Bronchiolitis is an acute viral lower respiratory tract infection, most commonly caused by respiratory syncytial virus (RSV), predominantly affecting infants under 2 years of age and characterized by small airway inflammation, edema, and mucus plugging leading to wheezing and respiratory distress.

Bronchiolitis in Children

Epidemiology

Understanding risk factors helps you identify which infants are at risk of severe disease requiring hospitalisation or intensive care:

Risk Factor	Why It Matters (Mechanism)
Prematurity (< 37 weeks, especially < 32 weeks)	Premature infants have smaller airways, less elastic recoil, reduced maternal antibody transfer (IgG crosses placenta predominantly in 3rd trimester), and immature immune responses
Age < 3 months	Smallest airway calibre; obligate nasal breathers; immature immune system; reduced ability to clear secretions
Chronic lung disease / Bronchopulmonary dysplasia (BPD)	Already compromised lung function and reduced respiratory reserve
Congenital heart disease (especially haemodynamically significant)	Cannot tolerate the increased work of breathing; pulmonary congestion exacerbates respiratory distress
Immunodeficiency	Impaired viral clearance → prolonged/more severe illness
Neuromuscular disease	Poor cough reflex, weak respiratory muscles → inability to clear secretions
Exposure to tobacco smoke	Impairs mucociliary clearance, increases airway reactivity, damages epithelium
Lack of breastfeeding	Breast milk provides secretory IgA and other immune factors that protect mucosal surfaces
Crowded living conditions / daycare attendance	Increased viral exposure
Older siblings	Major vector for bringing respiratory viruses home from school/daycare
Low socioeconomic status	Multifactorial: crowding, nutrition, access to care
Male sex	Males have slightly smaller airways relative to lung size in infancy
Down syndrome	Combination of smaller airways, hypotonia, congenital heart disease, and immune dysfunction

High-Risk Infants

When assessing a baby with bronchiolitis, always screen for: prematurity, CHD, CLD/BPD, immunodeficiency, and neuromuscular disease. These are the children who may need closer monitoring, earlier escalation, and possibly prophylaxis with palivizumab or nirsevimab.

Anatomy and Function: Why Small Airways Matter

To understand bronchiolitis, you need to appreciate infant airway anatomy and why it makes them vulnerable:

Aetiology (Microbiology)

RSV accounts for 50–80% of bronchiolitis cases ^[1]^[2]. The remainder are caused by other respiratory viruses:

Pathogen	Proportion	Key Notes
Respiratory Syncytial Virus (RSV)	50–80%	Most common cause; two subtypes (A and B); type A generally causes more severe disease
Rhinovirus	10–20%	Second most common; associated with recurrent wheezing/asthma risk
Parainfluenza virus	5–10%	Types 1–4; type 3 most associated with bronchiolitis (types 1&2 more associated with croup)
Adenovirus	~5%	Can cause severe necrotising bronchiolitis → bronchiolitis obliterans (rare but important)
Influenza virus	~5%	Seasonal; important to consider during flu season
Human Metapneumovirus (HMPV)	5–10%	Paramyxovirus family; similar clinical picture to RSV; increasingly recognised in Hong Kong
Bocavirus, coronavirus, enterovirus	Rare	Co-infections common (~20–30% of cases)

Pathophysiology

Understanding the pathophysiology explains every clinical feature. Let's walk through what happens step by step:

Step 4: Downstream Consequences

Classification

Bronchiolitis can be classified by severity (most clinically useful) and by aetiology:

Feature	Mild	Moderate	Severe
Feeding	Normal or slightly reduced	Reduced (< 50% of normal)	Unable to feed / requires NG or IV fluids
Respiratory rate	Mildly elevated	Moderately elevated (> 60/min)	> 70/min or apnoea
Oxygen saturation	≥ 95% on room air	90–94% on room air	< 90% on room air
Work of breathing	Mild subcostal recession	Moderate recession, nasal flaring	Severe recession, grunting, see-saw breathing
Behaviour	Alert, interactive	Irritable but consolable	Lethargic, exhausted, poorly responsive
Management	Can usually manage at home	Requires hospitalisation	May require PICU / respiratory support

Note on age-appropriate respiratory rates (normal for age):

Neonate (< 1 month): 30–60/min

1–12 months: 25–50/min

1–3 years: 20–30/min

Tachypnoea in an infant < 12 months is generally defined as RR > 50/min, though some use > 60/min as the threshold for concern.

