Consumptive Coagulopathies in the Critically III

  • R. Scherer
  • W. J. Kox
Conference paper
Part of the Yearbook of Intensive Care and Emergency Medicine 1993 book series (YEARBOOK, volume 1993)


Trauma, shock, and sepsis are frequently complicated by coagulation disorders which contribute to the development of multiorgan failure [1]. Especially in trauma patients, intrinsic and extrinsic activation of the clotting cascade is started by the release of tissue factor and contact activation following vascular damage. In septic patients, lipopolysaccharides (LPS) accelerate procoagulant turnover by activating neutrophils and hence mediators like elastase or platelet activating factor (PAF), and factor XII. The application of cristalloids and colloids in order to maintain normovolemia further dilutes both the procoagulant and inhibitor potential of the plasmatic coagulation. Plasma factors and platelets are lost by traumatic, surgical or diffuse bleeding. However, with ongoing activation of the coagulation cascade, dilution and loss become less important compared to changes in the dynamics of procoagulant and inhibitor turnover.


Thrombin Generation Coagulation Disorder Prothrombin Complex Concentrate Procoagulant Activity Split Product 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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© Springer-Verlag Berlin Heidelberg 1993

Authors and Affiliations

  • R. Scherer
  • W. J. Kox

There are no affiliations available

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