A wheeze is a high-pitched, continuous musical sound produced by turbulent airflow through narrowed airways, commonly heard in children with asthma, bronchiolitis, or viral-induced wheezing, particularly in those under 5 years of age.

Wheeze in Children

Epidemiology

Understanding the natural history of early wheeze is critical — not all infant wheezers become asthmatic:

Phenotype	Description	Prognosis
Transient early wheezers	Wheeze only in first 3 years; triggered by viral infections; never atopic	Resolve by age 6; related to small airway calibre at birth
Persistent wheezers	Wheeze begins < 3 years and persists beyond age 6	Often develop asthma; frequently atopic
Late-onset wheezers	No wheeze in first 3 years; begin wheezing after age 3–6	Usually atopic asthma

The modified Asthma Predictive Index (mAPI) helps predict which wheezing toddlers will develop persistent asthma (see Diagnosis section later).

Risk Factors

Risk Factor	Mechanism / Explanation
Genetics	Multiple genes implicated (e.g., IL-3, IL-4, TNF-α, ADAM33, ORMDL3/GSDMB on chromosome 17q21). Family history of asthma/atopy is the single strongest risk factor ^[1]^[4]
Atopy	Predisposition to mount IgE responses to common allergens; ↑serum IgE correlates with ↑asthma prevalence ^[1]^[4]. Often manifests as the "atopic march" (eczema → food allergy → allergic rhinitis → asthma)
Gender	M > F in children (boys have relatively smaller airways for lung size); F > M in adults ^[1]^[4]
Prematurity / Low birth weight	Disrupted alveolar and airway development; bronchopulmonary dysplasia (BPD) predisposes to chronic wheeze
Obesity	More common and difficult to control if BMI > 30 kg/m²; proposed mechanisms include altered lung mechanics (reduced FRC), systemic inflammation from adipocyte cytokines (leptin, adiponectin), and comorbidities ^[1]^[4]
Small airway calibre	Infants inherently have narrow airways (resistance ∝ 1/r⁴ by Poiseuille's law) — a small amount of mucosal oedema or mucus causes proportionally greater obstruction than in adults

Factor	Notes
Indoor allergens	Fecal pellets of house dust mites (dominant in HK), pets, cockroaches ^[1]^[4]
Outdoor allergens	Alternaria (Ascomycete fungus); pollen uncommon in HK ^[1]^[4]
Environmental tobacco smoke (ETS)	Both prenatal (maternal smoking) and postnatal; increases airway hyperreactivity and impairs lung growth ^[1]^[4]
Outdoor air pollution	Mainly acts as a trigger rather than a cause ^[1]^[4]
Infections	Mainly as trigger; RSV bronchiolitis in infancy is associated with subsequent recurrent wheeze (whether causal or a marker of predisposition is debated) ^[1]^[4]
Exercise, cold air	Triggers — exercise-induced bronchoconstriction occurs 5–15 min after exertion and may take 30–60 min to resolve (distinct from simple exertional dyspnoea which stops within 5 min of rest) ^[1]^[4]
Medications	NSAIDs (classical), OC pills, cholinergic agents, β-blockers, prostaglandins ^[4]
Occupational exposure	5–15% of adult-onset asthma; relevant for adolescent exposures in certain settings ^[4]

Anatomy and Function of the Paediatric Airway

Understanding why children wheeze so readily requires appreciating how the paediatric airway differs from the adult airway:

Feature	Infant/Young Child	Clinical Implication
Airway calibre	Smaller absolute diameter (neonatal trachea ~4 mm vs adult ~20 mm)	By Poiseuille's law, resistance ∝ 1/r⁴ — halving the radius increases resistance 16-fold. Even 1 mm of mucosal oedema in an infant airway causes dramatic obstruction
Cartilage support	Less developed, more compliant	Airways prone to dynamic collapse during forced expiration
Mucous glands	Proportionally more goblet cells	Greater mucus production relative to airway size
Collateral ventilation	Pores of Kohn and channels of Lambert poorly developed until ~6 years	Atelectasis develops more easily distal to obstruction
Chest wall compliance	Very compliant (cartilaginous ribs)	Generates less negative pleural pressure to keep small airways patent; intercostal/subcostal recession appears early
Diaphragm	Fewer type I (fatigue-resistant) fibres until ~2 years	Respiratory muscle fatigue occurs earlier
Alveolar number	~50 million at birth → 300 million by age 8	Reduced gas exchange reserve in young infants

Aetiology (with Hong Kong Focus)

The causes of wheeze in children span a wide range — the key is to think anatomically and by age:

Aetiology by Age Group

Cause	Key Features	Pathophysiology
Bronchiolitis (most common)	RSV peak season (winter in HK); coryzal prodrome → cough → wheeze → ↑WOB; age < 12 months	RSV infects bronchiolar epithelium → necrosis, oedema, mucus plugging → small airway obstruction. Infants affected most because their small airways are most vulnerable
Tracheo/bronchomalacia	Persistent wheeze from birth; worse with crying/feeding/URTI; improves with prone positioning	Deficient cartilage rings → dynamic airway collapse during expiration; may be primary or secondary to vascular compression
Congenital heart disease (CHD) with LV failure	Tachypnoea, poor feeding, failure to thrive, hepatomegaly	L→R shunts (VSD, PDA) → pulmonary overcirculation → interstitial oedema → peribronchial cuffing → airway compression and wheeze
Vascular ring/sling	Fixed wheeze (biphasic or expiratory); stridor; dysphagia	Anomalous great vessels encircle or compress the trachea/main bronchi (e.g., double aortic arch, aberrant right subclavian + ligamentum arteriosum)
Congenital lobar emphysema / CPAM	Progressive respiratory distress; hyperinflated hemithorax	Air trapping in congenitally abnormal lobe → compression of adjacent lung
Gastro-oesophageal reflux (GOR) with aspiration	Recurrent wheeze, cough; worse after feeds; vomiting/posseting	Microaspiration of gastric contents → chemical pneumonitis → airway inflammation; also reflex vagal bronchospasm
Cystic fibrosis	Recurrent chest infections, failure to thrive, steatorrhoea, classical triad: ↑sweat Cl⁻ + recurrent lung infections + pancreatic insufficiency	CFTR mutation (AR, chr 7) → defective Cl⁻ channel → thick, dehydrated airway secretions → impaired mucociliary clearance → chronic infection/inflammation ^[5]

Cause	Key Features	Pathophysiology
Viral-induced wheeze (most common in this age group)	Triggered exclusively by viral URTI (no interval symptoms); rhinovirus, RSV	Viral infection → airway inflammation, oedema, mucus hypersecretion → obstruction of small, compliant airways
Foreign body (FB) aspiration	Sudden onset wheeze/cough in previously well child; often unwitnessed; unilateral/localised wheeze; history of choking episode	FB lodges in bronchus (right main bronchus more common due to wider, more vertical angle) → partial or complete obstruction → air trapping (ball-valve effect) or atelectasis
Asthma (beginning to manifest)	Recurrent wheeze with interval symptoms; triggers include exercise, allergens; atopic comorbidities	Chronic eosinophilic airway inflammation → bronchial hyperreactivity → episodic bronchospasm, mucosal oedema, mucus plugging
Post-infectious bronchiolitis obliterans	Persistent wheeze following severe infection (e.g., adenovirus)	Fibroproliferative obliteration of small airways

Cause	Key Features	Pathophysiology
Asthma (most common by far)	Recurrent episodic attacks of wheezing, chest tightness, breathlessness, cough ^[1]^[4]; triggers, diurnal variation (worse at night/early morning) ^[4]; ±signs of atopy ^[4]	See detailed asthma pathophysiology below
Exercise-induced bronchoconstriction	Wheeze/cough 5–15 min into or after vigorous exercise (especially in cold, dry air)	Water and heat loss from airway surface during hyperventilation → airway cooling → rebound hyperaemia and oedema; osmolar changes trigger mast cell degranulation
Allergic bronchopulmonary aspergillosis (ABPA)	In CF or severe asthma patients; central bronchiectasis; ↑IgE; eosinophilia	Hypersensitivity (type I and III) to Aspergillus fumigatus colonising airways → intense eosinophilic inflammation → mucus plugging, bronchiectasis
Vocal cord dysfunction (VCD) / Inducible laryngeal obstruction	"Wheeze" is actually inspiratory stridor; exercise-triggered; normal spirometry between episodes; not responsive to bronchodilators	Paradoxical adduction of vocal cords during inspiration → upper airway obstruction mimicking asthma
Psychogenic dyspnoea	Hyperventilation, chest tightness; no objective wheeze; often anxious adolescent	Functional; no airway pathology

Foreign Body — The Great Mimic

Foreign body aspiration must be suspected in any child with sudden-onset unilateral wheeze, especially aged 1–3 years (peak oral exploration). The classic history of a choking episode may be absent in up to 40% of cases. A normal CXR does NOT exclude FB. If clinical suspicion exists, proceed to rigid bronchoscopy ^[1].

Pathophysiology of Wheeze — General Principles

All causes of wheeze share a final common pathway: narrowing of the intrathoracic airway lumen during expiration. The mechanisms differ:

Pathophysiology of Asthma (The Most Common Cause of Recurrent Wheeze in Children)

This deserves special attention given its importance:

Classification

Pattern	Definition	Typical Causes
Acute wheeze	Single episode or first presentation	Bronchiolitis, FB, anaphylaxis, acute asthma exacerbation
Episodic (viral) wheeze	Wheeze only during viral URTI; asymptomatic between episodes	Common in preschool children; typically outgrown
Multi-trigger wheeze	Wheeze with viral infections AND other triggers (exercise, allergens, emotions)	More likely to be asthma; more likely to persist
Chronic/persistent wheeze	Wheeze present most days	Asthma, structural lesion, CF, BPD, post-infectious bronchiolitis obliterans

Type	Sound Character	Implies
Generalised (bilateral) wheeze	Polyphonic (multiple pitches), bilateral	Diffuse small airway disease: asthma, bronchiolitis, COPD (adults) ^[4]
Localised (unilateral/fixed) wheeze	Monophonic (single pitch), localised	Focal obstruction: foreign body, tumour ^[4]

Monophonic vs Polyphonic

Polyphonic wheeze = many airways narrowed to different degrees → multiple notes simultaneously → think diffuse disease (asthma, bronchiolitis)
Monophonic wheeze = single airway obstruction producing a single note → think focal lesion (foreign body, endobronchial tumour, structural anomaly) This distinction is high yield and clinically very useful.

Asthma severity is assessed retrospectively from the level of treatment required to control symptoms and exacerbations ^[4]:

Severity	Treatment Step	Example
Mild	Well-controlled with Steps 1 or 2	SABA PRN or low-dose ICS
Moderate	Well-controlled with Step 3	Low-dose ICS/LABA
Severe	Well- or poorly controlled with Steps 4 or 5	Medium/high-dose ICS/LABA ± add-on

Clinical Features

Symptom	Mechanism / Pathophysiology
Wheeze (expiratory, high-pitched, musical)	Turbulent airflow through narrowed intrathoracic airways; worse on expiration because positive intrathoracic pressure further compresses already narrowed airways
Cough	Irritation of cough receptors in inflamed/oedematous airway mucosa; vagal afferent stimulation; mucus stimulating cough reflex. May be the only symptom in "cough-variant asthma" ^[4]
Breathlessness / dyspnoea	↑airway resistance → ↑work of breathing; air trapping → hyperinflation → diaphragm flattened and working at mechanical disadvantage; V/Q mismatch → hypoxaemia
Chest tightness	Perception of ↑work of breathing; hyperinflation stretching the chest wall; may also reflect smooth muscle contraction perceived via vagal afferents
Feeding difficulty (infants)	Respiratory distress makes coordinating suck-swallow-breathe impossible; obligate nose breathers (neonates) are especially affected by nasal congestion
Sleep disturbance / nocturnal symptoms	Diurnal variation in cortisol, vagal tone, adrenaline levels → worsening bronchoconstriction at night (see above)
Diurnal variation	Characteristically worse at night or early morning for asthma ^[4]
Exercise intolerance	Exercise → ↑minute ventilation → airway cooling/drying → osmolar shift triggers mast cell degranulation → bronchospasm. Attacks occur 5–15 min after brief exertion; resolve 30–60 min after stopping ^[4]

