With regard to fat embolism syndrome (FES), outline the precipitants, clinical features, diagnosis and management
Orthopaedic (most common)
Long bone fracture (esp femur)
Elective Orthopaedic surgery
Sickle cell disease
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
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
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
|Traumatic||Unrelated to trauma|
- 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
Symptoms of fat embolism
- Confusion is usually the earliest symptom (60%), but seizures and focal neurological signs have also been reported (all resolve completely)
- 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.
- Purtscher’s retinopathy:
- cotton wool exudates
- macular oedema
- macular haemorrhage
- retinal haemorrhages
- visible fat droplets on ophthalmoscopy
- Renal impairment
- Anaesthetists often note a sudden drop in end-tidal CO2 concentration during a stable steady state.
- 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
- 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.
- Specific management not supported by very strong evidence:
- 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)
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