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- Dilated submucosal esophageal veins connecting the portal and systemic circulations
- Most commonly results from portal hypertension (typically a result of cirrhosis)
- Variceal rupture: most common fatal complication of cirrhosis; severity of liver disease correlates with presence of varices and risk of bleeding.
- 30% of cirrhotic patients have varices at the time of diagnosis. This increases to 90% at 10 years.
- 1-year rate of first variceal bleeding is 5% for small varices, 15% for large varices.
Portal hypertension is common in chronic liver disease (CLD) in children. No clear guidelines for screening; pharmacologic or endoscopic treatment is equivalent.
- 50% of patients with esophageal varices experience bleeding at some point.
- Variceal bleeding: 10–20% mortality in the 6 weeks following the episode
- Gender: male > female
Etiology and Pathophysiology
- Portal hypertension causes the formation of portacaval anastomoses to decompress the portal circulation. This leads to a congested submucosal venous plexus with tortuous dilated veins, particularly in the distal esophagus. Variceal rupture results in hemorrhage.
- Pathophysiology of portal hypertension:
- Increased resistance to portal flow at the level of hepatic sinusoids caused by
- Intrahepatic vasoconstriction due to decreased nitric oxide production and increased release of endothelin-1 (ET-1), angiotensinogen, and eicosanoids
- Sinusoidal remodeling causes disruption of blood flow.
- Increased portal flow caused by hyperdynamic circulation due to splanchnic arterial vasodilation through mediators such as nitric oxide, prostacyclin, and TNF
- Causes of portal hypertension:
- Extrahepatic portal vein obstruction (EHPVO)
- Massive splenomegaly with increased splenic vein blood flow
- Severe right-sided heart failure, constrictive pericarditis, and hepatic vein obstruction (Budd-Chiari syndrome)
- Cirrhosis (accounts for most cases of portal hypertension)
- Less frequent causes are schistosomiasis, massive fatty change, diseases affecting portal microcirculation as nodular regenerative hyperplasia, and diffuse fibrosing granulomatous disease as sarcoidosis.
Cirrhosis is rarely hereditary.
- In cirrhotic patients, thrombocytopenia and splenomegaly are independent predictors of esophageal varices.
- Noncirrhotic portal hypertension
- Increased bleeding risk for known varices is associated with varix size, endoscopic signs (red wale marks, cherry-red spots), vessel wall thickness, and abrupt increase in variceal pressure (i.e., Valsalva maneuver).
- MELD/Child-Pugh score; presence of portal vein thrombosis; high hepatic venous pressure gradient (HVPG)
Prevent underlying causes: Prevent alcohol abuse, administer hepatitis B vaccine, needle hygiene, IV drug use (needle exchange programs reduce risk of hepatitis); specific screening and therapy for hepatitis B and C, hemochromatosis
Commonly Associated Conditions
- Portal hypertensive gastropathy; varices in stomach, duodenum, colon, rectum (causes massive bleeding, unlike hemorrhoids); rarely at umbilicus (caput medusae) or ostomy sites
- Isolated gastric varices can occur due to splenic vein thrombosis/stenosis from hypercoagulability/contiguous inflammation (most commonly, chronic pancreatitis).
- Other complications of cirrhosis: hepatic encephalopathy, ascites, hepatorenal syndrome, spontaneous bacterial peritonitis, hepatocellular carcinoma
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