eMedicine Specialties > Gastroenterology > Colon

Angiodysplasia of the Colon

Author: Alan BR Thomson, MD, MSc, PhD, Professor, Department of Medicine, Division of Gastroenterology, University of Alberta Faculty of Medicine
Coauthor(s): Andrea Duchini, MD, Assistant Professor of Medicine, Associate Medical Director of Liver Transplantation, Division of Transplantation, Department of Surgery, The Methodist Hospital-Cornell University, Houston; John Godino, MD, Staff Physician, Department of Internal Medicine, Brooke Army Medical Center; Peter Wong, MD, Director of Gastroenterology Clinical Service/Manometry and Physiology, Brooke Army Medical Center; Assistant Professor, Department of Medicine, Division of Gastroenterology, University of Texas Health Science Center at San Antonio
Contributor Information and Disclosures

Updated: May 27, 2009

Introduction

Background

Angiodysplasia is the most common vascular lesion of the gastrointestinal tract, and this condition may be asymptomatic, or it may cause gastrointestinal (GI) bleeding.1 The vessel walls are thin, with little or no smooth muscle, and the vessels are ectatic and thin (see Image 2 or below).

Angiodysplasia identified on cecum wall during co...

Angiodysplasia identified on cecum wall during colonoscopy.

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Angiodysplasia identified on cecum wall during co...

Angiodysplasia identified on cecum wall during colonoscopy.


Phillips first described a vascular abnormality that caused bleeding from the large bowel in a letter to the London Medical Gazette in 1839. During the 1920s, neoplasms were considered the major source of GI hemorrhage. However, in the 1940s and 1950s, diverticular disease was recognized as an important source of bleeding. In 1951, Smith described active bleeding from a diverticulum visualized through a sigmoidoscope. An association between colonic angiodysplasia and aortic stenosis was described by Heyde in 1958.2

Vascular abnormalities as a source of active bleeding were controversial. In 1960, Margulis and colleagues identified a vascular malformation in the cecum of a 69-year-old woman who presented with massive bleeding.3 This diagnosis was accomplished with operative mesenteric arteriography.

Galdabini first used the name angiodysplasia in 1974; however, confusion about the exact nature of these lesions resulted in a multitude of terms that included arteriovenous malformation, hemangioma, telangiectasia, and vascular ectasia. These terms have varying pathophysiologies, with a common presentation of GI bleeding.

Angiodysplasia is a degenerative lesion of previously healthy blood vessels found most commonly in the cecum and proximal ascending colon. Seventy-seven percent of angiodysplasias are located in the cecum and ascending colon, 15% are located in the jejunum and ileum, and the remainder is distributed throughout the alimentary tract. These lesions typically are nonpalpable and small (<5 mm).

Angiodysplasia is the most common vascular abnormality of the GI tract. After diverticulosis, it is the second leading cause of lower GI bleeding in patients older than 60 years. Angiodysplasia may account for approximately 6% of cases of lower GI bleeding. It may be observed incidentally at colonoscopy in as many as 0.8% of patients older than 50 years. The prevalence for upper GI lesions is approximately 1-2%.

Small bowel angiodysplasia may account for 30-40% of cases of GI bleeding of obscure origin. Retrospective colonoscopic analyses have shown that 12.1% of 642 persons without symptoms of irritable bowel syndrome (IBS), and 11.9% of those with IBS had colonic angiodysplasia.4

Angiodysplasia may present as an isolated lesion or as multiple vascular lesions. Unlike congenital or neoplastic vascular lesions of the GI tract, this lesion is not associated with angiomatous lesions of the skin or other viscera.

Clinical presentation in patients with angiodysplasia is usually characterized by maroon-colored stool, melena, or hematochezia. Bleeding is usually low grade, but it can be massive in approximately 15% of patients. In 20-25% of bleeding episodes, only tarry stools are passed. Iron deficiency anemia and stools that are intermittently positive for occult blood can be the only manifestations of angiodysplasia in 10-15% of patients. Bleeding stops spontaneously in greater than 90% of cases but is often recurrent.

For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education articles Gastrointestinal Bleeding, Rectal Bleeding, Diverticulosis and Diverticulitis, and Irritable Bowel Syndrome.

