We present a case of severe neurologic decline secondary to paradoxical cerebral fat embolism (CFE) following bilateral femur fractures after a road traffic accident (RTA).

Fat embolism syndrome (FES) is a triad of petechial rash, deteriorating mental status and progressive respiratory insufficiency, caused by embolization of fat particles into multiple organs. When neurological signs and symptoms predominate, cerebral fat embolism must be kept high in differential. It usually occurs within 24–72 hours of trauma with traumatic long-bone fractures or an orthopedic surgery. Its incidence ranges from 0.9-11% with a mean mortality rate around 10%. Pathophysiology involves either paradoxical embolism or lung filtration. 

Case report. 

17-year-old, boy with type 1 diabetes mellitus, presents after having a RTA resulting in bilateral femoral and L1 spine burst fractures with mesenteric contusions. On scene, he had a self-resolving loss of consciousness followed by GCS 14 in ER with some confusion and unremarkable CT head. Had gradual improvement throughout the day, being more conversant within 24 hours. Later, he suddenly developed paroxysmal sympathetic hyperactivity with GCS 7 and normal CT head, followed 2 hours later by episodes concerning for decorticate posturing, requiring Lorazepam and Levetiracetam load with maintenance. He underwent internal fixation and intubated subsequently the next day. MRI brain obtained within 48 hours showed “starfield pattern” on DWI sequence, characteristic for CFE. Echocardiography showed patent foramen ovale. Mental status improved gradually over two-weeks with ability to follow simple commands. Managed supportively, underwent tracheostomy and peg-tube placement and transferred to a rehab hospital. 

FES complicated with CFE is an uncommon, but fatal sequela of RTA. A missed diagnosis of neurologic dysfunction due to CFE may inappropriately guide assessment of patient’s prognosis and subsequently decisions regarding escalation or even withdrawal of care.