Aneurysmal Subarachnoid Hemorrhage: Strategies for Preventing Vasospasm in the Intensive Care Unit

Michael N. Diringer, MD; Allyson R. Zazulia, MD


Semin Respir Crit Care Med. 2017;38(6):760-767. 

In This Article

Abstract and Introduction


This article addresses the intensive care unit (ICU) management of patients with aneurysmal subarachnoid hemorrhage (SAH), with an emphasis on the prevention of cerebral vasospasm and delayed cerebral ischemia (DCI), which are major contributors to morbidity and mortality. Interventions addressing various steps in the development of vasospasm have been attempted, with variable success. Enteral nimodipine remains the only approved measure to potentially prevent DCI. Since oral and intravenous administrations are limited by hypotension, direct administration via sustained-release pellets and intraventricular administration of sustained-release microparticles are being investigated. Studies of other calcium channel blockers have been disappointing. Efforts to remove blood from the subarachnoid space via cisternal irrigation, cisternal or ventricular thrombolysis, and lumbar cerebrospinal fluid drainage have met with limited and variable success, and they remain an area of active investigation. Several interventions that had early promise have failed to show benefit when studied in large trials; these include tirilazad, magnesium, statins, clazosentan, transluminal angioplasty, and hypervolemia.


Subarachnoid hemorrhage (SAH) refers to bleeding that occurs primarily within the subarachnoid space. The most common cause of SAH is trauma, but among cases of spontaneous SAH, rupture of an intracranial saccular aneurysm accounts for approximately 85%.[1] Other causes of spontaneous SAH include bleeding from arteriovenous malformations, moyamoya syndrome, bleeding disorders, cocaine and stimulant abuse, and extension of intracerebral hematomas. In up to one-fifth of cases, no source of bleeding is identified.[2]

Acute aneurysmal SAH results from the sudden extrusion of blood from a defect in the wall of an arterial aneurysm. The duration of the bleeding event determines the impact of the primary injury, and ranges from a severe headache to syncope to sudden death in about a quarter of patients.[3] The amount of blood in the subarachnoid space sets the stage for secondary injury from hydrocephalus,[4] vasospasm, and delayed cerebral ischemia (DCI).[5,6] The focus of treatment is anticipating, preventing, and managing these secondary complications.

In addition to the neurologic consequences of SAH, intense activation of the sympathetic nervous system occurs, which can produce a variety of extracranial consequences including hypertension, stunned myocardium,[7] neurogenic pulmonary edema,[8] abnormal renal function, and systemic inflammatory response syndrome (SIRS).[9]