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OVERVIEW

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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.

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FIGURE 1-1.

A Acute metabolic stress response to acute injury.

Reproduced with permission from Baker SS, Baker RD, Davis AM: Pediatric Nutritional Support Energy Metabolism. Jones & Bartlett; 2007

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FIGURE 1-1.

B GH, growth hormone; IGF-1, insulin-like growth factor I; U3MH, urinary 3-methyl histidine.

Reproduced with permission from Mehta N, Jaksic, T. The Critically ill Child. In: Duggan W, Walker., ed. Nutrition in Pediatrics. 4 ed. Hamilton, Ontario: B. C. Decker Inc.; 2008

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NEUROENDOCRINE/AUTONOMIC NERVOUS SYSTEM RESPONSE

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Evolution of the stress response in mammals has resulted in the development of an intricate system of reflex neural injury-induced stimuli that trigger the central nervous system (CNS), causing alterations in the hypothalamic-anterior pituitary axes, including the adrenal (increased cortisol secretion), the somatotrophic (increased GH secretion), the thyrotrophic (decreased triiodothyronine [T3] and increased reverse T3 [rT3] secretion), and the gonado-/lactotrophic (decreased testosterone, increased prolactin) axes.3,6 The CNS also acts through the peripheral sympathetic nervous system ...

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