Pulmonary Medicine and Critical Care Carle Foundation Hospital
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Introduction: Dextromethorphan is a cheap, over the counter antitussive. Maximum adult dose is 120mg/24hrs. At high doses (2mg/kg), its N-methyl-D-aspartate (NMDA) receptor antagonism produces dissociative and hallucinogenic effects, similar to ketamine and PCP.1 National Poison Data System (NPDS) data show peak abuse in 2006-2007, highest among teenagers.3 Despite a 56.3% decrease through 2015, absolute numbers remain high.2,3 Toxicity causes hypertension, tachycardia through central sympathetic drive and prolonged catecholamine activity.4,5,6 Persistent sympathetic overactivity contributes to cardiac remodeling which eventually leads to end organ damage.7
Description: A 38-year-old male with no prior medical history presented with two weeks of progressive dyspnea, abdominal distention and bipedal edema. He was clammy and tachycardic. Labs showed elevated aminotransferases (200s-300s U/L), and troponin 537ng/L. He was intubated for impending respiratory failure. Echocardiogram showed dilated LV, global hypokinesis and ejection fraction (EF) of 30–35%. Right and left heart catheterization showed mild combined pre and post capillary pulmonary hypertension and non obstructive CAD. ICU diuresis and inotropic support were followed by GDMT with sacubitril-valsartan and spironolactone. He disclosed 20 years of DXM misuse-up to 100 tablets daily and recently averaging approximately 270 mg per day.
Discussion: Chronic DXM abuse in cardiotoxicity is under-recognized and rarely reported. The lack of alternate etiologies and non-ischemic pattern suggests causality. The NMDA receptor blockade and serotonergic effects triggers sustained sympathetic surge, causing tachycardia, hypertension, and increased myocardial oxygen demand. Prolonged catecholamine excess has been implicated in stress cardiomyopathy and may contribute to ventricular remodeling and systolic dysfunction.1,8 Co-formulants like pseudoephedrine causes vasoconstrictive effects. Management is similar to other non-ischemic cardiomyopathies, with focus of cessation of the offending agent. This case adds to the limited literature suggesting a causal relationship between long-term DXM toxicity and non-ischemic cardiomyopathy, and also highlights the importance of recognizing chronic OTC drug abuse as a potential etiology of new onset heart failure.
