• Neurocritical care · Jan 2007

    Cerebral infarction associated with acute subarachnoid hemorrhage.

    • J Michael Schmidt, Fred Rincon, Andres Fernandez, Charles Resor, Robert G Kowalski, Jan Claassen, E Sander Connolly, Brian-Fred M Fitzsimmons, and Stephan A Mayer.
    • Neurological Intensive Care Unit, Division of Stroke and Critical Care, Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
    • Neurocrit Care. 2007 Jan 1; 7 (1): 10-7.

    BackgroundCerebral infarction is a common complication of aneurysmal subarachnoid hemorrhage (SAH), but usually occurs several days after onset as a complication of vasospasm or aneurysm repair. The frequency, causes, and clinical impact of acute infarction associated with the primary hemorrhage are poorly understood.MethodsWe evaluated the presence of cerebral infarction on admission CT in 487 patients admitted within 3 days of SAH onset to our center between July 1996 and September 2002. Infarctions due to angiography or treatment complications were rigorously excluded. Outcome at 3 months was assessed with the modified Rankin Scale.ResultsA total of 17 patients (3%) had acute infarction on admission CT; eight had solitary and nine had multiple infarcts. Solitary infarcts usually appeared in the vascular territory distal to the ruptured aneurysm, whereas multiple infarcts tended to be territorial and symmetric. Global cerebral edema (P < 0.001), coma on presentation (P = 0.001), intraventricular hemorrhage (P = 0.002), elevated APACHE-II physiological subscores (P = 0.026) and loss of consciousness at onset (P = 0.029) were associated with early cerebral infarction. Mortality (P = 0.003) and death or moderate-to-severe disability (mRS 4-6, P = 0.01) occurred more frequently in the early cerebral infarction group.ConclusionsEarly cerebral infarction on CT is a rare but devastating complication of acute SAH. The observed associations with coma, global cerebral edema, intraventricular hemorrhage, and loss of consciousness at onset suggest that intracranial circulatory arrest may play a role in the pathogenesis of this disorder.

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