Childhood

Asthma
1

ZUHAIR M AL-MUSAWI
 Objectives
 Asthma, definition, etiology, types, and
clinical manifestations.
 Evaluation of Asthma Exacerbation Severity,
diagnosis, and differential diagnosis.
 Asthma
Chronic inflammatory disorder of the airways in which
.many cells and inflammatory mediators play a role

The chronic inflammation causes recurrent episodes of

wheezing, breathlessness, chest tightness, and
.coughing, particularly at night or in the early morning
These episodes are usually associated with widespread
reversible airflow obstruction

The inflammation also causes increased airway

hyperresponsiveness (AHR) to a variety of stimuli
 Childhood Asthma
 Asthma is a common chronic illness among
children with widely variable prevalence in
different countries (0.8% - 37.6%)
 The prevalence is more in the developed
countries
 Boys are more likely to have asthma than girls
with ratio of 1.4:1
 In Iraq, the prevalence of childhood asthma is
about 16% of general pediatric population
 Etiology
 The exact cause of childhood asthma has not
been determined and a combination of
environmental and genetic factors is suggested
 Environmental factors:
 Allergen exposure
 Respiratory infections
 Exposure to air Pollutants
 Exposure to tobacco smoke
 Genetic factors:
 Atopy
 Phenotypes of Childhood Asthma
 Transient early wheezing
 Common in early preschool years
 Recurrent cough/wheeze, primarily triggered by
common respiratory viral infections
 Tends to resolve during the preschool years, without
increased risk for asthma in later life
 Phenotypes of Childhood Asthma
 Persistent atopy-associated asthma
(allergic asthma)
 Begins in early preschool years
 Associated with atopy in early preschool years:
 Clinical:
 Atopic dermatitis in infancy
 Allergic rhinitis
 Food allergy
 Biological
 Early inhalant allergen sensitization
 Increased serum immunoglobulin E
 Increased blood eosinophils
 Highest risk for persistence into later childhood and
adulthood
 Phenotypes of Childhood Asthma
 Nonatopic wheezing
 Wheezing/coughing beginning in early life, often with
RSV infection
 Resolves in later childhood without increased risk of
persistent asthma
 Associated with AHR in early life

 Late-onset asthma in females, associated

with obesity and early-onset puberty
 Onset between 8 and 13 years of age
 Associated with obesity and early-onset puberty
 Specific for females
Phenotypes of Childhood Asthma
 Risk Factors for Persistent Asthma
 Major RFs:
 Parental asthma

 Eczema

 Inhalant allergen sensitization

 Minor RFs:
 Allergic rhinitis

 Wheezing apart from colds

 Blood eosinophils of ≥4%

 Food allergen sensitization

 Pathophysiology
 The symptoms of asthma are due to airflow
obstruction resulting from the cumulative
effects of:
 Smooth muscle constriction around airways
 Airway wall edema
 Intraluminal mucus accumulation
 Inflammatory cells infiltration of the submucosa
 Basement membrane thickening
Normal Asthmatic
bronchiole bronchiole
 Airways Inflammation
 Inflammatory cells mostly involved in asthmatic
airways inflammation include:
 Th2 Lymphocytes
 Eosinophils
 Mast cells
 Neutrophils
 Cytokines regulates airways inflammation include
(IL-4, IL-5 & IL-13)
 Inflammatory mediators mostly released include:
 Cysteinyl leukotrienes (LTC4, LTD4 & LTE4)
 Histamine
 PG-F2α
 Clinical Manifestations of
Childhood Asthma
 Chronic symptoms of asthma include intermittent
dry coughing and expiratory wheezing. Older
children also report shortness of breath and chest
tightness.

 Respiratory symptoms are usually worse at night,

especially during prolonged exacerbations
triggered by respiratory infections or inhalant
allergens.
 Clinical Manifestations of
Childhood Asthma
 Daytime symptoms are often linked with physical
activities or play.

