Pathophysiology of polytrauma

Pathophysiology of polytrauma Immediate and early trauma deaths are determined by primary brain injuries, or significant blood loss (haemorrhagic shock), while late mortality is caused by secondary brain injuries and host defence failure. First hits (hypoxia, hypotension, organ and soft tissue injuries, fractures), as well as second hits (e.g. ischaemia/reperfusion injuries, compartment syndromes, operative interventions, infections), induce a host defence response. This is characterized by local and systemic release of pro-inflammatory cytokines, arachidonic acid metabolites, proteins of the contact phase and coagulation systems, complement factors and acute phase proteins, as well as hormonal mediators: it is defined as systemic inflammatory response syndrome (SIRS), according to clinical parameters. However, in parallel, anti-inflammatory mediators are produced (compensatory anti-inflammatory response syndrome (CARS). An imbalance of these dual immune responses seems to be responsible for organ dysfunction and increased susceptibility to infections. Endothelial cell damage, accumulation of leukocytes, disseminated intravascular coagulation (DIC) and microcirculatory disturbances lead finally to apoptosis and necrosis of parenchymal cells, with the development of multiple organ dysfunction syndrome (MODS), or multiple organ failure (MOF). Whereas most clinical trials with anti-inflammatory, anti-coagulant, or antioxidant strategies failed, the implementation of pre- and in-hospital trauma protocols and the principle of damage control procedures have reduced post-traumatic complications. However, the development of immunomonitoring will help in the selection of patients at risk of post-traumatic complications and, thereby, the choice of the most appropriate treatment protocols for severely injured patients. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Injury Elsevier

Pathophysiology of polytrauma

Injury, Volume 36 (6) – Jun 1, 2005

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Publisher
Elsevier
Copyright
Copyright © 2005 Elsevier Ltd
ISSN
0020-1383
eISSN
1879-0267
DOI
10.1016/j.injury.2004.12.037
Publisher site
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Abstract

Immediate and early trauma deaths are determined by primary brain injuries, or significant blood loss (haemorrhagic shock), while late mortality is caused by secondary brain injuries and host defence failure. First hits (hypoxia, hypotension, organ and soft tissue injuries, fractures), as well as second hits (e.g. ischaemia/reperfusion injuries, compartment syndromes, operative interventions, infections), induce a host defence response. This is characterized by local and systemic release of pro-inflammatory cytokines, arachidonic acid metabolites, proteins of the contact phase and coagulation systems, complement factors and acute phase proteins, as well as hormonal mediators: it is defined as systemic inflammatory response syndrome (SIRS), according to clinical parameters. However, in parallel, anti-inflammatory mediators are produced (compensatory anti-inflammatory response syndrome (CARS). An imbalance of these dual immune responses seems to be responsible for organ dysfunction and increased susceptibility to infections. Endothelial cell damage, accumulation of leukocytes, disseminated intravascular coagulation (DIC) and microcirculatory disturbances lead finally to apoptosis and necrosis of parenchymal cells, with the development of multiple organ dysfunction syndrome (MODS), or multiple organ failure (MOF). Whereas most clinical trials with anti-inflammatory, anti-coagulant, or antioxidant strategies failed, the implementation of pre- and in-hospital trauma protocols and the principle of damage control procedures have reduced post-traumatic complications. However, the development of immunomonitoring will help in the selection of patients at risk of post-traumatic complications and, thereby, the choice of the most appropriate treatment protocols for severely injured patients.

