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An Overview of Viral Hepatitis: A Through E
MAY 1994, VOL 59, NO 5
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An Overview of Viral Hepatitis A THROUGH E Phyllis Lisanti, RN; Dorothy Talotta, RN
H
epatitis refers to inflammation and injury of the liver. It is a response by the liver to viruses, bacteria, drugs, toxic substances, and infections. Viral hepatitis is an acute inflammatory disease caused by several different strains of viruses. In viral hepatitis, the hepatocytes (ie, epithelial cells of the liver) are damaged either directly (as in hepatitis D virus [HDV]) or by the body’s immune response to the viruses; in either case, there is altered cellular function. The extent of inflammation and necrosis will depend on the individual’s direct or immune response to the virus.
Pathology
T
h e degree of functional impairment depends on the amount of hepatocellular damage. The hepatitis viruses invade the liver, replicate, and damage the liver regardless of the route of transmission. Liver damage includes inflammation and mononuclear cell infiltration in the parenchyma and portal ducts, hepatic cell necrosis, increases in the size and
Phyllis Lisanti, RN, PhD, is an undergraduate program director and clinical assistant professor, division of nursing, New York University, New York City. She earned her bachelor of science degree in nursing from the University of Pennsylvania, Philadelphia; her master of science degree in nursing from City University of New York, New York City; and her doctorate of philosophy in research and theory development
number of Kupffer cells, and cellular collapse. The accumulation of necrotic tissue in the lobules and ducts results in architectural changes in the liver. The overall effect of the infection influences bilirubin excretion and all liver functions. Symptoms of viral hepatitis are systemic and may vary from patient to patient according to the severity of the infection (Table 1). Five distinct hepatitis viruses have been identified and account for the majority of cases of viral hepatitis in this country.’ All nurses who come in contact with blood and body secretions need to be aware of the transmission modes of these viruses and how to protect themselves from exposure. The hepatitis A virus (HAV) and hepatitis B virus (HBV) have been recognized for many years. The diseases caused by these viruses were known in the past as “infectious” and “serum” hepatitis, respectively. Together, HAV and HBV account for approximately 70% of cases of acute viral hepatitis in the United States (30% of cases due to HAV; 40% to HBV).* More recently, portions of the viruses
from New York University, New York City.
Dorothy Talotta, RN, EdD, is an associate professor, College of New Rochelle (NY) School of Nursing. She earned her bachelor of science and master of science degrees in nursing from City University of New York, New York City, and her doctorate of education in nursing education from Teachers College, New York City. 997
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Table 1
Common Manifestations, Pathophysiologic Bases Pathophysiologic base
Manifestation jaundice, clay-colored stools
0
dark urine. increased serum bilirubin
urobilin in blood excreted through kidneys instead of bowel
abdominal pain
stretching of capsule surrounding liver during inflammation
anorexia, nausea, vomiting, diarrhea, constipation
changes in stomach or bowel, alteration in digestion
fatigue, weakness
reduced energy metabolism by liver
fever, flu-like symptoms, myalgias, arthralgia
0
bleeding tendencies
inflammatory process
bile salt accumulation in skin
pruritis 0
decreased prothrombin synthesis and reduced vitamin K absorption
anemia
reduced red blood cell life span due to liver enzyme changes
lethargy, irritability, deterioration of handwriting, asterixis
hepatic encephalopathy indicating worsening of infectious process
responsible for two forms of non-A, non-B hepatitis have been cloned. These viruses are the hepatitis C virus (HCV)and the hepatitis E virus (HEV).The HCV,a portion of which was cloned in 1988, causes a parenterally transmitted non- A, non-B hepatitis that accounts for approximately 20% of hepatitis cases in this country.3 The HEV, a portion of which was cloned in 1990, causes an enterically transmitted non-A, non-B hepatitis. The HEV is not recognized as endemic in the United States, but a few cases have been documented in travelers returning from other c o ~ n t r i e s . ~ The HDV was first identified in 1977 and is 998
impaired conjugated bilirubin excretion
also known as delta hepatitis. The HDV requires the presence of HBV infection. It is highly pathogenic and can confound and intensify the course of HBV i n f e ~ t i o nThe .~ HDV is believed to account for approximately 5% to 10% of hepatitis cases:
Overview of Viruses
E
ach virus has its own characteristics that distinguish it from the others (Table 2). The following is a brief overview of each of the five identified hepatitis viruses. Hepatitis A virus. The HAV is found in the
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Table 2
Characteristics of Etiologic agent
Route/mode of transmission
Incubation period Infectious period
Prevention
Prophylaxis/postexposure treatment Risk factors
Diagnostic tests
Hepatitis A virus (HAV) Single-stranded ribonucleic acid (RNA) virus; virus of the entero virus group (replicates in liver) Fecal-oral route; spread by feces, saliva, contaminated water, household and sexual contacts; parenteral (rare) 14 to 42 days Highest concentration of virus in stool during 2 weeks before onset of symptoms; ends 1 week after symptoms subside No vaccine; universal and enteric precautions; good personal hygiene; clean water supply; clean restaurant workers Postexposure immune globulin within 2 weeks of exposure Close personal contact; handling feces and contaminated articles; eating raw shellfish; working with animals imported from endemic areas Immunoglobulin M antibody to HAV (develops early, lasts 6 to 12 months); immunoglobulin G antibody to HAV (indicates life-
Hepatitis B virus (HBV) Double-stranded deoxyribonucleic acid hepadenovirus Percutaneous/permucosal exposure to blood; sexual contact; HBV can survive on surfaces for 1 week and lead to unknown exposures 28 to 180 days From before symptoms occur; may be life-long if individual becomes chronic carrier Vaccine; universal precautions; control of blood, blood products, skin piercing instruments; good personal hygiene Vaccine and HBV immune globulin therapy for postexposure; interferon alpha-2b for chronic state Health care workers; patients with multiple blood transfusions and dialysis; homosexually active males; morticians; people with tattoos; IV drug users Hepatitis B surface antigen; hepatitis B core antigen positive (and others)
Course of disease
Acute, self-limited; rarely fulminant; chronic form not known
Hepatitis B may be acute with insidious onset; can become chronic; may progress to cirrhosis and/or end-stage liver disease
Prognosis’
Rarely fatal, mortality 0.6%; no carrier state; life-long immunity
Mortality 0.5% to 2.0%; individuals can become immune; high risk of becoming a chronic carrier; chronic HBV associated with liver cancer
Note 1. J M Heeg, D A Coleman, “Hepatitis kills,” RN 55 (April 1992) 60-66.
