Portal hypertension is one of the main consequences of cirrhosis. It can result in severe complications, including bleeding of esophagogastric varices as well as spontaneous bacterial peritonitis or hepatorenal syndrome as complications of ascites. We describe in brief the pathophysiology of portal hypertension and review the current management of its complications, with emphasis on variceal bleeding and ascites. Pathophysiologic background Portal hypertensionPortal hypertension is defined as an increase in blood pressure in the portal venous system. The portal pressure is estimated indirectly by the hepatic venous pressure gradientthe gradient between the wedged (or occluded) hepatic venous pressure and the free hepatic venous pressure. A normal hepatic venous pressure gradient is less than 5 mm Hg.In cirrhosis, portal hypertension results from the combination of increased intrahepatic vascular resistance and increased blood flow through the portal venous system (Fig. 1). According to Ohm's law, portal venous pressure (P) is the product of vascular resistance (R) and blood flow (Q) in the portal bed (P = Q × R). Intrahepatic resistance increases in 2 ways: mechanical and dynamic. The mechanical component stems from intrahepatic fibrosis development; various pathologic processes are thought to contribute to increased intrahepatic resistance at the level of the hepatic microcirculation (sinusoidal portal hypertension): architectural distortion of the liver due to fibrous tissue, 1 regenerative nodules, 1 and collagen deposition in the space of Disse.2 The dynamic component results from a vasoconstriction in portal venules secondary to active contraction of portal and septal myofibroblasts, to activated hepatic stellates cells and to vascular smoothmuscle cells.3-5 Intrahepatic vascular tone is modulated by endogenous vasoconstrictors (e.g., norepinephrine, endothelin-1, angiotensin II, leukotrienes and thromboxane A 2 ) and enhanced by vasodilators (e.g., nitric oxide). In cirrhosis, increased intrahepatic vascular resistance results also from an imbalance between vasodilators and vasoconstrictors. 6Portal hypertension is characterized by increased cardiac output and decreased systemic vascular resistance, 7 which results in a hyperdynamic circulatory state with splanchnic and systemic arterial vasodilation. Splanchnic arterial vasodilation leads to increased portal blood flow, which in turn leads to more severe portal hypertension. Splanchnic arterial vasodilation results from an excessive release of endogenous vasodilators such as nitric oxide, glucagon and vasointestinal active peptide.An increase in the portocaval pressure gradient leads to the formation of portosystemic venous collaterals in an attempt to decompress the portal venous system. Esophageal varices, drained predominantly by the azygos vein, are clinically the most important collaterals because of their propensity to bleed. Esophageal varices can develop when the hepatic venous pressure gradient rises above 10 mm Hg. 8-10All factors that increase ...

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ARFI is highly feasible and reproducible, and provides diagnostic accuracy similar to Fibroscan. This new device seems noteworthy for the widespread noninvasive diagnosis of liver fibrosis.

LSE requires no learning curve: a novice is able to obtain a reliable result after a single training session, whatever the professional status. However, success rate will progressively increase. An LSE with less than four valid measurements should not be considered as reliable.