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Unfallchirurgie

, Volume 14, Issue 1, pp 3–11 | Cite as

Neue erkenntnisse der pathogenese des schockgeschehens in der traumatologie

  • G. Schlag
  • M. Redl
Experimentelle Arbeiten
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New finding on the pathogenesis of the shock process in traumatology

Abstract

Der frühe hypovolämisch-traumatische und der daraus resultierende späte, sogenannte septische Schock sind in der Traumatologie von zentraler Bedeutung. Beide Schockarten werden durch verschiedene, miteinander vernetzte Mediatorsysteme sowohl auf humoraler als auch zellulärer Ebene getriggert. Im hypovolämisch-traumatischen Schock stehen das Perfusionsdefizit (partielle Ischämie mit Reperfusionsschäden via Xanthin-Xanthinoxidase-System) und die Aktivierung der humoralen Achse durch Traumen im Vordergrund. Daran ist vor allem die Gerinnung, Fibrinolyse, das Kallikrein- und Komplementsystem entscheidend beteiligt. Reaktionsprodukte dieser Systeme führen zur Aktivierung speziell von. Thrombozyten und Granulozyten. Diese beiden können auch miteinander reagieren, z.B. über platelet activating factor, und so schlußendlich zum autoagressiven Gewebsschaden führen. Granulozyten spielen eine zentrale Rolle wegen der Ausschüttung von Sauerstoffradikalen und neutralen Proteinasen, z.B. Elastase, deren Plasmaspiegel (Inhibitorkomplexe) als Aktivierungsmarker von Granulozyten und Prädikator von Organversagen verwendet werden kann. Dem Gastrointestinaltrakt kommt im Rahmen der Schockentwicklung eine große Bedeutung zu, da es durch den Zusammenbruch der Darmbarriere für Endotoxin und Bakterien zur “septischen Herausforderung” kommt und damit zu Endotoxinämie, Bakteriämie, septischem Schock und zum Multiorganversagen. Im Zuge dessen kommen weitere Mediatorsysteme, speziell die der Makrophagen, hinzu wie z.B. das Interleukin 1 oder Cachectin. Ähnlich wie für aktivierte PMN-Elastase konnten wir in der Sepsis auch für Neopterinaktivierte Makrophagen einen Zusammenhang bezüglich Organversagen finden. Durch die Wirkung der aktivierten zellulären Elemente in der Mikrozirkulation, speziell auf der Ebene des Endothels und Interstitiums, kommt es zur Gewebsschädigung, die letztendlich zum (Multi) Organversagen führt.

Abstract

Traumatology deals with two different types of shock — the early hypovolemic-traumatic, and the late, so called septic shock, which is often associated with multi-organ failure. Both types of shock are triggered by several mediator systems of humoral and cellular origin, with numerous interactions between each other. In hypovolemic-traumatic shock central events are a perfusion deficit (ischemia with reperfusion injury via the xanthin-xanthinoxidase system) and activation of the humoral axis — of coagulation, of fibrinolysis, of the complement and kallikrein-kinin system by injured tissue. Coagulation and complement are responsible for the activation of platelets and granulocytes respectively. These cells further interact with each other e.g. via platelet activation factor, which finally causes tissue damage. Granulocytes play a central role because of their ability to release oxygen radicals and neutral proteinases, which can be monitored (elastase) and probably used to predict organ failure. The gut area is less resistant to the events of shock and therefore is a “locus minoris resistentiae” for further development of endotoxinemia, bacteremia, septic shock and multi-organ failure without a tvpical septic focus. By this “septic challenge” further mediator systems get involved, especially those of macrophages like interleukin-1 or cachectin. Similar to the activation marker of PMN-elastase, we could demonstrate that it was possible to use neopterin for monitoring macrophage activation in sepsis and organ failure. By the action of these cellular elements in microcirculation at the endothelial and interstitial level tissue damage occurs, which finally leads to individual and multi-organ failure.

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Copyright information

© Urban & Schwarzenberg 1988

Authors and Affiliations

  • G. Schlag
    • 1
  • M. Redl
  1. 1.Ludwig-Boltzmann-lnsütiit für experimentelle TraumatologieWien

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