hepatitis
(hep‵ă-tīt'ĭs 
)
[hepato- + -itis]
Inflammation of the liver, usually caused by exposure to an infectious agent (such as a hepatitis virus), a toxin (such as alcohol), or a drug (such as acetaminophen). The illness may be mild or life-threatening, chronic or acute. Chronic cases may be detected only by the discovery of elevated liver enzymes in the blood. Acute cases are marked by jaundice, hepatic enlargement, occasional bleeding, altered mental status, and multiple organ system failure. Usually, a history of any type of hepatitis (esp. after age 10), is a contraindication to being a blood donor.
Pathology: Damage to liver cells is caused by direct injury from the causative agent or indirectly as a result of inflammatory or autoimmune responses. During acute inflammation, the swollen hepatocytes are less able to detoxify drugs; to produce clotting factors, cholesterol, plasma proteins, bile, and glycogen; to store fat-soluble vitamins; or to perform other functions. All hepatitis viruses may cause fulminant hepatitis, but hepatitis B and D are the most common causes. Drug overdoses, ingestion of toxins, and shock are also responsible for rapid liver deterioration.
Patient Care: Patients are not generally hospitalized unless they experience significant liver damage or complications; the more severely affected patients need supportive medical and psychological care. Patients at home should be instructed about the nature and course of the illness, its care and treatment, and signs and symptoms of complications. When hepatitis is food-borne, thorough hand washing, safe food hand ling, and thorough cleaning of dishes and silverware are necessary to prevent transmission to other members of the household. The patient should avoid intimate contact with others until antigen and antibody levels are reduced. The patient is advised to schedule frequent rest periods and to rest between major activities. Diversionary activities should be included to help reduce anxiety. Good nutrition is encouraged (small, frequent, high-calorie, low-protein, nutrient-dense meals and fluids to 4 qt (4 L)/day). Fluid intake and output, and weight, color, consistency, and frequency of stools should be recorded. The hospitalized patient is assessed for complications (hepatic coma, pneumonia, vascular problems, and pressure ulcers) and is advised to avoid alcohol during the period of acute illness and for at least 6 months after recovery. Depression may occur because of the patient’s concerns about the illness, but the depression may also be linked to changes in body chemistry or adverse drug reactions. Hepatitis is the primary reason for liver transplants, and the concerns of potential need and treatment should be explained to the patient. Emotional support and reassurance should be offered because there may be considerable interference with the patient's habits and lifestyle.
SEE: Stand ard Precautions Appendix; hepatitis A; autoimmune hepatitis; hepatitis E; fulminant hepatitis.
SEE: Nursing Diagnoses Appendix.
h. A Hepatitis caused by hepatitis A virus (HAV), an RNA virus without an envelope. Hepatitis A was formerly called infectious hepatitis, which is still in use.
Approx. 90,000 people are infected every year, about half of whom develop clinically obvious signs and symptoms.
Because hepatitis A can be contracted through contaminated water or food, young adults and children in institutional settings and travelers in areas with minimal sanitation are at greatest risk for infection; small epidemics have been seen among people eating at restaurants that served contaminated shellfish.
Patients frequently experience anorexia, nausea, malaise, joint pains, fever, or jaundice. The course of the illness is usually mild although it can be severe; the incubation period is 2 to 6 weeks, the acute stage lasts 2 to 12 weeks, and complete recovery takes weeks to months.
Hepatitis A does not produce a carrier state and does not cause chronic hepatitis. The two antibodies produced in response to hepatitis A antigen serve as markers for infection; one of these, IgG anti-HAV, provides immunity against reinfection.
No drugs specifically treat hepatitis A. Immune globulin containing IgG anti-HAV antibodies may be prescribed for family members; it provides passive immunity for 6 to 8 weeks. Preventive education focuses on good personal hygiene, esp. washing of the hand s; use of good judgment in choice of food and eating places, and , in some areas of the world, basic sanitation. Hepatitis A vaccine prevents infection either before or immediately after exposure to the virus and is recommended for health care workers, travelers to developing countries, day care workers, people with liver disease, and others at high risk.
