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HIV for the ED

HIV for the ED. Navpreet Sahsi. Special thanks to Dr. Margriet Greidanus and Dr. James Huffman for their help and allowing use of some of their slides or images for this presentation. Outline. Epidemiology HIV Basics HIV in the ED, in the post HAART ERA Primer on Needlestick injuries.

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HIV for the ED

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  1. HIV for the ED Navpreet Sahsi

  2. Special thanks to Dr. Margriet Greidanus and Dr. James Huffman for their help and allowing use of some of their slides or images for this presentation.

  3. Outline • Epidemiology • HIV Basics • HIV in the ED, in the post HAART ERA • Primer on Needlestick injuries

  4. Epidemiology • Worldwide: 59 million persons infected, with 20 million deaths worldwide. • US – Currently more than one million individuals currently infected, with greater than fourty thousand new patients diagnosed each year • Canada - ???

  5. How many Canadians have a positive HIV Diagnosis? (June 2008) • A) 30,000 • B) 60,000 • C) 90,000 • D) 120, 000

  6. Answer • B) 60, 000 Public Health Agency of Canada 2008 Surveillance report.

  7. http://www.avert.org/canada-hiv.htm

  8. What Province has the highest proportion of HIV cases? • A) BC • B) Alberta • C) Ontario • D) Quebec • E) Nunavut

  9. Answer • B) Ontario – currently accounts for 39% of the nations HIV cases • BC, Ontario, Quebec, and Alberta account for 85% of our population, and 95% of our HIV cases • Currently 3 reported HIV positive cases in Nunavut since 2002 (epidemic?)

  10. HIV Basics From Wikipedia: “HIV enters……. macrophages and CD4+T cells by the adsorption of glycoproteins on its surface to receptors on the target cell followed by fusion of the viral envelope with the cell membrane and the release of the HIV capsid into the cell.[74][75]Entry to the cell begins through interaction of the trimeric envelope complex (gp160 spike) and both CD4 and a chemokine receptor (generally either CCR5 or CXCR4, but others are known to interact) on the cell surface.[74][75] gp120 binds to integrin α4β7 activating LFA-1 the central integrin involved in the establishment of virological synapses, which facilitate efficient cell-to-cell spreading of HIV-1.[76] The gp160 spike contains binding domains for both CD4 and chemokine receptors.[74][75] The first step in fusion involves the high-…..” • Ummm……..what?

  11. Better?

  12. The real basics • HIV – single stranded RNA virus • Primarily attacks host cells involved in immune function – primarily CD4 T cells • Makes copies into host genome’s DNA • High viral load early – until immune system kicks in • Accounts for acute symptomatic phase • Slowly weakens immune system -> badness

  13. How HIV Works 3. Integration into host cell’s nucleus HIV 4. Reproduction of viral components 1. Attachment to host cell • Assembly of new HIV viruses • Reverse transcriptase makes DNA from the virus’s RNA 6. Release

  14. Basics • Modes of Transmission • Unprotected vaginal or anal intercourse with an infected partner • Sharing needles with infected partner • Contact with infected blood • Perinatal transmission

  15. Virus is passed in infected body fluids • High concentration in blood, semen, vaginal fluid and breast milk • Low levels in almost every other fluid (incl. sweat, urine, csf, tears, bone marrow, alveolar fluid, synovial fluid, amniotic fluid and saliva • small likelihood of transmission Risk Factors - Viral load (higher load = higher risk) - CD4 count < 200 cells/microL - Other STD’s – especially ulcerative lesions

  16. Seroconversion (detectable antibody response to HIV) • Sources vary, but most sources state that most patients seroconvert to positive HIV serology in 4 to 10 weeks • > 95 % within six months • Median time to exposure 63 d

  17. Natural History • Viral transmission • Primary HIV infection (acute HIV infection) • Seroconversion • Clinically latent period (+/- lymphadenopathy) • Early symptomatic HIV infx • AIDS • Advanced HIV infx (CD4 < 50)

  18. Natural History of HIV Infection Viral Load Number of CD4 cells / Viral Load CD4 Count 2 4 6 0 2 6 8 10 4 years weeks

  19. Natural History of HIV Infection Viral Load Clinical Latent Period Viral Transmission Number of CD4 cells / Viral Load Advanced AIDS Primary Infection Early HIV Infection AIDS CD4 Count 2 4 6 0 2 6 8 10 4 weeks

  20. Acute HIV infection • Usually develop 2 – 4 weeks post exposure and last for less than 14 days • Presentation is nonspecific and frequently missed • Diagnosis is missed in up to 75 percent of patients due to low index of suspicion • In a small case series from Seattle only 5 of 19 patients (26 %) in HIV surveillance program who sought care from ED’s and walk-in’s were diagnosed with acute HIV infection

  21. What is the most common initial presentation with acute HIV? • A) Fever • B) Pharyngitis • C) Rash • D) Headache • E) Lymphadenopathy

  22. A) Fever - > 90% • B) Pharyngitis - > 70 % • C) Rash – 40- 80 % • D) Headache – 30 – 70 % • E) Lymphadenopathy – 40 – 70 % • Presentation very similar to flu-like or mononucleosis-like syndrome. • After six months of infection, plasma viremia reaches a steady state • Viral load is most important predictor of progession of disease in early stages

