Abstract
Burns account for around 700,000 emergency department visits every year resulting in around 50,000 admissions to hospital in the United States [1]. Around 50% of these admissions have burns of less than 10% total body surface area (TBSA) and, as such, have near normal metabolic rates. For the remainder, the rise in metabolic rate is linked to burn size and for those with severe thermal injuries (>40% TBSA) the change in patient metabolism is, if left unchecked, set to last for more than 12 months. The change contributes, at least in part, to long term deleterious effects on the individual. It has been previously shown that the ensuing period of hypermetabolism and catabolism following a severe burn leads to impaired immune function, decreased wound healing, erosion of lean body mass, and hinders rehabilitative efforts delaying reintegration into normal society. However, the magnitude and longevity of these changes has yet to be fully elucidated. Strategies for attenuating these maladaptive responses may be divided into pharmacological and non-pharmacological. Non-pharmacological approaches include prompt, early excision and closure of wounds, pertinacious surveillance for and treatment of sepsis, early commencement of high protein high carbohydrate enteral feeding, elevation of the immediate environmental temperature to 31.5°C (±0.7°C), and early institution of an aerobic resistive exercise program.
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References
American Burn Association (2000) Burn Incidence and Treatment in the US: 2000 Fact Sheet. Available at: http://www.ameriburn.org/resources_factsheet.php Accessed November 2006
Goodall M, Stone C, Haynes BW Jr (1957) Urinary output of adrenaline and noradrenaline in severe thermal burns. Ann Surg 145:479–487
Pereira C, Murphy K, Jeschke M, Herndon DN (2005) Post burn muscle wasting and the effects of treatments. Int J Biochem Cell Biol 37:1948–1961
Hart DW, Wolf SE, Chinkes DL, et al (2000) Determinants of skeletal muscle catabolism after severe burn. Ann Surg 232:455–465
Mlcak RP, Jeschke MG, Barrow RE, Herndon DN (2006) The influence of age and gender on resting energy expenditure in severely burned children. Ann Surg 244:121–130
Hart DW, Wolf SE, Mlcak R, et al (2000) Persistence of muscle catabolism after severe burn. Surgery 128:312–319
Sheridan RL (2001) A great constitutional disturbance. N Engl J Med 345:1271–1272
Roubenoff R, Roubenoff RA, Cannon JG, et al (1994) Rheumatoid cachexia: cytokine-driven hypermetabolism accompanying reduced body cell mass in chronic inflammation. J Clin Invest 93:2379–2386
Pomposelli JJ, Flores EA, Bistrian BR (1988) Role of biochemical mediators in clinical nutrition and surgical metabolism. JPEN J Parenter Enteral Nutr 12:212–218
Finnerty CC, Herndon DN, Przkora R, et al (2006) Cytokine expression profile over time in severely burned pediatric patients. Shock 26:13–19
Chance WT, Dayal R, Friend LA, Sheriff S (2006) Possible role of CRF peptides in burn-induced hypermetabolism. Life Sci 78:694–703
Chalmers DT, Lovenberg TW, De Souza EB (1995) Localization of novel corticotropin-releasing factor receptor (CRF2) mRNA expression to specific subcortical nuclei in rat brain: comparison with CRF1 receptor mRNA expression. J Neurosci 15:6340–6350
Barret JP, Jeschke MG, Herndon DN (2001) Fatty infiltration of the liver in severely burned pediatric patients: autopsy findings and clinical implications. J Trauma 51:736–739
Gore DC, Chinkes DL, Hart DW, et al (2002) Hyperglycemia exacerbates muscle protein catabolism in burn-injured patients. Crit Care Med 30:2438–2442
Flakoll PJ, Hill JO, Abumrad NN (1993) Acute hyperglycemia enhances proteolysis in normal man. Am J Physiol 265:E715–721
Chai J, Wu Y, Sheng ZZ (2003) Role of ubiquitin-proteasome pathway in skeletal muscle wasting in rats with endotoxemia. Crit Care Med 31:1802–1807
Biolo G, Fleming RY, Maggi SP, et al (2002) Inverse regulation of protein turnover and amino acid transport in skeletal muscle of hypercatabolic patients. J Clin Endocrinol Metab 87: 3378–3384
Klein GL, Bi LX, Sherrard DJ, et al (2004) Evidence supporting a role of glucocorticoids in short-term bone loss in burned children. Osteoporos Int 15:468–474
Paddon-Jones D, Sheffield-Moore M, Cree MG, et al (2006) Atrophy and impaired muscle protein synthesis during prolonged inactivity and stress. J Clin Endocrinol Metab (in press)
Ballard-Croft C, Horton JW (2002) Sympathoadrenal modulation of stress-activated signaling in burn trauma. J Burn Care Rehabil 23:172–182
Takahashi H, Tsuda Y, Kobayashi M, et al (2004) Increased norepinephrine production associated with burn injuries results in CCL2 production and type 2 T cell generation. Burns 30:317–321
Takahashi H, Kobayashi M, Tsuda Y, et al (2005) Contribution of the sympathetic nervous system on the burn-associated impairment of CCL3 production. Cytokine 29:208–214
