CHILD HOOD ASTHMA

Kussia .A (MD)
 Asthma is a chronic inflammatory condition of the
airways resulting in episodic reversible airflow
obstruction and air ways heperresponsiveness.
 Is a serious global health problem with increasing
prevalence in many developing countries rising
treatment costs and burden for patients and
communities.
ETIOLOGY
 combination of environmental exposures and inherent
biologic and genetic susceptibilities
 In genetically predisposed child immune responses to
common airways exposures can stimulate prolonged
pathogenic inflammation and aberrant repair of
injured airways
 These pathogenic processes in the growing lung
during early life adversely affect airways growth and
differentiation, leading to altered airways at mature
ages
 Genetics
 The familial association of asthma
 high degree of concordance in identical twins
 asthma is polygenic ( interaction of many genes )
 Epigenetic modification of genes
 Environment
 Recurrent wheezing episodes in early childhood are
associated with common respiratory viruses
 Home allergen exposures in sensitized individuals
can initiate airways inflammation hypersensitivity ,
and are strongly linked to disease severity and
persistence.
EPIDEMIOLOGY
 Childhood asthma is among the most common
causes of childhood emergency department visits,
hospitalizations, and missed school days
 Worldwide, childhood asthma appears to be
increasing in prevalence, despite considerable
improvements in management
 Childhood asthma seems more prevalent in
affluent nations, and is strongly linked with other
allergic conditions ( hygiene hypothesis)
 Approximately 80% of all asthmatic patients report
disease onset prior to 6 yr of age
 Only few children with recurrent weezing will
develop persistent asthma in later child hood
  Early childhood risk factors for persistent asthma

MAJOR MINOR

Parental asthma allergic rhinitis

eczema wheezing apart from colds

inhalant allergen sensitization ≥4% peripheral blood

eosinophils

food allergen sensitization

PATHOGENESIS
 Air way inflammation
 Inflammation has a central role in the
pathophysiology of asthma
 airway inflammation involves an interaction of
many cell types and multiple mediators
 Lymphocytes
 A shift, or predilection, toward the Th2-cytokine
profile resulted in the eosinophilic inflammation
characteristic of asthma .
 Generation of Th2 cytokines (e.g. IL-4, IL-5, and
IL-13) could also explain the overproduction of
IgE, presence of eosinophils, and development of
airway hyperresponsiveness
 Mast cells -Activation of mucosal mast cells
releases bronchoconstrictor mediators (histamine,
cysteinyl-leukotrienes, prostaglandin
 Mast cells also release a large number of cytokines
 Eosinophils- Eosinophil infiltration is a
characteristic feature of asthmatic airways
 Asthma…..‘chronic eosinophilic bronchitis’
 Eosinophils contain inflammatory enzymes,
generate leukotrienes, and express a wide variety of
pro-inflammatory cytokines
 Increases in eosinophils often correlate with greater
asthma severity
 Other cells neutrophils, basophils ,epithelial cells
 Bronchoconstriction
 In acute exacerbations of asthma, bronchial smooth
muscle contraction occurs quickly to narrow the
airways in response to exposure to a variety of
stimuli including allergens
 Allergen-induced acute bronchoconstriction results
from an IgE-dependent release of mediators from
mast cells that includes histamine , leukotrines and
prostaglandins
 Airway edema
 As the disease progresses air way edema , a result of
inflammation further limits air flow and contributes to
clinical symptoms
 Airway hyperresponsiveness
 an exaggerated bronchoconstrictor response to a wide
variety of stimuli is a major feature of asthma
 Inflammation , abnormal neuronal regulation and
structural changes contribute to air way
hyperresponsivenss
 Airway remodeling
 Permanent structural changes can occur in the airway
these are associated with a progressive loss of lung
function that is not fully reversible or treatable by
current therapy
 These include thickening of the sub-basement
membrane, subepithelial fibrosis, airway smooth
muscle hypertrophy and hyperplasia, blood vessel
proliferation and dilation, and mucous gland
hyperplasia and hypersecretion
Pathogenesis of asthma
Types of Childhood Asthma
 (1) TRANSIENT NONATOPIC WHEEZING
 Primarily triggered by common respiratory viral
infection
 Resolves during the preschool/lower school years
 (2) PERSISTENT ATOPY-ASSOCIATED 
ASTHMA
 Begins in early preschool years
 Associated with atopy in early preschool years
 persists into later childhood and often adulthood
 SEVERITY CLASSIFICATION
 Intermittent
 Persistent:
 Mild
 Moderate
 Severe
 CONTROL CLASSIFICATION
 Well controlled
 Not well controlled
 Very poorly controlled
 MANAGEMENT PATTERNS
 Easy-to-treat
 Difficult-to-treat:
 Exacerbators
 Refractory
CLINICAL MANIFESTATION
 Intermittent dry coughing and expiratory wheezing
 shortness of breath and chest congestion and
tightness in older children
 Respiratory symptoms can be worse at night
 Daytime symptoms, often linked with physical
activities (exercise-induced) or play
 asthma symptoms in children can be subtle
 Bronchodilator response supports the diagnosis of
asthma
 The presence of risk factors( family history , atopy or
allergy)
 Trigering factors
 During clinic visits , examination may be subtle
emphasizing the importance of clinical history
 During exacerbations, expiratory wheezing and a
prolonged exhalation phase can usually be appreciated
by auscultation
 Rhonchi and crackles can sometimes be heard
 Segmental crackles and poor breath sounds
indicate segmental atelectasis
 Severe respiratory distress indicates severe
exacerbation
 Absence of wheezing may indicate extreme air
flow limitation
Laboratory findings
 Pulmonary Function Testing
 Forced expiratory airflow measures
 Spirometry is feasible in children >6 yr of age
 Diagnosing and monitoring asthma and in
assessing efficacy of therapy
 particularly helpful in children with asthma when
physical signs of asthma do not occur until airflow
obstruction is severe.
Lung function abnormalities in asthma
TREATMENT
 Management of asthma has the following
components
(1) Assessment and monitoring of disease activity
(2) Asthma education
(3) Identification and management of precipitating
factors and co morbid conditions
(4) Pharmacotherapy
Goal of asthma Management
 Control chronic symptoms
 Prevent acute exacerbations
 Maintain normal lung function
 Maintain normal activity and growth
 Minimize hospitalization
 Prevent /minimize drug side effects
Regular assessment and monitoring