 Asthma symptoms may occur at any time, but it

usually follows certain triggering factors.
 Asthma Triggers
 Common viral infections of the respiratory tract
 Exposure to aeroallergens in sensitized patients:
 House dust mites
 Animal allergens
 Pollens
 Fungal allergens
 Exposure to environmental triggers (air pollutants)
 Exercise
 Exposure to cold and dry air
 Crying and laughing
 Drugs (β-blockers and aspirin)
 Co-morbid conditions (GERD, sinusitis, rhinitis)
 Acute Asthmatic Attacks
 Most acute asthmatic attacks have a slow
onset and last for several days.

 During asthma exacerbations, expiratory

wheezing and a prolonged expiratory phase
can usually be heard by auscultation. Crackles
can sometimes be heard, resulting from excess
mucus production and inflammatory exudate in
the airways.
 Acute Asthmatic Attacks
 In severe exacerbations, there is respiratory
distress, which manifests as inspiratory and
expiratory wheezing, poor air entry,
suprasternal and intercostal retractions, nasal
flaring, and accessory respiratory muscle use.

 In very severe exacerbations, airflow may be

so limited that wheezing cannot be heard.
Evaluation of Asthma Exacerbation Severity
Evaluation of Asthma Exacerbation Severity
Evaluation of Asthma Exacerbation Severity
Diagnosis of Childhood Asthma
 Establishing a diagnosis of asthma involves a
careful process of history taking, physical
examination, and diagnostic studies.
 For an individual child, this process first involves
obtaining a history of episodic or chronic
symptoms of airflow obstruction (wheezing,
breathlessness, chest tightness, and
coughing).
 These symptoms may occur or worsen with viral
infections, exercise or the exposure to animals,
smoke, pollen, mold, and airborne chemicals or
dust.
 Diagnosis of Childhood Asthma
 Physical examination of an asthmatic child is
generally normal if performed in the absence of
an acute exacerbation.
 Abnormal findings may suggest severe disease,
suboptimal control or associated atopic
conditions.
 Abnormalities that may be observed include an
increased anterior-posterior diameter of the
chest due to air trapping, decreased air entry,
wheezing and prolonged expiratory phase on
auscultation.
 Diagnosis of Childhood Asthma

 Response to treatment with bronchodilators

(decreased respiratory rate, decreased cough or
wheezing) supports the diagnosis of asthma.

 The onset of action of inhaled bronchodilators is

usually rapid and the benefits can last 4-6 hours
 Diagnosis of Childhood Asthma

Spirometry and other

lung function tests are
usually used for children
aged more than 5 years
to determine the
 presence of airflow
obstruction and to
 establish reversibility to
bronchodilator therapy.
 Diagnosis of Childhood Asthma
Lung function abnormalities in asthma
include:
 Airflow limitation:
 Low FEV1 (relative to percentage of predicted).
 FEV1/FVC ratio <0.8.

 Response to inhaled bronchodilators

(reversibility test):
 Improvement in FEV1 ≥12%.

 Exercise challenge:
 Worsening in FEV1 ≥15%.

 Daily peak flow monitoring:

 Day to day and/or AM-to-PM variation ≥20%.
 Lung Function Abnormalities

Volume-Time Curve

 Blue line:
line Normal subject
 Red line:
line Asthmatic patient (V-T curve showed reduced FEV1)
 Diagnosis of Childhood Asthma
 Direct bronchial provocation test with
methacholine or histamine can be used to tests
for AHR that is clinically useful to aid in the
diagnosis of asthma. Asthmatic airways are
usually hyperresponsive and less methacholine
or histamine is needed to induce airflow
obstruction.
 Measuring exhaled nitric oxide (FeNO) as a
marker of airway inflammation, has been found
to be helpful in confirming the diagnosis of
asthma in addition to monitoring asthmatic
inflammation and adjusting therapy.
 Diagnosis of Childhood Asthma

