, and
longitudinal tears, complete rupture, and tears of the superior peroneal retinaculum, resulting in peroneal tendon
subluxation or dislocation, may occur. The medial ankle is also systematically palpated beginning with the medial
malleolus and deltoid ligament and should include the tarsal navicular. The insertion of the posterior tibial tendon is
found just anterior and inferior to the talonavicular joint. The metatarsal squeeze test is then performed by compressing
the metatarsal heads together. The ankle, subtalar, and metatarsal phalangeal joints are evaluated and compared with
the contralateral side. Testing sensation helps rule out a nerve injury, most commonly the peroneal nerve.
Once the pertinent ankle structures have been palpated, manual muscle testing of the ankle musculature should be
performed. In the acute ankle, this is unnecessary and often painful, but in chronic ankle sprains, residual weakness may
contribute to functional ankle instability and risk of reinjury ( 60).
Considerable disability may result from a simple ankle sprain ( 61). Treatment of this injury consists of three phases. The
initial phase consists of addressing acute symptoms. Rest, ice, compression, and elevation (RICE) are effective initially.
Modalities such as electrical stimulation may be of benefit but are not well studied. Immobilization is generally avoided
unless the injury is severe and the ankle is functionally unstable in a brace. The second phase is rehabilitation, which
must address three separate aspects of ankle function: range of motion, strength, and proprioception. The third phase
consists of functional progressions of cutting, pivoting, and jumping activities, which prepare the athlete for return to
sports participation. This phase of rehabilitation is particularly important in sports like basketball and in various forms of
dance, which require agility and also jumping ability.
During all phases of rehabilitation, it is important to protect the healing ankle ligaments. Elastic braces offer no true
mechanical support but may function by providing tactile information to the brain regarding the relative position of the foot
and ankle (62,63,64,65,66 and 67). Ankle taping in sports is a popular method of limiting the motion of the ankle and
subtalar joints. It is used for both treatment and prevention of injuries. The effectiveness of ankle taping is questioned
(68,69,70 and 71) because quality of taping cannot be controlled and tape loosens with time. Tape is effective in limiting
the ankle at the extremes of motion. Karlsson and Andreasson ( 72) demonstrated that patients with unstable ankles had
improved peroneal muscle reaction time when taped. Taping loses 40% of its effectiveness after 10 minutes of playing. A
lace-up stabilizer may be more effective than tape and can be applied without assistance. It also offers the advantages of
lower cost and independent application.
Bracing as the sole treatment after an ankle sprain has been clearly shown to be effective in a number of studies
(73,74,75 and 76). In comparison with a cast, it allows early-protected mobilization of the ankle, maintains stability,
reduces muscle atrophy, and functional instability. Feurebach et al. ( 77) demonstrated improved position sense with
application of an ankle orthosis, and Tropp ( 78) recommended application of an ankle orthosis during the rehabilitation
period to reduce the risk of recurrent injury. Ankle bracing has been shown to reduce the incidence of ankle sprains in
soccer and basketball players who have a prior history of ankle sprains, but not in players with no prior history of injury.
Most important, there is evidence that prophylactic bracing does not impair athletic performance ( 76). Many types of
ankle braces are available for use in sports ( Fig. 57.15). The choice of brace type should be based on patient preference
and physician experience, although some braces have clearly been studied more than others ( 66). Braces range in
shape and form from tubular elastic supports or figure-of-eight straps to custom-molded orthotics that effectively limit
subtalar motion. Intermediate designs include leather or synthetic lace-up designs with side compartments for placement
of struts to limit motion. The use of a soft foam foot orthosis has recently been shown to reduce postural sway in patients
with acute ankle sprains and may be looked on as an adjunct to the treatment of ankle sprains. The orthosis is postulated
to maintain the neutral position of the foot and reduce stress on the ATFL ( 79). An off-the-shelf brace may be effective if
sized correctly and of sufficient strength. The use of high-top shoes alone has not been shown to be effective in the
prevention of ankle sprains in one prospective study but was associated with a protective effect in another study ( 80,81).
FIGURE 57.15. Functional ankle braces. The degree of injury and patient preference help determine the appropriate
brace to use for each patient.
When athletes offer persistent reports of giving way, swelling, and pain, and symptoms are not controlled by
rehabilitation and bracing, reconstructive surgery of the ankle ligaments is considered. Although many different
procedures have been explored in the literature, athletes and ballet dancers often do well with the modified Brostrom
direct repair with imbrication. The advantage of this procedure in an athlete is that no other muscle-tendon units are
sacrificed, patients generally have a reasonable range of motion following surgery, and are able to participate in preinjury
activities (82).
Lateral ankle sprains may produce subtalar instability. Elongation or tearing of the interosseous talocalcaneal ligament
results in diastasis of the subtalar joint and allows anterior displacement of the calcaneus. Disruption of the talocalcaneal
ligament only occurs after the ATFL and CFL are torn. Patients report both posterior foot pain and instability. Braces for
ankle instability and taping are usually not helpful. Physical examination demonstrates tenderness in the sinus tarsi or
posterior facet line. The anterior drawer test is often positive to a lesser degree than in true ankle instability and may be
associated with a click. Thermann et al. (83) described dorsiflexing the ankle and jerking the foot into internal rotation
while varus stressing the calcaneus. If subtalar instability is present, a medial shift of the calcaneus at the talocalcaneal
joint is perceptible. Stress radiographs (Broden views) may be helpful. Nonoperative management consists of bracing
and activity modifications. Multiple ligament reconstruction procedures have been advocated in the literature ( 84).
Anterior Impingement Syndrome
Anterior ankle impingement syndrome is characterized by ankle pain with limited and painful dorsiflexion due to either
soft tissue or bony obstruction ( Fig. 57.16) There appears to be a high incidence of repetitive ankle sprains in sports that
require repetitive forced ankle dorsiflexion (e.g., dance, soccer, football, and gymnastics), and patients often describe
minor repetitive trauma with the foot in dorsiflexion. The reported incidence in dancers is as high as 59%, although most
are asymptomatic (85,86). Morris first described the condition in 1943 ( 87). McMurray coined the term “footballer's ankle”
in 1950 (88), and O'Donoghue used “impingement exostosis of the tibia and talus” in 1954 ( 89). The mechanism of injury
is believed to be a combination of joint capsule strain from ankle sprains, followed by repetitive microtrauma to the
cartilage covering the anterior surface of the distal tibia, which results in a repetitive cycle of inflammation, scarring of the
capsule, calcification, and subsequent spur formation. The spurs may ultimately fragment and cause formation of loose
bodies. Patients often complain of anterior ankle and midfoot pain radiating to the lateral malleolus. Initially, the pain is
present only after prolonged activity and often subsides with rest. Chronic impingement is often accompanied by
complaints of instability and stiffness, making squatting, sprinting, and climbing stairs difficult. The physical examination
demonstrates decreased dorsiflexion with pain on palpation of the anterior tibial ridge. Tightness of the
gastrocnemius-soleus complex is often present.
FIGURE 57.16. Anterior ankle impingement in a ballet dancer. Note: “Kiss” lesion of anterior talus.
Plain radiographic evaluation demonstrates osteophytes on the anterior lip of the distal tibia and a “kiss lesion” may be
present on the anterior talar neck ( 86). X-ray studies in maximum plantarflexion and dorsiflexion often demonstrate the
tibiotalar impingement. Computed tomography (CT) and MRI are useful in diagnosing other causes of pain such as soft
tissue impingement, assessing the amount of cartilage damage, and assessing subtalar instability. Intraarticular injection
of lidocaine (Xylocaine) can be both diagnostic and therapeutic.
Treatment usually consists of arthroscopic or open resection of the symptomatic spur. Studies have shown that 90% of
osteophytes were situated well within the attachment of the joint capsule, making them accessible to arthroscopic
debridement (85). The size of the osteophyte also contributes to surgical planning, and large osteophytes occasionally
require open procedures.
Soft tissue impingement is the most common cause of chronic pain after an ankle sprain. This can occur along the
syndesmosis anterior gutter, the interval between the tibia and the fibula under the ankle, or posteriorly in the
syndesmosis and posterior gutter. Chronic lateral ankle pain is much more common than medial ankle pain after a sprain.
Anterolateral impingement of the ankle is the most common type of soft tissue impingement ( 90). In 1950, Wolin et al.
(91) described the “meniscoid band” between the tibia and fibula. In 1982, Waller ( 92) termed the pathology the
anterolateral corner compression syndrome. These injuries are thought to be the result of singular or repetitive inversion
injuries. Typically, the patient complains of vague anterior pain, usually along the anterior and anterolateral aspect of the
ankle, occasionally involving the syndesmosis and sinus tarsi. Pain is usually absent at rest and present with most
activities, limiting a patient's ability to participate in a given sport. Often, the patient has seen several physicians and is
frustrated by his or her lack of progress.
The physical examination may reveal tenderness along the syndesmosis anterior gutter, including the ATFL and CFL,
and the posterior subtalar joint and sinus tarsi may also be involved. Radiographic evaluation may reveal calcification or
heterotopic bone in the interosseous space consistent with previous injury to the distal syndesmosis or ossicles along the
tip of the fibula and lateral dome consistent with injuries to the ATFL. In many instances, the radiographs are normal, as
are the bone scan and CT scan. MRI may be helpful, and an MRI arthrogram may be the most effective test. Stress
radiographs are usually negative.
At surgery, patients may have synovitis and fibrosis of the lateral gutter and chondromalacia of the talus and fibula. In
some patients, thick bands can be identified and excised. The bands are the result of adhesions that develop along the
lateral malleolar joint and may contain torn fibers of the capsule and ligament, as well as chronic synovial tissue.
Inflammatory tissue may be seen not only in the lateral gutter but also in the syndesmosis and articular space between
the tibia and the fibula. Basset et al. ( 93) found syndesmotic impingement occurring with a separate distal fascicle of the
ATFL. With tearing of the ATFL, laxity occurs and the talar dome extrudes in dorsiflexion, leading to impingement of the
talus against the fascicle.
Posterior Impingement Syndrome
Posterior ankle impingement (Fig. 57.17) has been described under many names including os trigonum syndrome, os
trigonum impingement, posterior block of the ankle, and talar compression syndrome ( 94,95,96 and 97). It has been
defined as impingement occurring at the anatomic interval between the posterior tibial articular surface and the os calcis
(98). This impingement can be due to compression of many structures including the os trigonum, large posterior process
of the calcaneus, large posterior process of the talus, hypertrophic posterior capsule, calcific debris, and inflamed soft
tissue. Hedrick found that it could involve any anatomic structure in the posterior tibia, talus, or os calcis interval, and
could be visualized as a nut in a nutcracker ( 99). There is frequently an associated flexor hallucis longus (FHL) tendinitis.
Any sport involving forced plantarflexion, including ballet, soccer, and down hill running, may cause posterior ankle
impingement. The athlete describes posterolateral pain increased with ankle plantarflexion or dorsiflexion of the great
toe. Palpation often reveals pain posterior to the medial malleolus and occasionally a palpable click. Hyperplantar flexion
increases the pain, but hyperplantarflexion combined with anterior translation to distract the impinging structure may
reduce the pain. Lateral radiographs in maximal plantarflexion may show the impingement element. A bone scan may
show increased uptake in the posterior tibia, talus, or calcaneus. MRI is helpful in demonstrating associated FHL
tendinitis, capsular synovitis, and the size and shape of any bony impingement. Initial management consists of relative
rest from offending activities, ankle strengthening, proprioception training, and as-needed use of nonsteroidal
antiinflammatory drugs (NSAIDs), ice, and occasionally, injection and short periods of immobilization for symptomatic
relief. Surgery is performed when symptoms are intractable.
FIGURE 57.17. Posterior impingement of the ankle with large os trigonum which was fractured.
Peroneal Tendon Syndromes
Injuries to the peroneal tendons are common. The peroneal tendons pass posterior to the lateral malleolus running
through a discrete tendon sheath. The superior and inferior peroneal retinaculae and the fibular groove provide stability.
The peroneus brevis inserts into the base of the fifth metatarsal, a prominent body landmark on the lateral side of the
midportion of the foot. The peroneus longus runs deep to the peroneus brevis. It courses below the cuboid bone and the
deep plantar layer of the foot and inserts on the base of the first metatarsal and medial cuneiform. The peroneus brevis
functions to evert the foot. The peroneus longus contributes to eversion, but also depresses the first metatarsal.
Injuries to the peroneal tendons can be acute or chronic and may occur in conjunction with, or be confused with, ankle
sprains. Patients usually give a history of resisted inversion-type injury mechanism, which can result in a longitudinal tear
of the peroneal tendons, usually the peroneus brevis ( Fig. 57.18) (100). Acute injuries result in swelling, tenderness, and
ecchymosis in the groove of the posterior surface of the lateral malleolus, similar to an ankle sprain. However, the
greatest tenderness is posterior to the lateral malleolus at the level of the torn superior peroneal retinaculum, in contrast
to patients with classic ankle sprains, in whom tenderness is greatest over the ATFL, CFL, and anterolateral gutter.
Diagnosis of peroneal subluxation or dislocation is made by demonstrating the subluxation as the foot goes from
dorsiflexion and eversion into plantarflexion. This can be accomplished by circumducting the foot, or by resisting
plantarflexion in the dorsiflexed or everted foot. Radiographs are abnormal in 15% to 50% of cases. A lateral malleolar
rim fracture may be present with peroneal dislocation ( 101). Proximal migration of an os peroneii or base of the fifth
metatarsal avulsion indicates peroneal rupture. MRI is often diagnostic. In peroneal tendon injuries diagnosed acutely,
immobilization in a short leg cast with the foot in slight equinus position may allow the injury to heal. Patients with chronic
tenderness over the peroneal tendons and recurrent dislocations of these tendons should be treated surgically. Peroneal
tendon tears are usually longitudinal within the body of the tendon and, when present in isolation, may be repaired
primarily. These patients may present with peroneal tendon dislocation ( 102,103).
FIGURE 57.18. Hypertrophic peroneal tendons following multiple sprains. A longitudinal tear was present.
Flexor Hallucis Longus Pathology
FHL tendinitis occurring behind the medial malleolus is common among dancers and has been termed “dancer's
tendinitis” ( Fig. 57.19) (104). This condition does occur in nondancers and has been associated with running, climbing,
or activities that require sudden direction changes. Dancers usually report posteromedial ankle pain with or without
clicking or grating especially when the dancer is on demi-pointe. Initially, symptoms resolve after warmup and return
when the performance ends. Partial tearing of the fibers within the fibrous tunnel behind the medial malleolus may lead to
tenosynovitis and eventual nodule formation. The nodular thickening produces triggering, which becomes more severe
with time. The physical examination reveals tenderness localized behind the medial malleolus or at the fibro-osseous
groove of the FHL at the level of the subtalar joint, often with associated crepitus. Dorsiflexing and plantarflexing the
great toe with the ankle in the neutral position can demonstrate triggering. Similar symptoms are present in the
nondancer. MRI has been found to be superior to ultrasound for detecting pathology of the FHL ( 105). Initial treatment is
nonoperative, focusing on dance technique, ankle strength and flexibility, and FHL strength and flexibility. Surgical
intervention for recalcitrant cases or complete tears is highly successful.
FIGURE 57.19. FHL tendon tear in a professional dancer.

Osteochondral Lesions of the Talus
Monro first described the osteochondritis dissecans (OCD) lesion of the ankle joint in 1956. Kappis described the
osteochondral lesion of the talus in 1922 ( 106), while Koenig is credited with coining the term “osteochondritis dissecans”
in 1888 believing the etiology was secondary to avascular necrosis ( 107). Osteochondral lesions of the talus (OLT) are a
common cause of pain following an inversion injury. Several different terms have been used to describe this lesion
including transchondral fracture, osteochondral fracture, osteochondritis dissecans, and talar dome fracture ( Fig. 57.20).
Although the etiology of this problem remains controversial, many patients give a history of either previous ankle sprain
or inversion ankle injury. Lateral lesions are shallow and wafer-shaped and are thought to result from impaction of the
talus on the fibula by strong inversion of the dorsiflexed foot. Posteromedial lesions are deeper and cup shaped and may
result from inversion, plantarflexion, and external rotation of the tibia on the talus. Osteochondral lesions must be
considered in the differential diagnosis of the chronic ankle sprain, but a high index of suspicion is sometimes necessary
to detect these lesions. Patients usually report a vague pain and are sometimes unable to localize their pain to a specific
area. The pain is often accompanied by swelling and a noticeable limp. The physical examination also may be
unremarkable or demonstrate some minor loss of motion and pain in a specific area. There may be associated swelling
or instability. Standard anterolateral (AP), lateral, and mortise x-ray studies may be helpful in demonstrating the lesions;
however, MRI is the test of choice in evaluating the entire extent of the lesion. Osteochondral lesions occur bilaterally 10
percent of the time.
FIGURE 57.20. Osteochondral lesions of the talus. A: The location of the medial lesions tends to be more posterior, and
the lateral lesions tend to be more anterior. B: The shape of the lateral lesion is usually shallow and water-like and
frequently displaced; the medial lesions tend to be deeper, cup-shaped, and usually nondisplaced. (From Mann R,
Coughlin. Surgery of the foot and ankle, 6th ed. St. Louis: Mosby–Year Book, 1993.)
Several classification systems for these lesions have been devised, and Ferkel et al. ( 108) have developed a CT scan
staging system that appears to correlate best with the pathology and subsequent results of treatment. Pritsch et al. ( 109)
also developed an arthroscopic staging system to classify the cartilage quality overlying the lesion. They believe that this
system was a more useful indicator of the patient's prognosis. In this system, cartilage is considered to be grade I if it is
intact, firm, and shiny; grade II if it is soft, spongy, and intact; in grade III, the cartilage is frayed. Conti and Taranow ( 110)
have published a classification of OCD lesions that takes into account the status of the cartilage based on its
arthroscopic appearance and the condition of the bone based on it MRI appearance. The have suggested that if the
overlying cartilage is viable that a retrograde drilling technique with local bone grafting can result in highly satisfactory
results. By preserving the soft but viable overlying cartilage, it is hoped that the incidence of late arthrosis will be
lessened.
Nonoperative treatment is indicated for stage I or II lesions that can be adequately documented radiographically. Stage III
lesions in young patients (e.g., 18 years old or younger) are treated initially conservatively, but if they do not respond,
surgical treatment is indicated. In adults, all stage III and IV lesions that are symptomatic are treated surgically, and stage
I and II lesions are treated surgically if they continue to be symptomatic despite conservative treatment. Arthroscopy
provides an accurate diagnosis, demonstrating if the lesion is stable or not, and surgical treatments such as excision,
debridement, currettage, and transmalleolar or retrograde drilling with calcaneal bone grafting can be performed.
Arthroscopic treatment also allows early range-of-motion and strengthening exercises, with approximately 85% good to
excellent results (111). Recent use of mosaicplasty has been reported ( 112), although long-term results are not available.
Grafts are harvested from the intact femoral condyle as in cases of knee OCD.
THE FOOT
Running Footwear
Running footwear (Fig. 57.21) has blossomed into a multimillion dollar business, and a wide variety of shoes are
available to the athlete. With more choices available, there is understandably much confusion regarding the choice of
shoe. Although there are certain guidelines for proper selection of footwear, for a given sport, individual preference is a
major factor in patient satisfaction. The selection of the shoe must take into consideration of the sport, whether or not the
shoe is for training or competition, the playing surface, and the ability of the shoe to accommodate the addition of an
orthotic or brace. An ideal athletic shoe would facilitate performance, protect the foot from injury, and be economical.
Runners and other athletes usually find a specific brand and size of shoe (usually through trial and error) that they are
most comfortable in.
FIGURE 57.21. Running shoes differ by modifying different components of the same basic design.
In general, running and jogging shoes should be self-fitting, light weight, and aerated. They should be contoured to
provide some rocker affect. Shoe stability is a function of the last. The last is a model approximating the weight-bearing
foot over which the shoe is made. This explains the differences in shoe sizes from manufacturer to manufacturer when
one brand of shoes may fit an individual better than a similarly sized shoe from another company. A straight-last shoe is
the most rigid design, and a curved or banana-last is the most flexible. Most lasts are termed intermediate.
The midsole provides cushioning. A board-last is designed to increase the support provided by the shoe. With this
modification, the upper is glued to a firm board before being attached to the midsole. A slip-last is very flexible by virtue
of the fact that the upper is attached to the midsole without a stiffening board. A combination last has a board only in the
rear of the shoe. A patient with pronation problems may benefit from the maximum stability provided by a straight-board
last and a firm midsole. Similarly, a rigid cavus foot will benefit from a slip last with a soft midsole. When shoe instability
is required, a firmer midsole may be needed. The outsole is the interface between the shoe and playing surface. A stiff
outsole tends to be heavier and more durable than a blown rubber outsole that is filled with air pockets. The outsole can
be made from a combination of solid and blown rubber to provide increased durability at the heel while allowing greater
flexibility in the forefoot. The treads are designed to aid in shock absorption and to provide traction. Individual preference
and the playing surface play a large role in the selection of an appropriate tread pattern. Two common styles are the
herringbone and waffle tread.
A beveled heel and outflared sole are modifications to provide maximum stability at heel contact. Plastic heel stabilizers
act to reinforce the heel counter at the base. Other modifications may be added to the shoe for specific problems. The
addition of an arch support or a soft heel wedge for posterior tibial tendinitis are examples.
Orthotics are devices designed to maximize function in two ways. First, they correct a biomechanical problem, so athletes
do not waste energy compensating for a problem. They may also be used to reduce discomfort by changing the timing
and position of the foot as it moves through the gait cycle. Orthotics must use sound principles based on the normal gait
pattern.
Orthotics may be classified as flexible, semirigid, and rigid ( Fig. 57.22). A flexible orthotic acts mostly to cushion the foot
and provides only minimal support. Semirigid orthotics balance the need for a device that will provide support yet
accommodate for the changing shape of the foot and gait. Rigid orthotics do not allow the foot to move from a rigid lever
to a flexible unit capable of accepting uneven ground and providing shock absorption and are generally not
recommended. They are generally manufactured from acrylic materials and are often associated with neuroma formation,
nerve impingement, plantar fasciitis, and stress fractures.
FIGURE 57.22. Foot orthotics. Rigid (left), semirigid (middle), and flexible (right) orthotics are shown.
One of the most common indications for an orthotic prescription is to control subtalar pronation in a person with pes
planus (i.e., flat feet). By reducing baseline pronation, the foot is able to assume a supinated position that allows the foot
to form a rigid lever for stability at toe-off and heel strike. The high incidence of pes planus in the general population and
the popularity of running sports create an environment of potential abuse of this technology.
Fractures of the Foot

