Transcript Understanding Asthma, the Role of Allergens and Vocal Cord

Understanding Asthma, the Role
of Allergens and Vocal Cord
Dysfunction
Christopher Mjaanes, MD
Disclosures
• Meda Pharmaceuticals Inc., Speakers Bureau
– No direct conflict of interest
Objectives
• Understand the basic pathophysiology of asthma
• Be able to distinguish between intermittent and
persistent asthma
• Understand the difference between asthma severity and
asthma control
• Recognize potential asthma triggers, particularly
allergens
• Determine different asthma management strategies,
including medications
• Be able to recognize vocal cord dysfunction
• Distinguish between vocal cord dysfunction and asthma
Asthma Background
• Asthma prevalence in the US is rising, affecting
7.3% of the population in 2001 and 8.4% of the
population in 2010
– This was 1 in 12 people in the US in 2010
• Current asthma affects children more than adults
(9.5% vs 7.7%) and blacks more than whites or
hispanics
Source: National Surveillance of Asthma: United States, 2001-2010
Definition
• Asthma is a chronic inflammatory disorder of the
airways
• Airway inflammation is an essential component
of asthma
– Not all airway inflammation is “allergic” although
this type of asthma accounts for 80% of all asthma
NAEPP 2007 Expert Panel Report 3 Summary Report 2007.
Immunol 2007;120 (5): Supplement.
J Allergy Clin
Airway Inflammation
• Features of asthmatic airway inflammation
include:
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Neutrophils – particularly seen in fatal asthma
Eosinophils
Lymphocytes
Mast cell activation
Epithelial cell injury
• Airway inflammation contributes to airway
hyperresponsiveness, airflow limitation,
respiratory symptoms, and disease
chronicity
Hyperresponsiveness
• There is a predisposition for the airways of
asthmatics to “over-react” to stimuli
• Colds, smoke, allergens, etc., trigger an
exaggerated response with mucous production,
inflammation and bronchospasm
• Can be thought of as the “twitchiness” of the
airways
• Controlling inflammation can decrease (not
eliminate) hyperresponsiveness
Airflow Limitation
• This is what makes asthma an obstructive lung
disease
• Many factors contribute to airflow limitation
– Bronchospasm
– Airway secretions and mucous plugging
• In some patients, persistent changes in airway
structure occur
– Airway remodeling
• Airway wall fibrosis, mucous hypersecretion, smooth muscle
hypertrophy, and angiogenesis
Pathophysiology
• Gene interaction with environment
• Important to the development and expression
of asthma
• Atopy, the genetic predisposition for
IgE response to aeroallergens is strongest
identifiable factor
• Viruses cause exacerbations and contribute to
the development
National Education and Prevention Program. Expert panel report 3,
www.nhlbi.nih.gov/guidelines/asthma/asthgdln/htn
Diagnosis
Key points
• Episodic symptoms of airflow obstruction or
hyperresponsiveness
•
Acute asthma symptoms are a manifestation of
airflow limitation
• Airflow obstruction is at least partially reversible
(12% and 200 mL or more)
• Alternative diagnoses are excluded (But other
lung diseases often co-exist)
NAEPP 2007 Expert Panel Report 3 Summary Report 2007.
Allergy Clin Immunol 2007;120 (5): Supplement.
J
Diagnosis
• History
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There is no single symptom that indicates asthma
Commonly reported symptoms include: cough, chest
tightness, dyspnea and wheezing
Symptoms are often worse at night and can awaken
patients from sleep
Cough, dyspnea and wheeze begin and persist after
exercise, not during
There is often an association between specific
triggers and symptoms
• Although both symptoms and triggers are individualspecific
Diagnosis
Additional Points
• Eosinophilia in blood or sputum. (May be normal
during corticosteroid treatment.)
