Cirrhosis is a common chronic progressive clinical liver disease with diffuse liver damage formed by the long-term or repeated action of one or more etiologies. There are many etiologies, which can be divided into viral hepatitis cirrhosis, alcoholic cirrhosis, metabolic cirrhosis, biliary cirrhosis, hepatic venous return obstruction cirrhosis, autoimmune cirrhosis, toxic and drug cirrhosis, malnutrition cirrhosis, and cryptogenic cirrhosis. In China, most of them are post-hepatitis cirrhosis, and a few are alcoholic cirrhosis and schistosomal cirrhosis. Pathological histology has extensive hepatocyte necrosis, nodular regeneration of residual hepatocytes, connective tissue proliferation and fibrous septum formation, leading to structural destruction of liver lobules and pseudobullet formation, and progressive deformation and hardening of the liver to cirrhosis. In the early stage, due to the strong compensatory function of the liver, there are no obvious symptoms, but in the later stage, liver function damage and portal hypertension are the main manifestations, and there are multi-system involvement. Clinical manifestations 1. Compensated stage (generally Child-Pugh grade A) may have clinical manifestations of hepatitis, or may be insidious. There may be mild weakness, abdominal distension, mild enlargement of liver and spleen, mild jaundice, liver palm and spider nevus. (2) Loss of compensation stage (generally Child-Pugh grade B and C) with liver function damage and portal hypertension syndrome. (1) Systemic symptoms Weakness, emaciation, dull face, low urine, lower limb edema. (2) Gastrointestinal symptoms Loss of appetite, abdominal distension, gastrointestinal dysfunction or even malabsorption syndrome, hepatogenic diabetes mellitus, polyuria, polyphagia and other symptoms may occur. (3) Bleeding tendency and anemia Gingival bleeding, epistaxis, purpura, anemia. (4) Endocrine disorders Spider nevus, liver palm, skin pigmentation, menstrual disorders in women, gynecomastia, parotid enlargement. (5) Hypoproteinemia Bilateral lower limb edema, oliguria, peritoneal effusion, pleural effusion of hepatic origin. (6) Portal hypertension Abdominal effusion, pleural effusion, splenomegaly, hypersplenism, establishment of portal collateral circulation, esophagogastric-fundus varices, abdominal wall varices.