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Rescue of Nimodipine-Induced Refractory Vasoplegia With Hydroxocobalamin in Subarachnoid Hemorrhage: A Case Report.
Critical care explorations. 2020 October
BACKGROUND: We report a case of refractory vasoplegia after nimodipine administration that was unresponsive to triple vasopressor therapy and was rescued by IV hydroxocobalamin.
CASE SUMMARY: An 84-year-old male presented comatose from a subarachnoid hemorrhage and developed severe hypotension unresponsive to three vasopressors following a single dose of enteral nimodipine. Multisystem point-of-care ultrasonography ruled out alternate etiologies of shock, indicating that this was likely a vasoplegic state caused by nimodipine. We administered 5 grams of IV hydroxocobalamin over 15 minutes due to the possibility of impaired nitric oxide metabolism as the driver of vasoplegia. This led to immediate improvement in hemodynamics and rapid discontinuation of vasopressors. The patient experienced chromaturia but no other adverse effects due to hydroxocobalamin.
CONCLUSIONS: Nimodipine administration is a standard practice for patients with aneurysmal subarachnoid hemorrhage to reduce unfavorable outcomes from cerebral vasospasm. Although mild hypotension is a common side effect of nimodipine, in rare cases, it may become profound, leading to refractory vasoplegia. There is no evidence-base for reversal agents for nimodipine-induced vasoplegia, and this case is the first to demonstrate successful use of hydroxocobalamin as a potential rescue therapy. We also propose an algorithm for treatment of vasoplegia with consideration of medications that act on nitric oxide-mediated vasodilation and their side-effect profiles.
CASE SUMMARY: An 84-year-old male presented comatose from a subarachnoid hemorrhage and developed severe hypotension unresponsive to three vasopressors following a single dose of enteral nimodipine. Multisystem point-of-care ultrasonography ruled out alternate etiologies of shock, indicating that this was likely a vasoplegic state caused by nimodipine. We administered 5 grams of IV hydroxocobalamin over 15 minutes due to the possibility of impaired nitric oxide metabolism as the driver of vasoplegia. This led to immediate improvement in hemodynamics and rapid discontinuation of vasopressors. The patient experienced chromaturia but no other adverse effects due to hydroxocobalamin.
CONCLUSIONS: Nimodipine administration is a standard practice for patients with aneurysmal subarachnoid hemorrhage to reduce unfavorable outcomes from cerebral vasospasm. Although mild hypotension is a common side effect of nimodipine, in rare cases, it may become profound, leading to refractory vasoplegia. There is no evidence-base for reversal agents for nimodipine-induced vasoplegia, and this case is the first to demonstrate successful use of hydroxocobalamin as a potential rescue therapy. We also propose an algorithm for treatment of vasoplegia with consideration of medications that act on nitric oxide-mediated vasodilation and their side-effect profiles.
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