Gerinnungsstörungen bei Sepsis

C.-E. Dempfle

doi:10.1055/s-0037-1619655

Hämostaseologie, Table of Contents

Hamostaseologie 2005; 25(02): 183-189
DOI: 10.1055/s-0037-1619655

Original Article

Schattauer GmbH

Gerinnungsstörungen bei Sepsis

Sepsis-associated coagulation disorders

C.-E. Dempfle

¹I. Medizinische Klinik, Universitätsklinikum Mannheim

› Author Affiliations

Abstract

Zusammenfassung

Bei Patienten mit Sepsis findet sich in den meisten Fällen eine Gerinnungsaktivierung mit intravasaler Fibrinbildung. Ein vermindertes Hämostase-und Inhibitorpotenzial ist oft nachweisbar und kann zu Blutungen im Rahmen einer Verbrauchskoagulopathie führen. Ursache des Gerinnungsfaktoren-und Inhibitorenmangels ist nur zum Teil ein Vebrauch durch die Gerinnungsaktivierung. Relevant sind auch Plasmaverlust und hepatische Synthesestörung. Bestimmte Formen (z.B. Meningokokken-und Pneumokokkensepsis) können auch zu einer Purpura fulminans führen, die sich durch mikrovaskuläre Thrombosen mit Nekrosen und Blutungen sowie sehr niedrige Protein-C-Konzentrationen auszeichnet.

Bei der Verbrauchskoagulopathie-induzierten Blutung zielt die Therapie primär auf eine Substitution von hämostatischen Komponenten. Bei Sepsis-induzierter Purpura fulminans ist das Ziel eine Unterbrechung der Gerinnungsaktivierung und Verbesserung der Fibrinolyse (z. B. durch Gabe von Protein C oder rekombinantem aktiviertem Protein C).

Unfraktioniertes oder niedermolekulares Heparin wird zur Thromboembolieprophylaxe empfohlen, aber Ergebnisse klinischer Studien zum Einsatz von Heparin speziell bei Sepsis liegen nicht vor. Die Indikation für Antithrombinkonzentrate ist primär die Substitution bei nachgewiesenem Antithrombinmangel, beispielsweise im Rahmen der Therapie venöser Thromboembolien mit Heparin oder -derivaten oder bei extrakorporalen Zirkulationsverfahren unter Verwendung von Heparin. Zugelassene Indikation für rekombinantes aktiviertes Protein C (Drotrecogin alfa, aktiviert) ist die schwere Sepsis, unabhängig vom Vorhandensein einer Sepsis-induzierten Gerinnungsstörung oder Verbrauchskoagulopathie.

Summary

Coagulation activation with intravascular fibrin formation is a general finding in patients with sepsis. Low coagulation factors may be caused by disseminated intravascular coagulation, as well as by loss of plasma and impaired hepatic synthesis in the course of sepsis. The leading clinical symptom in consumption coagulopathy is bleeding. Therefore, treatment mainly consists of substitution of coagulation factors and platelets. Meningococcal and pneumococcal, as well as some other infections may lead to sepsisinduced purpura fulminans, a condition associated with microvascular thrombosis, necrosis, and haemorrhage. A typical laboratory sign is a very low plasma protein C level. Treatment with protein C concentrate or recombinant activated protein C (Drotrecogin alfa, activated) has been shown to be beneficial in sepsis-induced purpura fulminans.

Unfractionated heparin or low molecular weight heparin has been recommended for prophylaxis of venous thrombosis, but there are no clinical studies specificially on patients with sepsis. Antithrombin concentrate is used in patients with antithrombin deficiency treated with heparin for acute venous thrombosis or embolism, extracorporeal circulation procedures or other invasive procedures. There is no indication for general use of antithrombin concentrate in patients with sepsis even in patients with low plasma antithrombin levels. Drotrecogin alfa, activated, is used for treatment of patients with severe sepsis. Its use is not limited to patients with sepsis-induced disseminated intravascular coagulation, although these patients appear to benefit especially from this therapy.

Schlüsselwörter

Sepsis - disseminierte intravasale Gerinnung - Therapie

Keywords

Sepsis - disseminated intravascular coagulation - treatment

Full Text

References

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