
Emergency War Surgery NATO Handbook: Part II: Response of the Body to Wounding: Chapter X: Compensatory and Pathophysiological Responses to Trauma
United States Department of Defense
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Reviewed
Trauma produces a sympatheticoadrenal response which partially initiates a hypermetabolic state. Following resuscitation, oxygen consumption increases to supranormal levels. The extent of hypermetabolism is proportional to the severity of injury. The hyperdynamic response is mediated by elevated levels of the counter regulatory hormones: catecholamines, glucagon, and cortisol, which acutely maintain blood glucose levels and later maintain an accelerated body catabolism while opposing the anabolic functions of insulin. In the early post-injury period, insulin levels are low, contributing to hyperglycemia. With time, insulin levels rise toward normal, even in the presence of persistent hyperglycemia. There appears to be an altered tissue receptor sensitivity to insulin in peripheral tissues. Additionally, hepatic glucose production from peripheral precursors is elevated proportionately to the extent to injury. Epinephrine promotes glycogenolysis, also contributing the hyperglycemia; high concentrations of epinephrine may even inhibit the production of insulin.
Anaerobic glucose utilization at the injury site represents up to 80% of the consumed glucose. The byproducts produced by the wound, lactate and pyruvate, are recycled to the liver where gluconeogenesis occurs. Accelerated peripheral proteolysis occurs during the hypermetabolic state, resulting in a erosion of lean body mass and an increased nitrogen excretion. Amino acids from skeletal muscle are mobilized and serve as additional substrates for hepatic gluconeogenesis. In order to prevent the depletion of lean body mass in the hypermetabolic injured patient, nutritional support should be initiated following resuscitation. Nutritional support must provide sufficient protein and carbohydrate to match the elevated energy demands of the patient. The hypermetabolic response is exaggerated by post traumatic complications such as sepsis, and is especially detrimental in casualties who are already at the limits of their metabolic reserves.
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