Important History Points in Paediatric Wheeze

Age of onset: neonatal onset → congenital anomaly; < 12 months → bronchiolitis; > 3 years → asthma more likely
Pattern: episodic vs persistent; viral-only vs multi-trigger
Triggers: exercise (esp cold air), allergens (dust mites, molds, furry animals, cockroaches; pollen uncommon in HK), pollutants/irritants (cigarette smoke, strong fumes), viral URTI, medications (NSAIDs, β-blockers) ^[4]
Interval symptoms: does the child wheeze between episodes? (suggests multi-trigger/asthma)
Personal history of atopy: eczema, allergic rhinitis ^[4] — atopic march
Family history: asthma, atopy, CF
Birth history: prematurity, ventilation, BPD
Growth: failure to thrive → consider CF, immunodeficiency, cardiac disease
Choking episode: sudden onset → foreign body
Response to bronchodilator: improvement strongly suggests reversible airway obstruction (asthma); no response → consider other diagnoses
Red flags: neonatal onset, failure to thrive, focal/persistent signs, persistent moist cough with purulent sputum, no response to standard therapy

Sign	Mechanism / Pathophysiology
Expiratory wheeze on auscultation	Air forced through narrowed airways → turbulent flow → vibration of airway wall; expiratory because intrathoracic pressure rises during expiration, further narrowing airways
Prolonged expiratory phase	Air trapping — it takes longer to exhale through narrowed airways
Tachypnoea	Compensatory ↑respiratory rate to maintain minute ventilation despite ↑airway resistance and ↓tidal volume
Tachycardia	Sympathetic activation from hypoxia, distress, and ↑work of breathing; also a side effect of β₂-agonist therapy
Intercostal/subcostal/sternal recession	↑negative intrapleural pressure generated to overcome airway resistance → soft tissue sucked inward. More prominent in infants/young children due to highly compliant chest wall
Use of accessory muscles (sternocleidomastoid, scalenes)	Additional inspiratory muscles recruited when diaphragm and intercostals cannot generate sufficient force alone
Nasal flaring (infants)	Alar muscles contract to reduce nasal resistance and increase airflow — a sign of significant respiratory distress in infants
Head bobbing (infants)	Sternocleidomastoid contraction during accessory muscle use causes rhythmic head extension with each breath
Hyperinflated / barrel-shaped chest	Chronic air trapping → ↑residual volume → AP diameter increases; ribs become more horizontal. Indicates chronic/severe obstruction
Chest hyperinflation on CXR	Normal or hyperinflated ± lobar collapse (secondary to mucus obstruction) ^[4]
Hyperresonance on percussion	Hyperinflated lungs contain more air → more resonant to percussion
Reduced air entry (ominous if wheeze disappears)	Severe obstruction → airflow so reduced that insufficient to generate wheeze = "silent chest" — this is a pre-arrest sign
Pulsus paradoxus (> 15 mmHg in children)	Exaggerated drop in systolic BP during inspiration; large negative intrathoracic pressure swings during obstructed breathing → ↑venous return to RV → interventricular septum bows into LV → ↓LV filling and stroke volume
Cyanosis	Severe V/Q mismatch and/or hypoventilation → hypoxaemia → deoxyhemoglobin > 5 g/dL → visible blue discolouration
Signs of atopy: eczema, allergic rhinitis	±signs of atopy: allergic rhinitis, eczema ^[4] — suggests atopic asthma phenotype
Digital clubbing	Chronic suppurative lung disease ^[1] — if present with wheeze, think CF, bronchiectasis, NOT simple asthma. Clubbing is NOT a feature of asthma
Harrison's sulcus	Chronic chest hyperinflation → diaphragmatic traction on lower ribs → permanent horizontal groove at diaphragmatic insertion

Silent Chest = Emergency

When wheeze disappears in a dyspnoeic child, do NOT be reassured. A "silent chest" means airflow is so severely reduced that no turbulence (and therefore no wheeze) is generated. This indicates critical airway obstruction and is a pre-arrest sign requiring immediate escalation.

Sign	Possible Aetiology
Wheeze alone (no other abnormalities)	Intrathoracic airway lesion: asthma, foreign body ^[1]
Crepitations with wheeze	Parenchymal disease (pneumonia, bronchiolitis) ^[1]
Failure to thrive + wheeze	Serious systemic illness including pulmonary (CF, immunodeficiency, cardiac disease) ^[1]
Feeding difficulties + wheeze	Aspiration lung disease, serious systemic illness ^[1]
Daily moist/productive cough + wheeze	Suppurative lung disease (CF, bronchiectasis, PCD) ^[1]
Digital clubbing + wheeze	Chronic suppurative lung disease ^[1]
Hypoxia/cyanosis + wheeze	Airway or parenchymal disease, cardiac disease ^[1]
Neurodevelopmental abnormality + wheeze	Aspiration lung disease ^[1]
Recurrent pneumonia + wheeze	Immunodeficiency, congenital lung abnormalities, tracheo-oesophageal H fistula ^[1]
Chest wall deformity + wheeze	Chronic airway or parenchymal disease ^[1]

Important Associations and Special Entities

Bronchospasm (10–20%): wheezing and dyspnoea often during flushing episodes ^[6]
Mechanism: release of histamine, serotonin, and prostaglandins from neuroendocrine tumour

High Yield Summary

Wheeze = continuous, high-pitched, musical sound from turbulent flow through narrowed intrathoracic airways — it is a SIGN, not a diagnosis.
All that wheezes is not asthma — in infants think bronchiolitis, congenital anomalies, FB, cardiac causes; in older children asthma dominates but always consider alternatives.
Infant airways are especially vulnerable to obstruction: small calibre (resistance ∝ 1/r⁴), compliant walls, more mucous glands, less cartilage support.
Asthma = chronic inflammatory disorder → widespread, variable, reversible airflow obstruction + bronchial hyperreactivity ^[4].
Asthma prevalence ~8.6% in HK; M > F in children; 75% diagnosed < 7 years ^[4].
Asthma pathophysiology: Th2-driven eosinophilic inflammation → early phase (mast cell degranulation → bronchospasm/oedema/mucus) + late phase (eosinophil recruitment → epithelial damage → hyperreactivity) + chronic remodelling (smooth muscle hyperplasia, goblet cell hyperplasia, fibrosis) ^[4].
Triggers in HK: dust mites (dominant indoor allergen), ETS, exercise (cold air), viral URTI; pollen uncommon ^[4].
Classic asthma features: episodic wheeze + cough + chest tightness + dyspnoea; diurnal variation (worse at night/early morning); ±atopy; resolves with trigger avoidance or treatment ^[4].
Red flags against simple asthma: neonatal onset, FTT, clubbing, focal wheeze, persistent wet cough, no bronchodilator response, associated cardiac signs.
Foreign body: sudden-onset, unilateral/localised wheeze in a toddler — normal CXR does NOT exclude it → rigid bronchoscopy if clinical suspicion.
Wheeze + crepitations → parenchymal disease; wheeze + FTT → CF/immunodeficiency/cardiac; wheeze + clubbing → chronic suppurative lung disease (NOT asthma) ^[1].
Silent chest (absence of wheeze in a dyspnoeic child) = pre-arrest sign requiring immediate escalation.

Active Recall - Wheeze in Children

Differential Diagnosis of Wheeze in Children

The differential diagnosis of wheeze in children is considerably broader than in adults. The key principle is that wheeze is a sign, not a diagnosis — your job is to work backwards from the physical sign to the underlying pathology. The approach differs fundamentally by age, acuity (acute vs chronic/recurrent), and distribution (generalised vs localised).

Let me walk you through this systematically.

Major Differential Diagnoses — Organised by Age Group

Diagnosis	Key Differentiating Features	Why It Causes Wheeze
Acute viral bronchiolitis (most common)	Age < 12 months (peak 2–6 months); winter season in HK; coryzal prodrome 1–3 days → cough → wheeze → ↑work of breathing; caused by RSV in ~60–80%	RSV infects bronchiolar epithelial cells → cell necrosis, sloughing into lumen → mucosal oedema + mucus plugging + inflammatory debris → obstruction of small airways. Infants' airways are tiny — even minor oedema causes disproportionate narrowing (Poiseuille's law: R ∝ 1/r⁴)
Congenital heart disease with LV failure	Tachypnoea, poor feeding, failure to thrive, hepatomegaly, cardiac murmur; CXR: crackles ± expiratory wheeze ^[7]	Left-to-right shunt (VSD, PDA, AVSD) → pulmonary overcirculation → pulmonary venous congestion → peribronchial cuffing (fluid-thickened bronchial wall compresses airway lumen) ^[7] → airway narrowing → wheeze. Also interstitial oedema reduces airway calibre
Tracheo/bronchomalacia	Persistent wheeze from birth; characteristically worse with crying, feeding, URTI; improves in prone position; may have biphasic or expiratory wheeze	Deficient cartilage rings → airway wall lacks structural support → dynamic collapse during expiration when intrathoracic pressure exceeds intraluminal pressure
Vascular ring/sling	Fixed wheeze ± stridor from birth; stridor component often biphasic; dysphagia (oesophageal compression); not responsive to bronchodilators	Anomalous great vessels (e.g., double aortic arch, pulmonary artery sling) encircle or compress trachea/bronchi from outside → fixed narrowing
Aspiration lung disease	Feeding difficulties ^[1]; cough/wheeze during or after feeds; vomiting, posseting; neurodevelopmental abnormality ^[1]	Microaspiration of feeds or gastric contents → chemical pneumonitis → airway mucosal inflammation → bronchospasm and oedema. Recurrent aspiration causes chronic airway inflammation
Cystic fibrosis	Failure to thrive ^[1], daily moist/productive cough ^[1], recurrent chest infections, steatorrhoea; digital clubbing ^[1] if chronic	CFTR dysfunction → thick, dehydrated airway secretions → impaired mucociliary clearance → chronic infection → bronchial wall inflammation and oedema → airway obstruction
Congenital lobar emphysema / CPAM	Progressive respiratory distress; unilateral hyperinflated hemithorax on CXR	Congenitally abnormal lobe traps air → progressive overexpansion → compression of adjacent normal lung
Bronchopulmonary dysplasia	History of prematurity and prolonged ventilation/oxygen; chronic respiratory symptoms from neonatal period	Arrested alveolar development + airway injury from barotrauma/volutrauma and oxygen toxicity → airway inflammation, smooth muscle hypertrophy, and fibrosis

Cardiac Wheeze in Infants

A baby with wheeze who is NOT responding to bronchodilators, has poor weight gain, and has a cardiac murmur or hepatomegaly may have congenital heart disease with left heart failure. The wheeze is caused by peribronchial oedema from pulmonary venous congestion, NOT bronchospasm — hence why salbutamol doesn't help. Always examine the liver and feel the precordium in any wheezy infant.

Diagnosis	Key Differentiating Features	Why It Causes Wheeze
Episodic viral wheeze (most common in this age group)	Wheeze ONLY during viral URTI; completely asymptomatic between episodes; no atopic features; typically outgrown by age 5–6	Viral infection (rhinovirus, RSV) → airway inflammation, mucosal oedema, mucus hypersecretion → obstruction of small, compliant toddler airways. No underlying chronic inflammation (unlike asthma)
Foreign body aspiration	Sudden onset in previously well child; history of choking episode (may be absent in ~40%); localised/unilateral wheeze ^[3]^[4]; peak age 1–3 years (oral exploration phase)	FB lodges in bronchus (right more common — wider, more vertical) → partial obstruction → ball-valve effect (air enters on inspiration but cannot escape on expiration) → distal air trapping → localised wheeze. Complete obstruction → atelectasis
Multi-trigger wheeze / Early asthma	Wheeze with viruses AND other triggers (exercise, allergens, cold air); interval symptoms between episodes; atopic comorbidities (eczema, allergic rhinitis)	Chronic Th2-driven eosinophilic airway inflammation → bronchial hyperreactivity → bronchospasm + mucosal oedema + mucus plugging in response to multiple triggers
Croup (viral laryngotracheobronchitis)	Age 6 months to 6 years (peak 2 years); barking cough, hoarseness, stridor ^[8]; worse at night ^[8]; preceded by coryzal symptoms	Parainfluenza virus (most common) → subglottic mucosal inflammation and oedema → narrowing of the subglottic region (narrowest part of paediatric airway). Primarily causes stridor (extrathoracic obstruction), but if inflammation extends to bronchi ("laryngo-tracheo-bronch-itis"), lower airway wheeze may also be present ^[8]
Protracted bacterial bronchitis	Chronic wet cough > 4 weeks; responds to prolonged antibiotics (2–4 weeks amoxicillin-clavulanate); no features of alternative diagnosis	Bacterial infection of bronchial mucosa (non-typeable H. influenzae, M. catarrhalis, S. pneumoniae) → chronic neutrophilic airway inflammation → mucosal oedema and excess mucus → airway narrowing
Anaphylaxis	Acute onset after allergen exposure (food, insect sting, drug); wheeze/bronchospasm + urticaria + angioedema ± hypotension ^[9]; respiratory compromise: dyspnoea, wheezes, bronchospasm, stridor ^[9]	IgE-mediated mast cell degranulation → massive histamine/leukotriene release → bronchospasm + mucosal oedema + ↑vascular permeability → upper and lower airway obstruction

