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In the metabolically stressed patient, protein turnover is doubled when compared to healthy subjects.13-15 This process redistributes amino acids from skeletal muscle to the liver, wound, and tissues taking part in the inflammatory response. The mediators of the inflammatory response, acutely needed enzymes, serum proteins, and glucose, are thereby synthesized from degraded body protein stores. The well-established increase in hepatically derived acute phase proteins (including C-reactive protein, fibrinogen, transferrin, and -1-acid glycoprotein), along with the concomitant decrease in transport proteins (albumin and retinol binding protein) is evidence of this protein redistribution.

As substrate turnover is increased during the pediatric stress response, rates of both whole body protein degradation and whole body protein synthesis are accelerated. However, protein breakdown predominates, leading to a hypercatabolic state with ensuing net negative protein and nitrogen balance.16 Protein loss is evident in elevated levels of excreted urinary nitrogen during critical illness. Evidence of severe protein loss includes skeletal muscle wasting, weight loss, delayed wound healing, and immune dysfunction.17

The increase in protein breakdown associated with the metabolic stress response takes place for two fundamental reasons. First, the body needs to reroute its amino acid utilization from structural proteins to those required for the inflammatory response and wound healing. In addition, the body appears to have an increased need for glucose production during times of metabolic stress, and rates of gluco-neogenesis are accelerated during illness and injury.18-20 Accelerated glucose production is necessary, because glucose is a versatile energy source used by tissues involved in the inflammatory response. It has been shown, for example, that glucose utilization by leukocytes is significantly increased in settings of inflammation.21 Unfortunately, the nutritional provision of additional dietary glucose to critically ill patients does not suppress the body's need for increased glucose production, and therefore, net protein breakdown to fuel glucose production continues to predomi-nate.19,22,23

Although increased muscle protein catabolism is a successful short-term adaptation during critical illness, it is limited and ultimately harmful to the pediatric patient who has reduced protein stores and elevated protein demands at baseline. Without elimination of the inciting stress, the progressive breakdown of diaphragmatic, cardiac, and skeletal muscle can lead to respiratory compromise, fatal arrhythmia, and loss of lean body mass. Moreover, a prolonged negative protein balance may have a significant impact on the child's growth and development. Healthy, nonstressed neonates require a positive protein balance of nearly 2 g/kg/d.24,25 In contrast, critically ill, premature neonates requiring mechanical ventilation have a protein balance of -1 g/kg/d.26,27 Critically ill neonates who require extracorporeal membrane oxygenation (ECMO) have exceedingly high rates of protein loss with a net protein balance of -2.3 g/kg/d.13

The protein catabolic response is concerning, because it is well known to correlate with morbidity and mortality in the surgical patient. Fortunately, amino acid supplementation in critically ill children tends to promote increased nitrogen retention and positive protein balance.23,28 The mechanism appears to be an increase in protein synthesis, although the rate of protein degradation remains constant.29,30 The

Gaining Weight 101

Gaining Weight 101

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