Seizur-Like Activity and Recurrent Cardiac Arrests in a Healthy 24-Year-Old: Loperamide Abuse; a Case Report and Literature Review

Abstract

SESSION TITLE: Poisoning and Drug Overdose 2 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Loperamide is a relatively safe OTC anti-motility agent. However, at higher doses it can produce palliation for opiate withdrawal or even frank euphoria. We present an atypical case of loperamide toxicity with seizure like activity and recurrent cardiac arrests, treated successfully with Isoproterenol. CASE PRESENTATION: 24-year-old female transferred for seizure like activity. Her hospital stay was complicated with recurrent cardiac arrests, including pulseless electrical activity (n=1) and subsequently ventricular tachycardia (n=2) successfully resuscitated with standard ACLS protocol. Workup was remarkable for prolonged QTc at 645 milliseconds with no electrolyte imbalances, cardiac enzymes, negative CT brain, video electroencephalogram, and lumbar puncture. Coronary CT confirmed normal cardiac and coronary anatomy. Transthoracic echocardiogram revealed normal structure and function. Trial of IV Isoproterenol achieved normalization of QTc. DISCUSSION: Loperamide is a μ-opioid receptor agonist with poor oral bioavailability, limited GI absorption, and is metabolized by the liver. At super high doses, it is actively transported through the blood brain barrier via an efflux transporter. Our patient reported one year history of loperamide abuse and was treated successfully with isoproterenol infusion making ours the second case reported. The pro-arrhythmic mechanisms of loperamide induced dysrhythmia has been studied using cloned human cardiac sodium and potassium channels. Loperamide inhibits both the Nav1.5 sodium channel and especially the human ether-a-go-go-related gene potassium channel. This study attributed the QRS prolongation to the inhibition of the sodium channel and further devolution into Torsades to the potassium channel inhibition. CONCLUSIONS: Loperamide is increasingly abused for treatment of opioid withdrawal and euphoria. Because it is available without prescription, is not routinely tested for, and does not have a classic clinical presentation, diagnosis of loperamide overdose requires heightened clinical suspicion. Despite an FDA warning, loperamide abuse is on the rise. Therefore, general population and clinicians should be more attuned to the potential of cardiac toxicity, QTc prolongation, and death from loperamide abuse. Further studies need to be done focused on elucidating optimal treatment strategies and improved initial diagnostics. Reference #1: Swank, K et al. (2017). Adverse event detection using the FDA post-marketing drug safety surveillance system: Cardiotoxicity associated with loperamide abuse and misuse. Journal of the American Pharmacists Association, Vol 10 Reference #2: Eggleston, W et al. (2016). Cardiac Dysrhythmias After Loperamide Abuse - New York 2008 - 2016. Morbidity and Mortality Weekly Report, Vol 65 Reference #3: Kang, J; Compton, D; Vas, R; Rampe, D (2016). Proarrhythmic mechanisms of the common anti-diarrheal medication loperamide; revalations from the opioid abuse epidemic. Naunyn-Schmiedeberg’s Archives of Pharmacology, Vol 389 DISCLOSURE: The following authors have nothing to disclose: Abhinav Mittal, Rahul Sangani, Monica Cerone, Robert Stansbury No Product/Research Disclosure Information