Gastric varices are swollen, enlarged veins in the lining of the stomach. They develop when blood that normally flows through the liver gets blocked and rerouted, forcing it through smaller veins that aren’t built to handle the pressure. These veins balloon outward and become fragile. Gastric varices occur in roughly 10 to 30% of people with liver cirrhosis, and their biggest danger is bleeding, which carries a mortality rate around 30%.
Why Gastric Varices Form
The root cause is almost always portal hypertension, a condition where pressure builds up in the portal vein, the large vessel that carries blood from your digestive organs to your liver. When the liver is scarred (as in cirrhosis), it resists incoming blood flow. That blood has to go somewhere, so it detours through smaller veins in the stomach and esophagus. These detour routes, called collateral channels, gradually stretch and weaken under the excess pressure.
Three factors drive this process: increased resistance inside the liver’s blood vessels, widening of arteries in the digestive system that sends even more blood toward the blockage, and changes in the anatomy of small veins near the stomach and lower esophagus. Together, these create a perfect setup for varices to grow.
Cirrhosis from alcohol use or hepatitis is the most common underlying condition, but it’s not the only one. A blood clot in the portal vein or splenic vein can block flow and produce the same effect. Budd-Chiari syndrome, which blocks the veins draining blood out of the liver, is a rarer cause. In parts of Africa, South America, the Middle East, and East Asia, schistosomiasis (a parasitic infection) can damage the liver and spleen enough to trigger portal hypertension and gastric varices.
Types and Location in the Stomach
Not all gastric varices look or behave the same. Doctors classify them into four types based on where they sit in the stomach and whether they connect to varices in the esophagus.
- GOV1: Esophageal varices that extend down along the inner curve (lesser curvature) of the stomach. This is the most common type.
- GOV2: Esophageal varices that extend along the outer curve (greater curvature) toward the upper dome of the stomach (the fundus). These account for about 15% of gastric varices and tend to be more complex because they’re fed by multiple veins.
- IGV1: Isolated varices in the fundus with no connection to esophageal varices. These are particularly prone to severe bleeding.
- IGV2: Isolated varices found elsewhere in the stomach or even in the duodenum (the first part of the small intestine).
The type matters because it determines how blood flows through the varices, which directly affects treatment options and bleeding risk. GOV1 varices behave a lot like esophageal varices and are managed similarly. IGV1 and GOV2 varices involve deeper, more complex blood flow patterns and often need different interventions.
Symptoms and Warning Signs
Gastric varices usually cause no symptoms at all until they bleed. Most people discover them during an endoscopy done for another reason or as part of screening after a cirrhosis diagnosis. The varices themselves don’t cause pain or discomfort.
When they do bleed, the signs can be dramatic. Vomiting blood (which may look bright red or like dark coffee grounds) is the most obvious sign. Black, tarry stools indicate blood that has moved through the digestive tract. Because gastric varices tend to bleed more heavily than esophageal varices, blood loss can be rapid, causing lightheadedness, a racing heart, drops in blood pressure, and in severe cases, loss of consciousness. The cumulative risk of bleeding reaches as high as 44% over five years.
How They’re Diagnosed
An upper endoscopy is the primary way gastric varices are found. During this procedure, a thin, flexible camera is passed through the mouth into the stomach, giving a direct view of the stomach lining. Varices appear as raised, rounded folds or clusters beneath the mucosa. The doctor evaluates their size, location, and any signs they might be at risk of bleeding, such as red spots on the surface.
Imaging studies like CT scans with contrast or ultrasound of the portal vein system are often used alongside endoscopy. These help map out the blood flow patterns feeding the varices, which is critical for planning treatment, especially for the more complex types like IGV1 and GOV2.
Bleeding Risk and Severity
Gastric variceal bleeding is less common than esophageal variceal bleeding, but when it happens, it tends to be worse. The mortality rate from an acute gastric variceal bleed is around 30%. Even after initial treatment, about 16.7% of patients die within six weeks of the bleeding episode. Several factors increase the danger: the size of the varices, how advanced the underlying liver disease is, and whether bleeding is still active when treatment begins.
People with more severe liver disease (measured by scoring systems that assess liver function) face the highest risk. Large varices in the fundus of the stomach, particularly IGV1 type, bleed more heavily because the veins in that location are larger and under greater pressure.
Treatment for Active Bleeding
When gastric varices bleed, the priority is stopping the hemorrhage quickly. The approach depends on the type of varix.
For GOV1 varices (those extending along the lesser curvature), treatment is similar to esophageal varices and often involves banding during endoscopy. For GOV2 and isolated gastric varices, the standard endoscopic treatment is injection of a tissue adhesive, essentially a medical-grade glue that hardens inside the varix and seals it off. This achieves immediate hemostasis in 89 to 100% of cases. The most common side effect is abdominal pain, occurring in about 18% of patients. Re-bleeding from ulcers at the injection site happens in roughly 8% of cases, but these episodes are typically manageable.
For patients with severe liver disease who are bleeding from GOV1 or GOV2 varices, current guidelines recommend a procedure called TIPS (transjugular intrahepatic portosystemic shunt) within 72 hours, ideally within 24 hours. TIPS creates a new pathway inside the liver for blood to flow through, directly lowering the portal pressure that caused the varices in the first place.
BRTO as an Alternative
For certain patients, particularly those with isolated gastric varices and a specific type of natural blood vessel detour called a gastrorenal shunt, a procedure called balloon-occluded retrograde transvenous obliteration (BRTO) is an option. A catheter is threaded through a vein to reach the shunt feeding the varices, a balloon is inflated to block flow, and a hardening agent is injected to close off the varices. The obliteration rate for technically successful procedures is about 94%, and it controls active bleeding in roughly 95% of cases. BRTO also resolves hepatic encephalopathy (confusion caused by toxins the damaged liver can’t clear) in virtually all patients who have it. Not everyone is a candidate: the procedure requires a specific shunt anatomy that’s present in 39 to 85% of patients with gastric varices.
Preventing the First Bleed
For people whose gastric varices have never bled, the goal is keeping it that way. Blood pressure-lowering medications called non-selective beta-blockers are the first-line approach. These drugs reduce the amount of blood flowing into the portal system, which lowers pressure on the varices. Beyond preventing bleeding, they also help prevent other complications of advanced liver disease.
More invasive procedures like TIPS or BRTO are not currently recommended for preventing a first bleed in patients with otherwise stable (compensated) liver disease. If a first bleed does occur and is successfully treated, beta-blockers become part of ongoing prevention to reduce the chance of it happening again.
Living With Gastric Varices
A gastric varices diagnosis typically means you’ll need regular monitoring, usually with periodic endoscopies to check whether the varices are growing or developing signs of impending bleeding. How often depends on the severity of your liver disease and the size of your varices. Managing the underlying cause of portal hypertension, whether that means treating hepatitis, stopping alcohol use, or addressing a blood clot, is the most important thing you can do to slow progression.
For people with cirrhosis, gastric varices are one piece of a larger picture. Keeping liver disease as stable as possible through treatment adherence, nutrition, and avoiding liver toxins directly affects variceal risk. In some cases, liver transplantation ultimately resolves both the portal hypertension and the varices by replacing the scarred liver entirely.