title: [Pathophysiology of sepsis].
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.
authors.forename: Christian
authors.initials: C
authors.lastname: Ertmer
authors.forename: Sebastian
authors.initials: S
authors.lastname: Rehberg
mesh_terms: D002318:Cardiovascular Diseases / Q000209:etiology / Q000276:immunology*; D004730:Endothelium, Vascular / Q000276:immunology*; D005858:Germany; D006801:Humans; D007154:Immune System Diseases / Q000209:etiology* / Q000276:immunology*; D007113:Immunity, Innate / Q000276:immunology; D018448:Models, Immunological; D009102:Multiple Organ Failure / Q000209:etiology / Q000276:immunology*; D018805:Sepsis / Q000150:complications / Q000276:immunology*