Energy expenditure in critically ill children

Objectives: To measure energy expenditure in critically ill children and compare it with the energy expenditure predicted by recommended formulas, and relate the measured energy expenditure to nutritional and clinical indices. Design: A prospective, clinical study. Setting: Tertiary care pediatric intensive care unit in a university children's hospital. Patients: A total of 37 patients with critical illness who were mechanically ventilated for greater than or equal to 24 hrs were studied. Interventions: None. Measurements and Main Results: Chronic protein-energy malnutrition (CPEM) and acute protein-energy malnutrition were defined by the Waterlow's stages and fat and protein stores were classified as defined by Frisancho, Ryan, and Martinet. Severity of illness was assessed by the Pediatric Risk of Mortality Score, the Therapeutic intervention Scoring System, and indices of organ failure. Oxygen consumption, carbon dioxide production, and the respiratory quotient were measured by indirect calorimetry, and energy expenditure (MEE) was calculated using the modified Weir formula. Resting energy expenditure (PBMR), predicted energy expenditure, and caloric intake were calculated using recommended formulas. A total of 77 measurements were made in 37 children. MEE was significantly lower than PBMR as estimated by air equations except the Talbot equations. MEE was significantly lower than predicted energy expenditure and the recommended dairy allowances. On the first day, the MEE/PBMR ratio was <0.9 in 56.8%, 0.9-1.1 in 21.6%, and >1.1 in 21.6% of patients. MEE did not differ significantly among disease groups or between medical and surgical patients. There was no difference in MEE with or without neuromuscular blockade. MEE was tower in the presence of multiple organ system failure (MOSF) (1019 + 166 kcal/m(2) without MOSF vs. 862 + 241 with MOSF; p = .025). A total of 21% had CPEM and 8.1% had acute protein-energy malnutrition. Multivariate stepwise regression analysis showed that the protein intake, midarm muscle area, midarm fat area, the use of vasoactive agents, and sedation correlated with MEE (p < .05). With CPEM, MEE was correlated to the severity of illness (p < .05). Patients at risk for protein stores depletion (midarm muscle areas 1 and 2) had a higher incidence of MOSF compared with nutritionally normal children (p < .05), whereas patients with fat stores depletion (midarm fat area 2) had a higher probability of death (50% vs. 6%, respectively). Conclusions: Recommended daily allowances and energy expenditure predicted by using a stress-related correction to the resting energy expenditure grossly overestimate MEE. MEE is close to PBMR and in many patients, it is lower than PBMR. MEE that is lower than PBMR is associated with a higher morbidity. Nutritional repletion should thus be based on MEE to avoid the problems of over- or underfeeding.