Stacpoole P W, Wright E C, Baumgartner T G, Bersin R M, Buchalter S, Curry S H, Duncan C, Harman E M, Henderson G N, Jenkinson S
University of Florida, College of Medicine, Gainesville 32610.
Am J Med. 1994 Jul;97(1):47-54. doi: 10.1016/0002-9343(94)90047-7.
To determine the pathogenesis and clinical course of lactic acidosis in adults receiving standard medical care.
Placebo arm of a 5-year prospective, randomized, blinded study comparing placebo and dichloroacetate as specific lactate-lowering therapy. Each patient received intravenous saline placebo in addition to conventional therapy.
Intensive care units of 10 tertiary care hospitals in North America.
One hundred twenty-six patients with lactic acidosis, defined as arterial blood lactate greater than or equal to 5 mmol/L and either arterial pH of less than or equal to 7.35 or base deficit greater than 6 mmol/L. Patients were followed for up to 6 months.
Mean +/- SD demographic entry data for 126 patients included: age 56 +/- 17 years, lactate 10.4 +/- 5.5 mmol/L, pH 7.24 +/- 0.14, calculated base deficit 14.1 +/- 5.4, arterial systolic blood pressure 103 +/- 29 mm Hg, Glasgow Coma score 7.9 +/- 4.9, and APACHE II score 19.2 +/- 8.1. Despite fluids and pressors, 32% of patients had systolic blood pressures of less than or equal to 90 mm Hg in association with sepsis (59%), cardiac failure (18%), or hemorrhage (18%). The most common causes of lactic acidosis in the absence of shock were sepsis (49%), liver disease (15%), and respiratory failure (12%). The median survival was 38.5 hours. Survival at 24 hours was 59%. Arterial pH predicted 24-hour survival better than base deficit or bicarbonate level. Percent survival was 41% at 3 days and 17% at 30 days. Only 21% of patients survived to leave the intensive care unit, and 17% were discharged from the hospital. In patients receiving sodium bicarbonate, neither acid-base nor hemodynamic status improved.
In this first prospective study of the clinical course of acute lactic acidosis in adults, nearly all subjects had both hemodynamic and nonhemodynamic (metabolic) underlying causes, many of which independently predicted survival and most of which were refractory to standard care.
确定接受标准医疗护理的成年患者乳酸酸中毒的发病机制和临床病程。
一项为期5年的前瞻性、随机、双盲研究的安慰剂组,该研究比较安慰剂和二氯乙酸作为特定的降乳酸疗法。每位患者在接受常规治疗的基础上还接受静脉生理盐水安慰剂治疗。
北美10家三级护理医院的重症监护病房。
126例乳酸酸中毒患者,定义为动脉血乳酸大于或等于5 mmol/L,且动脉pH小于或等于7.35或碱缺失大于6 mmol/L。对患者进行长达6个月的随访。
126例患者的平均±标准差人口统计学入组数据包括:年龄56±17岁,乳酸10.4±5.5 mmol/L,pH 7.24±0.14,计算碱缺失14.1±5.4,动脉收缩压103±29 mmHg,格拉斯哥昏迷评分7.9±4.9,急性生理与慢性健康状况评分系统II(APACHE II)评分19.2±8.1。尽管进行了补液和使用血管活性药物治疗,但32%的患者因脓毒症(59%)、心力衰竭(18%)或出血(18%)而出现收缩压小于或等于90 mmHg。在无休克情况下,乳酸酸中毒最常见的病因是脓毒症(49%)、肝病(15%)和呼吸衰竭(12%)。中位生存期为38.5小时。24小时生存率为59%。动脉pH比碱缺失或碳酸氢盐水平更能预测24小时生存率。3天时生存率为41%,30天时为17%。只有21%的患者存活至转出重症监护病房,17%的患者出院。接受碳酸氢钠治疗的患者,酸碱状态和血流动力学状态均未改善。
在这项关于成年患者急性乳酸酸中毒临床病程的首次前瞻性研究中,几乎所有受试者都存在血流动力学和非血流动力学(代谢)方面的潜在病因,其中许多因素可独立预测生存率,且大多数病因对标准治疗无效。