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{{CMG}} {{AE}} {{NKS}}
{{CMG}}; {{AE}} {{NKT}}
==Overview==
==Overview==
In [[medicine]] ([[gastroenterology]]), '''angiodysplasia''' is a small, acquired [[blood vessel|vascular]] malformation of the [[gut]]. It is a common cause of otherwise unexplained [[gastrointestinal bleed]]ing and [[anemia]], especially after sixth decade of life. Lesions are often multiple, and frequently involve the [[cecum]] or [[ascending colon]], although they can occur at other places. Treatment may be with endoscopic interventions, medication, or occasionally surgery.


==Historical Perspective==
==Historical Perspective==
The first case of angiodysplasia was described in a letter to the London Medical Gazette by Phillips as a vascular abnormality causing bleeding from the large bowel in 1839. However, the term "Angiodysplasia" was coined by Galdabini in 1974. Due to the unknown etiology of these lesions, multiple terms have been used, like arteriovenous malformation, [[telangiectasia]], [[angioma]], and [[hemangioma]].<ref name="AthanasoulisGaldabini1978">{{cite journal|last1=Athanasoulis|first1=C. A.|last2=Galdabini|first2=J. J.|last3=Waltman|first3=A. C.|last4=Novelline|first4=R. A.|last5=Greenfield|first5=A. J.|last6=Ezpeleta|first6=M. L.|title=Angiodysplasia of the colon: A cause of rectal bleeding|journal=Cardiovascular Radiology|volume=1|issue=1|year=1978|pages=3–13|issn=0342-7196|doi=10.1007/BF02551967}}</ref>
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.


==Classification==
==Classification==
One system of classification is based on location, size, and number of angiodysplasias. <ref name="pmid9852467">{{cite journal| author=Schmit A, Van Gossum A| title=Proposal for an endoscopic classification of digestive angiodysplasias for therapeutic trials. The European Club of Enteroscopy. | journal=Gastrointest Endosc | year= 1998 | volume= 48 | issue= 6 | pages= 659 | pmid=9852467 | doi=10.1016/s0016-5107(98)70080-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9852467  }} </ref>
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.
{| class="wikitable"
|+Classification of gastrointestinal angiodysplasia
!Location
!Size
!Number of lesions
|-
|Gastric
|Minute (<2 mm in diameter)
|Unique (n = 1)
|-
|Duodenal
|Intermediate (2 to 5 mm)
|Multiple (n = 2 to 10)
|-
|Jejunal
|Large (>5 mm)
|Diffuse (n > 10)
|-
|Colonic
|
|
|-
| colspan="3" |For example, "D-S2-N3" signifies multiple angiodysplasias of intermediate size in the duodenum.
|}
Another system of classification uses endoscopic techniques to classify angiodysplasia depending on size, bleeding and surrounding venous dilatation. <ref name="pmid18155439">{{cite journal| author=Yano T, Yamamoto H, Sunada K, Miyata T, Iwamoto M, Hayashi Y | display-authors=etal| title=Endoscopic classification of vascular lesions of the small intestine (with videos). | journal=Gastrointest Endosc | year= 2008 | volume= 67 | issue= 1 | pages= 169-72 | pmid=18155439 | doi=10.1016/j.gie.2007.08.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18155439  }} </ref>
 
Type 1: Angioectasias:
 
Type 1 a - punctulate erythema (< 1 mm), with or without oozing
 
Type 1 b - patchy erythema (a few mm), with or without oozing
 
Type 2: Dieulafoy's lesions:
 
Type 2 a - punctulate lesions (< 1 mm), with pulsatile bleeding
 
Type 2b - pulsatile red protrusion, without surrounding venous dilatation
 
Type 3 - pulsatile red protrusion, with surrounding venous dilatation
 
Type 4 - other lesions not classified into any of the above categories.
 
==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>
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.


==Differentiating {{PAGENAME}} from Other Diseases==
==Differentiating {{PAGENAME}} from Other Diseases==
Angiodysplasia must be differentiated from other diseases that cause [[hematochezia]], [[melena]], and [[iron deficiency anemia]] like, [[diverticulitis]], [[hemorrhoids]], [[colon cancer]], [[Upper gastrointestinal bleeding|upper GI bleed]] and [[inflammatory bowel disease]].
Angiodysplasia must be differentiated from other diseases that cause [[hematochezia]], [[melena]], and [[iron deficiency anemia]] like, [[diverticulitis]], [[hemorrhoids]], [[colon cancer]], [[Upper gastrointestinal bleeding|upper GI bleed]] and [[inflammatory bowel disease]].
==Epidemiology and Demographics==
==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 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 (epidemiology)|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.
 
Angiodysplasia affects men and women equally regardless of race and is more prevalent after sixth decade of life.


==Risk Factors==
==Risk Factors==
The most important risk factors for angiodysplasia include:
The most important [[risk factors]] for active bleeding from angiodysplasia include advanced age, cardiovascular [[Comorbidities|co-morbidities]], [[von Willebrand disease]], [[end-stage renal disease]], and [[Antiplatelet drug|antiplatelet]] or [[anticoagulant]] use.
 
#Age (>60 years)
#[[Aortic stenosis]]
#[[von Willebrand disease]] (VWD)
#[[Chronic kidney disease]]
 
==Screening==
==Screening==
There are no specific indications for screening angiodysplasia.
There are no specific indications for [[screening]] angiodysplasia.


==Natural History, Complications, and Prognosis==
==Natural History, Complications, and Prognosis==
===Natural History===
===Natural History===
The natural history of angiodysplasia in asymptomatic people is benign and the risk of bleeding is low.
The natural history of angiodysplasia in [[asymptomatic]] people is benign and the risk of bleeding is low.


===Complications===
===Complications===
Anemia, hemodynamic instability from massive blood loss.
[[Anemia]], [[hemodynamic instability]] from massive blood loss.


===Prognosis===
===Prognosis===
Line 90: Line 38:


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


===Physical Examination===
===Physical Examination===
Signs and symptoms of [[Iron deficiency anemia physical examination|iron deficiency anemia]] like can be found in patients with occult bleeding.
Signs and symptoms of [[Iron deficiency anemia physical examination|iron deficiency anemia]] can be found in patients with occult bleeding.


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


===Laboratory Findings===
===Laboratory Findings===
Complete blood count, renal function tests, liver function tests and coagulation studies to diagnose any underlying medical conditions.<br />
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.
===Imaging Findings===
===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.<br />
[[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.<br />
===Other Diagnostic Studies===
Hdelical CT angiography or magnetic resonance angiography can be used in case the conventional methods fail to show bleeding sources.<br />
==Treatment==
==Treatment==
===Medical Therapy===
===Medical Therapy===
<br />
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.
===Surgery===
===Surgery===
<br />
In severe cases or cases not responsive to either endoscopic or medical treatment, [[surgical resection]] may be necessary to stop the bleeding.
===Prevention===
===Prevention===
Primary or secondary prevention is currently not available.<br />
[[Primary prevention|Primary]] or [[secondary prevention]] is currently not available.<br />
==References==
==References==
{{reflist|2}}
{{reflist|2}}

Latest revision as of 10:39, 15 October 2021

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Overview

Historical Perspective

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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]

Overview

Historical Perspective

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.

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

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.

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

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.

Risk Factors

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.

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 can be found in patients with occult bleeding.

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

Laboratory Findings

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.

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.

Treatment

Medical Therapy

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.

Surgery

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

Prevention

Primary or secondary prevention is currently not available.

References

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