Arteriovenous malformations (AVMs) are abnormal connections between arteries and veins that bypass the network of tiny capillaries. A gastric AVM is a vascular anomaly located specifically in the stomach lining or wall. While AVMs can occur anywhere, their presence in the gastrointestinal tract frequently causes bleeding. The primary manifestation of a gastric AVM is chronic or acute gastrointestinal hemorrhage.
The Physical Structure and Mechanism of Gastric AVMs
The stomach’s vascular system normally uses a dense capillary bed to regulate and reduce the force of arterial blood flow before it enters the veins. In a gastric AVM, arteries connect directly to veins, completely bypassing this pressure-reducing network. This direct connection forces high-pressure arterial blood into the low-pressure venous system.
Veins are not structurally designed to withstand this increased pressure and flow volume. Consequently, the affected veins and venules dilate, becoming tortuous, thin-walled, and fragile—a process known as ectasia. These weakened vessels lie close to the stomach’s inner mucosal surface.
The constant, forceful flow places immense stress on the delicate walls of these ectatic vessels, making them prone to erosion or rupture, especially from digestion and contact with stomach acid. When they break, they bleed directly into the stomach, causing the gastrointestinal hemorrhage that characterizes the condition.
Primary Factors and Acquired Conditions Driving AVM Formation
Many gastric AVMs are acquired later in life, resulting from degenerative changes or systemic illnesses. The most common risk factor is the natural process of aging. Over time, the blood vessel walls can weaken and degenerate, increasing the likelihood of abnormal arterial-venous connections forming in the stomach lining.
Chronic Kidney Disease (CKD)
A strong association exists between chronic kidney disease (CKD) and gastrointestinal angiodysplasias (AVMs). The prevalence of these lesions is significantly higher in patients with renal failure compared to the general population. This link is attributed to the accumulation of uremic toxins, which impair endothelial cell function, leading to vascular inflammation and reducing the vessel lining’s ability to repair itself.
Heyde’s Syndrome
This specific acquired condition is characterized by aortic stenosis, gastrointestinal bleeding from AVMs, and an acquired clotting disorder. The mechanism involves the high-velocity, turbulent flow created by blood forced through a narrowed aortic valve. This high shear stress physically breaks down the von Willebrand factor (vWF), a protein crucial for platelet adhesion and blood clotting. The resulting deficiency impairs the body’s ability to stop bleeding from the fragile AVMs.
Chronic stress or mechanical microtrauma to the stomach wall is also hypothesized to play a role in the formation of some acquired AVMs. Repeated distension or long-term localized irritation may contribute to localized vascular degeneration. Aging, CKD, and aortic stenosis represent the most established acquired causes of gastric AVMs.
Genetic Syndromes and Congenital Causes
Some gastric AVMs are congenital, meaning they are present from birth due to inherited genetic mutations. The most well-known hereditary condition associated with widespread AVMs is Hereditary Hemorrhagic Telangiectasia (HHT), also called Osler-Weber-Rendu syndrome. HHT is an autosomal dominant disorder, meaning a person only needs to inherit one copy of the mutated gene to develop the condition.
The genetic basis of HHT involves mutations in genes that affect the transforming growth factor-beta (TGF-\(\beta\)) signaling pathway. This pathway instructs cells on how to properly form and maintain blood vessels. Disruption in this signaling leads to the formation of structurally weak and abnormal vessels, including small red spots called telangiectasias and larger AVMs throughout the body.
In the stomach, this predisposition results in multiple small telangiectasias or larger AVMs that cause chronic bleeding. HHT affects multiple organs, and the gastrointestinal manifestations often lead to significant iron-deficiency anemia due to steady, long-term blood loss. The presence of multiple AVMs across different organ systems suggests a congenital etiology, distinguishing it from isolated acquired lesions.
Identifying Symptoms and Diagnostic Confirmation
Gastric AVMs typically manifest through signs of gastrointestinal bleeding, which can be chronic or acutely severe. Chronic blood loss is the more frequent presentation, often leading to iron-deficiency anemia over time. Patients experience symptoms like persistent fatigue, pallor, and shortness of breath due to a low red blood cell count.
Acute, massive bleeding may present as hematemesis (vomiting bright red blood or dark, “coffee-ground” material). Alternatively, blood passing through the digestive tract results in melena (black, tarry stools). Because the malformations can bleed intermittently, the source of the hemorrhage may be difficult to pinpoint immediately.
The primary method for confirming the diagnosis is an upper endoscopy, also known as esophagogastroduodenoscopy (EGD). During an EGD, a doctor inserts a flexible tube with a camera down the esophagus to visually inspect the stomach lining. The AVMs typically appear as characteristic bright red, flat, or slightly raised cherry-red spots or abnormal groupings of vessels on the mucosal surface. For complex cases or to map the feeding blood vessels, techniques like computed tomography angiography or conventional angiography may be used, which involve injecting a contrast dye to visualize the abnormal vascular network.