High-Dose Intra-Arterial Nicardipine Results in Hypotension Following Vasospasm Treatment in Subarachnoid Hemorrhage

Abstract

Intra-arterial (IA) nicardipine is often used to treat cerebral vasospasm associated with subarachnoid hemorrhage (SAH). While hypotension has been noted to be a dose-limiting side effect of intravenous infusions, this has seldom been reported for IA administration. We reviewed a consecutive series of patients who received IA nicardipine for SAH-associated vasospasm. Nicardipine was titrated to angiographic response, with blood pressure and intracranial pressure monitoring. We analyzed data using Wilcoxon signed rank, Student's t-test, Spearman's correlation, and χ(2) statistics as appropriate. A P value <0.05 was considered significant. Thirty patients underwent 50 procedures in which nicardipine was the sole chemical vasodilator (median dose, 15mg). Median mean arterial pressures (MAP) decreased from 118 to 100mmHg (P<0.001), with an intra-operative low of 80mmHg. Both intra-operative and post-operative decreases in MAP were directly related to nicardipine dose (r (s)=0.352, P=0.022 and r (s)=0.308, P=0.047, respectively). Hypotension (MAP<70mmHg) occurred in 22%, and 44% required initiation of or increases in vasopressor therapy. After the first treatment, 11 of 16 patients treated with vasodilator therapy alone, and 5 of 14 patients who underwent additional balloon angioplasty (68.8 vs. 35.7%, P=0.141), required further endovascular treatments due to recurrent vasospasm on subsequent days. Intra-arterial nicardipine is associated with significant intra-operative blood pressure lowering, an increased requirement for intra-operative vasopressor therapy, and a tendency toward re-treatment when used as initial monotherapy for vasospasm.