CHILDHOOD ASTHMA

Worldwide
In children = the most common
chronic disease
Account for large proportion of
health-care spending, and lost
time for school (and work)
All medical practisioner should
be aware
CHILDHOOD ASTHMA
Over the last decade, research in
verious aspect of the biology of
asthma are rapidly developing

Certain differences of opnion
may exist between authors
CHILDHOOD ASTHMA
DEFINITION
MECHANISMS OF DISEASE
CLINICAL PRESENTATION
PROGNOSIS
TREATMENT
DEFINITION I
There is no universally accepted definition

CIBA GUEST SYMPOSIUM, 1959
the condition of subjects with widespread
narrowing of the bronchial airways which
changes its severity over short periods of
time either spontaneously or under
treatment..
DEFINITION II
AMERICAN THORACIC SOCIETY (ATS), 1962 :
A disease characterized by an increase
responsiveness of the trachea and brochi
to various stimuli and manifested by
widespread narrowing of.(see CIBA)

ATS, 1975:
A diseaseand manifested by slowing of
forced expiration which changes in
severity either
DEFINITION III
WHO, 1975:
A chronic condition characterized by
recurrent bronchospasm resulting from
a tendency to develop reversible
narrowing of the airway-lumina in
response to stimuli of a level or
intensity not inducing such narrowing in
most individuals
DEFINITION IV
ATS, 1987:
A clinical syndrome characterized by
increased responsiveness of
tracheobronchial tree to a variety of
stimulisymtoms ofparoxysms of
dyspnea, wheezing, and cough, which
may varyhistologicallyevidence of
mucosal edema of the bronchi;
infiltration of the bronchial mucosa or
submucosa with inflammatory cells,
especially eosinophils; and shedding of
epithelium and obstruction of peripheral
airways with mucus
DEFINITION V
NATIONAL ASTHMA EDUCATION, 1991
A lung disease with following
characteristics :
1. Airway obstruction that is reversible
either spontaneously or with treatment
2. Airway inflammation
3. Increased airway responsiveness to a
variety of stimuli
DEFINITION VI
KONSENSUS UKK-PULMONOLOGI,
IDAI, 2000:

batuk dan/atau mengi yang
episodik yang telah terbukti bukan
disebabkan oleh penyakit lain
MECHANISM OF DISEASE
The exact mechanisms is still unclear

for decades, asthma had been regarded
as a classical type I hypersensitivity
reaction (IgE triggered release of mast
cell mediators intermittent
bronchoconstriction)

MECHANISM OF DISEASE
It is now acknowledged that this
mechanisms play a very important role but
they do not explain recently described
biological & clinical features of the disease
MECHANISM OF DISEASE
The factors responsible chronic changes
are not well understood. It is likely that
different pathogenetic mechanisms may
be present in different patients. It is now
widely believed that asthma is a
heterogeneous disease, with different
phenotypes and clinical expressions that
depend on age, gender, genetic,
background, and environmental
exposures.

MECHANISM OF DISEASE
There are 2 main pathogenetic
mechanisms responsible for recurrent
wheezing during childhood :

1. Altered reactivity to viral infections
2. Allergic airway inflammation
VIRUS
Wheeze
Host suspect
Sosec
factors
Smoking
Gen Atopy
Immune
response
Age
Viral Resp.Infection and wheezing mechanisms of association
Air way epithelial
injury
Inflammation BHR
Bronchoconstriction
Air way narrowing
Mediator
cytokines
Wheezing associated with allergic airway inflammation
ALLERGEN
Mast cell
act. (IgE)
Release of
chemotactil
mediators:
NCF,ECFA.
PAF, LTB4
Release
lysosomal
hydrolase
proteoglycans
Release of
vasoactive
mediators:
Hist., leukotines,
PAF, adenosine,
PGD2
Vasoperbeability
smooth muscle
contraction
Tissue damage
repair
Celular infiltrate
PAF, LTC
4

Low mol
weight
Activating factors
Eos
Neutr
Mono
T cells
Bas
Macro
Early Asthmatic reaction
Late Asthmatic reaction
PATHOPHYSIOLOGY
Chemical mediators
Bronchoconstriction, mucosal edema, exes.secret
Airway obstruction
Nonuniform
ventilation
Atelectasis Hyperinflation
Mismatching V/P
Decreased
compliance
Increased work
of breathing
Alveolar
Hypoventilation
PaCO
2

PaO
2

Acidosis
Decreased
surfactant
Pulmonary
vasoconstriction
DIAGNOSIS
Mostly can be diagnosed based on data
from anamnesis & physical diagnosis

