Angiodysplasia
Basics
- Dysplastic blood vessel formation within the mucosal and submucosal layers of the gastrointestinal (GI) tract
- Also known as angioectasias, arteriovenous malformations (AVMs), and telangiectasias
Description
- 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
Epidemiology
Incidence
The exact incidence of angiodysplasia is unknown.
Prevalence
- 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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Citation
Domino, Frank J., et al., editors. "Angiodysplasia." 5-Minute Clinical Consult, 33rd ed., Wolters Kluwer, 2025. Medicine Central, im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688488/all/Angiodysplasia.
Angiodysplasia. In: Domino FJF, Baldor RAR, Golding JJ, et al, eds. 5-Minute Clinical Consult. Wolters Kluwer; 2025. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688488/all/Angiodysplasia. Accessed November 17, 2024.
Angiodysplasia. (2025). In Domino, F. J., Baldor, R. A., Golding, J., & Stephens, M. B. (Eds.), 5-Minute Clinical Consult (33rd ed.). Wolters Kluwer. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688488/all/Angiodysplasia
Angiodysplasia [Internet]. In: Domino FJF, Baldor RAR, Golding JJ, Stephens MBM, editors. 5-Minute Clinical Consult. Wolters Kluwer; 2025. [cited 2024 November 17]. Available from: https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688488/all/Angiodysplasia.
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