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ILLUSTRATED ORTHOPEDIC PHY SICAL ASSE SSMENT. Third Edition ISBN: 978-0-323-04532-2
Copyright © 2009, 2001 by Mosby, Inc., an affiliate of Elsevier Inc.

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to determine the best treatment and method of application for the patient.

The Publisher

ISBN: 978-0-323-04532-2

Vice Presidel1l and Publisher: Linda Duncan


Senior Acquisitions Editor: Kcllie F. White
Senior Developmental Editor: Jennifer Watrous
Associate Developmental Editor: Kelly Milford
Publishing Services Manager: Julie Eddy
Senior Project Manager: Andrea Campbell
Designers: Renee Duenow, Jessica Williams

Working together to grow


libraries in developing countries
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ELSEVIER �?��,��� SaiJre t-llunddtion
DEDICATION

For Linda,

Inspiration Everlasting

For

PiS, VR, iG, KB, MAB, CG, LA, CR, KR, DR, RM , RS, iC, PS, MLP, DRG NIR , ,

is, MF, RH, MRN, SAA, EIW, MAN, LLS, FLvw, RMS MRA, SMR, ID, CMC, MC, ADS ...
,

and all other patients, past and present, participating in my continued search for their wellness ...

For iRB

... because many scientific premises first illuminate in eddies of single malts, plumes of Cuban smoke, and at the
end of tight lines ...a consummate physician/scientist ...

And finally,

For my mother:

An Irish woman who bore a Welsh son. I am blessed by her endless creativity and, compassion, and gift of gab.
Were it not for her, I would have less to say ... how very dull.
ABOUT THE A U T H O R

Dr. Ronald C. Evans is a Doctor of Chiropractic and a 1976 System of the ACA and a Forum Acquisitions Editor for the
graduate of Northwestern Health Sciences Univeristy, and ACA Press.
Chaired its Chiropractic Orthopedics Residency Program Dr. Evans was an appointee by Iowa Governor Terry E.
from 1980 to 1984. He is a Diplomate of the American Branstad to the Iowa Health Reform Council, the Iowa
Board of Chiropractic Orthopedists (DABCO) and Exam- Health Regulation Review Task Force, and the Iowa Comm-
iner Emeritus of that Board. He is a Fellow of the Academy unity Health Management Information System (CHMIS).
of Chiropractic Orthopedists (FACO) and Examiner Emeri- He is the CEO of the Iowa Chiropractic Physicians Clinic,
tus of that Board. Dr. Evans is a Fellow of the International (ICPC) a single-specialty independent provider network for
College of Chiropractors (FICC), and has lectured in ortho- Iowa and surrounding Midwestern states.
pedics and neurology for 35 years, speaking extensively Dr. Evans is the recipient of the Chiropractic Orthopedist
throughout the United States, Canada, New Zealand and of the Year Award (1984) and the Distinguished Service
Australia, and Scotland. Dr. Evans has lectured on the cam- Award (1994) from the American College of Chiropractic
puses of Northwestern Health Sciences, Drake University, Orthopedists, receiving the ACCO Distinguished Service
Texas College of Chiropractic, Logan University/College of Award again for 2001-2002. The Council on Chiropractic
Chiropractic, Southern California University of Health Sci- Orthopedics recognized Dr. Evans for Lifetime Achieve-
ences, and Palmer College of Chiropractic, Western States ment in 1992 and he received the President's Citation for
Chiropractic College, as well as at the Center for Alternative Distinguished Service by the American Board of Chiroprac-
Medicine Research, Harvard Medical School. Dr. Evans has tic Orthopedists in 1991. Dr. Evans received the Award of
addressed diverse audiences that include the Association of Excellence in 1993-1994, the Presidential Award in 1994,
Trial Lawyers of Iowa, the American Bar Association, the and the Outstanding ICS Member in 1996-1997, all from the
Australian Chiropractor's Association, the Defense Research Iowa Chiropractic Society. Most recently, he received the
Institute of the American Bar Association, the American Iowa Board of Chiropractic Examiners Service Award:
Public Health Association, and the Royal Academy of Iowa Chiropractic Society 1990-2001. Dr. Evans received
Physicians and Surgeons. the Distinguished Service Award from the Academy of
Dr. Evans is retired from an 11-year term of office on the Chiropractic Orthopedists in March 2003.
Iowa Board of Chiropractic Examiners, serving as chairper- Dr. Evans' writings include Orthopedic Test and Signs, A
son of the Board for nearly half that term. He maintains a Compendium, NWUHS, 1979, third edition, 1984, 1985;
private practice in Des Moines, and is the senior chiroprac- Differential Diagnosis of Conditions Presenting Neck and
tic orthopedic staff of a multi-provider, multi-disciplinary ArmPain,NWCC, 1980, second edition, 1984,1985; Ortho-
health care facility specializing in the non-surgical manage- pedic Considerations of the Low Back and Lower Extremity,
ment of orthopedic and neurological disorders. He is a NWUHS, 1980, second edition, 1984, 1985; The Impair-
Trustee of the Foundation for Chiropractic Education and ment Rating, NWCC, 1981, second edition, 1984; "The
Research, and served as Editorial Advisor for its publication Injured Worker: Role of the Chiropractor," Journal of the
"Staying Well" for many years. Dr. Evans is the Vice Presi- Australian Chiropractor's Association; 1985; 15(2); "Malin-
dent of FCER and continues to serve the FCER as the Chair- gering and Symptom Embellishment," Chapter 15, Chiro-
man of its Department of Defense Committee. Dr. Evans is practic Family Practice, Williams & Wilkins, 1990; Thoracic
the Chair of the Evidence-Based Resource Center of FCER. Spinal Examination Procedures; audio lecture for DC
He was an appointee to the RAND Consensus Panel for the TRACTS bimonthly publications, 1989, 1990; "Truncal
study of the Appropriateness of Manipulative Care for the Pain," Chapter 5, as a contribution to Scoliosis, by D. Asper-
Cervical Spine. He is an appointee, by the Secretary of gren, Williams & Wilkins, 1991; "Back School; a statistical
Defense of the United States, to the Oversight Advisory correlation to demonstrate efficacy of a Back School Educa-
Committee for Chiropractic Health Care, Department of tion Program in the therapeutic regimen: a one year study,"
Defense, now serving as a Senior Member of that Commit- completed 12/31/82; "CPT/ICD-9 coding and reference
tee, as well as its successor committee, the Chiropractic glossary" for Iowa Chiropractic Society; The Role of The
Healthcare Benefits Advisory Committee. Dr. Evans has Doctor of Chiropractic In Health Care Reform in The State
served as an Editorial Advisor for DC TRACTS, and is a of Iowa Within the Context of the Principles of Reform Of
Prepublication Book Reviewer for Lippincott Williams & the Iowa Health Reform Council; Notice of Intended Action
Wilkins Publishers; Elsevier, and Aspen Publishing. He is Insurance Division [191], New Chapter 75, "Iowa Individ-
an Associate Editor for the Journal of Neuromusculoskeletal ual Health Benefits Plans"; Managed Care In The United

vii
ABOUT THE A U T H O R ( C O N T I N U E D )

States Perspectives on Chiropractic Health Care Delivery Memorex," Iowa Trial Lawyers Association Medical
in Total Managed Care Systems, 1995; Noticed Rules, Damages Seminar June 9, 1995; Testing Methodology
Chapter 110, "Center for Rural Health and Primary Care," and Protocol of the American Board of Chiropractic
New Section. 514c. 11 Patient Access to Types of Physicians Orthopedists, Evans RC, Brandt JR; Evans RC, Rosner
Under Managed Care Health Plan or Indemnity Plan With A L . "Alternatives in Cancer Pain Treatment: The Applica-
Limited Provider Network; Analysis of the Final Report on tion of Chiropractic Care," Seminars in Oncology Nursing
the Physician Utilization Study as authorized by Iowa State 2005;21(3):184-189. His textbooks include The Illustrated
Senate, Senate File 2470(1996) and completed by Donald Essentials in Orthopedic Physical Assessment, 1993; Illus-
G. Hamm, Jr., FS A William M. Mercer, Incorporated, as the trated Orthopedic Physical Assessment, 2001; and Instant
Clinical and Cost Effectiveness of Various Types of Physi- Access to Orthopedic Physical Assessment, 2002; and Iatro-
cians for the Iowa Division of Insurance January 6, 1997 by genic Tendinopathy Associated with Levaquin (Levofloxa-
Ronald C. Evans, DC, FACO, FICC, and Anthony I. Rosner, cin); case report, 2008.
Ph.D. February 10, 1997; Fibromyalgia: A Conservative Dr. Evans holds the copyright and trademark for the
Perspective on Definition, Diagnosis and Management, a Greenfield Babinski Neurological Reflex Hammer;
video presentation for FCER 5/95; Identifying and Under- IMPSTAT (a computer program for the Evaluation and
standing Lateral Elbow Pain with Emphasis on Lateral Epi- Rating of Physical Impairments (coauthored with Logic
condylitis; Alternative Medicine: Implications for Clinical Unlimited, Inc.); and he is the co-developer of E X A M -
Practice Chiropractic Health Care; Basic Chiropractic M A K E R , a computerized exam-making program, based on
Testing and Evaluation Techniques PAIN: "Is it real, or is it multi-statistical permutations, with Logic Unlimited, Inc.
PREFACE

The basic observation of a patient's painful stance and Readers will enjoy the "At the View Box," contributions of
aggravating movements usually allows the formulation of Dr. Timothy Mick, DC, DACBR, as well as the expanded
the presenting signs and symptoms into a recognizable con- critical thinking elements. Illustrated Orthopedic Physical
stellation of a disease syndrome. The essence of orthopedic Assessment, Third Edition, remains clinically relevant and
diagnosis is the clinically demonstrable or reproducible useful for both the student and the practicing clinician.
signs of disease or injury. The scope and organization of Illustrated Orthopedic
Many physicians associate an aura of mysticism with the Physical Assessment, Third Edition, makes it a suitable com-
ease and speed with which the orthopedic specialist arrives panion for the clinician at all levels of sophistication, pro-
at a diagnosis. In fact, the specialist's development of inter- gressing from the initial procedures of orthopedic diagnosis
viewing, observation, and physical testing skills allows pro- to the requirements of the advanced student and the experi-
ceeding directly to the heart of the patient's problem. enced practitioner. Included in the thirteen chapters are diag-
I have been privileged in clinical practice to be chal- nostic facts in orthopedics, organized in a manner most
lenged by the myriad orthopedic health problems presented likely to be useful during the examination of patients. The
by my patients. I believe that my early and fumbling years book's compact physical dimensions invite constant use as
were well tolerated by these gracious people. They became a reference volume on the physician's office desk, in the
well in spite of my efforts. They have remained loyal instrument bag, and in the clinical setting; its functional
indeed. internal design, with liberal use of Orthopedic Gamuts,
In these latter years of practice, many of the early patients offers a convenient vehicle for refreshing one's memory
return with new diseases. These maladies are often much about seldom encountered and easily forgotten clinical
more difficult to diagnose and treat. My skills as an ortho- orthopedic phenomena.
pedic specialist have been honed to a fine edge out of neces- Only the unusual reader and clinician could master
sity. Some of these patients will not outlive me to give me the contents of Illustrated Orthopedic Physical Assessment
yet another chance to get it right. by studying it in sequence from beginning to end. Rather,
The perspective of the role of the physician in modern the student or clinician should digest the principles and
medicine has changed. Physicians are no longer viewed as procedures in segments as general diagnostic knowledge
the omnipotent beings they were formerly thought to be. The progresses. First, the reader should become familiar with
physician is expected to recognize personal skill limitations Chapters 1 and 2 and the descriptions of the "Cardinal
and make appropriate consultations and referrals. Patients Signs and Symptoms". From these chapters, the clinician
expect the correct diagnosis the first time around. At the should explore the regional chapters. As contact with
least, they deserve that. patients increases and specific questions arise, the reader
This book is created to alleviate the frustration and dis- should become familiar with the "Comments" for each
comfort for two parties in their respective quests for health diagnostic procedure. The "Comments" section of each
and wellness. First are the physicians and orthopedic spe- test or sign amplifies the knowledge of an underlying
cialists, who labor mightily in pushing, pulling, poking, pathology that is often discovered with the pertinent test or
bending, and twisting patients' body parts in the sometimes procedure.
less than compassionate search for the cause of the suffering. Chapter 13 presents rationale and procedures for inves-
Second are the patients who have been not-so-gently pushed, tigating malingering or non-organically-based complaints.
pulled, poked, bent, and twisted into inhuman configurations Included with Chapter 13 are numerous medical record
as they wait furtively for the discovery of the cause of their forms, outcomes assessment forms, and pain scale analogs.
anguish. I salute both parties for their endurance in seeking Each chapter of Illustrated Orthopedic Physical Assess-
the origin of disease and discomfort. ment, Third Edition, has a specific format. The format lends
Although the first edition of Instant Access to Orthopedic to the quick referencing of tests and maneuvers and cross-
Physical Assessment was an unqualified success—voted into referencing of associated procedures.
the 1994-1995 Top 250 Books of the Year by Doody's Each chapter begins with indexing of the tests found
Health Sciences Book Review Journal—it could be made to therein. Each chapter also begins with cross-reference
be better. Much of what made the first edition so successful tables for the syndrome assessed and by the syndrome sus-
succeeded into a second edition, and now a third edition. pected. Further, each chapter presents the separate protocols
There are many major changes to the contents: increasing for the regional joint assessment procedures and for assess-
the information on disease assessment, including more illus- ment of pain in the particular joint or region. These are
trations, and creating many more Orthopedic Gamuts. presented as testing procedural flow charts. These charts

ix
PREFACE ( C O N T I N U E D )

identify the test procedure(s) used to objectify the symptoms than one test or sign. In a problem-oriented situation,
of pain, paralysis, weakness, and loss of sensation. The chart eponyms are routinely used in the physical evaluation
provides a plan of examination and selections of tests for process. Familiarity with the terms and techniques used
the joint. in determining regional problems enables the physician
Each chapter begins with a set of axioms. Axioms are and assistant to record and clarify an orthopedic examina-
self-evident or universally recognized truths. Axioms are tion. Following the name of the test, maneuver, or sign is
also established rules, principles, or laws. An axiom used in identification of the specific pathology the test is suited to
this text is also a principle accepted as true, without proof elicit.
as the basis for argument. A test is part of the physical examination in which direct
Each chapter introduction addresses the various unique contact with the patient is made. It also may be a chemical
considerations or pathologies of the focal joint. The intro- test, x-ray, or other study. All tests described in his book will
ductory section contains the index of the tests presented and relate to the physical examination.
illustrated in the chapter. A sign is elicited by a test or a particular maneuver. A
Laced throughout a chapter are Orthopedic Gamuts. sign can be simply a visual observation (e.g., antalgia), and
The various gamuts present a range or spectrum of facts or it is an indication of the existence of a problem perceived
concepts in assessing orthopedic disease. The gamuts in by the examiner.
each chapter may represent universal orthopedic precepts as A maneuver is a complex motion or series of move-
well as specific regional principles and maxims. The gamuts ments, used either as a test or treatment. A maneuver is also
serve as diagnostic rubric in examining a patient. a method or technique.
Essentia] anatomy is presented in each chapter. The A phenomenon is any sign or objective symptom or any
essential anatomy section is not all-encompassing, but rather observable occurrence or fact.
discusses only the typical tissues that can be examined in A law is a description of a phenomenon that is so thor-
orthopedic physical procedures. oughly tested and accepted that it is regarded as a principle
Essential motion assessment for the joint is included. governing like phenomena.
These illustrations depict the expected full ranges of move- For each testing procedure in the book, a general
ment for the joint. The discussion further identifies the comment is presented about the pathologic condition tar-
amount of lost motion that can affect the activities of daily geted by the test. Numerous citations from current research
living. literature annotate the discussions of underlying patholo-
Essential muscle function for each joint is also included. gies. Following the comment section is a bulleted delinea-
This section identifies the musculature that is the prime tion of how the test is conducted. Each procedure is supported
mover of the joint, the innervation, and the action of the by photo illustrations and legends.
muscle, and limited discussion of the muscular anatomy. Each test is cross-referenced with other supportive tests
Essential imaging elements are addressed in each and procedures as "Next Steps/Procedures". Where perti-
chapter, specific for the region or joint discussed. Again, not nent, a "Clinical Pearl" identifies the subtle nuances or
all imaging techniques or modalities are discussed, only finesse of the tests that the author has gleaned from empiri-
those procedures germane to the physical orthopedic testing cal practice.
of a patient. For selected tests or procedures, At the Viewbox case
Each test, maneuver, sign, law, or phenomenon is pre- studies are presented. The case studies exemplify the typical
sented separately. The common usage name for the test, as and salient diagnostic image findings for the disease pathol-
identified in Stedman's, Taber's, Mosby's, Dorland's, or ogy discussed. The case studies have been graciously sup-
Churchill's medical dictionaries, is the heading for the test. plied from the teaching library of Dr. Timothy Mick, DC,
Equally, common synonyms and eponyms follow this DACBR.
name. At the close of each chapter, a "critical thinking" section
Eponyms for certain examinations vary from locale to is included. The critical thinking section is a range of ques-
locale or among institutions within the same area. Such tions germane to the specific region or joint of the chapter.
observations are a reflection of the training center's influ- The questions pertain largely to information contained in
ence. This is especially true where the names of prominent this text, but may occasionally require the reader to cross-
local physicians or clinicians or researchers are frequently reference with other pieces of literature or current scientific
used for these examinations. On occasion, the same test is journals. The answers for each question are contained in this
given two or more names, or the name can apply to more reference as well.

x
PREFACE ( C O N T I N U E D )

The references are listed for each chapter. The biblio- authors. Their works are exemplary in great scientific
graphic listing is new, updated, and extensive. In some writing, strongly contributing to the fund of knowledge of
instances, the bibliography reflects older volumes or works modern physicians. The artwork and line drawings used in
than are commonly found in scientific literature today. These these works are unsurpassed.
older references are the original work of the creators of Although the various tests and procedures in this book
various tests or procedures in this book. Preserving are presented in an anatomical or regional format, the appli-
the books in these reference lists is an attempt to pre- cation of the tests is accomplished in a more natural flow of
serve a continuum in the development of orthopedic examination procedures. The natural flow of the examina-
investigation. tion usually moves the patient from the standing position,
In an effort to accurately depict tissues and pathology through sitting, supine, and side-lying positions to the prone
involved in orthopedic disease and injury, numerous new position. Appendix A is a Listing of Tests, Alphabetically
illustrations are included in Illustrated Orthopedic Physical and Anatomically; Appendix B is a Listing of Tests Accord-
Assessment, Third Edition. Largely the new illustrations are ing to the Position of the Patient. A Glossary of Abbrevia-
from the outstanding and benchmark works of selected tions is also included.

-
xi
ACKNOWLEDGMENTS

Many individuals come to mind for their contributions to sense of photographic composition are unparalleled and
the continuum of this reference work, and they are indeed add to the advancement of the images used in various chap-
too numerous to list. They are, especially, the physicians ters. In many instances, the clinical photography of Dr.
who attend my lectures and symposia and take the time Skibsted is unsurpassed in depicting important positions
to tell me about or demonstrate for me various orthopedic and postures. Dr. Skibsted not only grasped the concept
tests and signs. I am sure that in many instances the unin- and framing issues of the illustrations, he worked tire-
formed or casual onlookers thought that grown men were lessly to perfect the quality of this book. I am ever
wrestling in public, when, in fact, we were exchanging the indebted.
latest testing procedures. I will always be grateful to these For the third edition, Mrs. Linda K. Evans saw to it that
keepers of the empirical body of medicine and science. manuscripts for both Illustrated Orthopedic Physical Assess-
Without their thirst for knowledge and scientific evidence ment, Third Edition, and Instant Access to Orthopedic Phys-
and support, this book could not be written or continue in ical Assessment, Second Edition, were ready, accurate, and
its evolution. finished ahead of time. Her zeal to make these editions as
More specifically, I must acknowledge three great mentors successful as the previous ones is unparalleled. She made
in chiropractic orthopedics: Dr. Joseph J. Sweere, Dr. the task of revision more interesting and less heavy. I will
Russell G. Hass (dec), and Dr. Robert N. Solheim (dec). seek her guidance for future works.
It was my fortune to be their student in orthopedic health For the third edition—and to quote, "It takes a village"
science. Their challenges kept me advancing in my funda- —to produce the stunning new color images for the various
mental knowledge in orthopedic medicine, and their educa- tests and maneuvers. At the outset, Logan University/
tional excellence caused me to grow. This book is a product College of Chiropractic president Dr. George Goodman,
of that growth. Their guidance and vitality have been the and Dr. Elizabeth Goodman, Ms. Ann Carter, Assistant to
breath of life for the entity of orthopedic specialization Drs. Goodman, and Ms. Kim Sullivan, Graduation &
within the scope of chiropractic practice. Perhaps more Event Planner at the Purser Center, are commended for their
especially, I acknowledge Dr. John F. Allenberg, former generosity in providing a magnificent location for the author,
President, Northwestern University of Health Sciences, as crew, editorial photographer, and models, in the production
the individual responsible for my completion of the arduous, of the art. The Purser Center is unparalleled in its beauty and
if not overwhelming, residency program at Northwestern. functionality. Certainly, the college administration and staff
Although I may have had the talent and intellect for the task, saw to every need for this project, ensuring its success. I am
he provided the necessary stimulus at the right times to help grateful to the ITC company for providing the set backdrop
me see the endeavor to completion. Without that, I would and carpet, without which, the art would be less charming.
not be a chiropractic orthopedist. Mr. Jim Visser, primary still photographer, and Mr.
It is hard to define the driving force that propels one to Chuck Leroi, and his videographic assistants Matt
aspire to excellence. Samuel C. Evans, DC, my father, and Aiskenen, and Ryan Cannon, could not have worked harder
partner in practice, in his life and love of quietly but effi- to achieve any higher degree of excellence with the color
ciently caring for people, embodied the greatest attributes in photos and illustrations and video footage. They both pushed
health science and art. His dedication to truth in science and the models to exceed their known abilities, squeezing out
compassion in ministering to the sick and injured inspired every detail of movement or position. Their collective work
me to greater heights as a physician and as a person. This embodies the constant search for perfection, serving as a
book, the editions before it, and those that will come after, guide for me to create prose equal to the illustrations. I look
is penned with eternal respect, admiration, and humility for forward to working with both in future endeavors.
his lifetime work and contribution to the human condition. The primary photographic models include Ms. Kim
The greatest man I ever knew. Alvis, Mr. Sean Brasfleld, Ms. Candyse Burns, Mr. Ryan
My contemporary, Dr. James R. Brandt, continued to Collart, Mr. Ochuko Ekpere, Ms. Angela Fain, Dr. LT
serve in the development of the third edition of this text, as Faison, Ms. Sheena Gordon, Mr. John Knott, Mr. Patrick
well as for its companion, Instant Access to Orthopedic Milford, Ms. Julie Mowczuo, Mr. Gary Taylor, and Ms.
Physical Assessment, Second Edition. Dr. Brandt remained Annie Walters. Both Mr. Brasfield and Dr. Faison rose far
steadfast in critical assessment of the work and dedicated to above the call of duty in providing either specialized and
making me strive for excellence in my writing. critical equipment for the photos, or in helping recruit suit-
Dr. Kim A. Skibsted contributed to the third edition with able models for the shoot. Each of the models demonstrated
astute clinical photography. Dr. Skibsted's keen eye and interminable patience in achieving just the right position or

xiii
ACKNOWLEDGMENTS (CONTINUED)

look of a test or procedure. I am grateful for their stamina ask for more of an editor. Her activities in compiling the
and physical pliability. It is worthwhile noting that some of manuscript schedules, arranging the photo shoot, arranging
these able models subsequently entered successful practice for the models and organizing the video and audio studios,
as chiropractic physicians. as well as keeping everyone on the same page were invalu-
Ms. Bailey Schechinger is a superb model for the clini- able. I could not have done any of the work without her at
cal illustrations. She was tireless, well-poised, and eager to the "director's table." Ms. Andrea Campbell, Senior Project
learn the meanings and usefulness of the procedures. Because Manager, juggled communication with numerous staff con-
of this, she helped make this book better. stantly. She was the last stop before the "work" becomes a
The Mosby/Elsevier staff for this edition included: Ms. book. She is the sous chef for my manuscripts: I gave her
Jennifer Watrous, Senior Developmental Editor, Health the ingredients and she turned them into something everyone
Professions 1 department of Editorial. I am pleased that Ms. will like to look at and want to read. Ms. Campbell helped
Watrous elected to engage in the work on my new editions. to sort out the art problems and keep track of what needed
She worked diligently on the second edition of Illustrated to be redrawn and what needed replacing (according to my
Orthopedic Physical Assessment, and it has been exciting to seemingly interminable corrections). Quite a task. I am ever
have her working on the third. Her attention to detail previ- grateful for her skills. Ms. Kellie White, Senior Acquisi-
ously made the book into a definitive reference. That same tions Editor, Health Professions I department of Editorial.
perseverance with editing my writing this time pushes the Worked with me from the earliest stages of Illustrated
book yet one notch higher. It is always a pleasure to work Essentials in Orthopedic Physical Assessment, through to
with people who truly want to see a project succeed. Ms. Illustrated Orthopedic Physical Assessment, Second Edition,
Watrous exemplifies this trait. Ms. April Falast, Editorial and Instant Access to Orthopedic Physical Assessment, and
Assistant, Health Professions I department of Editorial. We now for Illustrated Orthopedic Physical Assessment, Third
could not have completed the work on time or in an orga- Edition, and Instant Access to Orthopedic Physical Assess-
nized fashion without Ms. Falast's creative work in making ment, Second Edition. Ms. White continues to provide the
the photographic masters from the second edition. The necessary latitude and unwavering encouragement for the
enlarged illustrations were the perfect tool for both the stills development of both books to evolve them into nationally
and videos. I am sure this was hard work, but the resulting recognized, definitive works. She embodies the attributes of
photo catalog is unsurpassed. I am also grateful for her atten- a senior editor for which every author hopes. She and her
tion to the needs of the models. Without Ms. Falast's leader- excellent staff brought professionalism, interest, and dedica-
ship, I am certain the freezing models would simply have tion to the project. I have now written two editions under
left the building, along with Elvis. Ms. Kelly Milford, Asso- her guidance, with great result. The current revisions will
ciate Developmental Editor, Health Professions 1 depart- surpass both our expectations, which I attribute to her skills
ment of Editorial, is exceptional in her work. Her attention at marshaling all the creative elements, models, photogra-
to detail and dedication to completion of the project kept the phers, and the author, to their best. Developing a book with
manuscripts, models, photographers, and the author moving her and for her is a joy. Elsevier is both astute and fortunate
forward. I am ever indebted to her patience in waiting for to have Ms. White in its Editorial leadership, and I am for-
the final draft(s). Her professionalism is unsurpassed, espe- tunate to enjoy her friendship and creative counsel. I will
cially tested in frequent e-mail and tele-conference contact continue to strive to give her the best manuscripts. I look
from the beginning until the first bound copy. One could not forward to future collaborations.

xiv
Solving a patient's health problem can be a demanding exer- Diagnosis purely by comparison with previous cases is
cise of orthopedic medical detection and logical deduction. reserved for the physician or orthopedic specialist who is
Each health problem is a new diagnostic jigsaw puzzle for very experienced and very accurately remembers the cases,
which the pieces must be found and fitted together in a care- but this combination is not the norm. The entry level physi-
fully organized manner. cian or orthopedic specialist will come nearer to diagnostic
Each examination or investigation should have a plan for accuracy by progressing logically through the medical
including or excluding a specific member of a "short list" of investigation paradigm.
suspected conditions. It is always the failure to have such Despite all this, however, the right approach will never
an organized plan or approach that makes the diagnosis of be achieved until one misconception is laid to rest. This
orthopedic health problems so artificially difficult. Certainly, misconception is that the exact solution of an orthopedic
common or customary steps must be followed, but not blind problem does not matter very much and that such a solution
routine or blunderbuss investigations. will be of academic interest only, with no useful nonsurgical
treatment. Such a view is nonsense. It is true that health
science is frustrated in treating motor neuron disease; no
cure exists for hereditary ataxia, and no reliable method
exists to prevent relapses in disseminated sclerosis. Contrary
to many beliefs, these diseases occupy only a small part of
the orthopedist's time.
Think for a moment of the transformation in the last 30
years in the treatment of cervical spine trauma, interverte-
bral disc prolapse, carpal tunnel syndrome, and deficiency
neuropathies. Think of the influence of physiologic thera-
peutics in hypersensitivity states and in acute episodes of
soft-tissue disease, of the continuing progress of manipula-
tive therapy in certain facets of the migraine headache
process, mechanical lower-back disorders, and in trigeminal
neuralgia. Consider the advances of chiropractic orthopedics
in treating various forms of benign spinal compression.
Finally, the solution of an orthopedic problem takes time.
A solution cannot be rushed, and the examiner must never
allow the approach to be influenced by the exhortations of
optimistic colleagues to "just glance at this case while
passing" or to "just run over the musculoskeletal system, it
won't take 5 minutes." It will, it always does, and so it
should.

