Cirrhosis is a chronic, progressive, diffuse change in the liver due to various causes. It is characterized by repeated, long-term damage to hepatocytes from one etiology or several etiologies, resulting in hepatocyte degeneration and necrosis. Extensive hepatocyte degeneration and necrosis is followed by regeneration of intrahepatic connective tissue and diffuse proliferation of fibrous tissue. At the same time, intrahepatic hepatocytes regenerate and form regenerative nodules, and normal liver lobule structure and blood vessel formation are destroyed, forming pseudobullets. After a considerable period (several years or even decades), the liver gradually becomes deformed and hardens in texture, and this physiopathological change is clinically referred to as cirrhosis. Cirrhosis is relatively common in China, mostly post-hepatitis cirrhosis and, to a lesser extent, alcoholic cirrhosis and schistosomiasis cirrhosis. Since cirrhosis can be reversed or no longer progress after active prevention and treatment in the early stage, but the late stage will seriously affect the quality of life of patients and even endanger their lives, so the prevention and treatment of cirrhosis is very important. The causes of cirrhosis can be divided into the following 8 categories: 1. Hepatitis virus: the most common are hepatitis B virus, hepatitis C virus and hepatitis D virus infections. Some people with hepatitis B virus infection develop chronic hepatitis, and a small percentage of chronic hepatitis B develops into cirrhosis. About half of acute hepatitis C develops into chronic hepatitis, and 10-30% of them develop cirrhosis. Hepatitis D virus depends on hepatitis B virus before hepatitis can occur, and some patients develop cirrhosis. 2, alcohol factors: long-term heavy drinking leads to liver cell damage, fatty degeneration, necrosis, liver fibrosis, and in severe cases, cirrhosis. 3, biliary stasis: long-term chronic biliary stasis, resulting in inflammation of liver cells and bile duct reaction, and even necrosis, forming biliary liver sclerosis. 4, stasis factors: long-term recurrent chronic cardiac insufficiency, constrictive pericarditis and hepatic vein obstruction can cause liver stasis, causing necrosis and degeneration of hepatocytes due to lack of oxygen, which eventually leads to cirrhosis. Among them, cirrhosis caused by the heart is called cardiogenic cirrhosis. 5, drug or chemical toxic factors: long-term use of certain drugs, such as diphenhydramine, cinchon, methyldopa, etc. can lead to drug-related hepatitis, and finally develop into cirrhosis. Long-term exposure to certain chemical toxins, such as carbon tetrachloride, arsenic, phosphorus, etc. can cause toxic hepatitis and develop into cirrhosis. 6, metabolic disorders: copper metabolism disorders, seen in the liver bean nucleus degeneration. Iron metabolism disorders, seen in hemophilia, galactosemia, fibrous cysticercosis, alpha-antitrypsin deficiency, glycogen storage disease, tyrosine metabolism disorders, hereditary hemorrhagic capillary dilation, the above conditions are related to genetic metabolic defects, can lead to cirrhosis. 7, parasitic infection: schistosome infection is common in the south of China, which can lead to schistosomiasis and further cause liver fibrosis leading to cirrhosis. Human infection with Toxoplasma gondii can lead to cirrhosis after untimely treatment. 8, other factors: a high degree of malnutrition can cause cirrhosis, and a small number of cirrhosis of the liver for unknown reasons. It is easy to confirm the diagnosis of cirrhosis in patients with typical symptoms, but some patients can have no typical clinical symptoms and are in the insidious compensatory stage, so it is difficult to confirm the diagnosis. Therefore, the diagnosis of cirrhosis is a comprehensive diagnosis. 1.History of viral hepatitis, long-term alcoholism, long-term malnutrition, schistosomiasis or chemical poisoning, etc. 2.Symptoms: loss of appetite, ascites, nausea, diarrhea, mild enlargement of liver and spleen, vascular nevus in the early stage (compensated stage), ascites, bleeding tendency, jaundice, liver palm, splenomegaly and reduction of liver volume in the late stage (decompensated stage) 3, liver function examination: normal or mildly abnormal liver function in the compensated stage, significantly abnormal liver function in the decompensated stage, decreased plasma albumin, increased globulin, its ratio inverted, and significantly increased protein electrophoresis gamma globulin. 4.Blood picture examination: leukocytes and platelets are reduced in hypersplenism, and in severe cases, whole blood cells are reduced. 5.Barium esophagogram or endoscopy with esophageal or gastric fundic varices. 6.B ultrasound examination: changes in liver size, surface and morphology, echogenic changes, thickening of portal vein and splenic vein, ascites, visible liquid dark areas, and increased spleen volume. 7.Hepatic histological examination: those with fibrous septum formation and small nodular or mixed nodular hyperplasia can confirm the diagnosis. Liver cirrhosis generally takes a comprehensive treatment approach. Liver preservation and enzyme reduction, anti-liver fibrosis, anti-hepatitis B or C virus, etc. Blood-activating and stasis-transforming herbs have their unique advantages in the treatment of liver fibrosis and cirrhosis.