A Practical Approach to HIV/AIDS: Part 1

Authors: Kamoga Dickson, MD (EM Resident Physician, Makerere College of Health Sciences, Kampala, Uganda); Jessica Pelletier, DO, MHPE (APD/Assistant Professor of EM/Attending Physician, University of Missouri-Columbia) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case

A 17-year-old male presents to the emergency department (ED) for sexually transmitted infection (STI) testing. He has been having unprotected receptive anal intercourse with two male sexual partners over the past 6 months. The patient denies any current symptoms but states that he just wants to get “checked out.” He has no chronic medical conditions, does not take any medications, and does not use any drugs or alcohol. Vital signs are within normal limits, with BP 110/70 mmHg, HR 60 bpm, RR 18 breaths/min, O2 saturation 98% on RA, T 37 C. His physical examination is reassuring. Sexually transmitted infection (STI) testing is sent for chlamydia, gonorrhea, syphilis, trichomonas, and HIV, and he receives prophylactic ceftriaxone and doxycycline. The syphilis and trichomonas tests come back negative in the ED, but his rapid HIV test is positive.

How should clinicians approach the diagnosis and management of HIV in the ED?

Introduction

Human Immunodeficiency Virus (HIV) has represented a massive global health challenge since its recognition in the early 1980s.¹ Over the decades, HIV has transitioned from being a terminal illness to a manageable chronic condition for many individuals due to improved knowledge in the diagnosis and treatment of the disease globally.² The development of antiretroviral treatment (ART) in the 1990s, coupled with the adoption of the ‘treat-all’ strategy by WHO in 2015, has been fundamental in bringing HIV transmission and mortality rates down.^3,4

Despite these advances, HIV continues to pose a considerable public health burden, particularly in low- and middle-income countries.⁵ As of 2023, approximately 38 million people worldwide are living with HIV, with sub-Saharan Africa bearing the highest burden, accounting for nearly 67% of all cases.⁶ The region also experiences the highest rates of HIV-related morbidity and mortality. Other regions, such as Asia, Latin America, and Eastern Europe, have also seen significant increases in HIV prevalence.⁶

HIV infects and destroys CD4+ T-helper cells by binding to CD4 receptors (CCR5 or CXCR4), allowing fusion with the host cell membrane and subsequent integration of its viral RNA into the host genome. The progressive depletion of CD4+ cells and eventual immune dysfunction makes the body susceptible to opportunistic infections and malignancies.⁷ The disease spreads primarily through unprotected sexual contact, sharing of contaminated needles, blood transfusions, and from mother to child during childbirth or breastfeeding.⁸

By depressing the immune system, HIV affects all organ systems and may present with opportunistic infections such as tuberculosis, Pneumocystis jiroveci pneumonia, or cryptococcal meningitis.⁹ Though these infections have significantly reduced recently due to advancements in the use of highly active antiretroviral treatment (HAART), they still occur in individuals who are naïve to HAART or those with sub-optimal adherence.⁹

Historically, the management of HIV and its complications was primarily the domain of primary care and infectious disease (ID) specialists. However, with the global evolution of emergency medicine (EM), more HIV patients now engage with EDs, often presenting with acute complications or in an undifferentiated state before receiving a formal diagnosis.¹⁰ The advent and widespread use of HAART has markedly increased the life expectancy of persons living with HIV (PLHIV), consequently heightening the prevalence of chronic, non-communicable diseases such as hypertension, cardiovascular disease, diabetes, and cancers within this population.¹¹ These cardiovascular complications have further increased ED visits by HIV-positive patients by three times compared to individuals without HIV.¹²

EM has become a pivotal component of HIV care globally, serving as a critical intersection between inpatient admissions and outpatient clinic follow-ups.¹⁰ As such, emergency physicians need to possess a strong understanding of HIV diagnosis and treatment principles. This article provides a practical guide to managing HIV/AIDS in the ED, equipping ED physicians with the knowledge needed to deliver optimal care to these patients.

