MyEClinic
MyEClinic
Health Dictionary Find a Doctor

Angiodysplasia

For patient information click here

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

Synonyms and keywords: Colonic angiodysplasia; colonic arteriovenous malformation; vascular ectasia of the colon; angioectasia

Overview

Overview

Please help WikiDoc by adding more content here. It’s easy! Click here to learn about editing.

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

Template:WS Template:WH

Historical Perspective

Historical Perspective

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

Overview

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

Historical Perspective

Discovery

  • Angiodysplasia was first reported in 1839 by Phillips as a vascular lesion causing bleeding from the large intestine.
  • Dr. E.C. Heyde discovered the association between aortic stenosis and angiodysplasia in 1958.[1]
  • Margulis, while performing operative mesenteric arteriography on a patient who presented with massive bleeding, detected a vascular malformation in the large bowel in 1960.
  • The term angiodysplasia was coined by Galdabini in 1974.[2]
  • The association between gastrointestinal bleeding in angiodysplasia and von Willebrand disease was first described by Ramsey et al in 1976.[3][4]

References

  1. ↑ Hasan F, O’Brien CS, Sanyal A, Dalton HR (2004). “Aortic stenosis and gastrointestinal bleeding”. J R Soc Med. 97 (2): 81–2. doi:10.1258/jrsm.97.2.81. PMC 1079297. PMID 14749406.
  2. ↑ Athanasoulis CA, Galdabini JJ, Waltman AC, Novelline RA, Greenfield AJ, Ezpeleta ML (1977). “Angiodysplasia of the colon: a cause of rectal bleeding”. Cardiovasc Radiol. 1 (1): 3–13. doi:10.1007/BF02551967. PMID 311247.
  3. ↑ Selvam S, James P (2017). “Angiodysplasia in von Willebrand Disease: Understanding the Clinical and Basic Science”. Semin Thromb Hemost. 43 (6): 572–580. doi:10.1055/s-0037-1599145. PMC 5949878. PMID 28476066.
  4. ↑ Ramsay DM, Buist TA, Macleod DA, Heading RC (1976). “Persistent gastrointestinal bleeding due to angiodysplasia of the gut in von Willebrand’s disease”. Lancet. 2 (7980): 275–8. doi:10.1016/s0140-6736(76)90729-7. PMID 59851.

Template:WH Template:WS

Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nikita Singh, M.B.B.S.[2]; José Eduardo Riceto Loyola Junior, M.D.[3]

Overview

Angiodysplasia can be classified in multiple ways. The most often used classifies it according to findings on endoscopy.

Classification

There are multiple systems of classification of angiodysplasia. One system of classification is based on location, size, and number of angiodysplastic lesions. [1] Another system uses endoscopic findings to classify angiodysplasia into: [2]

Type 1: Angioectasias

Type 2: Dieulafoy’s lesions

Type 3: Pulsatile red protrusion, with surrounding venous dilatation

Type 4: Other lesions not classified into any of the above categories.

References

  1. ↑ 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.
  2. ↑ 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.

Template:WS Template:WH

Pathophysiology

Pathophysiology

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

Overview

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

Pathophysiology

  • The exact pathogenesis of angiodysplasia is still unknown.
  • According to a theory, angiodysplasia develops due to chronic obstruction of submucosal veins coupled with the effect of ageing, ultimately leading to the formation of small arterio-venous collaterals.[1]
  • Some studies have revealed increased levels of angiogenic factors like vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang1), Ang2, etc., in small bowel and human colonic angiodysplasia.[2][3]
  • It has also been proposed that aortic stenosis, von Willebrand disease, and chronic renal failure by various mechanisms contribute to development of angiodysplasia.[1]

Associated Conditions

The following conditions have been reported to be associated with angiodysplasia:

Gross Pathology

  • Angiodysplasia is particularly difficult to recognise on gross examination of a resection specimen without the use of specific injection techniques.[8]
  • Angiodysplasia can be seen easily on endoscopy. The most common appearance on endoscopy is a flat, red lesion with a fern-like or regular margin.

