All kinds of liver injury factors cause serious damage to hepatocytes (including hepatic parenchymal cells and blastocytes), so that their metabolism, secretion, synthesis, detoxification and immune function are severely impaired, which is called hepaticin-sufficiency. The patient often presents with a series of clinical signs such as gangrene, bleeding, 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. Early symptoms 1. Jaundice has 3 characteristics: (1) Jaundice appears and deepens rapidly within a short period of time, such as total bilirubin > 171 μmol/L, along with other manifestations of severe impairment of liver function, such as bleeding tendency, prolonged prothrombin time, and elevated ALT. If there is only deeper jaundice without other serious liver function abnormalities, it indicates intrahepatic biliary sludge. (2) The jaundice lasts for a long time, and the general pattern of jaundice waxing and waning is deepening, persisting, and receding in 3 stages, and if the jaundice does not subside after 2 to 3 weeks, it suggests a serious condition. (3) jaundice appears after the condition does not improve, the general rule of acute jaundice hepatitis, when the jaundice appears, appetite gradually improved, nausea and vomiting reduced. If the symptoms do not improve after 1 week after the appearance of jaundice, you need to be alert for heavy hepatitis. 2, persistent hypothermia at the beginning of the disease can have a low fever, jaundice after the appearance of body temperature dropped to normal. If jaundice is accompanied by persistent hypothermia, it suggests hepatocellular necrosis or endotoxemia. 3, general condition is very poor such as weakness, lethargy, no appetite, and even unable to take care of themselves. 4.Obvious gastrointestinal symptoms such as frequent nausea, vomiting, eructation, marked abdominal distension, loss of bowel sounds, and intestinal paralysis. 5, bleeding tendency such as skin bruising, purpura, epistaxis, gum bleeding, a few upper gastrointestinal bleeding, etc., suggesting coagulation dysfunction and liver failure. 6, rapid appearance of ascites because of the long half-life of albumin (about 2 weeks), generally 2-3 weeks after the disease before the appearance of hypoalbuminemia, more than 2 to 8 weeks of the disease have ascites. 7, personality changes such as the original cheerful personality, sudden change to melancholy, or the opposite. Reversal of sleep rhythm, repetitive language, inability to conceive, disorientation, behavioral quirks, behavioral eccentricities, and open defecation are all signs of hepatic encephalopathy. This is followed by impaired consciousness and entry into hepatic coma. 8, Progressive liver shrinkage, liver odor, fluttering tremor, increased muscle tone, positive cone bundle sign, ankle clonus, etc., suggest severe liver damage. 9. Accelerated heart rate and hypotension, associated with endotoxemia or internal bleeding.