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INFECTION

While managing patients, the anesthesiologist is exposed to a multitude of communicable diseases, most of which present no significant threat to healthy people.[30] The greatest concerns stem from contact with patients infected with HIV, hepatitis C, or hepatitis B. As a rule, the probability of becoming infected from a needle contaminated with one of these viruses is 0.3%, 3%, and 30%, respectively. This section concentrates on these three catastrophic diseases while also addressing tuberculosis. In March 1992, OSHA issued comprehensive, enforceable standards designed to minimize occupational exposure to blood-borne pathogens. The employer is responsible for maintaining an exposure control plan that protects all health care workers who have the potential for contact with blood or blood products. Protective equipment, including gloves, gowns, and eye shields, must be supplied by the employer at no cost to the employee. The standard also provides for hand-washing facilities, proper receptacles for contaminated materials, methods for handling contaminated laundry, and management of waste, among many other things.[31] Ten years later, the Needlestick Safety and Protection Act provided additional safeguards against percutaneous exposure with the use of needle safety devices.

Acquired Immunodeficiency Syndrome

Since the early 1980s, health care workers have feared contracting acquired immunodeficiency syndrome (AIDS) as a result of occupational exposure.[32] Yet HIV, which is responsible for the syndrome, is a relatively fragile virus. With proper attention to cleanliness and care in performing invasive procedures, the likelihood that the disease will develop in an anesthesiologist during the course of patient management is exceedingly low.

Two human immunodeficiency viruses, HIV-1 and HIV-2, are responsible for infections in humans. The former is found worldwide, and the latter occurs principally in northwest Africa, although it is now spreading into Europe.[33] Both are retroviruses that attach to cells with CD4 surface antigen (predominantly T-helper lymphocytes) and ultimately replicate by integrating virally produced DNA into the nucleus of the host cell.[34]

Initial infection with HIV follows within 2 to 10 weeks of inoculation. It is usually a self-limited, nonspecific, febrile viral syndrome lasting 1 or 2 weeks. An individual is considered to be both infected with HIV and infective if the results of both a serologic screening test, the enzyme-linked immunosorbent assay (ELISA), also called enzyme immunoassay (EIA), and a supplemental, more sensitive test, either Western blot or indirect fluorescent antibody, are repeatedly positive. ELISA tests are relatively easy to perform in a clinical laboratory but may be subject to false-positive results. Supplemental tests are time consuming but are necessary for confirmation. Results of the tests become positive within weeks of inoculation, but the median latency for the first opportunistic disease may be as long as 11 years. [34]

Epidemiology of AIDS

The apparent incidence, death rates, and other epidemiologic features of AIDS are influenced by the methods used to obtain these values. Although AIDS has been a reportable disease in the United States, infection with HIV has not. Because the incidence of HIV is derived from studies of population cohorts rather than individual cases, its numerical significance is less precise than data concerning AIDS.[35]

On January 1, 1993, the criteria for defining AIDS were expanded from those of 1987 to include objective laboratory data and illnesses not previously used in confirming the diagnosis. With these changes, all HIV-infected patients with CD4 T-lymphocyte counts of less than 200/µL, as well as those with opportunistic infections, including pulmonary tuberculosis, recurrent pneumonia, and cervical cancer, were defined as having AIDS. The result was an apparent 200% increase in cases of the disease reported in early 1993.[36] At that time, nearly 900,000 persons in the United States were estimated to be infected with HIV. In spite of these methodologic changes, the proportional rate of the annual increase in cases of HIV continued to decline in the late 1990s.[37] [38] Despite these overall declines, the incidence of AIDS increased in certain subpopulations, including black men and women and persons born after 1960.[37] [38] Since 1993, infection with HIV/AIDS has been the leading cause of death in persons 25 to 44 years old.[39] More than one in five of those infected are female, and perinatal transmission of HIV-1 occurs in as many as 25% of the offspring of infected mothers. Transplacental infection and possible transmission by breast milk have been implicated.[34]

With advancing technology, surveillance of AIDS in the United States continues to evolve. In January 2000, the surveillance case definition for HIV infection was revised to include a single definition for adults, adolescents, and children older than 18 months. The revised criteria include positive results or reports of a detectible quantity of HIV nucleic acid or plasma HIV RNA.[40]

AIDS and Health Care Workers

Health care workers account for 5% of cases of AIDS in the United States. Although occupationally related infections have been reported, the vast majority of the


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cases have been attributed to nonvocational contact.[41] However, epidemiologic data, coupled with the observation that more than 4% of 2300 patients treated at an urban emergency department had unrecognized HIV infection, [42] suggest that the potential for health care workers to have contact with an unidentified carrier of the disease is significant. By mid-2001, the Centers for Disease Control and Prevention (CDC) had documented 57 cases of occupationally acquired HIV infection in the United States.[43] Of these, 48 were due to percutaneous exposure. Of 1746 reported cases of AIDS in physicians, only 6 were directly linked to occupational exposure.

