[Neuroendocrine response to critical illness and nutritional pharmacology]

Injury and infection produce significant alterations in metabolic homeostasis. Host humoral factors, such as the counterregulatory hormones epinephrine, cortisol, and glucagons, play important roles in metabolic changes postinjury. Hyperglycemia associated with insulin resistance is common in critically ill patients, even those who have an uneventful course postinjury. The use of exogenous insulin to maintain blood glucose at a level no higher than 110 mg per deciliter, known as intensive insulin therapy, has reduced morbidity and mortality among critically ill patients. Glucocorticoids and various proinflammatory cytokines are important regulators of muscle proteolysis in stressed patients. With regard to nutritional support, enteral feeding is superior to parenteral feeding and early feeding is better than late feeding. Immune-enhancing diets has been shown in several recent studies to improve outcome in critically ill patients. Moreover, various hormones, including insulin, growth hormone, and insulin-like growth factor-1, may blunt muscle cachexia. Other treatments including cytokine antibodies, induction of heat-shock protein, and calcium antagonists, may prevent the catabolic response to stress, and these methods are important considering the significant clinical consequences of protein catabolism.