Mechanism of Prevention of Postburn Hypermetabolism and Catabolism by Early Enteral Feeding

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This study was performed to investigate the mechanism whereby immediate enteral feeding after burn injury reduces postburn hypermetabolism and hypercatabolism. Fifty-seven burned guinea pigs (30% TBSA) were divided into three groups: A (N = 19), given 175 kcal/kg/day beginning 2 hours after burn; B (N = 20), given 175 kcal/kg/day with an initial 72-hour adaptation period; and C (N = 18), given 200 kcal/kg/day with the same adaptation period as B. Resting metabolic expenditure (RME) on PBD 13 was lowest in group A (109% of preburn level), compared with group B (144%, p < 0.001) and group C (137%, p < 0.01). On PBD 1, group A had the greatest jejunal mucosal weight and thickness (p < 0.001), and mucosal weight had negative correlations with plasma cortisol (r = 0.829, p < 0.001) and glucagon (r = 0.888, p < 0.001). Two weeks after burn, urinary vanillyl mandelic acid (VMA) excretion, plasma cortisol, and glucagon were lowest in group A (p < 0.05 to p < 0.01). These hormones also significantly correlated with RME (p < 0.01 to p < 0.001). These findings suggest that immediate postburn enteral feeding can prevent hypermetabolism via preservation of gut mucosal integrity and prevention of excessive secretion of catabolic hormones.

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