Bronchial Asthma in Children

Asthma is the commonest chronic respiratory disease of childhood — a reversible, episodic airway obstruction driven by chronic eosinophilic (Th2-type) airway inflammation, bronchial hyper-responsiveness and remodelling. These notes are built around the current GINA framework with the cut-offs, drug-of-choice picks and acute-attack algorithms that NEET PG repeatedly tests.

Definition & core concept

Asthma is defined by a history of variable respiratory symptoms (wheeze, breathlessness, chest tightness, cough — worse at night/early morning) together with variable expiratory airflow limitation. The three pathological pillars are:

1. Chronic airway inflammation (eosinophils, mast cells, Th2 lymphocytes, IL-4/IL-5/IL-13).
2. Bronchial hyper-responsiveness — exaggerated bronchoconstriction to triggers.
3. Reversible airflow obstruction — reverses spontaneously or with a bronchodilator.

High-yield: The single most characteristic feature distinguishing asthma from other wheezy disorders is reversibility / variability of airflow obstruction, not the wheeze itself.

The hallmark on examination is a prolonged expiratory phase with polyphonic, bilateral expiratory wheeze. A "silent chest" in an acutely breathless child is an ominous sign of impending respiratory failure, not improvement.

Etiology, triggers & pathophysiology

Asthma is multifactorial — genetic atopic predisposition interacting with environmental triggers. The atopic march (atopic dermatitis → allergic rhinitis → asthma) is a classic high-yield sequence. A personal/family history of atopy is the strongest risk factor.

Common Indian paediatric triggers:

Category	Examples (Indian setting)
Aeroallergens	House-dust mite (Dermatophagoides), cockroach, pollen, fungal spores, pet dander
Infections	Viral URTI (rhinovirus, RSV) — commonest trigger of acute exacerbations in children
Irritants	Biomass/chulha smoke, passive (parental) tobacco smoke, mosquito-coil & incense smoke, vehicular pollution
Physical	Exercise, cold air, laughing/crying
Drugs/food	Aspirin/NSAIDs, beta-blockers; food additives (sulphites)
Others	GERD, emotional stress, menstruation in adolescents

Pathophysiology flow: Trigger/allergen exposure → mast-cell degranulation + Th2 activation → release of histamine, leukotrienes (LTC4/D4/E4), prostaglandins, IL-4/5/13 → eosinophil recruitment → bronchial smooth-muscle contraction + mucosal oedema + mucus hypersecretion → airflow obstruction → air-trapping & V/Q mismatch → hypoxaemia. Chronic inflammation → airway remodelling (basement-membrane thickening, smooth-muscle hyperplasia, goblet-cell metaplasia) → fixed obstruction.

High-yield: Early acute asthma shows hypocapnia (low PaCO₂) due to tachypnoea. A rising or "normal" PaCO₂ in a distressed child signals fatigue and impending respiratory failure — an ICU red flag.

Clinical features

• Recurrent episodic wheeze, cough (classically nocturnal/early-morning), dyspnoea, chest tightness.
• Symptom-free intervals between attacks (helps distinguish from structural causes).
• Cough-variant asthma: chronic dry cough as the only symptom.
• Exercise-induced bronchoconstriction: symptoms 5–15 min after exertion.
• Signs in acute attack: tachypnoea, accessory-muscle use, intercostal/subcostal retractions, hyperinflated chest, prolonged expiration, wheeze, pulsus paradoxus, tachycardia.

Phenotypes of childhood wheeze (loci-Tucson concept):

Phenotype	Features
Transient early wheeze	Onset <3 yr, resolves by ~6 yr; linked to small airways/prematurity/smoke; not atopic
Non-atopic (viral) wheeze	Triggered by viral infections; usually resolves by school age
Persistent atopic asthma (IgE-mediated)	Atopic background, persists into adulthood, true asthma

Diagnosis & investigation of choice

Diagnosis is clinical in young children. Objective confirmation needs lung-function testing, feasible only >5–6 years (when reliable spirometry can be performed).

Spirometry — investigation of choice for confirming reversible obstruction:

• Obstructive pattern: FEV₁/FVC reduced (<0.85–0.90 predicted in children; <0.75–0.80 used in adults).
• Bronchodilator reversibility: improvement in FEV₁ ≥12% (and ≥200 mL in older children/adults) after inhaled salbutamol — diagnostic.

Peak expiratory flow (PEF):

• Diurnal variability >13% in children (>10% averaged over 2 weeks) supports asthma.
• Useful for home monitoring, not first-line diagnosis.

Bronchial provocation test (methacholine/exercise challenge): a fall in FEV₁ ≥10–15% post-exercise indicates exercise-induced bronchoconstriction; used when spirometry is normal but suspicion is high.