XV
1 Principles in Assessing
Musculoskeletal Disorders, 1
2 Assessing Cardinal Musculoskeletal
Symptoms and Signs, 48
3 Cervical Spine, 75
4 Shoulder, 205
5 Elbow, 324
6 Forearm, Wrist, and Hand, 375
7 Thoracic Spine, 467
8 Lumbar Spine, 535
9 Pelvis and Sacroiliac Joint, 699
10 Hip, 765
11 Knee, 843
12 Lower Leg, Ankle, and Foot, 929
13 Malingering, 1004
Glossary of Abbreviations, 1141
Appendix A, 1149
Appendix B, 1151
Answers to Critical Thinking
Questions, 1153

xvii
AXIOMS IN ASSESSING MUSCULOSKELETAL l)I�llllll'II)ll (,\\\l I t I
DISORDERS
Eliciting the patient's history is the quintessential skill
ORTHOPEDlC EVALUATlON
in orthopedics.
PROCESS
• An examiner needs to learn about the patient's major The orthopedic evaluation process has three phases:
pre enting symptoms, the chronology of the disorder. I. History taking
and its impact on the patient's activities of daily living, 2. Examination
as well as ancillary information that include history 3. Diagnosis
and involvement of other systems.
The orthopedic examination is the focal activity in
assessing the patient's musculoskeletal complaint.
The orthopedic examination process is adapted to the l)I�lIllll'II)I( l,\\\l I I'
specific needs of the patient's musculoskeletal system,
CLlNlCAL ASSESSMENTS
such as inspection, palpation, and observation.
In clinical practice, assessments occur all day, every
day, including:
I . Elucidating complaints
INTRODUCTION 2. Establishing impact of the complaints
Health care providers assess patients every day in clinical 3. Checking the complaint consistency with specific
practice. Commonly, clinical practice is impossible wiLhoUl diagnoses
structured assessments and tests. Examination procedures 4. Performing a general physical examination

appear to be straightforward: results are either positive or 5. Performing special physical examinations

negative. However, all assessment and testing in clinical 6. Performing laboratory and imaging tests

practice is based on the assumption of uncertainty: Does the 7. Interpreting test results

patient have a disease? The probability of a particular disease 8. Formulating a diagnosis


can be established only by performing a test or a chain of 9. Commencing lreaunent
test.s. 10. Evaluating treatment efficacy

The accuracy of a test for detecting a disease or a condi­ I I . Referring to a specialist, as needed
tion is determined by sensitivity and specificity. A high
sensitivity (or a high specificity) does not uffice to make a
test lIseful in clinical practice: a test should be as sensitive dependent on how likely the existence of the disease is
as possible. The sensitivity and specificity of examination before the procedure is actually conducted. This likelihood
procedures and tesLS can often be found in the literature. is dependent on the prevalence of the disease.
Sensitivity and specificity are important characteristics of The decision on whether to perform a new test depends
evidence-based physical assessment procedures but only in on the resu lt of the previous test. Procedures with the lowest
the context of a specific disease or condition. burden. risk. and costs for the patient are performed first,
The probability of a disease or condition after having and those with the highest burden. risk. or costs are reserved
performed a test (Bayes theorem) is dependent on two for specific patients in which the prior probability is highest.
things: (I) the specificity and sensitivity of the procedure Examination procedures in the context of a low prior prob­
(test characteristics) and (2) the probability of the disease or ability of disease is rarely, if ever. informative. The yield of
condition before conducting the procedure. Interpretation of diagnostic testing will increase the prior probability in the
Bayes' theorem is that the probability of having a disease is range of approximately 50%. Very experienced clinicians
not only dependent on the lest or examination procedure intuitively apply these rules and arrange rheir diagnostic
result and the characteristics of the procedure, but is also process in such a way that the highest possible yield (a
2 CHAPTER I Principles in Assessing Musculoskeletal Disorders

llRIIIIlJ'1 \lIt t;AM1J I I l BOX I-I


BAYES THEOREM PRECIS IN ORTHOPEDIC DIAGNOSIS

Rules of Thumb rationale for use in clinical I. HistOry


situations: 2. Examination
I. Highly sensilive and specific lest, will not perform 3. Determination of disability lPILS):
very well in the clinical context if the a priori prob­ ,F:revcntable causes of disability
ability is very low, Independent living
2, No single diagnostic test exists that tums an a priori hifeslyle

risk of disease of less than 10% into a probabil.ity that SOCial support

makes a clinician sufficiently convinced to establish


a diagnosis,
3, lhting is most valuable if the a priori probability of
the disease is somewhere in the range of 40% to From the moment of the first encounter with a pmient,
60%, the examiner is simultaneously observing and examining the
4, Diagnostic tests can turn such a probability into a movements and mannerisms of the patient. as well as listen­
sufficiently high posttest probability onto which to ing to what is being said, The diagnostic process is complex;
base further action. the examiner needs to establish the physical issues that are
of greatest imponance to the patient (those most disrupting
to the activities of daily living) and try to differentiate the
anatomic and pathologic aspects of any disease or injury that
OIU 1101'1 \lIt t;AMlIl I 4
might be present.
PRECIS OF PHYSICAl The history provides much information about what dif­
EXAMINATION ficulties the patient is experiencing and the impact of these
difficulties on the patient. Orthopedic examination is essen­
Sensitivity and speciticity do not exclusively make a

tial to define the structures involved; together. these pro­
diagnostic test as appropriate for clinical use,
cesses allow differentiation of orthopedic disorders into
• Test results that are considered normal or abnormal various diagnostic cat.egories (Box I-I).
should always be interpreted in the context of the
individual patient.
The probability of having a disease is not totally HISTORY TAKING
dependent on the test result and the characteristics of
A carefully elicited history is a most crucial element in
the test.
onhopedic assessment. An experienced examiner can form
The probability of having a disease is also dependent
an idea of the extent and magnitude simply frol11 the patiem's
on how prevalent the disease is before the test is actu­
history. I n the modern era of electronic patient medical
ally conducted,
record keeping, the examiner has new lools and melhods for
Testing in the context of a low probability of disease
not only capturing patient infomlation. but also tracking
is rarely. if ever, informative.
clinically significant changes.
Highly sophisticated and costly diagnostic techniques
Health care providers arc increa�ingly under pressure to

may fail as easily as simple, cheap, diagnostic


deliver efficient and high-quality care. Irnponant reasons for
maneuvers.
this pressure arc the ageing population. increasing demands
and expectations by patients, rbing medical cOst.l.. and a
decrea.l.c of full-time cmployed spccialists. Various innova­
highly probable diagnosis) will be oblained at the lowest tions in information technology have been proposed to
possible burden, risk, and costs for the patient. Less experi­ enhance the efficiency and quality of health cart.!. Conse­
enced clinicians may learn from experienced colleagues by quences of these innovations are altered health care pro­
recalling Bayes theorem and implemcming ils principles in cesses. as well as a redefinition or responsibilities and a
everyday clinical practice. change in workload for caregivers and patients involved in
Health care provider� cannot function adequately without these processes. A health care innovation that is increasingly
physical examination procedures. In the real world, examin­ applied in 1l1:;IIlY medical specialties is telcmedicine (TM).
ers accomplish ciinicul practice appropriately witholll a TM can be defined as "the use of telecommunications tech­
deJailed knowledge of the principles of tests, However, the nology for medica,1 diagnostic. monitoring and therapeutic
benefits from physical testing can be easily increased by purpoSC!\ when distance andlor time scparmcs the partici­
recognizing that Lhese tests do nothing more than increase pants" (Bcrgholll ct al. 2006).
the probability of a certain condition or diagnosis. Test A recent Institute of Medicine (10M) report charactcr­
results are never infallible. i/cd increased utilization of advances in health care informa-
CHAPTER I Principles in Assessing Musculoskeletal Disorders 3

I
(lRI I I(l I'II) III,A�\lI11 , OIU Illll'lllll I;A�Il'1 1 (,

An integrated electronic patient record (EPR) is essen­ WORKlNG DIAGNOSIS


tial for the future of health care services.
Essential steps in formulating a working diagnosis
The EPR assists in the sharing of patient infomlation
include:
and helps promote efficiency.
I. History taking
The most important resource for the development of
2. Observation
the EPR is the patient.
3. Palpation
Computer systems can take appropriate directed
4. Orthopedic testing
medical histories from patients based on chief com­
5. Clinical laboratory and imaging procedures
plaint.

lion technology (IT) (e.g.. automation of clinical, financial.


and administrallve transactions) as essential 10 improving
llR1 IIlll' Illlt l,\"l'l 17

quality and efficiency. preventing errors. and enhancing OBSERVATION AND INSPECTION
comumcr confidence in the health care sy�lem. Research
shows that IT loo h •. such as computerized clinical decision
Observation and inspection of the patient occur
suppon <iy,lcm .. and computerized physician order entry.
anytime during the examination or history
can Improve phy...ician perrormance and puticm outcomes
interview, especially when the patient is not aware
(Nowill..,ki et al . 2007).
of the observation. In this way, the examiner notes:
Clearly. IT ha!\ had an cxtraordinilry impact on the provi­
I. Antalgia or deformities of poslure

,ioll of health service.... Over 40 years ha� passed since the


2. Gait disturbances, especially if the patient needs

vision of a comprehensive electronic patient record (EPR)


assistance

system wa<.; first e<.;tahlished. Integration of the EPR has been


3. Spinal synunelry, including prominences or eleva­

less than successful partly because it relics heavily on tions, flattening or depressions, scoliosis, or abnor­

physician<.; and other highly skilled professionab for daw


malities of the anteroposterior curValure

acquisition. Some EPR systems ha....e 3l1emplCd to improve


4. Surface scars and wounds

physician usc and acceptance by st3ndardiLing medical


prose or creating templates; acceptance is Mill suboptimal
(Benamia. Elinson. Zarnke. 2(07).
Bun and Hmg found that although 73Ck of physician
CHIEF COMPLAINT
offices u..,ecl computer.., for billing. only 17% lIsed them for
mainw1l1ing medical records and 8ift. for ordering prescrip­ Patients who have more than one complaint, such as those
tion.... The proponion of U.S. physicians who have adoptcd with pain of spinal origin coupled with other body region
electronic health rccords is estimated to be between 20% and symptoms or extremity problems. must be guided in ranking
25tH (Schleyer. Spallck. Hernandez, 2(07). the complaints in priority. Although patients occasionally
The complaint history of a musculoskeletal condition seek attention for stiffness or some other joint-related com­
covers certain essential points. History of trauma helps dif­ plaint, most patients with musculoskcletal conditions do so
ferentiate between acquired ligamentous (soft-tissue) insuf­ for reasons related to pain, especially when it compromises
ficiency, inherent laxity, and past instability. Ii" trauma or the activities of daily living.
overuse caused t.he problem, the examiner must determinc The basic elements of examining the patient include
whether the patient stopped the injurious activity immedi­ observation and inspection. palpmion. neurologic evalua­
ately and self-treated the resulting condition. Finding tion. vilal signs, range-of-motion studies, clinical laboratory
lraumali/ed joints and adjacent Mructures neglected. decon­ 'lUdies. orthopedic tests, and diagnostic imaging.
ditioned. weakened. or atrophied caused by prolonged Mo ...t examiner� perfonn routine cOll1prehcn�ivc cxal11l1la­
periods of protection is common. tiom, on patients with even minimal initial chief compl:lint�
An accurate description of the traumatic event. including (Phelps. Rodriguez. 2005).
the exact position of the part at the moment of injury, is
essential.
OBSERVATION AND INSPECTION
The exact site of the pain is also important. Patients
often identify pain in one location. such as the hip, but The first impressions-observations made while taking the
point somewhere else, such as the sacroiliac joint. The more patient's history-are often the most revealing.
distal the pain is, the morc accurately patients detine its Reasoning within the�c (pain-based dinical) categories
location. appears LO be useful in helping providers and patients under-
4 CHAPTER I Principles in Assessing Musculoskeletal Disorders

stand and account for c1inicaJ presenwuons of pain. Such 5 questions for an orUmpedic specialist. Once all five ques­
reasoning influences planning of phy.!.ical assessments and tions are answered, a differential diagnosis can usually be
lreatment (Smart. Doody, 2007). established (Box 1-2).
A useful approach in the clinical examination of the neu­ A rapid general screening examination suffices initially.
romusculoskeletal system is to seek answers to the Critical Abnormal joints are subjected to a more focused regional
orthopedic examination procedure.
The examiner must detennine the presence of active or
current inHammation. the presence of irreversible joint
ORl lllll'llll( (,A�HlI I X
damage from past. injury or inflammation, and existing
PAIN-BASED CLINICAL mechanical defects. These findings are not mutually exclu­
REASONiNG sive.
The distribution of joint involvement is important in
Five main categories of pain-based clinical
reaching a diagnosis. Certain patterns characterize specific
reasoning are:
disorders. The number of involved joints may also be of
• Biomedical (structural-functional source)
diagnostic significance.
Psychosocial (perception-interpretation of pain)
Learning what exacerbate!> or relieves the symptom
Pain mechanisms (underlying pathophysiologic
pattern is important. Equally important is how long the com­
factors)
plaints have existed (Table I-I) .
• Chronicity (temporal aspects of pain)
Several other features may be of diagnostic importance.
Irritability or severity (degree of pain)
Some of these features produce skin signs or nodules. Exam­
ples include rheumatoid nodules (Fig. I-I), gouty tophi
(Fig. 1-2), dermatomyositis (Fig. 1-3), and psoriatic arU"itis
(Fig. 1-4).
(lRllltll'l niL (,AMlil I ')

DETERMINING EXTENT OF
INJURY BOX 1-2

Other characteristic features of diagnostic CR.ITlCAL QJlESTIONS IN OR.THOPEDIC


importance in determining the extent of the disease PHYSICAL EXAMINATION
or injury:
I. Are any joints abnormal'?
1. Is involvement symmetric or asymmetric?
2. What is the nature of the abnormality?
2. Are large or small joints affected? 3. What is the extent of the involvement'?
3. Is the distribution of the condition peripheral or axial? 4. Are Olher features of diagnostic importance present?
4. Does the condition affect upper versus lower limbs, 5. Do the answers to questions I tJlrough 4 provide sufficient
or vice versa? data?

fAKlrl·t

JOINT PATTERNS IN ORTHOPEDiC/RHEUMATIC DISORDERS

Peripheral! Upper!
Number or JOints Large/SmaU Central Lower
Diagnosis Symmetry lnvolved* .Joints Distribution Limb Predilection

Rheumatoid arthritis Symmetric M ono-, oli g o-. polyarth rit is Large/sm all Pe ripheral Uppe rllow er MCPs. PIP,.
MTPs. DIPs
Ankylosing spondylitis Cenlral Sacroiliac
joints. hip,
sh ou lder
Psoriatic arthritis Asymmetric PO lyart hri tis Large/sma ll Peri pheral Uppcrllower DIPs, sacro i li ac
join ts
Reactive arthritis A!iymmctric 01 igoarthri lis/Polyanhri lis Large P eriph eral Lower Sacroiliac
join L'I. DIPs
(toes)
Gou t As ym me tri c MonoarthritislOligoarthritis Large/s ma ll P eri ph era l Lower m ore First MTP,
than upper Knee. Hip

DIPs. Distal interphalangeal joints: Mep.\'. mctacarpoph,lIangeal joints: MTP\. mClalarsophalangcills; PIPs. proxirmll interphalangeal joints.
*Monourthritis dellotes inflammation in a single joint. oligoarthritis Jenoles two to four joint1.. lind polyu
� 1hrilis
CHAPTER I Principles in Assessing Musculoskeletal Disorders 5

FIG. 1-3 Skin and nail fold lesions seen in dermatomyosi­


lis. Patches (A) and periungual edema and nail fold (B).
FIG. I-1 A, Rheumatoid nodules. B, Large nodules may (From Klippel JH. Dicppc PA: Rhe"l/IlllOlog.\; vol 1-2. cd 2, London. 1998.

develop in the olecranon bursa as well as in the subcutane­ Mo!.by.)

ous (issue. (From Klippel JH. Dieppc PA: Rhelllll(l(% gy. 1'0//-2. ed 2.

London. 1998, Mosby.,

F IG. 1-4 Psorialic anhritis, with swelling of the distal inter­


phalangeal joint and pitting in the adjacent fingernails. (From

Klippel HI, Dicppc PA: R"elll/llifOlog.\� vol 1·2. cd 2. London. 1998.

Mosby.)

PALPATION

Palpation is the process of assessing the physical character­


F I G. 1-2 Gouty tophi represent deposits of urate crystals. istics of joints and contiguous structures by touching or
(From Klippel JH. Dicppc PA: Nlli'1I/1I0to/OKI'. '0'011-2. cd 2. London. 1998. feeling the palienes body. The purpose of palpation is to
Mo�by.)
locate and substantiate areas of tenderness, swelling, and
abnormal muscle LOne. Palpmion allows the examiner to
identify a localized increase or decrease in surface tempera­
The answers to the Critical 5 questions usually provide ture and the presence of induration and mass. Palpation is
sufficient information to establish a differential diagnosis. classically performed with the fingerlips or Wilh the blum
They mu�l. Ir not, the examiner will need 10 retrace each end of a cotton·lip applicator. However, instruments can be
examination step ullIil a logical and credible diagnosis can used in percussion (gently tapping with a renex hammer).
be reached. Wilh vibralion (using a C-128 lUning fork).
6 CHAPTER I Principles in Assessing Musculoskeletal Disorders

() I� I I I () 1'1 I ) I ( (, \ \\ I I I III

SPINAL PALPATION
Effective spinal palpation can be accomplished with
the patient in the silling or kneeling variants of
Adam's position:
• In palpating various structures, the examiner assesses
the skin and subcutaneous tissue. Rolling of the skin
(Kibler's test) can be perfonned. The examiner
observes for surface temperature, hypesthesia, hyper­
hidrosis, and muscle splinting.
• Tenderness of muscles and tendons and their attach­
ments is assessed, in both the anatomic resting posi­
tion and through various ranges of motion. FIG. 1-5 From top to bottom, the Greenfield Babinski reflex
hammer, Taylor reflex hammer, Buck's neurologic hammer,
and Babinski reflex hammer.

Tendon sheaths and bursae are palpated for thickness,


crepitus (especially silken versus snowball crepitus), and
tenderness. The joints are palpated for all anatomic compo­
nents to include bones, capsule, ligaments, any specialized
structures, swelling. a change of shape or defornlity, posi­
tional deficits, and tenderness. Palpation also aids in estab­
lishing the integrity of local circulation.
Using a stethoscope or similar instrument improves crep­
itation grading by enhancing the auditory component in con­
junction with palpation and is especially useful with patients
who display mild or moderate crepitation grade subclassifi­
cations.

NEUROLOGIC EVALUATION

The neurologic evaluation involves locating the lesion;


testing deep tendon, superficial, and pathologic reftexes
(Fig. 1-5); testing cranial nerve and brainstem function;
measuring body parts (mensuration); grading muscular
strength; and testing the gross sensory modalities
(Fig. 1-6).
FiG. 1-6 Single-tipped cotton applicators are both eco­
Cerebral dysfunction is determined during the consulta­
nomical and versatile and can be used in the following set­
lion by nOling the patient's mannerisms and orientation to
tings: in emergency rooms, examining rooms, outpatient
time, space, and body pans (usually noted in the chan as
clinics, and laboratories and on dressing cans. Sterile tongue
oriented x3). Funher evaluations of lesions in the cerebrum
depressors are usually made from white Birchwood that is
require advanced imaging procedures and electroneurodiag­
'/..-inch thick. These tongue depressors are evenly cut and
nos tie testing.
highly polished for smooth and clean edges, ends, and sur­
Cerebellar lesions are characterized by repeated
faces.
cogwheel-type muscle actions while the patient's eyes arc
open. The posterior columns of the spinal cord are the source
of the dy function when repeated muscle actions are smooth sign in the second edition of his Lehrbuch der Nen1en·
and occur while the patient's eyes arc open. However, these kmnkheiten des Metlsc/len (1851). After discussing a reduc­
same muscular actions cannot be repeated as smoothly with tion of the motor power in the lower extremities. Romberg
the eyes closed. Brainstem dysfunction is discerned through stales, ··The individual keeps his eyes on his feet to prevent
testing of the cranial nerves. The type and quality of paraly­ his movements from becoming still morc unsteady. If he is
sis, reflexes, muscle lone, clonus. atrophy, fasciculation, and ordered to close his eyes while in the erect posture. he at
reaclions of degeneration can differentiate spinal cord lesions once commences to tolter. The insecurity of his gait also
from lower motor neuron disorders. exhibits itself more in the dark·' (Romberg. 1853). Romberg
Moritz Heinrich Romberg (1795-1873), the founder of thought lhe sign was pathognomonic of tabes dorsalis (Cole.
clinical neurology in Germany. described his now famous Michael. Roben, 2(03).
CHAPTER I Principles in Assessing Musculoskeletal Disorders 7

I
(}1�111(} 1 'lll l ( (,\\11 I I I I (liZ I II(1 1' I Il l( (, \ \\ I I I I 1

DEEP-TENDON REFLEXES CRANIAL NERVES AND BASIC


FUNCTION
I . Scapulohumeml C5-C6
2. Biceps C5-C6 I: Smell
3. Radial C5-C6 II: Vision
4. Triceps C7-C8 IJI : Light accommodation
5. Wrist C7-C8 I I I, IV, V I : Eye movement
6. Ulnar C8-T I v: Sensation (wink)
7. Patellar L2-L4 VII: Facial muscle (taste)
8. Hamstring L4-S I VIII: Auditory (balance)
9. Achilles 51-52 IX: Taste (gag)
x: Voice (swallow)
XI: Shoulder (shrug)
XII: Tongue (motor)
tlIZIII(lI'l l l l ( (,\\111 1 1'

SU PERFICIAL REFLEXES
J . Corneal IJ I, V lll� I I Illl'l 111( (,\ \I I I I I,
2. Upper abdominal 17-T9
COMMONLY ACCEPTED
3. Lower abdominal T I (}..T 12
DEEP-TENDON REFLEX
4. Cremasteric
GRADING SCHEME
5. Gluteal
6. Plantar 0 = Absent
7. T l 2-L2 I = Diminished or hyporeactive
8. L4-LS 2 = Average
9. S I -S2 2+ = Slightly exaggerated (hyperreactive)
3 = Exaggerated (hyperreactive)
4 = Associated with myoclonus

tl l Zllltl l'lllIl (,\\11 I I 1\

PATHOLOGIC REFLEXES comraction in the opposite upper or lower extremities


(Jendrassik maneuver).
J. Hoffmann
lendrassik faci litation is different between age groups
2. Babinski
and weight bearing versus non-weight bearing. Young
3. Chaddock
patients often demonstrate a significant lendrassik facilita·
4. Oppenheim
tion effect in the standing position, whereas. very often, no
5. Bechterew-Mendel
difference is seen in the elderly patients.
6. Rossohmo
Mensuration of body parts is used to determine atrophy
7. Gordon
and functional and anatomic abnormalities (Fig. J.7).
8. Schaeffer
Grip strength testing examines the functjon of the ulnar
nerve and can help differentiate myoneural dysfunction
from malingering activity ( Fig. \·8). The examiner can use
Deep·tendon renexes help the examiner locate the lower three methods of grip strength evaluation (one trial, the
motor neuron lesion and differentiate it from an upper motor mean of three trials. and the best of three trials) when using
neuron lesion. the Jamar dynamometer. Two different sLHtic grip tests are
Superficial renexes differentiate lower motor neuron the five-rung test and the maximal static grip test.
lesions from upper motor neuron lesions. Thc five-rung tc�t involve� perrorming one repetition (trial)
Pathologic renexes determine the presence of upper with the handle or the Jamar dynamometer on each of the
molor neuron lesions. rive handle sCllings. whereas the ma"imal static grip tc�t
Cranial nerve function is dClcmlined by testing brainslcm involves performing three repetitions with the handle on
activity. either lhe second or third sCILing (Fess. 1992: Joughin el 31.
On occasion, eliciting a particular renex is difficult; dis· 1993).
lrJclion techniques are helpful in such situations. If Jcss­ The main difference between the static grip test and the
than-nannal reactivity is encountered in the upper or lower rapid exchange grip ( REG) maneuver is the duration of the
extremities, the patient is directed to perfonn an isometric muscular contraction during gripping.
8 CHAPTER I Principles in Assessing Musculoskeletal Disorders

FIG. I-750ft linen tape is marked in inches on one side


and centimeters on Ihe other. The fast-read ing clinical ther­
FIG. 1-8 Manin Vigorimetcr aneroid dynamomeler (left)
mometer.
and Jamar hand grasp mechanical five-position dynamom­
eter (right).

lll: I l Illl'l l ll( (, \\\1, I I 1(,

COMMON AREAS OF
MENSURATION tll:!IILlI'1I11( (,\\\1'1117

I. Excursion of the chesl during inspiralion and CERVICAL SPINE EXTRINSIC


expiration MUSCULATURE WITH SPECIFIC
2. Upper-extremity circumference (brachium and ante­ NERVE ROOTS NOTED
brachium); measured in the noncontracled and con­
I. Deltoid (CS)
tracted state
2. Biceps (C6)
3. Lower-extremity circumferences ( thigh and calf);
3. Wrist extensors (C6)
measured in the noncontracted and contracted states
4. Triceps (C7)
4. Leg length (measured standing versus supine or
5. Wrist flexors (C7)
prone); differentiates a functional shan leg from an
6. Finger extensors (C7)
anatomic shan leg
7. Finger flexors (C8)
8. Finger abductors (T1)

During lhe stalic grip lcst, the duration of muscular contrac­


tion of each hand grip is 3 10 5 seconds. whereas during Lhe
REG maneuver. lhe hands alternate rapidly. resulting in a
�hortcr duration of each grip (Ics� than 1 .5 sccond� per grip) LlI:!IILlI'1 \ll( (,\\\tI1 11K
(Taylor c( al.2000).
A positil'e REG test i!<t obtained when REG l'Ocores
THORACOLUMBAR EXTRINSIC
arc greater than static grip scores. which indicates a l'!oub·
MUSCULATURE AND SPECIFIC
maximal or a feigned effort. A lIeglll;\'e REG test is obtained
ASSOCIATED NERVE ROOT
when slatic grip scores arc greater than REG scores. indical­
LEVElS
ing a maximal or a sincere eITon (Shechlman. Taylor. I. Hip flexors (L2-L3)
2002). 2. Knee extensors (L3-L4)
Cervical intrinsic muscle lesling relates to the cervical 3. Ankle extensors (L4--LS)
spine functions of flexion, extension, lateral flexion, and 4. Hip extensors (L4--LS)
rotation. 5. Knee nexors (L5-5 I)
Thoracolumbar imrinsic muscle function is associated 6. Ankle flexors ( 5I-52)
with trunk flexion. extension. lateral flexion. and rotation.
CHAPTER I Principles in Assessing Musculoskeletal Disorders 9

FIG. 1-9 From top to bottom, the Wanenberg pinwheel:


Boley two-point discrimination gauge: von Frey ancsthe­
,imctcr: Buck camel hair brush. pin. and neurologic hammer: FIG. J-IO Aluminum alloy tuning forks. available in C-64.
and u Serol China marker. C- 1 28. C-256. C-5 1 2. C- 1 024. C-2048. and C-4096 vibra­
tions. The lower-frequency luning forks are the usual choices
for bone vibration conduction studies.

Testing of the gross sensory modalities allows for evalu­


ation of the derl1latomcs involved in superficial and deep
sensations and proprioception (Fig. 1 -9).
The superficial scnsation� include light touch. pain. and
temperature. Light touch is mediated by the dorsal columns C4 C6 C4

and easily examined with a colton ball. Pilin receptors are


mediated by the lateral spinothalamic tracts and are tested
by a pinprick and hot and cold temperatures. Temperature.
or thermal scnsalian. mediated by the dorsal columns is
tested with warm ( not hot) and cool (not cold) tempera­
tures.
The deep sensat ions arc vibration and deep pressure per­
ception. The do"al columns of the spinal cord (Fig. 1 - 1 0)
mediate vibration. tested with a C-128 or lower-rrequency
luning rork. Deep pressure is ICMcd by squeezing any mus­
cular part of the body and is mediated in the dorsal
columns.
Proprioception. or joint po\ition �en\e. i� mediated by the
dorsal columns and can be tc;ted by having the patient point
to a particular part of the body while keeping the eyes
closed.

PAIN AND PATTERNS OF PAIN

Pain thal arises with activity and decreases with rest is l i kely C7
to ha\'c mechan ical causc�. The pain may be position depcn­ DERMATOMES MYOTOMES SCLEROTOMES
dent; most case\ of mechanical spinal pain have both a F I G. 1-1 1 Primary pallern� of pain originating in the �pioe:
provocative and palli:.ni\'e arc of l11otioo. derma tomes. myotol11e�. and sclerotomes. Demonstrated for
Spinal pain is the most difficult to differentially diagnose. lhe right upper extremity. (From Saidofl' DC. McDonough A: Cr;lj·
The three primary patterns are dermatogenous. myogenous. all 1H.lIl/l\'(/n ill therapf'lIlic in/(·n'f''''i(JI/.�, IIpper f'\lI"('milies, 51 Louis.
and sclcratogenous (Fig. I - I I). 1997. Moshy,)
10 CHAPTER I Principles i n Assessing Musculoskeletal Disorders

A dermatome is the area of sensation atlributed to a par­ VITAL SIGNS


ticular nerve root level. Dermatomal pain is often described
as sharp. stabbing, and well demarcated. It may result from Vital signs include the brachial blood pressure, peripheral
herniated discs, stretch injuries, or tumors. pulse rate, respiration rate, height. weight, and vital capac­
Pain referral within muscular or fascial tissue is myoge­ ity. The instrumentation for these measurements includes
nous pnin. Areas known as (rigger poiflls refer pain 10 distant stethoscopes, spirometers, scales, tape measures. and blood
sites. Trigger points are evident in patients with myofascial pressure cuffs (Fig. 1 - 1 4).
pain syndromes. Specific sites of tenderness that do not
result from referred pain are termed tellder poillfs. Tender
R ANGE OF MOTION
points develop in patients wilh varied sort-tissue, rheumatic.
and collagen-vascular disorders, such as systemic lupus ery­ Of a l l the orthopedic tests that an examiner can perform on
thematosus and fibromyalgia. a patient, none is more crucial than range-of-motion (ROM)
Pain referred from somatic structures such as cartil age. testing of the affected articulation. Range of motion testing
l igament, joint capsule, or bone often does not follow der­ often reveals the origin of the patient's discomfort. because
matome patterns, as does nerve root pain. This pain is known movement may reproduce the pain. The patient is examined
as sclera/agel/otis pain. Patients may describe this type of symmetrically for aClive ROM of all the joints that may be
pain as dull, achy, diffuse, and difficult to pinpoint. Sclera­ involved in the dysfunction or injury (Fig. 1 - 1 5). The exam­
logenous pain is one of the morc common spinal pain iner then takes the patient through passi,'e ROM, evaluating
patterns. the e/ldleel (i.e., spri nginess) of the affected joint.
Any movable joint in the body, including the spine. can
Local Versus Referred Pain be tested for ROM. ROM is assessed bilaterally by compar­
Patients with referred pain often point to large generalized ing findings with a given set of normal values. Normal
areas. whereas patients with localized lesions can be more values can vary dramatically, depending on the reference
specific. A patient complaining of unrelenting spinal pain. source used, An examiner must exercise careful professional
demonstrating ful l , pain-free range of motion presents a judgment to ensure objectivity. Any ROM that is less than
problem. The patient likely has either viscerosomatic pain, normal may indicale or be the result of muscle spasm, sprain.
which mandates further diagnostic te ting, or pain resulting strain. joint subluxation, general anhrilic degeneration. post­
from a psychosocial cause. If referred pain from a diseased surgical condition. or obesity.
organ system is mimicking a local orthopedic problem, the Recenll),. Childs and colleagues found in a clinical trial that
examiner should not hesitate to order appropriate tests. spinal stiffness was one of five predictors of which patients
Every effort should be made to objectify the patient's wilh low back pain would respond favorably to a particular
report of pain and discomfort. Measurement instruments physical lherapy manipulation. In their slUdy. they used a
such as the visual analog scale (Fig. 1 - 12) are reliable and manual assessment to grade the relative stiffness of the L4�
valid for examining a patient's pain. The McGill Short L5 and L5-S I joints. A palpable difference in the �tiffncs�
Form Questionnaire (Fig. 1 - 13) is helpful for pain mea­ at these joints helped predict which patients were more
surement in a clinical setting. likely to respond favorably to manipulative therapy. Manual
Pain is associated with a very high disability rate, sig­ palpation methods have been notoriousl), difficult to quan­
nificantly affecting the three domains evaluated by the liry and suffer from a lack of objectivity. Interexaminer
Sheehan Disability Scale, which assesses patient functional
impairment in three domains: work impairment. social
impairment. and impainnent of family l i fe or home respon­
sibilities. Two further items gather data on patient-perceived
stress and social support.
OINT END-FEEL CATEGORIES
In passive joint motion assessment, the end-feel is
important. The accepted end-feel categories are:
Bone-to-bone: an abrupt halt to movement when two
hard surfaces meet
Capsular end-feel: a lealhery resistance to movement
On Ihe hoe below.
- place a mark mdlcalmg your pam le\el
with a slight amount of give at the very end of the
range
Springy block: a usually pathologic end-feel, gener­
ally representing an intraarticular displacement
o 10 Tissue approximation: no further joint movement
F IG. 1 - 12 Visual analog scale for objective pain measure­ available
ment. (From Mulone TR. McPoil TG. Nit7. AJ: Orthopedic mill sports • Empty feel : usually pathologic
p/n·Jical ,lteropy. cd 3. SI Loub. 1 997. Mo:.b).)
CHAPTER I Principles in Assessing Musculoskeletal D isorders 1 1__

I
Check only one item for each category to describe your pain today.

2 3 4

1 Flickering 1 Jumping 1 Pricking t Sharp


2 Quivering 2 Flashing 2 Boring 2 Cutting
3 Pulsing 3 Shooting 3 Drilling 3 Lacerating
4 Throbbing 4 Stabbing
5 Beating 5 Lancinating
6 Pounding

5 6 7 8

1 Pinching 1 Tugging 1 Hot 1 Tingling


2 Pressing 2 Pulling 2 Burning 2 Itchy
3 Gnawing 3 Wrenching 3 Scalding 3 Smarting
4 Cramping 4 Saaring 4 Stinging
5 Crushing

9 10 11 12

1 Dull 1 Tender 1 Tiring 1 Sickening


2 Sore 2 Taut 2 Exhausting 2 Suffocating
3 Hurting 3 Rasping
4 Aching 4 Splitting
5 Heavy

13 14 15 16

1 Feartul 1 Punishing 1 Wretched 1 Annoying


2 Frightlul 2 Grueling 2 Blinding 2 Troublesome
3 Terrifying 3 Cruel 3 Miserable
4 Vicious 4 Intense
5 Killing 5 Unbearable

17 18 19 20

1 Spreading 1 Tight 1 Cool 1 Nagging


2 Radiating 2 Numb 2 Cold 2 Nauseating
3 Penetrating 3 Drawing 3 Freezing 3 Agonizing
4 Piercing 4 Squeezing 4 Dreadful
5 Tearing 5 Torturing

F I G . 1 - 1 3 McGill Short Form Pain QuesLionnaire. (From Malone TR. McPoil TG . Nitl AJ: Ortho·

pe(Jic (Il1d sports phYJiC(l/ ther(/I)): ed 3. S( Louis, 1 997. Mosby: rrom Mel7.acker R: The McGill Pain Quc�tion·

naire: major propenics and scoring methods. Pain 1:277. 1975.)

reliability or chiropractic palpation of segmental fixation is joint and periarticular structures through their respective
typically poor to 5!light. Inlracxaminer reliability iii usually arcs and end-range motions. Stability lesting involves stress­
rated :,omcwhat beuer. in the moderate to !o.ubMantial range. ing ligamentous tissues and joint capsules (Fig. 1 - 1 6).
depending on the experience of the exami ner. Similarly.
Miffness mcasures commonly used by physical therapi5!ts
MUSCULAR ASSESSMENT
show liulc interex3miner agreement. Childs and colleagues
were able to achicve acceptable reliability in the lumbar Movement resLrictions in a joint's passive ROM are nOI
mobility tClit they used by reducing the assc:,sment to three exclusively articular. Muscular hypertonicity limits passive
level>: ( I ) hypomobilc. (2) normal. and (3) hypcrmobilc movement and often occurs in association with articular
(Owen, C( .1. 2(07). lesions Uoint dysfunction). Chronic joint problems are also
commonly associated with myofascilis.

