Overview
Fat Embolism Syndrome
Topic Overview
Summary
Fat embolism syndrome (FES) is a clinical syndrome following release of fat droplets into the circulation, typically after long bone fractures or orthopaedic surgery. It presents with the classic triad of respiratory distress, neurological dysfunction, and petechial rash, usually 12-72 hours post-injury. Diagnosis is clinical using Gurd's criteria. Treatment is supportive; early fracture fixation may reduce risk.
Key Facts
- Timing: 12-72 hours after injury (peak 24-48 hours)
- Classic triad: Respiratory failure + neurological dysfunction + petechial rash
- Risk factors: Long bone fractures (especially femur, tibia), pelvic fractures, orthopaedic surgery
- Diagnosis: Clinical (Gurd's criteria) — no specific test
- Treatment: Supportive (oxygen, ventilation, fluids)
- Prevention: Early fixation of long bone fractures
Clinical Pearls
Petechial rash in axillae/conjunctivae + hypoxia 24-72h post-fracture = think FES
FES is a clinical diagnosis — there is no specific confirmatory test
Early fracture fixation (within 24h) may reduce FES incidence
Why This Matters Clinically
FES can rapidly deteriorate to ARDS and multi-organ failure. Early recognition allows supportive care and monitoring. All clinicians managing trauma must be aware of this time-dependent complication of long bone fractures.
Visual Summary
Visual assets to be added:
- Petechial rash photograph (chest, axillae)
- Fat embolism pathophysiology diagram
- Gurd's criteria infographic
- CXR showing ARDS pattern
Epidemiology
Incidence
- Clinical FES: 0.5-2% of long bone fractures
- Subclinical fat embolism: Up to 90% (detectable fat in circulation, asymptomatic)
- Multiple fractures: Higher incidence
- Mortality: 5-15% (higher if ARDS develops)
Demographics
- Age: All ages; more common in young adults (trauma population)
- Sex: Male predominance (trauma epidemiology)
Risk Factors
| Risk Factor | Notes |
|---|---|
| Long bone fractures | Femur, tibia — highest risk |
| Pelvic fractures | Significant marrow content |
| Multiple fractures | Cumulative risk |
| Delayed fixation | Over 24-48h increases risk |
| Intramedullary nailing | Reaming increases risk |
| Orthopaedic surgery | Hip/knee arthroplasty |
Pathophysiology
Fat Release
- Fracture disrupts bone marrow → fat globules enter venous circulation
- Fat enters pulmonary circulation (lungs first affected)
- May cross to systemic circulation (via pulmonary shunts or directly if foramen ovale patent)
Two-Hit Hypothesis
Mechanical Theory:
- Fat globules physically obstruct pulmonary capillaries
- V/Q mismatch → hypoxaemia
Biochemical Theory:
- Fat hydrolysed to free fatty acids by lung lipase
- Free fatty acids cause:
- Endothelial damage
- Increased capillary permeability
- ARDS-like picture
- Platelet aggregation
- Coagulopathy
Neurological Involvement
- Fat emboli cross to cerebral circulation
- Cause microinfarcts, petechial haemorrhages
- Encephalopathy, confusion, coma
Petechial Rash
- Fat emboli in dermal capillaries
- Non-thrombocytopenic petechiae
- Classic distribution: Axillae, chest, conjunctivae
Clinical Presentation
Timeline
Classic Triad (All Three Present in Only ~50%)
| Feature | Frequency | Description |
|---|---|---|
| Respiratory | 75-95% | Dyspnoea, tachypnoea, hypoxia, ARDS |
| Neurological | 60-80% | Confusion, agitation, drowsiness, coma |
| Petechial rash | 20-50% | Axillae, chest, conjunctivae — pathognomonic but transient |
Other Features
Differential Diagnosis
Symptom onset
12-72 hours post-injury (rarely earlier)
Peak
24-48 hours
Clinical Examination
Systematic Assessment
Respiratory:
- Tachypnoea
- Hypoxia (SpO₂ may drop despite supplemental O₂)
- Crackles on auscultation (ARDS pattern)
Neurological:
- GCS assessment
- Confusion, agitation, drowsiness
- Focal neurological signs (uncommon)
Skin:
- Petechial rash — look in:
- Axillae
- Anterior chest
- Conjunctivae
- Neck
- Oral mucosa
- Rash may be transient (disappears within hours)
Ophthalmic:
- Fundoscopy: Cotton wool spots, retinal haemorrhages
Investigations
No Specific Diagnostic Test
