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  • Title: Hyperlactataemia and metabolic acidosis following paracetamol overdose.
    Author: Gray TA, Buckley BM, Vale JA.
    Journal: Q J Med; 1987 Oct; 65(246):811-21. PubMed ID: 3449887.
    Abstract:
    Plasma lactate concentrations and acid-base status were determined in 53 patients poisoned with paracetamol. Eleven patients (Group 1) had plasma paracetamol concentrations below the standard treatment decision line; 19 cases (Group 2) presenting within 15 h of overdose had plasma paracetamol concentrations above the treatment line and received N-acetylcysteine. The remaining 23 patients (Group 3) arrived at hospital too late (more than 15 h after overdose) for treatment with N-acetylcysteine to be completely effective. Compensated metabolic acidosis was present on admission in 55 per cent of Group 1 and 42 per cent of Group 2 patients, and a further 21 per cent of cases in Group 2 had an uncompensated metabolic acidosis. Half the patients in Group 3 were acidotic: 22 per cent had a compensated and 26 per cent an uncompensated metabolic acidosis. On admission, the mean plasma lactate concentration was elevated in both Group 2 and Group 3 patients though not in Group 1 cases. Plasma lactate concentration then fell to normal in patients in Group 2 but became mildly elevated again in some cases at a time which coincided closely with the peak in serum aspartate aminotransferase activity. In patients presenting within 15 h of overdose there was a significant correlation between the elevation in plasma concentrations of lactate and paracetamol at admission. In patients presenting late (Group 3), plasma lactate remained elevated for longer than in Group 2 and acidosis and hyperlactataemia were prominent features in the four patients who died. This study demonstrates first that hyperlactataemia, with or without significant acid-base disturbance, is common following paracetamol overdose particularly in those who are severely poisoned. As uncompensated metabolic acidosis is found in 20 per cent of patients who present early and require protective therapy, it should be sought and corrected if it does not remit spontaneously. Second, half the patients presenting too late for effective treatment are acidotic and those with an uncompensated metabolic acidosis resistant to correction have a poor prognosis. Paracetamol poisoning should be considered in the differential diagnosis of metabolic acidosis of unknown aetiology.
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