varices

Varices are dilated veins that develop when there is increased pressure in the portal venous system, a condition known as portal hypertension. They most commonly form in the esophagus and stomach, but can also occur in the rectum or other parts of the gastrointestinal tract. The elevated pressure drives the formation of collateral vessels that bypass the liver, a process often seen with liver cirrhosis, alcoholic liver disease, hepatitis, or portal vein thrombosis.

The principal clinical concern with varices is rupture and bleeding. Variceal hemorrhage presents with vomiting blood, black or tarry stools, dizziness, or signs of shock. Many varices exist without symptoms until a bleed occurs. Bleeding risk increases with larger varices, certain endoscopic features (such as red wale signs), and worsening liver function. Rebleeding after an initial bleed is common and substantially affects prognosis.

Diagnosis is usually made by endoscopy, which directly visualizes varices, assesses their size, and guides treatment. Noninvasive assessment of portal hypertension can include Doppler ultrasound and liver imaging; these help evaluate underlying disease and plan management.

Management focuses on preventing first bleed, controlling active hemorrhage, and preventing rebleeding. Primary prevention uses nonselective beta-blockers or endoscopic variceal ligation for medium to large varices. In an acute bleed, resuscitation, antibiotics, and vasoactive therapy (eg, octreotide or terlipressin) are used, followed by endoscopic variceal ligation or sclerotherapy; TIPS (transjugular intrahepatic portosystemic shunt) is considered if bleeding cannot be controlled. Gastric variceal bleeding may require cyanoacrylate glue. Secondary prophylaxis combines beta-blockers with repeat endoscopic therapy, and TIPS is used for recurrent cases.

Overall prognosis depends on the level of portal hypertension and liver function, with management of the underlying liver disease being crucial.