PORTAL-HYPERTENSION

Portal hypertension arises from an elevated resistance to portal flow combined, in many cases, with an increased portal venous inflow. The p athogenesis of the hyperdynamic circulation in portal hypertensive sta tes, with its subsequent increase in splanchnic blood flow, continues to be a central focus of research in this area. Further evidence conti nues to accumulate in experimental models that nitric oxide may be a k ey mediator in the peripheral vasodilation seen in portal hypertension ; however, the pathogenesis of the increase in nitric oxide remains ob scure. Contradictory human studies have been reported on whether the g astric mucosa in portal hypertensive gastropathy participates in this hyperemic response. A wide array of noninvasive technology is being ex amined in order to detect the presence of esophageal varices. With reg ard to therapy, several trials have shown benefit with the administrat ion of octreotide in the management of acute variceal bleeding. Three randomized controlled trials have shown the advantages of esophageal v ariceal band ligation over sclerotherapy in the management of variceal hemorrhage. Increasing experience with transjugular intrahepatic port al-systemic stent has highlighted the risks and benefits associated wi th its use: its precise role in the management of variceal hemorrhage is still under examination.