Pathophysiology

The exact mechanism of development of angiodysplasia is not known, but chronic venous obstruction may play a role.5,6 This hypothesis accounts for the high prevalence of these lesions in the right colon and is based on the Laplace law. The Laplace law relates wall tension to luminal size and transmural pressure difference in a cylinder, whereby the wall tension is equal to the pressure difference multiplied by the radius of the cylinder. In the case of the colon, wall tension refers to intramural tension, the pressure difference is that between the bowel lumen and the peritoneal cavity, and cylinder radius is the radius of the right colon. Wall tension is highest in bowel segments with the greatest diameter, such as the right colon.

This theory involving chronic venous obstruction suggests that repeated episodes of colonic distention are associated with transient increases in lumen pressure and size., which results in multiple episodes of increasing wall tension with obstruction of submucosal venous outflow, especially where these vessels pierce the smooth muscle layers of the colon. Over many years, this process causes gradual dilation of the submucosal veins and, eventually, dilation of the venules and arteriolar capillary units feeding them. Ultimately, the capillary rings dilate, the precapillary sphincters lose their competency, and a small arteriovenous communication forms. This accounts for the characteristic early-filling vein observed during mesenteric angiography.

The developmental theory of angiodysplasia accounts for several clinical and pathologic features, including occurrence in older individuals, location in the cecum and proximal right colon, and prominent submucosal veins that dilate after traversing the muscularis propria. In addition, it also accounts for the lack of pathologic changes in arterioles supplying vascular ectasias and the absence of any mucosal lesion associated with them. Previous studies demonstrating that colonic motility, increased tension in the bowel wall, and increased intraluminal pressure can diminish venous flow lend further support to this theory. Dilated submucosal veins have been one of the most consistent histologic findings and may represent the earliest abnormality in colonic angiodysplasia. This histologic feature supports the theory of chronic venous obstruction in the genesis of angiodysplasia.

Of note, the aforementioned pathophysiologic mechanisms responsible for the development of cecal lesions are unlikely to apply to lesions in the upper GI tract, despite being morphologically identical.

A link between a deficiency of high molecular-weight multimers of von Willebrand factor, aortic stenosis, and colonic angiodysplasia has been proposed.

Frequency

There may be an association between colonic angiodysplasia and true diverticula.7  Portal hypertension colopathy, a form of colonic angiodysplasia, has been described.8 Vascular ectasia of the entire GI tract has been reported in a patient receiving high-dose chemotherapy and autologous stem cell transplantation for relapsing Hodgkin disease.9

United States

The prevalence of angiodysplasia is 0.8% in healthy patients older than 50 years who are undergoing screening colonoscopy.

Foutch et al noted the prevalence of angiodysplasia to be 0.83% from 3 prospective studies in which screening colonoscopies were performed in 964 asymptomatic individuals (mean age, 62 y).10

Patients with von Willebrand disease may have an increased incidence of GI bleeding from colonic angiodysplasia.11,12,13,14,15,16,17

International

No widespread studies to determine the international incidence of angiodysplasia have been conducted, but the incidence probably is similar to that in the United States.

Mortality/Morbidity

  • Bleeding from angiodysplasia is usually self-limited, but it can be chronic, recurrent, or even acute and life threatening.
  • Approximately 90% of bleeding angiodysplasias spontaneously cease bleeding, presumably because of its venous nature.
  • Mortality is related to the severity of bleeding, hemodynamic instability, age, and the presence of comorbid medical conditions.

Race

No racial predilection exists in cases of angiodysplasia of the colon.

Sex

Angiodysplasia of the colon occurs with equal frequency in men and women.

Age

Most patients found to have angiodysplasia are older than 60 years; of these patients, most are older than 70 years. However, case reports exist of occurrence in young people.

Clinical

History

Many patients with angiodysplasia are asymptomatic, and the lesions are incidentally found, such as with screening colonoscopy. Clinical presentation  and physical examination are related to GI bleeding or its consequences.

