Last updated: November 15, 2023

Summarytoggle arrow icon

Angiodysplasia is a degenerative disorder of gastrointestinal (GI) blood vessels in which abnormal connections between veins and capillaries are formed, potentially leading to upper and/or lower GI bleeding of variable severity. The precise cause of angiodysplasia is unclear, but it is often linked to von Willebrand disease, end-stage renal disease, and the use of left ventricular assist devices. Diagnosis typically involves endoscopy or imaging studies such as angiography or CT angiography. Endoscopic hemostatic therapy is the first-line treatment, supported by pharmacotherapy (e.g., octreotide, bevacizumab) if lesions are persistent or endoscopic intervention is not feasible.

Epidemiologytoggle arrow icon

  • Prevalence: increases with age; predominantly affects individuals > 60 years of age [1]
  • Small bowel angiodysplasia is the most common cause of obscure GI bleeding in individuals > 50 years of age. [1][2][3]

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

Pathophysiologytoggle arrow icon

  • Most accepted hypothesis: Low-grade intermittent obstruction of submucosal veins associated with aging and other conditions leads to the formation of angiodysplasias. [1]
  • Lesions consist of ectatic, thin-walled vessels that contain endothelium alone or small amounts of smooth muscle. [1][3]
  • Veins are the most commonly affected vessel, but arteriovenous and arterial changes may also occur.

Clinical featurestoggle arrow icon

Presentation and severity vary from occult to life-threatening upper or lower GI bleeding.

Most patients with angiodysplasias present with chronic compensated episodic bleeding.

Diagnosticstoggle arrow icon

The diagnostic approach varies according to the severity and presentation of bleeding. See “Gastrointestinal bleeding” for an initial evaluation and diagnostic approach to overt GI bleeding.

Laboratory studies [1][5][6]

Endoscopy (preferred method) [1][2]

Imaging [1]

  • Indications
    • Recurrent bleeding and inconclusive results with all other techniques
    • Endoscopy is unavailable or contraindicated.
  • Modalities
  • Findings
    • Simultaneous arterial and early venous filling (suggests early shunting)
    • Dilated vasculature
    • Contrast extravasation at the site of active bleeding

Angiodysplasias often occur in multiple locations in the GI tract. [1][3]

Differential diagnosestoggle arrow icon

See “Differential diagnoses of upper GI bleeding” and “Differential diagnoses of lower GI bleeding.”

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

General principles [2][5][6]

  • Approach to treatment depends on the severity of bleeding; see "Treatment of GI bleeding.”
  • Consult specialists early (e.g., gastroenterology, interventional radiology).
  • Hemostatic treatment is indicated for patients with overt GI bleeding or complications (e.g., severe anemia).
  • For incidentally found lesions and other nonbleeding lesions, treatment is generally not required. [1]

Spontaneous cessation of bleeding from angiodysplasia occurs in approx. 90% of cases. [3]

Endoscopic therapy (preferred initial therapy) [1][3]

Re-bleeding occurs in up to one-third of patients with angiodysplasia despite endoscopic therapy and is more frequent in small bowel lesions. [2]

Pharmacological therapy [1][3]

Angiographic therapy [1][3]

  • Indications include:
    • Signs of hypovolemic shock
    • Lesions refractory to, or inaccessible via, endoscopic therapy
    • Endoscopy is contraindicated. [1]
  • Techniques

Surgical therapy [1][3]

Surgical therapy is reserved for patients with a clearly defined source of bleeding.

  • Indications include:
    • Severe active bleeding refractory to other therapies [1]
    • Recurrent chronic bleeding that requires multiple blood transfusions
  • Technique
    • Intraoperative enteroscopy or guided endoscopic therapy
    • Partial surgical resection

Patients with aortic stenosis and multiple angiodysplastic lesions who do not respond to standard endoscopic treatment may require aortic valve replacement. [1][3]

Referencestoggle arrow icon

  1. Laine L, Barkun AN, Saltzman JR, Martel M, Leontiadis GI. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol. 2021; 116 (5): p.899-917.doi: 10.14309/ajg.0000000000001245 . | Open in Read by QxMD
  2. Karstensen JG, Ebigbo A, Aabakken L, et al. Nonvariceal upper gastrointestinal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) Cascade Guideline. Endosc Int Open. 2018; 06 (10): p.E1256-E1263.doi: 10.1055/a-0677-2084 . | Open in Read by QxMD
  3. Sami SS, Al-Araji SA, Ragunath K. Review article: gastrointestinal angiodysplasia - pathogenesis, diagnosis and management. Alimentary Pharmacology & Therapeutics. 2013; 39 (1): p.15-34.doi: 10.1111/apt.12527 . | Open in Read by QxMD
  4. Jackson CS, Gerson LB. Management of Gastrointestinal Angiodysplastic Lesions (GIADs): A Systematic Review and Meta-Analysis. Am J Gastroenterol. 2014; 109 (4): p.474-483.doi: 10.1038/ajg.2014.19 . | Open in Read by QxMD
  5. Jackson CS, Strong R. Gastrointestinal Angiodysplasia. Gastrointest Endosc Clin N Am. 2017; 27 (1): p.51-62.doi: 10.1016/j.giec.2016.08.012 . | Open in Read by QxMD
  6. Song AB, Sakhuja R, Gracin NM, Weinger R, Kasthuri RS, Al-Samkari H. Systemic bevacizumab for refractory bleeding and transfusion-dependent anemia in Heyde syndrome. Blood Adv.. 2021; 5 (19): p.3850-3854.doi: 10.1182/bloodadvances.2021004810 . | Open in Read by QxMD

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