STABILITY TESTING
CLINICAL L ABORATORY
Because clinical examination reveals the degree of ligamen­
tous or joint sprain, the examiner must be able to Lest accu­ For the examiner concemed with musculoskeletal disorders.
rately for joint instability (Table 1 -2). Stability testing moves differential diagnosb becomes a chal lenge. Complete blood
12 CHAPTER I Principles i n Assessing Musculoskeletal Disorders

F I G . 1 - 1 5 From top to bottom, stainless steel goniometer


measures movement or joints rrom 0 to 180 degrees. Bubble
inclinometers measure the angular motion from 0 to 360
degrees. Finger or small joint goniometer measures the
movement or interphalangeal joints or fingers and toes.
Plastic radiographic goniometer provides standard orthope­
F IG . 1 - 1 4 Wall-mounted sphygmomanometer and stetho­ dic measurements of joint mOl ion and neutral position.
scope (Ie[t). Portable blood pressure curr (top right). Most
significant heart sounds occur in the frequency range of 200
to 500 Hz. bUl human auditory sensitivity is l i m i ted to those
,ounds below 1000 Hz. Stethoscopes ampliry the lower rre­
quencies (bollo/ll right).

lAB l 1 1-2

I N J U RED LIGAMENT REst DUAL FUNCTtON

Residual
Extent of Joint Motion, Residual Residual functional
Failure Sprain Damage· Subluxation Strength Functional Length Capacity

Mi nimal Finol degree Less thun onc lhird of None RClaincd or Nonnal Retained
fibers failed: slightly
includes Illost decreased
sprains with few to
some fibers failed.
Microlcars also exist.
Partial Second degree One-third to two- In geneml. minimal Marked Increased. still within Marked
lhirds ligament or no increased decrease. functiomll range compromise:
damage; significant motion. At risk for but may later act requires
damage. but pans Remaining fibers complete as a check rein healing to
of the ligament are in ligament re�ist failure rather than subtle regai n
sti l l functional . openi ng. control of joint function
Microtcars may exist. motions
Complete Third degree More than two-thirds Depcnw. on Little to none Lost Severely
to complete failure: !>CCondary None Lost compromised
continuity remains re\lrainlS or lost
In pan. Depcnd� on Lost
Conti nui ty lost and .!.econdary
gross separation restrai nts
between fibers

·E�limate of damnge i� often difficult: however. the different I) pc.. li"led can u,uall) be diffcrentiated. NOle: Antcrior IInci po..tcrior crucimc IC:lr.. commonly
c:tiSI with liule 10 no .Ihnonnlll laxilY. Thc c:taminalion for medial and Imeral 1igamentou<; injury is u..ually more :lecumte.
From Fcagin JA. edilor: Th(' ("rllcia/ ligaftlenl.\. New York. 1988. Chun:hill Li"ing�tonc.
CHAPTER I Principles in Assessing Musculoskeletal Disorders 13

FIG. 1-16 Lachman (eM of the anterior crucialc l igament. (From Scuderi GR. McCann PD. Bruno
PJ: SWJrI\' medicine: (Jrind/,Ies ofprimary C(l�. 51 Louis. 1 997. Mosby.)

Ll I�I II LlI' I I) I ( (, \\\l I I _'tl

RESISTED MUSCLE MOVEMENT LA BORATORY RESULTS


INTERPRETATIONS
In assessing muscle tissue, resisted movements are
the most revealing. Standard interpretations of For laboratory testing in orthopedic evaluations,
resisted muscle tesling movements include: results interpretation errors usually Involve one or
Painful and strong is equated with a m i nor lesion of four areas:
muscle or tendon. False-positive results
Painful and weak equates with a major lesion of the False-negative results
muscle or tendon. Measurcmcnt error
Painless and weak equates with neurologic injury or • Differences in groups of patients compared with indi­
complete rupture of the muscular auachment. vidual patients
Painless and strong is normaL

and urine tests can help determine a diagnosis. Diseases of


INDIVIDUAL BLOOD AND
the heart. liver. kidney. pancreas. and prostate can mimic
URINE TESTS
back pain of spinal origin.
Mo" laboratory te;ting has l imited utility for orthopedic
Acid Phosphates
diagnosis (Table 1 -3)_ As an example, in rheumatoid Dietary deficiencies in phosphorus arc rare but may be seen
arthritis, the diagnosis is often established from the history with alcoholism and malnutrition_ Low levels of phosphorus
and physical examination; for systemic lupus erythemato­ (hypophosphatemia) may also be caused by or associated
sus, from the laboratory test antinuclear antibody (ANA); with:
for gout, from a synovial nuid examination; and for anky� Hypercalcemia (high levels of calcium), especially as
losing spondylitis, from a radiograph. In common disorders a result of hyperparathyroidism
such as osteoarthritis. fibromyalgia, or muscular strains and Overuse of diuretics (drugs that encourage urination)
sprains. essentially no diagnostic role exists for laboratory Severe burns
tests except to exclude other diagnostic possibilities. Diabctic ketoacidosis ( after treatment)
The simplest orthopedic screen includes rheumatoid Hypothyroidism
arthritis factor. ANA, and uric acid, although more elaborate Hypokalemia (low levels of potassium)
screens arc available, which may include erythrocyte sedi­ Chronic antacid use
mentation rate. C-reactive protein. antislreptolysin-O liter. Rickets and osteomalacia (caused by vitamin-D defi­
protein clectrophore�is. quantitative immunoglobulins. and ciencies)
ANA subsets such as anti-Ro and anti-LA. anti-Sm. and Higher-than-nom,,1 levels of phosphorus (hyperphos­
anticentromcre antibodics. phatemia) may be caused by or associated with:
14 CHAPTER I Principles in Assessing Musculoskeletal Disorders

TAIlI F Ll

LABORATORY STUDIES USEFUL I N DIAGNOSING low BACK SYNDROMES


Test Measurement Low Back Implication

Complete blood count A measure of volume of circulating red May be diminished in systemic diseases (e.g.. neoplasm)
Hematocrit hemoglobin blood cells and in chronic spinal infections.
White blood count and differential Amount and type of circulating white Total white blood cell and shifts in differential Illay be
blood cells prescnt in spinal infections or occasionally in
spondyJoarthropalhics.
Sedimentation rate NonspecifiC test of inHammation Increased in spinal infections. may be increased in
neoplasms and spondylo3nhropalhies.
Chemistry A measure of circulating calcium and Calcium is elevated in hyperp.trathyroidism, may be
Calcium phosphorus elevated with primary and secondary osseous tumors.
Phosphoru� alterations in the distribution of calcium and phosphorus
accompany many metabolic disorder!\: but arc norma.l in
osteoporosis.
Alkaline pho�phi1tase Enzyme associated with bone rannalian; May be elevated in primary or secondary osseous
therefore: elevation implies increased neoplasllls.
bone formalion.
Acid phosphatase An enzyme associated with tumors Increased in prostatic tumors.
metastatic to bonc
Serum proteins (albumin globulin Measurement of amount and type Elevations of one fraction of globulin are associated with
protein electrophoresis) protcin circulating multiple myeloma.
HLA·B27 antigen A circulating antigen Usually individuals with spondyloarthropaLhies arc HLA·
827 positive. NOle 6·8% of men have this antigen and
therefore its presence is not confinnaLory of a
spondyloarthropathy.

fiLA. Human leukocyte antigen.


Adaptcd from Pope ML: OCl"II{J(J/;OIUll low back paill. asseSSIllt'/It, IY'I!(I/f1U.'f/I (lnd prcl'elll{(}I/. SI Louis. 1991, Mosby.

• Kidney failure Then the amylase values will return to normal in a few days.
Hypoparathyroidism (underactive parathyroid gland) In chronic pancreatitis, amylase levels will initially be mod­
Diabetic ketoacidosis (when first seen) erately elevated bul often decrease over time with progres­
Phosphate supplementation sive pancreas damage.
Amylase levels may also be significantly increased in
Alkaline Phosphatase patients with pancreatic duct obstruction. cancer of the pan­
Increased serum alkaline phosphatase is seen in states of creas, and gallbladder allacks. Urine and blood amylase
increased osteoblaSlic activity (hyperparathyroidism, osteo­ levels may also be elevated wilh a variety of other condi­
malacia. primary and mctastatic neoplasms), hepatobiliary tions, such as ovarian cancer, lung cancer, tubal pregnancy,
diseases charaClCriL.ed by some degree of inlra- or extrahe­ mumps, intestinal obstruction, or perforated ulcer, but
patic cholestasis. and in sepsis. chronic inHammatory bowel amylase tests are not generally used to diagnose or Illonilor
disease, and thyrotoxicosis. Isoenzyme determination may these disorders. Decreased blood and urine amylase levels
help detennine the organ or tissue responsible for an alkaline may indicate permanent damage to the amylase-producing
phosphatase elevation. cells in the pancreas. Increased blood amylase levels with
Decreased serum alkaline phosphatase may not be clini­ normal to low urine amylase levels may indicate decreased
cally significant. However, decreased serum levels have kidney function or the presence of a macroamylase. a benign
been observed in hypothyroidism. scurvy. kwashiorkor. complex of amylase and other proteins that accumulates in
achondroplastic dwarfism, deposition of radioactive materi­ the blood.
als in bone, and in the rare genetic condition hypophospha­ Given that reference values for amylase vary from labo­
tasia. ratory to laboratory, depending on the test method used, no
universally accepted numberexisls that can be called nornlal
A mylase or high.
In acute pancreatitis, amylase in the blood increases (often
to four to six times higher than the highest reference value, Anti-Nuclear A ntibody
sometimes called the upper limit of normal). The increase Anti-nuclear antibody (ANA) tests are performed using dif­
occurs within 12 hours of injury to the pancreas and gener­ ferent assays (indirect immunoHuorescence microscopy or
ally remains elevated until the cause is successfully treated. by enzyme linked immunoabsorbent assay). and results are
CHAPTER I Principles in Assessing Musculoskeletal Disorders 15

reported as a liler with a particular type o f immunofluores­ the diffuse form is associated with autoantibodies to the
cence pattern (when positive). Low-level titers are consid­ anti-ScI-70.
ered negative, whereas increased lilers, such as I : 320, are A positive result on the ANA may also show up in
positive and indicate an elevated concentration of ANAs. patients with Raynaud disease. rheumatoid arthritis. der­
ANA shows up on indirect immunofluorescence as fluo­ matomyosilis, mixed connective tissue disease. and other
rescent patterns in cells that arc fixed to a slide that is autoimmune conditions.
evaluated under a microscope. Different patterns are associ­ Because symptoms may come and go. months or years
ated with a variety of autoimmune disorders. Some of the may be required to show a pattent that might suggest SLE
morc common patlems include: or any of the other autoimmune diseases.
Homogenous (diffuse)-associated with systemic lupus A negative ANA result makes SLE an unlikely diagnosis.
erythematosus (SLE) and mixed connective tissue Immediately repeating a negative ANA test is not usually
disease necessary: however. because of the episodic nature of auto­
Speckled-associated with SLE. Sjogren syndrome. immune diseases. repeating the ANA test at a future date
sclerodemta. polymyositis. rheumatoid arthritis. and may be worthwhile.
mixed connective tissue disease Aside from rare cases. further autoantibody (subset)
Nucleolar-associated with scleroderma and poly­ testing is not necessary if a patient has a negative ANA
myositis result.
Outline pattern (peripheraJ)-associated with SLE
An example of a positive resul t might be positive a/ Antislrepto(ysin-O Titer
J : 320 ,Ii/wioll ",i,h a homoge"ous pallem. Antistreptolysin-O ( A SO) titer test results can be reported
A positive ANA test result may suggest an autoimmune in several different ways: however. the interpretation is gen­
disease, but further specific testing is required to assist in erally the same: The higher the result is. the more antibody
making a final diagnosis. ANA test results can be positive that is present in the blood (unless a titer is perfonned. which
in people without any known autoimmune disease. Although is a ratio and therefore is interpreted differently).
this finding is not common. the frequency of a false positive The ASO antibody is either absent or present in very
ANA result increases as people get older. low concentrations in patients who have not had a recent
Approximately 95% of patients with SLE have a positive streptococcal (strep) infection. Antibodies are produced
ANA test result. If a patient also has symptoms of SLE. such approximately a week to a month after the initial slrep infec­
as anhritis. a rash. and autoimmune thrombocytopenia. then tion. ASO levels peak at approximately 4 to 6 weeks after
the patient probably has SLE. In cases such as these. a the illness and then taper off but may remain at detectible
positive ANA result can be useful to support the SLE diag­ levels for several months after the strep infection has
nosis. Two subset tests for specific types of autoantibodies. resolved.
such as anti-dsDNA and anti-Sm. may be ordered to help If the test is negative. or if ASO is present in very low
confimt that the condition is SLE. concentrations. then the patient 1110St likely has not had a
A positive ANA can also mean that the patient has drug­ recent strep infection. especially if a sample taken 1 0 to 1 4
induced lUpus. This condition is associated with the devel­ days later is also negative or minimal.
opment of aUloanlibodies to histones, which are water-soluble If the ASO level is high or is rising. then a recent strep
proteins rich in the amino acids lysine and arginine. An anti· infection has likely occurred. ASO levels that are initially
histone test may be ordered to support the diagnosis of high and then decline suggest that an infection has occurred
drug-induced lupus. and may be resolving.
Other conditions in which a positive ANA test result may The ASO test does not predict whether complications
be seen include: will occur after a strep infection, nor do they predict the
Sjogren syndrome: Between 40% and 70% of patients severity of the disease. If symptoms of rheumatic fever or
with this condition have a positive ANA test result. glomerulonephritis are present, an elevated ASO level may
Even though this finding supports the diagnosis, a be used to confirm the diagnosis.
negative result does not rule it out. The examiner may
want to test for two subsets of ANA: anti-SS-A (Ro) and Bence-Jones Protein
anti-SS-B (La). The frequency of autoantibodies to A Bence-Jones protein is a monoclonal globulin protein
SSA in patients with SjOgren syndrome can be 90% or found in the blood or urine. The isolated finding of a Bence­
greater. Jones protein is known as monoclonal gammopathy of
Scleroderma: Approximately 60% to 90% of patients uncertain significance. Finding this protein in the context of
with scleroderma have a positive ANA finding. In patients end-organ manifestations such as renal failure, lytic bone
who may have this condition. ANA subset tests can help disease. or anemia. or large numbers of plasma cells in the
distinguish two forms of the disease. l imited versus bone marrow of patients can be diagnostic of multiple
diffuse. The diffuse form is more severe. Limited disease myeloma.
is most closely associaled with the anticentromere patlem The proteins are antibody immunoglobulin-free light
of ANA staining (and the anticentromere test), whereas chains (paraproteins) and are produced by neoplastic plasma
16 C HAPTER I Principles i n Assessing M usculoskelelal Disorders

cells. The lighl chains can be delecled by healing or eleclro­ Calcium


phoresis of concentrated urine. Light chains precipitate A nonnal calcium result with other nom13l laboratory results
when heated 10 50· 10 60· C and re-dissolve aI 90· 10 100· means lhal Ihe patient has no problems with calcium melab·
C. These tests arc essential in patients who may bave Bence­ olism (use by the body).
Jones proteins in their urine because these proteins do not Because approximately one half of the calcium in Ihe
react with the reagents normally used in urinalysis dipsticks. blood is bound by albumin (a prolein). Ihese IwO lesls are
This circumstance lead� to false-negative results in people usually ordered logelher. Calcium values musl be inlerpreled
with Bence-Jones proteins in their urine undergoing stan­ in combination with albumin 10 delenlline if the calcium
dard urinaly�is. Various rarer conditions can produce Bence­ concentration of serum is appropriate. As albumin level�
Jones proteins. such as Waldenstrom macroglobulinemia rise, calcium rises as well. and vice versa.
and other mal ignancies. A high calcium level is called hypercalcemia, requiring
trearment for the underlying condition. Hypercalcemia is
Bilirubin usually caused by:
VeM.'boT/u Hyperparathyroidism ( i ncrease in paralhyroid gland
Excessive bilirubin kills developing brain cells in infanls funclion): This condilion is usually caused by a benign
and may cause mental retardation. physical abnonnalities, lumor on Ihe paralhyroid gland. This fonn of hypercal­
or blindness. Bilirubin in newborns must not become 100 cemia is usually mild and can be present for many years
high. When Ihe level of bilirubin is above a crilical lhresh­ before being nOliced.
old, special treatments arc initiated to lower it. An excessive Cancer: Cancer can cause hypercalccmia when it �preads
bilirubin level may resull from Ihe breakdown of red blood to the bones, which releases calcium into the blood. or
cells ( R BCs) caused by Rh blood Iyping incompatibililY. when cancer causes a hormone similar to parathyroid
(The mOlher is Rh negalive I Rh-I. lhe father is Rh posilive hormone to increase calcium levels.
I Rh+l. and Ihe felUs is Rh+: Ihe mOlher develops antibodies Olher causes of hypercalcemia include:
again;! Ihe newbom's RBCs. which are destroyed.) Hyperthyroidism
Sarcoidosis
Idl///.\ alld Childrell Tuberculosis
Bi lirubin level� can be used (0 idcIHify liver damage or Bone break!>. combined with bed rest or not moving
disease or to monitor the progression of jaundice. A conju­ for a long periods
gated bilirubin that is elevated may indicate some kind of Excess vitamin D intake
blockage of Ihe liver or bile duCI. hepmilis. lrauma 10 lhe Kidney lransplantation
l iver, a drug reaction. or long-Icnn alcohol abuse. Inherited High prolein levels (e.g .. if a lourniquel is used for 100
di,orders caused by abnonnal bilirubin melabolism (Gilbert, long while blood is collecled)
ROlOr. Dubin·Johnson. or Crigler·Najjar syndromes) may In this case, free or ionized calcium remains normal. High
also cause increased levels. levels of ionized calcium occur with all the conditions previ­
ously menlioned. excepl high prolein levels.
Blood Urea Nitrogen Low calcium levels. called hypocalcemia. mean that the
Increased blood urea nilrogen (BUN) levels suggesl impaired patient has insufficieJ1l calcium i n the blood or Ihal Ihe
kidney function. This elevation may be caused by acute or patient has insufficienl prolein in Ihe blood. The moS!
chronic kidney disease. damage. or failure; i t may also be common cause of low total calcium is low protein levels.
caused by a condilion Ihal resulls in decreased blood How especially low albumin. When low prolein i< Ihe problem.
(0 the kidneys, slich as congestive heart failure, shock. stress, the ionized calcium level remains normal.
recent heart attack, or severe bums; to conditions that cause Low calcium. known as hypocalcemia, is caused by many
Ob!<llflictiOIl of urine now: or to dchydrmion. conditions:
B U N concentrations may be elevated in the setting of Low prolein levels
excessive prolein catabolism (breakdown). significanlly Underaclive paralhyroid gland ( hypoparalhyroidism)
i ncrea!>.ed protein in the diet. or ga!>.lIointestinal bleeding Decreased dietary imake of calcium
(becau,e of Ihe prolein, presenl in the blood). Decreased levels of vitamin 0
Low BUN levels are not common and are not usually a Magnesium deficiency
cause for concern. They may be seen in severe liver disease, Excessive phosphorus
malnutrition. and sometimes when a patient is overhydnlled Acute inflammation of the pancreajo,
(excessive nuid volume): bUI Ihe B U N lesl is nol normally Chronic renal failure
used to diagnose or monitor these conditions. Calcium ions becoming bound 10 prole in (alkalosis)
Both decreased and increased B U N concentrations may Bone disease
be seen during a normal pregnancy. Malnutrition
I f one kidncy is fully funclional, B U N concenlralions Alcoholism
may be nonnal even when significant dysfunction is presem Causes of low ionized calcium Icvels include all of these
in Ihe olher kidney. condition except low protein levels.
C HAPTER I Principles in Assessing Musculoskeletal Disorde" 17

Chloride Glucose
Increased levels of chloride (hyperch/oremia) usually indi­ High levels of glucose most frequently indicate diabetes, but
cate dehydration, but high levels can also occur with any many other diseases and conditions can also cause elevated
other problem that causes high blood sodium. Hyperchlore­ glucose. The following information summarizes the meaning
mia also occurs when excessive base is lost from the body of the test results. These points are based on the clinical
( producing metabolic acidosis) or when a person hyperven­ practice recommendations of the American Diabetes Asso­
tilates (causing respiratory alkalosis). ciation (Table 1 -4).
Decreased levels of chloride (hypoch/oremia) occur with Some of the other diseases and conditions that can result
any disorder that causes low blood sodium. Hypochloremia in elevated glucose levels include:
also occurs with prolonged vomiting or gastric suction. • Acromegaly
chronic diarrhea. emphysema or other chronic lung disease Acute stress (response to trauma, hean attack, and
(causing respiratory acidosis), and with loss of acid from the stroke for instance)
body (causing metabolic alkalosis). • Chronic renal failure
Cushing syndrome
Cholesterol Drugs (e.g., conicosteroids, tricyclic antidepressants.
In a routine setling in which testing is perfonncd to screen diuretics, epinephrine, estrogens [birth control pills
for risk factors, the test results arc grouped in three catego­ and hormone replacement medications I, lithium, phe­
ries of risk: nytoin [ Dilantin"'" salicylates)
Desirable: A cholesterol level below 200 mg/dL Excessive food intake
(5. 1 8 mmol/L) is considered desirable and reflects a low Hyperthyroidism
risk of heart disease. Pancreatic cancer
Borderline high: A cholesterol level of 200 to 240 mg/dL Pancreatitis
(5. 1 8-6.22 mmol/L) is considered 10 reflect moderate Low to nondetectible urine glucose results are considered
risk. normal. Anything that raises blood glucose levels also has
High risk: A cholesterol level above 240 mg/dL the potential to elevate urine glucose levels. Increased urine
(6.22 mmol/L) is considered high risk. glucose levels may be seen with medications such as estro­
gens and chloral hydrate and with some forms of renal
Creatinine disease.
Increased creatinine levels in the blood suggest diseases Moderately increased levels may be seen with prediabe­
or conditions that affect kidney function, including the tes. This condition, if left untreated. often leads to type 2
fol lowing: diabetes.
Damage to or swelling of blood vessels in the kidneys Low glucose levels (hypoglycemia) are also seen
(glomerulonephritis) caused by. for example, infection or with:
autoimmune diseases Adrenal insufficiency
Bacterial infection of the kidneys (pyelonephritis) Drinking alcohol
Death of cells in the kidneys' small tubes (acute tubular Drugs (e.g., acetaminophen, anabolic ;tcroids)
necrosis) caused. for example, by drugs or toxins Extensive liver disease
Prostate disease, kidney stone. or other causes of urinary Hypopituitarism
tracl obstruction • Hypothyroidism
Reduced blood flow to the kidney caused by shock, dehy­ Insulin overdose
drmion. congestive hean failure. atherosclerosis, or com­ Insulinomas (insulin-producing pancreatic tumors)
plications of diabetes Starvation
Creatinine can also increase temporarily as a result of
muscle injury. Low levels of creatinine are not common and
are not usually a cause for concern and can be seen with Heavy Metal Screens
conditions that result in decreased muscle mass. Creatinine Heavy metals are increasingly responsible for the produc­
levels are generally slightly lower during pregnancy. tion of free radicals. as well as undermining the illlernal
ell v;romnellf and body chemistry. The main concern is not
Creatinine Phosphokinase so much the type of metal that may be detected but rather if
A high creatinine phosphokinase (CK) level, or one that metals in their ionic form are present. Chemical analyses can
goes up from the first to the second or later samples, gener­ establish the exposure to excessive amounts of toxic sub­
ally indicales some damage to the heart or other muscles; it stances. Many analytical procedures can be performed if the
can also indicate that the patient's muscles have experienced problem warrants me investment of time and the client is
heavy use. If the patient has experienced a heart allack and willing to pay for the procedure. Although screening samples
the CK is high, a more specific test (troponin or CK-MB) for cenain groups of chemicals is possible. analyzing for
should be ordered to determine if the patient's heart is everything or checking for poisons is not feasible. Heavy
damaged. metals include arsenic. cadmium. calcium. cobalt, copper,
18 C HAPTER I Principles i n Assessing Musculoskeletal Disorders

TAIl L E 1 -4

SUMMARY or GLUCOSE TOLERANCE TESTS AND I NTERPRETATtONS

Fasting Blood Glucose


From 70 to 99 rng/dL £3.9 to 5.5 mmol/L) Normal glucose tolerance
From 1 00 LO 125 OlgldL {5.6 to 6.9 mmoVL) Impaired fasting glucose (prediabclc..'iI)
1 26 mgldL (7.0 mmol/L) and above on more than one tcsling occasion Diabetes

Oral Glucose Tolerance Test (OG1T) [except pregnancy] (2 hours after a 75-gram glucose drink)
Lc�s Lhan 1 40 mgldL (7.8 mmollL) Nonllai glucose tolerance
From 140 10 200 mgldL (7.8 10 1 1 . 1 mmollL) Impaired glucose lo\cram:e (pre-diabetes)
Over 200 mgldL ( 1 1 . 1 Illmul/L) on more limn one testing occasion Diabetes

Gestational Diabetes Screening: Glucose Challenge Test (1 hour after a 50-gram glucose drink)
Less than 140* mg/dL (7.8 mmoVL) Normal glucose tolerance
1 40· mgldL (7.8 rnmollL) and over Abnormal. needs OGTI (�ce below)

Gestational Diabetes Diagnoslic: OGT'I' ( I OO-gram glucose drink)


Fu!.ting· 95 mg/dL (5.3 mmolfL)
I hour after glucose load 180 mgidL ( 1 0.0 mmollL)
2 hours after glucose load' 155 IllgidL (8.6 mmollL)
3 hours after glucose load' 140 mgidL (7.8 mmol/L)

"'Some use ,\ cUloff of > I JO mg/LIL (7.2 mmollL) bccau..c that identitic!; 901H of women with ge�w.lional diuOOlc.... compureel to SOIk idcmilicd using the
lhreshold or >140 mgldL (7.8 mmoIlL).
If two or more val ue... :u-c ubove the criteria. gestutionul diabetes is diagnosed.
A 75-gr:lI11 glucose load may be used. although thh method is not as v.cll validated as the IOO-gram OGTI: the 3-hour ..ample b not dr:lV.n iPS gram... is
u�cll.

cyanide. f1 uoride, iron, lead, magnesium, manganese. Below-normal hemoglobin levels may lead to anemia
mercury, molybdenum, phosphorus, potassium, selenium. that can be the result of:
sodium, and zinc. Iron deficiency or deficiencies in essential vitamins of
other elements such as vitamin B 1 2, folate. vitamin
Hematocrit B6
Decreased hematocrit indicates anemia, such as that caused • lnherited hemoglobin defects. such as sickle cell
by iron deficiency or other deficiencies. Further testing anemia or thalassemias
Illay be necessary to detennine the exact cause of the Other inherited derects arfecting the RBCs
anemia. CilThosis of the liver (during which the liver becomes
Other conditions that can result in a low hematocrit scarred)
include vitamin or mineral deficiencies, recent bleeding, cir­ Excessive bleeding
rhosis of the liver, and malignancies. Excessive destruction of RBCs
The 1l10�t common cause of increased hematocrit is dehy­ Kidney disease
dration, and with adequate fluid intake, the hematocrit • Other chronic illnesses
returns to normal. However, increased levels may reflect a Bone marrow failure or aplastic anemia
condition called pol.\'cythemia \Iera-thm is, when a peniOll Cancers lhat afrect the bone marrow
ha, more than the normal number of RBCs. Increa,ed hema­
tocrit can be caused by a problem with the bone marrow or. Human Leukocyte Antigen-B27
more commonly. as compensation for inadequate lung func­ Human leukocyte antigen ( H LA)-B27 will be present or
tion (the bone marrow manufacLUres more RBCs to carry absent. I f it is present. then the HLA-B27 antigen ( protein
enough oxygen throughout the body). structure) exists on the surface or the body's while blood
cell> (WBCs) ,uld nucleated cells. I f a patient has HLA-B27
Hemoglobin and has symptoms such as chronic pain. innammalion. and
Normal values in an adult nre 1 2 to 1 8 gJdL ( 1 00 mm/dL) degenerative changes to his bones (as seen on X-ray exam­
of blood. Above-nonnal hemoglobin levels may be the result ination), then it supports a diagnosis of ankylosing spondy­
or: litis (AS), Reiter syndrome. or another autoimmune disorder
Dehydration thal is a'Sociated with the presence or HLA-B27. This cir­
Excessive production of RBCs in the bone marrow cumstance is especially true ir the patient is young. male
Severe lung disease gender. and ir the patient experienced the first symptoms
Several other conditions before the age of -10.
CHAPTER I Principles in Assessing Musculoskeletal Disorders 19

The presence o f HLA-B27 may also seen w i t h other and unjaundiced patients. Values under 1 000 units arc of no
autoimmune conditions huch as: help in the differential diagnosis of jaundice, but values
Isolated acute anterior uveitis above 1000 units are highly indicative of b i liary ob;truction.
• Undifferentiated spondyloarthropathies The differentiation of intra- from extrahepatic obstruction,
• Entcropathic synovitis as well as of malignant from benign jaundice. cannot gener­
I f HLA-B27 is not present. then the symptoms arc likely a l l y be e;tablished by this single tesl.
the result of an HLA-B27-associated autoimmune disorder.
( Exceptions to this rule, however. arc approxi mately 10% of Lipase
patients with AS and 40% to 50% of those with Reiter syn­ In acute pancreatitis, l i pase levels are freq uently very high,
drome w i l l be negative for HLA-B27.) often 5 to 1 0 times higher than the highest reference value
At this time. identifying the presence of HLA-B27 does (often cal led the upper limit of normal). In acute pancreati­
not predict the likel ihood of developing an autoimmune tis. l i pase concentrations rise within 24 to 48 hours of an
disease. If a patient does have an associated disorder. the acute pancremic atlack and may remain elevated for approx­
presence of HLA-B27 cannot be used to tell which disease imately 5 to 7 days. Concentrations may also be increased
is present, how quickly it will progress, its severity. prog­ with pancreatic duct obstruction. pancreatic cancer. and
nosis. or the degree of organ involvement. other pancreatic diseases.
Moderately increased l ipa;e values may occur in other
Lactic Dehydrogenase Compression Test n conditions such as kidney disease (caused by decreased
Elevated levels of lactic dehydrogenase (LDH) and changes clearance from the blood), salivary gland infl ammation, a
in the ratio of the LDH isocl1tymcs usually indicalc some bowel obstruction, or peptic ulcer dise,,-,e, although the
type of tissue damage. LDH levels w i l l usually rise as the l ipase test is not nOnllally lIsed to monitor these conditions.
cellular destruction begins. peak after some time period. and Decreased li pase levels may indicate pennanent damage to
then begin to fal l . For instance. when someone has a heart the l i pase-producing cells in the pancreas.
allack, blood levels of total LDH will rise within 24 to 48
hour;, peak in 2 to 3 days, and return to normal in 1 0 to 1 4 lipidS
days. The lipid profile includes IOtal cholesterol, high-density
Elevated levels of LDI-I may be seen with: l ipoprotein ( H D L ) cholesterol (often called good choles­
Cerebrovascular accident (CVA. stroke) terol). low-density l ipoprotein (LDL) cholesterol (often
Drugs (c.g .. anesthetics, aspirin, narcotics. procain­ called bad cholesterol). and triglycerides. The report w i l l
amide_ alcohol) sometimes includc additional calcu lated valucs such a'\
Hemolytic anemia H DULDL ratio or a risk score based on lipid profile results,
Pernicious anemias ( megaloblastic anemias) age. sex, and other risk factors.
I nfectiolls mononucleosis A normal level for fasting triglycerides is less than
I ntestinal and pul monary infarction (tissue deat h ) 1 50 mgldL ( 1 .70 mmoI/L). Having high triglycerides
Kidney disease without also having high cholesterol is unusual. Most treat­
Liver disease ments for heart disease risk will be aimed at lowering LDL
Muscular dystrophy cholesterol. However, the type of treatment used to lower
Pancreatitis LDL cholesterol may differ depending on whether triglyc­
Some cancers erides are high or normal.
With .!tome chronic and progressive conditions. and Triglycerides that arc very high (greater than 1 000 mgldl
;ol11e drugs. moderately elevated LDH levels may 1 1 1 .30 mmol/L]) increases the risk of developing pancreati­
per�isl. tis. Treatment to lower trig lycerides should be started a;
Low and normal levels of LDH do not usually indicate a soon as possible.
problem. Low levels are sometimes seen when a patient
ingests large amounts of ascorbic acid (vitamin C). Lupus Erythematosus Cell Prep
The lupus erythematosus (LE) cell prep was the primary
Latex Agglutination diagnosis of SLE for nearly 50 years. having a sensitivity of
Various rapid tests identifying bacterial antigen from body nearly 50%. This test has been replaced by a more sensitive
nuids are becoming increasingly avail able. One of these test. ANA. which measures the binding of a patient's serum
technique;. latex agglutination. is frequently used 10 test antibodies to HEp-2 cell nuclei.
cerebrospinal fluid in chi ldren being eval uated for possible The results of each of the lupus anticoagulant te", lead
meningitis. Early diagnosis of meningitis can lead to prompt either toward or away from the likeli hood of having a lupus
treatment. anticoagulant. Although the tests performed may vary. they
u,u,lIly begin with a prolonged panial thromboplastin time
Leucine Aminopeptidase ( PTT ) .
Serum leucine aminopeptidase determination is a useful If the PTT or lupus anticoagulant (LA)-PTT is prolonged,
screening procedure for hepatobi l iary disease in jaundiced and mixing it with normal pooled plasma does not correct
20 C HAPTER I Principles in Assessing Musculoskeletal Disorders

the result, then an inhibitor is likely present. If the pro­ Chronic antacid use
longed test corrects when phospholipid is added, then a Rickets and osteomalacia (caused by vitamin-D
lupus anticoagulant is likely present. (After heparin con­ deficiencies)
tamination. a lupus 3micoagulalll is the most common H igher-than-normal levels of phosphorus ( hyperphos­
reason for a prolonged PTr.) phatemia) may be caused by or associated with:
If the PTr is not prolonged, a lupus anticoagulant may Kidney failure
not be present, the test reagents may contain too much Hypoparathyroidism (underactive parathyroid gland)
phospholipid. or the test may not be sufficiently sensitive •
Diabetic ketoacidosis (when first seen)
to pick up the lupus anticoagulant. The LA-sensitive PTr Phosphate supplementation
may need to be performed.
If a dilute Russell viper venom time or modified Russell Potassium
viper venom time test is prolonged and does not correct Increased potassium levels indicate hyperkalemia. Increased
when mixed with normal pooled plasma but does corrCCl levels may also indicate the following health conditions:
with Ihe addition of phospholipids, then a phospholipid Excessive dietary potassium intake ( Fruits are par­
antibody is likely present. ticularly high in potassium; therefore, excessive
If a thrombin time lest is nonnal, then heparin contamina­ intake of fruits or juices may contribute to high
tion is excluded. potassium.)
If a fibrinogen test is nonnal. then fibrinogen is likely Excessive imrdvenous potassium intake
sufficient for normal clot formation. Acute or chronic kidney failure
Other tests that may be performed 10 help confinn the Addison disease
diagnosis of a lupus anticoagulant include: Hypoaldosteronism
Platelet neutralization (This test uses platelets as a Injury to tissue
source of phospholipids.) Infection
Hexagonal ( I I ) phase phospholipid assay (Staclot-LA Diabetes
test) Dehydration
Kaolin clotting time Cenain drugs can also cause hyperkalemia in a small
Tissue thromboplastin inhibition lest percentage of patients. Among these drugs are nonsteroidal
"'
Venereal Disease Research Laboratory (VORL) or untiinnammatory drugs (e.g., Advil"'. MOlIin , Nuprin- ).
rapid plasma reagin (RPR) (These tests are used to beta-blockers (e.g.. propranolol atenolol). angiotensin­
detect syphilis. Their reagents arc made of cardiolipin converting enzyme inhibitors (e.g .. captopril. enulapril.
and they may give a false positive result for both lisinopril). and potassium-sparing diuretics (e.g .• triam­
anlicardiolipin antibodies and for lupus anticoagu­ terene. amiloride. spironolactone).
lant.) Decreased levels of potassium indicate hypokalemia.
Coagulation factors (These tests may be ordered to Decreased levels may occur in several conditions. particu­
rule out factor deficiencies that may cause a prolonged larly:
PTr and bleeding episodes.) Dehydration
Prothrombin lime •
Vomiting
Other tests that may be performed in addition to lupus Diarrhea
anticoagulant testing include: Deficient potassium intake ( rare)
Anticardiolipin and anti-beta2-glycoprotein I antibod­
ies to check for anti phospholipid syndrome Protein-Bound Iodine
Platelet count (Mild to moderate thrombocytopenia is Iodine binds to protein. mainly thyroxin. in the plasma. The
often seen a10ng with the lupus anticoagulant and may thyroid honnone is precipitated by protein-denaturing
be caused by anticoagulant I heparinl therapy.) agents. and the amount of iodine in a protein precipitate
generally indicates the amount of thyroid hormone present
Phosphorus and is thus an index of thyroid activity. Various values are
Dietary deficiencies in phosphorus are rare but may be seen given for thyroid function: hypothyroidism. 0 to 3.5 mcg!
with alcoholism and malnutrition. Low levels of phosphorus mL of protein-bound iodine: euthyroidism. 3.5 to 8.0 g!mL:
(hypophosphatemia) may also be caused by or associated hyperthyroidism, values higher than 8 mcg!mL.
with:

Hypercalcemia (high levels of calcium) especially as Red Blood Cell Count
a result of hyperparathyroidism A high RBC count may indicate congenital heart disease.

