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In the multiply traumatized patients, the distinguising feature is the hypermetabolic response to the insult. These response includes an alteration in energy needs and productions, preferential catabolism of body glucose, fat and protein stores,. limitation of intake by anorexia,. decreased intestinal absorption if the gut is poorly perfused,. production of immune cells and acute phase proteins,. fever,. sodium and fluid retention due to the influence of hormones and oxidative stress. The degree of hypermetaboism is proportional to the severity of the injury, and is influenced by the type of injury. The hypermetabolic response is thought to maximize a healing reponse to injury. This cataboism is partly mediated by the counter-regulatory hormones, ACTH, GH, catecholamines and glucagon. These hormones maintain the supply of glucose and result in hyperglycemia to provide energy and precursors to maintain the metabolic and immunological response. In addition to the hormonal response, the invasion of pathogens and the injury itself will activate the immune system to elicit widespread metabolic changes. This activation of immune response leads to the production of the immunoglobulin, complement proteins and cytokines. The pro-inflammatory cytokines, the key mediators of inflammation, are IL-1, IL-6 and TNF, which not only mediate and modulate immune system activity but also cause widespread metabolic changes. These widespread metabolic changes are.control the other cytokine production, .protect healthy tissues from the effects of free radicals and other oxidant molecules,.remove from the blood stream nutrients that may assist pathogen multiplication. However, excessive or inappropriate production of cytokines has been associated with morbidity and mortality. Since in these hypermetabolic patients, nutritional support should therefore always commence as early as possible in order to provide sufficient energy and avoid further complications.
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