Histology

References

  1. ↑ 1.0 1.1 Sami SS, Al-Araji SA, Ragunath K (2014). “Review article: gastrointestinal angiodysplasia – pathogenesis, diagnosis and management”. Aliment Pharmacol Ther. 39 (1): 15–34. doi:10.1111/apt.12527. PMID 24138285.
  2. ↑ Holleran G, Hussey M, Smith S, McNamara D (2017). “Assessment of serum angiogenic factors as a diagnostic aid for small bowel angiodysplasia in patients with obscure gastrointestinal bleeding and anaemia”. World J Gastrointest Pathophysiol. 8 (3): 127–132. doi:10.4291/wjgp.v8.i3.127. PMC 5561433. PMID 28868182.
  3. ↑ Holleran G, Hall B, O’Regan M, Smith S, McNamara D (2015). “Expression of Angiogenic Factors in Patients With Sporadic Small Bowel Angiodysplasia”. J Clin Gastroenterol. 49 (10): 831–6. doi:10.1097/MCG.0000000000000260. PMID 25319741.
  4. ↑ 4.0 4.1 Warkentin TE, Moore JC, Anand SS, Lonn EM, Morgan DG (2003). “Gastrointestinal bleeding, angiodysplasia, cardiovascular disease, and acquired von Willebrand syndrome”. Transfus Med Rev. 17 (4): 272–86. doi:10.1016/s0887-7963(03)00037-3. PMID 14571395.
  5. ↑ Pate GE, Chandavimol M, Naiman SC, Webb JG (2004). “Heyde’s syndrome: a review”. J Heart Valve Dis. 13 (5): 701–12. PMID 15473466.
  6. ↑ Tariq T, Karabon P, Irfan FB, Goyal S, Mayeda MM, Parsons A; et al. (2019). “Secondary angiodysplasia-associated gastrointestinal bleeding in end-stage renal disease: Results from the nationwide inpatient sample”. World J Gastrointest Endosc. 11 (10): 504–514. doi:10.4253/wjge.v11.i10.504. PMC 6885446 Check |pmc= value (help). PMID 31798771.
  7. ↑ Marie I, Ducrotte P, Antonietti M, Herve S, Levesque H (2008). “Watermelon stomach in systemic sclerosis: its incidence and management”. Aliment Pharmacol Ther. 28 (4): 412–21. doi:10.1111/j.1365-2036.2008.03739.x. PMID 18498445.
  8. ↑ Koga H, Iida M, Nagai E, Aoyagi K, Matsumoto T, Takesue M; et al. (1996). “Jejunal angiodysplasia confirmed by intravascular injection technique in vitro. Report of a case and review of the literature”. J Clin Gastroenterol. 23 (2): 139–44. doi:10.1097/00004836-199609000-00017. PMID 8877645.
  9. ↑ Thelmo WL, Vetrano JA, Wibowo A, DiMaio TM, Cruz-Vetrano WP, Kim DS (1992). “Angiodysplasia of colon revisited: pathologic demonstration without the use of intravascular injection technique”. Hum Pathol. 23 (1): 37–40. doi:10.1016/0046-8177(92)90008-q. PMID 1544666.
  10. ↑ Accordino R, Paties C, Inzani E, Civardi C, Cremonesi V, Lagasi L; et al. (1995). “[Angiodysplasia of the right colon]”. Minerva Chir. 50 (7–8): 703–6. PMID 8532207.

Template:WS Template:WH

Causes

Causes

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

Overview

The exact etiology of angiodysplasia is unknown. However, many conditions have been associated with angiodysplasia.

Causes

The exact cause of angiodysplasia is unknown. However, there are various conditions associated with angiodysplasia. For more information on associated conditions, click here.

References


Differentiating Angiodysplasia from other Diseases

Differentiating Angiodysplasia from other Diseases

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

Overview

Angiodysplasia must be differentiated from other diseases that cause hematochezia, melena, and iron deficiency anemia, such as hemorrhoids, diverticular disease, and colon cancer.

