ASTHMA IN CHILDREN

DEFINITION

Asthma is a heterogeneous chronic airway disease very common in childhood, usually

characterized by respiratory symptoms including wheeze, breathlessness, chest tightness
and cough, together with variable expiratory airflow obstruction
Asthma is a highly prevalent disease that involves a complex interplay of environmental
factors, airflow obstruction, bronchial hyperresponsiveness, and inflammation. The
dominant feature that leads to clinical symptoms is smooth muscle contraction and
inflammation, which results in narrowing of the airway and obstruction 
EPIDEMIOLOGY

Asthma is very common - it is estimated to occur in 5% to 10% of the population; 30%

of patients are symptomatic by 1 yr of age, whereas 80-90% of asthmatic children have
their first symptoms before 4-5 yr of age.
In childhood, there is a 2:1 male/female preponderance but the sex ratio equalizes by age
30.
RISK FACTORS FOR DEVELOPING ASTHMA:
GENETIC CHARACTERISTICS

Atopy
 The body’s predisposition to develop an antibody called immunoglobulin E (IgE)
in response to exposure to environmental allergens
 Can be measured in the blood
 Includes allergic rhinitis, asthma, hay fever, and eczema
RISK FACTORS FOR DEVELOPING ASTHMA:
ENVIRONMENTAL EXPOSURE
CLEARING THE AIR:
INDOOR AIR EXPOSURES & ASTHMA EXACERBATION
Biological Agents
 Sufficient evidence of causal relationship Chemical Agents
 Cat  Sufficient evidence of causal relationship
 Cockroach  Environmental tobacco smoke (among pre-school
 House dust mite aged children)
 Sufficient evidence of association
 Sufficient evidence of an association
 NO2, NOX (high levels)
 Dog
 Limited or suggestive evidence of association
 Fungus/Molds
 Environmental Tobacco Smoke (among school-aged,
 Rhinovirus older children, and adults)
 Limited or suggestive evidence of  Formaldehyde
association  Fragrances
 Domestic birds
 Chlamydia and Mycoplasma pneumonia
 RSV
PATHOPHYSIOLOGY

 Airflow obstruction may be caused by chronical smooth-muscle spasm, airway-wall

swelling and excessive secretions in the airway lumen.
 The lumen is filled with mucus containing epithelial cells, neutrophils, basophils,
mononuclears, eosinophils and lymphocytes.
 The mucosa has been desquamated and the basement membrane is thickened and
finally the bronchial smooth-muscle is hypertrophied.
PATHOPHYSIOLOGY

 Bronchial smooth-muscle spasm and hypertrophy may arise from several

mechanisms:
 the bronchial smooth-muscle spasm is vagally innervated, and vago-vagal reflexes
may cause construction;
 mucosal irritant receptors may be stimulated by stimuli include: inhaled allergens
(dust mites, pollens), vegetable proteins, viral infection, cigarette smoke, air
pollutants, odors drugs (nonsteroid anti-inflammatory agents, receptor
antagonists), cold air and exercise.
Cycle of chronic inflammation in patients with asthma.

Faoud T. Ishmael J Am Osteopath Assoc 2011;111:S11-S17

PATHOGENESIS OF ALLERGIC ASTHMATIC INFLAMMATION.

 Allergens are endocytosed by antigen presenting cells (APCs) and presented to naive T cells.
Environmental and inflammatory factors activate the respiratory epithelium to release thymic stromal
lymphopoietin (TSLP) and other inflammatory mediators that recruit leukocytes to the lung and skew
the function of dendritic cells toward an allergic response.
 Dendritic cells induce the differentiation of T cells into T-helper 2 (Th2)-specific helper cells, as
well as Th17 cells. The Th2 cells induce immunoglobulin E (IgE) antibody production from B
cells via interleukin 4 (IL-4) and IL-13 stimulation. Immunoglobulin E binds to receptors on the
surfaces of mast cells and basophils and, in the presence of allergen, release mediators that
induce bronchoconstriction and enhance the inflammatory response. Production of IL-5 from Th2
cells increases eosinophil levels.
 Inflammatory mediators released from eosinophils, T cells, macrophages, and neutrophils result in
damage to the airway, bronchoconstriction, stimulation of epithelial cell inflammatory pathways, and
remodeling of the lung.
 Pathogenesis of allergic asthmatic inflammation.

Faoud T. Ishmael J Am Osteopath Assoc 2011;111:S11-S17

 Exposure to antigen typically produces an immediate response in which airways
obstruction develops in minutes and then resolves a second wave of bronchoconstriction,
the so-called late reaction, develops 6 to 10 h later.

