Gray T A, Buckley B M, Vale J A
West Midlands Poisons Unit, Dudley Road Hospital, Birmingham.
Q J Med. 1987 Oct;65(246):811-21.
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.
对53例扑热息痛中毒患者测定了血浆乳酸浓度和酸碱状态。11例患者(第1组)血浆扑热息痛浓度低于标准治疗决策线;19例(第2组)在过量服药15小时内就诊,血浆扑热息痛浓度高于治疗线,接受了N - 乙酰半胱氨酸治疗。其余23例患者(第3组)到医院就诊太晚(过量服药超过15小时),N - 乙酰半胱氨酸治疗无法完全有效。第1组55%的患者和第2组42%的患者入院时存在代偿性代谢性酸中毒,第2组另外21%的病例存在失代偿性代谢性酸中毒。第3组一半的患者存在酸中毒:22%为代偿性,26%为失代偿性代谢性酸中毒。入院时,第2组和第3组患者的平均血浆乳酸浓度升高,而第1组患者未升高。第2组患者的血浆乳酸浓度随后降至正常,但在某些情况下又再次轻度升高,此时与血清天冬氨酸转氨酶活性峰值密切吻合。在过量服药15小时内就诊的患者中,入院时血浆乳酸浓度升高与扑热息痛浓度之间存在显著相关性。在就诊较晚的患者(第3组)中血浆乳酸升高的时间比第2组更长,酸中毒和高乳酸血症是4例死亡患者的突出特征。本研究首先表明,扑热息痛过量后高乳酸血症很常见,无论是否伴有明显的酸碱紊乱,尤其是在重度中毒患者中。由于20%早期就诊并需要保护性治疗的患者存在失代偿性代谢性酸中毒,如果不能自发缓解,应予以查找并纠正。其次,就诊太晚无法进行有效治疗的患者中有一半存在酸中毒,而那些失代偿性代谢性酸中毒难以纠正的患者预后较差。在不明病因的代谢性酸中毒鉴别诊断中应考虑扑热息痛中毒。