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Hepatitis Viruses Hepatitis C virus (HCV) Single-stranded RNA virus; little specific information available Parenteral/percutaneous/permucosal exposure to blood and blood products; sexual, personal contact suspected; possible fecal-oral route 14 to 180 days Before onset of symptoms; may persist for lifetime if individual becomes a carrier No vaccine; universal precautions; control of blood, blood products, skin piercing instruments; good personal hygiene Standard immunoglobulin for postexposure; interferon alpha-2b for chronic HCV Same as HBV
Hepatitis D virus (HDV) Defective, incomplete, singlestranded RNA virus that is dependent on HBV for replication Appears as a coinfection or superinfection with hepatitis B; transmitted same as HBV
Fecal-oral route; spread via feces and contaminated water
15 to 64 days Not known
15 to 60 days Not known
Same as HBV
No vaccine; universal and enteric precautions
Hepatitis E virus (HEV) Unenveloped, singlestranded RNA virus
Same as HBV (interferon alpha- No postexposure pro2b trials are under study) phylaxis available Same as HBV
Often seen after natural disaster in developing regions of the world
Antibody to HCV; tests have high false-positive and false-negative results; lack sensitivity and specificity
Antibody to HDV
None available-must rule out all other forms of hepatitis
Insidious onset; 40% to 60% become chronic carriers; 20% of acute HCV may progress to cirrhosis
Acute onset; may resolve without sequelae; may lead to serious fulminant hepatitis; more likely leads to chronic HDV and liver failure Mortality 30% in chronic cases; high risk of chronic liver disease; can become a chronic carrier; immunity to HBV provides immunity to HDV
Acute process; 99% of patients recover uneventfully
Mortality 1% to 2%; high risk for chronic liver disease and chronic carrier state (50% of infected individuals); possible association with liver cancer
Chronic cases not reported; mortality 1% to 2% (10% in pregnant women)
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blood, feces, saliva, and urine of infected individuals, but transmission is primarily by the fecal-oral route. The virus also may be carried by raw shellfish from polluted waters. Transmission of HAV can occur through person-to-person contact or through contaminated food or water. The highest concentration of virus (in the stool) occurs during the two-week period before the onset of jaundice. Because people with HAV are infectious before symptoms appear, they can transmit the disease unknowingly at that time. Transmission of HAV by blood transfusion is rare; however, blood donated during the prodromal phase of the disease, during which the virus is in the blood for a brief period, can contain HAV. It would not be known that the donor was infected because blood is not tested for anti-HAV. Poor personal hygiene, poor sanitation, and intimate contact (eg, household contact, sexual contact) facilitate transmission of HAV, and HAV infection is common in institutional settings. Those living in developing areas of the world are also at higher risk.7 In the United States, there is a higher incidence of HAV antibody in lower socioeconomic groups.8 Nosocomial transmissions to health care workers have occurred among health care workers caring for infected patients who were not diagnosed. Lack of glove use and inadequate hand washing are responsible for these transmissions? Environmental sanitation and hand washing before eating or handling food are effective means of preventing the spread of HAV. Hepatitis B virus. The highest concentration of HBV is in the blood and serous fluids of carriers and acutely infected people. The virus also is present in other body fluids in lower concentrations. Blood and blood products remain the best vehicles for transmission; however, body fluids such as vaginal secretions, semen, and serous fluid also can transmit the virus. The HBV also is present in urine, saliva, and feces in lower concentrations. The virus is stable and can survive for seven days or more in, for example, dried blood on a surface.I0 The HBV is prevalent in people born in highly endemic areas and their descendants. 1002
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People engaging in homosexual activity and IV drug use and those with many sexual partners also have high rates of infection. Prison inmates, people in institutions for the developmentally disabled, people who come into close contact with HBV carriers, people undergoing hemodialysis, and people receiving certain plasma products also are at increased risk." Transmission of HBV to health care workers occurs via puncture injuries, blood contact with mucous membranes (eg, the splashing of bloody fluids into the eyes), and blood contact with skin cuts or other portals of entry. Between 6% and 30% of nonimmunized health care workers who are exposed to HBV through one needle stick and who do not receive postexposure prophylaxis become infected. This is much higher than the risk of acquiring HIV from exposure to infected blood through one needle stick (ie, 0.5%).'* Various tests exist for HBV antibodies, and the US Food and Drug Administration requires testing of the nation's blood supply for the hepatitis B surface antigen (HBsAG). Blood banks began voluntary testing for the antibody to the hepatitis B core antigen in 1986, and they began testing for alanine aminotransferase in 1987. The alanine aminotransferase test is used primarily to determine liver disease and could signal possible hepatitis infection. In spite of screening procedures, HBV accounts for approximately 5% to 10% of posttransfusion hepatitis.13 Hepatitis B also is transmitted perinatally; therefore, the Immunization Practices Advisory Committee of the Centers for Disease Control and Prevention recommends that all pregnant women receive prenatal testing for HBsAG. The committee also recommends a comprehensive strategy to prevent HBV infection that includes universal vaccination of infants and adolescents. l 4 Hepatitis C virus. Worldwide, HCV (ie, parenterally transmitted non-A, non-B hepatitis) is responsible for the majority of bloodbome nonA, non-B hepatitis cases. The HCV is involved in most posttransfusion cases of hepatitis; however, only one in 10 cases of HCV can be traced to blood transfusion.15 One study of