 Asthma severity
 Intrinsic intensity of disease

 Directs the initial level of therapy

i) Intermittent asthma
ii) Persistent asthma
 Mild

 Moderate

 Severe
 Asthma control
 Symptom control
 Minimization of adverse events
 Responsiveness to therapy
 How difficult is asthma control achieved
 Classification of asthma severity and control is
based on the impairment and risk
 Impairment consists of an assessment
 Symptoms frequency ( day and night)
 SABA usage for quick relief
 Activity level
 Airflow compromise evaluated by spirometry in
children 5 yr and older
 Risk refers to
 likelihood of developing severe asthma
exacerbations
 Persistent asthma should be considered in children
with risk factors and 4 or more episodes of
wheezing / a year or 2 or more exacerbations
requiring systemic steroid therapy
Asthma education
 Basic facts of asthma
 Proper techniques of drug administration
 Precipitating factors
 Asthma management plan
 Daily control
 Exacerbation treatment
 Follow up
 Potential drug adverse effect
Precipitating factors and co morbid conditions

asthma precipitating factors

 Treating Co morbid Conditions
 Sinusitis
 Rhinitis- nasal congestion reduces air
humidification ,warming and filtration
 GERD –Aspiration of gastric contents
 - reflux bronchospasm
Asthma pharmacotherapy
CLASS ExAMPLE
• Short acting
ß2 agonists
salbutamol
albuterol
terbutalin
• Long acting
Salmeterol
formoterol

Inhaled corticosteroids Beclomethasone

Fluticasone
budesonide
Leukotrine pathway Montelukast( > 1yr)
modifiers zafirlukast ( > 5 yrs)
Nonsteroidal anti- Cromolyn
nedocromil
inflammatory
Agents
Methylxanthines Theophylline

Anti– Omalizumab
Immunoglobulin E
 Goal of pharmacotherapy is to achieve well
controlled asthma by reducing impairment and risk
 All persistent asthmas should be treated with anti-
inflammatory controller medication as a
monotherapy or in combination based on asthma
severity
 Intermittent asthmas should be treated with short
acting bronchodilators ( SABA) as needed
 Children < 4 yrs
 with moderate or severe persistent asthma medium-dose
ICS monotherapy (step 3)
 combination therapy ( Step 4) treatment for
uncontrolled asthma
 Children > 4 yrs
 With moderate persistent asthma medium dose ICS
PLUS ajuvant therapy
 Children with severe persistent asthma (treatment Steps
5 and 6) should receive high-dose ICS and LABA
“Step-Up, Step-Down” Approach
 Air flow limitation may decrease delivery of ICS at
initial treatment necessitating high dose ICS or
combination treatment
 If asthma not well controlled treatment should be

increased ( step up)

 If a child has had well-controlled asthma for at least 3

mo, decreasing the dose or number of the child’s

controller medication(s) to the minimum
required medications to maintain well-controlled
asthma ( step down)
Stepwise Approach for Managing Asthma in
Children
Management of exacerbations
 Assessment of severity
 Airflow obstruction during exacerbations can

become extensive, resulting in life-threatening

respiratory insufficiency
 Mild

 Moderate

 Severe
 SYMPTOM Mild moderate Severe Imminent
respiratory
failure
41
Breathlessness walking At Rest At Rest
Talks In Sentence Phrases Words
Alertness Alert Usually Usually Confused
agitated agitated
SIGNS
RR Increased Increased Increased
Accessory Usually not commonly usually Paradoxical
Muscle Use respiration
Wheeze Moderate, Loud, Inspiratory & Silent Chest
Expiratory Expiratory Expiratory
Pulse Rate Normal +20 >+20 Bradycardia
Pulses <10mmhg 10-25mmhg >25mmhg Absent
Paradoxus Mgt. Of Asthma 9/2/21
 Functional
Assessment
42
PEF 40-69% <40% <25%

PaO2 Normal >60mmhg <60mmhg

Pco2 <42mmhg <42mmhg >42mmhg

SaO2 >95% 90-95% <90%

Treatment of Asthma exacerbation
 Supplemental oxygen
 Hydration / avoid dehydration
 SABA Q 20 minutes for 1 hr , then q 4-6 hrly
 Short-course systemic corticosteroid for moderate
to severe exacerbations
 Anticholenergic ( Ipratropium bromide)
 Patients not responding for standard treatment may
benefit from parentral epinephrine
,methylxanthines or magnesium sulphate
 Patients recicieving magnesium sulphate and
methylxanthines require monitoring serum drug
level
 Rarely, a severe asthma exacerbation in a child
results in respiratory failure, and intubation and
mechanical ventilation become necessary
 PROGNOSIS
 In children, management of severe exacerbations is
usually successful, even when extreme measures
are required
 Only 1/3 of recurrent swheezer continue to have
persistent asthma into later childhood