The biochemical alterations underlying post-burn hypermetabolism

Abstract

A severe burn can trigger a hypermetabolic state which lasts for years following the injury, to the detriment of the patient. The drastic increase in metabolic demands during this phase renders it difficult to meet the body’s nutritional requirements, thus increasing muscle, bone and adipose catabolism and predisposing the patient to a host of disorders such as multi-organ dysfunction and sepsis, or even death. Despite advances in burn care over the last 50 years, due to the multifactorial nature of the hypermetabolic phenomenon it is difficult if not impossible to precisely identify and pharmacologically modulate the biological mediators contributing to this substantial metabolic derangement. Here, we discuss biomarkers and molecules which play a role in the induction and mediation of the hypercatabolic condition post-thermal injury. Furthermore, this thorough review covers the development of the factors released after burns, how they induce cellular and metabolic dysfunction, and how these factors can be targeted for therapeutic interventions to restore a more physiological metabolic phenotype after severe thermal injuries.

Feeding During Resuscitation After Burn Injury

“…The cornerstones of burn management include adequate fluid resuscitation and sufficient nutrition to accommodate increased caloric and protein requirements following burn injury. Metabolic demands are increased after thermal injury by a complex cascade of reactions caused by proinflammatory cytokines, stress hormones, and a sustained rise in catecholamine production and circulation resulting in increased rates of glycolysis, lipolysis, and protein catabolism that persist long after the initial injury . Protein and micronutrient losses through burned surfaces also require replenishment.…”

“…The continual breakdown of glycogen results in sustained hyperglycemia, which poses increased risk of wound infections, fatty liver infiltration, and suppression of the immune system . Collectively, these changes result in substantially increased energy requirements that are grossly proportional to TBSA burned (Figure ); thus, accounting for increased resting energy requirements is of utmost importance in caring for patients after burn injury.…”

“…Metabolic demands are increased after thermal injury by a complex cascade of reactions caused by proinflammatory cytokines, stress hormones, and a sustained rise in catecholamine production and circulation resulting in increased rates of glycolysis, lipolysis, and protein catabolism that persist long after the initial injury. 1,2 Protein and micronutrient losses through burned surfaces also require replenishment. The rapid increase in metabolism after burn places patients at risk for severe malnutrition and subsequent infection, sepsis, and death.…”

Immune and metabolic alterations following trauma and sepsis – An overview

“…Jeschke and colleagues describe potential mechanisms of cellular and metabolic dysfunction after burn injury [15]. According to the authors despite the last five decades of research little is known with regard to the factors that contribute to the metabolic derangement in burn trauma.…”

Energy metabolism in amyotrophic lateral sclerosis: assessment of body composition and energy expenditure

“…Clinical conditions characteristically associated with hypermetabolism include hyperthyroidism McAuliffe, 1989), pheochromocytoma (McCullagh andEngel, 1942), malignancy (Purcell et al, 2016), burns (Auger et al, 2017) and significant trauma (Rogobete et al, 2017). Given reports of hypermetabolism in ALS, the clinical consequences and possible mechanisms of hypermetabolism in other disorders will be considered.…”