Question 16

College answer

Precipitants:                                               
Trauma-related 
Orthopaedic (most common) 
Long bone fracture (esp femur) 
Pelvic fracture 
Elective Orthopaedic surgery 
Non-orthopaedic 
Liposuction 
BM harvest/transplant 
Nontrauma-related 
Acute pancreatitis  
Sickle cell disease 
 
Clinical features                                              
Typically develops 24-72 hours following insult. 
Classic clinical triad (neurological, respiratory, cutaneous), none of which is specific for FES. 
•    Respiratory – the most common presenting feature. Dyspnoea, hypoxia, ARDS  
•    Neurological – confusion, reduced level of consciousness, seizure, focal deficit, retinal changes (petechiae) 
•    Petechial rash – usually in non-dependent areas, including neck, axillae, anterior chest, head, subconjunctiva. Only in 1/3 of cases, and often not until 3-5 days after insult. 
Other – fever, thrombocytopenia, coagulation abnormalities (incl DIC), anaemia, tachycardia, myocardial depression, renal/liver dysfunction, high ESR 
 
Diagnosis 
Based on the clinical features in the setting of known precipitant 
CXR may reveal bilateral patchy infiltrates 
No single diagnostic test – BAL sampling for lipids has been described – no other tests shown to be useful 
Several sets of diagnostic criteria proposed 
 
Management                                               
Prevention clearly preferable if possible – e.g. surgical timing (following fracture) and technique Fixation of fracture 
No specific therapy. Supportive only. 
Steroids controversial – proposed anti-inflammatory effect but limited data to support 
 

Discussion

Precipitants

• One long bone fracture: 1-3% chance
• Chance increases in proportion of number of fractures, and size of involved bones
• 33% with bilateral femoral fractures

Clinical features

Symptoms of fat embolism

• Confusion is usually the earliest symptom (60%), but seizures and focal neurological signs have also been reported (all resolve completely)
• Dyspnoea
• Tachypnoea
• Haemoptysis
• Usually, with a latent period (say, some days after the manipulation of a fracture).

Signs of fat embolism

• Respiratory features are present in 95%: moist crepitations over all lung fields, hypoxia, cyanosis. ARDS-like picture develops
• Fat globules may be seen in the sputum!
• Petechial rash (in 30-60%) - alone, enough to make the diagnosis according to Schonfelds criteria.
• Fever
• Tachycardia
• Purtscher’s retinopathy: 
  • cotton wool exudates
  • macular oedema
  • macular haemorrhage
  • retinal haemorrhages
  • visible fat droplets on ophthalmoscopy
• Jaundice
• Renal impairment
• Anaesthetists often note a sudden drop in end-tidal CO₂ concentration during a stable steady state.

Diagnosis

Laboratory features:

• Thrombocytopenia
• Anaemia (sudden decrease) -70% of patients
• High ESR
• Fat macroglobulinaemia
• Hypocalcemia (due to free fatty acids binding calcium)
• Elevated serum lipase
• DIC-like coagulopathy
• ABG: respiratory alkalosis with hypoxia and an unexplained shunt
• ECG: right heart strain, RBBB

Characteristic imaging:

• CXR: florid embolism may develop into a "flocculent" patchy widespread opacities, "snowstorm appearance".
• CT chest: non specific; focal areas of ground glass opacification
• CT brain: diffuse white-matter petechial hemorrhages consistent with microvascular injury.
• TOE: may actually catch the passing of fatty globules within the heart, but afterwards - useless.

Management:

• Specific management not supported by very strong evidence:
  • Corticosteroids
  • Aspirin
  • Heparin infusion (which supposedly encourage lipase activity and discourages the formation of platelet aggregates).
  • N-acetylcysteine (based on rat studies only)
• Boring, non-specific treatment:
  • O₂ supplementation
  • Positive pressure ventilation
  • Correction of coagulopathy
  • Replacement of platelets
  • Correction of the source problem (i.e. reduction of fractures)