– More common in adults than children
• Eosinophilic airway inflammation can be detected
by exhaled nitric oxide testing
• Positive allergy tests and elevated serum IgE level
are common
• Determination of obstruction and reversibility
– Spirometry and peak flow measurement, pre- and
post-bronchodilator
Differential Diagnosis of Asthma
Dependent on Patient Age
• Children
– Bronchiolitis and
bronchitis
– Foreign body aspiration
– Pneumonia
– GERD
– Malacia (tracheal or
laryngeal)
– Cystic fibrosis
– VCD
• Adults
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COPD
Bronchiectasis
Sarcoidosis
Bronchitis
Chronic cough
Pulmonary embolism
Heart Failure
GERD
Tumor
Aspration
VCD
A word about severity and control…
• Asthma severity is used to establish initial
therapy
– Severity: the intrinsic intensity of the disease
process. Severity is measured most easily and
directly in a patient not receiving long-termcontrol therapy
• This is NOT modifiable
– Control: the degree to which the manifestations of
asthma (symptoms, functional impairments, and
risks of untoward events) are minimized and the
goals of therapy are met.
Severity and Control
• Both severity and control include the domains of
current impairment and future risk
• Impairment: frequency and intensity of
symptoms and functional limitations the patient
is experiencing or has recently experienced
• Risk: the likelihood of either asthma
exacerbations, progressive decline in lung
function (or, for children, reduced lung growth),
or risk of adverse effects from medication
The Four Components of Asthma
Management
• Assessment and monitoring of control
• Education for partnership in care
• Control of environmental and co-morbid
factors
• Pharmacologic therapy
NAEPP 2007 Expert Panel Report 3 Summary Report 2007.
Clin Immunol 2007;120 (5): Supplement.
J Allergy
Goals of Asthma Control
• Reduce impairment.
• Prevent chronic symptoms.
• Use short acting beta agonists infrequently.
• Maintain normal or optimal pulmonary
function.
• Maintain normal activity.
• Meet patients’ and families’ expectations of
and satisfaction with asthma care .
NAEPP 2007 Expert Panel Report 3 Summary Report 2007. J
Allergy Clin Immunol 2007;120 (5): Supplement.
Goals of Asthma Control
• Reduce risk.
• Prevent exacerbations and minimize need for
ED visits or hospitalization.
• Prevent/reduce progressive loss of lung
function.
• Provide optimal pharmacotherapy with
minimal adverse effects
NAEPP 2007 Expert Panel Report 3 Summary Report 2007. J
Allergy Clin Immunol 2007;120 (5): Supplement.
Assessment and Monitoring
• Identify precipitating factors
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Including environmental control measures
Monitor at each follow up
• Identify comorbidities
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Re-assess at each follow up
• Classify severity of both impairment and risk
NAEPP 2007 Expert Panel Report 3 Summary Report 2007.
J Allergy Clin Immunol 2007;120 (5): Supplement.
Periodic Assessment Measures
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Signs and symptoms
History of exacerbations
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Adherence to pharmacotherapy
Spirometry is essential for monitoring control
Quality of life questionnaires
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Acute care visits, hospitalizations, systemic steroids
Asthma Control Test (ACT)
Patient-provider communication and satisfaction
NAEPP 2007 Expert Panel Report 3 Summary Report 2007. J
Allergy Clin Immunol 2007;120 (5): Supplement.
Additional Assessment Measures
• Effectiveness of environmental control
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Anti-dust Mites Measures
Pets (and mice)
Water damage and humidity
Occupational exposures
Airborne irritants:
• Volatile organic chemicals
• Tobacco smoke
Control of Environmental Factors
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Identify allergens by history, skin and/or in
vitro testing
Reduce exposure if possible
Avoid exposure to tobacco smoke and
other environmental irritants
Repair water damage
Avoid humidifiers and prolonged use of
dehumidifiers
NAEPP 2007 Expert Panel Report 3 Summary Report 2007.
Allergy Clin Immunol 2007;120 (5): Supplement.
J
Major Environmental Allergens
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Indoor
Dust mite
Cockroach
Cat and dog
Mouse and rat
Mold
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Outdoor
Grass pollen
Weed pollen
Tree pollen
Mold
Importance of Allergic Sensitization in
Asthma
• In the US, ~56% of acute asthma cases are attributable
to allergy
• Specific allergen sensitization is a more important risk
factor than total IgE
• Greater than 80% of school age children with asthma
are sensitized to ≥1 common aeroallergen
• The greater the number of positive skin tests  the
more severe the patient’s asthma
Arbes S et al, JACI 2007 Nov 120: 1139-45.
Gergen PJ et al, JACI 2009 Sept 124: 447-53.
Carroll WD et al, Arch Dis Childhood 2006 May 91: 405-9.
Major Outdoor Allergens
• Pollen from grasses, trees, weeds, and mold spores.
