Which vessels are most commonly affected by varices in patients with cirrhosis?

Vessels Affected in Cirrhosis Varices

In cirrhosis, the most commonly affected vessels are esophageal varices, followed by gastric varices, and less commonly rectal varices, all developing as a consequence of portal hypertension. 1

Esophageal Varices

• Esophageal varices develop in approximately 50% of patients with cirrhosis and are the most common type of varices 1
• They form in the intrinsic and extrinsic gastro-esophageal veins at the cardia, serving as collateral circulation to divert portal blood into the systemic circulation 1
• The prevalence of esophageal varices correlates with the severity of liver disease: present in 40% of Child A patients but in 85% of Child C patients 1
• Patients without varices develop them at a rate of 8% per year, with an HVPG ≥10 mmHg being the strongest predictor for development 1

Gastric Varices

• Gastric varices are less prevalent than esophageal varices, occurring in 5-33% of patients with portal hypertension 1
• They are classified into two main categories:
  • Gastroesophageal varices (GOV): Extensions of esophageal varices 1
    • Type 1 (GOV1): Extend along the lesser curvature of the stomach (most common) 1
    • Type 2 (GOV2): Extend along the fundus, typically longer and more tortuous 1
  • Isolated gastric varices (IGV): Occur in the absence of esophageal varices 1
    • Type 1 (IGV1): Located in the fundus, tortuous and complex 1
    • Type 2 (IGV2): Located in the body, antrum, or around the pylorus 1
• The presence of IGV1 fundal varices should prompt investigation for splenic vein thrombosis 1

Rectal Varices

• Rectal varices develop in the anal canal where the superior hemorrhoidal vein (portal system) anastomoses with the middle and inferior hemorrhoidal veins (caval system) 1, 2
• They form as portosystemic collaterals when portal pressure increases above the threshold HVPG of >10-12 mmHg 2
• Although less common than esophageal or gastric varices, they carry significant mortality when bleeding occurs 2

Other Portosystemic Collaterals

• Para-umbilical veins in the falciform ligament of the liver (causing caput medusae) 1
• Collaterals in the abdominal wall and retroperitoneal tissues 1
• Veins from the liver to the diaphragm 1
• Collaterals in the lienorenal ligament, omentum, and lumbar veins 1
• Diversion from diaphragmatic, gastric, pancreatic, splenic, and adrenal veins into the left renal vein 1

Pathophysiology of Variceal Formation

• Portal hypertension develops initially due to increased resistance to blood flow caused by architectural distortion of the liver from fibrous tissue and regenerative nodules 1
• Active intrahepatic vasoconstriction accounts for 20-30% of the increased resistance, primarily due to decreased nitric oxide production 1, 2
• Portal hypertension persists despite collateral formation because of:
  • Increased portal venous inflow from splanchnic arteriolar vasodilation 1
  • Insufficient portal decompression through collaterals which have higher resistance than normal liver 1
• Varices develop when the hepatic venous pressure gradient (HVPG) exceeds 10-12 mmHg 1, 2

Risk Factors for Variceal Bleeding

• Size of varices (large varices >5 mm have highest risk) 1, 3
• Decompensated cirrhosis (Child B/C classification) 1, 2
• Presence of red wale marks or red spots on varices 1, 2
• Higher portal pressure gradient (HVPG >20 mmHg) 1, 2
• Continued alcohol consumption in alcoholic cirrhosis 1, 4

Clinical Implications

• Variceal hemorrhage occurs at a yearly rate of 5-15%, with mortality of at least 20% at 6 weeks 1, 5
• Patients with HVPG ≥20 mmHg have higher risk of early rebleeding (83% vs 29%) and higher 1-year mortality (64% vs 20%) 1
• Late rebleeding occurs in approximately 60% of untreated patients within 1-2 years 1, 5
• Gastric varices bleed less frequently but more severely than esophageal varices 5
• The risk of bleeding is greatest immediately after a bleeding episode and slowly declines thereafter 5