A 32-year-old male presented with severe palpitations and syncope. He had a history of prior alcohol, opiate, and methamphetamine abuse, but otherwise no known medical conditions. He admitted to taking, over the prior 10 days, up to 200 mg daily of loperamide (maximum recommended dosage 16 mg per day) and multiple doses of famotidine daily (estimated up to 500 mg per day). Both medications were obtained over the counter. He did not take any other medications, supplements, or recreational substances.\nHis initial vital signs were as follows: blood pressure 121/76 mmHg; pulse 62 beats/min; temperature 98 F; and oxygen saturation 97%, breathing ambient air. He appeared disheveled, but otherwise had no abnormal physical exam findings. His presenting electrocardiogram (ECG) showed sinus tachycardia at 101 beats/min, first-degree atrioventricular (AV) block, nonspecific intraventricular conduction delay, and prolonged QT interval (Fig. ). Serum electrolytes, blood counts, cardiac troponin (I), renal, liver, and thyroid function were normal. Transthoracic echocardiogram showed normal chamber size and function and normal valves.\nShortly after admission, he had recurrent symptoms (syncope preceded by palpitations) that occurred during sustained monomorphic VT (Fig. ). VT terminated spontaneously. Loperamide and famotidine were discontinued, and he was treated with intravenous magnesium and supportive care. During hospitalization, he had frequent multifocal premature ventricular complexes and runs of both monomorphic and polymorphic VT. After 5 days, his PR interval, QRS duration, and QT interval normalized and VT resolved. He was discharged and strongly encouraged to abstain from recreational drug use. At 6 months follow-up, he had maintained abstinence from recreational drugs and his ECG continued to be normal (Fig. ).
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 -).