Clinical Features

Symptom	Pathophysiological Basis
Preceding coryzal symptoms: fever (~70%), nasal congestion, nasal discharge ^[1]^[2]	Initial viral replication in the nasopharyngeal epithelium triggers local inflammation and pyrogenic cytokine release
Cough ^[1]^[2]	Irritation of airway epithelium and cough receptors by inflammation, debris, and mucus; initially dry, then wet/productive
Breathlessness (SOB) ^[1]^[2]	Increased airway resistance from oedema and mucus → increased work of breathing → perceived dyspnoea
Reduced feeding / poor feeding	Combination of nasal obstruction (infants are obligate nasal breathers — they can't breathe while feeding), tachypnoea (can't coordinate suck-swallow-breathe), and general malaise
Irritability	Hypoxia, discomfort from respiratory distress, general illness
Apnoea (particularly in premature infants and neonates < 1 month)	Likely multifactorial: immature central respiratory drive, vagal-mediated reflex from nasopharyngeal secretions, respiratory muscle fatigue. Apnoea may be the presenting feature in very young infants BEFORE other typical signs appear

Apnoea Warning

Apnoea may be the presenting complaint in very young infants (< 6 weeks) with bronchiolitis, even BEFORE wheeze or respiratory distress develop. Always ask about apnoeic episodes and consider bronchiolitis in the differential of neonatal apnoea during RSV season. Risk factors for apnoea include: age < 2 months, history of prematurity, and history of apnoea of prematurity.

Sign	Pathophysiological Basis
Low-grade fever (typically < 39°C)	Pyrogenic cytokines (IL-1, IL-6, PGE₂) from the inflammatory response acting on the hypothalamic thermoregulatory centre. High fever (> 39°C) should raise suspicion of bacterial superinfection
Nasal congestion and rhinorrhoea	Mucosal inflammation and oedema in the nasal passages
Tachypnoea	Compensatory increase in respiratory rate to maintain minute ventilation in the face of increased dead space and V/Q mismatch
Wheezing ^[1]^[2]	High-pitched, polyphonic, predominantly expiratory — caused by turbulent airflow through narrowed small airways. The narrowing is worse during expiration (dynamic compression) → hence the expiratory predominance
Crackles (crepitations) ^[1]^[2]	Fine inspiratory crackles caused by the sudden opening of collapsed small airways and alveoli during inspiration (like "popping" open). Also from air bubbling through secretions/debris
Signs of respiratory distress ^[1]^[2]	Subcostal, intercostal, and suprasternal recession (retractions) — the highly compliant infant chest wall is "sucked in" by the large negative intrapleural pressures generated to overcome increased airway resistance
Nasal flaring	Reflex dilation of the nares to reduce nasal airway resistance and facilitate airflow
Tracheal tug	Visible descent of the trachea with each inspiration — indicates significant use of accessory muscles
Head bobbing (in infants)	Sternocleidomastoid contraction pulling the head forward with each breath — sign of severe respiratory effort
Hyperinflation (barrel chest, hyperresonance to percussion)	Air trapping due to ball-valve mechanism → increased FRC → thorax held in inspiration
Palpable liver and spleen	NOT hepatosplenomegaly — the hyperinflated lungs push the diaphragm down, displacing the liver and spleen below the costal margin. This is a common trap
Grunting	Expiration against a partially closed glottis — a physiological mechanism to generate auto-PEEP, maintaining alveolar patency and preventing collapse. Grunting is a sign of severe disease
See-saw (paradoxical) breathing	The compliant chest wall collapses inward while the abdomen protrudes during inspiration — suggests severe respiratory distress and potential impending respiratory failure
Cyanosis	Late sign — occurs when deoxyhaemoglobin > 5 g/dL. Indicates significant hypoxaemia and warrants urgent intervention
Reduced SpO₂	V/Q mismatch → inadequate oxygenation. SpO₂ < 92% on room air is generally an indication for supplemental oxygen
Dehydration signs (reduced urine output, dry mucous membranes, sunken fontanelle)	Reduced oral intake + increased insensible losses from fever and tachypnoea