• Pollen and mold counts vary geographically and by season.
• Seasonal peaks in pollens cause allergic rhinitis (“hay fever”) and
can exacerbate asthma.
• The National Allergy Bureau (NABTM) maintains a current and user
friendly website of pollen counts
• http://www.aaaai.org/global/nab-pollen-counts.aspx
• Pollen counts are predicted to rise with climate change
Burge HA, Rogers CA. Outdoor allergens. Environ Health Perspect. 2000;108(S4):653
Shea KM, et al. Climate change and allergic disease. J Allergy Clin Immun.
2008;122(3):443–53
http://www.vcbio.science.ru.nl/en/virtuallessons/pollenintro/
Follow-up and Monitoring
• 1 to 6 month intervals, depending on
degree of control
• Evaluate patient’s symptoms, satisfaction
and compliance
• Include spirometry to assess control and
guide step-up or step-down drugs
NAEPP 2007 Expert Panel Report 3 Summary Report 2007.
Allergy Clin Immunol 2007;120 (5): Supplement.
J
Vocal Cord Dysfunction (PVFM)
• Incidence is unknown
• Newman et al., 40% of adults seen for refractory
asthma had PVFM
– 30% in combination with asthma
– 10% as sole diagnosis
• Among healthy, physically active adolescents and
young adults the incidence has been reported to
be between 8% and 27%
• Reported in up to 5% of Olympic athletes
Description
• Upper airway obstruction
• Adduction of the true vocal folds
– Primarily on inhalation
• Sometimes during exhalation
• Usually very abrupt onset
• Spectrum of presentation
– Severe respiratory distress to mild dyspnea
Symptoms/Signs
More common:
• Difficulty breathing
– “Air hunger”
• Throat or neck tightness
• Cough
• Stridor or laryngeal
wheezing
• Lightheadedness
• Dizziness
Other:
• Dry cough
• Chest tightness
• Neck/chest retractions
• Dysphagia
• Globus pharyngeus
• Choking
• Suffocating
• Dysphonia
• Intermittent aphonia
• Throat clearing
• Paresthesias of hands, feet,
around mouth
Self-reported Triggers
• Upper respiratory
infections
• Eating
• Talking
• Laughing
• Singing
• Coughing
• Acid Reflux
• Physical Exertion
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Post-nasal Drip
Weather Changes
Emotional Stress
Strong Scents
– E.g., perfume
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Smoke
Fumes
Solvents
Air Pollution
Hicks, et al. Prim Care Clin Office Pract. 35 (2008): 81-103
Pathophysiology
• PVFM
– Non-physiologic closure of the true vocal folds on
inspiration with or without concommitant closure
on expiration
• Adduction may be complete, along the entire length of
the cords
• Adduction may be along the anterior two-thirds leaving
a “posterior chink”
– Expiratory-only closure may be a PVFM variant
Differential Diagnosis
• Infectious
– Croup, epiglottitis, laryngitis, pertusis, etc.
• Inflammatory
– Wegener’s granulomatosis, laryngeal sarcoid, etc.
• Traumatic
– Caustic ingestion, thermal injuries, etc.
• Allergic
– Atypical asthma, anaphylaxis, exercise-induced asthma,
hereditary angioedema, etc.
• Pulmonary
– Asthma, COPD, gastric or laryngopharyngeal reflux with
aspiration, hyperventilation syndrome, etc.
• Congenital anomalies
– Laryngomalacia, laryngeal cleft, subglottic stenosis, intrathoracic
vascular ring, laryngeal web
• Psychiatric and Neurologic
Diagnosis
• Diagnosis relies on four areas:
– Clinical history and physical exam
– Pulmonary function testing
– Measures of oxygenation
– Provocation testing with laryngoscopy
Vocal Cord Dysfunction
Clinical History
• Patients point to or grab their throat when describing
symptoms
• May have worsening of symptoms when using
metered-dose or dry powder inhalers
• May have some relief when using nebulized
medications
• Symptoms of hyperventilation may be reported in up
to 76% of patients
• Common associated risk factors or triggers*
Risk Factors/Triggers
• Female gender
• GERD
• Upper Airway Inflammation
– Rhinitis, sinusitis, etc.
• Prior traumatic event involving breathing
– Near drowning, suffocation, etc.
