• First Oral Contraceptive Approved for Acne – Norgestimate/ethinyl estradiol
• Asymptomatic Shedding and Transmission of Herpes Simplex Virus
• Occupational Exposure to HIV
• Update on Drugs
  • Norgestimate/ethinyl estradiol Ortho Tri-cyclen® tablet - Ortho
  • Sodium sulfacetamide lotion 10% Klaron® - Dermik
  • Tazarotene Tazorac® - Allergan
  • Loratidine Claritin® - Schering
  • Levofloxacin Levaquin® - Ortho
  • Butenafine HCI 1% cream Mentax® - Penederm
  • Amlexanox paste Aphthasol® - Block Drug Company
  • Cefuroxime axetil Ceftin® - Glaxo Wellcome

Although according to the Centre for Disease Control statistics, the risk of contracting HIV following occupational exposure is less than one half of one per cent, the fear associated with accidental exposure to HIV is something we can all appreciate! The common sense approach to treatment outlined below provides a plan of therapeutic action based on current therapeutic experience and should go a long way towards allaying such fears.

Stuart Maddin, Editor

What Constitutes Occupational Exposure?

Exposure to known or suspected HIV positive blood or infectious body fluid by means of a needlestick or a cut with a sharp object such as a scalpel or other surgical instrument.

Risk of Transmission

The risk of seroconversion after a documented percutaneous exposure has been estimated to be 0.32% per needlestick injury.^1-4 In the USA, between 1978 and June 1996, there were 51 cases of occupational HIV transmission documented: 44 had percutaneous exposure, five had mucocutaneous exposure, one had both percutaneous and mucocutaneous exposures, and one had an unknown route of exposure. Forty-six exposures were to blood from an HIV-infected person, one to visibly bloody fluid, one to an unspecified fluid, and three to concentrated virus in a laboratory. Twenty-four of these health care workers developed AIDS. A further 108 cases of occupational exposure have been classified as possible transmission of HIV; percutaneous or mucocutaneous exposure to HIV was reported, but HIV seroconversion specifically resulting from the occupational exposure was not documented.⁴ The risk of occupational infection resulting from mucous membrane exposure is still too low to accurately measure, although one study has calculated it to be 0.09%.^2,5

During a specific exposure, the risk of occupational HIV infection is affected by the relative immunity of the health care worker, the volume of inoculum, the quantity of virus, depth of penetration, type and size of needle (the risk is considerably greater with hollow-bore needles), and the actual injection of blood.^5,6 For mucocutaneous exposures, large volumes of blood, prolonged duration of contact, and a portal of entry appear to be common factors in the few individuals who have become infected.⁵ During surgical procedures, factors associated with increased risk include the type of procedure, a longer duration of procedure, and the use of hands rather than instruments to hold material for suturing. Recapping needles is the single most common (and potentially avoidable) hazard.⁵

Management of Occupational Exposure to HIV

• Testing

The source patient should be tested for HIV after appropriate counselling and obtaining informed consent. Health care workers who sustain massive, definite, or possible parenteral exposures should undergo baseline serum testing for HIV, hepatitis B and hepatitis C, or have their serum frozen and stored.⁵ When the source patient is potentially infected with HIV, follow-up HIV testing of the worker is generally performed at six weeks, three months, and six months. The exposed worker should be informed about the symptoms of an acute retroviral infection and should observe precautions to prevent possible secondary transmission. Seroconversion should occur within six months of exposure.⁵

• Treatment

Because most occupational exposures to HIV do not result in infection transmission, potential toxicity must be carefully considered when prescribing post exposure prophylaxis.⁴

• The Centre for Disease Control recommends postexposure prophylaxis (PEP) for workers after high-risk occupational exposure. For exposures with a lower, but non-negligible risk, PEP should be offered, balancing the lower risk against the use of drugs having uncertain efficacy and toxicity. For exposures of negligible risk, PEP is not justified.⁴
• Zidovudine, (ZDV, Retrovir®, Glaxo Wellcome and generics) 600 mg per day should be considered for all PEP regimens, because it is the only agent for which data support the efficacy of PEP in the clinical setting. In a case control study among health care workers, zidovudine PEP was associated with a decrease of approximately 79% in the risk for HIV seroconversion after percutaneous exposure to HIV-infected blood.^8,9 In a prospective trial, the direct effect of ZDV prophylaxis may have contributed to an observed 67% reduction in perinatal HIV transmission.¹⁰ Some failures of zidovudine PEP have occurred.³
• Lamivudine (3TC, Epivir®, Glaxo Wellcome) 150 mg twice daily should usually be added to ZDV for increased antiretroviral activity and activity against many ZDV-resistant strains.⁴

