Managing portal hypertension in patients with liver cirrhosis

Abstract

Portal hypertension is one cause and a part of a dynamic process triggered by chronic liver disease, mostly induced by alcohol or incorrect nutrition and less often by viral infections and autoimmune or genetic disease. Adequate staging - continuously modified by current knowledge - should guide the prevention and treatment of portal hypertension with defined endpoints. The main goals are interruption of etiology and prevention of complications followed, if necessary, by treatment of these. For the past few decades, shunts, mostly as intrahepatic stent bypass between portal and hepatic vein branches, have played an important role in the prevention of recurrent bleeding and ascites formation, although their impact on survival remains ambiguous. Systemic drugs, such as non-selective beta-blockers, statins, or antibiotics, reduce portal hypertension by decreasing intrahepatic resistance or portal tributary blood flow or by blunting inflammatory stimuli inside and outside the liver. Here, the interactions among the gut, liver, and brain are increasingly examined for new therapeutic options. There is no general panacea. The interruption of initiating factors is key. If not possible or if not possible in a timely manner, combined approaches should receive more attention before considering liver transplantation.

Treatment of Oesophageal Varices in Liver Cirrhosis

“…Although it is advised to titrate NSBB until a 25% reduction of basal heart rate has been reached, there is evidence that lower dosages may be equally effective [20,28,31], probably with less side effects. Carvedilol, an NSBB with additional alpha-1 adrenoceptor blocking properties, induces a better haemodynamic response than propranolol and may prevent progression of varices [32]. It is also advised for primary prophylaxis of bleeding.…”

Eosinophils Control Liver Damage by Modulating Immune Responses Against Fasciola hepatica

“…However, we failed at detecting parasites in the peritoneum in our experimental infections in mice. Last, eosinophils could also derive from the blood due to portal hypertension produced by fibrosis in livers (42), since infected mice with severe clinical signs present hemorrhagic ascites which is a marker of advanced liver injury (43,44). Thus, the eosinophils found in the peritoneal cavity could represent an attempt of the host to allow eosinophil recruitment to the liver to fight against the parasite.…”

Efficacy Analysis of Gastric Coronary Venous TH Glue Embolization with Splenectomy for Treating Cirrhotic Portal Hypertension

“…To further reduce the bleeding rate during or after operation, we have also made some modifications in the surgical mode: anatomy in situ. (1) The previous recommendation for the surgery is that the spleen be lifted out or partially removed from the abdominal cavity before the treatment of spleen pedicle. Our experience is to perform the anatomy in situ as much as possible, not lifting the spleen out prematurely.…”

“…Portal hypertension is a clinical syndrome affecting patients with or without cirrhosis, in which hemodynamic changes in the portosystemic circulation lead to complications such as variceal bleeding, ascites, and portosystemic encephalopathy. [1][2][3] Upper gastrointestinal bleeding caused by esophageal varices is its most serious complication, with an annual bleeding rate of 5-15% and a rebleeding rate of 60% within 1 year. 4 The surgical treatment of portal hypertension primarily aims to prevent esophageal variceal bleeding.…”