Asma in Children Dr SAK Indriyani SpA MKes 16062009

7/22/2019 Asma in Children Dr SAK Indriyani SpA MKes 16062009

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dr. SAK Indriyani, SpA, MKes

Department of Child Health RSU Mataram



2

Prevalence increased Asthma: attack or not attack

Bronchoconstriction changed into chronicinflammation remodelling

Advance in management



3

F Definition of asthma has varied depending onthe purposes

F National consensus: suspected asthma if: cough

and/or wheeze that episodic, nocturnal,reversible, activity, atopy (+)

F Asthma attacks: Episodes of rapidlyprogressive increase in symptomps.



4

PATHOGENESIS

1. Immunologic mechanism of respiratory tract

Antigen

Naïve T lymphocyteTh-0

Dendritic cell IL-12 (-)

IL-12 (+) (-)

Th-2 response

IL-4, IL-13 IL-9 IL-3, IL5

Th-1 response IL-4 IL- GM-CSF

(IFN-, IL-2. Lympho…….)

IgE Mast cell Basophils Eosinophils

Cell mediated immunity and

Neutrophile inflammation Mediators of inflamations (eg. Histamine,

prostaglandine, leukotrines etc)

Asthma symptoms Bronchial hyperresponsiveness

Airway obstruction

Figure 1. Asthma pathogenesis (PNAA 2004)



2. Chronic & acute inflammation

Allergen immediate allergy reaction, some of this

followed by delayed reaction

Immediate phase reaction

# Ig E specific (mast cell, macrophage, basophils)

preform mediator & newly form mediator

bronchoconstriction, sensoric nerve stimulation,

mucous hypersecretion, vasodilatation, vascular

breakage



Delayed phase reaction

# Inflammation mechanism in asthma

# Respiratory tract cell aktivation

cytokines release to circulation

Proinflammatory leucocyte stimulation

(eosinofil & others precursor from bone marrow)

3. Remodelling process



ENVIRONMENT

Allergens, pollutants, infections, etc

Epithelium

Dendritic cell

(Myo) T cell

Fibroblast

Matrix Cytokines

Blood vessels Nerve Smooth muscleMacropha

IgE Mast cell Eosinophile

Basophile

REMODELING

INFLAMATIONMediators

ASTHMA

Figure 2. Inflammation & remodelling in asthma (PNAA 2004)

i ll di d l i



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Genetically Predisposed Population

Inducer (I)

Indoors allergens ? Avoidance

Alternaria, etc

Immune responseTh2, IgE, IgG4, IgG1

Enhancer (E)

Rhinovirus Avoidance

Ozone Anti-inflamatories

-2 agonist ImmunotherapyInflammation

Th2, Mast cell,

Eosinophils

BHR

Triggers

Exercise/Cold air -2 agonist

Histamin/Methacoline

Wheezing

Figure 3. Factors related with asthma (PNAA 2004)



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Upper respiratory tract :

Nose

Sinus

Throat

Lower respiratory tract :

Bronchus

Bronchiolus

AlveolusUpper & lower respiratory tract is connected

50-80% child with asthma + rhinitis

20% child with rhinitis + asthma



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Trigger

(dust, animal feather, kapok, etc)

Bronchus Bronchus

Still wide(not susceptible, not sensitive,

stable)



1

trigger

(dust, animal feather, kapok, etc)

Bronchus

No attack attack

• Respiratory tract muscle constrictio

• Edema mucous

• Hypersecretion & sticky

Bronchus

Hyperactive:

• too susceptible

• too sensitive

• not stable/easy to constric



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Inhalant Chemical

Stress

Activity (exercise)

Drugs

Foods



13

Triggers



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Asthma

Triggers

Acute attacks

• Inhalant

• House dust mite

•

Smoke• Food

Failed of

long term

management



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Triggers

Airway obstruction

ununiform pulmonary

ventilation hyperinflation

atelectasis mismatchcompliance

ventilation-perfution abnormality

surfactant alv.hypoventilation Resp.rate

acidosis

pulmonary

v.constriction

b.constriction, oedema, secretion

PaCO2

PaO2



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Class. Asthma disease Clinical parameter,

medication need,

lung function test

Infrequent episodic

asthmaPersistent asthma

Frequent episodic

asthma

Attack frequency < 1x /month often> 1x /month

Attack duration < 1 week Almost all year

No remission1 week

Between attack No symptom Symptom at noon & niFrequent symptom

Sleep & activity Normal Very disturbingFrequent disturbPhysical exam. If not

in attack conditionNormal Always abnormaMaybe abnormal

Controller No need Need steroidNeed steroid

Lung function test

(not attack)PEF/FEV1 >80%

PEF/FEV1 <60%

Variability 20-30%PEF/FEV1 60-80%

Variability in

lung function (attack)>15% < 50%< 30%



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Class. diseases Severity of attack

