Fat embolism syndrome (FES) occurs in long-bone fractures and classically presents with the triad of hypoxia, petechia, and altered mental status, or the criteria of Gurd and Wilson.1 The Lindeque criteria (femur fracture, pH <7.3, increased work of breathing) are also used.1,2 FES is a potentially fatal complication, with mortality rates ranging from 10% to 36%.1,3 FES typically occurs within 24 to 72 hours after initial insult, with one study finding an average of 48.5 hours after injury and an incidence of 0.15% to 2.4%.4 The overall FES rate is <1% in retrospective reviews and 11% to 29% in prospective studies.5 FES may present without one or all of the Gurd and Wilson criteria,6 and cerebral fat embolism (CFE) can be even more difficult to diagnose. Patients with CFE typically present with a wide array of postoperative neurologic deficits, commonly in the 24- to 72-hour window in which FES typically occurs. Correct diagnosis and management of CFE require a high index of suspicion and knowledge of the diagnostic work-up. In the postoperative setting, it can be difficult to distinguish CFE-related neurologic deficits from the normal sequelae of anesthesia, pain medications, and other factors.
In this article, we report the case of a 42-year-old woman who developed CFE after reamed intramedullary nail fixation of femoral and tibial shaft fractures. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 42-year-old woman with no past medical history was injured when a horse reared and fell on her. Initial emergent computed tomography (CT) was negative for intracranial hemorrhage, and injury radiographs were obtained (Figures 1A, 1B).
About 9 hours after surgery and 36 hours after injury, the patient was unresponsive. Vital signs, including oxygen saturation, were within normal limits, but she was unable to verbalize. Physical examination revealed symmetric facial musculature but also generalized weakness and diffuse hypertonicity and hyperreflexia. Initial laboratory results, including complete blood cell count, electrolyte panel, and troponin levels, were unremarkable. Naloxone was administered to rule out opioid overdose. An immediate code stroke and neurology consultation was requested. An emergent CT scan of the brain was negative; an urgent magnetic resonance imaging (MRI) scan showed multiple punctate T2/FLAIR (fluid attenuated inversion recovery) hyperintensities with restricted diffusion, predominantly in a parasagittal white matter distribution (Figure 2).
The patient slowly and steadily improved. She was verbal by postoperative day 3 (POD-3), upper motor neuron signs resolved by POD-4, encephalopathy resolved by POD-7, and she was discharged to a rehabilitation center. Unresolved post-stroke symptoms included mild visual field deficits in the right eye (20/25 vision, central scotoma) and amnesia regarding the events immediately surrounding the surgery. There were no other neurologic or cognitive deficits. The patient was non-weight-bearing on the operative extremity and ambulating with assistance, and she started range-of-motion exercises. After 1 week, she was discharged home with crutches.
The patient followed up with neurology and ophthalmology for routine post-stroke care. At 2- and 6-month neurology follow-ups, she was still amnestic regarding her acute stroke event but did not exhibit any confusion, memory problems, speech deficits, facial droop, headaches, or weakness. According to neurology, the encephalopathy was completely resolved, and the patient was completely recovered from the event. Levetiracetam and aspirin were discontinued at 2 months. At the 2-month ophthalmology follow-up, the patient had 20/20 vision in both eyes and nearly complete resolution of the central scotoma. Ophthalmology confirmed symptom relief and recommended return to routine eye care and 1-year follow-up.
The patient began weight-bearing as tolerated on POD-14 and had no hardware or other complications. At 6-month orthopedics follow-up, range of motion of the affected knee was 0° to 120°, and rotation, length, and varus/valgus and anteroposterior knee laxity were all symmetric to the contralateral extremity. The patient walked with a cane for balance and had a mild limp. The affected thigh still had mild atrophy, but strength was 5/5 throughout. The patient denied pain or hardware sensitivity in the affected extremity and was very pleased with the result.