Protein, Energy and Their Interaction in Critically Ill Children

Critically ill patients are in a catabolic state, characterized by three major metabolic changes. First, there is an increased protein turnover with enhanced hepatic protein synthesis and muscle protein breakdown. Second, during critical illness there is increased lipolysis, or the breakdown of triglycerides to free fatty acids (FFA) and glycerol. And third, insulin resistance causes hyperglycemia due to ongoing endogenous glucose production (glycogenolysis and gluconeogenesis) and blunted peripheral uptake. These metabolic derangements are caused by various endogenous and exogenous triggers, including increased inflammatory cytokines (Tumor Necrosis Factor α, interleukin-1, interleukin-6, and interleukin-8), catecholamines and glucocorticoids, all in which insulin resistance plays a central role.This response to injury is universal and has been beneficial all through evolution at the acute onset of severe disease or trauma. However, modern medicine has improved survival rate and critical illness has become a process which lasts not just mere hours but can last for days or even weeks. Early last century Sir David P. Cuthbertson described the short initial hypometabolic “ebb” phase, followed by the prolonged hypermetabolic “flow” phase during adult critical illness. Persistent glucose overload and breakdown of skeletal muscle and adipose tissue releasing large amounts of amino acids and FFA are the result. Unfortunately, although plasma substrate levels may be increased, their availability to peripheral tissues may be blunted (because of factors such as insulin resistance and inhibition of lipoprotein lipase), while plasma levels of other substrates (e.g. specific amino acids, cholesterol) may be insufficient to meet metabolic demands. As a result, these metabolic changes, beneficial in the initial phase from a teleological viewpoint, become detrimental during prolonged critical illness.

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