THE

ALAN

R.

FAT

GURD

and

R.

From

The

fat

embolism

undiagnosed.
of skin

The

and

mucosa

is not

A distinction

must

pathologically.

often

picture

BELFAST,

Victoria

always

(Sevitt

clinical
emboli

IRELAND

Belfast

a complication

of major

confusion,

trauma,

respiratory

frequently

distress

passes

and

petechiae

seen.

between

fat

the

embolism

clinical

is often

entity
found

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

trauma

NORTHERN

Hospital,

of cerebral

be made

Post-mortem,

SYNDROME

I. WILsoN,

the Royal

syndrome,
classical

EMBOLISM

1957,

DIAGNOSIS

OF

TABLE

FAT

EMBOLISM

THE

and
after

fat

embolism

deaths

from

demonstrated
causes

other

than

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

SYNDROME

Injury
Latent

period

Major

features-

I) Respiratory

insufficiency;

involvement;

Minor

features-

Laboratory

In this

series

100 cases

3) Petechial

2) Cerebral
rash

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

features-I)

of the

Anaemia;

2)

Thrombocytopenia;

3) High

erythrocyte

4) Fat

macroglobulaemia

syndrome

seen

sedimentation

over

a period

rate;

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

after
fractures.
feature
was not
onset

pointed
It was
merely

out

that

pathological

found
necessary
the demonstration

of fat macroglobulaemia,

fat was

to assess
of fat

or an increase

in the

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

of fat droplets

with

or without

clinical

seen,

blood
globules

often

values
but

number

in considerable

quantities,

daily
because
the important
the finding
of either
a recent

of globules,

or a change

in their

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

evidence

of their
THE

JOURNAL

presence.
OF

BONE

AND

JOINT

SURGERY

THE

FAT EMBOLISM
PRESENT

Of
males

100

the
ranged

sixteen

patients

from

seventy-seven

fourteen

to sixty-six

years

STUDY

were

to ninety-one

(average

male

and

years

twenty-three

(average

thirty-nine).

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

409

SYNDROME

The

mean

The

female.

thirty-three)

and

average

age

ages

of the

was

of the

females

from

thirty-four

and

half

In seven

the

cases

syndrome

followed

fracture
fracture,

injury

with
two or more
long
ten tibial
fracture
and four

with

either

TABLE
NATURE

OF
FAT

THE

minor

100

IN

EMBOLISM

CASES

Thus

fractured

calcaneus.

two

she developed
bruising

and

patellae.

Femoral

shaft

30

fracture

Tibial

fracture

10

Pelvic

fracture

minor
no

from

was

step

involved

fracture

fracture

ladders,

both

in a car

accident

a severe

fat embolism

syndrome

mandible.

A youth

was

severely

stairs

and

was

and

died

thirty-six

none

was

found

elderly

or

crush

49

fell

A girl

man

a classical

clinically

a fractured

An

developed

patients

fell

down

syndrome

radiologically

injuries

of the

and
upper

OF

Number

fractures

Trauma:

abdomen,

six hours

chest

or no demonstrable

SYNDROME

Multiple

Trauma:

injury

involved
fractures.

11

INJURY

Injury

fracture.

bone

bones
pelvic

and

after
badly

being

later;

for

admitted

with

and

bilateral

had

two
no

Two

without

injury

unattended

bruised;

necropsy.

arms

soft-tissue

lay

assaulted

hours
at

and

sustaining

days

hypothermia,
fractured

after

injury

fracture

had

patients

sustained

evident

and

six hours;

been

he

found
severe

fracture.

PRESENTATION

In all cases
varied

from

latent

period

There
recorded

hours

of

fifteen

two

days

was

observed

rash

was

days

after

marked

in

of a femoral

was

found

in the

sign

in only

Respiratory
uncommon
anaemia.
VOL.