  • The estimated incidence of active GI bleed in patients with angiodysplasia is less than 10%. However, because these lesions may be located throughout the GI tract and because the rate of bleeding may be variable, the clinical presentation ranges from hematemesis or hematochezia to occult anemia. Bleeding is usually chronic or recurrent and, in most cases, low grade and painless because of the venous source.
  • Angiodysplastic lesions are often present in more than one location within the GI tract, and the presentation may vary during a patient's clinical course.
    • GI bleeding from small bowel lesions has occurred in as many as 22% of patients in whom angiodysplasia of the colon was the presumed index source of bleeding.
    • In 40-60% of patients with gastric and duodenal angiodysplasia, multiple lesions are observed at endoscopy. Colonic lesions will be associated in 15-20% of these patients. In addition, angiodysplastic lesions in the colon are more frequently multiple than single. To diagnose and treat patients with suspected angiodysplasia, the diffuse location of lesions and the propensity for multiplicity must be considered. A possible association of true colonic diverticula and angiodysplasia has been proposed and should be kept in mind.
  • Hematemesis is frequently observed in patients with angiodysplasia of the upper GI tract. Presentation with hemodynamically well-compensated, chronic bleeding is typical and often suggests the diagnosis. Patients with upper tract lesions may have had bleeding from days to years.
  • Bleeding from colonic lesions is most often chronic and low grade, but as many as 15% of patients present with acute massive hemorrhage. Patients with colonic angiodysplasia may present with hematochezia (0-60%), melena (0-26%), hemoccult positive stool (4-47%), or iron deficiency anemia (0-51%).
    • Melena occurs in at least one fourth of patients with colonic bleeding.
    • Spontaneous cessation of bleeding (occurring in 90% of patients) is the rule for angiodysplastic lesions located in any part of the GI tract.

Physical

Physical examination in a patient suspected of having angiodysplasia should include assessment of their hemodynamic stability and the likely origin of blood loss.

  • Extracolonic angiodysplasias occur in 17% of persons with colonic lesions.18
  • Vital signs may demonstrate tachycardia, hypotension, and postural changes based on the amount of blood loss.
  • Stool is typically guaiac positive. Because bleeding may be intermittent, alternating positive and negative guaiac stools can be found.
  • In most cases, bleeding presents as bright red blood, but it can also be maroon in color or melena.
  • A microcytic hypochromic anemia, reflecting iron deficiency, is observed in 10-15% of cases.
  • Hemodynamic instability may occur if bleeding is massive. This is observed in 15% of cases.

Causes

The exact cause of angiodysplasia is unknown, but theories include the following:

  • Degenerative changes of small blood vessels associated with aging (most widely accepted theory)
  • Long-term local hypo-oxygenation of the microcirculation from cardiac, vascular, or pulmonary disease
    • Angiodysplasia has been reported to be associated with aortic stenosis. Heyde first reported this association in 1958, describing Heyde syndrome as the combination of calcific aortic stenosis and GI bleeding due to angiodysplasia of the colon.2 He reported on 10 patients with GI bleeding of unknown origin who had clinical signs of aortic stenosis and speculated that these patients bled from sclerotic GI vessels.2  One month later, Schwartz et al suggested a similar association.19 Catell was quoted in a clinicopathologic conference on such a case in 1965. He suggested that these patients bled from a vascular lesion in the ascending colon that the pathologists could not demonstrate. Catell recommended a blind right hemicolectomy, which, in his experience, had resulted in cessation of bleeding in these patients.
    • Mucosal hypoperfusion from cardiac disease was later postulated to be the underlying cause for development of angiodysplasia. Studies using echocardiograms indicated that only a few patients with angiodysplastic lesions had significant valvular heart disease, such as aortic stenosis. More patients had aortic sclerosis than aortic stenosis. Aortic valve replacement or colectomy may be effective in the cessation of recurrent bleeding or after correction of heart failure in hypertrophic subaortic stenosis.20   In most persons with angiodysplasia, cardiac findings have no importance in the development of angiodysplasia, although in Japan the most prevalent underlying condition in patients with colonic angiodysplasia was cardiovascular disease (56%).21 Critiques of the literature by Imperiale and Ransohoff found a lack of conclusive evidence to support the association of aortic stenosis, angiodysplasia, and GI bleeding22
    • Hypoperfusion or hypo-oxygenation from cardiac or pulmonary disease possibly results in ischemic necrosis of an existing angiodysplastic lesion. The observation that low cardiac output usually is a late occurrence in the course of aortic valve disease has not supported this possibility. In addition, the low cardiac output associated with mitral stenosis is not associated with a propensity for bleeding in angiodysplastic lesions.
    • Cessation of angiodysplastic bleeding after aortic valve replacement in severe aortic stenosis
  • Pate et al suggested that Heyde syndrome consists of bleeding from presumably latent angiodysplasia as a result of a hematologic defect, such as a lack of high molecular weight von willebrand factor multimers.20
  • Bleeding angiodysplastic lesions in the upper GI tract have been found with a high prevalence in patients with chronic renal failure requiring dialysis.23  However, this has not been a consistent finding. Patients with chronic renal failure are more likely to have coagulopathies that are related to quantitative and qualitative platelet defects and abnormal function and structure of von Willebrand factor.
  • Bleeding from angiodysplastic lesions in the upper and lower GI tract has been reported in patients with von Willebrand disease. Because factor VIII complex is synthesized partly in vascular endothelial cells, patients with von Willebrand disease and angiodysplasia have been proposed to have an underlying endothelial defect that may be related to the subsequent development of the 2 disorders. However, as with renal failure, the coagulopathy is more likely responsible for bleeding than for the development of the lesions.
  • Roskell et al demonstrated a relative deficiency of collagen type IV in the mucosal vessels in angiodysplasia compared to controls.24  The authors proposed that this deficiency may be related to the patients' susceptibility to ectasia and hemorrhage.
  • In a small study, Junquera et al observed an increased expression of angiogenic factors in human colonic angiodysplasia.25  This study noted that vascular immunoreactivity for basic fibroblast growth factor was observed in 7 (39%) specimens from patients with colonic angiodysplasia, whereas either very limited or no immunostaining was found in sections from specimens of patients with colonic cancer and healthy margins.
  • Patients with scleroderma may also have a higher incidence of angiodysplasia throughout the GI tract, including the colon.

