Fat Embolism Syndrome

Fat embolism syndrome is a serious consequence of embolisation of fat globules:

Epidemiology and Risk Factors

Primary risk factor is number of fractures:

  • Single long bone fracture
    1-3%.
  • Bifemoral fractures
    Up to 33%.

Pathophysiology

Two major mechanisms of injury:

  • Mechanical
    Mechanical obstruction of capillary beds, which explains:
    • Right heart dysfunction
    • Paradoxical embolism
  • Biochemical
    Degradation of fat into pathogenic free fatty acids, which explains:
    • Delayed presentation
    • ARDS
    • Cardiac dysfunction

Aetiology

Majority are trauma related, and include:

  • Marrow-containing bone fractures
    • Long bone
    • Pelvis
  • Orthopaedic surgery
  • Fat injury
    • Burns

Non-trauma related:

  • Bone related
    • Bone marrow transplant
    • Bone tumour lyses
    • Osteonecrosis
  • Fat related
    • Liposuction
    • Pancreatitis
  • Other
    • DM
    • Steroid therapy
    • Fatty liver disease
    • Haemoglobinopathies
      • Sickle-cell

Clinical Manifestations

Presentation usually:

  • Occurs 12-72 hours after injury
    May occur up to 2 weeks.
  • Classical triad of hypoxia, neurological findings, and rash
  • Respiratory changes
    Due to pulmonary embolism.
    • Dyspnoea
    • Tachypnoea
    • Hypoxaemia
  • CVS changes
    • Obstructive shock
    • Right heart dysfunction
  • Neurological features
    Due to cerebral embolism. Heterogenous appearance:
    • Confusion
    • Drowsiness
    • Seizures
  • Haematological
    • Anaemia
    • Thrombocytopaenia
    • Petechiae
      • Red-brown rash
      • Occurring in ~33% of cases
      • In non-dependent regions
      • Due to:
        • Microvascular haemorrhage
        • Paradoxical embolism

Diagnostic Approach and DDx

Differential diagnoses include:

  • Other sources of embolism
    • PE
    • AFE
    • Tumour embolism
    • Foreign body embolism
    • Air embolism
  • Pulmonary oedema
    • Pneumonia
    • Heart failure
    • ARDS
  • Vasculitis

Investigations

None are diagnostic:

  • Bloods
    • FBE
      • Anaemia
      • Thrombocytopaenia
    • UECs
      • Hypocalcaemia
        Due to free fatty acid binding.
  • CXR
    May reflect developing ARDS.
  • CR chest
    Focal ground glass opacification.
  • MRI Brain

Notably, aspiration of fat from a wedged PAC is neither sensitive nor specific.

Management

Preventative:

  • Medullary venting hole drilled prior to reaming
    Reduced major embolic events on TOE.
  • Early fixation of fractures

Therapeutic is entirely supportive:

  • ABC approach
  • Maintain adequate oxygenation and ventilation
  • Right heart support

Marginal and Ineffective Therapies

Include:

  • Methylprednisolone prophylaxis
    • 1.5mg/kg IV Q8H for 7 doses
    • Hypothesised to reduce perivascular haemorrhage
    • No RCT evidence supporting use
  • Heparin
    Theorised to remove lipaemia by stimulating lipase activity.

Complications

Include:

  • Death
    5-15%, usually due to:
    • Respiratory failure
    • Obstructive shock
    • Brian death

Prognosis

Most recover spontaneously.

References

  1. Gupta A, Reilly CS. Fat embolism. Contin Educ Anaesth Crit Care Pain. 2007 Oct 1;7(5):148–51.