56B.

involvement

and

tachypnoea

even
The
NO.

when
arterial

3,

AUGUST

was
with

between

clinical

seventeen

arterial
oxygen
1974

hypoxia
tension

rales
was

the

the

onset

of symptoms.

time

hours.

patient

developed

fifteen

days

of onset

and

This

The

recorded

symptoms

after

the original

the severity

In thirty-four

cases

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

the

of the
earliest

otherwise
dysfunction
A petechial

cases.
FEATURES

in seventy-five
over

was

the

of forty-six

fracture,

presentation.

predominant

moist

and

time

be misleading:

may

CLINICAL

dyspnoea

injury

average

usually
drowsiness
and
pyrexia
heralded
more
patients
with dyspnoea,

twenty

presenting

case

an

cerebral,

tachycardia
first

in one

between

with

remanipulation

variation

were

period
days,

correlation

symptoms

the

a latent

to fifteen

significant
course.

unexplained
was

was

four

of embolism
injury.
No
subsequent

there

the

marked,
monitored

whole

patients,
of the

lung

presumably
in

only

most

because
fifty

of whom

had

Cyanosis

was

fields.
cases.

of
In

concomitant
twenty-four

410

A. R. GURD

cases

the

ranged

minimum

from
Fifty-two

showed

p02

level

was

less

than

51 to 80, and in nine patients

patients
had radiographic

typical

R. I. WILSON

50 millimetres

of

mercury;

it was greater
than
examination
of the

patients.
was some

cerebral

involvement

their

in eighty
and
and

patients,

seventeen

1). Of seven
of mercury.
Haemoptysis

of whom

eleven

fully orientated
on admission,
twenty-five
deeply
comatose

it

cases

In forty-three

diffuse

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

in

81.
chest.

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

bilateral

AND

the

films

patients
with
Two patients
occurred
in
had

and
during

of

associated
these
nine
the peak of

symptoms.

FIG.

An

antero-posterior

A petechial

rash

anterior

axillary

fold

and the
detected

conjunctiva.
only with

Pyrexia

radiograph

was

observed

and
The
aid

the

of 394

the

of the

of the neck

degrees

Celsius

or

above

in eighty-three

cases.

Ophthalmoscopy

was

normal

in fifty-four.

Retinal

exudates

seventeen

became

retinal
within

vessels
in two.
ten days.
Some

oliguric,

one

became

than

Daily
haemoglobin
20 per cent was

three

Five
renal

were

anuric

2).

appearances.

typically

It was also
of the

and

it was
found

rash

of

recorded

haemorrhages

required

seen

at times

120

per

were

dialysis,

over

noted

the

mucosa

it could

minute

in sixty-three

patients
became
jaundiced
involvement
was manifest
and

first

in the buccal

varied:

tachycardia
was

and

typical

or

be
more

patients

in seven,

and

and

fat

but the pigmentation

in twenty-two
patients;
one had haematuria
and

incontinent.
LABORATORY

in sixteen

showing

patients;
(Fig.

distribution
and intensity
of a magnifying
glass.

noted

in the
subsided

fields

in fifty-seven

root

were

droplets
always

lung

hours.

estimations
found
in forty

Daily

platelet

INVESTIGATIONS

were recorded
in sixty-eight
patients,
the maximum
fall

counts

were

monitored

patients.
being from

in only
THE

JOURNAL

thirty-eight
OF

BONE

A drop
of more
l63 to 8l grams
cases:
AND

a drop
JOINT

SURGERY

of

THE

50 per

cent

or more

was

found

FAT EMBOLISM

411

SYNDROME

in twenty-three,

with

minimum

values

of under

90,000,

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

of petechiae.

TREATMENT

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

ward

endotracheal
require

care

full

required

was

were

500,000

units

infusion

for
56B,

with
twenty-six

NO.

received
given

two

physiotherapy

care

required

fibrillation
and
for hypocalcaemia.