Differentiating Angiodysplasia from other Diseases

Angiodysplasia must be differentiated from other diseases that cause hematochezia, melena, and iron deficiency anemia such as:

Diseases Clinical manifestations Para-clinical findings Gold standard
Symptoms Physical examination
Lab Findings Imaging Histopathology
Abdominal pain Lower GI Bleed Changes in bowel habits, weight loss Characteristic physical examination findings Pertinent laboratory findings Ultrasound/CT scan Endoscopy MRI
Diverticulitis[1][2][3][4][5][6][7][8] + + – Left lower quadrant abdominal tenderness, fever Leukocytosis, elevated ESR and CRP Radiological test of choice – CT of abdomen and pelvis with contrast which shows segmental bowel wall thickening, pericolic inflammation, abscess (30% cases) Endoscopy is not indicated in acute diverticulitis due to the risk of perforation Findings similar to CT scan Varying grades of inflammation seen in surgical specimens Abdominal computerized tomography (CT) scan
Hemorrhoids[9][10][11][12][13][14][12] – (anal pain) + – Skin tags, fistulas/fissures, prolapsed hemorrhoid Complete blood count may show iron deficiency anemia Ultrasound – “mosaic pattern” of anal cushion in grade III and IV internal hemorrhoids Anoscopy – bulging, dilated purplish-blue veins MRI is not recommended for the assessment of hemorrhoids Abnormally dilated, vessels within submucosal arteriovenous plexus Anoscopy
Colon cancer[15][16][17][18][19][20][21][22][23][24][25] +/- +/- + Lymphadenopathies, abdominal mass, hepatomegaly (metastasis) Complete blood count – iron deficiency anemia, tumor marker – CEA, methylated circulating DNA markers CT scan shows soft tissue mass causing narrowing of colonic lumen or asymmetric bowel wall thickening. Colonoscopy reveals mass protruding from the mucosa to the lumen which may sometimes bleed on touching MRI is better than CT to detect liver metastasis Majority of colorectal cancers are adenocarcinomas characterised by glandular formation Colonoscopy
Massive upper GI bleed[26][27][28][29][30] + + – Hemodynamic instability, upper abdominal tenderness, pale skin Complete blood count in acute bleeding – normocytic anemia. Elevated BUN-to-Creatinine ratio >30:1 CT angiography localises the site of GI bleed Upper GI endoscopy can play a diagnostic and therapeutic role in localising and stopping the bleed MRI is not indicated NA Endoscopy
Inflammatory bowel disease[31][32][33][34][35][36][37][38][39][40] + +/- + Tachycardia, fever, occult blood on digital rectal examinaton, anal fistulas
  • Complete blood count – microcytic anemia, leukocytosis.
  • Elevated ESR, CRP,
  • Elevated fecal calprotectin (non-specific),
  • Low serum vitamin B12 and folate levels,
  • Anti-Saccaromyces cerevisiae antibodies (ASCA) – Crohn’s disease.
  • Anti-neutrophil cytoplasm antibodies (p-ANCA)-Ulcerative colitis.
 CT scan – Ulcerative colitis presents as thinning of bowel wall whereas, active Crohn’s disease presents as bowel wall thickening with hyperenhancement of mucosa. Colonoscopy in:
  • Ulcerative colitis – edematous mucosa, decreased vascular markings, erosions.
  • Crohn’s disease – discontinuous ulcers, cobblestone appearance of mucosa.
 Pelvi MRI for perianal involvement UC- crypt abscess

Crohn’s- transmural involvement, granulomas

Endoscopy
Angiodysplasia[41][42][43][44] – Occult – Signs of anemia, systolic ejection murmur (if aortic stenosis), rarely, orthostasis or hypotension CT angiography – focal areas of contrast enhancement, early filling veins Upper GI endoscopy and colonoscopy: discrete, small foci with arborizing pattern from a visible central artery
 MRA may be used Tortuous, dilated veins, venules and capillaries in the colonic mucosa and submucosa Endoscopy

