Critical care medicine · 1991
Evolution of energy expenditure and nitrogen excretion in severe head-injured patients.
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Bruder N, Dumont J C, François G
Аннотация
OBJECTIVE: The aim of the study was to estimate the influence of therapeutic changes on the level of energy expenditure (EE) and N excretion in a homogeneous group of patients usually considered hypermetabolic.
DESIGN: EE and N excretion of head-injured patients were measured simultaneously at phases 1 and 2 (patients treated 4 +/- 3 and 18 +/- 8 days after injury, respectively).
SETTING: Acute care hospital.
PATIENTS: Eight severe head-injured patients, mean weight 63.1 +/- 6.1 (SD) kg, mean age 21 +/- 3.8 (SD) yr.
INTERVENTIONS: At phase 1, all patients were sedated with fentanyl (6.7 +/- 1.9 micrograms/kg.hr) plus flunitrazepam (9.1 +/- 4.8 micrograms/kg.hr) and were mechanically ventilated. All patients received continuous total parenteral nutrition. The nonprotein caloric intake averaged 1092 +/- 200 kcal/day, including 77% glucose and 23% fat (Intralipid 20%). The total N intake averaged 7 +/- 5 g/day, consisting of crystalline amino acids. At phase 2, no patient received any sedative and all were breathing spontaneously via tracheostomy. All patients received parenteral and/or enteral nutrition. The nonprotein caloric intake averaged 1929 +/- 200 kcal/day consisting of 65% carbohydrates and 35% fat. The total N intake averaged 13 +/- 2 g/day.
MEASUREMENTS AND MAIN RESULTS: The EE was significantly higher at phase 2 than at phase 1 (2121 vs. 1737 kcal), but the interindividual variability was low at both phases. N excretion was high at the two periods of the study and not correlated to the level of EE. The RQ was 0.75 at both periods, indicating predominant fat oxidation.
CONCLUSIONS: We could not demonstrate any parallelism in the evolution of EE and protein catabolism in head-injured patients. The therapeutics (mechanical ventilation, sedation, and nutrition) have a major effect on EE but little on N excretion.
DESIGN: EE and N excretion of head-injured patients were measured simultaneously at phases 1 and 2 (patients treated 4 +/- 3 and 18 +/- 8 days after injury, respectively).
SETTING: Acute care hospital.
PATIENTS: Eight severe head-injured patients, mean weight 63.1 +/- 6.1 (SD) kg, mean age 21 +/- 3.8 (SD) yr.
INTERVENTIONS: At phase 1, all patients were sedated with fentanyl (6.7 +/- 1.9 micrograms/kg.hr) plus flunitrazepam (9.1 +/- 4.8 micrograms/kg.hr) and were mechanically ventilated. All patients received continuous total parenteral nutrition. The nonprotein caloric intake averaged 1092 +/- 200 kcal/day, including 77% glucose and 23% fat (Intralipid 20%). The total N intake averaged 7 +/- 5 g/day, consisting of crystalline amino acids. At phase 2, no patient received any sedative and all were breathing spontaneously via tracheostomy. All patients received parenteral and/or enteral nutrition. The nonprotein caloric intake averaged 1929 +/- 200 kcal/day consisting of 65% carbohydrates and 35% fat. The total N intake averaged 13 +/- 2 g/day.
MEASUREMENTS AND MAIN RESULTS: The EE was significantly higher at phase 2 than at phase 1 (2121 vs. 1737 kcal), but the interindividual variability was low at both phases. N excretion was high at the two periods of the study and not correlated to the level of EE. The RQ was 0.75 at both periods, indicating predominant fat oxidation.
CONCLUSIONS: We could not demonstrate any parallelism in the evolution of EE and protein catabolism in head-injured patients. The therapeutics (mechanical ventilation, sedation, and nutrition) have a major effect on EE but little on N excretion.