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HCV in the United States indicates that the percentage of people with a history of blood transfusion significantly decreased between 1982 and 1988, while the percentage of people reporting parenteral drug use increased signifi~ant1y.I~ In 1990, tests to detect the HCV antibody were licensed, and blood now is routinely screened for anti-HCV. Tests for anti-HCV will detect only 85% of blood infected with HCV, however, because approximately two-thirds of HCV-infected individuals do not develop the antibody for five to 12 months. Because of this screening, however, parenteral drug users are expected to be identified as those most at risk for hepatitis C.I7 In addition to transfusion recipients and parenteral drug users, dialysis patients are at high risk for hepatitis C.lS Some risk factors for acquiring HCV are frequent contact with blood in the course of health care work, household contact with infected individuals, and personal contact with individuals who have had hepatitis.I9 Further investigation of sexual activity and person-to-person contact in disease transmission is needed. Although health care workers are at risk for HCV infection, the rate at which infection occurs following puncture injuries is not known.20 Hepatitis D virus. All groups at increased risk for hepatitis B are considered at increased risk for infection with HDV.2‘ Because hepatitis D occurs with hepatitis B as either a coinfection or a superinfection, those at high risk for hepatitis B should be vaccinated. Hepatitis E virus. Hepatitis E (ie, enterically transmitted non-A, non-B hepatitis) has occurred in Mexico, West and North Africa, and parts of Asia; however, it is not known whether HEV is present in the United States or Western Europe. The HEV is transmitted by the fecal-oral route, and those who travel to parts of the world where HEV is present may be at risk if they ingest contaminated water or food or if they have close contact with infected individuals. The best means of preventing HEV infection is avoiding water or food that may be contaminated.22
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Perioperative Nursing Care
B
efore surgery, it is important that the perioperative nurse question the patient about his or her history of liver disease, including hepatitis. Nurses who provide care to patients with a history of hepatic dysfunction should be aware of the physiologic alterations-and their implications for nursing care-that may occur secondary to liver disease. Physiologic alterations include changes in glucose homeostasis, protein synthesis, and fat metab0lism.2~ Glucose homeostasis. Glycogenolysis and gluconeogenesis are impaired with resulting hypoglycemia. Because of impaired uptake and release of glucose, there may be an abnormal glucose tolerance curve.24Impairment of glucose homeostasis necessitates continually monitoring the patient for changes in glucose levels. Protein synthesis,fat metabolism. Alterations in protein synthesis affect the production of coagulation factors that result in clotting abnormalities and increase the risk of bleeding.25In situations in which the prothrombin time is prolonged, vitamin K may be ordered.2hThe changes in protein synthesis also may decrease protein binding sites necessary for drug binding. The inability of drugs to bind with protein can lead to elevated drug plasma levels. The nurse should monitor the patient for signs of bleeding and drug toxicity. Alterations in protein synthesis also may lead to hypoalbuminemia, which warrants close observation of the patient’s fluid and electrolyte balance. Careful monitoring is necessary because alterations in fat metabolism may lead to metabolic acid0sis.2~ The patient’s metabolism of drugs also is affected. Drugs that require hepatic metabolism (eg, diazepam, lidocaine, morphine, meperidine) can have a prolonged effect on the patient.** Medications such as chlorpromazine, aspirin, acetaminophen, and many sedatives have the potential to damage the liver and should be administered as infrequently as possible.2y One of the problems of operating on a patient with hepatitis is the risk of disease transmission to health care providers. Health care workers whose tasks involve contact with 1003
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blood or body fluids should be vaccinated against hepatitis B. Health care workers also need to practice universal precautions to protect themselves and to prevent cross contamination.
General Nursing Care ‘ursing care of the hospitalized hepatitis patient includes attention to nutrition, fluid volume, comfort, and rest. Because the patient may suffer from anorexia, frequent small meals are important. The largest meal may be best tolerated in the morning, as anorexia often worsens during the day. A highprotein, high-carbohydrate diet that is moderate in fat allows recovery of liver cells. If the patient has problems digesting or metabolizing fat or protein, the amounts of these nutrients should be decreased. If there is a danger of hepatic encephalopathy, a low-protein diet is indicated to decrease accumulation of serum ammonia. Problems with fat metabolism result from alterations in the production and excretion of bile and could require adjustment of fat intake. Nasogastric feedings, total parenteral nutrition, and IV fluids may be necessary. Pruritis associated with jaundice may cause severe discomfort and altered skin integrity. Maintaining ventilation, using cotton clothing, applying skin emollients, and avoiding alkaline soaps benefit the patient. Patients suffering from acute symptoms require bed rest. If hepatic encephalopathy occurs, the patient requires oral or rectal neomycin to decrease intestinal bacteria that synthesize ammonia. This decreases the patient’s serum ammonia levels. Lactulose may be used to cause ammonia and hydrogen ion coupling. The resultant compound is then excreted in feces. Diarrhea may occur with the use of lactulose, so the nurse monitors the patient’s electrolyte levels during lactulose therapy.
Patient Education
B
efore the patient is discharged, the nurse teaches the patient and his or her family members about the disease and precau-
1004
tions for preventing its spread. The nurse emphasizes follow-up care (eg, liver function tests, serum HBsAg), ample rest, proper nutrition, and avoidance of over-the-counter medications (eg, acetaminophen) and alcohol. For hepatitis A patients, the nurse stresses the importance of thorough hand washing and the need to disinfect articles soiled with feces. Patients infected with HAV must not prepare food for consumption by others while the disease is symptomatic, nor should they share articles such as eating utensils, toothbrushes, or toys.30 Patients in the acute stage of hepatitis B and non-A, non-B hepatitis should avoid sexual activity until they test negative for HBsAg or until their partners receive their complete series of HBV vaccine. People who are carriers of HBV must understand that their blood and bodily secretions are infectious, and people in close contact with HBV carriers should receive HBV vaccine. People with a history of non-A, non-B hepatitis and those who carry the HBV should not donate blood.
