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Acetaminophen (paracetamol in the UK, Europe) is a common analgesic found in many nonprescription and
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prescription products After absorption, it is metabolized mainly by glucuronidation and sulfation, with a small fraction metabolized via the P450 mixed-function oxidase system (2E1) to a highly toxic reactive intermediate This toxic intermediate is normally detoxified by cellular glutathione With acute acetaminophen overdose (> 140 mg/kg, or 7 g in an average adult), hepatocellular glutathione is rapidly depleted and the reactive intermediate attacks other cell proteins, causing necrosis Patients with enhanced P450 2E1 activity, such as chronic alcoholics and patients taking INH, are at increased risk of developing hepatotoxicity Hepatic toxicity may also occur after chronic accidental overuse
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of acetaminophen eg, as a result of taking two or three acetaminophen-containing products concurrently or intentionally exceeding the recommended maximum dose of 4 g/d
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Administer activated charcoal (see p 1362) within 1 2 hours of the ingestion Although charcoal may interfere with absorption of the oral antidote acetylcysteine, this is not considered clinically significant
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Shortly after ingestion, patients may have nausea or vomiting, but there are usually no other signs of toxicity until 24 48 hours after ingestion, when hepatic aminotransferase levels begin to increase With severe poisoning, fulminant hepatic necrosis may occur, resulting in jaundice, hepatic encephalopathy, renal failure, and death Rarely, massive ingestion (eg, serum levels over 500 1000 mg/L) can cause early onset of acute coma, hypotension, and metabolic acidosis unrelated to hepatic injury The diagnosis after acute overdose is based on measurement of the serum acetaminophen level Plot the serum level versus the time since ingestion on the acetaminophen nomogram shown in Figure 38 1 Ingestion of sustained-release products or coingestion of an anticholinergic agent, salicylate, or opioid drug may cause delayed elevation of serum levels and may render the nomogram useless The nomogram is not useful after chronic overdose
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B Specific Treatment
Although the general recommendation is to treat if the serum acetaminophen level is above the toxic line on the nomogram (Figure 38 1), many clinicians prefer to use the lower line as a guide to treatment, as it provides a 25% safety margin Begin treatment with a loading dose of N-acetylcysteine, 140 mg/kg orally, followed by 70 mg/kg every 4 hours Dilute the solution to 5% with water, juice, or soda If vomiting interferes with oral N-acetylcysteine administration, consider giving the antidote intravenously (see below) The most widely used oral Nacetylcysteine protocol in the United States calls for 72 hours of treatment However, other regimens have demonstrated equivalent success with 20 48 hours of treatment A 20-hour intravenous regimen was recently approved by the FDA (Acetadote) Treatment with N-acetylcysteine is most effective if started within 8 10 hours after ingestion If the precise time of ingestion is unknown or if the patient is at higher risk of hepatotoxicity (eg, alcoholic, liver disease, chronic use of P450-inducing drugs), then use a lower threshold for initiation of N-acetylcysteine (in some case reports, a level of 100 mg/L at 4 hours was suggested in very high-risk patients) The conventional oral formulation may also be given intravenously using a micropore filter and a slow rate of infusion Call a regional poison control center or medical toxicologist for assistance
Kanter MZ Comparison of oral and iv acetylcysteine in the treatment of acetaminophen poisoning Am J Health Syst Pharm 2006 Oct 1;63(19):1821 7 [PMID: 16990628] Lavonas EJ et al Intravenous administration of N-acetylcysteine: oral and parenteral formulations are both acceptable Ann Emerg Med 2005 Feb;45(2):223 4 [PMID: 15671984]
300 200 Plasma or serum acetaminophen concentration (mcg/mL) 100 80 60 50 40 30 20 No toxicity 10 8 6 5 4 3 200 at 4 hours Probable toxicity
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