Nutritional Monitoring in the lCU: Rational and Practical Application

Abstract

The metabolic response to injury can induce a state of hypermetabolism that results in the rapid loss of the body nitrogen, so that a critical reduction in lean body mass that affects morbidity and mortality can occur in a short period of time. The process also induces a redistribution of the body nitrogen away from the skeletal mass and toward the viscera and areas of increased metabolic activity, such as the surgical wound, the zone of inflammation, and toward cells producing mediators. Exogenously administered nitrogen is not very effective in reducing the rate of catabolism. It can, however, increase the rate of protein synthesis. In so doing, the rate of net catabolism is reduced. The modified amino acids appear to be much more effective in achieving these ends than do the standard amino acid formulas. Visceral protein synthesis is difficult to use as an index of visceral protein malnutrition in the settings where the metabolic response to injury is also present. These proteins and the acute-phase reactants may not have the sensitivity and specificity to discriminate between visceral protein malnutrition and the changes induced by the metabolic response to injury. The practical clinical endpoint, then, in managing the nitrogen economy during the metabolic response to injury is to provide adequate nitrogen intake, achieving 2 to 4 gm of positive nitrogen balance whenever possible. Caloric (energy) equilibrium can be achieved. Calories in excess of demand or glucose in excess of the ability to effectively oxidize, however, can have detrimental effects in some settings. Expired gas analysis can be useful in this context. Achieving caloric equilibrium does not appear to be essential. The reduction in malnutrition as a cofactor in morbidity and mortality appears to come from achieving nitrogen equilibrium. These alterations in metabolism induced by metabolic stress and the changes in nutrient requirements have been called metabolic support and are summarized in Table 3. The end-points of metabolic support, whenever possible, become 2 to 4 gm of positive nitrogen balance with an amino acid load that will achieve that balance; support of visceral protein synthesis as judged by acute-phase reactant and hepatic protein (e.g., transferrin) synthesis; and avoiding complications of excess VCO2 and urea production (BUN less than 110 mg per cent) (Fig. 5).