It is the most common vascular lesion of the gastrointestinal tract. This condition may be asymptomatic or may cause gastrointestinal bleeding.
The walls of the vessel are thin, with little or no smooth muscle and the vessels are ectatic and thin.
Angiodysplasia is a degenerative lesion of previously healthy blood vessels that are found most frequently in the cecum and the proximal ascending colon .
Seventy-seven percent of the angiodysplasias are located in the cecum and the ascending colon, 15% are located in the jejunum and ileum, and the rest is distributed throughout the alimentary tract. These injuries are typically non-palpable and small.
After diverticulosis , angiodysplasia is the second cause of low digestive hemorrhagein patients older than 60 years. Angiodysplasia may represent approximately 6% of cases of low gastrointestinal bleeding.
Angiodysplasia can be observed incidentally on colonoscopy in up to 0.8% of patients older than 50 years.
Angiodysplasia of the small intestine may represent 30-40% of cases of obscure gastrointestinal hemorrhage. In a recent retrospective colonoscopic analysis, it was shown that 12.1% of 642 people without symptoms of irritable bowel syndrome (IBS) and 11.9% of those with IBS had colonic angiodysplasia.
The arteriovenous malformation (AVM) of the colon is one of the causes of low digestive hemorrhage.
Unlike small vascular ectasia or angiodysplasia, the colonic AVM tends to be solitary, large and endoscopically identified as flat or as a bright red elevated lesion.
Angiodysplasia can occur 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.
Types of angiodysplasia
The type of angiodysplasia is based on the location of the enlarged blood vessels. Your doctor may classify your case as angiodysplasia of the colon (enlargement of the blood vessels in the colon) or angiodysplasia of the stomach (increase of the blood vessels in the stomach).
In addition, this condition can be divided into the following categories according to location:
- Colonic and gastric angiodysplasia.
- Angiodysplasia of the stomach and intestine.
- Angiodisplasia cecal.
- Duodenal and small bowel angiodysplasia.
Angiodysplasia can occur without pain and go unnoticed, or you may have subtle symptoms. Anemia is a symptom of this condition because it causes injuries and hemorrhage in the gastrointestinal tract .
Anemia is when your red blood cell count is lower than normal. This can cause a reduction in the flow of oxygen throughout the body and trigger a variety of symptoms.
You may experience any of the following symptoms with angiodysplasia:
- Difficulty breathing.
- Pale skin.
- Accelerated heartbeat.
Angiodysplasia can also cause hemorrhage in the rectum. The blood loss can vary from mild to severe, and the blood may appear bright red or black and tarry.
Rectal bleeding can also be a sign of colon cancer and other disorders of the gastrointestinal tract.
Causes and risk factors of angiodysplasia
The cause of angiodysplasia is unknown. But normal spasms that occur in the gastrointestinal tract may be responsible for the enlargement of blood vessels.
This enlargement leads to the development of small pathways between a vein and an artery, which can leak with blood. In addition, the weakening of the blood vessels related to age can also cause angiodysplasia.
This could explain why the condition is more common in older people.
Other risk factors for angiodysplasia include a history of heart disease, such as aortic stenosis , as well as taking an anticoagulant medication.
If you have symptoms of angiodysplasia, your doctor may order a series of tests to detect abnormalities and hemorrhages in the gastrointestinal tract.
These may include:
- High endoscopy : In this test, your doctor examines the lining of your esophagus and stomach by inserting a tube with an attached camera into your throat and stomach.
- Stool test : Your doctor may ask you for a stool sample to detect traces of blood.
Complete blood count (CBC). This blood test evaluates your number of red blood cells. The results can confirm or rule out anemia.
- The colonoscopy : This procedure involves inserting a tube with a camera attached to the anus to examine their intestines. Your doctor can see the lining of your large intestine and check for bleeding and other abnormalities.
- Angiogram : This x-ray creates images of the blood vessels and helps identify the location of the bleeding. Your doctor may recommend an angiogram if a colonoscopy does not reveal any injury, but your doctor suspects you have an active hemorrhage.
Treatment options for angiodysplasia
Sometimes, bleeding caused by angiodysplasia stops on its own without medical intervention. But you may need treatment to control bleeding and reverse anemia.
Treatment depends on the severity of the condition and if you have anemia. If you do not have anemia, your doctor may delay the treatment of the disease until you begin to have symptoms.
The treatment may include:
- Angiography : In this procedure, your doctor uses a thin plastic tube to give medicine to a bleeding blood vessel. This medicine closes the blood vessel and stops bleeding.
