THE

ALAN R. GURD

FAT
and
From

EMBOLISM
R. I. WILsoN,
Victoria

SYNDROME
BELFAST,
Hospital,

NORTHERN
Belfast

IRELAND

the Royal

The undiagnosed.
of skin

fat
and

embolism The
mucosa

syndrome, classical
is not

often
seen.

a complication confusion, clinical

of major respiratory entity

found after

trauma, distress embolism

from

frequently and

passes petechiae

picture
always fat

of cerebral between
embolism

A distinction
pathologically. trauma (Sevitt 1957,

must
Post-mortem,

be made

the

and

fat
deaths

demonstrated
causes other than

is often

clinical emboli

1962, Bergentz 1968). It is also found evidence of the syndrome (Warren 1946, Scully is of doubtful significance in cases where the clinical

in deaths following fracture without 1956). The finding of pulmonary fat features of the syndrome are absent.

TABLE
DIAGNOSIS OF THE FAT

I
EMBOLISM SYNDROME

Injury Latent Major Minor

period
featuresfeaturesfeatures-I) I) Respiratory
involvement;

insufficiency;
3) Petechial rash

2) Cerebral

1) Pyrexia; 2) Tachycardia; 3) Retinal changes; 4) Jaundice; 5) Renal changes Anaemia;

3) High

Laboratory

2)

Thrombocytopenia;

erythrocyte
macroglobulaemia

sedimentation

rate;

4) Fat

In this

series

100 cases

of the

syndrome

seen

over

a period

of four

years

are

analysed.

Certain clinical features were looked for in suspected cases (Table I) and in addition blood samples were checked for pathological fat globules. A positive diagnosis was made on finding at least one major feature, four minor features, and fat macroglobulaemia (Gurd 1970). The assessment of pathological fat globulaemia has been criticised by Nolte, Olofsson, Schersten and Lewis (1974), who report finding large fat globules as often in normal patients and in patients with fractures as in proven cases of fat embolism syndrome. In the original description of the test it was pointed It was merely out that pathological fat was blood globules number seen, often in considerable quantities, after fractures. feature was not onset found necessary the demonstration to assess of fat values but daily because the important the finding of either a recent or a change in their

of fat macroglobulaemia,

or an increase

in the

of globules,

appearance associated with the onset of the clinical As with the post-mortem finding of pulmonary in the asymptomatic patient is probably irrelevant. finding which is specific in fat embolism is one of of the condition under discussion here is made association with accepted clinical features. The embolism syndrome rather than the misleading embolism
408

condition. fat emboli, so, too, fat macroglobulaemia Bergentz (1968) asserts that the only intravascular fat droplets. The diagnosis when fat macroglobulaemia is found in condition is then referred to as the fat term fat embolism, which denotes the of their
THE JOURNAL

of fat droplets

with

or without

clinical

evidence

presence.
OF BONE AND JOINT SURGERY

THE

FAT EMBOLISM PRESENT

SYNDROME STUDY

409

Of males

the ranged

100
from

patients fourteen

seventy-seven to ninety-one

were years

male

and (average

twenty-three thirty-three)

female. and

The
of the

ages
females

of the
from

sixteen half

to sixty-six

years

(average

thirty-nine). fracture fracture, with

TABLE

The

mean

average

age

was

thirty-four bones pelvic

and involved fractures.

years. Forty-nine cases followed multiple (Table II). Thirty followed femoral shaft
In seven cases

with two or more long ten tibial fracture and four either
11
IN

the

syndrome

followed

injury

minor

bone

injury

or no demonstrable

NATURE

OF FAT

THE

INJURY

100

CASES

OF

EMBOLISM

SYNDROME

Injury Multiple
Femoral Tibial Pelvic Trauma: Trauma:

Number
.

fractures
shaft fracture fracture minor no fracture
.

49 30

10
4 4

fracture
.

fracture

fracture.

Thus

two

patients

fell

from

step

ladders,

both

sustaining

soft-tissue

injury

and

fractured bruising patellae. developed

clinically crush

calcaneus. a severe a fractured elderly

radiologically of the

A girl

was

involved syndrome A youth down and

none

in a car was and thirty-six

found and at

accident after badly hours

necropsy. without

and being assaulted

lay

unattended admitted and two had fracture

patients fracture.

for with bilateral

six hours; fractured injury been found

severe

she developed and An

or injuries

fat embolism mandible. man fell

and upper

six hours severely was

hypothermia, after he

stairs died
was chest

bruised; later; no
Two evident

days

a classical

syndrome
abdomen,

had

sustained

arms

PRESENTATION

In all cases
varied latent from period four of

there
hours fifteen

was
days

a latent
in one

period
days, case with may

between
an average

injury
time

and the fracture, time

the

onset

of symptoms.
hours. The

This
recorded

to fifteen

of forty-six

be misleading: of a femoral between the

patient fifteen

developed days and after

symptoms the original of the earliest

of embolism injury. No subsequent There recorded

unexplained
was observed

two

days

after

remanipulation was in the found

significant course. was marked

correlation variation cerebral,

of onset

the severity cases the

clinical

presentation.

