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Ischemic and Pseudomembranous Colitis

Colitis ischaemica et colitis pseudomembranacea

For medical students2 min readUpdated 2026-10-10

Ischemic and pseudomembranous colitis are severe pathological conditions of the large intestine wall characterized by distinct morphological changes. The former is caused by compromised blood supply, while the latter results from an infectious agent inducing fibrinous inflammation.

Primary pathogen*Clostridium difficile* in pseudomembranous colitis
Cause of ischemiaArterial occlusion, hypotension, and venous stasis
Ischemia morphologyErosions, hemosiderosis, and progression to fibrosis
PseudomembranesFormation of superficial fibrin plaques

Ischemic Colitis: Causes and Pathogenesis

The disease develops as a result of impaired blood supply to the large intestine. The primary factors include circulatory disorders such as atherosclerotic lesions of the mesenteric arteries (vascular occlusion), arterial hypotension, and venous stasis. An additional risk factor is hypercoagulation associated with malignant tumor growth or the use of oral contraceptives.

The pathogenesis is based on the development of segmental ischemia of the bowel wall. In severe cases, the process leads to critical manifestations: arterial or venous intestinal infarction and subsequent gangrene.

Morphological Features of Chronic Ischemia

Chronic blood flow impairment in the large intestine leads to the following changes:

  1. Necrosis of the superficial layers of the mucosa.
  2. Formation of acute erosions capable of undergoing repair.
  3. Focal accumulation of hemosiderosis in the lamina propria.
  4. Spread of the inflammatory process to the deeper layers of the wall with granulation tissue formation, resulting in fibrosis and the formation of narrowings, or strictures.

Microscopic examination demonstrates a characteristic feature: the epithelium is completely preserved only in the deep portions of the crypts, accompanied by marked edema of the submucosal layer.

Pseudomembranous Colitis

This pathology is an infectious enterocolitis etiologically linked to the activity of Clostridium difficile.

The pathomorphological picture is characterized by the development of fibrinous inflammation in the wall of the large intestine. Superficial plaques called pseudomembranes form in areas of mucosal necrosis. Histological examination reveals a key diagnostic sign: viable epithelium is preserved exclusively at the very base of the crypts.

Frequently asked questions

What are the macroscopic changes in the bowel wall during acute infarction resulting from ischemia?

Acute intestinal infarction secondary to ischemia leads to wet gangrene. Macroscopic changes in the bowel wall are characterized by the following features:

  • Tissue swelling — the wall becomes edematous.
  • Foul odor — caused by putrefactive microorganisms.
  • Absence of a demarcation zone — the boundary of the lesion is indistinct.
Which zones of the large intestine are most frequently affected in ischemic colitis?

Ischemic colitis most commonly affects the splenic flexure of the colon. Depending on hemodynamic conditions, typical involvement zones include:

  • Splenic flexure — represents a watershed area of blood supply and is the most common site of involvement.
  • Left hemicolon — the disease as a whole is typically characterized by predominantly left-sided involvement.
  • Right hemicolon — more frequently involved in low-flow states.
What are the main causes of ischemic colitis?

The key causes include circulatory disorders (mesenteric artery atherosclerosis, hypotension, venous stasis) and hypercoagulable states associated with tumors or oral contraceptive use.

What is the primary morphological outcome of chronic intestinal ischemia?

Chronic ischemia leads to the extension of inflammation into deeper wall layers, proliferation of granulation tissue, and progression to fibrosis with subsequent stricture formation.

What is the causative agent of pseudomembranous colitis and what is its morphology?

The disease is caused by Clostridium difficile. Morphologically, it manifests as fibrinous inflammation and the formation of superficial plaques (pseudomembranes) in areas of necrosis.

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