Fat Embolism Syndrome

Reviewed and revised 22nd June 2014

OVERVIEW

A syndrome caused by systemic embolisation of fat globules released into the circulation following trauma or surgical procedures

PATHOGENESIS

Mechanical theory

• fat globules embolise throughout circulation causing microvascular occlusion
• causes ischaemia and microvascular injury
• in pulmonary capillaries this leads to pulmonary hypertension and increased RV pressure

Toxic intermediaries theory

• embolised fat degraded in plasma to several products including FFAs
• results in production of toxic metabolites & agglutination/degradation of fat emboli

CLINICAL FEATURES

• variable!
• typically develops within 24-72 hours post injury
• associated with trauma or surgery

• RESP – hypoxia, hypotension, sudden tachypnoea, haemoptysis, crackles, globules of fat in sputum
• NEURO – confusion, drowsiness, seizures, retinal exudates
• CVS – tachycardia, myocardial depression, right heart strain
• SKIN – petechial rash (conjunctival, anterior chest, axillae)
• HAEM – DIC, anaemia (e.g. due to alveolar haemorrhage)
• RENAL – oliguria, lipiduria, proteinuria, haematuria
• HEPATIC – jaundice
• METABOLIC – fever

Classic Triad

1. respiratory compromise
2. neurological abnormalities – transient and usually reversible
3. petechial rash ((distribution is related to fat particles floating in the aortic arch, like oil in water and embolized to non dependent skin areas via aortic arch vessels (subclavian or carotid arteries))

Risk Factors

• long bone & pelvic #
• IM nails
• hip or knee arthroplasty
• DM
• soft tissue injury
• liposuction
• bone marrow harvest
• burns
• acute pancreatitis
• sickle cell crisis
• TPN infusion

• difficult to diagnose
• Gurd, Lindeques and Schonfeld criteria may be used for diagnosis

INVESTIGATIONS

• Thrombocytopenia, anemia, hypofibrinogenemia, and increased  ESR (non-specific findings)
• sudden decrease in Hb by 20% may be seen
• fat globules (urine, blood, sputum, BAL  – either free or within macrophages) (insensitive test)
• coagulopathy
• large A-a gradient
• CXR: diffuse bilateral opacitities
• CT chest may be normal
• MRI brain: may show typical white matter changes along the boundary zones of major vascular territories
• Showers of bone marrow fat globules may be seen on TOE intra-operatively in conjunction with episodes of desaturation

GURD CRITERIA

• Diagnosis requires the presence of at least one major criteria and at least four minor criteria

Major criteria

• petechiae
• high A-a gradient
• CNS depression
• pulmonary oedema

Minor criteria

• tachycardia
• low grade temperature
• retinal emboli
• fat in urine or sputum
• decreased HCT
• thrombocytopaenia
• increased ESR

MANAGEMENT

Management is supportive

• immobilize fracture
• optimise oxygenation
• protective lung ventilation
• avoid hypovolemia (some use albumin based fluids as albumin binds free fatty acids)
• DVT and peptic ulcer prophylaxis
• these therapies have been suggested but are considered ineffective: steroids, heparin, alcohol, and dextran

Prevention

• early surgery
• avoidance of intermedullary fixation
• limiting elevation of intramedullary pressure (venting holes)
• ?aspirin or heparin (unclear)
• ? methylprednisolone (unclear)

PROGNOSIS

• uncertain as often clouded by coexistent disease processes
• overall mortality 5-15%
• fulminant form with acute cor pulmonale, respiratory failure, and/or embolic phenomena may lead to death within  hours
• acute symptoms typically resolves over days-to-weeks in survivors
• persistent neurological deficits may occur
• longterm pulmonary sequelae, like ARDS, typically resolve within a year

References and Links

• Akhtar S. Fat embolism. Anesthesiol Clin. 2009 Sep;27(3):533-50, table of contents. doi: 10.1016/j.anclin.2009.07.018. PMID: 19825491.
• Shaikh N. Emergency management of fat embolism syndrome. J Emerg Trauma Shock. 2009 Jan;2(1):29-33. PMC2700578.
• Shaikh N, Parchani A, Bhat V, Kattren MA. Fat embolism syndrome: clinical and imaging considerations: case report and review of literature. Indian J Crit Care Med. 2008 Jan;12(1):32-6. PMC2760911.