Concept The development of acute hepatic failure in viral hepatitis is called severe hepatitis. Acute hepatic failure is defined as a rapid onset of severe hepatic insufficiency with a decrease in prothrombin activity to less than 40%, a rapid rise in serum bilirubin and a rapid decrease in ALT (enzyme-jaundice separation), and a significant decrease in cholinesterase activity. Acute liver failure with significant hepatic encephalopathy within 10 days of onset is called fulminant liver failure (acute severe hepatitis), and acute liver failure with significant hepatic encephalopathy between 10 and 8 weeks of onset is called subfulminant liver failure (subacute severe hepatitis). Cases of chronic active hepatitis, hepatitis B surface antigen carriers or cirrhosis with clinical manifestations similar to those of subacute severe hepatitis are called chronic severe hepatitis by our scholars. The most common cause of FHF is hepatitis virus infection, followed by drug or toxicity, while other causes are rare. The epidemiology of acute hepatitis E is similar to that of acute hepatitis A, but it causes more FHF than hepatitis A. In Xinjiang, China, the epidemiology of acute hepatitis E is similar to that of acute hepatitis A, but it causes more FHF than hepatitis A. The epidemiology of acute hepatitis E is similar to that of acute hepatitis A, but it causes more FHF than hepatitis A. In Xinjiang, China, there was an epidemic of hepatitis E from 1986 to 1988, and among 199 cases with clinical and pathogenic studies, 16 cases had acute FHF (8.04%), and all of them had hepatic coma; among 17 cases in pregnant women, 6 cases (35.3%) had severe hepatitis, and among 68 cases in non-pregnant women, 2 cases (2.9%) had severe hepatitis, which suggests that pregnant women have severe disease after HEV infection and more cases of FHF than non-pregnant women. This suggests that pregnant women with HEV infection have more severe disease and more FHF than non-pregnant women. FHF and subfluvial hepatitis caused by HBV infection alone and co-infection with HDV were reported to account for 25%, 60% and 65% respectively. It has been confirmed that the risk of FHF is much higher in patients with HBV and HDV co-infection than in those with HBV infection alone. HCV causes 23-44% of FHF and sub-FHF patients seen in Europe. In addition, non-hepatitis viruses such as CMV and HSV co-infected with HBV can also cause FHF. (i) Necrotic type: characterized by acute massive necrosis with consistent old and new necrosis, disappearance of hepatocyte lysis, only a small number of hepatocytes remaining around the lobules, dilated and congested liver sinusoids, sparse inflammatory cells, more neutrophilic leukocyte infiltration visible, early hepatic lobular reticular scaffold and structure of the hilar region preserved, residual hepatocytes There is bile stasis in the residual hepatocytes and small bile ducts. (ii) Edematous type In addition to focal necrosis of the liver parenchyma, the more prominent feature is the extensive balloon-like transformation of the hepatocytes, which are extruded from each other and form a vegetative cell pattern. Subacute heavy hepatitis Sub-massive, massive necrosis and bridging-like necrosis of varying age can be seen, with intensive infiltration of lymphocytes and other infiltrates in the necrotic area, collapse of the reticular scaffold, marked concentration in the portal duct area, massive hyperplasia of small bile ducts, proliferation of residual hepatocytes into clusters, significant biliousness of hepatocytes and small bile ducts, and highly deformed liver tissue structure. Chronic severe hepatitis Those with secondary submassive or massive hepatic necrosis on the basis of chronic active hepatitis or cirrhosis, i.e., fresh submassive or massive necrosis with a background of chronic old lesions. Dense inflammatory cell infiltration, significant bruising, and highly distorted liver tissue architecture.