Esophageal Varices-I: Introduction

Esophageal varices are enlarged, twisted veins located primarily in the submucosa of the lower esophagus and stomach. These dilated, tortuous vessels may extend higher into the esophagus or into the stomach. They develop due to increased pressure in the portal venous system, typically from liver cirrhosis, which scars and damages the liver, impeding normal blood flow.

Portal hypertension impairs blood transport from the gastrointestinal system to the liver through the hepatic portal vein. Venous blood from the intestinal tract and spleen seeks alternative routes through collateral circulation, creating new pathways to redirect blood flow. These fragile collateral vessels in the esophagus and stomach lack elasticity and expand under elevated pressure, forming varices prone to rupture.

Esophageal varices can result from portal vein thrombosis, hepatic vein obstruction, right-sided heart failure, splenomegaly with increased splenic vein blood flow, and chronic alcohol consumption. Abnormalities in the splenic vein or superior vena cava, hepatic venothrombosis, and constrictive pericarditis also contribute to variceal development by increasing pressure in the portal venous system.

Esophageal varices lack the elasticity of typical blood vessels, making them easily ruptured. The elevated pressure from collateral circulation causes these fragile vessels to expand and become thin-walled. This combination of structural weakness and increased hemodynamic stress makes them susceptible to rupture and can cause massive hemorrhages in the upper gastrointestinal tract.

Hemorrhage from esophageal varices can be triggered by muscular exertion, constipation, sneezing, coughing, vomiting, esophagitis, irritation from poorly chewed foods or irritating fluids, and reflux of stomach contents. Certain medications may also precipitate bleeding. Recognizing these risk factors is vital for prompt medical attention and management to prevent life-threatening complications.

When portal hypertension impairs normal blood flow through the damaged liver, venous blood from the gastrointestinal system and spleen cannot reach the heart's right atrium through the standard route. The body compensates by creating new pathways called collateral circulation to redirect blood flow. These alternative vessels develop in the esophagus and stomach, but lack the structural integrity of normal vessels.

Liver cirrhosis scars and damages the liver, severely impairing normal blood flow through the portal vein and causing portal hypertension. This increased pressure forces blood to seek alternative pathways through collateral circulation in the esophagus and stomach. The resulting fragile, dilated vessels are the esophageal varices that carry significant risk of rupture and severe bleeding.