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A Guide to Primary Care of People with HIV/AIDS Chapter 9: Management of Opportunistic Diseases 9 Figure 9-1 Decline in the Incidence of Opportunistic Infections in HIV-1-Infected Individuals Receiving Potent Combination Declining U.S. Incidence of OIs Antiretroviral with Potent ARV Therapy Therapy No. of OIs per 100 person-years 20 15 10 5 2 0 MAC CMV PCP 1994 1995 1996 1998 Source: Adapted from Palella FJ Jr, Delaney KM, Moorman AC, et al. Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators. N Engl J Med. 1998;338:853-860. Copyright 1998 by the Massachusetts Medical Society. Modified with permission (data extrapolated through 2000). developing a specific OI is determined by the degree of immunosuppression, as measured by the CD4 cell count. The CD4 threshold of risk differs for each specific OI (see Table 9-1). It is uncommon for an OI to occur in HIV-infected individuals with CD4 cell counts above its threshold. For patients with the same CD4 cell count, those with high viral loads (plasma HIV RNA levels >100,000 copies/mL) have a greater risk for developing an OD than those with a low viral load. Other factors that contribute to increased risk for ODs include previous exposure to or infection with a specific pathogen, prior occurrence of an OD, environmental exposure in the absence of a host response, and the use of ART. What malignancies are associated with HIV infection? The most common are Kaposi sarcoma (KS) and lymphomas. There is also a modest increase in the frequency of cervical cancer. In general, these 3 forms of malignancies correlate with immunosuppression, meaning the frequency increases with low CD4 cell counts, but the association is less strong than it is with the traditional AIDS-defining ODs. The rate of KS is approximately 20,000-fold higher with HIV infection compared with the general population, the frequency of non-Hodgkin lymphoma is 200- to 600-fold more frequent with HIV infection, and the rate of cervical cancer is 5-fold greater. Both lymphomas and KS are less frequent in the era of ART. 2000 PNEUMOCYSTIS JIROVECI (CARINII) PNEUMONIA (PCP) What are the clinical manifestations of PCP in patients with HIV infection? PCP usually presents as an acute or subacute respiratory illness associated with fever, dyspnea, nonproductive cough, and fatigue. Physical findings on examination include tachypnea, fever, and inspiratory rales. Rarely, disseminated Pneumocystis occurs in HIV-infected patients with profound immunosuppression. Laboratory abnormalities associated with PCP include leukocytosis, hypoxemia, an elevated lactate dehydrogenase (LDH), and chest radiographic findings of localized or diffuse interstitial infiltrates. Occasionally, nodular or cavitary lesions may be observed. Pneumothorax in patients with advanced HIV is almost always associated with underlying Pneumocystis infection. The degree of hypoxemia is a measure of disease severity; severe PCP is defined as an arterial blood gas PO 2 of 35 mm Hg. The diagnosis is confirmed by demonstrating the presence of P. jiroveci organisms in sputum or tissue samples obtained by sputum induction, bronchoscopy with bronchoalveolar lavage, or tissue biopsy. In the rare circumstance in which acute PCP presents very early with a normal chest radiograph, a gallium scan may demonstrate diffuse uptake in the lung compatible with an interstitial inflammatory process; however, this diagnostic test is nonspecific. How should you manage PCP? The preferred initial treatment for PCP in HIV-infected individuals is trimethoprim-sulfamethoxazole (TMP- SMX). Route of administration (oral or parenteral) is generally based on the severity of the disease. For those with severe PCP, parenteral therapy with trimethoprim 15-20 mg/kg and sulfamethoxazole 75-100 mg/kg, in 6-8 hour divided doses, is recommended. In addition, adjunctive treatment with corticosteroids, in a dose equivalent to 40 mg twice a day of prednisone for the first 5 days, followed by a tapering schedule of 40 mg/ day for days 6-10, and then 20 mg/day to complete 21 days of therapy, should be initiated as soon as possible after starting treatment but preferably within the first 72 hours. For patients with mild to moderate PCP (PO 2 >70 mmHg and AaO 2 gradient
A Guide to Primary Care of People with HIV/AIDS Chapter 9: Management of Opportunistic Diseases Table 9-2. Alternative Regimens for the Treatment of Pneumocystis carinii Pneumonia in Those Unable to Tolerate Trimethoprim and Sulfamethoxazole Disease Presentation Severe (PO 2 35 mm Hg) Alternative Treatment Regimens Pentamidine 3-4 mg/kg/d IV IV Trimetrexate 45 mg/M 2 /d IV + Leucovorin 0.5 mg/kg IV q6h Primaquine 15-30 mg/d (base) po + Clindamycin 600-900 mg IV q8h Mild-moderate Trimethoprim 15-20 mg/kg/d po + Dapsone 100 mg/d po q8h Primaquine 15-30 mg/d (base) p.o. + Clindamycin 300-450 mg po q6-8 hours Atovaquone suspension 750 mg po bid What adverse reactions occur with treatment for PCP? Patients should be carefully monitored for adverse reactions to treatment and response to therapy. Many patients will demonstrate acute worsening of signs and symptoms and have radiographic abnormalities in the first 3-5 days of treatment. This is the rationale for adjunctive corticosteroids in those with severe PCP. Five to 7 days of treatment may be required before a clinical response is observed, defined as a reduction in fever, and improvement in hypoxemia, respiratory symptoms, and radiographic abnormalities. Adverse reactions to treatment are common in patients with AIDS. Many patients can be treated through these with supportive care and adjunctive medications to ameliorate symptoms; however, severe adverse reactions may require substituting alternative treatment regimens. Adverse effects most often associated with TMP-SMX include skin rash (rarely, Stevens-Johnson syndrome or toxic epidermal necrolysis), fever, hepatotoxicity, leukopenia, thrombocytopenia, renal dysfunction, and hyperkalemia. Major side effects of pentamidine include pancreatitis, renal dysfunction, dysglycemia, electrolyte abnormalities, and cardiac dysrhythmias. Toxicities commonly observed with trimetrexate include bone marrow suppression (particularly in those who are not treated with leukovorin), fever, rash, and hepatitis. Dapsone may cause fever, skin rash, and methemoglobinemia with hemolysis (particularly in those with G-6-PD deficiency). Primaquine also causes methemoglobinemia and anemia, and clindamycin toxicities include nausea, rash, hepatitis, Clostridium difficile toxin-associated diarrhea, and rarely toxic megacolon. Atovaquone is associated with nausea, vomiting, diarrhea, rash, fever, and hepatitis. Is secondary prophylaxis or maintenance therapy required after treatment of the acute episode of PCP? All patients with a CD4 count of 200 cells/mm 3 and is sustained for at least 3 months. Prophylaxis should be restarted if the CD4 count declines to
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