Bronchial Asthma

• Asthma is a chronic inflammatory condition

of the lung airways resulting in episodic
airflow obstruction.
• Airway inflammation is associated with airway
hyperreactivity or bronchial
hyperresponsiveness (BHR), which is defined
as the inherent tendency of the airways to
narrow in response to a variety of stimuli.
 Epidemiology
• Worldwide, childhood asthma appears to be
increasing in prevalence.
• Asthma prevalence correlated well with
reported allergic rhinoconjunctivitis and atopic
eczema prevalence
• Approximately 80% of all asthmatics report
disease onset prior to 6 yr of age.
• A disparity in asthma outcomes links high rates
of asthma hospitalization and death with
poverty, ethnic minorities, and urban living.
 Epidemiology
• There is good evidence that asthma occurs in
families.
• Childhood asthma seems particularly common
in modern metropolitan locales and is strongly
linked with other allergic conditions.
• Children living in rural areas of developing
countries and farming communities are less
likely to develop asthma and allergy.
 Risks of persistent asthma
• Parental asthma • Male gender
• Allergies • Low birthweight
– Food allergy • Environmental tobacco
– Inhalent allergens smoke exposure 
• Severe lower respitatory
tract infection
– Bronchiolities requring
admission
– Wheezing apart from
colds
 Types of Childhood Asthma

• There are 2 main types of childhood asthma:

• (1) recurrent wheezing in early childhood, primarily
triggered by common viral infections of the respiratory
tract.
• (2) chronic asthma associated with allergy that persists
into later childhood and often adulthood.
• Triad asthma, characteristically associated with
hyperplastic sinusitis/nasal polyposis and hypersensitivity
to aspirin and non-steroidal anti-inflammatory
medications (ibuprofen), rarely has its onset in childhood.
• The most common persistent form of childhood asthma is
that associated with allergy.
Etiology and pathogenesis of
asthma.
 What is the Pathophysiology?
• Trigger Factor
• Mast cell
– Mediators : histamine,prostaglandin,leukotrienes,as well
as cytokines.
• Inflammatory cells
• Sustained Inflammatory response
– Contraction of airway smooth muscles
(Bronchoconstriction)
 Pathophysiology (Cont.)
– Airway wall swelling (mucosal edema)
– Airway hyper responsiveness
• Chronic changes
– Hypertrophy of the smooth muscles, thickening of the
basement membrane
– Airway remodeling
 Pathophysiology:
•  Interactions between environmental and genetic
factorsairway inflammationlimits airflow
functional and structural changes(bronchospasm,
mucosal edema, and mucus plugs)
• Airway obstruction causes increased resistance to
airflow and decreased expiratory flow rates.
• decreased ability to expel air and may result in
hyperinflation.
• The resulting overdistention helps maintain airway
patency, thereby improving expiratory flow; however,
it also alters pulmonary mechanics and increases the
work of breathing.
 What are the Triggering Factors?
• Domestic dust mites
• Air pollution
• Tobacco smoke
• Occupational irritants
• Cockroach
• Animal with fur
• Pollen
 Triggering Factors ( cont.)
• Respiratory (viral)
infections
• Chemical irritants
• Strong emotional
expressions
• Drugs ( aspirin, beta
blockers)
 What causes the chronic
inflamation
• 1) Susuptible individual 
environmental/infectious triggers  Helper T
lymphocytes and other immune cells that
produce pro-allergic, proinflammatory cytokines
(IL-4, IL-5, IL-13) and chemokines (eotaxin).
• 2) breach in normal immune regulatory
processes (regulatory T lymphocytes that
produce IL-10 and transforming growth factor
[TGF]–β) that dampen effector immunity and
inflammation when they are no longer needed.
How airway narrowing develops
Asthma is a condition of the airways where
there is difficulty in breathing due to

