Esophageal varices are swollen, bulging veins in the lining of the lower esophagus, the tube that connects your throat to your stomach. They develop when scar tissue or disease in the liver forces blood to find alternate routes back to the heart, causing small veins in the esophagus to balloon under pressure they weren’t designed to handle. The main danger is rupture: these thin-walled veins can burst and cause life-threatening bleeding. About 30 to 40% of people with early-stage cirrhosis have them, and that number jumps to 85% in people with advanced liver disease.
How Liver Disease Creates Varices
Your portal vein carries roughly 1,500 milliliters of blood per minute from your digestive organs to your liver for processing. When the liver is scarred (cirrhosis), that blood flow meets resistance. With nowhere to go, pressure builds in the portal vein, a condition called portal hypertension. Normal portal pressure sits between 5 and 10 mmHg; in people with significant blockage, it can climb to 15 or 20 mmHg.
Because the portal venous system has no valves, high pressure pushes blood backward and forces it through smaller, alternative vessels. One key set of these detour vessels runs along the wall of the lower esophagus, connecting the portal system to veins that drain into the chest. These vessels were never meant to carry heavy blood flow. Over time, the increased volume causes them to stretch, twist, and weaken. Research suggests a portal pressure gradient of at least 10 mmHg is needed before varices begin to form, and the body also grows entirely new small blood vessels in response to the pressure, further expanding the problem.
What Causes Them
Cirrhosis from any cause is the most common reason. Chronic alcohol use, hepatitis B and C, and fatty liver disease are the leading drivers. Less commonly, blood clots in the portal vein or parasitic infections that scar the liver (like schistosomiasis) can raise portal pressure enough to trigger varices without traditional cirrhosis. Any condition that blocks blood flow through or out of the liver can set the process in motion.
Symptoms Before and During a Bleed
Varices themselves produce no symptoms until they bleed. You won’t feel them forming, and they don’t cause pain or difficulty swallowing. Most people discover they have varices either through screening or when a bleed happens.
A ruptured varix is a medical emergency. The hallmark sign is vomiting bright red blood or material that looks like coffee grounds. You may also pass black, tarry stools, which indicate digested blood moving through the intestines. Rapid blood loss can cause lightheadedness, a racing heartbeat, pale skin, and fainting. Because the portal vein carries such a high volume of blood, variceal bleeds can be severe and fast.
How Varices Are Found and Classified
The standard way to diagnose esophageal varices is an upper endoscopy, where a thin, flexible camera is passed through the mouth into the esophagus and stomach. During this procedure, a doctor can see the varices directly and classify them by size:
- Small (F1): Straight, slightly raised veins that don’t flatten when air is pumped into the esophagus.
- Medium (F2): Enlarged, winding veins that take up less than one-third of the esophageal opening.
- Large (F3): Bulging veins that occupy more than one-third of the esophageal opening.
Size matters because larger varices are more likely to rupture. Red marks on the surface of a varix, visible during endoscopy, also signal higher bleeding risk.
Not everyone with cirrhosis needs an endoscopy right away. Current guidelines allow doctors to use two noninvasive measurements to gauge risk: liver stiffness (measured by a painless ultrasound-based scan) and platelet count from a blood test. If liver stiffness is below 15 kilopascals and platelets are above 150,000 per microliter, the chance of having significant varices is low enough that endoscopy can often be safely postponed. When liver stiffness is 20 kPa or higher, or platelets drop below 150,000, screening endoscopy is recommended.
Preventing a First Bleed
Once varices are found, the priority is keeping them from ever rupturing. The first-line approach is a class of blood pressure medications that reduce the force of blood flowing into the portal system. Carvedilol is the most potent option for lowering portal pressure, though propranolol and nadolol are also used. These medications slow the heart rate and relax blood vessels feeding the portal system, easing the pressure on fragile esophageal veins. For people with fluid buildup in the abdomen (ascites), dosing is adjusted more carefully, and carvedilol is generally avoided because it can lower blood pressure too much in that setting.
For medium or large varices, especially when someone can’t tolerate these medications, endoscopic band ligation is an alternative. During this procedure, small rubber bands are placed around the base of each varix through an endoscope, cutting off blood flow so the vein shrinks and scars down. Sessions are repeated every two weeks until the varices are eliminated or reduced to a size too small to band.
What Happens During an Acute Bleed
Acute variceal bleeding requires emergency treatment. In the hospital, the immediate goals are stabilizing blood pressure, replacing lost blood, and stopping the hemorrhage. Endoscopic band ligation is the primary tool for controlling an active bleed, and it succeeds in about 96% of cases during the first session. Medications that constrict blood vessels in the portal system are given simultaneously through an IV.
For patients at high risk of failing standard treatment, or when endoscopic therapy and medications don’t stop the bleeding, a procedure called TIPS may be used. This involves threading a catheter through a neck vein into the liver, where a small metal stent is placed to create a new channel for blood to bypass the scarred liver tissue. TIPS controls acute bleeding in about 95% of cases and dramatically lowers the chance of rebleeding (around 19% compared to 44% with endoscopic therapy alone). The tradeoff is a higher risk of hepatic encephalopathy, a condition where toxins normally filtered by the liver build up and cause confusion and cognitive changes.
Preventing Rebleeding
Surviving a first variceal bleed doesn’t mean the danger has passed. Without preventive treatment, the risk of bleeding again within one year is as high as 60%. That’s why secondary prevention is aggressive: most patients receive both medication and repeat band ligation sessions.
TIPS is generally reserved for people who keep rebleeding despite medication and endoscopic treatment. For some patients with very advanced liver disease, a liver transplant is the only way to resolve portal hypertension permanently.
How Dangerous Variceal Bleeding Is
Variceal hemorrhage remains one of the most serious complications of liver disease. In one study of patients hospitalized for variceal bleeding, about 22% died within six weeks. The severity of the underlying liver disease was the strongest predictor of outcome. Among patients with the most advanced liver dysfunction, the six-week mortality rate reached nearly 77%, compared to roughly 31% in those with moderately impaired liver function. Uncontrolled bleeding accounted for most early deaths, while liver failure was the second leading cause.
These numbers underscore why screening and prevention matter so much. Catching varices before they bleed, starting medications early, and following through with band ligation sessions can substantially change the trajectory for people living with cirrhosis.