Chest X-rays are

usually normal, but
hyperinflation can
be seen in patients
with long lasting and
poorly controlled
disease.
 Diagnosis of Childhood Asthma
Biomarkers:
 Peripheral blood eosinophils count:
Peripheral blood eosinophilia usually associated
with allergic airways inflammation, but it is non-
specific, and sputum eosinophils count is preferred.
 Total serum IgE:
Total serum IgE may be used to differentiate
between atopic and nonatopic asthmatics prior to
allergen-specific IgE determination. Also it is
helpful in predicting severity and monitoring
response to therapy in children with allergic asthma.
 Diagnosis of Allergic Asthma
 The diagnosis of allergic asthma requires the
assessment of sensitization to aeroallergens by
performing a screening test for the most common
aeroallergens in the area by:
 Allergen-specific IgE immunoassay or

 Skin prick test

 Based on the results of these tests, asthmatic

children are divided into allergic (one or more
inhalation allergen test positive) or non-allergic
asthmatics.
 Diagnosis of Allergic Asthma
 Allergic asthmatic children in Kerbala are mostly
sensitized to (Cat, house dust mite, dog and
fungal allergens)
 Differential Diagnosis of
Childhood Asthma
Upper respiratory tract conditions:
 Allergic rhinitis
 Chronic rhinitis
 Sinusitis
 Adenoidal or tonsillar hypertrophy
 Nasal foreign body
Differential Diagnosis of Childhood Asthma
Middle respiratory tract conditions:
 Laryngotracheobronchomalacia
 Laryngotracheobronchitis (e.g., pertussis)
 Laryngeal web, cyst, or stenosis
 Vocal cord dysfunction
 Vocal cord paralysis
 Tracheoesophageal fistula
 Vascular ring, sling, or external mass compressing
on the airway (e.g., tumor)
 Foreign body aspiration
 Chronic bronchitis from environmental tobacco
smoke exposure
 Toxic inhalations
Differential Diagnosis of Childhood Asthma
Lower respiratory tract conditions:
 Bronchopulmonary dysplasia (chronic lung
disease of preterm infants)
 Viral bronchiolitis
 Gastroesophageal reflux
 Causes of bronchiectasis:
 Cystic fibrosis
 Immune deficiency  
 Allergic bronchopulmonary mycoses (e.g.,
aspergillosis)  
 Chronic aspiration  
 Immotile cilia syndrome, primary ciliary dyskinesia
Differential Diagnosis of Childhood Asthma
Lower respiratory tract conditions:
 Bronchiolitis obliterans
 Interstitial lung diseases
 Hypersensitivity pneumonitis
 Pulmonary eosinophilia, Churg-Strauss vasculitis
 Pulmonary hemosiderosis
 Tuberculosis
 Pneumonia
 Pulmonary edema (e.g., congestive heart failure)
 Medications associated with chronic cough:   
 Acetylcholinesterase inhibitors  
 β-Adrenergic antagonists  
 Angiotensin-converting enzyme inhibitors
 SKILLS
 Spirometry: lung function tests are
usually used for children aged more than
5 years.
 Peak flowmeter: for school age children.
 Childhood
Asthma
2

ZUHAIR M AL-MUSAWI
 Objectives
 Goals of treatment.
 What are the controller and reliever drugs.
 Assessment of Asthma Severity.
 The Stepwise Treatment Approach.
 Drug Therapy for Childhood Asthma.
 Treatment of Acute Asthmatic Attacks: mild,
moderate, severe, and life threatening.
 Prognosis of childhood asthma.
 Treatment of Childhood Asthma
Goals of pediatric asthma treatment includes:
 Improvement in asthma symptoms
 Reductions in frequency, severity & durations of
exacerbations
 Normalization of lung function
 Normalization of AHR
 Reduction in chronic inflammation of the airways and
airways remodeling
 Normal development of lung function
 Normal psychosocial development
 Reduced SABA (Short-Acting Beta2-Agonist)
 Minimal adverse effects of therapy
 Treatment of Childhood Asthma
 Current treatment of childhood asthma is mainly
depends on pharmacological approach.
 Drugs used can be classified as controllers or
relievers:
 Controllers are drugs taken daily on a long
term basis to keep asthma under clinical control
chiefly through their anti-inflammatory effects.
 Relievers are used on need, which acts quickly
to reverse bronchoconstriction and relieve its
symptoms
 Controller Drugs
 Inhaled corticosteroids (ICS)
 Leukotriene modifiers:
 Leukotriene receptor antagonists
 5-lipoxygenase inhibitor
 Inhaled long-acting β2-agonists (LABAs)
 Theophylline
 Cromolyn sodium and nedocromil
 Anti-IgE (omalizumab)
 Systemic corticosteroids (SCS)
 Reliever Drugs

 Inhaled Short-acting β2-agonists (SABAs)

(salbutamol MDI is the most widely used)
 Anticholinergic drugs (Ipratropium)
 Systemic corticosteroids (SCS)
 Aminophylline
 Magnesium sulphate
Treatment of Childhood Asthma
Other treatment options for allergic asthma
that may aid pharmacotherapy includes:

 Specific allergen immunotherapy that shows

some benefit in children, particularly with house
dust mite allergens.

 Allergen avoidance when there is sensitization

or a clear association between allergen
exposure and symptoms.
Treatment of Childhood Asthma
Management of childhood asthma requires:
 Assessment and monitoring of disease activity
(asthma severity & asthma control)
 Identification and management of precipitating
factors and co-morbid conditions that may
worsen asthma
 Appropriate selection of medications according
to the patient's needs
 Education to enhance the patient's and family's
knowledge and skills for self-management
 Assessment of Asthma Severity
 Asthma severity is the intrinsic intensity of the
disease.
 The two general categories are intermittent and
persistent asthma
 Persistent asthma is further subdivided into
mild, moderate and severe.
 The Stepwise Treatment Approach
 Management of intermittent asthma is simply
the use of SABA as needed for symptoms and
for pre-treatment in those with exercise-induced
bronchospasm (Step 1 therapy).
 The preferred treatment for all patients with
persistent asthma is daily inhaled
corticosteroid (ICS) therapy, as monotherapy
or in combination with adjunctive therapy (Steps
2-6 therapy).
 Drug Therapy for Childhood
Asthma
 Inhaled therapy is the cornerstone of asthma
treatment for children of all ages.
 Young children often cannot generate adequate
inspiratory flow to effectively use dry-powder inhaler
(DPI) devices.
 Metered-dose inhaler (MDI) devices with spacers
supplied with face masks can be used for children
less than 5 years of age.
 DPIs and MDIs with or without spacers are generally
used more efficiently by older children.
 Inhalers & Spacers
MDI DPI

Spacer
with face
mask
 Inhaled Corticosteroid (ICS)
Inhaled corticosteroids are the most effective
controller therapy for asthma in children of all ages
 Inhaled Corticosteroid (ICS)
 The clinical effects of ICS therapy include:
 reduction in severity of symptoms
 improvement in asthma control and quality of life
 improvement in lung functions
 diminished airway hyperresponsiveness
 prevention of exacerbations
 reduction in systemic corticosteroid courses,
emergency care, hospitalizations, and deaths due to
asthma
 The use of ICS does not induce remission of asthma and
symptoms usually returns when treatment is stopped.
Asthma control usually deteriorates within weeks to
months after ICS discontinuation.
 Inhaled Corticosteroid (ICS)

 Generally, inhaled corticosteroids have lower

bioavailability than oral systemic corticosteroids;
hence, the risk of potential side effects is
substantially reduced with ICS therapy.

