April 11, 2024

Fat embolism syndrome is first coined by Dr. Von Bergmann

Fat Embolism

Fat emboli pass through the bloodstream and lodge within blood vessels

Fat Embolism Syndrome

The serious manifestation of fat embolism occasional cause multisystem dysfunction, lungs are more involved than the brain (Physiological responses)

Onset: 24-72 hours of insult

Closed fracture > Open fracture (Increase Intraosseous pressure)

Risk Factors for Fat embolism syndrome

General Factors

  • Males
  • Age 10-39 ages
  • Post-traumatic hypovolemic state
  • Decrease cardiopulmonary reserves

Injury-related factors

  • Multiple fractures
  • B/L femur fractures
  • Femur shaft fractures
  • Lower extremity fractures
  • Traumatic fractures
  • Concomitant pulmonary injury

Surgery related fractures

  • Intramedullary reamed/unreamed nailing after femoral fractures
  • Joint replacement after femoral fracture
  • Bilateral procedure
  • Joint replacement with a high-volume prosthesis


The exact mechanism is unknown

Mechanical hypothesis

  • Increase in intramedullary pressure
  • Forces fat/marrow in blood
  • Lodges into bloodvessels
  • Passes from the pulmonary artery to cerebral circulation/renal which can cause dysfunction

Biochemical hypothesis

  • Toxicity of free radicals
  • Affects pneumocytes producing abnormality in gas exchanges
  • Shock, sepsis, hypovolumia
  • Auguments FFA effects

Fat emboli

  • Obstruct lung vessels (20um)
  • Platelets and fibrins adhere to it
  • Can cause Inflammatory changes later lead to ARDS

Clinical Features

  • Pulmonary dysfunction
  • Neurological signs
  • Dermatological signs (petechias)

Other findings:

  • Retinopathy
  • Lipiduria
  • Fever
  • DIC
  • Myocardial depression
  • Thrombocytopenia/ Anemia
  • Hypocalcemia
Triad of Fat Embolism Syndrome

Snow storm is characteristic feature seen in CXR

Gurd and Wilson Criterias

Two major criteria or 1 major and 4 minor criteria is diagnostic of Fat Embolism syndrome

Major Criteria

  1. Petechial rashes
  2. Neurological signs (Confusion, drowsiness, coma)
  3. Respiratory symptoms (Tachypnoea, Dyspnoea, B/L crepts, Hemoptysis, Patchy shadow in CXR)

Minor Criteria

  1. Pyrexia >39.4 C
  2. Jaundice
  3. Retinal changes: Fat/ petechias
  4. Renal Changes: Anuria/ Oliguria
  5. Tachycardia > 120/ min

Laboratory features:

  1. ESR >71mm/hr
  2. Hb decrease > 20 % of admission value
  3. Platelets decrease > 50 % of admission value
  4. Fat macroglobulinemia

Schonfeld FES Index

Score >5: Diagnosis of FES

Petechial Rashes5
Diffuse alveolar infiltrate4
Hypoxemia PaO2 < 70mmHg, FiO2 100%3
Fever (>100.4 F)
Heart Rate >120 beats/min1
Respiratory rate >30 /min1
Schonfeld FES Index

Laboratory studies

Important laboratory investigations for FES are:

  • ABG
  • Urine and Sputum examination
  • Hematological tests
  • Biochemical tests

Treatment and Management


Immobilization + Early internal fixation of fractures

Fixation within 24 hours yields a 5 folds reduction in the incidence of ARDS

Continuous SpO2 monitoring

High dose corticosteroids (Controversial)

Supportive Medical Care

Maintainance of adequate oxygenation and ventilation (High flow O2 )

Maintainance of hemodynamic stability

Administration of blood products


Prophylaxis of DVT



Recommended for volume resuscitation, balanced electrolytes solution, binds to fatty acids and decreases the extent of lung injury


No evidence

Proposed for treatment: Clear lipemic plasma

Fat embolism syndrome vs Cerebral Injury

FeaturesFat Embolism SyndromeCerebral Injury
Lucid Interval18-24 hours6-10 hours
Pulse raterapid >120/minslow
Onset of comarapidslow
Localizing signabsentpresent
Decerebrate rigidityearlyterminal
Fat embolism syndrome vs Cerebral Injury