Diagnosis	Key Differentiating Features	Why It Causes Wheeze
Asthma (most common by far)	Recurrent episodic attacks of wheezing, chest tightness, breathlessness, cough ^[3]^[4]; triggers: exercise (esp cold air), allergens, pollutants, viral URTI, medications (NSAIDs, β-blockers) ^[3]^[4]; diurnal variation (worse at night/early morning) ^[3]^[4]; ±signs of atopy (allergic rhinitis, eczema) ^[3]^[4]; response to bronchodilator	Chronic eosinophilic airway inflammation → bronchial hyperreactivity → smooth muscle hyperplasia → ↑bronchoconstriction; goblet cell hyperplasia → ↑mucus secretion; fibrosis → airway wall thickening ^[3]^[4]
Bronchiectasis	Chronic dyspnoea, cough and airflow obstruction; prominent cough with mucopurulent sputum production ± haemoptysis; diagnosed by CXR/HRCT demonstrating airway dilatation ('tram-line' appearance) ^[3]^[4]	Permanently dilated and damaged airways → loss of mucociliary clearance → chronic infection → inflammatory exudate and mucus plug small airways → airway obstruction → wheeze
Bronchiolitis obliterans	History of severe previous infection (adenovirus, Mycoplasma) or post-transplant; persistent wheeze and exercise intolerance; poor response to bronchodilators; mosaic attenuation on HRCT	Fibroproliferative obliteration of small airways → fixed obstruction of bronchioles → air trapping and wheeze
Central airway obstruction	Exertional dyspnoea ± monophonic wheeze; flow-volume loop characteristic for upper airway obstruction (expiratory plateau) ^[3]^[4]; may be due to luminal or extraluminal masses ^[3]	Tumour, lymphadenopathy, or other mass compresses central airway → fixed narrowing → monophonic wheeze (single note because only one airway is narrowed)
Vocal cord dysfunction / Inducible laryngeal obstruction	"Wheeze" actually loudest over larynx/neck (not lung fields); inspiratory > expiratory; exercise-triggered; normal spirometry between episodes; flattened inspiratory loop on flow-volume curve; does NOT respond to bronchodilators; often anxious adolescent	Paradoxical adduction (closure) of vocal cords during inspiration → upper airway obstruction. This is technically stridor, not true wheeze, but is frequently misdiagnosed as "refractory asthma"
Allergic bronchopulmonary aspergillosis	In CF or poorly controlled asthma; central bronchiectasis; ↑total IgE; blood/sputum eosinophilia; positive Aspergillus IgE/precipitins	Type I + III hypersensitivity to Aspergillus → intense eosinophilic inflammation → mucus plugging of central airways → wheezing
Psychogenic dyspnoea / Hyperventilation	Chest tightness, air hunger; no objective wheeze on auscultation; often adolescent with anxiety; normal SpO₂; perioral/digital tingling (hypocapnic alkalosis)	No actual airway pathology; patient reports "wheeze" but it is absent on examination. Important to distinguish from organic causes

The lecture slides ^[1] provide a systematic approach to identifying the cause of cough in children. When wheeze is the dominant associated sign:

Question	Features	Likely Diagnosis
Is this a lower respiratory tract illness?	Tachypnoea (> 60 for < 2 months, > 50 for 2–12 months, > 40 for > 1 year), respiratory distress with increased work of breathing, chest signs (crepitations or wheeze/rhonchi), fever	Acute bronchiolitis, Pneumonia (viral, bacterial), Asthma ^[1]
Is this an allergic/atopic illness?	Seasonal and diurnal variation, association with rhinitis, posture, 'clearing of throat', triggers (dust, pollutant, pollen etc.)	Post-nasal drip from allergic rhinitis, Reactive airway/asthma ^[1]
Is this an acute exacerbation of a chronic respiratory disorder?	Failure to thrive, finger clubbing, chest deformity, features of atopy	CF, bronchiectasis, chronic lung disease ^[1]

Specific cough associations with wheeze ^[1]:

Wheeze → Intrathoracic airway lesion (e.g., asthma, foreign body)
Crepitations → Parenchymal disease
Digital clubbing → Chronic suppurative lung disease
Failure to thrive → Serious systemic including pulmonary illness
Feeding difficulties → Aspiration lung disease, serious systemic illness
Recurrent pneumonia → Immunodeficiency, congenital lung abnormalities, tracheo-oesophageal H fistula

This is a point where students frequently get confused ^[8]^[10]:

Feature	Wheeze	Stridor
Origin	Intrathoracic (lower) airway	Extrathoracic (upper) airway
Phase	Predominantly expiratory (inspiratory = severe)	Predominantly inspiratory (expiratory = severe)
Mechanism	During expiration, +ve intrathoracic pressure narrows intrathoracic airways that are already diseased → turbulent flow ^[8]	During inspiration, −ve intrathoracic pressure collapses extrathoracic airways that are already narrowed → turbulent flow ^[8]
Typical causes	Asthma, bronchiolitis, FB in bronchus	Croup, laryngomalacia, FB at larynx, epiglottitis
Loudest	Over lung fields	Over trachea/neck

Pathophysiology ^[8]: During inspiration, negative intrapleural pressure dilates intrathoracic airways but collapses extrathoracic airways → extrathoracic obstruction presents as stridor. During expiration, positive intrapleural pressure collapses intrathoracic airways but dilates extrathoracic airways → intrathoracic obstruction presents as wheeze ^[8].

Diagnosis	Why You Must Know It	Key Clue
Primary ciliary dyskinesia (PCD)	Chronic wet cough from birth, recurrent otitis media, situs inversus (50% — Kartagener syndrome), neonatal respiratory distress	Immotile cilia → impaired mucociliary clearance → chronic airway secretions → wheeze; think of it when there is situs inversus + chronic respiratory symptoms
Immunodeficiency	Recurrent pneumonia ^[1]; failure to thrive; unusual or opportunistic infections	Inability to clear respiratory pathogens → chronic/recurrent lower airway infection → airway inflammation → wheeze
Tracheo-oesophageal fistula (H-type)	Recurrent pneumonia ^[1]; cough and wheeze with feeds; recurrent aspiration	Abnormal connection between trachea and oesophagus → aspiration of feeds into airway → chemical pneumonitis and chronic airway inflammation
Carcinoid syndrome	Bronchospasm (10–20%): wheezing and dyspnoea often during flushing episodes ^[11]	Rare in children; when present: episodic flushing + diarrhoea + wheeze due to histamine/serotonin release
Eosinophilic oesophagitis / GORD	Chronic cough and wheeze in atopic child; symptoms worse after feeds or supine	Refluxate → microaspiration and/or vagal reflex bronchospasm
Mediastinal mass	Progressive wheeze + dyspnoea; orthopnoea (worse lying flat); SVC syndrome (facial swelling)	Lymphoma/thymoma compresses trachea or bronchi → fixed monophonic wheeze

Feature	Asthma	Bronchiolitis	Foreign Body	CHD/HF	CF	VCD
Age	Usually > 3y	< 12m	1–3y (peak)	Any	Any	Adolescent
Onset	Episodic, recurrent	Acute, single	Sudden	Gradual	Chronic	Exercise-triggered
Wheeze pattern	Generalised, polyphonic	Generalised	Localised, monophonic	Generalised	Generalised	Inspiratory "wheeze"
Cough	Dry, nocturnal	Wet	Paroxysmal	Wet if pulm oedema	Chronic productive	Absent or minimal
Atopy	+++	−	−	−	−	−
Growth	Normal	Normal	Normal	FTT	FTT	Normal
Clubbing	Never	No	No	Cyanotic CHD	Yes (late)	No
Bronchodilator response	Yes	Minimal/None	No	No	Variable	No
CXR	Normal/hyperinflated	Hyperinflated	Unilateral hyperinflation or normal	Cardiomegaly, pulm oedema	Hyperinflation, bronchiectasis	Normal

High Yield Exam Point

The differential of generalised wheeze in children = asthma, bronchiectasis, bronchiolitis obliterans, viral bronchiolitis. The differential of localised wheeze in children = foreign body, tumour. ^[3]^[4]

In a preschool child with recurrent wheeze, distinguish episodic viral wheeze (wheeze only with URTI, asymptomatic between) from multi-trigger wheeze (wheeze with viruses AND exercise/allergens/cold air) — the latter is more likely true asthma and more likely to persist.

Always remember: wheeze → intrathoracic airway lesion (e.g., asthma, foreign body) ^[1]. But the absence of wheeze in a dyspnoeic child ("silent chest") is a pre-arrest sign ^[3].

Active Recall - Differential Diagnosis of Wheeze

References

^[1] Lecture slides: GC 141. A child with cough acute and chronic cough in children.pdf, p15, p20 ^[3] Senior notes: Adrian Lui Pediatrics.pdf, p170–172 (Asthma — Clinical Features and D/dx) ^[4] Senior notes: Ryan Ho Respiratory.pdf, p97–98 (Asthma — Clinical Features and D/dx) ^[7] Senior notes: Ryan Ho Cardiology.pdf, p73 (Acute Decompensated HF) ^[8] Senior notes: Adrian Lui Pediatrics.pdf, p155, p161 (Stridor vs Wheeze, Croup) ^[9] Senior notes: Ryan Ho Critical Care.pdf, p24 (Anaphylactic Shock) ^[10] Senior notes: Ryan Ho Fundamentals.pdf, p55 (Adventitious Sounds — Wheezes) ^[11] Senior notes: Ryan Ho Endocrine.pdf, p66 (Carcinoid Syndrome — D/dx of episodic flushing)

Diagnosis of Wheeze in Children — Criteria, Algorithm, and Investigations

Diagnostic Criteria for the Most Common Causes of Wheeze

A. Asthma (The Most Common Cause of Recurrent Wheeze in Children > 5 years)

Diagnosis is predominantly clinical based on compatible Hx ± PE ^[3]^[4]

Both of the following must be present:

History of characteristic symptom pattern: Variable symptoms of wheezes, cough, chest tightness, SOB ^[3]^[4]
- More than one type of symptom (wheeze, cough, dyspnoea, chest tightness)
- Symptoms worse at night or early morning ^[3]^[4]
- Symptoms vary over time and in intensity
- Triggered by exercise, allergens, cold air, viral URTI, laughter ^[4]
- ±Signs of atopy (allergic rhinitis, eczema) ^[4]
Confirmed variable expiratory airflow limitation: at least once during the diagnostic process

Test	Criterion for Children	Explanation
FEV₁/FVC ratio	≤ 85% in children (cf. ≤ 75% in adults) ^[3]; GINA 2024 uses ≤ 90% in children ^[4] as a more sensitive cut-off	Normal ratio is higher in children than adults because paediatric airways are proportionally more patent relative to lung volume. A ratio of 0.85 in a child is already abnormal, whereas in an adult it might be borderline
Bronchodilator reversibility	≥ 12% increase in FEV₁ after 200–400 µg salbutamol (10–15 min post-inhalation) ^[3]^[4]	Note: the 200 mL absolute increase required in adults is NOT mandated in children (their lungs are smaller, so a 12% relative change may be < 200 mL)
PEF diurnal variability	> 10% variability in twice-daily PEF over 1–2 weeks ^[3]^[4] (calculated as daily amplitude percent mean = [daily max − daily min] / mean of daily max and min) ^[3]	Reflects the hallmark of asthma: variable airflow obstruction. Morning dip is characteristic
Exercise challenge	> 10% decrease in FEV₁ (and > 200 mL in adults) after 6 min exercise ^[3]^[4]	Exercise → airway drying/cooling → mast cell degranulation → bronchospasm
Bronchoprovocation test	≥ 20% decrease in FEV₁ post-methacholine/histamine at standard dose ^[3]^[4] OR ≥ 15% decrease post-hyperventilation, hypertonic saline or mannitol ^[3]^[4]	Not routinely done — only when lung function at rest is normal ^[3]^[4]. Tests bronchial hyperreactivity directly. High sensitivity but lower specificity (positive in some non-asthmatics)
ICS therapeutic trial	Significant improvement in FEV₁ or symptoms after 4 weeks of inhaled corticosteroid treatment ^[3]^[4]	If the child improves, this supports the diagnosis retrospectively

FEV₁/FVC in Children vs Adults

A common mistake: applying the adult cut-off (FEV₁/FVC < 0.70 or < 75%) to children. Children normally have FEV₁/FVC ratios of 0.85–0.90+. Using the adult threshold will miss genuine obstruction in children. GINA specifies ≤ 90% for children ^[4] as the threshold, though some paediatric guidelines use ≤ 85% ^[3]. The principle is the same — use age-appropriate normal values.

