Esophageal Varices
Basics
Basics
Basics
Description
Description
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
Epidemiology
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
Etiology and Pathophysiology
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
Risk Factors
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
General Prevention
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
Commonly Associated Conditions
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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