Physiological and metabolic response to isolated closed-head injury. Part 1: Basal metabolic state: correlations of metabolic and physiological parameters with fasting and stressed controls.
Studies of the metabolic and physiological response to closed-head injury have intimated the presence of persistent hypermetabolism. To more fully define and evaluate the metabolic response to head trauma, a prospective study was conducted in patients with isolated closed-head injuries. Metabolic and cardiopulmonary data were obtained for a 7-day period. Patients with multiple injuries or infections, or those who received steroids, were excluded. The basic treatment regimen utilized hyperventilation, bed rest with head elevation, intracranial pressure monitoring, mild fluid restriction, and mannitol as needed. No exogenous nutritional support was given. Intrastudy trends and comparsion with data from unstressed fasting patients and stressed patients were noted. Mean Glasgow Coma Scale scores were 4.4 +/- 1.5 initially, but rose to a mean of 8.2 +/- 3.7 by Day 7. While the responses of cardiac index, CO2 production, lactate/pyruvate ratio, and arteriovenous O2 content difference (AVO2D) were initially elevated, these parameters declined over the course of 7 days. The AVO2D was equivalent to the fasting level by Day 5. Metabolic data, including most amino acid levels in plasma, showed an initial equivalence to stress control levels and a pattern similar to that in non-stressed control subjects by Day 7. Nitrogen and 3-methyl histidine excretion were persistently elevated for the full 7 days. Patients with isolated closed-head injury seemed to be initially hypermetabolic, but this process appeared to resolve by 1 week; the persistent nitrogen excretion may reflect equilibration of muscle mass to the existing level of activity (bed rest). After the first few days, nitrogen excretion may give an erroneous index of the level of metabolic stress and the type or amount of nutritional support needed.
Deutschman
C S
CS
Konstantinides
F N
FN
Raup
S
S
Thienprasit
P
P
Cerra
F B
FB
D000293:Adolescent; D000328:Adult; D000596:Amino Acids / Q000097:blood; D001930:Brain Injuries / Q000097:blood / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D002245:Carbon Dioxide / Q000378:metabolism; D005260:Female; D006801:Humans; D007773:Lactates / Q000032:analysis; D008137:Longitudinal Studies; D008297:Male; D009584:Nitrogen / Q000652:urine; D010101:Oxygen Consumption; D011773:Pyruvates / Q000032:analysis; D014655:Vascular Resistance
D000596:Amino Acids; D007773:Lactates; D011773:Pyruvates; D002245:Carbon Dioxide; D009584:Nitrogen