Esophageal Varices

How esophageal varices form

Blood from the intestines normally flows through the portal vein into the liver. In cirrhosis, scarring increases resistance, raising pressure in the portal system (portal hypertension). Blood finds detours back to the heart through smaller veins, including those in the wall of the lower esophagus and stomach. These veins stretch and become varices. They have thin walls and can burst under pressure.

Roughly half of people with cirrhosis have varices at diagnosis, and new varices develop over time. Large varices with red marks on endoscopy, and more advanced liver disease, carry the highest bleeding risk.

Causes

• cirrhosis from alcohol, metabolic dysfunction-associated fatty liver disease, hepatitis C, hepatitis B, autoimmune and genetic liver diseases
• portal vein thrombosis (clot)
• schistosomiasis, a parasitic infection, in some parts of the world
• Budd-Chiari syndrome (blocked liver veins)

Signs and symptoms of esophageal varices

Varices themselves cause no symptoms. Signs usually reflect the underlying liver disease:

• tiredness
• yellow skin or eyes (jaundice)
• a swollen belly from fluid (ascites)
• spider-like blood vessels on the skin
• easy bruising
• confusion (hepatic encephalopathy)

Signs of bleeding varices

• vomiting large amounts of bright red blood or coffee-ground material
• black, tarry, sticky stools (melena), or maroon stools
• lightheadedness, fainting, fast heartbeat, pale clammy skin
• confusion

Variceal bleeding is one of the most serious complications of cirrhosis and needs emergency treatment.

Diagnosis

• upper endoscopy: a camera passed through the mouth shows varices, their size and high-risk signs
• non-invasive screening: under Baveno VII guidance, people with compensated cirrhosis with a liver stiffness under 20 kPa on elastography and platelets over 150,000 can often avoid screening endoscopy
• blood tests: liver function, blood count, clotting
• imaging: ultrasound or CT showing an enlarged spleen and collateral veins

Preventing a first bleed

For people at high risk:

• non-selective beta blockers: carvedilol or propranolol lower portal pressure. Current guidance increasingly favors carvedilol for people with clinically significant portal hypertension, which also reduces other complications of cirrhosis
• endoscopic band ligation: small rubber bands placed around varices to cut off their blood flow, repeated until they are eliminated. Used when beta blockers are not tolerated or contraindicated

Treatment of bleeding varices

This happens in hospital, usually intensive care:

1. Resuscitation: IV fluids and blood transfusion, avoiding over-transfusion, which can raise portal pressure
2. Vasoactive medicines: octreotide (or terlipressin) to reduce blood flow to the varices
3. Antibiotics: reduce infection and death risk
4. Urgent endoscopy within 12 hours: band ligation to stop bleeding
5. Balloon tamponade or esophageal stent: temporary measures if bleeding cannot be controlled
6. TIPS (transjugular intrahepatic portosystemic shunt): a stent placed through the liver to lower portal pressure, used early in high-risk patients or when bleeding recurs

Preventing rebleeding

After a bleed, the risk of another is high. Prevention combines:

• a non-selective beta blocker
• repeated band ligation sessions
• TIPS for selected patients
• evaluation for liver transplantation

Managing the underlying liver disease

• stop drinking alcohol completely
• treat hepatitis B or C with antiviral medicine
• weight loss and diabetes control for fatty liver disease
• avoid NSAIDs such as ibuprofen, which increase bleeding and kidney risk
• vaccination against hepatitis A and B, flu and pneumococcus
• liver cancer surveillance every 6 months
• consideration for liver transplant in advanced disease

Outlook

The outlook depends largely on how advanced the liver disease is. A variceal bleed still carries significant mortality, around 15% to 20% at 6 weeks in many studies, but this has fallen with modern treatment. Preventive treatment greatly reduces the risk of a first bleed.

Frequently asked questions

What are the signs and symptoms of esophageal varices?

Varices cause no symptoms until they bleed. Bleeding causes vomiting of blood or coffee-ground material, black tarry stools, dizziness, fainting and a racing heart. Underlying cirrhosis may cause jaundice, belly swelling, easy bruising and confusion.

What causes esophageal varices?

They are caused by portal hypertension, which is high pressure in the veins carrying blood to the liver. The most common cause is cirrhosis from alcohol, fatty liver disease or viral hepatitis. Blood clots in the portal vein are another cause.

How are esophageal varices treated?

Varices at risk of bleeding are treated with beta blockers such as carvedilol, or with band ligation during endoscopy. Bleeding varices need emergency care with medicines, antibiotics, endoscopic banding and sometimes a TIPS procedure.

Can esophageal varices go away?

They can shrink if portal pressure falls, for example after stopping alcohol, curing hepatitis C or after a liver transplant. Banding eliminates existing varices, but new ones can form if portal hypertension persists, so monitoring continues.

How long can you live with esophageal varices?

It depends mainly on the severity of the liver disease. Many people with compensated cirrhosis and treated varices live for years. A bleed or decompensated cirrhosis worsens the outlook, which is why prevention and liver transplant assessment matter.