Diagnosis is clinical using Gurd's criteria
Supportive Investigations
| Investigation | Findings |
|---|---|
| ABG | Hypoxaemia (PaO₂ under 60), may have respiratory alkalosis initially |
| CXR | Bilateral infiltrates (ARDS pattern) — may be initially normal |
| FBC | Thrombocytopenia (50%), anaemia |
| Coagulation | May be deranged |
| CT Head | If altered mental status — often normal; may show petechial haemorrhages |
| MRI Brain | More sensitive — "starfield" pattern of microinfarcts |
| Urinary fat globules | Neither sensitive nor specific |
| Bronchoalveolar lavage | Fat-laden macrophages (not specific) |
Classification & Staging
Gurd's Criteria (Diagnosis if ≥1 Major + ≥4 Minor, or ≥2 Major)
Major Criteria:
- Petechial rash
- Respiratory symptoms + bilateral infiltrates on CXR
- Cerebral signs unrelated to head injury
Minor Criteria:
- Tachycardia over 110/min
- Pyrexia over 38.5°C
- Retinal changes (cotton wool spots, haemorrhages)
- Jaundice
- Renal changes (oliguria)
- Anaemia (acute drop in Hb)
- Thrombocytopenia (over 50% drop)
- High ESR (over 71 mm/hr)
- Fat globules in urine/sputum
Schonfeld's FES Index
Alternative scoring system based on weighted clinical features
Management
Prevention
- Early fracture fixation (within 24 hours if possible)
- Consider damage control orthopaedics in severely injured polytrauma
- Debate on reamed vs unreamed nailing (reaming may increase fat release)
- Adequate resuscitation — avoid hypotension
Supportive Treatment
| Intervention | Details |
|---|---|
| Oxygen | Titrate to maintain SpO₂ over 94% |
| Ventilatory support | NIV, CPAP, or intubation/IPPV if required |
| IV fluids | Maintain euvolaemia |
| DVT prophylaxis | LMWH when safe |
| Monitoring | ICU for moderate-severe cases |
There Is No Specific Treatment
- Steroids: Some evidence for prophylaxis but not for treatment; routine use not recommended
- Heparin: Theoretical benefit (fat hydrolysis) but not proven; not recommended
- Albumin: No evidence
- Ethanol infusion: Theoretical (inhibits lipase) but not used
Monitoring
- Serial ABGs
- Neurological observations
- Repeat CXR
- Treat precipitating injury definitively when stable
Complications
Acute
- ARDS: May require prolonged ventilation
- Neurological sequelae: Persistent confusion, cognitive impairment
- Multi-organ failure
- DIC
Long-Term
- Most survivors recover fully
- Persistent cognitive impairment possible (especially if severe cerebral involvement)
- Rarely: Permanent neurological deficit
Prognosis & Outcomes
Mortality
- Mild FES: Under 5%
- Severe FES with ARDS: 10-20%
- Multi-organ failure: Higher mortality
Recovery
- Most patients recover fully with supportive care
- Neurological symptoms usually resolve
- Respiratory function recovers once ARDS resolves
Evidence & Guidelines
Key Guidelines
- No specific international guideline
- BOA fracture management standards mention FES prevention
- Early fracture fixation recommended by major trauma guidance
Key Evidence
- Early fixation (under 24h) for femoral fractures reduces FES incidence
- Steroids for prophylaxis: Some supportive data but not standard practice
- Damage control orthopaedics in polytrauma may reduce systemic complications
Patient & Family Information
What is Fat Embolism Syndrome?
Fat embolism syndrome can happen after breaking a large bone like the thigh bone (femur). Fat from the bone marrow gets into the bloodstream and can affect the lungs and brain.
Warning Signs
- Difficulty breathing
- Confusion or unusual behaviour
- Small red spots on the skin (chest, armpits)
Treatment
- Oxygen and breathing support
- Close monitoring in hospital
- Fixing the fracture with surgery
Outlook
Most people recover fully with treatment.
Resources
References
Primary Sources
- Gurd AR. Fat embolism: an aid to diagnosis. J Bone Joint Surg Br. 1970;52(4):732-737. PMID: 5487573
- Mellor A, Soni N. Fat embolism. Anaesthesia. 2001;56(2):145-154. PMID: 11167474
Key Studies
- Giannoudis PV, et al. Fat embolism: the reaming controversy. Injury. 2006;37 Suppl 4:S50-58. PMID: 16978631
- Akhtar S. Fat embolism. Anesthesiol Clin. 2009;27(3):533-550. PMID: 19825491