Overview of Acute Viral Hepatitis

Acute hepatitis must first be differentiated from other disorders that cause similar symptoms. In the prodromal phase, hepatitis mimics various nonspecific viral illnesses and is difficult to diagnose. Anicteric patients suspected of having hepatitis based on risk factors are tested initially with liver tests, including aminotransferases, bilirubin, and alkaline phosphatase. Acute hepatitis often manifests in the icteric phase and so should be differentiated from other disorders causing jaundice Jaundice Jaundice is a yellowish discoloration of the skin and mucous membranes caused by hyperbilirubinemia. Jaundice becomes visible when the bilirubin level is about 2 to 3 mg/dL (34 to 51 micromol/L)... read more (see figure Simplified diagnostic approach to possible acute viral hepatitis Simplified diagnostic approach to possible acute viral hepatitis ).

Acute hepatitis can usually be differentiated from other causes of jaundice by

ALT is typically higher than AST, but absolute levels correlate poorly with clinical severity. Values increase early in the prodromal phase, peak before jaundice is maximal, and fall slowly during the recovery phase. Urinary bilirubin usually precedes jaundice. Hyperbilirubinemia in acute hepatitis varies in severity, and fractionation has no clinical value. Alkaline phosphatase is usually only moderately elevated; marked elevation suggests extrahepatic cholestasis and prompts imaging tests (eg, ultrasonography).

Liver biopsy is usually not needed unless the diagnosis is uncertain.

If laboratory results suggest acute hepatitis, particularly if ALT and AST are > 1000 IU/L (16.7 microkat/L), PT/INR is measured to assess liver function.

Manifestations of portosystemic encephalopathy Portosystemic Encephalopathy Portosystemic encephalopathy is a neuropsychiatric syndrome that can develop in patients with liver disease. It most often results from high gut protein or acute metabolic stress (eg, gastrointestinal... read more combined with bleeding diathesis or prolongation of INR suggest acute liver failure Acute Liver Failure Acute liver failure is caused most often by drugs and hepatitis viruses. Cardinal manifestations are jaundice, coagulopathy, and encephalopathy. Diagnosis is clinical. Treatment is mainly supportive... read more , indicating fulminant hepatitis Fulminant Hepatitis Fulminant hepatitis is a rare syndrome of rapid (usually within days or weeks), massive necrosis of liver parenchyma and a decrease in liver size (acute yellow atrophy); it usually occurs after... read more .

If acute hepatitis is suspected, efforts are next directed toward identifying its cause. A history of exposure may provide the only clue of drug-induced or toxic hepatitis. The history should also elicit risk factors for viral hepatitis.

Prodromal sore throat and diffuse adenopathy suggest infectious mononucleosis rather than viral hepatitis.

In patients with findings suggesting acute viral hepatitis, the following studies are done to screen for hepatitis viruses A, B, and C:

If any are positive, further serologic testing may be necessary to differentiate acute from past or chronic infection (see tables Hepatitis A Serology Hepatitis A Serology , Hepatitis B Serology Hepatitis B Serology* , and Hepatitis C Serology Hepatitis C Serology ).

If serologically confirmed HBV infection is severe, anti-HDV is measured.

If the patient has recently traveled to an endemic area or is immunosuppressed, IgM antibody to HEV (IgM anti-HEV) should be measured if the test is available.

Biopsy is usually unnecessary but, if done, usually reveals similar histopathology regardless of the specific virus:

HBV infection can occasionally be diagnosed based on the presence of ground-glass hepatocytes (caused by HBsAg-packed cytoplasm) and using special immunologic stains for the viral components. However, these findings are unusual in acute HBV infection and are much more common in chronic HBV infection.

Good personal hygiene helps prevent transmission, particularly fecal-oral transmission, as occurs with HAV and HEV.

Blood and other body fluids (eg, saliva, semen) of patients with acute HBV and HCV infection and stool of patients with HAV infection are considered infectious. Barrier protection is recommended, but isolation of patients does little to prevent spread of HAV and is of no value in HBV or HCV infection.

Posttransfusion infection is minimized by avoiding unnecessary transfusions and by screening all donors for hepatitis B and C. Screening has decreased the incidence of posttransfusion hepatitis B and hepatitis C, which are now extremely rare in the US.

Immunoprophylaxis can involve active immunization using vaccines and passive immunization.

Vaccines for hepatitis A and hepatitis B are available in the US.

Routine vaccination for hepatitis A and B is recommended in the US for all children and for adults at high risk (see Adult Immunization Schedule).

A vaccine for hepatitis E is not available in the US but is available in China.

Standard immune globulin prevents or decreases the severity of HAV infection and should be given to nonimmune family members and close contacts of patients. Hepatitis B immune globulin (HBIG) probably does not prevent infection but prevents or attenuates clinical illness.

No product exists for immunoprophylaxis of HCV or HDV. However, prevention of HBV infection prevents HDV infection. The propensity of HCV for changing its genome hampers vaccine development.