Injury, Int. J.

Care Injured (2006) 37S, S3S7

www.elsevier.com/locate/injury

Fat embolism syndrome:

history, definition, epidemiology
Max Talbot1, Emil H Schemitsch2
1

1 Canadian Field Hospital, Canadian Forces (The views and opinions expressed in this article are those
of the author alone and do not necessarily state or reflect the views, opinions and conclusions of the
Canadian Forces Health Services Group, the Canadian Forces, the Department of National Defence or
the Government of Canada.)
Department of Orthopaedics, St Michaels Hospital, Toronto, Canada

KEYWORDS:
Fat embolism;
epidemiology.

Summary1 The first clinical case of fat embolism was described over 100 years
ago and significant progress has been made in the understanding of this condition since then. Gurds criteria, consisting of major and minor clinical features,
is the most commonly used diagnostic tool in the literature. Due to the lack of
a gold standard for diagnosis, clinical criteria cannot be validated. It is now
recognized that although fat embolization occurs in the majority of patients
with long bone fractures, clinical signs and symptoms occur only in 1 10% of
patients with fractures.

History
The first animal model of fat embolism was described over 330 years ago by Lower who injected
intravenous milk into dogs [1]. Magendie performed
more elaborate studies in the early 19th century
and observed that intravenous injection of oil led
to mechanical obstruction of small vessels by fat
globules [1]. Virchow reported that injection of intravenous oil produced pulmonary edema [1]. These
experiments were undertaken without knowledge of
human fat embolism syndrome (FES).
The first human case of posttraumatic fat embolism was described by Zenker in 1862 in a patient
with a severe crush injury. Fat was observed in the
pulmonary capillaries at autopsy [1]. Scuderi, who
extensively reviewed the condition in 1934, stated
at that time the treatment of this condition is not

Abstracts in German, French, Italian, Spanish, Japanese,

and Russian are printed at the end of this supplement.

very illuminating [1]. However, in 1914 Tanton proposed that adequate fracture immobilization could
help prevent the syndrome [2].
In the 1920s, the two theories of fat embolism
that remain to this day were put forward. Gauss
established the mechanical theory [3] in which he
defined three conditions for fat embolism to occur:
injury to adipose tissue, rupture of veins within
the zone of injury, and some mechanism that will
cause the passage of free fat into the open ends of
blood vessels. Gauss thought that this mechanism
was that blood vessels in bone were bound tightly
to their bony channels thus remaining open, unlike
veins elsewhere in the body that tend to collapse and
thrombose. Lehman proposed a biochemical theory
to explain FES, hypothesizing that plasma mediators
can mobilize fat from body stores and cause it to
form large droplets [4].
Following the emergence of intramedullary (IM)
nailing in the 1940s, a number of surgeons were
concerned about the potential complication of fat
embolism [5, 6]. Peltier determined that solid nails

00201383/$ see front matter # 2006 Published by Elsevier Ltd.

doi:10.1016/j.injury.2006.08.035

S4

M Talbot, E H Schemitsch

caused greater increases in intramedullary pressure

than hollow nails [5]. Shortly after, he reported a
case of fatal FES following IM nailing of a closed
femur fracture [6]. He advised that prevention of
FES should be based on preventing shock, using a
hollow nail design, and driving the nail in slowly
with a pause between hammer blows [6].
As with all traumatic conditions, a great deal
has been learned about FES during armed conflict.
In World War II, the incidence of FES was noted to
be approximately 0.8% in a series of 1,000 combat
wounds [7]. A study of 110 combat fatalities from
the Korean War found that 93% had pulmonary fat
at autopsy, but this was only moderate to severe
in 19% of cases [8]. However, the authors were not
convinced that pulmonary fat embolism could induce pulmonary dysfunction and stated that serious
pulmonary embarrassment may result from embolic
fat in occasional cases, but such cases must be quite
uncommon. In Vietnam, technological advances
made it possible to diagnose more subtle cases.
Collins notes a high incidence of arterial hypoxemia
in 69 wounded soldiers and attributed this to FES
after carefully excluding thoracic injuries and hypoventilation as causes of hypoxemia [9]. He noted
a strong association between hypoxemia and femur
fractures from high velocity missiles. Cloutier was
able to conduct a prospective study of 50 Vietnam
battle casualties and found five classic cases of FES
among them [10].

Major features

Minor features

Petechial rash

Tachycardia

Respiratory symptoms
Pyrexia
plus bilateral signs with
positive radiographic
changes
Cerebral signs
unrelated to head
injury

Retinal fat or petechiae

There is no universally accepted definition of FES.

