Angiodysplasia overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nikita Singh, M.B.B.S.[2]

Angiodysplasia was first reported in 1839 by Phillips as a vascular lesion causing bleeding from large intestine. Heyde discovered the association between aortic stenosis and angiodysplasia in 1958. The term angiodysplasia was coined by Galdabini in 1974.

There are multiple systems of classification of angiodysplasia. One system of classification is based on location, size, and number of angiodysplastic lesions. Another system uses endoscopic findings to classify angiodysplasia.

The exact pathogenesis of angiodysplasia is unknown. It has been proposed that chronic obstruction of submucosal veins coupled with the effect of ageing, ultimately leading to the formation of small arterio-venous collaterals. Angiogenic factors have also been found to play a role in the development of angiodysplasia.

Angiodysplasia must be differentiated from other diseases that cause hematochezia, melena, and iron deficiency anemia like, diverticulitis, hemorrhoids, colon cancer, upper GI bleed and inflammatory bowel disease.

Angiodysplasia is the most common vascular malformation of the GI tract and accounts for 20% of major episodes of lower intestinal bleeding. The prevalence of angiodysplasia is less than 1% in healthy patients older than 50 years undergoing screening colonoscopy. The incidence of angiodysplasia is equal in both men and women. Majority of the affected population is older than 60 years. The most common location of angiodysplasia of the gastrointestinal tract is the colon.

The most important risk factors for active bleeding from angiodysplasia include advanced age, cardiovascular co-morbidities, von Willebrand disease, end-stage renal disease, and antiplatelet or anticoagulant use.

There are no specific indications for screening angiodysplasia.

The natural history of angiodysplasia in asymptomatic people is benign and the risk of bleeding is low.

Anemia, hemodynamic instability from massive blood loss.

Prognosis is favorable in asymptomatic cases and in cases where bleeding is controlled.

Many patients with angiodysplasia lack symptoms. Others present with GI bleeding or its consequences. Patients may present with rectal bleeding (0-60%), melena (passing black tarry bloody stool) (0-26%), occult blood positive stool (4-47%), or iron deficiency anemia (0-51%). Spontaneous cessation of bleeding (90%) is the rule for lesions located in any part of the GI tract.

Symptoms include hematochezia (60%), melena (26%), hematemesis observed in angiodysplasia of the upper GI tract.

Signs and symptoms of iron deficiency anemia can be found in patients with occult bleeding.

A systolic ejection murmur can be heard if associated with aortic stenosis.

No specific laboratory findings are found in angiodysplasia. Complete blood count may show microcytic hypochromic anemia due to iron deficiency. Fecal occult blood testing is positive when bleeding is active.

Endoscopy is the imaging modality of choice for the diagnosis of angiodysplasia. Lesions appear like flat, 5- to 10 mm, cherry-red, fern-like pattern of vessels.

Treatment is not required for incidentally found, asymptomatic, non-bleeding lesions. However, it is considered for non-bleeding angiodysplasia with symptoms of occult or overt GI bleed. The invasiveness of therapy depends on clinical severity of anemia, hemodynamic stability and recurrence of symptoms. Although endoscopic techniques are the first choice, hormonal therapy, thalidomide and octreotide are the pharmacological options that have been tried for patients with significant co-morbidities who cannot undergo invasive procedures.

In severe cases or cases not responsive to either endoscopic or medical treatment, surgical resection may be necessary to stop the bleeding.

Primary or secondary prevention is currently not available.

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