PORTAL-HYPERTENSION

Portal hypertension arises from an elevated resistance to portal flow combined, in many cases, with an increased portal venous inflow. The pathogenesis of the hyperdynamic circulation in portal hypertensive states, with its subsequent increase in splanchnic blood flow, continues to be a central focus of research in this area. Further evidence continues to accumulate in experimental models that nitric oxide may be a key mediator in the peripheral vasodilation seen in portal hypertension; however, the pathogenesis of the increase in nitric oxide remains obscure. Contradictory human studies have been reported on whether the gastric mucosa in portal hypertensive gastropathy participates in this hyperemic response. A wide array of noninvasive technology is being examined in order to detect the presence of esophageal varices. With regard to therapy, several trials have shown benefit with the administration of octreotide in the management of acute variceal bleeding. Three randomized controlled trials have shown the advantages of esophageal variceal band ligation over sclerotherapy in the management of variceal hemorrhage. Increasing experience with transjugular intrahepatic portal-systemic stent has highlighted the risks and benefits associated with its use: its precise role in the management of variceal hemorrhage is still under examination.