Hepatitis is applied to a broad category of clinicopatho-logic conditions that result from the damage produced by a vi-ral, toxic, pharmacologic, or immunemediated attack on the liver. The common pathologic features of hepatitis are hepato-cellular necrosis, which may be focal or extensive, and inflam-matory cell infiltration of the liver, which may predominate in the portal areas or may extend into the parenchyma. Physical examination may show an enlarged tender liver and icteric mu-cous membranes. Laboratory evidence of hepatocellular dam-age is invariably found in the form of elevated transaminase levels. Independent of the cause of hepatitis, the clinical course may range from subclinical or mild to severe hepatocel-lular dysfunction with evidence of impairment of coagulation, marked jaundice, and disturbance of neurologic function.
Acute hepatitis implies a condition lasting less than 6 months, culminating either in complete resolution of the liver damage with return to normal liver function and structure or a rapid progression of the acute injury toward extensive necrosis and a fatal outcome.
Chronic hepatitis is defined as a sustained inflammatory process in the liver lasting longer than 6 months and is often impossible to differentiate from acute hepatitis on histologic criteria alone. Inflammatory cell extending beyond the limits of the portal tracts surrounding isolated nests of hepatocytes (piecemeal necrosis) and portal and/or central areas of the hepatic lobules connected by inflammation, necrosis, and col-lapse of architecture (bridging necrogis) are seen in severe forms of chronic hepatitis. However, these features may also be noted in uncomplicated acute hepatitis that ultimately re-solves completely. A purely histologic diagnosis of chronic hep-atitis usually requires evidence of progression toward cirrhosis,such as significant fibrous deposition and disruption of the hep-atic lobular architecture.
Treatment
No specific treatment exists for acute viral hepatitis. Management is largely supportive and includes rest, mainte-nance of hydration, and adequate dietary intake. Most patients show a preference for a low-fat, highcarbohydrate diet. Vita-min supplementation is of no proven value, although vitamin K may be indicated if prolonged cholestasis occurs. Activity is re-stricted to limit fatigue. Alcohol should be avoided until liver enzymes return to normal. Measures to combat nausea can in-clude small doses of metoclopramide and hydroxyzine. Hospi-talization is indicated in patients with severe nausea and vomit-ing or in those with evidence of deteriorating liver function,such as hepatic encephalopathy or prolongation of the pro-thrombin time. In general, hepatitis A may be regarded as noninfectious after 2 to 3 weeks, whereas hepatitis B is poten-tially infectious to sexual contacts throughout its course, al-though the risk is low once HBsAg has cleared. Although hep-atitis C may also be transmitted to sexual contacts, the risk of this is considered less than for hepatitis B.