Conclusion
T
he perioperative nurse should be aware that there are five identified hepatitis viruses. Each virus presents unique challenges for the perioperative nurse providing patient care; therefore, knowledge of the hepatitis viruses, their modes of transmission, and their pathologies enables nurses to provide quality patient care while protecting themselves, other patients, and other health care workers from the disease. 0 Notes I . A M Kools, “Hepatitis A, B, C, D, and E: Update on testing and treatment,” Postgraduate Medicine 91 (Feb 15, 1992) 109-114. 2. Ibid. 3. Ihid. 4. I b i d ; M M Jackson, D C McPherson, “Hepatitis A through E---current and future trends,” Today’s OR Nurse 13 (October 1991) 7-12. 5 . J H Hoofnagle, “Type D (delta) hepatitis,” Journal of the American Medical Association 261 (March 3, 1989) 1321-1325.
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6. Kools, “Hepatitis A, B, C, D, and E: Update on testing and treatment,” 109-114. 7. I D Gust, “The epidemiology of viral hepatitis,” in Viral Hepatitis and Liver Disease, ed G N Vyas, J L Dienstag, J H Hoofnagle (Orlando, Fla: Grune & Stratton, 1984) 415-421. 8. J L Dienstag et al, “Hepatitis A virus infection: New insights from seroepidemiologic studies,” The Journal of Infectious Diseases 137 (March 1978) 328-340. 9. Jackson, McPherson, “Hepatitis A through E 4 u r r e n t and future trends,” 7-12. 10. J M Heeg, D A Coleman, “Hepatitis kills,” RN 55 (April 1992) 60-66. 11. Centers for Disease Control and Prevention, “Protection against viral hepatitis: Recommendations of the Immunization Practices Advisory Committee,” Morbidity and Mortality Weekly Report 39 (RR-2) (Feb 9, 1990) 1-26. 12. Centers for Disease Control and Prevention, Guidelines for Prevention of Transmission of Human Immunodeficiency Virus and Hepatitis B Virus to Health-Care and Public-Safety Workers, pub1 no 89107 (Atlanta: US Department of Health and Human Services, 1989). 13. E Rubin, J L Farber, eds, Essential Pathology (Philadelphia: J B Lippincott Co, 1990) 404,406. 14. Centers for Disease Control and Prevention, “Hepatitis B virus: A comprehensive strategy for eliminating transmission in the United States through universal childhood vaccination: Recommendations of the Immunization Practices Committee,” Morbidity and Mortality Weekly Report 40 (RR-13) (NOV22, 1991) 1-25. 15. Heeg, Coleman, “Hepatitis kills,” 60-66. 16. M J Alter et al, “Risk factors for acute non-A, non-B hepatitis in the United States and association with hepatitis C virus infection,” Journal of the American Medical Association 264 (Nov 7, 1990) 223 1-2235. 17. Jackson, McPherson, “Hepatitis A through E 4 u r r e n t and future trends,” 7-12. 18. Alter et al, “Risk factors for acute non-A, nonB hepatitis in the United States and association with hepatitis C virus infection,” 223 1-2235. 19. Centers for Disease Control and Prevention, “Protection against viral hepatitis: Recommendations of the Immunization Practices Advisory Committee,’’ 1-26. 20. Jackson, McPherson, “Hepatitis A through E-current and future trends,” 7-12. 21. L Lettau et al, “Nosocomial transmission of delta hepatitis,” Annals of Internal Medicine 104 (May 1986) 631-635. 22. Centers for Disease Control and Prevention, “Protection against viral hepatitis: Recommendations of the Immunization Practices Advisory Committee.” 1-26.
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23. K Litwack, Post Anesthesia Care Nursing (St Louis: Mosby-Year Book, Inc, 1991). 24. C M Porth, Pathophysiology: Concepts of Altered Health States, third ed (Philadelphia: J B Lippincott Co, 1990) 724. 25. Litwack, Post Anesthesia Care Nursing. 26. S W Ames, C R Kneisl, Essentials of Adult Health Nursing (Menlo Park, Calif Addison-Wesley Publishing Co, 1988). 27. Litwack, Post Anesthesia Care Nursing. 28. Ibid. 29. Luckmann and Sorensen’s Medical-Surgical Nursing: A Psyc hophysiologic Approach, fourth ed, J M Black, E MatassarkJacobs, eds (Philadelphia: W B Saunders Co, 1993). 30. Clinical Nursing, third ed, J M Thompson et al, eds (St Louis: Mosby-Year Book, Inc, 1993).
Suggested reading Centers for Disease Control and Prevention. “Public health service inter-agency guidelines for screening donors of blood, plasma, organs, tissues, and semen for evidence of hepatitis B and hepatitis C.” Morbidity and Mortality Weelky Report 40 (RR-4) (April 19, 1991) 1-17. Choo, Q L, et al. “Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome.” Science 244 (April 21, 1989) 359-362. Cottone, J A. “Recent developments in hepatitis: New virus, vaccine, and dosage recornmendations.” Journal of the American Dental Association 120 (May 1990) 501-508. Lemon, S M. “Type A viral hepatitis: New developments in an old disease.” The New England Journal of Medicine 313 (Oct 24, 1985) 10591067. Meeker, M H; Rothcock, J C. Alexander’s Care of the Patient in Surgery, ninth ed. St Louis: Mosby-Year Book, Inc, 1991. Reece, S M. “Immunization strategies for the elimination of hepatitis B.” Nurse Practitioner 18 (February 1993) 42-45,49-50. Reyes, G R, et al. “Isolation of a cDNA clone from the virus responsible for enterically transmitted non-A, non-B hepatitis.” Science 247 (March 16, 1990) 1335-1339. Rizzetto, M, et al. “Immunofluorescence detection of new antigen-antibody system (deltdanti-delta) associated to hepatitis B virus in liver and in serum of HBsAg carriers.” Gut 18 (December 1977) 997-1003. Robinson, W E. “Biology of human hepatitis viruses,” in Hepatology: A Textbook of Liver Disease, ed D Zakim, T D Boyer. Philadelphia: W B Saunders Co, 1990. Sarver, D K. “Hepatitis in clinical practice. 1. Hepatitis A and B.” Postgraduate Medicine 79 (March 1986) 194-200, 209-214. 1005
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An Overview of Viral Hepatitis A THROUGH E Phyllis Lisanti, RN; Dorothy Talotta, RN
H
epatitis refers to inflammation and injury of the liver. It is a response by the liver to viruses, bacteria, drugs, toxic substances, and infections. Viral hepatitis is an acute inflammatory disease caused by several different strains of viruses. In viral hepatitis, the hepatocytes (ie, epithelial cells of the liver) are damaged either directly (as in hepatitis D virus [HDV]) or by the body’s immune response to the viruses; in either case, there is altered cellular function. The extent of inflammation and necrosis will depend on the individual’s direct or immune response to the virus.
