High-Dose Intra-Arterial Nicardipine Results in Hypotension Following Vasospasm Treatment in Subarachnoid Hemorrhage
- First Online:
- Cite this article as:
- Rosenberg, N., Lazzaro, M.A., Lopes, D.K. et al. Neurocrit Care (2011) 15: 400. doi:10.1007/s12028-011-9537-4
- 234 Downloads
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 χ2 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, 15 mg). Median mean arterial pressures (MAP) decreased from 118 to 100 mmHg (P < 0.001), with an intra-operative low of 80 mmHg. Both intra-operative and post-operative decreases in MAP were directly related to nicardipine dose (rs = 0.352, P = 0.022 and rs = 0.308, P = 0.047, respectively). Hypotension (MAP < 70 mmHg) 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.