Allergy Grand Rounds

Allergy Grand Rounds
By:Sarbjit S. Saini, M.D.
JHAAC

Chief complaint
* 13 yr old male referred in June 2004 for evaluation of severe chronic urticaria
* Referred by pediatric allergist in VA
* Significant illnesses:
o include Type I DM for 2.5 yrs
o ADHD
o mood disorder

History of Present Illness-I
History of Present Illness-II
History of Present Illness-III
Other atopic history
* No history of eczema or food allergy
* Allergic rhinitis symptoms
* Exercise-related asthma age 9 treated with prn albuterol prior to activity
* Reported qhs cough, but denied wheezing
Medications
* Zoloft, 50 mg qd**
* Oxcadazepine (Trileptal) 300 mg/600 mg **
* Adderall 30 mg bid
* Quetiapine (Seroquel) 200 mg qd
* Fexofenadine 180 mg qd ( off 1 wk)
* Cetirizine 10 mg qd ( off 1 week)
* Cyclosporine 100 mg bid (off 1 wk)
* Humulin 7 U/4 U, Humulin R 5 U/ 4 U
* Epipen, Albuterol

Past Medical History
* Type I DM for 2.5 yrs
* ADHD
* Mood disorder, possible bipolar
o exacerbated by steroids
o suicidal ideation due to urticaria
* Chicken pox as child
* Salivary gland surgery
* Normal birth history, negative history of other infections
Family History
* Younger Sister with eczema
* PGM with asthma
* Paternal cousins with asthma
Environmental Hx
* Apt dweller x 5 yrs
* Dog since 1999
* 3 hamsters

Social Hx
* 7th grader
* Lives with mom and sister
Physical Exam
* T-99.7, HR-121, BP-109/75, HT-5, WT-125,RR-22
* General: no obvious pubertal signs,central obesity, moon facies
* HEENT: “allergic shiners”,erythematous nasal mucosa, prominent turbinates
o Normal TMs, oropharynx, neck
* Resp: CTA, normal I:E ratio, CV: nl S1, S2 tachy
* Abdomen: benign Ext: no joint swelling
* Skin: urticaria on face, arms, feet, back, chest; no pigmentation

Recent labs
* CBC-WBC 7.3 HCT-41.2, Plts-331
* HbA1C-8.6 (4-6) Jan 2004
* Negative studies: ANA, H. Pylori Ab,anti-thyroid peroxidase antibodies, WESR
* Normal C3, C4, CH50; TSH, thyroxine, T3 and T4
* RASTS- negative for crab, lobster, fish garlic and insulin

Cyclosporine related labs
* Jan 2004 reduced Hct-12.1 HB- 37.2
o CsA: 37 ng/ml trough
* March 2004 Normal studies
* June 2004
o CsA: 46 ng/ml trough
o CBC, Mg, Cr, K normal
Impression/ Recommendations
* Severe CIU/angioedema h/o significant steroids requirements
o No clear drug (insulin), food or systemic etiology
o Avoiding NSAIDs
* Consider alternate diagnoses:
o Hx of autoimmunity with Type I DM
o Rheumatologic?-joint symptoms, bruising
o Obtain a skin Biopsy to verify urticaria vs. other
+ Consider immunofluorescence

Follow-up on Recommendations
* Rheum evaluation: Repeated ANA, RF, dsDNA, ANCA, Urine and SPEP- all normal
o showed IgA of < 20, no other etiology for joints
* October 04 -Csa 100 mg qd and fexofenadine with good control
* Prednisone used only single day since 6/2004
* No skin biopsy to date- attempted
* Glucose under better control
CU in children : association with thyroid autoimmunity
* 187 CU pts (6- 18 yr) followed 7.5 yrs
* Tests: CBC, sed, Chem, Antibodies to Hep B, HSV, EBV,CMV, mycoplasma, ASO, ANA, C3, C4, Thyroid function and antibodies,Ua, chest and sinus X-rays, food skin tests, ice cube test
* Results: 8/187 antithyroid Ab (4.3%), all girls
o 3x -1.27% rate seen in pediatric population
o Much less than 14 to 33% range in adults
o 5 +ANA, 4 + family Hx of autoimmunity
Cyclosporine in Urticaria
* CBC, Mg, K, renal function q 2 wks for first 3 months, CsA levels
* Gingival hypertrophy
* BP monitoring
* Dose: 2-6 mg/kg/d similar to RA and psoriasis (2.5 mg/kg/day)
* Tx dose 8 mg/kg/d; trough levels 100 ng/ml

