A SEVER CASE OF CALCIUM CHANNEL BLOCKER TOXICITY REQUIRING HYPERINSULINEMIA EUGLYCEMIA AND LIPID EMULSION TREATMENT

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Calcium channel blocker (CCB) is a significant drug exposure reported to the American Association of Poison centers (1). Medical care of patients poisoned with CCBs can be complex as profound bradycardia and hypotension might be challenging to control, with insufficient evidence on which medical therapy is best (2). Calcium channel blockers directly block calcium L-type channels in the heart and blood vessels leading to hypotension and circulatory collapse in overdose cases. Dihydropyridines are generally less notorious for causing bradycardia than non-dihydropyridine. Amlodipine has a relatively long half-life, and therefore toxicity with amlodipine tends to cause prolonged circulatory collapse (3).This case was particularly challenging since calcium channel blockers were combined with three additional medications, including a benzodiazepine and a GABA receptor agonist (zolpidem). This combination made cardiopulmonary collapse an inevitable consequence. CASE PRESENTATION: A 32-year-old man presented to the emergency department in a stable clinical condition about an hour after intentionally ingesting a total of 300 mg of amlodipine, 1500 mg of bupropion, 3 mg alprazolam, and an unknown amount of zolpidem in a suicidal attempt. Soon after arriving at the emergency room, he started to have slurred speech, and his blood pressure started dropping—treatment initiated with activated charcoal. Subsequently, the patient became more lethargic, requiring emergent sedation, intubation, and mechanical ventilation for airway protection. Additional treatments included hyperinsulinemia euglycemia treatment (HIET), calcium gluconate, sodium bicarbonate, and lipid emulsion.The patient quickly became hemodynamically unstable with a refractory distributive shock requiring high doses of four different vasopressors (norepinephrine, vasopressin, phenylephrine, and epinephrine). Initial laboratory results showed metabolic acidosis (pH of 7.14). Complete blood count and chemistry were unremarkable. Chest x-ray, electrocardiogram, and echocardiogram were essentially normal. After stabilization in the intensive care unit, all vasopressors were successfully weaned off, and the patient was extubated on day 4 of admission. He was transferred out to an inpatient psychiatric unit on day 8 of admission. DISCUSSION: Aside from the initial therapy with intravenous fluids and atropine for bradycardia, there is no agreed-upon algorithms for CCBs toxicity treatment.Hyperinsulinemia euglycemia treatment (HIET) was originally shown to improve survival in dogs poisoned with verapamil in a controlled environment. CONCLUSIONS: Management of calcium channel blocker toxicity is based on maintaining adequate circulation with the use of IV fluids, vasopressors, calcium, high-dose insulin, glucagon, and other therapies that have been documented. REFERENCE #1: Kent R. Olson, Andrew R. Erdman, Alan D. Woolf, Elizabeth J. Scharman, Gwenn Christianson, E. Martin Caravati, Paul M. Wax, Lisa L. Booze, Anthony S. Manoguerra, Daniel C. Keyes, Peter A. Chyka & William G. Troutman (2005) Calcium Channel Blocker Ingestion: An Evidence-Based Consensus Guideline for Out-of-Hospital Management, Clinical Toxicology, 43:7, 797-822. REFERENCE #2: DeWitt CR, Waksman JC. Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity. Toxicol Rev. 2004;23(4):223-38. REFERENCE #3: Vimal Upreti, V. R. Ratheesh, Pawan Dhull, and Ajay Handa.Shock due to amlodipine overdose. Indian J Crit Care Med. 2013 Nov-Dec; 17(6): 375–377. DISCLOSURES: No relevant relationships by Matthew Apedo, source=Web Response no disclosure on file for Setana Idriss; No relevant relationships by Mazin Shaikhoun, source=Web Response