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 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. ).