CsA and Urticaria-RDBCT
* 30 subjects, severe CIU unresponsive to H1 tx and positive ASST ( +HRA)
o 4mg/kg CsA (n=20) or placebo (n=10) for 4 wks
o All subjects followed for up to 20 wks, all on daily 20 mg cetirizine
* Outcome: +< 25% of baseline UAS, relapse > 75% of UAS
* Results: 8/19 + at week 4, 6 relapse wk 6
o Noted reductions in HRA and ASST

CsA in CIU:Adults
* Open trial in 35 CIU with 3(0-3)
o Low dose CsA 3 mos, 68% response (13/19) with few SEs1
* DB trial :40 pts CsA 5 mg/kg x 8 wks, then 4 mg/kg x 8 wks vs. cetirizine 10 mg/d2
o All cetirizine crossed to active CsA
o 3 pts reduced CsA for Cr rise
o On tx- 22 had relapse, 10 resolved spon 12 with H1
o Off tx- 16/40 in remission at 9 mos

Immunosuppression in Adolescents: Cyclosporin
* 80% of liver, kidney, cardiac Tx > 5 yr survivors on CsA
* Nephrotoxicity: 4-5 % in cardiac and liver
o 10% in RA dosed > 4 mg/kg avg 19 mos
* HTN (20-30%)
* Hyperlipedemia (10% of cardiac)
* Post-tx lymphoproliferative disease:5-17%
* Cosmetic-Gingival hyperplasia, hirsutism

Allergy Grand Rounds.ppt

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A case of refractory, severe,steroid-dependent asthma

A case of refractory, severe,steroid-dependent asthma
By: Bruce S. Bochner, M.D.

* 24 y/o AA female referred in 2/99 from southern Maryland for evaluation and management of uncontrolled asthma
* At the time, 20 weeks pregnant (G5, P4)
* Last two pregnancies were complicated by uncontrolled asthma and oral steroid use throughout the pregnancy
* H/O asthma since age 12, frequent episodes of wheezing & cough without any obvious triggers or seasonal pattern
* Review of accompanying records revealed that her FEV1 can range from 30% to 80% predicted on any given visit

* Early on, exacerbations 1x/yr, necessitating ER visits
* Initially treated with Cromolyn, Vanceril and Albuterol
* Since 1992, worsening asthma, increased ER visits and for 1998 at least 6 hospitalizations
* In 1992, found to have multiple positive skin tests, tried on ImTx w/o improvement; in fact, exacerbations of wheezing with most shots
* Frequent courses of antibiotics for bronchitis or sinusitis

* At the time of her 2/99 visit:
o Daily nocturnal symptoms
o Wheezing with minimal activity
o Normal CXR
o managed with Prednisone 30 mg qAM, Flovent 110 2 puffs BID, Serevent 2 puffs BID, Alupent 2 puffs q3h and nebs PRN, Atrovent 4 puffs BID, Accolate 20 mg BID, and Cromolyn q3h

* Drug allergy Hx: acute rashes from Penicillin, Codeine, Ceclor; Erythromycin caused GI upset
* Environ. Hx: Born and raised in MD, lives in a separate home, no pets
* Family Hx: All of her four kids (two different fathers) have asthma; current pregnancy is with a third father

