Nutrition

Abstract

Severe brain injury, whether from trauma or stroke, constitutes a massive metabolic insult. There is a consensus in the literature that patients with acute neurologic injury are hypermetabolic (increased energy expenditure) and hypercatabolic (increased protein degradation). This hypermetabolism is evidenced by increased oxygen consumption which peaks within 5–12 days and generally resolves thereafter unless there are infectious complications, continued steroid administration, persistent seizure activity, or decerebrate posturing. These will all prolong the hypermetabolic response. Correlations have been shown between severity of brain injury and energy requirements. The mechanism of the hypermetabolic response following neurologic injury has been only partially defined. It is now believed that the primary mediators of this hypermetabolic/hypercatabolic response are the catecholamines, glucocorticoids, glucagon, and the now more recently identified cytokines. Release of these counterregulatory hormones is markedly increased. Circulating levels of insulin also tend to be high in the stressed state, although tissue responsiveness is severly blunted as a result of insulin resistance caused by the other hormones. The most evident metabolic change is a shift from storage to utilization of protein, fat, and glycogen reserves. It is important to keep in mind that the metabolically stressed patient does not exhibit the normal adaptation to starvation because of the changes in the hormonal milieu The typical 70 kg man has approximately 225 g of glycogen stores in the liver and muscle, which will be exhausted in less than 24 h of fasting. After this, the nonstressed individual begins to break down adipose tissue preferentially to spare tissue protein and significantly reduces the need for glucose. The stressed patient, on the other hand, continues to use glucose as a primary source of energy, catabolizing muscle protein to provide substrate for gluconeogenesis. Glucose is the major fuel used by injured tissues and by the cells involved in repair and immune processes. Adipose tissue is also mobilized at an accelerated rate under stressed states, with free fatty acids providing a significant fuel source for the liver and skeletal muscle.