VOL.

chest

intubation;

ventilation
Antibiotics

Digoxin

with

respiratory

all the routine

to the fifty-four

in twelve
with right
A protease

intravenously
three
3,

to six
AUGUST

cases,

oxygen

by mask

six

with

by

a further

was

sufficient.

Thirty-four

and 40 per cent oxygen,

Ten comatose
patients

care of the unconscious

patients
with moderate
uncontrollable

heart
failure.
Eight
inhibitor
(Trasylol)
followed

days.
1974

and

assisted
ventilation
had tracheostomies.

patient.
or severe
tachycardia,

patients
were given
was given to thirty
200,000

units

six

lung

eight
with
who did not
involvement.

four

with

atrial

intravenous
calcium
patients
in a dose of
hourly

by

continuous

412

with

A. R. GURD

Seventy-seven
epilepsy,
one

AND

R. I. WILSON

patients
recovered
fully,
seven
recovered
with scotomata
and five with personality

of the deaths
were from
eight from other
traumatic

severe
pulmonary
causes.

insufficiency

with some
residual
changes)
and sixteen
of the

fat

embolism

deficit
died.

(one
Eight

syndrome

and

DISCUSSION
In

this

series

100 cases

of

a combination
ofwell
globules
of pathological
operations,

minor

Tedeschi,

globules

to

the

demonstration
The origin

fat embolism

syndrome,

known
but variable
clinical
fat.
Fat macroglobulaemia

trauma

and

Kropp

and

Castelli,

the

of

in a variety
Tedeschi

pathogenesis
of their
of the

of

presence
pathological

the

findings

of
1968).

medical
illnesses
Although
the

clinical

helpful
fat

picture

diagnosis

(Bryans
relationship

remains

in diagnosis.
has remained

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

the

made

from

and Eiseman
1955:
of these
large fat

obscure,

controversial

mechanical
from
the

was

plus the demonstration

of circulating
has been
shown
to occur
after
minor

for

and the metabolic.

marrow
of injured

we

have

found

the

more

than

a century.

In the mechanical
bones,
driven
out

by

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

increased

local

lactic

factors
which

results
further

activates
kinins,

tissue

acid
in the
increases

syndrome

carbohydrate

metabolism

In addition,

formation
the local

tissue
proteases
which
are very

embolism

hypoxia;

production.

of microthrombi
oxygen
deficiency

only

one

activation

of

and

there

the

coagulation

(disseminated
intravascular
and the metabolic
acidosis.

which
in turn
liberate
potent
in the production

is probably

is altered

post-traumatic

coagulation)
A lowered
pH

vasoactive
polypeptides,
of post-traumatic
shock.

particular

facet

of the

is an

among

them
the

Indeed

post-traumatic

shock

the
fat

syndrome.

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

of

Over

a third

the

patients
of the
undiagnosed

remained
Pulmonary

and

valuable

investigated
or
Defective

degree

had

bilateral

arterial

PO2
pCO2.

gas

of alveolar

the

diffuse
in

minimum

reduced

so

they

was

both

had

a lowered
normal

of

to

were

involvement

evidence

proved

admitted
cases

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

common

pulmonary

diagnosis

and

values

of under

in injured

transfer

across

oedema

that

for

patients
the

develops

feature,

oedema.

usually

monitoring

when

Carbon
THE

JOURNAL

of

(1970)

OF

is caused

by

dioxide

is not

BONE

AND

those

believes

in conjunction

membrane

syndrome.

estimation
half

Ross

found

dyspnoea

tension
Almost

of mercury.

alveolar/arteriolar

in this

tachypnoea,

oxygen

treatment.

50 millimetres
is diagnostic

with

Arterial

with
the

JOINT

severe

retained
SURGERY

THE FAT EMBOLISM

because
it diffuses
across
the course
of the disorder

the membrane
veno-arterial

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

413

SYNDROME

at a much
faster
rate than does oxygen.
shunting
plays an important
role (Sproule,

is also helpful,
of consolidation,

the

significant
congested

positive
features
hilar
shadows

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

were

and

ten

in whom

cerebral

been
here

patients,

by Wertzberger
drowsiness
alert

respiratory

features

appear

stressed
confusion,

and

to occur

orientated

involvement

predominate

and Peltier
(1968)
and coma appeared

was

is less

on

common

pulmonary

features

who

or absent.
than

being evenly
and
at times
pathology,

of the fat embolism

and by Ross (1970).

