Surgical Intensive Care Medicine 2016
DOI: 10.1007/978-3-319-19668-8_44
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Trauma

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Cited by 2 publications
(2 citation statements)
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“…In both sepsis ( 19 ) and poly-trauma, ( 20 , 21 ) a state of hyper-inflammation is observed initially as the host responds to the infection or traumatic stress with marked production of pro-inflammatory mediators, e.g., cytokines and polypeptides. A failing circulatory system is associated with activation of the hypothalamic-pituitary-adrenal (HPA) axis and increased sympathetic drive, contributing to metabolic changes and to increased energy expenditure ( 22 , 23 ).…”
Section: Pathophysiological and Cellular Abnormalities Following Hostmentioning
confidence: 99%
“…In both sepsis ( 19 ) and poly-trauma, ( 20 , 21 ) a state of hyper-inflammation is observed initially as the host responds to the infection or traumatic stress with marked production of pro-inflammatory mediators, e.g., cytokines and polypeptides. A failing circulatory system is associated with activation of the hypothalamic-pituitary-adrenal (HPA) axis and increased sympathetic drive, contributing to metabolic changes and to increased energy expenditure ( 22 , 23 ).…”
Section: Pathophysiological and Cellular Abnormalities Following Hostmentioning
confidence: 99%
“…This section refers specifically to the response mechanisms observed in sepsis and poly-trauma that we use as a template for attempting to understand what is likely to be occurring in ME/CFS. In both sepsis (Mello et al, 2016) and poly-trauma, (Keel and Trentz, 2005;Rosenblatt and Delmonico, 2016) a state of hyper-inflammation is observed initially as the host responds to the infection or traumatic stress with marked production of pro-inflammatory mediators, e.g. cytokines and polypeptides.…”
Section: Non-specific Changes In Response To Severe Acute Injurymentioning
confidence: 99%