- Cauterization : Once your doctor identifies the site of bleeding, you can use cauterization to close part of the vein and stop bleeding. This procedure can be done using an endoscope, a flexible tube that goes through the mouth into the stomach and the upper part of the small intestine.
- Surgery : If you have severe bleeding from the colon, surgery may be the only option to stop bleeding. In this case, your doctor may remove the right side of your colon.
The doctor may also prescribe or recommend over-the-counter iron supplements in cases of anemia. Iron can stimulate the production of red blood cells.
It is important that you do not ignore the signs of angiodysplasia. Contact your doctor if you experience unusual fatigue, weakness, dizziness, or rectal bleeding. If left untreated, angiodysplasia can cause severe blood loss.
And in cases of extreme anemia, you may need a blood transfusion. Hemodynamic instability can be the result of massive bleeding.
There does not seem to be any way to prevent angiodysplasia.
Deepening in angiodysplasia
The exact mechanism of development of angiodysplasia is not known, but chronic venous obstruction can play an important role.
This hypothesis explains the high prevalence of these lesions in the right colon and is based on Laplace’s law. The law of Laplace relates the voltage of the wall with the luminal size and the difference of transmural pressure in a cylinder, so that the voltage of the wall is equal to the pressure difference multiplied by the radius of the cylinder.
In the case of the colon, wall tension refers to the intramural tension, the difference in pressure is between the intestinal lumen and the peritoneal cavity, and the radius of the cylinder is the radius of the right colon. Wall tension is highest in the intestinal segments with the largest diameter, such as the right colon.
This theory, which implies chronic venous obstruction, suggests that repeated episodes of colonic distension are associated with transient increases in pressure and lumen size, resulting in multiple episodes of increased wall tension with obstruction of the submucosal venous flow.
This condition occurs especially when these vessels perforate the smooth muscle layers of the colon. For many years, this process has caused the gradual dilation of the submucosal veins and, finally, the dilation of the venules and the arteriolar capillary units that feed them.
Ultimately, the capillary rings dilate, the precapillary sphincters lose their competence and a small arteriovenous communication is formed.
The theory of the development of angiodysplasia explains several clinical and pathological characteristics, which include the presence in older individuals, the location in the cecum and the right proximal colon, and prominent submucosal veins that dilate after traversing the muscularis propria.
In addition, it also explains the lack of pathological changes in the arterioles that supply vascular ectasias and the absence of mucosal injury associated with them.
Previous studies that showed that colonic motility, increased tension in the intestinal wall and increased intraluminal pressure can decrease venous flow provide further support for this theory.
Dilated submucosal veins have been one of the most consistent histological findings and may represent the earliest abnormality in colonic angiodysplasia.
It is noteworthy that the physiopathological mechanisms mentioned above responsible for the development of cecal lesions probably do not apply to lesions in the upper gastrointestinal tract, despite being morphologically identical.
It is also believed that increased expression of angiogenic factors, such as basic fibroblast growth factor (FCFb) and vascular endothelial growth factor (VEGF), plays a role in the pathogenesis of colonic angiodysplasia.
A link has been proposed between the mechanical alteration of high molecular weight multimers of von Willebrand factor, due to turbulent blood flow through a narrowed valve in patients with aortic stenosis and colonic angiodysplasia.
Colonic angiodysplasia and true diverticula may be associated. Hypertensive portal colopathy, a form of colonic angiodysplasia, has been described.
Vascular ectasia of the entire gastrointestinal tract has been reported in a patient receiving high doses of chemotherapy and autologous stem cells for the recurrence of Hodgkin’s disease .
Angiodysplasia, a vascular malformation, is the most common cause of recurrent lower intestinal hemorrhage in patients with renal insufficiency. Lesions are multiple in 40-75% of cases and are often located in the stomach and duodenum, but can also affect the colon and jejunum.
The diagnosis is improved with endoscopy, which has a much higher sensitivity compared to angiography.
Capsular endoscopy may reveal the site of small bowel hemorrhage when regular endoscopy fails, and therapeutic intervention usually includes coagulation with argon plasma.
Although the exact cause of angiodysplasia is unknown, theories include degenerative changes of small blood vessels associated with aging (most widely accepted theory) and long-term local hypooxygenation of the microcirculation of cardiac, vascular or pulmonary diseases.
Reports indicate that angiodysplasia is associated with aortic stenosis. Heyde et al. reported for the first time this association in 1958 and described Heyde’s syndrome as the combination of calcified aortic stenosis and gastrointestinal bleeding due to angiodysplasia of the colon.
