A 43-year-old female patient with a past medical history of substance use disorder (SUD) was brought to the hospital by emergency medical services (EMS) presenting with multiple episodes of dizziness, shortness of breath, and palpitations. EMS reported ventricular tachycardia (VT) while in transit to the hospital for which she was externally defibrillated 10 times without any resolution of the ventricular arrhythmia. The patient’s past medical history was positive for depression and substance abuse of hydrocodone dating back to 2007. The patient’s husband denied any history of cardiac arrhythmias, structural heart disease, or ischemic heart disease. The patient’s husband denied using any medications, including herbal supplements, but reported drug allergies to amoxicillin and erythromycin. The patient’s social history revealed that she worked at a consignment store and had a history of alcohol and marijuana abuse. The patient’s husband also revealed recreational usage of loperamide at approximately 400 mg in the last 24 hours before the presentation. On physical exam in the emergency department, she appeared to be in moderate distress with pain from the external defibrillations. Her vital signs consisted of an elevated pulse of > 200 beats per minute (bpm), an elevated blood pressure of 157/80, and an increased respiratory rate at 24/minute. The pulmonary exam revealed decreased breath sounds bilaterally with symmetrical chest wall expansion. The cardiovascular exam revealed tachycardia with no murmurs reported. Examination of the head and neck showed moist mucous membranes with no jugular venous distension. The gastrointestinal exam was negative for distention, tenderness, rebound, guarding, hepatomegaly, or splenomegaly. The musculoskeletal exam revealed warm and well-perfused upper and lower extremities free of clubbing, cyanosis, and edema. In the processes of placing the electrocardiogram (EKG) electrodes onto the patient in the emergency room, the patient became unresponsive and the two lead EKG monitors showed polymorphic VT with a heart rate of 220 per minute and blood pressure of 84/58. The patient was immediately defibrillated once again before being sedated, intubated, and started on an amiodarone drip. The patient’s vitals were stabilized for 15 minutes before she went into another episode of polymorphic VT despite the amiodarone drip. The patient underwent synchronized cardioversion, and once her vitals stabilized, she underwent a cardiac catheterization which showed patent coronaries and a normal ejection fraction. The patient got transferred to the Medical Intensive Care Unit (MICU) for continuous monitoring and was started on a lidocaine drip in addition to the amiodarone drip. Her EKG in the MICU is shown below in Figure .\nIn the MICU, the patient continued to have polymorphic VT episodes despite medical management and went in and out of VT episodes approximately 16 times with each episode lasting between 30 seconds to two minutes. Subsequently, the patient had a transvenous cardiac pacer placed which stabilized her vital signs. After 72 hours, the pacer was removed, and the patient remained stable on amiodarone and lidocaine. Transthoracic echocardiogram in the MICU revealed a normal ejection fraction with no valvular abnormality. Serum electrolytes were within normal limits, and the urine drug screen was also negative. After the temporary pacer was removed, the patient subsequently remained in sinus rhythm with a heart rate of 70 bpm, QRS duration of 98 ms, and a QTc interval of 456 ms as seen in Figure .\nAfter five days of hospitalization, the effects of the loperamide had completely resolved, and the patient remained in normal sinus rhythm on amiodarone until discharge and followed up a month later.
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.