Increased contribution of protein oxidation to energy expenditure in head-injured patients.

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Abstract
Six patients with acute head injury (initial GCS 4.8 +/− 1.7) were studied to determine the contribution of protein oxidation to resting energy expenditure (REE). Patients were studied on the second or third day post-injury and prior to implementation of nutritional support. Variables measured included REE by indirect calorimetry (normalized to percent predicted energy expenditure calculated from the Harris-Benedict equation). 24-hr urinary nitrogen excretion, calorie, and nitrogen intake. All patients received dexamethasone (39 +/− 2 mg/day) and three received pentobarbital. Mean REE was widely variable, ranging from 43 to 128% of predicted (mean, 90 +/− 31%). Mean 24-hr urinary nitrogen excretion was 16.5 +/− 5.8 g. The contribution of protein oxidation to REE was 30 +/− 4%. The contribution of protein oxidation to REE did not parallel REE (r = -0.237, p = NS) or REE expressed as percent predicted (r = -0.258, p = NS). The contribution of protein oxidation to energy expenditure is greater in acute heat trauma than previously described soft tissue injury and sepsis. The observed excessive nitrogen catabolism and increased contribution of protein oxidation to resting energy expenditure suggest accentuated protein requirements in respect to energy needs in head-injured patients.