| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
British Medical Bulletin 55:726-743 (1999)
© 1999 The British Council
research-article |
Systemic responses to trauma
Emergency Medicine, University of Manchester, Hope Hospital Salford, UK
Correspondence to Mr Bernard A Foëx, Emergency Medicine, Clinical Sciences Building, Hope Hospital, Salford M6 8HD, UK
Abstract
The systemic responses trauma can be divided into cardiovascular, immunological, and metabolic. The cardiovascular responses are seen immediately after a traumatic insult. The Pattern of response depends on wheter the insult is mainly haemorrhagic, tissue damage, or a combination of the two. The response may be quite different for penetrating vascular trauma, compared with a crush injury to a limb. The immunological, or inflammatory, consequences of trauma usally become apparent several hours or days after the initial insult, although it is increasingly clear that they may be triggered by the very early cardiovascular changes. These have been implicated in the development of multiple organ failure. The metabolic responses are of greatest importance in the longer term: after succesful resuscitation and after the definitive treatment of the patient's injuries. The meatbolic responses need to be taken into account during the recovery from treatment and during the rehabilitation of the patient.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
K. W. Mathis and P. E. Molina Central acetylcholinesterase inhibition improves hemodynamic counterregulation to severe blood loss in alcohol-intoxicated rats Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2009; 297(2): R437 - R445. [Abstract] [Full Text] [PDF] |
||||
![]() |
K Anam, M Amare, S Naik, K. Szabo, and T. Davis Severe tissue trauma triggers the autoimmune state systemic lupus erythematosus in the MRL/++ lupus-prone mouse Lupus, April 1, 2009; 18(4): 318 - 331. [Abstract] [PDF] |
||||
![]() |
H. Takahashi, Y. Tsuda, M. Kobayashi, D. N. Herndon, and F. Suzuki CCL2 as a trigger of manifestations of compensatory anti-inflammatory response syndrome in mice with severe systemic inflammatory response syndrome J. Leukoc. Biol., April 1, 2006; 79(4): 789 - 796. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Tsuda, H. Takahashi, M. Kobayashi, T. Hanafusa, D. N. Herndon, and F. Suzuki CCL2, a product of mice early after systemic inflammatory response syndrome (SIRS), induces alternatively activated macrophages capable of impairing antibacterial resistance of SIRS mice J. Leukoc. Biol., August 1, 2004; 76(2): 368 - 373. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. H. Cooke, K. L. Ryan, and V. A. Convertino Lower body negative pressure as a model to study progression to acute hemorrhagic shock in humans J Appl Physiol, April 1, 2004; 96(4): 1249 - 1261. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. B. C. Coumans, Y. Garnier, S. Supcun, A. Jensen, T. H. M. Hasaart, and R. Berger The Role of Nitric Oxide on Fetal Cardiovascular Control During Normoxia and Acute Hypoxia in 0.75 Gestation Sheep Reproductive Sciences, July 1, 2003; 10(5): 275 - 282. [Abstract] [PDF] |
||||
![]() |
H. Takahashi, T. Tashiro, M. Miyazaki, M. Kobayashi, R. B. Pollard, and F. Suzuki An essential role of macrophage inflammatory protein 1{alpha}/CCL3 on the expression of host's innate immunities against infectious complications J. Leukoc. Biol., December 1, 2002; 72(6): 1190 - 1197. [Abstract] [Full Text] [PDF] |
||||