Infrequent episodic asthma

Frequent episodic asthma

Persistent asthma

Mild

Moderate

Severe

Respiratory arrest

imminent



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The classification should be include class. diseaseand severity of asthma attacks, example: Infrequent episodic asthma without asthma attacks

Infrequent episodic asthma with mild asthma attacks Frequent episodic asthma with severe asthma attacks

Frequent episodic asthma without asthma attacks

Persistent asthma with severe asthma attacks



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Mild Moderate Severe Respiratory

arrest immin

Breathless Walking

Can lie down

Talking

Infant-softer

Shorter cry

Difficult feedingPrefers sitting

At rest

Infant stops

feeding

Hunchedforward

Talks in Sentences Phrases Words

Allertness Maybe agitated Usually agitated Usually agitated Drowsy or confus

Respiratory rate Increased Increased Often >30x/min



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Normal rates of breathing in awake children:

Age Normal rates

<2 months <60/min

2-12 months <50/min

1-5 years <40/min6-8 years <30/min

Accessory

muscles and

suprasternal

retractions

Usually not Usually Usually Paradoxial

thoraco-

abdominal

movement

Wheeze Moderate, oftenonly end

expiratory

Loud Usually loud Absence ofwheeze

Pulse/min <100 100-200 >120 Bradycardia

Infants 2-12 months <160/min

Preschool age 1-2 years <120/min

School age 2-8 years <110/min

Pulsus

paradoxus

Absent

<10 mmHg

Maybe present

10-25 mmHg

Often present

20-40 mmHg

Absence

suggests



2

Pulsus

paradoxus

Absent

<10 mmHg

Maybe present

10-25 mmHg

Often present

20-40 mmHg

Absen

sugge

PEF after initial

bronchodilator

%predicted or

% personal

best

Over 80% Approx. 60-80% <60% predicted or

personal best or

response lasts <2

hrs

PaO2 (on air)

and/or

PaCO2

Normal

Test not usuallynecessary

<45 mmHg

>60 mmHg

<45 mmHg

<60 mmHg

possible cyanosis

>45 mmHg

SaO2% >95% 91-95% <90%



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Cost ?

Avai labi l ity ?



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Minimal (ideally no) chronic symptomps Minimal (infrequent) exacerbations

No emergency visits

Minimal (ideally no) use of as needed ß2 -agonist

No limitations on activities (exercise)

(Near) Normal lung function

Minimal (or no) adverse effects from medicine



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Rapid resolution of acute symptoms To reduce hypoxemia

Normal lung function as soon as possible

Reevaluation to prevent asthma attacks



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At home

At emergency room



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Known of asthma symptoms Nebulized ß2 agonist

If not available: MDI with or without spacer ororally



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At home

At emergency room



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Asthma attacks algorithms

Emergency roomAssess severity.of attacks

Early treatment• nebulized -agonist 3x, interval 20 min

• 3rd nebulized + anticholinergic

Moderate attacks(nebulized 2-3x,partial response)

• O2

• reassessment mode-

rate ODC • IV line

Mild attacks(nebulized 1x,

good response)

• observe 1-2 jam,

discharge

• symptoms (+)

moderate attack

Severe attacks(nebulized 3x,

poor response)

• O2

• IV line

• reassessment seve

admission

• Chest X-ray



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One Day Care (ODC)• Oxygen therapy

•

Oral steroid• Nebulized / 2 hour

• Observe 8-12 hours,

if stable discharge• Poor response in 12 hrs,

admission

Admission room• Oxygen therapy

• Treat dehydration andacidosis

• Steroid IV / 6-8 hours

• Nebulized / 1-2 hours

• Initial aminophylline IV,

then maintenance

• Nebulized 4-6x

good response per 4-6

• If stable in 24 hours

discharge

• Poor response ICU

Discharge

•

give -agonist(inhaled/oral)