Epidemiology

Since the start of the epidemic in the 1980s, HIV has killed over 40 million people globally, with the highest number being in Sub-Saharan Africa.¹³ Globally, 39.9 million (36.1 million–44.6 million) people are living with HIV, with an annual incidence of 1.3 million (1 million–1.7 million) people. 630,000 (500,000–820,000) people die from HIV/AIDS-related illnesses annually. 88.4 million people have become infected with HIV since the start of the epidemic.¹³

The Joint United Nations Program on HIV/AIDS (UNAIDS) set targets for ending the HIV pandemic by 2030. These 95-95-95 targets aim to have 95% of PLHIV know their status, 95% receive treatment, and 95% of people receiving HAART have viral suppression. As of 2023, these targets have grown closer, with 86% of PLHIV knowing their status, 77% accessing treatment, and 72% virally suppressed globally.¹³ The current United States (U.S.) government freeze on global aid, specifically the stoppage of the U.S. President’s Emergency Plan for AIDS Relief (PEPFAR) program, is anticipated to have extremely negative impacts on reaching these goals.¹⁴

67% of the global HIV cases occur in sub-Saharan Africa (SSA). Other regions with a high HIV prevalence include Asia, with 5.8 million PLHIV, Latin America, and Eastern Europe.⁶ Certain groups bear a disproportionate burden of HIV globally. These include men who have sex with men (MSM), sex workers, intravenous drug users (IVDU), adolescent girls, and young women (especially in SSA due to gender inequality and lack of education).¹⁵

There are two distinct strains of HIV, HIV-1, and HIV-2, both causing HIV infection but differing in epidemiology, pathogenicity, and treatment response. HIV-1 is more widespread and virulent, driving the global pandemic. In contrast, HIV-2 is primarily localized to West Africa, with limited cases in Europe and India, and has lower transmissibility compared to HIV-1.¹⁶

Risk Factors

HIV can affect anyone, regardless of sexual orientation, race, ethnicity, gender, age, or location. However, some groups face a higher risk due to factors like engaging in high-risk behaviors. These include:¹⁷

• Unprotected Sex: High-risk behaviors like condomless sex and multiple partners, especially among youth, drive HIV transmission.
• Mother-to-Child: HIV can be passed during pregnancy, birth, or breastfeeding but is preventable with proper care.
• STI: Having concurrent STIs such as chlamydia, gonorrhea, syphilis, bacterial vaginosis, and herpes increase their risk of getting HIV.
• IVDU: Sharing needles among injection drug abusers.
• The use of alcohol or drugs before sex can affect decision-making about whether to engage in sex or to use condoms during sex.
• Having sex with multiple partners.
• Young men who have sex with men, particularly Black/African American and Hispanic/Latino individuals, face high rates of new HIV diagnoses. Anal sex is the highest risk among forms of sexual intercourse for transmitting HIV.

Pathophysiology

HIV is an RNA retrovirus that targets the immune system, primarily infecting CD4+ T lymphocytes, macrophages, and dendritic cells. The virus spreads through unprotected sex, blood transfusions, injection drug use, and from mother to child.¹⁸

Once in the body, the virus follows a natural progressive course that starts with an initial period of influenza-like illness, which clinicians can easily miss. The subsequent latent phase is asymptomatic. During the latent phase, the virus replicates and destroys CD4+ lymphocytes, leading to AIDS (CD4 + count <200  cells/mm³ of blood) and death if unchecked.¹⁹

Figure 1. Natural progression of HIV/AIDS. Source: By Sigve – Own work, CC0, https://commons.wikimedia.org/w/index.php?curid=15383502

Once an individual is infected, the virus replicates via seven key steps leading to the establishment of HIV disease:

1. Fusion: HIV attaches to host cells, CD4+ lymphocytes, or macrophages via CCR5 or CXCR4 chemokine co-receptors, respectively.²⁰ CCR5 Antagonists (e.g., maraviroc) block the CCR5 co-receptor, and fusion inhibitors (e.g., enfuvirtide) prevent viral fusion with the host cell, thus blocking this replication stage.
2. Entry: The virus and its genetic material merge with the cell membrane and enter the host cell.
3. Reverse Transcription: HIV RNA is copied into proviral DNA by reverse transcriptase, an error-prone enzyme. These errors result in frequent mutations, which can create HIV that is resistant to the host’s immune system and antiretroviral drugs. This stage occurs in the cytosol. Two classes of drugs: Nucleoside Reverse Transcriptase Inhibitors (NRTIs) (e.g., tenofovir, emtricitabine) and Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) (e.g., efavirenz, nevirapine) block this stage of replication by inhibiting the reverse transcriptase enzyme.²¹
4. Integration: The proviral DNA is transported across the nucleus, integrated into the host cell’s DNA, and duplicated with each cell division. Integrase Strand Transfer Inhibitors (INSTIs) (e.g., raltegravir, dolutegravir) block the integration of viral DNA into the host genome.²²
5. Transcription and translation: The proviral DNA is transcribed into HIV RNA and translated into HIV proteins.
6. Assembly: The HIV proteins are assembled into virions at the host cell’s inner membrane, which bud off and are released into the circulation.
7. Cleavage: Protease, another HIV enzyme, cleaves the viral proteins, converting the immature virion into a mature, infectious virion. Protease Inhibitors (PIs) (e.g., lopinavir, darunavir) prevent protease from cleaving viral proteins, resulting in non-infectious virions.²³

 Antiretroviral drugs target specific stages of the HIV replication cycle to disrupt it.