- Infections – the most important infectious agents that evoke acute exacerbations
of asthma are: respiratory syncytial virus, parainfluenza virus in young children and
rhinovirus and influenza virus in older children;
- the mechanism by which viruses induce exacerbation of asthma may be related to
the production of T-cell derived cytokines that potentiate the infiltration of inflammatory
cells into already susceptible airways.

- Endocrine factors – asthma may worsen in relation to pregnancy and menses,

especially premenstrually; it improves at some children at puberty.
 - Psychologic factors -
The psychologic factors participate in the induction and/or continuation of any
given acute exacerbation; it is not very well established but probably varies from patient
to patient and in the same patient from episode to episode.

- Exercise – is one of the most common precipitants of acute episodes of asthma.

Exercise provokes bronchospasm to some extent in every asthmatic patient and in some is
the only trigger that produces symptoms; activities such as ice hockey, cross-country
skiing, ice skating produce a more severe attack of asthma then walking.
DIAGNOSING ASTHMA:
MEDICAL HISTORY

 Symptoms
 Coughing
 Wheezing
 Shortness of breath
 Chest tightness
 Symptom Patterns
 Severity
 Family History
CLINICAL MANIFESTATIONS

 The symptoms of the asthma consists of a triad of dyspnea, cough and wheezing.
 Dyspnea and tachypnea with prolonged expiration is associated with use of the
accessory muscle of respiration.
 Cough may be present without wheezing or wheezing may be present without
cough.
 Tachycardia and a paradoxical pulse often develops, which may be present to
varying degrees depending upon the stage and severity of the attack.
 Troublesome cough, particularly at night
 Awakened by coughing
 Coughing or wheezing after physical activity
 Breathing problems during particular seasons
 Coughing, wheezing, or chest tightness after allergen exposure
 Colds that last more than 10 days
 Relief when medication is used
 Wheezing sounds during normal breathing

 Hyperexpansion of the thorax

 Increased nasal secretions or nasal polyps

 Atopic dermatitis, eczema, or other allergic skin conditions

DIAGNOSIS OF ASTHMA SEVERITY

DIAGNOSIS PEF % of personal

DAYS/W NIGHTS/W
step best

SEVERE PERSISTANT CONTINUAL FREQUENT ≤ 60%

MODERAT PERSISTENT DAILY ≥5/MONTH 60-80

MILD PERSISTANT 2/W 3-4/MONTH ≥ 80

MILD INTERMITANT ≤2/W ≤2/MONTH ≥80

LABORATORY EVALUATION

Blood eosinophilia may be of more than 250-400 cells/mm3 occurs in asthma. The Ig
E may be increased. Allergy skin testing and rast (radioallergoabsorbent test) or other in
vitro determinations of specific Ig E are useful in identifying potentially important
environmental allergens.
The response of the asthmatic patient to exercise testing is quite characteristic.
Measurement of pulmonary function immediately before exercise, immediately after
exercise and 5 to 10 min later, usually shows decreases in peak expiratory flow
rate(PEFR) and in forced expiratory volume in 1 sec(FEV1) of at least 15% without
premedication.
CHEST ROENTGENOGRAMS

Shows hyperinflations during acute attacks.

Atelectasis may occurs, in during acute
exacerbations.

Image Asthma with upper lobe

atelectasis
PULMONARY FUNCTION TESTING

Total lung capacity, functional residual capacity, and residual volume are increased.
Vital capacity is usually decreased. Dynamic test of air flow, forced vital capacity
(FVC), FEV1, PFR and maximum expiratory flow between 25 and 75% of the vital
capacity may also show reduced values.
Determination of arterial blood gases and pH is important in evaluation of the patient
with asthma during an exacerbation.
PULMONARY FUNCTIONAL TESTS
(PFT)

 Increase in forced expiratory volume in one second FEV1 of 12% or more after
bronchodilators
 Variable airflow obstruction of 20% or more with serial spirometry or peak
expiratory flow (PEF)
 Not under the age of 3-4 years
DIFFERENTIAL DIAGNOSIS

•The differentiation of asthma from other diseases is usually not difficult and
include:
- congenital malformations (of the respiratory, cardiovascular or
gastrointestinal systems);
- foreign bodies in the airway of the esophagus;
- bronchiolitis;
- cystic fibrosis;
- immunologic deficiency diseases;
- hypersensitivity pneumonitis.
- GERD
 TREATMENT

 The current guidelines emphasize 4 important components of asthma care: (1)

assessment and monitoring, (2) education, (3) control of environmental factors and
comorbid conditions, and (4) medications

