Refractory Vasoplegia Following Nimodipine Administration in Aneurysmal Subarachnoid Hemorrhage: A Case Series

Introduction: Following aneurysmal subarachnoid hemorrhage (aSAH), approximately 30% of patients experience delayed cerebral ischemia (DCI). Nimodipine, a cerebroselective dihydropyridine calcium channel blocker, reduces this risk of DCI with <5% of patients experiencing hypotension or bradycardia. We review four patients admitted to our Neurosciences Intensive Care Unit following aSAH who developed nimodipine-induced refractory vasoplegia. We discuss these four cases and detail the interventions used to counter their bradycardia and hypotension. Methods: We performed a retrospective chart review to examine vasopressor use and interventions required to combat hypotension and bradycardia as well as patient demographics and comorbidities to identify risk factors for nimodipine-induced vasoplegia. Similar case studies were reviewed. We performed a literature search to suggest treatment options for nimodipine toxicity and assess the risk of Nimodipine dose adjustments in possibly increasing DCI occurrence. Results: Patients required 6.5 medications on average to treat vasoplegia. Transvenous pacing and intubation were required for two patients. On average, vasoplegia lasted 18 hours and patients were slowly weaned off vasopressors. Risk factors for vasoplegia include liver and kidney disease. Nimodipine formulation may contribute to vasoplegia. Dose adjustments of nimodipine may increase risk of DCI. Conclusion: In our literature review, nimodipine is generally well-tolerated and reduces DCI. Mild to moderate hypotension requiring vasopressor support should be expected. In cases of refractory vasoplegia resulting in cardiovascular collapse, we recommend cessation of nimodipine and treating as calcium channel blocker toxicity along with the use of nitric oxide scavengers given nimodipine’s mechanism of action and the mechanism of vasoplegia.