There is a paucity of data documenting the metabolic response to catab
olic stress in childhood in general and about protein turnover in crit
ically ill children in particular. Despite a high overall morbidity an
d mortality rate there is little information on which to base decision
s to improve the management either by dietary therapy or by use df gro
wth factors. Protein turnover is a key metabolic process that signific
antly alters during the catabolic state. Protein kinetics are easy to
quantify using various stable isotope models, with some having advanta
ges in the critically ill child. The 1-C-13 leucine technique is the m
ost widely used and best validated model to date, requiring accurate e
stimation of CO2 production. There is also uncertainty about the bicar
bonate kinetics and pool sizes in ventilated children whose respirator
y function is severely impaired. The value of the N-15 glycine (end pr
oduct) 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-D-5 phenylalanine technique has the advanta
ge of not requiring the measurement of CO2 production or C-13 enrichme
nt, but the model has not yet been validated in critically ill childre
n. Despite it is of obvious value to measure protein turnover, few stu
dies in critically ill children have been done.