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 32-year-old man with a history of polysubstance use including heroin was found combative and delirious in his room by staff at his sober living facility. Multiple empty boxes of loperamide were found in his backpack at the scene by emergency medical services. He was given intravenous (IV) fluids and transported to the emergency department (ED). In the ED, he was notably agitated. On physical exam, he was noted to be tachycardic with a regular pulse of 128 beats per minute and a blood pressure of 123/77 millimeters of mercury (mmHg). He was tachypneic with mild respiratory distress, diaphoretic, and oriented to person only. He was intubated for airway protection using etomidate and succinylcholine. An initial electrocardiogram (ECG) showed a regular, wide-complex tachycardia with a prolonged QTc of 473 milliseconds (ms) and QRS of 140 ms, with an RSR’ pattern in lead aVR. This was determined to be sinus tachycardia with a left bundle branch block by the consulting cardiologist and electrophysiologist (). The patient’s electrolyte levels were within normal limits.\nAcutely, in conjunction with poison control the decision was made to manage the patient with 0.4 milligram (mg) IV naloxone, 400 mg IV lidocaine, and one gram IV magnesium. The patient also received 50 milliequivalent (mEq) IV sodium bicarbonate for presumed sodium channel toxicity from the high-dose loperamide. An initial troponin I was elevated to 0.084 nanograms (ng) per milliliter (mL) (reference 0.000–0.045 ng/mL). A point-of-care ultrasound (POCUS) demonstrated left ventricular anterior wall hypokinesis. He underwent emergent cardiac catheterization, which revealed left ventricular anterior wall hypokinesis, angiographically normal cardiac arteries with a left ventricle ejection fraction (LVEF) of 45%, and an elevated left ventricular filling pressure of 23 mmHg.\nDuring his hospitalization, the patient’s QT peaked one day after admission to 616 ms with a QTc 573 ms and a QRS of 120 ms (). At that time the patient admitted to taking over 100 mg of loperamide as well as an unknown amount of gabapentin as an alternative to opioids on the day of admission. His dysrhythmia resolved and QTc normalized within four days of admission with no further exposure to loperamide. A subsequent transthoracic ECG showed a LVEF of 55% and no evidence of diastolic dysfunction or hypokinesis of the anterior wall. At discharge, his ECG showed a QTc of 442 ms and a QRS of 98 ms (). A loperamide serum concentration was not measured during hospitalization. Urine toxicology screen on admission was negative for opiates as loperamide is not included in the standard panel of drugs screened.