With supratherapeutic ingestions, up to 50% of absorbed APAP is metabolized by CYP2E1, leading to production of N-acetyl-p-benzoquinone imine (NAPQI), the hepatotoxic metabolite. With therapeutic dosing, APAP is metabolized primarily via glucuronidation and sulfation to nontoxic metabolites. Poisoning can occur through single or repeated ingestions. IntroductionĪcetaminophen (APAP) toxicity is among the most common medication-related overdoses and accounts for nearly half of all liver transplantations in the United States. This case highlights the potential benefit of a triple strategy of NAC, fomepizole, and early hemodialysis in massive acetaminophen overdose, potentially sparing complications of prolonged intubation and ICU hospitalization. The patient had complete clearance of acetaminophen by 32 hours after presentation and normalization of her acid base and hemodynamic status without any organ failure. She was treated with gastric decontamination with activated charcoal, IV NAC, fomepizole, and hemodialysis. We present a case of a 20-year-old female presenting with an acute ingestion of over 120 grams (1764.7 mg/kg) and an acetaminophen concentration of 5880 μmol/L who developed refractory shock, decreased level of consciousness, and metabolic acidosis requiring mechanical ventilation and vasopressor support. In such ingestions, the role of adjuvant treatments such as fomepizole and extracorporeal removal is unclear. However, there is less clarity in the management of massive overdoses (acute, single mg/kg with 4-hour equivalent concentrations ~6000 μmol/L) which are often associated with metabolic acidosis and multiorgan dysfunction. There is strong evidence for N-acetylcysteine (NAC) as a safe and effective antidote for acetaminophen toxicity. Acetaminophen overdose is one of the most common causes of acute hepatic failure in the developed world.

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