Spirometry is generally not reliable in children under 5–6 years (they cannot perform forced expiratory manoeuvres reproducibly). Diagnosis is therefore based on:

Clinical pattern recognition: episodic wheeze with multiple triggers, interval symptoms, atopic comorbidities, family history
Modified Asthma Predictive Index (mAPI): used to estimate the probability that a wheezing preschooler will develop persistent asthma

mAPI Criteria
Major criteria (any 1)	Parent with asthma; physician-diagnosed eczema; sensitisation to ≥ 1 aeroallergen
Minor criteria (any 2)	Sensitisation to milk, egg, or peanut; wheezing unrelated to colds; blood eosinophils ≥ 4%
Positive mAPI	≥ 4 wheezing episodes/year + 1 major OR 2 minor criteria → ~77% chance of active asthma at age 6–13
Negative mAPI	~95% chance of NOT having asthma at school age

Therapeutic trial: a trial of low-dose ICS for 2–3 months with assessment of response is often the most pragmatic diagnostic tool in this age group. Clear improvement supports asthma; no improvement should prompt consideration of alternative diagnoses.

Investigation Modalities — Detailed Interpretation

1. Bedside / First-Line Investigations

2. Spirometry (School-Age Children ≥ 6 years)

Spirometry involves a maximal inhalation followed by a rapid and forceful complete exhalation into a spirometer ^[3].

Parameter	What It Measures	Normal in Children	Asthma Pattern	Why
FEV₁	Volume exhaled in first second of forced expiration	≥ 80% predicted (age/height/sex matched)	↓ during exacerbation; may be normal between attacks	Narrowed airways → slower emptying → less volume in 1 second
FVC	Total volume exhaled during forced expiration	≥ 80% predicted	Normal or mildly ↓ (air trapping)	FVC relatively preserved as total lung capacity is normal; may ↓ if severe air trapping prevents complete exhalation
FEV₁/FVC	Ratio indicating obstruction	≥ 85–90% in children ^[3]^[4]	↓ (≤ 85–90%)	The hallmark of obstructive disease: FEV₁ falls more than FVC because narrowed airways limit early flow more than total volume
FEF₂₅₋₇₅	Mid-expiratory flow rate (small airway function)	≥ 65% predicted	↓ (often the earliest abnormality)	Small airways contribute to resistance late in expiration; early small airway disease shows here first

Pattern	Appearance	Implies
Normal	Triangular expiratory limb with rapid peak flow then smooth descent	No obstruction
Intrathoracic obstruction (asthma/COPD)	'Scooped out' concave expiratory limb ^[3]^[4]	Diffuse small airway narrowing → flow limitation particularly at low lung volumes → concavity
Fixed upper airway obstruction	Flattened inspiratory AND expiratory limbs (plateau) ^[3]	Obstruction does not change with respiratory phase → equally limits both flow directions
Variable extrathoracic obstruction	Flattened inspiratory limb, normal expiratory	Extrathoracic lesion collapses during inspiration (negative pressure) but opens during expiration
Variable intrathoracic obstruction	Flattened expiratory limb, normal inspiratory	Intrathoracic lesion collapses during expiration (positive pressure) but opens during inspiration

Flow-Volume Loop Logic

The shape of the flow-volume loop tells you WHERE the obstruction is and WHETHER it is fixed or variable. A 'scooped out' concave expiratory limb ^[4] is classic for diffuse intrathoracic obstruction (asthma, COPD) because as lung volume decreases during forced expiration, the already-narrowed small airways compress further, progressively limiting flow. The result is a curve that dips below the normal triangular shape — like someone scooped out the middle.

3. Chest X-Ray (CXR)

CXR: normal or hyperinflated ± lobar collapse (secondary to mucus obstruction) → mainly to exclude alternative d/dx ^[3]^[4]

CXR Finding	Possible Diagnosis	Why It Appears
Hyperinflation (flattened diaphragms, > 6 anterior ribs visible, increased AP diameter)	Asthma (acute exacerbation), bronchiolitis	Air trapping → ↑FRC → lungs cannot deflate fully
Lobar collapse	Asthma (mucus plugging) ^[3]^[4], FB (complete obstruction)	Mucus plug or FB completely blocks a bronchus → distal air reabsorbed → lobe collapses
Unilateral hyperinflation	Foreign body (ball-valve obstruction)	FB allows air in during inspiration but traps it during expiration → one lung stays inflated
Cardiomegaly ± upper lobe venous diversion ± Kerley B lines	Congenital heart disease with heart failure	Pulmonary venous congestion from left heart failure → interstitial then alveolar oedema ^[7]
Peribronchial thickening / cuffing	Bronchiolitis, asthma, heart failure	Fluid or inflammatory cells in peribronchial interstitium → thickened bronchial walls visible on CXR as ring shadows ("doughnuts") end-on or "tram-lines" in long-section
Bilateral perihilar infiltrates	Acute pulmonary oedema	Alveolar flooding from pulmonary venous hypertension
Bilateral bronchiectatic changes	CF, PCD, immunodeficiency	Chronic airway infection → permanent structural airway dilatation
Right-sided aortic arch	Vascular ring	May explain fixed wheeze/stridor from birth

Allergic status: skin prick test, total/allergen-specific IgE, serum eosinophil count ^[3]^[4]

Test	What It Does	Interpretation	Clinical Utility
Skin prick test (SPT)	Introduces allergen into epidermis; measures wheal-and-flare response	Positive: wheal ≥ 3 mm above negative control at 15 min → sensitisation to that allergen	Identifies specific triggers for avoidance; supports atopic phenotype; available from age ~6 months
Total serum IgE	Measures overall IgE level	Elevated in atopic conditions, ABPA, parasitic infections	Non-specific; supports atopic tendency but does not identify specific allergens
Allergen-specific IgE (RAST)	Measures IgE directed against specific allergens	Positive = sensitisation (not necessarily clinical allergy)	Useful when SPT not possible (severe eczema, antihistamine use, dermatographism)
Blood eosinophil count	Measures circulating eosinophils	> 0.3 × 10⁹/L or > 4% suggests eosinophilic inflammation	Supports atopic/eosinophilic asthma phenotype; helps guide biologic therapy selection

Airway inflammation tests ^[3]^[4]:

Test	Cut-Off	What It Means	Limitations
Sputum eosinophil count	> 2% ^[3]^[4]	Active eosinophilic airway inflammation	Requires induced sputum (difficult in young children); time-consuming
Exhaled breath nitric oxide (FeNO)	> 50 ppb → associated with good short-term response to ICS ^[4]; > 35 ppb suggestive of eosinophilic inflammation in children	NO is produced by inducible NO synthase (iNOS) upregulated in eosinophilic airway inflammation; higher FeNO = more inflammation	Affected by viral infection, atopy (can be elevated without asthma), smoking (↓), age, height; available from ~5–6 years with proper technique

FeNO in Clinical Practice

FeNO is NOT diagnostic of asthma alone — it reflects eosinophilic airway inflammation. A child with allergic rhinitis but no asthma may have elevated FeNO. Its real value is in:

Supporting diagnosis when spirometry is inconclusive
Predicting ICS response (high FeNO → likely to respond well to ICS)
Monitoring adherence (falling FeNO on ICS treatment suggests good adherence and response)

Not routinely done — only when lung function at rest is normal ^[3]^[4]

These tests directly provoke bronchial hyperreactivity:

Test	Method	Positive Result	When to Use
Methacholine challenge	Inhale increasing doses of methacholine (muscarinic agonist → direct smooth muscle contraction)	≥ 20% fall in FEV₁ at standard dose ^[3]^[4]	Normal spirometry but clinical suspicion of asthma
Mannitol / hypertonic saline challenge	Inhale osmolar stimulus → draws water from airway → ↑osmolarity triggers mast cell degranulation	≥ 15% fall in FEV₁ ^[3]^[4]	More specific for asthma than methacholine; useful for exercise-induced bronchoconstriction
Exercise challenge	Standardised treadmill or free-running for 6–8 min at 80–90% max HR	> 10% fall in FEV₁ ^[3]^[4]	To confirm exercise-induced bronchoconstriction

Why methacholine is more sensitive but less specific: methacholine directly contracts smooth muscle regardless of cause — anyone with hyperreactive airways (including post-viral, allergic rhinitis) may test positive. Mannitol/hypertonic saline/exercise work via the indirect pathway (mast cell degranulation), which is more specific to asthmatic inflammation.

The lecture slides outline a comprehensive list of investigations to be ordered according to history and PE, and developmental appropriateness ^[14]:

Investigation	When to Order	What You Are Looking For
CXR ^[14]	First-line for any atypical wheeze; progressive symptoms; red flags	See above
Peak flow ± lung function study ^[14]	Recurrent wheeze in children ≥ 6 years	Confirm variable airflow obstruction (asthma)
CBC with differentials ^[14]	Recurrent infections; suspected immunodeficiency; eosinophilia	Eosinophilia (asthma/ABPA); lymphopenia (immunodeficiency); neutrophilia (bacterial infection)
Mantoux test / PPD / Interferon-based test for TB ^[14]	Endemic area; contact with TB; chronic cough with FTT; immigrant	Active or latent TB (rare cause of wheeze but important in HK)
Sputum or gastric aspirate for TB ^[14]	Suspected pulmonary TB	AFB smear and culture; young children cannot expectorate → gastric aspirate (swallowed sputum)
HRCT ^[14]	Suspected bronchiectasis, CF, interstitial lung disease, bronchiolitis obliterans	Airway dilatation ("tram-lines" = bronchiectasis); mosaic attenuation (BO); ground-glass opacities (ILD)
Nasal NO / Cilia study ^[14]	Suspected primary ciliary dyskinesia (chronic wet cough from birth, situs inversus, neonatal distress)	Low nasal NO (< 77 nL/min); abnormal ciliary beat pattern/frequency on high-speed video microscopy; electron microscopy of ciliary ultrastructure
Sweat test ^[14]	Suspected CF: chronic productive cough, FTT, steatorrhoea, recurrent infections, digital clubbing	Sweat chloride ≥ 60 mmol/L = diagnostic of CF; 30–59 mmol/L = intermediate (needs CFTR genetic testing)
Immunoglobulin pattern ^[14]	Recurrent sinopulmonary infections; failure to thrive; unusual organisms	Low IgG, IgA, IgM → primary antibody deficiency; low IgG subclasses
pH probe / impedance study ^[14]	Wheeze associated with feeds, vomiting; aspiration suspected	Quantifies gastro-oesophageal reflux episodes; correlates with respiratory symptoms
Video fluoroscopy ^[14]	Suspected aspiration during swallowing; neurodevelopmental abnormality; recurrent aspiration pneumonia	Demonstrates penetration/aspiration of contrast during swallowing
Bronchoscopy with BAL ^[14]	Persistent/unexplained wheeze; suspected FB; suspected chronic infection; structural anomaly	Direct visualisation (FB removal, tracheomalacia); BAL cell differential (eosinophilic vs neutrophilic); microbiology (lipid-laden macrophages suggest aspiration)
Echocardiography	Cardiac murmur, hepatomegaly, failure to thrive, cardiomegaly on CXR	Structural heart disease; LV function; pulmonary hypertension
Flexible nasopharyngoscopy / laryngoscopy	Suspected VCD; stridor component; recurrent croup	Paradoxical vocal cord adduction (VCD); laryngomalacia; subglottic stenosis

This is critical for guiding immediate management. The assessment combines clinical features with objective measures:

Feature	Mild	Moderate	Severe	Life-Threatening
Can speak	Full sentences	Phrases	Unable to complete sentences in one breath ^[9]	Unable to speak
SpO₂	≥ 95%	92–95%	< 92%	< 92%
Respiratory rate	Normal for age	Increased	RR ≥ 25 (older child) ^[9]	Shallow/irregular
Heart rate	Normal for age	Mildly ↑	HR ≥ 110 ^[9]	Bradycardia (pre-arrest)
PEF	> 75% best/predicted	50–75%	33–50% of best or predicted ^[9]	< 33%
Accessory muscles	None	Some	Marked use	Exhaustion / poor effort
Wheeze	End-expiratory	Throughout expiration	Loud, inspiratory + expiratory	Silent chest (ominous — airflow too reduced to generate wheeze)
Consciousness	Normal	Normal	Normal/agitated	Drowsy / confused (CO₂ narcosis)
Other	—	—	—	Cyanosis, bradycardia, hypotension, inability to breathe

The Silent Chest

It is not uncommon for wheezes to be absent during severe asthma exacerbation due to severely reduced airflow ('silent chest') ^[3]. This is paradoxical: the most severe obstruction produces the least audible wheeze because airflow is so reduced that insufficient turbulence is generated. If a previously wheezy child suddenly becomes "quiet" but remains distressed, this is a pre-arrest sign — escalate immediately.

