This refers to a single or staggered ingestion of excessive paracetamol over 8 hours or less. Provided that time of ingestion is well-defined, risk assessment and the decision to treat (or not) with the antidote, N-acetylcysteine (NAC), is straightforward and guided by a serum paracetamol level plotted on a nomogram. Where the nomogram cannot be utilised, the decision to treat is based on serum paracetamol and hepatic transaminase levels.
References
- Daly FS, Fountain JS, Murray L et al. Guidelines for the management of paracetamol poisoning in Australia and New Zealand – explanation and elaboration. A consensus statement from toxicologists consulting to the Australasian Poisons Information Centres. Medical Journal of Australia 2008; 188:296-301.
- O’Grady JG. Acute liver failure. Postgraduate Medical Journal 2005; 81:148-154.
- Prescott LF. Paracetamol (acetaminophen). A critical bibliographic review. 2nd edn. Taylor and Francis, London 2001.
- Prescott LF, Illingworth RN, Critchley JA. Intravenous N-acetylcysteine: the treatment of choice for paracetamol poisoning. British Medical Journal 1979; 2:1097.
- Rumack BH. Acetaminophen hepatotoxicity: the first 35 years. Journal of Toxicology-Clinical Toxicology 2002; 40:3-20.
- Rumack BH, Matthew H. Acetaminophen poisoning and toxicity. Pediatrics 1975; 55:871-876.
- Schiødt FV, Bondesen S, Tygstrup N et al. Prediction of hepatic encephalopathy in paracetamol overdose: a prospective and validated study. Scandinavian Journal of Gastroenterology 1999; 34(7):723-8
- Silvalotti MCA, Yarema MC, Juurlink DN et al. A risk quantification instrument for acute acetaminophen overdose patient treatment with N-acetyl cysteine. Annals of Emergency Medicine 2005; 46(3):263-271.
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