Pathology
T
h e degree of functional impairment depends on the amount of hepatocellular damage. The hepatitis viruses invade the liver, replicate, and damage the liver regardless of the route of transmission. Liver damage includes inflammation and mononuclear cell infiltration in the parenchyma and portal ducts, hepatic cell necrosis, increases in the size and
Phyllis Lisanti, RN, PhD, is an undergraduate program director and clinical assistant professor, division of nursing, New York University, New York City. She earned her bachelor of science degree in nursing from the University of Pennsylvania, Philadelphia; her master of science degree in nursing from City University of New York, New York City; and her doctorate of philosophy in research and theory development
number of Kupffer cells, and cellular collapse. The accumulation of necrotic tissue in the lobules and ducts results in architectural changes in the liver. The overall effect of the infection influences bilirubin excretion and all liver functions. Symptoms of viral hepatitis are systemic and may vary from patient to patient according to the severity of the infection (Table 1). Five distinct hepatitis viruses have been identified and account for the majority of cases of viral hepatitis in this country.’ All nurses who come in contact with blood and body secretions need to be aware of the transmission modes of these viruses and how to protect themselves from exposure. The hepatitis A virus (HAV) and hepatitis B virus (HBV) have been recognized for many years. The diseases caused by these viruses were known in the past as “infectious” and “serum” hepatitis, respectively. Together, HAV and HBV account for approximately 70% of cases of acute viral hepatitis in the United States (30% of cases due to HAV; 40% to HBV).* More recently, portions of the viruses
from New York University, New York City.
Dorothy Talotta, RN, EdD, is an associate professor, College of New Rochelle (NY) School of Nursing. She earned her bachelor of science and master of science degrees in nursing from City University of New York, New York City, and her doctorate of education in nursing education from Teachers College, New York City. 997
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Table 1
Common Manifestations, Pathophysiologic Bases Pathophysiologic base
Manifestation jaundice, clay-colored stools
0
dark urine. increased serum bilirubin
urobilin in blood excreted through kidneys instead of bowel
abdominal pain
stretching of capsule surrounding liver during inflammation
anorexia, nausea, vomiting, diarrhea, constipation
changes in stomach or bowel, alteration in digestion
fatigue, weakness
reduced energy metabolism by liver
fever, flu-like symptoms, myalgias, arthralgia
0
bleeding tendencies
inflammatory process
bile salt accumulation in skin
pruritis 0
decreased prothrombin synthesis and reduced vitamin K absorption
anemia
reduced red blood cell life span due to liver enzyme changes
lethargy, irritability, deterioration of handwriting, asterixis
hepatic encephalopathy indicating worsening of infectious process
responsible for two forms of non-A, non-B hepatitis have been cloned. These viruses are the hepatitis C virus (HCV)and the hepatitis E virus (HEV).The HCV,a portion of which was cloned in 1988, causes a parenterally transmitted non- A, non-B hepatitis that accounts for approximately 20% of hepatitis cases in this country.3 The HEV, a portion of which was cloned in 1990, causes an enterically transmitted non-A, non-B hepatitis. The HEV is not recognized as endemic in the United States, but a few cases have been documented in travelers returning from other c o ~ n t r i e s . ~ The HDV was first identified in 1977 and is 998
impaired conjugated bilirubin excretion
also known as delta hepatitis. The HDV requires the presence of HBV infection. It is highly pathogenic and can confound and intensify the course of HBV i n f e ~ t i o nThe .~ HDV is believed to account for approximately 5% to 10% of hepatitis cases:
Overview of Viruses
E
ach virus has its own characteristics that distinguish it from the others (Table 2). The following is a brief overview of each of the five identified hepatitis viruses. Hepatitis A virus. The HAV is found in the
MAY 1994, VOL 59, NO 5
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Table 2
Characteristics of Etiologic agent
Route/mode of transmission
Incubation period Infectious period
Prevention
Prophylaxis/postexposure treatment Risk factors
Diagnostic tests
Hepatitis A virus (HAV) Single-stranded ribonucleic acid (RNA) virus; virus of the entero virus group (replicates in liver) Fecal-oral route; spread by feces, saliva, contaminated water, household and sexual contacts; parenteral (rare) 14 to 42 days Highest concentration of virus in stool during 2 weeks before onset of symptoms; ends 1 week after symptoms subside No vaccine; universal and enteric precautions; good personal hygiene; clean water supply; clean restaurant workers Postexposure immune globulin within 2 weeks of exposure Close personal contact; handling feces and contaminated articles; eating raw shellfish; working with animals imported from endemic areas Immunoglobulin M antibody to HAV (develops early, lasts 6 to 12 months); immunoglobulin G antibody to HAV (indicates life-
Hepatitis B virus (HBV) Double-stranded deoxyribonucleic acid hepadenovirus Percutaneous/permucosal exposure to blood; sexual contact; HBV can survive on surfaces for 1 week and lead to unknown exposures 28 to 180 days From before symptoms occur; may be life-long if individual becomes chronic carrier Vaccine; universal precautions; control of blood, blood products, skin piercing instruments; good personal hygiene Vaccine and HBV immune globulin therapy for postexposure; interferon alpha-2b for chronic state Health care workers; patients with multiple blood transfusions and dialysis; homosexually active males; morticians; people with tattoos; IV drug users Hepatitis B surface antigen; hepatitis B core antigen positive (and others)
Course of disease
Acute, self-limited; rarely fulminant; chronic form not known
Hepatitis B may be acute with insidious onset; can become chronic; may progress to cirrhosis and/or end-stage liver disease
Prognosis’
Rarely fatal, mortality 0.6%; no carrier state; life-long immunity
Mortality 0.5% to 2.0%; individuals can become immune; high risk of becoming a chronic carrier; chronic HBV associated with liver cancer
Note 1. J M Heeg, D A Coleman, “Hepatitis kills,” RN 55 (April 1992) 60-66.
