46-year-old male was presented in the ER after cardiac arrest. Patient had two-hour flight before he started feeling light-headed and passed out at the airport. The airport emergency services found him in ventricular fibrillation and provided him with two shocks before he regained consciousness. Subsequent EKG showed normal sinus rhythm and prolonged QT (QTc-589 msec); EKG is not available. Upon arrival to ER, patient was alert and oriented but amnesic about past events. Patient was taken for cardiac catheterization which revealed nonobstructive coronaries and normal ejection fraction. Electrolytes were unremarkable except potassium of 3.1 which was replaced. Complete blood counts, renal function, serum troponin, and serum magnesium were within normal limits. MRI of brain revealed no significant abnormalities. Shortly after coronary angiogram, patient again went to cardiac arrest and resuscitated with one shock. Cardiac monitor showed torsades de pointes ventricular tachycardia () with hemodynamic instability. Patient was intubated for airway protection and received IV magnesium and IV amiodarone. Toxicology screen was unremarkable except benzodiazepine he received during intubation (midazolam) for sedation. EKG showed normal sinus rhythm, nonspecific ST-T wave abnormality, and prolonged QT (QTc-620 msec) (). Echocardiogram revealed structurally normal heart. Acute pulmonary embolism was also ruled out with computed tomography pulmonary angiogram. Patient's spouse reported that patient has been taking large amount of Loperamide for irritable bowel syndrome for more than 5 years. However, she was not able to quantify the amount of Loperamide. Patient persistently experienced multiple episodes of sustained ventricular tachycardia requiring multiple defibrillation in setting of significantly prolonged QTc (>600 msec) on multiple serial EKGs. Patient was treated with metoprolol, lidocaine, and magnesium infusion. Over the period of 7 days, patient stopped having sustained ventricular tachycardia. Frequency of nonsustained ventricular tachycardia was also reduced and patient was extubated after several days of CCU monitoring. Lidocaine and magnesium were discontinued and metoprolol was continued. Loperamide levels were not obtained. After extubation, patient denied having similar episode in the past, chest pain, palpitations, syncope, shortness of breath, and any family history of sudden cardiac death or cardiac diseases. However, patient admitted that he has been self-medicating with over-the-counter 2 mg Loperamide approximately 50 tablets a day for diarrhea predominant irritable bowel syndrome for more than 5 years. He also admitted having approximately 100 pills of Loperamide daily for the last 2 days before admission. Since patient was buying over-the-counter Loperamide from different pharmacy; we could not determine exact frequency of purchase. Patient denied using illicit drug use, herbal supplements, or concurrent p-glycoprotein inhibitors. Serial EKG monitoring showed gradual decrease in QTc. However, serial EKG monitoring off Loperamide for several days revealed normal sinus rhythm and QTc of 472 msec () and 456 msec (). Only one EKG revealed QTc of 432 msec (). Thus, patient's QTc interval did not completely normalize after several days off all QTc prolonging medications and subsequently he received dual chamber automated cardioverter defibrillator (AICD) before discharge for secondary prevention of cardiac arrhythmia related death. Since majority of patient's QTc interval was >440 msec even after a week of stopping all QT prolonging medications, at this time, we think that patient may have subclinical long QT syndrome which was unmasked by Loperamide. However, electrophysiological studies were not performed to verify the diagnosis. Patient was instructed not to use Loperamide again.
A 35-year-old male with a history of AICD placement for long QT syndrome by a local cardiologist six months ago presented to the ED by ambulance for altered mental status and frequent shocks from AICD secondary to a loperamide overdose. He was unable to provide a history of more than “yes" or "no” because of his agitation, so the most history was obtained from emergency medical services (EMS), with confirmation by the patient. EMS stated that the patient was having dinner with his spouse when the spouse noticed that he had a brief loss of consciousness for several seconds. The spouse stated that when the patient awoke, he became very anxious, diaphoretic, and irritable; it was unclear if the defibrillator had fired at that time. On arrival, EMS gave the patient 2 mg of naloxone IV without any effect. They stated that en route to the facility, they noted that the AICD had fired several times, causing the patient much anxiety and pain. EMS also stated that they found a bag full of loperamide tablets inside a purse-string bag near the patient, which they brought into the department for identification. They stated that the patient had a history of IV drug abuse and had overdosed on loperamide in the past when he had been unable to obtain opiate medications. In the ED, the patient was anxious and diaphoretic and was shocked by his defibrillator every three to four minutes for runs of polymorphic ventricular tachycardia (Torsades). A review of symptoms was negative, except for tachycardia, anxiety, and diaphoresis. Initial vital signs were a heart rate of 120, respiratory rate of 24, oxygen saturation 99% on room air, and blood pressure 138/64. Physical exam showed that the patient could not hold an extended conversation; he was anxious, had reactive mydriasis, and an AICD in place in the left chest, without signs of infection; otherwise, the physical was normal.\nPotassium was found to be 2.7 so IV potassium, magnesium, bicarbonate, and saline were started with lidocaine chosen as an antiarrhythmic (with which cardiology and poison control had agreed). The remaining basic labs, as well as toxicology and cardiac enzymes, were normal. Lorazepam was also used to control agitation. The electrocardiogram (ECG) showed tachycardia, which was different from the patient’s baseline atrial-paced rhythm. This ECG (Figure ) was obtained when the patient was not in polymorphic ventricular tachycardia, which was only shown on the monitor for several seconds before being detected and electrically cardioverted by the AICD. Chest X-ray was normal. After treatment in the ED and intensive care unit (ICU), the shocks eventually became less frequent as electrolytes normalized. The patient was eventually removed from the lidocaine drip and discharged home five days later with the normalization of ECG over time (Figures -).