A Guide to Primary Care of People with HIV/AIDS - Canadian Public ...

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