Figure 2. HIV replication process. Source: Jmarchn, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons

Clinical Presentation

The clinical presentation of HIV is highly dependent on the World Health Organization (WHO) clinical stage of the disease.

Table 1. HIV staging. Modified from: Consolidated Guidelines on the Use of Antiretroviral Drugs for Treating and Preventing HIV Infection: Recommendations for a Public Health Approach. 2nd edition. Geneva: World Health Organization; 2016. ANNEX 10, WHO clinical staging of HIV disease in adults, adolescents and children. Available from: https://www.ncbi.nlm.nih.gov/books/NBK374293/

Diagnosis

Diagnosis of HIV depends on the clinical phase.

New-onset HIV (Acute HIV – 2 to 4 weeks)

The early HIV stage – also known as acute retroviral syndrome (ARS) or seroconversion stage – presents with nonspecific complaints. Common symptoms include fever, fatigue, rash, lymphadenopathy, pharyngitis, and myalgia. Symptoms overlap with common ED diagnoses, making clinical suspicion vital; this is based on the patient’s history and risk factors for exposure. Some patients (approximately 10% to 60%) of individuals with acute HIV infection are asymptomatic.²⁴

Tests Used:

• HIV RNA (Nucleic Acid Amplification Test): This test detects viral RNA within 10-14 days of exposure and is highly sensitive for early infection.
• Fourth-Generation HIV Test: Detects both HIV p24 antigen and antibodies. Can identify infection within 2-4 weeks.
• Baseline Tests: Consider screening for other STIs and hepatitis.
• Antibody tests are negative during this stage and should never be reliably used for diagnosis.²⁴
• Patients diagnosed with new-onset HIV need a baseline complete blood count (CBC), renal function tests (RFTs), and liver function tests (LFTs), as the results of these tests may modify the selection of HAART by ID.¹⁰

Pearl: Patients with acute HIV symptoms often present undiagnosed to the ED, where early recognition, risk assessment, and timely referral for ART initiation are critical. Consider giving Post-Exposure Prophylaxis (PEP) if a patient presents within 72 hours of possible exposure and has a negative baseline HIV test.

Asymptomatic HIV/Latent phase

Following the ARS stage, HIV progresses into a stage of clinical latency. This stage lasts weeks to years; diagnosis is usually made incidentally during screening.²⁵

Tests Used:

• Fourth-generation HIV Tests: Detect both HIV antibodies and the p24 antigen.
• HIV RNA: Detects viral RNA directly. Highly sensitive and effective throughout the latent phase, particularly in cases where antibody tests might be ambiguous.
• Rapid Antibody Tests: Detect antibodies to HIV-1 and HIV-2. Effective during the latent phase once seroconversion is complete (typically 3-12 weeks post-infection).
• Western Blot and Immunoassays (Confirmatory Tests): Used to confirm initial reactive results from antibody or antigen/antibody tests.
• CD4 Count and Viral Load: Assess immune function and viremia, respectively.

AIDS (Advanced HIV Infection)

AIDS is diagnosed when CD4 counts drop <200 cells/mm³ or in the presence of AIDS-defining illnesses (e.g., Pneumocystis pneumonia, Kaposi sarcoma, cryptococcal meningitis).²⁵

Tests Used:

• HIV Testing as above: Confirmatory testing to establish HIV status if previously undiagnosed.
• CD4 Count: Assesses immune status.
• Viral load: To assess baseline before HAART initiation
• Opportunistic infection workup: Specific tests based on presenting symptoms (e.g., chest X-ray, sputum studies for Pneumocystis and tuberculosis, CSF analysis for cryptococcal meningitis, CMV work-up, etc.)²⁶

Pearl: The ED plays a vital role in HIV care, requiring clinicians to diagnose at all stages, initiate PEP, manage AIDS complications, and ensure continuity with outpatient services.