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Hepatitis Viruses Hepatitis C virus (HCV) Single-stranded RNA virus; little specific information available Parenteral/percutaneous/permucosal exposure to blood and blood products; sexual, personal contact suspected; possible fecal-oral route 14 to 180 days Before onset of symptoms; may persist for lifetime if individual becomes a carrier No vaccine; universal precautions; control of blood, blood products, skin piercing instruments; good personal hygiene Standard immunoglobulin for postexposure; interferon alpha-2b for chronic HCV Same as HBV
Hepatitis D virus (HDV) Defective, incomplete, singlestranded RNA virus that is dependent on HBV for replication Appears as a coinfection or superinfection with hepatitis B; transmitted same as HBV
Fecal-oral route; spread via feces and contaminated water
15 to 64 days Not known
15 to 60 days Not known
Same as HBV
No vaccine; universal and enteric precautions
Hepatitis E virus (HEV) Unenveloped, singlestranded RNA virus
Same as HBV (interferon alpha- No postexposure pro2b trials are under study) phylaxis available Same as HBV
Often seen after natural disaster in developing regions of the world
Antibody to HCV; tests have high false-positive and false-negative results; lack sensitivity and specificity
Antibody to HDV
None available-must rule out all other forms of hepatitis
Insidious onset; 40% to 60% become chronic carriers; 20% of acute HCV may progress to cirrhosis
Acute onset; may resolve without sequelae; may lead to serious fulminant hepatitis; more likely leads to chronic HDV and liver failure Mortality 30% in chronic cases; high risk of chronic liver disease; can become a chronic carrier; immunity to HBV provides immunity to HDV
Acute process; 99% of patients recover uneventfully
Mortality 1% to 2%; high risk for chronic liver disease and chronic carrier state (50% of infected individuals); possible association with liver cancer
Chronic cases not reported; mortality 1% to 2% (10% in pregnant women)
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blood, feces, saliva, and urine of infected individuals, but transmission is primarily by the fecal-oral route. The virus also may be carried by raw shellfish from polluted waters. Transmission of HAV can occur through person-to-person contact or through contaminated food or water. The highest concentration of virus (in the stool) occurs during the two-week period before the onset of jaundice. Because people with HAV are infectious before symptoms appear, they can transmit the disease unknowingly at that time. Transmission of HAV by blood transfusion is rare; however, blood donated during the prodromal phase of the disease, during which the virus is in the blood for a brief period, can contain HAV. It would not be known that the donor was infected because blood is not tested for anti-HAV. Poor personal hygiene, poor sanitation, and intimate contact (eg, household contact, sexual contact) facilitate transmission of HAV, and HAV infection is common in institutional settings. Those living in developing areas of the world are also at higher risk.7 In the United States, there is a higher incidence of HAV antibody in lower socioeconomic groups.8 Nosocomial transmissions to health care workers have occurred among health care workers caring for infected patients who were not diagnosed. Lack of glove use and inadequate hand washing are responsible for these transmissions? Environmental sanitation and hand washing before eating or handling food are effective means of preventing the spread of HAV. Hepatitis B virus. The highest concentration of HBV is in the blood and serous fluids of carriers and acutely infected people. The virus also is present in other body fluids in lower concentrations. Blood and blood products remain the best vehicles for transmission; however, body fluids such as vaginal secretions, semen, and serous fluid also can transmit the virus. The HBV also is present in urine, saliva, and feces in lower concentrations. The virus is stable and can survive for seven days or more in, for example, dried blood on a surface.I0 The HBV is prevalent in people born in highly endemic areas and their descendants. 1002
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People engaging in homosexual activity and IV drug use and those with many sexual partners also have high rates of infection. Prison inmates, people in institutions for the developmentally disabled, people who come into close contact with HBV carriers, people undergoing hemodialysis, and people receiving certain plasma products also are at increased risk." Transmission of HBV to health care workers occurs via puncture injuries, blood contact with mucous membranes (eg, the splashing of bloody fluids into the eyes), and blood contact with skin cuts or other portals of entry. Between 6% and 30% of nonimmunized health care workers who are exposed to HBV through one needle stick and who do not receive postexposure prophylaxis become infected. This is much higher than the risk of acquiring HIV from exposure to infected blood through one needle stick (ie, 0.5%).'* Various tests exist for HBV antibodies, and the US Food and Drug Administration requires testing of the nation's blood supply for the hepatitis B surface antigen (HBsAG). Blood banks began voluntary testing for the antibody to the hepatitis B core antigen in 1986, and they began testing for alanine aminotransferase in 1987. The alanine aminotransferase test is used primarily to determine liver disease and could signal possible hepatitis infection. In spite of screening procedures, HBV accounts for approximately 5% to 10% of posttransfusion hepatitis.13 Hepatitis B also is transmitted perinatally; therefore, the Immunization Practices Advisory Committee of the Centers for Disease Control and Prevention recommends that all pregnant women receive prenatal testing for HBsAG. The committee also recommends a comprehensive strategy to prevent HBV infection that includes universal vaccination of infants and adolescents. l 4 Hepatitis C virus. Worldwide, HCV (ie, parenterally transmitted non-A, non-B hepatitis) is responsible for the majority of bloodbome nonA, non-B hepatitis cases. The HCV is involved in most posttransfusion cases of hepatitis; however, only one in 10 cases of HCV can be traced to blood transfusion.15 One study of