Overu�e of diuretics (drugs that encourage urination) dehydration. obstructive lung disease. or bone marrow
Severe bUnls overproduction. A high RBC count is also seen in bela­
Diabetic ketoacidosis (after treatment) thalassemia trait, a benign condition with little or no anemia.
Hypothyroidism A low RBC count may indicate anemia. bleeding. kidney
Hypokalemia (low levels of potassium) disease. bone marrow failure (for instance. from radiation or
CHAPTER I Principles in Assessing Musculoskeletal Disorders 2\

a tumor). malnutrition. o r other call�es. A l o w count may mine whether other deficiencies or excesses exiM. Frequently
abo indicate nutritional deficiencies of iron. foJ:.uc. vitamin the balance among thcsc different substances. and the
B 12, and vitamin 86. changes in them. arc just as important as the concemratiolls.
Calcium can be used as a diagnostic test jf the patient pres­
Rheumatoid A rthritis Factor (RA Latex) Test ents wilh symptoms thai suggest:
A mpid latex .Iide agglutination te,t ror the qualitative and Kidney stones
semi-quantitative determ ination of rheumatoid arthritis • Bone disease
factor in human serum. The presence of these aUlOalllibodies eurologic disorders
to human immunoglobu l i n G (IgG ) is a userul diagnostic The lotal calcium lesl is Ihe leS( mo;! rrequenlly ordered
tool ror aClive rheumHloid arthrilis ( R A J becau,e high li tres to cvaluatc calcium status. I n most cases. it is a good rencc­
indicate severe disease. tion of the amount of free calcium involved in Il1cLabolism
since the balance between free and bound is usually �lable
Serum Glutamate Oxaloacetale Transaminase and predictable. However. in !'tome patients. the balance
Very high levels or aspanate aminOlransremse (AST) ( more between bound and free cnlciull1 is disturbed and total
than 10 Lime!' the highcM nOfmal lcvel) are usually the result calcium is not a good reflection of calcium status. In thoo,e
of acute hepatitis. oflen caw.,cd by a virus infection. In acute circumstances. measurement of ioniL.cd calcium i!\ neces­
hepat ili,. AST level> u,ually stay high ror approx imately I sary. Some conditions where ionized calciull1 should be the
to 2 months but can take as long as 3 to 6 l110lllhs to return test of choice include: critically i l l patients who are receiv­
to normal. I n chronic hepatitis. AST levels are usually not ing transfusions or I V fluids. patients undergoing major
a:-. high as they arc in acute hepat itis. often les� than four surgery, and paticnts with blood protein abnormalities like
time� the highe�t normal level. I n chronic hepatitis. AST low albumin. Large fluctuations in ionized calcium can
onen varies between nonnal and slightly increased: there­ cau!\c the hean to slow down or to beat too rapidly. can cause
fore. examiner.!> w i l l typically order the test frequently to muscles to go into spasm (tetany). and can causc confusion
determ ine the pattem. or even coma. In critically i l l patients, it is extremely im por­
In '!'ol1le di seases of the liver. especially when the bile tant to know the ionized calcium levcl to be able to i ntervene
duct� are blocked. or with cirrhosis and cenain cancers of and prevent serious cOll1p l i cations. These include the fol­
the liver. AST may be close to normal. but it i l1crease� more lowing:
often than alanine aminotnll1,remse (ALT). When liver I . Kidney di scase. becausc low calcium is especially
damage is the result of alcohol, AST often increases much common i n those wilh kidney failure:
more than A LT. (This pattem is seen with a few Olher liver 2. Symptoms of too much calcium. such a!\ fatigue.
dise,,,es.) AST i, also increased arter heart anacks and wilh weakness. loss of appetite. nausea. VOITIltlllg. con­
mu�cle injury. usually to a much greater degree than is stipation. abdominal pain. urinary frequency. and
A LT. increased thirM:
3. Symptoms of low calcium. such as cramp� i n your
Serum Ionized Calcium abdomen. muscle cramps. or tingling fi ngers: or
Blood calcium is tested to screen for. di agnose. and monitor 4. Olher diseases that have been associaled with abnor­
a range of conditions relating to the bones. hean, nerves. mal blood calcium. such as thyroid d isease. inteMinal
kidneys. and leelh. Blood calcium level> do not directly lell disease. cancer. or poor nutrition.
how much calcium i s in the bones. but ralher, how much An ion ized calcium test b, ordered when the patient ha�
calcium is circulating i n lhe blood. numbness around the mouth and i n the hands and feet and
A total calcium level is often measured as pan of health muscle spasms in the same areas. These can be symptoms
screen ing. It is incl uded in the comprehensive metabolic of low levels of ionized calcium. However. when calcium
panel (CMP) and the basic metabolic panel ( B M P)-groups levels rail slowly. many people have no symploms at a l l . The
of tests that are performed together to di agnose or monitor patient may need calcium moniLOring when they have cenain
a variety of conditions. When an abnormal total calcium kinds or cancer (particularly breast. lung. head and neck,
result is obtai ned. it i s viewed as an indicator or some kind kidney. and multiple myeloma), have kidney disease, or
of underlying problem. To help diagnose the underlying have had a kidney transplant. Monitoring may also be neces­
problem. additional tests are often done to measure ionized sary when the patient is being treated for abnormal calcium
calcium. urine calcium, phosphorous, magnesium. vitamin levels to evaluate the effecti veness of treatment� such as
D. and paralhyroid hormone (PTH). Parathyroid hormone calcium or vitamin D supplements.
and vitamin D arc responsible for maintaining calcium con­ Calcium absorpLion. usc. and excretion are regulated and
centrations in the blood within a narrow range of values. Slabil iLed by a reedback loop involving PTH and vitamin D.
Measuring calcium and PTH together can help determine Conditions and diseases that di�rupt calcium regulation can
whether the parathyroid gland is runclioning normally. Mea­ cause inappropriate acute or chronic elevmions or decreases
suring urine calcium can hclp determinc whether the kidneys in calcium and lead to symptoms or hypercalcemia or hypo­
are excreting the proper amount of calcium. and testing for calcemia. In most cases. total calcium is measured because
vitamin D, phosphorus. and/or magnesium can help deler- the test is more easily performed than the ionized calcium
22 CHAPTER I Principles in Assessing M usculoskeletal Disorders

test and requires no special handling of the blood ample. proLein is present. The value of protein electrophoresis
TOlal calcium is usually a good reflection of free calcium lies in the proportions of proLeins and in the pauerns Lhey
since the free and bound forms are typically each about half creaLe on the elecLrophoresis graph. The value of immuno­
of the total. However. because about half the calcium in fixation electrophoresis is in identifying the presence of
blood is bound to protein . lOlal calcium lest results can be a panicular Lype of i m munoglobulin. For example. certain
affected by high or low levels of protein. In such cases. it is conditions or diseases may be associated with decreases
morc useful to measure free calcium directly using an or i ncreases in various serum proteins, as reflected as
ionized calcium test. follows:
Albumin
Normal Calcium Decreased: with malnutrition and malabsorption.
A normal lOla) or ionized calcium resulL together with pregnancy. kidney disease (especially nephroLic syn­
other normal lab results generally means that calcium drome), liver disease, inflammatory conditions, and
metabolism is normal and blood levels arc being appropri­ proLein-losing syndromes
ately regulated. II/creased: with dehydration
• Alpha, globulin
IIigil To/al Calcillm-llypercalcemia Decreased: in congenital emphysema (CII-antitrypsin
Two of the morc common causes of hypercalcemia are: deficiency, a rare genetic disease) or severe liver
1. Hyperparathyroidism. an increase in parathyroid disease
gland function: This condition is usually caused by a Increased: in acute or chronic inflammatory diseases
benign tumor of the parathyroid gland. This fonn of Alpha, globulin
hypercalcemia is usually mild and can be present for Decreased: WiLh hyperthyroidism or severe liver
many years before being noticed. disease. hemolysis (RBC breakage)
2. Cancer: Cancer can cause hypercalcemia when iL • II/creased: with kidney disease ( nephrotic syndrome).
spreads to the bones, which releases calcium into the acute or chronic inflammatory disease
blood. or when a cancer produces a honnone similar BeLa globulin
to PTH, resulting in increased calcium levels. Decreased: with malnutrition. cirrhosis
Some oLher causes of hypercalcemia include: Increased: with hypercholesterolemia, iron deficiency
1 . Hyperthyroidism anemia, some cases of multiple myeloma. or mono­
2. Sarcoidosis clonal gammopaLhies of undetermined significance
3. Tuberculosis (MGUS)
4. Prolonged immobilizaLion Gamma globulin
5. Excess Vitamin D i ntake Decreased: variety of genetic i m mune disorders. and
6. Kidney LransplanL in secondary immune deficiency
• Increased: polyclonal-chronic inflammatory disease.
Low Tolal Calciwll-Uypoca[cemia RA, SLE. cirrhosis. chronic liver disease. aCULe and
The most common cause of low total calcium is: chronic infection, recent immunization.
I. Low blood proLein levels. especially a low level of • Increased: monoclonal-Waldenstrom macroglobu­
albumin. I n this condiLion. only the bound calcium is linemia. muhiple myeloma. MGUS
low. Ionized calcium remains normal and calcium TOLal protein
metabolism is being regulaLed appropriaLely. Low total protein levels can suggest a liver disorder, a
Some oLher causes of hypocalcemia include: kidney disorder. or a disorder i n which protein is nOL digesLed
I . U nderacLive parathyroid gland (hypoparaLhyroid­ or absorbed properly. Some laboraLories also report the cal­
ism) culated raLio of albumin LO globulins ( NG raLio). Normally,
2. InheriLed resistance LO the effecLs of parathyroid albumin slighLly exceeds globulins. giving a normal A/G
hormone raLio of slighLly over I . Because disease SLates affect Lhe
3. Extreme deficiency in dietary calcium relaLive changes i n albumin and globulins i n differenL ways.
4. Decreased levels of viLamin D this ratio may provide a clue to the physician as to the cause
5. Magnesium deficiency of the change in proLein levels. A low NG raLio may renect
6. Increased levels of phosphorus overproducLion of globulins. such as seen in muhiple
7. Acute i nflammalion of the pancreas ( pancrealitis) myeloma or autoimmune diseases, or underproduction of
8. Renal failure albumin. such as occurs with cirrhosis, or selective loss of
9. MalnUlriLion albumin from the circulaLion, as occurs with nephroLic syn­
10. Alcoholism drome. A high NG raLio suggesLs underproducLion of immu­
noglobulins. as may be seen in some genetic deficiencies
Serum Protein Electrophoresis and in some leukemias. More specific tests, such as albumin.
Protein and i m munofixation electrophoresis tests give liver enzyme tests, and serum protein elecLrophoresis. must
the examiner a rough eSlimate of how much of each be performed to make an accurate diagnosis.
CHAPTER I Principles in Assessing M uscu.loskeletal Disorders 23

Sodium GII/cose
Hyponatremia is rarely caused by decreased sodium intake Normally, urine contains no glucose. A poslLJve glucose
(deficient dietary intake or deficient sodium in intravenous occurs in diabetes. The number of people who have glucose
fluids). Most commonly. hyponatremia is caused by sodium in their urine with normal blood glucose levels is small;
loss (Addison disease, diarrhea, excessive sweating, diuretic however, any glucose in the urine would raise the possibility
administration, or kidney disease). In some cases. hypona­ of diabetes or glucose intolerance.
tremia is caused by increased water (drinking too much
water, heart failure, cirrhosis, kidney diseases that cause Proteiu
protein loss [ nephrotic syndrome]). In a large number of Normally no protein is detectable on a urinalysis strip.
diseases (particularly those involving the brain and the Protein can indicate ki dn ey damage, blood in the urine, or
lungs, many kinds of cancer, and with some drugs), the body an i n fection. Up to 10% of children can have protein in their
makes too much 3Illidiurclic hormone, causing the patient urine. Certain diseases require the use of a special. more
to keep too much water in the body. sensitive (and more expensive) test for protei n called a
A high blood sodium level means the patient has hyper­ microalbumin test. A microalbum i n test is useful in screen­
natremia, almost always caused by excessive loss of water ing for early damage to the kidneys from di abetes, for
(dehydration) withollt enough water intake. Symptoms instance.
include dry mucous membranes. lhirsl, agitation, restless­
ness, acti ng irrationally, and coma or convulsions if levels Illood
rise extremely high. In rare cases, hypernatremia may be NormaJl y, urine comains no blood. Blood can indicate an
caused by increased salt intake without enough water, i n fection, kidney stones, trauma. or bleeding from a bladder
Cushing syndrome, or insufficient antidiuretic hormone or kidney tumor and may be hemolyzed (dissolved blood)
(diabetes insipidus). or nonhemolyzed (intacl RBCs). R are ly, musc le inju ry can
Sodium urine concentrations must be evaluated in asso­ cause myoglobin to appear in the urine, which also causes
ciation with blood levels. Concentrations may mirror blood the reagent pad to indicate blood falsely.
levels or be the opposite. The body normally excretes excess
sodium; thus the concentration in the urine may be elevated Bilirubin
because it is elevated i n the blood . .It may also be elevated Normally, urine cOlllains no bilirubin or u rob i l inogen. These
in the urine when the body is losing excessive sodium. In substances are pigments that arc cleared by the l iver. I n livcr
this case. the blood level would be normal to low. I f blood or ga ll bladder disease, they may appear in the urine as
sodium levels are low as a resull of i nsufficient intake. then well.
urine concentrations will also be low.
Nitrate
Uric Acid Normally negative. nitrate i n the urine usually indicates a
Higher-than-normal uric acid levels mean that the body is urinary tract infection.
not handling the breakdown of purines well. .Increased con­
centrations of uric acid can cause crystals to form in the Leukocyte Esterase
joints. which leads to the joint inHammation and pain char­ Leukocyte esterase is normally negative. Leukocytes are the
acteristics of gout. Uric acid can also form crystals or kidney WBCs (or pus cells). WBCs in the urine suggest a urinary
stones lhat can damage the kidneys. tract infection.
Low levels of uric acid in the blood are seen much less
commonl y than high levels and are seldom considered Sediment
cause for concern. Although low values can be associated I tems such as mucous cells and squamous cells arc com­
with some kinds of liver or kidney diseases, exposure to monly seen. Abnormal findings would include >15 RBCsl
toxic compounds, and rarely as the result of an i nherited hpf (hematuria)-additional i nvestigation must be donc to
metabolic defect, these conditions are typically identified by determi n e the source of the hematuria (renal or postrenal);
other tests and symptoms and not by an isolated low uric or >10 WBCs/hpf (pyuria)-additional investigation must
acid result. be done to determine the source of the pyuria (renal or
postrenal); or the presence of crystals, casts, renal tubular
Urinalysis cells. or bacteria (bacteria can be presen t if contamination
pH was present at the time of collection).
Acid ity of urine is measllred by the pH.
White Blood Cell Count
.S'pecijil: Grat'ily An elevated number of white blood cells ( WBCs) is called
Specific gravity (SO) measures how dilute the urine is. leukocytosis, which can result rrom bacterial infections.
Water has a SG of 1.000 . Most urine is approximately1.0 10, inflammation, leukemia, trauma, or stress.
but it can vary greatly depending on when the patient drank A decreased WBC cou n t is called leukopenia. which
Iluids last or if the patient is dehydrated. can result from many differen t situations, such as chemo-
24 CHAPTER I Principles i n Assessing Musculoskeletal Disorders

lhcrapy, radiation therapy. or diseases of the Immune fall below 1 0 mg/L, clinically active inflammation is no
system. longer present.
Blood and serum panels that are lIseful in the differential • RA latex
diagno1'>is include:
Bone panel Liver Function Tests
Alkaline phosphatase Alkaline phosphatase
Calcium B i lirubin-total and direct
Complete blood eOllnt (CBC) Cholesterol
Table 1 -5 explains whm increases or decreases in ench of Gamma-giutamyl transpeptidase (GGT) or peptidase
the components of the esc may mean. Elevated GGT levels indicate that something is going on
wiLh the liver but nOI specifically what. In general, the higher
the level is, the greater the inslI!1 will be to " liver. Elevated
SPEClTIC PROFILES
levels Illay be caused by liver disease. but they may aho be
Arthritis Panel caused by congestive heart failure. alcohol consumption.
ANA screen and use of many prescription and nonprescription drugs.
C-reactive protein (CRP) including nonsteroidal antiinflammatory drugs. lipid­
A high or increasing amount ofCRP in the blood suggests lowering drugs. antibiotics. histamine blockers ( used to treat
an acute infection or inflammation. In a healthy person, CRP excess slOmach acid production), antifungal agents. seizure
is usually less than 10 mg/L. Most infections and inflamma­ control medications. antidepressants. and hormones slich as
tions re>lilt in CRP levels above 1 00 mg/L. l f the CRP level testosterone. Oral contraceptives (birth control pills) and
drops. it means inflammation is being reduced. When results clofibrate can decrease GGT levels.

TAB l E 1-5

SUMMARY OF CBC COMPONENTS AND INTERP RETATIONS

Test Name IncreascdU1>ecrcased

WBC White blood cell May be increased with i nfections, inflammation, cancer. leukemia;
decre;'lscd with some medications (such as methotrexate). some
autoimmune conditions, some severe infections. bone marrow fuilurc.
and congenital marrow aplasia ( marrow docsn't develop normally)
% Neutrophil NeutrophillBandfSeg This is a dynamic population that varies somewhat rrom day to day
% Lymph!'> Lymphocyte depending on what is going on in the body. Significant increase!'> in
% Mono Monocyte panicu lar types are a.s�ociated with di frerent temporary/acute amVor
% Eo!'> Eosinophi l chronic conditions. An example or this is lhe increased number or
o/r- Ba�o Basophil lymphocytes seen with lymphocytic leukemia. For more informalion,
Neul rophil Neu troph illBandfSeg see Blood S mear and WBC.
Lymphs Ly mphocyte
Mono Monocyte
Eos Eosinophi l
Ba'io Basophil
RBC Red blood cell Decreased wil.h anemia: incrcased whcn too many made and with fluid
loss due 10 di arrhea, dehydration. burns
Hgh Hcmoglobin Mirrors RBe resu l�
Het Hematocri t Mirrors RBe results
MeV Mean corpu scular volumc Increased with BI: and Folate deficiency: dec reased wilh iron deficiency
and thalassemia
MCH Mean corpuscular hemoglobin Mirrors MCV results
MCHC Mean corpu !'>cular hemoglobin concentration May be del'reased when MCV is decrca!'>cd; increases limited to amount
of Hgb that will fil in.�ide a RBe
RDW Red blood cell distribution width Increased ROW i ndicutc:-. mixed popu lati on of RBCs: immature RBClt
tend to be larger
Platelet Platelet Decreased or increa�ed with conditions lhat affect platelet production:
decreased when greater numbers used. a.s with bleeding: decreased with
some inherited disorders (such as Wiskott-Aldrich. Bernnrd·Soulicr),
with Systemic lupus erythcmatoslI:', pernicious anemia, hypersplenism
(splcen takcs 100 many Olll of circuhuion), leukcmia. and chemotherapy
MPV Mean platelet volu me Vary with platclet production; younger platelets are larger than older ones
CHAPTER I Principles in Assessing Musculoskeletal Disorders 25__

LDH (See previous discussion.) such a s temporal arteritis. polymyalgia rheumatica, and
Serum glutamate pyruvate transaminase (SGPT) (See rheumatoid arthritis� it call also be used as a crude measure
previolls discussion.) of response in Hodgkin disease.
Serum glutamate oxaloacetate transaminase (SGOT) The use of ESR as a screening test in asymptomatic
Total protein-albumin and globulin persons is limited by its low sensitivity and specificity. When
a moderate suspicion of disease exists, the ESR may have
Parathyroid Function and Calcium Metabolism some value as a sickness index.
Alkaline phosphatase An elevaled ESR in Ihe absence of other findings should
Serum calcium n01 trigger an extensive laboratory or radiographic evalua­
Serum phosphorm. tion.
Total protein Uric acid
Urine calcium •
Synovial fluid analysis, including culture
Pancreas function lests Synovial fluid analysis is inexpen:-.ive and may be diag­
Amylase nostic in patients with bacterial infections or crystal-induced
CBC synovitis. According to lhe American College of Rheuma­
Glucose tolerance lology (ACR) clinical guidelines committee, Ihis analysis
Lipase should be performed in dle febrile patienl with an acule flare
of established arthritis to rule oul superimposed seplic arthri­
Joint Pain or Swelling Tests tis. In other situations. its main value is to permit classifica­
ANA screen tion into an inflammatory or noninflammatory category.
CBC Thus, synovial fluid analysis should be performed if il is
Heavy metal screen readily obtainable and the diagnosis is uncertain after history
RA latex interview. physical examinatioll, und standard laboratory
Scdimclllalion rate tests (Table 1 -6).
Although it is frequently ordered. the erythrocyte sedi­ The WBC count, differential counL. cultures, Gram slain,
mentation rate (ESR) is not a useful screening (eM; it is and polarized light microscopy are the mosl valuable sludies,
useful only for diagnosing three diseases: ( I ) myeloma, ( 2 ) Noninflammatory fluids generally have fewer than 2000
"
temporal arteritis, and ( 3 ) polymyalgia rheumatica (in which WBCs/ml11 with fewer Ihan 75% polymorphonuclear leu­
it may exceed 100 nlln/hour). kocytes. The ACR commiltee suggests Ihal unexplained
ESR is commonly lIsed for a di fferential diagnosis for innammutory fluid, panicularly in a febrile patient, is
Kawasaki disease. and it Illay be increased in some chronic assumed to be inrected until proven otherwise by appropri­
infective conditions such as tuberculosis and infective endo­ ate culture.
carditis. The ESR is a componenl of the Pediatric Crohn Normal joints contain a small amount of synovial fluid
Disease AClivily Index (PDCAI), an index for assessmenl of with the following characteristics:
severity of innaml11atory bowel disease in children. Highly viscous
The clinical usefulness of ESR is limited to monitoring Clear
the response to therapy in certain inflammatory diseases Essentially acellular

TAB I F 1-6
CATEGORJ[S OF SYNOVIAL F LU I D BASED UPON CLIN ICAL AN D LABORATORY F I N D I NGS

Measure Normal Noninflammatory Inflammatory Septic Hemorrhagic

Volume, IllL (knee) <3.5 Often >3.5 Oflen >3.5 Often >3.5 Usually >3.5
Clurity Tnmsparenl Transparent Translucent-opaque Opaque Bloody
Color Clear Yellow Yellow to opalescent Yellow to green Red
Viscosity H igh High Low Variable Variable
Wac. per mlll3 <200 200-2.000 2000- 1 0.000 >100.000* 200-2.000
PMN<;. percent <25 <25 ;,50 ,,75 50-75
Culture Negative Negative Negative Often positive Negative
Total protcin. gldl 1-2 1-3 3-5 3-5 4-6
LDH (comp<lrcd to Vcry low Very low High Variable Similar
level!. In blood)
Glucose. mgldl Nearly equal Nearly equal to blood >25. lower than blood <25. much lower Nearly equal 10 blood
10 blood than blood

LDH, Laclic dehydrogenase: PMN, polymorphonuclear ce tl: WOc, white blood cell.
·Lower with infcctiol1\ caused by partially treated or low virulence organi!'!tns
26 CHAPTER I Principles in Assessing Musculoskeletal Disorders


Protein conccnLration approximately one-third thaL of TAB L E 1 -7
plasma
SUMMARY OF THYRO I D-STIMUlATING HORMONE
Glucose concentration similar to that in plasma
TEST RESULTS AND INTERPRETATIONS
If a synovial effu�ion is present and anhrocentesi� is
indicated, joint nuid should be routinely analyzed for TSH T4 T3 Interpretation
volume, clarity, color, viscosity, crystals cell counL differ­
High Normal NOnllal Mild (subclinical)
ential. Gram stain. and culture. In certain circumstances. the
hypothyroidism
presence and type of crystals should also be assessed. Syno­ High Hypothyroidi"m
Low Low or normal
vial fluid is subsequently categorized as either normal. non­ Low Nonnal Normal Mild ( ..ubclinical)
inflammatory. inflammatory, septic, or hemorrhagic based hypcnhyroidi!im
on the clinical and labonuory analysis. The differential diag­ Low High or normal High or Hyperthyroidism
nosis of each of these specific calegories is broad and nOI normal
necessarily exclusive: Low Low or normal Low or normal Rare pilUitury
NOllinjfallllJl(l[ory effusions may be caused by degenera­ (secondary)
hypothyroidism
tive joint disease (osteoarthritis). trauma. osteochondritis
dissecans. neuropathic arthropathy, subsiding or early
n. Triiodothyronine: T-I. thyroxinc� TSN. lhyroiu-\timul;lling hurmone.
innammation, hypertrophic oSleoarthropathy. and pig­
mented villonodular synovitis.
Illfiall/II/atory effusions may be caused by RA, acule hormone medication in patients who are being treated for an
crystal-induced synovitis. reactive arthritis (formerly underactive (or removed) thyroid gland. In rare cases. a low
Reiler syndrome), ankylosing spondylilis, psoriatic TSH resuh may indicale damage 10 the piluilary gland that
arlhriti�. arthritis associated wilh inflammatory bowel prevents it from producing adequate amounts of TSH.
disease, rheumatic fever, SLE. hyperuophic osteoar­ Whelher high or low, an abnormal TSI I indicates an
thropathy, and scleroderma. Rheumalic fever, SLE, and excess or deficiency in the amount of thyroid hormone avail·
scleroderma can also cause a noninflammatory effusion. able 10 the body, bUI il does nOI indicate Ihe reason why. An
Septic effusions may be caused by bacleria. mycobacte­ abnormal TSH lest result is usually followed by additional
ria, or fungus. testing to investigate the cause of the increase or decrease.
Hemorrhagic effusions may be caused by hemophilia or Table 1 -7 summarizes test results and their potelllial
other hemorrhagic dimhesis, scurvy, trauma with or meaning.
withoul fraclure, neuropalhic arthropathy, pigmenled vil­
lonodular synovitis. synovioma, hemangioma. and other Thyroxille
benign neoplnsms. In general. high free or tOlal T4 results may indicale an
overaclive thyroid gland (hyperthyroidism). and low free or
Thyroid Profile 10lal T4 resulls may indicale an underactive thyroid gland
Free Thyroxine Jilt/ex (hypothyroidism). The test resuils alone are nOI diagnoslic
The free thyroxine index ( Ff l or T7) is a mathematical but will prompt t.he examiner to perform additional teMing
computation thm allows lhe laboratory to estimate the free 10 invesligale the cause of Ihe excess or deficiency. Both
Ihyroxine index from Ihe Ihyroxine (T4) and lriiodOlhyro­ decreased and increased T4 results are associated with a
nine (T3) uplake leSls. The resuhs lell how much thyroid variety of temporary and chronic thyroid conditions. Low
hormone is free in the blood stream 10 work on the body. T4 resuils in conjunction wilh a low TSH level. or high T4
Unlike Ihe T4 alone, Ffl is not affected by estrogen resuils along wilh a high TSH, may indicate a piluitary gland
levels. condition.
Table 1 ·8 summarizes lest results and their potential
Thyroid·Stimulating Hormoll(' meaning.
A high Ihyroid-stimulaling hormone (TSH) resuh often
means an underactive thyroid gland that is not responding T,.iiodot"yrollille
adequalely 10 the slimulalion of TSH because of some IYpe Increased or decreased thyroid hormone results indicate an
of acute or chronic thyroid dysfunction. In rare instances, a imbalance bel ween Ihe body's requiremenls and supply, bUI
high TSH resuh can indicate a problem wilh Ihe pituilary they do not lell the examiner specifically whal i s cau,ing Ihe
gland. such as a tumor that produces unregulated levels excess or deficiency.
of TSH, in what is known as secondary hyperThyroidism. Table 1 -9 summarizes test results and their potential
A high TSH value can also occur when palienls wilh a meaning.
known thyroid disorder (or those who have had their thyroid If a patient is being treated with antithyroid medication
gland removed) are receiving inadequate thyroid hormone for hyperthyroidism and Ihe T3 (or, morc frequeJ1lly, the T4
medicatioll. or TSH) is normal, then the medication is likely controlling
A low TSti resull can indicate an overactive thyroid the condition. If the T3 (or T4) is elevaled, Ihen Ihe medica­
gland (hyperthyroidism) or excessive amOUI1lS of dlyroid lion is not sufficient to control the condition, and the palient
CHAPTER I Principles in Assessing Musculoskeletal Disorders 27