References

  1. ↑ Swanson SM, Strate LL (2018). “Acute Colonic Diverticulitis”. Ann Intern Med. 168 (9): ITC65–ITC80. doi:10.7326/AITC201805010. PMC 6430566. PMID 29710265.
  2. ↑ Laurell H, Hansson LE, Gunnarsson U (2007). “Acute diverticulitis–clinical presentation and differential diagnostics”. Colorectal Dis. 9 (6): 496–501, discussion 501-2. doi:10.1111/j.1463-1318.2006.01162.x. PMID 17573742.
  3. ↑ Laméris W, van Randen A, van Gulik TM, Busch OR, Winkelhagen J, Bossuyt PM; et al. (2010). “A clinical decision rule to establish the diagnosis of acute diverticulitis at the emergency department”. Dis Colon Rectum. 53 (6): 896–904. doi:10.1007/DCR.0b013e3181d98d86. PMID 20485003.
  4. ↑ Hawkins AT, Wise PE, Chan T, Lee JT, Glyn T, Wood V; et al. (2020). “Diverticulitis: An Update From the Age Old Paradigm”. Curr Probl Surg. 57 (10): 100862. doi:10.1016/j.cpsurg.2020.100862. PMC 7575828 Check |pmc= value (help). PMID 33077029 Check |pmid= value (help).
  5. ↑ Hulnick DH, Megibow AJ, Balthazar EJ, Naidich DP, Bosniak MA (1984). “Computed tomography in the evaluation of diverticulitis”. Radiology. 152 (2): 491–5. doi:10.1148/radiology.152.2.6739821. PMID 6739821.
  6. ↑ Doringer E (1992). “Computerized tomography of colonic diverticulitis”. Crit Rev Diagn Imaging. 33 (5): 421–35. PMID 1418606.
  7. ↑ Destigter KK, Keating DP (2009). “Imaging update: acute colonic diverticulitis”. Clin Colon Rectal Surg. 22 (3): 147–55. doi:10.1055/s-0029-1236158. PMC 2780264. PMID 20676257.
  8. ↑ Pesce A, Barchitta M, Agodi A, Salerno M, La Greca G, Magro G; et al. (2020). “Comparison of clinical and pathological findings of patients undergoing elective colectomy for uncomplicated diverticulitis”. Sci Rep. 10 (1): 8854. doi:10.1038/s41598-020-65727-1. PMC 7264214 Check |pmc= value (help). PMID 32483125 Check |pmid= value (help).
  9. ↑ Kluiber RM, Wolff BG (1994). “Evaluation of anemia caused by hemorrhoidal bleeding”. Dis Colon Rectum. 37 (10): 1006–7. doi:10.1007/BF02049313. PMID 7924705.
  10. ↑ Lohsiriwat V (2015). “Treatment of hemorrhoids: A coloproctologist’s view”. World J Gastroenterol. 21 (31): 9245–52. doi:10.3748/wjg.v21.i31.9245. PMC 4541377. PMID 26309351.
  11. ↑ Lohsiriwat V (2013). “Approach to hemorrhoids”. Curr Gastroenterol Rep. 15 (7): 332. doi:10.1007/s11894-013-0332-6. PMID 23715885.
  12. ↑ 12.0 12.1 Mounsey AL, Halladay J, Sadiq TS (2011). “Hemorrhoids”. Am Fam Physician. 84 (2): 204–10. PMID 21766771.
  13. ↑ Sanchez C, Chinn BT (2011). “Hemorrhoids”. Clin Colon Rectal Surg. 24 (1): 5–13. doi:10.1055/s-0031-1272818. PMC 3140328. PMID 22379400.
  14. ↑ Aimaiti A, A Ba Bai Ke Re MMTJ, Ibrahim I, Chen H, Tuerdi M (2017). “Sonographic appearance of anal cushions of hemorrhoids”. World J Gastroenterol. 23 (20): 3664–3674. doi:10.3748/wjg.v23.i20.3664. PMC 5449423. PMID 28611519.
  15. ↑ Hamilton W, Round A, Sharp D, Peters TJ (2005). “Clinical features of colorectal cancer before diagnosis: a population-based case-control study”. Br J Cancer. 93 (4): 399–405. doi:10.1038/sj.bjc.6602714. PMC 2361578. PMID 16106247.
  16. ↑ Majumdar SR, Fletcher RH, Evans AT (1999). “How does colorectal cancer present? Symptoms, duration, and clues to location”. Am J Gastroenterol. 94 (10): 3039–45. doi:10.1111/j.1572-0241.1999.01454.x. PMID 10520866.
