Fat Embolism Syndrome

Reviewed and revised 22nd June 2014


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


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


  • 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


  • 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


  • 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 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


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


  • 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.

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.