Background:
The classic triad of fat embolism syndrome consists of pulmonary distress, mental status change, and petechial rash. Typically, symptoms manifest 24–48 hours after a long bone fracture, but case reports have demonstrated fat embolism syndrome without long bone fracture. These cases are initiated by a stress response, mobilizing free fatty acids into the circulation.
Case Description:
Herein, we present the case of a 70-year-old male who presented with the left-sided hemiparesis and was subsequently found to have tandem lesions of the right internal carotid artery (ICA) and right middle cerebral artery (MCA) warranting emergent mechanical thrombectomy (MT). The ensuing pathology report determined the source of ischemic stroke to be caused by fat embolism, a rare and intriguing case of cryptogenic large vessel occlusion (LVO) with unique features distinguishing it from other reports in the literature.
Conclusion:
According to the biochemical theory, a catecholamine surge can precipitate fat globules forming in the circulatory system, leading to tissue hypoxia, injury, and ischemia. While the majority of cerebral fat emboli cause reversible ischemia of small diameter vessels, our case presents with LVO and tandem lesions in both the ICA and MCA resulting in infarct and residual hemiparesis.
Cerebral fat embolism syndrome after long bone fracture: A case report
