Angiodysplasia overview: Difference between revisions
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==Classification== | ==Classification== | ||
There are multiple systems of classification of angiodysplasia. One system of classification is based on location, size, and number of | 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. | ||
==Pathophysiology== | ==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. <ref name="pmid31210709">{{cite journal| author=García-Compeán D, Del Cueto-Aguilera ÁN, Jiménez-Rodríguez AR, González-González JA, Maldonado-Garza HJ| title=Diagnostic and therapeutic challenges of gastrointestinal angiodysplasias: A critical review and view points. | journal=World J Gastroenterol | year= 2019 | volume= 25 | issue= 21 | pages= 2549-2564 | pmid=31210709 | doi=10.3748/wjg.v25.i21.2549 | pmc=6558444 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31210709 }} </ref> 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.<ref name="pmid12878741">{{cite journal| author=Vincentelli A, Susen S, Le Tourneau T, Six I, Fabre O, Juthier F | display-authors=etal| title=Acquired von Willebrand syndrome in aortic stenosis. | journal=N Engl J Med | year= 2003 | volume= 349 | issue= 4 | pages= 343-9 | pmid=12878741 | doi=10.1056/NEJMoa022831 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12878741 }} </ref> | 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. <ref name="pmid31210709">{{cite journal| author=García-Compeán D, Del Cueto-Aguilera ÁN, Jiménez-Rodríguez AR, González-González JA, Maldonado-Garza HJ| title=Diagnostic and therapeutic challenges of gastrointestinal angiodysplasias: A critical review and view points. | journal=World J Gastroenterol | year= 2019 | volume= 25 | issue= 21 | pages= 2549-2564 | pmid=31210709 | doi=10.3748/wjg.v25.i21.2549 | pmc=6558444 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31210709 }} </ref> 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.<ref name="pmid12878741">{{cite journal| author=Vincentelli A, Susen S, Le Tourneau T, Six I, Fabre O, Juthier F | display-authors=etal| title=Acquired von Willebrand syndrome in aortic stenosis. | journal=N Engl J Med | year= 2003 | volume= 349 | issue= 4 | pages= 343-9 | pmid=12878741 | doi=10.1056/NEJMoa022831 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12878741 }} </ref> | ||
Revision as of 18:17, 10 September 2021
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Angiodysplasia Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Angiodysplasia overview On the Web |
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American Roentgen Ray Society Images of Angiodysplasia overview |
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Risk calculators and risk factors for 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.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 angiodysplastic lesions. 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)
von Willebrand disease (VWD)
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
- ↑ 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. - ↑ 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.