* PE:
o Vitals: BP 105/66, P 112, RR 18, Wt 168 lbs, peak flow best effort 130 liters/min
o GEN: Mild Cushingoid facies, no rashes
o HEENT: Nasal exam normal, no lymphadenopathy or thyromegaly
o LUNGS: Diffuse expiratory wheezing and prolonged expiratory phase; sounds were in chest but not neck
o HEART: Normal S1, S2.
o EXTREMITIES: No peripheral edema

* SPIROMETRY
o FEV1: 1.1 liters (36% predicted), FVC: 1.62 liters (42% predicted), ratio 0.68. Post-bronchodilator FEV1 1.89 liters (79% increase), FVC 2.34 liters (44% increase)

* TREATMENT CHANGES
o At this visit, patient was switched from Flovent to Pulmicort 4 puffs bid
o The rest of her medications were continued
o Inhaler technique was observed to be correct
o Husband verified medication adherence.

* Delivered the baby on continuous nebs. Baby and Mom did fine. 5 weeks postpartum admitted to Hopkins Bayview for 5 days for worsening SOB, wheezing and leg pain
* On admission, wheezing; PEF 100 liters/min
* V/Q scan and leg dopplers normal
* FEV1 28% predicted; flow-volume loops normal
* CT scan of sinuses revealed pan-sinusitis
* 24-hr pH probe documented significant GERD
* Discharged on 24-day steroid taper with markedly improved lung function at discharge; started on antibiotics and Prilosec

* Since 2000, multiple ER visits
o two prolonged intubations in 2000 and 2001
+ 2000: complicated by full respiratory arrest and persistent doll’s eyes
+ 2001: complicated by bilateral pneumothoraces requiring chest tubes and a DVT; s/p IVC filter
* Multiple meds tried in 2000-2001 included Advair, Pulmicort respules, Theophylline, and Methotrexate. None had a significant impact on our ability to taper oral steroids.

* In 10/01, sent for an outpatient evaluation by me to National Jewish (made possible through philanthropic help from NJC, AAFA and her local church) with dx of severe, labile steroid-dependent asthma
* Diagnosis quickly confirmed when she required admission for worsening SOB and wheezing

* Skin tests positive to dust mites, grasses, alternaria
* Alpha-1 antitrypsin: normal
* CF genotyping: normal
* No peripheral blood eosinophilia
* Total IgE: 123 IU/ml
* Chest CT: no interstitial disease
* Bone densitometry: normal
* Sinus CT: mild sinusitis
* Oral steroid kinetics normal

* Seen by Drs. Barry Make and Sally Wenzel
* After stabilization with IV steroids and nebs, underwent bronchoscopy
* Found to have some collapsibility of her larynx with exhalation which they felt would be helped with CPAP
* Sleep study found sleep apnea for which CPAP was also recommended

* Bronchoscopy (on IV steroids) revealed prominent basal lamina thickening and a mild inflammatory infiltrate, primarily lymphocytic

* After 3 weeks, sent back to Baltimore on the following regimen:
o Serevent 3 puffs q12
o QVAR 6 puffs bid
o Atrovent 4 puffs qid
o Uniphyl 400 mg qhs
o Singulair 10 mg qhs
o Zyflo 600 mg qid
o Prilosec 40 mg qd
o Supplemental Calcium
o Prednisone 40 mg q am, 20 mg q afternoon
o Nasonex 1 spray bid
o CPAP

* Within 2 months, back to pre-Denver management
* 2002 to 2003
o Managed primarily with Prednisone (40-80 mg/day), Prilosec and Albuterol
o Extremely Cushingoid; now weighs 240 lbs
o Tried Xopenex w/o any additional benefit
* September 2003
o Started Xolair one vial q month (completely covered by her insurer)
o Still had ER visits but no hospitalizations while on Xolair
o Despite this, after seven months, Prenisone, q3h albuteral requirements and FEV1 remained unchanged
o She became frustrated, so we discussed other options (Enbrel) and stopped Xolair

Pathophysiology of allergic airway inflammation
Model of IgE-dependent acute and chronic allergic inflammatory reactions
Leukocyte recruitment in allergic disease
Soluble Tumour Necrosis Factor Alpha (TNF-a) Receptor (Enbrel) as an Effective Therapeutic Strategy in Chronic Severe Asthma
Respiratory Cell & Molecular Biology
Study design
* Open label, single center study
* Subjects with chronic severe asthma on oral corticosteroids, high dose inhaled corticosteroids, salmeterol, and/or theophylline
* 25 mg of Enbrel administered subcutaneous twice a week for 12 weeks
* Subjects aged 18-65 years
* FEV1 of at least 50% predicted
* Demonstrated a reversibility of at least 9%
* Lung function, methacholine response performed before and after treatment
* Asthma control symptom questionnaire completed before and after the trial
* Diary cards issued to assess peak flows and use of rescue medication

Results

* 15 subjects enrolled in the trial
* 11 female, 4 male
* Mean age of the patients: 41 yrs
* Mean duration of asthma: 24 years
* Mean dose of oral prednisolone: 12.1mg/day
* Mean dose of inhaled corticosteroids
o 2500 ľg/day of beclomethasone or equivalent
* Mean dose of nebulised albuterol: 8 mg/day

Changes in FEV1 with Enbrel

WEEK 1 WEEK 12
Changes in Symptom Scores with Enbrel
Symptom score (Juniper Scale)
Adverse effects
* Skin rashes (4)
* Injection site reactions (4)
* Respiratory tract infections (7)
* Weakly positive ANA (3)

Conclusions
Treatment with Enbrel in patients with chronic severe asthma:

* Improves lung function (FEV1, FEV1/FVC, morning and evening PEF)
* Markedly improves asthma control
* Markedly improves airway hyperresponsiveness
* Markedly reduces the need for rescue medications as all the subjects completely withdrew from their nebulised albuterol by the end of the study

* April - early June 2004
o Started Enbrel 25 mg sq twice weekly (completely covered by her insurer) after PPD was negative; husband trained on administration technique
o Two weeks later, she was admitted for an asthma exacerbation associated with nausea, fatigue, myalgias and unexplained fevers to 102° despite Enbrel and prednisone; discovered Prilosec had been stopped
o Infectious workup unrevealing; IV steroids given
o Enbrel dosing held for 2 weeks, fever resolved
o Enbrel restarted and 1 week later she was admitted for another asthma exacerbation
o Enbrel discontinued

* June 21: planned to restart Xolair but got admitted again
* Discharged June 22
* Seen June 23
o FEV1 60%; FVC 93%
o Diffuse wheezing on Prednisone 80 mg
o Restarted Xolair 300 mg q 4 weeks
o Restarted Serevent diskus 1 puff BID
* What next????

Our ongoing work on TNFa and allergic inflammation

* There is a tissue-specific pattern of chemokines/cytokines/adhesion molecules involved in human allergic inflammation
* This pattern is TNF- dependent
* The primary source of TNF- released in human allergic inflammation is the mast cell

Etanercept in late phase cutaneous allergic inflammation: study overview

* Randomized DBPC Trial
* To evaluate effects of etanercept (Enbrel) on cutaneous allergen LPR in 10 perennial allergic rhinitis/dust mite sensitive patients
* 15 visits to JHAAC over 8.5 wks
* Lead investigators: Lisa Beck, Ed Conner, Bruce Bochner

Study Purpose

* To evaluate the clinical effects of etanercept on cutaneous allergen challenge late phase responses
* To evaluate the effects of etanercept on the allergen dose response
* To characterize a variety of biomarkers in the cutaneous late phase responses
* To assess limited pharmacokinetic data of etanercept in the serum and nasal washings

DBRPC Crossover Study Design
A case of refractory, severe,steroid-dependent asthma.ppt

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Occupational Exposures to Bloodborne Pathogens