TAB L E 1·8 the most useful in this range. When patients in Ihe gray lone
have decrea\ed levels of free "SA. lhey have a higher prob­
SUMMARY OF THYROX I N E (T4) TFST RESULTS
ability of proslate cancer; when Ihey have elevated levels o f
AND I NTERPRETATIONS
free PSA. the risk is dimin ished. The ratio of free to total
T4 T8H T3 Interpretation PSA can help the examiner decide whelher a proslate biopsy
should be performed.
Nannal HIgh NOnllal Mild (�ubcJinic<ll)
When the complexed PSA (cPSA) test is used as a screen­
hypoLhyroidi..m
ing tool. increa.\cd leyels may indicate an increased ri\k of
Low High Low or nonna1 Ilypothyroidi..m
Nannal Low Nonnni Mild huOclinicnl) prostate C�1J1cer. whereas lower Icvels indicate a decreu\cd
hyperthyroidism risk.
High or normal Low High or nomlal Hypcnhyroidi"m In addition to lhe inlroduction of the free PSA and cPSA
Low or normal Low Low or nonna! Rare pituitary tests. efforts have been made to increase the u"iefulnes!o. of
(!ooccondary ) the total PSA as a screening 100\. A l lhough none of these
hypothyroidi..m efforts have been widely accepted yet. researchers are study­
ing them. and some examiners are using them. These factors
n. Triiuollihyronlllc; 14. thyroxine; TW/, thyroill-..llIl1ulallllg hormone.
include:
PSA velocilY. This tesl mea,ures the change In PSA con­
centrations over time. If the PSA continues 10 risc sig­
nificantly over time. such as 3 or more years. then proslatc
TABLE I ·')
canccr is morc l i kely present. I f it climbs rapidly. then lhe
SUMMARY Of TRIIODOTHYRO N I N E (D) TEST patient may have a morc aggre...sive form of cancer.
RESULTS AND INTERPRETATIONS •
PSA doubling lime. This leM i!o. another version of the
T3 T4 T8H Interpretation PSA velocity. 11 measures how rapidly Ihe PSA concen­
tration doubles.
Nonnal Nannal High Mild bubclimcal)
PSA densilY. This te'l is a comparison o f Ihe PSA con·
hypothyroidi..m
centration and the volume o f the prostate (as metlsurcd
LO\I, or nc.mnal Lo" High Hypothyroidism
r\onnal Nonnal Low Mild (..ubclinical)
by ultrasound). Paliel11S with larger prostates tend to

hyperthymidi..m produce morc PSA; thus. thi'i factor is an adjuslment to


High or nonnal High or 00011al Low Hypcnhyroidh,m compensate for the SilC.
Low or normal Low or 110mlal Lo" Rare pituita!) Age-specific PSA ranges. Given Ihat PSA le,e1s nalurally
hccondaryl increase as a man ages. experts have proposed thal nonnal
hypolhyroidi'im ranges be tai lored to a man's age.
During trealment for prostale cancer. the PSA level
7J, Triiodulh)roninc; T.J, Ihyro'(illl:: TSH. Ih)roji.J-_�lillluJaling hormone.
should begin to fall. At the end of treatment. it should be al
very low or undetectable levels i n the blood. I f concentra­
tions do not fall to very low levels. Ihen lhe trcalment ha,
may be experiencing symptoms associated with hyperthy­ not been fully effective. After Ireatment. Ihe PSA lesl is
roidi!o.ITI. perfonned at regular intervals to monitor the patient for
recurrence. Because even tiny increases can be signi ficant.
Prostate Profile patients may want to have their monitoring PSA tests per­
I'ro.\llIl(·.Sp(·ciji(' \ IIli/.:(·11 fonned by the same laboralory each time so Ihal testing
The normal value for lOWI proslale·specific anligen (PSA) \'arialion is kept to a minimum.
has heen ScI at less Ihan 4.0 ng/mL blood. Some experls
believe lhat Ihis level should be lowered to 2.5 ng/mL to IJro.\ltItil- \cill Phmpllllla.\"l!
detect more C3SC!o. of pro"tate cancer. Other" argue that this Pro'tatic acid phosphatase (PAP) is an enlyme produced by
change would exacerbate overdiagnosing and overtreating the prostate. It may be found in increased amount.s in mcn
cancers that are not clinically signilicant. who have prostate cancer or other diseases. This same
Mosl experls agree thai palients with a total PSA level enzyme is also found in significant amounts in female
grealer than 10.0 ng/mL are aI an increased risk for pros laiC ejaculate.
cancer (more than a 67CJr chance. according to the American The highesl levels of PAP are found in melaslasized pros·
Cancer SocielY). Levels belween 4.0 and 1 0.0 ng/mL may tate cancer. Diseases of the bone (e.g .. Pagel di,ease. hyper­
indicate pro'itatc cnncer (approx imntcly a 25% chance. parathyroidism). diseases of blood cells (e.g .• sickle-cell
according to the Americnn Cancer Society). benign prm,tntc disease. multiple myeloma). or lysosomal storage disease,
hyperplasia. or pro'itutitis. Thc'ie conditions are more (e.g .. Gaucher disease) will sho\\ moderalely increased
common in older adult males. as is a general increase in levels.
PSA levels. Concentrations of total PSA between 4.0 and Certain medicmioJ1!o. can cau-,e temporary increa!o.c!o. or
10.0 ng/mL arc often called the gra\" :olle. The free PSA is decreases ill PA P levels. Manipulation of the prostate gland
28 CHAPTER I Principles in Assessing M usculoskeletal D isorders

through massage. biopsy. or rectal examination before a tcst lligll-Dellsity Lipoproteill Cilolesterill
can increase the level. LDL cholesterol
• Triglycerides
Hypertension ( Coronary Risk Profile)
Cholesterol Health Screen
• Coronary risk indicator • Albumin
This is a group of tests and health faclOrs have been Low albumin levels can suggest liver di\ease. Other liver
proven to indicate a patient's chance of having a coronary enlYme tests are ordered to detemline exactly which type of
evenl. They havc been refined to indicate the degree of risk: liver disease. Low albumin levels can also reflect diseases
slight, moderate, or high. in which the kidneys cannot prevent albumin from leaking
Perhap� the most important indicators for cardiac risk are from the blood into the urine and being losl. In this case. the
those of the personal health history. Age, hereditary factors. amount of albumin (or protein) in the urine also may be
weight. smoking. blood pre sure, exercise h istory, and dia­ measured. Low albumin levels can ;]Iso be seen in inflam­
betes arc all important in determining risk. The lipid profile mation. shock. and malnutri tion. Low albumin levels may
is the most important blood test for risk assessmenl. Other also suggest conditions in which the body does nOl properly
tests, bOlh invasive and noninvasive, may be used in cardiac ab,orb and digest protein (e.g .• Crohn di,ea,e. 'prue) or in
risk assessment. Noninvasive tests may include an electro­ which large volumes of protein are 10M from the intes­
cardiographic stress lest, thallium SlrcSS lest. electrocardio­ tines.
gram, computed tomographic scan. and echocardiogram. High albumin levels usually reflect dehydration.
I nva�ivc tests include an arteriogram and cardiac catheter­ NG ratio (See previous discussion.)
ization. Alkaline phosphatase
The lipid profile measures cholesterol. triglycerides. HDL Anion gap
(good cholesterol), and LDL (bad cholesterol). Triglycerides Anion gap can be classified as high. normal. or. in
are the major form of fat found in the body. and their func­ rare cases, low. A high anion gap indicates a lo�s of bicar­
tion is to provide energy for the cells. The de,irable ranges bonate without a subsequent increase in chloride. Electro­
for the components of the lipid profile include the follow­ neutrality is mail1lained by the increased production of
ing: anions such as ketones, lactate. phosphate. and sulfate; lhese
Cholesterol <200 mg/dL (5. 1 8 mmollL) anions are not part of the anion-gap calculation. and there­
HDL cholesterol >40 mg/dL ( 1 .04 mmollL) fore a high anion gnp results. In patiel1l� with a normal
LDL cholesterol < 1 00 mg/dL* (2.59 mmol/L) anion gap. the drop in bicarbonate is compensated for by
Triglycerides < 1 50 mg/dL ( 1 .70 mmollL) an increase in chloride and hence i ... also known til., hyper­
If any or all of the results arc significantly outside these chlorcmic acidosis.
ranges, the risk of a cardiac event is increased. If they are
only slightly outside the desirable level. diet, exercise, med­
ication. or any combination of these treatments may be suf­ Higtt Illiol/ Gap
ficient to reduce the abnormal levels. thereby reducing The bicarbonate 10M is replaced by an lInmea�ured anion.
ri�k. and thus a high anion gap will be present in the following
Another test gaining importance is serum homocysteine. disorders:
Homocysteine is un amino acid that comes from the normal Lactic acido�is
breakdown of proteins in the body and appears to be a beller Ketoacidosis
test than cholesterol testing for predicting heart disease, Diabetic ketoacidosis
stroke. and reduced blood now to the hands and feel. Lipo­ Alcohol abuse
protein A (Lpl a J ) is a lipoprotein consisting of an LDL Toxins:
molecule with another protein (apolipoprotein A) attached Ethanol
to il. Lp(a) is similar to LDL but does not respond to typical Ethylene glycol
strategies to lower LDL such as dict. exercise, or most lipid­ Lactic acid
lowering drugs. Given that the level of Lp(a) appears to be Methanol
genetically determined and not easily altered. the presence Paraldehyde
of a high level of Lp(a) may be used to identify individuals Aspirin
who might benefit from more aggressive treatment of other Cyanide. coupled with elevated venous oxygenation
risk factors. A fairly new test, high-sensitivity (hsCRP), may Iron
be measured on apparently healthy patients to detemline if Isoniazid
they are at risk for a coronary event. evcn if their lipid levels The mnemonic MUDPILES is used to remember the
are normal or borderline elevated. causes of a high anion gap.
Methanol/metformin
*Oplim:tl le'o'cl, will depend on the number and type of ri-;k facloN prcsclll Uremia
and whether testing i.. being used in primary or secondary intervention I!iabetic ketoacidosis
CHAPTER I Principles i n Assessing Musculoskeletal Disorders 29

faraldehyde/propylene g l yco l Blood, which consists largely of the protein hemoglobin,


In reClion/ischcl11i vi
.. son i azid is broken down by digestive enzymes of the upper GI
Lactate tract into amino acids.
Ethylene glycol/ethanol The amino acids. which origimlte from the hemoglobin,
S.al icylate,/starvation are reabsorbed by the lower G I tracl.
Some people. especi al ly those not in the emergency Urea is a break-down product of amino acid catabolism;
room. find the mnemonic KILU easier to remember and also therefore, the protein meal from an upper GI bleed shows
more useful cli ni cal ly : lip in the blood as urea.
Ketone; Because of decreased muscle mass. elderly patients may
Ingestion have an e le vated B U N/creatinine ratio at baseline.
,Lactic acid Calcium
Uremia Calculated LDL
All of lhe componeJ1ls of M UDPILES are also covered CBC
with the KILU device. with the added imperative that these Chloride
th ings can kill a patie nt . Cholesterol
Ketones: morc slraigillfofward than remembering dia­ CholeslCrol-HDL ratio
betic ketosis, starvation ketosis, and so forth. Creatinine
Ingeslion: methanol. metfonnin. paraldehyde, propylene GGT (Sec earlier discussion.)
glycol. i;oniazid. ethylene glycol. ethanol. and sal icy­ G lobul i n
lales are covered by i ngestion. These substances can Globulins are roughly divided into alpha. beta. and
be considered as a single group-illgesliolls-during gamma globulins. These values can be separtlled and mea­
the initial con�idcration. especially when nOt triaging sured in the laboratory by techniques called electrophoresis
a patient in the emergency room. and densitometry. The gamma fraction includes the variou�
LaclicAcid: including that caused by infection and shock types of alllibodies ( immunoglobulins M, G, and A).
(U,ually the bicarbonate lost is replaced by a chloride Normal values are:
anion. and thus the anion gap is normaL) Serum globulin: 2.0 to 3.5 g/dL
Gastrointestinal loss of bicarbonate (e.g., diarrhea) IgM component: 75 10 300 mgldL
( ote: Vomiting causes hypochloremic alkalosis.) IgG component: 650 to 1 850 mgldL
Renal loss of bicarbonate (e.g.. proximal renal tubular IgA component: 90 to 350 mgldL
acidosis) I ncreased gamma globu l i n proteins may i ndicate:
Uremia: Renal dysfunction (e.g .. renal failure. hypoal­ Multiple myeloma
doslcronism, distal renal tubular acidosis) Chronic inflammatory disease (e.g., RA, SLE)
A low anion gap i� re l at ive ly rare but may occur from the Hyperimmun ization
presence of abnormal positively charged proteins. as in mul­ Acute infection
tipl e myelom a or in the settin g of a low serum albumin
, Waldenstrom macroglobulinemia
level. Glucose
Bilirubin (IOtal) HDL
BUN (See earlier discussion.) • Ionized calcium
BUN-creatinine ratio LDH
The B UN/creatinine ratio is a rmio of two laboratory test Phosphorus
values: the BUN and serum creatinine. It is used in the Potas� i U 111
United States. Elsewhere (Canada. Europe). urea is used • Serum glutamate ox aloaccta te transaminase
instead of BUN; thus. it is the urea-lo-creatinine ratio, also Serum glutamate pyruvate transaminase
urea-creatinine ratio. and urea/creatinine ratio. Sod i um
The BUN/creatinine ratio is predictive of prerenal failure, T4 radioimmunoassay ( R I A )
if the BUN-to-creatinine r'Jtio is greater than 20 or the T4 b y RIA i s the most widely used thyroid test of a l l . I t
urea-Io-creatinine ratio of marc than 0. 1 0 and urea of more i s frequently called a T7, which means that a resin T3 uptake
than 1 0. I n prerenal fai lure, urea rises out of proportion (RT3u) has been accomplished 10 correc t for certain medica­
to the creatinine because of enhanced proximal tubular tions such as birth control pills, other hormones. seizure
reabsorption . medication. cardiac dru gs, or even aspirin that may alter the
The BUN/creatinine ratio is useful for the diagnosis of routine T4 tesl. The T4 renects the amount of T4 in
upper gastrointestinal ( G I ) bleeding in patients who do not the blood. If the patient does not take any type of thyroid
exhibit overt vomiting of blood. In children. a B U N/cremi­ medication. this test is u su al ly a good measure of thyroid
nine ratio of 30 or above has a sens i tivity of 68.80/0 for upper functi on .

GI b leeding and a specificity of 98%. • Total carbon dioxide


The reason the urea concentration increases in upper GI Carbon dioxide levels that arc higher or lower than
bleeds is as follows: nonnal suggest that the body is having troublc mainwining
30 CHAPTER I Principles in AssessLng Musculoskeletal Disorders

Normal synovial nuid is a hypocellular. avascular con­


nective tissue. In disease, the synovial Huid increases i n

SYNOVIAL FLUID volume and can b e aspirated. Synovial Auld is a transudate


of plasma supplemented with high molecular weight. sac­
For three significant aspects, analysis of synovial charide-rich 1110lecules. The 1110st notable of these is
fluid differs from other body fluids: hyal uronan (hyaluronic acid). which is produced by fibro­
I . Neoplastic processes rarely arfect synovial joints. blast-derived type B synoviocyte ( Box 1-3). Variation in the
2. Recognition of noncellular paniculate material, such volume and composition of synoviai lluid reRects pathologic
as microorganisms and crystals and cartilage frag­ processes within the joint.
ments. is essential for defining the disease process
affecting the joint.
3. Diagnostic information comes not only from recogni­ ORTHOPEDIC TESTS
tion of cell types but also from their quantification. In the orthopedic physical examination, a test is positive or
a sign is present when the procedure dupl icates the patient's
complaint or symptom. Tests are based on joint, muscle, or
its acid-base balance or that the electrolyte balance is upset, nerve function. If testing causes different pain or symptoms,
perhaps by losing or retaining fluid. Both of these imbal­ it may indeed be significant, but the result is nOI positive for
ances may be the result of a wide range of dysfunctions. the findings that Ihe test was designed to elicit.
Total protein During an examination, the examiner must use techniques
Triglycerides that defeat the human tendency of exaggeration. The exam­
Uric acid iner must conduct several tests and multiples of similar tests
• Synovial fluid so that the patient is not aware of which specific tissue func­
tion is being examined. Wilh lime and exposure to a myriad
of orthopedic disorders. examiners develop the skill and

IIOX 1-3 accuracy necessary to reach diagnoses efficiently. However.


interpreting the results of examination processes in a clini­
N O RMAL SYNOVIAL F L U I D
caJly meaningful way requires the examiner to consider the

OsmOlarity 296 mO,mIL reliability of the clinical measurements and tests.


pH 7.44 Interpretation and analysis of examination procedures
Carbon dioxide pressure 6.0 kPa (range 4.7-7.3) depend not only on Ule reliability and validity of such mea­
Oxygen prc�surt! <4.0 kPa sures, bUI also on the sensitivity and specificity of the signs
Potassium 4.0 mmoJIL elicited by the test procedures.
Sodium 136 mmoUL
Calcium 1 .8 mmollL
Urea 2.5 mmoUL DIAGNOSTIC IMAGING MODALITIES
Uric acid 0.23 mmollL IN ORTHOPEDICS
Glucose tOO mmollL
I maging procedures are important to the diagnosis and man­
Chondroitin sulfate 40 "'gIL
Hyaluronate 2. t 4 gIL agement of an orthopedic condition. The decision to use any
Cholesterol Small amounts diagnostic imaging procedure, especially ionizing imaging
TOl..lI prolein -25 gIL procedures, should be based on a demonstrated need and
Albumin -8 gIL should be used only after an adequate medical history is
(Xt-antitrypsin 0.78 mcglL obtained and a physical examination is conducted. The deci­
CcnllopJasmin -43 I1lgIL sion to use any imaging procedure must also be based on
Haptoglobin -90 mgIL
the assumption lhat the results of the eXIDllination. even if
(X.:z-macroglobin 0.31 gIL
negative, will significantly affect the treatment of the patient.
Laclofcrrill 0.44 mglL
The value of the information gained from the imaging exam­
IgG 2.62 gIL
ination must be worth the possible detrimental effects of the
IgA 0.85 gIL
procedure. In imaging modalities tJlat use ionizing radiation
IgM 0. 1 4 gIL
lL-I� 20 pglmL (plain-film radiography, fluoroscopy, and CT), the possible
IL-2 1 5 . t U/mL effect of radiation on the patient or future offspring must be
TNF-ct 1 .38 hglmL considered (Fig. 1 - 1 7 ).
INF-ct 350 U/mL
INI'-o 13.7 U/mL Plain-Film Radiography (Conventional
Radiography)
IgA. Imml.lll/)gfo/JII/ifl A; IgG. imfllllllog/oi>u/ifl G; IgM. imlllllllog!obllUn
Plain-film radiography. or conventional radiography. pro­
M: IL. imerle"k;lI: INF. illft:ljI!l"Ofl: TNF. tulllor-necrosis/aclor:
Adapted from Klippel lH. Dieppe PA: RlwulI/lIw/agy. \'0/ /·2. ed 2. London. vides a wide and di verse array of diagnostic data about
1998. Mosby. musculoskeletal problems. such as soft-tissue injury. bony
CHAPTER I Principles in Assessing Musculoskeletal Disorders 31

malalignment, loss of integrity of the osseous structures. and The patienl's history and clinical evaluation are guides
joint space abnormality. that help determine which portion or portions of the body
Plain-film X-ray examination is an efficient way to dis­ requires plain-film imaging and how many different views
cover dislocations, fracLUres, the static component of ana­ should be produced (Fig. 1 - 1 8 ) .
tomic subluxations. certain types of stress injuries. metastatic Radiography i s a useful tool in the initial assessment
disease, some types of primary tumors, metabolic disease, of rheumatologic disorders because it may providc specific
degenerative arthropathic diseases (Table 1 - 10). and abnor­ infomlalion thaI contributes to establishing a diagnosis.
malities in the growth plate. Various rhcumatologic disorders have unique fealUres that
Soft-tissue structures require careful scrutiny on film can be easily detcclCd with plain-film radiographs. Abnor­
because they may offer subtle clues to serious or underlying malities on plain-film radiographs can be detected with a
pathologic abnormalities. high degree of sensitivity. Serial radiography is useful in
A radiologic evaluation of the traumatized sites should measuring structural damage, and features such as erosions.
include films of the adjacent joints. If a need exists for joint space narrowing. and disease-specific findings can hclp
special projections, other radiologic investigation may be gauge response to therapy (Dry. 2003).
necessary (Table I - I I ).
Care must be taken to investigate the possibility of asso­ Tomography
ciated injuries in trauma victims (Table 1 - 1 2). Patients may Conventional tomography is also known as thill-section
not realize that such injuries have occurred. radiography, planigraphy, and linear tomography. Conven­
tional tomography is largely replaced by CT. However, some
circumstances. such as evaluating sublle alteralions of bone
density and ruling out fracture, necessitate conventional
lA I\ L E 1 · 1 0
tomography. CT scans are used for more detailed apprecia­
PLAtN- F t LM EVALUATION t N DEGENERATIVE tion of skeletal pathologic processes, which can help evalu­
ARTH ROPATHIC DISORDERS ate suspected intervertebral disc protrusions or herniations,

Diagnosis Site of Plain-Film findings facet disease. or central canal and lateral recess stenosis. I f
spinal disease is suspected and is not well idenlified o n plain
Psoriatic anhritis Hand. sacroiliac joints (common): films and the patient is not responding to care, a CT scan is
pubis symphysis, hip, knee (less
indicated. A CT scan is especially useful for the appreciation
common)
of bone and caJcifications and surpasses magnetic resonance
Rheumatoid arthritis Wrist and hand, shoulder. knee.
imaging ( M R I ) in this regard.
cervical spine. hip
CT has been useful in a wide variely of musculoskeletal
Spondyloarthropathy Sacroiliac joints. thoracolumbar spine
Osteoarthritis Lumbosacral spine, hip, knee. foot disorders, including those related 10 trauma (Fig. 1 - 1 9), back
and ankle, hand pain (e.g., herniated nucleus pulposus) (Fig. 1 -20), and met­
abolic bone disease (e.g .. osteoporosis, tumor and soft-tissue
masses).
Two thirds of patients with multiple injuries suffer from
blunt chest trauma. and severe thoracic trauma is associated
with multiple injuries in 70% lO 90% of cases (LoCicero J
3rd. MallO •. 1989; Pinilla. 1982).

f i G . 1 - 1 7 From left to right and top 10 bottom, An arias of


I/ormal roelllgell variants fhat may simulate disease (by
Theodore E. Keats). gonadal shielding, sandbag, DuPont F I G . 1-18 Displacemenl of fat pads in the elbow by joint
Quanta Delail Rare Earth X-ray casselle screens, and com­ effusion. (From Klippel JH. Dieppe PA: RheumatOlogy. vol 1-2. ed 2.
patible film. London. 1 998. Mosby.)
32 C HAPTER I Principles in Assessing Musculoskeletal Disorders

O R1 1101'1 \l I L GAMli r I 2\

ARTHRITIDES: D IAGNOSIS AND CLINICAL PROGRESSION ASS.ESSMENT


STEPS IN RHEUMATOID ARTHRITIS, PSORIATlC ARTHRITlS, ANKYLOSIS
SPONDYLITlS, AND OSTEOARTHRITIS
Rheumatoid arthritis radiographs of pelvis, sacroiliac joints, and axial spine
Serial radiographs (posteroanterior [PAl view) of hands, annually or every other year
wrists, and feet at baseline and at 6-month intervals for Serial radiographs ( l ateral and AP views) of cervical,
a minimum of 2 years after onset thoracic, and lumbar spine annually or every other year
Monitoring frequency decreased after 2 years in patients Radiographs (PA view) of hands and feet at baseline;
without erosions at 2 years fol low-up radiographs based on clinical features
• Distinguishing radiographic features: bilateral symmetri­ Distinguishing radiographic features: cervical lesions not
cal involvement of the small joints ( hands, wrists, and typically associated with instability and subluxations of
feel),juxtaanicular osteopenia, lack of proliferative bone the lower five vertebrae as in rheumatoid arthritis, less­
response, marginal erosions. joint space narrowing. severe hip lesions than in rheumatoid arthritis without
Psoriatic arthritis protrusions, osteophytcs along the margin of articular
• Serial radiographs (PA view) of hands, wrists. and feet canilage of the femoral head, marginal syndesmophytes
(and spine and other joints if symptoms are present) at in consecutive vertebrae. sacroiliilis. 'bamboo spine,'
baseline and at 6-month intervals for a minimum of 2 smaller and more localized erosions, and less frequent
years after onsel joint space narrowing and osteopenia compared with
• Distinguishing radiographic features: asymmetric and rheumatoid arthritis
possibly oligoarticular joint involvement, initially mar­ Osteoarthritis
ginal erosions lhat become irregular and ill defined, distal • Radiographs (PA view) of the hrulds and fect annually
interphalangeal joint involvement, abnormalities in pha­ • Radiographs of the hips (AP pelvic in supine position)
langeal tufts and at sites of uuachmcnts of tendons and and knees (standing, weight-bearing AP with full knee
ligaments to the bone, possible spondylitis, paramarginal extension) annually
syndesmophytes in nonconsecutive vertebrae, sausage Distinguishing radiographic features of osteoanhritis:
digits, proliferative bone changes, and ankylosis osteophytes, subchondral sclerosis
Ankylosing spondylitis Distinguishing radiographic features of erosive osteoar­
Serial radiographs (anteroposterior IAPI view) of pelvis. thritis: distribution in distal joints of fingers similar to
sacroiliac joints. and axial spine that of psoriatic anhritis; centrally located erosions; ero­
• If early ankylosing spondylitis is suspected, repeat pelvic sions typically absent i n metacarpophalrulgeal joints
radiographs 6 months from baseline; otherwise, serial

Adapted from Ory PA: Radiography in the aSSCS\IllC'llt of mu,>culoskeletal condj(ion�, Ik�/ Prtlc/ R('\ Clin Rlll'lflll 17(�1:495·5 1 2 . 2003.

Among hlum injuril!!oi 10 the chest. lung contllsion is Discography


con!'lidcred one of the mo�t important factors contrihuting to Although effective, discography has been a controversial
the incre"lsed morbidity and mortality of patients with mlll� imaging modality for spinal disc disease. Clinicians use
riple injuries (Johnson. Cogbi ll. Winga, 1986: Schild el al. discography for specific cases of spinal pain that arc recal­
1 986). citrant to conventional therapy.
The usual diagnostic work-up in rhe emergency Discography is an important diagno�tic procedure in which
department for blunt injuries to the chest includes a routine disc pressure comrolled by need le injection is correlated
chest x-ray taken in the supine position m
; d an ultrasound. with degree of lumbar pain rcp<Jrred by the patient. Although
Despite this approach. significam injuries such as pneumo­ imaging studic'i. such MRI. call be used to document paLho­
thoraces. hemothoraces. and lung contusions can be missed logic changes in the disc. some studies have 'ihown a poor
during the initial trauma assessmem (W:'lgner, Jamieson, con'e1ation between MRI findings and clinical symptoms
(989). because di!'lc degeneration and hernimion incrc<'lsc wil.h
CT scanning is accurate in visualizing intrathoracic inju­ normal aging (Boden el at. 1990).
ries. In addilion, the availabil i ty, reliability, and low com­ The high incidence of asymptollliltic findings on MRI
plication rate of CT scans has led to its widespread use in makes imcrprelalion of patienl ,,(udies morc difficult becau\c
the evaluation of blunt trauma. each imaging finding must be closely correlated 10 symp­
Clinicians often use the noninvasive technique of quan­ LOIllS Ihat can be relatively nonspecific in mallY palicllls.
litatjvc CT to mea�ure bone mineral density. MRI alone is not able 10 differentiate \ymplOmatic from
CHAPTER I Princi ples in Assess ing Musculoskeletal Disorders 33

TA B l E I- I I
PREFFRR£D RADIOGRAP HIC VI EWS I N SKE LETAL TRAUMA

Arca Specific Views Area Specific Views

Skull POSlCroanlerior or anteroposterior Caldwell Sternum. Posteroanterior


Townes sternoclavicular Right and left anterior obliques with
Uilcral (one lateral should be upright) joinLS cephalad angle of lube
Lateral
Facial bones Waters Elbow Anteroposterior
Modified Waters Lateral
Caldwell Capitellum
Lateml
Cervical spi nc Anteroposterior Radioulnar joims A meroposlerior or posteroanterior
Coned odontoid or oflhopanlogram (forearm) Lateral
Odontoid
Lateral (cross�table or upright)
Swimmer latem! (cross-table)
BOlh obliques, when possible
Thomcic spine Anteroposterior Wrist and hand Posteroanterior
Lateral (cross-table or routine) Oblique imerna!. ex.temal. or both
Swimmer (coned to upper thoracic spine) Lateral
Navicular views. if needed
Lumbar spine Anteroposterior Pelvis, acetabulum Anl.eroposterior
L<llcral (cross-table or upright) Obliques (Judet)
Lateral {coned to L5-S I }
Sacrum Anteroposterior (tube-angled cephalad) Hip. proximal part Anteroposterior pelvis
Lateral of femur Frog·leg or cross-table lateral
Obliques
Chest Posteroanterior or anteroposterior Femur Anterol>osterior (to include hip and knee)
Left lateral (may not be possible in Lrauma) Lateral (to include hip and knee)
Lateral decubitus (pneumothorax.. pleur'c11 Ouid)
Ribs Anteroposterior or posteroanterior Distal part of femur Anteroposterior
Oblique and knee Latcml
Tunncl
Internal oblique
Shoulder Anteroposterior (internal rOlation) Tibia. fibula Antcroposterior (to include ankle and knec)
Anteroposterior (ncutml) Lateral (to include both joints)
Transscapular lat.eral (NeeI')
Axi llary
Humerus Anteroposterior (to include elbow and shoulder) Ankle Anteroposterior
Latcml (10 include both joints) Oblique (mortise)
Lateral
Clavicle Anteroposterior or posteroanterior (to include Calcancus Tangential
both joints with and without weight bearing) Lateral
FOOl Laternl
Anteroposterior
Oblique
Lateral

From Gu:;tilo RB. Kyle RF. Templeman DC: Fr(lCfU"e� ami (/islocmio//'\', 1'01 I. 51 Louis. 1993. Mosby,

asymptOmatic degenerative disc Changes (Scuderi et al. in Lhe sagittal, coronal, o r axial planes, a s well a s a n y other
pres:;). oblique plane desired. The MRI can i mage neuro logi c struc­
tures and other soft tissues and can reveal disc degeneration
Magnetic Resonance Imaging before any other imagi ng method. Indications for MRI are
M R I is a computerized, thin-section imaging proced ure that similar 10 those for CT. M R I is superior to CT for the
uses a magnetic field and radio·frequency waves rather than evaluation of suspected spinal cord tumors or damage intra­ .

ionizing radiation. M R I can produce thin-section images in cranial disease. and various types of central nervous system
34 CHAPTER I Principles in A"essing Musculoskelelal Disorders

" IZI II"I' I I) l l (,\\\1 1 1 ' j

ASSESSMENT ABILITIES AND


LIMITATIONS OF PLAIN-FILM
RADIOGRAPHY
r------
I . Plain- if lm radiography is Ihe leasl expensive and mosl
widely ..vailable imaging lechnique.
2. Radiography offers higher spalial resolulion than any
other modalily, providing exlremely high contrast for
cortical and trabecular bone.
3. Radiography affords only a projectional viewing per­
spective.
4. Projeclion of three-dimensional anatomy onlo a 1\\'0-
dimensional film results in morphologic distortion
and superimposilion of overlapping struclures.
5. The sensitivily for trabecular bone los> is relalively
poor.
6. As much as 30% 10 50% of lrabecular bone must be
removed before Ihe change becomes perceplible on
convenlional radiographs.
7. The contrast for soft lissues Ihal are not calcified or
fauy is relatively poor.
8. Radiography cannOI directly visual ize Ihe articular
cartilage, inflamed synovial lissue, joint effusion,
bone marrow edema, or intraanicular fat pads.

(1IZIII " I' I I) I ( (,\\\1 I I "

ASSESSMENT A B I LITIES AND


LIMITATIONS OF COMPUTED
TOMOGRAPHY
I . The grealeS! advantage of CT over convenlional radi­
ography is its lomographic nalure.
2. CT provides high contrast belween bone and adjacem F I G. 1-19 Complex acetabular fraclure. A, Anlcropo,lerior
tissues and is excellent for evaluating osseous struc­ plain film. B, Axial computed tomography scan. (hum GU'lilo
lures. R H . Kyle RF. T�mplcman DC· rraC"lIln.'\ mul di,hlnllimu. \01 I Sl l.oui,
3. CT offers slightly grealer SOh-lissue contra>! than 1993. M<hhY.1
radiography.
4. Image contrasl is insufficienl lo visual ile the articular
canilage or synovial tissue or to discrimjnate between
lendonilis and tendon ruplure. cilha diagnmm. or operative planning. A "'OfHiv..ue rna..... In

5. CT reveals only Ihe surfaces of these struclures; il the hand may be a manifc..tallon of ncopla...m. congenital

does nOI disclose intra substance changes that may malformation. infection. other inOammalory proce ...... or

precede gross morphologic disruption. trauma. Infcctiou... and traumallc cau ..c... arc more prc\alcOi
111 pediatric palicllI!'I than ncopla,ia or congcmtal malfonna-
lion. The evaluation of the...e ma,...c!'l ...hould IIlclude an
a....e
. .... menl of the extent of the ...oft-u......ue. m...cou.... and

di «asc (e.g .. multiple sclerosis). M R I is especially lIseful in ncurova,cular II1volvement. Of all Ihe lIunging ImxJalllle"

identifying small di fferences among similar soft tissues and MRI i ... he..., ..uiled for ,hi... role (Jimene/. Jaramillo. Con­

surpa"es CT in Ihis regard. nolly. 2(05 ).


The evaluation of a child with a \uspccted ..oft ti"..uc mass In Ihe management of low back pain and lumbar degen­
III the hand i.., .
1 chal lenge. Imagmg evaluation ... houkl t>egin erative kyphosis disorder!'!, paraspinal muscles are subjected
with radiograph... that l11a) reveal the diagno..i!'!. Further to many slUdies using ultrasound, CT. needle eleclromyog­
imaging ....
· ith uhra...ound. CT. or MRI is often required for raphy (EMG). and histopalhologic analysis. MRI can evalu-
CHAPTER I Principles in Assessing Musculoskeletal Disorders 35

fA 1l 1 E 1- 1 2

I N I U RI ES ASSOCIATW WITH SKELETAL TRAUMA

Fracture Associated Injury

Bone and bone Remote additional spinal fracture


Spine Scapula fracture
Chest wall Sacrum fracture or dislocated
Anterior pelvic arch sacroiliac joint
Femoral shaft Fracture or fraclUrc-dislocation of
Tibia (severe) hip
Calcaneus Dislocated hip
Fractured thoracolumbar spine

Bone and viscera Ruptured mcscnlcry or small bowel


Chance fracture of spine Laceration of liver. spleen. kidney.
Lower ribs or diaphragm
Pelvis Ruptured bladder or urethra
Pelvis Ruptured diaphmgm F I G . 1-20 Axial image showing a right paracentral hernia­

Ruptured aona
lion of the nucleus pulposus. (From Brier SR: Prim(lr" {"(Ire orOw­
Bone and vascular
Ribs I . 2. or 3 Myocardial contusion /u'lJicl. 51 Lou i )l. 1 999. Mo�by.)