In thirty-four

symptoms
tachycardia
first in

were
twenty

usually drowsiness and pyrexia heralded more patients with dyspnoea, in only seventeen
CLINICAL

or confusion. In twenty-nine, specific signs. Respiratory tachypnoea or haemoptysis.

otherwise dysfunction A petechial

rash

was

the

presenting

sign

cases.
FEATURES

Respiratory dyspnoea uncommon anaemia.

VOL.

involvement tachypnoea when arterial

3,
AUGUST

was with

predominant rales was was over hypoxia

in seventy-five the whole in marked, monitored presumably only

patients, of the lung fifty because

most fields. of cases.

of whom Cyanosis concomitant twenty-four In

had was

and The
NO.

moist tension

even

arterial oxygen
1974

56B.

410 cases ranged showed the minimum p02 level

A. R. GURD

AND

R. I. WILSON
of mercury; in seventeen cases

was

less

than

50 millimetres

it

from Fifty-two typical

51 to 80, and in nine patients patients had radiographic bilateral diffuse

it was greater than examination of the

81. chest.

In forty-three 1). Of seven of mercury. Haemoptysis eleven and during

the

films

patchy areas of consolidation (Fig. normal radiographs, two had a p02 level of under 80 millimetres with clinically normal lungs had moderate radiological changes. twenty-two There patients. was some cerebral involvement and and in eighty patients,

patients with Two patients occurred in had of associated these nine the peak of

of whom

head injuries. Sixty-nine were awake became confused, thirty-five drowsy,

their symptoms.

fully orientated on admission, twenty-five deeply comatose

FIG.

I lung fields showing typical appearances.

An

antero-posterior

radiograph

of the

A petechial anterior and the detected

were

rash fold the

was and The aid degrees

observed the root

in fifty-seven of the neck (Fig.

patients; 2). of the

typically rash

it was found varied: of 120 noted

first at times

seen

over

the be more
and

axillary

It was also

in the buccal

mucosa

conjunctiva. only with of 394

distribution and intensity of a magnifying glass. Celsius

cases.

it could or and

Pyrexia
noted

or exudates

above and

and

tachycardia
was recorded

per

minute in seven,

in eighty-three

Ophthalmoscopy

in sixty-three

patients

was

normal

in fifty-four. retinal within

Retinal

haemorrhages

were

fat

droplets always
seventeen

in the subsided
became

vessels in two. ten days. Some

three were

Five renal
anuric

patients became jaundiced involvement was manifest

and required dialysis,

oliguric,

but the pigmentation in twenty-two patients; one had haematuria and

one

became

incontinent.
LABORATORY INVESTIGATIONS

than

Daily haemoglobin 20 per cent was hours.

estimations found in forty platelet

were recorded in sixty-eight patients, the maximum fall were monitored in only
THE

patients. being from thirty-eight

OF BONE

A drop of more l63 to 8l grams cases:

AND JOINT

in sixteen

Daily

counts

a drop
SURGERY

of

JOURNAL

THE

FAT EMBOLISM

SYNDROME

411 values of under

90,000,

50 per

cent

or more

was

found

in twenty-three,

with

minimum

cubic

millimetre in twelve patients. In eighty-seven cases the erythrocyte sedimentation rate was raised, with values of 30 to 50 millimetres in sixteen cases, 51 to 70 millimetres in seventeen cases, and over 71 millimetres in fifty-four cases. Fat globules larger than 8 microns were found circulating in all cases. The amount of circulating fat did not appear to correlate with the clinical severity of the condition.

..

FIG.

A photograph

showing COURSE

the distribution AND TREATMENT

of petechiae.

Thirty-six patients recovered without any treatment. In the remaining cases treatment was directed towards: 1) the restoration of circulating volume with fresh blood or a physiological substitute; 2) the correction of acidosis; and 3) immobilisation of the affected part. Additional treatment was primarily concerned with respiratory support. In twenty cases routine
required

ward full

care

with

chest
care

physiotherapy

and

oxygen

by mask

was

sufficient.