In most
to follow
the onset of hypoxia.

admission,

minimal

other

Later
in
Brady
and

became

Systemic

pulmonary

deeply

comatose

fat embolism

fat

embolism,

where
but

does

occasionally.
Haemorrhage

*
Hypovolaemia
*
Release
of Catecholamines
/

j
ReactIve

Activation

of Coagulation
+
Microthrombus
Formation

Vasoconstriction

\
Tissue

Hypoxia

kCI
Activation

D0]

of Proteases
+
Release
of

Vasoactive

Polypeptides

(Kinins)
SHOCK

and

LFAT

EMBOLISM

SYNDROME
3

FIG.

A suggested

on

Petechial
the second

haemorrhages,
to fourth
days

particularly
the
the conjunctiva.
the

hands

and

very

easily

and

Bergentz

feet

of

(1968)

fine

of the rationale

one

changes
streaks

patient

unless
quote

of the fat embolism

first noted
by Benestad
after injury.
Initially

anterior
axillary
fold,
On occasions
petechiae

overlooked

fat embolism.
Pathological
exudates,

scheme

in

the

root of the
can be found

this

series.

patient

20 per
may

the

be

is studied

cent

for

found

of haemorrhage

the
on

and

in 1911,
they

occur

are

a classical
finding,
usually
the front
of the chest,

across

neck,
the mucosa
all over and they

The rash
carefully

incidence

oedema

of the mouth
and
were even noted
on

may last only a few days

every day.
Both Peltier
of petechiae

retinoscopy.

macular

syndrome.

Classically,
are

found

in diagnosed

cases

multiple
(Newman

and is
(1965)

white
1948,

of

fluffy
Kearns

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.

56B,

haemorrhage.
NO.

3,

AUGUST

It
1974

is much

more

likely

that

this

anaemia

follows

an

increased

414
tendency

cells

of

red

(Gelin

to

AND

followed

by

aggregate,

R. I. WILSON
trapping

in the

form
may explain
the clinical

of the fat embolism

not been a routine

haemolysis

of

the

aggregated

syndrome
in fact means
to give fracture
patients

the prevention
prophylactic

of shock.
treatment

In many
of shock

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

Westermark

1967).

Adequate

volume

substitution

________________

is essential,
solutions
or
Fonkalsrud,
showed
that

w-

------

and

1956).

Prevention
hospitals
it has

and

cells

A. R. GURD

can
.

in fat

gives

capacity

to

much

blood

with

metabolic

early

fracture.
The role

of proteases

it was

not

the

has

of a controlled

conclusions

cannot

yet be drawn.
It is difficult
specific
treatment
amongst
measures
spontaneous

unpredictable.
analysis
that

An
the

the first

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

routine
15 per

measures
cent

died

appeared

to be failing.

from

fat

the

given

embolism

showing
on the

In the
syndrome,

first

been

Unfortunately

as part

statistical

study.
naturally

Trasylol

patients.

given

and

production

under

by

enzyme
thirty

as

of the

in the

inhibition

occurring

of

necessary,

is currently

Protease
in

interfering

Correction

immobilisation

of shock-This

trial

without
is also

is adequate

used

Bergentz

the
postaround
30 to 35,
oxygen-carrying

flow.

acidosis

(1962)
blood

keep

satisfactory

of the

too

Maloney
of stored

haematocrit

which

colloidal
Miller,

embolism.

attempts

traumatic

cell-free
blood.

