• J A Kruse, S A Zaidi, and R W Carlson.
• Am. J. Med. 1987 Jul 1;83(1):77-82.

AbstractLactic 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.

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