Angiodysplasia of the Colon Clinical Presentation

  • Author: Alan BR Thomson, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Jun 15, 2011
 

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.

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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.[22]
  • 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.
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Causes

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.[23]

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.[24]

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.[25]

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%).[26] 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[27]

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 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.[25]

Bleeding angiodysplastic lesions in the upper GI tract have been found with a high prevalence in patients with chronic renal failure requiring dialysis.[28] 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 but can also be an effective treatment for coexistent bleeding angiodysplasias and acquired von Willebrand disease.[29]

Roskell et al demonstrated a relative deficiency of collagen type IV in the mucosal vessels in angiodysplasia compared to controls.[30] 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.[31] 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 rate of bleeding with the new continuous flow left ventricular assist devices (CF-LVAD) has not been studied. The rate of postoperative bleeding is similar to that of the prior generation pulsatile LVAD, but GI bleeding due to angiodysplasia and AVMs is more common and appears to be related to the blood flow rheology of these devices. Acquired von Willebrand disease develops in some patients due to the reduction in high molecular weight (HMW) multimers of von Willebrand's factor (vWF). Similar to acquired von Willebrand disease seen in patients with aortic stenosis, the shear stress of the CF-LVAD may cause proteolysis of the HMW multimers of vWF. 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 are noted. Screening of patients for angiodysplasia and von Willebrand disease before CF-LVAD implant may allow for effective preemptive treatment.[32]

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.[33]

Aortic valve replacement corrects the vWF abnormalities with long-term resolution of GI bleeding.[34] Resolution of anemia usually follows aortic valve replacement.[35]

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.[36]

GI angiodysplasia is a very common cause of digestive hemorrhage among patients with chronic renal insufficiency.[37]

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.[38]

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.[39] GAVE is often associated with systemic illnesses, such as cirrhosis of the liver, autoimmune connective tissue disorders, bone marrow transplantation, and chronic renal failure.[40]

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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, The Methodist Hospital

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 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.

Specialty Editor Board

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.

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

Disclosure: Medscape Salary Employment

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.

Alex J Mechaber, MD, FACP  Senior 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

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 & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Anca Tapardel, MD, Narmin Kassam, MD, and Peter Wong, MD, to the development and writing of this article.

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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 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.
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