Nutritional support of the critically ill child.pdf

Nutritional support of the critically ill child.pdf

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Nutritional support of the critically ill child

Nutritional support of the critically ill child Michael S.D. Agus, MD,* and Tom Jaksic, MD, PhD? The pediatric metabolic response to injury and operation is proportional to the degree of stress and causes an increase in the turnover of proteins, fats, and carbohydrates. Thereby, substrates are made readily available for the immune response and wound healing. Because this process requires energy, the resting energy expenditure of ill patients increases. Whole-body protein degradation rates are elevated out of proportion to synthetic rates, and negative protein balance also ensues. Neonates and children are particularly susceptible to the loss of lean body mass and its attendant increased morbidity and mortality caused by an intrinsic lack of endogenous stores and greater baseline requirements. An appropriately designed mixed fuel system of nutritional support replete in protein does not quell this metabolic response but can result in anabolism and continued growth in ill children. In addition, the use of adequate analgesia and anesthesia is a readily available and proven means of reducing the magnitude of the catabolism associated with operation and injury. Finally, as hormonal- and cytokine-mediated metabolic alterations are better understood, therapeutic interventions may become available to directly modulate the metabolic response to illness, thus potentially further improving clinical outcome in pediatric surgical patients. Curr Opin Pediatr 2002, 14:470–481 ? 2002 Lippincott Williams Wilkins, Inc. Surgery, trauma, and sepsis are accompanied by a con- stellation of metabolic aberrations that tend to be pro- found and predictable. Sir David P. Cuthbertson de- scribed the fundamental aspects of this metabolic response to injury in the adult over 50 years ago [1,2]. By observing patients with long bone fractures and utilizing complementary animal models, he determined that the excessive output of nitrogen following the stress of injury was a result of the catabolis

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