Consumptive Coagulopathies in the Critically III
Trauma, shock, and sepsis are frequently complicated by coagulation disorders which contribute to the development of multiorgan failure . 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.
KeywordsThrombin Generation Coagulation Disorder Prothrombin Complex Concentrate Procoagulant Activity Split Product
Unable to display preview. Download preview PDF.
- 8.Preissner KT (1990) Biological relevance of the protein C system and laboratory diagnosis of protein C and protein S deficiencies. Clin Sei 78: 351–364Google Scholar
- 10.Niewiarowski S, Holt JC (1987) Biochemistry and physiology of secreted platelet proteins. In: Colman RW, Hirsh J, Marder VJ, Salzman EW (eds) Hemostasis and thrombosis, 2nd edn. Lippincott, Philadelphia, pp 618–630Google Scholar
- 18.Song KS, Kim BS, Lee SY (1991) Diagnostic efficacy of D-dimer assay in evaluating disseminated intravascular coagulation. Thromb Haemost 65: 1235 (Abst)Google Scholar
- 27.Mann KG (1984) Membrane-bound enzyme complexes in blood coagulation. In: Spaet TH (ed) Progress in hemostasis and thrombosis. Grüne & Stratton, New York, pp 1–23Google Scholar
- 28.Archipoff G, Beretz A, Freyssinet JM, et al. (1991) Heterogeneous regulation of constitutive thrombomodulin or inducible tissue-factor activities on the surface of human saphenous-vein endothelial cells in culture following Stimulation by interleukin-1, tumour necrosis factor, thrombin or phorbol ester. Biochem J 273: 679–684PubMedGoogle Scholar