Esophageal Varices: Pathophysiology, Approach, and Clinical Dilemmas

Portal hypertension is one of the most significant complications of both acute and chronic liver diseases. It generally develops as a result of an increase in vascular resistance at the prehepatic, intrahepatic, or postherpetic level. An increase in portal blood flow may also contribute. The dominant cause of portal hypertension relates to liver cirrhosis which increases resistance through the hepatic sinusoids. Gastroesophageal varices are the most important clinical manifestation of this syndrome and are associated with a high risk of upper gastrointestinal hemorrhage and its attendant high mortality. This special issue includes nine evidence-based reviews. They discuss the pathophysiology of portal hypertension as well as its clinical manifestations and management. Selected topics and controversies related to esophageal varices are covered, including noninvasive diagnostic methods, bleeding prophylaxis in adults and children, rescue treatments, and the clinical dilemma of portal vein thrombosis. H. Maruyama and O. Yokosuka review the current concepts of the pathophysiology of portal hypertension and esophageal varices. Portal hypertension is initially caused by distortion of the hepatic vascular bed, which in turn leads to increased resistance to portal blood flow. This phenomenon is associated with intrahepatic endothelial dysfunction with a resultant imbalance between vasodilators such as nitric oxide and prostaglandins vasoconstrictors including endothelin. An important consequence of increased resistance to portal blood flow is splanchnic vasodilatation with consequent sodium and water retention. As a result of the plasma's expansion, and the reduction in peripheral resistance, a hyperdynamic circulation develops. Consequently, there is a significant increase in the blood flow through the portal vein which further contributes to portal hypertension. Esophageal varices appear and may bleed when the HVPG exceeds 12 mmHg. A comprehensive review of the clinical manifestations of portal hypertension is presented by S. A. Al-Busafi et al. Portal hypertension is a common clinical syndrome defined as the elevation of hepatic venous pressure gradient (HVPG) above 5 mmHg. Its gastrointestinal manifestations include the development of esophageal varices, gastric varices, and intestinal vasculopathy. Approximately 5–15% of cirrhotics develop esophageal varices annually. The majority of patients with cirrhosis are expected to develop this condition over their lifetime. Beyond its gastrointestinal effects, portal hypertension may also affect other vital organs resulting in extrahepatic manifestations. Y.-I. Chen and P. Ghali present an overview of strategies to prevent and manage portal hypertension. The one-year rate of first variceal hemorrhage is 5% for small varices and 15% for large varices. Six-week mortality rate following …