Pathophysiology of portal hypertension and variceal bleeding

Abstract

Portal hypertension results from an interaction of abnormal intrahepatic resistance and increases in portal blood flow. Intrahepatic resistance is probably multifactorial in nature and may include compression of hepatic veins by regenerating nodules, collagen deposition in sinusoids and venules, hepatocyte enlargement, and constriction of sinusoids by contractile myofibroblasts. The increase in splanchnic blood flow observed is incompletely understood, but it may involve circulating vasodilators and alteration in volume and sodium balance. The end result of these interactions is the development of increased portal pressure and portosystemic collaterals, the most important of which are esophageal varices. The rupture of esophageal varices is a devastating complication of portal hypertension. Increased portal pressure is necessary for the development and rupture of varices but apparently not sufficient, because many patients with elevated portal pressures never bleed. Presumably, local factors must be involved. Variceal wall tension is probably the best single descriptor of risk from variceal hemorrhage. The wall-tension formula unites the contributions of portal pressure, varix size, and wall thickness to variceal rupture. Lowering portal pressure, reducing varix size, and supporting varices in scar tissue may all lower the risk of hemorrhage.