QJM Advance Access originally published online on January 7, 2008
QJM 2008 101(2):121-125; doi:10.1093/qjmed/hcm139
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Does the patient history predict hepatotoxicity after acute paracetamol overdose?
From the Scottish Poisons Information Bureau, Royal Infirmary of Edinburgh, 51 Little France Crescent Edinburgh, UK
Address correspondence to W.S. Waring, Scottish Poisons Information Bureau, Royal Infirmary of Edinburgh, 51 Little France Crescent, Edinburgh, EH16 4TJ, UK. email: s.waring{at}ed.ac.uk
Received 8 August 2007 and in revised form 4 September 2007
| Abstract |
|---|
Background: Initial management of patients who were presented to hospital after acute paracetamol overdose depends on the suspected amount ingested and more than 12 g is potentially fatal. However, the validity of this approach has received comparatively little attention.
Methods: The present study is sought to establish whether the stated paracetamol dose might predict systemic exposure and risk of hepatotoxicity. A prospective observational study of consecutive patients presenting to the Emergency Department due to acute paracetamol overdose was performed. Serum paracetamol concentrations between 4 and 15 h post-ingestion were compared with the Rumack-Matthew 200-line nomogram, and hepatotoxicity was defined by prothrombin time ratio >1.3 or alanine transaminase
1000 U/l.
Results: There were 987 patients, and the stated quantity of paracetamol ingested was 0–12 g in 475 (48.1%), >12 g in 349 (35.4%) and unknown in 163 (16.5%). Ingestion of >12 g was associated with paracetamol concentration above the 200-line in 31.8% (95% CI 27.1–36.9%) vs. 3.2% (1.9–5.2%), P < 0.0001 by
2 proportional test, and associated with hepatotoxicity in 6.9% (4.6–10.1%) vs. 1.3% (0.5–2.8%), P = 0.0001.
Conclusions: Therefore, ingestion of >12 g predicted higher paracetamol exposure and increased risk of hepatotoxicity and supports the validity of patient history in this context.