Assessment and monitoring

 Once the patient's condition is classified and therapy has been initiated, continual
assessment is important for disease control. Asthma control is defined as "the degree
to which the manifestations of asthma are minimized by therapeutic intervention and
the goals of therapy are met.  
 In order to assess asthma control and adjust therapy, impairment and risk must be
assessed. 
 Assessment of impairment focuses on the frequency and intensity of symptoms
and the functional limitations associated with these symptoms. 
 Risk assessment focuses on the likelihood of asthma exacerbations, adverse
effects from medications, and the likelihood of the progression of lung function
decline; spirometry should be measured every 1-2 years or more frequently for
uncontrolled asthma. 
 Because asthma varies over time, follow-up every 2-6 weeks is initially necessary
(when gaining control of the disease) and then every 1-6 months thereafter.
EDUCATION OF THE PATIENT

 Education continues to be important in all areas of medicine and is particularly

important in asthma. Self-management education should focus on teaching
patients the importance of recognizing their own their level of control and signs of
progressively worsening asthma symptoms. 
 Both peak flow monitoring and symptom monitoring have been shown to be
equally effective; however, peak flow monitoring may be more helpful in cases in
which patients have a history of difficulty in perceiving symptoms, a history of
severe exacerbations, or moderate-to-severe asthma.
 Educational strategies should also focus on environmental control and avoidance
strategies and medication use and adherence (eg, correct inhaler techniques and use
of other devices).
  The use of written asthma action plans in partnership with the patient (make sure to
review the differences between long-term control and quick-relief medications)
 Education through the involvement of other members of the healthcare team (eg,
nurses, pharmacists, physicians), and education at all points of care (eg, clinics,
hospitals, schools) are examples of various educational tools that are available and
are important tools for good patient adherence and understanding.
CONTROL OF ENVIRONMENTAL FACTORS AND COMORBID
CONDITIONS 

 As mentioned above, environmental exposures and irritants can play a strong role in
symptom exacerbations. Therefore, in patients who have persistent asthma, the use
of skin testing or in vitro testing to assess sensitivity to perennial indoor allergens is
important. Once the offending allergens are identified, counsel patients on
avoidance from these exposures. In addition, education to avoid tobacco smoke is
important for patients with asthma.  
 Lastly, treatment of comorbid conditions that may affect asthma as mentioned above
must be appropriately managed. These include bronchopulmonary aspergillosis,
gastroesophageal reflux disease (GERD), obesity, obstructive sleep apnea, rhinitis,
sinusitis, depression, and stress.   
MEDICATIONS TO TREAT ASTHMA

 Two major categories of medications are:

– Long-term control
– Quick relief

Long-Term Control
 Taken daily over a long period of time
 Used to reduce inflammation, relax airway muscles, and improve symptoms and lung
function
– Inhaled corticosteroids
– Long-acting beta2-agonists
– Leukotriene modifiers
QUICK-RELIEF

 Used in acute episodes

 Generally short-acting beta2agonists
BRONCHODILATOR, BETA2-AGONISTS

Albuterol sulfate (Proventil HFA, Ventolin HFA, ProAir HFA)

 Oral inhaler: 90 mcg per inhalation, 2 inhalations q4-6h; more inhalations may be
used in severe, acute episodes; more frequent dosing can be used to treat acute
symptoms
Nebulizer: 2.5 mg via nebulization of 0.5% solution in 2-3 mL of sodium chloride
solution q4-6h
PIRBUTEROL ACETATE (MAXAIR AUTOHALER)

 PO inhalation: 1-2 inhalations q4-6h; not to exceed 12 inhalations q24h

Nonracemic form of the beta2-agonist albuterol

Levalbuterol (Xopenex)

 MDI: 45-90 mcg (1-2 inhalations) q4-6h

 Nebulizer: 0.63 mg by nebulizer q8h
LONG-ACTING BETA2-AGONISTS

Salmeterol (Serevent Diskus)

 <4 years: Not established
>4 years:1 inhalation (50 mcg) q12h

Formoterol (Foradil Aerolizer)

 <5 years: Not established
>5 years: 12 mcg inhaled (contents of 1 cap inhaled PO) bid at least
12 h apart
 Methylxanthines ( not so used)
Theophylline (Theo-24, Theochron, Uniphyl)
 Initial dose: 10 mg/kg PO sustained-release tablets and capsules; not to exceed 300
mg/d
First dose adjustment: 13 mg/kg PO; not to exceed 450 mg/d
Second dose adjustment: 16 mg/kg PO; not to exceed 600 mg/d

