BACKGROUND AND PURPOSE: Delayed cerebral infarction (DCI) is an important cause of poor outcome after subarachnoid hemorrhage. Cerebral perfusion is a predictor for DCI. Because acute hydrocephalus may impair cerebral perfusion, we evaluated the predictive value of the extent of acute hydrocephalus on the development of DCI. METHODS: We retrieved data on 321 patients admitted within 4 days after aneurysmal subarachnoid hemorrhage from our prospectively collected database. Ventricular enlargement was quantified by measuring the bicaudate index and the width of the third ventricle. Ventricular sizes were analyzed as continuous variables and after categorization into quartiles. The relationship between these variables and the development of DCI was analyzed by means of the Cox proportional hazards model. RESULTS: DCI occurred in 76 patients (23.7%). Hazard ratios for occurrence of DCI of the continuous variables were 1.01 (95% CI: 0.97 to 1.06) for the bicaudate index, 1.00 (95% CI: 1.00 to 1.01) for the age-adjusted bicaudate index, and 0.99 (95% CI: 0.92 to 1.06) for the width of the third ventricle in univariable analysis. The adjusted hazard ratio for the highest quartile of the bicaudate index versus the lowest quartile was 0.9 (95% CI: 0.5 to 1.8). No linear trend could be recognized in consecutive quartiles. CONCLUSIONS: Acute hydrocephalus is not a risk factor for occurrence of DCI, even when the extent of hydrocephalus is taken into account. However, we cannot exclude the possibility that extensive hydrocephalus leading to coma does increase the risk for DCI if no therapeutic intervention were done.
BACKGROUND AND PURPOSE:Delayed cerebral infarction (DCI) is an important cause of poor outcome after subarachnoid hemorrhage. Cerebral perfusion is a predictor for DCI. Because acute hydrocephalus may impair cerebral perfusion, we evaluated the predictive value of the extent of acute hydrocephalus on the development of DCI. METHODS: We retrieved data on 321 patients admitted within 4 days after aneurysmal subarachnoid hemorrhage from our prospectively collected database. Ventricular enlargement was quantified by measuring the bicaudate index and the width of the third ventricle. Ventricular sizes were analyzed as continuous variables and after categorization into quartiles. The relationship between these variables and the development of DCI was analyzed by means of the Cox proportional hazards model. RESULTS:DCI occurred in 76 patients (23.7%). Hazard ratios for occurrence of DCI of the continuous variables were 1.01 (95% CI: 0.97 to 1.06) for the bicaudate index, 1.00 (95% CI: 1.00 to 1.01) for the age-adjusted bicaudate index, and 0.99 (95% CI: 0.92 to 1.06) for the width of the third ventricle in univariable analysis. The adjusted hazard ratio for the highest quartile of the bicaudate index versus the lowest quartile was 0.9 (95% CI: 0.5 to 1.8). No linear trend could be recognized in consecutive quartiles. CONCLUSIONS: Acute hydrocephalus is not a risk factor for occurrence of DCI, even when the extent of hydrocephalus is taken into account. However, we cannot exclude the possibility that extensive hydrocephalus leading to coma does increase the risk for DCI if no therapeutic intervention were done.