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8 - Nutrition
- Edited by Lindsey T. A. Rylah, St Andrew's Hospital, Billericay
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- Book:
- Critical Care of the Burned Patient
- Published online:
- 02 December 2009
- Print publication:
- 08 October 1992, pp 105-119
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- Chapter
- Export citation
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Summary
Introduction
The importance of nutritional support in the management of critically ill trauma and/or burned patients is well accepted. Nutritional support is a prerequisite for survival following major burn injuries; however, many questions regarding optimal nutrition in critically ill man remain unanswered and warrant further investigation. Major burn injury presents unique nutritional problems as a result of extreme hypermetabolism and an increased demand for energy-yielding substrates.
The goal
The overall goal of administering nutritional support to critically ill burned patients is to improve survival as well as to decrease associated morbidity. In order to accomplish this goal, nutritional support must minimize the erosion of lean body mass effectively and help to maintain immunocompetence. Loss of vital protein stores, a process referred to as ‘auto-cannibalization’, often occurs following major burn injury, as metabolic demands are usually greater than the available energy (calorie) supplies. Additional factors which increase metabolic demands include infections and associated traumatic injuries. An unmatched metabolic demand will eventually result in protein-calorie malnutrition, cachexia, weight loss and an increased morbidity and mortality. By contrast, the administration of nutritional support may result in closely matched caloric supply and demand, thereby improving survival.
Hypermetabolism
The victims of major burns are always at risk from nutritional deficiencies because of an exaggerated and prolonged hypermetabolic state. There is a continued demand for additional protein and total calories during this period. Cuthbertson first described the metabolic consequences of burn injury as an initial ‘ebb’ or hypometabolic phase (24–48 hours) and a subsequent ‘flow’ or hypermetabolic phase (after 48 hours). Others have suggested a correlation between hypermetabolism and circulating ‘stress’ hormones such as catecholamines or circulating lipopolysaccharide.