Restricted diffusion and poor clinical outcome in cerebral fat embolism syndrome.

Cerebral fat embolism syndrome (CFES) is a neurologic syndrome occurring in up to 60% of patients with fat embolism syndrome (FES). The defining features of FES include respiratory, neurologic and dermatologic features. The classical explanation is release of fat emboli into the circulation after long bone fractures, but the clinical syndrome of FES only occurs in 0.5-3% of cases, typically within 12-72 hours1. The pathophysiologic mechanism appears to involve a combination of mechanical occlusion by fat emboli in the microvasculature, and biochemical toxicity of free fatty acids locally released from embolic material1. Neurologic presentation may include confusion, seizure, focal neurologic deficits or coma. Magnetic resonance imaging (MRI) is the diagnostic test of choice, usually demonstrating multifocal punctate lesions preferentially involving the cerebral white matter. These are hyperintense on T2-weighted images, and demonstrate enhancement on gadolinium-enhanced T1 sequences2,3. Diffusion weighted Restricted Diffusion and Poor Clinical Outcome in Cerebral Fat Embolism Syndrome