Disturbances of oxygen supply or cellular oxygen metabolism are common in critically ill patients. An understanding of dysoxia, or oxygen limited energy depletion, requires an understanding of the normal physiology of cell oxygen metabolism, and the compensatory mechanisms that supply high energy molecules under conditions of hypoxia. Understanding disorders associated with hyperlactataemia requires consideration of the cellular response in dysoxia, and pathology specific derangements in lactate metabolism. Much has recently been discovered about the causes of lactic acidosis in sepsis, and about the role of lactate in monitoring critically ill children.

This review discusses how cells produce energy for metabolism under normal and hypoxic conditions; what happens to lactate produced during these processes; the clinical situations in which lactic acidosis has been described; the reasons why excess lactate may occur in sepsis; the evidence that a high lactate concentration is not simply a surrogate for tissue dysoxia; the relevance of lactate in the management of critically ill children; and suggested strategies to manage high blood lactate.