Fulminant hepatic failure is caused by a variety of causes of mass production of hepatocyte necrosis and severe liver function damage, so how to prevent progressive liver shrinkage, let us take a look at it: where a variety of liver injury factors cause serious damage to hepatocytes (including liver parenchymal cells and wither cells), so that its metabolism, secretion, synthesis, detoxification and immune function is severely impaired, this situation is called liver insufficiency ( This condition is called hepaticin-sufficiency. Patients often have a series of clinical syndromes such as gangrene, hemorrhage, secondary infection, renal dysfunction, and hepatic encephalopathy. Hepatic failure (hepaticfailure) generally refers to the advanced stage of hepatic insufficiency, and the main clinical manifestations are hepatic encephalopathy and hepatorenal syndrome (functional renal failure). The clinical symptoms are complex and varied due to the involvement of multiple organs in the course of the disease. The onset of the disease is rapid, and the evolution of the disease progresses rapidly. 1, first of all, we should start from the etiology, actively prevent hepatitis B. Universal hepatitis B vaccination, especially for high-risk groups can effectively prevent hepatitis B and D. Since chronic hepatitis C overlap infection with hepatitis A is easy to cause fulminant liver failure, therefore, hepatitis A vaccination for patients with chronic hepatitis C and non-immune high-risk groups can prevent fulminant liver failure caused by HAV. Prevention of drug-induced liver failure should be taught to patients about drugs, especially when new symptoms appear during drug use, and should be discontinued promptly. Combining alpha-interferon with chemotherapy for tumor patients with hepatitis B, especially HBeAg-negative HBV mutant strain infection, can prevent the occurrence of acute severe hepatitis. Others include careful consumption of wild mushrooms, prevention of heat stroke, treatment of intractable arrhythmias, and avoiding excessive liver resection during surgery. 2. It is to prevent the occurrence of progressive liver shrinkage in patients with acute liver disease. Patients with prothrombin activity <50%, especially those over 40 years old with significant jaundice should be admitted to hospital promptly and treated actively for the cause. Patients applying sedative, hepatotoxic and nephrotoxic drugs should be discontinued immediately if they develop symptoms of acute liver disease. If a patient develops acetaminophen toxicity, N-acetylcysteine should be given intravenously immediately to prevent severe liver damage. Women with late pregnancy who develop irritable thirst, nausea and vomiting should be alerted to fatty liver in pregnancy and it is advisable to terminate the pregnancy as soon as possible to save the life of mother and child. High doses of D-penicillamine should be given as soon as possible in young patients presenting with acute Wilson's disease. For herpes simplex hepatitis should be given intravenous acyclovir as soon as possible. 3. Further deterioration of fulminant liver failure should be prevented. When hepatic encephalopathy appears, all the above measures should be carried out as soon as possible even late at night and transferred quickly to a liver disease treatment center. Comatose patients should be given tracheal intubation as soon as possible, agitated individuals should be restrained, and all possible therapeutic measures should be taken to alter the natural course of the disease.