Fulminant liver failure is a syndrome of massive production of hepatocellular necrosis and severe hepatic impairment caused by multiple etiologies, with no previous history of liver disease and the onset of hepatic encephalopathy within 8 weeks of the disease. It has an acute onset, rapid progression and high mortality rate. Early diagnosis and treatment can reduce the mortality rate. Early symptoms of progressive hepatic shrinkage include jaundice, persistent hypothermia, hypothermia, gastrointestinal symptoms, bleeding tendency, progressive liver shrinkage, liver odor, fluttering tremor, accelerated heart rate, hypotension, etc. Late symptoms manifest as hepatic encephalopathy, cerebral edema when there are ankle clonus, slowed breathing, irregular rhythm, coagulation dysfunction and bleeding bleeding sites such as skin, gums, nasal mucosa, bulbar conjunctiva and gastric mucosa. symptoms. The following is the examination method of the late symptoms: manifestation of hepatic encephalopathy, followed by the following symptoms, the migratory stages of which are not easily separated distinctly. 1, cerebral edema when there is ankylosing clonus, cone bundle sign positive when there is already cerebral edema, or there is bulbar conjunctival edema, pupil dilatation fixed, breathing becomes slower, irregular rhythm, optic papillary edema are indicative of cerebral edema performance. 2, coagulation dysfunction and bleeding bleeding sites such as skin, gums, nasal mucosa, bulbar conjunctiva and gastric mucosa are common. (1) Platelet quality and quantity abnormalities in FHF are smaller than normal, and electron microscopy shows vacuoles, pseudopods and blurred plasma membranes. Platelets are normal in the absence of hepatic encephalopathy. Thrombocytopenia can be caused by bone marrow suppression, hypersplenism, and depletion by intravascular coagulation. (2) Impaired coagulation factor synthesis All coagulation factors in plasma are reduced, especially factor VII is synthesized outside the liver, but increased. The prothrombin time is significantly prolonged. (3) DIC with local secondary fibrinolysis plasma plasmin and its activating substances are reduced, while fibrin/fibrinogen degradation products are increased. 3, Infections are most common with respiratory tract infections, other hair urinary infections, mostly G-bacilli, G+ cocci, but also anaerobic bacteria and mycobacterial infections. 4, renal failure in FHF with abnormal renal function up to 70%, acute tubular necrosis accounts for half. There is hypernatremia, isotonic urine and tubular necrosis. It is associated with hepatocyte necrosis, endotoxemia, improper application of diuretics, gastrointestinal bleeding resulting in hypovolemia and hypotension. Renal failure has been reported to be the leading cause of death in FHF, which is worth noting. 5.Disorders of electrolyte acid-base balance, low blood sodium, low blood calcium, low blood magnesium, low blood potassium, respiratory alkalosis, low metabolic alkalosis and metabolic acidosis, etc. 6, other hypoglycemia, hypoxemia, pulmonary edema, cardiac arrhythmia, portal hypertension and acute pancreatitis, etc.