Variceal bleeding is a life-threatening type of internal hemorrhage that occurs when swollen, fragile veins in the esophagus or stomach rupture. These swollen veins, called varices, develop when blood pressure builds up in the portal vein, the major vessel that carries blood from your digestive organs to your liver. About 50% of people with cirrhosis have varices, and once they rupture, the six-week mortality rate is roughly 22%.
How Varices Form
Your liver normally filters all the blood arriving through the portal vein with relatively low pressure. The pressure difference across the liver, measured as the hepatic venous pressure gradient, is typically 3 to 5 mmHg. When liver disease stiffens or scars the organ, blood can’t flow through easily, and pressure backs up. Once that gradient reaches 10 mmHg or higher, the condition becomes clinically significant portal hypertension.
With nowhere else to go, blood reroutes through smaller veins that weren’t designed to handle the volume. These detour vessels run along the lining of the esophagus and stomach, where they balloon outward just beneath the surface. The combination of high pressure, increased blood flow, and thin vessel walls creates a setup where even minor stress can cause a rupture and rapid, heavy bleeding into the digestive tract.
What Causes the Underlying Pressure Buildup
Liver cirrhosis is by far the most common cause. Chronic alcohol use, hepatitis B and C infections, and fatty liver disease all produce the kind of scarring that obstructs blood flow and raises portal pressure. Each year, an estimated 5 to 15% of people with cirrhosis either develop new varices or see existing ones grow larger.
Less commonly, portal hypertension can develop without cirrhosis. Blood clots in the portal vein or splenic vein, parasitic infections like schistosomiasis, and certain blood disorders can all raise pressure enough to force collateral veins to expand. In these cases the liver itself may function normally, but the plumbing leading to it is blocked.
Recognizing the Symptoms
The most dramatic sign is vomiting blood. The blood may be bright red or dark brown, sometimes described as looking like coffee grounds. Black, tarry stools are another hallmark, indicating that blood has passed through the digestive tract. Some people also notice rectal bleeding.
When the bleeding is slower or less obvious, the warning signs are subtler: lightheadedness, difficulty breathing, fainting, chest pain, or unexplained abdominal pain. If a large amount of blood is lost quickly, shock can set in. Signs of shock include a rapid pulse, rapid breathing, pale or clammy skin, confusion or agitation, and a sharp drop in blood pressure. This is a medical emergency that requires immediate treatment.
How Doctors Classify Varices
Varices are categorized by where they sit and how large they’ve grown. Esophageal varices form in the lower esophagus and are the most common type. Gastric varices appear in the stomach and are further divided based on their exact location: some extend downward from the junction between the esophagus and stomach, while others develop in isolation in the upper dome of the stomach (called fundal varices) or elsewhere in the stomach lining.
During an upper endoscopy, a doctor examines the varices for size, color, and surface markings. Small, straight varices carry less immediate risk than large, coiled ones that occupy a third or more of the esophageal opening. Blue-colored varices and those with red markings on their surface, such as red wale marks or cherry-red spots, signal a higher chance of rupture. This grading system, originally developed by the Japanese Society for Portal Hypertension in 1980 and refined since, helps guide treatment decisions.
Emergency Treatment for Active Bleeding
When varices rupture, the priority is stopping the hemorrhage and stabilizing blood volume. Two approaches happen in parallel: medications that reduce blood flow to the portal system and an endoscopic procedure to seal the bleeding vein directly.
Vasoactive drugs work by constricting the blood vessels feeding the portal system, lowering pressure at the site of the bleed. These are given intravenously as soon as variceal bleeding is suspected, often before endoscopy even begins, and typically continue for two to five days.
The primary endoscopic technique is band ligation. A flexible scope is guided down the throat, and small elastic bands are placed around the base of each bleeding varix. The banded tissue loses its blood supply, shrivels, and eventually scars over, sealing the vessel permanently. Band ligation has largely replaced the older technique of injecting a chemical solution directly into the varix (sclerotherapy), because ligation causes fewer complications while controlling bleeding equally well or better. It also lowers the rate of rebleeding compared to sclerotherapy.
When Standard Treatment Isn’t Enough
In roughly 10 to 20% of cases, bleeding can’t be controlled with medications and endoscopy alone. For these situations, a procedure called TIPS (transjugular intrahepatic portosystemic shunt) serves as a rescue option. A radiologist threads a catheter through the neck vein into the liver and creates a small channel connecting the portal vein to a hepatic vein, essentially building a bypass that relieves pressure. TIPS is supported by the highest level of clinical evidence for both refractory variceal hemorrhage and prevention of rebleeding.
The tradeoff is that by diverting blood around the liver, TIPS can worsen liver function and increase the risk of hepatic encephalopathy, a condition where toxins the liver normally filters build up and affect brain function. For this reason, it’s reserved for cases where other treatments have failed rather than used as a first-line approach.
Preventing the First Bleed
Once varices are found, the goal shifts to keeping them from ever rupturing. The preferred first step is a type of blood pressure medication called a non-selective beta blocker. These drugs slow the heart rate and reduce the volume of blood flowing into the portal system, lowering pressure on the fragile veins. For patients already taking one of these medications, screening endoscopy is often unnecessary because the treatment plan wouldn’t change regardless of what the scope shows.
Beta blockers aren’t safe for everyone with cirrhosis. They’re typically avoided in people with very low blood sodium levels (below 130), active kidney injury, an active abdominal infection called spontaneous bacterial peritonitis, or fluid buildup in the abdomen that no longer responds to water pills. In each of these situations, the drug’s effect on blood pressure and heart output can do more harm than good. For patients who can’t take beta blockers, preventive band ligation during endoscopy is the main alternative.
Prognosis and Rebleeding Risk
Survival after a variceal bleed depends heavily on overall liver health. Doctors assess this using scoring systems that factor in lab values like bilirubin and albumin along with clinical signs such as fluid retention and mental status changes. Higher scores on these scales correlate with worse outcomes, including greater odds of rebleeding and death. One study found that a simple combination of albumin level, bilirubin level, and whether rebleeding occurred in the hospital could accurately predict six-week survival.
The rebleeding rate within six weeks of an initial episode is around 30%, which is why ongoing prevention is critical. After surviving a first bleed, most patients are placed on a combination of beta blockers and repeated band ligation sessions, spaced weeks apart, until the varices are fully eliminated. Even after obliteration, periodic endoscopic surveillance continues because new varices can form as long as the underlying portal hypertension persists.