BACKGROUND: Delayed cerebral ischemia is common after aneurysmal subarachnoid hemorrhage (aSAH) and is a major contributor to poor outcome. Yet, although generally attributed to arterial vasospasm, neurological deterioration may also occur in the absence of vasospasm.
OBJECTIVE: To determine the relationship between delayed infarction and angiographic vasospasm and compare the characteristics of infarcts related to vasospasm vs those unrelated.
METHODS: A retrospective review of patients with aSAH admitted from July 2007 through June 2011. Patients were included if they were admitted within 48 hours of SAH, had a computed tomography scan both 24 to 48 hours following aneurysm treatment and ≥7 days after SAH, and had a catheter angiogram to evaluate for vasospasm. Delayed infarcts seen on late computed tomography but not postprocedurally were attributed to vasospasm if there was moderate or severe vasospasm in the corresponding vascular territory on angiography. Infarct volume was measured by perimeter tracing.
RESULTS: Of 276 aSAH survivors, 134 had all imaging requisite for inclusion. Fifty-four (34%) had moderate or severe vasospasm, of whom 17 (31%) had delayed infarcts, compared with only 3 (4%) of 80 patients without vasospasm (P < .001). There were a total of 29 delayed infarcts in these 20 patients; 21 were in a territory with angiographic vasospasm, but 8 (28%) were not. Infarct volume did not differ between vasospasm-related (18 ± 25 mL) and vasospasm-unrelated (11 ± 12 mL) infarcts (P = .54), but infarcts in the absence of vasospasm were more likely watershed (50% vs 10%, P = .03).
CONCLUSION: Delayed infarcts following aSAH can occur in territories without angiographic vasospasm and are more likely watershed in distribution.
ABBREVIATIONS: ACA, anterior cerebral artery
aSAH, aneurysmal subarachnoid hemorrhage
CSD, cortical spreading depression
DCI, delayed cerebral ischemia
Neurocritical Care Section, Department of Neurology, Washington University School of Medicine, Saint Louis, Missouri
Correspondence: Michael N. Diringer, MD, Neurocritical Care Section, Department of Neurology, Washington University School of Medicine, 660 South Euclid, Campus Box 8111, St. Louis, MO 63110. E-mail: email@example.com
Received September 13, 2012
Accepted December 11, 2012