RT Book, Section A1 Chwals, Walter J. A2 Goday, Praveen S. A2 Mehta, Nilesh M. SR Print(0) ID 1105178408 T1 The Acute Metabolic Response to Injury in Children T2 Pediatric Critical Care Nutrition YR 2015 FD 2015 PB McGraw-Hill Education PP New York, NY SN 978-0-07-179852-5 LK accesspediatrics.mhmedical.com/content.aspx?aid=1105178408 RD 2024/10/08 AB In response to a variety of injurious stimuli, such as trauma, sepsis, and acute inflammatory conditions, a series of metabolic changes occur that characterize the acute metabolic stress (AMS) response in humans (Figs. 1-1A and 1-1B). This response is basically stereotypical in nature in all patient populations (children and adults).1-4 This response may vary to some degree with respect to the nature (e.g., sepsis, burn,) and severity of the insult, as well as factors that impact the endogenous metabolic reserve and/or reserve mobilization capacity (e.g., malnutrition, recent previous tissue injury, underlying systemic disease, age, pharmacologic intervention,) of the acutely injured host. In infants, especially those born prematurely, functional immaturity is a particularly important response-modifying variable.5 Among the early features of the injury response is the release of cytokines, followed rapidly by important alterations in the hormonal environment. Increased counter-regulatory hormone concentrations are associated with insulin and growth hormone (GH) resistance. As a result of this response, a sequence of metabolic events is initiated that includes the catabolism of endogenous stores of protein, carbohydrate, and fat to provide essential substrate intermediates and energy necessary to fuel the ongoing response process. Amino acids from catabolized proteins flow to the liver where they provide substrate for the synthesis of acutephase proteins and glucose (gluconeogenesis). Therefore, the AMS response represents a hypermetabolic, hypercatabolic state that results in the loss of endogenous tissue stores with associated increases in glucose and free fatty acid (FFA) production and oxidation, increased energy expenditure, and increased protein turnover and breakdown. Growth, which is an anabolic process, is thought to be inhibited during periods of AMS. As the AMS response resolves, adaptive anabolic metabolism ensues to restore catabolic losses. In children, this phase is characterized by the resumption of somatic growth.