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HIV and Associated Infections in the ICU 131
2.2.1. HIV-Associated Organ Damage. HIV directly damages many
organ systems, either through direct cellular toxicity or secondary to
associated host inflammatory responses. This may be manifest as HIVinduced
myocarditis/cardiomyopathy, myelopathy, enteropathy,
encephalopathy/dementia, interstitial pneumonia, emphysema,
dermatitis/pruritus, as well as affective and psychotic disorders (25-35).
In addition, conditions such as HIV-induced anemia and thrombocytopenia
appear to be mediated by humoral immunity, with target damage arising
from antigen-antibody complexes rather than from cytokine-induced
inflammation (36).
While these and other examples of HIV-induced organ damage are well
characterized in the literature, their identification remains difficult in the
ICU. Each may be sufficiently severe to require ICU management, yet
none may be diagnosed except by exclusion. As a group, these conditions
have convincing (and often multiple) clinical imitators, typically related to
opportunistic infections or toxic medication effects. Furthermore, clinical
signs such as pulmonary infiltrates may be caused by several of these
entities, by opportunistic infection, by drug toxicities, or by any number of
non-HIV-related conditions.
Once established, some HIV-induced organ damage, such as
cardiomyopathy and dementia, are not significantly reversible, though
effective antiretroviral therapy may halt progression. In contrast, others
conditions (e.g., enteropathy, pruritus) potentially resolve with therapy.
Thus, bona fide HIV-induced organ damage may be a realistic ICU
indication for institution of HAART in the absence of infectious
contraindications. Corticosteroids play an unclear role in the management
of HIV-induced organ damage, though they appear to be beneficial in the
management of immune mediated anemia and thrombocytopenia, in concert
with intravenous immunoglobulin and splenectomy.
2.2.2. HIV-Related Drug Toxicities. Just as HIV-induced organ damage
can result in ICU admissions, so too can the untoward effects of
antiretroviral therapies. For example, 2’,3’-dideoxinosine (ddI) may result
in peripheral neuropathy at therapeutic doses. Similarly, stavudine (d4T)
therapy may result in mitochondrial toxicity with lactic acidosis. To
further complicate this problem, the use of either of these drugs along with
parenteral pentamidine may result in severe pancreatitis (19). Therefore,
the intensivist must diligently review the medication lists of HIV-infected
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