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 29-year-old female with history of heroin abuse and depression presented after being found altered and confused. At the time, the patient was known to be taking an estimated 300 tablets of loperamide daily for “chronic stomach issues” (1 tablet is 2 mg for an approximate total of 600 mg). Her husband reported that within the past year, he would witness her taking at least one entire bottle of loperamide with roughly 96 tablets up to 3 times per day. There were no other medications reported, including use of any antidepressants.\nOn presentation, she was tachycardic to 156 BPM (beats per minute) and hypotensive to 70/40 mm Hg. Initial electrocardiogram (ECG) showed polymorphic VT with prolonged QTc of 669 ms ( and ). Subsequently, she developed recurrent episodes of VT that degenerated into torsades de pointes, resulting in multiple cardioversions and her admission to the cardiac intensive care unit.\nPreliminary laboratory findings were unremarkable except for the following: leukocytosis 18 bil/L, anion gap 16, and lactate 2.2 mmol/L. Chemistries showed a sodium 136 mmol/L, potassium 4.3 mmol/L, calcium 2.2 mmol/L, and magnesium 1.6 mmol/L. Urine drug screen was positive for cannabinoids, and her chest X-ray was normal. A serum loperamide level was ordered but would not result until after her discharge.\nAfter cardioversion in the emergency room, the patient was stabilized. Repeat ECG shortly after demonstrated a QTc of 515 ms. Poison control was contacted immediately and recommended supportive management. Unfortunately that evening, she began having frequent episodes of nonsustained VT triggered by positional change and vomiting (). Additional intravenous magnesium sulfate was given but symptoms persisted. A sodium bicarbonate infusion at 150 mEq/h was initiated per the recommendations of the electrophysiologist on call.\nSeveral hours later, the patient further decompensated into sustained VT. Electrical cardioversion with 120 J was required to maintain hemodynamic stability. Given her tenuous status and recurrent VT storm, she was intubated and sedated to suppress sympathetic overstimulation. Subsequently, an isoproterenol infusion was started at 2 µg/min to reduce the number of subsequent VT episodes.\nAfter 8 hours without VT, isoproterenol was reduced to 1 µg/min and the bicarbonate infusion was discontinued. Her transthoracic echocardiogram was completed and shown to be normal. Isoproterenol was stopped on day 3, and the patient was extubated. By then, she was free of VT for more than 24 hours and her QTc improved to 500 ms. No additional anti-arrhythmics were started, and the patient was downgraded and later discharged from the hospital ().\nThe final results of her serum loperamide and desmethyl loperamide (the primary metabolite of loperamide) were elevated to 26 ng/mL (normal is <10 ng/mL) and 160 ng/dL (normal is <20 ng/dL), respectively.