FAT EMBOLISM SYNDROME(FES)

DR AFTAB HUSSAIN
History
First diagnosed in 1873 by Dr Von Bergmann

In 1879 Fenger and Salisbury published description of

Fat embolism syndrome
Fat Emboli: Fat particles or droplets that
travel through the circulation

Fat Embolism: A process by which fat

emboli passes into the bloodstream and
lodges within a blood vessel.

Fat Embolism Syndrome (FES): serious

manifestation of fat embolism occasionally
causes multi system dysfunction, the lungs are always
involved and next is brain
 FE vs. FES
Fat embolization is a well-known complication of
skeletal trauma and surgery involving
instrumentation of the femoral medullary canal.

 Fat embolism syndrome (FES) is a physiological

response to fat within the systemic circulation.

Fat embolization and FES are not synonymus.

The embolization of fat can be detected in almost all

patients who sustain a pelvic or femoral fracture, but
the incidence of FES is less than 1%.
Fat Embolism Syndrome
Mortality: 10-20%
Clinical diagnosis, No specific laboratory test is
diagnostic.
Mostly associated with long bone and pelvic
fractures, and more frequent in closed fractures.
Single long bone fracture has 1-3% chance of
developing FES, and increases with number of
fractures.
Onset is 24-72 hours from initial insult.
Causes of fat embolism
TRAUMA RELATED:
Blunt trauma: Long bone (Femur, tibia, pelvic) factures
orthopedic procedures
Soft tissue injury(chest compression with or without rib
fracture)
Burn
Liposuction
Bone marrow harvesting and transplant.
NON TRAUMA RELATED
Pancreatitis
Diabetes mellitus
Osteomyelitis and panniculitis
Bone tumor lysis
Steroid therapy
Sickle cell hemoglobinopathy
Alcoholic liver disease
Fat infusion
Most common cause of FES is blunt trauma.

90 % occurs after blunt trauma complicated by long-

bone fractures

Closed fractures had higher incidence compared to

open fractures. The intramedullary bone pressure is
lower in case of open fractures, which reduces the
bulk of fat emboli propelled into the blood stream.
Non-traumatic fat embolism
It occurs due to the process of fat or marrow necrosis
or by the increased concentration of lipids in the
blood.
It may be caused by agglutination of chylomicrons
and VLDL by high levels of plasma CRP.
As in Acute pancreatitis in patients with types I, IV,
and V hyperlipidaemia and avascular necrosis of bone
in patients with corticosteroid-induced
hyperlipidaemia.
Drug-related causes of FES

 Infusion of lipids at rates greater than the normal

clearance capacity of lipids.

 Agglutination of lipid emulsion particles with fibrin.

Agglutination of endogenous or infused exogenous

fat such as Intra lipid.
FES can occur in SC
crisis.
Bone marrow necrosis
as a result of hypoxia
may release fat.
Risk factors
Pathophysiology of FES
Exact mechanism unknown, but two main hypothesis

1. Mechanical Hypothesis

2. Biochemical Hypothesis
Mechanical Hypothesis
Obstruction of vessels and capillaries

Increase in inter medullary pressure forces fat and

marrow into bloodstream.

Bone marrow contents enter the venous system

and lodge in the lungs as emboli.
Smaller fat droplets travel through the pulmonary
capillaries into the systemic circulation: Embolization to
cerebral vessels or renal vessels also leads to central
nervous system and renal dysfunction
Biochemical Hypothesis
Toxicity of free fatty acids

Circulating free fatty acids directly affect the

pneumocytes, producing abnormalities in gas
exchange.

Coexisting shock, hypovolemia and sepsis impair liver

function and augment toxic effects of free fatty acids.
 Hormonal changes caused by trauma or sepsis
induce systemic release of free fatty acids as
chylomicrons.

Acute-phase reactants( C-reactive proteins) cause

chylomicrons to coalesce.

 It explains non traumatic forms of fat embolism

syndrome and why symptoms take 12 hours to
develop.
FE in ARDS
Fat emboli obstructs
lung vessel (20microns),
platelets and fibrin
adhere to it
Lipase increases FFA
Inflammatory changes-
>endothelial damage-
>ARDS
CLINICAL FEATURES
Asymptomatic for the first 12-48 hours

Pulmonary Dysfunction
Neurological (nonspecific)
Dermatological Signs
Pulmonary
Hypoxia, rales, pleural friction rub
ARDS may develop.
CXR usually normal early on, later may show
‘snowstorm’ pattern- diffuse bilateral infiltrates
CT chest: ground glass opacification with interlobular
septal thickening.
Neurological findings
Usually occur after respiratory symptoms
Incidence- 80% patients with FES
Minor global dysfunction is most common-ranges
from mild delirium to coma.
Seizures/focal deficits
Transient and reversible in most cases.
CT Head: general edema, usually nonspecific
MRI brain: Low density on T1, and high intensity T2
signal, correlates to degree of impairment.
Dermatological findings
Petechie
Usually on conjunctiva, neck, axilla, upper limbs.
Results from occlusion of dermal capillaries by fat
globules and then extravasations of RBC.
Resolves in 5-7 days. Usually fast resolving.
Pathognomic, but only present in 20-50% of patients.
Early Signs
Dyspnea
Tachypnea
Hypoxemia
Triad of FES
Hypoxemia
Neurological abnormalities
Petechial rash
Other findings
Retinopathy (exudates, cotton wool spots,
hemorrhage)
Lipiduria
Fever
DIC
Myocardial depression (Right heart strain)
Thrombocytopenia/Anemia
Hypocalcemia.
Diagnostic Criteria
Gurd criteria most
commonly used.