  17. ↑ Rizk SN, Ryan JJ (1994). “Clinicopathologic review of 92 cases of colon cancer”. S D J Med. 47 (3): 89–93. PMID 8184311.
  18. ↑ Saidi HS, Karuri D, Nyaim EO (2008). “Correlation of clinical data, anatomical site and disease stage in colorectal cancer”. East Afr Med J. 85 (6): 259–62. doi:10.4314/eamj.v85i6.9622. PMID 18817021.
  19. ↑ Moreno CC, Mittal PK, Sullivan PS, Rutherford R, Staley CA, Cardona K; et al. (2016). “Colorectal Cancer Initial Diagnosis: Screening Colonoscopy, Diagnostic Colonoscopy, or Emergent Surgery, and Tumor Stage and Size at Initial Presentation”. Clin Colorectal Cancer. 15 (1): 67–73. doi:10.1016/j.clcc.2015.07.004. PMID 26602596.
  20. ↑ Astin M, Griffin T, Neal RD, Rose P, Hamilton W (2011). “The diagnostic value of symptoms for colorectal cancer in primary care: a systematic review”. Br J Gen Pract. 61 (586): e231–43. doi:10.3399/bjgp11X572427. PMC 3080228. PMID 21619747.
  21. ↑ Symonds EL, Pedersen SK, Baker RT, Murray DH, Gaur S, Cole SR; et al. (2016). “A Blood Test for Methylated BCAT1 and IKZF1 vs. a Fecal Immunochemical Test for Detection of Colorectal Neoplasia”. Clin Transl Gastroenterol. 7: e137. doi:10.1038/ctg.2015.67. PMC 4737873. PMID 26765125.
  22. ↑ Sun J, Fei F, Zhang M, Li Y, Zhang X, Zhu S; et al. (2019). “The role of mSEPT9 in screening, diagnosis, and recurrence monitoring of colorectal cancer”. BMC Cancer. 19 (1): 450. doi:10.1186/s12885-019-5663-8. PMC 6518628 Check |pmc= value (help). PMID 31088406.
  23. ↑ Song L, Li Y (2015). “SEPT9: A Specific Circulating Biomarker for Colorectal Cancer”. Adv Clin Chem. 72: 171–204. doi:10.1016/bs.acc.2015.07.004. PMID 26471083.
  24. ↑ Niekel MC, Bipat S, Stoker J (2010). “Diagnostic imaging of colorectal liver metastases with CT, MR imaging, FDG PET, and/or FDG PET/CT: a meta-analysis of prospective studies including patients who have not previously undergone treatment”. Radiology. 257 (3): 674–84. doi:10.1148/radiol.10100729. PMID 20829538.
  25. ↑ Shia J, Schultz N, Kuk D, Vakiani E, Middha S, Segal NH; et al. (2017). “Morphological characterization of colorectal cancers in The Cancer Genome Atlas reveals distinct morphology-molecular associations: clinical and biological implications”. Mod Pathol. 30 (4): 599–609. doi:10.1038/modpathol.2016.198. PMC 5380525. PMID 27982025.
  26. ↑ Wilkins T, Wheeler B, Carpenter M (2020). “Upper Gastrointestinal Bleeding in Adults: Evaluation and Management”. Am Fam Physician. 101 (5): 294–300. PMID 32109037 Check |pmid= value (help).
  27. ↑ Hopper AD, Sanders DS (2011). “Upper GI bleeding requires prompt investigation”. Practitioner. 255 (1742): 15–9, 2. PMID 21932501.
  28. ↑ Gralnek IM, Dumonceau JM, Kuipers EJ, Lanas A, Sanders DS, Kurien M; et al. (2015). “Diagnosis and management of nonvariceal upper gastrointestinal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) Guideline”. Endoscopy. 47 (10): a1–46. doi:10.1055/s-0034-1393172. PMID 26417980.
  29. ↑ Srygley FD, Gerardo CJ, Tran T, Fisher DA (2012). “Does this patient have a severe upper gastrointestinal bleed?”. JAMA. 307 (10): 1072–9. doi:10.1001/jama.2012.253. PMID 22416103.
  30. ↑ Richards RJ, Donica MB, Grayer D (1990). “Can the blood urea nitrogen/creatinine ratio distinguish upper from lower gastrointestinal bleeding?”. J Clin Gastroenterol. 12 (5): 500–4. doi:10.1097/00004836-199010000-00004. PMID 2229992.