Journal

InjuryElsevier

Published: Jun 1, 2005

References

  • Lethal injuries and time to death in a level I trauma center
    Acosta, J.A.; Yang, J.C.; Winchell, R.J.
  • Fas ligand mediates activation-induced cell death in human T lymphocytes
    Alderson, M.R.; Tough, T.W.; Davis-Smith, T.
  • Reliable variables in the exsanguinated patient which indicate damage control and predict outcome
    Asensio, J.A.; McDuffie, L.; Petrone, P.
  • Postinjury neutrophil priming and activation: an early vulnerable window
    Botha, A.J.; Moore, F.A.; Moore, E.E.
  • Femur fracture induces site-specific changes in T-cell immunity
    Buzdon, M.M.; Napolitano, L.M.; Shi, H.J.
  • Metalloproteinase inhibition prevents acute respiratory distress syndrome
    Carney, D.E.; McCann, U.G.; Schiller, H.J.
  • Interleukin 13 and inflammatory markers in human sepsis
    Collighan, N.; Giannoudis, P.V.; Kourgeraki, O.
  • IL-10 enhances resolution of pulmonary inflammation in vivo by promoting apoptosis of neutrophils
    Cox, G.
  • Cerebrovascular hypoxic and autoregulatory responses during reduced brain metabolism
    Donegan, J.H.; Traystman, F.J.; Koehler, R.C.
  • Complement activation in injured patients occurs immediately and is dependent on the severity of the trauma
    Fosse, E.; Pillgram-Larsen, J.; Svennevig, J.L.
  • Neutrophil-mediated tissue injury and its modulation
    Fujishima, S.; Aikawa, N.
  • Damage control: extremities
    Hildebrand, F.; Giannoudis, P.; Kretteck, C.; Pape, H.C.
  • Metabolic response to severe injury
    Hill, A.G.; Hill, G.L.
  • Ischaemia–reperfusion injury to the intestine
    Kong, S.E.; Blennerhassett, L.R.; Heel, K.A.
  • Role of nitric oxide in inflammation
    Laroux, F.S.; Pavlick, K.P.; Hines, I.N.
  • Fas and the art of lymphocyte maintenance
    Lenardo, M.J.
  • The role of the gastrointestinal tract in postinjury multiple organ failure
    Moore, F.A.
  • Production of cytokines following brain injury
    Morganti-Kossmann, M.C.; Lenzlinger, P.M.; Hans, V.
  • Xanthine oxidase activity and blood glutathione redox ratio in infants and children with septic shock syndrome
    Nemeth, I.; Boda, D.
  • Conversion of external fixation to intramedullary nailing for fractures of the shaft of the femur in multiply injured patients
    Nowotarski, P.J.; Turen, C.H.; Brumback, R.J.; Scarboro, J.M.
  • The timing of fracture treatment in polytrauma patients: relevance of damage control orthopedic surgery
    Pape, H-C.; Giannoudis, P.; Krettek, C.
  • Sequential metabolic changes following induction of systemic inflammatory response in patients with severe sepsis or major blunt trauma
    Plank, L.D.; Hill, G.L.
  • The metalloproteinase matrilysin proteolytically generates active soluble Fas ligand and potentiates epithelial cell apoptosis
    Powell, W.C.; Fingleton, B.; Wilson, C.L.
  • The central effectors of cell death in the immune system
    Rathmell, J.C.; Thompson, C.B.
  • Early goal-directed therapy in the treatment of severe sepsis and septic shock
    Rivers, E.; Nguyen, B.; Havstad, S.
  • The systemic inflammatory response syndrome in acute liver failure
    Rolando, N.; Wade, J.; Davalos, M.
  • Role of systemic inflammatory response syndrome and infection in the occurrence of early multiple organ dysfunction syndrome following severe trauma
    Smail, N.; Messiah, A.; Edouard, A.
  • The role of the complement system in traumatic brain injury
    Stahel, P.F.; Morganti-Kossmann, M.C.; Kossmann, T.
  • Evidence for a role of kallikrein–kinin system in patients with shock after blunt trauma
    Sugimoto, K.; Hirata, M.; Majima, M.
  • Role of lipopolysaccharide and tumor necrosis factor-alpha in induction of hepatocyte necrosis
    Wang, J.H.; Redmond, H.P.; Watson, R.W.; Bouchier-Hayes, D.

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