An arteriovenous malformation (AVM) in the colon is an abnormal tangle of blood vessels directly connecting an artery and a vein. This bypasses the usual capillary network that regulates blood flow and pressure. These vascular lesions most commonly develop within the submucosal layer of the colon wall. Colonic AVMs are a frequent cause of lower gastrointestinal bleeding, ranging from subtle, chronic blood loss to more significant, acute episodes.
Age and Degenerative Changes
Colonic arteriovenous malformations are primarily seen in older adults, strongly linked to the natural aging process. These lesions are generally considered acquired rather than present from birth. Over time, colonic blood vessels, especially small arteries and veins, undergo degenerative changes, leading to weakened and fragile walls.
This weakening makes vessels more susceptible to everyday physiological stresses. Chronic, low-grade trauma or pressure within the colon, sustained over decades, can further compromise their integrity. This prolonged strain, combined with age-related vascular deterioration, facilitates abnormal connections, allowing higher-pressure arterial blood to flow directly into the lower-pressure venous system.
The progressive dilation and tortuosity of these weakened vessels eventually culminate in the characteristic tangled appearance of an AVM. This degenerative process explains why AVMs are rare in younger individuals and become increasingly prevalent with advancing age.
Mechanical Stress and Vascular Weakness
The colon’s dynamic internal environment plays a significant role in the development and enlargement of arteriovenous malformations. The muscular layers of the colon constantly contract and relax through peristalsis, propelling digested material. This continuous muscular activity, along with fluctuating pressures inside the bowel, exerts repetitive mechanical stress on the blood vessels embedded within the colonic wall.
This repeated physical stress, particularly on vessels already compromised by age-related degeneration, can lead to the gradual dilation of submucosal veins. Higher arterial pressure, transmitted directly into these weakened, dilated veins, contributes to their expansion and eventual rupture, creating direct arteriovenous shunts. Localized muscular contractions may also intermittently obstruct venous outflow, further increasing pressure within the colon wall’s venous system.
Such focal pressure increases, combined with potential temporary reduced blood flow (ischemia) from intense contractions, can promote abnormal growth and dilation of existing vessels. This sustained biomechanical strain transforms previously healthy vessels into the fragile, ectatic structures characteristic of an AVM. The physical forces within the colon contribute to the structural changes that define these vascular lesions.
Systemic Conditions as Contributing Factors
Beyond age and local mechanical forces, certain systemic medical conditions significantly increase susceptibility to colonic AVMs. Chronic kidney disease (CKD) is a well-established contributing factor. Patients with CKD often experience a buildup of uremic toxins, which can directly impair the integrity and function of blood vessel walls throughout the body, including the colon.
This altered vascular integrity makes vessels more fragile and prone to developing abnormal connections. Additionally, CKD can lead to various bleeding abnormalities, such as platelet dysfunction, which may exacerbate bleeding from existing AVMs or contribute to their formation. The combination of weakened vessels and impaired clotting mechanisms creates a heightened risk.
Aortic stenosis, a narrowing of the aortic heart valve, is another condition linked to colonic AVMs, often through a mechanism known as Heyde’s syndrome. In this syndrome, the turbulent blood flow across the narrowed aortic valve can shear and degrade high molecular-weight multimers of von Willebrand factor, a protein crucial for blood clotting. This acquired deficiency in von Willebrand factor can lead to an increased tendency to bleed from existing AVMs or potentially promote their development. Other less common associations include certain inherited bleeding disorders, which can also contribute to vascular fragility and an increased predisposition to these lesions.