Asthma may have ascribed erroneously to
allergic cough, allergic bronchitis,
wheezy bronchitis, or chronic bronchitis
DIAGNOSIS
For special cases (asthma varians; asthma
with nocturnal-cough), the diagnosis of
asthma can be establish with:
PEFR/FEV
1
before & after bronchodilator
Daily-card
Bronchial-provocation-test
Exercise-testing
ASTHMA
Cough
(night)
Cough
wheezing
Wheezing
dypsneu
Wheezing
dypsneu cyanotic
Triggers:, infection, alergen, Exercise, Weather
BRONCHIAL HYPERACTIVITY
Genetic + Inducer (Infection, Pollution Allergen) ??
FEV
1
< < < N <
Bronchospasme Bronchospasme
+inflammation EAR
LAR
CLINICAL MANIFESTATIONS
Asthma exacerbation
triggers
symptomless
Signs & symptoms of exacerbation:
Cough
Weezing
Tachypnea
Dyspnea with prolonged expiration and used
of accessory muscles
Signs & symptoms of exacerbation:

Cyanosis
Hyperinflation
Pulsus paradoxus
Abdominal pain due to sternuous
use of diaphragm & abdominal
muscles
Somnolent
Barrel chest, harrison sulci
Clubbing of the finger
4 CLINICAL VARIATION OF ASTHMA
Y
X
Z
I Wheezing +
APE
PEFR (APE) Normal
III
IV
II
0 2 5 10 15 years
?
?
PROGNOSIS
Severe persistent asthma (5%)
Moderate persistent astma (20%)
Mild asthma (75%)
MANAGEMENT OF CHILDHOOD ASTHMA
BASED ON : ASTHMA = INFLAMATION
I. Controlling acute exacerbation
II. Preventing acute exacerbation
III. Patient and family education

the GOAL:
optimal growth and development
asthmatic child activity = non asthmatic child
TREATMENT
Basic concepts of avoiding allergens,
improving bronchodilation, and reducing
mediator-induced-inflamation

Pharmacologic therapy is mainstay of
treatment of asthma

Consist of relievers (I)
controllers (II)
I
Relievers
Exacerbation

II
Controllers
A. Symphatheticomimethics
1. - Agonist
2.
1-2
Agonist
3.
2
Agonist
B. Xantines
C. Anticholinergic
MANAGEMENT OF ACUTE EXACERBATION
TO RELIEVE THE CHILD FROM SUFFERING,
caused by:

BRONCHOCONSTRICTION
COMPLICATION
MANAGEMENT OF ACUTE EXACERBATION
Acute exacerbation
Cough
Wheezing
Mild dyspneu
Moderate dyspneu
Severe dyspneu
Moderate-severe dyspneu
+ complication :
- Hypoxemia/cyanosis
- Acidosis
- Respiratory failure
- SIADH
Bronchospasme
Bronchospasme
Inflammation :
oedema
cell infiltration
Hypersecretion
Bronchodilator
. Simpatetikomimetik
. Adrenalin s.c
. B-2-agonist s.c.,
inhalers (salbutamol
terbutalin)
. Xanthin : Aminofilina I.v.
. Anticolinergik : IC, Inhal
Narrowing bronchial lumina
DYSPNEU, WHEEZING, PROLONGED EXPIRATION
Bronchodilator
+ Anti-inflammation
. Steroid systemic
Prednisone
Prednisolone
Dexamethasone
Bronchodilator
antiinflammation
steroid-sytemic
O
2

NaHCO
3
Fuild 1:4
Ventilator
Broncho-
dilator
Avoid
from patient
Triggers
Early asthmatic reaction
= brochospasme
Late asthmatic rx
=brochospasme
+ inflammation
(oedem, infilt.cell,
mukous)
COMPLICATION
Hypoxemia
Acidosis
dehydration
Resp. failure
Cor-pulm.
Atelectasis
Bronchiektasis
CONTROLLING ACUTE EXACERBATION
MILD, MODERATE, SEVERE EXACERBATION
O
2
,

Adrenalin sc/
2
agonist
GOOD
Wheezing-
Dyspneu-
Conscious
Disccharge
- Bronchodilator for 5-7 days
PARTIAL
Wheezing <
Dyspneu <
Mental status: N
O
2

2
agonist nebul
every 20
Steroid, po
GOOD
Discharge
-Bronchodilator
+ steroid , po
for 5-7 days
POOR
admitted
POOR

MILD, MODERATE, SEVERE EXACERBATION
O
2
,

Adrenalin sc/
2
agonist
POOR
Wheezing
Dyspneu
Mental status:
O
2
Salbutamol nebulizer every 20
Steroid
IVFD 1:4, 5/4 M
Bicarbonat Natricus 1-2 mEq/kbBW
GOOD
Discharge
admitted
SQA
Continue salbutamol
WORSE
Ventilator
Target:
1. Chronic symptoms <<
2. Freq. acute exacerbation <<
3. Hospitalized (-)
4.
2
- agonist <<
5. Sleep and activity disorder (-)
6. Drug side effect (-)
7. APE : normal
8. Daily APE variant < 20 %
=====> Indication :
Acute exacerbation >1 x /week
Night cough > 2 x /month




Preventing acute exacerbation
Thank you