varici

Varici, or varices, are dilated veins that form when blood flow through the portal venous system is obstructed or redirected, most often due to portal hypertension from liver disease. The most clinically important varices are esophageal and gastric (gastroesophageal varices); varices can also occur in the rectum (anorectal varices). They are fragile and prone to rupture, and bleeding from esophageal varices is a major cause of death in cirrhosis.

Causes and pathophysiology: Portal hypertension, typically from cirrhosis due to alcohol, viral hepatitis, or nonalcoholic fatty liver disease, drives formation of collateral variceal vessels. Other causes include hepatic venous outflow obstruction and heart failure. The resulting high pressure dilates submucosal veins and predisposes to rupture.

Symptoms and diagnosis: Many varices are asymptomatic until bleeding. When bleeding occurs, it presents as hematemesis or melena and can cause shock. Diagnosis is usually by upper GI endoscopy, which also grades variceal size and stigmata of recent bleeding. Liver function and portal pressure are assessed to guide management.

Management and prevention: Primary prevention for high-risk varices includes nonselective beta-blockers (eg, propranolol, nadolol) or preventive endoscopic ligation. Acute variceal bleeding requires resuscitation, antibiotics, vasoactive therapy, and urgent endoscopic hemostasis. Secondary prevention combines ongoing beta-blockade with repeated endoscopic treatment to reduce rebleeding. Addressing the underlying liver disease, abstinence from alcohol, vaccination, and antiviral therapy where appropriate are important for prognosis.