Occupational Exposures to Bloodborne Pathogens
By:Arjun Srinivasan
Johns Hopkins Hospital

Outline
* What’s an exposure?
* 1st step in all exposures - Clean the site!!
* Specific pathogens
o Hepatitis C
o Hepatitis B
o HIV

Scope of the Problem
Impossible to measure the psychological stress that an exposure places on a health care worker
At Risk Exposures
1. Percutaneous injury
Hollow needle > Solid sharp
Visible blood
Deep injury
Device in patient’s artery or vein
2. Splash on non-intact skin
3. Splash on mucous membrane

Risks From Body Fluids
* Known to be infectious:
o Blood
o Any fluid visibly contaminated with blood
o Semen
o Vaginal secretions
o Concentrated virus (used in labs)
* Potentially infectious
o CSF
o Pleural fluid
o Pericardial fluid
o Peritoneal fluid
o Amniotic fluid
o Synovial fluid
o Tissue samples
* Not Infectious (if not visibly bloody)
o Tears
o Saliva
o Urine
o Feces
o Sweat
o Emesis

The Solution to Pollution . . .
* Exposure site should be cleaned IMMEDIATELY! This may be the most important part of PEP
* Skin wounds should be washed with soap and water
* No evidence that antiseptics are useful and caustic agents (bleach) may do more harm than good
* Mucous membranes should be flushed thoroughly with water
* Eyes should be irrigated with a liter of saline

A word from our lawyers . . .
* ALL exposures should be reported to the proper people (Occupational health, Employee health etc.)
* Disability claims can be denied if follow up reporting was not done right

Hepatitis C
Hepatitis C: Risk of Exposure
Hepatitis C: Risk of Disease
Post Exposure Recommendations
* Clean the site immediately
* Hepatitis B immune globulin has NOT been effective
* Interferon is NOT recommended at this time
Hepatitis C: Follow Up
* Enzyme linked immunoassay (EIA) is screening test of choice
* ALL exposed HCWs should have LFTs monitored
* Average interval between exposure and seroconversion with EIA is 8-10 weeks
* Follow up guidelines vary - CDC recommends follow up at 4-6 months
Hepatitis C: Follow up issues
* EIA is falsely positive in up to 50% of HCW and falsely negative in 5% - results must be confirmed by RIBA or VL
* PCR may catch infection earlier but detection is highly variable
* Immediate referral for treatment if HCW seroconverts
Hepatitis C: Counseling
* Risk of transmission to infants and partners is thought to be low
* Exposed HCW do not need to modify sexual practices, stop breast feeding or refrain from becoming pregnant
* Should not donate blood

Hepatitis B
Hepatitis B: Risk of Exposure
Hepatits B: Outcome of Infection
* In patients who are infected with Hep B:
o 25% get jaundice
o 5% require hospitilization
o 6-10% become chronically infected
o .125% die of fulminant hepatitis

Hepatitis B: Good News
* Most HCWs have been vaccinated and vaccine offers virtually complete protection to responders
Hepatitis B: Bad News
* Some employees are NOT vaccinated
* 6-10% of vaccinees do NOT develop antibody
* Really bad news:
CDC estimates that 50-75 HCW die from Hep B each year
Hepatitis B: Post Exposure
* Clean the site immediately
* Determine the vaccine status of the HCW
* Determine the surface antigen status of the source patient

Hep B: HCW Never Vaccinated
* HCW should receive vaccine ASAP
1. Source patient is sAg positive:
HCW should also receive one dose of Hep B immune globulin (HBIG) .06ml/kg (1 vial=5 ml) ASAP and absolutely within 7 days of exposure
2. Source patient sAg neg or unknown
Vaccine alone
Hep B: HCW Vaccinated (one or more doses)
* Source patient should be tested for sAg AND HCW should be tested for sAb
* If HCW has adequate Ab >10 IU/mL (now or at any time) then no additional treatment
* IF HCW has inadequate Ab:
1. If pt is sAg negative:
HCW should get booster dose of vaccine (or complete series)
2. If pt is sAg positive:
HCW should receive HBIG AND a booster dose of vaccine at different sites (complete series if necessary)
If HCW has inadequate Ab:
3. Unknown source:
Give vaccine booster or complete series
Vaccine non-responders
* If HCW has inadequate Ab after 3 dose series they should get another series: 30-50% chance of responding to 2nd series
* If no response to 2nd series HCW should be considered susceptible
* PEP for known non-responders exposed to Hep B positive or high risk unknown sources: 2 doses of HBIG- 1 at exposure then 4 weeks later
Hep B: Follow Up Testing
* Hepatitis B sAg is the test of choice as it rises in about 6 weeks
* LFTs should be monitored at regular intervals
Post Exposure Counseling
* Risk of transmission to infants and partners is thought to be low
* Exposed HCW do not need to modify sexual practices, stop breast feeding or refrain from becoming pregnant
* Should not donate blood
HIV
HIV: Risk of Exposure
* Risk of transmission from percutaneous expsosures involving HIV positive pts estimated at 0.3%
* Risk from mucous membrane exposure estimated at 0.1%
* As of 2000 there were 56 confirmed and 138 possible cases of occupational transmission in the US
Rationale for PEP
* HIV infects dendritic cells and then regional lymph nodes before becoming systemic
* AZT blocks infectivity of HIV infected dendritic cells
* Goal of PEP is to halt viral replication before systemic infection is established

Does It Work?
* Several animal studies showing efficacy
* Peri-natal prophylaxis has been effective
* Retrospective study showed that risk of seroconversion after exposure was 81% lower in HCWs who took AZT PEP.
Time is Virus
What To Use?
* Before: AZT+3TC +/- IDV or NFV
* Now: Becoming more difficult to answer!
* Regimens may need to be tailored based on the treatment history of the source patient -Surveillance study from 1998-1999 found that 39% of virus from source patients had some NRTI resistance and 10% had some PI resistance.

Nucleoside Reverse Transcriptase Inhibitors (NRTI)
* Still form the backbone of most regimens
* AZT has been formally studied thus it should be included if possible
* Addition of 3TC is recommended because:
1. It appears non-toxic
2. It has some synergistic effect with AZT with respect to mutations
* If source patient’s virus is felt to be resistant to AZT or 3TC alternatives include:
* d4T + 3TC
* d4T + ddI
* Role of abacavir?
* Role of tenofovir?
Protease Inhibitors (PI)
* Are very potent anti-virals and work very well in patients
* BUT they have significant side effects and can cause HCW to stop PEP altogether
* PI should be recommended primarily when the exposure is high risk
* Any PI can be used but indinavir and nelfinavir have been used the most
Non Nucleoside Reverse Transcriptase Inhibitors (NNRTI)
* Not much experience using these for PEP
* Use should be reserved for situations when source patient’s virus is thought to be resistant to all PIs
* Nevirapine should probably be avoided as PEP: from 1997-2000 there were 22 reports of serious toxicity in HCW taking it for PEP

Toxicity of PEP
Side Effects of PEP
PEP Counseling
* Clean the site immediately
* Determine the HIV status of the source
* Determine the extent of the exposure
PEP management: Source Patient Testing
* Crucial 1st step as most exposures do NOT involve HIV positive patients
* Rapid test kit (SUDS) is available and yields an answer in about 30 minutes
* Rapid test is an EIA that is >99.9% sensitive
* Testing of blood on sharps is NOT recommended
* Patient consent is required in Maryland
HIV RNA Testing of Source
* No official recommendations and test is not approved for this indication
* Should be reserved for cases where there is a suspicion of acute retroviral conversion