Hepatitis A is transmitted by fecal-oral contact. To prevent the spread of the disease, those infected should not be involved in food preparation.acute anicteric h.Hepatitis marked by a slight fever, gastrointestinal upset, and anorexia but without jaundice.
alcoholic h.Hepatitis marked by the destruction of large numbers of hepatocytes due to excessive ingestion of alcohol. Fever, jaundice, altered mental status, and enlargement of the liver are common findings. It can be treated with abstinence, corticosteroids, pentoxifylline, and supportive therapy.
amebic h.A syndrome marked by a tender, enlarged liver; pain over the liver; fever; and leukocytosis in a patient with amebic colitis. This term is inaccurate because the liver changes are not due to an infestation of that organ with amebae but are a part of the nonspecific reaction to the infection in the intestinal tract. Nevertheless, a liver abscess will occasionally develop, and the walls of the abscess will contain amebae.
Metronidazole plus iodoquinol, or chloroquine phosphate plus either emetine or dehydroemetine are used to treat amebic hepatitis. These latter two drugs are toxic and should be given only if their course can be carefully observed with a cardiac monitor. The drugs should not be given to a patient who has cardiac disease or is pregnant. Needle aspiration of the abscess may be required.
autoimmune h.Persistent hepatitis and hepatic necrosis in the presence of hypergammaglobulinemia and autoantibodies and in the absence of other common causes of liver injury. The disease is more common in women than in men; it is associated with HLA-DR3 and -DR4 major histocompatibility antigens. It responds to immunosuppressive drug therapy.
h. B Hepatitis caused by hepatitis B virus (HBV), a double-strand ed DNA virus. It may appear as an asymptomatic, acute, chronic, or fulminant infection. Acute infection often is marked by jaundice, nausea and vomiting, joint pains, rashes, and marked elevations in serum liver function tests. Chronic infection typically is asymptomatic and may be detected only by blood tests until it causes late complications (cirrhosis, portal hypertension, or hepatocellular carcinoma). Fulminant hepatitis B infection occurs when the patient suffers hepatic encephalopathy within 8 weeks of the onset of the disease.
The virus is transmitted by exposure to the blood or bodily fluids of an infected person. The incubation period is approx. 2 to 6 months. Acute infection usually resolves in less than 6 months. When HBV surface antigen does not clear from the blood within 6 months, chronic hepatitis is said to have developed. Each year in the U.S., about 300,000 people are infected with HBV. Worldwide, chronic hepatitis affects about 300 million people.
Those at greatest risk for infection include intravenous drug abusers, people with multiple sex partners, men who have sex with men, infants born of HBV-infected mothers, and health care workers. Blood banks now routinely screen for HBV antigens, which has greatly reduced the transmission of infection by transfusion.
Patients who are hepatitis B surface antigen or hepatitis B core antigen positive should not be treated with rituximab or ofatumumab. These monoclonal antibody therapies can cause fatal reactivation of hepatitis B infection.The primary antigenic markers used to diagnose hepatitis B infection include 1) hepatitis B surface antigen (HBsAg), the first marker to appear in the blood and is sometimes detected before serum levels of hepatic enzymes rise; 2) hepatitis Be antigen (HBeAg) and hepatitis B DNA, markers of active viral replication and high infectivity; and 3) hepatitis B core antibodies (antibodies against the core antigen of hepatitis B), which indicate infection of a patient with HBV. IgM antibodies against the core antigen (IgM anti-HBc) are present early in the course of infection and may sometimes be the only detectable evidence of an acute infection. IgG antibodies against the core antigen (anti-HBc) are present in any patient infected with the virus, either acutely or at some time in the past.
