Hepatitis, viral
Hepatitis, viral: Excerpt from Handbook of Diseases
A fairly common systemic disease, viral hepatitis is marked by hepatocellular destruction, necrosis, and autolysis, leading to anorexia, jaundice, and hepatomegaly. In most patients, hepatic cells eventually regenerate with little or no residual damage. Advanced age and serious underlying disorders make complications more likely. The prognosis is poor if edema and end-stage liver disease develop.
There are six types of hepatitis:
❑ Type A (infectious or short-incubation hepatitis) is rising among homosexuals and in people with immunosuppression related to human immunodeficiency virus (HIV) infection. It’s usually self-limiting and without a chronic form. About 40% of cases in the United States result from hepatitis A virus.
❑ Type B (serum or long-incubation hepatitis) is also increasing among HIV-positive individuals.
Clinical tip Hepatitis B is considered a sexually transmitted disease because of its high incidence and rate of transmission by this route.
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. Acute signs and symptoms usually begin insidiously and last for 1 to 4 weeks. Urticaria or arthralgia that’s experienced before any signs of jaundice is highly suggestive of hepatitis B infection. A chronic, potentially infectious state develops in about 10% of infected adults and in 70% to 90% of infected infants. This chronic state is associated with progressive liver disease in some individuals. Fulminant hepatitis can ensue, and there’s an increased risk of primary hepatocellular carcinoma.
❑ Type C accounts for about 20% of all viral hepatitis cases and is primarily transmitted through blood and body fluids or obtained during tattooing.
❑ 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 hepatitis is confined to people who are frequently exposed to blood and blood products, such as I.V. drug users and hemophiliacs. It’s transmitted parenterally and, less commonly, sexually.
❑ Type E (formerly grouped with type C under the name non-A, non-B hepatitis) occurs primarily in people 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.
❑ Type G is a newly discovered form of hepatitis. Transmission is by the blood-borne route, and it more commonly occurs in those who receive blood transfusions.
Causes
The major forms of viral hepatitis result from infection with the causative viruses: A, B, C, D, E, or G.
Type A hepatitis
Hepatitis A is highly contagious and usually transmitted by the fecal-oral route. It may also be transmitted parenterally.
Clinical tip I.V. drug abusers and recipients of multiple blood product transfusions are at increased risk for hepatitis A.
Hepatitis A usually results from ingestion of contaminated food, milk, or water. Outbreaks of this type are commonly traced to ingestion of seafood from polluted water.
Type B hepatitis
Once thought to be transmitted only by the direct exchange of contaminated blood, hepatitis B is now also known to be transmitted by contact with human secretions and stool passed by health care workers, recipients of plasma-derived products, and hemodialysis patients. As a result, nurses, physicians, laboratory technicians, and dentists are frequently exposed to type B hepatitis, commonly as a result of wearing defective gloves.
Transmission also occurs during intimate sexual contact and through perinatal transmission.
Type C hepatitis
Although hepatitis C 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 and receiving tattoos.
Clinical tip Most patients with hepatitis C are asymptomatic. Hepatitis C virus is associated with a high rate of chronic liver disease (chronic hepatitis, cirrhosis, and an increased risk of hepatocellular carcinoma), which develops in 50% to 80% of those infected. People who have chronic hepatitis C are considered infectious.
Type D hepatitis
Hepatitis D is found only in patients with an acute or a 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, a type D infection can’t outlast a type B infection.
Hepatitis D is rare in the United States, except in I.V. drug abusers.
Type E hepatitis
Hepatitis E is transmitted enterically (oral-fecal and waterborne routes), much like type A. Because this virus is inconsistently shed in feces, detection is difficult.
Type G hepatitis
Hepatitis G, a newly identified virus, is transmitted by the blood-borne route, similar to hepatitis C.
Signs and symptoms
Assessment findings are similar for the different types of hepatitis. Typically, signs and symptoms progress in three stages — prodromal (preicteric), clinical (icteric), and recovery (posticteric).
Prodromal stage
In the prodromal stage, the patient typically complains of easy fatigue, 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 vital signs may reveal a temperature of 100° to 102° F (37.8° to 38.9° C). As the prodromal stage draws to a close, 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.
Clinical jaundice stage
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 can’t remove bilirubin from the blood, but it 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, and 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.
Recovery stage
During the recovery stage, most of the patient’s symptoms decrease or subside. On palpation, a decrease in liver enlargement may be noted. The recovery stage commonly lasts from 2 to 12 weeks, although sometimes this stage lasts longer in patients with hepatitis B, C, or E.
Diagnosis
In suspected viral hepatitis, a hepatitis profile is routinely performed. This study identifies antibodies specific to the causative virus, establishing the type of hepatitis as follows:
❑ 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: The 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) 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; the diagnosis may also be determined by ruling out hepatitis C.
❑ Type G: Detection of hepatitis G antigen supports diagnosis; the patient may be otherwise symptomless.
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 (PT) 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. (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 alfa-2b and the more recently FDA-approved peginterferon alfa-2a. Instead, the patient is advised to rest in the early stages of the illness and to combat anorexia by eating small, high-protein meals.
Clinical tip The largest meal should be eaten in the morning because nausea tends to intensify as the day progresses.
Protein intake should be reduced if signs of precoma — lethargy, confusion, and mental changes — develop.
In acute viral hepatitis, hospitalization is usually required only for patients with severe symptoms (severe nausea, vomiting, change in mental status, and PT greater than 3 seconds above normal) or complications. Parenteral nutrition may be required if the patient experiences persistent vomiting and can’t maintain oral intake.
Antiemetics (diphenhydramine or prochlorperazine) 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
❑ Before the patient is discharged, discuss restrictions and how to prevent a recurrence of hepatitis. (See Preventing a recurrence of hepatitis.)
❑ Enteric precautions are used when caring for patients with type A or E hepatitis. Practice standard precautions for all patients.
❑ Stress the importance of thorough hand washing.
❑ Inform visitors about isolation precautions.
❑ Provide rest periods throughout the day. Schedule treatments and tests so the patient can rest between bouts of activity.
❑ Because inactivity may make the patient anxious, include diversional activities as part of his care. Gradually add activities as the patient begins to recover.
❑ Encourage the patient to eat. Provide small, frequent meals. Minimize medications.
❑ Force fluids (at least 4,000 ml/day). Encourage the anorectic patient to drink fruit juices. Also offer ice chips and effervescent soft drinks to maintain hydration without inducing vomiting.
❑ Administer supplemental vitamins and commercial feedings. If symptoms are severe and the patient can’t tolerate oral intake, provide parenteral nutrition and hydration.
❑ Monitor the patient’s weight daily, and record intake and output. 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 any other complications while awaiting liver regeneration and repair.
Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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