Cytokines and inflammatory pathways in the pathogenesis of multiple organ failure following abdominal aortic aneurysm repair

Eur J Vasc Endovasc Surg. 2001 Dec;22(6):485-95. doi: 10.1053/ejvs.2001.1522.

Abstract

Multiple organ failure is a common mode of death following abdominal aortic aneurysm repair, particularly after rupture. Cytokines are the principal mediators of the inflammatory response to injury and high levels of circulating cytokines have been associated with poor outcome in major trauma and sepsis. Abdominal aortic aneurysm repair results in an ischaemia-reperfusion injury to the tissues distal to the site of aortic clamping. The inflammatory response in these tissues causes the release of cytokines, principally Interleukins 1-beta, 6, and 8, and Tumour Necrosis Factor alpha. If released in large enough concentrations, these cytokines may enter the circulation and gain access to organs distant to the site of initial injury. Circulating cytokines cause dysfunction of the renal, cardiovascular, respiratory, nervous and musculo-skeletal systems. The combination of these individual changes in organ function is the multiple-organ dysfunction syndrome, which may progress to multiple organ failure.

Publication types

  • Review

MeSH terms

  • Aortic Aneurysm, Abdominal / surgery*
  • Aortic Rupture / physiopathology
  • Cardiovascular System / physiopathology
  • Central Nervous System / physiopathology
  • Cytokines / physiology*
  • Humans
  • Kidney / physiopathology
  • Liver / physiopathology
  • Multiple Organ Failure / etiology
  • Multiple Organ Failure / physiopathology*
  • Reperfusion Injury / etiology
  • Reperfusion Injury / physiopathology
  • Systemic Inflammatory Response Syndrome / etiology
  • Systemic Inflammatory Response Syndrome / physiopathology*

Substances

  • Cytokines