Sternum Laceration of pelvic arterial lree


Pelvis Laceration of femoral artery
Obtai third femur Popliteal ancl)' laceration
Knee dislocation

OIU 1101'1 J) I ( (, ·\ M ll I I 2 7
Adapted from Roger� IF. Hendrix RW: Evaluating the multiple injured
patient radiographically. Orillop CIi" Norlll Am 2 1 (3):444. 1990. fOR CERTAIN PATHOLOG [ C
COND [ TlONS, MAGNETIC
RESONANCE IMAG[NG [ S THE
D LAGNOSTIC PROCEDURE O f
CHOICE
O RI II O I' I Il I ( (,,\ �1l1 1 1 '>(,
I . Spinal disc disease
USES Of DISCOGRAPHY 2. Medullary tumor
3. Mulliple sclerosis
To rule out disc involvement. especially as a cause of
4. Cerebral edema
postoperative pain
5. Spinal stenosis
To detennine the appropriate level for spinal fusion
To test the potential effectiveness of chemonucleoly­
6. Metastatic disease
7. Hemiated disc
sis
8. Discilis (or infection)
To visualize internal disc anatomy
9. Meniscal lear ( fibrocartilage abnormalities)
10. Central nervous system tumor
I I . Soft-tissue tumor

ate fatly infiltration in the muscles and the fascia status


overlying the muscles. The MRI enables the examiner to
distinguish between muscle and fibrous tissue.
The ratigue or the lumbar muscles is probably one or the
mO!<lt important cau�el-, or pain in lumbar degenerative (l JU II () I' I J) I ( (, \\\11 I I .> H
kypho�is deformity because the lumbar extensors overwork
to maintain secure balance (Takcmitsu et al. 1 988).
ASSESSMENT A B [ L 1 T 1 ES NO
Experts also �uggest that weakness is a consequence.
L 1 M [ TATIONS O F MAGNETIC
rather than a cause. of low back pain. whereby pain limits
RESONANCE [ MAG[NG
movement and muscle atrophy OCCUf!<l (Slokes. Young. I . Diarthrodial joints are panicularly suitable for MRI.
1984). 2. MRI is unparalleled in its ability to depict soft-tissue
For patients who have sustained head trauma with skull detail.
fractures. MRI is an efficient way to identify the early signs 3. MRI is the only modality lhat can examine all com­
of cerebral edema. The test procedure of choice for diagnos­ ponents of the joint simultaneously.
ing metaslalic disease is an M R I scan (Table 1 - 1 3 ).
36 CHAPTER I Principles in Assessing Musculoskeletal Disorders

TA l\! [: 1 - 13

MAGNETIC RESONANCE IMAGING VERSUS COMPUTED TOMOGRAPHY

Anatomic Area Indications Recommended Procedure

Brain (including brainslcm) Inilial evaluation (e.g., demyelination disease seizures) MRt
Previous normal cr MRI
Previous abnormal CT CT or MRI*
Unchanged abnormal CT with increase in symptoms MRI
Contrast aJ lergy MRI
Acute trauma CT
Pituitary tumors MRI
Ear, nose. throat, and eye Neurosensory hearing loss (e.g., \0 rule out acoustic neuroma) CT
Conductive hearing loss CT
Cancer staging (including laryngeal cancer) CT or MRI'"
CholeMealOTna of temporal bone CT
Fractures of facial bones CT
Thyroid or parathyroid dysfunction (artcr US) MRI
Sinus conditions CTor MRI*
Orbital disease MRl or CT*
Disease of optic t:racLS and chiasm MRI
Internal derangement of lemporonmndibu,lar joint MRt
Musculoskeletal spine Lower back or radicular pain in younger person MRI
Lower back or radicular pain in older person MRI or CT*
Cervical disk disease MRt
Spinal stenosis MRt
Cervical CTor MRI*
Lumbar MRI
Tumors MRt
Metaslalic disease
Hips Early detection or aseptic necrosis MRt
Congenital hip dislocation or reduction US
Extremities Tumors, disease. or injury to muscle. ligaments. or c<lrtilage MRI
Confirmation or calcificution or rracture CT
Chest Diseases or the hi la MRI
Diseases or the mediastinum MRI or CT*
Lung disease CT
Abdomen and pelvis General survey (e.g., to rule oul !Ulnar) CT
Li\'er disease CTor MRI*
Renal cell cancer staging MRI
Prostate disease MRI. CT. or US
B ladder disease MRl orCT
Abdominal aortic aneurysm MRJ*
Other

cr. Computed tomography: MRI. mugnctlc resonunce imaging: US. ultrasonography.


*Consult r.ldiologiSi for imaging options.
From Brier SR: Primary eMf! ortlwpedicx. 51 Loui!l. 1 999, Mosby; originally councsy of Roben Goodman. MD. Soulh Sun·olk MRI. Pc. Bayshore. New
York.

The guideline ror using the imaging modalities 10 best


advaIHagc can be summaril.cd as follows: Using slate of IIle Contrast A rthrography
art M R techniques with high resolulion, at lcasi lwo plancs, The conventional usc of arthrography in musculoskeletal
fast sequences, phaSed-array coils, and established technical disease involves the use of air to distend a synovial joint and
parameters. M R I can answer all clillical questions. This a radiopaque contrast agent to outline anatomic structures,
guidelinc applies 10 conditions treated conservatively or sur­ The injection of contrast material into the joint space results
gically, as well as to all manifestations of degenerative spine in a radiographic outline of the cartilage. menisci, ligaments.
disense. In particul;u. only MRI can identiry abnormalities or synovium. Conventional arthrography is used in diagnos­
within the spinal cord as syringomyelia or myelopathy ing the scope and magnitude of orthopedic trauma to the
:schmar, 1 998),
(Krcu shoulder, wrist. knee. and ankle (Table 1 - 1 4).
CHAPTER I Principles in Assessing Musculoskeletal Disorders 37

TA B l E 1-14
JOI NTS TYPICALLY STUDIED WITH COMPUTED
TOMOG RAPHIC ARTHROGRAPHY FOLLOWING
TRAUMA

Joint To Observe

Knee Meniscus. cruciate and colhlleral


ligaments. hYlilinc cartilage tears,
osteochondral delects
Shoulder ROlator cuff, glenoid labrum disruption
Hip Hyaline cartilage integrity and teurs.
pro!!lhctic joint loosening
Wrist Triangular fibrocartilage, intercarpal
ligament imcgrilY
Elbow Hyaline cartilage integrity.
osteochondral defects
A n kle LigamenLous lears. osteochondral
defects
Temporomandibular Disc and condylar integrity

Adapted from GUl>lil(} RB. Kyle RF. Templeman DC: FraclI!res allli (Ii:.-
!oCll/iol1:'i, 1'01 I. 5t Loui .... 1993. Mosby. A

0 1( 1 1 1 0 1' 1 Il l l l,,\MIII I 2<)

ASSESSMENT ABILITlES AND


LIMITATlONS OF RADlONUCLIDE

SCANNING
I , The principal advantage of scintigraphy over oLher
imaging modalities is its ability to help in identifying
tissues or organs with abnormal physiologic Or bio­
chemica.l properties.
2, Increased skeletal uptake can be seen at sites of ele­
vated blood flow or increased bone metabolism,
3, Scintigraphy is a convenient way of surveying the
enlire skeleton for multifocal processes,

COl1lra�l-cnhanccd cartilage imaging can visualize early


degenerative cartilage lesions before substantial morpho­
lugic changes occur. The application or contrast agent can
B
he performed a� either direct or indirect M R arthrography.
Despite the advantages of indirect MR arthrography using F I G. 1-2 1 Normal bone scans. (From Earl), PJ, Sodcl DB: Prin­

intravenolllo. contrast material. direct M R arthrography has dples (lml practice of mtl.·lea,. IIU!tiicifll!. Sl Louis. 1 995. Mosby.)

gained increasing popularity il:-; a safe diagnmaic 1001 in


assessing subtle illlraanicuiar derangements. including the
evalu�lIion of articular cartilage especially in the shoulder,
the hip, the ankle. ilnd the postoperative knee (Guntern lomography ( SPECT) scans, are valuable in diagnostic
C\ a1. 2003: Kassarjian CI al. 2005: McCauley. 2005: Schmid imaging because of their highly sensitive and noninvasive
CI ul. 2003), nature. Whole-body scanning for metastatic and infectious
di seases, as well as in flammatory and ischemic processes. is
Radionuclide Scanning possible with scintigraphy (Fig. 1 -2 1 ),
Examinations conducLed wiLh the use of nuclear medicine Highly active individuals (e.g.. competitive athletes) are
techniques, including bone scans. posiLron emission LOmog­ prime candidates for bone scanning when the diagnosis
raphy (PET) scans. and single-photon emission computed is uncertain. A bone scan may show increased uptake or
38 CHAPTER I Principles in Assessing Musculoskeletal Disorders

the radioactive isotope consistent with a Slfess fracture


(Fig. 1 -22).
Because of the high incidence of falsc-ncgalivc radiographs
early in the course of stress fractures, additional diagnostic
imaging is oftcn indicted. Radionuclide bone scanning has
traditionally been the Lest of choice in this situation but is
being supplanted by M R I . An increased uptake observed on
a bone scan correlates with increased bone activity caused
by fatigue failure and confinns the diagnosis of stress frac­
ture (Sehils et al . 1 992).
Despite being sen�itivc. bone scanning is nOI specific
and can yield false-positive rates between 1 3% and 24%.
Additionally. localiJ.ing the precise anatomic location of
injury can be difficult (Steinbronn. Bennet!. Kay. 1994).
Bone scanning has become common in the evaluation of
child abuse. Very young chi ldren typically do not develop
stress fractures of multiple fracture sites in normal living
situations (Fig. 1 -23).

Video Fluoroscopy
Video fluoroscopy is used when a function study of the joint
is warranted. Video fluoroscopy should be used when a
biomechanical abnormality is present but is not adequately
demonstrated by plain-film stress surveys or other examina­
tion methods.
Three-dimensional mOlion visualization in the context of
clinical and biomechanical analyses of the musculoskeletal
�ystcl1l is becoming a key instrument for investigating its
complex mechani�rnJ, and the awkward characteristics
(Lcardini cl al. 2006).
Conventional inslrumented gait analysis with skin­
mounted markers has the disadvantage of measuring arte­
facts because of skin movement relative to the underlying
bones. Video fiuoro!'ocoPY i!'o a well-established mcthod of
marc accurately mca\uring knee joint kinematics by avoid­
ing the usc of skin markers. The small field of view of the
image intensifier and thc ability only to gain kinematic data
are lhe two main dbadvantagcs of this system (Zihlmann
ct .1. 2006).

Diagnostic Ultrasound
Diagnostic ultra ound, a sound wave echo study. is particu­
larly useful for evalualing soft tissues. The diagnostic ultra­
sound does not provide the same quality of image as CT or
MRI.
Diagnostic ultrasound requires high-resolution equip­
ment. including a high-frequency transducer. Diagnostic B
ultrasound perfomls well in the detection of rotator cuff tears
FIG. 1-22 Radiographic film (A) and bone scan (B) dem­
and other tendon abnormalities, as well as in identifying
onstrating Slress fracture. (From Nichola... JA, Hen-hm:!n EB: The
some metabolic disease. In cases of suspected pediatric hip
lower exm'mity mul .fpillt' in .�/}()rtf meliil'illt!, cd 4. St Louis, 1995.
disease. diagnostic u ltrasound is the recommended primary
Mosby.)
imaging technique.
Preoperative ultrasound-guided marking of calcium dcposits
significa11lly enhances the clinical re�ults of arthroscopic
removul of calciulll deposits. The success of this type of
surgery is largely dependcnl on the exact localil.ation and
removal of calcium deposits. Complete removal of calcium
CHAPTER I Principles in Assessing Musculoskeletal Disorder. ___ 39
_ _.....

IIOX 1·4

STRENGTHS AN D L IM ITATIONS O F
MYElOGRAPH I C ST U D I E S

Strengths
Studies 01" the subarachnoid space arc poss.ible.
Inlraarachnoid lesions are shown.
Demarcation of multi-disc levels is shown.
Information on surgical scars is provided.
• AS'icssment of ftexion and extension dynamic arc possihle,

Limitations
Lesions removed from outside of the thecal sac can be
missed.
Study variations are problematic.


Detail shown in the dorsal spine is poor.
Postoperative studies arc impossihle to read with accur.J.cy.
Testing. procedure is invasive.

From Brier SR: Primlln- cart' onho/H·t!in. St Loui�, 1999. Mosh)'.

Myelography
A B
Traditional myelographic techniques involve Ihe inlroduc­
FI G 1-23 A, Whole-body scintigraphy. B, Normal bone lion of 'imall amounts of water-soluble contrast medium into
scan is shown for comparison. (Fmm Klippel JH. Dieppc PA the subarachnoid space, either through a lumbar approach
Rht'lIInuw!og\', "01 1·2. eel 2. London. 1 998. Mo�by.) below the level of the conus medullaris or at the level of
C I -C2 through a posterolateral approach. Standard films of
the spinal canal are made to determine the presence or
absence of a filling defect. In cases of acute spinal trauma,
1l1�l l l ll l' I I) 1 1 (,\\\1 I 1 ,(I myelography may be used in conjunction with CT (Fig.
1 -24).
ASSESSMENT A BILIT I ES AND
Myelography remains valuable in evaluating intrinsic
L I MITATIONS OF
spinal cord lesions, nerve root lesiom and dural tear!) asso­
ULTRASONOGR APHY
• .

ciated with severe trauma ( Box 1-4).


I . U ltrJsonography offers direct multiplanar tomogra­ Depending on patient selcction and therapeutic strategy. the
phy without any need for image reformatting. role of plain CT and MRI. as well as myelography comhlncd
2. U ltrasonography can also provide i mages in real time, with myclo-CT. in the diagnmtic evaluation of dcgenerative
without any exposure to ionizing radiation. change\ of the ,;pinc is judged diffcrently ( Krcl.t\chmar.
3. The modality is inexpensive and widely available. 1 998).
4. Ultrasonography offers relatively good soft-tissue In paticnt, with di\k dlsca\c. plain-film cr for initial
contrast and is panicularly effective at helping diagnmtic examination is rccommcnded. if the complaints
to identify fluid collections such as bursitis and are non\pccific (Thornbury ct al. 1 99 1 . 1 993).
abscesses. If the clinical finding:o, \uggest a herniated dis�. MRI
5. Ultrasound waves cannot penetrate bone. should he given prcfcrence ovcr myclog.raphy comhined
with myclo-CT. Thc U\C of non ionic contrast media without
meningeal irritation or neurotoxicity ha� reduced the mor­
bidity of myelography < Krett...chmar. 199K).
dcro�lt... correlatc!'! with good or excellent clinical rcsult\
c Porccllini cl ::II. 2()().l: Rupp. Scil. Kohn. 2(00 ).
Thermography
Identlrying the COUI"\C of the calcium dCPQI;it i\ therefore Using temperature differentials of the body. Ihermography
extremely importanl. The prescnce of a calcium dcpo\lI with illustrates neurovascular changes in injury or dh�ease. Ther­
an atypical cour\c and location more proximal 10 the joint mograms do not provide speci ic
f information regarding the
complicates the opcmlion c\'cn further Failure to locate the cause of nerve fiber irritation (e.g .. herniated disc. scar
calcium dcpo.. 11 can make the ...urgical process extremely tissue_ myospasm).
fnlslratmg and may rcsult in a vcry long operativc time Reflex sympathetic dywophy is pan of a spectrum of
( Kayscr ct al. :W(7). sympathetically mediated pain syndromes that usually occur
40 CHAPTER I Principle> in As;essing Musculoskeletal D i sorders

(\1(l 11(l1' 1 1) 1 ( (,\\\ 1 ' 1 I ; )

ASSESSMENT A BILITIES AND


LIMITATIONS OF
I- __ T
--=
....:.
H .E
.:...: RMOG
::..:. ..: RA!'.H_
Y_
I . The thermographic examination is conducted with the
use of contact liquid cl)'slal detectors or electronic
infrared sensors.
2. Thennography is extremely scnsiti\'c to Ill icro\'ascu­
lar changes in the skin.
3 . ThemlOgraphy IS excellent f"r differentiati ng between
a neurologic and vascular abnormality.
4. Thennography has a greater degree of 'cns l l l \ lIy in
documenling neurovascular abnormality than any
other imaging sy\lcm.
5. Thermography has a greater degree of spec i ficity of
image than mdionuclide hone scan.
6. Thermography has a lesser degree of speci licity of
Image resolution than CT or ,\1RI.

Motor and trophic \ymptom.... ho\\c\cr. characlcri/c mmplex


regional pam ,yndromc, hut arc not found after acute
trauma. Thc\c latter 'ymptom, ob\iou,l) need time to
de\cJop. and the durallon of d .. ,ea,e clear!} "::panuc"
complex regional pam ,,)ndrome' (\\ccb) ,\Ild trJlllna (da)"
(811-)"'lell1 ct al. 2000 ).

Electrodiagnostic Testing
Although electrodiagnostic testing provides valuahle infor­
mation. it docs not stand alone as a diagnostic entity (Table
I - I S). The data obtained must be correlated w i lh the phySi­
cal examination findings and case hi\lory.
Electrodiagnostic testing can potentially dliTerent i ate
asymptomatic dh
, k hcmialions rrom symptomatic ones. A
minimal amount of dencn'aLion can occur in asymptomat ic
..,pines.
With �urface measurement of motor nerve conduction.
velocity provides a "aluable anci llary procedure In the diag­
no�is of various pcriphcral nerve lesions in both thc upper
and lowcr extrcmities. This form of testing involves stimu­
F I G . 1-24 Lumbar myelogram ( A ). with computed tomog­ lating a peripheral ncrve at two ...eparatc po...itions along it ...
raphy aX1i.I1 imuge (8) through the T 1 2 body. (hom GU... lilo RB. COUfl)C and recording the action potentials obscrved on an
Kyle RF Fm('tllrt'\' rllld d/\lowtfOlI\, vol 1. SI l.oui ... 1�J3. �10,hy. ) oscilloscopic scrcen. Slow conduction time'> indicate nCf\'C
entrapment syndromes across the poi III HI whir h thc il11puhc�
are delayed.
Thc electrical rcsponses of nCf\OllS system sensory trad"
in an extremity after a \ccm i ngly minor injury or \ urgical are SOIl1l11o.\ellsory-e\'okl'l1 potentials (SSEPs). SSEPs evalu­
procedure . atc varioul) pathologic variation!) from the peripheral nene
Even Lhough certain ...imilarilic... cxi--I helwccn aculccomplcx through the spinal cord to the \omatoscll..,ory region of the
regional pmn \yndromc\ (n:tlcx \yrnpathclic dy\lrophyJ and brain. SSEPs assess discascs of thc "'pinal cord. trauma
patient... \\ IIh acule trauma. detailed illvc\tigauol1 or the.....: to thc spine. ncuromuscular diseasc. and demyelinating
...ign ... n!\ic.lh ...lriking di fference... . The dinical ... imi lnril)­ disorders.
compn ...c\ pam. hypcralgc...ia. and ..,ome prc... umahly auto· U,ing needle electrodes, needle EMG is \\ idely u,ed to
nomic di,turhancc\ (edema and ,kill tcmpcnllurc change..,), diagnosc nCf\'C root le... ions at the level of the 'pille. EMG
CHAPTER I Principles in Assessing Musculoskeletal Disorders 4,...
1 _----'

lAll L I I 1 5

STRENGTHS A N D liMITATIONS O F ELECfRODIAGNOSTIC TESTING

Testing Modality Strengths Limitations

Nerve conduction velocity Helpful in ruling OUI peripheral cntrapmcni neuropathic Provides imperfect sensitivity; limiled locali/..alion
conditions (c.g., prolonged latencies exhibited in and determination of injury severity; Liming of
carpal tunnel syndrome, tarsal tunnel syndrome) lind study an imponant factor
ulnar neuropathic variations
F waves Provides screening for lale mOlor response with distal Evaluates motor reflex only: possibly evailimes
sweeps staning at the fool abnonnal findings only in lhe presence of
multiple-level injury
l-I reflex Equivalent of ankle join! reflex: evaluates Provides assessment of S I nerve root only
monosynaptic reflex with sensory and mOlor S I
function
SSEP, Helpful in documenting sensory pathway dislUrbances Offers imperfect localization: findings arc rarely
in proximal neural injury and central conduction abnonnal if results of other electrodiagnostic
delays, as in myopathies and multiple sclerosis tests within nomlal limits
Needle EMG Useful in assessing conductivity of ncuntl tissues: Unable to detect denervation potentiab for 14 to
helpful in determining sile and severity of lesion; 28 days aftcr injury: provides imperfect
may be helpful in carly assessment of recovery. 5.Cnsitivity: study timing an imponant factor:
screening for fibrillation potentiab. and signs of proxinu11 lesions sometimes inaccessible
denervation from nerve rOOI compre�sion disorders anatomically: effectiveness reduced after
surgery

EMG. Eh..'Ctmmyography: SSEPs. .;omutoscmory-c\lokcd potential!..


Adapted from Brier 5R: Priman' ('lirt' ortl/Of1l'dic.�, 5t Loui!., 1 999. Mo<,hy.

llltl l llll'l nil l,,\'\\ ll l I \2

ASSESSMENT A BILlTlES AND


LIMITATIONS OF NERVE
CONDUCTlON VELOCITY
I . Studies of nerve conduction velocity (NCV) can rule
out peripheral neuropathic conditions.
2. Routine NCV tests are not specific for conditions
such as radiculopathy, but they may be helpful i n
cases o f chronic pain that have a questionable spinal
origin.

F I G . 1-25 The IMEX portable Doppler (righl). audibly


lllU IIll l' l llIl t, " I ll I I II monitors pulses in noisy environments when palpation is

ASSESSMENT A BILITIES AND queslionable or not possible or when the pulse is especially

L1 MlTATlONS OF weak or rapid. The Doppler also aids in the assessment

ELECTROMYOGRAPHY of circulation distal to fractures, burns. and other injuries


Lo quickly determine the extent of injury. Transmission
I. Electromyography (EM G) shows fibrillation poten­ gel (Iefl) is used to couple the Doppler head to the skin
tials and possible motor unit changes in denervated surface and eliminate air gaps that can degrade sound
muscles. transmission.
2. Denervation of paraspinal muscle, indicates that the
patient has a lesion at the nerve root level.
3. The usual finding of needle EMG in a palient who has
dorsal root disease is normal.
4. It does not provide any information with respect to
the locus of injury (e.g., root, nerve, muscle) and, in
fact, often rcneclS associated tissue injury rather than
neurovascular dysfunction.
42 CHAPTER I Principles in Assessing Musculoskeletal Disorders

differentiates a central spinal lesion from a peripheral neu­ Laser Doppler flowmetry is a valuable noninvasive method
ropathic condition. Resuhs of the procedure are accurate i n for investigation of the very early skin vcnoartcriolar dys­
differentiating disease o f a neuromuscular origin. functions. for evaluation of focal autonomic dysrcgulation
and skin vasomotor abnormalities in patients with Raynaud
Doppler Ultrasonic Vascular Testing phenomenon. Laser Doppler-recorded vcnoartcriolar reflex
Doppler vascular testing allows the assessment of pulses in testing i� a simple procedure and an adequatc addilional
noisy environments or when pulses are weak. This lest is diagnostic 1001. which contribute� to diagno�c Raynaud phe·
efticient when palpation of a pulse is questionable or not nomcnon and differentiate primary frolll secondary Raynaud
possible. The Doppler instrument aids in the assessment of phenomenon (Stoyncva. 200�).
circulation distal to fracture sites. burns, and other injuries
lhal potentially compromise vascular tissue, quickly deter­
mining the extent of injury (Fig. 1 -25).
CHAPTER I Principles in Assessing Musculoskeletal Disorders 43

C R I I I CA L 1 11 1 N 1\.1 N (;
I . In the complaint history of a musculoskeletal condi- S. How are the two tests penormed?
lion, what essential points hould be included for 9. How would you describe the presentation of a patient
proper history taking by an experienced examiner? with scleralogenous pain?
2. Name the five essential steps in drawing a working 10. Why is serial radiography useful i n a patient with
diagnosis for your patient. rheumatoid arthritis?
3. Name the Cr;t;cal 5 questions in orthopedics. I I . What area or areas would you monitor?
4. Describe lendrassik maneuver. 1 2. How Frequent should radiography be used?
5. You have a patient who is complaining of unrelenting 1 3. You have just diagnosed a case of AS. How frequent
spinal pain who demonstrates full and pain-free range should you penorm serial studies of this patient?
of motion. What two problems should you consider 14. What areas should be monitored?
with this presentation? 1 5. A question of causation arises in a child with multiple
6. Describe the difference and what information can be complaints. What imaging procedure would you rec-
obtained from the five rung test and the max;mal om mend for this child?
stalic grip when using a Jamar dynamometer. 1 6. SSEPs are useful in the evaluation of various patho-
7. What are the significances of the clinical findings of logic conditions. What part of the nervous system is
the static grip test and the REG test? evaluated with this process?
44 CHAPTER I Principles in Assessing Musculoskeletal Disorders

B I B L I OG RA P H Y

American Medical Association: Guides 10 the evaf,utl;Ofl of penncmelll Damhra MR, Griffith JA: Gri[fi,h 's 5 mill/lie clinical conmlr. Baltimore,
impairmen', cd 4. Chicago. 1 993. American Medical Association. 1997, Williams & Wilkins.
Anderson KN. Andcn.on LE: Mosby 's pocket dictionary oj medidne, Oat/. FL: H(mdbO()A oj nuclear 11Il!(Jicine, cd 2, St Louis. 1993. Mosby.
mln.ing, &. alfiell Ilea/th. cd 2. SI Louis. 1 994. Mosby. DelillO A. S nyder· Mackler L: The diagnostic process: cxamples in onho­
Ar..tbi A Cl al: Discriminative ability of dual-encrgy X-my absorpliomctry pedic physical therapy. Ph.\·s Tiler 75:203. 1995.
. lection ill i dcntiry ing palienls with oSlcoporOlic fr'dclurcs, BOlle
site 'iC Derby R et til: P153. The influence of pain tolcrancc and psychological
40(4): 1060. 2007. factors on discography in chronic axial LBP palientl>. Spine J 5{4.
Ashford RF. Nagclburg S, Adkins R: Senshivity of the Jamar dynamometer suppl 1 ): S I 84. 2005.
in detecting submaximal grip eITort. J Hand 5/lrg 2 1 (3):402. Dicken�on AH: Spinal cord phamlacology of pain. HI' J AIIlII!SIIt 75:193.
1996. 1995.
Atkinson G. Nevill A. Hopkin!> WG: TypicAl error vers u::; limib of agree­ Dislcr DG. et til: Fal-l>uppressed three-dimensional spoiled grudient-ccho
men!. Sports Met! 30 (5):375, 2000. MR imaging ol" hyal ine can ilage defects in the knee: compurison with
Atkinson G. Nevill AM: Statistical methods for as..'icssing: measurement standard MR i muging and unhroscopy. AJR 167: 127. 1996.
crror (reliability) ill vari:lblcs rele....ant (0 �ports med ic ine. Sports Med Doheny M: Color atlas ami text of osteOtmhritis. London. 1 994. Wolfe.
26(4):2 17. 1 998. Doheny M. Doherty J: Clillical examillatiOIl ill rht'/l/1I(Itology, London,
Ballou SP. Kushner I: C·reactivc prole in and [he acute phase response. Adv 1 992. Wolfe.
Il1Iefll Med 37:313. 1 992. Doheny M. George E: Se/fm·.'wrsmefll pil:tllre le.�IS iTl rht'IlIIllIWlof.:.I',
Barboi AC, Barkhaus PE: Elcclrodiagnoslic testing in neuromuscul ar dis· London. 1 995, Mosby-Wolfe.
orders. Neurologic Clill 22(3):619. 200·L Doody C. McAteer M: Clinical reasoning of CAper! and novice phyioio­
Barkauska:; Vl-I c{ al : fleallh & 11h.\·J,·iaJ/ U.W!SSI1U!fIl. cd. 2. St Loui,. 1998. therapists in an olltpatient orthopaedic '>elling. PI/\'siorhl.'1"(//H'
Moshy. 88(5):258. 2002.
Barker S et al: Guidance for pre-manipulative testing of the cervical spine. Dray A: Inflammatory mediutor!<. of pain, Br J AII(/(,.'I,II 75: 125. 1995.
Pln'.\·iorhemp,v 87(6):3 t 8. 200 I . Emly (>l Sodee DB: Prillcil)/t'.\ afl(J pral'licf! oIIIlIclear medidlll'. 5[ Louis,
Beaton DE. O'Dri'<Coll SW. Richards RR: Grip strength testing using the 1 995. Mo�by.
BTE work simulator and the Jamar dynamometer: a compllr.IIi\"c
. Epstei n 0 et al: Clillic(i/ f'.mmilUllitm, cd 2, London. 1 997, Moshy.
,tudy, J Hand SI/I'g 20(2):293. 1995. Fc"lgin JA. The crucial ligmllellls: ditl,f:II(}.'lis find trt'lllml'nf oj li,f:tllllt'lIlO/I.\
Bechman 1 1 et al: Gelling the most from <l 20-m inute visit Am J Castl'o' illjurie.\· almllt the kllee. New York. 1988, Churchill Livingstone.
e11lemI 89:662. 1994. Feldmann E: Cllrrt'1II dia,S:lImi.\ in 1U.
' llroloMY. St Louis. 1994. Mosby.
Birklein F. Kun7.eI W. 5iewekc N: Despite clinical similarities there arc Freemont AJ. DCllton J : Atlt/.\" oI n'IIMit/I]llIi" C\'IOI'Cllholo1{Y, \'01 18. Dar­
�ignificunt di fferences between acute limb lrauma nnd complex dreclu. Netherl:'lI1ds. 1991. Kluwcr Acadcmic.
regional pllin 'yndrome I (CRPS I). 1'(liIl 93(2):165. 200 1 . Freemont FJ e[ al: The diagnostic value of ,yno\,ial lIuid cytoo.nalysis: a
Bland J M . Altm:1Il Dei : Mea�urcrnenl error and correlalion cocmcient�. reW>:'Ciosment. AI/II Rheum Dis 50; 1 0 1 . 1 9 9 1 .
liMJ 1 1 3(7048):41. 1 996. Galvcl R e l a l : Cross-sectional cvaluation ofpa[icnt functioning and hc. .lth­
Bogduk N. Aprill C. Derby R: Discognlphy. I n White AH. 5chofferman relntcd quality of life in patients wilh neurop:lthie p:lin uncler \tanclurd
JA, editors: Spille ('(Ill!. vol t . $[ Loui�. 1995. Mosby. care conditions. Ellr J Paill 1 1 (.3):2..14, 2007,
Botwin KP, Gruhcr RD, Savare�c R: Lumbar discogr.lphy. Tech Rex Al1l!srh Gc H-Y ct al: Hypoalgcsia to pressure pain in referrcd pain arcas triggered
Paill Mumlg 9{ I ):3, 2005. by spatial summation of experimental muscle pain from unilateral or
Bowlus B: Mosln" " regiollal (t(la.� of 11I1I/1lI11 tll/arom,\', St Louis. 1 997. bi lmcml trapcLiu� mu�cle�. Ellr J fluill 7(6):53 1 , 200.3.
Mo�hy. Gemmell 1-1, Miller P: Should chiropmctor, recommend provoc'.Iti\"c di,­
Brannan SR. JernlnJ DA: Synovial fluid analysi�. J Emert< Me,J 30(3):33 1 . cogmphy for diugnostic purposes in patients with chmnk low back
1006. pain'! Clill Chiro(Jr 8( I ):20. 2005.
Brier SR: Primary care onllOp('(lic:x. $t Louis. 1999, M o�by. Ghanem N et al: MRI and di scography in Lnlumatic intcr\'cnebral disc
Bushong SC: Rat/ia/ogic .H:ie/Wl' JOl' t{'(·llI/ologi.I·I: pln'.lic.\·, hi% g\; (/Ild lesions, C/irl IIIWgi1lg 3 1 (2): 1 47. 2007.
pmtf!Ni()I/, cd. S, St Louis. 1 993. Mosby. Goker B Ct al: The effects of minor hip flexion. lIbduction or adduction ..nd
Canale T: C(1II1/,/Jell \ operatil't' orthopaedic.I·, vol I-t cd 9. 5t Louis. 1 998. x-ray benm angle on the radiogr:lphic join! �pace width of the h ip.
Moshy. o.\({'(}(lr1hl' Carlif 1 3(5):379. 2005.
Cardinal E, Lafortune M. Bums P: Powcr Doppler US in synovit is: reality Goldie BS: Onhopaedic diaK'lOsis OI/(l matW!:t'lIIellf a Ruide 10 Ihl' care nJ
or arti fact? RadiO/OJ.!)' 200:868, 1996. orthopaedic ptllielll�', cd 2. Oxford. UK. 1 998, ISIS Medical Media.
Chance PF: Survcy of inherited peripheral nerve disenscs. Elecrroellceplw· Greenstein G� Clinical (/sse!>slIIl't/f oj tll!lIroIIllISCuill.l"AI'II'wl di.'iordel'.\, SI
loW Cijll Nt'flmphy.\·;ol 103( I ): 1 2 . 1 997. Louis. 1 997. Mosby.
Chandnani VP. ct al: Knee hy"line cartilage evaluatcd wit h MR imaging: GlIckd C. Nidecl.:cr A: Diagnosis of tcars in rot:llor-t·lIlT-inJuries. EIll' J
•1 cadaveric study involving l11ulliple imaging sequences and intra..r­ R(ldio/ 25(3):168. 1 997.
ticular inje(�li()1I of gadolinium and saline solution. Radiology 1 78:557. Gustilo RB. Ky le RF. Temple-m.tIl DC: Pmcfllre,f mtel (li.�/oc(/tioll�. SI
1991. Loui�. 1993. Mosby.
Chiodo A e t a l : Needle EMG h'IS tI lower false positive rate than M R I in Haack E. Tkach J: FaM MR imaging: techniques and clinical appl icalion�.
a�ymptom:uic older adu lt� bei ng evaluated for lumhar spi nal !'Ienosis. AJR 155:95 1 . 1990.
CIi" Nellrophy.liol 1 1 8H ):75 1 . 2007. Hall LD. Tyler JA: Can quanlitativc m:lgnctic resonance imag ing detcct
Cipriano JJ: PhOiographi(' /lUll/lUll oj re.�i(lf/(/I onlwp(wdic alld fI('llI"olo!)i­ and monitor [he progres,ion of carly osteoanhriti:.;'! In Kuetncr KE,
('til ti'.H. ed J. Ballimore. 1997. Willi:uns. & Wilkin:;. Goldberg VM. cdjto�: O,weo"rthritic diwmll'rs. RO�lllonl. III. 1 995.
Coldham F. Lewi, J. Lee H: TIle rcli;lbilily of onc "s. three grip trial� in American Academy of Onhopaedic Surgeons.
�Y lllptolllatic ,lnd asymptomatic iouhj(,'Cts. J fI(II/(J 771t.'r 19(3):318. Hamilton J. Manriquc L. Scurborough N: Development of an intervcrtebral
2006. disc model for testing a nc\\ d i scogntph y syMcm. J Paill 7(4. suppl
Conwell TO: Docllml'l1Iil/,� pmiel/l pmjfft.'.I'.\· "d(lily offiCI! charting seminar" 1 ):526. 2006.
,homugh (lC("fll'(lte qllick pmC"edure.l. cd 1 1 . L<lkewood. CO. 1990. H:U1lcy A: Pf(lcric(I/j()illf (I,�.\I!,f.\'III('1lt loll'('/' (jllmlnlllt. cd 2, St Louis. 1995.
Clinical Advancement Plu� Seminars. Mosby.
CHAPTER I Principles in Assessing M usculoskeletal Disorders 4S

