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
In medicine (gastroenterology), angiodysplasia is a small, acquired vascular malformation of the gut. It is a common cause of otherwise unexplained gastrointestinal bleeding 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
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.[1]
Classification
One system of classification is based on location, size, and number of angiodysplasias. [2]
| 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 | ||
| 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. [3]
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
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. [4] 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.[5]
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
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Prevention
References
- ↑ Athanasoulis, C. A.; Galdabini, J. J.; Waltman, A. C.; Novelline, R. A.; Greenfield, A. J.; Ezpeleta, M. L. (1978). "Angiodysplasia of the colon: A cause of rectal bleeding". Cardiovascular Radiology. 1 (1): 3–13. doi:10.1007/BF02551967. ISSN 0342-7196.
- ↑ Schmit A, Van Gossum A (1998). "Proposal for an endoscopic classification of digestive angiodysplasias for therapeutic trials. The European Club of Enteroscopy". Gastrointest Endosc. 48 (6): 659. doi:10.1016/s0016-5107(98)70080-x. PMID 9852467.
- ↑ Yano T, Yamamoto H, Sunada K, Miyata T, Iwamoto M, Hayashi Y; et al. (2008). "Endoscopic classification of vascular lesions of the small intestine (with videos)". Gastrointest Endosc. 67 (1): 169–72. doi:10.1016/j.gie.2007.08.005. PMID 18155439.
- ↑ 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.