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 38-year-old female with an extensive history of poly-substance abuse presented after an outside hospital cardiac arrest that was recognized in the field to be caused by ventricular fibrillation of uncertain duration in the field. Her family reported daily use of two boxes of loperamide (144 tabs, 288 mg) daily for an indefinite period of time for the purpose of controlling symptoms of heroin withdrawal. She formerly used codeine and suboxone for opioid withdrawal symptom control but no longer had access to those treatments. Other than the polysubstance abuse, she was not known to have any known chronic medical illness and was not taking any prescription medications. There was no family history of cardiac arrhythmias or sudden cardiac death (SCD). The patient was successfully resuscitated in the field as per ACLS protocol with defibrillation, and, for airway protection, was intubated. She was initially taken to an outside facility and then emergently transferred to a tertiary care center. Hypothermia protocol was not initiated because of non-availability at the outside hospital. At the time of arrival, electrocardiogram (EKG) revealed a wide complex undetermined atrial rhythm at a rate of 58 bpm with prolonged QT and QTc intervals (). The patient had no available baseline EKG for comparison. Emergent coronary angiography indicated normal coronary arteries. Urine toxicology screen was negative. The regional poison control center was notified and recommended sodium bicarbonate and lipid infusions. Electrolytes, including potassium, magnesium, and calcium, were maintained within normal limits through intravenous supplementation.\nDue to bradycardia, the patient was started on an isoproterenol drip. The following day, her telemetry alarmed for a very wide QRS; EKG showed wide complex tachycardia () that culminated with a ventricular cardiac arrest. She was successfully resuscitated as per ACLS protocol with amiodarone push and lidocaine infusion. Six hours later, she developed sustained polymorphic ventricular tachycardia without loss of pulse that responded to magnesium supplementation. A temporary transvenous pacer was inserted with overdrive strategy. She was reliably paced as shown in the EKG (). Shortly after that, however, she developed a third ventricular fibrillation cardiac arrest that was successfully resuscitated as per ACLS protocol with multiple shocks (>10 times). Higher electrolytes levels were targeted with a potassium goal of 4.5 mmol/L and magnesium goal of 2–2.5 mg/dL. It was expected that the loperamide side effect would last for 24–48 hours. On Day 3, she was extubated without any residual neurologic deficit. She remained bradycardic when the pacemaker was turned down (EKG, ). Isoproterenol was weaned. On Day 5, she developed another episode of ventricular fibrillation that responded to four shocks of 200 Joules. Isoproterenol infusion was restarted transiently due to bradycardia. She was discharged to the medical floor on Day 6. However, on Day 11, she had multiple episodes of Torsade de Pointes (TdP), that were self-limiting and without symptoms. She was readmitted to the ICU due to these episodes, and temporizing measures were restarted (lidocaine and isoproterenol) with positive results. The patient threatened to leave the ICU against medical advice, so AICD/DDD ICD was placed to prevent ventricular fibrillation cardiac arrest given her recurring TdP. Repeat EKG () showed progressive shortening of the QTc and QT intervals. The patient changed her mind about leaving the ICU after the AICD placement and was discharged after medical stabilization two days later. She followed as outpatient with the EP team. She denied any symptoms or any further use of loperamide. Office EKG showed normal sinus rhythm at a rate of 85 bpm with normal QTc at 437 msec. Device interrogation demonstrated normal sensing and pacing pacemaker. She was enrolled in remote device monitoring every three months and has had no detected device shocks.