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Angiodysplasia of the Colon

  • Author: Hussein Al-Hamid, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Jul 27, 2016
 

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 below).

Angiodysplasia identified on the cecum wall during Angiodysplasia identified on the 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 once considered 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. In a recent retrospective colonoscopic analyses, it was 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]

Colonic arteriovenous malformation (AVM) is one of the causes of lower GI bleeding. Unlike small vascular ectasia or angiodysplasia, colonic AVM tends to be solitary, large in size, and identified endoscopically as flat or as an elevated bright red lesion.[5]

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.

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Pathophysiology

The exact mechanism of development of angiodysplasia is not known, but chronic venous obstruction may play a role.[6, 7] 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.

Increased expression of angiogenic factors, like basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), is also believed to play a role in the pathogenesis of colonic angiodysplasia.[8]

A link between the mechanical disruption of high molecular-weight multimers of von Willebrand factor, due to the turbulent blood flow through a narrowed valve in patients with aortic stenosis, and colonic angiodysplasia has been proposed.

Colonic angiodysplasia and true diverticula may be associated.[9] Portal hypertension colopathy, a form of colonic angiodysplasia, has been described.[10] 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.[11]

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Etiology

Angiodysplasia, a vascular malformation, is the most common cause of recurrent lower intestinal hemorrhage in patients with renal failure. Lesions are multiple in 40-75% of cases and are often located in the stomach and duodenum but can also affect the colon and the jejunum. Diagnosis is improved by endoscopy, which has a much higher sensitivity compared with angiography. Capsular endoscopy may reveal the hemorrhage site in the small intestine when regular endoscopy fails, and therapeutic intervention usually includes argon plasma coagulation.[12]

The exact cause of angiodysplasia is unknown, but theories include degenerative changes of small blood vessels associated with aging (most widely accepted theory) and 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.[13]

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 the 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.[14]

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%).[15] Critiques of the literature by Imperiale and Ransohoff found a lack of conclusive evidence to support the association of aortic stenosis, angiodysplasia, and GI bleeding[16]

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 has been reported in patients with severe aortic stenosis.

Pate et al suggested that the 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.[14]

Bleeding angiodysplastic lesions in the upper GI tract have been found with a high prevalence in patients with chronic renal failure requiring dialysis.[17] 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.

Moreover, degenerative aortic stenosis is associated with increased destruction of high molecular weight multimers of von Willebrand factor which can promote bleeding from intestinal angiodysplasias. Aortic valve replacement is the first line therapy for advanced stage of valve disease but can also be an effective treatment for coexistent bleeding angiodysplasias and acquired von Willebrand disease.[18]

Roskell et al demonstrated a relative deficiency of collagen type IV in the mucosal vessels in angiodysplasia compared to controls.[19] 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.[8] 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.

The incidence of GI bleeding after implantation of the continuous-flow left-ventricular assist devices (CF-LVAD) varies between 18% and 40% in many studies, and it is believed to be higher compared to the older generation pulsatile LVAD. GI bleeding due to angiodysplasia and arteriovenous malformations (AVMs) is more common and appears to be related to the blood-flow rheology of these devices.[20, 21]

A study from the University of Minnesota showed that 51 of 233 (22%) patients who underwent CF-LVAD (Heartmeate 2) implantation between 2005 and 2013 had GI bleeding.[21] Acquired von Willebrand disease is believed to be the proposed mechanism in some patients due to the reduction in high molecular weight (HMW) multimers of von Willebrand factor (vWF) from the shear stress affecting blood flow in the CF-LVAD .[21] In addition to acquired von Willebrand's disease, activation of the fibrinolytic system and a loss of platelet numbers and function during CF-LVAD support is a possibility.[21] The low pulse pressure and the secondary intestinal hypoperfusion is another proposed mechanism for GI bleeding after CF-LVAD. Screening of patients for angiodysplasia and von Willebrand disease before CF-LVAD implant may allow for effective preemptive treatment.[20, 21]

