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Book ChapterDOI

Metabolic changes following major burn injury: How to improve outcome

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TLDR
This chapter will discuss the metabolic changes seen following a major burn and how different treatment options affect outcome.
Abstract
The changes in patient metabolism following a major burn may be seen for more than 12 months after the initial injury. The ensuing period of hypermetabolism and catabolism post-burn leads to impaired immune function, decreased wound healing, erosion of lean body mass, and hinders rehabilitative efforts delaying reintegration into normal society. The typical changes in metabolism are the development of a hyperdynamic circulation [1], increased body temperature [2], increased protein catabolism with peripheral protein wasting [3], increased lipolysis leading to fatty infiltration of the liver [4], increased glycolysis and futile substrate cycling 5. These changes are responsible for much of the morbidity and mortality seen with such an injury and as such are important targets for available treatments including: early excision and grafting; aggressive 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. Several pharmacotherapeutic options are also available to further reduce erosion of lean body mass; these include anabolic agents such as recombinant human growth hormone, insulin, oxandrolone and beta-blockade with propranolol. This chapter will discuss the metabolic changes seen following a major burn and how different treatment options affect outcome.

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Citations
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Journal ArticleDOI

Improved burn wound healing by the antimicrobial peptide LLKKK18 released from conjugates with dextrin embedded in a Carbopol gel

TL;DR: This work obtained an efficient, safe and non-expensive formulation that improves burn wound healing, maintains a moist environment within the wound, is easy to apply and remove, and has potential to prevent infection due to the presence of an antimicrobial peptide.
Journal ArticleDOI

Release of insulin from PLGA-alginate dressing stimulates regenerative healing of burn wounds in rats

TL;DR: Application of ASD-containing insulin-loaded PLGA particles on burns every 3 days stimulates faster and more regenerative healing, suggesting insulin as a potential therapeutic agent in burn healing and, because of its long history of safe use in humans, could become one of the treatments of choice when repair and regeneration are critical for proper tissue function.
Journal Article

Risk factors for mortality among hospitalised adult burn patients in a Malawian tertiary hospital burns unit

TL;DR: The main predictors of death were burn size, scalds, time to presentation, and length of hospital stay, which can be improved by paying more attention to these factors.
Posted ContentDOI

Risk factors of mortality of hospitalised adult burn patients a malawian tertiary hospital burns unit

TL;DR: Risk factors for mortality are connected by their association with post-burn hypermetabolism and further studies are needed to identify the best and cost-effective ways of preventing death in burn patients.
Posted ContentDOI

Metabolic consequences of non-severe burn injury are associated with increased plasma markers of inflammation and cardiovascular disease risk

TL;DR: In this article , longitudinal plasma was collected from adults with non-severe burn injuries (n=35) within 48 hours of admission to hospital and at 6 weeks post-surgery, as well as non-burn controls.
References
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Journal ArticleDOI

Foxo Transcription Factors Induce the Atrophy-Related Ubiquitin Ligase Atrogin-1 and Cause Skeletal Muscle Atrophy

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Journal ArticleDOI

The IGF-1/PI3K/Akt Pathway Prevents Expression of Muscle Atrophy-Induced Ubiquitin Ligases by Inhibiting FOXO Transcription Factors

TL;DR: Akt is not only capable of activating prosynthetic pathways, as previously demonstrated, but is simultaneously and dominantly able to suppress catabolic pathways, allowing it to prevent glucocorticoid and denervation-induced muscle atrophy.
Journal ArticleDOI

Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy

TL;DR: Atrogin-1 is one of the few examples of an F-box protein or Ub-protein ligase (E3) expressed in a tissue-specific manner and appears to be a critical component in the enhanced proteolysis leading to muscle atrophy in diverse diseases.
Journal ArticleDOI

NF-κB Controls Cell Growth and Differentiation through Transcriptional Regulation of Cyclin D1

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