Jones Fracture
The Jones fracture (named for Sir Robert Jones) is a fracture of the base of the fifth metatarsal at the junction of the
metaphysis and the diaphysis. Jones suffered this particular injury while dancing in the early part of the twentieth century.
The fracture must be differentiated from the more common fracture of the base of the fifth metatarsal within the
metaphyseal region (Fig. 57.12). The fifth metatarsal is different from the other metatarsals in that it is the most mobile,
but the motion is limited to abduction and adduction. The axis between the metatarsals and the floor decreases from
approximately 20 degrees for the first metatarsal to 5 degrees or nearly parallel to the floor for the fifth metatarsal, so the
entire diaphysis bears weight while the other metatarsals bear weight on their condyles. These differences can result in
fractures at the diaphyseal junction of the immobile metaphyseal base during forced adduction. This has been described
as a “natural fulcrum” ( 113). Angular deformities such as genu varus, ankle varus, hindfoot varus, or forefoot supination
compound the stresses on the lateral forefoot ( 114). The vascular anatomy of the fifth metatarsal has been well defined
by Sherreff et al. (115). The intraosseous blood supply comes from three principle sources: the periosteal, metaphyseal,
and nutrient arteries. A watershed zone is formed at the metaphyseal diaphyseal junction corresponding to the level for
fracture healing. Jones fractures can be acute, or they can be chronic stress fracture injuries. The acute fracture occurs
more commonly in patients over the age of 21 with equal frequency in men and women (116). A chronic stress fracture is
related to increased frequency of normal loads applied beneath the fifth metatarsal had over a short period of time. This
is more common in 15- to 21-year-old male athletes. Treatment is controversial. It is clear that if cast immobilization is
tried, the patient must not bear weight on the foot ( Fig. 57.23). Treatment of the patient with an acute nondisplaced Jones
fracture consists of a non–weight-bearing cast for 6 to 8 weeks, and often times up to 12 weeks. Operative management
is indicated for fracture displacements greater than 2 mm, high-performance athletes, or signs of intramedullary sclerosis
(diaphyseal stress fracture). The well-known sequelae of prolonged immobilization and non–weight bearing must be
weighed against the relatively safe and easy internal fixation that can be performed as an outpatient. Current
recommendations involve percutaneous placement of a 4.5-mm screw. The postoperative regimen consists of 5 to 7 days
in a splint followed by weight bearing in a cast brace. Full activity is permitted at 12 weeks. When nonunion results, a
bone stimulator or bone grafting, or both, may be necessary.
FIGURE 57.23. A: Jones fracture weight bearing was not restricted in cast. B: Resultant nonunion of fracture at 3
months.
Avulsion Fracture of the Fifth Metatarsal
The avulsion-type fracture of the fifth metatarsal is the most common fracture of the proximal fifth metatarsal. The most
commonly accepted mechanism of injury has been a sudden inversion of the hindfoot by the contracting peroneus brevis,
causing a bony avulsion. More recent studies have shown that the lateral band of the plantar aponeurosis is the more
likely structure responsible for the avulsion ( 117). Often, the patient is able to walk and delays seeking medical care.
Treatment of the avulsion fracture depends on the amount of displacement and whether the fracture is intraarticular or
extraarticular ( Fig. 57.24). For extraarticular nondisplaced fractures, symptomatic treatment is recommended. For
displaced extraarticular fractures, short leg weight-bearing casts or a removable non–weight-bearing boot for 4-6 weeks
are used. A symptomatic fibrous union often develops. Intraarticular fractures displaced greater than 2 mm or involving
greater than 30% of the joint require internal fixation. Smaller fragments can be excised with reattachment of the
peroneus brevis.
FIGURE 57.24. Avulsion fracture of fifth metatarsal.

