The hypermetabolic response to burn injury and modulation of this response: an overview

Abstract

Burn injuries are followed by a profound hypermetabolic response, which is characterised by circulatory, physiological, catabolic and immune system changes. This response can persist for up to 24 months post burn. It is mediated by a 50-fold elevation in plasma catecholamines, cortisol and inflammatory cells. This leads to whole body catabolism, significantly elevated resting energy expenditure (REE) and multi-organ dysfunction. These patients have a number of metabolic derangements, including increased REE, increased cardiac work, increased myocardial oxygen consumption, marked tachycardia, severe lipolysis, liver dysfunction, severe muscle catabolism, increased protein degradation, insulin resistance and growth retardation. Early excision and grafting is the cornerstone of management. No treatment modality supersedes early wound coverage. Early enteral nutrition, thermoregulation and resistance training are other components of care. Basic management should be correctly executed before pharmacological agents are employed.