• routine drugs

• viral infection:

oral steroid

• Outpatient clinic in

24-48 hours

Notes:

• In severe attack, directly use -agonist + anticholinergic

• If nebulizers not available, use adrenalin SC 0.01 ml/kg/times

with maximal dose 0.3 ml/times•Oxygen therapy 2-4 l/min should be early treatment in moderate

and severe attack



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Initial assessment of severity asthma attacks

Nebulized ß2-agonist, interval 20 minute

3rd nebulization: anticholinergic agent

Severe attacks: directly with anticholinergic agent If nebulizer not available:

MDI with Spacer

Adrenalin SC



3

Good response post nebulization

Observe: 1-2 hours

Discharge if good response

Treat as moderate attacks if symptoms still remai Use routine drugs

Out patient clinics

M f h k



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Management of asthma attacks

Mild

Nebulization

Observe 1-2 hours

DISCHARGE

Moderate

Routine drugs

Outpatient clinic



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Partial response post nebulization ODC admission

Oxygen therapy

Oral steroid

IV line

Repeated nebulization

Good response: discharge

Poor response: admission

MANAGEMENT OF ASTHMA ATTACK



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MILD

Nebulization

Observe: 1-2 hours

DISCHARGE

MODERATE

Oxygen

Nebulization

IVFD

Oral steroid

ODC SEVERE

???



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Dehydration Metabolic acidosis

Atelectasis



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Poor response postnebulization Oxygen therapy IV line: rehydration and treat acidosis

Corticosteroids (IV) Initial Aminophylline (IV), then maintenance Repeated nebulization Chest X-ray

Good response : Discharge Poor response : Intensive care

MANAGEMENT OF ASTHMA ATTACKS



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MANAGEMENT OF ASTHMA ATTACKS

MILD

Nebulization

Observe 1-2 hours

DISCHARGE

MODERATE

Oxygen

Nebulization

IVFD

Oral steroid

ODC SEVERE

•O2, steroid

• Nebulizatio

• Hydration•Aminophyll

• Rö

•ICU ?



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Adrenalin: maximal dose, and effects

Salbutamol SC: be careful

MgSO4: not significant

Inhaled steroid : high dose (1600 mg)

Asthma attacks



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Stable asthma

(No attack)

Infrequent

episodic

Frequent

episodicPersistent

Reliever (+)

Controller (-)

Reliever (+)

Controller (+)

Reliever (+)

Controller (+)

Assess the

severity of attacks

Assess class

of disease

AVOIDANCE



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-agonis short acting) Steroid anti inflammation

Terbutalin Budesonid

Salbutamol Fluticason

Orsiprenalin Beclometason

Heksoprenalin Non steroid anti inflammation

Fenoterol Chromoglikat

Xantin Nedokromil

Teofilin -agonis long acting)

Procaterol

Bambuterol

SalmeterolKlenbuterol

Longterm management



4

Low dose steroid

Flix 2 x 50 mcg or Bud/BDP 2 x 100 mcg

Normal dose steroid

Flix 2 x 100 mcg or Bud/BDP 2 x 200 mcg

Increase steroid

(high dose)

Normal Steroid + LABA (long

acting agonist)

Steroid + ALR

(Antileucotriene

Oral Steroid

A thm m n m nt



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Allergen

avoidance

ImmunotherapyPharmacotherapy

EDUCATION

Asthma management

COSTS

GINA, 2002



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Trigger avoidance: dust house mite Stay away from pet

Before & during pharmacotherapy

GINA, 2002



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Pharmacotherapy

Reliever :• 2 agonis : inhaler, nebulized, oral

• Epinefrin : subcutan

• Teofilin/aminofilin : oral, I.V.

• Anticholinergic(ipratropium br) : inhaler

• Steroid : oral, I.M.

Controller :

• Steroid : inhaler

• LABA : inhaler, oral

• Antileukotrien : oral

PNAA, 2002



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About asthma Compliance

Practical guideline in home

Patient-family-doctor relationship

GINA,2002



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Known as desensitization Still controversial

Multifactorial trigger



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Asthma prevalence in childhood: Classification of asthma: infrequent episodic

asthma, frequent episodic asthma, persistentasthma

Acute asthma attacks: mild, moderate, severeattack

Asthma management in childhood: controversial In Indonesia: National Consensus for asthma

management in childhood



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Asma in Children Dr SAK Indriyani SpA MKes 16062009

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