The dancer's fracture involves the fifth metatarsal middle to distal diathesis. The mechanism of injury involves rolling over
on the outer border of the foot while in the demi-pointe position (on the balls of the feet) or when landing from a jump on a
supinated foot. A long oblique fracture running from proximal medial to distal lateral is seen on the AP view of the foot.
On the lateral view, the fracture runs proximal plantar to distal dorsal. Even in elite dancers, this fracture can usually be
treated nonoperatively with early weight bearing in a removable boot. Pain-free walking can be expected in 6 weeks and
return to full activity at 19 weeks.
Tarsal Navicular Stress Fractures
This stress fracture is most commonly associated with basketball players, but can be seen in participants of any sport
involving jumping and running. Symptoms are often vague, and delay in diagnosis is common. Torg et al. ( 117) noted that
stress fractures were more common in the central third of the bone because of relative avascularity in that area. Khan et
al. (118) conducted a study of 86 cases of navicular stress fractures, and only two cases did not involve the central third.
Those cases involved only dorsal fragments. The physical examination may demonstrate limited dorsiflexion, limited
subtalar motion, or both. Tenderness over the navicular at the proximal dorsal border, called the N spot by Khan, is
characteristic. Symptoms may be reproduced by hopping (119). The diagnosis can be made by bone scan combined with
CT scan or by MRI. In Khan's series, initial plain films were positive in only 14% of cases.
Tarsal navicular stress fractures should be treated in a non–weight-bearing cast for 6 to 8 weeks. A routine CT scan is
not indicated to determine fracture healing, and follow-up bone scans remain positive after clinical union. The duration of
non–weight bearing usually leaves the lower leg badly deconditioned and a prolonged course of rehabilitation is required
to return an athlete to play. The use of orthotics after a stress fracture is controversial because no specific biomechanical
abnormality has been described in these cases.
STRESS FRACTURE OF THE HALLUX SESAMOID
Athletes with sesamoid stress fractures have a history of an insidious onset of poorly localized pain during or after an
athletic activity that is relieved by rest. There is no history of a traumatic event. Pain is increased with hyperextension
and palpation over the involved sesamoid. Failure to recognize the sesamoid stress fracture can lead to prolonged
disability. Diagnosis can be made through serial radiographs at least 3 weeks apart. A bone scan will show increased
uptake. Treatment consists of a short leg weight-bearing cast for 6 weeks, with repeat clinical examination and
radiographs and recasting, if necessary. Although most stress fractures heal with activity modification or limitation,
sesamoid stress fractures behave differently. Symptoms often persist and lead to excision of the involved sesamoid.
Early excision after an initial period of immobilization may allow the athlete to return to activity sooner. Sesamoid hallux
stress fracture is also at increased risk for nonunion. Orava and Hulkko ( 120) reviewed their experience with nonunion of
stress fractures and had more cases of nonunion of this injury than any other fracture (15 of 37 stress fractures).
Treatment with stiffer, thicker soled shoes and relative rest was effective in 10 of 15 cases.
Fractures of the sesamoid are the result of direct or indirect trauma ( Fig. 57.13). Direct trauma may result from a fall from
a height, an object falling onto the foot, or from a crushing injury. Indirect trauma is less common and results from a
sudden hyperextension of the metatarsophalangeal (MTP) joint. Unlike the sesamoid stress fracture, patients are often
able to remember a specific traumatic event. Point tenderness and pain with dorsiflexion and resisted plantarflexion of
the MTP are common findings. Pain is greatest at toe-off. Diagnosis may be confirmed with radiographs. True fractures
show a jagged and irregular margin with fragments that are usually equal in size ( Fig. 57.25A and Fig. 57.25B). A bone
scan will show increased uptake. In contrast, bipartite or multipartite sesamoids will have a smooth outline, often with
unequally sized fragments. Bipartite sesamoids are unilateral in 75% of patients. Recommended treatment includes a
short leg walking cast with a walking heel to transfer weight off the forefoot. This cast is worn for 3 weeks, and then the
patient is placed in a stiff soled shoe with a metatarsal pad. Relief of symptoms may take 4 to 6 months. If symptoms
persist longer than 6 months, operative intervention is warranted. A recent study has shown autogenous bone grafting of
the hallux sesamoid nonunion to be effective ( 121). Gross motion of the nonunion site was a poor prognostic indicator.
Autogenous bone grafting has a low morbidity and preserves the sesamoid, which is of great benefit in the athlete. If
bone grafting fails, the success of later sesamoidectomy appeared to be ineffective.
FIGURE 57.25. A and B: Fracture of the sesamoid in a basketball player.
Other Sesamoid Problems
The two sesamoids of the great toe lie within the tendon of the flexor hallucis brevis (FHB). The FHB then inserts onto
the base of the proximal phalanx. The sesamoids are suspended under the hallux metatarsal head by the slinglike
mechanism composed of the metatarsal phalangeal collateral ligaments and the sesamoid ligaments. They move anterior
to posterior within a medial and lateral groove beneath the distal first metatarsal, separated by a ridge or crista. The
primary functions of the sesamoids include increasing the mechanical advantage of the FHB, or increasing its lever arm,
protecting the FHL tendon, and absorbing the weight-bearing stress on the medial forefoot. The ancient Hebrews
believed that the medial sesamoid was indestructible and was the seed from which the whole body was resurrected after
death. Although it is not indestructible, the sesamoids bear three times the weight of the body, with the medial sesamoid
taking the majority of the force. Unfortunately, these small but important bones and support structures are subject to a
variety of acute and chromic injuries in the athlete. These conditions can be quite debilitating and require prompt
diagnosis and treatment.
The sesamoid bones are formed from multiple ossification centers and nonunion of the centers leads to the radiographic
appearance of bipartite, tripartite, and quadripartite sesamoid bones ( 122,123). The most common sesamoid problem in
the athletic population is caused by repetitive stress on the sesamoids and is termed sesamoiditis. This is a common
problem in athletes who require maximum dorsiflexion of the great toe, but may also be associated with trauma from
direct pressure of the athletic shoe. Athletes at risk include joggers, sprinters, figure skaters, ballet dancers, and
basketball and football players. The diagnosis of sesamoiditis is a diagnosis of exclusion. The problem is manifested by
the insidious onset of pain and tenderness with weight bearing under the first metatarsal head, usually in the region of
the medial rather than the lateral sesamoid. There may be associated tenderness to palpation over the involved
sesamoid accompanied by swelling. Passive dorsiflexion and resisted plantar flexion of the first MTP joint often increases
the pain. Treatment of sesamoiditis consists of changing the weight-bearing profile of the foot to decrease the load
underneath the first metatarsal head. This is best accomplished through activity modification and the use of orthotics with
metatarsal pads and custom arch supports. Taping the great toe in neutral or slight plantar flexion also may relieve
pressure on the sesamoids, as may use of a J- or U-shaped pad under the sesamoids ( 124). Some authors advocate
intraarticular corticosteroid injections, but this should be done with extreme care because it may lead to permanent skin
atrophy at the injection site. Sesamoiditis usually responds well to nonoperative management.
Osteochondritis of the sesamoids is a rare condition that can affect either sesamoid. The etiology remains unclear.
Current theories include the development of the condition after a trauma or crush injury, after a stress fracture with
subsequent repair of the process, or due to decreased circulation. It is characterized by pain on weight bearing and
tenderness to palpation of the involved sesamoid. The metatarsal head is usually not tender. Radiographic changes,
seen most clearly on axial views, include mottling, flattening, elongation, and fragmentation; however, they may not
appear for 9 to 12 months. These changes can lead to painful arthritis of the sesamoid metatarsal articulation.
Nonoperative management of osteochondritis involves reducing weight-bearing stress as with sesamoiditis, but is rarely
effective. It may diminish the symptoms, but once fragmentation or collapse occurs, excision of the involved sesamoid is
indicated. Careful attention should be paid to repair of the FHB tendon. A poor repair of the defect left from excision of
the medial sesamoid may lead to hallux valgus, and an insufficient repair of the lateral sesamoid may lead to hallux
varus. Neuritis of the medial plantar digital nerve or Joplin nerve as it passes plantar to the lateral sesamoid and passes
dorsal to the FHL tendon may occur. The diagnosis should be suspected when the pain beneath the lateral sesamoid is
accompanied by hypesthesia of the medial hallux. The treatment of this problem is to unload the lateral sesamoid,
although surgery is occasionally necessary when this fails. Subsequent neuroma formation may produce similar
symptoms (125).
Plantar Heel Pain
Plantar heel pain is a common problem among athletes. Many terms have been used to describe plantar heel pain
including bone bruise, runners heel, policeman's heel, heel pain syndrome, subcalcaneal heel pain, medial calcaneal
neuritis, calcaneodynia, fat pad syndrome, calcaneal periostitis, and heel spurs ( 126,127,128 and 129). The differential
diagnosis of diagnosis of plantar heel pain is extensive and includes both common and rare conditions ( 130). Diagnosis
is often difficult because there are many problems with similar presentations in a small anatomic region. Frequently, the
source of pain is difficult to identify, leading some physicians to lump diagnosis into the term heel pain syndrome (HPS)
(131). Heel pain is one of the most common reasons for an athlete to visit a physician and represents about 10% of
running injuries ( 132). The differential diagnosis of heel pain is extensive, and includes Reiter syndrome and ankylosing
spondylitis for men and rheumatoid arthritis in women. Most commonly, a running athlete or patient who had begun an
exercise program, gained weight (including pregnancy), or increased the intensity of his or her training may be prone to
this disorder. High-impact aerobics and occupations that require walking on hard surfaces may also lead to this painful
disorder.
The plantar fascia is a strong band of collagen extending form the anterior aspect of the calcaneal tuberosity to the base
of each proximal phalanx. The distal attachment divides to allow the passage of the flexor tendons to the toes. Therefore,
there are 10 distal attachments of the plantar fascia. The insertion of the plantar fascia distal to the metatarsal
phalangeal joints also gives rise to the windlass mechanism of the foot. The windlass mechanism elevates the
longitudinal arch with toe dorsiflexion, leading to greater foot stability as midstance ends and toe-off begins. The heel is
covered by a fat pad whose main function is shock absorption. It has been estimated that 20% to 25% of the contact
force at heel strike may be absorbed by the heel fat pad ( 133). There are nerve endings in the fat pad that can also be a
source of pain.
The tibial nerve gives off the medial calcaneal nerve at the level of the medial malleolus that innervates the heel pad and
skin. The first branch of the lateral plantar nerve, the posterior branch of the lateral plantar nerve or Baxter's nerve,
passes deep between the abductor hallucis and the medial head of the quadratis planti. The medial and lateral plantar
nerves also pass deep to the abductor hallucis. Pronation of the foot, mass lesions, and scarring or hypotrophy of the
plantar fascia are some causes of nerve entrapment. Distribution among men and women is equal. The majority of
patients are between 40 and 60 years of age. Studies have shown a significant relationship to obesity, prolonged
standing on hard surfaces, and athletic overuse in runners ( 132,135).
A typical history for plantar fasciitis is gradual onset of stabbing heel pain with the first few steps in the morning. Pain
gradually diminishes during the day with walking. By the end of the day or in the early evening, the heel aches. The early
morning pain is believed to be related to the plantarflexed position patients assume while in bed. While the Achilles
tendon and plantar fascia are relaxed, a contracture can develop during the night. On awaking, the first steps will then
stretch these tissues ( 136).
Physical examination should begin with evaluation of the entire lower extremity including gait and station. Ankle range of
motion with the knee flexed and extended will demonstrate gastrocnemius versus soleus tightness. Evaluation of the foot
position (i.e., pes planus or pes cavus), pronation or plantarflexion of the first ray are biomechanical abnormalities that
can predispose the patient to plantar fasciits. The insertion of the plantar fascia is more medial than lateral and is not
generally beneath the calcaneus as much as along the anterior medial border. Occasionally, the pain may be distal to the
insertion, especially when a history of discrete trauma to that area is elicited. Care must be taken to palpate a plantar
fibroma or other mass in the fascia when the tender area is distal to the calcaneal insertion. Forceful sustained
dorsiflexion of the toes and compression of the plantar fascia in the midarch region inconsistently may cause pain at the
insertion of the plantar fascia on the calcaneus. Tapping over the tarsal tunnel or over the nerve to the abductor digiti
minimi may demonstrate the Tinel sign. Kibler et al. ( 137) studied the strength and range of motion of running athletes
with unilateral plantar fasciitis and noted peak deficits in plantarflexion strength from 17% to 44%; dorsiflexor strength
was found to be within normal limits. Decreased dorsiflexion range of motion was also noted. Ankle inversion and
eversion strength were not tested.
Plain radiographs often demonstrate a heel spur. In actuality, the heel spur is a rigid bone within the substance of the
flexor digitorum brevis muscle, one of the intrinsic muscles of the foot. This bony ridge is seldom responsible for heel
pain. Rarely, the spur itself may fracture causing pain in this region. The spur is seen in a discrete percentage of feet
without pain referable to the heel. The presence of a heel spur on a radiograph can never be considered synonymous
with plantar fasciitis or HPS. Radiographs are important in demonstrating fracture, tumors, or arthrosis. Bone scans are
helpful in detecting osseous pathology and often demonstrate increased uptake in plantar fasciitis ( 138). MRI
demonstrates thickening of the plantar fascial medial column in chronic cases and can also be used to evaluate other
soft tissue and bony pathology ( Fig. 57.26).
FIGURE 57.26. Plantar fasciitis on MRI. Note: Edema of calcaneus with thickening of plantar fascia.
Initial treatment consists of patient education and both pharmacologic and physical therapy modalities. The natural
history of this condition is such that resolution of the pain my take 1 to 2 years. The patient must be informed of the
length of time that the condition may persist so that appropriate scheduling of athletic events, training, and cross-training
may be incorporated into the treatment plan. It is helpful to develop an outline of the treatment options to minimize the
inevitable frustration both the patient and the physician may experience. On the initial visit, most patients are started on a
five-part program consisting of plantar fascia and Achilles' stretching, use of a night splint, heel cup, heel pads, or an
orthotic, a home exercise program, and as needed use of NSAIDs. Heel pads act to shield the shock absorption function
of the plantar fascia but do not share the function of the plantar fascia in maintaining the medial longitudinal arch of the
foot. Use of prefabicated night splint that holds the ankle in 5 degrees of dorsiflexion, increasing the flexibility of the
gastrocnemius and soleus muscles and the plantar fascia, is effective in reducing morning stiffness and pain ( 136).
Taping the arch may also be effective. It is important to educate the patient about appropriate footwear. Shoes with a
more rigid sole (i.e., cross-training shoes) will increase the dorsiflexion of the toes during gait and decrease the stress
placed on the plantar fascia. Overpronation can be controlled with a shoe that has a medial heel counter. In the case of
acute severe plantar fasciitis or for those who have failed the initial five-part program, injection of cortisone preparation
with a local anesthetic into the insertion of the plantar fascia is considered an appropriate next step. Wolgin et al. ( 139)
studied patient's response to various treatments of plantar fasciitis and noted that steroid injection had the lowest rating
among patients. The authors noted that their findings were weakened by the fact that many injections were performed by
physicians outside the study and proper technique when injecting could not be ensured. The injection should be
performed on the medial side to avoid leakage of cortisone into the heel pad. The skin can be sprayed with ethyl chloride
before the injection to decrease the pain from the needle. The patient should be told that the heel may be tender for
several days following the injection and that the pain relief following injection may be permanent for days, weeks, or
months. Rupture of the plantar fascia after multiple cortisone injections may occur ( 140). Casting of the ankle in
dorsiflexion for 2 to 4 weeks is also appropriate for patients in whom therapy has failed, especially if previous injections
or concern for rupture is an issue. Heel fat pad atrophy may be treated with heel cups or appropriate orthotics.
Tarsal tunnel or entrapment of the nerve to the abductor digiti minimi are best evaluated with an EMG and nerve
conduction studies. Nonoperative management consists of correcting biomechanical abnormalities identified on the
physical examination that may predispose the patient to these conditions. Pes planus, planovalgus, and overpronation
may lead to traction neuropathies, and attempts should be made to correct these problems with stretching, strengthening,
orthotics, and appropriate shoewear (see later).
Surgery for plantar fasciitis is best reserved as a last resort for those patients with intractable pain for 1 or more years'
duration. Although there are many different operations described in the literature for the treatment of plantar fasciitis, the
most commonly performed procedures are those intended to release the medial attachment of the plantar fascia from the
anterior inferior aspect of the calcaneus. The release is performed through an oblique incision on the medial side of the
foot. The fascia over the abductor hallucis is released circumferentially, and then the underlying fascia over the nerve to
the abductor digiti minimi is released. The medial column of the plantar fascia is then identified, and a 1-cm segment is
excised. Weight bearing is protected until the incision has healed and then the five-part program is restarted. Alternatives
to surgery such as extracorporeal shock-wave therapy are still in their infancy but show promise ( 141).
Accessory Navicular Syndrome
The foot is the interface between the body and the ground, and the longitudinal arch of the foot serves to provide a shock
absorber for the body. Therefore, the foot must protect the other joints of the lower extremity by damping the energy
imparted on the leg with each step. The arch is supported by several intrinsic and extrinsic factors. The shape of the
bones in the foot is such that a gentle arch is formed. Strong ligaments hold the bones of the foot together but allow
motion to occur. The plantar fascia extends from the anterior aspect of the calcaneus inferiorly to the base of each
proximal phalanx. The posterior tibial tendon winds behind the medial malleolus and inserts primarily on the plantar
medial surface of the navicular. The navicular is located at the apex of the longitudinal arch so that the posterior tibial
tendon acts as a dynamic support of this configuration ( 142). A congenital nonunion of the two centers of ossification may
occur on the navicular with the smaller of the two halves in the medial position. The portion of the posterior tibial tendon
inserts on this medial piece and chronic stresses can cause a microfracture of the synchondrosis or cartilaginous
connection between the two halves. This manifests itself as arch pain and weakness or the posterior tibial tendon, similar
to posterior tibial tendinitis. Giest ( 143) classified the accessory navicular syndrome into three types on the basis of the
size and location of the ossicle, and the presence or absence of a synchondrosis ( 143). Type I is a small accessory bone
within the substance of the posterior tibial tendon, without attachment to the body of the navicular. Type II is an
accessory navicular with a synchondrosis that has the appearance of a cartilaginous unit containing islands of hyaline
and fibrocartilage ( Fig. 57.27). Type III is a cornual navicular that probably represents an end stage of type II ( Fig.
57.28). If the synchondrosis is injured, tension and shearing forces of the posterior tibial tendon can exacerbate the injury
and result in separation of the synchondrosis. Treatment of this syndrome is usually a short period of immobilization, with
weight bearing as tolerated. Rarely, we have used steroid injections in intractable cases. Orthotics and posterior tibial
tendon therapeutic exercises exacerbate symptoms. Excision of a type II or type III accessory navicular is rarely
necessary (144).
FIGURE 57.27. Type II accessory navicular.
FIGURE 57.28. Type III accessory navicular.
Midfoot Sprains
Tarsometatarsal joint injuries are uncommon, and the majority occur as result of high-velocity trauma, in particular motor
vehicle accidents and falls. Lisfranc injuries involve disruption of the tarsometatarsal complex and are often associated
with fractures. These injuries have been shown to produce significant long-term morbidity. Multiple studies have shown
that low-velocity trauma does occur to the joint. Several studies have been conducted evaluating this injury in the athletic
population ( 145,146 and 147). Meyer et al. (145) studied collegiate football players over a 5-year period of time, and
found midfoot injuries occurred in 4% of the players. Offensive linemen sustained 29.2% and defensive backs 20.8% of
the injuries (145). The athletes were assessed by performing pronation and supination, and dorsiflexion and
plantarflexion maneuvers on the forefoot, and by assessing swelling and discomfort. Athletes were treated variably, with
non-weight bearing on crutches and short leg casts, with or without weight bearing in others. Following the initial
treatment, a molded arch support with an ankle brace was provided depending on the position played. A progressive
rehabilitation program was provided for all players. Mean return to play time was 6.3 days for the skill position players
and 15.0 days for linemen. The mean time to full healing was 30.9 days for skilled position players, and 39.6 days for
linemen. Shapiro et al. (146) studied nine athletes with injuries to the Lisfranc joint. They described a pronation/external
rotation mechanism of injury in all cases. Compression of the midfoot from side to side reproduced pain in the interval
between the bases of the first and second metatarsals, and dorsal and plantar deviation of the first metatarsal head while
holding the second metatarsal head immobilized also caused pain. Lateral weight-bearing x-rays did not show signs of
flattening on the longitudinal arch. Seven of the nine patients were treated with immobilization and crutches, and one
patient with severe diastasis had surgical intervention. One patient refused treatment. Return to play averaged 12 weeks.
Only three athletes returned the same season. Curtis et al. ( 147) retrospectively reviewed 19 athletes with midfoot
sprains, and found three were unable to return to play. Their athletes were treated in casts until asymptomatic, and then
treated with physical therapy. Seven of their patients also sustained a fracture. Poor functional results were noted when
diagnosis was delayed.
Turf Toe
Turf toe refers to a ligament injury of the first MTP joint and is a common injury to soccer and football players. The term
turf toe refers to the observation that the injury is more common on the artificial playing surfaces. Turf toe occurs when
the proximal phalanx is jammed into the dorsal articular surface of the metatarsal head as the plantar capsule restricts
dorsiflexion beyond its normal limit ( Fig. 57.29). Along with forced dorsiflexion, the MTP joint may also be associated with
valgus stress. The use of soft-soled nonleather playing shoes that lack the stiffness to restrict dorsiflexion has been
implicated. The mechanism of injury is typically a tackle in which the player's foot is planted on the nonyielding playing
surface and the player or opponent falls on the leg, forcing the great toe into hyperdorsiflexion. The spectrum of injury
includes sprained collateral ligaments, dorsal joint compression, plantar plate avulsion, and dislocation and fracture of
the sesamoid. The physical examination demonstrates a dorsally tender, red, stiff, and swollen MTP joint. Radiographs
often demonstrate only soft tissue swelling. Ligamentous injury to the MTP joint may also occur by hyperplantar flexion
and valgus forces. Sesamoid and midfoot injuries have the same mechanism of injury and must be considered in the
differential diagnosis. Treatment consists of local care and taping of the great toe to limit hyperdorsiflexion. Modifying
shoewear to reinforce the forefoot, either with an orthotic with a first MTP extension (Morton extension) or a 0.51-mm
spring steel insert is effective in most cases ( 148).
FIGURE 57.29. Turf toes occurs with hyperflexion of the metatarsophalangeal joint of the great toe and is commonly seen
in football played on synthetic fields.
Other Tendon Problems
Any tendon crossing the ankle joint to insert on the foot may be subject to disease. As noted in the section on Achilles
tendon injuries, accurate assessment of the tendons involved determines treatment. The posterior tibial tendon may be
injured at its insertion on the tarsal navicular proximally as it winds around the medial malleolus. The athlete may have
trouble standing on his or her toes or running because the posterior tibial tendon acts as a strong plantarflexor and helps
position the hindfoot in pronation, the position of stability. Patients may not have the swelling and acute pain often seen
with Achilles' tendinitis. Posterior tibial tendon tears occur primarily in middle-aged people with a history of diabetes,
obesity, and hypertension (149). Jahss (150) reported a possible association with multiple steroid injections. However, in
athletes, several case reports of posterior tendon dislocation have been reported ( 151,152 and 153). The mechanism of
injury is not well known but may be dorsiflexion and inversion. Woods and Leach ( 154) reported on posterior tendon
tears in athletic people. They noted that the pain may be confused with arch pain, and patients initially had good function.
The anterior tibial tendon is easily palpable anteriorly ( Fig. 57.30). Pain in this structure may be caused by a
hyperplantarflexion injury of the foot as in football and soccer. Diagnosis is made by direct palpation of the tendon and by
resisted dorsiflexion of the foot causing pain over the tendon.
FIGURE 57.30. Tibialis anterior tendinitis. Note: Mild edema around tibialis anterior tendon.
Nerve Injuries in the Athlete
Nerve entrapment is a common cause of foot pain and disability but is often poorly diagnosed. Entrapment is most
commonly caused by compression as the nerve courses over or through a fascial structure. It can also be impinged
against bony structures. The clinician must have a high index of suspicion. A careful history as well as a static and
functional physical examination must be performed. Entrapment symptoms are often present only during athletic activity
and standard static tests may be unrevealing. Electromyelography (EMG) and nerve conduction velocity (NCV) are
helpful but not always diagnostic. Plain radiographs are less helpful unless a bony entrapment is present.
Interdigital Neuroma
Interdigital neuromas are common problems that usually occur in older patients but can be present in young athletes
(155,156 and 157). Activities that require the ankle to plantarflex while the toes dorsiflex will cause compression of the
interdigital nerve under the intermetatarsal ligament. Ballet, running, and basketball are a few of the most common sports
associated with this condition. The third web space is most commonly involved, followed by the second. Patients report
localized tenderness that radiates into the toes and proximally into the midfoot. Palpation in the intermetatarsal space as
the forefoot is squeezed often recreates the pain, including the referred pain. A lumbar spine etiology must always be
considered and ruled out. Nonoperative treatment consists initially of a wider shoe and metatarsal or neuroma pads. If
this is unsuccessful, a corticosteroid injection may be tried. Multiple injections may lead to fat pad atrophy or damage to
the plantar plate and collateral ligament, and should be avoided. If nonoperative management fails, surgery is indicated.
The nerve is resected through a dorsal incision and, if possible, the intermetatarsal ligament should be left intact. When
the athlete returns to competition, it is often beneficial to strap the forefoot circumferentially with tape.
Tarsal Tunnel Syndrome
Tarsal tunnel syndrome is an entrapment of the tibial nerve at the level of the ankle. The tunnel is formed by the flexor
retinaculum or lacinate ligament, the medial wall of the calcaneus, the posterior talus, the distal tibia, and medial
malleolus. Contents of the tunnel include the posterior tibial artery and veins, the tibial nerve and its branches, and the
tendons of the posterior tibialis, flexor digitorum longus, and flexor hallucis longus muscles. The tibial nerve branches
from 0 to 2 cm above a line drawn from the medial malleolus to the calcaneal tuberosity. The tibial nerve can be
compressed at multiple locations. A “high” tarsal tunnel syndrome occurs when the nerve is compressed at the lower
edge of the gastrocnemius muscle. A classic location is behind the medial malleolus under the flexor retinaculum. The