Inflammation Swelling Excess mucus

• Or a combination of all three

Asthma
 Clinical features
• Intermittent dry cough
• Shortness of breath
• Recurrent wheezing
• Chest pain
• Associated triggering factors
 Clinical features
• Expiratory wheezing and a prolonged
expiratory phase
• Crackles (or rales) and rhonchi result from
excess mucus production and inflammatory
exudate in the airways.
• Segmental crackles and poor breath sounds
can indicate lung segmental atelectasis
 Diagnosing Asthma in Young Children –
Asthma Predictive Index
• > 4 episodes/yr of • Major criteria
wheezing lasting >1 – Parent with asthma
– Physician diagnosed
day affecting sleep in atopic dermatitis
a child with one – Airway allergens
MAJOR or two • Minor criteria
MINOR criteria – Physician diagnosed
allergic rhinitis
• High specificity 97%
– Eosinophilia (>4%)
and positive predictive
– Wheezing apart from
value 77% for colds
persistent asthma into – Food allergy
later childhood.
 Differential Diagnosis Wheezing
• Asthma
• Congenital Anomalies with airway impingement: Vascular
rings, tracheobronchial obstruction, mediastinal mass
• Bronchopulmonary dysplasia
• Cystic fibrosis
• Gastroesophageal reflux
• Foreign Body Aspiration
• Heart Failure
• Sinusitis and allergic rhinitis
• Bronchiolitis
• Pertussis
• Tuberculosis
• Immune system Disorders
 Diagnosis
• Lung function test(spirometry)
– FEV1 -Forced Expiratory volume in 1 second
– FEV1/FVC-(FVC-forced vital capacity)
– Applicable for those aged greater than 6 months
– It is an objective measure of airflow limitation.
– Forced expiratory airflow measures are
• helpful in diagnosing and monitoring asthma and in
assessing efficacy of therapy.
• helpful in children with asthma who are poor perceivers of
airflow obstruction or when physical signs of asthma do not
occur until airflow obstruction is severe.
 Spirometry
- Airflow obstruction is defined as FEV1
reduced to less than 80 %predicted and
an FEV1/FVC ratio of less than 0.8 (80 %)

- FEV1/FVC appears to be a more sensitive

measure of impairment than FEV1,
whereas FEV1 may be a more useful
measure of risk for future exacerbations
• PEF-peak expiratory flow rate< 80% of
personal best.
• CXR-hyperinflation , important to rule out
asthma masquarders.
• Allergy prick skin testing
Peak expiratory flow rate
 Management of Asthma

Goals;
• Control chronic and nocturnal symptoms
• Maintain normal activity levels and exercise
• Maintain near-normal pulmonary function
• Prevent acute episodes of asthma
• Minimize emergency department (ED)
visits and hospitalizations
• Avoid adverse effects of asthma medications
 SYMPTOM CLASSIFICATION
• Severe Persistent Step 4FEV1/FVC <60%
– Day: continual PEF Variability >30%
– Night: frequent
• Moderate Persistent Step 3FEV1/FVC 60-80%
– Day: daily PEF Variability >30%
– Night: >1/week
• Mild Persistent Step 2FEV1/ FVC>80%
– Day: >2/week (<1/day) [3-6/week] PEF Variability 20-30%
– Night: >2/month
• Mild Intermittent Step 1FEV1/ FVC >80%
– Day: <2/week PEF Variability <20%
– Night: <2/month
 DAILY MEDICATIONS
Preferred Treatment:
• Step 4
– High-dose inhaled corticosteroids, AND
– Long-acting beta2-agonists
• Step 3
– Low-to-medium dose inhaled corticosteroids, AND
– Long-acting beta2-agonists
• Step 2
– Low-dose inhaled corticosteroids
• Step 1
– No daily medication needed
Children Less than 5 yrs
Children age 5-12 yrs
 STEPPING
• STEP DOWN: Review treatment every 1 to 6 months; a
gradual stepwise reduction in treatment may be possible.
- decreasing ICS (inhaled corticosteroid) dose by about
25% every 2 to 3 mo, as long as good asthma control is
maintained
-Change tid to bid
• STEP UP: If control is not maintained, consider step up.
First, review patient medication technique, adherence and
environmental control.
 Standard Therapy

