Bloodborne pathogens. Can you become infected from your older patient?

1. Exposure to bloodborne pathogens in the workplace creates acute anxiety in health care workers (HCWs); however, HCWs are at a greater risk for contracting the hepatitis B virus (HBV) than for contracting the human immunodeficiency virus (HIV). 2. A postexposure management program (PEMP) provides an education of the risk of infection and risk-reduction techniques; a mechanism for assessment of the source patient's risk factors and for obtaining source patient HBV and HIV serologic status; a setting in which the HCW can be periodically and confidentially tested for HIV antibody; and a formal assessment of the HCW for AZT chemoprophylaxis. 3. As in other areas of nursing practice, it is possible to be exposed to potentially infectious body fluids when caring for older patients. It is important that health care providers protect themselves with hepatitis B immunization and decrease exposure risk by the rigorous practice of universal precautions with patients in all age groups.

Management of health-care workers exposed to blood and body fluids.

1. The risk of transmission of HIV from an infected patient to a percutaneously exposed HCW is about 1 in 200 to 300. 2. The exposure, the source patient and the HCW recipient must be assessed to determine the risk of HIV infection to the recipient. 3. Azidothymidine (AZT, zidovudine) is the only drug currently licensed by the FDA for the treatment of HIV infection.

Management of health care workers exposed to blood and body fluids in the workplace.

Management of HCWs with "sharps" injuries and other workplace exposures is a growing concern in this era of multiple, blood-borne, potentially fatal infectious diseases. HCWs and institutions are advised to become knowledgeable about exposure risks and mechanisms for decreasing them.

The evolution of lymphadenopathy and hypergammaglobulinemia are evidence for early and sustained polyclonal B lymphocyte activation during human immunodeficiency virus infection.

To examine whether polyclonal activation of B lymphocytes as measured by hypergammaglobulinemia contributes to lymphadenopathy in human immunodeficiency virus (HIV) infection, correlates of adenopathy were examined in 240 homosexual men. Lymph node size was measured in 12 sites semiannually over 4 years. Both adenopathy and hyperglobulinemia developed within 1 year after seroconversion and persisted at high levels. Adenopathy declined near diagnosis of AIDS whereas serum IgG decreased 8-16 months after diagnosis. Adenopathy attributable to HIV occurred in all palpable node groups. By logistic regression, HIV-positive men were best discriminated from HIV-negative men by size of posterior cervical nodes and the number of sites with enlarged nodes. In a repeated measures model of covariance, adenopathy in HIV-positive men was associated with more CD4+ cells (P less than .002), elevated serum globulins (P less than .01), and lower platelet counts (P less than .05). Adenopathy declined over time (P less than .001) and with diagnosis of AIDS or AIDS-related complex (P less than .03). Thus, adenopathy and hypergammaglobulinemia are correlated and follow a similar course through various stages of HIV infection, suggesting that both are caused by polyclonal B cell activation.

The spectrum of HIV infection: what happens clinically.

When a person contracts HIV, the initial acute infection is followed by a prolonged asymptomatic or mildly symptomatic period; lab values may be completely normal. By the time AIDS is diagnosed, the cell-mediated immune system is irreversibly damaged; virtually all patients die within 5 years. The pace of progression of HIV disease varies widely among patients and is therefore difficult to predict for any one individual.