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Review
. 2016 Oct 1;388(10052):1417-1426.
doi: 10.1016/S0140-6736(16)31469-6.

The metabolic stress response to burn trauma: current understanding and therapies

Craig Porter  1 , Ronald G Tompkins  2 , Celeste C Finnerty  3 , Labros S Sidossis  4 , Oscar E Suman  3 , David N Herndon  3
Affiliations
Review

The metabolic stress response to burn trauma: current understanding and therapies

Craig Porter et al. Lancet. .

Abstract

Major burns provoke a profound stress response, which is unrivalled in terms of its magnitude and duration. Evidence suggests that the pathophysiological stress response to severe burn trauma persists for several years after injury. Thus, there is a pressing need for novel strategies that mitigate this response and restore normal metabolic function in patients with burns. This is the first in a Series of three papers about the care of people with burns. In this paper, we review the current knowledge of the stress response to burn trauma, with a focus on hypermetabolism, muscle wasting, and stress-induced diabetes. We highlight recent developments and important knowledge gaps that need to be pursued to develop novel therapeutic strategies to improve outcomes in burn survivors.

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Conflict of interest statement

Conflict of Interest

The authors have no relevant conflict of interest to disclose. C.P. drafted the manuscript and produced the Figures. R.G.T., L.S.S., O.E.S., C.F.F., and D.N.H. critically reviewed the manuscript. All authors approved the final version of the manuscript.

Figures

Figure 1
Figure 1
Long-term stress response to injury. (A) The genomic response to injury in white blood cells in individuals who had undergone a lipopolysaccharide injection (sepsis), blunt trauma (trauma), or severe burns (burn) (adapted from reference 6). (B) Hypermetabolic response to injury in septic patients (sepsis), blunt trauma (trauma), or severe burns (burn) (adapted from references –12).
Figure 2
Figure 2
(A) Altered mitochondrial function in adipose tissue of burn victims, where mitochondrial thermogenesis is increased after burn (adapted from reference 20). (B) Altered mitochondrial function in skeletal muscle of burn victims, where mitochondrial thermogenesis is increased after burn (adapted from reference 27).
Figure 3
Figure 3
(A) Total energy expenditure (TEE) in a burn victim with a 50% increase in TEE. The proportion of normal metabolic rate attributable to ATP or heat production is adapted from reference . The proportion of burn induced hypermetabolism attributable to ATP or heat production is adapted from reference . (B) The proportion of TEE attributable to heat and ATP production in healthy individuals and burn victims based on data in Figure 3A. (C) Absolute kcal values for heat and ATP production in healthy individuals and burn victims based on data in Figure 3A.
Figure 3
Figure 3
(A) Total energy expenditure (TEE) in a burn victim with a 50% increase in TEE. The proportion of normal metabolic rate attributable to ATP or heat production is adapted from reference . The proportion of burn induced hypermetabolism attributable to ATP or heat production is adapted from reference . (B) The proportion of TEE attributable to heat and ATP production in healthy individuals and burn victims based on data in Figure 3A. (C) Absolute kcal values for heat and ATP production in healthy individuals and burn victims based on data in Figure 3A.
Figure 4
Figure 4
Long-term catabolic stress response to massive burns. Images of a child with a 95% TBSA burn at their hospital admission and at 3, 6, 12 and 24 months post-injury.
Figure 5
Figure 5
Skeletal muscle and burn wound protein synthesis and breakdown rates in burn victims determine by isotopic dilution. Protein net balance is equal to protein breakdown subtracted from protein synthesis. Data are adapted from reference .
See this image and copyright information in PMC

Comment on

References

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