Clinical applications of lactate testing in patients with sepsis and septic shock

Hyperlactatemia is very common in patients with sepsis and septic shock and is closely associated with poor prognosis. The third international consensus definition for sepsis and septic shock recently revised the definition of septic shock. Serum lactate concentration >2 mmol/L was added as a key component in the definition of septic shock. Moreover, the Surviving Sepsis Campaign (SSC)recommended lactate normalization in patients with elevated lactate levels as a marker of tissue hypoperfusion. Therefore, lactate-guided sepsis and septic shock management is preferred rather than central venous oxygen saturation (ScvO₂) for monitoring patients’ tissue hypoperfusion. Hyperlactatemia occurs when glycolytic flux is increased via anaerobic metabolism such as tissue hypoperfusion and β-adrenergic stimulation by endogenous/exogenous catecholamines. Moreover, decreased serum lactate removal due to hepatic and renal dysfunction promotes hyperlactatemia. Thus, lactate-guided treatments should aim to reduce glycolytic flux and enhance lactate removal. To reduce glycolytic flux, tissue oxygen delivery is increased by increasing the cardiac output with sufficient volume resuscitation and improving the hemodynamic state and oxygen contents are increased by treating anemia and providing enough oxygen supply. Moreover, the early reduction of adrenergic vasopressors is important in reducing glycolytic flux. To enhance lactate removal, hepatic and renal function should be preserved by removing toxic materials and correcting the reversible cause of dysfunction. Dichloroacetate and thiamine induce an aerobic pyruvate metabolism in Krebs cycle and may help reduce serum hyperlactatemia. However, the most important treatment is controlling the underlying infection.