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Revue médicale suisse · Dec 2013
[Hyperlactatemia and lactic acidosis in the critically ill patient].
- Nawfel Ben-Hamouda, Laurence Haesler, and Lucas Liaudet.
- Service de médecine intensive adulte et Centre des brûlés, CHUV, 1011 Lausanne. mohamed-nawfel.ben-hamouda@chuv.ch
- Rev Med Suisse. 2013 Dec 11; 9 (410): 2335-40.
AbstractHyperlactatemia is associated with an ominous prognosis in critical illness and must be rapidly detected. Lactate is produced by glycolysis through reduction of pyruvate, itself oxidized in the mitochondria. It is transported to the liver and converted to glucose through gluconeogenesis (Cori's cycle). Hyperlactatemia can result from excessive production or reduced clearance. Excess production can occur in aerobic conditions, following an increase in pyruvate generation, or in anaerobic conditions, due to impaired pyruvate oxidation. Reduced lactate clearance occurs as a result of liver hypoperfusion or hepatic failure. Lactate/pyruvate ratio, as well as the concomitant existence of metabolic acidosis (lactic acidosis), help distinguish the different mechanisms leading to hyperlactatemia, which are reviewed in detail in this article.
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