Bronchial Asthma

Dr.Nabila Sherlala
Peadiatric Consultent

Objective:
By the end of this session you will know the background
of the Br.asthma.

Content:
Definition
Epidemiology
Pathophysiology
C/p
Diagnosis,D/D
Managment.
Prognosis.

Definition:
Bronchial asthma is a chronic, reversible inflammatory
disorder of the airways associated with airway hyper
responsiveness that leads to recurrent episodes of
wheezing, breathlessness, cough.

Epidemiology
Asthma is a common condition.
Incidence; 5.8-6%.
It is the commonest chronic medical condition in

children.
The cost of asthma about a billion pounds per year.

 Age: approximatly 80% <6years.

Sex: male>female with reversal in early adultdhood.
Incidence and morbidity is increased recently in all

age,especialy in children <6years.

Common in industralized countries such as
canada,uk,newzeland,USA,europe.

Increase in incidence because of urbnization,air

polusion,passive smoking,hygene theory,improved the way of

the diagnosis.
Mortality is decreased for the last decades,because of

improved diagnosis,good long term ttt.

Pathophysiology:
The pathophysiology:
Airway inflammation
Intermittent airflow obstruction
Bronchial hyper responsiveness

The mechanism of inflammation in

asthma
May be acute, sub acute, or chronic.
The presence of airway edema and mucus
secretion also contributes to airflow obstruction
and bronchial reactivity.
Varying degres of
mononuclear cell and eosinophil infiltration
mucus hypersecretion,
desquamation of the epithelium.
smooth muscle hyperplasia
airway remodeling .

 T lymphocytes play an important role in the regulation

of
airway inflammation through the release of numerous
cytokines.
Fibroblasts,neutrophils, endothelial cells, and epithelial
cells,
contribute to the chronicity of the disease.

Airway hyper responsiveness or

bronchial hyper reactivity in asthma:
This is an exaggerated response to numerous
exogenous and endogenous stimuli.
The mechanisms involved include;
direct stimulation of airway smooth muscle
and indirect stimulation by pharmacologically
active
substances from mediator-secreting cells such as
mast
cells.
The degree of airway hyper responsiveness
generally
correlates with the clinical severity of asthma.

Airflow obstruction:
Can be caused by a variety of changes, including
Acute bronchoconstriction,
Airway edema,
Chronic mucus plug formation,
Airway remodeling.

Atopy:
The genetic predisposition for development of an IgE
mediated response to common aeroallergens is the
strongest identifiable predisposing factor for developing
asthma.

Cause:
Asthma is multifactorial disease caused by
environmental and genetic factors.
This view also suggests that removing or reducing
airborne pollutants should be successful at reducing the
problem.

.
Environmen
Biologic
t
and
allergen.
genetic
infection.
Age
risk
microbes.
Immune.
pollutant
lung
stress
repair
Innate and adaptive
Immune
development
( Atopy)
Respiratory infection.
Lower
Aeroallergens.
airway
ETS.
injury
pollutants / toxicants.
Persistent inflammation.
Aberran
AHR.
t repair
Remodeling.
Air ways growth and
differentiation .
Asthma

Environmental:
Environmental tobaco exposure(mother)
Aeroallergen(pollens)
Molds
Pets(cats,dogs,rabbit,horse...)
Air pollusion,strong odor or fume.
Dust mites.
Viral infection(Rhinovirus,RSV,Adenovirus,Influnza)
Psychological factors.
Cold air,dry air
Exercise

Clinical manifestations:
1.Intermitent dry cough
2-Expiratory wheezing
3-Shortness of breath,chest tightness.
4-Exersice intolerance(exersice induced asthma).

Diagnosis:
1-History:
Improvement of all these symptoms with asthma

ttt.
provocation of these symptoms by previous factors.
H/O other allergic condition(A/R,A/C,A/D,food allergy)
parentral asthma.

2-Examination:
1-during attack: signs of R/D.
Wheezing,ronchi.
air entry bilaterally.
Prolonged expiratory phase.
Crackles,rales.
2-Between attacks: Almost normal.
Signs of chronic illness(short
stature,chest
deformity,cautary marks).

