Kruse J A, Zaidi S A, Carlson R W
Am J Med. 1987 Jul;83(1):77-82. doi: 10.1016/0002-9343(87)90500-6.
Lactic acidosis unrelated to tissue hypoxia has been described in patients with liver disease. This raises questions regarding the utility of the arterial lactate level as an indicator of tissue hypoperfusion in critically ill patients with hepatic dysfunction. The incidence of hyperlactatemia in a group of critically ill patients with liver disease and its association with clinical indicators of circulatory shock as well as hospital mortality were examined. The medical records of all patients admitted to the medical intensive care unit of Detroit Receiving Hospital between July 1, 1984, and June 30, 1985, with parenchymal liver disease and a total bilirubin level of more than 2 mg/dl were reviewed. Patients were excluded if lactate was not assayed. The severity of liver disease was assessed by Child's classification. Shock was defined as a systolic blood pressure of less than 90 mm Hg and at least two of the following: urine output of less than 20 ml/hour, evidence of decreased skin perfusion, or acutely altered mentation. These criteria were met in 35 patients; three patients had two medical intensive care unit admissions separated by more than one week. There were two patients in Child's class A, three in class B, and 30 in class C. Shock was identified in 27 of the 38 medical intensive care unit admissions. In the group with shock, the maximal lactate level ranged from 1.2 to 30 mM (mean, 9.6). The lactate level was significantly lower (p less than 0.0005) in the group without shock, ranging from 0.6 to 2.0 mM (mean, 1.3). The mean bilirubin level was significantly higher in the group without shock (16.7 mg/dl) than in the group with shock (8.5 mg/dl). A maximal arterial lactate concentration of more than 2.2 mM was significantly associated with hospital mortality. Thus, lactic acidosis in critically ill patients with liver disease is associated with clinical evidence of shock and with increased hospital mortality.
肝病患者中已出现与组织缺氧无关的乳酸性酸中毒。这引发了关于动脉血乳酸水平作为肝功能不全重症患者组织灌注不足指标的效用的疑问。研究了一组肝病重症患者的高乳酸血症发生率及其与循环性休克临床指标以及医院死亡率的关联。回顾了1984年7月1日至1985年6月30日期间入住底特律接收医院内科重症监护病房、患有实质性肝病且总胆红素水平超过2mg/dl的所有患者的病历。未检测乳酸的患者被排除。采用Child分级评估肝病严重程度。休克定义为收缩压低于90mmHg且至少具备以下两项：尿量少于20ml/小时、皮肤灌注减少的证据或急性精神状态改变。35例患者符合这些标准；3例患者有两次间隔超过一周的内科重症监护病房入院记录。Child A级有2例患者，B级有3例，C级有30例。38次内科重症监护病房入院记录中有27次发现休克。休克组的最大乳酸水平为1.2至30mM（平均9.6）。无休克组的乳酸水平显著更低（p<0.0005），为0.6至2.0mM（平均1.3）。无休克组的平均胆红素水平（16.7mg/dl）显著高于休克组（8.5mg/dl）。动脉血最大乳酸浓度超过2.2mM与医院死亡率显著相关。因此，肝病重症患者的乳酸性酸中毒与休克的临床证据及医院死亡率增加相关。