Phase	PaO₂	PaCO₂	pH	Interpretation
Early/Mild	↓ or Normal	↓ (respiratory alkalosis)	↑	Hyperventilation (tachypnoea) blows off CO₂. Hypoxia from V/Q mismatch stimulates ventilation
Moderate	↓	Normal	Normal	"Normalisation" — this is actually an ominous sign: the child is tiring and can no longer hyperventilate to compensate
Severe/Late	↓↓	↑ (respiratory acidosis)	↓	Respiratory muscle fatigue → hypoventilation → CO₂ retention. This child is heading for respiratory arrest

Teaching point: a "normal" PaCO₂ in a tachypnoeic wheezing child should alarm you. A child breathing at 50/min SHOULD be blowing off CO₂ and having a low PaCO₂. If PaCO₂ is "normal" (5.3 kPa / 40 mmHg), it means the child is failing to compensate — they are getting worse, not better. This is a pre-intubation ABG.

Clinical Scenario	Key Investigation	Why
Recurrent wheeze, atopic child > 6 years	Spirometry + BDR	Confirm variable airflow obstruction → asthma
Recurrent wheeze, child 1–5 years, multi-trigger	Clinical assessment + therapeutic ICS trial	Cannot do reliable spirometry; response to ICS supports asthma
First episode wheeze, infant < 12 months, winter	Clinical diagnosis (± NPA for RSV)	Bronchiolitis; investigations rarely change management
Sudden-onset unilateral wheeze, toddler	CXR (inspiratory/expiratory) → rigid bronchoscopy	Foreign body — CXR may be normal; bronchoscopy is definitive
Wheeze + failure to thrive + chronic productive cough	Sweat test ^[14]	CF — must exclude in any child with chronic respiratory symptoms + FTT
Wheeze + situs inversus + chronic wet cough	Nasal NO + cilia study ^[14]	PCD — immotile cilia → chronic airway secretion retention
Wheeze + cardiomegaly/murmur/hepatomegaly	Echocardiography	Congenital heart disease with heart failure
Wheeze + recurrent pneumonia in unusual locations	Immunoglobulin pattern ^[14]; barium swallow / video fluoroscopy ^[14]	Immunodeficiency or structural anomaly (H-type TOF)
Wheeze unresponsive to treatment + inspiratory component	Direct laryngoscopy	Vocal cord dysfunction; structural upper airway lesion

High Yield Summary — Diagnosis of Wheeze in Children

Asthma diagnosis is predominantly clinical — variable symptoms of wheeze/cough/dyspnoea/chest tightness + confirmed variable expiratory airflow limitation ^[3]^[4].
Spirometry in children: FEV₁/FVC ≤ 85–90% indicates obstruction (NOT the adult < 70% cut-off) ^[3]^[4]. Bronchodilator reversibility: ≥ 12% increase in FEV₁ ^[3]^[4].
Preschool children (< 6 years): spirometry unreliable → use clinical pattern, mAPI, and therapeutic ICS trial.
PEF variability > 10% over 1–2 weeks supports asthma ^[3]^[4]. Exercise challenge: > 10% fall in FEV₁ ^[3]^[4].
Bronchoprovocation (methacholine): ≥ 20% fall in FEV₁ — only when lung function at rest is normal ^[3]^[4].
CXR is mainly to exclude alternative diagnoses — normal or hyperinflated ± lobar collapse in asthma ^[3]^[4]. NOT routinely needed for simple bronchiolitis or typical asthma exacerbation.
FeNO > 50 ppb predicts good ICS response ^[4]. Sputum eosinophils > 2% confirms eosinophilic inflammation ^[3]^[4].
A "normal" PaCO₂ in a tachypnoeic wheezing child is an ominous sign — indicates impending respiratory failure.
Silent chest = pre-arrest sign ^[3] — wheeze disappears when airflow is critically reduced.
Investigations for alternative diagnoses ^[14]: sweat test (CF), nasal NO/cilia study (PCD), immunoglobulins (immunodeficiency), pH probe/video fluoroscopy (aspiration), HRCT (bronchiectasis/BO), bronchoscopy (FB/structural).

Active Recall - Diagnosis of Wheeze in Children

References

^[3] Senior notes: Adrian Lui Pediatrics.pdf, p171–172 (Asthma — Diagnosis) ^[4] Senior notes: Ryan Ho Respiratory.pdf, p98 (Asthma — Diagnosis) ^[7] Senior notes: Ryan Ho Cardiology.pdf, p73 (ADHF — CXR findings) ^[9] Senior notes: Ryan Ho Critical Care.pdf, p13–14 (Acute Severe Asthma; Lower Airway Emergencies) ^[12] Lecture slides: GC 141. A child with cough acute and chronic cough in children.pdf, p14 (Acute cough investigations) ^[13] Lecture slides: GC 141. A child with cough acute and chronic cough in children.pdf, p13 (Physical examination) ^[14] Lecture slides: GC 141. A child with cough acute and chronic cough in children.pdf, p26 (Investigations)

Management of Wheeze in Children

A. Acute Asthma Exacerbation in Children

This is the most common acute wheezing emergency in paediatrics. The management follows a stepwise escalation approach.

Step 1: Initial Assessment (First 5 Minutes)

Always assess inhaler technique and adherence before stepping up! ^[3]

ABCDE approach — is the child in immediate danger?
Assess severity (see Diagnosis section) — mild/moderate vs severe vs life-threatening
Key features to identify immediately:

Life-threatening features ^[4]^[9]	Action
Silent chest	Immediate escalation
Hypotension	IV access, fluid bolus, ICU
PEF < 33% of best/predicted	ICU referral
Cyanosis	High-flow O₂
Confusion / altered consciousness	Prepare for intubation
Bradycardia	Pre-arrest — call for help
Exhaustion / poor respiratory effort	Impending arrest

Features warranting ICU care ^[3]^[4]: Life-threatening features present; deterioration in PEF/FEV₁; worsening or persistent hypoxia or hypercapnia; respiratory failure requiring IPPV; respiratory or cardiorespiratory arrest

Step 2: Immediate Treatment

Oxygen

Controlled O₂ therapy aiming SpO₂ 93–95% ^[4] by nasal cannulae or face mask
High-flow O₂ to keep SpO₂ 94–98% in acute severe/life-threatening episodes ^[9]
Why 93–95% target? Over-oxygenation can worsen V/Q mismatch (by releasing hypoxic pulmonary vasoconstriction in poorly ventilated areas) and suppress respiratory drive (less relevant in children than adults, but still applies in severe asthma with CO₂ retention)

Inhaled Short-Acting β₂-Agonist (SABA)

Drug: Salbutamol ("sal-BUTA-mol" — selective β₂-adrenoceptor agonist)
Mechanism: binds β₂ receptors on airway smooth muscle → activates adenylyl cyclase → ↑cAMP → phosphorylation and inhibition of myosin light chain kinase (MLCK) → smooth muscle relaxation → bronchodilation ^[4]
Onset: 1–5 minutes (rapid); Duration: 4–6 hours

Paediatric dosing (age-appropriate formulations):

Severity	Route	Dose	Frequency
Mild-moderate	MDI + spacer ^[4]	4–10 puffs (100 µg/puff)	Every 20 min for first hour ^[4], then Q1–4H as needed
Severe	Nebuliser with O₂	2.5 mg (< 5 years) or 5 mg (≥ 5 years) ^[9]	Repeated / back-to-back nebulisation ^[9], then Q1–2H
Life-threatening / refractory	IV (if available)	15 µg/kg bolus then 1–5 µg/kg/min infusion	Continuous; requires cardiac monitoring

MDI + Spacer = Nebuliser

Use of MDI + spacer or DPI is associated with similar improvement in lung function compared to nebuliser ^[4]. In fact, MDI + spacer is preferred in mild-moderate exacerbations because:

Faster to administer
Less staff-dependent
Lower risk of cardiac side effects (more controlled dosing)
Teaches the child the technique they will use at home

Reserve nebulisers for severe or life-threatening exacerbations where the child cannot coordinate with a spacer or needs continuous delivery.

Side effects of salbutamol (all dose-related):

Tremor: β₂ receptors on skeletal muscle → direct stimulation
Tachycardia/palpitations: β₂-mediated peripheral vasodilation → reflex tachycardia; at high doses, some β₁ cross-reactivity
Hypokalaemia: β₂ stimulation drives K⁺ into cells via Na⁺/K⁺-ATPase activation — monitor K⁺ with frequent/continuous nebulisation
Lactic acidosis: β₂-mediated glycogenolysis → ↑lactate

Systemic Corticosteroids

Drug: Oral prednisolone (preferred if child can swallow) or IV hydrocortisone (if vomiting/unable to take PO/severe) ^[3]^[4]^[9]
Mechanism: corticosteroids suppress the inflammatory cascade at multiple levels — ↓transcription of pro-inflammatory cytokines (IL-4, IL-5, IL-13), ↓eosinophil survival, ↓mast cell mediator release, ↓vascular permeability (reducing mucosal oedema), upregulate β₂-receptor expression (restoring bronchodilator responsiveness)
Onset: takes 3–4 hours to show clinical effect (genomic mechanism requires protein synthesis) — hence give early
Oral is as effective as IV ^[4] — there is no benefit to IV over oral if the child can tolerate oral medication

Paediatric dosing:

Route	Drug	Dose	Duration
Oral	Prednisolone	1–2 mg/kg/day (max 40 mg < 12y; max 50 mg ≥ 12y)	3–5 days ^[3]^[4] (no taper needed for short courses)
IV	Hydrocortisone	50–100 mg Q6–8H ^[4] (adjust by weight: 4 mg/kg Q6H in young children)	Until able to take oral

Prednisolone tablets for 3–5 days is adequate for most patients ^[3]. Short courses (≤5 days) do NOT require tapering as the hypothalamic-pituitary-adrenal axis has not yet been suppressed.

Inhaled Short-Acting Muscarinic Antagonist (SAMA) — Ipratropium Bromide

Drug: Ipratropium bromide ("ipra-TROP-ium" — anti-muscarinic/anti-cholinergic)
Mechanism: blocks muscarinic M₃ receptors on airway smooth muscle → prevents acetylcholine-mediated bronchoconstriction; also ↓mucus secretion from submucosal glands
Why add to SABA? Complementary mechanism — SABA works via β₂ (sympathetic) pathway while SAMA blocks the parasympathetic pathway. Together = synergistic bronchodilation
Associated with ↓hospitalisation and ↑PEF/FEV₁ improvement compared to SABA alone in moderate-severe attacks ^[4]

Paediatric dosing:

Route	Dose	Frequency
Nebuliser	250 µg (< 5y) or 500 µg (≥ 5y) ^[9]	Q4–6H; can give Q20 min in first hour for severe attacks
MDI + spacer	4–8 puffs (20 µg/puff)	Q4–6H

Side effects: dry mouth, urinary retention (rare in children), paradoxical bronchospasm (rare — due to hypertonic nebuliser solution, not the drug itself)

IV Magnesium Sulphate (MgSO₄) — For Severe/Refractory Cases

Consider IV MgSO₄ if refractory or severe ^[3]^[9]
MoA: thought to ↓Ca²⁺ influx in airway smooth muscles ^[4] → smooth muscle relaxation → bronchodilation. Also inhibits mast cell degranulation and acetylcholine release from nerve endings
Dosing: 1.2–2 g IV (adults) / 40–50 mg/kg IV (max 2 g) over 20 minutes ^[4]^[9]
Caution: hypotension, CKD (↑risk of hyperMg → paralysis) ^[4]
Paediatric note: particularly useful in children as an escalation step before considering IV salbutamol or aminophylline; relatively safe and well-tolerated

IV Aminophylline — Last Resort

Consider IV aminophylline if refractory or severe ^[3]
Mechanism: phosphodiesterase inhibitor → ↑cAMP → bronchodilation; also adenosine receptor antagonist → reduces mast cell mediator release
Narrow therapeutic profile with poor efficacy ^[4] — risk of toxicity (seizures, arrhythmias) is significant
Paediatric dosing: Loading dose 5 mg/kg IV over 20 min (omit if already on theophylline), then maintenance infusion 0.5–1 mg/kg/hr; requires serum level monitoring (target 10–20 mg/L)
Generally avoided in modern paediatric practice unless in PICU setting with failure of all other therapies

Step 3: Reassessment

Reassessment in ALL patients 1 hour after initial treatment ^[3]:

Assess: clinical status, response to treatment, lung function measurement (PEF, FEV₁) ^[3]

Response	Action
Satisfactory response	Controlled O₂ to aim 93–95%, gradual weaning; continue steroids 3–5 days; continue SABA Q1–2H ^[3]
Unsatisfactory response	↑dose of SABA; add inhaled ipratropium bromide ^[3]; consider IV MgSO₄
Life-threatening / deteriorating	ICU admission ^[3]^[4]; IV salbutamol or aminophylline; prepare for intubation and IPPV

Step 4: Discharge Planning

Home when symptoms cleared, PEF/FEV₁ > 75% predicted/best ^[3]