Latta
and
transfusion

result

(1968)

using
fresh

to each
recovery

to evaluate
the routine

patient
occurs

because
and
is

The
only
attempt
at
be made is to compare

can

thirty-three

patients,

only

routine

treatment

and

a second

rou

for whom

was

of sixt

available,

-seven

cases

where
protease
lnhIbltlOn
therapy
was
available
but only given
to thirty
when
group
60 per cent recovered
fully and
while

in the

full in 85 per cent and the mortality

only
5 per cent
(Table
controlled
trials
with
protease
inhibition
in patients
with the

second

III).
shock

group

recovery

Zimmerman
lung syndrome

was

(1972),
and

in
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

even more difficult

protease
inhibition
effects

were

observed

prognostic
as early

sign.
Protease
as possible.
This,

inhibition
of course,

ought
makes

to be used
evaluation

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

that
side-

treated.
THE

JOURNAL

OF

BONE

AND

JOINT

SURGERY

THE
The

established

case-Here

the

aim

the

correction

of anaemia

and

the

tracheostomy
unit.

and

mechanical

Antibiotics

Digoxin

are

may

be

intravenously
enough
treatment

of treatment

indicated

for

of blood

for

to result
in tetany,
is given in Table

and

with

tachycardia,

but
IV.

this

was

not

RESULTS

IIEFORE

or

P#{176}2 Besides

care

respiratory

heart

care

involvement.

failure,

of these

include

intensive
and

hypocalcaemia

in any

may

to be in an

right
that

observed

arterial

or severe

suggested

TABLE
COMPARATIVE

ought

moderate

(1966)

adequate

respiratory

patients

arrhythmias

Volz

an

viscosity,

such

all patients

hypocalcaemia.

415

SYNDROME
is to ensure

lowering

ventilation,

required

for

FAT EMBOLISM

can

cases.

calcium
be

severe

A summary

of

III

AND

AFTER

THE

ADVENT

OF

TRASYLOL

Mortality
Number
of
cases

Group

Trasylol

Partial
recovery

Full
recovery

Fat
embolism
syndrome

Overall

33

20(60#{176}c)

5(15#{176},)

67

30

57(835#{176})

3(45#{176},,)

TABLE
SCHEME

Shock

OF

IV
TREATMENT

prevention

1) Restoration

of circulating

volume

a) fresh

blood

h) physiological

2) Maintenance
3) Protease
4) Early

of normal

inhibition
and

Established

adequate

immobilisation

of the injured

part

syndrome

I) Maintenance
2) Care

substitute

pH

of normal

arterial

of the unconscious

3) Non-specific

drugs

P#{176}2

patient
a) antibiotics
h) Digoxin
c) calcium

SUMMARY

1.

A distinction

must

be made

embolism
demonstrated
with no prior evidence
2.

hundred

cases

studied

in

and

feature,

four

3.

One

minor

Sixteen

eight

4.

detail

from

The

other

the
5.

patients

production

56

B,

NO.

3,

AUGUST

may

fat

have

syndrome,

be

encountered
criteria

is the

found
over

been

a clinical

after

a period
defined.

death

entity,

and

following

of four
These

years
include

fat

fracture
have
one

been
major

macroglobulaemia.

from

1974

best

of shock

syndrome
are briefly
discussed.
For the established
case the aim

oxygen.
VOL.

syndrome

diagnostic
and

fat embolism

severe

pulmonary

insufficiency

of the

syndrome,

causes.

of shock

in the

the
which

died-eight

traumatic

prevention

of proteases

of the
the

features

of the

between

pathologically,
of the syndrome.

measure
and

of treatment

the

for
place

prevention

of the

of protease

is to ensure

syndrome.

inhibition

an adequate

The

role

in treatment
pressure

of arterial

of

416

A. R. GURD

AND

R. I. WILSON

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.

to study
Respiratory

patients
under their care, and Dr R. C.
Intensive
Care Unit, Royal
Victoria

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THE

JOURNAL

OF

BONE

AND

JOINT

SURGERY