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Key Points

  1. Children have reduced metabolic reserves and are particularly susceptible to the adverse effects associated with the catabolic response to critical illness.

  2. The metabolic response to injury is proportional to the degree of stress.

  3. Both protein degradation and protein synthesis increase during illness; however, quantitatively the former predominates. Hence, net negative protein balance ensues.

  4. Adequate supplementation of protein is the most important nutritional intervention in children during illness.

  5. In illness the breakdown of existing skeletal muscle stores and consequent release of amino acids is driven by increased requirements. These needs include amino acids to synthesize new proteins and the conversion of these amino acids to form glucose through the process of gluconeogenesis. During the metabolic stress state, this catabolic process is refractory to inhibition by the supplementation of dietary glucose.

  6. Energy expenditure can be measured either directly or indirectly. Direct calorimetry is very precise but not practical as a method to use in sick children. Indirect calorimetry requires a leak-free system, which can be difficult to achieve in children with uncuffed endotracheal tubes or not breathing calmly. Other indirect methods include deuterated water and 13C-labeled bicarbonate, which have been shown to correlate with indirect calorimetry.

  7. In neonates and children, the increase in resting energy expenditure associated with surgery is very brief and is measured in hours.

  8. Free fatty acids are the primary source of energy in stressed patients. In neonates, with limited stores, this makes them more susceptible to develop essential fatty acid deficiency. The quantity of lipid necessary to obviate fatty acid deficiency is relatively limited. Newer experimental data support the use of lipid-limited omega-3 formulas, in highly selected patients with cholestasis and a long-term requirement for parenteral nutrition.

  9. During illness neural pathways, hormones, and inflammatory mediators mediate the prolonged metabolic response. The ability to effectively modulate these responses could result in an amelioration of the net negative protein balance that exists during stress states. Neural pathway modulation is achieved with adequate sedation and analgesia and has been shown to decrease the hypercatabolic state in ill neonates. Hormonal and inflammatory mediator modulation remains experimental at this time.


Surgery, trauma, and sepsis are accompanied by a constellation of metabolic aberrations that tend to be profound and predictable. Sir David P. Cuthbertson described the fundamental aspects of this metabolic response to injury in the adult over 50 years ago. 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 catabolism of whole-body protein rather than merely the loss of muscle mass surrounding the site of injury. Diet, particularly protein intake, affected the degree of catabolism. Regardless of the etiology of the injury, the metabolic response seemed to be stereotypic and was characterized by a short “ebb” phase marked by relative hypometabolism followed by a subsequent prolonged rise in metabolic activity termed the “flow” ...

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