FAT EMBOLISM

SYNDROME
(FES)
Harun Rosidi

FES-Introduction
FES

may be defined as a complex

alteration of haemostasis which occurs as
an infrequent complication of fractures of
the pelvis and/or long bones and
manifests clinically as acute respiratory
insufficiency.
First described in 1862 by Von Bergmann
as a triad of confusion, dyspneu and
petechiae following fracture of long bones

Introduction-FES

FES commonly follows long bone fractures

although it is also associated with other
nontraumatic causes such as fatty liver,
prolonged corticosteroids use, acute pancreatitis
and osteomyelitis
Classic presentation consists of asymptomatic
interval (12-48 hours ) followed by pulmonary
and neurologic manifestations combined with
petechial hemorrhage.

Introduction-FES
Biphasic

clinical course-

Initial symptoms probably caused by

mechanical occlusion of multiple blood
vessels with fat globules which is often
temporary and incomplete
Late presentation thought to be caused by
hydrolysis of fat globules to more irritant free
fatty acids which migrate to other organs

Incidence
Exact

incidence and mortality not known

Hoyt et al studied the incidence of
pulmonary complications in trauma victims
during a three year study period and found
that 11.2 % trauma patients develop fat
embolism

FES-Risk factors
Most

common after skeletal injury and

more likely in long bone and pelvic
fractures
More likely in closed rather than open
fractures
More common when there is movement of
unstable bone fragments and reaming of
medullary cavity during internal fixation

FES-Risk factors
Multiple

fracture more at risk than single

fracture
Young men with fractures are more at risk
than older men and children

FES-Pathophysiology
Two

theories

Mechanical theory

Biochemical theory

Pathophysiology
Mechanical

theory

Physical obstruction of pulmonary and

systemic vasculature with embolized fat.
Increased intramedullary pressure forces
marrow into injured venous sinusoids, from
which fat travels to lung and occludes
pulmonary capillaries.
Fat emboli can cause cor-pulmonale if no
adequate pulmonary vasodilatation occur

Pathophysiology
Biochemical

theory -proposed by

Baker et al

Circulating free fatty acids are directly toxic to

pneumocytes and capillary endothelium,
causing interstitial hemorrhage, edema and
chemical pneumonitis
It is also possible that shock, hypovolemia
and sepsis can exacerbate the toxic effects of
free fatty acids

Clinical Presentation
Must

have high index of suspicion and

thorough knowledge of FES for diagnosis
to be made.
An asymptomatic period of about 12-48
hours precedes clinical manifestations
Fulminant form presents as acute corpulmonale, respiratory failure and later
death within few hours of injury

Clinical Presentation
Tachycardia

Tachypneu
Elevated

temperature
Hypoxemia
Hypocapnia
Thrombocytopenia

Clinical Presentation
Hypoxaemia

Occuring in nearly all patients with FES

PaO2 below 60 mmHg

Attributed to ventilation-perfusion inequality

and intrapulmonary shunting

Clinical Presentation
Acute

cor-pulmonale

Manifested
by
respiratory
distress,
hypoxemia, hypotension and elevated central
venous pressure.
Pulmonary insufficiency occurs in 75% and
10% progress to respiratory failure
Chest X-ray may show Snow storm
appearance, increased pulmonary markings
and dilated right side of the heart

Clinical Presentation
CNS

signs-occur in up to 86% patients

Acute confusion
Stupor
Coma
Rigidity
convulsions

Clinical Presentation
Petechial

rash that appears on upper

anterior portion of body-occur in 50-60%
pts

Neck
Chest
Upper arm
Axilla
Shoulders
Oral mucous membrane and conjunctivae

Diagnosis
Gurds

Criteria for diagnosis

Major Features
(at least one)

1.
2.
3.

Minor Features
(at least four)

1.
2.
3.
4.
5.

Laboratory Features
(at least #1)

1.
2.

3.
4.

Respiratory Insufficiency
Cerebral Involvement
Petechial Rash
Pyrexia
Tachycardia
Jaundice
Retinal Changes
Renal Changes
Fat Macroglobulinemia
Anemia
Thrombocytopenia
High ESR

Diagnosis
Schonfelds Fat Embolism Index
Symptom

Score

Petechiae

Diffuse Alveolar infiltrates

Hypoxemia ( PaO2 <9,3 kPa)

Confusion

Fever > 38oC

Heart Rate > 120 beats/min

Respiratory Rate > 30/min

A score > 5 is considered diagnostic

Laboratory Tests
Non-specific

Serum lipase level-which can be misleading in

bone trauma
Cytologic examination of urine, blood and
sputum with Sudan or oil red O staining to
detect fat globules-not sensitive
Haematocrit-decreased within 24-48 hours
due to intra alveolar haemorrhage

Laboratory tests
Blood

lipid level-not helpful because

circulating fat levels does not correlate
with severity of syndrome
Deranged coagulation and
thrombocytopaenia

Management
Prophylactic

measure-

Early immobilization and reduction of long

bone fracture

Management
Supportive

measures-

Maintenance

of

adequate

intravascular

volume as shock can exacerbate lung injury

caused by FES

Albumin has been recommended for volume

resuscitation. It balances electrolyte solution
and also binds to the toxic fatty acids

Management
Supportive

measures-

Mechanical ventilation and PEEP to maintain

arterial oxygenation

High dose corticosteroids still controversial

Maintain perfusion by optimizing cardiac

output through use of inotropes

Haematocrit to be kept above 30% w/p RBC

Morbidity and mortality

Most

commonly
self-limiting
and
pulmonary function returns to normal if
adequate supportive care given

Mortality

is about 5-15% and is closely

correlated to respiratory complications

Most

long term morbidity is secondary to

focal cerebral neurologic deficits

Conclusion
FE

usually sub clinical, occurring mostly in

long bone fracture particularly tibia and
femur

Clinical

diagnosis is still the cornerstone of

diagnosing FE

Respiratory

insufficiency, petechiae and

CNS changes still pathognomic of FES

Conclusion
Management

consists of
prophylactic
measures and aggressive supportive care
which includes early immobilization and
reduction of fracture, possible mechanical
ventilation, volume replacement and
analgesia.
Fortunately, most patients survive FES
without sequelae today