The pathophysiological phenomenon of fat embolization (FE) must be differentiated from FES, which
is defined by the presence of clinical signs and
symptoms resulting from embolic showers.
Gurd proposed diagnostic criteria in 1970 that
are still widely used today [11]. They are divided
into major features and minor features (Table 1).
Gurd stated that the diagnosis of FES could be
made if one major feature plus four minor features
plus fat macroglobulinemia were present. These
criteria have been adapted by other authors who
stated that one of the following combinations of
major and minor features was needed to make the
diagnosis: two major [12 15]; one major and three
minor [16, 17]; two major and two minor [16]; or
one major and two minor [18] features. Most authors
have also dropped the requirement for presence of
fat macroglobulinemia from the necessary criteria
[12 19]. None of these authors, including Gurd, have
provided justification for the number of features
needed for the diagnosis.
Other diagnostic systems have been proposed.
Schonfeld proposed a fat embolism index that gives
points for different diagnostic criteria [20] (Table 2).
A diagnosis of FES is made with a score of 5 or more.
Schonfeld acknowledges that this system is not useful for patients with cerebral, thoracic, or abdominal
injuries. Vedrinne developed a scoring system with
the polytrauma patient in mind [21] that uses pulmonary infiltrates, neurological status, petechiae,
platelet count, retinal changes, total blood lipids,
and the presence of long bone fractures to assess
patients. Finally, in a study of pediatric patients,
Weisz made the diagnosis of FES when one of three
signs was present: retinal embolism, positive skin,
lung or kidney biopsy, or histological findings at
autopsy [22].

Urinary fat globules or

oligoanuria

Points
Diffuse petechiae

Sudden drop in Hg-level

Alveolar infiltrates

Sudden thrombocytopenia

Hypoxemia (<70 mm Hg)

High erythrocyte
sedimentation rate

Confusion

Fever >38C

Heart rate >120/min

Respiratory rate >30/min

Fat globules in sputum

FES = 1 major feature + 4 minor features + fat
macroglobulinemia
Table 1: Gurds criteria.

Definition

FES = 5 or more points

Table 2: Fat embolism index.

Fat embolism syndrome: history, definition, epidemiology

A number of investigators have sought a gold

standard test for the diagnosis of FES but such a
test remains elusive. The absence of a diagnostic
gold standard makes it impossible to evaluate the
value of these clinically-based evaluation systems. A
correlation with autopsy findings would perhaps be
feasible but fatal cases are rare events.
In the future, advances in diagnostic imaging and
in laboratory tests may help with the diagnosis of
FES. In polytrauma patients, it can be difficult to
attribute pulmonary or brain dysfunction to fat
emboli. A number of authors have described the MRI
appearance of cerebral FES [19]. The appearance of
pulmonary FES on high-resolution CT scans has also
been described [23]. Another approach has been to
evaluate cells staining positive for fat globules in
bronchoalveolar lavage (BAL) fluid which, although
it seemed promising at first [13], has conflicting data
[14, 21, 24, 25]. These modalities are examples of
tests that could help refine Gurds criteria. At this
time, the diagnosis of FES remains clinical [26].

Epidemiology
The phenomenon of fat embolism is extremely common among trauma patients, especially those with
long bone or pelvic fractures [27]. However, in the
context of trauma, fat embolism is also common
following extensive injury to subcutaneous fat, such
as occurs in severe beatings [28, 29]. Fat emboli can
be demonstrated in a number of ways. Gurd showed
that 67% of trauma patients without evidence of FES
had circulating fat globules [30]. Allardyce studied
43 cases of femoral shaft fractures and found that
95% of patients had circulating fat globules in blood
draining from the fracture site [31]. Urinary fat
droplets are also a frequent finding after trauma
[16, 32, 33]. Mudd found pulmonary fat in 68% of
patients dying from blunt trauma, most of whom
had associated fractures [34].
The first study to use ultrasound to detect embolic particles was performed in 1972 [35]. This
technology has since been used by many authors
to study the phenomenon of fat embolism. Pell et
al performed transoesophageal echocardiograms in
24 patients undergoing nailing of a lower extremity
fracture [36]. In 41% of cases, embolic showers were
detected, with 16% being graded as severe. The
same group performed a second study that showed
embolic phenomena in 94% of pathological femurs
(59% severe), 62% of femur fractures (6% severe),
and 94% of tibial fractures (none severe) undergoing IM nailing [37]. Blood sampling from the right
atrium confirmed that fat was responsible for these