In Heyde syndrome, the association of aortic stenosis and bleeding from angiodysplasia appears to be related to subtle alterations in plasma coagulation factors. vWF is the strongest possible link between aortic stenosis and bleeding associated with GI angiodysplasia. Aortic valve replacement appears to offer the best hope of long-term resolution of the bleeding.[22]

Aortic valve replacement corrects the vWF abnormalities with long-term resolution of GI bleeding.[23] Resolution of anemia usually follows aortic valve replacement.[24]

Hereditary hemorrhagic telangiectasia (HHT), also known as Osler-Weber-Rendu disease, is an autosomal dominant disorder of the fibrovascular tissue. It is characterized by the classic triad of mucocutaneous telangiectasias, recurrent hemorrhages, and familial occurrence. Gastric angiodysplasia of the fundus and body of the stomach is observed. Histopathologic study shows dilated capillaries lined by flat endothelial cells in the papillary dermis.[25]

GI angiodysplasia is a very common cause of digestive hemorrhage among patients with chronic renal insufficiency.[26]

About two third of patients with systemic sclerosis who have gastric antral vascular ectasia (GAVE) have diffuse cutaneous systemic sclerosis and the remainder have limited cutaneous systemic sclerosis. The mean disease duration at diagnosis with GAVE was 22 months for diffuse systemic sclerosis and 84 months for limited cutaneous systemic sclerosis (p = 0.025); diffuse cutaneous systemic sclerosis is associated with earlier development of GAVE, as well as more severe anemia requiring more therapeutic interventions.[27]

GAVE appears to be related to autoimmune disorders or to hepatic cirrhosis, whereas radiation proctitis is the result of pelvic irradiation, most commonly used for the treatment of pelvic malignancies. Argon plasma photocoagulation (APC) is the most commonly used endoscopic modality in the treatment of GAVE and radiation proctitis.[28] GAVE is often associated with systemic illnesses, such as cirrhosis of the liver, autoimmune connective tissue disorders, bone marrow transplantation, and chronic renal failure.[29]

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Epidemiology

United States statistics

The incidence per 100,000 person-years of hospitalizations due to upper GI ulcer bleeding and perforation has decreased over time, from 54.6 and 3.9 in 1996 (R² = 0.944) to 25.8 and 2.9 in 2005 (R² = 0.410), respectively. In contrast, the incidence of colonic diverticular and angiodysplasia bleeding per 100 000 person-years increased over time from 3.3 and 0.9 in 1996 (R² = 0.443) to 8 and 2.6 in 2005 (R² = 0.715), respectively. Recent recorded drug intake showed an increased frequency of anticoagulants with colonic diverticular and angiodysplasia bleeding, whereas NSAID and low-dose aspirin use were more prevalent in peptic ulcer bleeding and colonic diverticular bleeding, respectively.[30]

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).[31]

Angiodysplasia is the most common reason (50%) for occult GI bleeding. The pooled completion rate was 84%. The pooled retention rates were approximately 2%.[32]

Angiodysplasia accounts for 20-30% of GI bleeding episodes in patients with end-stage renal disease[33] and up to 50% of recurrent GI bleeding in this patient population.[34]

Patients with von Willebrand disease may have an increased incidence of GI bleeding from colonic angiodysplasia.[35, 36, 37, 38, 39, 40, 41]

International statistics

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.

Colonic angiodysplasia in Japanese patients is predominantly located in the left colon, whereas in Western patients it is mainly located in the right colon. The percentage of colonic lesions with a size of more than 5 mm or elevated type detected in Japanese patients was significantly higher than in Western patients .[42] Two cases have been reported in Nigeria.[43]

Race-, sex-, and age-related demographics

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

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

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.[44]

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Prognosis

The prognosis in patients with angiodysplasia is favorable because most angiodysplasias spontaneously cease bleeding (90% of cases).

