Subarachnoid Hemorrhage

Aneurysmal subarachnoid hemorrhage (aSAH) occurs when a cerebral aneurysm (most commonly at the anterior communicating artery, posterior communicating artery, or MCA bifurcation) ruptures, flooding the subarachnoid space with arterial blood. The initial hemorrhage causes a transient spike in ICP approaching MAP, producing transient global cerebral ischemia (causing the 'thunderclap headache' and frequent LOC). Blood in the subarachnoid space triggers inflammatory cascades: oxyhemoglobin breakdown products cause endothelial dysfunction and free radical damage. Cerebral vasospasm peaks at days 4-14 (delayed cerebral ischemia [DCI]) through multiple mechanisms: nitric oxide scavenging by free hemoglobin, endothelin-1 upregulation, inflammation-mediated vessel narrowing, and cortical spreading depolarizations. DCI is the leading cause of morbidity in SAH survivors and occurs in ~30% of patients. Additional complications include acute hydrocephalus (blood obstructing CSF drainage), rebleeding (4-12% in first 24 hours without treatment), cardiac stunning (neurogenic stunned myocardium), and neurogenic pulmonary edema from catecholamine surge.