A 29-year-old female with history of heroin abuse and depression presented after being found altered and confused. At the time, the patient was known to be taking an estimated 300 tablets of loperamide daily for “chronic stomach issues” (1 tablet is 2 mg for an approximate total of 600 mg). Her husband reported that within the past year, he would witness her taking at least one entire bottle of loperamide with roughly 96 tablets up to 3 times per day. There were no other medications reported, including use of any antidepressants.\nOn presentation, she was tachycardic to 156 BPM (beats per minute) and hypotensive to 70/40 mm Hg. Initial electrocardiogram (ECG) showed polymorphic VT with prolonged QTc of 669 ms ( and ). Subsequently, she developed recurrent episodes of VT that degenerated into torsades de pointes, resulting in multiple cardioversions and her admission to the cardiac intensive care unit.\nPreliminary laboratory findings were unremarkable except for the following: leukocytosis 18 bil/L, anion gap 16, and lactate 2.2 mmol/L. Chemistries showed a sodium 136 mmol/L, potassium 4.3 mmol/L, calcium 2.2 mmol/L, and magnesium 1.6 mmol/L. Urine drug screen was positive for cannabinoids, and her chest X-ray was normal. A serum loperamide level was ordered but would not result until after her discharge.\nAfter cardioversion in the emergency room, the patient was stabilized. Repeat ECG shortly after demonstrated a QTc of 515 ms. Poison control was contacted immediately and recommended supportive management. Unfortunately that evening, she began having frequent episodes of nonsustained VT triggered by positional change and vomiting (). Additional intravenous magnesium sulfate was given but symptoms persisted. A sodium bicarbonate infusion at 150 mEq/h was initiated per the recommendations of the electrophysiologist on call.\nSeveral hours later, the patient further decompensated into sustained VT. Electrical cardioversion with 120 J was required to maintain hemodynamic stability. Given her tenuous status and recurrent VT storm, she was intubated and sedated to suppress sympathetic overstimulation. Subsequently, an isoproterenol infusion was started at 2 µg/min to reduce the number of subsequent VT episodes.\nAfter 8 hours without VT, isoproterenol was reduced to 1 µg/min and the bicarbonate infusion was discontinued. Her transthoracic echocardiogram was completed and shown to be normal. Isoproterenol was stopped on day 3, and the patient was extubated. By then, she was free of VT for more than 24 hours and her QTc improved to 500 ms. No additional anti-arrhythmics were started, and the patient was downgraded and later discharged from the hospital ().\nThe final results of her serum loperamide and desmethyl loperamide (the primary metabolite of loperamide) were elevated to 26 ng/mL (normal is <10 ng/mL) and 160 ng/dL (normal is <20 ng/dL), respectively.
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 -).