Adjuncts: FeNO (fractional exhaled nitric oxide) — marker of eosinophilic inflammation, predicts ICS response. Total/specific IgE, absolute eosinophil count, skin-prick tests identify atopy/triggers. Chest X-ray is NOT routine — done to exclude differentials (foreign body, structural lesion) or in first severe episode; may show hyperinflation.

High-yield: Bronchodilator reversibility of FEV₁ ≥12% is the classic spirometric criterion. In an exacerbation, SpO₂ <92% on room air is the key cut-off marking severe attack / need for admission.

Severity & control assessment

GINA shifted the paradigm from "severity" to assessing control to guide step-up/step-down therapy. For children ≤5 yr, control over the past 4 weeks:

Parameter (past 4 weeks)	Well controlled	Partly controlled	Uncontrolled
Daytime symptoms >few min, >1/week	None	—	—
Night waking/coughing due to asthma	None	1–2 of these	3–4 of these
Reliever needed >1/week	None	—	—
Any activity limitation	None	—	—

(Well controlled = none; partly = 1–2; uncontrolled = 3–4 features present.)

Acute exacerbation severity (key clinical grading):

Feature	Mild–Moderate	Severe	Life-threatening
Talks in	Sentences/phrases	Words	Unable to speak
SpO₂ (room air)	>94%	90–94%	<90%
Pulse	<100–120	>120–125	Bradycardia
Sensorium	Normal/agitated	Agitated	Drowsy/confused
Chest	Wheeze	Loud wheeze	Silent chest
PEF	>50% predicted	33–50%	<33%

High-yield: Silent chest, cyanosis, bradycardia, drowsiness, feeble respiratory effort and a normalising PaCO₂ are signs of life-threatening asthma demanding ICU care.

Management — controller & reliever therapy

The twin pillars: reliever for quick symptom relief and controller for long-term inflammation control.

• Reliever (rescue) drug of choice: inhaled SABA — salbutamol (albuterol). GINA now also endorses as-needed low-dose ICS-formoterol as preferred reliever in older children/adolescents (anti-inflammatory reliever strategy).
• Controller drug of choice: inhaled corticosteroid (ICS) — the single most effective anti-inflammatory long-term controller (budesonide, fluticasone).

Stepwise control therapy (children 6–11 yr, GINA principle) — step up if uncontrolled, step down once controlled ≥3 months:

Step 1 (as-needed low-dose ICS-formoterol / SABA + ICS) → Step 2 (daily low-dose ICS, OR daily LTRA, OR ICS taken whenever SABA used) → Step 3 (low-dose ICS-LABA, OR medium-dose ICS) → Step 4 (medium-dose ICS-LABA + refer to specialist) → Step 5 (high-dose ICS-LABA + add-on: tiotropium/anti-IgE omalizumab/anti-IL-5).

High-yield: ICS is the controller of choice; SABA is the reliever of choice. LABA must never be used as monotherapy in asthma (increased mortality) — always combined with ICS.

Other controllers:

• LTRA (montelukast): add-on/alternative; useful in exercise-induced asthma, concomitant allergic rhinitis, aspirin-sensitive asthma, in young children who cannot use inhalers. (Note neuropsychiatric warning.)
• LAMA (tiotropium): add-on in older children with severe asthma.
• Biologics: Omalizumab (anti-IgE) for severe allergic asthma with elevated IgE; mepolizumab/benralizumab (anti-IL-5) for severe eosinophilic asthma; dupilumab (anti-IL-4Rα).

Delivery device — by age (high-yield):

Age	Preferred device
<4 yr	pMDI + spacer with face mask
4–6 yr	pMDI + spacer with mouthpiece
>6 yr	pMDI + spacer / dry-powder inhaler

High-yield: A pMDI with a spacer is as effective as a nebuliser for delivering bronchodilators in most acute attacks and is preferred (less infection risk, better deposition). Always rinse mouth after ICS to prevent oral candidiasis and dysphonia.

Acute severe asthma — emergency management

Stepwise approach (memorise the order):

1. Oxygen — target SpO₂ 94–98% in children.
2. Inhaled SABA — nebulised salbutamol (2.5 mg <5 yr; 5 mg ≥5 yr) or pMDI-spacer; repeat / back-to-back ("continuous") nebulisation in severe cases.
3. Inhaled ipratropium bromide (anticholinergic) added to salbutamol in severe attacks — improves bronchodilation.
4. Systemic corticosteroids early — oral prednisolone 1–2 mg/kg/day (max 40–60 mg) or IV hydrocortisone/methylprednisolone if vomiting. Steroids reduce relapse and admission.
5. IV magnesium sulphate (25–50 mg/kg, max 2 g over 20 min) for severe attacks unresponsive to initial therapy — smooth-muscle relaxant.
6. IV salbutamol / aminophylline in refractory cases (in ICU, with monitoring).
7. Heliox (helium-oxygen 70:30/80:20) — reduces airway resistance/turbulence; adjunct in severe refractory obstruction.
8. Consider non-invasive ventilation → intubation for impending/actual respiratory failure.

