Clinical Classification of Fulminant viral Hepatitis

Acute fulminant viral hepatitis

Presents an acute onset with jaundice. Within two weeks, develops into extreme hypodynamia, pronounced gastrointestinal symptoms, hepatic encephalopathy of degree
II or above (IV degrees total), prothrombin activity less than 40% without other reasons, liver dullness and progressive shrinking, and progressive deepening of jaundice.
Patients with mild jaundice but with other above-mentioned symptoms should be highly suspected.

Subacute fulminant viral hepatitis

Presents an acute onset with jaundice. Between 15 to 24 weeks, develops into extreme hypodynamia, pronounced gastrointestinal symptoms, prothrombin activity less
than 40% without other reasons, progressive deepening of jaundice (serum total bilirubin increasing at >17.1 μmol/L/d, or >340 μmol/L). Subacute fulminant hepatitis
which initially presents with hepatic encephalopathy of degree II or above is termed encephalopathy type (including brain edema, hernia, etc.). Cases initially presenting
with ascites and related symptoms (including pleural effusion, etc.) are known as ascites type.

Chronic fulminant viral hepatitis
The pathogenesis of chronic fulminant hepatitis includes:
(1) History of chronic hepatitis or cirrhosis;
(2) History as a carrier of chronic hepatitis B virus;
(3) Neither (1) nor (2), but with signs of chronic liver disease (liver palms, arterial spider, etc.). Radiological changes (increased gamma globulin, and decreased or even
inverted albumin/globulin ratio);
(4) Hepatitis confirmed by biopsy;
(5) Complicated overlapping infection by HBV, HCV, or other hepatitis viruses.
The clinical onset may be the same as subacute fulminant hepatitis, and with the progression of disease, may reach the diagnostic criteria of fulminant viral hepatitis
(prothrombin activity less than 40%, and serum total bilirubin >340 μmol/L) beyond a course of 24 weeks.
To facilitate determination of treatment efficacy and prognosis, the subacute and chronic fulminant viral hepatitis can be divided into three stages:
Early stage: the basic diagnostic criteria are met, such as extreme hypodynamia, pronounced gastrointestinal symptoms, progressive deepening of jaundice, serum total
bilirubin >340 μmol/L, prothrombin activity between 30% and 40%, or pathologically confirmed. No obvious encephalopathy, nor ascites are present.
Mid-stage: easily detectable encephalopathy or ascites, bleeding tendency (bleeding or bruising), prothrombin activity between 20% and 30%.
Late stage: Intractable complications, such as hepatorenal syndrome, gastrointestinal bleeding, severe bleeding tendency (at injection sites), severe infection, electrolyte
imbalance, or hepatic encephalopathy of degree II and above, cerebral edema, with prothrombin activity less than 20%.
Histopathological Diagnosis
Acute fulminant viral hepatitis
Simultaneous necrosis of liver cells with necrotic area over 2/3 of liver parenchyma, or sub-massive necrosis, or bridging necrosis with severe degeneration of living
liver cells. When 50% or more of liver cells remain after the acute phase, liver regeneration can be expected. A poor prognosis may be predicted in case of diffuse
microvesicular steatosis.
Subacute fulminant viral hepatitis
Mixed past and present sub-massive necrosis. Mesh fiber collapse in the relatively old necrosis area, with deposition of collagen fibers. Residual liver cell proliferation
groups, with large amount of small bile duct hyperplasia and cholestasis.
Chronic fulminant viral hepatitis
With a chronic liver disease (chronic hepatitis or cirrhosis) background, massive (lobular) or sub-massive fresh necrosis of liver cells.
                                                                                                    Box 1: Diagnosis of Fulminant Viral Hepatitis [3].