etiology is multifactorial and includes mass lesions, heel valgus, over pronation, subtalar laxity, and a symptomatic os
trigonum (155). The patient complains of pain along the distribution of the tibial nerve and often has a Tinel sign. EMG
and NCV are helpful unless the compression only occurs during activity. Nonoperative management consists of orthotics
and shoewear modifications directed at any abnormal foot biomechanics. Surgical intervention should be directed at
releasing the nerve at the specific site of entrapment. MRI to visualize masses or entrapment is helpful. Extensive
release should be avoided to speed recovery.
First Branch of the Lateral Plantar Nerve
Compression of the first branch of the lateral plantar nerve causes heel pain and is often associated with plantar fasciitis.
Entrapment occurs under the abductor hallucis. The patient may complain of pain on the plantar heel lateral and proximal
to the location of classic plantar fasciitis. EMG and NCV may be useful. Nonoperative management is similar to that used
for plantar fasciitis, and may be effective ( 158). For recalcitrant conditions, surgical decompression involving release of
the deep fascia around the abductor hallucis, or release of the fascia deep to the abductor hallucis overlying the nerve
with or without a proximal plantar fasciectomy ( 155,157).
Medial Plantar Nerve
Medial plantar nerve entrapment or “jogger's foot” occurs in the region of the master knot of Henry ( 155). The nerve
exists from under the flexor retinaculum and courses deep to the abductor hallucis. It then runs along the plantar surface
of the FDL and through the master knot of Henry and then down along the medial aspect of the foot. There is no gender
predilection, although the condition tends to occur in patients who run with increased heel valgus or hyperpronation.
There may be a history of ankle instability after an injury. The patients complain of burning or aching pain in the arch that
radiates distally into the medial forefoot or proximally to the ankle. The physical examination may demonstrate
tenderness just plantar to the navicular tuberosity at the region of the master knot of Henry. Tinel sign may be present.
Nonoperative management consists of orthotics to control the neutral position of the foot and accommodate the condition.
Surgical decompression involves release of the fascia over the FHL and the calcaneonavicular ligament.
Deep Peroneal Nerve
Deep peroneal nerve entrapment or anterior tarsal tunnel syndrome can occur in several locations, like classic tarsal
tunnel syndrome (155,157). The deep peroneal nerve lies between the extensor hallucis longus (EHL) and extensor
digitorum longus (EDL) in the distal one third of the leg. The nerve divides 1 cm above the ankle joint, giving off a lateral
branch to the EDB and a medial branch that continues along the dorsalis pedis artery. The medial branch may be
compressed as it passes under the inferior extensor retinaculum and over the dorsal talonavicular joint. Entrapment can
also occur at the superior edge of the inferior extensor retinaculum, where the nerve passes under the EHB or where the
EHL tendon crosses over the nerve. Dorsal osteophytes around the talonavicular joint or an os intermetatarseum can
also entrap the deep peroneal nerve and has been described in runners ( 155). The patient complains of burning or
aching on the dorsal midfoot, with occasional paresthesias or numbness in the first web space. Care should be taken to
look for proximal sources of compression, in particular lumbar radiculopathy and common peroneal nerve compression at
the fibular head. Ankle plantarflexion or dorsiflexion may increase symptoms. Asymmetry of the EDB when compared with
the unaffected side may also be present. Accompanying ankle instability should be ruled out. EMG and NCV can be
helpful, and plain radiographs should be obtained to look for osteophytes. Nonoperative management consists of dorsal
padding to relieve pressure of the nerve, altering lacing patterns on shoes to decrease nerve compression, and ankle
bracing and rehabilitation in cases in which instability or functional instability may contribute to symptoms. Recalcitrant
cases are treated with surgical decompression with or without excision of osteophytes.
Superficial Peroneal Nerve
Superficial peroneal nerve entrapment or anterolateral compartment syndrome usually occurs where the superficial
peroneal nerve exits from the deep fascia, approximately 10 to 12 cm proximal to the tip of the lateral malleolus.
Predisposing factors include recurrent ankle sprains with stretching of the nerve, previous fasciotomy with scar formation,
or fascial defects with local muscle herniation. The patient reports pain and occasionally numbness and tingling over the
distal anterolateral leg and dorsal foot and ankle that is generally exacerbated with activity. As with the deep peroneal
nerve, physical examination should begin with the lumbosacral spine to rule out an accompanying radiculopathy, and
evaluate the fibular neck to rule out entrapment proximally. Tenderness where the nerve exits from the fascia or Tinel
sign may be present. Nonoperative management includes use of transcutaneous electrical stimulation (TENS) to reduce
symptoms, and therapeutic trials of gabapentin and tricyclic antidepressants. Injection may be helpful. Relief with
conservative measures is uncommon. Surgical intervention involves releasing the area of entrapment or neurectomy for
refractory cases (155,157).
Sural Nerve
Entrapment of the sural nerve can occur anywhere along its course. The sural nerve originates between the two heads of
the gastrocnemius muscle and travels laterally down the lateral border of the Achilles tendon. Approximately 2 cm above
the ankle joint, it gives off a branch that supplies sensation to the lateral heel. The sural nerve continues inferior to the
peroneal sheath and branches as it reaches the base of the fifth metatarsal. Its terminal branches supply sensation to the
lateral aspect of the fifth toe and fourth web space. Patients report radiating pain and paresthesias along this distribution.
The physical examination may demonstrate local tenderness and Tinel sign. Nonoperative and operative management is
similar to superficial peroneal nerve entrapment ( 155,157).
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58 Abdominal Injuries
58
ABDOMINAL INJURIES
RUSSELL D. DUMIRE
ANDREW B. PEITZMAN
Mechanism of Injury
Initial Evaluation
Abdominal Wall Injuries
Hernia
Spleen
Liver
Renal Injuries
Pancreatic Injuries
Intestinal Tract Injury
Bladder Injury
Conclusion
Chapter References
Over the past several decades, we have seen tremendous growth in the number of those participating in athletic activities
and organized sports, especially in the younger age groups and among women. Approximately one half of American boys
from age eight through 16 years and one fourth of similarly aged girls participated in some type of organized competitive
athletic event at sometime during the year, resulting in 30 million adolescents each year in this country alone
participating in sporting events ( 1,2). Of this 30 million, approximately 25% to 30% participated in organized athletic or
exercise programs, while 40% participated in nonorganized events such as neighborhood football or baseball games.
Most American high schools and approximately 75% of middle schools offer competitive sports programs ( 3). In addition,
the recent interest and health issues among the adult population has resulted in an increase in adult participation in both
exercise and organized athletic programs. As participation rates increase, so will the number of sports-related injuries. In
addition, the younger participants are entering during an era of increased expectations, resulting in increased intensity,
duration, and frequencies of practices, which, in turn, result in more injuries because most injuries occur during the
practice sessions as opposed to during the actual competition.
Catastrophic sporting injuries, fortunately, are quite rare. The vast majority of injuries are minor and usually self-limited.
However, approximately 7% to 10% of sporting injuries involve the abdomen, whereas 10% of all reported abdominal
injuries are a result of athletic participation. The reported overall injury rates in organized collegiate athletics in the
United States are 39 per 100 athletes, with 40% of these injured athletes being referred to a physician and 71% of those
referred requiring further diagnostic evaluation such as x-ray or laboratory workup ( 4). Only 6% to 10% of the injured
athletes require hospitalization. However, the overall cost for the diagnosis and acute management of these
sports-related injuries is approximately 1.3 billion dollars per year in the United States ( 5). It should be noted that these
data take into account all injuries, with the vast majority being made up of musculoskeletal injuries, whereas very few of
these injuries are actually abdominal. Contact sports such as American football, hockey, soccer, rugby, wrestling, and the
martial arts are the activities most frequently associated with abdominal injuries. Noncontact sports such as gymnastics,
baseball, basketball, and softball also have a small but significant incidence of abdominal injuries. Other recreational
activities associated with abdominal injuries include bicycling, motorcycles, jet-skis, downhill skiing, ATVs, and horseback
riding. ATV-associated injury may result in serious intraabdominal injury whose patterns resemble those of motor vehicle
crashes. In the next section, we discuss some of the anatomic considerations as well as mechanisms of injury that should
raise our level of concern for the possibility of abdominal injuries sustained during athletic participation. As previously
mentioned, sports-related abdominal injuries are, in fact, quite rare and it is exactly this fact that makes these injuries
particularly dangerous in that the possibility of intraabdominal injury is often overlooked. This may lead to delay or
missed diagnosis of significant intraabdominal injury. Abdominal injuries are rarely immediately life-threatening, and their
symptoms are often insidious in onset, which makes diagnosis difficult in many instances. However, outcomes related to
abdominal injury are directly related to prompt recognition and treatment. Therefore, as health care providers, coaches,
officials, and parents, we must be aware of the possibility of such injuries based on the history and mechanism of injury.
Prevention is obviously the first option but is not always possible. Therefore, prompt recognition of injury, followed by
appropriate initial evaluation and diagnostic modalities, will provide the optimal outcome for the injured athlete.
Unlike the catastrophic sporting injury such as a severe head injury or cervical spine fracture, whose manifestations are
immediately obvious, abdominal injuries are often difficult to diagnose and evaluate, especially in young athletes.
However, the end-result of missing a significant intraabdominal injury may be just as debilitating. Significant
intraabdominal injury may be present despite the lack of external signs or symptoms. It is precisely for this reason that we
must familiarize ourselves with the intraabdominal anatomy, and when a mechanism of injury suggests the potential for
abdominal injury, we must ensure that the injured athlete receives appropriate evaluation before resuming the activity or
competition. Only through this increased awareness for the potential of significant abdominal injury can we maximize our
efforts to detect and treat these rare but significant injuries.
The abdominal cavity is bound by the diaphragm superiorly, pelvic floor inferiorly, muscle and the lower ribs laterally, and
spine and musculature posteriorly. For practical purposes, the abdomen may be divided into four distinct regions ( Fig.
58.1). These regions consist of the intrathoracic, free, pelvic, and retroperitoneal abdomen. The intrathoracic abdomen is
that portion directly under the diaphragm and lying within the protection of the lower ribs. The contents include the liver,
spleen, stomach, diaphragm, and the first portion of the duodenum. Because of their intrathoracic position, examination
of the organs contained within this portion of the abdomen is often difficult. Approximately 25% of the time, injury to
organs in this portion of the abdominal cavity (especially the solid organs) are associated with rib fractures ( 6,7 and 8).
However, because of the incomplete ossification of the ribs in children, significant intraabdominal trauma may occur with
little external evidence of trauma. Therefore, the mechanism of injury should raise the suspicion of significant underlying
abdominal trauma. The free abdomen contains the small intestine and the majority of the large bowel, as well as the
dome of the bladder and uterus. As most of the organs contained within this cavity are hollow organs, injuries resulting in
perforation of one of these organs often produces peritonitis, which may be diagnosed on physical examination. The
hallmark of injury to a hollow organ is abdominal pain, which progressively worsens with time and is aggravated with
motion. The pelvic abdomen lies within the bony pelvis and includes the sigmoid colon, bladder, ureters, proximal
urethra, uterus, tubes, and ovaries. Trauma to these organs due to low velocity blunt injury is rare owing to the protection
offered by the pelvic bony structure. However, any force significant enough to fracture the pelvis may result in injury to
one of these underlying organs. Between 40% and 60% of pelvic fractures may have associated abdominal, thoracic, or
other bony injuries (9). Of note, the rectum and urethra are particularly susceptible to injury when they are associated
with pelvic fractures. The retroperitoneal abdomen contains the second and third portions of the duodenum, kidneys,
ureters, pancreas, and great vessels. Visceral injury in this portion of the abdomen is difficult to diagnose by physical
examination because most injuries to organs in this area result in few if any external signs, with the exception of the
kidneys, which may exhibit gross or microscopic hematuria following injury. Common mechanisms of injury include direct
abdominal trauma, falls from a height, deceleration injury, and direct blows.
FIGURE 58.1. The solid abdominal viscera are fragile and easily injured but are well protected by the
musculoaponeurotic and skeletal components of the abdominal parietes. A: Anterior view. B: Posterior injured but is well
protected by the musculoaponeurotic and skeletal view.
MECHANISM OF INJURY
Abdominal injuries are generally classified as either penetrating or blunt. Penetrating injuries are broken down further
into high-velocity wounds such as gunshot wounds, low-velocity wounds such as stab wounds, and impalement injuries.
We will not be discussing the presentation and management of gunshot and stab wounds. Impalement wounds present
an interesting problem in that they must be treated as both a penetrating and a blunt injury. For example, a participant in
a bicycle race runs over an embankment, is thrown from his bicycle, and is subsequently thrown onto a tree branch,
which is impaled into the abdominal cavity. One must consider not only the damage done by the penetration of the object
into the abdominal cavity, but also the potential damage done by the blunt force trauma secondary to the fall and the
deceleration. While keeping these facts in mind, the victim should be transported to the nearest appropriate medical
facility with the impaled object secured in place. If the size of the impaled object impedes the ability to extricate or
transport the victim, the object may be cut and then secured so as to prevent excessive motion, which might possibly
produce further internal damage. On arrival at the medical center, two large caliber intravenous catheters should be
inserted and surgical consultation should be obtained. Under most circumstances, the patient should be taken to the
operating room, where the object may be removed and surgical exploration can be performed to control internal bleeding
as well as repair damage done by the impaled object.
Blunt abdominal trauma is by far the most common mechanism of abdominal injury associated with sporting events.
Common mechanisms include events such as a collision between two moving objects such as two football players
running into each other ( Fig. 58.2) or through direct blows to the abdomen by a fast-moving baseball or through multiple
blows sustained during a boxing match. Other mechanisms include deceleration injuries, which are often sustained in
falls.
FIGURE 58.2. A direct blow may rupture a viscus without bony fracture. Hemorrhage may be slow and subtle or massive.
INITIAL EVALUATION
The evaluation of the blunt abdominal trauma victim can be difficult in that the initial presentation may range from frank
peritoneal irritation to vague and nonspecific abdominal symptoms. Only 22% of patients with blunt abdominal trauma
present with obvious signs of intraabdominal injury and, of these, approximately 80% have significant intraabdominal
injuries (7). On the other hand, approximately 12% of patients sustaining significant blunt abdominal trauma will present
with an initially negative physical examination despite the fact that approximately 43% of these patients have actually
sustained significant intraabdominal injury ( 10). Also, 20% of patients with significant retroperitoneal injuries may present
initially with a negative physical examination. Another consideration is evaluation of the abdomen in the patient with
concurrent altered level of consciousness or cervical spine injury. Altered sensorium, whether the cause be secondary to
closed head injury or intoxication, confounds the physical examination and mandates further diagnostic evaluation. The
initial approach in evaluation of the injured athlete should start with a detailed history and physical examination of the
abdomen. Knowledge of the mechanism of injury may raise suspicion for the existence of intraabdominal injuries as well
as dictate possible further diagnostic evaluation based on physical findings. One of the most important concepts in the
evaluation of patients with suspected abdominal trauma is that of sequential abdominal examinations. Any athlete
sustaining abdominal trauma and experiencing persistent or progressive abdominal discomfort warrants further
diagnostic evaluation.
In general, the diagnostic pathway taken in the evaluation of the injured athlete is initially dictated by the patient's
hemodynamic stability. In the stable patient, a thorough history and physical examination may reveal the need for further
diagnostic evaluation. Examination of the abdomen should include a complete visual inspection, including the back and
flanks. Contusions may not show up for several hours after the initial injury, and in children, there may be few external
signs of injury despite the existence of significant intraabdominal pathology. Following visual inspection, the abdomen
should be palpated in all quadrants, any tenderness, rigidity, or masses should be noted. Remember that whole blood is
not a peritoneal irritant in small to moderate amounts. Therefore, we must rely on other physical findings such as pulse
rate, respiratory rate, capillary refill, and blood pressure to provide clues of significant blood loss. Based on these
findings, no further evaluation or diagnostic tests may be required. However, if any doubt exists, appropriate radiographic
or laboratory evaluation is required. If no abnormalities are found, the patient may be discharged home with instructions
to follow up if the pain persists or worsens over the next 12 to 24 hours. Sporting activities may be resumed at the
patient's discretion.
In the unstable patient, the initial approach is to stabilize the patient and restore circulating volume, followed by a rapid
diagnostic evaluation. An unstable patient is defined as any patient with a compromised airway or a deteriorating
hemodynamic status manifested by a systolic blood pressure less than 90 mmHg or a pulse rate greater than 120 beats
per minute. These patients require rapid stabilization and immediate diagnostic evaluation. Initial stabilization is
accomplished with 2 L of crystalloid solution in the adult population or 20 mL per kg of similar solution in the pediatric
population. If the patient quickly stabilizes and remains stable, further diagnostic evaluation typically includes a computed
tomography (CT) scan of the abdomen. The accuracy of the CT scan ranges from 95% to 98% with the additional
advantage of delineating the extent of injury to the various involved organs ( 8). This is important in that the vast majority
of solid organ injuries, such as the spleen and liver, which may be managed nonoperatively based on these findings. An
additional modality available in most modern emergency rooms is ultrasound. Ultrasound has the benefit of being fast,
inexpensive, and most important, repeatable at the bedside. However, the results of the study are operator dependent
and require some degree of skill in both the performance and the interpretation of the results. The reported sensitivity of
ultrasound ranges from 60% to 90%. In the patient who initially stabilizes with fluids and then again becomes unstable, a
more aggressive approach is warranted. Any patient with overt peritoneal symptoms requires operative intervention
without further or abdominal diagnostic workup. In the absence of peritoneal signs in the unstable patient with potential
abdominal injury, the diagnostic peritoneal lavage (DPL) remains the procedure of choice; however, the focused
abdominal ultrasound is replacing the DPL in many institutions.
ABDOMINAL WALL INJURIES
Abdominal wall strains or contusions due to direct blows are common athletic injuries especially among the contact sports
but also may be seen with any activity associated with rigorous conditioning exercises that result in overexertion of these
muscles. The primary concern with these conditions is to distinguish them from pain associated with intraabdominal
injury. Muscle wall strains or contusions are usually self-limited conditions that resolve with time and rest. A history of
vigorous exercise period preceding the onset of pain is very suggestive of strain, and the physical examination may help
to confirm this diagnosis. Abdominal wall pain is usually very well localized, nonradiating, aggravated by tensing of the
muscles, and somewhat relieved by relaxation of the same muscles. There should be no evidence of peritoneal irritation,
and the vital signs should typically completely within normal limits. If the history and physical examination are consistent
with the diagnosis of abdominal wall strain or contusion, no further diagnostic evaluation is required and treatment should
consist of rest and ice to the affected area to the first 48 hours, followed by heat to the same area thereafter as needed.
The athlete may resume activity as pain permits.
Occasionally the contraction of the muscle can be so intense as to rupture the inferior epigastric artery or a branch
thereof, resulting in a rectus hematoma. This condition is characterized by the abrupt onset of severe and intense
abdominal pain, and often there is a palpable mass in the area of the rectus muscle where the rupture has occurred. This
mass is usually exquisitely tender, firm, and tends to be immobile. Approximately 80% of these ruptures of the epigastric
artery occur below the level of the umbilicus and often periumbilical ecchymosis can be appreciated ( 11,12 and 13). This
condition is usually diagnosed by physical examination; however, owing to the intense pain, there is often associated
nausea and vomiting. If any doubt exists, the diagnosis may be confirmed by ultrasound or CT examination, which
demonstrates the rectus hematoma. The CT scan has the further benefit of allowing inspection of the internal organs and
ruling out potential intraabdominal injury or associated injuries. Treatment consists of rest with ice to the affected area
during the first 48 hours, followed by application of heat to the same area as needed thereafter. Activity may be resumed
once the pain resolves; however, abdominal exercises should be progressed over a 2- to 3-week period. Occasionally,
the resolving hematoma will leave a persistently palpable nodule. However, this requires no therapy, as long it is not a
source of persistent pain, in which case excision of this granulomatous tissue may be warranted in order to relieve the
persistent discomfort. Rarely, the hematoma continues to expand or is so painful that surgical evacuation of the
hematoma and ligation of the inferior epigastric artery is required. The incision required for this process is typically quite
small and usually does not violate the posterior fascia; therefore, the athlete may resume normal activity within 2 to 3
weeks.
HERNIA
The hernia is a defect in the abdominal wall (natural or acquired), which allows the passage of preperitoneal or
abdominal contents. Hernias occur in approximately 1% to 2% of the population, with a vast majority (approximately 80%)
localized in the inguinal region and approximately 80% of these are diagnosed in men. However, as female athletic
participation continues to increase, we may begin to see a rise in the proportion of hernias being diagnosed in women.
Most hernias in athletes are diagnosed during routine physical examinations in a relatively asymptomatic state, and it is
not until the athlete engages in strenuous activity that he or she begins to appreciate discomfort or bulging in the groin. It
is difficult to say that all asymptomatic hernias require repair. However, the natural history of a hernia is gradual
enlargement with progression from asymptomatic to symptomatic. There is also a 5% lifetime risk of incarceration or
strangulation or both ( 9,14,15 and 16). Therapy is obviously individualized, but in the athlete who will continue with
strenuous activity and most likely increase his level of exertion and participation with time, it is prudent to recommend
repair of the hernia at the athlete's earliest convenient time. Also, repairs are technically much easier and are associated
with lower recurrent rates when the hernias are small. There is no doubt as to the management of the symptomatic
hernia. All symptomatic hernias require repair, with the cessation of strenuous activity before the repair.
The operative repair of both congenital and acquired hernias is straightforward and can usually be accomplished with the
athlete as an outpatient. Recurrence rates range from 1% to 5% for indirect hernias and 2% to 15% for direct hernias ( 9).
Routine conditioning activities may be resumed at 3 to 4 weeks after repair, and full activity may usually be resumed by 8
to 12 weeks. The advent of laparoscopic hernia repair has further shortened the recovery period, and the highly
competitive athlete may resume full activity within 3 to 4 weeks. Laparoscopic repair is typically reserved for the recurrent
or bilateral hernias but is useful for the unilateral repair in the highly motivated athlete or in the patient who is required to
return to strenuous activities as soon as possible (such as the individual whose job performance requires heavy lifting
and who cannot tolerate long periods of absence from the job). To date, the laparoscopic repair is not recommended in
the pediatric population. Long-term data on recurrence rates for the laparoscopic approach are not yet available;
however, short-term data reveal an approximate 3% recurrence rate, which is similar to that of the conventional repair
(14,17).
SPLEEN
The spleen is the second most commonly injured intraabdominal organ due to blunt abdominal trauma. However,
because of its propensity for bleeding, it remains the most common organ injury requiring operative intervention. The
spleen is situated deep in the left upper quadrant under the ninth through the 11th ribs. The spleen contains
approximately 25% of the body's reticuloendothelial tissue and receives about 5% of the cardiac output, which explains
the important role of the spleen in immunocompetency. The immunologic importance of the spleen has been recognized
since the early 1950s, and this knowledge has swayed our approach to splenic trauma from the routine splenectomy to
nonoperative management and attempts at splenic salvage whenever possible. The spleen is responsible for clearing the
circulation of circulating bacteria (especially encapsulated organisms) and has a significant role in the cell-mediated
immunity with antigen presentation as well as production of mediators of the compliment system such as tuftsin and
properdin. Full immunogenic competence is usually achieved by the age 2 to 5 years and splenectomy before this age
significantly increases the child's lifetime risk of overwhelming infection due to encapsulated organisms, in particular
Streptococcus pneumoniae, Meningococcus, Escherichia coli, and Haemophilus influenzae. The spleen of a child is
typically larger than that of an adult, reaching its maximum size by the age 13 years and subsequently decreasing in size
by about 30% to achieve the adult size of 150 to 250 g. This larger spleen in children predisposes them to splenic injury.
However, the thicker capsule and higher elastin content of the spleen is somewhat protective and allows for easier repair
salvage if required. Any condition that causes splenomegaly may predispose the spleen to rupture; of particular note is
mononucleosis. Approximately 0.1% to 0.2% of patients with mononucleosis sustain splenic rupture; therefore, athletes
with or recovering from mononucleosis and concurrent splenomegaly should refrain from training activities and contact
sports for at least 2 to 3 weeks following the complete resolution of the splenomegaly because even insignificant trauma
may result in rupture ( 18,19).
Approximately 8% of adult splenic injuries and 20% of pediatric splenic injuries are direct result of sporting activities
(6,11,20). Sporting injuries account for approximately 10% of all splenic injuries due to blunt force trauma. The spleen
may be injured by direct compressive effects such as a blow to the left upper quadrant or by shear force, such as that
resulting from a deceleration injury such as in a fall. To help understand the physiology behind splenic injury, it is
important to review splenic anatomy. The spleen is attached and fixed into its position by four primary points; the
splenophrenic ligament, which attaches the spleen to the diaphragm; the splenorenal ligament, which attaches the spleen
to the superior pole of the left kidney; the gastrosplenic ligament, which attaches the hilar aspect of the spleen to the
greater curvature of the stomach and contains the short gastric vessels; and the splenocolic ligament, which attaches the
inferior pole of the spleen to the splenic flexure of the transverse colon. These points of attachment explain some of the
common sites of capsular injuries to the spleen. When the body comes to a sudden stop, the internal organs tend to
continue in motion. However, with the spleen being fixed in its position any forward motion may result in tears at its point
of attachment with resultant bleeding. Direct blows to the left upper quadrant can cause the spleen to fracture typically