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HCV in the United States indicates that the percentage of people with a history of blood transfusion significantly decreased between 1982 and 1988, while the percentage of people reporting parenteral drug use increased signifi~ant1y.I~ In 1990, tests to detect the HCV antibody were licensed, and blood now is routinely screened for anti-HCV. Tests for anti-HCV will detect only 85% of blood infected with HCV, however, because approximately two-thirds of HCV-infected individuals do not develop the antibody for five to 12 months. Because of this screening, however, parenteral drug users are expected to be identified as those most at risk for hepatitis C.I7 In addition to transfusion recipients and parenteral drug users, dialysis patients are at high risk for hepatitis C.lS Some risk factors for acquiring HCV are frequent contact with blood in the course of health care work, household contact with infected individuals, and personal contact with individuals who have had hepatitis.I9 Further investigation of sexual activity and person-to-person contact in disease transmission is needed. Although health care workers are at risk for HCV infection, the rate at which infection occurs following puncture injuries is not known.20 Hepatitis D virus. All groups at increased risk for hepatitis B are considered at increased risk for infection with HDV.2‘ Because hepatitis D occurs with hepatitis B as either a coinfection or a superinfection, those at high risk for hepatitis B should be vaccinated. Hepatitis E virus. Hepatitis E (ie, enterically transmitted non-A, non-B hepatitis) has occurred in Mexico, West and North Africa, and parts of Asia; however, it is not known whether HEV is present in the United States or Western Europe. The HEV is transmitted by the fecal-oral route, and those who travel to parts of the world where HEV is present may be at risk if they ingest contaminated water or food or if they have close contact with infected individuals. The best means of preventing HEV infection is avoiding water or food that may be contaminated.22
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Perioperative Nursing Care
B
efore surgery, it is important that the perioperative nurse question the patient about his or her history of liver disease, including hepatitis. Nurses who provide care to patients with a history of hepatic dysfunction should be aware of the physiologic alterations-and their implications for nursing care-that may occur secondary to liver disease. Physiologic alterations include changes in glucose homeostasis, protein synthesis, and fat metab0lism.2~ Glucose homeostasis. Glycogenolysis and gluconeogenesis are impaired with resulting hypoglycemia. Because of impaired uptake and release of glucose, there may be an abnormal glucose tolerance curve.24Impairment of glucose homeostasis necessitates continually monitoring the patient for changes in glucose levels. Protein synthesis,fat metabolism. Alterations in protein synthesis affect the production of coagulation factors that result in clotting abnormalities and increase the risk of bleeding.25In situations in which the prothrombin time is prolonged, vitamin K may be ordered.2hThe changes in protein synthesis also may decrease protein binding sites necessary for drug binding. The inability of drugs to bind with protein can lead to elevated drug plasma levels. The nurse should monitor the patient for signs of bleeding and drug toxicity. Alterations in protein synthesis also may lead to hypoalbuminemia, which warrants close observation of the patient’s fluid and electrolyte balance. Careful monitoring is necessary because alterations in fat metabolism may lead to metabolic acid0sis.2~ The patient’s metabolism of drugs also is affected. Drugs that require hepatic metabolism (eg, diazepam, lidocaine, morphine, meperidine) can have a prolonged effect on the patient.** Medications such as chlorpromazine, aspirin, acetaminophen, and many sedatives have the potential to damage the liver and should be administered as infrequently as possible.2y One of the problems of operating on a patient with hepatitis is the risk of disease transmission to health care providers. Health care workers whose tasks involve contact with 1003
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blood or body fluids should be vaccinated against hepatitis B. Health care workers also need to practice universal precautions to protect themselves and to prevent cross contamination.
General Nursing Care ‘ursing care of the hospitalized hepatitis patient includes attention to nutrition, fluid volume, comfort, and rest. Because the patient may suffer from anorexia, frequent small meals are important. The largest meal may be best tolerated in the morning, as anorexia often worsens during the day. A highprotein, high-carbohydrate diet that is moderate in fat allows recovery of liver cells. If the patient has problems digesting or metabolizing fat or protein, the amounts of these nutrients should be decreased. If there is a danger of hepatic encephalopathy, a low-protein diet is indicated to decrease accumulation of serum ammonia. Problems with fat metabolism result from alterations in the production and excretion of bile and could require adjustment of fat intake. Nasogastric feedings, total parenteral nutrition, and IV fluids may be necessary. Pruritis associated with jaundice may cause severe discomfort and altered skin integrity. Maintaining ventilation, using cotton clothing, applying skin emollients, and avoiding alkaline soaps benefit the patient. Patients suffering from acute symptoms require bed rest. If hepatic encephalopathy occurs, the patient requires oral or rectal neomycin to decrease intestinal bacteria that synthesize ammonia. This decreases the patient’s serum ammonia levels. Lactulose may be used to cause ammonia and hydrogen ion coupling. The resultant compound is then excreted in feces. Diarrhea may occur with the use of lactulose, so the nurse monitors the patient’s electrolyte levels during lactulose therapy.
Patient Education
B
efore the patient is discharged, the nurse teaches the patient and his or her family members about the disease and precau-
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tions for preventing its spread. The nurse emphasizes follow-up care (eg, liver function tests, serum HBsAg), ample rest, proper nutrition, and avoidance of over-the-counter medications (eg, acetaminophen) and alcohol. For hepatitis A patients, the nurse stresses the importance of thorough hand washing and the need to disinfect articles soiled with feces. Patients infected with HAV must not prepare food for consumption by others while the disease is symptomatic, nor should they share articles such as eating utensils, toothbrushes, or toys.30 Patients in the acute stage of hepatitis B and non-A, non-B hepatitis should avoid sexual activity until they test negative for HBsAg or until their partners receive their complete series of HBV vaccine. People who are carriers of HBV must understand that their blood and bodily secretions are infectious, and people in close contact with HBV carriers should receive HBV vaccine. People with a history of non-A, non-B hepatitis and those who carry the HBV should not donate blood.
