Key result
Continuous intra-arterial nimodipine infusion resulted in a favorable functional outcome (mRS ≤2) at discharge in 80% of patients with refractory cerebral vasospasm, compared to 70% treated with conventional intra-arterial nimodipine.
Why the study?
Does continuous intra-arterial nimodipine infusion improve functional outcomes at discharge in patients with refractory cerebral vasospasm after aneurysmal subarachnoid hemorrhage compared to conventional intra-arterial nimodipine?
Cohort (n=274)
No
Does continuous intra-arterial nimodipine infusion improve functional outcomes at discharge in patients with refractory cerebral vasospasm after aneurysmal subarachnoid hemorrhage compared to conventional intra-arterial nimodipine?
Absolute Event Rate: 80% vs 70%
Continuous intra-arterial nimodipine infusion may serve as a viable salvage treatment for refractory cerebral vasospasm following aneurysmal subarachnoid hemorrhage, potentially yielding favorable functional outcomes despite longer hospital stays.
May support CIAN as salvage in refractory vasospasm; leaves open need for randomized confirmation.
OBJECTIVE: Delayed cerebral ischemia (DCI) is a severe complication following aneurysmal subarachnoid hemorrhage (aSAH), potentially leading to functional impairments. Cerebral vasospasm (CVS) is one of the primary mechanisms of DCI. In cases of medically refractory CVS, intra-arterial (IA) nimodipine is a rescue treatment, but its effectiveness can be insufficient. We hypothesized that continuous IA nimodipine infusion (CIAN) could serve as a salvage treatment, and we evaluated its effectiveness and safety. METHODS: We evaluated 274 patients with aSAH admitted between October 2017 and February 2024, identifying those who received IA nimodipine and those who also received CIAN. Characteristics of the patients, length of stay, and modified Rankin scale (mRS) score at the time of discharge were compared between the conventional IA nimodipine and the CIAN groups. RESULTS: Of the 274 patients, 15 received IA nimodipine, and five of those underwent CIAN. More females were observed in the medically refractory CVS group compared with the non-refractory group (87% [13/15] vs. 66% [171/259]), but there was no sex difference between the CIAN and conventional IA nimodipine groups. CIAN was initiated at a mean of 9 days after the onset of aSAH and continued for 21-81 hours. Two complications were noted, including severe brain edema and suspected heparin-induced thrombocytopenia. However, radiological assessments showed no new lesions. The CIAN group exhibited a longer duration of abnormal findings on transcranial Doppler compared to the conventional IA group (16.0±10.1 vs. 9.4±7.9 days), as well as longer neurocritical care unit (17.4±10.1 vs. 14.1±7.0 days) and hospital stays (46.6±28.7 vs. 29.5±13.2 days). Nonetheless, more achieved a favorable outcome (mRS ≤2) in the CIAN group (80% [4/5] vs. 70% [7/10]). CONCLUSION: CIAN is a viable salvage treatment for refractory CVS, providing a prolonged vasodilatory effect compared to conventional IA nimodipine, with favorable outcomes.
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Lee et al. (2025) conducted a cohort in Refractory vasospasm after aneurysmal subarachnoid hemorrhage (n=274). Continuous intra-arterial nimodipine infusion vs. Conventional single-session intra-arterial nimodipine infusion was evaluated on Favorable outcome (mRS ≤2) at discharge. Continuous intra-arterial nimodipine infusion resulted in a favorable functional outcome (mRS ≤2) at discharge in 80% of patients with refractory cerebral vasospasm, compared to 70% treated with conventional intra-arterial nimodipine.
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