along a plane that is parallel to that of the segmental vessels traversing the spleen. More severe blows to the left upper
quadrant can result in stellate lacerations, which tend to cross the segmental vessels and produce bleeding which can
result in rapid physiologic deterioration. Approximately 25% of splenic lacerations have an associated rib fracture.
However, in children, the chest wall is very pliable owing to the incomplete ossification of the ribs, and significant
underlying damage can occur despite little external evidence of trauma.
The athlete who has sustained a splenic injury tends to complain of left upper quadrant pain, which may be referred to
the left shoulder in 25% of the cases (i.e., Kehr sign). Because bleeding from the spleen can be brisk, in the majority of
the cases, the athlete may be pale, cool; have a weak, thready pulse; and complain of thirst, all of which are signs of
hypovolemia and impending hemodynamic collapse. Nausea and vomiting are also common in children. Any athlete with
a history of trauma to the left upper quadrant and any of these findings requires urgent evaluation because an
unrecognized splenic injury can be fatal.
The evaluation of a patient with suspected splenic injury depends on the stability of the patient. Approximately 93% to
95% of children and 57% of adults with splenic injury present to the emergency room in stable condition and are suitable
for further diagnostic evaluation such as a CT scan ( 21). The remaining patients are hemodynamically unstable and
require urgent resuscitative efforts and evaluation by either a focused abdominal ultrasound or a DPL if the vital signs do
not rapidly stabilize with fluid resuscitation. If the patient does stabilize following fluid resuscitation and does not require
ongoing resuscitative efforts to maintain hemodynamic status, the patient may be sent to undergo a CT scan for
evaluation. Approximately 3% to 5% of patients with spleen injuries from blunt abdominal trauma present in extremis and
require urgent operative evaluation and resuscitation in the operating room. If a patient undergoes CT scan and has an
identifiable isolated splenic injury, there is an excellent chance that this patient may be managed nonoperatively.
Approximately 60% to 80% of adult patients with isolated splenic injuries and 95% to 98% of children can be successfully
managed nonoperatively as long as they remain hemodynamically stable ( 21). In fact, only 10% of children managed
nonoperatively even require a blood transfusion. The decision to manage nonoperatively is based on several criteria. Of
primary importance is the ability to examine the patients sequentially for changes in physical examination and physiologic
parameters, as well as the ability to repeat diagnostic evaluation such as CT scan or ultrasound. The factor that most
accurately predicts the success of nonoperative management in children is hemodynamic status, regardless of splenic
grade or hemoperitoneum based on CT results. However, in the adult population, the degree of hemoperitoneum, the
absence of an arterial blush on the CT scan, and the grade of splenic laceration are the best predictors for the success of
nonoperative management (21). In the adult population, the two variables associated most with nonoperative failure are
the finding of a large hemoperitoneum and the presence of an arterial blush on the CT scan.
LIVER
The mechanisms of injury producing hepatic injury are similar to those that produce splenic injury; however, the injury
occurs to the right side of the body. Blows to the right upper quadrant may result in injury patterns ranging from simple
hepatic contusions with no subsequent intraabdominal bleeding to significant fractures of the hepatic parenchyma,
producing catastrophic intraabdominal bleeding requiring emergent operation. Because the susceptible surface of the
liver is in close approximation to either the diaphragm or the anterior abdominal wall, minor injuries to the liver often
spontaneously tamponade and require no further therapy. The liver is also subject to deceleration-type injury that
typically occurs at points of attachment. These points include the triangular ligaments that attach both the right and left
lobes to the undersurface of the diaphragm and the falciform ligament, which is one of the more common sites associated
with deceleration-type hepatic injuries.
Treatment of hepatic injuries is dependent on the severity of the injury and the stability of the patient. By far the most
common type of injury associated with sporting events is a simple hepatic contusion resulting in right-sided abdominal
pain and possibly some diaphragmatic irritation with referred pain to the right chest and shoulder. The first step in
treating such injuries obviously is the recognition of the potential of the underlying injury based on the mechanism of
injury. Any athlete sustaining a blow to the right upper quadrant and complaining of persistent right upper quadrant pain
should receive further evaluation. This evaluation may be as simple as a physical examination. However, if the
examination reveals a possible underlying injury, further diagnostic evaluation, including a CT scan, may be warranted.
Again, the CT scan is the preferred method of evaluation because it allows accurate diagnosis of the injury and ability to
classify and grade the injury. If a small subcapsular hematoma is appreciated with no significant intraabdominal bleeding,
treatment may be as simple as avoidance of sporting activity for 3 to 4 weeks, followed by gradual return to full activity
over another 2 to 3 weeks. More significant injuries to the liver resulting in some intraabdominal bleeding may produce
symptoms ranging from right upper quadrant tenderness to nausea, vomiting, and even signs of hypovolemia such as
tachycardia, pallor, and diaphoresis. Any athlete who reports or manifests any of these symptoms requires immediate
evaluation at an emergency facility. CT examination may reveal a small hepatic laceration with some intraabdominal
bleeding, and further therapy will be dictated based on the patient's hemodynamic status. Because most patients remain
hemodynamically stable or quickly stabilize with minimal fluid resuscitation, most hepatic injuries of this degree may be
treated nonoperatively. Nonoperative management of these hepatic injuries includes hospitalization and serial abdominal
examinations, including serial hematocrits for the first 24 to 36 hours. The patient is confined to bed rest for 3 to 5 days,
after which he is gradually allowed to increase his activity to normal daily activity excluding sporting activities. The
follow-up CT scan is obtained in approximately 6 weeks. Typically, the small liver injuries are completely healed by 2 to 4
weeks, as documented by CT scan. Full healing, however, must be documented before allowing the athlete to resume
normal activity, and depending on the degree of laceration, this can take up to 3 to 6 months ( 22,23). Finally, in rare
instances, the hepatic laceration may be to such a degree that the athlete does not stabilize with fluid resuscitation and
requires emergent operative intervention to control the bleeding. Typically, all that is required in these instances is
evacuation of blood from the abdomen and packing the liver with hemostatic agents as well as manual compression for
several minutes. Rarely, the liver is injured to such an extent that portions must be resected in order to remove the
devitalized tissue. This type of injury is typically a result of massive energy transfer and is usually more common in motor
vehicle crashes than in sporting mishaps.
RENAL INJURIES
When considering only sports-related injuries, the kidney remains the most commonly injured organ among sports
participants. Approximately 15% to 50% of all renal injuries are a result of sporting activities, and as many as 30% of
renal injuries in children are sports related ( 4,5). By far, the most common activity causing renal injuries is American
football, resulting in direct blows to the flank and back. However, sports such as soccer, rugby, hockey, and wrestling are
associated with renal injuries due to blows to the back. Long-distance runners and basketball players also may suffer
renal injury due to microtrauma due to repetitive trauma to the kidney from running long distances or back and forth down
the basketball court. As many as 25% of long-distance runners and basketball players can be noted to have microscopic
hematuria following their activities. This microscopic hematuria is invariably associated with no evidence of trauma when
diagnostic studies are performed and resolves on its own without sequela. In fact, this occult hematuria without
radiographic evidence of injury is common among many sports such as boxing, football, basketball, and long-distance
runners. Unless gross hematuria is present or microscopic hematuria does not clear over 48 to 72 hours, no further
evaluation is warranted.
The mechanism of injury for renal injury is similar to most sporting injuries in that it may be due to a direct blow to the
overlying area of the flank or back or through repeated microtrauma such as repeated jumping or long-distance running.
The upper third of the right kidney and the upper half of the left kidney lie above the protection of the twelfth ribs and the
lower poles extend below the ribs and are protected only by the surrounding muscle and perinephric fat. In children, the
kidneys are somewhat larger and protrude further below the protection of the rib cage, the perinephric fat pad is less well
developed and affords much less protection and the intrinsic nature of the juvenile kidney is much more susceptible to
injury. All of these properties predispose children to renal injury when suffering direct blows to the back or flank. An
athlete is particularly susceptible to kidney injury when the muscles around the back are relaxed such as when a receiver
is jumping for a football and the defender tackles him from the side. Whenever an athlete sustains a flank or back injury
and complains of flank pain, a renal injury must be considered. The presentation of renal injuries can be quite variable in
that they may present with minor flank pain without evidence of hematuria to severe flank pain, gross hematuria, and
cardiovascular compromise. With this in mind, a very quick and easy screening test for any athlete suspected of having
renal trauma is to remove him or her from participation and ask the athlete to void. If the specimen contains gross
hematuria, the athlete requires further evaluation and should not be allowed to return to participation. However, as many
as 25% of patients with severe renal injuries and 40% of patients with renal pedicle injuries may present without
hematuria. Therefore, the absence of hematuria does not rule out a renal injury, and in fact, the degree of hematuria
does not correlate with the degree of injury.
Once an initial evaluation of the injured athlete reveals that there may be a kidney injury, further diagnostic evaluation is
required. Physical examination may be unremarkable, with flank tenderness on the affected side or severe muscle
tenderness, ecchymoses, and even a flank mass may be appreciated if the perinephric bleeding is significant. If gross
hematuria is present, the bladder may also fill with blood and clot, resulting in overdistension of the bladder and inability
to void. Therefore, patients with significant gross hematuria must be considered for early Foley catheterization to
evacuate the bladder of clot and to monitor the amount of bleeding. As with most other solid organ injuries, the diagnostic
method of choice if available is the CT scan. The CT scan is a rapid diagnostic tool that accurately delineates the extent
of renal injury, quantifies the degree of perinephric bleeding, and identifies extravasation from the collecting system, as
well as other associated intraabdominal injuries which may be present.
Treatment of renal injuries varies with the extent of intrinsic injury. The majority of renal injuries consist of minor
contusions with minimal perinephric bleeding. These patients may be treated with bed rest until the gross hematuria
clears, followed by a period of restricted activity for approximately four weeks, at which point they may be gradually begin
conditioning exercises over a period of a couple weeks. Normal activity may be resumed within 4 to 6 weeks after the
injury. More serious renal injuries resulting in significant parenchymal fractures or devascularization require more
intensive treatment and follow-up. Patients sustaining this type of renal injury are treated initially in similar fashion with
bed rest until the gross hematuria clears and then gradual progression of activity to normal daily activity with the
exclusion of strenuous or athletic activity. These patients often require repeat CT evaluation at approximately 2 to 3
months to evaluate the extent of healing and require sequential physical examinations to monitor for impaired renal
function, formation of kidney stones, and even the remote possibility of development of hypertension secondary to renal
pedicle or parenchymal injury. Once complete healing of the kidney is documented, the athlete may resume normal
activity. Of special note, patients with congenital kidney malformation such as polycystic kidney disease and congenital
horse shoe kidneys should be extensively counseled on the possibility of damage and the inherent risk of contact sports.
Although these entities do not preclude their participation in athletics, it does, however, predispose the kidneys to injury,
especially with contact sports. Any athlete with these preexisting conditions should be well aware of the risk and the
possible consequences of their participation.
PANCREATIC INJURIES
Pancreatic injuries following blunt low-velocity injuries such as those incurred during athletic participation are, fortunately,
quite rare, with an incidence of only 2% to 3% of athletic injuries ( 24). The pancreas lies deep within the abdomen, with
its body crossing directly over the body of L-2. Because of the close association to other major intraabdominal structures,
such as the inferior vena cava and duodenum, associated injuries can occur in 12% ( 8).
Diagnosis of isolated pancreatic injury can be extremely difficult because few if any symptoms may be present
immediately following injury. The mechanism of injury may raise your suspicion as to the possibility of an injury; however,
all diagnostic modalities during the initial postinjury period may be negative. The serum amylase level is negative in
approximately 30% to 40% of patients with pancreatic injury, and the CT scan often misses acute pancreatic injuries if no
peripancreatic hematoma or associated abdominal injury is present.
The mechanism of injury associated with sports-related pancreatic injuries is usually a focused blow to the abdomen or
back, such as with a baseball, football helmet, or foot (Karate blow or kick from a horse) ( 24,25 and 26). The only initial
reports may be vague abdominal or back pain that progressively worsens over 6 to 24 hours and is often associated with
progressive nausea and vomiting. This history should raise the suspicion of a pancreatic injury, and a repeat CT may
now reveal peripancreatic inflammation or fluid accumulation. The primary concerns in dealing with pancreatic injuries
are to determine the integrity of the pancreatic duct, which may require an endoscopic retrograde
cholangiopancreatography, and to exclude associated injuries, which may require an operative exploration. The
operative considerations in pancreatic injury are beyond the scope and focus of this chapter. If a fracture through the
body of L-2 is identified, the incidence of pancreatic injury increases significantly and many centers perform surgical
exploration based on this finding alone.
INTESTINAL TRACT INJURY
Hollow viscus injury is an uncommon sports-related injury, but it has been reported secondary to blunt trauma sustained
during sporting activities. The two proposed mechanisms of injury causing hollow viscus injury include direct compressive
injuries resulting in bowel injury or, more commonly, a closed-loop phenomenon, which results in overpressurization of
the closed loop and subsequent perforation ( Fig. 58.3). The portions of the bowel most vulnerable to this injury are those
portions adjacent to points of attachment such as a second portion of the duodenum, the ligament of Treitz, and the
ileocecal area ( Fig. 58.4). Also, any abdominal adhesions that may be a result of prior intraabdominal procedures or
infections may predispose that portion of the bowel to twisting or obstruction during compressive episodes, resulting in
perforation. Evaluation of an injured athlete for suspected hollow viscus injury is exceptionally difficult in that symptoms
may initially be sparse and nonspecific. This difficulty is particularly noticeable in children in that even with significant
intraabdominal injury, their only problem in 40% to 60% of the cases is generalized abdominal tenderness. In general,
symptoms of hollow viscus injury include progressive abdominal pain. This pain may be aggravated with motion, which is
consistent with peritoneal irritation. As the pain progresses, the athlete typically will begin to report nausea and vomiting
as well. Although these injuries are not as dramatic as exsanguinating bleeding from solid organ injury, a missed hollow
viscus injury is just as devastating in that the subsequent peritonitis and sepsis may be fatal.
FIGURE 58.3. In bicycle handlebar trauma, force is applied to the abdominal and retroperitoneal structures, particularly
the duodenum and pancreas, compressing them against the spinal column. (From Valentine MW. Bicycle handlebar
injuries in children Emerg Med 1988;20:37, with permission.)
FIGURE 58.4. A: Cross-section, coronal plane, cephalad view of a CT scan of the abdomen showing an intramural
duodenal dermatoma resulting from a football injury. B: The transition area of the duodenum between the tightly
anchored and loosely tethered attachments of the small bowel to the mesentary. The transition area becomes stressed
when the athlete is stopped suddenly, which can happen in football, cycling, or equestrian events. (From Henderson JM,
Puffer JC. Abdominal pain in a football player. Phys Sportsmed 1989;17:48.)
Again, evaluation of an athlete suspected of having an intraabdominal injury includes a detailed history of the mechanism
of injury and a physical examination. If the initial evaluation reveals peritoneal signs, or an initial kidney, ureter, and
bladder examination (KUB) shows free air under the diaphragm, no further diagnostic workup is required and the patient
is taken to the operating room for exploratory laparotomy and repair of the injury. If, however, the physical exam is
equivocal and the KUB is nonspecific, a CT scan, which is much more sensitive for the detection of free air in the
abdomen, may be obtained. However, the CT scan does lack sensitivity for small bowel injury and may potentially miss
these injuries. Therefore, a negative CT scan does not exclude the possibility of a bowel injury. If all diagnostic studies
are negative, the patient should be closely observed for at least 24 hours with sequential abdominal examinations. If
exploratory laparotomy is required, a midline incision is used, and the abdomen is thoroughly explored. The injury is
identified, and if possible, the perforation is primarily repaired. However, if significant devascularization has occurred, a
segmental resection and anastomosis may be required.
Two other gastrointestinal tract injuries due to blunt abdominal injury must be mentioned. The first is a simple mesenteric
laceration. This results typically from a deceleration injury in which the fluid-filled bowel continues in the forward motion;
however, the mesentery is fixed to the retroperitoneum. Therefore, the mesentery may be torn, and if this tear traverses a
mesenteric vessel, significant intraabdominal bleeding may occur. Although the hollow viscus is intact, the bowel may be
ischemic if enough of the mesentery is torn so as to compromise the blood flow to that portion of the bowel. This type of
mesenteric bleeding may be so severe as to cause significant abdominal distention as well as signs of hypovolemia and
shock including tachycardia, low blood pressure, pallor, and diaphoresis. Small mesenteric lacerations are probably more
common than we realize and often go undiagnosed. However, larger lacerations resulting in significant abdominal
bleeding may result in hemodynamic compromise, which requires emergent operation. Evacuation of the abdominal
hemorrhage and ligation of the bleeding vessel is required in these instances. If the laceration is large enough to
devascularize a segment of bowel, this portion of bowel is resected and a primary anastomosis is performed.
The second condition, which is probably more common in children, is the duodenal hematoma ( Fig. 58.4). Owing the
extreme pliability of the child's abdominal wall and the flaring of the rib cage, the duodenum is much more vulnerable to
injury in the pediatric age group. In blunt injury to the epigastrium, in a child may result in a small hemorrhage in the
duodenal wall in the second portion of the duodenum. This hemorrhage may enlarge over 24 to 48 hours and typically
the child will begin to complain of nausea, vomiting, and abdominal pain approximately 24 to 48 hours following the
incident. Typical mechanisms of injury resulting in this type of injury in children include handlebar injury ( 26), as well as
direct blow to the epigastrium such as in martial arts competition and in boxing matches ( Fig. 58.3). Duodenal
hematomas may also result from deceleration injuries such as a fall from a height or a very vigorous football tackle. The
duodenum becomes retroperitoneal at its second portion, is attached firmly to the retroperitoneum in its second and third
portions, and becomes loose in the abdomen at the ligament of Treitz. The common locations of duodenal hematomas
are the junction of the second portion of the duodenum and also occasionally at the ligament of Treitz. Typically, the
athlete with the duodenal hematoma will complain of persistent abdominal pain with progressive nausea and vomiting
over 24 to 48 hours. Evaluation of an athlete with these symptoms should consist of a Gastrografin swallow, which often
reveals the duodenal hematoma or the classic coil spring or stacked coin appearance on an upper gastrointestinal study.
Treatment of duodenal hematomas is conservative and expectant in that most resolve on their own in 5 to 7 days. Most
would agree that conservative treatment should be tried for up to 2 weeks and, if necessary, to total parenteral nutrition
used in order to provide nutritional supplementation. If the hematoma persists past 2 weeks, most would also agree that
exploration is indicated, not only to evaluate the hematoma but also to exclude the coexistence of another intraabdominal
injury. Postoperative treatment would include just nasogastric decompression and nutritional supplementation through
parenteral routes. Return to athletic activity following routine duodenal hematoma should be possible within 3 to 4 weeks
following resolution of symptoms.
BLADDER INJURY
Injury to the urinary bladder is an uncommon sports-related injury in that the bladder lies deep within the protection of the
bony pelvis. However, when the bladder is full, the dome may extend above the pelvic brim into the free abdomen and
make the bladder susceptible to rupture. Bladder injuries may range from simple contusions of the bladder to perforation
of the dome of the bladder. Typically, the athlete with the bladder injury reports suprapubic pain as well as generalized
abdominal tenderness and possibly peritoneal irritation. Any athlete complaining of the inability to void following an
abdominal injury should be regarded as having a possible bladder or urethral injury until proven otherwise and further
diagnostic evaluation is warranted. Typically, the diagnostic evaluation of a suspected bladder or urethral injury begins
with a retrograde urethrogram. After the urethrogram is negative, a full cystogram can be obtained. If the cystogram
shows an extraperitoneal perforation, the majority of these injuries may be managed with simple drainage. Intraperitoneal
perforation requires operative intervention to repair the laceration ( 29,30).
Urethral injuries are also uncommon injuries associated with sporting events. Typically, the male urethra is most
vulnerable owing to its longer course under the pubic brim. Any force significant to fracture the pelvis or separate the
pubic symphysis may be significant enough to disrupt the urethra. In addition, direct blows to the perineum, such as
kicks, may traumatically disrupt the urethra without associated pelvic fracture. Physical examination of a patient with
urethral injury may reveal blood at the urethral meatus, a perineal, or scrotal hematoma, or rectal examination may reveal
a bulging hematoma around the prostate or a high-riding prostate gland. When urethral injury is suspected, the initial
evaluation begins with a retrograde urethrogram. If no urethral injury is appreciated, the Foley catheter may be inserted
and a cystogram may be performed. If the urethral injury is identified, attempts to pass a Foley catheter should be
avoided and a urology consult should be obtained. Any athlete who reports the inability to void following pelvic or
abdominal trauma should be suspected of having urethral or bladder injury until proven otherwise.
CONCLUSION
As previously mentioned, significant sports-related abdominal trauma is uncommon. The mortality and morbidity
associated with abdominal trauma is directly proportional to the amount of time taken to receive definitive treatment. This
includes the potential time delay in the recognition, diagnosis, and treatment of abdominal injury. Any athlete suspected
of having abdominal trauma following an activity should be immediately removed from that activity and receive a thorough
physical examination. If the examination is consistent with an insignificant injury or muscle wall contusion, the athlete
may resume activity as tolerated. However, if the examination reveals the potential for underlying injury, the athlete
should be transported to the nearest emergency facility where an appropriate diagnostic evaluation maybe undertaken.
This evaluation should always include a thorough history of the mechanism of injury as well as detailed physical
examination of the abdominal cavity and all of its contents. The diagnostic workup is dictated by the patient's physiologic
condition, and if the patient remains physiologically stable, further evaluation may include a CT scan. If the patient is
unstable, evaluation with a focused abdominal ultrasound or a diagnostic peritoneal lavage maybe indicated to confirm
abdominal bleeding and, if indicated, operative intervention.
With the recent interest in athlete and health-related activities in the United States, it is not surprising that we are seeing
more and more sports-related injuries. Although preventive measures may help to decrease a number of these injuries,
prompt recognition and detection of such injuries is the single most important factor in the treatment of abdominal-related
sports injuries.
CHAPTER REFERENCES
1. Rooks D. Musculoskeletal assessment and training: the young athlete. Clin Sports Med 1988;7:3.
2. Stanitski C. Common injuries in preadolescent and adolescent athletes: recommendations for prevention. Sports Med 1989;7:32–41.
3. Garrick JG. Injuries in high school sports. Pediatrics 1978;61:465–469.
4. Coady C. Emergencies in sports. The young athlete. Clin Sports Med 1981;7:625–640.
5. Hergenroeder A. Prevention of sports injuries. Pediatrics 1998;101:1057–1063.
6. Amaral J. Thoracoabdominal injuries in the athlete. Clin Sports Med 1997;16:739–753.
7. Davis J. Diagnosis and management of blunt abdominal trauma. Ann Surg 1976;183:672.
8. Peitzman A. The trauma manual. Philadelphia: Lippincott-Raven, 1998.
9. Greenfield Lazar. Surgery; scientific principles and practice. Philadelphia: Lippincott-Raven, 1997.
10. Diamon D. Sports related abdominal trauma. Clin Sports Med 1989;8.
11. Bergquist D. Abdominal injuries from sporting activities. Br J Sports Med 1982;16:76–79.
12. Deshazo WF. Hematoma of the rectus abdominis in football. Phys Sports Med 1984;12:73–75.
13. Kenny P. Abdominal pain in athletes. Clin Sports Med 1986;6: 885–204.
14. Arrequi M. Laparoscopic inguinal herniorrhaphy. In: Cameron J, ed. Current Surgical Concepts, 6th ed. St. Louis: CV Mosby, 1999.
15. Kalson J. Chronic groin pain in athletes. Recommendation for treatment and rehabilitation. Sports Med 1994;17:141–147.
16. Smedberg SG, Roos H. Herniorrhaphy in athletes with groin pain. Am J Surg 1985;140:378–382.
17. Stoker DL. Laparoscopic verses open inguinal hernia repair: a randomized prospective trial. Lancet 1994;343:1243–1245.
18. Haines JD. When to resume sports after infectious mononucleosis. How soon is safe? Postgrad Med 1987;81:331–333.
19. Maki D. Infectious mononucleosis in the athlete: diagnosis, complications, and management. Am J Sports Med 1982;10:162–173.
20. Bergquist D. Abdominal trauma during 30 years: analysis of a large case series. Injury 1981;13:93–99.
21. Powell M, Peitzman A. Management of blunt splenic trauma: significant differences between adults and children. Surgery,
122:97:654–660.
22. Cywes S. Blunt liver trauma in children; non-operative management. J Pediatr Surg 1985;20:14–18.
23. Nichols A. Abdominal and thoracic injuries. In: Athletic Injuries and Rehabilitation. Philadelphia: WB Saunders, 1996:485–498.
24. Harrison JD. Pancreatic injury in association with football. Injury 1985;16:232.
25. Nielson, TH. Pancreatic transection during karate training. Br J Sports Med 1986;20:82–83.
26. Spearnon AL. Bicycle handlebar injuries in children. J Pediatr Surg 1986:21:118–119.
27. Valentine MW. Bicycle handlebar injuries in children. Emerg Med 1988;20:37.
28. Henderson JM, Puffer JC. Abdominal pain in a football player. Phys Sportsmed 1989;17:48.
29. Blalock N. Bladder trauma in long distance runners. Am J Sports Med 1979;7:239–241.
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59 Chest Injuries
59
CHEST INJURIES
CLAIRE CHASE
STEPHEN Z. TURNEY
Chest Wall
Rib Fractures
Flail Chest
Scapular Fractures
Sternal Fractures
Costochondral Injuries/Intercostal Muscle Strains
Clavicular Injuries
Traumatic Asphyxia
Pneumothorax
Hemothorax
Pulmonary Injuries
Aortic Disruption
Myocardial Contusion
Cardiac Rupture and Pericardial Tamponade
Commotio Cordis
Iatrogenic Injuries Secondary to Cardiopulmonary Resucitation
Chapter References
Chest trauma is common in the United States, ranking third in incidence behind head and extremity injuries. The Major
Trauma Outcome Study, reviewing nationwide data as of September 1987, reported a 30.6% incidence of chest injury in
all types of trauma patients (1). A total of 10% were caused by a blunt mechanism. The chest wall was injured in 50% of
these patients, pneumothorax or hemothorax was present in 45%, and pulmonary injury occurred in 26% of patients. Less
common were cardiac (9%) and aortic and great vessel injuries (4%).