Age Group	Key Considerations
Neonates (< 1 month)	May present with apnoea, temperature instability (hypothermia or fever), poor feeding rather than typical wheeze; lower threshold for septic workup
1–6 months	Classical presentation; highest risk age group for severe disease
6–12 months	Still common; usually less severe than younger infants
12–24 months	Less common; consider alternative diagnoses (asthma, foreign body, pertussis) if presentation atypical
> 2 years	Bronchiolitis diagnosis becomes less likely; recurrent wheezing more suggestive of asthma

High Yield Summary

Bronchiolitis — Key Points for Exams:

Definition: Acute URTI followed by LRTI in children < 2 years — a clinical diagnosis
Peak age: 1–9 months; most common in winter
Aetiology: RSV (50–80%) is dominant; other viruses include rhinovirus, parainfluenza, adenovirus, influenza, HMPV
Pathophysiology: Viral → epithelial necrosis + oedema + mucus → small airway obstruction → air trapping (ball-valve) + atelectasis → V/Q mismatch → hypoxaemia. Bronchospasm is a minor component (hence why bronchodilators don't really work)
Clinical course: Worst on day 2–3; most recover within 2 weeks; 50% have recurrent wheezing
Key symptoms: Coryzal prodrome (fever ~70%, nasal congestion, discharge) → cough, SOB, wheeze/crackles, ± respiratory distress
Danger signs: Apnoea (especially < 6 weeks), grunting, cyanosis, poor feeding, lethargy, quiet chest
Risk factors for severe disease: Prematurity, age < 3 months, CHD, CLD/BPD, immunodeficiency, neuromuscular disease
Why infants are vulnerable: Poiseuille's law (R ∝ 1/r⁴) — small baseline airway calibre means even minimal oedema causes massive increase in resistance
Adenovirus can cause bronchiolitis obliterans (rare but permanent damage) ^[1]^[2]
Palivizumab: monoclonal antibody against RSV F protein; IM injection Q1 month; reduces hospitalisation but limited by cost and need for multiple injections ^[1]^[2]

Active Recall - Bronchiolitis (Definition, Epidemiology, Aetiology, Pathophysiology, Clinical Features)

Differential Diagnosis of Bronchiolitis

When you're standing in front of a wheezy, tachypnoeic infant in the emergency department, your first job is to confirm that this really is bronchiolitis — and not something else masquerading as it. The differential diagnosis is essentially: "What else causes wheeze, respiratory distress, crackles, or cough in a young child?"

Let me walk you through the systematic approach, grouped by mechanism.

The lecture slides provide a structured approach to acute cough in children ^[1]:

Question to Ask	Features	Likely Common Diagnosis
Is this an acute URI?	Coryzal symptoms, fever, sore throat	URI
Is this a croup syndrome?	Stridor, "barking" or "croupy" cough, hoarseness, ± fever	Viral croup, recurrent spasmodic croup, bacterial tracheitis
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
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
Is this an acute exacerbation of a chronic respiratory disorder?	Failure to thrive, finger clubbing, chest deformity, features of atopy	To be continued (chronic cough differential)

This framework tells you: once you've identified that the child has a lower respiratory tract illness (tachypnoea, respiratory distress, wheeze/crackles), your main differentials are acute bronchiolitis, pneumonia, and asthma ^[1].