  31. ↑ Seyedian SS, Nokhostin F, Malamir MD (2019). “A review of the diagnosis, prevention, and treatment methods of inflammatory bowel disease”. J Med Life. 12 (2): 113–122. doi:10.25122/jml-2018-0075. PMC 6685307 Check |pmc= value (help). PMID 31406511.
  32. ↑ Rosen MJ, Dhawan A, Saeed SA (2015). “Inflammatory Bowel Disease in Children and Adolescents”. JAMA Pediatr. 169 (11): 1053–60. doi:10.1001/jamapediatrics.2015.1982. PMC 4702263. PMID 26414706.
  33. ↑ Nocerino A, Nguyen A, Agrawal M, Mone A, Lakhani K, Swaminath A (2020). “Fatigue in Inflammatory Bowel Diseases: Etiologies and Management”. Adv Ther. 37 (1): 97–112. doi:10.1007/s12325-019-01151-w. PMC 6979464 Check |pmc= value (help). PMID 31760611.
  34. ↑ Satsangi J, Silverberg MS, Vermeire S, Colombel JF (2006). “The Montreal classification of inflammatory bowel disease: controversies, consensus, and implications”. Gut. 55 (6): 749–53. doi:10.1136/gut.2005.082909. PMC 1856208. PMID 16698746.
  35. ↑ van Rheenen PF, Van de Vijver E, Fidler V (2010). “Faecal calprotectin for screening of patients with suspected inflammatory bowel disease: diagnostic meta-analysis”. BMJ. 341: c3369. doi:10.1136/bmj.c3369. PMC 2904879. PMID 20634346. Review in: Ann Intern Med. 2011 Jan 18;154(2):JC1-12
  36. ↑ Pan Y, Liu Y, Guo H, Jabir MS, Liu X, Cui W; et al. (2017). “Associations between Folate and Vitamin B12 Levels and Inflammatory Bowel Disease: A Meta-Analysis”. Nutrients. 9 (4). doi:10.3390/nu9040382. PMC 5409721. PMID 28406440.
  37. ↑ Alkhouri RH, Hashmi H, Baker RD, Gelfond D, Baker SS (2013). “Vitamin and mineral status in patients with inflammatory bowel disease”. J Pediatr Gastroenterol Nutr. 56 (1): 89–92. doi:10.1097/MPG.0b013e31826a105d. PMID 22832510.
  38. ↑ Strobel D, Goertz RS, Bernatik T (2011). “Diagnostics in inflammatory bowel disease: ultrasound”. World J Gastroenterol. 17 (27): 3192–7. doi:10.3748/wjg.v17.i27.3192. PMC 3158394. PMID 21912467.
  39. ↑ Spiceland CM, Lodhia N (2018). “Endoscopy in inflammatory bowel disease: Role in diagnosis, management, and treatment”. World J Gastroenterol. 24 (35): 4014–4020. doi:10.3748/wjg.v24.i35.4014. PMC 6148432. PMID 30254405.
  40. ↑ Gee MS, Harisinghani MG (2011). “MRI in patients with inflammatory bowel disease”. J Magn Reson Imaging. 33 (3): 527–34. doi:10.1002/jmri.22504. PMC 3078716. PMID 21512607.
  41. ↑ Tonea A, Andrei S, Andronesi D, Ionescu M, Gheorghe C, Herlea V; et al. (2008). “[Difficulties in diagnosis and surgical treatment of the angiodysplasia of the gastrointestinal tract]”. Chirurgia (Bucur). 103 (5): 513–28. PMID 19260627.
  42. ↑ Danesh BJ, Spiliadis C, Williams CB, Zambartas CM (1987). “Angiodysplasia–an uncommon cause of colonic bleeding: colonoscopic evaluation of 1,050 patients with rectal bleeding and anaemia”. Int J Colorectal Dis. 2 (4): 218–22. doi:10.1007/BF01649509. PMID 3500991.
  43. ↑ Howard OM, Buchanan JD, Hunt RH (1982). “Angiodysplasia of the colon. Experience of 26 cases”. Lancet. 2 (8288): 16–9. doi:10.1016/s0140-6736(82)91153-9. PMID 6123752.
  44. ↑ Pounder DJ, Rowland R, Pieterse AS, Freeman R, Hunter R (1982). “Angiodysplasias of the colon”. J Clin Pathol. 35 (8): 824–9. doi:10.1136/jcp.35.8.824. PMC 497797. PMID 6980903.