3-Investigation:
1-PFT:
It helps to diagnose,monitoring,assessing the efficacy of
therapy.
Spirometry
Peak expiratory flow meter.
2-Radiology.
3-blood- IgE,eosinophilia.
4-Skin test.

 D/D:
Acute bronchiolitis
GERD
Bronchioctasis(CF,immune deficiency,PCD)
BPD
Bronchiolitis oblitrance
Pneumonia
Vocal cord paralysis
TEF
Vascular ring

Treatment:
1-Treatment of acute attack
2-Long term treatment.
1-Treatment of acute attack(quick reliever or rescue):

1-Short acting B2-agonist:

rapid onset of action
4-6 hr duration.

Ex: Salbutamol(ventoline)
Albuterol
Terbutaline.
.

Given by: Nebulizer

Inhaler
I.V infusion(icu)
Syr.tab--- no more recommended.
The nebulizer with O2 can be repeated 3/hr.(every 20 mint).
Can be give contious,1h,2h,4h,6h...

Side effect:

Tachycardia
Tremor
Vomiting
Hypokalemia

2- Anticholinergic agent: Bronchodilator

(Ipratropium bromide) (Atrovent)
Better to use in combination with B2 agonist.
Nebulizer
Inhaler(MDI).

3- O2-therapy:
Mask
Nasal pronge
Nebulizer with B2-agonist or anticholenergic.
4- Systemic GC therapy:
Mod-sever excerbation
Hasten recovery
Prevent recurence of symptoms.
Types Methylprednisolon(1-2mg/kg/day)
oral prednisolon(1-2mg/kg/day)
In single or twice for 310 days.

5- I.V theophylline:
Used only in sever life threatning asthma exacerbation.
Acute attack failed to responce to intensive previous therapy.
Close observation with ECG monitoring,drug level.

6- I.V mg sulfate(smooth muscle relaxent)

Close observation of BP to avoid hypotension.
7 M.V

Principles of optimal asthma management

1-Regular assessment & monitoring.
2-Control of factors contributes to asthma severity .
3-Asthma pharmacotherapy
4-Patient education.

Step up & step down approach

Step down therapy :
Initiating higher level controller therapy & once good asthma
control achieved reduce gradually the dose of the medications

Long term control or controller medications

1. Inhaled Glucocorticoids:
This is the Gold standered treatment of BA.
Can be MDI,DPI ( Turbuhalar, Diskus )
Advantage:
Reduce asthma symptoms.
Improve base line pulmonary function.
Decrease bronchial hyper responsiveness.
Less need of quick reliever & the need of
prednisone.
Decrease the tachyphlaxis of B-agonist.
Early use of inhaled Glucocorticoids even in mild
persistent asthma to prevent airway remodeling
and subsequent loss of therapeutic response.

2. Long acting inhaled B-agonists:

Salmetarol, Formetarol
Both of these not recommended as monotherapy in
control of asthma nor as quick reliever uses mainly
in combination with inhaled GC if optimal response
is not achieved or use in nocturnal asthma or in
exercise induced asthma.
Salmetrol used in children>4 years (servent.
Beglan,inaspir)
Formetarol used in children >6 years( oxis
turbohaler, 4.5ug, 9ug)

3. Leukotrines modifying agents:

A.
B.

Leukotrines receptors antagonists.

Leukotrines synthesis inhibitors.

4.

Immunotherapy:
It is consist of serial administrations of progressive
increasing doses of the allergen which the patient
is sensitive which finally lead to immunological
change in the way well not develop symptoms
after the contact with the allergen.

5. Omalizumab(Xolair):

If

Anti IgE Ab ( recombinant humanized monoclonal

anti Ig EAb).
S/C administration.
The dose & frequency depend on the wt. ,level of
IgE.
every 2-4 week.
IgE too high not effective.
Used in mod-sever asthma.
When used with inhaled steroid observe that
reduction in of dose of inhaled steroid.


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