Viral hepatitis
Viral hepatitis: Excerpt from Professional Guide to Diseases (Eighth Edition)
Viral hepatitis is a fairly common systemic disease, 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. However, old age and serious underlying disorders make complications more likely. The prognosis is poor if edema and hepatic enceph-alopathy develop.
Hepatitis occurs in these forms:
❑ Type A (infectious or short-incubation hepatitis) is rising among homosexuals and in people with immunosuppression related to human immunodeficiency virus (HIV) infection.
❑ Type B (serum or long-incubation hepatitis) also is increasing among HIV-positive individuals. Routine screening of donor blood for the hepatitis B surface antigen (HBsAg) has decreased the incidence of posttransfusion cases, but transmission by needles shared by drug abusers remains a major problem.
❑ Type C accounts for about 20% of all viral hepatitis cases and for most posttransfusion cases.
❑ Type D (delta hepatitis) is responsible for about 50% of all cases of fulminant hepatitis, which has a high mortality. Developing in 1% of patients, fulminant hepatitis causes unremitting liver failure with encephalopathy. It progresses to coma and commonly leads to death within 2 weeks. In the United States, type D is confined to people who are frequently exposed to blood and blood products, such as I.V. drug users and patients with hemophilia.
❑ Type E (formerly grouped with type C under the name non-A, non-B hepatitis) occurs primarily among patients who have recently returned from an endemic area (such as India, Africa, Asia, or Central America); it’s more common in young adults and more severe in pregnant women.
❑ Hepatitis G is a newly discovered form of hepatitis. Transmission is by the blood-borne route and it’s more common in those who receive blood transfusions.
Causes and incidence
The major forms of viral hepatitis result from infection with the causative viruses: A, B, C, D, E, or G.
Type A hepatitis is highly contagious and is usually transmitted by the fecal-oral route. However, it may also be transmitted parenterally. Hepatitis A usually results from ingestion of contaminated food, milk, or water. Many outbreaks of this type are traced to ingestion of seafood from polluted water. In 2001, there were more than 10,000 acute cases of hepatitis A infection reported in the United States.
Type B hepatitis, once thought to be transmitted only by the direct exchange of contaminated blood, is now known to be transmitted also by contact with human secretions and feces. As a result, nurses, physicians, laboratory technicians, and dentists are frequently exposed to type B hepatitis, in many cases as a result of wearing defective gloves. Transmission also occurs during intimate sexual contact as well as through perinatal transmission. An estimated 200,000 new cases of hepatitis B virus (HBV) and 5,000 deaths from HBV occur annually in the United States.
Although specific type C hepatitis viruses have been isolated, only a small percentage of patients have tested positive for them — perhaps reflecting the test’s poor specificity. Usually, this type of hepatitis is transmitted through transfused blood from asymptomatic donors. Hepatitis C accounts for 30,000 new infections and 8,000 to 10,000 deaths each year in the United States. Most exposures (60%) occur through the use of illicit I.V. drugs. However, sexual transmission is responsible for 20% of cases. More than 170 million people have the hepatitis C virus worldwide.
Type D hepatitis is found only in patients with an acute or chronic episode of hepatitis B and requires the presence of HBsAg. The type D virus depends on the double-shelled type B virus to replicate. For this reason, type D infection can’t outlast a type B infection. About 15 million people are infected with hepatitis D worldwide. It’s more common in adults than in children. People with a history of illicit I.V. drug use and people who live in the Mediterranean basin have a higher incidence.
Type E hepatitis is transmitted enterically, much like type A. Because this virus is inconsistently shed in feces, detection is difficult. In the United States, the prevalence of hepatitis E is less than 2%. It’s typically found in developing countries that lie near the equator. Incidence is highest among people ages 15 to 40.
Type G may be transmitted in a manner similar to that of hepatitis C. It may also be transmitted by sexual contact, and its incidence may be higher than previously suspected. It’s associated with acute and chronic liver disease, but studies haven’t clearly implicated the hepatitis G virus as an etiologic agent.
Other proposed causative factors, such as non-ABCDE viral hepatitis and type F, are under investigation.
Signs and symptoms
Assessment findings are similar for the different types of hepatitis. Typically, signs and symptoms progress in several stages.
In the prodromal (preicteric) stage, the patient typically complains of easy fatigue and anorexia (possibly with mild weight loss), generalized malaise, depression, headache, weakness, arthralgia, myalgia, photophobia, and nausea with vomiting. He also may describe changes in his senses of taste and smell.
