Hamostaseologie 1997; 17(04): 180-189
DOI: 10.1055/s-0038-1659994
Übersichtsarbeiten/Review Articles
Schattauer GmbH

Verbrauchskoagulopathie und Fibrinolyseaktivierung bei Lebererkrankungen

C.-E. Dempfle
1   Universität Heidelberg, Klinikum Mannheim, I. Medizinische Klinik
,
D. L. Heene
1   Universität Heidelberg, Klinikum Mannheim, I. Medizinische Klinik
› Author Affiliations
Further Information

Publication History

Publication Date:
27 June 2018 (online)

Zusammenfassung

Verminderte hepatische Synthese von Gerinnungsfaktoren und Inhibitoren sowie eine verminderte hepatische Klärfunktion begünstigen die Entwicklung von chronischen und akuten Verbrauchsreaktionen bei Patienten mit Lebererkrankungen. Auslöser dieser Verbrauchsreaktionen sind insbesondere direkte toxische Einflüsse mit Zellschädigung in den Lebersinusoiden und lokaler Aktivierung von zellulärer und plasmatischer Hämostase sowie die Einschwemmung insbesondere von Endotoxinen in die Zirkulation. Weitere Ursachen für eine Gerinnungsaktivierung sind Immunphänomene, etwa die Entwicklung von Antiphospholipid-Antikörpern, die häufig im Zusammenhang mit Hepatitiden beobachtet wird. Die Fibrinolyseaktivierung hingegen ist eher reaktiv und wird ausgelöst durch die Gerinnungsaktivierung einerseits und Endotoxin-vermittelte Mechanismen andererseits. Begünstigt wird die Entwicklung einer Verbrauchsreaktion durch spontane oder therapeutisch geschaffene Umgehungskreisläufe vom portalen in das kavale Stromgebiet, wodurch die hepatische Klärfunktion für Aktivatoren und aktivierte Gerinnungs- und Fibrinolysefaktoren weiter beeinträchtigt wird. Die Diagnose der pathologischen Gerinnungsaktivierung ist anhand etablierter Aktivierungsparameter der Gerinnung kaum zu stellen, da sich deren Kinetik ebenfalls durch die Lebererkrankung gravierend ändert. Hilfreich sind am ehesten serielle Messungen in Kombination mit der klinischen Einschätzung. Die Therapie konzentriert sich hauptsächlich auf die Ausschaltung der Auslöser und erst in zweiter Linie auf die hämostaseologische Therapie. Bei Einsatz von gerinnungshemmenden Substanzen wie dem Antithrombin III ist zu bedenken, daß der Patient mit Leberzirrhose oder anderen Lebererkrankungen durch das verminderte plasmatische und zelluläre Hämostasepotential stark blutungsgefährdet ist, so daß außer bei einer eindeutigen Indikation zur Gerinnungshemmung (wie der Hämodialyse oder der Anlage eines portosystemischen Shunts) auch das hämostatische Potential verbessert werden sollte. Neben Frischplasma hat sich hierbei insbesondere die Gabe von Thrombozytenkonzentraten als hämostatisch wirksam erwiesen.

 
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