Vaccination of healthcare workers

1. Dr. BALAMUGESH.T
Professor
Dept. of Pulmonary Medicine
CMC, Vellore

2. Scenario
 33 yr
 Nursing staff
 Past h/o allergic rhinitis
 Itching skin lesions, followed by cough, chest tightness
and breathlessness with wheeze in ward
 Following handling Inj Piptaz.

3. Occupational respiratory diseases
 Occupational allergies
 At risk population
 Diagnosis
 Smoke inhalation
 Infections
 Tuberculosis
 Influenza

4. Occupational allergies
 Under recognized
 Under diagnosed
 Under treated
 Under reported
 Common Occupational allergies
 Occupational asthma
 Occupational dermatitis
 Occupational rhinitis
 Occupational conjunctivitis

5. Occupational asthma
 Accounts for 5-10% of asthma in young adults
 New‐onset asthma:
 Hospital technicians (RR 4.63; 95% CI 1.87 to 11.5)
 Those using ammonia and/or bleach at work (RR 2.16;
95% CI 1.03 to 4.53).
Kogevinas M et al.
Lancet. 1999

6. Occupational asthma
 Of 182 cases of OA in HCWs over 10 years.
 75% - nursing, operating theatre, endoscopy and
radiology staff.
 70% - glutaraldehyde, latex and cleaning products
G. I. Walters et al. Occupational Medicine 2013;63:513–
516

7. Definition – occupational asthma
 Occupational asthma (OA) refers to
 de novo asthma or the recurrence of previously
quiescent asthma
 induced by
 sensitization to a specific substance, which is termed
sensitizer-induced OA, or
 exposure to an inhaled irritant at work, which is termed
irritant-induced OA (reactive airways dysfunction syndrome).
 Work related asthma
 Work exacerbated asthma + OA
OA

9. Agents causing OA
NEJM:
July
1995

10. Risk factors
 Level and duration of exposure
 Smoking
 Atopy
 Occupational rhinitis and conjunctivitis
 Genetic factors

11. Irritant-induced OA
 Exposure to airway irritants, in the absence of
sensitization
 New-onset asthma after exposure to very high levels of
alkaline dust from the collapse of the World Trade
Center
 16% of persons with high exposures at 1 year
 At 9 years 36% of them recovered.

12. Lower airway disease symptoms -
WTC dust exposure
 Irritant-induced asthma (of subacute onset),
 Nonspecific chronic bronchitis,
 Chronic bronchiolitis, or
 Aggravated preexistent obstructive pulmonary disease

13. Symptoms OA
 Cough,
 Breathlessness,
 Wheeze

14. Diagnosis
 History
 Examination
 PEFR
 Spirometry
 Serum IgE
 Skin prick test
 Methacholine challenge test

15. The Peak Flow Meter
like a thermometer for asthma
 Inexpensive clinic
instrument
 Monitoring
 Builds confidence in
treatment
 One ‘hard, fast blow’

16. Occupational asthma diagnosis
• Compatible history
• Detailed exposure history
• Spirometry with reversibility
• Bronchoprovocation test
• Establish the relationship
• Serial peak flow, BPT after exposure, Skin tests,
Immunoassay

17. Environmental Health Perspectives August 2000

18.  An estimated prevalence of sensitization among the
general healthcare worker population - 12.1 %
 4-7% : powder-free gloves
 It can be assumed that rates have decreased even
further with the increased use of non-latex gloves.
Latex allergy

19. Diagnostic tests for latex allergy
 Skin testing
 Extracts prepared with Hevea latex B and C serum
proteins
 Sensitivity 65 -96 % and specificity – 88-94 %
 Serology testing
 Hevea latex-specific IgE antibody
 Sensitivity – 70%, specificity - >95%

20. Glutaraldehyde induced asthma
 Cidex
 Agent used for disinfection

22.  The odour threshold of glutaraldehyde has been
reported to be 0.04 parts per million (ppm),
 Odour detection is a potential indicator that the
engineering controls are inadequate.
 Odour detection - unreliable

23.  Glutaraldemeter
 United Kingdom Health and Safety Executive which
also has established a 0.05 ppm Workplace Exposure
Limit (WEL)

24. Prevention
 Primary prevention
 reducing workplace exposure to potential
causal agents
 Substitution,
 Process modification,
 Respirator use,
 Engineering control with monitoring of
airborne exposure levels.

25. Secondary prevention
identify early evidence of subclinical
disease
 periodic medical surveillance by using tools such as
questionnaires, spirometry

26. Tertiary prevention
minimize effects of the workplace
environment on clinically manifest
disease
 Control of specific factors responsible for
disease onset or exacerbation/aggravation
 Change the person to another job.

27. Treatment
 Medical management of asthma
 Controller inhalers
 Rescue inhalers

28. Outcomes
 Factors predicting a worse outcome
 Smoking
 Lower PC20 at baseline, longer duration of exposure, and
the interval since removal of the patient from exposure
 Subjects with OA to HMW agents
 Typical plateau for improvement in spirometry is
around 1 year, whereas the plateau for improvement in
BPT occurs around 2 years

29. Smoke inhalation
Three types of injuries:
 Thermal injury to the upper airways,
 Chemical injury to the tracheobronchial tree, and
 Systemic poisoning due to carbon monoxide and/or
cyanide.

30. 95 people, including members of the staff

31. Thermal injury: airway compromise
 Intubation is justified if any of the following signs are
present:
 Stridor,
 Use of accessory respiratory muscles,
 Respiratory distress,
 Hypoventilation,
 Deep burns to the face or neck, or blistering or edema of
the oropharynx.

32.  Oropharygeal examination -if erythema
 Do Larygoscopy
 Upper airway edema or blistering seen during
laryngoscopic exam should prompt intubation.
 Bronchoscopy instead of laryngoscopy
 if there is a history of inhalation
of superheated particles or steam,

33. Carbon monoxide poisoning
 Headache, nausea, malaise, altered cognition,
dyspnea, angina, seizures, coma, cardiac
dysrhythmias, heart failure, or bright "cherry red" lips.
 Detected by co-oximetry
 Treatment
 100% oxygen
 Hyperbaric oxygen.

34. Cyanide poisoning
 Burning of certain compounds (eg, polyurethane,
acrylonitrile, nylon, wool, and cotton)
 Clinical suspicion for cyanide poisoning should be
high
 Unexplained lactic acidosis, low arterial carbon
dioxide tension
 Treatment
 high flow oxygen,
 use of antidotes ( eg, sodium thiosulfate PLUS
hydroxocobalamin)

35. Prevention

36. Influenza in HCW
Olga Anikeeva et al, Am J Public Health. 2009

37. Additional benefits of vaccination
 Prevent sickness absenteeism
 Protect transmission to patients

38. SUMMARY
 High index of suspicion required for occupational
respiratory diseases
 Preparedness for smoke inhalation management.

39. THANK YOU

40. Cleveland clinic,
Nov 2013

42. Features of Irritant-Induced
Occupational Asthma.

43. ASSOCIATIONS BETWEEN OCCUPATIONAL EXPOSURES
AND ASTHMA AMONG TEXAS HEALTH CARE WORKERS: