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Operational Medicine 2001
Emergency War Surgery
Second United States Revision of The Emergency War Surgery NATO Handbook
United States Department of Defense

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Emergency War Surgery NATO Handbook: Part II: Response of the Body to Wounding: Chapter X: Compensatory and Pathophysiological Responses to Trauma

Metabolic/Endocrine Response

United States Department of Defense


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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Operational Medicine 2001

Health Care in Military Settings

Bureau of Medicine and Surgery
Department of the Navy
2300 E Street NW
Washington, D.C
20372-5300

Operational Medicine
 Health Care in Military Settings
CAPT Michael John Hughey, MC, USNR
NAVMED P-5139
  January 1, 2001

United States Special Operations Command
7701 Tampa Point Blvd.
MacDill AFB, Florida
33621-5323

This web version is provided by The Brookside Associates Medical Education Division.  It contains original contents from the official US Navy NAVMED P-5139, but has been reformatted for web access and includes advertising and links that were not present in the original version. This web version has not been approved by the Department of the Navy or the Department of Defense. The presence of any advertising on these pages does not constitute an endorsement of that product or service by either the US Department of Defense or the Brookside Associates. The Brookside Associates is a private organization, not affiliated with the United States Department of Defense.

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