Hospital admission is a window of opportunity to review ^[3]:

Inhaler technique
Compliance
Environment

Upon discharge ^[3]:

Identify + avoid risk factors for current attack
Oral corticosteroids: prednisolone tablets × 3–5 days
Early outpatient or ward follow-up + review long-term treatment plan + review inhaler technique
- Mild/moderate: follow-up general or asthma clinic in 3–4 months
- Severe: ward follow-up in 1 week, then asthma clinic in 1 month

What NOT to Give in Acute Asthma

Avoid ^[4]:

Antibiotics (unless strong evidence of bacterial infection — most exacerbations are viral)
Aminophylline/theophylline (narrow therapeutic window, poor efficacy relative to risk)
Sedatives/cough suppressants (suppress respiratory drive → dangerous)
Mucolytics (no evidence of benefit; may worsen cough)

Part 2: Long-Term / Chronic Management of Asthma in Children

Identification of triggering factors through clinical history ^[3]^[4]

Assessment of asthma control by two domains ^[3]^[4]:

Domain	Well Controlled	Partly Controlled	Uncontrolled
Daytime symptoms	≤ 2×/week	> 2×/week
SABA reliever use	≤ 2×/week	> 2×/week	≥ 3 features of
Night waking	None	Any	partly controlled
Activity limitation	None	Any

Severity of asthma: assessed retrospectively from level of treatment required to control symptoms and exacerbation ^[3]^[4]:

Mild asthma: well-controlled with Steps 1 or 2 ^[3]^[4]
Moderate asthma: well-controlled with Step 3 ^[3] (or Step 3 or 4 ^[4])
Severe asthma: well- or poorly controlled with Steps 4 or 5 ^[3] (or Step 5 ^[4])

GINA 2023/2024 Stepwise Approach

The GINA guidelines offer two tracks ^[4]:

This is the preferred approach for children ≥ 12 years and adults because it ensures that every time the child uses their reliever, they also get an anti-inflammatory (ICS) dose — reducing the risk of undertreated inflammation.

Step	Controller	Reliever	When to Use
Step 1	None (or as-needed low-dose ICS-formoterol)	As-needed low-dose ICS-formoterol	Symptoms < 2×/month
Step 2	Low-dose ICS-formoterol daily	As-needed low-dose ICS-formoterol	Symptoms ≥ 2×/month but not daily
Step 3	Medium-dose ICS-formoterol daily	As-needed low-dose ICS-formoterol	Symptoms most days or waking ≥ 1×/week
Step 4	Medium/high-dose ICS-formoterol + add-on (LAMA or LTRA)	As-needed low-dose ICS-formoterol	Persistent despite Step 3
Step 5	High-dose ICS-formoterol + LAMA ± biologic	As-needed low-dose ICS-formoterol	Refer to specialist / severe asthma phenotyping

SMART = Single Maintenance and Reliever Therapy ^[3]: uses the same ICS-formoterol device for both daily maintenance and acute relief. Recommended for children ≥ 12 years as Steps 3–5 ^[3]. In QMH, SMART can be considered (using Symbicort) when there are concerns about adherence to controller and SABA overuse ^[3].

This is more commonly used in younger children (6–11 years) where ICS-formoterol combination data is still evolving:

Step	Controller	Reliever	When to Use
Step 1	ICS whenever SABA taken ^[4] (or low-dose ICS taken with each SABA dose)	As-needed SABA	Infrequent symptoms
Step 2	Low-dose ICS daily ^[4] (alternatives: daily LTRA, or add HDM SLIT)	As-needed SABA	Symptoms ≥ 2×/month
Step 3	Medium-dose ICS, or low-dose ICS + LABA, or add LTRA, or add HDM SLIT ^[4]	As-needed SABA	Symptoms most days
Step 4	Medium/high-dose ICS + LABA ± LAMA or LTRA or HDM SLIT ^[4]	As-needed SABA	Persistent despite Step 3
Step 5	High-dose ICS + LABA + add LAMA + phenotype-guided biologics	As-needed SABA	Specialist management

Feature	Difference
ICS dose definitions	"Low dose" in 6–11y is lower than in ≥ 12y (e.g., budesonide low = 100–200 µg vs 200–400 µg)
LABA	Can be added from Step 3; salmeterol or formoterol approved ≥ 4–6 years
SMART	Less evidence in 6–11y; more commonly used in ≥ 12y
Biologics	Omalizumab approved ≥ 6y; mepolizumab ≥ 6y; dupilumab ≥ 6y

Drug Details

Bronchodilators

Feature	Detail
Example	Salbutamol (Ventolin) ^[4]
Mechanism	β₂-agonist → ↑cAMP → smooth muscle relaxation (see above)
Onset / Duration	1–5 min / 4–6 hours
Route	MDI + spacer (preferred), nebuliser, IV (severe)
Paediatric dose (MDI)	100 µg/puff; 2–4 puffs PRN (up to 10 puffs in acute exacerbation)
Indication	Reliever for breakthrough symptoms; pre-exercise prophylaxis
Side effects	Tremor, tachycardia, hypokalaemia, lactic acidosis (high dose)
Contraindication	No absolute contraindications in acute wheeze
Important note	Over-reliance on SABA without controller → undertreated inflammation → ↑risk of severe exacerbation and death

Feature	Detail
Examples	Salmeterol, formoterol
Mechanism	Same as SABA but with longer lipophilic side chain → binds to receptor for 12+ hours
Key difference	Formoterol has rapid onset (1–3 min) → can function as reliever (basis of SMART); Salmeterol has slow onset (15–30 min) → controller only
Route	MDI + spacer or DPI
Indication	Step 3+ as add-on controller with ICS; NEVER as monotherapy (increases risk of asthma death if used without ICS — black box warning)
Contraindication	Monotherapy without ICS

Feature	Detail
Example	Ipratropium bromide
Mechanism	Blocks M₃ muscarinic receptors → ↓parasympathetic bronchoconstriction
Indication	Add-on in acute severe exacerbation; associated with ↓hospitalisation vs SABA alone in moderate-severe attacks ^[4]
Side effects	Dry mouth, urinary retention (rare), paradoxical bronchospasm (rare)

Feature	Detail
Example	Tiotropium (Spiriva Respimat)
Mechanism	Selective M₃ blockade → 24-hour bronchodilation
Paediatric approval	≥ 6 years as add-on at Step 4–5
Indication	Persistent symptoms despite medium/high-dose ICS + LABA

Anti-Inflammatory Agents

ICS: MAINSTAY of asthma treatment, regular use as controller ^[4]

Feature	Detail
Examples	Beclomethasone (Becloforte 250 µg, Beclotide 50 µg), budesonide (Pulmicort), fluticasone (Flixotide) ^[4]
Mechanism	Binds intracellular glucocorticoid receptor → translocates to nucleus → suppresses transcription of pro-inflammatory genes (IL-4, IL-5, IL-13, TNF-α, COX-2) + upregulates anti-inflammatory genes (lipocortin-1, β₂-receptor)
Effect	↑symptom control, ↓exacerbation, ↓mortality, ↓lung function decline ^[4]
Onset	Takes 2–4 weeks to reach full effect ^[4] — educate families to be patient and continue daily use
Side effects	Minimal systemic effect, but risk of oral candidiasis (5–10%) ^[4]
Prevention of oral candidiasis	Post-administration mouthwash or spacer use ^[4]
Treatment of oral candidiasis	Nystatin suspension for gargle or lozenge ^[4]
Growth effect	ICS may cause 0.5–1 cm reduction in growth velocity in the first 1–2 years; this effect is small and non-progressive; final adult height is minimally affected (0.7 cm on average). Benefits greatly outweigh risks
Contraindication	Hypersensitivity to components (very rare)

ICS Dose Equivalents (Children 6–11 years):

ICS	Low Dose	Medium Dose	High Dose
Beclomethasone dipropionate	100–200 µg/day	200–400 µg/day	> 400 µg/day
Budesonide	100–200 µg/day	200–400 µg/day	> 400 µg/day
Fluticasone propionate	50–100 µg/day	100–200 µg/day	> 200 µg/day

Montelukast ("monte-luka-st" — antagonist of the leukotriene receptor)

Feature	Detail
Examples	Montelukast (Singulair), zafirlukast ^[4]
Mechanism	Block action of leukotriene (arachidonic acid derivative) → ↓bronchoconstriction ^[4]. Leukotrienes (LTC₄, LTD₄, LTE₄) are 100–1000× more potent bronchoconstrictors than histamine and also ↑mucus secretion and vascular permeability
Route	Oral daily drug ^[4]
Indication	Steroid-sparing therapy in mild/moderate asthma; especially effective in exercise- and aspirin-induced asthma ^[4]
Paediatric dose	4 mg (2–5y), 5 mg (6–14y), 10 mg (≥ 15y) — once daily at bedtime
Side effect note	Can unmask previously undiagnosed Churg-Strauss syndrome ^[4]; FDA black box warning (2020) for neuropsychiatric events (agitation, sleep disturbance, depression) — discuss with families
Contraindication	Hypersensitivity; use with caution in patients with neuropsychiatric history

Anti-IgE Antibody ^[4]:

Feature	Detail
Example	Omalizumab ^[4]
Mechanism	Binds IgE → ↓activation of mast cells and basophils ^[4]
Route	SC injection Q2–4 weeks ^[4]
Indication	Atopic asthma (documented ↑IgE, +ve skin prick test) with suboptimal control despite max treatment, or steroid-sparing in steroid-dependent asthma ^[4]. Approved ≥ 6 years
Side effect	Anaphylaxis ^[4] (0.1–0.2%) — observe 2h post-injection

Anti-IL-5 Therapy ^[4]:

Feature	Detail
Examples	Mepolizumab, reslizumab (anti-IL5), benralizumab (anti-IL5 receptor) ^[4]
Mechanism	Block action of IL-5 → ↓eosinophilic airway inflammation ^[4]
Indication	Eosinophilic asthma with ↑serum eosinophil count ^[4]. Mepolizumab approved ≥ 6 years

Anti-IL-4/13 Therapy:

Feature	Detail
Example	Dupilumab
Mechanism	Blocks IL-4 and IL-13 signalling via IL-4Rα → ↓Th2 inflammation, ↓IgE class switching, ↓mucus production, ↓eosinophil recruitment
Indication	Moderate-severe eosinophilic or OCS-dependent asthma; approved ≥ 6 years

Feature	Detail
Example	Theophylline (oral), aminophylline (IV)
Mechanism	Non-selective phosphodiesterase inhibitor → ↑cAMP → bronchodilation; also adenosine receptor antagonist
Therapeutic profile	Narrow therapeutic index ^[4]; target level 10–20 mg/L
Side effects at toxicity	Arrhythmias (SVT/VT), hypotension, seizures ^[4]
Role in paediatrics	Largely superseded by LABAs and biologics; reserved for PICU refractory cases

Part 3: Specific Management by Aetiology

Management is supportive — there is no specific antiviral or anti-inflammatory therapy with proven benefit:

Intervention	Detail	Evidence
Supplemental O₂	If SpO₂ < 92% persistently; nasal cannulae or high-flow nasal cannula (HFNC)	HFNC provides humidified, heated O₂ with some CPAP effect — increasingly used
Feeding support	Small frequent feeds; NG tube feeds if unable to maintain oral intake; IV fluids if NG not tolerated	Respiratory distress impairs suck-swallow-breathe coordination
Nasal suctioning	Gentle bulb syringe or suction catheter before feeds and PRN	Infants are obligate nasal breathers; clearing nasal secretions improves feeding and breathing
Salbutamol	NOT routinely recommended	Multiple RCTs show no benefit in bronchiolitis — the obstruction is from mucosal oedema/debris, not bronchospasm
Corticosteroids	NOT recommended	No benefit shown; Cochrane reviews consistently negative
Antibiotics	NOT indicated unless secondary bacterial infection suspected	Bronchiolitis is viral
Hypertonic saline	3% nebulised NaCl may reduce hospital stay if admitted	Draws water into airway lumen → loosens secretions; evidence is modest
Palivizumab	Monoclonal anti-RSV antibody for prophylaxis (not treatment) in high-risk infants (ex-premature, BPD, haemodynamically significant CHD)	Given monthly IM during RSV season

Step	Action
If choking and conscious	Back blows (infant) or abdominal thrusts / Heimlich manoeuvre (child > 1 year)
If choking and unconscious	CPR + call for help; look in mouth before each ventilation
If partial obstruction	Keep child calm; do NOT attempt blind finger sweep; urgent transfer to hospital
Definitive management	Rigid bronchoscopy — diagnostic and therapeutic (visualise and remove FB under GA)
Post-removal	Repeat bronchoscopy if clinical concern for retained fragments; follow-up CXR