Template:WH Template:WS

Epidemiology and Demographics

Epidemiology and Demographics

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

Overview

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

Epidemiology and Demographics

Angiodysplasia is the most common vascular malformation of the GI tract and accounts for 20% of the major episodes of lower intestinal bleeding.

United States statistics

  • The incidence of colonic diverticular and angiodysplasia bleeding per 100,000 person-years increased over time, which may be attributed to an increased frequency of anticoagulant use.
  • The prevalence of angiodysplasia is less than 1% in healthy patients older than 50 years undergoing screening colonoscopy.[1]
  • Angiodysplasia accounts for up to 50% of episodes of recurrent GI bleeding in patients with end-stage renal disease.
  • The most frequent cause of GI bleeding in patients with von Willebrand disease is angiodysplasia.
  • According to a study, the prevalence of aortic stenosis in patients with endoscopically confirmed angiodysplasia is around 30%.
    [2]

International statistics

  • Extensive studies have not been performed to establish the incidence of angiodysplasia worldwide, but the incidence is in all likelihood similar to that in the United States.
  • Predominant location for colonic angiodysplasia in Japanese patients is left colon, whereas it is the right colon for Western patients. Additionally, Japanese patients have a higher incidence of lesions measuring more than 5 mm in size or of elevated type than their Western counterparts.[3]
  • Angiodysplasia affects all races equally.
  • The incidence of angiodysplasia is equal in both men and women.
  • Majority of the affected population is older than 60 years.

Location wise statistics:

Upper GI tract

Angiodysplasia is responsible for non-variceal upper gastrointestinal bleeding in 4–7% of patients.

Small bowel

In patients older than 50 years, the source of obscure gastrointestinal bleeding is most commonly small bowel angiodysplasia.

Colon

The most common location of angiodysplasia of the gastrointestinal tract is the colon. Within the colon, the cecum and ascending colon are the most frequent location of angiodysplasia in western patients, whereas, descending colon is the most likely site in Japanese patients.

Angiodysplasia of the colon can be accountable for 3% to 40% of the cases of lower GI hemorrhage which can be classified into mild, chronic, recurrent, or life-threatening.[4]

References

  1. ↑ 1.0 1.1 Lanas A, García-Rodríguez LA, Polo-Tomás M, Ponce M, Quintero E, Perez-Aisa MA; et al. (2011). “The changing face of hospitalisation due to gastrointestinal bleeding and perforation”. Aliment Pharmacol Ther. 33 (5): 585–91. doi:10.1111/j.1365-2036.2010.04563.x. PMID 21205256.
  2. ↑ Bhutani MS, Gupta SC, Markert RJ, Barde CJ, Donese R, Gopalswamy N (1995). “A prospective controlled evaluation of endoscopic detection of angiodysplasia and its association with aortic valve disease”. Gastrointest Endosc. 42 (5): 398–402. doi:10.1016/s0016-5107(95)70038-2. PMID 8566626.
  3. ↑ Ueno S, Nakase H, Kasahara K, Uza N, Kitamura H, Inoue S; et al. (2008). “Clinical features of Japanese patients with colonic angiodysplasia”. J Gastroenterol Hepatol. 23 (8 Pt 2): e363–6. doi:10.1111/j.1440-1746.2007.05126.x. PMID 17725595.
  4. ↑ Sami SS, Al-Araji SA, Ragunath K (2014). “Review article: gastrointestinal angiodysplasia – pathogenesis, diagnosis and management”. Aliment Pharmacol Ther. 39 (1): 15–34. doi:10.1111/apt.12527. PMID 24138285.
Risk Factors

Risk Factors

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

Overview

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

Risk Factors

The most important risk factors for active bleeding from angiodysplasia include:[1][2]


References

  1. ↑ Nishimura N, Mizuno M, Shimodate Y, Doi A, Mouri H, Matsueda K; et al. (2016). “Risk factors for active bleeding from colonic angiodysplasia confirmed by colonoscopic observation”. Int J Colorectal Dis. 31 (12): 1869–1873. doi:10.1007/s00384-016-2651-1. PMID 27596107.
  2. ↑ Tsai YY, Chen BC, Chou YC, Lin JC, Lin HH, Huang HH; et al. (2019). “Clinical characteristics and risk factors of active bleeding in colonic angiodysplasia among the Taiwanese”. J Formos Med Assoc. 118 (5): 876–882. doi:10.1016/j.jfma.2018.10.001. PMID 30348493.

