History of Metabolic Treatments in Burn Care
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Throughout the latter portion of the 20th century, major developments and advances within the specialty of burn care have been made. Several interventions and developments in reducing energy demands following burns have played a role in attenuating the metabolic response and reducing energy requirements. As a result, long-term function and prognosis have greatly improved. These interventions include early burn excision and wound closure with skin grafts or substitutes, early and aggressive enteral feeding, elevating environmental temperature to thermal neutrality, and pharmacological therapies to modulate the hypermetabolic response. Other developments include improved antimicrobial agents and treatment rationales, as well as efficacious topical antimicrobials and burn dressings that have led to prevention, earlier recognition, and treatment of sepsis.
Severe burn injuries induce an array of metabolic and physiologic processes to activate and respond in an attempt to restore homeostasis. The stress response following severe burns (approximately ≥ 40% total body surface area [TBSA]) is exaggerated and manifests detrimentally as hypermetabolism and associated profound catabolism. Features of the hypermetabolic response are known to include prolonged elevation in circulating catecholamines, cortisol, and glucagon.1 This results in associated elevation in gluconeogenesis, glycogenolysis, and muscle catabolism as well as other features including insulin resistance and impairment of lipolysis. Metabolic disturbances continue well past the acute phase following severe burns and may persist for more than a year after injury.
A large study from a burn unit in the United Kingdom covering the decade prior to 1954 showed 50% mortality in children with a burn of 50% TBSA.2 The authors later compared burn units from 1918–1948 and found that overall mortality was 50% in the 0–14 year age group of patients with 30% TBSA burns, and more than 90% mortality in patients with 40% surface area burns. Bull and Fisher2 of the UK Medical Research Council attributed the observed improvements at Jackson’s Birmingham unit in 1954 to factors including recognition of the value of transfusion for shock, control of infection, and early surgery. By the late 1990s, pediatric burn mortality in specialized burn units was less than 50% for 91%–95% TBSA burns.3 Factors that remain associated with poor outcomes include very young age, inhalation injury, delayed resuscitation, sepsis, and multi-organ failure.
The primary mediators of the catabolic response following burns are catecholamines,4 which rise up to 10-fold following burns with greater than 40% TBSA.5 Wilmore et al4,6 showed in 1974 and 1975 that following severe burns, metabolism and catecholamine levels could also be reduced by increasing ambient temperature to 33˚C, and also be modulated with alpha- and beta-adrenergic antagonists. They found the hypermetabolic response directly correlated with elevated catecholamine levels, which routinely increased 5-fold above normal following severe burns, and hence, promoted muscle catabolism and lipolysis. Wilmore and colleagues7 affirmed that burned extremities display increased glucose uptake and lactate production, and suggested that systemic responses act to increase peripheral blood flow in an attempt to supply the energy needs of the healing burn wound, thus, promoting hypermetabolism.
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