Management: clinical diagnosis (no absolute C/I to epinephrine in anaphylaxis) ^[9]

Step	Action	Paediatric Dose
1st and most important	IM epinephrine 1:1000 ^[9]	0.01 mg/kg (max 0.3 mg < 6y; max 0.5 mg ≥ 12y) — mid-outer thigh ^[9]
Repeat	Every 5–15 min as needed ^[9]	Same dose
Airway	Secure; intubate if angioedema threatens airway ^[9]	—
Breathing	100% O₂ ^[9]	—
Circulation	IV NS bolus 20 mL/kg ^[9]	Repeat as needed
Adjuncts	Antihistamines (chlorphenamine); steroids (hydrocortisone); bronchodilators (nebulised salbutamol) ^[9]	Age-adjusted doses

Always assess inhaler technique and adherence before stepping up! ^[3]

Age	Recommended Device	Technique
0–3 years	MDI + spacer + face mask	Parent holds mask firmly over child's nose and mouth; actuate MDI into spacer; child breathes tidally through mask for 5–10 breaths
3–5 years	MDI + spacer + mouthpiece	Child forms seal around mouthpiece; single slow deep breath after actuation + 10-second breath-hold (if able) or 5–10 tidal breaths
≥ 6 years	MDI + spacer or DPI	Slow deep inhalation (MDI + spacer) or fast deep inhalation (DPI); 10-second breath-hold

Why Spacers Matter

Without a spacer, ~80% of the MDI dose impacts on the oropharynx (causing local side effects and swallowed systemic absorption) and only ~10–20% reaches the lungs. A spacer:

Slows particle velocity → ↓oropharyngeal impaction
Allows large particles to sediment out → only fine particles (< 5 µm) inhaled
Eliminates need to coordinate actuation with inhalation (critical for young children)
Increases lung deposition to ~20–40%

High Yield Summary — Management of Wheeze in Children

Acute Management:

ABCDE first. Life-threatening features (silent chest, hypotension, cyanosis, confusion) → ICU ^[3]^[4].
O₂ to target SpO₂ 93–95% ^[4]; high-flow O₂ for severe/life-threatening.
Inhaled SABA (salbutamol) is first-line bronchodilator — MDI + spacer is as effective as nebuliser ^[4].
Systemic corticosteroids early — oral prednisolone is as effective as IV ^[4]; 3–5 days, no taper needed ^[3].
Add ipratropium for severe attacks — synergistic with SABA, ↓hospitalisation ^[4].
IV MgSO₄ for refractory severe — works by ↓Ca²⁺ influx in smooth muscle ^[4].
Aminophylline is last resort — narrow therapeutic index ^[4].
Reassess ALL patients at 1 hour ^[3]; discharge when PEF > 75% ^[3].

Long-Term Management: 9. Control-based stepwise approach — adjust treatment based on control assessment ^[3]^[4]. 10. ICS is the MAINSTAY controller — takes 2–4 weeks for full effect ^[4]; prevent oral candidiasis with spacer + mouth rinse ^[4]. 11. GINA Track 1 (preferred ≥ 12y): ICS-formoterol as both controller and reliever (SMART) ^[3]^[4]. 12. LABA must NEVER be used as monotherapy — always with ICS. 13. Biologics (omalizumab, mepolizumab, dupilumab) for severe asthma ≥ 6 years — phenotype-guided ^[4]. 14. Always check inhaler technique and adherence before stepping up! ^[3]

Cause-Specific: 15. Bronchiolitis: supportive only — salbutamol and corticosteroids NOT recommended. 16. Foreign body: rigid bronchoscopy is definitive. 17. Cardiac wheeze: treat underlying CHD + diuretics — salbutamol ineffective. 18. Anaphylaxis: IM epinephrine first and most important ^[9].

Active Recall - Management of Wheeze in Children

Complications of Wheeze in Children

Complications of wheeze depend entirely on the underlying cause and its severity/chronicity. We will organise this section by:

Complications of acute wheezing episodes (i.e., the acute exacerbation itself)
Complications of the underlying diseases causing wheeze (asthma, bronchiolitis, etc.)
Complications of treatment (iatrogenic)

The key principle: complications arise either from the direct pathophysiology of airway obstruction (hypoxia, air trapping, respiratory failure) or from the chronic inflammatory/structural damage that the disease inflicts over time.

1. Complications of Acute Wheezing Episodes

These complications are shared across most causes of acute wheeze because they all stem from the same final common pathway — airway obstruction → air trapping → V/Q mismatch → respiratory compromise.

Type	Mechanism	Clinical Features	When to Suspect
Type 1 Respiratory Failure (hypoxaemic)	V/Q mismatch from uneven airway obstruction → some alveoli ventilated poorly → ↓PaO₂ with normal/low PaCO₂ (because hyperventilation compensates for CO₂)	Tachypnoea, SpO₂ < 92%, cyanosis, agitation	Early-to-moderate exacerbation; child is working hard to compensate
Type 2 Respiratory Failure (hypercapnic)	Severe obstruction → respiratory muscle fatigue → hypoventilation → ↑PaCO₂ AND ↓PaO₂	Drowsiness, confusion, shallow breathing, "normal" PaCO₂ in a tachypnoeic child (ominous — see Diagnosis section)	Late/severe exacerbation; the child is tiring — this is a pre-arrest sign

Why does asthma cause Type 2 failure? In severe obstruction, the work of breathing becomes enormous (imagine breathing through a straw). The diaphragm — especially in young children with fewer type I fatigue-resistant muscle fibres — cannot sustain this effort. As muscles fatigue, tidal volume drops, dead space ventilation increases, and CO₂ accumulates. This is the pathway from "severe" to "life-threatening" to cardiorespiratory arrest.

Features warranting ICU care ^[3]^[4]:

Life-threatening features present (silent chest, hypotension, cyanosis, confusion)
Deterioration in PEF/FEV₁
Worsening or persistent hypoxia or hypercapnia
Respiratory failure requiring IPPV
Respiratory or cardiorespiratory arrest

Complication	Mechanism	Clinical Features
Pneumothorax	Severe air trapping → alveolar overdistension → rupture of alveolar wall → air escapes into pleural space	Sudden worsening dyspnoea, pleuritic chest pain, unilateral ↓air entry, hyperresonance; tension pneumothorax if air accumulates under pressure → mediastinal shift, cardiovascular collapse
Pneumomediastinum	Air dissects along perivascular sheaths from ruptured alveoli into mediastinum (Macklin effect)	Subcutaneous emphysema (crepitus in neck/chest), muffled heart sounds; usually self-limiting but can progress to pneumothorax
Subcutaneous emphysema	Extension of pneumomediastinum into subcutaneous tissues	Palpable crepitus over neck, chest wall, face

Why does air trapping lead to air leak? In obstructive airway disease, expiration is incomplete → progressive hyperinflation → alveolar pressure rises well above atmospheric pressure. If the pressure exceeds the structural integrity of the alveolar wall (especially at the junction between alveolar septa and perivascular connective tissue), the wall ruptures. The escaped air follows the path of least resistance — along the bronchovascular sheath to the mediastinum, then potentially into the pleural space or subcutaneous tissues.

This is particularly relevant in:

Severe acute asthma with significant air trapping
Bronchiolitis in ventilated infants (barotrauma/volutrauma)
Foreign body aspiration with ball-valve effect causing massive unilateral hyperinflation

Problem	Mechanism
Dehydration	↑respiratory rate → ↑insensible water loss from airways; ↓oral intake (too breathless to drink/eat); vomiting from swallowed air or medication side effects
Hypokalaemia	β₂-agonist therapy (salbutamol) drives K⁺ intracellularly via Na⁺/K⁺-ATPase; systemic corticosteroids cause renal K⁺ loss; important to monitor in children receiving frequent/continuous nebulised salbutamol
Lactic acidosis	β₂-agonist-mediated glycogenolysis → ↑serum lactate; also tissue hypoperfusion in severe cases
Hyponatraemia	Inappropriate ADH secretion (SIADH) can occur in severe respiratory disease; also from hypotonic fluid administration in dehydrated wheezing children

2. Complications of Specific Underlying Diseases

Complication	Mechanism	Clinical Relevance
Airway remodelling	Chronic uncontrolled eosinophilic inflammation → smooth muscle hyperplasia, goblet cell hyperplasia, subepithelial fibrosis, airway wall thickening ^[3]^[4]	Leads to fixed (irreversible) airflow obstruction — the component that does NOT respond to bronchodilators. This is why early and consistent ICS use is crucial
Growth impairment	Poorly controlled severe asthma → chronic hypoxia, systemic inflammation, ↓physical activity, ↓nutritional intake; also high-dose systemic corticosteroid use → growth suppression	More relevant to severe/frequent exacerbation-prone phenotype; ICS at standard doses cause minimal growth effect (~0.5–1 cm reduction in growth velocity in first 1–2 years, with minimal impact on final adult height)
Psychosocial impact	Chronic disease with recurrent exacerbations → school absenteeism, exercise avoidance, anxiety/depression, family stress, sleep disturbance	Must be actively addressed; asthma action plans and family-centred care improve outcomes
Reduced exercise capacity	Combination of exercise-induced bronchoconstriction + deconditioning from exercise avoidance	Paradoxically, regular exercise improves asthma control; children should be encouraged to exercise with appropriate pre-treatment
Samter's triad complications	Chronic rhinosinusitis + nasal polyposis + aspirin-exacerbated respiratory symptoms ^[4] — worsening cycle of inflammation	More relevant in older adolescents/adults; COX-1 inhibition shunts arachidonic acid to leukotriene pathway

Airway Remodelling Is the Key Long-Term Complication

The reason we insist on regular ICS use even when asymptomatic is to prevent airway remodelling. Every inadequately treated exacerbation contributes to cumulative structural damage. Over years, this produces irreversible fixed obstruction — essentially converting asthma into a COPD-like phenotype. ICS takes 2–4 weeks for full effect ^[4] — but the remodelling it prevents is permanent.

Complication	Mechanism	Notes
Apnoea	Particularly in premature infants and those < 6 weeks; mechanism may involve direct RSV effect on brainstem respiratory centre or vagal reflex from nasopharyngeal inflammation	An important reason for hospital admission in young infants with bronchiolitis — may present BEFORE significant lower respiratory signs
Respiratory failure	Severe small airway obstruction → V/Q mismatch → hypoxaemia; may progress to hypercapnic failure in exhausted infants	HFNC or CPAP used as respiratory support; intubation and ventilation if these fail
Secondary bacterial infection	Viral destruction of respiratory epithelium → impaired mucociliary clearance → bacterial superinfection (S. pneumoniae, H. influenzae)	Suspect if persistent/recrudescent fever after initial improvement; true secondary bacterial pneumonia is relatively uncommon (~1–2%)
Post-bronchiolitis recurrent wheeze	~30–40% of infants with severe RSV bronchiolitis develop recurrent wheeze in early childhood; mechanism debated (viral-induced airway remodelling vs. unmasking of pre-existing airway vulnerability)	Most outgrow this by school age; those who develop persistent multi-trigger wheeze may go on to true asthma
Dehydration / feeding failure	Respiratory distress impairs coordination of suck-swallow-breathe in infants; ↑insensible losses from tachypnoea	NG feeds or IV fluids often required for hospitalised infants
Air leak	Particularly in ventilated infants; mucus plugging causes ball-valve effect → hyperinflation → alveolar rupture	Pneumothorax, pneumomediastinum
SIADH	Inappropriate ADH secretion triggered by severe respiratory disease → dilutional hyponatraemia	Monitor serum Na⁺ in hospitalised infants; use isotonic fluids

Complication	Mechanism	Clinical Features
Complete airway obstruction	FB completely blocks bronchus → no airflow → respiratory arrest (if bilateral/tracheal) or lobar atelectasis (if unilateral)	Acute: choking, inability to cough/cry/speak. Chronic: persistent lobar collapse
Recurrent/non-resolving pneumonia	Retained FB → chronic mucosal irritation → bacterial colonisation → infection distal to obstruction	Recurrent pneumonia (≥ 2 episodes/year or ≥ 3 episodes anytime with radiographic clearing in between) should prompt investigation for structural cause including FB ^[16]
Bronchiectasis	Long-standing unrecognised FB → chronic infection → irreversible airway dilatation	Particularly if FB is organic (e.g., peanut) which incites intense granulomatous inflammation
Granulation tissue formation	Chronic irritation from retained FB → exuberant granulation tissue around FB → further narrowing and making extraction more difficult	Delayed presentation → complex bronchoscopic or surgical extraction needed
Post-obstructive emphysema	Ball-valve effect → progressive air trapping → hyperinflation distal to FB → compression of adjacent normal lung	Unilateral hyperinflation on CXR