Detailed Differential Diagnoses

Feature	Bronchiolitis	Viral-Induced Wheeze / Asthma
Age	Typically < 12–24 months, first or second episode	Older infants/toddlers; recurrent episodes (≥ 3)
Coryzal prodrome	Almost always present	May or may not be present
Wheeze character	Diffuse, bilateral, with crackles	Predominantly wheeze; crackles less prominent
Response to bronchodilators	Minimal/no response (obstruction is from oedema + mucus, not bronchospasm)	Significant improvement with salbutamol (bronchospasm is the dominant mechanism)
Atopic history	Not typically associated	Associated with personal or family history of atopy: eczema, allergic rhinitis ^[3]
Diurnal variation	No	Classically worse at night or early morning ^[3]
Triggers	Viral illness (specifically RSV season)	Exercise, cold air, allergens, pollutants, viral URTI ^[3]

Why the confusion? Both are triggered by viral infections and present with wheeze. The key distinction is:

Bronchiolitis = first or second episode of viral wheeze in an infant < 2 years
Viral-induced wheeze/asthma = recurrent episodes, especially if there is a personal or family history of atopy, response to bronchodilators, or the child is > 2 years

D/dx of generalized wheeze includes bronchiectasis, bronchiolitis obliterans, and viral bronchiolitis (in children) ^[3]^[4]

The Wheeze Threshold

In practice, the boundary between "bronchiolitis" and "viral-induced wheeze" is blurry. Many clinicians use the "rule of 3": if a child has had 3 or more episodes of wheeze, you should start thinking about a diagnosis of recurrent viral-induced wheeze or asthma rather than labelling each episode as bronchiolitis.

Pneumonia is inflammation of lung parenchyma, commonly due to infective agents — characterised by fever, chills, dyspnoea, cough with sputum, pleurisy; consolidation on CXR; alveoli filled with pus and fluid ^[2].

Feature	Bronchiolitis	Pneumonia
Predominant pathology	Small airway obstruction (bronchioles)	Alveolar consolidation (parenchyma)
Age	< 2 years	Any age
Fever	Low-grade (< 39°C, ~70%)	Often high-grade (> 39°C), especially bacterial
Cough	Wet or dry	Productive/wet; may be rust-coloured (pneumococcal)
Auscultation	Bilateral wheeze + crackles	Focal crackles/bronchial breathing/reduced air entry over consolidated area
CXR	Hyperinflation, peribronchial thickening, ± patchy atelectasis	Consolidation with air bronchograms (lobar) or patchy infiltrates (bronchopneumonia) ^[2]
Systemic toxicity	Usually mild	Bacterial pneumonia: child looks toxic — high fever, rigors, tachycardia
WBC	Normal or mildly elevated (lymphocyte predominant)	Raised WBC with neutrophilia in bacterial causes

Why can they overlap? Viral bronchiolitis and viral pneumonia are on a spectrum — both are caused by similar viruses (RSV, rhinovirus, HMPV), and the distinction often depends on whether the predominant pathology is in the airways (bronchiolitis) vs. alveoli (pneumonia). In reality, many infants have elements of both. Bacterial pneumonia is suggested by high fever, focal signs, and lobar consolidation on CXR ^[2]^[5].

Important: Antibiotics are only indicated in bronchiolitis if you suspect secondary bacterial infection (e.g., pneumonia, otitis media, sinusitis) ^[2].

Croup typically occurs in 6 months to 6 years (peak at 2 years), most common in autumn ^[6].

Feature	Bronchiolitis	Croup
Sound	Expiratory wheeze + crackles	Inspiratory stridor + barking cough (sea lion-like) ^[6]
Site of obstruction	Lower airway (bronchioles)	Upper airway (subglottic larynx/trachea)
Voice	Normal	Hoarseness ^[6]
Age	< 2 years	6 months – 6 years ^[6]
Season	Winter	Autumn ^[6]
Microbiology	RSV predominant	Parainfluenza virus predominant ^[6]

Why the distinction matters: The treatment is completely different. Croup responds to dexamethasone and nebulised adrenaline ^[6], while bronchiolitis is managed with supportive care ^[2]. Stridor = upper airway; wheeze = lower airway. If a child has both stridor AND wheeze, consider that the infection may span the entire airway (laryngotracheobronchitis extending into bronchiolitis), or consider alternative diagnoses.

