[Pathophysiology and therapy of sepsis-associated coagulation disorders].
Sepsis and septic shock are very complex and dynamic clinical syndromes. A systemic response to an infection or other triggers can induce a cascade consisting of toxins--leukocytes--cytokines--mediators of inflammation--endothelial cell dysfunction--activation of blood coagulation--intravascular fibrin deposition--alteration of microcirculation, resulting in a damage of organs. Multi organ failure and sepsis are therefore tightly connected. The associated disturbances of blood coagulation range between a simple activation of coagulation with a transient increase of activation markers (i.e. D-dimer), similar to an acute-phase reaction and full blown disseminated intravascular coagulation with consumption coagulopathy. This article summarizes these pathophysiological mechanisms, shows available diagnostic tools and differential diagnoses, and discusses therapeutic options for sepsis and multi organ failure.
Knöbl
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Klinische Abteilung für Hämatologie und Hämostaseologie, Universitätsklinik für Innere Medizin I, Währinger Gürtel 18-20, A-1090 Wien. Paul.Knoebl@akh-wien.ac.at
D000818:Animals; D001780:Blood Coagulation Tests; D004211:Disseminated Intravascular Coagulation / Q000503:physiopathology* / Q000628:therapy; D004730:Endothelium, Vascular / Q000503:physiopathology; D005342:Fibrinolysis / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D009102:Multiple Organ Failure / Q000503:physiopathology* / Q000628:therapy; D015539:Platelet Activation / Q000502:physiology; D012772:Shock, Septic / Q000503:physiopathology* / Q000628:therapy; D018746:Systemic Inflammatory Response Syndrome / Q000503:physiopathology* / Q000628:therapy; D013925:Thromboplastin / Q000502:physiology
D018836:Inflammation Mediators; D013925:Thromboplastin