Richter et al reviewed the clinical course of 101 patients with colonic angiodysplasia.[45] The cases of 15 asymptomatic individuals who had never bled were followed for as long as 68 months (mean, 23 mo), and no patient experienced bleeding during this observation period.[45] Therefore, one should conservatively manage nonbleeding angiodysplasia that is discovered as an incidental finding. Thirty-one patients with overt bleeding or anemia managed with blood transfusions alone had rebleeding rates at 1 year of 26% and 3 years of 46%. The high rate of rebleeding justifies treatment for angiodysplasia in symptomatic individuals.

Rebleeding after hemicolectomies occurs in 5-30% of patients, which is much less than that of endoscopic techniques.

Individuals with angiodysplasia lesions longer than 10 mm have higher transfusion requirements, a higher proportion of therapeutic procedures performed after CE, lower hemoglobin concentration, and a lower rebleeding rate. Patients with 10 or more angiodysplasia lesions had also higher transfusion requirements and lower hemoglobin levels, but no differences in the number of therapeutic procedures or rebleeding rate were noted between groups. Angiodysplasiawith a size of 10 mm or more suggests a worse clinical impact and a greater possibility of receiving a therapeutic procedure.[46]

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.

Complications

Hemodynamic instability may result from massive bleeding.

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Patient Education

If angiodysplasia is identified incidentally, most patients can be reassured because most remain asymptomatic.

Preventive treatment with endoscopic obliteration should be decided on a patient-to-patient basis and should not be done routinely.

For patient education resources, see the Digestive Disorders Center, as well as Gastrointestinal Bleeding (GI Bleeding), Rectal Bleeding, Diverticulosis and Diverticulitis, and Irritable Bowel Syndrome (IBS).

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Contributor Information and Disclosures
Author

Hussein Al-Hamid, MD Fellow, Department of Gastroenterology, Providence Hospital

Hussein Al-Hamid, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Roberto M Gamarra, MD Consulting Gastroenterologist, Digestive Health Associates, PLC

Roberto M Gamarra, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Crohn's and Colitis Foundation of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Marc D Basson, MD, PhD, MBA, FACS Associate Dean for Medicine, Professor of Surgery and Basic Science, University of North Dakota School of Medicine and Health Sciences

Marc D Basson, MD, PhD, MBA, FACS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Gastroenterological Association, Phi Beta Kappa, Sigma Xi

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

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 Surgical Association, American College of Surgeons, American Gastroenterological Association, American Medical 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, Western Surgical Association

Disclosure: Nothing to disclose.

John Godino, MD Staff Physician, Department of Medicine, Brooke Army Medical Center

John Godino, MD is a member of the following medical societies: American College of Physicians, American Medical Association

Disclosure: Nothing to disclose.

Andrea Duchini, MD Associate Professor of Medicine and Surgery, Director of Hepatology, University of Texas Medical Branch School of Medicine; Medical Director of Liver Transplantation, Department of Surgery, University of Texas Medical Branch School of Medicine

Andrea Duchini, MD is a member of the following medical societies: American College of Physicians, International Liver Transplantation Society, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Alan BR Thomson, MD Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada

Alan BR Thomson, MD is a member of the following medical societies: Alberta Medical Association, American College of Gastroenterology, American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, College of Physicians and Surgeons of Alberta, and Royal College of Physicians and Surgeons of Canada

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

Disclosure: Nothing to disclose.

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Algorithm for acute gastrointestinal (GI) bleeding. CBC = complete blood cell count; CXR = chest x-ray; EKG = electrocardiography; IVF = intravenous fluid; NG = nasogastric.
Angiodysplasia identified on the cecum wall during colonoscopy.
Double-contrast barium enema studies in a 44-year-old man known to have a long history of ulcerative colitis. These images show total colitis and extensive pseudopolyposis.
Double-contrast barium enema examination in a patient with Crohn colitis demonstrates numerous aphthous ulcers.
 
 
 
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