ENERGY-METABOLISM IN SEPSIS AND INJURY

The development of malnutrition is often rapid in critically ill patie nts with sepsis and severe trauma. In such patients, a wide array of h ormonal and nonhormonal mediators are released, inducing complex metab olic changes. Hypermetabolism, associated with protein and fat catabol ism, negative nitrogen balance, hyperglycemia, and resistance to insul in, constitute the hallmark of this response. Critically ill patients demonstrate a marked alteration in the adaptation to prolonged starvat ion: resting metabolic rate and tissue catabolism stay elevated, while ketogenesis remains suppressed. The response to nutrition support is impaired. Substrate use is modified in septic and traumatized patients . Glucose administration during severe aggression does not suppress th e enhanced hepatic glucose production and the lipolysis. This phenomen on, related to tissue insulin resistance, ensures a high flow of gluco se to the predominantly glucose-consuming cells, such as the wound, th e inflammatory, and immune cells, all insulin-independent cells. In ad dition, the elevated protein catabolism is difficult to abolish, even during aggressive nutrition support. Thus, in patients with prolonged aggression, these alterations produce a progressive loss of body cell mass and foster the development of malnutrition and its dire complicat ions. In this review, the relevant physiologic data and the nutritiona l implications related to energy metabolism in septic and injured pati ents are discussed, while potential therapeutic strategies are propose d. (C) Elsevier Science Inc. 1997.