Source Patient
1. Patient HIV negative - No PEP
2. Patient HIV positive
Low viral load / high CD4 = class 1
High viral load / low CD4 = class 2
3. Patient HIV positive, unknown CD4, VL
Use best judgement - err towards class 2
4. Unknown source
Exposure Types
1. Non-infectious fluids - No PEP
2. Mucous membrane, non-intact skin
Small volume
Large volume
3. Percutaneous injury
Less severe
More severe
HIV PEP Recommendations
Percutaneous injuries
Less severe
* Source pt HIV negative - No PEP
* Source pt class 1 - Recommend 2 drugs
* Source pt class 2 - Recommend 3 drugs
* Source of unknown status- Consider 2 drugs in setting where exposure to HIV positive pt likely or if pt has HIV risk factors

HIV PEP
More severe injury
* Source pt HIV negative - No PEP
* Source pt HIV class 1 or 2 - Recommend expanded 3-drug regimen
* Source of unknown status - Consider 2 drugs in setting where exposure to HIV positive pt likely or if pt has HIV risk factors
HIV PEP
Mucous membrane exposures
Small Volume
* Source pt HIV negative - No PEP
* Source pt class 1 - Consider 2 drugs
* Source pt class 2 - Recommend 2 drugs
* Source of unknown status- Consider 2 drugs in setting where exposure to HIV positive pt likely or if pt has HIV risk factors
Large volume
* Source pt HIV negative - No PEP
* Source pt class 1 - Recommend 2 drugs
* Source pt class 2 - Recommend 3 drugs
* Source of unknown status- Consider 2 drugs in setting where exposure to HIV positive pt likely or if pt has HIV risk factors
Duration of Treatment
* Current recommendation is 4 weeks but this is an arbitrary selection
* Animal studies suggest 10 days is too short but 28 days conferred protection
Resistance
* Becoming a significant problem now that so many patients are getting treated
* Treatment history can be helpful in the acute setting
* Recent history may be more important than remote
Resistance Issues
* Full medical history often not available when the exposure occurs - PEP should NOT be delayed
* Data from maternal transmission studies shows viral resistance does not preclude benefit
* Consultation with someone experienced in HIV treatment is recommended in cases where HIV resistance is possible
* PEP may need to be modified once more history is available
* Resistance testing is too slow to be of use right now

PEP and Pregnancy
* Women of child bearing age should be offered a pregnancy test before starting PEP
* BUT, recommendations on starting PEP should NOT change just because HCW is pregnant

HIV medications to avoid in Pregnant HCW
* d4T, ddI: have been associated with severe lactic acidosis in pregnant women
* Efavirenz: is teratogenic in primates
* Indinavir: causes hyperbilirubinemia in newborns if given near time of delivery

Post Exposure Testing
* Testing should be done at regular intervals (eg 6,12 weeks and 6 months)
* Testing should continue for 12 months if the HCW contracts HCV from the exposure
* Unclear if testing should be prolonged in exposures to pts with HIV and HCV or in HCW who have history of impaired Ab responses
* EIA is test of choice
* Viral loads and p24 assays should be reserved for suspected cases of acute seroconversion given high false pos rate
Counseling
* For 3 months following exposure HCW should avoid:
-unprotected sex
-donating blood
-sharing razors, toothbrushes
* HCW should consider stopping breast feeding (risk of perinatal transmission and drugs may get into breast milk)

Time to Seroconversion
* Most HCW seroconvert in 6-12 weeks with median time of 46 days
* 95% seroconvert within 6 months
* 100% seroconvert in one year
* Co-infection with HCV may delay HIV seroconversion

Acute Retroviral Conversion
* Symptomatic seroconversion develops in 50-90% of cases
* Average time from exposure to symptoms is 2-6 weeks
* ANY HCW who develops a flu-like illness in the follow up period should be encouraged to get HIV RNA testing

Resources
Conclusion

* People react very differently to exposures - be prepared for anything!
* The psychological impact of an exposure can be enormous
* Your patience and understanding may be the best PEP of all

Occupational Exposures to Bloodborne Pathogens.ppt

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