Hyperlactatemia in patients with sepsis is an indicator of the severity of stress response. Hyperlactatemia may possibly develop as a byproduct of overall acceleration in glycolysis in severe sepsis. This may well be an adaptive host mechanism designed to provide for efficient generation of energy in response to severe stress; however, some investigators have observed that patients with sepsis have decreased lactate clearance rather than increased lactate production. Skeletal muscle and lung tissue have been shown to produce lactate during sepsis. Therefore, hyperlactatemia may be caused by increased lactate production in the gut, liver, lungs, and skeletal muscles, decreased lactate clearance in the liver, or a combination of both.
