Çocuklarda Parasetamol Zehirlenmesine Yaklaşım
Synopsis
Paracetamol (acetaminophen) is one of the primary causes of drug toxicity presentations to pediatric emergency departments due to its widespread use and easy availability. Approximately 90% of the drug metabolized in the liver is excreted via conjugation, while less than 5% is converted into a toxic metabolite, NAPQI, by the CYP2E1 enzyme; during toxic dose ingestions, the depletion of glutathione leads to cellular damage and hepatic necrosis. In children, the acute toxic dose is defined as 200 mg/kg for those under 6 years of age, and 150 mg/kg or 10 grams for those over 6 years; in chronic ingestions, doses exceeding 150 mg/kg for two consecutive days or 100 mg/kg for three consecutive days are toxic. The clinical course consists of four stages: mild symptoms appear in the first 24 hours, transaminases rise between 24 and 72 hours, hepatic failure, encephalopathy, multiple organ failure, and the risk of death emerge between 72 and 96 hours, while surviving patients progress to the recovery phase between 4 days and 2 weeks. For diagnosis, serum paracetamol levels are evaluated using the Rumack-Matthew nomogram to determine risk. In treatment, activated charcoal is administered in the early hours to reduce absorption. The antidote N-acetylcysteine (NAC), a glutathione precursor, provides the highest efficacy in preventing hepatotoxicity when administered within the first 8 hours. In severe cases, liver transplantation is a life-saving option.
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