Intravenous Nimodipine Associated Severe Metabolic Acidosis and Haemodynamic Collapse in patient with Aneurysmal Subarachnoid Haemorrhage: A Case Report

Nimodipine is a dihydropyridine Calcium Channel Blocker (CCB) routinely used in the management of aneurysmal Subarachnoid Haemorrhage (aSAH) to prevent Delayed Cerebral Ischemia (DCI). While oral route of administration is the standard of care, intravenous (i.v.) nimodipine is occasionally used in critically ill patients. However, i.v. administration may lead to profound hypotension and uncommon metabolic derangements. A 54-year-old hypertensive female presented with aSAH secondary to ruptured left anterior communicating artery aneurysm. Following aneurysm clipping, the patient was monitored in ICU with standard neurocritical care and oral nimodipine. The patient was transitioned to i.v. nimodipine due to high clinical suspicion of cerebral vasospasm and DCI. Within 48 hours of i.v. nimodipine, the patient developed severe hypotension requiring high-dose vasopressor support, mixed metabolic acidosis, hyperchloremia, ketonemia, and hyperglycaemia. Workup for sepsis, postsurgical meningoencephalitis, and other causes was inconclusive. An adverse drug reaction related to i.v. nimodipine was suspected. Discontinuation of nimodipine and targeted metabolic support led to improvement of clinical symptoms. This case highlights the rare but potentially life-threatening adverse effects of i.v. nimodipine, including refractory hypotension and severe metabolic acidosis. Clinicians should exercise caution, maintain close monitoring, and consider drug-induced toxicity when unexplained metabolic and haemodynamic instability occurs. The present case emphasises that vigilant haemodynamic and metabolic monitoring during i.v. nimodipine therapy is essential.