Although the most common cause of blunt chest trauma is the motor vehicle accident, many contact sports involve
enough force to produce significant injury to the chest. The three most common mechanisms of injury to the thorax are
acceleration and deceleration, compression, and high-speed impact. Acceleration and deceleration involve the delay in
inertia of visceral organs compared with the skeletal inertia, resulting in injury to the viscera. This type of injury is typically
seen in motor vehicle accidents, although any rapid change in velocity can be the cause. Compression injuries occur
when the force applied to the chest exceeds the strength of the chest wall, as in falls or crush injury. High-speed impact
entails injury produced by a projectile or blunt object impacting against a discrete area of a stationary body.
CHEST WALL
The chest wall has two major functions: to protect and support the organs within it and to contribute to ventilatory efforts.
To generate a greater negative intrathoracic pressure or inspiration, the thoracic cavity must expand. The intercostal
muscles contract, causing an upward, outward movement of the chest wall. This, along with the descent of the
diaphragm, is a principal factor in the maintenance of the ventilatory pump. Even relatively minor injuries such as rib
fractures can cause a significant morbidity. The chest wall structures in their protective and supportive role can also
absorb much of the energy directed to the thorax; fractures of these structures can provide a clue to the presence of
massive forces and possible injury to internal viscera. These structures tend to be more compliant and flexible in the
younger athlete, so that fracture may not occur, despite forces sufficient to damage seriously intrathoracic organs.
RIB FRACTURES
Rib fractures are the most common chest injuries and the most commonly fractured ribs are in the middle level, or the
fourth through the seventh ribs. In the past, considerable efforts were made to diagnose each possible rib fracture
radiographically. This resulted in a substantial expenditure of time and finance. With recent interest in cost containment,
several studies have examined the efficacy of this practice ( 2,3 and 4).
The priorities of therapy are directed toward life-threatening intrathoracic injuries (e.g., pneumothorax, hemothorax, and
pulmonary contusion) that can be detected on an anteroposterior (AP) chest radiograph. The treatment for isolated rib
fractures is analgesia alone. Therefore, special views to detect additional rib fractures are a waste of resources, because
they will not change therapy.
There are notable exceptions to this rule: Multiple rib fractures, especially in elderly patients or those with chronic lung
disease, can cause serious difficulties in ventilation. These patients usually need to be admitted to the hospital for
aggressive pulmonary care, even if the rib fractures are an isolated injury.
Another special circumstance that received considerable attention in recent years is fracture of the first rib. Because of
the protected location and broad, thick dimensions of the first rib, it was assumed that a large amount of force is needed
to fracture it. Thus, the injury may serve as a “sentinel” to aortic rupture. Also, because of its proximity to the lung and
critical neurovascular structures, it was assumed that the ends of a fractured first rib have a greater likelihood to cause
local serious damage ( 5). Routine angiography in all patients with first rib fracture ( 6) has given way to more selective
use of contrast studies (7,8). Current diagnostic protocols generally reserve arteriograms for the patient with documented
upper-extremity vascular or neurologic deficits, or other signs of aortic injury (discussed later).
Less well-documented in the literature but of comparable special concern are fractures of the lower ribs, especially on the
left side. Because the energy needed to break the ribs overlying the spleen or liver could have been transmitted to the
solid viscera, special care in the evaluation for intraabdominal injury is warranted in these patients.
FLAIL CHEST
The term flail chest is used to describe the injury in which a segment of ribs has been isolated from the remainder of the
chest wall secondary to multiple rib fractures. This segment is displaced outwardly during expiration (and inwardly during
inspiration) in contrast to the rest of the thorax. Diagnosis is made on physical examination during respiration and may
not be obvious initially. The understanding of the significance of the flail segment has changed over the past few
decades. The typically serious respiratory difficulties encountered in patients with flail chest were at first hypothesized to
be purely a result of futile pendulum-like exchange of air from one lung to another. Termed pendelluft, this theory fell into
disfavor after such ventilatory movements could not be demonstrated in animal models ( 9). At present, more importance
is placed on the underlying pulmonary contusion to explain the respiratory manifestations of flail chest ( 10). However,
factors related purely to ventilatory dysfunction such as retained secretions and atelectasis secondary to rib pain and
splinting should not be discounted and need to be addressed in the care of the patient with flail chest. ( Fig. 59.1).
FIGURE 59.1. Chest film of a patient with left-sided flail chest. Multiple rib fractures and underlying lung contusion are
evident. (From Rodriguez A. Injuries of the chest wall, the lungs and the pleura. In: Turney SZ, Rodriguez A, Cowley RA,
eds. Management of cardiothoracic trauma. Baltimore: Williams & Wilkins, 1991:157–177, with permission.)
Just as the knowledge of the pathophysiology of flail chest has undergone an evolution, so has the therapy of the injury.
Mandatory prolonged mechanical ventilation for internal splinting, the standard of care for many years, has been
gradually replaced by a protocol of selective endotracheal intubation, particularly in the younger, cooperative patient
(11,12). In this management plan, intubation is carried out only if the patient exhibits significant difficulties in oxygenation
by arterial blood gas analysis or is in respiratory distress. Otherwise, therapy consists of aggressive pulmonary care and
adequate analgesia. Major advancements have been made with the use of epidural narcotics or local anesthetics,
providing pain relief while avoiding the respiratory depressive effects of systemic analgesia. This appears to be
particularly true with epidural local anesthetics, such as bupivacaine ( 13).
Intraoperative chest wall stabilization may have a role in the subset of patients with flail chest without pulmonary
contusion and who require intubation. The respiratory insufficiency in these patients is directly related to chest wall
instability rather than underlying lung injury. In this population, early (within 48 hours after injury) internal fixation of the
flail segment appears to reduce the incidence of pneumonia and facilitate early extubation ( 14).
SCAPULAR FRACTURES
Another strong, well-protected bone of the thoracic cavity is the scapula. Because of the significant force required to
damage it, fracture of the scapula (which is rare) has been cited as a marker for severe ipsilateral lung and chest wall
injury. In one series of 56 patients with scapular fractures, 54% had pulmonary contusions, 12.5% had ipsilateral brachial
plexus injuries, and 10.7% had ipsilateral subclavian, axillary, or brachial artery injury ( 15). Hospital admission is
probably warranted, even in isolated scapular fracture, to evaluate for delayed pneumothorax or pulmonary injury.
Because of the muscular encasement around the scapula, fractures usually heal without difficulty or permanent disability.
However, severely comminuted neck and glenoid fractures occasionally require open reduction with internal fixation. An
early program of range-of-motion exercises is essential in all patients with scapular fractures ( 16).
STERNAL FRACTURES
The majority of sternal fractures occur secondary to motor vehicle accidents, usually related to impact on the steering
wheel and possibly related to seat belt use. Much less commonly, the injury occurs after falls on direct blows to the chest.
Once regarded as another sentinel injury suggesting possible myocardial contusion or aortic rupture, isolated sternal
fracture was, in part, an indication for admission to a monitored unit and aortography. In recent studies, evidence is
accumulating to show that there is no statistically significant increase in aortic rib or myocardial contusion in isolated
sternal fracture (17,18). As in the case of isolated first rib fracture, other findings of aortic rib must be present to lead to
further diagnostic workup of that serious injury. Most sternal fractures are nondisplaced and require no therapy. The most
common sites of fracture are at the junction of the body and manubrium and through the body. Occasionally, open
reduction and internal fixation are required.
COSTOCHONDRAL INJURIES/INTERCOSTAL MUSCLE STRAINS
Separation of the costochondral or sternochondral articulations is quite common, even with relatively minor trauma to the
chest. Pain, which can be severe, may be localized or radiating along the intercostal nerve distribution. Physical
examination may reveal increased mobility or point tenderness over the involved articulation. Chest films are not usually
helpful in the diagnosis because of the radiolucency of the costal cartilages. Initial management is conservative, with rest
and application of local heat being the mainstays of treatment. If pain is persistent, instillation of local anesthetics or
intercostal nerve block can be performed. In particularly severe cases, surgical resection of the involved cartilage may be
necessary (13).
Direct injury and overuse strain of the chest wall muscles are common. Intercostal muscle pain is usually pleuritic in
nature: Exacerbation occurs with deep breathing, coughing, and sneezing. The pain is typically localized and sharp in
quality. Lateral and anterior compression of the chest wall generally does not worsen the pain, which distinguishes it from
pain associated with rib contusion and fracture. The accessory thoracic muscles such as the pectoralis muscles, teres
major, and latissimus dorsi may sustain direct trauma but more commonly are injured with overuse. There may be mild
tenderness on examination. Movement and tensing of the affected muscle worsens the pain and there is no pleuritic
quality. Therapy of all of these muscle strains consists of rest and antiinflammatory medications ( 19,20).
CLAVICULAR INJURIES
Clavicular fractures are common and can occur from either a direct blow to the clavicle or a lateral blow to the shoulders.
Approximately 80% of these occur in the middle third of the bone. Most heal without difficulty with a figure-of-eight
dressing and immobilization. Occasionally, fractures with widely displaced fragments require operative repair. Also,
fragments of bone, especially in the distal third of the bone, may impinge on the subclavian vessels. Rare late side
effects of callus formation include thoracic outlet obstruction with neurologic or vascular symptoms ( 21,22).
Sternoclavicular dislocation is relatively unusual secondary to the strong ligamentous support of the joint. Anterior
dislocation is much more common than posterior displacement. Either can occur from a lateral compression force applied
to the shoulders. Posterior dislocation can occur from direct force and rarely results in injury to the underlying trachea
and great vessels. The reduction can usually be performed with a closed technique and local anesthesia, although
reduction of posterior dislocations may be performed more easily under general anesthesia.
TRAUMATIC ASPHYXIA
A characteristic clinical syndrome of cyanotic discoloration of the neck and face with petechiae and subconjunctival
hemorrhage can occur when a large force is applied to the chest. The cause of the cutaneous changes is thought to be
reversal of blood flow through the valveless superior vena cava and jugular veins. Besides the constriction of the chest,
an essential element in the pathophysiology of the syndrome appears to be closure of the glottis during full inspiration at
the time of injury. Other than the rare occurrence of prolonged coma secondary to anoxia, long-term neurologic sequelae
do not appear to be significant ( 23). However, the underlying pulmonary and chest wall injury may be substantial ( 24).
Recognition of the dramatic but benign cutaneous signs should alert the clinician that a careful evaluation for more
serious associated injuries is necessary.
PNEUMOTHORAX
A pneumothorax results when the normally negative intrathoracic pressure is changed through the disruption of the
pleura and air enters the pleural space. This can occur either with penetrating trauma with direct parenchymal injury and
air leak or with blunt injuries. In the case of blunt injuries, pneumothorax can result either from direct impact or from a
fragment of fractured rib lacerating the lung.
Although the three types of pneumothorax (namely, tension, open, and simple) require a tube thoracostomy, the initial
approach varies somewhat. By far the most potentially lethal type is a tension pneumothorax, in which a flap valve
mechanism allows the accumulation of inspired air in the pleural space without allowing its escape. This can eventually
lead to mediastinal compression, hemodynamic compromise, and eventual death if it is not corrected. Prompt recognition
of the physical signs of tension pneumothorax—absent or diminished breath sounds with possible shift of the trachea to
the contralateral side, and especially if hypotension is present—should be followed by immediate decompression of the
pneumothorax. If tube thoracostomy is not possible at that time, adequate initial treatment can be achieved even with
placement of an intravenous catheter in the thorax. A general recommendation is insertion of a 14-gauge catheter into
the second intercostal space in the midclavicular line. A rush of air can sometimes be evident but not always. There is
usually rapid improvement in vital signs if the pneumothorax was the major cause of the compromise. This is followed by
placement of a tube thoracostomy as soon as it is feasible. Additional diagnostic evaluation may require bronchoscopy if
there is persistent large air leak. This is rarely from major tracheobronchial laceration or rupture.
An open pneumothorax occurs when there is a communication between the pleural cavity and the outside. If the opening
is greater than two-thirds the diameter of the trachea, air will begin to flow preferentially through the chest wall defect
rather than the trachea. To prevent ventilatory compromise, the wound should be covered and the covering secured on
three sides, with eventual placement of a chest tube at a site away from the wound. If a fully occlusive dressing is placed
on the wound, a chest tube must be inserted promptly to avoid creation of a tension pneumothorax ( Fig. 59.2).
FIGURE 59.2. Schematic representation of technique for insertion of a chest tube. 1, Proper location in the fifth
intercostal space, anterior axillary line. 2, Careful blunt dissection and penetration of the pleura with clamp. 3, Spreading
of intercostal tissues with clamp. 4, Digital dilatation of tube tract and exploration of pleural cavity. 5, Insertion of tube
with clamp. Use of a trocar is not recommended. (From Baker JL. Management of thoracic trauma by the emergency
physician. In: Turney SZ, Rodriguez A, Cowley RA, eds. Management of cardiothoracic trauma. Baltimore: Williams &
Wilkins, 1991:21, with permission.)
A simple pneumothorax, unless it is small and a reliable follow-up is possible, also requires a tube thoracostomy.
However, this usually can be done with less urgency than in the previous two types of pneumothorax. The placement of
chest tube for evacuation of air or fluid, or both, is now recommended in the fourth or fifth intercostal space in the anterior
axillary line, posterior to the border of the pectoralis major muscle. Previous recommendations to use the second
intercostal space in the midclavicular line has been abandoned because of the need for dissection through the pectoralis
major muscle and the lack of real benefit of using this position.
When there is a strong suggestion of the presence of a pneumothorax, such as when subcutaneous or mediastinal
emphysema is present, but none can be detected on chest film, there are some instances in which insertions of a
prophylactic chest tube is warranted. If the patient will not be followed reliably for a while, such as during transport to
another facility and during an operative procedure, or if the patient will be maintained on positive pressure ventilation, the
presence of the chest tube protects against the development of a tension pneumothorax.
HEMOTHORAX
Hemothorax may result from injury to the great vessels, the bronchial circulation, the lung parenchyma, or the intercostal
vessels. Accumulations greater than approximately 300 mL can be detected on chest x-ray study. All pleural fluid
collections in the acute trauma setting should be drained with a large-bore (at least 36 French) chest tube placed in the
fifth intercostal space. This is usually the only treatment needed: Bleeding resolves spontaneously, especially if the injury
is the low-pressure pulmonary vessels (25). However, if initial drainage is greater than 1500 mL, or continues at a rate of
more than 300 mL per hour for 3 consecutive hours, then urgent thoracotomy is usually indicated ( 26).
PULMONARY INJURIES
Blunt trauma to the thorax can result in injury to the lung parenchyma. With the increasing use of chest computed
tomography (CT) in the evaluation of thoracic trauma, several distinct traumatic lung lesions have been described. Lung
lacerations are being recognized more frequently with the use of chest CT ( 27). The injuries may be a result of shearing
energy or a direct tear by a broken rib. These different causes may be clinically significant, because the lacerations
secondary to pure blunt force may have more contused tissue present. This may result in more frequent problems with
hypoxia and infection. Most lung lacerations can be managed simply with placement of the chest tube. Persistent air leak
or bleeding may be an indication for thoracotomy.
Pulmonary hematoma results when the cavity formed by a laceration fills with blood. Radiographically, it can be
distinguished from a contusion by the more distinct margins and greater density of a hematoma. Although hematomas
take longer to resolve than contusions, they have a more benign clinical course, with rarely any effect on pulmonary
function being evident.
Pulmonary contusion is classically diagnosed as a infiltrate developing within the setting of acute trauma ( Fig. 59.3). The
detection on plain chest film must occur within approximately 6 hours of the injury, otherwise atelectasis or aspiration
pneumonia may be the cause of the infiltrate. CT is the more sensitive test with immediate recognition of the injury very
likely (28). The lesion is of great clinical significance. Because of the architectural disruption of the alveoli and the
adjacent microvasculature, the air space becomes filled with cells and fluid, causing shunting and subsequent hypoxia.
There also is atelectasis in associated areas of the lung that are not directly injured.
FIGURE 59.3. A: Chest film from patient with lung contusion. The contusion is seen as a fairly smooth density
peripherally in the right upper lobe. B: CT of the chest from another patient with bilateral lung contusions. Mottled
densities are present throughout both midlung fields.
Considerable controversy has surrounded the treatment of patients with pulmonary contusion. Because of the
derangement in the permeability of the alveolar membrane, it was thought that fluid restriction along with colloid
administration would prevent the severe sequelae of fluid overload ( 11). However, the current consensus is that
euvolemia is the most appropriate goal and that judicious use of crystalloid is not deleterious in these patients. Efforts
have been directed toward identifying a subset of patients in whom prompt intubation and mechanical ventilation are
important. Several criteria have been established, the clearest of which are the following:
1. Hemodynamic instability
2. Hypoxemia: The patient is unable to maintain a Pao 2:FIo2 ratio greater than 350.
3. Hypoventilation: The patient is unable easily to maintain a vital capacity greater than 12 to 14 mL per kg or has
sustained hypercapnia.
If nonmechanical ventilatory management is chosen, aggressive pulmonary therapy and adequate analgesia are
mandatory.
AORTIC DISRUPTION
Blunt traumatic rupture of the thoracic aorta and its major branches is a life-threatening injury seen especially in
high-speed motor vehicle accidents and falls. The hypothesized mechanism primarily involves deceleration (horizontal or
vertical) or crushing chest injuries with some flexion of the spine. At least three factors appear to be present:
1. A relative fixation of one portion of the aorta compared with another, for example, the aortic isthmus just distal to the
origin of the left subclavian artery. Deceleration of the proximal and distal segments occur at unequal rates, causing
a shearing force.
2. Compressive and bending stress on the aorta over the vertebral column.
3. Intraluminal hypertension at the time of injury, causing a burst stress ( 29,30 and 31).
Autopsy studies have shown that most aortic ruptures occur at the isthmus, followed by the distal descending and the
ascending aorta. Very few of the ascending aortic group survive long enough to present to a hospital ( Fig. 59.4). The
patients who do survive to be evaluated do so because of the containment of the hematoma within the fragile aortic
adventitial tissue. As described in the original natural history of this lesion by Parmley et al. ( 32), if the condition is left
untreated, 25% of these survivors will have delayed rupture within 24 hours of presentation and an additional 5% rupture
each day for 2 weeks after initial presentation.
FIGURE 59.4. Hypothetical composite survival curve of untreated blunt traumatic aortic rupture. (From Turney SZ,
Rodriguez A. Injuries to the great thoracic vessels. In: Turney SZ, Rodriguez A, Cowley RA, eds . Management of
cardiothoracic trauma. Baltimore: Williams & Wilkins, 1991:229–260, with permission.)
Diagnosis of aortic disruption often depends on the clinician's high index of suspicion based on mechanism of injury. All
patients who have withstood sufficient deceleration or compressive forces to have possibly caused aortic rupture should
be assumed to have injury until otherwise proven ( Fig. 59.5). An upright chest film may demonstrate some of the many
described radiologic signs suggestive of mediastinal hematoma. Among the most reliable are loss of the normal aortic
knob contour, widening of the mediastinum greater than 8 cm, and shift of the trachea or nasogastric tube to the right.
The diagnosis of aortic rupture is made definitively through aortography. Although there may be a role in the future for
helical CT scanning that can be performed rapidly in this setting, at the current time, it is used as an ancillary study when
the suspicion of the diagnosis is lower. Likewise, transesophageal echocardiography is promising in its level of sensitivity
in the detection of aortic rupture but it is not yet widely implemented. Operative repair is indicated if at all possible,
associated injuries permitting. The use of vasodilators and beta blockers to control blood pressure and aortic wall tension
before surgery should theoretically decrease the risk of rupture ( 33,34).
FIGURE 59.5. Possible forces acting on the aorta that result in blunt traumatic rupture. (Reprinted by permission from
Symbas PN. Cardiothoracic trauma. Philadelphia: WB Saunders, 1990.)
MYOCARDIAL CONTUSION
Blunt injury to the heart, whether secondary to steering column impact in a motor vehicle accident or a severe blow to the
chest during contact sports, is common. The estimated incidence ranges from 10% to 38% in patients with chest trauma
(35,36). One of the great difficulties in clearly defining the incidence is the lack of a precise diagnostic test. Fortunately,
most myocardial contusions do not cause severe clinical manifestations and heal without serious sequelae.
The histopathologic lesion is similar to that found with myocardial infarction, except that the contused tissue contains
more areas of hemorrhage with more myonecrosis. Also, the boundary between normal and injured tissue is more clearly
defined in contusions. The severity of injury can range from epicardial alone to full thickness ( 37).
The most common physical sign of myocardial contusion is sinus tachycardia, although any type of dysrhythmia is
possible. Functional pump disturbance, that is, cardiac failure, is uncommon except in the most severe cases of
contusion. There are no distinctive symptoms of the injury other than nonspecific chest pain, which is not always present
and may easily be a result of noncardiac thoracic injury. All of these factors result in myocardial contusion being a difficult
diagnosis to establish on initial presentation of the patient.
A further complication in the evaluation of myocardial contusion is the lack of a clearly accepted diagnostic test.
Electrocardiography (ECG) is the easiest but is not sensitive or specific: Contusion may not be accompanied by
dysrhythmia, and conversely, rhythm disturbances may be the result of other causes. However, persistent ECG
abnormalities are highly suggestive of contusion and the diagnosis should be pursued ( 29).
Creatine kinase MB band (CK MB) determinations have long been used to detect ischemically infarcted myo-cardium,
and the application was extended to the diagnosis of contused tissue. There has been considerable controversy in the
literature concerning the efficacy of the test, with varying reports of its specificity and sensitivity. However, CK MB serial
determinations remain a screening test in patients suspected of having a myocardial contusion. Cardiac troponin is a
protein found exclusively in the myocardium. Elevation of troponin is a very sensitive indicator of myocardial injury, both
trauma and ischemia induced. Because it is not present in skeletal muscle, increased troponin is also an extremely
specific indicator of cardiac contusion ( 38).
Once the diagnosis is probable, that is, the ECG or CK MB determinations, or both, are positive, more focused
evaluations are warranted. Again, the available tests have proven less than ideal. Radionuclide imaging with
technetium-99 is less accurate than was previously hoped ( 39). Radionuclide angiography (MUGA scan) has also been
proposed, with varying reported results ( 40,41). Perhaps the most useful of the imaging evaluations is echocardiography,
which can provide some indications of functional disturbance of wall motion and values, as well as a measurement of any
pericardial fluid present ( 42). Although transthoracic echocardiography has been the standard modality used, it can have
severe technical limitations in the critically ill trauma patient. Transesophageal echocardiography has been shown to
provide superior images of wall motion abnormalities especially of the commonly injured right ventricle ( 43,44).
Because of the tendency toward dysrhythmias in injured cardiac tissue, once the diagnosis of contusion is established,
cardiac monitoring should be instituted. No clear recommendations for the length of observation have been described,
but it should certainly continue until no acute symptoms are present. Long-term sequelae such as ventricular aneurysms
have been described but are rare.
CARDIAC RUPTURE AND PERICARDIAL TAMPONADE
Severe blunt injury to the chest wall can result in disruption of a free cardiac wall or, less commonly, the intraventricular
septum or valves. Most patients sustaining such an injury die quickly, particularly with free rupture into the pericardium
with tamponade. However, 10% to as many as 30% with lower pressure atrial ruptures may survive long enough to be
treated (45).
Free wall rupture will result in pericardial tamponade if the pericardium is intact, but massive hemothorax with
hypovolemic shock may be the result if there is associated pericardial rupture. Pericardial tamponade, with its
accompanying impaired cardiac filling and low output, has classically been diagnosed by the concurrence of shock,
distended neck veins, and narrowed pulse pressure. Unfortunately, the classic physical signs may not be easy to
appreciate in the setting of acute trauma. If the patient is relatively stable, the measurement of central venous pressure
(CVP) may provide supporting evidence: An elevated CVP in the presence of low systemic blood pressure is presumptive
evidence of cardiac tamponade. However, if shock is profound, CVP may not be elevated. Echocardiography usually is
conclusive diagnostically ( 46), but this requires specialized equipment and trained personnel.
The most direct method of diagnosis is an emergency subxiphoid retrosternal pericardiotomy performed in the operating
room. Free blood in the pericardial cavity confirms the diagnosis. Preliminary pericardial aspiration of even 20 to 50 mL
of blood, using a long subxiphoid needle, may improve hemodynamics temporarily, allowing time to prepare for surgery.
COMMOTIO CORDIS
Sudden death due to chest wall impact during sports activities is termed commotio cordis. This typically occurs in young
athletes struck in the midchest with a baseball or hockey puck or on collision with a fellow sports participant. Impact is
usually of low velocity. Cardiac arrest is immediate. In the rare survivors, cardiopulmonary resuscitation (CPR) was
rapidly instituted in the field ( 47,48). The mechanism of the injury is unclear, but timing of the impact in relation to the
cardiac cycle is probably very important. In animal models, ventricular fibrillation was consistently induced when the
experimental force was applied during the upstroke of the T wave. In this same study, the use of safety baseballs
decreased the incidence of ventricular fibrillation ( 49).
IATROGENIC INJURIES SECONDARY TO CARDIOPULMONARY RESUCITATION
Cardiac arrest can occur during sports activity, whether seen in the increasing proportion of older people engaging in
sports, in the small but definite subset of athletes who abuse arrhythmogenic recreational drugs, or in persons with no
known risk factors. With the prevalence of CPR training programs for the general population, closed cardiac massage is
being started in the field by bystanders more frequently. Although these efforts are laudable, overzealous attempts at
resuscitation (as well as mechanical cardiac resuscitation devices) can result in injury ( 50). Rib fractures, sternal
fractures, aortic rupture, and right ventricular rupture have been reported especially with improper positioning of the
hands on the sternum (they should be centrally located in the lower third of the sternum). The sports clinician should be
aware of the possibility of these injuries occurring during CPR.
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60 The Emotionally Intelligent Sports Medicine Practitioner
60
THE EMOTIONALLY INTELLIGENT SPORTS MEDICINE PRACTITIONER

