Hypermetabolism following Moderate to Severe Traumatic Acute Brain Injury: A Systematic Review

Elevations of metabolic rate following traumatic brain injury (TBI) have been reported previously, with estimates ranging from 32% to 2009% above normal values. Die aim of this systematic review was to describe the pattern of energy expenditure during the first 30 days following TBI. We searched six databases for trials that measured the energy expenditure at least once during the first 30 days post-injury and compared that value to one that would be predicted in the non-injured state. We identified 24 studies, three of which were randomized controlled trials (RCTs). The sample sizes of the included studies ranged from 6 to 80 (mean, 24.7), and the mean Glasgow Coma Scale (GCS) score of subjects was 4.8. Mean energy expenditure, expressed as a percentage of a predicted value, ranged from 75% to 2009%. The lowest values were reported in patients admitted in brain death. Several factors were found to have modulating effects on energy expenditure. The administration of paralyzing agents, sedatives, or barbiturates reduced metabolic rate by approximately 12-32%. Propranolol and morphine were associated with smaller decreases in energy expenditure. Factors that do not appear to augment the hypermetabolic response included the administration of steroids and method of feeding (enteral vs. parenteral). Based on our results, it was unclear if elevated temperature, the presence of extracranial injury, or the severity of injury further exacerbate hypermetabolism. We conclude that energy expenditure following TBI is highly variable, and the use of standard factors to estimate the energy needs of individual patients are inappropriate and should be discouraged.