 The use of MDIs with spacer devices produces

maximum drug delivery to the lungs and further
reduces the oral bioavailability.
 Side effects of ICSs
 Adverse effects of ICSs are closely related to the
dose of particular drug.
 Other factors include duration of therapy and oral
bioavailability.
 Minimum side effects (mostly local) are observed
with daily low-dose therapy, while serious
systemic adverse effects (like Suppressed growth
velocity and hypothalamic-pituitary-adrenal axis
suppression) are usually associated with long
term daily high-dose therapy.
 Side effects of ICSs
 Local side effects:  Systemic side effects:
 Oropharyngeal  Suppressed growth velocity
candidiasis  Hypothalamic-pituitary-adrenal
 Dysphonia
axis suppression
 Sore throat
 Decreased lower leg length
 Pharyngitis
 Reduced bone mineral density
 Reflex cough
 Osteoporosis and bone fractures
 Bronchospasm
 Increased susceptibility to
infections
 Cataracts and glaucoma

 Skin thinning and bruising

 Leukotriene Modifiers
 Leukotriene modifiers include leukotriene receptor
antagonists (LTRA) and a 5-lipoxygenase inhibitor
that are available as oral controller drugs for the
treatment of pediatric asthma.
 Two cysteinyl-leukotriene 1 receptor antagonists
are available, montelukast (for patients ≥1 year
of age) and zafirlukast (for patients ≥7 years of
age). The 5-lipoxygenase inhibitor zileuton is
available for patients ≥12 years of age.
Leukotriene Modifiers
 Leukotriene Modifiers
 Leukotriene modifiers have bronchodilator effect, reduce
symptoms, improve lung function, and reduce airway
inflammation and asthma exacerbations.
 Montelukast also provides protection against exercise-
induced bronchoconstriction within hours after
administration.
 Montelukast is highly safe drug and demonstrated a
safety profile more than that of inhaled corticosteroids in
asthmatic children.
 Hepatic dysfunction has been associated with zafirlukast
and zileuton treatment. Although most patients improved
with discontinuation of therapy.
 Theophylline
 Theophylline is a phosphodiesterase inhibitor
methylxanthine that acts primarily as
bronchodilator. In addition, it has modest anti-
inflammatory properties.
 On long term oral therapy, theophylline reduces
asthma symptoms and the need for rescue SABA
use and improves lung function.
 Theophylline has a narrow therapeutic index;
therefore, serum theophylline levels need to be
routinely monitored, especially if the patient taking
medications known to delay theophylline
clearance such as erythromycin, cimetidine and
ketoconazole.
 Systemic Corticosteroids (SCS)
 Systemic corticosteroids are used primarily to
treat asthma exacerbations and rarely used
as controller drugs.
 Oral corticosteroids should be preserved for
patients with severe disease who remain
symptomatic despite optimal use of other
controller agents
 Prednisolone, prednisone and
methylprednisolone are usually used.
 Systemic Corticosteroids (SCS)
 The oral corticosteroid dose should not exceed 20 mg
every other day to avoid serious adverse effects.

 Systemic adverse effects include; growth

suppression, hypothalamic-pituitary-adrenal axis
suppression, osteoporosis, proximal myopathy, fluid
retention, increased appetite, weight gain, capillary
fragility, hypertension, peptic ulceration, diabetes,
cataracts, and psychosis
 Treatment of Acute Asthmatic
Attacks

 The management of AAAs requires a prior

assessment of attacks severity
 The treatment lines are:
Treatment of Acute Asthmatic
Attacks
Treatment of Acute Asthmatic
Attacks
Treatment of Acute Asthmatic
Attacks
Treatment of Acute Asthmatic
Attacks
 Prognosis
 Approximately one third of preschool-aged
asthmatic children continue to have persistent
asthma into later childhood, and two thirds improve on
their own through their teen years.
 Asthma severity by the ages of 7-10 yr of age is
predictive of asthma persistence in adulthood.
 Children with moderate to severe asthma are likely to
have persistent asthma as adults. Children with milder
asthma are likely to improve over time, with some
becoming periodically asthmatic (disease-free for
months to years)
 SKILLS
 Types of Inhalers & Spacers and how they are
used.
 Types of nebulizers and how they are used.
Thank you