Injury from a needle is the most likely route of infection for anesthesiologists. Of 493 anesthesia personnel surveyed in a multicenter study, 32% reported having been stuck with a contaminated needle at least once in the preceding 12 months. Of those, only half sought treatment.[44] The risk of infection is greater with hollow-bore than with solid needles and is further increased with large-bore needles and deep intramuscular injection.[34] In a study evaluating percutaneous injuries in anesthesia personnel, nearly 90% were from hollow-bore needles, were self-inflicted, most commonly involved the non-dominant hand, and were deemed preventable. A significant number of the injuries occurred during disposal of contaminated needles.[45] The minimal dose of contaminated blood needed to infect humans is unknown, although one patient became HIV positive after the accidental intravenous injection of 100 to 200 µL of infected blood.[46] The likelihood of development of antibodies to HIV is related to the volume of the inoculum and the concentration of viral particles.[47] Consequently, most seroconversions have been associated with deep intramuscular injection of contaminated blood through large-bore needles.

The theoretical risk for occupational infection in anesthesiologists over a 30-year exposure period has been calculated to range from 0.05% to 4.5%, depending on the infectivity of the patient population; however, these estimates are based on incomplete data.[48] The overall risk of seroconversion in health care workers after documented percutaneous exposure to HIV-infected body fluids is usually said to be about 0.3%. Although seroconversion has been documented after nonintact skin has been in contact with infected blood, the incidence from this route is far lower than from needle injuries.[47] [49]

The risk of transmission of HIV from health care workers to patients, with the exception of errors in technique, is extremely small. No infections were identified in more than 19,000 patients who had been treated by 57 infected health care workers, including 29 dentists, 12 surgeons, and 16 physicians in nonsurgical specialties. The only documented infections have been in 6 of 1100 patients treated by a dentist in Florida.[50]

With proper attention to routine methods of disinfection, sterilization, and housekeeping, the AIDS virus on instruments, surfaces, and laundry can be destroyed. At concentrations of 5 orders of magnitude greater than normally found clinically, HIV may survive for several days after being dried. This situation represents an extreme, however. Several hours of drying generally inactivates 90% to 99% of viable virus. The amount of HIV usually found on contaminated surgical instruments and equipment used in anesthetic management can be killed with "high-level disinfection." Such disinfection involves careful cleaning, followed by exposure either to one of the commercially available germicides or to a 1:10 to 1:100 dilution of sodium hypochlorite (household bleach). These methods annihilate bacteria and viruses but may not be effective against bacterial spores. If the instruments are to be sterilized, they should be thoroughly cleaned first. Contaminated hospital linen should not be washed or rinsed in the operating room or another patient care area; instead, it should be placed directly in sealed, water-impenetrable bags. It can safely be laundered by normal methods. Infective waste, including secretions, blood, and other body fluids, should be incinerated or autoclaved. Alternatively, large volumes of fluids may be discarded in a sanitary sewer.[51] Personal protection and protection of patients are afforded by standard precautions.

The best defense is a good offense, and there is no substitute for strict adherence to universal precautions. If in spite these efforts you or a coworker are exposed to HIV, postexposure prophylaxis is available. Because most occupational exposures do not result in HIV transmission, the guidelines for postexposure prophylaxis weigh the relative risk of infection against the potential toxicity of treatment. The relative risk of infection depends on both the type and amount of blood exposure. The risk of transmission is increased by (1) percutaneous exposure, (2) devices contaminated with visible blood, (3) hollow-bore needles, and (4) high viral titer (i.e., a patient late in the course of the disease). The three classes of antiretroviral agents available for treatment—nucleoside reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, and protease inhibitors—are all associated with a number of toxicities. A basic two-drug regimen is most often recommended, with an expanded three-drug regimen reserved for high-risk exposure ( Table 88-1 ). The U.S. Public Health Service guidelines recommend that clinicians consider known drug resistance in their area or documented drug resistance in the source patient, or both, when selecting a prophylactic protocol.[52]

Evaluation for postexposure prophylaxis and baseline HIV testing should be completed within hours of exposure. Prophylaxis should begin as soon as possible inasmuch as animal studies show that prophylaxis is less effective if begun more than 24 to 36 hours after exposure. Because the time to no benefit in humans is unclear, the U.S. Public Health Service advises beginning prophylaxis up to 1 week after exposure. Four weeks of treatment is recommended if tolerated. Regardless of whether post-exposure prophylaxis is initiated, follow-up should include counseling and HIV antibody testing at 6 and 12 weeks, as well as 6 months after exposure.[52]

Health care workers are encouraged to contact the National Clinicians' Post-Exposure Prophylaxis Hotline (PEPline) at 1-888-448-4911 for expert advice. This hotline can be accessed 24 hours a day.

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