Flanagan R J, Mant T G
Hum Toxicol. 1986 May;5(3):179-82. doi: 10.1177/096032718600500305.
Coma and profound metabolic acidosis early in acute paracetamol poisoning have been described in three patients. Of five further patients (four female, one male, aged 17-80 years) with severe poisoning (plasma paracetamol concentration greater than 800 mg/l, 4-12 h postingestion), four were deeply unconscious on admission and two had a severe metabolic acidosis. Signs of hepatorenal damage were minimal and no additional poisons were detected except salicylates (plasma concentration 290 mg/l) in one instance. Plasma paracetamol half-lives were prolonged (median 9.4 h, range 4.8-39 h) and one patient sustained massive hepatic damage and a further patient died despite treatment with intravenous acetylcysteine. Paracetamol poisoning, when associated with exceptionally high plasma concentrations, can give rise to coma and metabolic acidosis in the absence of hepatic failure or other drugs. Although unusual, other such presentations may not have been recognized because a toxicology screen was not performed.
已有三名患者在急性对乙酰氨基酚中毒早期出现昏迷和严重代谢性酸中毒。另有五名严重中毒患者（四名女性，一名男性，年龄17 - 80岁）（摄入后4 - 12小时血浆对乙酰氨基酚浓度大于800 mg/l），其中四名入院时深度昏迷，两名有严重代谢性酸中毒。肝肾损害迹象轻微，除一例检测到水杨酸盐（血浆浓度290 mg/l）外，未检测到其他毒物。血浆对乙酰氨基酚半衰期延长（中位数9.4小时，范围4.8 - 39小时），一名患者发生大量肝损伤，另一名患者尽管接受静脉注射乙酰半胱氨酸治疗仍死亡。对乙酰氨基酚中毒在血浆浓度异常高时，可在无肝衰竭或其他药物的情况下导致昏迷和代谢性酸中毒。虽然不常见，但其他此类表现可能因未进行毒理学筛查而未被识别。