P. KEVIN ELKO
ROBERT O. BLANC
Goal Setting
Cognitive Skills for Sport
Athletic Competition and Anxiety
Imagery
Cognitive Imagery
The Athlete and Loss
Conclusion
Chapter References
There are unique challenges facing the sports medicine practitioner today. The stakes for the athlete are higher than
ever before. Because of the power of the media, athletic performance on and off the field is under the microscope.
Moreover, the athlete is looking to the sports medicine professional to reengage him or her in competition after an injury
at a quicker rate than has ever been expected before. Therefore, it is the modern day professional that is aware of all
possible treatment modalities in his or her “tool box” to assist the athlete in these challenges.
In this toolbox needs to be a compartment for mental skills to assist the athlete to perform well with conditioning on the
playing field and in the rehabilitation gym. Individuals that address this area of emotions are comprehensive in their
athletic intervention. However, it is an area that is still incomplete in their professional education. In a recent sports
medicine conference for those who work in the National Football League (NFL), a physician that organized the entire
event reiterated to me how he set up an outstanding conference covering every possible area of effective treatment for
an NFL physician. I asked him: “Every?” He reiterated: “Every.” I then asked him what he had organized in the area of the
psychology of performance and rehabilitation and he responded: “I never thought of that.” He then went on to say: “If I
have room I'll give you a call and we can include that area.” It is a sad commentary when something as important as the
mental approach is simply an afterthought. I never got the call.
In a study that assessed the data from interviews of 75 Canadian Olympic athletes in 19 different sports about their
experiences with sport psychology and the teaching of mental techniques to enhance performance 98% of those
interviewed said that more practitioners are needed in the field that could teach these types of mental techniques ( 1).
Yet, even with all of the known benefits of mental training in the athletic arena the sports medicine practitioner
underutilizes these tools. Bruce Ogilvie, a notable sport consultant for such professional teams as the Portland Trail
Blazers and the Los Angeles Lakers, claims that Americans are 25 years behind the Russians and Europeans in the
learning and utilization of performance-enhancing techniques ( 2).
Think of performances on the field and in rehabilitation that you have witnessed. Was the mental approach a factor? Bill
Bates, the longtime Dallas Cowboy and owner of three Super Bowl rings, told me he visualized himself performing every
performance before he performed them. Moreover, a positive mental state, in his opinion, is what returned him from every
injury. It is imperative that a practitioner in the sports medicine field have an idea of what is needed to assist the athletes
he or she works with. These techniques include effective goal setting, using imagery to improve performance, cognitive
strategy for coping and excelling, and assisting the grieving athlete through injury and trauma.
GOAL SETTING
Michael Johnson, the Olympic champion sprinter, had a goal to win the 200- and 400-meter sprints at the 1996 Summer
Olympics in Atlanta. The problem, however, was that the 200- and 400-meter sprints were traditionally run on the same
day. This would have almost made it impossible for him to win because of recovery time.
After setting this goal, Johnson remembered something his father asked him every time he set a goal when he was a
young person. “What are you going to do about it?” and “Now that you have a goal, how are you going to achieve it?”
Johnson developed a workout regimen with his coach that involved specific weight training, stretching, and running
intervals 5 days a week. In addition, he petitioned the Olympic Committee daily to move the 200- and 400-meter sprints
to different days.
There are two kinds of goals: product and process. A product goal is what the athlete is going to achieve, such as, “I will
become an all-conference athlete by next season,” or “I will be completely recovered from ACL surgery by the time the
season starts.” A process goal is what the athlete is planning to do to get the product goal, which means developing a
“prescription for success.” This is a plan that the athletes will follow very closely to hone their work habits and periodically
evaluate themselves. The athlete needs to fall in love, not with what they are trying to accomplish, but with the process of
accomplishing it. All the great ones have a high regard for the process.
Both goals, process and product, need to be very specific ( 3). The athlete needs to develop the discipline of specifically
focusing on exactly what is to be done every time he or she walks into the gym or the practice field. Abstract goals can be
deadly and allow the athlete an “arena for rationalization” of their progress. When goals are specific and measurable,
rationalization gives way to concrete evidence. Also, the measurable specific goal will act as motivation to stay with the
process. Feedback equals motivation, and there is no feedback without measurement.
Additionally, the goal needs to be attainable. One of the major killers of motivation is discouragement. When the athlete
feels that no matter what he or she does, he or she is not going to meet the standard set in his or her mind, the athlete
tends to quit; this is called discouragement. To battle discouragement, first set goals that are attainable. If it is impossible
to be recovered from knee surgery during the course of the same season of surgery, then the athlete is going to be
discouraged if that goal is set. To avoid this discouragement, emphasize process goals as opposed to product goals.
They can almost always achieve the process goal, or the step by step of recovery or peak athletic performance. The
product or results will take care of themselves.
The second way to deal with discouragement is to dispute internal sentences cognitively or one's own thinking when
discouraging thoughts occur. This next section outlines that process.
COGNITIVE SKILLS FOR SPORT
There are three main psychological aspects of mental performance: thoughts, feelings, and behavior. These three are
intertwined and interrelated; changes in one element will often produce changes in another. For example, if an athlete
changes the way he or she thinks about an event, he or she will usually feel differently and often perform differently.
Therefore, the foremost principle to keep in mind is that cognition (the way the athlete chooses to think) is the most
important determinant of emotion and will frequently be the main determinant in how athletes perform. Simply stated, we
feel how we think. Events do not makes us “feel good” or “feel bad”; we do it ourselves. Past or present events contribute
to how we feel but do not directly induce the emotion. Rather our internal events or perceptions and judgments of these
events are more powerful sources of our emotions than the events. In other words, the biggest obstacles athletes face on
the athletic field are the ones they place on themselves.
Chad Scott, a first-round draft pick of the Pittsburgh Steelers, tore his anterior cruciate ligament (ACL) before the 1998
season. When I went to talk to him about it and asked how he was dealing with it he said: “Do you know all I have to be
thankful for?” I said: “No, I don't.” He said: “Do you have a few hours?” He would walk around the training room chanting:
“Chopping down trees.” Meaning every day of rehabilitation he was hitting the tree one more time and eventually the tree
will fall, eventually his knee would be strong. Incidentally the trainers told me he recovered quicker than they would ever
have expected.
If it were events that cause an athlete to feel a certain emotion, then Chad Scott wouldn't have acted this way. He was
starting in his second season, on his way to initiating a great career and living a dream when the unfortunate event
happened. We have all seen athletes in his situation who were depressed, moping around daily, describing how awful it
is that life has dealt to them this card. His feeling and reaction was entirely different simply because his thinking was
different.
The athlete, and especially the injured athlete, often uses ineffective thinking, such as exaggeration (I will never play
again), overgeneralization (my decision on that first play cost us the season), unvalidated assumptions (the coach hates
me because he didn't say hello today), illogic (what is the use anyway), and faulty deductions (I do not have to
rehabilitate, I will be fine). It is often these five notions that are behind half-hearted performances and attempts by the
athletes. These cognitive errors that the athlete internally focuses on will sabotage ACL rehabilitation as well as play-off
performances.
Here, the practitioner needs to suggest to the athlete that his or her belief system is hurting him or her. Ellis ( 4) states
that belief systems come in two forms: irrational and rational. Both rational and irrational beliefs are evaluations of reality,
not descriptions of it. Therefore, irrational statements are not merely thoughts like: “Something might happen during the
game.” They are statements like: “Something might happen. And if it does it is awful and terrible. We will never recover,
and I will be embarrassed.”
According to Ellis, rational beliefs are consistent with reality and degree. They can be supported with evidence and are
empirically verifiable. Therefore, an irrational belief does not follow reality. It will lead with an inaccurate premise or lead
to inaccurate deductions, and it is not supported by evidence, it often represents an over generalization. Irrational beliefs
tend to be extreme evaluative exaggerations of a situation and are often reflected in descriptors such as “awful,”
“terrible,” or “horrible.”
After listening for and hearing the athlete state these types of beliefs, it may be suggested in a gentle way: “Try not to
judge or evaluate. Focus on the task of rehabilitating or performing, but do not label it as awful,” or “One day at a time;
one play at a time; do not look at the score.” It is this thinking that will influence the athlete's performance and recovery.
Get the athlete away from evaluative thoughts and more focused on the process of rehabilitation and performing. You
might even suggest “Chopping down trees.”
Following is an example of an interaction between an athletic trainer and an injured athlete. Here, the trainer is using
cognitive strategies to intervene with the athlete.
Athlete: I am never going to play again. I can't stand this any more.
Trainer: What do you mean?
Athlete: I can't stand it!
Trainer: You mean you do not like it, which is different from I can't stand it.
Athlete: I mean I can't stand it.
Trainer: There is no evidence that you cannot stand it. You will not cease to exist if you have to rehabilitate one more
day. If you tell yourself you cannot stand it, you will begin to believe what is not true. Moreover, that statement to yourself
is not helping you get better.
Athlete: So what can I say to get better?
Trainer: Don't judge, one day at a time. Or how about this one: I will get better over a long period of time all of a sudden.
Athlete: What does that mean?
Trainer: It means every day you are rehabilitating you are getting better even if the results do not show. If you stay on the
process we outlined and don't judge, chances are good you will get better. If you get discouraged you may not. One day
you will get better.
In this scenario, the trainer is trying to affect the athlete's “self-talk” with more motivating self-encouraging internal
dialogue.
ATHLETIC COMPETITION AND ANXIETY
Anxiety is a “transitory state which consists of feelings of apprehension and tension and a heightened activity of the
autonomic nervous system” (5). For an athlete, these manifestations of anxiety can be detrimental to performance.
However, it cannot be assumed that for all athletes the lower the anxiety, the better performance. Hanin ( 6) found that
some athletes perform best at low levels of anxiety, others at moderate levels, and still others at high levels. What is
needed is an individual approach to determine the athlete's best level of anxiety for optimal performance. In other words,
the practitioner that assumes the calmer an athlete is the better, will be just as remiss as the coach that thinks the more
“fired up” the athletes are, the better are the chances of winning.
The causes of heightened anxiety may vary, but most center on some form of the athlete's belief system; thus, even
self-defeating statements can trigger any or all these physical effects of anxiety. Therefore, athletes can reach a level of
optimal arousal by what they tell themselves. For some, they may need to tell themselves strong internal language to
reach a level of anxiety that “fits” their makeup. Others may need to tell themselves less evaluative internal statements to
reach a more relaxed state that historically has assisted them in their best performances. The best way to find out is to
discuss with the athlete past performances and determine where they fit on this anxiety spectrum.
IMAGERY
A physician in New York was one of the first to arrive at a jetliner that just crashed. Many of the passengers were
Colombian, and the doctor did not speak Spanish, so the only thing he understood was the injured passengers yelling
“Doctor.” The passengers had injured limbs that, in many cases, were barely hanging onto their bodies. The doctor went
passenger to passenger, treating whomever he could. Afterward, someone asked him how he dealt with the chaos, the
noise, police, and ambulance sirens and helicopters coming in and out. He responded: “What noise, it was the most quiet
surrounding I have ever been in. All I was aware of was the passengers and could hear and see nothing else. Time
slowed down.” This is a pretty good description of peak athletic performance. However, this mental state is difficult to
attain by chance. Many athletes that perform regularly at optimal levels adhere to practices that assist in reaching this
state.
One of these practices is mental imagery. Imagery is the ability to use all the senses to create or recreate an experience
in the mind. Thus, imagery is a sensory experience that occurs in the mind without environmental props ( 7). This imagery
is sometimes described as mental rehearsal. It is the activity in which the athlete “sees” himself or herself in a particular
environment performing in a desired way. The athlete closes the eyes, relaxes the body, and develops mental images
that produce the desired outcome. In this mental rehearsal, athletes often reproduce the same environment, often
referred to as the “zone,” that the doctor experienced at the crash. They will see their mind as quiet and focused, aware
of nothing other than the task in front of them, as if something has taken over making choices for them.
Imagery is an excellent means to maintain level of performance after injury. When the athlete cannot practice and
compete, he or she can mentally rehearse. This may not be quite as effective as physical practice, but it is effective and
will allow the athlete to return to the desired level quickly. It is something that can be used in rehabilitation, and is very
compatible with rehabilitative exercises. Moreover, imagery can reduce panic-stress images that the athlete often
experiences after an injury. Elimination of these images that cause vasoconstriction will allow normal blood flow to
resume and relax the muscle in the injured area, facilitating healing ( 8). Thus, imagery does not have to be used just for
athletic performance but can also be used to enact the mind-body partnership in the facilitation of the healing process.
The most effective techniques for performing imagery are first to relax, by sitting with your back straight and simply
listening to your breath leaving. As one does this and the mind clears and focuses on the breathing, the athlete develops
a visual scene. Included in this scene is auditory and tactile sense. The colors are as vivid as possible. The task is taking
place in real time. It is occurring in the athlete's mind at the same rate the task occurs in reality. The athlete is not a
camera in the atmosphere taking this picture but is inside his or her body, looking out through the eyes, experiencing this
image. Imagery will best assist the athlete when he or she has a reasonable idea of what these skills look and feel like,
and the motor performance is established. This helps keep an optimal performance planted in the mind to call on later.
This does not all occur the first time the athlete attempts to perform imagery but occurs with better clarity after practice. In
the advanced stages of the skill, athletes are able to develop sensations such as touch, muscular tensions and forces,
and the body's orientation in space. Eventually, the task the athlete is rehearsing is planted in what is called “muscle
memory.” When performing, the athlete will complete the task without much conscious awareness. He or she will tell you
that he or she was not thinking about the performance that just happened. The athlete will state that the body did it, not
the mind.
There are a few key principles to imagery. First, the athlete must visualize performance and outcome. The images need
to be real-game situations. The athlete needs to pay attention to details. This helps provide the mind with environmental
cues to react to. The imagery needs to be felt in the forearms, biceps, quadriceps, and whatever muscles and limbs are
completing the task. (The athlete needs to see the task from inside his or her body, not a big camera in the sky.)
Cognitive Imagery
It is possible for the athlete to imagine thinking differently than he or she already does. When an athlete has routinely
told himself or herself negative or irrational thoughts, these notions become personal truths of the athlete. Therefore,
even though these thoughts are not reality, they are for the person who is thinking them because he or she has thought
this so many times that it has become programmed in the athlete's mind to be the truth. One way to address this problem
is to get the athlete to begin to think differently with imagery.
The athlete simply thinks of the task that he or she is challenged with. This could be performing in front of a large crowd
or even putting in front of a few friends. Then the athlete hears the “self-talk” that he or she usually tells himself or herself
in these situations that causes the athlete to feel shaken: “I am going to miss this putt and look stupid,” or “I am going to
screw up in front of all these people and they are going to laugh at me and it will be awful.” Then, in the imagery, the
athlete feels the uneasy feelings that accompany these types of thoughts, nervousness, anger, or anxiety. Next, the
athlete changes the cognition in the imagery: “See the putt,” “Focus and be aware of the task only.” The problem here is
the nervousness may go away, but the easy feeling does not replace the old emotion. A rather strange emotion may
surface here that Maultsby ( 9) calls cognitive dissonance. The feeling of nervousness or anger is commonplace for the
athlete so when the thoughts are gone that produce the emotion, the practitioner will see that the emotions have been
somewhat programmed as well. An effective technique would then be to image a different, more desired emotion such as
calm or an energized focused positive state.
Following is a script between a doctor and an athlete who was helping him deal with the discomfort of a rehabilitating a
nagging shoulder injury.
Doctor: I want you to close your eyes and sit with your back straight. Place your feet flat on the floor.
Now, listen to your breath leaving and if your mind wonders come back to the calm sound of your breath leaving.
As you are listening to your breath I am going to slowly count from 1 to 10 and as I do let yourself get as relaxed as you
want to get. 1, 2, 3, 4, 5, 6, 7, 8, 9, 10.
Now I want you see yourself exercising your injured shoulder in rehabilitation. As the event of feeling discomfort begins,
listen and imagine hearing your old self-talk: “I can't stand this; it is awful and terrible to feel this way.”
Now, feel the upset feeling you get when you think these types of thoughts. The anxious feelings.
Next, change your self-talk: “Do not judge, keep pushing. The discomfort is helping my body get better.”
Finally, change the emotion. Imagine feeling relaxed and centered as you change the way you think about the process of
healing.
THE ATHLETE AND LOSS
The athlete needs to address loss frequently throughout his or her participation. The loss of physical skills due to injury,
the loss of dreams when the desired outcome is not obtained, the ending of a career of a teammate or themselves, and
even in severe instances, the death of a friend or fellow teammate.
In most research and writing related to the psychological aspects of sport, so-called “normal” psychological processes
have been increasingly overlooked. Athletics do not take place within a vacuum, and participants are not impervious to
factors outside the athletic playing field.
The final focus of this chapter is how to help these athletes when they have experienced these losses. (Such losses
include being involved when an athlete broke his C-4 vertebra and was paralyzed for life, a player was killed by a jealous
boy friend from the past, and the loss of three members of a high school soccer team due to a plane crash. There are
predictable responses when loss occurs.) The severity of the reaction often depends on the severity of the incident and
the mental health of the athlete or athletes. The challenge for the sports medicine practitioner is that athletes are less
likely to seek psychological assistance ( 10,11) and tend to exhibit severe psychopathology by the time they are
diagnosed with psychological difficulties ( 12).
Many different emotions are observed when an athlete is grieving a loss: shock, disbelief, anger, rage, helplessness,
sadness, and anxiety. Often, the athletes will become very detached. They often will have an inability to concentrate.
This is one factor the sports medicine practitioner needs to be aware of because it is a time an athlete can become
injured owing to decreased focus. Frequently after a loss, ranging from an ACL injury to the death of a family member,
the athlete can experience a loss of control, fearing the recurrence of the incident.
Physically, the athlete may experience fatigue, nightmares, hyperarousal, startle response, and psychosomatic
complaints. There are often abnormalities in sleep patterns, and the athlete frequently spends less total time sleeping.
While grieving, in relationships there is often an acting out of anger that is displaced from the incident that is happening.
Frequently, athletes can have aggressive interactions, displaying anger toward loved ones that is confusing. With an
unenlightened significant other, it can escalate to catastrophic levels.
The role of the sports medicine practitioner during these incidences is understanding and education. The understanding
is that the most normal people become abnormal when these losses occur. It is comforting to educate the athlete of this
factor as well as the coaches. The coaches are often scared and confused themselves, and can find comfort in the notion
they are “not crazy.” The fact of the matter is they are crazy at the time. But those who enter into the incident mentally
healthy process the event and leave it in the same condition.
Here, it pays to become a good listener. The sports medicine practitioner needs to divorce himself or herself from the
erroneous notion that practitioners can fix everything. They cannot. But the healing is often in the athlete being
understood and able to say how he or she feels without being judged. It is important to leave the interaction feeling cared
for. And this requires real skill, not flippant advice giving. Patience is needed to listen at the athlete with the goal of not
fixing but completely understanding what the grieving athlete is saying to you, which is impossible to do completely
unless you have experienced the exact same incident ( 13). If you have been through something similar, then it may be
wise to share some of what you experienced and how you got through it. But advise sparingly.
Know when to refer the athlete to a mental health counselor. If there are any severe emotions or behavior, advise the
athlete to get additional help. Refer him or her to a counselor that you are familiar with professionally. This is especially
true if the athlete has any thoughts of hurting himself or herself, or another. Be conservative here. If you have doubts as
to whether to refer or not, refer. Let the mental health professional decide if the athlete needs more assistance.
Exercising caution is a good practice here.
Finally, follow the same practice for yourself. When I have been asked to intervene in these cases, it has always been
the doctors and athletic trainers who have taken care of everyone else but have been omitted from the circle of care
themselves. You may need a good listener yourself as well as simply need a good counselor to debrief from what you
have been through.
CONCLUSION
In sports medicine, many are aware of the latest techniques when it comes to treating injuries. Most are current. But how
many work on being as good as they can be in the way they interact with the athletes. If you do not work on this area, you
can be better. The ones, in every field, that are among the elite are emotionally intelligent. They do not just practice the
science of medicine but include the art. In their practice, they have not forgotten one important thing—the athlete.
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CONTRIBUTING AUTHORS
Marlene Adrian, M.D. Pike Creek Sports Medicine Center, Wilmington, Delaware
Answorth A. Allen, M.D. The Hospital for Special Surgery, New York, New York
Maria Apreleva, Ph.D. Research Fellow, Orthopedic Biomechanics Laboratory, Harvard Medical School; and
Post-Doctoral Fellow, Orthopedic Biomechanics Laboratory, Beth Israel Deaconess Medical Center, Boston,
Massachusetts
Thomas D. Armsey II, M.D. Assistant Professor, Departments of Family Practice and Orthopaedics, University of
Kentucky, Lexington, Kentucky
Timothy A. Barker, M.D. Primary Care Sports Medicine Fellow, University of Pittsburgh Medical Center, St. Margaret
Hospital, Pittsburgh, Pennsylvania
Gloria M. Beim, M.D. President, Alpine Orthopaedics; and Chief, Medical Staff, Gunnison Valley Hospital, Gunnison,
Colorado
Craig Bennett, M.D. Assistant Professor, Department of Orthopaedic Surgery, University of Pittsburgh, Center for Sports
Medicine, Pittsburgh, Pennsylvania
Wilma F. Bergfeld, M.D. Professor, Department of Dermatology, The Cleveland Clinic Foundation, Cleveland, Ohio
Robert O. Blanc, M.S., A.T.C. Head Athletic Trainer, Sports Medicine Program, University of Pittsburgh, Pittsburgh,
Pennsylvania
Delmas J. Bolin, M.D. Clinical Instructor, Department of Family Medicine, University of Pittsburgh School of Medicine;
and Assistant Director, Primary Care Sports Medicine Fellowship, University of Pennsylvania Medical Center, St.
Margaret's Hospital, Pittsburgh, Pennsylvania
Paul A. Borsa, Ph.D., A.T.C. Assistant Professor, Department of Kinesiology, University of Michigan, Ann Arbor,
Michigan
James P. Bradley, M.D. Clinical Associate Professor, Department of Orthopaedic Surgery, University of Pennsylvania
Medical Center Health System; and Orthopaedic Surgeon, Department of Surgery, Shadyside Hospital, Pittsburgh,
Pennsylvania
Joseph A. Brosky, Jr. P.T., S.C.S., M.S. Assistant Professor, Department of Allied Health, Carroll College, Waukesha,
Wisconsin
Nancy Burke Reston, Virginia
Robert T. Burks, M.D. Professor, Department of Orthopedic Surgery, University of Utah, Salt Lake City, Utah
Neil A. Busis, M.D. Assistant Professor, Department of Neurology, Shadyside Hospital, Pittsburgh, Pennsylvania
David N.M. Caborn, M.D. Associate Professor, Department of Surgery, University of Kentucky; and Medical Director of
Sports Medicine, Department of Surgery, University of Kentucky Medical Center, Lexington, Kentucky
Peter J. Carek, M.D. Associate Professor, Department of Family Medicine, Medical University of South Carolina,
Charleston, South Carolina
Richard L. Carter, M.D. Assistant Professor, Department of Neurological Surgery, University of Miami, Miami, Florida
Claire Chase, M.D. Community Hospital at Dobbs Ferry, Dobbs Ferry, New York
Jerome V. Ciullo, M.D. Detroit Medical Center, Sports Medicine Center of Metro Detroit, Troy, Michigan
Jeremy R. Ciullo Sports Medicine Center of Metro Detroit, Troy, Michigan
Kevin M. Conley, M.S., A.T.C. Coordinator, Undergraduate Athletic Education, Department of Athletics, University of
Pittsburgh, Pittsburgh, Pennsylvania
Stephen F. Conti, M.D. Chief, Division of Foot and Ankle Surgery, Department of Orthopaedic Surgery, University of
Thomas Crisp, M.B.B.S. Department of Sports Medicine, The London Hospital Medical College; and Sport Injury Clinic,
The Royal London Hospital, London, England
Robert G. Devenyi, M.D., F.R.C.S.C., F.A.C.S. Team Ophthalmologist, Toronto Mapleleafs, National Hockey League;
and Director, Retinal Service, The University Health Network, University of Toronto, Toronto, Ontario, Canada
Russell D. Dumire, M.D. Staff Surgeon, Department of Surgery, Joint Trauma Training Center, Ben Traub Hospital,
Houston, Texas; and Assistant Professor, Department of Surgery, Uniformed Services University of the Health Sciences,
Bethesda, Maryland
P. Kevin Elko, Ph.D. Adjunct Professor, Sports Medicine Fellows, University of Pittsburgh School of Medicine and
Marshall University, McDonald, Pennsylvania
Mark Ferguson, M.B., Ch.B. Consultant, Department of Orthopaedics, University of the Witwatersrand, Johannesburg,
South Africa; and Staff, Centre for Sports Medicine, Rosebank Clinic, Johannesburg, South Africa
Richard T. Ferro, M.D., C.A.Q.S.M. Associate Professor, Department of Community and Family Medicine; Director, Duke
Primary Care Sports Medicine Fellowship; and Head Medical Team Physician, Duke University Medical Center, Durham,
North Carolina
Joseph F. Fetto, M.D. Associate Professor, Department of Orthopaedic Surgery, New York University Medical Center,
New York, New York
Peter J. Fowler, M.D., F.R.C.S. Fowler-Kennedy Sports Medicine Clinic, University of Western Ontario, London, Ontario,
Canada
Freddie H. Fu, M.D. David Silver Professor and Chairman, Department of Orthopaedic Surgery, Head Team Physician,
University of Pittsburgh, Pittsburgh, Pennsylvania
William E. Garrett, Jr., M.D. Chairman, Department of Orthopedics, University of North Carolina School of Medicine,
Chapel Hill, North Carolina
Wayne K. Gersoff, M.D. Department of Orthopaedics, University of Colorado Health Sciences Center, Denver, Colorado
Steven Goldstein, M.D. Associate Professor, Department of Neurology, University of Pittsburgh School of Medicine; and
Associate Professor, Department of Neurology, University of Pittsburgh Medical Center Stroke Institute, Pittsburgh,
Pennsylvania
Noelle Grace, M.D. Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania
Patrick E. Greis, M.D. Assistant Professor, Department of Orthopaedic Surgery, University of Utah, Salt Lake City, Utah
Larry Grollman, M.B.A., A.T.C. Director, Department of Sports Medicine, University of Pennsylvania Medical Center
Health System, Pittsburgh, Pennsylvania
Lyndon B. Gross, M.D., Ph.D. Assistant Professor, Department of Orthopaedic Surgery, St. Louis University; and
Orthopaedic Surgeon, Orthopedic and Sports Medicine, Incorporated, St. Louis, Missouri
Christopher D. Harner, M.D. Professor, Department of Orthopaedic Surgery, University of Pittsburgh Physicians; and
Medical Director, University of Pittsburgh Medical Center / Center for Sports Medicine, Pittsburgh, Pennsylvania
Laurence D. Higgins, M.D. Assistant Professor, Department of Surgery, Duke University Medical Center, Durham, North
Carolina
W. Douglas B. Hiller Lucy Henriques Medical Center, Kamuela, Hawaii
Richard Y. Hinton, M.D. Union Memorial Orthopaedics, Baltimore, Maryland
Henry H.P. Ho M.B., Ch.B., F.R.C.S. Senior Medical Officer, Department of Orthopaedics and Traumatology, Queen
Elizabeth Hospital, Kowloon, Hong Kong
Stacey C. Inglis Department of Athletics, University of Pittsburgh, Pittsburgh, Pennsylvania
Mary Lloyd Ireland, M.D. Kentucky Sports Medicine, Lexington, Kentucky
James J. Irrgang, M.S., A.T., P.T. Assistant Professor, Vice Chairman, Department of Physical Therapy, University of
Rebecca Jaffe, M.D., F.A.C.S.M., FAAFP Instructor, Department of Family and Community Medicine, Thomas Jefferson
University Medical School, Philadelphia, Pennsylvania
David M. Jenkinson, D.O. Department of Orthopaedic Surgery, University of Pittsburgh Physicians; and Primary Care
Sports Medicine, Center for Sports Medicine, Pittsburgh, Pennsylvania
Sarah W. Jenkinson University of Pennsylvania Medical Center, Center for Sports Medicine, Pittsburgh, Pennsylvania
Deryk G. Jones, M.D. Assistant Professor, Department of Orthopaedic Surgery, Tulane University Medical School; and
Staff, Department of Orthopaedic Surgery, Tulane Medical Center, New Orleans, Louisiana
Ruth Kamenski, M.S., P.T., O.C.S. Physical Therapist, Department of Physical Therapy, Ohio Valley General Hospital,
McKees Rocks, Pennsylvania
John B. King, M.B.B.S, F.R.C.S. Director, Department of Sports Medicine; Senior Lecturer, Department of Orthopaedic
and Trauma Surgery, The London Hospital Medical College; and Orthopaedic Surgeon, Royal London Hospital, London,
England
John J. Klimkeweicz, M.D. Chief, Department of Orthopaedic Surgery, Georgetown University Medical Center,
Washington, DC
Mark A. Knaub, M.D. Resident, Department of Orthopaedic Surgery, University of Pittsburgh; and Department of
Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
Julie M. Knowles, E.D.D., A.T.C., P.T. Pike Creek Sports Medicine Center, Wilmington, Delaware
Robert E. Leach, M.D. Professor, Department of Orthopaedics, Boston University Medical School, Boston,
Massachusetts; and Editor-in-Chief, American Journal of Sports Medicine, Waltham, Massachusetts
Wayne B. Leadbetter, M.D. Adjunct Professor, Department of Surgery, Uniformed Services University of the Health
Sciences, Bethesda, Maryland; and Department of Orthopedic Surgery, Shady Grove Adventist Hospital, Rockville,
Maryland
Scott M. Lephart, Ph.D. Director, Neuromuscular Research Laboratory, Center for Sports Medicine, University of
Pennsylvania Medical Center Health System, Pittsburgh, Pennsylvania
John C. Linz, M.D. Director, Division of Foot and Ankle Surgery, Department of Orthopaedic Surgery, University of
Cincinnati, Cincinnati, Ohio
John H. Lohnes, M.D. Department of Orthopedics, University of North Carolina, School of Medicine, Chapel Hill, North
Carolina
Donald W. Marion, M.D. Professor, Department of Neurological Surgery, University of Pittsburgh; and Interim Chief,
Department of Neurosurgery, University of Pennsylvania Medical Center-Presbyterian, Pittsburgh, Pennsylvania
Leslie S. Matthews, M.D. Union Memorial Hospital, Baltimore, Maryland
Thomas K. Miller Associate Professor, Department of Orthopaedic Surgery, University of Virginia; and Roanoke
Orthopaedic Center, Roanoke, Virginia
James D. Mills, M.D., F.A.C.C. Associate Director, Cardiovascular Services, Department of Medicine, York Hospital,
York, Pennsylvania
Jeffrey Minkoff, M.D. Chairman, Department of Orthopaedics, Cleveland Clinic Florida, Fort Lauderdale, Florida
Raymond R. Monto, M.D. Department of Orthopaedic Surgery, Martha's Vineyard Hospital, Oak Bluffs, Massachusetts
Morey S. Moreland, M.D. Professor, Department of Orthopaedics, University of Pittsburgh School of Medicine; and
William and Jean Donaldson Professor, Department of Pediatric Orthopaedic Surgery, Children's Hospital of Pittsburgh,
Matthew J. Morelli, M.S., A.T.C. UPMC Center for Sports Medicine, Pittsburgh, Pennsylvania
H. Andrew Motz, M.D. Instructor, Department of Orthopaedics, University of Colorado Health Sciences Center, Denver,
Colorado
David L. Muller Departments of Orthopaedics, Sports Medicine and Arthroscopy, Karolinska Hospital, Stockholm,
Sweden
Mark C. Mysnyk, M.D. Assistant Clinical Professor, Department of Orthopaedic Surgery, University of Iowa School of
Medicine, Iowa City, Iowa
Kathleen M.J. Nachazel, A.T.C. Athletic Training Coordinator, Department of Sports Medicine, University of
Pennsylvania Medical Center, Pittsburgh, Pennsylvania
Thomas C. Namey, M.D., F.A.C.P., F.A.A.S.P. Professor of Medicine, Nutrition, and Exercise Science, University of
Tennessee, Knoxville; and Chief, Section of Sports Medicine, University of Tennessee Graduate School of Medicine,
Knoxville, Tennessee
Ronald A. Navarro, M.D. Assistant Clinical Professor, Department of Orthopaedics, Harbor General—UCLA Medical
Center, Torrance, California; and Director, Orthopaedic Sports Medicine, Department of Orthopaedic Surgery, Kaiser
Foundation Hospital, Harbor City, California
Clive Noble, M.B., B.ch., F.C.S. Centre for Sports Medicine, Rosebank Clinic, Johannesburg, South Africa
John A. Nyland, M.D. Associate Professor, School of Physical Therapy, University of South Florida, Tampa, Florida
Kevin O'Toole, M.D. Department of Emergency Medicine, University of Pennsylvania Medical Center, Pittsburgh,
Pennsylvania
Mary L. O'Toole, Ph.D., F.A.C.S.M. Professor and Director, Women's Exercise Research Laboratory; and, Departments
of Obstetrics, Gynecology, and Women's Health, St. Louis University, St. Louis, Missouri
Susan M. Ott, D.O. Surgeon, Departments of Orthopedics and Sports Medicine, Guthrie Clinic, Sayre, Pennsylvania
Robert C. Pashby, M.D. Assistant Professor, Department of Ophthalmology, University of Toronto; and Chief,
Oculoplastic Service, Department of Ophthalmology, Hospital for Sick Children, Don Mills, Ontario, Canada
Thomas J. Pashby, M.D. (Retired) Professor, Department of Ophthalmology, University of Toronto, Toronto, Ontario,
Canada
Andrew B. Peitzman, M.D. Professor and Chief, Department of General Surgery, University of Pittsburgh; and Director,
Trauma and Surgical Critical Care, Department of General Surgery, Presbyterian University Hospital, Pittsburgh,
Pennsylvania
John J. Perry, M.D. Orthopedic Surgeon, Department of Orthopedic Surgery, Duke University Medical Center, Durham,
North Carolina; and Head, Department of Orthopedic Surgery, Mammoth Hospital, Mammoth Lakes, California
Russell S. Petrie, M.D. Staff, Department of Orthopedic Surgery, Hoag Memorial Hospital, Newport Beach, California
David J. Pezzullo, M.S., P.T., S.C.S., A.T.C. Assistant Professor, Department of Physical Therapy, University of
Pittsburgh; and Facility Director, Department of Physical Therapy, Centers for Rehabilitation Services, Pittsburgh,
Pennsylvania
Per A.F.H. Renstrom Departments of Orthopaedics, Sports Medicine, and Arthroscopy, Karolinska Hospital, Stockholm,
Sweden
Arlene S. Rogachefsky, M.D. Clinical Associate, Department of Dermatology, The Mount Sinai Medical Center, New
York, New York; and Skin Laser and Surgery Specialists of New York and New Jersey, Westwood, New Jersey
Ronald Roth, M.D. Associate Professor, Department of Emergency Medicine, University of Pittsburgh; and Chief,
Emergency Medicine, University of Pittsburgh Health System, Pittsburgh, Pennsylvania
Marc R. Safran, M.D. Codirector of Sports Medicine, Associate Professor, Department of Orthopaedic Surgery,
University of California, San Francisco, California
Karl A. Salesi Coordinator, Athletic Trainer, Department of Athletics, University of Pittsburgh, Pittsburgh, Pennsylvania
Julia (Chuan-Hsiu Liu) Shaw, M.S. Physical Therapist, Center for Sports Medicine, Pittsburgh, Pennsylvania
Ian Shrier, M.D. Jewish General Hospital, Herzl Family Practice Centre, Montreal, Quebec, Canada
Mark B. Silbey, M.D. Bradenton Orthopaedic Associates, Bradenton, Florida
Barry G. Simonson, M.D. Attending Physician, Department of Orthopaedic Surgery, North Shore University Hospital,
Manhassett, New York
Dan M. Somogyi, M.D. Primary Care Sports Medicine, University of Pennsylvania Medical Center, Pittsburgh,
Pennsylvania
Steven Stecker, M.D. Associate Staff, Department of Orthopaedic Surgery, Cleveland Clinic Florida, Fort Lauderdale,
Florida
David A. Stone, M.D. Assistant Professor, Departments of Orthopaedic Surgery and Family Practice, University of
Kathleen A. Swanik, Ph.D., A.T.C. Assistant Professor, Department of Kinesiology, Temple University, Philadelphia,
Pennsylvania
James S. Taylor, M.D. Cleveland Clinic Foundation, Cleveland, Ohio
Matthew M. Tomaino, M.D. Associate Professor, Department of Orthopaedic Surgery, University of Pittsburgh Health
System, Pittsburgh, Pennsylvania
Thomas H. Trojian, M.D. Department of Sports Medicine, University of Connecticut, Storrs, Connecticut
Stephen Z. Turney, M.D., F.A.C.S. Maryland Institute of Emergency Medical Service, University School of Medicine,
College Park, Maryland (retired)
Gerard P. Varlotta, D.O. Clinical Associate Professor, Director of Sports Rehabilitation, Department of Rehabilitation
Medicine, New York University School of Medicine, Rusk Institute, New York, New York
Vincent Verdile, M.D., F.A.C.E.P. Professor and Chair, Department of Emergency Medicine, Albany College; and
Emergency Physician, Department of Emergency, Albany Medical Center Hospital, Albany, New York
Robert L. Waltrip, M.D. Chief Resident, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh,
Pennsylvania
Robert G. Watkins, M.D. Professor, Department of Orthopedics, University of Southern California; and Director, Spine
Surgery, University of Southern California University Hospital, Los Angeles, California
Robert G. Watkins IV, M.D. Professor, Department of Orthopedics, University of Southern California, Los Angeles,
California
Lawrence R. Wechsler, M.D. Professor, Department of Neurology, University of Pittsburgh; and Director, Department of
Neurology, University of Pittsburgh Medical Center Stroke Institute, Pittsburgh, Pennsylvania
Jeffery R. Weiss, M.S., P.T., A.T.C. Director of Rehabilitation, Allegheny Valley Hospital, Natrona Heights, Pennsylvania
Jennifer B. White, M.D. Department of Athletics, University of Pittsburgh, Pittsburgh, Pennsylvania
James R. Williams, M.D. Resident, Department of Orthopaedic Surgery, University of Pittsburgh Physicians, Pittsburgh,
Pennsylvania
Lytton A. Williams, M.D. Assistant Professor, Department of Clinical Orthopedic Surgery, University of Southern
California, Los Angeles, California
Savio L.-Y. Woo, Ph.D., D.Sc. Ferguson Professor, Department of Orthopaedic Surgery; Director, Musculoskeletal
Research Center, University of Pittsburgh, Pittsburgh, Pennsylvania

