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  • Dysplastic blood vessel formation within the mucosal and submucosal layers of the gastrointestinal (GI) tract
  • Also known as angioectasias, arteriovenous malformations (AVMs), and telangiectasias


  • Most common vascular abnormality of the GI tract
  • Lesions are usually small (<1 cm).
  • Most common in the right colon and small bowel but can occur anywhere in the GI tract
  • If bleeding occurs, it is often recurrent and chronic resulting in iron deficiency anemia. Bleeding can also be acute.
  • 2/3 of cases in patients >70 years of age


The exact incidence of angiodysplasia is unknown.

  • Lesions increasingly detected with advancements in endoscopic imaging
  • Prevalence of incidental, asymptomatic angiodysplasias in patients undergoing screening colonoscopy estimated at 0.8%
  • Accounts for 5–6% of all GI bleeds
  • Accounts for 4–7% of all upper GI bleeds
  • Estimated cause of 3–40% of all lower GI bleeds
  • In obscure GI bleeding, angiodysplasias found in 30–60% of small bowel examinations
  • 40–60% of patients with angioectasia have more than one lesion. Up to 20% are synchronous lesions located in different parts of the GI tract.

Etiology and Pathophysiology

  • Exact pathophysiology is unknown.
  • Lesions develop from chronic, low-grade obstruction of submucosal veins as a result of increased smooth muscle contractility. Subsequent capillary congestion results in formation of arteriovenous collaterals.
  • Chronic obstruction leads to local hypoxia, causing induction of vascular growth factors and the development of abnormal vessels.
  • Increased production of vascular endothelial growth factor (VEGF) occurs with tissue hypoxia.
  • A defect (or absence) in von Willebrand factor (VWF) is associated with increased angiogenesis and increased angiodysplasia formation.
  • Right colon, with wide diameter and high wall tension, is the most common location for lesions (62%).

Commonly Associated Conditions

  • Aortic stenosis (Heyde syndrome; increased mucosal hypoxia with concomitant VWF deficiency)
  • von Willebrand disease (VWD)
  • End-stage renal disease (ESRD; platelet dysfunction)
  • Left ventricular assist devices
  • Hereditary hemorrhagic telangiectasia (HHT or Osler-Weber-Rendu; increased VEGF)

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