Arteriovenous malformations (AVMs) are abnormal connections between arteries and veins that bypass the normal capillary network. These vascular lesions occur throughout the body, but the small intestine is a frequent location, where they are often medically termed angiodysplasia or angioectasia. Small intestinal AVMs are the most common cause of bleeding in the lower gastrointestinal tract for older adults.
Understanding Arteriovenous Malformations in the Small Intestine
Small intestinal AVMs are distinct from the larger AVMs found in other organs. These gastrointestinal lesions are typically acquired over time, appearing small, flat, and frequently multiple within the intestinal wall. They represent a cluster of dilated, tortuous vessels located primarily in the submucosa, the layer just beneath the inner lining of the gut.
The structural problem lies in the vessels themselves, which lack the typical muscular layer that provides strength and allows for controlled constriction. Without this supportive tissue, the vessels become fragile and balloon-like, making them highly susceptible to rupture and chronic bleeding. The resulting condition is a significant cause of obscure gastrointestinal bleeding, which is bleeding from an unknown source that persists after initial evaluation.
The Primary Mechanism: Age-Related Degeneration and Chronic Stress
The most common cause of small intestinal AVMs is a long-term, degenerative process linked directly to aging, with the vast majority developing in people over 60 years old. This involves chronic, intermittent obstruction of the small veins that drain blood from the intestinal wall. The normal muscular contractions of the small intestine, which propel food forward, intermittently squeeze the veins that pass through the muscular layers of the gut wall.
Over decades, this chronic tension and intermittent blockage of venous outflow leads to increased pressure within the small submucosal vessels. This pressure causes the delicate venules to gradually dilate, become tortuous, and lose their muscular support structure. This process eventually leads to the formation of a tiny, direct communication between the high-pressure artery and the low-pressure vein, bypassing the resistance of the capillary bed.
This chronic venous congestion also contributes to localized hypoxia, or low oxygen levels, in the intestinal lining and submucosa. The low oxygen tension may stimulate the production of growth factors that promote the dilation and abnormal proliferation of new, but structurally weak, blood vessels. The high-pressure arterial blood then flows directly into these fragile, thin-walled vessels, causing them to break down and bleed easily into the intestinal lumen. The acquired nature of these lesions and their increasing prevalence with age strongly support this theory of mechanical and degenerative vascular breakdown.
Systemic Conditions That Increase AVM Risk
While age and mechanical stress are the primary drivers, several systemic diseases act as significant risk factors for small intestinal AVMs. One of the strongest associations is with Chronic Kidney Disease, particularly End-Stage Renal Disease (ESRD). Patients with ESRD frequently develop AVMs, which account for a substantial percentage of their gastrointestinal bleeding episodes.
The reasons for this link involve uremia, the buildup of toxins in the blood due to kidney failure, which impairs the structural integrity of blood vessel walls. Additionally, hormonal and metabolic imbalances associated with kidney failure can lead to platelet dysfunction, meaning the lesions bleed more readily.
Another notable association is with Aortic Stenosis, a narrowing of the heart’s aortic valve, a condition sometimes referred to as Heyde’s Syndrome when coupled with gastrointestinal bleeding from angiodysplasia. The turbulent, high-velocity blood flow across the narrowed valve mechanically damages von Willebrand factor (vWF), a large blood protein essential for clotting. The reduction of vWF leads to an acquired bleeding disorder, making any AVM prone to hemorrhage.
Underlying inherited Coagulopathies, such as Von Willebrand Disease, also compound the risk by impairing the body’s natural ability to clot blood. Though rare, Genetic Syndromes like Hereditary Hemorrhagic Telangiectasia (HHT) cause multiple vascular malformations throughout the body, but this represents a congenital, not acquired, cause.
Why Diagnosis Is Challenging in the Small Intestine
The location of arteriovenous malformations within the small intestine presents a significant diagnostic hurdle, often leading to prolonged periods of occult, or hidden, bleeding and chronic anemia. The small intestine is situated between the stomach and the large intestine. Standard endoscopic tools, such as an upper endoscopy (EGD) and a colonoscopy, cannot reach the majority of this middle segment of the digestive tract.
Consequently, the source of bleeding often remains obscure until specialized diagnostic tools are utilized. Patients typically present with vague symptoms like fatigue and weakness due to iron-deficiency anemia, or they may have black, tarry stools, which are non-specific signs of upper or mid-gastrointestinal bleeding. The intermittent nature of the bleeding, where the AVM may stop and restart bleeding spontaneously, further complicates detection.
To visualize the small intestine, physicians must use advanced techniques such as capsule endoscopy, where the patient swallows a pill-sized camera that transmits images as it travels through the bowel. For therapeutic intervention, deep enteroscopy, which involves specialized endoscopes pushed or guided deep into the small bowel, is necessary to reach and treat the lesions with methods like argon plasma coagulation. These specialized procedures highlight the anatomical difficulty in diagnosing and treating these small, fragile vascular lesions.