2014•Neurosurgery QuarterlyRequires access

Ischemic Lesion on Computed Tomography after Subarachnoid Hemorrhage

Vladimir Vrsajkov, Jasna Jevđić, Dunja M. Mihajlović, Vesna Pajtić, Aleksandra Lazukić, Jelena Pantić-Vrsajkov

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Abstract

Objective: The aim of our study was to evaluate the frequency of angiographic vasospasm and computed tomography (CT) detectable cerebral ischemia after subarachnoid hemorrhage, the relationship between these events, and the impact on outcome. Patients and Methods: We prospective enrolled 54 patients with subarachnoid hemorrhage treated from March 2011 to January 2013. CT and CT angiography of brain were obtained on the ninth day of rupture regardless of neurological status. The control brain CT and CT angiography were obtained earlier if clinical symptoms implied delayed cerebral ischemia. The outcome was assessed after 6 months using the extended Glasgow Outcome scale scale. Results: Fifty-four percent of the patients recruited had CT angiography vasospasm and 46% had cerebral ischemia on CT scans. Our study shows a strong correlation between angiographic vasospasm and cerebral ischemia visible on CT (P=0.001) and severity of vasospasm and frequency of ischemia (P=0.03). Twenty percent of the patients showed ischemia with no demonstrable vasospasm confirming multiple cause of delayed cerebral ischemia. Logistic regression model has shown the strong impact of angiographic vasospasm (P=0.004, odds ratio=6.85; 95% confidence interval, 1.83-26.65) and arterial hypertension (P=0.02, odds ratio=4.32; 95% confidence interval, 1.16-16.01) on the development of cerebral ischemia. Angiographic vasospasm (P=0.01) and cerebral ischemia (P=0.005) were associated with worse 6-month outcome. Conclusion: A strong association exists between angiographic vasospasm and cerebral ischemia on CT although some ischemia occurs in area without vasospasm.

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Objective: The aim of our study was to evaluate the frequency of angiographic vasospasm and computed tomography (CT) detectable cerebral ischemia after subarachnoid hemorrhage, the relationship between these events, and the impact on outcome. Patients and Methods: We prospective enrolled 54 patients with subarachnoid hemorrhage treated from March 2011 to January 2013. CT and CT angiography of brain were obtained on the ninth day of rupture regardless of neurological status. The control brain CT and CT angiography were obtained earlier if clinical symptoms implied delayed cerebral ischemia. The outcome was assessed after 6 months using the extended Glasgow Outcome scale scale. Results: Fifty-four percent of the patients recruited had CT angiography vasospasm and 46% had cerebral ischemia on CT scans. Our study shows a strong correlation between angiographic vasospasm and cerebral ischemia visible on CT (P=0.001) and severity of vasospasm and frequency of ischemia (P=0.03). Twenty percent of the patients showed ischemia with no demonstrable vasospasm confirming multiple cause of delayed cerebral ischemia. Logistic regression model has shown the strong impact of angiographic vasospasm (P=0.004, odds ratio=6.85; 95% confidence interval, 1.83-26.65) and arterial hypertension (P=0.02, odds ratio=4.32; 95% confidence interval, 1.16-16.01) on the development of cerebral ischemia. Angiographic vasospasm (P=0.01) and cerebral ischemia (P=0.005) were associated with worse 6-month outcome. Conclusion: A strong association exists between angiographic vasospasm and cerebral ischemia on CT although some ischemia occurs in area without vasospasm.

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Available abstract

Objective: The aim of our study was to evaluate the frequency of angiographic vasospasm and computed tomography (CT) detectable cerebral ischemia after subarachnoid hemorrhage, the relationship between these events, and the impact on outcome. Patients and Methods: We prospective enrolled 54 patients with subarachnoid hemorrhage treated from March 2011 to January 2013. CT and CT angiography of brain were obtained on the ninth day of rupture regardless of neurological status. The control brain CT and CT angiography were obtained earlier if clinical symptoms implied delayed cerebral ischemia. The outcome was assessed after 6 months using the extended Glasgow Outcome scale scale. Results: Fifty-four percent of the patients recruited had CT angiography vasospasm and 46% had cerebral ischemia on CT scans. Our study shows a strong correlation between angiographic vasospasm and cerebral ischemia visible on CT (P=0.001) and severity of vasospasm and frequency of ischemia (P=0.03). Twenty percent of the patients showed ischemia with no demonstrable vasospasm confirming multiple cause of delayed cerebral ischemia. Logistic regression model has shown the strong impact of angiographic vasospasm (P=0.004, odds ratio=6.85; 95% confidence interval, 1.83-26.65) and arterial hypertension (P=0.02, odds ratio=4.32; 95% confidence interval, 1.16-16.01) on the development of cerebral ischemia. Angiographic vasospasm (P=0.01) and cerebral ischemia (P=0.005) were associated with worse 6-month outcome. Conclusion: A strong association exists between angiographic vasospasm and cerebral ischemia on CT although some ischemia occurs in area without vasospasm.

Key concepts: Medicine, Vasospasm, Subarachnoid hemorrhage, Ischemia, Cerebral vasospasm, Odds ratio, Angiography, Confidence interval

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