Standard asthma treatment should include short-acting beta

2-agonists, systemic glucocorticoids, and supplemental
oxygen
1.Short-acting beta 2-agonists
- inhaled short-acting beta 2-agonists (SABA, eg albuterol,
salbutamol
-can be administered continuously or intermittently (via
nebulizer or metered dose-inhaler [MDI] with spacer)
2.Glucocorticoids
Systemic —  to decrease airway inflammation and secretions
may be given as prednisone, prednisolone, or
methylprednisolone. Dose-1 mg/kg every 12 hours for a total
of five days
Route — Oral is preferred to IV administration since it is less
invasive and equally efficacious.
Taper in patients a course longer than 10 days and may be
tapered by decreasing the dose by 50 % every two to three
days
• Inhaled — are not as effective as systemic glucocorticoids for
severe asthma exacerbations and should not be used as a
substitute for systemic glucocorticoids.
3.Supplemental oxygen 
It should be provided by nasal cannula or face mask as needed
to maintain an oxygen saturation of ≥ 92 %.
All nebulized medications should be delivered with oxygen,
generally at a flow rate of 6 to 8 L/min.
Status asthmaticus
• It is severe exacerbation of asthma that does
not improve with standard therapy..
 Acute asthma…
 Intial assessment
(hx, P/E, Ix O2 saturation…)
 O2 to achieve saturation >90%
 Inhaled SABA by nebulizer or MDI with valved
holding champer up to 3 doses 1st hour
 Oral systemic corticosteroides
 Reassessment

If there is good response

 FEv1 or PEV>70%
 No sign of distress
 P/E normal DISCHARGE
If mild improvement
• inhaled SABA(short actinf beta agonists) every 60 minutes
• oral systemic corticosteroides
• Continue treatment 1-3 hrs if there is improvement and decide within <4 hours

•
Sever exaserbation
– FEV1 or PEF<40%
– P/E sever sx at rest ,accessory muscle use, chest retraction
– Mentation drowseness,confusion
– No improvement after the initial treatment
consider adjuvant therapy
POOR RESPONSE
 admit to ICU
 o2
 inhaled SABA hourly
 IV steroid
 consider adjuvant therapy
 possible intubation and mechanical ventilation
 Risk of asthma morbidity and
mortality
Psychosocial
BIOLOGIC
 Poverty   and Crowding   
 Previous severe asthma exacerbation
 Mother <20 yr old  , less than high school
  
education   
 Severe air obstruction  
 Inadequate medical care     Inaccessible   
   Hx of repeated attacks 
and Unaffordable   
 Severe airways AHR   No regular medical care (only emergent)
 Increasing and large diurnal variation   
in peak flows      No care sought for chronic asthma
 Decreased chemosensitivity and symptoms   
perception of dyspnea      Delay in care and  Inadequate hospital
 Poor response to systemic care
corticosteroid therapy     Psychopathology in the parent or child   
 Male gender    Family problems  
 Low birthweight
 Prognosis
Recurrent coughing and wheezing occurs in 35% of pre–school-age children.
⅓ - persistent asthma into later childhood,
⅔ -improve on their own
Asthma severity by the ages of 7–10 yr of age is predictive of asthma
persistence in adulthood.
Children with moderate to severe asthma and with lower lung function
measures are likely to have persistent asthma as adults.
Children with milder asthma and normal lung function are likely to improve
over time, with some becoming periodic (disease-free mo to yr);
however, complete remission for 5 yr in childhood is uncommon
 References
• Nelson text book of Pediatrics 18th ed
• Up tudate 18.2
• emedicine