Nutrition in the intensive care unit

Nutritional support has become a routine part of the care of the critically ill patient. It is an adjunctive therapy, the main goal of which is to attenuate the development of malnutrition. The effectiveness of nutritional support is often stymied by an underlying hostile metabolic milieu. The design of a nutritional support regimen must, therefore, take into consideration this disordered metabolic situation.Acute stress caused by accidental or surgical injury, sepsis, burns or other serious illnesses, such as myocardial infarction, results in the outpouring of counter-regulatory endocrine hormones, cytokines and lymphokines. This results in changes in substrate utilization and substance synthesis rates, as well as catabolism and hypermetabolism. Consequently, there is loss of fat and lean body (muscle) mass, a problematic situation that has been dubbed 'auto-cannibalism'. Thus, it is not surprising that this abnormal metabolic milieu causes disordered utilization of exogenously administered nutrients. Conventional nutritional strategies, such as providing the equivalents of a usual human diet, frequently do not prevent or attenuate the loss of muscle and fat tissue. As a result, many investigational efforts have been directed at overcoming or circumventing the obstacles placed by this disordered milieu.The metabolic response to stress is characterized by major alterations in glucose metabolism. The increased secretion of the counter-regulatory (to insulin) hormones cortisol, catecholamines and glucagon [1] results in elevated endogenous glucose production that is secondary to accelerated hepatic gluconeogenesis (Fig. 1). This increased glucose production, coupled with peripheral tissue resistance to insulin, results in reduced glucose utilization and causes hyperglycaemia. Insulin levels are usually within the normal or mildly elevated range, but are not sufficiently elevated to prevent hyperglycaemia. Hyperglycaemia may also be due to reduced nonoxidative glucose