He reported on 10 patients with gastrointestinal bleeding of unknown origin who had clinical signs of aortic stenosis and speculated that these patients were bleeding from GI sclerotic vessels. One month later, Schwartz et al suggested a similar association.
On this case it was also suggested that these patients were bleeding from a vascular lesion in the ascending colon that the pathologists could not demonstrate.
A right blind hemicolectomy was recommended , which, in his experience, had caused the cessation of hemorrhage in these patients.
Hypoperfusion of the mucosa of heart disease was postulated later as 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 hemorrhage or after correction of heart failure in subaortic hypertrophic stenosis.
In most people with angiodysplasia, cardiac findings are not important in the development of angiodysplasia, although in Japan the underlying condition most prevalent in patients with colonic angiodysplasia was cardiovascular disease (56%).
Critics of the Imperiale and Ransohoff literature found a lack of conclusive evidence to support the association of aortic stenosis, angiodysplasia, and digestive hemorrhage.
Hypoperfusion or hypooxygenation of heart or lung disease possibly results in ischemic necrosis of an existing angiodysplastic lesion.
The observation that low cardiac output is usually late 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 to hemorrhage in angiodisplastic lesions.
The cessation of angiodysplastic hemorrhage after aortic valve replacement in patients with severe aortic stenosis has been reported.
Specialist have suggested that Heyde’s syndrome consists of hemorrhage from an allegedly latent angiodysplasia as a result of a hematological defect, such as the lack of von Willebrand factor multimers of high molecular weight.
Angiodisplastic haemorrhagic lesions have been found in the upper gastrointestinal tract with a high prevalence in patients with chronic renal failure requiring dialysis. 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 the abnormal function and structure of von Willebrand factor.
Bleeding of angiodysplastic lesions in the upper and lower gastrointestinal tract has been reported in patients with von Willebrand disease.
Because the factor VIII complex is partially synthesized in vascular endothelial cells, it has been proposed that patients with von Willebrand disease and angiodysplasia have an underlying endothelial defect that may be related to the subsequent development of the 2 disorders.
However, as with renal failure, coagulopathy is more likely responsible for bleeding than the development of the lesions.
On the other hand, degenerative aortic stenosis is associated with greater destruction of high molecular weight multimers of von Willebrand factor that may promote bleeding of intestinal angiodysplasias.
Aortic valve replacement is the first-line therapy for the advanced stage of valvular disease, but it can also be an effective treatment for coexisting hemorrhagic angiodysplasia and von Willebrand’s acquired disease.
In Heyde syndrome, the association of aortic stenosis and angiodysplasia hemorrhage seems 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 seems to offer the best hope for long-term resolution of bleeding.
Aortic valve replacement corrects vWF anomalies with the long-term resolution of GI bleeding. The resolution of anemia usually follows the replacement of the aortic valve.
Hereditary hemorrhagic telangiectasia (HHT), also known as Osler-Weber-Rendu disease, is an autosomal dominant disorder of fibrovascular tissue. It is characterized by the classic triad of mucocutaneous telangiectasias, recurrent hemorrhages and family presence.
Gastric angiodysplasia of the fundus and body of the stomach is observed. The histopathological study shows dilated capillaries lined by flat endothelial cells in the papillary dermis.
GI angiodysplasia is a very common cause of gastrointestinal bleeding in patients with chronic renal failure.
The prognosis in patients with angiodysplasia is favorable because most angiodysplasias stop bleeding spontaneously (90% of cases).
Individuals with angiodysplasia lesions larger than 10 mm have higher transfusion requirements, a greater proportion of therapeutic procedures performed after CE, a lower hemoglobin concentration, and a lower rebleeding rate.
Patients with 10 or more angiodysplasia lesions also had higher transfusion requirements and lower hemoglobin levels, but no differences in the number of therapeutic procedures or rate of rebleeding between groups were observed.
Angiodysplasia with a size of 10 mm or more suggests a worse clinical impact and a greater possibility of receiving a therapeutic procedure.
Morbidity and mortality
Bleeding from angiodysplasia is usually self-limiting, but it can be chronic, recurrent or even acute and potentially fatal. Approximately 90% of hemorrhagic angiodysplasias spontaneously cease hemorrhaging, presumably due to their venous nature.
Mortality is related to the severity of bleeding, hemodynamic instability, age and the presence of comorbid medical conditions.
If angiodysplasia is identified incidentally, most patients can be calm because most remain asymptomatic.
Preventive treatment with endoscopic obliteration should be decided from patient to patient and should not be done routinely.