Esophageal varices are abnormally enlarged veins located in the lower third of the esophagus.

These varices develop primarily as a complication of portal hypertension, a condition characterized by increased blood pressure in the portal venous system, most often caused by liver cirrhosis.

Pathophysiology of Esophageal Varices

The esophagus has a complex venous drainage system involving veins that connect the portal and systemic circulations. Normally, the portal vein carries blood from abdominal organs such as the intestines, pancreas, and spleen to the liver, where it is filtered.

When portal hypertension occurs, commonly from liver cirrhosis, blood flow is obstructed or impaired, causing blood to divert into smaller collateral blood vessels that are not designed to accommodate high volumes of blood flow. The dilation of these collateral vessels in the submucosal layer of the esophagus results in esophageal varices.

The normal pressure gradient between the portal vein and the systemic venous system is around 3 to 7 mmHg, but when it exceeds approximately 10 to 12 mmHg, portal hypertension is established. This leads to the development of tortuous, thin-walled veins that can measure from 1 mm to 2 cm in diameter in the esophagus. The increased pressure and fragility of these veins significantly raise the risk of rupture and hemorrhage.

Etiology and Risk Factors

Liver cirrhosis is the primary cause of portal hypertension and subsequent esophageal varices. Cirrhosis results in scarring of liver tissue, restricting blood flow, and causing portal vein pressure to rise.

Other less common causes include portal vein thrombosis, schistosomiasis (a parasitic infection), Budd-Chiari syndrome (hepatic vein obstruction), severe right-sided heart failure, and rare liver diseases such as Wilson's disease and primary biliary cirrhosis.

The severity of liver disease correlates with the risk of variceal development and bleeding. Patients with advanced fibrosis and decompensated liver function are at substantial risk for the formation of these varices.

Clinical Presentation and Symptoms

Esophageal varices often remain asymptomatic until bleeding occurs. The first sign of variceal hemorrhage may be sudden and severe, characterized by vomiting of large volumes of blood (hematemesis) and passing black, tarry stools (melena), indicating upper gastrointestinal bleeding.

Other clinical signs associated with underlying liver disease may include jaundice (yellowing of the skin and eyes), easy bruising or bleeding due to impaired clotting factor synthesis, and ascites (fluid accumulation in the abdominal cavity). Bleeding from esophageal varices is a medical emergency requiring immediate intervention due to the risk of hypovolemic shock and death if untreated.

Diagnostic Approaches

The gold standard for diagnosing esophageal varices is esophagogastroduodenoscopy (EGD), which allows direct visualization of the esophageal mucosa and identification of varices. Endoscopy not only confirms the presence of varices but also helps classify their size and risk of bleeding. This procedure can also be therapeutic if variceal band ligation or sclerotherapy is performed to prevent or control bleeding.

Management and Treatment

Preventing first variceal bleeding and treating active hemorrhage are critical goals. Primary prophylaxis includes the use of non-selective beta-blockers such as propranolol, which reduce portal pressure by decreasing cardiac output and inducing splanchnic vasoconstriction. Endoscopic band ligation is another effective prophylactic approach for patients with medium to large varices at high bleeding risk.

In cases of active variceal bleeding, immediate resuscitation with fluids and blood transfusions is essential. Endoscopic intervention to ligate or sclerose varices is the mainstay of treatment. In refractory cases, transjugular intrahepatic portosystemic shunt (TIPS) placement can reduce portal pressure to control bleeding.

Additionally, antibiotic prophylaxis is administered to reduce the risk of infections such as spontaneous bacterial peritonitis, which often complicates cirrhosis and variceal bleeding.

Prognosis and Complications

The prognosis of patients with esophageal varices largely depends on the extent of liver disease and the effectiveness of bleeding control. Bleeding from varices is associated with significant mortality, especially if recurrent. Preventive measures and early detection are crucial to improving outcomes.

Dr. Guadalupe Garcia-Tsao, a highly distinguished physician-scientist, emphasizes the critical nature of esophageal varices in liver disease management, "Esophageal varices are dilated submucosal veins in the esophagus that develop as a complication of portal hypertension, primarily due to cirrhosis. Their rupture can lead to life-threatening bleeding."

Esophageal varices are dilated veins in the lower esophagus that develop due to portal hypertension, mainly caused by liver cirrhosis. These varices pose a critical health risk because they can rupture and cause life-threatening bleeding.

Diagnosis primarily relies on endoscopic examination, while management focuses on preventing bleeding through medication and endoscopic techniques, and treating hemorrhage promptly if it occurs. The prognosis depends heavily on liver disease severity, underlining the importance of early recognition and treatment to prevent fatal complications.