Viral Hepatitis

Viral hepatitis is a fairly common systemic disease. It's marked by hepatic cell destruction, necrosis, and autolysis, leading to anorexia, jaundiCe, and hepatomegaly. In most patients, hepatic cells eventually regenerate with little or no residual damage. allowing recovery. However, old age and serious underlying disorders make complications more likely. The prognosis is poor if edema and hepatic encephalopathy develop.

More than 70,000 cases of viral hepatitis are reported annually in the United States. Today, six types of viral hepatitis are recognized, and a seventh is suspected.

Causes

Hepatitis is inflammation of the liver. Several different viruses cause viral hepatitis. They are named the hepatitis A, B, C, D, and E viruses.

All of these viruses cause acute, or short-term, viral hepatitis. The hepatitis B, C, and D viruses can also cause chronic hepatitis, in which the infection is prolonged, sometimes lifelong.

People who are most at risk for developing viral hepatitis are workers in the health care professions, people with multiple sexual partners, intravenous drug users, and hemophiliacs who receive blood clotting factors

Signs and Symptoms

Investigate the patient's history for the source of transmission. For example, you may learn that he was recently exposed to individuals with hepatitis A or B, underwent recent blood transfusions, used I.V. drugs, or had hemodialysis for renal failure.

Assessment Tip Look for evidence of recent ear piercing or tattooing (significant because contaminated instruments can transmit hepatitis), travel to a foreign country where hepatitis is endemic, or living conditions that are, or were, overcrowded.

Be sure to ask about alcohol consumption, which is especially significant in suspected cirrhosis. An alcoholic patient often deliberately underestimates how much he drinks, so you may need to interview family members as well.

Check the patient's employment history for occupational exposure. For instance, the patient may work in a hospital or laboratory, where the risk of viral exposure from contaminated instruments or waste could be high. Also probe the patient's background for possible exposure to toxic chemicals, such as carbon tetrachloride, which can cause nonviral hepatitis.

Assessment findings are similar for the different types of hepatitis. Typically, signs and symptoms progress in several stages. In the prodromal (preictal) stage, the patient generally complains of easy fatigue and anorexia, possibly with mild weight loss. He may also report generalized malaise, depression, headache, weakness, arthralgia, myalgia, photophobia, and nausea with vomiting. He may describe changes in his senses of taste and smell.

Assessment of vital signs may reveal fever, with a temperature of 100° to 102° F (37.8° to 38.9° C). As the prodromal stage draws to a close, usually within 1 to 5 days before the onset of the clinical jaundice stage, inspection of urine and stool specimens may reveal dark-colored urine and clay-colored stools.

If the patient has progressed to the clinical jaundice stage, he may report pruritus, abdominal pain or tenderness, and indigestion. Early in this stage, he may complain of anorexia; later, his appetite may return. Inspection of the sclerae, mucous membranes, and skin may show jaundice, which can last for 1 to 2 weeks. Jaundice indicates that the damaged liver is unable to remove bilirubin from the blood; it doesn't indicate disease severity. Occasionally, hepatitis occurs without jaundice.

During the clinical jaundice stage, skin inspection may reveal rashes, erythematous patches, or hives, especially if the patient has hepatitis B or C. Palpation may disclose abdominal tenderness in the right upper quadrant, an enlarged and tender liver and, in some cases, splenomegaly and cervical adenopathy.

If you assess the patient during the recovery or posticteric stage, you find most symptoms are decreasing or have subsided. On palpation, you may notice a decrease in liver enlargement. The recovery phase generally lasts from 2 to 12 weeks, sometimes longer in patients with hepatitis B, C, or E.

Diagnostic tests

In suspected viral hepatitis, a hepatitis profile is routinely performed. This study identifies antibodies specific to the causative virus, establishing the type of hepatitis:

• Type A. Detection of an antibody to hepatitis A virus (anti-HAV) confirms the diagnosis.
• Type B. The presence of hepatitis B surface antigens (HBsAg) and hepatitis B antibodies (anti-HBs) confirms the diagnosis.
• Type C. Diagnosis depends on serologic testing for the specific antibody 1 or more months after the onset of acute illness. Until then, the diagnosis is principally established by obtaining negative test results for hepatitis A, B, and D.
• Type D. Detection of intrahepatic delta antigens or immunoglobulin (lg) M antidelta antigens in acute disease (or IgM and IgG in chronic disease) establishes the diagnosis.
• Type E. Detection of hepatitis E antigens supports the diagnosis; however, the diagnosis may also consist of ruling out hepatitis C.
• Type G. Detection of hepatitis G ribonucleic acid supports diagnosis. Serologic assays are being developed.

Additional findings from liver function studies support the diagnosis:

• Serum aspartate aminotransferase and serum alanine aminotransferase levels are increased in the prodromal stage of acute viral hepatitis.
• Serum alkaline phosphatase levels are slightly increased.
• Serum bilirubin levels are elevated. Levels may continue to be high late in the disease, especially if the patient has severe disease.
• Prothrombin time is prolonged. (Prothrombin time more than 3 seconds longer than normal indicates severe liver damage.)
• White blood cell counts commonly reveal transient neutropenia and lymphopenia followed by lymphocytosis.
• Liver biopsy is performed if chronic hepatitis is suspected. (This study is performed for acute hepatitis only if the diagnosis is questionable.)

Treatment

Persons believed to have been exposed to hepatitis A and the household contacts of patients with confirmed cases should be treated with standard immunoglobulin. Travelers planning visits to areas known to harbor such viruses should receive hepatitis A vaccine.

Hepatitis B globulin is given to individuals exposed to blood or body secretions of infected individuals. The immunoglobulin is effective but very expensive. Hepatitis B vaccine should be given to people at risk for exposure. This group includes neonates of hepatitis B virus (HBV)-positive mothers, sexual contacts of HBV-positive individuals, hemodialysis patients, health care workers, and male homosexuals. There is no vaccine against hepatitis C, but it has been treated with alfa interferon.

In the early stages of the disease, the patient is advised to rest and combat anorexia by eating small, high-calorie, high-protein meals. (Protein intake should be reduced if signs of precoma -lethargy, confusion, mental changes - develop.) Large meals are usually better tolerated in the morning because many patients experience nausea late in the day.

In acute viral hepatitis, hospitalization usually is required only for those patients with severe symptoms or complications. Parenteral nutrition may be required if the patient has persistent vomiting and is unable to maintain oral intake.

Antiemetics (trimethobenzamide or benzquinamide) may be given half an hour before meals to relieve nausea and prevent vomiting; phenothiazines have a cholestatic effect and should be avoided. For severe pruritus, the resin cholestyramine, which sequesters bile salts, may be given.