More on Angiodysplasia of the Colon

Overview: Angiodysplasia of the Colon
Differential Diagnoses & Workup: Angiodysplasia of the Colon
Treatment & Medication: Angiodysplasia of the Colon
Follow-up: Angiodysplasia of the Colon
Multimedia: Angiodysplasia of the Colon
References
Further Reading
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Keywords

angiodysplasia of the colon, colonic angiodysplasia, angiodysplasia, arteriovenous malformation, AVM, angiomatosis, vascular ectasia, hemangioma, telangiectasia, vascular lesion of the gastrointestinal tract, gastrointestinal bleeding, GI bleeding, GI hemorrhage, gastrointestinal hemorrhage, rectal bleeding, blood in stool, colonoscopy

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Contributor Information and Disclosures

Author

Alan BR Thomson, MD, MSc, PhD, Professor, Department of Medicine, Division of Gastroenterology, University of Alberta Faculty of Medicine
Alan BR Thomson, MD, MSc, PhD is a member of the following medical societies: American Federation for Aging Research, American Federation for Clinical Research, American Gastroenterological Association, American Geriatrics Society, American Physiological Society, Canadian Association of Gastroenterology, Gastroenterology Research Group, New York Academy of Sciences, and Royal Society of Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Andrea Duchini, MD, Assistant Professor of Medicine, Associate Medical Director of Liver Transplantation, Division of Transplantation, Department of Surgery, The Methodist Hospital-Cornell University, Houston
Andrea Duchini, MD is a member of the following medical societies: American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and International Liver Transplantation Society
Disclosure: Nothing to disclose.

John Godino, MD, Staff Physician, Department of Internal Medicine, Brooke Army Medical Center
John Godino, MD is a member of the following medical societies: American College of Physicians and American Medical Association
Disclosure: Nothing to disclose.

Peter Wong, MD, Director of Gastroenterology Clinical Service/Manometry and Physiology, Brooke Army Medical Center; Assistant Professor, Department of Medicine, Division of Gastroenterology, University of Texas Health Science Center at San Antonio
Peter Wong, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Medical Editor

Marco G Patti, MD, Professor of Surgery, Director, Center for Esophageal Diseases, University of Chicago Pritzker School of Medicine
Marco G Patti, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Surgeons, American Gastroenterological Association, American Medical Association, American Surgical Association, Association for Academic Surgery, Pan-Pacific Surgical Association, Society for Surgery of the Alimentary Tract, Society of American Gastrointestinal and Endoscopic Surgeons, Southwestern Surgical Congress, and Western Surgical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

James L Achord, MD, Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine
James L Achord, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Mississippi State Medical Association, New York Academy of Sciences, Sigma Xi, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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