MAXIMAL PARENTERAL GLUCOSE-OXIDATION IN HYPERMETABOLIC YOUNG-CHILDREN- A STABLE-ISOTOPE STUDY

Background: During periods in which nutrition support of critically il l young children must be parenteral, glucose infusions are administere d at up to 10 or more mg.kg(-1).min(-1) to meet predicted energy needs . However. data in adults suggest that such high glucose loads exceed the ability to oxidize glucose in the hormonal milieu that, characteri zes critical illness. The purpose of this study was to determine if th ese high glucose loads are oxidized by critically ill young children. Methods: Ten young children ri; serious bums were enrolled in a stable isotope study of glucose metabolism. These five boys and five girls w ere an average age of 5.2 years (range, 1 to 11 years), weight of 18.4 kg (range, 10 to 31 kg) and burn size of 51.6% of the body surface (r ange, 35% to 86%). During clinically required episodes of parenteral n utrition support, we used the [C-13(6)]glucose tracer to assess the ef ficacy of glucose oxidation at both 6 and 8 mg . kg(-1) . min(-1). Ser um glucose was recorded and indirect calorimetry was performed. Result s: The fraction of exogenous glucose oxidation fell from 59% +/- 6% to 47% + 5% (p < .06). Although there was a significantly increased leve l of total glucose oxidation (3.2 to 3.8 mg . kg(-1) . min(-1)), this increment (29% +/- 9%) was accompanied by a significant decrease in th e efficiency of energy production, because the bulk of the additional glucose above 5 mg . kg(-1) . min(-1) was not being oxidized. Plasma g lucose concentration did not change (145 +/- 4 vs 137 +/- 4 mg/dL, p < .01) and whole-body expired gas respiratory quotients remained consist ent with a mixed fuel oxidation, implying that there exists an increas ed rate of exogenous glucose uptake by tissues in nonoxidative pathway s. Conclusions: Maximum glucose oxidation in severely burned children occurs at intakes approximating 5 mg . kg(-1) . min(-1). Exogenous glu cose in excess of this amount enters nonoxidative pathways and is unli kely to improve energy balance. Clinical markers such as serum glucose levels or expired respiratory quotient may not detect inefficient glu cose utilization.