Other indexes are

Schonfeld Index
Lindeque Index
Gurd & Wilson Criteria
Schonfeld Fat Embolism Syndrome
Index

It ranks signs and symptoms of FES in relation to

their incidence of presentation.

Score >5 required for diagnosis of fat embolism

syndrome
Schonfeld FES Index
sign score

Petechial rash 5

Diffuse alveolar infiltrate 4

Hypoxemia pao2<70 mm Hg, FIO2-100% 3

confusion 1

Fever ( >100.4 F) 1

Heart rate >120 beats/min 1

Respiratory rate >30/min 1

Lindeque's criteria
Acc. to Lindeque FES can be diagnosed on the basis
of respiratory system involvement alone.
Laboratory Studies
 Arterial Blood Gases (ABGs)

Urine and sputum examination

Haemotological Tests

Biochemical tests
Imaging
• Chest x-ray
– shows multiple flocculent shadows (snow storm
appearance). picture may be complicated by infection
or pulmonary edema.
Imaging contd.

MRI Brain
- Image showing minimal hypodense changes
in periventricular region, which are more evident in
DWI and T2WI as areas of high signals.
Treatment and management
Prophylaxis
Immobilization and early internal fixation of
fracture.
Fixation within 24 hours has been shown to yield
a 5 fold reduction in the incidence of ARDS.
Continuous pulse oximeter monitoring in high-
risk patients may help in detecting desaturation
early, allowing early institution of oxygen and
possibly steroid therapy.
High doses of corticosteroids.
Treatment and management contd.

Supportive Medical Care

Maintenance of adequate oxygenation and ventilation

Maintenance of hemodynamic stability.
Administration of blood products as clinically
indicated.
Hydration
Prophylaxis of deep venous thrombosis .
Nutrition.
Treatment and management contd.
Oxygenation and ventilation

 High flow rate oxygen is given to maintain the

arterial oxygen tension in the normal range.

 Mechanical ventilation and PEEP may be required to

maintain arterial oxygenation.
Treatment and management contd.
Hemodynamic stability
Maintenance of intravascular volume is important,
because shock can exacerbate the lung injury caused
by FES.
Albumin has been recommended for volume
resuscitation in addition to balanced electrolyte
solution, because it not only restores blood volume
but also binds with the fatty acids and may decrease
extent of lung injury
Steroids
Steroid prophylaxis is controversial to prevent FES.
It causes blunting of inflammatory response and
complement activation
Prospective studies suggests prophylactic steroids
benefit in high risk patients.
Preoperative use of methylprednisolone may prevent
the occurrence of FES
Once FES established, steroids have not shown
improved outcomes.
Results of Randomized, Controlled Trials of Corticosteroids for Prevention of Fat
Embolism Syndrome
Dose Model Timing Duration of Effect on
study disease
incidence
30mg/kg Dog Before event 60min None
10mg/kg q8h Human At admission No data Declining
for 24 hrs trauma
7.5mg/kg q6h Human Within 12hrs 2 days Declining
for 12hrs or Trauma
placebo
Heparin
Heparin has also been proposed for treatment as it
"clears" lipemic plasma in vivo by causing the release
of lipoprotein lipase into the circulation, but no
evidence exists for its use in FES.
Prognosis
The fulminant form presents as acute cor pulmonale,
respiratory failure or embolic phenomena, leading to
death within a few hours of injury.

Most death contributed to pulmonary dysfunction

Hard to determine exact mortality rate

Estimated less than 10%

The incidence of FES ranges from < 1 to 29% in
different studies.
 Actual incidence of FES is not known, as mild cases
often go unnoticed.
A high index of suspicion is needed to diagnose FES.
A combination of clinical criteria and MRI brain will
enable early and accurate diagnosis of FES.
Refrences
Altaf Hussain: “A Fatal Fat Embolism.” The Internet Journal of Anesthesiology,
2004. Volume 8 Number 2.

Fabian T. “Unraveling the fat embolism syndrome”. N Engl J Med 1993;329:961–

63

U. Galway, J. E. Tetzlaff & R. Helfand : “Acute Fatal Fat Embolism Syndrome In

Bilateral Total Knee Arthroplasty – A Review Of The Fat Embolism
Syndrome”. The Internet Journal of Anesthesiology. 2009 Volume 19 Number
2

Latif, A., Bashir, A., Aurangzeb. "Fat Embolism and Fat Embolism Syndrome;
Management Trends." Professional Med J 15.4 (2008): 407-413.

Harrisons principles of Internal medicine 18th edition.

Nissar Shaikh, Emergency management of fat embolism syndrome.” J Emerg

Trauma Shock. 2009 Jan-Apr; 2(1): 29–33
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