[Pathophysiological mechanisms of organ dysfunction in sepsis].
Sepsis is defined as the systemic inflammatory response to an infection. The occurrence of organ dysfunction increases the severity of sepsis. Complex interactions between multiple immunomodulating mediators and various cell populations, activated secondarily to the initial infectious insult, promote the development of organ dysfunction in sepsis. Although septic organ dysfunction has long been considered as the end result of chaotic, uncontrolled and deregulated inflammatory cascades, it might instead represent an adaptive response to avoid the occurrence of irreversible tissue damage and end-organ injury. In this article, we review the major mechanisms involved in organ dysfunction during sepsis, and also present the concept of organ dysfunction as an adaptive response to the septic process.
Service d'anesthésiologie, CHUV, 1011 Lausanne. belinda.calderari@chuv.ch
Belinda
B
Calderari
Lucas
L
Liaudet
D016470:Bacteremia / Q000150:complications / Q000276:immunology / Q000503:physiopathology*; D001424:Bacterial Infections / Q000276:immunology / Q000503:physiopathology*; D016207:Cytokines / Q000276:immunology; D042783:Endothelial Cells / Q000276:immunology; D004730:Endothelium, Vascular / Q000276:immunology; D006801:Humans; D009000:Monocytes / Q000276:immunology; D009102:Multiple Organ Failure / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D009504:Neutrophils / Q000276:immunology; D009569:Nitric Oxide / Q000096:biosynthesis / Q000276:immunology; D018384:Oxidative Stress / Q000276:immunology; D018805:Sepsis / Q000503:physiopathology
D016207:Cytokines; D009569:Nitric Oxide