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 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.