Complication	Mechanism	Notes
Bronchiectasis	Chronic neutrophilic airway infection → protease-mediated destruction of airway wall → irreversible dilatation	Progressive; the hallmark of advanced CF lung disease
Chronic infection	Impaired mucociliary clearance → bacterial colonisation: early = S. aureus, H. influenzae; late = P. aeruginosa, Burkholderia cepacia	Pseudomonas acquisition is a particularly poor prognostic marker
ABPA	Allergic sensitisation to Aspergillus fumigatus ^[5] → Type I + III hypersensitivity → central bronchiectasis, mucus plugging	15% of CF patients have asthma-type symptoms ^[5]
Pneumothorax	Rupture of subpleural blebs from chronic air trapping and bullous disease	~5–8% of CF patients; recurrence common
Massive haemoptysis	Erosion of hypertrophied bronchial arteries (part of chronic inflammatory neovascularisation)	Life-threatening; may require bronchial artery embolisation
Respiratory failure	End-stage lung disease → progressive decline in FEV₁ → chronic hypoxaemia → cor pulmonale	Lung transplantation is the definitive treatment for end-stage CF

Complication	Mechanism	Notes
Eisenmenger syndrome	Large unrepaired L-to-R shunt → destruction of pulmonary arterioles → irreversible pulmonary vascular disease → reversal of shunt → cyanosis ^[17]	Once established, the only curative option is heart-lung transplant; pregnancy is contraindicated (maternal mortality 30–50%) ^[17]
Heart failure progression	Continued pulmonary overcirculation → progressive LV volume overload → cardiac dilatation and failure	Manifests as worsening wheeze, tachypnoea, hepatomegaly, poor feeding, FTT
Recurrent lower respiratory tract infections	Pulmonary congestion creates a favourable environment for bacterial proliferation; also ↓immune defence from chronic hypoxia	Important cause of morbidity in unrepaired CHD
Failure to thrive	↑metabolic demand from cardiac workload + ↓caloric intake from feeding difficulty + ↓absorption from gut oedema	Growth monitoring is essential in any child with CHD
Pulmonary hypertension	Chronic ↑pulmonary blood flow → endothelial damage → medial hypertrophy → intimal fibrosis → ↑PVR	Precursor to Eisenmenger syndrome; early surgical correction prevents this

Treatment	Complication	Mechanism	Prevention/Management
Inhaled SABA (salbutamol)	Tremor, tachycardia	β₂ stimulation of skeletal muscle and cardiac β₁ cross-reactivity	Dose-related; usually self-limiting; use MDI + spacer for more controlled dosing
	Hypokalaemia	β₂-mediated K⁺ shift into cells via Na⁺/K⁺-ATPase	Monitor K⁺ with frequent nebulisation; replace as needed
	Lactic acidosis	β₂-mediated glycogenolysis	Monitor lactate; avoid over-interpreting as "tissue hypoperfusion"
ICS	Oral candidiasis (5–10%) ^[4]	Local immunosuppression + altered oral flora from steroid deposition on oropharyngeal mucosa	Prevention: spacer use + post-inhalation mouth rinse/gargle. Treatment: nystatin suspension ^[4]
	Dysphonia	Steroid myopathy of laryngeal muscles from local deposition	Use spacer to reduce oropharyngeal deposition; voice rest
	Growth suppression	Systemic absorption → ↓GH-IGF1 axis (mild)	~0.5–1 cm/year in first 1–2 years; minimal effect on final adult height; monitor growth centiles
	Adrenal suppression	High-dose ICS → sufficient systemic absorption to suppress HPA axis (rare at standard doses)	Use lowest effective ICS dose; educate about sick-day steroid rules if on high-dose ICS
Systemic corticosteroids	Weight gain, growth suppression	Catabolic effects, ↑appetite, fluid retention, ↓bone formation	Short courses (3–5 days) for exacerbations → minimal risk; long-term OCS → significant risks
	Adrenal suppression	Exogenous steroid → negative feedback on CRH/ACTH → adrenal atrophy	Relevant if > 2 weeks of daily systemic steroids; requires gradual tapering
	Osteopenia	↓osteoblast activity, ↑osteoclast activity, ↓calcium absorption	Monitor bone health in children on frequent OCS courses
	Immunosuppression	Global suppression of immune response	↑risk of infections; avoid live vaccines during courses
	Behavioural/mood changes	CNS effects of corticosteroids (irritability, hyperactivity, sleep disturbance)	Common in children; warn families; usually resolves when course ends
IV aminophylline	Arrhythmias (SVT/VT), hypotension, seizures ^[4]	Narrow therapeutic index; phosphodiesterase inhibition → ↑cAMP in cardiac and CNS tissue	Monitor serum levels (target 10–20 mg/L); avoid if possible
LTRA (montelukast)	Can unmask Churg-Strauss syndrome ^[4]; neuropsychiatric effects (agitation, sleep disturbance, depression — FDA black box warning)	Mechanism unclear; possibly ↓steroid use unmasks underlying eosinophilic vasculitis; direct CNS effects of leukotriene modulation	Discuss with families; monitor mood/behaviour; discontinue if significant neuropsychiatric effects
Biologics (omalizumab)	Anaphylaxis ^[4]	Immune reaction to monoclonal antibody protein	Observe for 2 hours post-injection; ensure anaphylaxis kit available
Mechanical ventilation (for severe exacerbation)	Barotrauma, volutrauma, ventilator-associated pneumonia	Positive pressure ventilation in hyperinflated lungs → alveolar rupture; prolonged intubation → nosocomial infection	Use lung-protective ventilation strategies; minimise duration

Steroid Phobia — A Real Problem

One of the most impactful "complications" is actually parental non-adherence driven by steroid phobia. Families often stop ICS when the child seems well, fearing side effects. This leads to undertreated inflammation → exacerbations → more emergency OCS courses (which ironically carry greater systemic steroid exposure). Education about the safety profile of ICS at standard doses — and the distinction between inhaled (topical, minimal systemic effects) and oral (systemic, significant side effects) steroids — is essential at every visit.

Even beyond the specific disease, chronic wheeze in a child has important developmental, psychological, and functional consequences:

Domain	Impact	Explanation
Growth and development	↓growth velocity, ↓exercise capacity	Chronic hypoxia (even mild) + ↑metabolic demand + ↓caloric intake + medication effects; particularly relevant in CF, severe asthma, CHD
School performance	↓attendance, ↓academic achievement	Recurrent exacerbations, hospitalisations, sleep disturbance (nocturnal symptoms) → fatigue, poor concentration
Physical activity	Exercise avoidance → deconditioning → worsening symptoms	Exercise-induced bronchoconstriction creates a vicious cycle; proper pre-treatment and encouragement are key
Psychological	Anxiety (child and parents), depression, ↓self-esteem, health-related QoL impairment	Chronic disease burden; fear of exacerbations; overprotective parenting
Family impact	Parental anxiety, work absenteeism, financial burden, sibling neglect	Family-centred care and support are essential components of management
Sleep disturbance	Nocturnal wheeze/cough → fragmented sleep → daytime fatigue	Reflects inadequate disease control; should prompt step-up of controller therapy

High Yield Summary — Complications of Wheeze in Children

Acute Complications:

Respiratory failure — Type 1 (hypoxaemic, early) → Type 2 (hypercapnic, late/ominous). A "normal" PaCO₂ in a tachypnoeic child = the child is tiring.
Air leak syndromes — pneumothorax, pneumomediastinum from alveolar rupture due to air trapping and hyperinflation.
Atelectasis — lobar collapse from mucus plugging; CXR may show lobar collapse secondary to mucus obstruction ^[3]^[4].
Dehydration and hypokalaemia — from insensible losses and β₂-agonist use.
Cardiorespiratory arrest — respiratory arrest precedes cardiac arrest in children; silent chest is the warning sign ^[3].

Disease-Specific: 6. Asthma: airway remodelling (smooth muscle hyperplasia, goblet cell hyperplasia, fibrosis) ^[4] → irreversible fixed obstruction if inflammation not controlled. 7. Bronchiolitis: apnoea (especially young/premature infants), post-bronchiolitis recurrent wheeze (~30–40%). 8. Foreign body: recurrent pneumonia ^[16], bronchiectasis, granulation tissue formation. 9. CF: bronchiectasis, chronic Pseudomonas infection, ABPA, pneumothorax, massive haemoptysis. 10. CHD: Eisenmenger syndrome ^[17] from unrepaired L→R shunt; heart failure progression; FTT.

Treatment-Related: 11. ICS: oral candidiasis (5–10%, prevent with spacer + mouth rinse) ^[4]; minimal growth suppression at standard doses. 12. SABA: hypokalaemia, tremor, tachycardia (dose-related). 13. Aminophylline: arrhythmias, seizures ^[4] — narrow therapeutic index. 14. Montelukast: neuropsychiatric effects; can unmask Churg-Strauss ^[4]. 15. Omalizumab: anaphylaxis ^[4].

Active Recall - Complications of Wheeze in Children

References

^[3] Senior notes: Adrian Lui Pediatrics.pdf, p172–173, p179 (Asthma — Diagnosis, Management, Complications) ^[4] Senior notes: Ryan Ho Respiratory.pdf, p97–107 (Asthma — Pathophysiology, Clinical Features, Acute Exacerbations, Drug Details) ^[5] Senior notes: Adrian Lui Pediatrics.pdf, p181 (Cystic Fibrosis) ^[16] Senior notes: Adrian Lui Pediatrics.pdf, p167 (Pneumonia — Complications and Recurrent Pneumonia) ^[17] Senior notes: Ryan Ho Cardiology.pdf, p186 (Eisenmenger Syndrome)

Wheeze

Definition

Epidemiology

Prevalence

Demographics

Temporal Patterns (Wheezing Phenotypes in Children)

Risk Factors

Host Factors

Environmental Factors

Anatomy and Function of the Paediatric Airway

Key Differences

Functional Consequences

Aetiology (with Hong Kong Focus)

Classification by Mechanism

Aetiology by Age Group

Neonates and Infants (0–12 months)

Toddlers and Preschool Children (1–5 years)

School-age Children and Adolescents (5–18 years)

Pathophysiology of Wheeze — General Principles

1. Bronchospasm (Smooth Muscle Contraction)

2. Mucosal Oedema

3. Mucus Hypersecretion and Plugging

4. Structural Remodelling (Chronic)

5. External Compression

6. Dynamic Collapse

Pathophysiology of Asthma (The Most Common Cause of Recurrent Wheeze in Children)

The Inflammatory Cascade

Early-Phase Response (Minutes)

Late-Phase Response (6–12 hours)

Chronic Inflammation and Remodelling

Why Symptoms Are Worse at Night/Early Morning

Classification

A. By Temporal Pattern (Important for Paediatric Practice)

B. By Localisation

C. By Severity (for Asthma — GINA Classification)

Clinical Features

A. Symptoms (with Pathophysiological Basis)

B. Signs (with Pathophysiological Basis)

C. Specific Signs That Point to Aetiology

Red Flags — When Wheeze Is NOT Simple Asthma

Important Associations and Special Entities

Samter's Triad (Aspirin-Exacerbated Respiratory Disease)

The "Atopic March"

Bronchiolitis → Recurrent Wheeze

CF-related Wheeze

Carcinoid Syndrome (Rare but Testable)

Active Recall - Wheeze in Children

References

Organising Framework

Major Differential Diagnoses — Organised by Age Group

A. Infants (0–12 months)

B. Toddlers and Preschool Children (1–5 years)

C. School-age Children and Adolescents (5–18 years)

Classification of Differentials by Distribution

The Lecture Slide Approach to Acute Cough with Wheeze

Critical Distinctions: Wheeze vs Stridor

Less Common but Must-Know Differentials

Approach to Narrowing the Differential

Summary Table: Key Differentiating Features

Active Recall - Differential Diagnosis of Wheeze

Guiding Principle: Wheeze Diagnosis Is Age-Dependent

Diagnostic Criteria for the Most Common Causes of Wheeze

A. Asthma (The Most Common Cause of Recurrent Wheeze in Children > 5 years)

Clinical Diagnostic Criteria (GINA 2023/2024 for Children ≥ 6 years)

Asthma in Preschool Children (< 6 years): Probability-Based Approach

B. Acute Viral Bronchiolitis (Infants < 12 months)

C. Foreign Body Aspiration

Diagnostic Algorithm for the Wheezy Child

Investigation Modalities — Detailed Interpretation

1. Bedside / First-Line Investigations

a. Pulse Oximetry (SpO₂)

b. Peak Expiratory Flow (PEF) — School-Age Children

2. Spirometry (School-Age Children ≥ 6 years)

Key Parameters and Interpretation

Bronchodilator Reversibility Test

Flow-Volume Loop Patterns

3. Chest X-Ray (CXR)

When to Order a CXR in a Wheezy Child

CXR Findings and Their Significance

4. Allergy Testing