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KEY POINTS
The acquired immunodeficiency syndrome (AIDS) is caused by human immunodeficiency virus (HIV), a sexually transmitted retrovirus, and characterized by depletion of T-helper (CD4) cells and severe immunodeficiency. Clinically, AIDS is defined as depletion of CD4 cells less than 200 cells/mm3 or development of AIDS qualifying opportunistic infection.
Effective antiretroviral therapy and chemoprophylaxis has increased the latency phase of HIV infection prolonging asymptomatic disease to several decades.
Pulmonary complications remain the leading cause of morbidity and mortality in HIV-infected patients. Bacterial pneumonia caused by streptoccocus pneumoniae, staphylococcus aureus and tuberculosis are common causes of respiratory illness.
The prevalence of respiratory failure from Pneumocystis jiroveci pneumonia (PCP) has significantly decreased over the past 2 decades with the use of highly active antiretroviral therapy and prophylaxis with trimethoprim-sulfamethoxazole.
Adjunctive corticosteroid therapy is recommended to prevent lung injury in severe cases of PCP pneumonia, defined as those with PaO2 of less than 70 mm Hg or alveolar-arterial oxygen gradient more than 35 mm Hg on room air.
HIV-infected patients have a higher incidence of pancreatitis due to older nucleoside reverse transcriptase agents, pentamidine, sulfa drugs, isoniazid as well as pathogens, such as cytomegalovirus and cryptosporidium.
Co-infection with hepatitis B and C viruses is common in HIV patients and can lead to chronic infection, high level of viremia, and early progression to end stage liver disease.
Neurological complications in HIV and AIDS patients can range from neurocognitive disorders (eg, HIV dementia) to life-threatening opportunistic infections associated with changes in mental status or seizures.
Metabolic and cardiovascular disorders are common in HIV-infected patients and are frequent causes of morbidity and mortality in the post-highly active antiretroviral treatment era.
It is usually safer to withhold HIV medications in the critically ill patient. However, if continuing or initiation of antiretroviral agents is warranted, consultation with an infectious disease specialist is recommended.
Immune reconstitution inflammatory syndrome is commonly seen 4 to 6 weeks after initiation of highly active antiretroviral treatment in treatment naive patients who are severely immune suppressed (CD4 < 50-100 cells/mm3) and have an opportunistic infection at the time of HIV diagnosis.
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Human immunodeficiency virus (HIV) is a sexually transmitted retrovirus composed of RNA (ribonucleic acid) genome and enzymes such as protease, reverse transcriptase and integrase; enveloped within an outer shell that has binding sites for two cell receptors, CCR5 and CXCR4. CXCR4 is a coreceptor found on CD4+ T cells and CCR5 is found on CD4+ T helper cells, macrophages, and dendritic cells. In the first 2 to 3 weeks of acute infection, macrophages and CD4+ T cells are depleted rapidly as the virus replicates within these cells. Clinically, this period manifests as a febrile viral syndrome commonly with symptoms of atypical rash and lymphadenopathy. Seroconversion eventually follows 2 to 4 weeks after primary HIV infection as humoral immunity develops. As the immune system recognizes and destroys systemic viral particles and infected cells, the body enters ...