A 32-year-old male presented with severe palpitations and syncope. He had a history of prior alcohol, opiate, and methamphetamine abuse, but otherwise no known medical conditions. He admitted to taking, over the prior 10 days, up to 200 mg daily of loperamide (maximum recommended dosage 16 mg per day) and multiple doses of famotidine daily (estimated up to 500 mg per day). Both medications were obtained over the counter. He did not take any other medications, supplements, or recreational substances.\nHis initial vital signs were as follows: blood pressure 121/76 mmHg; pulse 62 beats/min; temperature 98 F; and oxygen saturation 97%, breathing ambient air. He appeared disheveled, but otherwise had no abnormal physical exam findings. His presenting electrocardiogram (ECG) showed sinus tachycardia at 101 beats/min, first-degree atrioventricular (AV) block, nonspecific intraventricular conduction delay, and prolonged QT interval (Fig. ). Serum electrolytes, blood counts, cardiac troponin (I), renal, liver, and thyroid function were normal. Transthoracic echocardiogram showed normal chamber size and function and normal valves.\nShortly after admission, he had recurrent symptoms (syncope preceded by palpitations) that occurred during sustained monomorphic VT (Fig. ). VT terminated spontaneously. Loperamide and famotidine were discontinued, and he was treated with intravenous magnesium and supportive care. During hospitalization, he had frequent multifocal premature ventricular complexes and runs of both monomorphic and polymorphic VT. After 5 days, his PR interval, QRS duration, and QT interval normalized and VT resolved. He was discharged and strongly encouraged to abstain from recreational drug use. At 6 months follow-up, he had maintained abstinence from recreational drugs and his ECG continued to be normal (Fig. ).
A 32-year-old man with a history of polysubstance use including heroin was found combative and delirious in his room by staff at his sober living facility. Multiple empty boxes of loperamide were found in his backpack at the scene by emergency medical services. He was given intravenous (IV) fluids and transported to the emergency department (ED). In the ED, he was notably agitated. On physical exam, he was noted to be tachycardic with a regular pulse of 128 beats per minute and a blood pressure of 123/77 millimeters of mercury (mmHg). He was tachypneic with mild respiratory distress, diaphoretic, and oriented to person only. He was intubated for airway protection using etomidate and succinylcholine. An initial electrocardiogram (ECG) showed a regular, wide-complex tachycardia with a prolonged QTc of 473 milliseconds (ms) and QRS of 140 ms, with an RSR’ pattern in lead aVR. This was determined to be sinus tachycardia with a left bundle branch block by the consulting cardiologist and electrophysiologist (). The patient’s electrolyte levels were within normal limits.\nAcutely, in conjunction with poison control the decision was made to manage the patient with 0.4 milligram (mg) IV naloxone, 400 mg IV lidocaine, and one gram IV magnesium. The patient also received 50 milliequivalent (mEq) IV sodium bicarbonate for presumed sodium channel toxicity from the high-dose loperamide. An initial troponin I was elevated to 0.084 nanograms (ng) per milliliter (mL) (reference 0.000–0.045 ng/mL). A point-of-care ultrasound (POCUS) demonstrated left ventricular anterior wall hypokinesis. He underwent emergent cardiac catheterization, which revealed left ventricular anterior wall hypokinesis, angiographically normal cardiac arteries with a left ventricle ejection fraction (LVEF) of 45%, and an elevated left ventricular filling pressure of 23 mmHg.\nDuring his hospitalization, the patient’s QT peaked one day after admission to 616 ms with a QTc 573 ms and a QRS of 120 ms (). At that time the patient admitted to taking over 100 mg of loperamide as well as an unknown amount of gabapentin as an alternative to opioids on the day of admission. His dysrhythmia resolved and QTc normalized within four days of admission with no further exposure to loperamide. A subsequent transthoracic ECG showed a LVEF of 55% and no evidence of diastolic dysfunction or hypokinesis of the anterior wall. At discharge, his ECG showed a QTc of 442 ms and a QRS of 98 ms (). A loperamide serum concentration was not measured during hospitalization. Urine toxicology screen on admission was negative for opiates as loperamide is not included in the standard panel of drugs screened.