HIV for the Emergency Physician - Calgary Em

HIV for the Emergency Physician - Calgary Em

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

Answer B) 60, 000 Public Health Agency of Canada 2008 Surveillance report. http://www.avert.org/canada-hiv.htm What Province has the highest proportion of HIV cases? A)

BC B) Alberta C) Ontario D) Quebec E) Nunavut 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?) 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 47 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? Better?

The real basics HIV single stranded RNA virus Primarily attacks host cells involved in immune function primarily CD4 T cells Makes copies into host genomes DNA High viral load early until immune system kicks in Accounts for acute symptomatic phase Slowly weakens immune system -> badness

How HIV Works HIV 1. Attachment to host cell 2. Reverse transcriptase makes DNA from the viruss RNA 3. Integration into host cells nucleus

4. Reproduction of viral components 5. Assembly of new HIV viruses 6. Release Basics Modes of Transmission Unprotected vaginal or anal intercourse with an infected partner

Sharing needles with infected partner Contact with infected blood Perinatal transmission 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 STDs especially ulcerative lesions 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 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) Number of CD4 cells / Viral Load Natural History of HIV Infection ad o lL a r Vi

4 CD t un Co 0 2 4 weeks

6 2 4 6 years 8 10

0 2 4 weeks 6 2 4

6 AIDS 8 t un Co Early HIV Infection Clinical Latent Period

Advanced AIDS ad o lL a r Vi 4 CD Number of CD4 cells / Viral

Load Natural History of HIV Infection 10 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 EDs and walk-ins were diagnosed with acute HIV infection What is the most common initial presentation with acute HIV? A) Fever

B) Pharyngitis C) Rash D) Headache E) Lymphadenopathy A) Fever - > 90% B) Pharyngitis - > 70 % C) Rash 40- 80 % D) Headache 30 70 % E) Lymphadenopathy 40 Presentation

70 % 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 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 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 (38.5C) or diarrhea

for more than one month - Idiopathic thrombocytopenic purpura - Pelvic inflammatory disease, especially if complicated by a tubo-ovarian abscess Candida Oral Hairy Leukoplakia Herpes Zoster Probability of progression to AIDS (%)

Probability of developing AIDS within 3 years (N=1,637) Viral Load (copies/mL) Ann Intern Med AIDS AIDS Diagnosis occurs when a person: 1. Has antibodies against HIV in their blood

AND 2. Is diagnosed with one or more AIDSdefining illnesses In the US (but not Canada or Europe) the AIDS definition also includes all HIVinfected individuals with a CD4 count lower than 200 cells/L or a CD4 L or a CD4 percentage less than 14% What are the opportunistic infections that are considered AIDS defining illnesses? 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 Kaposis sarcoma

Lymphoma (CNS or Burkitts) Mycobacterium avium complex Mycobacterium

tuberculosis (pulmonary) Pneumocystis pneumonia Recurrent bacterial pneumonia Progressive multifocal leukoencephalopthy Recurrent Salmonella septicemia Toxoplasmosis of the brain HIV wasting syndrome Pneumocystis carinii (PCP) Tuberculosis

Apical infiltrates Kaposis Sarcoma Toxoplasmosis Lymphoma 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% Kaposis Sarcoma 10.7% Disseminated M. Avium infection -4.8% Tuberculosis 4.5% Advanced HIV CD4

< 50 Median time of survival 12- 18 months in the absence of ARVs Presence of end-stage disease including disseminated MAC or disseminated CMV So learning about advanced HIV/ AIDS is great, and we all love looking at pictures of Kaposis Sarcomas, but does this even matter anymore?

http://www.youtube.comwatchv=DGJDzufJKlc 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

Times have changed In 80s hospitalizations in HIV population were mainly due to opportunistic infections and conditions related to patients 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

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 Who gets HAART? Controversial For still debated sure CD4 < 350 cells/microL Pregnancy HIV associated nephropathy or

neuropathy Co-infection with HBV or HCV receiving therapy History of AIDS-defining illness ?? Age > 50 Discordant couples CD4 > 350 Cardiovascular disese 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.. How NRTIS Work HIV

Nucleoside reverse transcriptase inhibitors (NRTIs) latch onto the new strand of DNA that reverse transcriptase is trying to build How NNRTIS Work HIV Non-nucleoside reverse transcriptase inhibitors (NNRTIs) hook onto reverse transcriptase and stop it from working How PIs Work HIV

Protease inhibitors (PIs) prevent final assembly and completion of new HIV viruses within the cell HAART Most patients are on a combination of drugs from all three classes Side effects many look up specifics Things of note All ARVs have potential for hepatotoxicty (any class)

