Ischemic colitis pathophysiology

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

Ischemic colitis is the result of a sudden reduction in blood flow that is insufficient to meet the metabolic demands of the region of the colon. Ischemic changes 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.

• The physiology of blood supply is as follows:^[1]
  • Colon receives blood from the superior and inferior mesenteric arteries.
  • Blood supply from these arteries overlap, with abundant collateral circulation.
  • There are weak points, or “watershed” areas, at the borders of the territory supplied by each of these arteries. and are vulnerable to ischemia when blood flow decrease due to hypotension.

• Rectum receives blood from the inferior mesenteric artery and the internal iliac artery which is rarely affected by colonic ischemia due to its dual blood supply.

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

• The colon receives between 10% and 35% of the total cardiac output.
• If blood flow to the colon drops by more than about 50%, ischemia will develop.
• The arteries feeding the colon are very sensitive to vasoconstrictors and during periods of low blood pressure the arteries will collapse.
• Vasoconstricting drugs such as ergotamine, cocaine, or vasopressors can also cause colonic ischemia which results in non-occlusive ischemic colitis.

• A range of pathologic findings are seen in ischemic colitis, corresponding to the spectrum of clinical severity.
  • In the mildest form mucosal and submucosal hemorrhage and edema are seen, possibly with mild necrosis or ulceration.
  • With more severe ischemia, a pathologic picture resembling inflammatory bowel disease (i.e. chronic ulcerations, crypt abscesses and pseudopolyps) may be seen.
  • In the most severe cases, transmural infarction with resulting perforation may be seen.
  • After recovery, the muscularis propria may be replaced by fibrous tissue, resulting in a stricture.
  • Following restoration of normal blood flow, reperfusion injury may contribute to the damage to the colon.

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