Abstract

There is a paucity of data documenting the metabolic response to catabolic stress in childhood in general and about protein turnover in critically ill children in particular. Despite a high overall morbidity and mortality rate there is little information on which to base decisions to improve the management either by dietary therapy or by use of growth factors. Protein turnover is a key metabolic process that significantly alters during the catabolic state. Protein kinetics are easy to quantify using various stable isotope models, with some having advantages in the critically ill child. The 1-13C leucine technique is the most widely used and best validated model to date, requiring accurate estimation of CO2 production. There is also uncertainty about the bicarbonate kinetics and pool sizes in ventilated children whose respiratory function is severely impaired. The value of the 15N glycine (end product) technique is more limited because the time to achieve isotopic equilibrium is lengthy and considerable concerns about the validity of the model exist. The ring-D5 phenylalanine technique has the advantage of not requiring the measurement of CO2 production or 13C enrichment, but the model has not yet been validated in critically ill children. Despite it is of obvious value to measure protein turnover, few studies in critically ill children have been done.

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