Thirty-four eight with who did not involvement. with atrial

respiratory

endotracheal require

intubation; were two received given

with twenty-six

assisted ventilation had tracheostomies.

and 40 per cent oxygen, Ten comatose patients patient. or severe tachycardia, lung four

ventilation Antibiotics was

all the routine to the fifty-four cases, six

care of the unconscious patients with moderate with uncontrollable

Digoxin

required

in twelve with right A protease

fibrillation and for hypocalcaemia. 500,000

infusion
VOL.

heart failure. Eight inhibitor (Trasylol) followed by a further

patients were given was given to thirty 200,000

units six

intravenous calcium patients in a dose of hourly by continuous

units
for

intravenously
three 3, to six
AUGUST

days.
1974

56B,

NO.

412 Seventy-seven epilepsy, one

A. R. GURD

AND

R. I. WILSON

with

patients recovered fully, seven recovered with scotomata and five with personality severe pulmonary causes. insufficiency

with some residual changes) and sixteen of the fat embolism

deficit died. syndrome

(one Eight and

of the deaths were from eight from other traumatic

DISCUSSION In this series of

100 cases

of

the

fat embolism

syndrome, findings

the

diagnosis

was

made

from

a combination ofwell globules of pathological operations,

Tedeschi,

known but variable clinical fat. Fat macroglobulaemia and

and

plus the demonstration of circulating has been shown to occur after minor (Bryans relationship obscure, for and Eiseman 1955: of these large fat we more have than found a century. by the

minor
Castelli,

trauma
Kropp

in a variety
Tedeschi

of 1968).

medical illnesses Although the picture remains controversial

globules

to

the

pathogenesis of their of the presence pathological

of

the helpful fat

clinical

demonstration The origin

in diagnosis. has remained mechanical from the

Basically two concepts have evolved, the theory it is alleged that fat is liberated

and the metabolic. marrow of injured

In the mechanical bones, driven out

an increase of intramedullary pressure and transmitted via the draining veins to the pulmonary capillaries, where it lodges. The metabolic theory suggests that emboli arise in the plasma from conglomeration and fusion ofa pre-existing physiological suspension oftiny chylomicrons (usually less than one micron), possibly due to some biochemical change initiated by injury. Other changes occur which augment the embolic effect of the large fat globules, such as agglutination of the formed elements of blood-particularly platelets and red cells-and an increase in the viscosity of plasma and whole blood (Bergentz, Gelin, Rudenstam and Zederfeldt 1961). Aggregation of platelets, chylomicrons and red cells can be produced by injection of thromboplastic substances, which also cause the formation of fat droplets (Bergentz 1961, Adkins, Foster and OSaile 1962). The pathological sequence of events is not yet proven, but the triggering mechanism appears to be an over-compensation in response to injury, haemorrhage, decreased venous return and increased cardiac output (Fig. 3). Reactive vasoconstriction
follows, causing local tissue hypoxia; carbohydrate metabolism is altered and there is an

increased factors which activates kinins,

embolism

lactic results further

acid in the increases

production. formation the local

In addition, of microthrombi oxygen deficiency

post-traumatic

activation

of

the

coagulation

(disseminated intravascular and the metabolic acidosis. vasoactive polypeptides, of post-traumatic shock.
facet of the post-traumatic

coagulation) A lowered pH among

Indeed shock

tissue proteases which are very

syndrome

which in turn liberate potent in the production

only one particular

them the
syndrome.

the fat

is probably

An association between pulmonary fat embolism and intravascular coagulation has frequently been reported (Bradford, Foster and Nossel 1970; Saldeen 1970; Soloway and Robinson 1972). It has been said that fat embolism potentiates shock (Porter 1917), but in reality the reverse applies (Peltier 1965, Volz 1966). It is our impression that the clinical syndrome is not uncommon: it occurred in 19 per cent
Over

of

the

a third

remained
Pulmonary

patients of the undiagnosed

involvement

admitted
cases were

to
so the

had
was in

they diffuse
diagnosis

the Royal Victoria Hospital, Belfast, with major trauma. mild that no treatment was required, and these might have not been screened both clinically and for fat macroglobules.
most and common for feature, usually with tachypnoea, dyspnoea

and
proved

evidence
valuable

of had arterial

bilateral
both

pulmonary of under patients

the

oedema.
monitoring

Arterial
treatment.

