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Pathophysiologisch f\u00fchren die \u00fcberschie\u00dfende Immunantwort auf \u201epathogen associated molecular patterns\u201c (PAMPs) und \u201edamage associated molecular patterns\u201c (DAMPs), die Aktivierung des Komplementsystems, die Bildung neutrophiler extrazellul\u00e4rer Fallen (NETs) sowie die Sch\u00e4digung des endothelialen Glykokalyx zu einer prothrombotischen und antifibrinolytischen Mikroumgebung mit Mikrothrombosen, Organfunktionsst\u00f6rungen und erh\u00f6hter Letalit\u00e4t. Etwa 20\u201325\u202f% der intensivpflichtigen Sepsispatient*innen erf\u00fcllen die Kriterien einer SIC. Diagnostisch stehen derzeit verschiedene Scoresysteme wie der ISTH-SIC-, ISTH-overt-DIC- und JSTH-DIC-Score zur Verf\u00fcgung, deren Aussagekraft jedoch limitiert ist, da sie \u00fcberwiegend h\u00e4morrhagische Parameter erfassen, obwohl die Sepsis typischerweise durch einen thrombotisch dominierten Ph\u00e4notyp gekennzeichnet ist. Viskoelastische Point-of-Care-Verfahren erm\u00f6glichen eine dynamische und bettseitige Beurteilung der Gerinnung einschlie\u00dflich der h\u00e4ufig vorliegenden Hypofibrinolyse bzw. des \u201efibrinolytic shutdown\u201c, der mit ung\u00fcnstigem Outcome assoziiert ist. F\u00fcr diese spezifische Fragestellung sind die Verfahren bislang jedoch weder ausreichend validiert noch als diagnostischer Standard etabliert. Daten und Empfehlungen zu spezifischen therapeutischen Optionen sind eingeschr\u00e4nkt. Grundlegend ist eine konsequente Thromboseprophylaxe bei Patienten mit Sepsis, wobei niedermolekulare Heparine gegen\u00fcber unfraktioniertem Heparin Vorteile hinsichtlich ven\u00f6ser Thromboembolien zeigen. Gerinnungsmodulierende Therapien wie Antithrombin, rekombinantes Thrombomodulin oder aktiviertes Protein\u00a0C konnten in gro\u00dfen randomisierten Studien bislang keinen konsistenten \u00dcberlebensvorteil nachweisen. Experimentelle Ans\u00e4tze, die auf NETs, die Komplementaktivierung oder die Modulation der Fibrinolyse abzielen, erscheinen mechanistisch vielversprechend, bed\u00fcrfen jedoch weiterer klinischer Evaluation. Insgesamt erfordert die SIC eine individualisierte, pathophysiologisch orientierte Diagnostik und Therapie.<\/jats:p>","DOI":"10.1007\/s00101-026-01748-1","type":"journal-article","created":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T10:03:35Z","timestamp":1792577015000},"page":"789-800","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Sepsisinduzierte Koagulopathie","Sepsis-induced coagulopathy"],"prefix":"10.1007","volume":"75","author":[{"given":"Martin","family":"Mirus","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul L.","family":"Petrick","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Schmoch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felix C. 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