Alterations in protein, carbohydrate, and fat metabolism in injured and septic patients.
The physiological and biochemical responses of the body following major injury or severe infection are characterized by hypermetabolism, accelerated gluconeogenesis, and the mobilization of substrates from the carcass to be utilized by visceral organs. These responses in the febrile patient are supported by an elevated cardiac output which insures perfusion of vital organs and provides additional bloodflow to the area of inflammation and/or injury. Because of the accelerated substrate flux and increased catabolism, weight loss and negative nitrogen balance are profound. Cumulative losses rapidly approach near-lethal limits if adequate nutritional support is not instituted. Nutritional maintenance will support the febrile response, maintain body nitrogen and acute phase protein synthesis, and assure an ongoing energy supply. Reparative tissue appears to preferentially utilize substrate, but if malnutrition occurs, wound healing and tissue repair may be limited. The effects of nutritional support on immunological function in these critically ill patients are only now being dissected. Clearly, immunosuppression is related to the initial insult and abnormalities in host defense mechanisms occur almost immediately in patients well nourished before illness. In addition, nutrient depletion and erosion of body mass are also associated with immunological dysfunction so that these two factors combine to impair the patient's resistance to subsequent infection. Present therapy should maintain balance of essential nutrients while complications associated with specialized techniques of nutrient support are minimized. Control of the patient's environment, minimizing pain and discomfort, preventing "bad rest" effect through exercise are all techniques of supportive care, but responses are ablated with resolution of the infection or wound closure, and every effort should be directed toward this goal.
D000818:Animals; D001424:Bacterial Infections / Q000378:metabolism*; D001921:Brain / Q000378:metabolism; D050260:Carbohydrate Metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D009132:Muscles / Q000378:metabolism; D009584:Nitrogen / Q000378:metabolism; D011506:Proteins / Q000378:metabolism*; D018805:Sepsis / Q000378:metabolism; D012756:Sheep; D014947:Wounds and Injuries / Q000378:metabolism*
D011506:Proteins; D005947:Glucose; D009584:Nitrogen