Protective IgG antibodies to the HB surface antigen (HBsAB), which develop late in the disease, persist for life and protect against reinfection. As hepatitis B surface antibody levels rise, HBsAg levels fall, indicating resolution of acute infection. Antibodies against hepatitis B core antigen and hepatitis Be antigen are not protective. Approx. 5% to 10% of patients develop chronic infection.
Hepatitis B vaccine, which contains the HB surface antigen, provides active immunity and is recommended for those at increased risk (children, health care workers, hemodialysis patients, intravenous drug abusers). All pregnant women should be screened for infection. Hepatitis B immune globulin, which contains antibodies against HBV, provides passive immunity to those who have not been vaccinated and are exposed to the virus.
Drug therapies, including pegylated interferon (given for 48 weeks) and either nucleoside or nucleotide analogues (which block viral DNA synthesis) can suppress hepatitis B viral replication if given continuously for years. Commonly used antiviral drugs include entcavir, tenofovir, and lamivudine.
ABBR: HCV
A chronic blood-borne hepatitis believed to affect roughly 3,200,000 people in the U.S. It was formerly known as non-A, non-B hepatitis.About 20,000 to 40,000 new cases occur each year in the U.S., most of which result from needle sharing during intravenous drug abuse. A smaller number of infections are acquired as a result of exposure to tainted blood at work, e.g., in health care. About 6% of cases are the result of the transmission of the virus from mother to child during childbirth. Tattooing, body piercing, and cocaine snorting are associated with some cases. Sexual transmission of the virus is rare. Long-term infection develops in 55% to 85% of those infected, and 5% to 20% develop cirrhosis over 20 to 30 years. The disease is identified more often in people born between 1945 and 1965 than in any other age group. Chronic hepatitis C infection has become the preeminent cause of cirrhosis, liver cancer, and death from liver failure in the U.S.
HCV is caused by a single-strand ed RNA virus transmitted from person to person by exposure to blood or body fluids. In the past it was the most common form of hepatitis transmitted by transfusions of blood or blood products and by organ transplantation.
Signs and symptoms of acute infection are often milder than those of hepatitis A and B. They may include nausea, malaise, fevers, or jaundice, or the disease may not be recognized.
Infection with HCV is usually identified years after exposure when an asymptomatic person is found to have repeatedly elevated liver enzymes on routine blood tests. Antibodies to HCV or HCV RNA in the blood confirm the infection. Antibody production is stimulated by HCV RNA, but antibodies against HCV do not destroy the virus or provide immunity. Patients who are antibody positive typically undergo additional testing, including assessments of their viral load (the concentration of HCV per mL of blood), HIV status, and genotype. Genotype determination is used to guide therapy, since some genotypes of HCV are more susceptible to treatment than others.
Prevention of hepatitis C in health care professionals stresses using safely engineered sharps, providing safe sharps disposal, limiting contact with blood and body fluids, and properly sterilizing instruments. Public health teaching regarding prevention for the general public includes use of properly sterilized instruments for body piercing and single-use needles for tattooing, avoidance of sharing needles, and taking advantage of needle-replacement programs (for injection drug users). Maternal-to-child transmission during childbirth occurs commonly, but neither cesarean delivery nor avoiding breast-feeding prevents vertical transmission of HCV from mother to child.
The United States Preventive Services Task Force recommends that all people born in the U.S. between 1945 and 1965 be screened for infection with hepatitis C virus.
A variety of antiviral agents can be used to treat HCV infection. Antiviral agents such as pegylated alpha interferon in combination with ribavirin can be used alone to treat hepatitis C genotypes 2 and 3. Treatment eradicates the virus in about two thirds or more of cases. Direct-acting antiviral agents, such as telaprevir, boceprevir, or sofosbuvir, may cure hepatitis C genotypes 1, 4, 5, or 6 if given in combination for prolonged courses (usually 48 weeks). The treatment can cause significant side effects, including high fevers, chills, malaise, muscle aches, and other flulike symptoms; it also causes decreases in white blood cell and platelet counts.
