Angiodysplasia overview

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Angiodysplasia from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

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Other Imaging Findings

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Treatment

Medical Therapy

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

Overview

Historical Perspective

Angiodysplasia was first reported in 1839 by Philips 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 Galbadini in 1974.

Classification

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

Pathophysiology

Exact etiology of angiodysplasia is unclear. Various theories appear in the literature. According to one theory, ageing and intermittent, low-grade obstruction of submucosal veins in the muscularis propria layer leads to the formation of small arterio-venous collaterals. Another theory states that due to chronic hypoxia angiogenic factors like vascular endothelial growth factor (VEGF) and basic fibroblast growth factor increase which contribute to the development of angiodysplasia. [1] A proposed mechanism that may lead to the development of angiodysplasia in aortic stenosis is the development of acquired von Willebrand disease (VWD) from mechanical disruption of von Willebrand factor multimers during their passage from the stenotic aortic valve.[2]

Differentiating Angiodysplasia overview from Other Diseases

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.

Epidemiology and Demographics

The prevalance of angiodysplasia is 0.8% in adult population but it accounts for 20% of major episodes of lower intestinal bleeding.

Angiodysplasia affects men and women equally regardless of race and is more prevalent after sixth decade of life.

Risk Factors

The most important risk factors for angiodysplasia include:

Age (>60 years)

Aortic stenosis

von Willebrand disease (VWD)

Chronic kidney disease

Screening

There are no specific indications for screening angiodysplasia.

Natural History, Complications, and Prognosis

Natural History

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

Complications

Anemia, hemodynamic instability from massive blood loss.

Prognosis

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

Diagnosis

Diagnostic Criteria

History and Symptoms

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.

Physical Examination

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

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

Laboratory Findings

Complete blood count, renal function tests, liver function tests and coagulation studies to diagnose any underlying medical conditions.

Imaging Findings

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.

Other Diagnostic Studies

Hdelical CT angiography or magnetic resonance angiography can be used in case the conventional methods fail to show bleeding sources.

Treatment

Medical Therapy

Endoscopic treatment is the therapy of choice in which cautery or argon plasma coagulation (APC) is used. Other options are mechanical hemostasis using clips, sclerotherapy. First-line medications are antifibrinolytics tranexamic acid or aminocaproic acid. Estrogens can be used to stop bleeding from angiodysplasia. In difficult cases, there have been positive reports about octreotide and thalidomide,

Surgery

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

Prevention

Primary or secondary prevention is currently not available.

References

  1. García-Compeán D, Del Cueto-Aguilera ÁN, Jiménez-Rodríguez AR, González-González JA, Maldonado-Garza HJ (2019). "Diagnostic and therapeutic challenges of gastrointestinal angiodysplasias: A critical review and view points". World J Gastroenterol. 25 (21): 2549–2564. doi:10.3748/wjg.v25.i21.2549. PMC 6558444 Check |pmc= value (help). PMID 31210709.
  2. Vincentelli A, Susen S, Le Tourneau T, Six I, Fabre O, Juthier F; et al. (2003). "Acquired von Willebrand syndrome in aortic stenosis". N Engl J Med. 349 (4): 343–9. doi:10.1056/NEJMoa022831. PMID 12878741.

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