oxygen

tension
Almost half

estimation
of those

investigated a lowered
normal or Defective

minimum
PO2 pCO2. transfer

values in injured
across

50 millimetres is diagnostic

of mercury. when
membrane

Ross

(1970)

believes with
the severe

found

in conjunction
is caused by

reduced gas

alveolar/arteriolar

degree

of alveolar

oedema

that

develops

in this

syndrome.
THE

Carbon
JOURNAL OF

dioxide
BONE AND

is not
JOINT

retained
SURGERY

THE FAT EMBOLISM

SYNDROME

413 Later in Brady and

because it diffuses across the course of the disorder

the membrane veno-arterial

at a much faster rate than does oxygen. shunting plays an important role (Sproule, the significant congested positive features hilar shadows other features pulmonary

Gilbert 1964). Chest radiography distributed, small fleck-like areas

is also helpful, of consolidation,

being evenly and at times pathology,

dilatation of the right heart. Radiographs also help to exclude such as pneumothorax (Fig. 4). The importance of arterial hypoxia in producing the cerebral syndrome has cases reported There and
cerebral appear

of the fat embolism

been here

stressed confusion,

by Wertzberger drowsiness alert and was

and Peltier (1968) and coma appeared on admission, or absent.

than pulmonary

and by Ross (1970). In most to follow the onset of hypoxia. who became
fat

were in whom

ten

patients,
predominate occasionally.

orientated minimal
common

deeply

comatose where
but does

respiratory

involvement
is less

Systemic

fat embolism
embolism,

features to occur

Haemorrhage

* Hypovolaemia * Release of Catecholamines /

j
ReactIve Vasoconstriction

Activation

\
Tissue kCI Activation Hypoxia D0]

of Coagulation + Microthrombus Formation

of Proteases + Release of
Polypeptides

Vasoactive

(Kinins)
SHOCK

I
LFAT
A suggested scheme EMBOLISM

and
SYNDROME
FIG.

of the rationale

of the fat embolism

syndrome.

on

Petechial the second

haemorrhages, to fourth days

first noted by Benestad after injury. Initially the

this

in 1911,
they occur

are

across

a classical finding, usually the front of the chest, of the mouth and were even noted on and is (1965) cases white 1948, of

particularly the the conjunctiva.

the hands and

anterior axillary fold, On occasions petechiae

feet of one patient in

root of the can be found

series.

neck, the mucosa all over and they

very and

easily Bergentz

overlooked (1968)

unless
quote

the 20 per

patient cent found and for

is studied the on

The rash carefully

may last only a few days every day. Both Peltier of petechiae Classically, are found in diagnosed multiple (Newman

incidence retinoscopy. oedema

fat embolism. Pathological exudates, fine

changes streaks

may

be

fluffy Kearns

of haemorrhage

macular

1956, Adams 1971). Scotomata may occur and usually resolve completely (Duke-Elder 1954). Oliguria is not uncommon and complete anuria does occur. Renal involvement is so frequent in fat embolism that Sevitt (1960) has suggested needle biopsy of the kidney as an aid to the diagnosis of obscure cases. Adebahr (1957) believes the sudden drop in the haemoglobin value, occurring even after adequate blood replacement at the time of injury, is due to pulmonary
VOL.

haemorrhage.
NO.

It
1974

is much

more

likely

that

this

anaemia

follows

an

increased

56B,

3,

AUGUST

414 tendency of red cells to aggregate,

A. R. GURD followed

AND by

R. I. WILSON trapping and haemolysis of the aggregated

cells

(Gelin

1956). of the fat embolism not been a routine syndrome in fact means to give fracture patients the prevention prophylactic of shock. treatment In many of shock

Prevention hospitals it has

in the

form may explain the clinical and

of transfusions, sedatives, analgesics or general anaesthesia (Bergentz 1968). This why fracture patients subjected to immediate internal fixation appear to develop syndrome less often than patients treated conservatively (Saikku 1954, Liljedahl 1967). Adequate volume substitution is essential, solutions or Fonkalsrud, showed that can
. 1

Westermark

using fresh Latta and transfusion

cell-free blood. Maloney of stored keep

colloidal Miller, (1962) blood Bergentz

________________
------

w-

result

in fat attempts
haematocrit

embolism. to

(1968)
traumatic

which
capacity

gives much

satisfactory
blood

the postaround 30 to 35, oxygen-carrying

interfering

of the

without is also

too

with
acidosis

flow.

Correction
necessary,

of
as

metabolic

is adequate fracture. The role

of shock-This Protease

early

immobilisation in the
by the

of the production
study. naturally

of proteases
is currently inhibition

under

occurring
used in

enzyme
thirty patients.

