Ischemic colitis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Hamid Qazi, MD, BSc [2]

Overview

Ischemic colitis is the result of a sudden reduction in blood flow that is insufficient to meet the metabolic demands of the region of colon. Ischemic change will subsequently extend from the mucosa to the serosa. Mucosal injury will develop in 20 minutes to 1 hour, and transmural infarction occurs within 8 to 16 hours. Reperfusion injury can occur with the release of reactive oxygen species, which cause lipid peroxidation within cell membranes, causing cell necrosis.

Pathophysiology

The pathophysiology of ischemic colitis is as follows:[1][2][3][4]

Colonic Blood Supply

Development of Ischemia

Microscopic Pathology

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By Nephron Source: Own work, CC BY-SA 3.0

Micrograph of a colonic pseudomembrane, a finding that may be associated with ischemic colitis. H&E stain.

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References

  1. Rosenblum JD, Boyle CM, Schwartz LB (1997). "The mesenteric circulation. Anatomy and physiology". Surg Clin North Am. 77 (2): 289–306. PMID 9146713.
  2. Granger DN, Rutili G, McCord JM (1981). "Superoxide radicals in feline intestinal ischemia". Gastroenterology. 81 (1): 22–9. PMID 6263743.
  3. Brandt LJ, Boley SJ, Goldberg L, et al: Colitis in the elderly. Am J Gastroenterol 76:239, 1981.
  4. Washington, Christopher; Carmichael, Joseph (2012). "Management of Ischemic Colitis". Clinics in Colon and Rectal Surgery. 25 (04): 228–235. doi:10.1055/s-0032-1329534. ISSN 1531-0043.

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