Esophageal Varices

BASICS

DESCRIPTION

  • Dilated submucosal esophageal veins connecting the portal and systemic circulations
  • Most commonly results from portal hypertension (usually 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.

EPIDEMIOLOGY

Incidence

  • 30% of cirrhotic patients have varices at the time of diagnosis; 90% of cirrhotic patients will have varices at 10 years.
  • 1-year rate of first variceal bleeding is 5% for small varices and 15% for large varices.

Prevalence

  • 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:
    • Prehepatic:
      • Extrahepatic portal vein obstruction
      • Massive splenomegaly with increased splenic vein blood flow
    • Posthepatic:
      • Severe right-sided heart failure, constrictive pericarditis, and hepatic vein obstruction (Budd-Chiari syndrome)
    • Intrahepatic:
      • 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.

Genetics

Cirrhosis is rarely hereditary.

RISK FACTORS

  • Cirrhosis. 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)

GENERAL PREVENTION

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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