Management and Disposition

Asymptomatic HIV exposure

Patients within 72 hours of HIV exposure who have a baseline negative HIV test should be offered PEP. It is critical to ensure that the patient is also negative for hepatitis B, as emtricitabine plus tenofovir (Truvada) can temporarily suppress hepatitis B and then cause rebound viral activity, leading to liver damage.¹⁰ Further details on PEP can be accessed here: https://www.emdocs.net/emdocs-podcast-episode-82-hiv-post-exposure-prophylaxis/

If patients have had a high-risk sexual encounter as their source of HIV exposure, the following additional prophylaxis medications:

• Ceftriaxone 500 mg intramuscular (IM) once PLUS doxycycline 100 mg per os (PO) twice daily (BID) X 7 days to cover gonorrhea, C. trachomatis, Ureaplasma, and Mycoplasma species
  • Ceftriaxone dosing should be increased to 1 g for patients ≥150 kg²⁷
  • Doxycycline PEP will also cover syphilis²⁸
• For females: add metronidazole 500 mg PO BID X 7 days to cover vaginalis²⁷ and offer emergency contraception.
  • Within 3 days: Levonorgestrel (LNG) 1.5 mg PO once OR 0.75 mg BID X 2 doses
  • Within 5 days: Ulipristal acetate (UPA) 30 mg PO once²⁹
• Hepatitis B immune globulin if unvaccinated/not immune PLUS the hepatitis B vaccine series³⁰
• Note that many of these medications are associated with nausea. Patients may need antiemetics in the ED and at discharge to ensure medication tolerance.

Patients with asymptomatic HIV exposure and negative HIV testing may be discharged home. They should be notified that if any testing for other sexually transmitted diseases (i.e., chlamydia, gonorrhea, etc.) comes back positive, they will receive a call from the hospital (if follow-up calls are available) or from the health department. These patients will need to follow up with primary care (or ID) for repeat testing for lab monitoring and to set up follow-up testing.¹⁰

New-Onset HIV

Initiation of HAART is typically preceded by HIV viral load and resistance genotyping, assessment of liver and renal function, pregnancy testing, and ruling out hepatitis B co-infection. Since many of these tests will not come back during the ED course, initiation of HAART in the ED is uncommon (though not impossible). Local protocols should be followed to ensure rapid referral to ID.³¹

In patients with a new diagnosis of HIV who do NOT have findings concerning for AIDS (Table 1, Stage 4), they may be stable for discharge with outpatient follow-up with ID. If outpatient follow-up is difficult due to social issues (such as transportation or financial barriers), ED clinicians should discuss the case with ID in the ED (where available) to determine an appropriate HAART regimen and follow-up plan.

AIDS

Patients with AIDS should be admitted to the hospital. Those with sepsis should receive broad-spectrum antibiotics based on local hospital antibiograms. They should receive additional antifungal coverage and specific empiric treatment for opportunistic infections based on the history and exam after discussion with ID.  Initiation or resumption of HAART in patients with AIDS should be discussed with ID, as there is a risk of developing immune reconstitution syndrome (IRIS). Patients with CD4 counts ≤50 cells/mm³ are at the highest risk of developing IRIS. This condition is typically treated symptomatically but may occasionally require corticosteroids (which should only be initiated after discussion with ID).^32–37

Prognosis

Asymptomatic HIV exposure

For patients with asymptomatic HIV exposure, the risk of seroconversion will differ based on the level of risk of exposure (Table 2).

Table 2. Risk of HIV seroconversion stratified by exposure type.

New-Onset HIV

Patients who are compliant with HAART and maintain near-normal CD4 counts may expect a life expectancy similar to that of the general population.⁴³

AIDS

Patients with AIDS, unfortunately, have a poor prognosis. Patients who start HAART with a CD4 count <200 cells/mm³ may have a life expectancy reduction of as much as 15 years compared to those who start HAART at a higher CD4 count.⁴⁴

Prevention

The Centers for Disease Control and Prevention (CDC) recommends several strategies for preventing HIV infection (Table 3).

Table 3. HIV prevention/harm reduction strategies.⁴⁵

Pearls and Pitfalls

• HIV infection is an RNA retrovirus causing immunosuppression that can be transmitted via occupational or non-occupational exposures.
  • High-risk exposures warrant PEP for both HIV and possible concomitant infections.
• New-onset HIV should be ruled out in patients with potential exposures and flu-like illness.
• HAART should only be initiated in the ED with input from ID.
• Patients engaging in high-risk sexual behavior or IVDU should be counseled regarding prevention strategies.

Further Reading

FOAMed:

• https://www.emdocs.net/emdocs-podcast-episode-46-hiv/
• https://www.emdocs.net/emdocs-podcast-episode-82-hiv-post-exposure-prophylaxis/
• https://www.emdocs.net/the-em-educator-series-hiv-aids-fever/
• https://www.emdocs.net/pneumocystis-jirovecii-pneumonia-and-hiv-a-practical-guide-for-ed-diagnosis-and-management/
• https://www.emdocs.net/em3am-cns-toxoplasmosis-in-hiv-aids/
• https://www.emdocs.net/cryptococcal-meningitis-ed-presentations-evaluation-and-management/
• https://www.emdocs.net/em3am-oropharyngeal-candidiasis/

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