A 26-year-old male, with history of heroin abuse, was brought to the ER after a transient episode of loss of consciousness. His vital signs upon arrival were heart rate of 50 beats/min, blood pressure of 125/60 mmHg, respiratory rate of 14 breaths/minute, and temperature of 98.9°F. He was lethargic and had symmetrical constricted pupil bilaterally, absent bowel sounds, and a normal neuromuscular, cardiac, and respiratory exam. His initial laboratory tests showed sodium of 142 mmol/L, potassium of 4.2 mmol/L, calcium of 9.1 mg/dL, and magnesium of 1.8 mg/dL; extended urine drug screen was positive only for opiates. Blood alcohol level was within normal limits. No abnormalities were noted on CT scan of the head. EKG showed sinus bradycardia with normal PR, QRS, and QT/QTc intervals (). Soon after presentation he developed shortness of breath, diaphoresis, and sustained ventricular tachycardia with ventricular rate of 220 beats/minute. He was defibrillated 2 times with 200 J before sinus bradycardia was attained again. After defibrillation his bradycardia worsened with heart rate of 40 beats/min; however, the patient remained symptom-free. Over the course of one hour he had 2 episodes of self-limiting Torsades de Pointes (TdP) each lasting less than 10 seconds and a third ending up in pulseless ventricular tachycardia ( shows one such episode of TdP caught on telemetric monitoring). He was defibrillated again and prompt CPR was initiated. Pulse was regained immediately and he continued to have sinus bradycardia with heart rate of 40 beats/minute. He was given 2 gm of magnesium IV and overdrive pacing was started with isoproterenol. A goal heart rate of 90 beat/minute was maintained for 48 hours. No further ventricular arrhythmias were noted; once isoproterenol was discontinued his heart rate remained between 50 and 60 beats/min. Transthoracic echocardiogram showed a normal left ventricular ejection fraction and no valvular or structural abnormalities. Cardiac angiography did not reveal any coronary pathology either. On day 3 of admission the patient admitted to taking loperamide for the past two months to relieve diarrhea associated with heroin withdrawal. Recently he had read on an internet blog that high doses of loperamide can give a similar “high” to heroin. A day prior to admission he started increasing his daily dose of the medicine to attain a euphoric state. On the day of admission his maximum ingested dose reached up to 192 mg of loperamide. At this point a serum loperamide level was sent that came back, 2 ng/mL (expected peak level after ingestion of 8 mg oral dose is 2 ng/mL or less). The patient remained hemodynamically stable and was discharged to drug rehabilitation facility on day 8 of hospitalization.
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.