**1. Introduction**

Hepatic fibrosis, nodular rigeneration, distortion of hepatic architecture are the histopathological characters of liver cirrhosis. The main outcome of this pathological condition is the portal hypertension (PH) by the disruption of the hepatic blood flow, beside the damage of liver metabolic functions. Moreover the alteration of the splanchnic blood flow and the block of portal flow can be localized also in the prehepatic and posthepatic site. The prehepatic causes of PH are portal vein thrombosis, splenic vein thrombosis, arteriovenous fistula, blood overflow in the splanchnic district; the posthepatic causes are the Budd-Chiari syndrome, inferior vena cava obstruction, right-sided heart failure [1]. The liver cirrhosis is a remarkable medical problem in the world. Cirrhosis and hepatic chronic diseases are an important cause of morbidity and mortality worldwide, but with many differences in the geographic distribution. The global mortality rate ranges from 2% to 4% of total deaths in 2017, with decrease from the rate variance 1%–9%, evaluated in 1990 [2]. The more evident clinical evolutions of liver cirrhosis are PH, damage of coagulation, digestive hemorrhage, ascites, hepatic encephalopathy, hepatocarcinoma.
