IS THE METABOLIC RESPONSE TO INJURY DIFFERENT WITH OR WITHOUT SEVERE HEAD-INJURY - SIGNIFICANCE OF PLASMA GLUTAMINE LEVELS

Acute brain injury is the single largest cause of trauma center deaths. Injury that does not involve the brain directly can lead to a cascade of changes in neuroendocrine system function. In order to evaluate the effect of head injury in severely traumatized patients on the response of body fuel mobilization and utilization, 42 adult patients were studied in the early ''flow'' phase of injury in the fasting state. They were divided into two groups: (1) multiple trauma patients without head injury (MI group, n=21); and (2) multiple trauma patients with severe head injury (HMI group, n=21). This enabled evaluation of the influence of injured brain on the general response to body injury. Kinetic measurements of protein (primed-constant infusion of N-15 glycine), glucose (C-14 and H-3 isotopic glucoses), fat (two-stage glycerol infusion), and energy metabolism (indirect calorimetry) were made along with hormone and substrate determinations. The results of this integrated approach demonstrated similar hormonal and metabolic changes between these two groups of patients. However, hepatic glucose production and whole body lipolysis rates were significantly decreased in HMI patients. In addition, hyperglycemia and hypoglutaminemia were more pronounced in injured patients with associated head injury. Glutamine release, which forms a significant net release of brain amino acids in normal subjects may be impaired in HMI patients. Associated brain injury appears to moderate the systemic effect of trauma.