Trasylol as part

has
Unfortunately

been

it was trial

not and

given statistical

of a controlled cannot to evaluate the routine because and is

conclusions

yet be drawn. It is difficult specific treatment amongst measures spontaneous given to each recovery patient occurs

An the

FI;. 4 antcro-postcrior radiograph of the lung fields typical diffuse patchy appearances, complicated left side by a pneumothorax.

unpredictable. analysis that the first

only showing on the routine

can

The only attempt at be made is to compare patients,

was

thirty-three
treatment

for whom
available,

and

a second g

rou

of sixt y

-seven

cases

routine 15 per

measures cent died

appeared from the

to be failing. fat embolism

In the syndrome,

first

where protease lnhIbltlOn therapy was available but only given to thirty when group 60 per cent recovered fully and while in the second group recovery (1972), and was in the III). shock Zimmerman lung syndrome

full in 85 per cent and the mortality only 5 per cent (Table controlled trials with protease inhibition in patients with the

fat embolism syndrome, has reduced the mortality from almost 70 per cent with routine therapy alone to 39 per cent when using Trasylol in addition. Three cases in this present study died of massive pulmonary embolism whilst on protease inhibition treatment. In retrospect we noted that Trasylol was not commenced until the pCO2 had begun prophylactically to rise, which is a bad and therefore given prognostic as early sign. Protease as possible. This, inhibition of course, ought makes to be used evaluation that side-

even more difficult protease inhibition

effects were observed

as so many cases recover spontaneously. It is our clinical impression with Trasylol has a place in the treatment of this syndrome. No
in the thirty cases treated.
THE JOURNAL OF BONE AND JOINT

SURGERY

THE The established case-Here the aim

FAT EMBOLISM of treatment

SYNDROME is to ensure an adequate arterial

415
P#{176}2 Besides

the
unit.

correction
Antibiotics

of anaemia and mechanical

are indicated

and

the
for

lowering and
all patients

of blood such
with

viscosity, patients

respiratory ought
respiratory

care

may intensive

include care calcium be severe of

tracheostomy Digoxin intravenously enough treatment may

ventilation, for but IV. tachycardia, Volz this was

to be in an heart failure, cases.

moderate

or severe

involvement.

be for

required

arrhythmias (1966) not suggested observed

III
AFTER THE

or in any

right that

and can

hypocalcaemia.

hypocalcaemia of these

to result in tetany, is given in Table

COMPARATIVE

A summary

TABLE
RESULTS IIEFORE AND

ADVENT

OF

TRASYLOL

Mortality Group Number of cases 33 67 Trasylol Partial recovery 4 3 Full recovery 20(60#{176}c) 57(835#{176}) Overall 9 7 Fat embolism syndrome
5(15#{176},)

A B

0 30

3(45#{176},,)

TABLE
SCHEME OF

IV
TREATMENT

Shock

prevention of circulating volume pH a) fresh blood substitute

h) physiological

1) Restoration 2) Maintenance 3) Protease 4) Early Established and

of normal

inhibition adequate syndrome immobilisation of the injured part

I) Maintenance 2) Care

of normal

arterial
patient

P#{176}2

of the unconscious drugs

3) Non-specific

a) antibiotics h) Digoxin c) calcium

SUMMARY

1.

A distinction

must

be made

between

the which

fat embolism may be

syndrome, found over after

a clinical death of four

These

entity,

and fracture have

fat

embolism demonstrated with no prior evidence 2. One hundred

in four from detail minor

pathologically, of the syndrome. of the

the features and causes.

following years
include

cases
and

syndrome
fat

encountered
criteria have

a period
defined.

been
major

studied feature,

diagnostic

been

one

macroglobulaemia.

3.
eight

Sixteen The

of the
other

patients
traumatic

died-eight is the best

from

severe

pulmonary for place prevention

insufficiency of the

of the syndrome.

syndrome, The role of

4. the 5.

prevention in the

of shock production

measure and the

of proteases

of shock

of protease

inhibition

in treatment pressure of arterial

syndrome are briefly discussed. For the established case the aim

of treatment

is to ensure

an adequate

oxygen.
VOL.

56

B,

NO.

3,

AUGUST

1974

416

A. R. GURD

AND

R. I. WILSON to study Respiratory patients under their care, and Dr R. C. Intensive Care Unit, Royal Victoria

We wish to thank our orthopaedic colleagues for permission Gray, Dr D. L. Coppel and Dr W. F. K. Morrow of the Hospital. Belfast, for their invaluable help. REFERENCES
ADAMS,
ADEBAHR,

C. B. T. (1971):
G R.
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OSAILE,

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Pathokgie

iu,d

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H., and
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WESTERMARK,

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PORTER,

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