What, How, and How Much Should Patients with Burns be Fed?

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Metabolic changes after severe burn injury

Severe burns covering more than 40% total body surface area (TBSA) are typically followed by a period of stress, inflammation, and hypermetabolism, characterized by a hyperdynamic circulatory response with increased body temperature, glycolysis, proteolysis, lipolysis, and futile substrate cycling.5, 6, 7 These responses are present in all trauma, surgical, or critically ill patients, but the severity, length, and magnitude are unique for patients with burns.4, 8 Marked and sustained increases

rhGH

Intramuscular administration of rhGH at doses of 0.2 mg/kg as a daily injection during the acute burn phase favorably influenced the hepatic acute phase response,138, 139 increased serum concentrations of its secondary mediator IGF-I,140 improved muscle protein kinetics, maintained muscular growth,141, 142 decreased donor site healing time by 1.5 days,143 improved resting energy expenditure, and attenuated hyperdynamic circulation.144 These beneficial effects of rhGH are mediated by IGF-1, and

Insulin

Insulin probably represents one of the most extensively studied therapeutic agents, and novel therapeutic applications are continually being explored. Insulin decreases blood glucose levels by mediating increased peripheral glucose uptake by skeletal muscle and adipose tissue, and suppressing hepatic gluconeogenesis. It also increases DNA replication and protein synthesis via control of amino acid uptake, increases fatty acid synthesis and decreases proteiolysis.166 The latter action makes

Summary

Severely burned patients have profound nutritional requirements secondary to the prolonged postburn hypermetabolic, hypercatabolic response. Enteral nutritional support should be initiated early to optimize total burn care and decrease long-term morbidity. Neither nonpharmacologic nor pharmacologic strategies are sufficient to abate completely the catabolic response to severe burn injury. All therapeutic strategies have contributed to some extent to the improvements in morbidity and mortality

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      Providing total nutritional estimations in the early critical hypermetabolic stage immediately after a burn increases risk of overfeeding, and any damage to the intestinal mucosa from delayed enteral feeding will lead to poor nutrient absorption [24]. Overfeeding leads to serious metabolic derangements such as hyperglycaemia, hyperuremia, hypercapnia, and fluid issues including dehydration; it may compromise organ function such as kidney and liver, as well as further increase metabolic rate and escalate catabolism [4,24]. The mainstay of nutritional intervention for burns injury in the resuscitation stage is the delivery of nutritional substrates to attenuate metabolic derangements, and to maintain gut integrity through which we expect to minimise bacterial translocation and diarrhoeal events, thereby paving the way for metabolic tolerance of increased intake and achievement of total estimates without compromising homeostasis further down the track.

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    There are no financial ties between any of the authors and any corporate entity or product mentioned in this manuscript.

    Supported by SHC Grant #8660, SHC Grant # 8490, SHC Grant # 8640, SHC Grant # 8760, SHC Grant # 9145, NIH Training Grant #2T32GM0825611, NIH Center Grant #1P50GM60338-01, NIH Grant #5RO1GM56687-03, NIH R01-GM56687, NIH Grant # R01-HD049471, NIDDR H133A020102, NIDDR H133A70019, NIGMS U54/GM62119, American Surgical Association.

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