• Competitive athletics
• Excessive voice demands
– Singing, drama, public speaking, telecommunications
• Severe emotional stress
• Playing a wind instrument
Psychologic Factors
• 1842, Dunglison reported first cases of PVFM; called
“hysteric croup”
• 1975, Patterson called the disease Munchausen’s
stridor
• Anxiety has been seen in up to 34% of adults and
25% of kids with respiratory disorders*
• Estimated 20% of PVFM attacks are triggered by
stress in the general population
– Increased PVFM in soldiers as a reaction to combat
– Increased PVFM in highly, competitive athletes
• Approximately 5% of US Olympic athletes with VCD†
* Hicks, et al. Prim Care Clin Office Pract. 2008;35: 81-103
† Rundell KW, et al. Chest. 2003;123:468-74
Treatment
• Multidisciplinary approach
• Guided by comorbidities
• Patient education is critical
– Avoidance/minimization of triggers
– Direct visualization enhances patient
understanding and engagement in treatment
• Acute episode management
• Chronic management
Acute Treatment
• Patient reassurance
• Breathing techniques: panting, sniffing,
pursed-lip breathing on exhalation, nasal
inhalation
• Heliox therapy (70:30, 80:20)
• Anxiolysis
• Consider nebulized lidocaine
Chronic Management
• Comorbid disease management
• Speech therapy
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Patient education
Supportive counseling
Respiratory restraining
Management and suppression of laryngeal abusive
behaviors
– Voice therapy
– Desensitization to specific irritants
• Psychotherapy if indicated
Selected References
• National Heart, Lung and Blood Institute Asthma
Education and Prevention Program. Expert Panel
Report 3 (EPR-3): Guidelines for the Diagnosis and
Management of Asthma. Full Report 2007.
Bethesda, Maryland: National Institutes of
Health, US Department of Health and Human
Services, National Heart, Lung and Blood
Institute; 2007.
• Hicks M, Brugman SM, Katial R. Vocal Cord
Dysfunction/Paradoxical Vocal Fold Motion. Prim
Care Clin Office Pract. 35 (2008): 81-103.
Post-Test: Q1
Which of the following cells do not contribute to
airway inflammation in asthma?
A.
B.
C.
D.
Neutrophils
Lymphocytes
Red blood cells
Eosinophils
Q2
Which of the following are essential features of
asthma?
A. Airway inflammation
B. Airway “twitchiness”/hyperresponsiveness
C. Airway obstruction
D. All of the above
Q3
Which is not a symptom of asthma?
A. Cough
B. Wheezing
C. Stridor
D. Shortness of breath
E. Response to albuterol
Q4
A 18 year old male reports coughing and chest
tightness 3 to 4 days per week, nighttime cough
about once per week and albuterol (which clears
his symptoms) use twice per week. His asthma
is:
A. Persistent
B. Intermittent
C. A figment of his imagination
Q5
You can change your patient’s severe asthma to
mild asthma by giving them more prednisone?
A. True
B. False
Q6
Which is NOT a common outdoor allergen?
A. Rose flower pollen
B. Birch tree pollen
C. Alternaria
D. Ragweed pollen
Q7
You determine that the 27 year old female you
are seeing has mild persistent asthma. She has
never been on controller therapy. Which is the
most appropriate first line control medication?
A. Fluticasone/salmeterol, 250/50 , BID
B. Budesonide, 90 mcg, once daily
C. Omalizumab, IM, twice monthly
D. Montelukast 10 mg plus Fluticasone, 220
mcg, nightly
Q8
The 16 year old soccer player you are seeing
reports severe shortness of breath, coughing
and wheezing within 1 to 2 minutes of starting
to run, which improves within minutes of resting
only to return as soon as he runs again. His most
likely issue is:
A. Exercise induced bronchospasm
B. Vocal cord dysfunction
C. GERD with aspiration
Q9
Which is not a recommended environmental
control to reduce indoor allergen exposure?
A. Cover pillows and mattress with anti-dust
mite encasements
B. Remove animals from the home
C. Remove flowering plants from the home
when pollinating
D. Eliminate potential sources of water damage
and mold
Q10
Which is not a risk factor/trigger for vocal cord
dysfunction?
A. Gastroesophageal reflux
B. Post-nasal drainage from allergies
C. Competitive athletics
D. Answering post-test questions about VCD in a
relaxing, no-pressure-added conference
setting