Key messages

• Acetaminophen is predominantly metabolized in the liver; 90 per cent of the drug undergoes glucuronidation or sulfation to a non-toxic inactive compound, which is excreted in the urine, and 5 per cent is oxidized to W-acetyl-p-benzoquine imine which is rendered non-toxic by glutathiones.

• In acetaminophen poisoning there is an increase in the formation of the toxic W-acetyl-p-benzoquine imine, which saturates the glutathione defense mechanism and causes hepatic necrosis.

• The presence of symptoms or signs in acetaminophen poisoning should be treated as an indicator of hepatotoxicity. Liver function tests start to become deranged from 12 h with the serum aspartate aminotransferase peaking at 72 h.

• Any patient with a plasma acetaminophen level after 4 h which is greater than the standard treatment line or greater than half the standard line in a high-risk patient should be treated with the antidote W-acetylcysteine. The antidote should also be given if the timing is suspect or inaccurate.

• The management of fulminant hepatic failure resulting from acetaminophen overdose is based on resuscitation and preparation for urgent and safe transfer to a specialist liver failure unit.

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