Unusual complications of paracetamol poisoning.

Every physician is only too familiar with acute failure, and who showed histological features consistent with toxic myocarditis, such as diffuse myocardial hepatic necrosis as the most common complication of severe paracetamol poisoning. The frequency with damage with interstitial oedema or bands of necrosis and haemorrhage.10,11,13–15 It is likely that other which paracetamol is used for self-poisoning may, however, give rise to complacency through familiarfactors contributed to toxicity, as such lesions have also been found in fulminant hepatic failure not due ity, and the less common complications may be missed. The purpose of this review is to act as a to paracetamol poisoning.6,16,17 Electrocardiographic abnormalities have been reported in paracetamolreminder of these more unusual complications. Although there have been many reports of toxic induced fulminant hepatic failure as preterminal events.13,18–21 Instances of bradycardia,22 pericardial effects on other body systems, these have often occurred in the presence of hepatic or multi-organ rub23 and endocarditis24 have been mentioned after paracetamol overdose. Ohtani and colleagues25 failure, and in such circumstances it is difficult to distinguish between cause and effect. reported cardiac failure occurring 16 days after a paracetamol overdose sufficient to cause renal failure; however, it is difficult to see how paracetamol could have caused late myocardial damage in this Cardiotoxicity case. Not surprisingly, ECG changes have been reported following overdosage with combination preNon-specific ECG changes, mostly of the ST segment parations of dextropropoxyphene and paracetamol,26 and T wave,1–8 and changes suggestive of pericardand in one such case were clearly attributable to itis,6,9 have been reported in patients with paracethypothermia.27 In 20 unselected cases of fatal paraamol overdose without hepatic encephalopathy, but cetamol poisoning there was no evidence of myocarsuch reports are rare given the number of paracetditis at postmortem examination.28 amol-poisoned patients per year, especially in Two potential mechanisms for paracetamol cardiothe UK. In the case reported by Will and Tomkins,1 toxicity have been postulated.29 It was suggested that the ECG changes may have been due to viral paracetamol may deplete sulphydryl groups to interinfection since the patient had a sore throat and fere with production of nitric oxide and lead to atypical monocytes in the blood film. coronary ischaemia,8 while arrhythmias may be Symptomatic or clinically apparent disturbances precipitated by metabolic complications of paracetof cardiac function appear to be very rare after amol poisoning such as hypoxia,6,30 hyperkalaeparacetamol overdose in the absence of encephalomia,6,31 acidosis6,32 and a rise in serum free fatty pathy.6,9–12 Most of the claims made for paracetamol acids.33,34 No systematic assessment of paracetamol cardiotoxicity have been based on post-mortem findings in patients who developed fulminant hepatic cardiotoxicity per se has been reported using sensit-