  23. Natural History of HIV – Clinical Latent Period • Clinical latent period • Generally no findings except for possible lymphadenopathy • Persistent generalized lymphadenopathy (PGL) referred to as enlarged lymph nodes involving at least two non-contiguous sites other than inguinal nodes • Lymphoid tissue serves as the major reservoir for HIV. Lymphoid tissue traps free virus and infected CD4 T cells

  24. Natural History of HIV - Early symptomatic HIV infection AIDS indicators – can also occur with other disease processes, but are typically more frequent or more severe with an HIV infection - Thrush - Vaginal candidiasis that is persistent, frequent, or difficult to manage - Oral hairy leukoplakia - Herpes zoster involving two episodes or more than one dermatome - Peripheral neuropathy - Bacillary angiomatosis - Cervical dysplasia - Cervical carcinoma in situ - Constitutional symptoms such as fever (38.5°C) or diarrhea for more than one month - Idiopathic thrombocytopenic purpura - Pelvic inflammatory disease, especially if complicated by a tubo-ovarian abscess

  25. Candida

  26. Oral Hairy Leukoplakia

  27. Herpes Zoster

  28. Probability of developing AIDS within 3 years Probability of progression to AIDS (%) (N=1,637) Viral Load (copies/mL) Ann Intern Med 1997;126:946

  29. AIDS

  30. AIDS Diagnosis occurs when a person: • Has antibodies against HIV in their blood AND • Is diagnosed with one or more AIDS-defining illnesses • In the US (but not Canada or Europe) the AIDS definition also includes all HIV-infected individuals with a CD4 count lower than 200 cells/μL or a CD4 percentage less than 14%

  31. What are the opportunistic infections that are considered AIDS –defining illnesses?

  32. AIDS-Defining Illnesses • Candidiasis of esophagus, trachea or lungs • Cervical Cancer (invaisive) • Coccidiomycosis • Cryptococcosis • Cryptosporidiosis • Isosporiosis • Cytomegalovirus disease • HSV (>1month duration) • Disseminated histoplasmosis • HIV encephalopathy • Kaposi’s sarcoma • Lymphoma (CNS or Burkitt’s) • Mycobacterium avium complex • Mycobacterium tuberculosis (pulmonary) • Pneumocystis pneumonia • Recurrent bacterial pneumonia • Progressive multifocal leukoencephalopthy • Recurrent Salmonella septicemia • Toxoplasmosis of the brain • HIV wasting syndrome

  33. Pneumocystis carinii (PCP)

  34. Tuberculosis Apical infiltrates

  35. Kaposi’s Sarcoma

  36. Toxoplasmosis

  37. Lymphoma

  38. Natural History of HIV – AIDS • 10% of pts will develop an AIDS defining diagnosis with a CD4 count above 200/mm3 • Most common AIDS diagnosis (prior to HAART) • P. carinii pneumonia - 42.6% • Esophageal candidiasis – 15% • Wasting – 10.7% • Kaposi’s Sarcoma – 10.7% • Disseminated M. Avium infection -4.8% • Tuberculosis – 4.5%

  39. Advanced HIV • CD4 < 50 • Median time of survival 12- 18 months in the absence of ARV’s • Presence of end-stage disease – including disseminated MAC or disseminated CMV

  40. So learning about advanced HIV/AIDS is great, and we all love looking at pictures of Kaposi’s Sarcomas, but does this even matter anymore?

  41. http://www.youtube.comwatchv=DGJDzufJKlc

  42. The HAART Era • Recommended reading • Venkat et al. Care of the HIV-Positive Patient in the Emergency Department in the Era of Highly Active Antiretroviral Therapy. Ann Emerg Med. 2008; 52:274-285

  43. Times have changed… • In 80’s hospitalizations in HIV population were mainly due to opportunistic infections and conditions related to patient’s poor immune response to other pathogens • Primarily in patients under 40 years old • In 1993 33.3 % of HIV-related admissions were due to infections caused by opportunistic infections or uncharacterized pneumonia

  44. Living longer…. • Now with the success of HAART, patients are living longer • For a 20 year old HIV-infected patient, mean life-expectancy has increased from 9.1 years (+/- 2.3 years) in 1993 to 23.6 years (+/- 4.4 years) in 2002 • Now illnesses related to cardiovascular disease, medication adverse effects, and malignancies (mainly lymphoma) have become more prevalent

  45. Who gets HAART? • Controversial – still debated • For sure • CD4 < 350 cells/microL • Pregnancy • HIV – associated nephropathy or neuropathy • Co-infection with HBV or HCV receiving therapy • History of AIDS-defining illness

  46. ?? • Age > 50 • Discordant couples • CD4 > 350 • Cardiovascular disese

  47. HAART drugs • Lots of fancy drugs that we never prescribe… • Basically 3 major groups • Nucleoside reverse transcriptase inhibitore (NRTIs) • Non – NRTIs • Protease inhibitors • Plus some new ones that are being used, but beyond the scope of this talk…..

  48. How NRTI’S Work HIV Nucleoside reverse transcriptase inhibitors (NRTI’s) latch onto the new strand of DNA that reverse transcriptase is trying to build

  49. How NNRTI’S Work HIV Non-nucleoside reverse transcriptase inhibitors (NNRTI’s) hook onto reverse transcriptase and stop it from working

  50. How PI’s Work HIV Protease inhibitors (PI’s) prevent final assembly and completion of new HIV viruses within the cell

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