Lactic Acidosis NNRTIs and PIs affect the cytochrome p450 system drug interactions! Cardiovascular Disease ACS All protease inhibitors cause hyperlipidemia, hyperglycemia and truncal obesity Increased time receiving HAART associated with 26% increased relative risk of MI/year Take

home: Consider HIV positive patients on prolonged ARV therapy at risk for ACS often at younger ages What is the most common respiratory pathogen in the post-HAART era? A) Pneumocysitis Jiroveci B) C. pneumonia C) Strep pneumo D) Legionella

E) TB Pulmonary C) Strep. Pnuemonia most common pneumonia Was PJP in pre-HAART era Similar presentation as non-HIV patients Can treat similarly if no immune compromise HIV

is an independant RF for COPD 0.5% will have pulmonary hypertension Not related to CD4 count Not related to specific HAART therapy Pneumocystis Jirvoveci Pneumonia Prolonged course (2 weeks) Typical symptoms of pneumonia nonspecific CXR interstitial infiltrates in 80%, otherwise N Treatment is TMP-SMX oral or IV

If oral, start 2 DS tabs q8h Renal ARF is now a leading cause of death in HIV-infected patients HIV nephropathy = HAART Due to HIV mediated viral or immunologic disease, as well as treatment-related effects PIs

associated with urolithiasis Rx is the same CNS T. Gondii and C. neoformans were predominant diseases pre-HAART but less common now Always CT before LP in workup of new neuro symptoms in patient with prolonged course of HIV infection

Increased risk of CVA aging population and medication effects Also think: AIDS dementia, lymphoma, Progressive multifocal leukoencephalopathy (encephalitis) Peripheral Nervous System Distal sensory neuropathies both HIV and HAART related (NRTs) Typically hypersensitivities to distal extremities +/- absent ankle reflexes

Discontinue meds and treat with gabapentin and NSAIDS Acute demyelinating polyneuropathy Presents like Guillain-Barre (ascending muscle weakness and sensory changes) Treated with plasmaphoresis Chronic

relapsing demyelinating polyneuropathy GI and Liver Diarrhea v. common problem C. Diff is the most likely bacterial pathogen (up to 36% of patients!) Assess and treat as you would non-HIV patients If

advanced AIDS need to think about cryptosporidium and microrsporidia need special stool studies Co-infection with Hep B/C causes most serious hepatic complications 2-3x more likely to develop chronic liver dz Shorter time to progression of AIDS If HAART meds stopped, severe exacerbations of Hep B can occur ARVs can cause an increase in all transaminases and unconjugated bili with no clinical liver disease

Hematologic and Oncologic Anemia of chronic disease is very common Hemolytic anemia can be severe associated with certain meds Neutropenia, thrombocytopenia secondary to disease progression Increased venous thromboembolic events (2-10x the risk) Coumadin has significant interactions with Protease inhibitors meds

Increased risk of TTP regardless of HAART Increased malignancies Hodgkins, anal cancer, lung cancer Any person with anal condylomata needs to be referred for anal cancer screening (HAART hasnt changed risk) Endocrine Protease inhibitors increase risk of hyperlipidemia and truncal

obesity Increased risk of insulin resistance and DM Psychiatric Depression 40% - need referral sig. dec. in compliance with HAART Demoralization different from depression in that it doesnt have anhedonia Need referral for counselling AIDS

mania - late Present in manic state with no history of previous disorders Associated with cognitive impairment (AIDS dementia) R/O meningoencephalitis, need CT, LP NNRTs can cause a psychosis, nightmares and increased irritability within first four weeks of therapy need to terminate med only for psychosis, the other symptoms will resolve

MSK/Rheumatologic Disease - Old: HIV associated arthritis/polymyositis - Now: Osteoporosis and osteonecrosis most common (usually of the hip) - Think chronic recurrent pain of hip - > surgical - - With HAART increased incidence of

infectious complications septic arthritis, osteomyeltits, diskitis) In HAART era, immune syndrome caused by ARVs has led some patients to develop sarcoidosis (mean time 9 months of therapy) - Symptomatic rx with corticosteroids Optho CMV retinitis reduced by 80% since onset of HAART therapy Any HIV + patient with any visual

loss or any macular edema needs urgent optho referral A Quick Primer on Needlestick Injuries Hypothetical case: Youre at the end of your shift and one of your resident collegues pulls you aside in the hallway (lets call him.I dunno.Kris McKrossin..with a

