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Dtsch Med Wochenschr 2016; 141(15): 1067-1073
DOI: 10.1055/s-0042-110742
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Sepsis
© Georg Thieme Verlag KG Stuttgart · New York

Pathophysiologie der Sepsis

Pathophysiology of sepsis
Christian Ertmer
1   Klinik für Anästhesiologie, operative Intensivmedizin und Schmerztherapie, Universitätsklinikum Münster
,
Sebastian Rehberg
2   Klinik für Anästhesiologie, Anästhesie, Intensiv-, Notfall- und Schmerzmedizin, Universitätsmedizin Greifswald
› Author Affiliations
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Publication History

Publication Date:
27 July 2016 (online)

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Zusammenfassung

Eine dysregulierte, d.h. systemische und überschießende, Immunantwort ist nach derzeitiger Lehrmeinung für die Entstehung des Sepsis-assoziierten Multiorganversagens verantwortlich. Dabei ist der im späteren Verlauf auftretenden Infekt-assoziierten Depression des Immunsystems ein mindestens ebenso hoher Stellenwert wie der in der Initialphase klinisch offenkundigen Inflammation beizumessen. Weitere zentrale Pathomechanismen stellen die septische Koagulopathie und die endotheliale Dysfunktion dar, die aufgrund von zahleichen Interaktionen auf Mediator- und Rezeptorebene lediglich zu didaktischen Zwecken isoliert von der Inflammation betrachtet werden können. Klinisch resultiert die charakteristische Symptomatik aus Störungen der Mikro- und Makrozirkulation mit einer verminderten mikrovaskulären Sauerstofftransportkapazität. Hinzu kommt die Störung des zellulären Energiestoffwechsels („zytopathische Hypoxie“), so dass selbst nach Wiederherstellung normaler Sauerstoffpartialdrücke Beeinträchtigungen der Organfunktionen entstehen. Diese sind zwar meist funktionell und potenziell reversibel, entwickelt sich jedoch ein Multiorganversagen steigt die Letalität auf bis zu 70%.

Abstract

Current evidence suggests that a dysregulated, i.e. systemic and extensive, immune response causes sepsis-induced multiple organ failure. Notably, this does not only imply the initial inflammatory reaction but also the delayed sepsis-associated depression of the immune system. Endothelial dysfunction and sepsis-induced coagulopathy represent additional major pathomechanisms. Based on multiple interactions between mediators und receptors all of these mechanisms can be discussed individually only for didactical purposes. Clinically, there are charateristic microcirculatory disorders and macrocirclatory changes resulting in an impaired oxygen transport capacity. Due to an additional cytopathic hypoxia, organ function might be impaired even if physiological partial pressures of oxygen are restored. Although these changes are often functional and potentially reversible, mortality increases up to 70% in case of multiple organ failure.

Schlüsselwörter

dysregulierte Inflammation - endotheliale Dysfunktion - Mikrozirkulationsstörungen - septische Koagulopathie - zytopathische Hypoxie

Keywords

dysregulated inflammation - endothelial dysfunction - microcirculatory dysfunction - septis-induced coagulopathy - cytopathic hypoxia
 

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