Oh M S, Carroll H J, Goldstein D A, Fein I A
Ann Intern Med. 1978 Dec;89(6):925-7. doi: 10.7326/0003-4819-89-6-925.
We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine.
我们研究了35例患者,以发现糖尿病酮症酸中毒恢复期高氯性酸中毒的发生情况。入院时,患者存在典型的正常氯性酸中毒,阴离子间隙增加与血清碳酸氢盐降低恰好平衡。相比之下,在18例苯乙双胍诱导的乳酸性酸中毒患者中,入院时阴离子间隙的增加远大于碳酸氢盐的降低。乳酸性酸中毒和酮症酸中毒之间的差异可能是由于乳酸的排泄速度比酮阴离子慢。酮症酸中毒患者接受治疗后,酸中毒主要变为高氯性且阴离子间隙正常。血清碳酸氢盐未能恢复正常归因于尿中酮阴离子的排泄。