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Viral hepatitis may result from infection with any of several different pathogens. Of greatest interest to the
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Infection Status of Source | ||||
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Exposure Type | HIV Positive Class 1 * | HIV Positive Class 2 * | Source of Unknown HIV Status † | Unknown Source ‡ | HIV Negative |
Less severe § | Recommend basic 2-drug PEP | Recommend expanded 3-drug PEP | Generally, no PEP warranted; however, consider basic 2-drug PEP ‖ for source with HIV risk factors ¶ | Generally, no PEP warranted; however, consider basic 2-drug PEP ‖ in settings where exposure to HIV-infected persons is likely | No PEP warranted |
More severe £ | Recommend expanded 3-drug PEP | Recommend expanded 3-drug PEP | Generally, no PEP warranted; however, consider basic 2-drug PEP ‖ for source with HIV risk factors ¶ | Generally, no PEP warranted; however, consider basic 2-drug PEP ‖ in settings where exposure to HIV-infected persons is likely | No PEP warranted |
From U.S. Public Health Service: Updated U.S. Public Health Service guidelines for the management of occupational exposures to HBV, HCV, and HIV and recommendations for postexposure prophylaxis. MMWR Recomm Rep 50(RR-11):1–42, 2001. |
Hepatitis B is a serious disease that may be life threatening, but it can be prevented. In the 1970s the prevalence of HBV infection in health care workers was 10 times higher than that in the general population. In the 1980s, it was estimated that 200 to 300 health care workers would die annually from the effects of hepatitis B. Fortunately, the introduction of an effective vaccine for hepatitis B has dramatically decreased the incidence, morbidity, and mortality of the disease.[47] Infection may be documented serologically by the appearance of HBV surface antigen (HBsAg), HBV surface antibody (anti-HBs), or HBV core antibody (anti-HBc) in serum. Before routine vaccination, the development of covert seropositivity for hepatitis B during residency was common. In a multicenter study involving hospitals in both rural and metropolitan areas, the overall prevalence of serologic indicators for hepatitis B in anesthesiology residents who had received neither hepatitis vaccine nor hepatitis B immune globulin (HBIG) was 17.8% in 267 tested. Most seropositive residents were unaware of having been exposed to hepatitis. No correlation was found between the incidence and geographic location, but the incidence of seropositivity increased in parallel with clinical experience. Thirty percent of residents with more than 11 total years of experience, including their current residency and previous work in other specialties, were seropositive for HBV. Routine use of gloves and attention to obtaining detailed histories from patients did not appear to decrease the incidence of infection.[54]
An estimated 200,000 new cases of HBV infection occur each year. Of these cases, jaundice will develop in 50,000, and 10,000 will require hospitalization. As many as 12,000 to 20,000 annually become asymptomatic carriers of HBsAg, with the total number of carriers in the United States estimated to be nearly 800,000. [55] It is this group that threatens nonimmunized anesthesiologists. The epidemiologic features of HBV and AIDS have much
Active immunization of seronegative health care workers with hepatitis
B vaccine is imperative for prophylaxis against infection. The first vaccine was
composed of inactivated particles of surface antigen prepared from the sera of HBsAg
carriers. Ninety percent of recipients of the vaccine became seropositive and thus
were protected against infection.[55]
Despite the
efficacy and the safety of the early vaccine, in the mid-1980s, substantial numbers
of anesthesia personnel refused to be immunized for unspecified reasons.[54]
Some were concerned that because the vaccine
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Treatment | ||
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Vaccination and Antibody Response Status of Exposed Workers * | Source HBsAg Positive | Source HBsAg Negative | Source Unknown or Not Available for Testing |
Unvaccinated | HBIG † × 1 and initiate vaccine series | Initiate HB vaccine series | Initiate HB vaccine series |
Previously vaccinated |
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Known responder ‡ | No treatment | No treatment | No treatment |
Known nonresponder § | HBIG × 1 and initiate revaccination or HBIG × 2 ‖ | No treatment | If known high-risk source, treat as though source were HBsAg positive |
Antibody response unknown | Test exposed person for anti-HBs | No treatment | Test exposed person for anti-HBs |
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1. If adequate, ‡ no treatment is necessary |
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1. If adequate, ‡ no treatment is necessary |
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2. If inadequate, § administer HBIG × 1 and vaccine booster |
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2. If inadequate, § administer vaccine booster and recheck titer in 1–2 mo |
Anti-HBs, HBV surface antibody; HBIG, hepatitis B immune globulin; HBsAg, hepatitis B surface antigen. | |||
From U.S. Public Health Service: Updated U.S. Public Health Service guidelines for the management of occupational exposures to HBV, HCV, and HIV and recommendations for postexposure prophylaxis. MMWR Recomm Rep 50(RR-11):1–42, 2001. |
Anesthesiologists in whom no antibodies are present in serum and who suspect that contact with HBV has occurred should be passively immunized with HBIG and should also receive a series of three injections of hepatitis B vaccine [47] ( Table 88-2 ). Previous vaccination and seroconversion eliminate the need for HBIG, whose acronym is an appropriate description of the discomfort that it produces after injection.
HCV is now recognized as one of the major causes of NANB hepatitis. This disease, whose symptoms and signs are nonspecific, is the predominant source of hepatitis from transfusion. Chronic hepatitis develops in more than 85% of hepatitis C infections, with 20% progressing
Important discoveries in the diagnosis of HCV were reported in 1989 when a segment of the genome of an NANB virus was isolated, cloned, and designated hepatitis C virus and when an assay for circulating anti-HCV antibodies was developed.[61] [62] Like HBV, HCV appears to be transmitted principally by infected blood. Studies using the anti-HCV assay have shown that HCV is responsible for up to 90% of transfusion-related NANB hepatitis.[63] With this assay, some have reported only a 1% to 2% incidence of antibody to HCV in health care workers (similar to that seen in volunteer donors), thus suggesting that HCV is not easily transmitted. [63] [64] Reports based on the same assay indicate that transmission of HCV by contaminated needles occurs in less than 4% of these injuries.[65] More sensitive assays for HCV are currently under investigation. One of these assays, detection of HCV RNA by polymerase chain reaction, documented a 10% incidence of HCV infection in health care workers.[66] This method is limited to laboratory investigation, it is not licensed for clinical use, and its accuracy is widely variable.[67] However, with further refinement, it may become an important method for precisely determining the incidence of occupationally acquired HCV infection.
At present, no effective postexposure treatment is available for HCV exposure. Instead, the recommendations for postexposure management are geared toward early recognition and intervention in chronic disease. Health care workers who are exposed to HCV should undergo baseline testing for anti-HCV and alanine aminotransferase activity as soon as possible after the injury, with follow-up testing 3 and 6 months after exposure.[67] Some institutions offer immune serum globulin to these persons as prophylaxis against infection. However, such prophylaxis is of little value because anti-HCV antibodies are not consistently found in production lots of immune globulin.[47]
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