Ätiologie und Pathophysiologie der disseminierten intravasalen Gerinnung

Zusammenfassung

Die disseminierte intravasale Gerinnung (disseminated intravascular coagulation, DIC) tritt bei einer Reihe von Krankheitsbildern auf. Es treten sowohl eine hämorrhagische Diathese mit teilweise dramatischen Blutungskomplikationen als auch Thrombosen in der Mikrozirkulation und in sehr seltenen Fällen in größeren Gefäßen auf. Klinisch steht die Blutung im Vordergrund, entscheidend für Morbidität und Mortalität ist jedoch ein Organversagen aufgrund der thrombotischen Mikrozirkulationsstörungen. Ursache für die DIC können sowohl eine Gewebstrauma als auch eine Schädigung des Gefäßendothels sein. Traumata unterschiedlicher Genese führen zur Freisetzung von Gewebsfaktor (Tissue-Faktor, TF) in die Zirkulation. Eine Schädigung des Gefäßendothels, die zur DIC führt, wird in dem größten Teil der Fälle von einer Sepsis verursacht. Auslöser ist die Einschwemmung von Endotoxin oder ähnlichen Substanzen in den Blutstrom. Dies führt zur Freisetzung einer ganzen Reihe von Mediatoren. So führen über die Stimulierung unterschiedlicher Systeme der Tumornekrosefaktor-a (TNF-a) und andere Zytokine zu einer Aktivierung des Gerinnungssystems. Die weitere Pathophysiologie einer DIC ist bei allen Grundkrankheiten ähnlich. In der Zirkulation befindliches Thrombin führt zur Ablagerung von Fibrinmonomeren und quervernetztem Fibrin in der Mikrozirkulation. Die gleichzeitige Zirkulation von Plasmin ist verantwortlich für die Bildung von Fibrinspaltprodukten, die die Polymerisation von Fibrinmonomeren und die Thrombozytenfunktion beeinflussen. Die Zerstörung von Gerinnungsfaktoren durch Plasmin verstärkt die Blutungsneigung.

Schlüsselwörter

DIC - Ätiologie - Pathophysiologie

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