Huwkim RJ: An orgalli':.t'ti aPPI"O{lch /0 1I111,\'{'ulo.lkeh'wl 1!.\'tIlllilltlliofl (lml Malnnga GA er al: Phy�ic<ll c)(amination of the knee: a review of the
hiS/(In' /(/kifl.�. SI Loui.�, 1995. Mosby. original tc\ot description and scientilk vulidity of common orthopedic
Haye!>. KW, Petersen C. Falc�mer J: An c;<.:unioalion of Cyriax's pa,,!-.h'c tests. Arch Pln'S Met! Rdwbil 84(4);592-603, 2003.
mOl ion IC..ts with patients having Ol>lcoanhrilis of the knee. Phys Tllt.'r Malone TR. McPoil TG. NitL AJ: Orthopedic lItIll ,\port.\" rhr,\ical ,heral)\'.
74:697. 1994. cd 3. 5t Louis. 1 997. Mosby.
Herndon WA: AculC and chronic injury: ils effect on growth in the young Mather:. LH: Clinit'rll Wll/lOml' pri"ciples. St Loui:-;. 1996. M()�by.
athlete. In Fruna WA. ci til. editors: Adl'(lI/('C.I ill .\11(}n� medicillt: Mat!!-uo T el al: Applicution of thermography for evaluution of mechanical
jiflll!.fS. vol J, Chicago. 1 99(). Year-Book Medical. load on the musde� of upper limb during whce1chuir driving.
Hillman TE c.1 ::1.1: A pr.lclical po!.lurC for hand grip dynamometry in the J /Jiomech 39(suppl 1 ):S537. 2006.
clinical \clting. eli" Mllr 2·H2):224. 2005. Maurisscn JPJ et a1; Factor..: affecting grip strength testing. Neflf"O/(uicol
Hinkle CZ; F/IIu/(llIIellla/,\ of (I1UlI01II\' (lilt! IIWI'l'IIIf!m: 1I lI'ol'/.;./J()oA (11/(1 Terafo/ 15(5):5-43-553. 2003.
gllidl', 51 Loui�, 1 997. Mosby. McDonnell MN et :11: Illlpainnenls in precl1..ion grip cOlTclutc with fUllc,
I-Iuckcll CB. Simmons ED. Zhcng Y: The signilicunce of annular tear of tional mcru;ure� in adult hemiplegia. Oill N('/tl'{lphysiof 1 1 7(7): 1474-
ccr\'ical disc for positi\'c discography by age in discogcnic pain. Spilll' 1 480. 2006.
J 5(4. suppl I ):S48. 2005. McKinnis LN: FundamclIl:Il .. of radiology for physical lhcrapisls. In Rich­
Ido K ct al: The validit) of upright myelography for diagnosing lumbar on J K. Igiar\b ZA. editor...: ('fillic(1f orriJolJedic- phnic:af liJemp\'.
nrd..
lIisc herniation. Cli" Nt'lIml Nellrmllrg 104( 1 ):30, 2002. Philadelphia. 1 994. W B Saunders.
Jahlonski S: Diclionory of l1ledit'al llcmnW1I.I' & abbrel'i(llio//\. cd 3. Phila­ McRae R: Clinicaf orll/o/Jaedic t'.Ulmilimioll. ell 3. Edinhurgh. 1990.
lIclphia. 1998. Hanlc)' & Bcll'us. Churchill Livingstone.
Jones MA: Clinical rca!>oning in manual Ih('rapy. Phn Tiler 72:875. y /IInlil"iIll' the primaf')' ClIre of
Mengel MB. Schwicocrt LP: Ambl/llIlOr
1 992. j(lIf1i/it!S. ed 2. Stamford. Conn. 1 996. Appklon & Lange,
Kang CH et al: MRI of paraspin1!1 muscll!� in lurnb:Jr dcgcncr:nivc kypho· Mennell JM: The Jl/1l.\·clilflJlie/l'fal .n'srem differelllia/ diagllosis/mm .1)"lIlp'
sb palients and control patients with chronic low hack pain. Clill toms (/Ild physical �;Km. Gaithersburg. Md. 1 992. Aspen.
Rat/io/ 62'5):.H9. 2007, Mercier LR. PeBid FJ: Practic(ll orth0l'edic.\·, cd 5. $1 Louis. 2000.
Kllti�ii B: Elt:'clmm\'o,t,:mphr ill clillical prtlcliu (/ ClUI' .�t/Uly appm(/ch. 51 Moshy.
Loui�. 1998. Mo�hy. Micheli U: Rcne)( sympathetic dystrophy mu) stem from ,>ports (news
KC':u� TE: Mltu oj lIonll(ll f'Ol'Tlfgt'/I 1·'(lri(1I/1S Ilwl lIIa.\' ,�imulm{' (lisease. cd brien. Phy.\ SpOrl,\ Ml'l' 18:35, 1990.
6. St Louis. 1996. Mosby. Middleton GO. McFarlin JE.. Lipsky PE: Prevalence and clinical impact of
Kessler RM. Herling 0; A...scs�melll of l1lusculo�keletal disorders. In libromyalgia in systemic lupus crythcmalOu,>. Anl/rili.1 Rht'um 8: 1 1 8 1 ,
Ke�sler RM. Herling D. editors: MallaMemt'll1 ojcommo/l IIII/scl/im/.:.· 1994.
('Iewl di.lmders. cd. 2. Philaddphi'l. 1990. J8 Lippincoll. Morenu JE Rc: "Ultrasound: i:. therc a fuwre in diagnostic imaging'!" J Am
Keltenb'lch G: WrilillK .\.().tl.p. IIolel'. Philadelphia. 1990. FA Oavi!'>. Coli RlIt/io/ 4( I ):78·79. 2007.
Khumna R. Berney SM: Clinical aspects of rheumutoid arthritis. Pm/I/)· Morse JL ct ul: Maximal dynamic grip force lind wrist torque: the effccts
IJIr.ni% ,l!.\· 1 2(3): 15.�· I 65. 2005. of gender. exertion dircction. angular velocity. and wrist angle. AJlpl
Kim H-S et al: Compari�on of the predictivc \'ulue of computed tomogra� Ergoll 37(6):737-742. 2006.
phy with myelogmphy vcr�us MRI u�ing exercise treadmill exam in Mosby·Year Book. Inc: £rpt'fl IO·mifll/le I'''n·.\·i('(// t'.\lIlIliflllti(lll, 5t Louis,
lumbar "pinal stenosis. Spill!' J .lIS. suppl 1 ):8-4·95. 2003. 1 997. Mosby.
Klcinrcn);inb. GJ ct al: Upper limb tension tests as tools in the ciillgnosis of Mower WR ct al: U�c of plain 1"..Ic1iogmphy to �crccn for cervical spine
nerve and pkxu� lesions: anutumical and biomechanical a.spects. C/ill injuries. AIm Ell/erg Med 38( 1 l: 1 -7. 200 1 .
Biolllecli 1 5( 1 ):9-1-4, 2000. Nardone OA CI ul: A modd for lhe di;lgnoslic medical inler\'icw: non­
Klippel JI-I. Dieppe PA: RJl£'lIIl1tlfuirW.I·. vol 1-2. ell. 2. London. 1998. verbal. verhal and cognitive a:.sessments. J Ct'fI IllleJ"ll Mn' 7:437.
M(hby. 1 992.
KonowitL KB: Rctlex !'ymp'lthy dy·arophy syndrome sometime� misdiag­ Nellina SM: The UP/,illCtJlI mall/llIl of III/r.\'illg {II"l1Clice. cd 6. Phihldelphia.
noscd. often mi..understooc.l, J Alii Chiro AJSOC 35:58. 1998. 1 996. J B Lippincoli.
LiHlca:.h:r AR. Nylund J. Robens CS: The validity of the motion palpation Newman J5 et al: Power Doppler sonography of synovili ..: asscssment of
test for dctermining patellofcmornl joint articular c:lrtilage damage. therapeutic rc�ponse-prelimin:lry ohservatiolls. R(u/i% ,/fY 1 98:582.
PhI'S n'er Sport 8(2 ):59·65. 2007. 1996.
Lander PH: Lumbar discogrllphy: CU/Tcnt concept!> and cOlHrover�ies, Ng GYE Filii ACC: Does elbow position affect strength and reproduc­
Sl'IIIi" Ullm.w//Ild CT MRJ 26(2);81-88. 2005. ibility of power grip measuremelll�? PhYJiOlher(l/1.\· 87(2):68·72.
Landewe RBM. "an der Hcijdc DMFM: Principles of a.�scs<;ment from a 200 1 .
clinical perspccli\'c. Bt',\1 P/,{/('I Res Cli" Rht'IIllUlwl 17(31:365-:'19. Nicholas JA. Hershmnn EB: Till' lower e.HremU\' & ,\],i"" ill .�porlS medi·
2003. t.:ille. ed 2. 5t Loui�, 1995. MOl>by.
Las�cre M et "I: Stnalle�t delectable difference in radiological progression. Nierc KR. Torney SKSK: Cliniciam' perccption ... of minor cervical in:sta­
J Rlu:'lIlIIlIlol I 26(3):7J 1 -7J9. 999. bility. M"" 7Jwr 9(3): I-l--H 50. 2004.
Lewis CB. Knortl KA: Orthopedic Wi,\en'llll!m a/ld Irtmtmelll oj the geri­ Pag:lIltl KO. Pag�IIl:l TJ: MO.\by :� m(1ll/wl o/diagnoslic /JlUllohomwry lesu.
Ulric II(I(i('l1(, SI Louis. 199J. Mo�hy. St Louis. 1 998. Mosby.
Licht PB, Chri�ten.,cn HW. Hoilund·Carlsen PF: I:> there a role for prema­ Palmgren PJ ct ill: Improvement after chiropnlctic cure in ccrvicoccph..lic
nipuJalive le<;ling before cervical manipuJillion'! J Mcmipulalil'e kinesthetic scnl'ihilifY and subjecti\-(' pain illlen,>ity in p;ltients with
Pllysio/ Ther 2J(Jl; 1 75-1 79. :WOO. nontraumatic chronic ned; pain. J Mallipiliruil'e Ph.l'l'iol Thel'
Long L. HUlltley A. Ern�1 E: Which complclllcntUl,) and alternative thera· 29(2):100- 106. 2006.
pics benclh which conditions? A �urvey of the opinions of223 profc�­ Paoloni JA. Appleyard Re. Murrell GAC: The Onhopaedic Research Insti­
sional organi7atiolls. COmplelll(!1If Titer Metl 9(3):! 78· 185. 200 1 . tute-Tenni� Elbow Testing Systcm: a nlodit1ed chair pick-up test­
Mader TJ, Ames A, Letourneau P: Pain Illilnagemcnt i n paediatric trauma internucr and intrarater reliability te�ting and validity for monitoring
patients with tong hone I'ructure. llljllry 37( 1 ): 6 1 ·65, 2006. I:lteml epicondy1osis, J Slwl/ltler Elbow SlIrg 13( I ):72· 77. 2004.
Magee OJ: On/wpe(Jic phnit:a/ (1.�.\'e.\"smelll, cd 3, Philadelphia, 1 997. W B Papach"r'..Il<unpou� X et ill: The effcct of contrast media on the synoviuJ
Saunder�. membrane. Eur J Radiol 55(3):-126-430. 2005.
Maher C. Adam:. R: Reliabilit� of pain and stifTncs:. as.,essments in L"linical Pascual E, Jovani V: Syno\iul fluid analysb. Be.1'I f'mel Res elill Rheum
manual lumbar �pinc examination, PI,y.\· TIIt'I' 74:80 1 . 1 99-4. 19(3):371 ·386. 2005.
46 CHAPTER I Principles in Assessing Musculoskeletal Disorders

Patlon K: Sflldetlt SllIl'il'tl/ Kllhle for (lI/tlWmr lind physi% 8J: S, Louis. Swmford JA: Descending conlrOl of pain. 8r J A!laesth 75:217. 1995.
1999. M01>by. Stevenson J: When lhe trauma pmieOl i:-; elderly. J Pt'ri(me.ffh Nun'
Peterfy CG et 31: MR imaging of the arthritic knee: improved discrimina­ 19(6):392·400. 200l.
tion of canil:lgc. synovium and effusion with pulsed saturation lrtms­ Stojilovic N et al: Analysi<; of prosthetic "nee wear debr!.. extracted from
fer and fal-suppressed Tl -weighlcd sequences. Radi% gy 1 9 1 :413. synovial fluid. Appl Slirface Sci 252( 10):3760-3766. 2006.
1994. Stone JA: MR myelography of the spine and MR peripheral nerve imaging.
Pincus T el til: Persistent back pain-why do physical therapy clinicians '...tax" Resoll (maging CIi" N Aill 1 1 (4):543-558. 2003.
cominuc tremmcnt? A mixed methods study of chiropractors. osteo­ Storm S el al: Compliance with elcctrodiagnostic guidclines for patients
palhs and physiothempists. ellr J Pain 10{ I ):67-76. 2006. undergOing carpal tunnel release. Arch PII,"s Med Relw/Ji{ 86( I ):8- 1 1 .
Pope MH: OC"lIfHuional loll' back paj,,: a.�sessmelll. IreD/mew. Olld prel'en­ 2005.
lio". $1 Loui!o>. 1 9 9 1 . Mosby Year Book. Sugimoto H et a1: Early-stage rheumatoid :Irthritis: diagnostic accuracy of
Raspc I-IH: Back pain. In Silman AJ, Hochberg M. editors: EpideminloRY MR imaging. Radiolngy 198:185. 1996.
of rile rllel/Illmic disea.'ies, Oxford. UK. 1993. Oxford University Tumai K et al: Dynamic magnetic rcsonan(�e imaging for the evaluation of
Press. synovitis in patients with rheumatoid arthritis. A /·thritis Rheum
Ra"':lud Pet 01: Assessing smallest deteclIlble change over time in continu� 37: 1 1 5 1 . 1994.
ous structural outcome measures: application to radiological changc Thibodeau G. Patlon K: Pocket reference to ll(,(,omptmy (ll/alUmy & phy.�·
in knee osteoarthritis. J eli" Epidemiol 52( 12): 1225·1 230. 1999. iolog.\'. ed 3. SI Louis, 1996. Mosby.
Ravel R: CIi1Jical laboralary medicillt, di"ical appliml;oll of labomlOrv Thibodeau GA. Patton KT: AIUlttJIIH' & I)hvsiolog\'. ed 3, St Louis. 1996.
dalll, ed. 6. 51 Louis. 1 995. Mo�by. Mosby.
Rogcrs LF. Hendrbt RW: Evaluating the multiple injured patients radio· Thibodeau GA. Patlon KT: A/UllOm\' & ph\·siology. ed 4, St lolli.... 1<)99.
graphically. Orr/WI) Clill North Alii 2 1 :437. 1990. Mosby.
Ross JS: Diagnostic imaRing. Spine. Sail Lake City, 2004. AmiThYs. Thompson JM: Clinical ollllilles for health (/.\'.I/;!.Hl1It'IIt. 51 Louis. 1997.
Sohin G. Demirtas M: An overview of MR arthrography with emphasis on Mosby.
the cumnt technique and applicutional hints and tips. Elir J Radiol Toghill PJ: £xamillillt-: (Jmiellf.l· all immdllClio/l to clinical lIIet/ieinf'.
58(3):41 6·430. 2006. London. 1990. Edward Arnold.
Saidoff DC. McDonough AL: Critical pathways ill thempelflic illlen't!I'­ Torg JS. Shepard RJ: Cur"'" therapy i/l sport.I' medicil/e. cd 3. St Loub.
tioll: lower I!xtremity, St Louis. 1997. Mosby. 1 995. Mosby.
Sasaki H et at: Grip strength predicts cause-specific mortality in middle­ Truub M et al: The use of chest computed tomogl1lphy versus chest x-my
aged and elderly persons. Am J Med 1 2(){4):337-342. 2007. in patients with major blunL trauma. I"jun' 38( 1 ):43-47. 2007.
Schrcudcrs TAR ct al: Strength measuremenls of the intrinsic hand muscles: Tredgeu MW. Davis TRC: Rapid repeal testing of grip strength for delec­
a rcview of the developlllelll :md evaluation of the ROllcrdam iOirin­ lion of faked hand weakness. J Hcmd 5ltrg 25(4):372-375. 2000.
�ic hand myomcter. J Halld Tiler 19(4):393-402. 2006. Tsunlike M et al: Age comparison of H-reflex modulation with the Jl!ndr.u;­
Schueller G: MRI atlas of onhopedics and trJuOlalology of the knee. Eur sik maneuver and postuf:ll complexity, CIi" NeltrophysioI I 1 4(5):945·
J Radiol 51 (3 ):293·238. 2004; from Teller P ct al. Ellr J Radiol 953. 2003.
5 1 (3)0293·298. Turnbull TJ. Dymowski JJ: Emergency department U!)C of hand-held
Schunlllcher HR. Klippe[ JH. Koopman WJ: Primer 0" rlu: rhellllUltj{, Doppler ultrasonography. Am J Emerg Metl 7(2):209-215. 1989.
disemes, ed 10. At[unlO. 199.'. Arthritis Foundation. Van De Kar THJ et al: Clinical value of c[cctrodiagnostic testing following
Schwartt ML. Al-Zahmni S: Diagnostic imaging of elbow injuries in the repair of peripheral nerve lesions: a pro�pective study. J Hand Sllrl:
throwing athlete. Oper Tech Sport.\' Med 4(2):84-90. 1 996. 27(4)0345-349. 2002.
Scuderi OR. McCann PD. Bruno PJ: S(XJm medicine: principles ofpriman' Weinstein SL. Buckwllher JA: Tur('k's orthopaedics prillciple.\ and Iht'ir
care. St Louis. 1997. Mosby. applicCllion. ed 5. Philadelphia. 1994. JB Lippincott.
Scutellari PN. Or/incolo C: Rheumatoid arthritis: sequences, £ur J Radiol White KP et al: Fibromyalgia in rheumatology practice: a survey of C..na·
27(suppl 1 ):S31 ·S38. 1998. dian rheummologists. J Rhe/lmaI01 22:722. 1995.
Seo K+S et al: In vitro measurement of pressure differences using manom­ Whitmore I. Willan P: Mllitiple choice questioll.l· ill 11/1111(111 {J/Il1lOmy.
ct,ry at v..rious injection speeds during discogmphy. �iJille J 7( I ):68- London. [995. Mosby.
73. 2007. Wiener E et al: Contrast enhanced cartilage imaging: comparison of ionic
Shankm:'111 GA: P'wullll!1enta/ l1n}w{Jl!dic 1I1l1t111gemelJl for the physical and non-ionic contrast "genls. Ellr J Rat/iol (in prcss. corrected
"wrapi.\·' (l.I·sisl(lIIt. St Louis. [997. Mosby. proof).
Shechtman O. Tnylor C: How do therdpists administer lhe rapid exchange Wolfe F el a!: The prevalence and characteristics of flbrornyalgi:1 in the
grip test? A sun'ey. J HlItul Ther 15( 1 ):53-6 1 . 2002. genera) population. Arthrili.'· Rheum 38: 19. 1995.
Sheehan DV H-SK. Raj BA: The measurement of disability. lilt Cli" Psy­ Woolf CJ: Somatic pain-pathogcnesi!. and prevention. Br.l AlIlIesli1 75: 169.
clloplwrmaml I I :S89-595. 1996. 1 995.
Sherbondy PS. Sebastiane!!i WJ: Slress fracmres of the medial malleolus Zatouroff M: Diagllosis ill color pln'.\·iml .fig/1.';' ill general mellieille. cd 2.
and di"tal fibula. Cli" Sports Med 25( I ): 1 29- [37, 2006. London. 1996. Mosby-Wo[re.
Sieper J et al: Ditlgnosing reactive nrthrilis: role of clinical seuing in the Zeitl K. McCutcheon H: Observation.!. and vital signs: ritual or \ ital for the
value of serologic and microbiologic as..ays. Arthritis Rhe//m monitoring of postoperalive patients? App/ Nun' Res 19(4):204-2 1 1 .
46(2):3 1 9·327. 2002. 2006.
Slipmnn CW et al: ProvQCnti\'c cervical discogr.tphy symptom mapping. Zcmbsch A el al: Positioning device for optimal active kinematic real-time
Spine J 5(4):381 -388. 2005. magnetic rcsonnnce imaging of lhe knee joint: a technical note. Clill
Smat1 K. Doody C: The clinical reasoning of pain by experienced museu­ Biomecll 1 3(4-5):308-3 13. 1998.
lo..keletal physiotherapists. Mall Tiler 12( 1 ):40-49. 2007. ZitcHi BJ. Duvis HW: At/lIS of(Jetlitlrl'i(' "/n'.\ical di(1,�rwsi.I·. ed 2. London.
Smith Re. Hoppe RB: The patient's story: intcgrJ.ting the palient and 1992. Wolfe.
physician cenlered approaches 10 interviewing. AIIII (litem Met!
1 1 50470. 1991.
51. Claire SM: Diagnosis and treatment of fibromyalgia syndrome, J Nell­
rrJlIlIl.fC Sy.ft 2:3. 1994.
CHAPTER I Principles in Assessing Musculoskeletal Disorders 47

C I TATI O N S
Benaroia M, Elinson R. Zarnke K: Patient-directed intelligent and interac­ minor chief complaints? Ami Ell/erg Mell 46(3. suppl 1 ):28-29.
live compulcr medicnl history-gathe-ring systems: a utility and feasi­ 2005.
bility study in !..he emergency departmenl, 1111 J Med Illform 76(4):283- Pinilla JC: ACUle respiratory failure in severe blunt chest trauma. .1 Trauma
238. 2007. 22(3);22 1 -226. 1 982.
Berghout RM CI al: Evalumion of general practitioner's time investmenl Porcellini G CI al: Arthroscopic treatment of calcifying tendinitis of the
during a store-and-forward teledermatology consultation. 1m J Met! shoulder: clinical and ultrasonographk follow-up finding� at two to
InJonll 76 (supplement): S384-839 1 . five years, J Sholl/der Elboll' 5t1rg 1 3(5):503-508, 2004.
Birklein F et al: Neurological findings i n complex regional pain syn­ Rupp S. Seil R. Kahn D: [Tendinosis calcarea of the rolawr curfl. Orrho­
dromes-analysis of 145 cases. Acta Neurol Sccmd 1 0 1 (4):262-269, pade 29(1 0);852-867. 2000.
2000, Schild H c\ al: [Computed tomography of lung contusiOI1. An experimental
Boden SO et al: Abnormal magnetic-resonance scans of the lumbar spine studyl, Fortscllr Geb ROlltg(!fIstr NllkleclrIlled 145(5): 5 1 9-526.
in a.,ymptomatic subjects. A prospective invcslig:ltion. 1 BOfle 10illl 1986.
S,,'II 72(3);403-408. 1990. Schils lP ct a1: Medial malleolar stress fraclUfcs in seven pUlien,-,; review
Cole M. Michael JA, Robert BD: Romberg's sign. In E1Icyciopedia uf /he of the clinical and imaging fc,llures. Radio/nKY 185( I ):219�2 2 1 .
lIel4l"Olog;cal .\·ciem.:es, New York. 2003. Academic Press. 1992.
Fess EE: Grip strength. In Casanova JS. cditor: Clillical asses,smellf recom­ Schleyer T. Spu.llck H, Hernandez P: A qualitative investigmion of the
mendarions cd 2. Chic3go, 1 992. American Society of Hand Thera­ content of dental paper-based and computer-based palient record
pists. form,u.s. J Am Meli Illform Assoc 14(4):5 1 5-526, 2007,
Gunlern DV el al: Articular canilage lesions of the glenohumeral joint: Schmid MR ci al: Cartilage lesions in the hip: diagnostic effectiveness of
diagnostic effectiveness of MR arthrogrJphy and prevalcnce in MR anhrogrdphy. Radiology 226(2):382-386, 2003.
patients with subacromial impingement syndrome. Radiology Scuderi GJ el al: Towards a more sdcntilic understanding of lumbar dis�
226( I); 165-1 70. 2003. cography in pmients with lumbar interverlebrul disc disease. SpintO J
Jimenez RM. Jaramillo D. Connolly SA: Imaging of the pediatric hand: (in press. corrected prooO.
soft tissue abnormaliticl>. £ur J Radio/ 56(31:344-357. 2005, Shechtman O. Taylor C: How do therapists administer the rapid c.xchallge
Johnson JA. Cogbill TH, Wingo ER: Determinants of outcome after pul� grip test? A survey. J Halld Ther 15( I ):53-6 1 , 2002.
monary contusion. J Trauma 26(8):695-697. 1 986. Sman K. Doody C: The clinical reasoning of pain by experienced muscu­
Joughin K ct al: An evaluation of rapid exchange and simultaneous grip loskeletal physiotherapi<;ts. MflfJ Ther 1 2( 1 ):40-49. 2007,
tests. J Hal/(l Surg 18(2):245�252. 1993. Slcinbronn OJ. Bennett GL. Kay DB: The usc of mugnetic resonance
Kassarjiun A et al: Triad of MR arthrographic findings in patients with imaging in the diagnosis of stress fractures of the foot and ankle: four
cllm�type femoroacetabular impingement. Radiology 236(2):588-592. case reports, Fool Ankle 1111 15(2):80-83. 1 994.
2005. Stoke!. M, Young A: The contribution of reflex inhibition to anhrogenous
Kayser R ct ..I: V:llue of preopcmlive ullrasound marking of calcium depos� muscle weaknes�. CIi" Sci 67( I ):7-14. 1 984.
it!> in patients who require surgie ..l treatment of calcific tendinitis of Stoyneva Z: Laser l)oppler�recorded vcnoaneriolar renex in Raynnud's
the shoulder, Arthroscopy 23( I ):43-50. 2007. phenomenon. AlIlo" Nellrosci 1 1 6{1�2):62-68. 200·t
Kretzschmar K: Dc.genentlivc discases of the spine. The role. of myelogra­ Takernitsu Y el <11: Lumbar degenerative kyphosis. Clinical. radiological
phy and myclo-CT. Ellr J RlIllioI 27(3):229-234. 1 998. and epidemiological studies, Spille 1 3 ( ! I ): 1 3 17·1 326. 1988.
Leardini A ct al: A ncw software 1001 for 3D Illotion analyses of the Taylor C, Shechtman 0: The u!>c of the rapid exchange grip tCM in detect­
musculo--skclctal system, CUn Biomech 21 (8):870-879. 2006. ing sincerity of effort, pan I: administr-.ltion of the tCSt. J Hand Tiler
LoCicero J 3rd, Mattox KL: Epidcmiology of cheM traum:L Surg C/ill North 13(31: 195-202. 2000.
Am 69( 1 ); 1 5-19. 1 989. Thornbury JR ct al: Disk-caused nerve compression in patients with acute
McCaulcy TR: MR imaging evaluation of the postoperative knee, Radiol­ low·back pain: diagno!'is with MR. cr myelography. nnd plain CT.
ogy 234( 1 );53-6 1 . 2005. Radiology 186(3);7 3 1 -738. 1993.
Nowin...ki CJ et al: The impact of converting to an electronic health record Thornbury JR CI al: Increasing the scientific quality of clinicnl ellicucy
on organizational culture and quality improvemcnt. 1m J Med Itifnrm studies of magnctic resonance imaging. IIII'e.H R(/{/ioI 26(9):829-835.
761"ppl 1 );5 174-5 1 83. 2007. 1991.
Ory PA: Radiography in the assessment of musculoskeletal conditions. Best Wagner RB. Jamieson PM: Pulmonary contusion. Evulunlion and classifi·
Pmc' Rt:.1 Oil/ Rhellm J 7(3):495�5 J 2. 2003. Calion by computed tomography. Surg CIi" N()rth Am 69( I ):31-40.
Owens JEF et al: The reliability of a posterior-to-anterior spinal stiffness 1989.
measuring sy�tcm ill a population of putients with low back pain. Zihlmann MS et al: 111ree�dimensional kinematics and kinctic!) oftolal knee
J Mllllipulalil·t: I'lIy.\·;ol Tiler 30(2): 1 1 6- 1 23. 2007. arthroplasty during level walking using single plane video·fluoros­
Phelps MA. Rodriguez RM: The comprehensive physical exam: when and copy and force plntes: a pilot study. Gail Post/In' 24(4):475-48 1 .
why do emergency medicine residents perform them on pUlients with 2006.
C H A PTER 2 Assess ing Cardi nal Musculoske letal Sym ptoms and S ig n s 69

TA B U 2- 1 2
TREMOR C LAS S I F I CAT I O N

Cause Type and Rate of Movement Description

Anxiety Fine, rapid. I () to 12/scl' I rregular, variahle


I ncreased by attempts to move part; decreased by relaxation of part
Parkinsonism Fine, regular. or coarse. 2 t o 5/sec Occurs at rest
May be i n h i bited by mov e me nt
Involves flexion of fi nger and thumb pill rollillg
Accompanied by rigidity. cogwheel phe n ome n a , brady k i nesia
Cen:hcllar tremor Variable rate Evident o n l y on mo ve m c n t (most prom i nent on linger-to-nose test)
Dysmetria (seen when patient i s asked to pat rapi d l y ; pats are of unequal force
and do not all arri ve at same point)
Essential or seni Ie Coarse. 3 to 7/sec I n volves the jaw. sometimes the lOngue, and sometimes the entire head
Metabolil' Disappears on complete relaxation or in re s pon se to a lcoho l
Yariahle
Patient is obv iously i l l ; if i l l ness i s a res u l t of hepatic fai' l u rc, patiel1l w i l l have
other signs, such as palpable l i ver, spider nevi

From Barkauskas YH et al: Health & physical assessmefl/. ed 2 , St Louis. 1 998. M osby.