Health care providers can provide invaluable education to affected patients by giving them written and verbal information on high-risk behavior, including the need to avoid needle sharing by users of intravenous drugs, having unprotected sex, snorting drugs, or drinking alcohol. Regular consumption of alcohol increases the risk of liver cancer dramatically for a person with HCV. Other recommendations for people infected with hepatitis C include not to donate blood, blood products, tissue, or semen; to avoid sharing cosmetic items or personal grooming items that may be contaminated by blood, e.g., toothbrushes or razors; not to use over-the-counter, herbal, or prescription medications unless they have been approved by a knowledgeable health care provider; and to be vaccinated against hepatitis A and B in order to avoid additional viral insults to the liver. Community support groups and Internet-based resources may help those infected to learn more about disease management, e.g., www.liverfoundation.org. Regular professional care may help optimize health and well-being.
chronic h.Hepatic inflammatory and necrotic changes that continue for more than 6 months. The most common causes are hepatitis B, C, and D viruses. Chronic liver inflammation may also result from abuse of alcohol or other drugs, exposure to toxic chemicals, fatty infiltration of the liver, or autoimmune processes. Patients may be asymptomatic or present with only elevated serum transaminase levels, fatigue, anorexia, malaise, or mild jaundice. In other patients, the disease actively progresses, eventually leading to cirrhosis and death. Depending on the underlying cause, corticosteroids, interferons, or antiviral agents may be used to manage chronic hepatitis. In alcoholic patients, abstinence from alcohol may allow the liver to heal.
h. D Hepatitis caused by the hepatitis delta virus (HDV). It is considered a defective virus because it can produce infection only when hepatitis B virus (HBV) is present and therefore can be prevented through hepatitis B vaccination. It is rare in the U.S. In healthy people, coinfection with HDV and HBV usually causes acute disease and recovery with immunity. In patients with chronic hepatitis B, it may produce severe acute disease or, more commonly, chronic progressive disease that may lead to cirrhosis. Mortality is approx. 10%. Hepatitis D antigens (HDV RNA) are found in the blood and liver and stimulate production of an antibody that is present only briefly during early acute infection.
SEE: hepatitis B.
Because hepatitis D only occurs in people already infected with hepatitis B, vaccination against hepatitis B helps prevent the spread of this virus.
h. E A form of hepatitis similar to hepatitis A, occurring primarily in regions with contaminated water supplies or in travelers returning from abroad. It is caused by an RNA virus that produces acute infection only.
fulminant h.Acute liver failure.
ABBR: IH
SEE: hepatitis A.
interface h.Hepatitis in which lymphocytes and plasma cells disrupt the border between hepatic portals and the parenchyma of the liver. SYN: piecemeal hepatitis.
ischemic h.Acute, severe hepatitis that results from an episode of hypotension, typically in someone with underlying heart or lung disease. This type of hepatitis may result in bleeding, encephalopathy, coma, or death.SYN: acute ischemic hepatocellular injury; hypoxic hepatitis.
Lábrea h.Santa Marta hepatitis.
SEE: hepatitis C.
piecemeal h.Interface hepatitis.
rapidly recurrent cholestatic h. C
Variant: recurrent cholestatic hepatitis
Hepatitis C infection occurring in a patient's transplanted liver shortly after organ transplantation. The disease causes early damage to the grafted organ and carries a poor prognosis.Santa Marta h.Fulminant hepatitis due to coinfection with hepatitis B and hepatitis D. SYN: Lábrea hepatitis.
serum h.A term formerly used for HBV infection.
toxic h.Hepatitis caused by the ingestion or absorption of toxins or drugs into the body. Included in the great number of agents known to cause this type of hepatitis are common drugs and chemicals (such as halothane, isoniazid, anabolic steroids, carbon tetrachloride, trichlorethylene) used in either the treatment of disease or in the workplace.