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.
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.