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Sports Injuries - Mechanisms, Prevention and Treatment 2nd Ed - F. Fu, D. Stone Lippincott 1994) WW

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Sports Injuries: Mechanisms, Prevention, Treatment 2nd edition (December 1994): by Freddie H.

SECTION 1: EVALUATION, TRAINING, AND SPECIAL CONCERNS

1 Customizing the Preparticipation Evaluation

2 Conditioning and Training

3 The Athletic Trainer

4 Environmental Factors in Athletic Performance

5 Biomechanics of Ligaments in Sports Medicine

8 Cardiovascular Evaluation of the Athlete

9 Ergogenic Drug Use in Sports

10 Special Concerns of the Pediatric Athlete

11 The Aging Athlete

12 Special Concerns of the Female Athlete

SECTION 2: SPORT-SPECIFIC INJURIES

21 Emergency Medical Care at Sports Events

28 Skating: Figure, Speed, Long-Distance, and In-Line

29 Judo and Karate

30 Canoeing and Kayaking

32 Nordic and Alpine Skiing

33 Power Lifting, Weight Lifting, and Bodybuilding

41 Track and Field

SECTION 3: MANAGEMENT AND TREATMENT OF SYSTEMIC AND REGIONAL INJURIES

46 Soft Tissue Athletic Injury

50 Treatment of Sports Eye Injuries

51 Cervical Spine and Spinal Cord Injuries

52 Lumbar Spine Injuries in Athletes

55 Hand and Wrist Injuries

57 Foot and Ankle Injuries

60 The Emotionally Intelligent Sports Medicine Practitioner

FREDDIE H. FU, M.D.

DAVID A. STONE, M.D.

Sports Injuries: Mechanisms, Prevention, Treatment

CUSTOMIZING THE PREPARTICIPATION EVALUATION

Purpose of the Preparticipation Evaluation

TABLE 1.1. OBJECTIVES OF THE PREPARTICIPATION EVALUATION ORGANIZED BY TYPE OF PREVENTION

TABLE 1.2. ADDITIONAL OBJECTIVES OF THE PREPARTICIPATION EVALUATIONa

TABLE 1.4. ABILITY OF PREPARTICIPATION EVALUATION FORMATS TO ACHIEVE DESIRED OBJECTIVESa

Timing and Frequency

Who Should Conduct the Examination?

COMPONENTS OF THE EVALUATION

TABLE 1.5. OBJECTIVES FULFILLED BY PREPARTICIPATION EVALUATION HISTORY QUESTIONS, DIVIDED BY

TABLE 1.8. POTENTIAL BIOMECHANICAL FACTORS CONTRIBUTING TO INJURY

TABLE 1.9. SPORTSPECIFIC MUSCULOSKELETAL INJURIESa

TABLE 1.11. DIAGNOSTIC CRITERIA FOR MARFAN SYNDROMEa

Hemoglobin and Ferritin

Electrocardiography and Echocardiography

APPENDIX A. OVERVIEW OF ALL STUDIES THAT SPECIFICALLY EVALUATED THE ENTIRE

Author N Athlete Methods Results

Goldberg et 701 High Station 80% identified by history, no details given

Author N Athlete Methods Results

APPENDIX B. MEDICAL CONDITIONS AND SPORTS PARTICIPATION

Sports Injuries: Mechanisms, Prevention, Treatment

CONDITIONING AND TRAINING

Conditioning of the Athlete

CONDITIONING OF THE ATHLETE

Measurement of Body Composition

Alternative Methods of Assessing Body Composition

Physiology of Strength Training

Adaptations to Strength Training

Modes of Strength Training

TABLE 2.1. DELORME'S PROGRAM

TABLE 2.2. SANDERS' MODIFIED PROGRAM

TABLE 2.3. KNIGHT'S DAILY ADJUSTED PROGRESSIVE RESISTANCE EXERCISE PROGRAM

Circuit Resistance Training

Measurement of Muscular Strength, Power, and Endurance