Assessment of the patient’s vital signs may reveal a fever of 100° to 102° F (37.8° to 38.9° C). As the prodromal stage ends, usually 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 reveal jaundice, which can last for 1 to 2 weeks. Jaundice indicates that the damaged liver is unable to remove bilirubin from the blood; however, its presence doesn’t indicate the severity of the disease. Occasionally, hepatitis occurs without jaundice.
During the clinical jaundice stage, inspection of the skin may detect rashes, erythematous patches, or urticaria, 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.
During the recovery (posticteric) stage, most of the patient’s symptoms decrease or subside. On palpation, a decrease in liver enlargement may be noted. The recovery phase commonly lasts from 2 to 12 weeks, although sometimes this phase lasts longer in the patient with hepatitis B, C, or E.Little is known about hepatitis G.
Diagnosis
A hepatitis profile, which identifies antibodies specific to the causative virus and establishes the type of hepatitis, is routine in suspected viral hepatitis.
❑ Type A: Detection of an antibody to hepatitis A confirms the diagnosis.
❑ Type B: The presence of HBsAg and hepatitis B antibodies confirms the diagnosis.
❑ Type C: Diagnosis depends on serologic testing for the specific antibody 1 or more months after the onset of acute hepatitis. Until then, the diagnosis is established primarily by obtaining negative test results for hepatitis A, B, and D.
❑ Type D: Detection of intrahepatic delta antigens or immunoglobulin (Ig) 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 be determined by ruling out hepatitis C.
❑ Type G: Detection of hepatitis G antigen supports the diagnosis but doesn’t clearly implicate infection; the patient may be otherwise asymptomatic.
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 in severe cases.
❑ Prothrombin time is prolonged (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; however, it’s performed for acute hepatitis only if the diagnosis is questionable.
Treatment
No specific drug therapy has been developed for hepatitis, with the exception of hepatitis C, which has been treated somewhat successfully with interferon alpha. Instead, patients are advised to rest in the early stages of the illness and to combat anorexia by eating small, high-calorie, high-protein meals. (Protein intake should be reduced if signs or symptoms of pre-coma — lethargy, confusion, and 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 the patient with severe symptoms or complications. Parenteral nutrition may be required if the patient experiences persistent vomiting and is unable to maintain oral intake.
Antiemetics may be given 30 minutes before meals to relieve nausea and prevent vomiting; phenothiazines have a cholestatic effect and should be avoided. For severe pruritus, the resin cholestyramine may be given.
Special considerations
Use enteric precautions when caring for patients with type A or E hepatitis. Practice standard precautions for all patients.
❑ Inform visitors about isolation precautions.
❑ Provide rest periods throughout the day. Schedule treatments and tests so that the patient can rest between bouts of activity.
❑ Because inactivity may make the patient anxious, include diversionary activities as part of his care. Gradually add activities to his schedule as he begins to recover.
❑ Encourage the patient to eat. Don’t overload his meal tray or overmedicate him because this will diminish his appetite.
❑ Encourage fluids (at least 4 qt [4 L] per day). Encourage the anorectic patient to drink fruit juice. Also offer chipped ice and effervescent soft drinks to maintain hydration without inducing vomiting.
❑ Administer supplemental vitamins and commercial feedings, as ordered. If symptoms are severe and the patient can’t tolerate oral intake, provide I.V. therapy and parenteral nutrition, as ordered by the physician.
❑ Record the patient’s weight daily, and keep intake and output records. Observe stools for color, consistency, and amount and record the frequency of bowel movements.
❑ Watch for signs of fluid shift, such as weight gain and orthostasis.
❑ Watch for signs of hepatic coma, dehydration, pneumonia, vascular problems, and pressure ulcers.
❑ In fulminant hepatitis, maintain electrolyte balance and a patent airway, prevent infections, and control bleeding. Correct hypoglycemia and other complications while awaiting liver regeneration and repair.
❑ Before discharge, emphasize the importance of having regular medical checkups for at least 1 year. The patient will have an increased risk of developing hepatoma. Warn the patient against using alcohol or over-the-counter drugs during this period. Teach him to recognize the signs of a recurrence.
❑ Inform the patient about the availability of support groups for people with all types of hepatitis and provide contact information if he’s interested.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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