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Background: Aluminum phosphide (AlP) is a highly toxic fumigant that is restricted in the USA. When exposed to humidity or water, AlP generates phosphine gas, a mitochondrial toxin that can produce cardiovascular collapse, respiratory failure, metabolic acidosis, and death. Hypothesis: The use of extracorporeal life support (ECLS) in patients with severe AlP toxicity increases chances of survival. Methods: Single-patient chart review. Case: A 3-year-old girl with no significant past medical history presented to the emergency department with 10 h of cough and vomiting. Symptoms started after her father placed AlP pellets throughout the house for rodent control. Of note, her 47-year-old mother, 16-year-old brother, and 21-year-old sister all presented at the same time with minor gastrointestinal and upper respiratory symptoms that resolved quickly. The patient's vital signs were BP 60/40 mmHg, HR 150 beats/min, RR 25 breaths/min, T 99.5 degreeF, O2 Sat 100%. She was noted to be somnolent and had dry mucous membranes with delayed capillary refill. Venous blood gas showed pH 7.32; PCO2 28 mmHg, calculated HCO3 14 mEq/L, and a lactate 4.2 mmol/L. Anion gap was 29 mmol/L. ECG showed diffuse ST segment depressions. She remained hypotensive despite intravenous fluids and was started on IV dopamine. She was transferred to an ECLS center 2 h after presentation. Shortly after transfer, the patient had a ventricular tachycardia arrest and was connected to veno-arterial ECLS after 90 min of resuscitation. She was started on IV N-acetylcysteine and oral vitamin E as well as intravenous L-carnitine. Her hospital course was complicated by ventricular dysrhyth-mias, seizures and bacteremia, hepatic injury, pulmonary edema and acute kidney failure requiring dialysis. Cardiac function slowly improved, and the patient was weaned off ECLS on day 15 of admission with an intact mental status and no reported neurologic sequelae. Discussion: Phosphine poisoning is challenging for the provider since it is often lethal, has no specific antidotes and rarely occurs in the USA. Conclusion: Early transfer to an ECLS-capable center and aggressive treatment in aluminum phosphide toxicity may be associated with better outcomes

OBJECTIVE: Loperamide, a non-prescription anti-diarrheal agent, is a peripheral mu-opioid receptor agonist that is excluded from the blood-brain barrier by p-glycoprotein at therapeutic doses. Overdoses of loperamide penetrate the central nervous system (CNS), leading to abuse. We report cardiac conduction abnormalities and dysrhythmias after ingestion of a recreational supra-therapeutic dose of loperamide confirmed with an elevated blood loperamide concentration. CASE DETAILS: A 48-year-old woman with a history of alcohol and benzodiazepine abuse presented to the emergency department (ED) with somnolence, weakness and slurred speech. She was taking 20 to 40 tablets of 2 mg loperamide 1-2 times/day for weeks along with clonazepam and whiskey. Vital signs were: blood pressure (BP), 124/90 mmHg; heart rate (HR), 88/min; respiratory rate(RR), 20/min; T, 36.9 degrees C; O2 saturation 100% on room air (RA). Glucose was 6.4 mmol/L. Electrocardiogram (ECG) had a ventricular rate of 58/min, QRS 164 ms, QT 582 ms with no discernable p-waves. Lactate was 3.5 mmol/L and potassium was 6.2 mEq/L. Labs were notable for an anion gap of 20 mEq/L, ethanol of 3.9 mmol/L, creatinine of 2.3 mg/dL and loperamide concentration of 210 ng/mL (average therapeutic plasma concentration 1.2 ng/mL). She became hypotensive, but responded to fluids. Following treatment for hyperkalemia with calcium, insulin, dextrose, and hypertonic sodium bicarbonate a repeat ECG had a ventricular rate of 66/min, QRS 156 ms, and QT 576 ms. Magnesium was given and pacer pads were placed. During the infusion of magnesium, her BP fell to 92/58 mmHg with a HR of 54/min, RR 14/min, O2 saturation of 97% on RA so the infusion was stopped. The ECG after the magnesium infusion had a ventricular rate of 51/min, QRS of 134 ms, and QT 614 ms. In the ICU she had multiple runs of non-sustained ventricular tachycardia that did not require therapy. Over the next 48 h she improved and was transferred to a floor bed. On day four of hospitalization the patient left against medical advice. At that time, her ECG showed sinus tachycardia with a heart rate 114/min, QRS 82 ms, QT 334 ms. DISCUSSION: Loperamide produces both QRS and QT prolongation at supra-therapeutic dosing. A blood loperamide concentration of 210 ng/mL is among the highest concentrations reported. Supra-therapeutic dosing of loperamide is promoted on multiple drug-use websites and online forums as a treatment for opioid withdrawal, as well as for euphoric effects. With the current epidemic of prescription opioid abuse, toxicity related to loperamide, an opioid agonist that is readily available without a prescription is occurring more frequently. It is important for clinicians to be aware of the potentially life-threatening toxicity related to loperamide abuse in order to provide proper diagnosis, management and patient education.