Klein GL, Wolf SE, Goodman WG, et al (1997) The management of acute bone loss in severe catabolism due to burn injury. Horm Res 48(Suppl 5):83–87
Przkora R, Barrow RE, Jeschke MG, et al (2006) Body composition changes with time in pediatric burn patients. J Trauma 60:968–971
Suman OE, Spies RJ, Celis MM, et al (2001) Effects of a 12-wk resistance exercise program on skeletal muscle strength in children with burn injuries. J Appl Physiol 91:1168–1175
Barrow RE, Wolfe RR, Dasu MR, et al (2006) The use of beta-adrenergic blockade in preventing trauma-induced hepatomegaly. Ann Surg 243:115–120
Herndon DN, Hart DW, Wolf SE, et al (2001) Reversal of catabolism by beta-blockade after severe burns. N Engl J Med 345:1223–1229
Hart DW, Wolf SE, Ramzy PI, et al (2001) Anabolic effects of oxandrolone after severe burn. Ann Surg 233:556–564
Przkora R, Jeschke MG, Barrow RE, et al (2005) Metabolic and hormonal changes of severely burned children receiving long-term oxandrolone treatment. Ann Surg 242:384–389
Wolf SE, Edelman LS, Kemalyan N, et al (2006) Effects of oxandrolone on outcome measures in the severely burned: a multicenter prospective randomized double-blind trial. J Burn Care Res 27:131–139
Herndon DN, Barrow RE, Kunkel KR, et al (1990) Effects of recombinant human growth hormone on donor-site healing in severely burned children. Ann Surg 212:424–429
Barret JP, Dziewulski P, Jeschke MG, et al (1999) Effects of recombinant human growth hormone on the development of burn scarring. Plast Reconstr Surg 104:726–729
Aili Low JF, Barrow RE, Mittendorfer B, et al (2001) The effect of short-term growth hormone treatment on growth and energy expenditure in burned children. Burns 27:447–452
Takagi K, Suzuki F, Barrow RE, et al (1998) Recombinant human growth hormone modulates Th1 and Th2 cytokine response in burned mice. Ann Surg 228:106–111
Takala J, Ruokonen E, Webster NR, et al (1999) Increased mortality associated with growth hormone treatment in critically ill adults. N Engl J Med 341:785–792
Ramirez RJ, Wolf SE, Barrow RE, Herndon DN (1998) Growth hormone treatment in pediatric burns: a safe therapeutic approach. Ann Surg 228:439–448
Lyman CA, Walsh TJ (1992) Systemically administered antifungal agents. A review of their clinical pharmacology and therapeutic applications. Drugs 44:9–35
Engelhardt D, Dorr G, Jaspers C, Knorr D (1985) Ketoconazole blocks cortisol secretion in man by inhibition of adrenal 11 beta-hydroxylase. Klin Wochenschr 63:607–612
Loose DS, Stover EP, Feldman D (1983) Ketoconazole binds to glucocorticoid receptors and exhibits glucocorticoid antagonist activity in cultured cells. J Clin Invest 72:404–408
Gore DC, Chinkes D, Heggers J, et al (2001) Association of hyperglycemia with increased mortality after severe burn injury. J Trauma 51:540–544
Van den Berghe G, Wouters PJ, Bouillon R, et al (2003) Outcome benefit of intensive insulin therapy in the critically ill: Insulin dose versus glycemic control. Crit Care Med 31:359–366
Pierre EJ, Barrow RE, Hawkins HK, et al (1998) Effects of insulin on wound healing. J Trauma 44:342–345
Aarsland A, Chinkes DL, Sakurai Y, et al (1998) Insulin therapy in burn patients does not contribute to hepatic triglyceride production. J Clin Invest 101:2233–2239
Ferrando AA, Chinkes DL, Wolf SE, et al (1999) A submaximal dose of insulin promotes net skeletal muscle protein synthesis in patients with severe burns. Ann Surg 229:11–18
Thomas SJ, Morimoto K, Herndon DN, et al (2002) The effect of prolonged euglycemic hyperinsulinemia on lean body mass after severe burn. Surgery 132:341–347
Pham TN, Warren AJ, Phan HH, et al (2005) Impact of tight glycemic control in severely burned children. J Trauma 59:1148–1154
Dandona P, Aljada A, Mohanty P, et al (2001) Insulin inhibits intranuclear nuclear factor kappaB and stimulates IkappaB in mononuclear cells in obese subjects: evidence for an antiinflammatory effect? J Clin Endocrinol Metab 86:3257–3265
Ferrando AA, Chinkes DL, Wolf SE, et al (1998) Acute dichloroacetate administration increases skeletal muscle free glutamine concentrations after burn injury. Ann Surg 228: 249–256
Herndon DN, Ramzy PI, DebRoy MA, et al (1999) Muscle protein catabolism after severe burn: effects of IGF-1/IGFBP-3 treatment. Ann Surg 229:713–720
Wolf SE, Woodside KJ, Ramirez RJ, et al (2004) Insulin-like growth factor-I/insulin-like growth factor binding protein-3 alters lymphocyte responsiveness following severe burn. J Surg Res 117:255–261
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Norbury, W.B., Jeschke, M.G., Herndon, D.N. (2007). Early Manipulation of Metabolic Changes due to Severe Burns in Children. In: Intensive Care Medicine. Yearbook of Intensive Care and Emergency Medicine, vol 2007. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-49433-1_70
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DOI: https://doi.org/10.1007/978-3-540-49433-1_70
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