Hypermetabolism remains a significant clinical problem after burn. Every organ system is transformed metabolically in response to severe burn trauma. With long-term consequences including cardiac dysfunction in as many as 60% long term,1 growth arrest for nearly a year after burn in children,2 and high incidence rates of depression, anxiety, and posttraumatic stress disorder(PTSD),3 the metabolic changes after burn clearly have far reaching and long lasting detrimental effects. The history and recognition of burn (and traumatic) hypermetabolism has an extensive history, with the principal changes beginning in the 1930s. Cuthbertson and colleagues monitored metabolism via nitrogen balances in healthy humans, patients with fractures, and patients with sepsis. Their preliminary studies revealed that increased nitrogen losses and temperature changes between the groups were not simply localized to the exact source of infection/trauma but involved a systemic response.4, 5 This concept of a systemic hypermetabolic response to trauma was extended to burns in the 1940s with various authors. Cope and colleagues monitored various aspects of burn hypermetabolism including oxygen consumption and thyroid function, while Truman Blocker monitored muscle protein breakdown using radiolabeled albumin.6, 7 Francis D. Moore and others then furthered the understanding of burn hypermetabolism in the early 1940s by further quantifying the causes of hypermetabolism, including sources of nitrogen and exudative ion losses.8, 9 Subsequently, Dr. Moore began using patient weights to guide fluid resuscitation and feeding, noting that weight loss signified a dire situation in trauma and burn patients, in part reflecting severe electrolyte and nutritional deficiencies.10 Based on their research, resuscitative protocols for severely burned individuals emerged.9 In the 1960s and 1970s, research continued to define key mediators of the systemic responses to trauma and burns. Moore and colleagues observed endocrine alterations in response to trauma, including elevated cortisol and catecholamine levels and decreased growth hormone levels.10-12 These contributions spawned further investigation in the field of burn hypermetabolism that would eventually provide a better understanding of this stress response while leading to therapeutic strategies that improve survival of patients with severe burns. The initial response to burns has 2 specific phases. An initial “ebb” phase during the first 1 to 3 days after-burn is characterized by a decrease in tissue perfusion and temporary decrease in metabolic rate similar to a short lived “fight or flight” response, possibly to preserve vital organ functions and central blood flow. Thereafter, a the hypermetabolic “flow” phase is initiated (Fig. 1), characterized by increased perfusion of superficial tissues, increased adrenergic stress, increased glucocorticoid levels, and increased levels of inflammatory cytokines. These alterations in hormone and cytokine levels drive many energy dependent biochemical processes in response to severe burn trauma, collectively resulting in a hypermetabolic response that necessitates a drastic increase in the caloric needs of severely burned individuals.13, 14 Therefore, the hypermetabolic response can be defined as an increase in the whole body oxygen consumption and resting metabolic rate. This response is created by various modifications in protein turnover, hepatic acute phase response, mitochondrial uncoupling, and various other metabolic pathway modifications, and has now been shown to last up to 2 years after-burn (Table 1).15 Open in a separate window Figure 1: Simulation of the overall timeline of the hypermetabolic response, with the ebb phase occurring in the first 1-3 days, and the flow phase occurring subsequently, and resolution (depending on which hormone/aspect is examined) occurring at some point during the next 2 years.
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May 16, 2024
Charlotte Ehle + 7
Open Access