High-yield: In acute severe asthma the first three immediate steps are Oxygen → inhaled SABA (salbutamol) → early systemic steroids. IV magnesium sulphate is the classic add-on for severe attacks not responding to first-line nebulisation.

High-yield: Antibiotics are NOT routine — most exacerbations are viral. Sedatives are contraindicated (respiratory depression). Mucolytics and chest physiotherapy are not helpful acutely.

Mnemonic for acute management — "O SHIT MA": Oxygen, SABA (salbutamol), Hydrocortisone/steroids, Ipratropium, Theophylline (aminophylline, refractory), Magnesium sulphate, Admit/Anaesthetist (ICU/intubation).

Complications

• Acute: status asthmaticus (refractory acute severe asthma), respiratory failure, pneumothorax/pneumomediastinum (from air-trapping/barotrauma), atelectasis (mucus plugging), dehydration, hypokalaemia (from beta-agonists).
• Chronic: airway remodelling with fixed obstruction, growth concerns (high-dose ICS — usually small, transient effect on velocity), oral candidiasis, recurrent school absenteeism, impaired quality of life.
• ABPA (allergic bronchopulmonary aspergillosis): suspect in poorly controlled asthma with central bronchiectasis, fleeting infiltrates, raised total IgE & Aspergillus-specific IgE/IgG, peripheral eosinophilia.

Key differentials

In young/infant wheeze, "all that wheezes is not asthma." Distinguish from:

Differential	Discriminating clue
Bronchiolitis	First wheeze in infant <2 yr, viral (RSV), seasonal
Foreign body aspiration	Sudden onset, unilateral/localised wheeze, choking history, asymmetric air entry
Cystic fibrosis	Failure to thrive, steatorrhoea, recurrent infections, clubbing, raised sweat chloride
GERD	Symptoms with feeds, recurrent aspiration
Vocal cord dysfunction	Inspiratory stridor, normal spirometry, adolescent
Congenital heart disease / vascular ring	Cardiac murmur, feeding difficulty, fixed wheeze
Primary ciliary dyskinesia	Situs inversus, chronic otitis/sinusitis, neonatal respiratory distress
Tuberculosis (India)	Chronic cough, contact, weight loss, lymphadenopathy

High-yield: Unilateral, sudden-onset wheeze with localised hyperinflation in a toddler = foreign body until proven otherwise — not asthma.

Recently asked / exam angle

• Reliever vs controller — SABA reliever, ICS controller: a near-guaranteed one-liner.
• Drug of choice for long-term control = inhaled corticosteroid.
• LABA monotherapy is contraindicated (must combine with ICS) — frequently tested.
• IV magnesium sulphate for severe acute asthma not responding to nebulisation.
• Spacer device selection by age (face mask <4 yr, mouthpiece 4–6 yr).
• Silent chest = severe/life-threatening, not improving.
• Rising/normal PaCO₂ in a tachypnoeic asthmatic = impending respiratory failure.
• Spirometry reversibility FEV₁ ≥12% as diagnostic criterion.
• Montelukast (LTRA) for exercise-induced asthma and asthma with allergic rhinitis; neuropsychiatric adverse-effect warning.
• Omalizumab (anti-IgE) for severe allergic asthma — mechanism-based MCQ.
• Recognising ABPA (raised IgE, Aspergillus sensitisation, central bronchiectasis) in steroid-dependent asthma.
• GINA "control-based" management and step-up/step-down concept.

Rapid revision

1. Asthma = chronic Th2 eosinophilic airway inflammation + hyper-responsiveness + reversible obstruction.
2. Reliever of choice = inhaled SABA (salbutamol); controller of choice = inhaled corticosteroid.
3. LABA never as monotherapy — always with ICS (mortality risk).
4. Spirometry confirms asthma: bronchodilator reversibility of FEV₁ ≥12%; reliable only >5–6 yr.
5. PEF diurnal variability >13% in children supports the diagnosis.
6. Acute severe attack order: O₂ (target 94–98%) → nebulised salbutamol ± ipratropium → early systemic steroids → IV MgSO₄ → aminophylline/heliox/ICU.
7. Silent chest, cyanosis, drowsiness, normalising PaCO₂ = life-threatening — call ICU.
8. Spacer with face mask <4 yr, mouthpiece 4–6 yr; pMDI+spacer ≈ nebuliser for acute relief.
9. Rinse mouth after ICS to avoid oral thrush and dysphonia.
10. Montelukast (LTRA) good for exercise-induced asthma and coexisting allergic rhinitis.
11. Omalizumab = anti-IgE for severe allergic asthma; anti-IL-5 (mepolizumab) for eosinophilic asthma.
12. Sudden unilateral wheeze in a toddler = foreign body; antibiotics & sedatives are not routine in acute asthma.