Conclusion
T
he perioperative nurse should be aware that there are five identified hepatitis viruses. Each virus presents unique challenges for the perioperative nurse providing patient care; therefore, knowledge of the hepatitis viruses, their modes of transmission, and their pathologies enables nurses to provide quality patient care while protecting themselves, other patients, and other health care workers from the disease. 0 Notes I . A M Kools, “Hepatitis A, B, C, D, and E: Update on testing and treatment,” Postgraduate Medicine 91 (Feb 15, 1992) 109-114. 2. Ibid. 3. Ihid. 4. I b i d ; M M Jackson, D C McPherson, “Hepatitis A through E---current and future trends,” Today’s OR Nurse 13 (October 1991) 7-12. 5 . J H Hoofnagle, “Type D (delta) hepatitis,” Journal of the American Medical Association 261 (March 3, 1989) 1321-1325.
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6. Kools, “Hepatitis A, B, C, D, and E: Update on testing and treatment,” 109-114. 7. I D Gust, “The epidemiology of viral hepatitis,” in Viral Hepatitis and Liver Disease, ed G N Vyas, J L Dienstag, J H Hoofnagle (Orlando, Fla: Grune & Stratton, 1984) 415-421. 8. J L Dienstag et al, “Hepatitis A virus infection: New insights from seroepidemiologic studies,” The Journal of Infectious Diseases 137 (March 1978) 328-340. 9. Jackson, McPherson, “Hepatitis A through E 4 u r r e n t and future trends,” 7-12. 10. J M Heeg, D A Coleman, “Hepatitis kills,” RN 55 (April 1992) 60-66. 11. Centers for Disease Control and Prevention, “Protection against viral hepatitis: Recommendations of the Immunization Practices Advisory Committee,” Morbidity and Mortality Weekly Report 39 (RR-2) (Feb 9, 1990) 1-26. 12. Centers for Disease Control and Prevention, Guidelines for Prevention of Transmission of Human Immunodeficiency Virus and Hepatitis B Virus to Health-Care and Public-Safety Workers, pub1 no 89107 (Atlanta: US Department of Health and Human Services, 1989). 13. E Rubin, J L Farber, eds, Essential Pathology (Philadelphia: J B Lippincott Co, 1990) 404,406. 14. Centers for Disease Control and Prevention, “Hepatitis B virus: A comprehensive strategy for eliminating transmission in the United States through universal childhood vaccination: Recommendations of the Immunization Practices Committee,” Morbidity and Mortality Weekly Report 40 (RR-13) (NOV22, 1991) 1-25. 15. Heeg, Coleman, “Hepatitis kills,” 60-66. 16. M J Alter et al, “Risk factors for acute non-A, non-B hepatitis in the United States and association with hepatitis C virus infection,” Journal of the American Medical Association 264 (Nov 7, 1990) 223 1-2235. 17. Jackson, McPherson, “Hepatitis A through E 4 u r r e n t and future trends,” 7-12. 18. Alter et al, “Risk factors for acute non-A, nonB hepatitis in the United States and association with hepatitis C virus infection,” 223 1-2235. 19. Centers for Disease Control and Prevention, “Protection against viral hepatitis: Recommendations of the Immunization Practices Advisory Committee,’’ 1-26. 20. Jackson, McPherson, “Hepatitis A through E-current and future trends,” 7-12. 21. L Lettau et al, “Nosocomial transmission of delta hepatitis,” Annals of Internal Medicine 104 (May 1986) 631-635. 22. Centers for Disease Control and Prevention, “Protection against viral hepatitis: Recommendations of the Immunization Practices Advisory Committee.” 1-26.
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23. K Litwack, Post Anesthesia Care Nursing (St Louis: Mosby-Year Book, Inc, 1991). 24. C M Porth, Pathophysiology: Concepts of Altered Health States, third ed (Philadelphia: J B Lippincott Co, 1990) 724. 25. Litwack, Post Anesthesia Care Nursing. 26. S W Ames, C R Kneisl, Essentials of Adult Health Nursing (Menlo Park, Calif Addison-Wesley Publishing Co, 1988). 27. Litwack, Post Anesthesia Care Nursing. 28. Ibid. 29. Luckmann and Sorensen’s Medical-Surgical Nursing: A Psyc hophysiologic Approach, fourth ed, J M Black, E MatassarkJacobs, eds (Philadelphia: W B Saunders Co, 1993). 30. Clinical Nursing, third ed, J M Thompson et al, eds (St Louis: Mosby-Year Book, Inc, 1993).
Suggested reading Centers for Disease Control and Prevention. “Public health service inter-agency guidelines for screening donors of blood, plasma, organs, tissues, and semen for evidence of hepatitis B and hepatitis C.” Morbidity and Mortality Weelky Report 40 (RR-4) (April 19, 1991) 1-17. Choo, Q L, et al. “Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome.” Science 244 (April 21, 1989) 359-362. Cottone, J A. “Recent developments in hepatitis: New virus, vaccine, and dosage recornmendations.” Journal of the American Dental Association 120 (May 1990) 501-508. Lemon, S M. “Type A viral hepatitis: New developments in an old disease.” The New England Journal of Medicine 313 (Oct 24, 1985) 10591067. Meeker, M H; Rothcock, J C. Alexander’s Care of the Patient in Surgery, ninth ed. St Louis: Mosby-Year Book, Inc, 1991. Reece, S M. “Immunization strategies for the elimination of hepatitis B.” Nurse Practitioner 18 (February 1993) 42-45,49-50. Reyes, G R, et al. “Isolation of a cDNA clone from the virus responsible for enterically transmitted non-A, non-B hepatitis.” Science 247 (March 16, 1990) 1335-1339. Rizzetto, M, et al. “Immunofluorescence detection of new antigen-antibody system (deltdanti-delta) associated to hepatitis B virus in liver and in serum of HBsAg carriers.” Gut 18 (December 1977) 997-1003. Robinson, W E. “Biology of human hepatitis viruses,” in Hepatology: A Textbook of Liver Disease, ed D Zakim, T D Boyer. Philadelphia: W B Saunders Co, 1990. Sarver, D K. “Hepatitis in clinical practice. 1. Hepatitis A and B.” Postgraduate Medicine 79 (March 1986) 194-200, 209-214. 1005