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The Hypermetabolic Response to Burn Injury and Interventions to Modify this Response

Journal

CLINICS IN PLASTIC SURGERY
Volume 36, Issue 4, Pages 583-+

Publisher

W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.cps.2009.05.001

Keywords

Hypermetabolism; Burns; beta-blockade; Catabolism; Catecholamines; Wasting

Categories

Funding

  1. Shriners Hospitals for Children [8660, 8490, 8640, 8760, 9145]
  2. National Institutes of Health [2T32GM0825611, 1P50GM60338-01, 5R01GM56687-03, R01-GM56687, R01-HD049471]
  3. National Institute on Disability and Rehabilitation Research [H133A020102, H133A70019]
  4. National Institute of General Medical Sciences [U54/GM62119]
  5. American Surgical Association
  6. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R01HD049471] Funding Source: NIH RePORTER
  7. NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000073] Funding Source: NIH RePORTER
  8. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM056687, U54GM062119, P50GM060338, R01GM087285, T32GM008256] Funding Source: NIH RePORTER

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Severe burn injury is followed by a profound hypermetabolic response that persists up to 24 months after injury. It is mediated by up to 50-fold elevations in plasma catecholamines, cortisol, and inflammatory cells that lead to whole-body catabolism, elevated resting energy expenditures, and multiorgan dysfunction. All of these metabolic and physiologic derangements prevent full rehabilitation and acclimatization of burn survivors back into society. Modulation of the response by early excision and grafting of burn wounds, thermoregulation, early and continuous enteral feeding with high-protein high-carbohydrate feedings, and pharmacologic treatments have markedly decreased morbidity.

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