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Hamostaseologie 1997; 17(04): 190-196
DOI: 10.1055/s-0038-1659995
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Hämostasedefekt im Rahmen von Lebertransplantationen

H. Riess
1   Medizinische Klinik und Poliklinik, Virchow-Klinikum, Humboldt-Universität Berlin
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Publication Date:
27 June 2018 (online)

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Zusammensetzung

Aufgrund der zentralen Bedeutung der Leber als Syntheseort wesentlicher Hämostasekomponenten und ihrer funktionellen Rolle im retikoendothelialen System führen fortgeschrittene Lebererkrankungen laboranalytisch zu verminderten Werten der hepatisch synthetisierten Hämostasefaktoren und Zeichen eines vermehrten Umsatzes der plasmatischen Gerinnung und Fibrinolyse. Bei der orthotopen Lebertransplantation (OLT) wird die vorbestehend gestörte Hämostase durch den langdauernden operativen Eingriff, die Entfernung der hä-mostaseologisch noch bedeutsamen, erkrankten Leber und der komplexen Transplantat-Wirt-Auseinandersetzung stark beeinträchtigt. Schwere Blutungskomplikationen, die fast ausschließlich nach Perfusion der Transplantatleber bei einem relevanten Anteil der Patienten auftraten, bestimmen die Prognose der Patienten. Während der präanhepatischen Phase finden sich nur geringe Abweichungen der Hämostase von der Ausgangssituation. Regelhaft treten zunehmende Zeichen der Hyperfibrinolyse während der anhepatischen Phase auf, die bei Reperfusion des Spenderorgans, in der postanhepatischen Phase, rasch in eine der disseminierten intravasalen Gerinnung vergleichbare Laborkonstellation übergehen. In dieser letzten Operationsphase werden auch Aktivierungen anderer Kaskadensysteme im Sinne der leukozytären Freisetzung von Proteasen und der Zytokinbildung beobachtert. Von den verschiedenen Versuchen der medikamentösen Hämostaseoptimierung führt die antifibrinolytische Therapie insbesondere mit Aprotinin bei prophylaktischer Applikation zur Reduktion der Blutungskomplikationen und zur Verminderung des Transfusionsbedarfes.

Schlüsselwörter

Lebertransplantation - Hyperfibrinolyse - Entzündung - Leukozytenaktivierung - Aprotinin
 

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