Loperamide overdose
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Various toxicities secondary to abuse: case report A 42-year-old man developed various toxicities, including seizure-like activity, cardiac arrest, lack of response to painful stimuli, elevated levels of AST, ALT, phosphate and ammonia, respiratory acidosis, hypoxic brain injury, bradycardia, prolonged QTc interval, hypotension, ventricular tachycardia, torsades de pointes, encephalopathy and acute pancreatitis following abuse and overdose of loperamide for Crohn’s disease. The man, whose medical history was notable for Crohn’s disease, chronic pancreatitis and use of narcotics, developed seizurelike activity. His spouse contacted the emergency medical services after being awoken by an audible fall. His family reported no signs of intoxication on the previous night; however, they stated that for the past several days, he had been complaining of frequent loose stools and severe abdominal pain, and also that he had been consuming a ’lot’ of loperamide [exact quantity not specified]. At home, he was found motionless and unresponsive, in a state of cardiac arrest. The man received cardiopulmonary resuscitation and epinephrine, resulting in the return of spontaneous circulation with normal sinus rhythm and strong pulses. He was intubated and ventilated on admission. Physical examination showed no obvious signs of trauma. He was unresponsive to painful stimuli. He began to exhibit bilateral upper extremity movements toward the endotracheal tubing following administration of naloxone. Initial complete metabolic panel revealed elevated AST, ALT, phosphate and ammonia. Analyses of arterial blood gases revealed respiratory acidosis. Initial hospital drug screening was found to be negative for opiates. Brain CT scan raised suspicion for hypoxic injury, whereas ECG demonstrated bradycardia and prolonged QTc interval. He was subsequently shifted to the ICU, where he was found to be hypotensive, with ventricular tachycardia compatible with torsades de pointes. He was transcutaneously paced and placed on dobutamine drip. EEG demonstrated nonspecific encephalopathy. He was placed on a temporary pacer and administered norepinephrine [levophed]. His family elected to have gift of life donation according to his wishes, and he expired on day 3 of admission. Autopsy findings verified underlying diverticulosis, myocyte hypertrophy, mild interstitial fibrosis, and hypertensive and atherosclerotic cardiovascular disease (coronary artery atherosclerosis). The findings were notable for ischaemic neurons. Focal haemorrhagic areas were observed around the pancreas, in addition to numerous fat necrosis within the adipose surrounding. Microscopic examination of the pancreas showed evidence of acute and chronic inflammation, focal haemorrhage and fat necrosis, with lymphocytic and neutrophilic infiltrates. The acute pancreatitis was attributed to loperamide. A loperamide metabolic panel revealed loperamide levels of 19 ng/mL with the metabolite desmethylloperamide present at 200 ng/mL. Based on these findings, the cause of death was determ
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