Alterations in Fuel Metabolism in Critical Illness

  • Barry A. Mizoch
Part of the Contemporary Endocrinology book series (COE, volume 4)


Claude Bernard (1), in the late 19th century, was one of the first to recognize that acute injury was associated with the development of hyperglycemia. His observation was subsequently confirmed by others who applied the terms “traumatic diabetes,” “diabetes of injury,” or “stress diabetes” to this state. It has been suggested that the evolutionary value of a hyperglycemic response to injury is to compensate for volume loss by promoting movement of cellular fluid into the intravascular compartment or liberating water bound to glycogen (2). It has also been proposed that hyperglycemia is beneficial by satisfying an increased requirement for glucose by cells active in the immune response to severe injury or infection (e.g., neutrophils, macrophages); the wound may be viewed from this perspective as an “organ of repair,” which generates a hyperglycemic milieu through the release of neuroendocrine and cytokine mediators (3). In 1942, Sir David Cutherbertson (4) introduced the terms “ebb” and “flow” to describe the phases of hypo- and hypermetabolism, which follow traumatic injury. The ebb phase begins immediately following injury; it is characterized by tissue hypoperfusion and peripheral vasoconstriction, which are accompanied by a decrease in metabolic activity. Hyperglycemia during the ebb phase roughly parallels the severity of injury; it is promoted by hepatic glycogenolysis secondary to catecholamine release, as well as by direct sympathetic stimulation of glycogen breakdown (5, 6). The ebb phase typically lasts 12–24 h, but may last longer depending on the severity of injury and adequacy of resuscitation. Restoration of oxygen delivery and metabolic substrate appear to signal the onset of the flow phase (also known as the catabolic phase).


Insulin Resistance Critical Illness Hepatic Glucose Production Circ Shock Glycogen Breakdown 
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  • Barry A. Mizoch

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