Unraveling NAGMA: A Case Series of Intravenous Nimodipine-Induced Metabolic Acidosis in Neuro-ICU Patients

Nimodipine, a calcium channel blocker of the dihydropyridine class, is used prophylactically in ruptured aneurysmal subarachnoid hemorrhage (aSAH) patients to reduce the incidence of poor outcome, delayed cerebral ischemia, and delayed ischemic neurological deficits. This case series reports nine instances of normal anion gap metabolic acidosis (NAGMA) in patients with aSAH following intravenous nimodipine administration in a neuro-intensive care unit (NICU) over 2 months. The patients, aged 4 to 68 years (seven male, two female), presented with acute headaches and were diagnosed with intracranial aneurysms, managed with aneurysmal clipping or coiling. Intravenous nimodipine (1-2 mg/hour) was initiated as per protocol, along with standard NICU care. After 48 to 72 hours, patients developed hyperventilation, respiratory alkalosis, and a significant decrease in bicarbonate, leading to NAGMA. Despite ruling out common causes like gastrointestinal losses and nephrotoxic drugs, renal tubular acidosis was suspected. The NAGMA resolved spontaneously 6 to 7 days postsurgery, coinciding with the discontinuation of intravenous nimodipine. A retrospective audit revealed a common factor: using a specific brand of intravenous nimodipine, a new arrival from the hospital supply. This phenomenon was later corroborated in a similar case from another hospital. The case highlights the importance of pharmacovigilance, postmarketing surveillance, and regulatory oversight in identifying rare drug-related adverse events, particularly in high-acuity settings like NICU.