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Dear Editor,
Paracetamol toxicity is caused by excessive use or overdose of the drug. It is the most common cause of acute liver failure (ALF) in the Western world.1 Acute liver failure secondary to paracetamol overdose characteristically presents as an initial gastrointestinal upset shortly after ingestion, often followed 24 to 48 hours later by hepatic injury. The hepatotoxicity results not from paracetamol itself, but from one of its metabolites, N-acetyl-p- benzoquinoneimine (NAPQI), which depletes the liver's natural antioxidant glutathione and directly damages cells in the liver, leading to ALF.2 It rapidly progresses to lactic acidosis, coma, and death in previously healthy patients with no underlying liver disease.
Acute liver failure (ALF) has a mortality of greater than 80 per cent (depending on aetiology) in the absence of liver transplantation.1 Many patients die before a suitable organ becomes available, and morbidity and mortality after transplant is also high.
The management of patients with ALF presents complex and challenging problems to all those involved in their care. Such patients inevitably have serious derangement of function in multiple organ systems and an evidence-based, coordinated approach is necessary to optimise clinical outcomes. Frequent clinical evaluation and assessment of various biochemical and haematological parameters forms the cornerstone of clinical care. The early institution of general supportive therapies, such as control of elevated intracranial pressure and haemofiltration for renal failure, as well as specific therapies (e.g., N-acetylcysteine for paracetamol overdose) can provide the opportunity for potential liver recovery, or allow sufficient time for graft procurement in patients requiring transplantation.3
We report here on a small retrospective study investigating whether the institution of a standard set of guidelines, which were based on the King's College criteria for the management of paracetamol toxicity, could have an...