the underlying aneurysm leading to decrease of immediate complications such as rebleeding, cerebral vasospasm remains the major cause for mortality and morbidity
after subarachnoid hemorrhage. The only FDA approved drug for treatment of cerebral vasospasm is the calcium antagonist Nimodipine that has shown beneficial effects on outcome. It is safe, cost efficient and the most widely studied drug for treatment of cerebral vasospasm. But it has reported side effects such as systemic hypotension, especially when used intravenously. The present paper reports about the occurence
of severe systemic catecholamine refractory hypotension after oral application of the standard dosage of 60 mg nimodipine. In those patients we were only able to establish a sufficient arterial blood pressure after application of methylene blue suggesting that at least part of the underlying mechanism was NO related vasoplegia. Keeping in mind that vasoplegia can occur even after oral nimodipine application we suggest that there should be a test dosage of 15-30 mg nimodipine applied to evaluate the impact on each patient and avoid potential lethal hypotension.