Negro F, Cerra F B
University of Minnesota, Minneapolis.
Crit Care Clin. 1988 Jul;4(3):559-72.
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).
对损伤的代谢反应可诱发一种高代谢状态，导致机体氮迅速丢失，从而在短时间内出现瘦体重的显著减少，进而影响发病率和死亡率。该过程还会引起机体氮从骨骼肌向内脏以及代谢活动增加的部位重新分布，如手术伤口、炎症区域以及产生介质的细胞。外源性给予氮在降低分解代谢速率方面效果不佳。然而，它可以提高蛋白质合成速率。这样一来，净分解代谢速率就会降低。与标准氨基酸配方相比，改良氨基酸在实现这些目标方面似乎更有效。在内脏蛋白质营养不良且同时存在对损伤的代谢反应的情况下，很难将内脏蛋白质合成用作内脏蛋白质营养不良的指标。这些蛋白质和急性期反应物可能不具备区分内脏蛋白质营养不良和由对损伤的代谢反应所诱导的变化的敏感性和特异性。因此，在对损伤的代谢反应期间管理氮平衡时，实际的临床终点是提供充足的氮摄入，尽可能实现2至4克的正氮平衡。可以实现热量（能量）平衡。然而，超过需求的热量或超过有效氧化能力的葡萄糖在某些情况下可能会产生有害影响。在这种情况下，呼出气体分析可能会有所帮助。实现热量平衡似乎并非至关重要。作为发病率和死亡率的一个辅助因素，营养不良的减少似乎源于实现氮平衡。由代谢应激引起的这些代谢改变以及营养需求的变化被称为代谢支持，总结于表3中。代谢支持的终点尽可能为2至4克的正氮平衡以及能实现该平衡的氨基酸负荷；通过急性期反应物和肝脏蛋白质（如转铁蛋白）合成来判断对内脏蛋白质合成的支持；以及避免过量二氧化碳产生和尿素生成的并发症（血尿素氮低于110毫克/百分比）（图5）。
