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 female with a past medical history of chronic back pain, fibromyalgia, chronic pain syndrome, and past opioid usage presented to our ED with atypical chest pain, palpitations, and shortness of breath. She also gave a history of near-syncopal episodes in the past. The day before she presented to the ED, the patient had a syncopal episode and "turning purple" at home, prompting her daughter to call the emergency medical services (EMS), but the patient canceled the EMS after she awakened from this episode (likely due to Torsade’s de Pointes). On arrival to the ED, she had an episode of polymorphic ventricular tachycardia, which was sustained, and the patient spontaneously self-converted to sinus rhythm with frequent premature ventricular contractions and ventricular bigeminy (Figure ). She had a persistently prolonged QT interval, and nonspecific ST changes were noted. She was put on telemetry, where 19 beats of Torsade’s were noted. The patient denied any known personal or family history of heart disease or any congenital QT syndrome. She is an everyday cigarette smoker and denied any alcohol or any other illicit drug use. Toxicology studies were unremarkable.\nLabs were normal except for hypokalemia, which was replaced. Her serial cardiac enzymes were normal imaging of the chest, abdomen, and pelvis was unremarkable. The patient received amiodarone and magnesium in the ED and was put on continuous telemetry. Despite this intervention the patient continued to show ventricular bigeminy and short runs of polymorphic ventricular tachycardia (Figure ). The patient was upgraded to the intensive care unit (ICU), for closer monitoring and evaluation. The electrophysiology and cardiology services were consulted. The patient underwent an echocardiogram, which showed a normal ejection fraction, normal right and left ventricular functions, and no valvular abnormalities. The patient later endorsed that she was on oxycodone, fentanyl patch, and hydrocodone for her chronic pain issues. Her primary care had weaned her off the medications, and she was not getting any more opioid prescriptions. She also confided that she had been consuming 200 tablets of 2 mg over-the-counter (OTC) loperamide every week to "extend her opioid analgesic prescription for her chronic pain issues" and that she had taken one high dose of 200 tablets of 2 mg all at once before today's ED visit. Due to the long half-life of loperamide, the patient was advised to continue admission to the ICU till the QT interval stabilizes. Further plan was made to send her home on life vest with outpatient follow-up for implantable cardiac defibrillator (ICD) therapy. She did not seem interested in any of the above-stated therapies and adamantly refused any outpatient or inpatient opiate rehabilitation. While all these discussions were taking place, the patient left the hospital against medical advice (AMA).\nThe patient again presented to our ED with chest pain, shortness of breath, nausea, and vomiting on the following day. She was still bradycardic in the '50s along with persistent, prolonged QT interval and ventricular bigeminy (Figure ). Electrophysiology and cardiology services were again consulted, and the patient also underwent coronary angiography, which did not show any significant blockage or evidence of structural heart disease. It was again reiterated to her about the importance of considering life vest versus ICD versus medical management. She was also advised to refrain from loperamide use entirely and to quit cigarette smoking. Despite all the advice and education from several physicians and hospital staff, the patient again left the hospital AMA and was unfortunately lost to follow up.