Aneurysm rupture

When an aneurysm ruptures, blood flows into the subarachnoid space. Patients may experience sudden onset of severe headache (often described as “the worst headache of my life”), altered level of consciousness, focal or global neurologic deficits, or coma, depending on the location and magnitude of the bleed. As the blood spreads in the subarachnoid space, signs of meningismus become evident. Obstructive hydrocephalus and increased ICP may occur. Categorizing the severity of rupture is achieved using the Hunt-Hess classification system, which is based on a 5-grade scoring scale. Grades 1 and 2 are associated with increasing headache, and grades 3 and 4, with increasing neurologic deficits; grade 5 signifies deep coma. Latter grades are associated with worse outcomes. Definitive diagnosis is made with imaging of the head (i.e., computed tomography or magnetic resonance imaging) or cerebral angiography.

Major causes of morbidity and death include rebleeding, cerebral vasospasm, and obstructive hydrocephalus. The worst among these causes continues to be vasospasm, the exact cause of which is unknown. If vasospasm is left untreated, permanent neurologic damage from ischemia is likely to occur. Vasospasm usually manifests at about 72 h after the rupture of the aneurysm. The initial clinical diagnosis of cerebral vasospasm is made with changes in neurologic status. Definitive diagnosis can be made with transcranial Doppler ultrasonography. Reference velocities are less than 120 cm/sec; velocities greater than this value are an indication that intracranial vessels are constricting.

Nimodipine is the standard drug used to manage vasospasm because it improves collateral blood flow (Table 134-1); however, it does not relieve the vasospasm of the main vessel. Optimal management entails the use of hypertension, hydration, and hemodilution (triple-H therapy) to overcome the vasospasm, which usually lasts for up to 14 days.