Skip to content

Fat Embolisation Syndrome

Summary

fleuron

  • Systemic manifestation of fat emboli in circulation, typically following trauma
  • Classic triad: respiratory distress, neurological symptoms, petechial rash
  • Diagnosis based on clinical presentation and imaging findings, primarily chest radiographs and brain MRI

Pathophysiology

  • Two proposed mechanisms:
    • Mechanical theory: fat globules from bone marrow enter circulation through torn venous sinusoids
    • Biochemical theory: plasma mediators cause systemic inflammation and coagulopathy
  • Fat emboli obstruct capillaries in various organs, leading to:
    • Pulmonary oedema and acute respiratory distress syndrome (ARDS)
    • Cerebral ischaemia and oedema
    • Cutaneous petechiae and other systemic manifestations

Demographics

  • Most common in young adults (20-30 years old)
  • Male predominance (3:1 male to female ratio)
  • Associated with:
    • Long bone fractures (especially femur and tibia)
    • Pelvic fractures
    • Orthopaedic procedures (e.g., intramedullary nailing)
    • Rare non-traumatic causes (e.g., pancreatitis, liposuction)

Diagnosis

  • Clinical diagnosis based on Gurd's criteria:
    • Major criteria: hypoxaemia, neurological symptoms, petechial rash
    • Minor criteria: tachycardia, fever, retinal changes, renal abnormalities
  • Laboratory findings:
    • Anaemia
    • Thrombocytopenia
    • Elevated inflammatory markers (ESR, CRP)
    • Fat globules in urine or sputum (not specific)

Imaging

  • Chest radiography:
    • Bilateral, diffuse, fluffy infiltrates ('snow storm' appearance)
    • Rapid onset within 24-48 hours of injury
  • CT chest:
    • Ground-glass opacities
    • Interlobular septal thickening
    • Centrilobular nodules
  • Brain MRI:
    • T2-weighted and FLAIR: multiple, scattered, hyperintense lesions in white matter
    • Diffusion-weighted imaging (DWI): 'starfield pattern' of multiple, punctate, hyperintense lesions
    • Susceptibility-weighted imaging (SWI): may show microhaemorrhages

panels-1

  • A 25-year-old patient presented with decreased GCS after a femoral fracture.
  • MRI showed punctate T2-hyperintensities with diffusion restriction and diffuse microhaemorrhages.

Treatment

  • Supportive care is the mainstay of treatment:
    • Oxygen therapy and mechanical ventilation if needed
    • Fluid resuscitation and haemodynamic support
    • Early fracture fixation to prevent further fat embolisation
  • Pharmacological interventions (limited evidence):
    • Corticosteroids: may reduce inflammation and oedema
    • Heparin: potential benefit in preventing further embolisation
  • Experimental treatments:
    • Albumin for binding free fatty acids
    • N-acetylcysteine as an antioxidant
  • Prognosis:
    • Mortality rate: 5-15%
    • Most patients recover fully within weeks to months

Differential diagnosis

Differential Diagnosis Differentiating Feature
Diffuse axonal injury Trauma-related haemorrhagic lesions at grey-white matter junction and corpus callosum on SWI; DWI restriction less numerous and punctate than fat embolism starfield pattern
Disseminated intravascular coagulation Similar multifocal DWI and SWI lesions; associated with sepsis or systemic causes; no fat-specific distribution
Cardiogenic or septic cerebral emboli Larger embolic infarcts in arterial territories; fewer and less uniformly distributed than fat embolism starfield pattern
Cerebral vasculitis Multifocal infarcts in multiple vascular territories; vessel wall enhancement on high-resolution MRI
Haemorrhagic cerebral metastases Larger lesions with surrounding vasogenic oedema; grey-white junction location; no starfield DWI-SWI pattern
Watershed infarction Infarcts in border-zone distributions between major vascular territories; related to haemodynamic compromise