Template:WS Template:WH

Screening

Screening

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

Overview

No screening protocol is available for angiodysplasia.

Screening

No screening protocol is available. Angiodysplasia is usually an incidental finding for endoscopy done for different reasons.

References

Template:WS Template:WH

Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

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

Overview

In asymptomatic people, the course of angiodysplasia is benign, and the bleeding risk is low. Consequently, treatment is not required for incidentally found lesions. Complications of angiodysplasia include iron-deficiency anemia, side effects from treatment e.g., subcutaneous emphysema, perforation of the bowel during argon plasma coagulation, re-bleeding post procedure, severe loss of blood from the GI tract, death from hypovolemic shock. Nevertheless, the prognosis of angiodysplasia in asymptomatic patients is good as the bleeding risk is low. Moreover, in 90% of cases, angiodysplasias stop bleeding spontaneously which might be the result of the venous nature of angiodysplasias.

Natural History

  • Small bowel angiodysplasia (SBA) contributes to 50% of obscure GI bleeding cases.[1]
  • SBA tends to re-bleed more than angiodysplasia of the colon and stomach.
  • In a retrospective study, re-bleeding occurred after about 11 months of diagnosis in 80% of patients, and 3.5% died as a direct result of bleeding.[1]
  • Multiple lesions and valvular heart diseases have been found to increase the risk of re-bleeding.
  • Apart from recurrence of bleeding, some other concerns in the natural history of angiodysplasia are transfusion requirements, hospital readmissions, and requirement endoscopic, pharmacological, or surgical therapy.
  • In asymptomatic people, the course of angiodysplasia is benign, and the bleeding risk is low. Consequently, treatment is not required for incidentally found lesions.[2]

Complications

Prognosis

  • The prognosis of angiodysplasia in asymptomatic patients is good as the bleeding risk is low.
  • In 90% of cases, angiodysplasias stop bleeding spontaneously which might be the result of the venous nature of angiodysplasias.[5]
  • Advanced age, severe bleeding and hemodynamic instability, and the presence of co-morbid medical conditions like coronary artery disease, type 2 diabetes mellitus may contribute to mortality in these cases.

References

  1. ↑ 1.0 1.1 Holleran G, Hall B, Zgaga L, Breslin N, McNamara D (2016). “The natural history of small bowel angiodysplasia”. Scand J Gastroenterol. 51 (4): 393–9. doi:10.3109/00365521.2015.1102317. PMID 26540240.
  2. ↑ Foutch PG, Rex DK, Lieberman DA (1995). “Prevalence and natural history of colonic angiodysplasia among healthy asymptomatic people”. Am J Gastroenterol. 90 (4): 564–7. PMID 7717311.
  3. ↑ Herrera S, Bordas JM, Llach J, Ginès A, Pellisé M, Fernández-Esparrach G; et al. (2008). “The beneficial effects of argon plasma coagulation in the management of different types of gastric vascular ectasia lesions in patients admitted for GI hemorrhage”. Gastrointest Endosc. 68 (3): 440–6. doi:10.1016/j.gie.2008.02.009. PMID 18423466.
  4. ↑ Ben Soussan E, Mathieu N, Roque I, Antonietti M (2003). “Bowel explosion with colonic perforation during argon plasma coagulation for hemorrhagic radiation-induced proctitis”. Gastrointest Endosc. 57 (3): 412–3. doi:10.1067/mge.2003.131. PMID 12612532.
  5. ↑ Al-Mehaidib A, Alnassar S, Alshamrani AS (2009). “Gastrointestinal angiodysplasia in three Saudi children”. Ann Saudi Med. 29 (3): 223–6. doi:10.4103/0256-4947.51786. PMC 2813652. PMID 19448365.

Template:WS Template:WH

Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Template:Gastroenterology

Template:WH Template:WS

Looking for the patient version?

Back to the patient-friendly article

Imprint

Privacy Policy

Terms and Conditions

© 2026 MyEClinic – IFTM Institut für Telematik in der Medizin GmbH