• A protease inhibitor (preferably indinavir4, Crixivan®, Merck) should be added after high-risk exposures and might be considered for lower-risk exposures if ZDV-resistant strains are likely.⁴ To avoid a potentially life-threatening drug interaction (e.g. cardiac arrhythmias, prolonged sedation), indinavir must not be administered concurrently with terfenadine, astemizole, cisapride, triazolam, or midazolam.¹¹
  
  For HIV strains resistant to both ZDV and indinavir or resistant to a protease inhibitor, or if these drugs are contraindicated or poorly tolerated, the optimal PEP regime is uncertain and expert consultation is advised.⁴

• PEP should be initiated promptly, preferably within 1-2 hours post-exposure. Even though animal studies suggest that PEP is ineffective when delayed more than 24-36 hours following exposure, in humans the interval after which there is no benefit from PEP is undefined. In patients who have experienced a high risk exposure, PEP might be initiated after a longer interval (e.g. 1-2 weeks), as even if the infection is not prevented, early treatment of acute HIV infection may be beneficial.^9,12
• The optimal duration of PEP is unknown, but because ZDV treatment for four weeks appears protective; if tolerated, PEP should probably be continued for four weeks.⁴
• Drug-toxicity monitoring should include a complete blood count and renal and hepatic chemical function tests at baseline and two weeks after starting PEP. If toxicity is noted, experts should be consulted and dose reduction or drug substitution considered. Further diagnostic studies may be indicated.⁴
• Finally, universal precautions including the routine use of appropriate barrier precautions and techniques to reduce the likelihood of exposure to bloodborne pathogens are even more important for hepatitis B and C and nosocomial infections than they are for HIV.⁶

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References

1. Henderson DK, Fahey B, Willy M, et al. Risk for occupational transmission of human immunodeficiency virus type 1 (HIV-1) associated with clinical exposures: a prospective evaluation. Ann Intern Med 1990;113:740-746.
2. Ippoloito G, Puro V, De Carli G. The risk of occupational human immunodeficiency virus infection in health care workers: Italian multicenter study. Arch Intern Med 1993;153:1451-1458.
3. Tokars JI, Marcus R, Culver DH, et al. Surveillance of HIV infection and zidovudine use among health care workers after occupational exposure to HIV-infected blood. The CDC Cooperative Needlestick Surveillance Group. Ann Intern Med 1993;118:913-919.
4. Provisional public health recommendations for chemoprophylaxis after occupational exposure to HIV. MMWR 1996;45:No. 22.
5. Fraser VJ, Powderly WG, Risks of HIV infection in the health care setting. Annu Rev Med 1995;46:203-211.
6. Gerberding JL, Lewis FR, Schecter WP. Are universal precautions realistic? Surg Clin North Am 1995;75:1091-1104.
7. McLeod WA. Personal communication. February 1997.
8. CDC. Case-control study of HIV seroconversion in health care workers after percutaneous exposure to HIV-infected blood – France, United Kingdom, and United States, January 1988- August 1994. MMWR 1995;44:929-933.
9. Gerberding JL. Prophylaxis for occupational exposure to HIV. Ann Intern Med 1996; 125:497-501.
10. Connor EM, Sperling RS, Gelber R, et al. Reduction of maternal-infant transmission of human immunodeficiency virus type 1 with zidovudine treatment. N Engl J Med 1994;331:1173-1180.
11. Drug Facts & Comparisons. St. Louis, Missouri: Facts and Comparisons, 1996.
12. Kinloch De Loes S, Hirschel BJ, Hoen B, et al. A controlled trial of zidovudine in primary human immunodeficiency virus infection. N Engl J Med 1995;333:408-413.

We are indebted to Dr. Alastair McLeod (Chair, Committee on Accidental Exposures to HIV, St. Paul’s Hospital, Vancouver, Canada) for his helpful suggestions, and to Rita Fahrner (San Francisco General Hospital) for information received.

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