Abstract Background Acute ischemic stroke in young adults is uncommon and warrants investigation for secondary etiologies. Cocaine is a potent cerebrovascular toxin that induces vasospasm, endothelial injury, and platelet activation, leading to both ischemic and hemorrhagic events. Although mechanical thrombectomy is an established therapy for large-vessel occlusion, reperfusion in the context of cocaine-induced vasculopathy increases the risk of hemorrhagic transformation. We present a fatal case of cocaine-associated right middle cerebral artery (MCA) occlusion complicated by reperfusion hemorrhage and malignant cerebral edema. Case Presentation A 45-year-old man with no known medical history was found unresponsive at home following suspected substance use. On arrival, he was obtunded (GCS 6; E1V1M4), blood pressure 165/100 mmHg, heart rate 110 bpm, and had left gaze deviation, right flaccid hemiplegia, and anisocoria. He was immediately intubated for airway protection. Laboratory evaluation revealed mild leukocytosis and hyperglycemia; urine toxicology was positive for cocaine.Non-contrast CT head showed no acute hemorrhage. CT angiography demonstrated a right M1 MCA occlusion. CT perfusion revealed a core infarct of 28 mL and a penumbra of 90 mL with a mismatch ratio of 3.2, indicating a substantial volume of salvageable tissue. Interventional neurology was consulted, and the patient underwent urgent mechanical thrombectomy achieving partial reperfusion (TICI 2b). He was admitted to the neuro-critical care unit for close monitoring.Approximately twelve hours later, he developed progressive bradycardia, loss of brainstem reflexes, and fixed pupils. Repeat CT demonstrated extensive hemorrhagic transformation of the right MCA territory with acute subarachnoid and subdural hemorrhage, 8 mm midline shift, and descending transtentorial herniation. Neurosurgery deemed the injury non-survivable, and decompressive craniectomy or external ventricular drain placement was not pursued. Despite maximal medical therapy—mannitol, hypertonic saline, head elevation, and hyperventilation—the patient progressed to brain death within 24 hours. His family elected for organ donation. Discussion This case highlights the paradox of reperfusion in drug-induced vasculopathy. Cocaine disrupts cerebrovascular autoregulation and endothelial integrity, predisposing to reperfusion-related hemorrhage even when imaging suggests viable tissue . Careful post-procedural monitoring, blood pressure control, and early neurosurgical collaboration are essential in such high-risk cases. Conclusion Cocaine-associated large-vessel occlusion represents a unique management challenge. While CT perfusion may guide intervention, clinicians must weigh reperfusion benefits against the elevated risk of hemorrhagic conversion. Early recognition of neurological decline and prompt multidisciplinary management remain crucial, though outcomes in malignant transformation are often fatal. This abstract is funded by: None
Nazeef et al. (2026) studied this question.