Nutrition and metabolism in burn patients

Abstract

Severe burn causes significant metabolic derangements that make nutritional support uniquely important and challenging for burned patients. Burn injury causes a persistent and prolonged hypermetabolic state and increased catabolism that results in increased muscle wasting and cachexia. Metabolic rates of burn patients can surpass twice normal, and failure to fulfill these energy requirements causes impaired wound healing, organ dysfunction, and susceptibility to infection. Adequate assessment and provision of nutritional needs is imperative to care for these patients. There is no consensus regarding the optimal timing, route, amount, and composition of nutritional support for burn patients, but most clinicians advocate for early enteral nutrition with high-carbohydrate formulas.Nutritional support must be individualized, monitored, and adjusted throughout recovery. Further investigation is needed regarding optimal nutritional support and accurate nutritional endpoints and goals.

Manejo De Las Quemaduras en Niños

“…Los bajos niveles de vitaminas A, C y D y Fe, Cu, Se y Zn afectan negativamente la cicatrización de heridas y la función esquelética e inmune. (Clark, 2017). Por lo que el médico pediatra no debe omitir compensar micronutrientes en adecuadas cantidades con el fin de obtener una cicatrización de buena calidad.…”

A ’metabolic bundle‘ including Oxandrolone in optimising the metabolic status of severely burn injured patients: a retrospective analysis of the first 50 patients

“…The resultant progressive loss of mean body mass, if unencumbered, is associated with increased morbidity and mortality [1], [2]. …”

“…The degree and duration of burn injury induced hypermetabolism far exceeds that which would be expected in comparison to that manifested by other causes of sepsis and trauma [2]. The metabolic rate can remain significantly elevated for over a year following initial injury [1], [3].…”

“…These are supplemented by free radicals, arachidonic acid and mediators of inflammation such as cytokines, tumor necrosis factor alpha (TNFα) and interleukins 1 and 6 (IL1, IL6) [7], [8]. At the cellular level oxygen demand is increased through ATP-consumption and heat generation [1], [2]. It is this greater understanding of the metabolic pathways involved that has permitted an emphasis shift from mortality to one of morbidity reduction through amelioration of the hypermetabolic state [1], [2].…”

“…At the cellular level oxygen demand is increased through ATP-consumption and heat generation [1], [2]. It is this greater understanding of the metabolic pathways involved that has permitted an emphasis shift from mortality to one of morbidity reduction through amelioration of the hypermetabolic state [1], [2]. …”