S5

echogenic masses. The severity of the embolic showering also correlated with the severity of decreased
end-tidal CO2 and hypoxemia.
Hypoxemia after long bone fractures is a frequent
occurrence, which in many cases could be represented by mild pulmonary dysfunction induced by
intravasated fat without full blown FES developing.
Moed et al found arterial hypoxemia in 35% of patients with fractures of the femur, tibia, or pelvis
using intermittent pulse oxymetry [38]. The use of
continuous pulse oxymetry has shown that these
events occur in nearly all patients with these injuries
[17]. McCarthy found hypoxemia (PaO2<80 mm Hg) in
74% and an elevated alveolar-arterial O2 gradient
(>20 mm Hg) in 100% of patients with uncomplicated
extremity fractures [32]. Whether this incidence
truly represents subclinical FES remains to be determined with certainty.
Despite the high frequency of embolic fat globules
entering the circulation, the incidence of FES (ie,
patients who develop signs and symptoms from the
emboli) is much lower. In 1974, Gurd reported that
the syndrome occurred in 19% of major trauma cases
admitted to a Belfast hospital [30]. Riska reported
an incidence of severe FES (ie, in need of respiratory
support) of 22% in a group of 384 multiply injured
patients with long bone fractures treated nonoperatively between 1967 and 1974. In subsequent years
(1975 1978), internal fixation was instituted as a
standard treatment and the incidence fell to 1.4%
in a similar group of 211 patients [39]. However, 9%
had milder forms of the syndrome not requiring respiratory support, making a total incidence of 10.4%.
In Pells echocardiographic study, 12.5% of patients
were diagnosed with FES [36]; all of whom were in
the group in which embolization was graded as severe. Allardyce reports an incidence of 11% [31].
Bulger and Fabian provide the best modern data on
the incidence of FES. Both conducted studies at level
1 trauma centers. Bulger retrospectively studied all
cases of FES over a 10-year period at Harborview
medical center [16]. They found 27 cases out of
3,026 patients with long bone fractures admitted
during that time period, which gives an incidence
of 0.9%. Fabian conducted a prospective study over
a 12-month period of patients with femoral, tibial,
and pelvic fractures [40]. In this population, the
incidence of FES was thought to be at least 11%.
They based the diagnosis on increased pulmonary
shunt fraction as inferred from an increased alveolar-arterial oxygen tension difference. The authors
emphasize that this is the minimum incidence of
FES given that many cases with concomitant chest
injuries may have gone undetected.
The timing of the fracture fixation also appears to
impact on the incidence of FES. Pinney reported on

S6

a series of 274 consecutive femoral shaft fractures

[18]. The overall incidence of FES was 4%, but all
cases occurred in the group that had IM nailing performed more than 10 hours after surgery. Ten Duis
studied 172 consecutive patients with isolated femoral shaft fractures over an 18-year period [15]. Overall, 3.5% of patients were diagnosed with FES. Their
data also suggest that early surgery might prevent
FES as all cases occurred in patients that underwent
fixation after 24 hours. Talucci did a retrospective
study of 100 patients undergoing IM nailing of the
femur [41]. They found that the incidence of FES was
11% in the group that had delayed fixation compared
to 0% in the early fixation group. These findings were
also confirmed by Bone in a prospective randomized
study of early versus delayed stabilization of femoral
shaft fractures [42]. The influence of the method of
fracture fixation on FES has not been directly studied
in humans, although one study showed no difference
in the rate of adult respiratory distress syndrome
(ARDS) when comparing plating versus nailing of
femoral shaft fractures [43].
The incidence of FES in children is said by some
authors to be up to 100 times lower than in adults
[27, 44], but the incidence might be higher when
signs and symptoms are carefully sought [22].
Mortality directly attributable to FES is relatively
low with modern ICU care. Fabian reports a mortality
rate of 10% [40], while Bulger reports a death rate
of 7% [16]. This compares favourably to the 10 20%
mortality rate reported by a panel of experts from
four different institutions in 1974 [45]. That same
year, Moreau also reported a mortality rate of 15%
in a series of 100 patients [44].

Summary
Fat embolism is a frequent occurrence in trauma
patients. Despite technological advances in diagnostic imaging and numerous attempts to find a
confirmatory laboratory test, the diagnosis remains
a clinical one. Diagnostic criteria have remained
essentially unchanged over the past 30 years. Early
fracture fixation and modern critical care should
help minimize the impact of fat embolism.

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Correspondence address:
Dr Emil H Schemitsch, MD, FRCS(C)
Department of Orthopaedics
St Michaels Hospital
Suite 800, 55 Bond St
Toronto, ON
M5B 1W8, Canada
e-mail: schemitsche@the-wire.com