K) He tells you that he poked himself in the finger while putting in a central line on a patient a few hours ago and is wondering if he needs postexposure prophylaxis. What do you tell Kris? If you dont know, ask! Report all cases OH & S Call line 234-7799 24 hrs a day/7 days a week

Ask the charge nurse Every ED has a pre-printed protocol on what to do in case of exposures and access to PEP starter kit If you do get poked/exposed Remove the contaminated clothes undergarments excepted

Allow immediate bleeding of the wound Wash the injured area well with soap and water, and apply an antiseptic If the eyes, nose, or mouth are involved, flush them well with large amounts of water Southern Alberta Clinic Guidelines 1 Is the source known HIV+? Yes: proceed to step 2 of protocol

No: Test source (with consent) using rapid point-of-care HIV test available through CLS at any Emergency Room or Chumir Centre If negative, and no risk of window period, reassure patient If source unknown or refuses testing and has risks for or symptoms of HIV, proceed to step 2 of protocol Consider source testing for HBV, HCV most guidelines suggest testing for this Rapid HIV Testing Sensitivity

and Specificity both >90% Done in the on-site rapid response labs Current turn around time 1 hr 24 min can take about 4 hrs from blood draw to get result Realistically takes about 24hrs unless in special circumstances Confirmed by Western Blot at Prov Lab Consider giving dose of PEP before results arrive (based on your pre-test probability) CDC now endorsing more liberal use of rapid point-of-care testing Southern Alberta Clinic Guidelines

2 Timing and Type of Exposure: Assess fluid type, volume, viral titre, mode of exposure Assess exact timing of exposure If exposure is not considered infectious for HIV/HBV/HCV (i.e. vomit, feces, etc. without blood ) reassure and arrange f/u if patient desires If exposure considered potentially infections go to 3

Southern Alberta Clinic Guidelines 3 Decision: Make a decision for or against PEP based on risk assessment (these are debatable) HIV + = start PEP HIV and no risk of source pt being in Window period = dont start PEP Unknown (source not tested or refuses testing) = evaluate risk (OHS and protocols binder)

Risk Assessment -Done by EP / OHS guidance in protocols and PEP kit High risk IVDU High risk sexual behaviour (MSM, sex w/IVDU, multiple sexual partners (3 or more

sexual partners/yr w/I past 5 yrs), prostitution Blood transfusion prior to 1985 Sex w/HIV + person Clinical suspicion of HIV infections by physicians Prior HIV test HIV as part of a Ddx Unexplained opportunistic infections (i.e. PCP, toxo, crypto, histo, TB, MAC)

Low Risk HIV Serology unknown but answers no to all high risk questions Unknown Source is not assessed Southern Alberta Clinic Guidelines

4 Drug Selection Best to start within 1-2 hrs, consider dose before Rapid HIV test returns depending on risk of source patient CHR has PEP kits prepared for us Basic Regimen: If Low risk exposure (unknown source or mucocutaneous exposure) Combivir: (AZT 300mg + 3TC 150mg) bid

Expanded Regimen: For most percutaneous to known HIV + IN CONTACT WITH ID Basic Regimen + Nelfinavir 1250mg bid Other: consider other drugs if source patient is already on antiretrovirals or if source patient is known to have resistant HIV

Southern Alberta Clinic Guidelines 5 Duration of Prophylaxis: Start ASAP and continue for 4 weeks 6 Discuss adverse reactions w/patient ED physician to order baseline

CBC, diff., ALT HBV, HCV, HIV serology Follow up? Follow Up Occupational exposures are sent to Odyssey Travel and Tropical Medicine Clinic 14th ST NW Dr. Rudy Zimmer Employee to make own

appointment phone # in the ED MD to fax referral form to Dr. Zimmer References

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 Rothman et al. Preventive Care in the Emergency Department: Should Emergency Departments Conduct Routine HIV Screening? Acad Emerg Med 2003; 10; 278- 285. Rothman et al. HIV and complications in Emergency Medicine. Emerg Med Clin N Am 2008; 26; 367-387. Emergency Med Reports HIV Positive Patient in the ED Part I and II,

Vol 27:9, Apr. 2006 FMC ED Charge Nurse Manual (PDF File) Management of Health Care workers exposed to HIV. www.uptodate.com When to Initiate Antiretroviral therapy in HIV-infected patients www.uptodate.com Primary HIV-1 Infection: Diagosis and Treatment www.uptodate.com Tintinalli, J. Emergency Medicine: A comprehensive study guide 6 th Ed. 2004. pgs. 925-935. Google Images Dr. Margriet Gredanus and Dr. James Huffman

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