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

Abstract

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.