Mast cell stabilizers

Cromolyn sodium (Intal)
 MDI: 2 inhalations q6h initially; once control achieved, may attempt gradual
downward titration to 2 inhalations q12h
Nebulizer: 20 mg in 2 mL nebulizer solution q6-8h
 Corticosteroids, inhaled
Ciclesonide (Alvesco)
 patients previously on bronchodilator therapy alone: 80 mcg bid; not to exceed 160 mcg bid
Patients on previous inhaled corticosteroids: 80 mcg bid; not to exceed 320 mcg bid
Patients on previous oral corticosteroids: 320 mcg bid; not to exceed 320 mcg bid
Beclomethasone (QVAR)
 <5 years: Not established
5-11 years: 40 mcg inhaled bid initially; may increase to 80 mcg bid
>11 years: Taking bronchodilators alone: 40-80 mcg inhaled bid initially; may increase to 320 mcg bid
Taking inhaled corticosteroids: 40-160 mcg inhaled bid initially; may increase to 320 mcg bid
Fluticasone (Flovent Diskus, Flovent HFA)
 MDI:88 mcg inhaled bid
Diskus:
<4 years: Not established
4-11 years: 50 mcg inhaled bid; may increase, not to exceed 100 mcg bid
Systemic corticosteroids

Prednisone (Deltasone, Orasone) and prednisolone (Pediapred, Prelone, Orapred)

 1-2 mg/kg/d PO for 3-10 d; not to exceed 60-80 mg/d

Methylprednisolone (Solu-Medrol)
 1 mg/kg IV q6h
 Leukotriene modifier

Zafirlukast (Accolate)
 <5 years: Not established
5-11 years: 10 mg PO bid
>12 years: Administer as in adults

Montelukast (Singulair)
 Chronic persistent asthma:10 mg PO hs
Exercise-induced asthma: 10 mg PO at least 2 h before exercise; do not repeat dose within 24h Pediatric
 Chronic persistent asthma:
6-23 months: 1 packet of 4 mg oral granules PO hs
2-5 years: 4 mg PO hs
6-14 years: 5 mg PO hs
>14 years: Administer as in adults
Exercise-induced asthma:
<15 years: Not established; some pediatric subspecialists recommend 5 mg PO qd
>15 years: Administer as in adults
 Monoclonal Antibody

Omalizumab (Xolair)
 <12 years: Not established
>12 years: 150-375 mg SC q2-4wk; inject slowly over 5-10 seconds because
of viscosity; not to exceed 150 mg per injection site
Precise dose and frequency established by serum total IgE level (IU/mL)
 Combination inhaled steroid/long-acting beta2-agonist

Budesonide and formoterol (Symbicort)

 <12 years: Not established
 >12 years: Patients previously on medium-to-high dose inhaled steroids: 2 inhalations of 4.5/160 PO
bid Patients previously on low-to-medium dose inhaled steroids: 2 inhalations of 4.5/80 PO bid.
Patients not currently receiving inhaled corticosteroids: 2 inhalations PO bid (strength depends on
asthma severity)
Do not exceed 2 inhalations of 160/4.5 daily

Fluticasone and salmeterol (Advair HFA, Advair Diskus)

 Anticholinergic Agent

 These agents may be added to beta2-agonist therapy for acute exacerbation.

Ipratropium (Atrovent)
 Nebulizer: 250 mcg (1.25 mL) inhaled via nebulizer tid MDI: 1-2 inhalations PO tid;
not to exceed 6 inhalations in 24 h
ASTHMA TREATMENT BY SEVERITY

 STEP 1 MILD INTERMITTENT

 No daily preventive therapy, treat only symptoms

 Short actig beta 2 agonist: ALBUTEROL face mask or spacer
STEP 2 MILD PERSISTENT

 Daily aintiinflamatory medications

 Cromolyn (Intal)
 Nedocromil (Tilade)
 Or LOW TO MEDIUM DOSE INHALED STEROIDS
 SHORT ACTING BRONCHODILATOR as needed by nebulizer or spacer
 Or ORAL BETA 2 AGONIST
STEP 3 MODERATE PERSISTENT ASTHMA

 High dose coticoid inhaler daily

(Beclomethasone, Fluticasone)
 Long acting daily bronchodilators (Salmeterol=SEREVENT)
 Short acting bronchodilator for symptoms
STEP 4 SEVERE AND PERSISTENT
SYMPTOMS

 Add oral prednisone to step3

 Daily antiinflamatory med

High doses inhaled corticosteroids

Systemic corticosteroids 0,25-2mg/day
ROLE OF ANTILEUKOTRIENES

 In patients with cronic asthma who are symptomatic even if they get moderate to high doses of
beclomethasone, AL reduce the rate of exacerbations that require systhemic corticosteroids
GINA – GLOBAL INITIATIVE FOR ASTHMA

 The GINA report is not a guideline, but an integrated evidence-based strategy focusing on
translation into clinical practice

HTTPS://GINASTHMA.ORG/WP-CONTENT/
UPLOADS/2019/04/GINA-2019-MAIN-POCKET-
GUIDE-WMS.PDF
GINA 2014