Cramps and Spasm


O RI H O P I D l l' ( ; ;\ , \HJ r 2 I I
Muscu lar spasm, or tremor (Table 2- 1 2), may occur at rest
or with movement. S pasms and tremors occur in the normal GAIT
ind i vidual with metabo l ic and electrolyte a l terations. Cramp­
Gait impairments of predominant neurologic origin
ing is a common complaint after excessive sweati ng and
include the following (in descending order of
subsequent hyponatremia, hypocalcemia, hypomagnese­
frequency):
mia, or hyperuricemia.
I . Di sorders of the corticospinal pathways (spasticity )
Exercise-associ ated muscle c ram pin g is a pai n fu l . involun­
2. Basal gangl ia ( parki nsonism)
tary contraction of skeletal muscle that occurs i mmed i a tel y
3 . Cerebel l u m and connections ( ataxia)
after e x e rc i se . Any athlete who e x h i bi t s repeated epi sodes
4. Cerebral cortex (gai t aprax ia)
of muscle spas ms should u n d ergo a comprehensive h is lOry
5 . Neuromuscul ar system ( weakness)
and p h y s ic al e x a m i n ation and. in most cases, l aborato ry
6. Sensation (atax ia)
studies to evaluate e l ectro l y te s . Athl etes should a l so have a
u r i n a l y s i s to c h ec k for blood or myoglob i n . The i n i ti a l
history shou l d i ncl ude questions pertai n i ng t o h ydra t io n
status, frequency of s t ret ch i n g . and the use of ergogenic
s upp l eme n t s s uc h as stero id s or creat i ne . Questions to define
the athlete's me d i c a l h i story should i n q u i re about how the Trousseau sign i s demonstrated by i nflating a sphygmo­
muscle crampi ng relates to temperature, d iet. fa m i l y history, manometer around the wrist area of the left hand to above
u r i ne color changes (myog l o b i nuria), and how l o ng the systolic blood pressure for 3 mi n u tes while observ i ng the
symptom� last ( Nad l er et ai, 2004). hand. Typ ical carpal spasm, which relaxes approxi mately 5
seconds after the cuff is released, is considered a positive
Tetany Trousseau sign.
Hypocalcemia and hypomagnesemia often cause the Tetany i s m o s t c ommo n l y caused by h ypoca l c e m i a . Low
invo l untary spasms of s keletal m uscle, which resemble levels of free or ion ized e x trace l l u lar c a l c i u m reduce the
cramping. Tetan ic cramps can be el icited by repeatedly per­ normal transmembrane pote n t i a l of the nerve by i ncreasing
c u ss i ng the motor nerve, which leads to a muscle gro u p so d i u m conductance, thus red u c i n g the threshold req u ired to
contraction-cramp-spasm at frequenc ies o f 1 5 t o 20 per cause depolarization. Normal serum ion ized c a l c i u m l evels
second. Chvostek s ign is the spasm of fac ial muscles pro­ range from 5.9 to 6.5 mg/d l . Levels fa l l i n g be l o w 4.3 mgldl
duced by tapping over the facial nerve near i t s foraminal can cause tetany. H y poca l cem ia i s observed in h y poparathy­
ex it. Chvostek s ign may also occur w i th normocalcemia, as roid i s m , v i ta m i n - D deficiency, m a l ab s orpt i o n s y n dromes.
wel l as w i th h y pocalcem ia. acute pancrea t i t i s . m a l i g n ancy, sep s i s . and drug effect.
Patients w i th hypocalcemic seizures demonstrate marked Hyper venti lat i o n lead i n g to respiratory a l k a l o s i s and sec­
Chvostek sign, positive Trousseau sign, sweaty hands, and ondary reduction of ionized c a l c i u m may prec i p i tate tetany
hyperreflexia (Ahmed et ai, 2004). (Freeman, M ichae l . R ob e rt . 2003).
70 CHAPTER 2 Assessing Cardinal Muscu loskeletal Symptoms and S i gns

Impairment of Gait
Finding a spinal or lower ex tremity orthopedic or neurologic O RI I I O I' I D I C l,A,\\ lJl 1- 1 -1-
di sorder that does not produce abnormal i ties of gait a t some IMPAIRED MICTURIT I ON
time during i ts course i s d ifficult.
Gait disturbances a fter a stroke a r e multifaceted a n d hence Localization of impaired micturition depends on the

must be studied from multiple perspectives. B iomechanical following:

measurements such as temporal distance parameters, kine­ 1 . Loss of bladder sensation

matics, kinetics, mechanical energy, and energy costs, as 2. Perineal sensory loss

well as electromyography, can evaluate the behavioral 3. Patulous anal sph i ncter
profile of gait and reflect CNS adaptation with respect to 4. Absence of the bulbocavernous and anocutaneous
internal and external demands. Electrophysiologic measure­ reflexes

ments such as stretch reflex, H-reflex, and cutaneous reflexes 5 . Sensory, motor, and reflex changes in the lower
can evaluate the integrity of spinal cord functions during gait extrem ities

and indirectly assess the integrity of the descending control


system (Lamontagne, Stephen son, Fung, 2007).

B1adder Control
Incontinence and other disturbances of urinary bladder fu nc­ bilateral-needle e1ectromyographic examination of the
tion are occasion al l y the fi rst man ifestation of d isease of the externaI anal sphincter and sometimes of the bulbocaverno­
spinal cord, as well as the rest of the nervous system. The sus muscle needs to be considered first. Detection of spon­
physiologic mechanism of micturition is complex. The terms taneous denervation activity, most appropriately in the bul­
atonic bladder and spastic bladder are no longer useful i n bocavernosus muscle, is common in the interval from 3
descri bing different levels of neurologic i n v olvement weeks to several months after a lower motor neuron i njury
because they are related mainly to l ocal factors i n the bladder ( Podnar, in press).

wall. A n associated history of erectile dysfunction or rectal


Compressive lesions to the cauda equina or conus medullaris incontinence should c learly suggest the presence of a
are a common cause of neurogenic lower urinary tract dys­ common neurogenic cause for urinary i n continence. The
function, although more peripheral lesions may also cause additional presence of sacral pain should suggest tumor in
sacral disease. [n patients with suspected focal sacral disease, the sacral region.
CHAPTER 2 Assessing Cardinal Musculoskeletal Symptoms and S igns 71

CRt n e A L T H t N Kt N C

I . What are the five groups of signs and symptoms dif­ 9. What are the two most common tumors of the dig its
ferentiating muscu loskeletal complaints? of the hand and on the dorsum of the foot?
2. Why can articular or periarticular pain radiate widely 1 0 . A hel iotropic rash and Gottron papules are character­
and be fe lt in a spot di stant from its originating istic and possibly pathognomonic cutaneous feature
tissue? of what condition?
3 . What typical sensations differentiate pain with nerve I I . Where can Gottron papules most commonly be
entrapment, vascular compromise, and articular or found?
joint involvement? 1 2 . The Leeds Assessment of Neuropathic Symptoms I
4 . In listening to a patient's description of pai n , i . e . , and S igns i s used in the assessment of what type of
when present, what relieves i t , what makes i t worse, conditions?
and what improves it, pain at rest, night, or with u se 1 3 . You have a very athletic patient with reoccurring
suggests what kinds of problems? episodes of muscle cramping with exercise . What
5 . What is the leading cause of accidental death in older would be your immed iate action steps for this case
adults? presentation?
6. What subgroup of patients is at high risk of develop­ 1 4 . Gait impairments from d isorders of the corticosp inal
ing chronic lower back pain ? pathways are mani fested by what?
7. What four issues are important in assessing a patient's 1 5 . Gait i m pairments from the cerebe l l u m and its
disability? connections are c haracterized by what?
8. After thoroughly examining the patient's painful part,
you have doubt of the source of the symptoms. What
would your next step be?
72 CHAPTER 2 Assessing Cardinal Musculoskeletal S),mptoms and Signs

B I B L I O G RAP H Y

Abrams W B , Berkow R: The Merck manual af geriatrics, Rahway, NJ , Craik RL, Oatis CA: Cait analysis t/leorv ond applicOliol/. St Lou i s , 1 995,
1 990, Merck Sharp & Dohme Research Laboratories. Mosby.
Adams JC, Hamblen DL: ()ulline af arthapaedics, ed I I , Edinb urgh, 1 990, Dambro MR. Griffith J A : Criffith 's 5 mil/ute clinical COl/suit, B a l t i more.
C h u rc h i l l Livingstone. 1 997, Williams & Wil kins.
Ahwee Leftwich S ct il l : H igh incidence d i s<l b i l i t ies: placement determi­ Daruwalla P, Darcy S : Personal and soc ietal attitudes to disability, Ann
nants and impl icliions for instruction and service deli very. In Scruggs Tourism Res 3 2 ( 3 ):549-570. 2005.
TE, Mastropieri M A , ed itors: Advances il1 learning alld behaviaral Demeter SL, Andersson G B J , S m i t h GM: Disability evaluotiol/, St Louis,
disabililies, vol 1 8 , Greenwich, Conn. 2005, JAI Press. 1 996, Mosby.
Alario A J : Praclical guide 10. the care of the pediatric palielll, St Louis, Dickenson A H : Spinal cord pharmacology of pain. Br J Anaesti"l 75: 1 93 ,
1 997, Mosby. 1 995.
Alberti A: Headache and sleep, Sleep Med Rev 10(6):43 1 -437, 2006. Dionysian E et a l : Prox imal interphalangeal joint stiffness: measurement
Anderson KN. Anderson LE: Masby's pockel diclianary of medicine, and an alysis, J Hand Surg 30(3):573-579, 2005.
nursin!!, & al/ied health. ed 2, St Louis, 1 994, Mosby. Doherty M: Calor atlas and lext of os tea arthritis, London, 1 994, Wolfe.
Atki nson G , Davenne D: Relationships between sleep, physical act i v i ty and Doherty M et a l : The "GALS" locomotor screen. AI/n Rheum Dis 5 1 : 1 1 65 ,
human hea l t h , Physiol Behav 90(2-3):229-235, 2007. 1 992.
Barkauskas Y H et al: Heallh & physical assessmenl, e d 2 , St Louis, 1 998, Doherty M , Doherty J: Clinical examination in rheUml1lOlagv, London,
Mosby. 1 992, Wolfe .
Bechman H et al: Getting the most from a 20 m i nute visit, A m J Casu'o­ Doherty M . George E : Self-assessment piclUre tests ill rhelllllatolog.l',
enlerol 89:662, 1 994. London, 1 995, Mosby-Wolfe.
Beighton L et a l : Articular mobility in an African population, Annu Rheum Dray A: InAam matory mediators of pain, Br J Anaesth 7 5 : 1 25 , 1 995.
Dis 3 2 : 4 1 3-4 1 7 , 1 97 3 . Epstein 0 e t al: Clinical examination, ed 2, London. 1 997, Mosby.
Boukhris S e t a l : Pain as t h e presenting symptom of chronic i n flammatory Farasyn A: Referred muscle pa i n is primarily peripheral in origin: the
demyel inating polyrad iculoneuropathy (CIDP), J /Vel/rol Sci 254( 1 - "barrier-dam" theory, Med H.l'patheses 68( I ) : 1 44- 1 SO, 2007.
2):33-38, 2007. Feldmann E: Current diagnosis in lIeuralagy, St Louis, 1 994, Mosby
Brotzman SB: Clinical onhopaedic rehabililalian, St Lou i s , 1 996, Ferezy J S : The chiropractic neuralogiCYlI examination, Gaithersburg, M d ,
Mosby. 1 992, Aspen.
Brown DE, Neumann RD: Onhopedic secrets, P h i l adelphia, 1 995, Hanley Field T e t al: Lower back pain and sleep disturbance are reduced follow i n g
& Belfus. massage therapy, J Badywark Mave Ther I I (2): 1 4 1 - 1 45 , 2007.
Bruc i n i M et a l : Pain thresholds and electromyographic features of periar­ Fi tzpatrick TB et a l : Color atlas and .'."lIopsis of clinical dermntology
ticular muscles in patients w i t h osteoarthritis of the knee, Pain COllllllan all" seriaus diseases, ed 2. New Yo rk, 1 992. McGraw- H i l I .
1 0( 1 ) : 57-66, 1 9 8 1 . Gatts S K , Wool l acott M H : How Tai C h i i mproves balance: biomechanics
Bucholz RW: Orthopaedic decision making, e d 2 , S t Louis, 1 996, Mosby. of recovery to a walking s l i p in i m paired seniors, Cait Posture
B u n ker TD, Schranz PJ : Clinical challenges in orlhapaedics: the shauldel; 25(2):205- 2 1 4 , 2007.
Oxford, U K , 1 998, ISIS Medical Media. Goldie BS: Orthopaedic diagnasis and management a guide to the care of
Calvino B , Grilo RM: Central pain control, Joint Bone Spine 73( I ) : I 0- 1 6, orthapaedic patielllS, ed 2, Oxford, U K , 1 998, I S I S Medical Media.
2006. Gracely RH, Undem BJ, Banzett RB: Cough, pain and dysp noea: s i m i lari­
Campbell J B , Campbe l l JM: Masb v s survival guide to medical abbrevia­ ties and d iffere nces. Pullll Pharmacol Ther 20(4):433-437, 2007.
tians & acronyms prefi�res & suffixes symbols Creek alphabet, Gramag l i a L et al : Worsen ing of chronic pa i n : the treatment. Arch CeronlOl
St Louis, 1 995, Mosby. Ceriatr 44(suppl 1 ): 207-2 1 1 , 2007.
Campbell IN, Meyer RA: Mechanisms of neuropath i c pain, Neuron Greenstein G M : Clillical assessment of neuralllusculoskeletal disorders,
52( I ):77-92, 2006. St Louis , 1 997, Mosby.
Canale ST: Call1pbell:5 operative arthapaedics, v o l 1 -4, ed 9, St Louis, G u nther M , B l ickhan R: Joint sti ffness of the a n k le and the knee in running,
1 998, Mosby. J Bio/1/ech 35 ( 1 1 ) : 1 459- 1 474, 2002.
Card i na l E, Lafortune M. Burns P: Power Doppler US in synovitis: rea l ity G u rwood AS, Drake J: G u i l l ain-Barre syndrome. J Am Optom Assoc
or artifact? Radialagy 200:868, 1 996. 77( I I ) : 540-546, 2006.
Chard MD et a l : Shoulder d i sorders in the elderly: a com m u n ity survey, Haack E, Tkach J : Fast M R imaging: techn iques and c l i nical applications,
A rthritis Rheum 34:766. 1 99 1 . AJR 1 55 : 95 1 , 1 990.
Cipriano J J : Phatagraphic nwnual af regional arthopaedic (lnd neurolagi­ Han ley M A et al: Self-reported treatments used for lower- l i mb phantom
cal test, ed 3, B a l t i more, 1 997, Wil liams & W i l k i n s . pain: descriptive fi n d i ngs. A rch Ph .l's Med Rehabil 87('2):270-277.
Cleeman E , Auerbach J D , Springfield DS: Tumors o f t h e shoulder girdle: 2006.
a review of 1 94 cases, J Shoulder Elbaw Surg 1 4 (5 ):460-465, 2005. Hanley M A et a l : Preampuration pain and acute pa i n pred ict c hronic pain
Cohn RE: Impairment rating examinatian and disabilitv evaluatial/, ed 3 . after lower extremity amputation, ./ Pain 8(2): 1 02- 1 09, 2007.
Wil kesboro, N C , 1 994, R Ernest Cohn. Hartley A : Practicaljaillt assessment 10wer quadral1l, ed 2, St Loui s . 1 995,
Col loca CJ , Keller TS: S t i ffness and neuromuscular reAex response of the Mosby.
human spine to posteroanterior manipulative t hr usts in patients with Hasse l l AB et a l : The relationship between serial measures of d i sease
low back pain. J Manipulative Physiol Ther 24(8):489-500, 200 1 . activity and outcome in rheumatoid arthritis, Q J ivied 86:60 I .
Col v i n LA, Power l: Neurobiology of chronic pain states, Anoesth Intensive 1 995.
Care Med 6( I ) : 1 0- 1 3 , 2005. Hawkins RJ : A n organized appraach 10 musculoskeletal examination ([lid
Conwe l l TD: Documenting patielll pragress "daily office charting seminar" history taking, St Louis, 1 995, Mosby.
thalVugh accurate quick procedures. ed I I , Lakewood, Colo, 1 990, H i n k le CZ: FUlldamel1lals of onalOmv & lIIal'emel1l {/ workbaak alld guide,
C l i n ical Advancement P l u s Seminars. St Louis, 1 997, Mosby.
Copeland SA et al: '/o illl stiffness of the upper limb, St Louis, 1 997, Mosby. Hofer M, M ahl aoui N, Prieur A-M: A c h i l d with a systemic febrile i l l ness­
Coutaux A et al: Hyperalgesia and allody n i a : peripheral mechanisms, Jaint d i fferential diagnosis and management , Best Pmct Res Ciill Rheumo­
Bane Spine 72(5): 359-37 1 , 2005. to/ 20(4 ) : 627-640, 2006.
CHAPTER 2 Assessing Cardinal Musculoskeletal Symptoms and Si ns 73

J agoda A , Riggio S: M i ld trau m a t ic brai n i nj u ry and the postconcussive Peterfy CG e t a l : M R i maging o f the arthri t i C knee: i m p roved d iscri m i na­
syndrome, C'fJ/crg Med Ciin North Am 1 8( 2 ) : 355-363, 2000. tion o f cartilage, synov i u m and effu s i on w i t h pulsed saturation
Karkin-Tai s A et al: 367 1 3-year study of pain in phantom l i m bs of ampu­ transfer and fat-su ppressed T I -weighted sequences, Radiology
tees-v i c t i m s o f war in Sarajevo (period 1 992-2005) , Eur j Pain 1 9 1 : 4 1 3 , 1 994.
1 0( suppl I ) : S98 -S 2 1 I , 2006. Peterfy CG, Genant HK: Emerging applications of magnetic resonance
Kat irj i B : Electromyography in clinical practice a case s(udy approach, imaging for e v a l u a t i ng the artic u l ar cartilage, Radial CIiI1 Nonh Am
S t Louis, 1 99 8 , Mosby. 34: 1 9 5 , 1 996.
Kl ine CR, Martin DP. Deyo RA: HeaJth consequences of pregnancy and Rach l i n ES: A'lyofascial pa;11 and fibromyalgia (rigger poin( monagemellt,
chi ldbirth as perceived by women and c l i n icians. Obs(el GynecoJ St Louis, 1 994, Mosby.
92(5 ) :842-848. 1 998. Raspe HH: Back pai n . In S iJ ma n AJ, Hochberg M . editors: Epidemiology
K l i ppel J H, Dieppe PA : Rllellma(ology, vol 1 -2 , ed 2, London, 1 998, of (he rheu/1/(//ic diseases, O x ford, U K , 1 99 3 , Ox ford Uni versity
Moshy. Press.
KurugHnti U et al: Strength and muscle coac t i va t i on in older adults after Robertson CM. Coopersm i t h CM: The systemic i n n a m matory response
lower l i m b strength tra i n i ng . Int j Illd ErgOIl 36(9 ) : 7 6 1 -766, 2006. syndrome, Microbes Infeel 8(5): 1 3 82- 1 3 89, 2006.
Lautcnbacher S. Kundcrmann B, Krieg 1-C: Sleep deprivation and pai n R u bens DJ et a l : Rheumatoid arthri tis : evaluation of w r i s t extensor tendons
perception, Sleep Med Rev 1 0( 5 ) : 357-369, 2006. w ith c l i n ical exa m i na t i o n versus MR imagi ng-a pre l i m i n ary report.
Lewis C B , KJlortz KA: O,.,hopedic assessmen( alld [remmellt of (he Radialogy 1 87 : 8 3 1 , 1 993.
geriel/ric pel/icllt, S t Lou i s , 1 99 3 , Mosby. Schumacher HR, Kl ippel J H, Koopman WJ : Primer 011 (he rheuma(ic
Lovejoy CO: The natural history of human gait and posture: Part 3 . The diseases, ed 10, At la nta, 1 99 3 , Arthri t i s Foundation.
knee, Gait Pos(ure 25(3): 325-34 1 . 2007. Smith RC, Hoppe R B : The patient's story: i n tegrating the patient and
Ly nch GS, Schertzer 1D. Rya l l J G : Therapeutic approaches for muscle physician centered approaches to i nterv i e w i ng, A n n In(ern Med
wa sting disorders. Pharmacol Ther 1 1 3 ( 3 ) :46 1 -487, 2007. 1 1 5 :470, 1 99 1 .
Magee D.J: Or(hopedic phl'sical a55eSSmen(, ed 3, Ph i l adelphia, 1 997. WE Spacek E e t a l : Disa b i l it y i n d uced by hand osteoarthriti s: are patients w i t h
Saunders. more s y m p t o m s a t d igits 2-5 i n terphalangeal joints d i fferent from
Makhsous M , Lin F. Zhang L-Q: M u l t i -axis passive and act i ve stiffness of those w it h mOre symptoms at the base of tbc thumb? Os(coarlhr
the glenohu meral j o i n t . Clin Biol1lech 1 9(2) : 1 07- 1 1 5 , 2004, Cartil 1 2( 5 ) : 366-373. 2004.
Malone TR. McPoil TG, N i t z AJ: Orthopedic and SP0rlS physicol (hempv, Stamford J A : Desce n d i n g con trol of p a i n , 8r j A naes(h 7 5 : 2 1 7 , 1 995.
ed 3, St Louis, 1 997, Mosby. Stein C : The control o f pain i n peripheral t i ssue by opioids, N Engl j Med
Mathews DA, Suchman AL. Branch WT: Making "connexions": enhanc i ng 3 3 2 : 1 68 5 , 1 995.
the therape utic pote n t i a l of pat ie n t-c l i n i cia n relationships, Ann In(em Stevens JC et al: Cond i t i ons assoc iated w i th carpal t u n nel syndrome, Mayo
k/ed 1 1 8:973. 1 99 3 . Clin Proc 67:54 1 , J 992.
McRae R: Clinical orlhopaedic e.romina(ion, ed 3, Ed in burgh, 1 990, Stochkendahl MJ e t a l : M a n u a l e x a m i na t i.on of the spine: a syste m a t i c
C h u rch i l l L i v ingstone. cri t ical l iterature rev iew of reproduc i b i l ity. j Manipulatil'e Physiol
Mengel M'B , Schwiebert LP: Al1IblllalOr)' medicine (he primary care of Ther 29(6):475-462, 2006.
families, ed 2, Stamford, Conn, 1 996, Appleton & Lange. Sugimoto H et a l : Early-stage rheumatoid arthrit i s : diagnostic accuracy of
Mennell J M : The musculaskele(al 5\'steul diffe rential diagnosis from M R imaging, Radi% gy 1 98 : 1 85, 1 996.
symplOl/1s and ph rsical signs. Gaithersburg, Md, 1 992, Aspen. Tan JC, Horn SE: Practical mnnual of physical medicine alld rehai?ili(a­
Mercier LR, Pellid Fl: PraClical or(/7.opedics, ed 5 , St Louis, 2000, Mo�by. (iOIl, St Louis, 1 998, Mosby.
Moriwaki K et a l : Ne uropat hic pain and prolonged regional i n flammation Thibodeau GA, Patton KT: AnalOmv & ph ysiology, ed 3, S t Louis. 1 996,
as two d i st i nct symptomatological components in complex regional Mosby.
IJa in syndrome w i t h patchy osteoporos is-a pi lot study, Po;n 72( 1- Thi bodeau G A , Patton KT: Packe( reference 10 accolllpany {/I1{/(O/ll V &
2): 277-282, 1 997. physiology, ed 3, St Louis, 1 996, Mosby.
Mosby-Year Book, Inc: Mosbr :, expert IO-minwe physical examination, Thompson J M : Clinical oLl(lines for hea/(h assessment, St Louis, 1 997,
S t Louis, 1 997. Mosby. Mosby.
Murphy AJ et al: Reliability of a test of musculotendinous sti ffness for the Togh i l l PJ: Examining pOlients an introduCiion (0 clinical medicine,
triceps-slirae, Phys The Sport 4(4) : 1 75- 1 8 1 , 2003. London, 1 990, Edward Aroold.
Nardone DA et a l : A model for the diagnostic medic.,1 interview: nonver­ Wakefield TS, Frank R G : The clinician :,. guide (0 neurornllsculoskele(al
bal, verbal and cogn i t i ve assessme nts, j Gen In(em Med 7:437, practice, Abbotsford, Wise, 1 995, A l lied Health of Wiscons i n ,
1 992. S.c.
Nettina SM: The Lippincott manual o[nllrsinf{ practice, ed 6, Philadelphia, We i n stein SL, Buckwalter JA: Turek 's orthopaedics prillCiples and their
1 996, Lippincott. applicOlion, ed 5, P h i l adelphia, 1 994, JB Lippincott.
Newton RW: Color (IIlas of pediatric neurology, St Lou is, 1 995, W h i te G : Levene:s color alias of dermalOlogy, ed 2 , London, 1 997,
Mosby-Wol fe. Mosby- Wolfe.
Ogi lv i e - H arris DJ, Saleh K: Genera l i zed synovial chondromatosis of the W h i te G : Regional dermatology, London, 1 994, Mosby-Wolfe.
knee: a comparison of removal of the loose bodies alone with W h i te KP e t a l : Fibromyalgia in rheumatology prac t ice: a $urvey of
arthroscopic synovectomy, Arlhroscopy 1 0: 1 66, 1 994. Canadian rheumatologists. j Rheul11a1o/ 22:722, 1 995.
Oleson M, Adler D . Goldsmith P : A comparison of forefoot s t i ffness i n Windsor RE, Lox DM: Soft (;ssue injuries: diagnosis and treallnefll,
running and ['tin n i ng shoe b e n d i n g s t i ffness, j Biamech 38(9): 1 8 86- Phi lade l p h i a , 1 998, Hanley & Belfus.
1 8 94, 2005. Wolfe F et a l : The prevalence and charac teristics of fibromyalgia i n the
Olson WH et al: Handbook of symp(om-oriel1fed neurology, ed 2, St Lou i s , general population, A rlh ri(is Rheum 38: 1 9, 1 995.
1 994, Mosby. Woo l f CJ : Somatic pain-pathogenes i s and prevent ion, B r j A llaesth 75: 1 69,
Patin JR, Hamot H B , S i nger J M : Replicated evidence o n the construct 1 995
v a l i d i ty of the SCAG (Sandoz C l i n i cal Assessment-Geriatric) scale, Ye amans DC et a l : Pai n , management of. In Inlel71atiollal en cyclopedia of
Prog NeLlropsych opharmacol Bio/ PsychiOlry 8(2):293-306, 1 984. rhe social & behavioral sciences, O x ford, U K , 200 1 , Pergamon.
Perilala RS e t al: Local i n fectious complications fol l o w i n g large j o i nt Zatouroff M : Diagnosis in colar physical signs il1 general medicine, ed 2,
replacement in rheumatoid arthritis patients treated w i t h methotrexate London, 1 996, Mosby-Wolfe.
versus those not treated w i t h methotrexate, A rlhritis Rheum 34: 1 46, Z i te l l i BJ, Davis HW: At/as of pedialric physical diagnosis, ed 2, London,
1 99 1 . 1992, Wolfe.
74 CHAPTER 2 Assessing Cardinal Musculoskeletal Symptoms and Signs

C I TAT I O N S
Ahmed M A S et a l : Chvostek's sign and hypocalcaemia i n c h i l d ren with Nadler SF et al: Sports and performing arts medic i n e . I . General. consider­
seizures. Seizure 1 3 (4):2 1 7-222, 2004. ations for sports and performi ng arts medicine, Arch Phys Med
Baalen AV, Stephani U: Fibration, fibri l lati o n , and fasc iculation: say what Rehabi/ 85(suppl 1 ) : 48-5 1 , 2004.
you see, Clin Neurophysiol (in press, corrected proof). Pal mgren PJ et al: Improvement after chiropractic care in cervicocephalic
Baker FC, Driver HS: Circadian rhythms, sleep, and the menstrual cycle, kinesthetic sensibility and subjective pain intensity i n patients w i th
Sleep Med (in press, corrected proof), nontraumatic chronic neck pain, 1 Manipulmive Physiol Ther
Callen JP. Dermatomyos it is, Lance t 3 5 5 (9 1 97 ) : 5 3-57, 2000. 29(2): 1 00- 1 06, 2006.
Carayon p, S m i t h MJ, Haims MC: Work orga n i zation, job stress, and work­ Pamuk ON, Yei l Y, Cak i r N: Factors that a ffect the number or tender points
related musculoskeletal di sorders, Human Faclors 4 1 (4):644-663, i n \ibromyalgia and chronic widespread pain patients who did not
1 999. meet the ACR 1 990 criteria for flbromyalgia: are tender points a
Costardi D et a l : The Ital i a n version of the pain assessment i n advanced reflection of neuropathic pai n ? Sem ;11 A rthritis Rhe um 36(2): 1 30- 1 34,
dementia (PAINAD) scale, Arch Gerontol Ceriatl' 44(2): 1 7 5 - 1 80, 2006.
2007. Panel ror the Pred iction and Prevention of Pressure U l cers in A d u l t s : Pres­
European Pressure Ulcer Adv isory Panel (EPUAP): Gotopu, EPUAP Rev sure ulcers in adulls: prediclion and preve11lion. Clin ical praClice
1 :3 1 - 33. 1 999. guideline number 3, Rockv il le, Md, 1992, Agency for Health Care
Freeman MC, Michael JA, Robert B D: Tetany. I n Encyclopedia of Ihe Policy and Research, P u b l ic Health Service, U . S . Department of
neurological s cien ces, New York, 2003 , Academic Press. Health and Human Services.
G i lbert RJ, Napadow Vl. Threc-dimensional muscular architecture of the Podnar S : Neurophysiology of the neurogenic lower uri nary tract d i sorders,
human tongue determined i n v i vo with diffu sion tensor magnetic C1in Neurophysiol ( i n press, corrected proof).
resonance imaging. Dysphagia 20( 1 ) : 1 -7, 2005. Poiraudeau S et al: Fear-avoidance beliefs about back pain in patients w ith
G i u mmarra Ml et al: Central mechanisms i n phantom l imb percepti o n : the subacute low back pai n . Pain 1 24(3): 305-3 1 1 , 2006.
past, present and fu ture, Brain Res Rev 54( 1 ) :2 1 9-232, 2007. Quevedo AS, Cogh i l l RC: A n i l l usion of proximal radiation of pain due to
Goldberg 8, Neptune RR: Compensatory strategies during normal walking distally directed inhibition, J Pain 8(3):280-286, 2007 .
in response to muscle weakness and increased h i p joint stifrn ess, Cail Sharma H, lane MJ, Reid R: Pigmented v i l ionod u J ar synovitis of the foot
PoslU re 25(3):360-367, 2007 . and ankle: forty years of experience from the Scottish bone tumOr
Grahame R: The hypermobi li t y syndrome, A nn Rh eulnalol Dis 49: 1 99- registry, 1 Fool Ankle Surg 45(5):329-336, 2006.
200, 1 990. S iegel KL, Kepple TM, Stan hope S l : A case study of gait compensat ions
Grahame R : Pain, d i stress and joint hyperlaxity. 10il1l Bone Spine 67 ( 3 ) : 1 57 - for hip muscle weakness in i diopathic i n fl a mmatory myopathy, C1in
1 63 , 2000. Biomech 22(3) : 3 1 9-326, 2007 .
Hausmanowa-Petrusewicz [: Electrophysiological find ings in childhood S i mmonds lV, Keel' RJ: Hypermobil i ty and the hypermo b i l i ty syndrome.
spinaJ muscular atrophies, Revue Neurologique J 44 ( 1 1 ) : 7 1 6-720, Manual Ther 1 2(4) :298-309, 2007 .
1 98 8 . S i va S, Pereira S P : Acute pancreatitis, Medicine 35(3): 1 7 1 - 1 77, 2007.
Jensen B R et al: Soft tissue architecture and i n tramu scular pressure i n the S iobodin G et a1: Varied presentations of en thesopathy, Semin Arihrilis
shoulder reg ion, Eur 1 Morphol 3 3 ( 3 ):205-220, 1 995. Rheum (in press, con'ected proof).
Kashdan TB et al: Fragile self-esteem and affective instab i l ity i n posttrau­ Vanderwee K et a l : The reliability of two observation methods or non­
matic stress d isorder, Behav Res Ther 44( 1 1 ): 1 609- 1 6 1 9 , 2006. blanchable erythema, grade 1 pressure ulcer, Appl Nurs Res 1 9(3): 1 56-
Koenigsberg HW et a l : Characterizing affective instabi l i t y in borderline 1 62 , 2006.
persona l ity d isorder, Am J Psychialry 1 59 ( 5 ) : 7 84-788, 2002. Visser B, van Dieeo JH: Pathophysiology of upper extremity muscle
Lamontagne A, Stephenson lL, Fung J: Physiological evaluation of gait disorders, J Eleclromyogr Kinesiol J 6( I ) : 1 - 1 6 , 2006.
disturbances post stroke, Clin Neurophysiol 1 1 8(4) : 7 1 7 -729, 2007 . Wid iger TA, Sankis LM: Adult psychopathology: issues and controversies,
Lankester B J A , W h i tehouse M, Gargan MF: Morquio syndrome, CUl'r Ann Rev Psychol 5 1 : 377-404, 2000.
Orthopaed 20(2): J 28- 1 3 1 , 2006. Zautra AJ et a l : Dai l y fatigue in women with osteoarthritis, rheumatoid
Lowery DJ et a l : A c l i n ical composite score accurately detects meniscal arthri tis, and fibromyalgia, Pain I 2S( 1 -2): 1 28- 1 3 5, 2007.
patho logy, AJ'/hroscopy 22( I I ) : 1 1 74- 1 1 79 , 2006. Zhang P, Chen X, Fan M: S ignal ing mechanisms inv olved in disuse muscle
Luyten FP et a l : Contemporary concepts of i nflammation, damage and atrophy, Med HYPOlheses (in press, corrected proot),
repair in rheumatic diseases, Besl PraC! Res C1in RheulnaI01 20( 5 ) : 829-
848, 2006.

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