Feature	Bronchiolitis	Foreign Body Aspiration
Onset	Gradual (coryzal prodrome → LRTI over days)	Sudden, often with a witnessed choking episode
Age	< 2 years	Typically 6 months – 3 years (when children explore with their mouths)
History	Contact with sick person, seasonal	History of playing with small objects, eating nuts/seeds
Examination	Bilateral wheeze and crackles	Unilateral wheeze or reduced air entry (localised to the affected side)
CXR	Bilateral hyperinflation	Unilateral hyperinflation (air trapping on affected side), mediastinal shift away from affected side on expiratory film
Fever	Usually present	Usually absent initially (may develop later if secondary infection)

Why this is a dangerous miss: A foreign body lodged in a bronchus can cause a ball-valve effect on one side, mimicking unilateral bronchiolitis. Always ask about a choking episode. If the wheeze is localised (monophonic, unilateral), think foreign body before bronchiolitis.

D/dx of localised wheeze includes tumour and foreign body ^[3]^[4].

Red Flag: Unilateral Wheeze

Bronchiolitis causes bilateral, symmetrical wheeze. If you hear unilateral wheeze or asymmetric air entry in any child, foreign body aspiration must be excluded — even if there is no clear history of choking (parents may not have witnessed it). Urgent rigid bronchoscopy is the definitive investigation.

This is a frequently tested differential because congestive cardiac failure (CCF) in infants can closely mimic bronchiolitis.

Feature	Bronchiolitis	CHD with Heart Failure
Wheeze mechanism	Airway oedema, mucus plugging, debris	Pulmonary oedema from elevated left atrial pressure causes peribronchial fluid cuffing → airway narrowing ("cardiac wheeze")
Feeding	Acutely reduced (nasal obstruction, tachypnoea)	Chronically poor feeding — sweating during feeds, prolonged feeding time, failure to thrive
Growth	Usually normal prior to illness	Failure to thrive — weight faltering is a key red flag
Murmur	Absent	Cardiac murmur present (e.g., pansystolic at LLSB for VSD, continuous murmur for PDA ^[7])
Hepatomegaly	Pseudo-hepatomegaly from hyperinflated lungs pushing diaphragm down	True hepatomegaly from venous congestion (tender, firm liver edge)
CXR	Hyperinflation, flat diaphragms, peribronchial thickening	Cardiomegaly + pulmonary plethora (increased vascular markings)
Recurrence	Seasonal	Persistent/progressive symptoms regardless of season
Response	Improves with supportive care over 1–2 weeks	Does NOT improve with bronchiolitis management; needs anti-failure treatment

Why this matters in Hong Kong: Congenital heart disease affects ~8 per 1000 live births. An infant presenting with "recurrent bronchiolitis" or "bronchiolitis that isn't getting better" may actually have an undiagnosed VSD, AVSD, or PDA with heart failure. Large PDA causes HF symptoms at 1–2 months, with hyperdynamic circulation, collapsing pulse, and continuous murmur at left infraclavicular area ^[7].

'Recurrent Bronchiolitis' = Think Cardiac

If a parent tells you their infant has been admitted "three times for bronchiolitis" or the bronchiolitis "never seems to fully resolve," always re-examine for cardiac murmurs, hepatomegaly, and failure to thrive. Order an echocardiogram. This could be an undiagnosed left-to-right shunt.

Pertussis is caused by Bordetella pertussis, presenting with coryzal symptoms followed by protracted whooping cough (short expiratory bursts followed by inspiratory gasp) ^[5]^[8].

Feature	Bronchiolitis	Pertussis
Cough character	Wet/productive, continuous	Paroxysmal — bursts of rapid coughs followed by an inspiratory "whoop"
Post-tussive vomiting	Uncommon	Common (the violence of the coughing paroxysms triggers vomiting)
Duration	Resolves in ~2 weeks	Prolonged course: catarrhal phase (1 week) → paroxysmal phase (3 months!) → convalescent phase ^[8]
Wheeze	Prominent	Usually absent
Apnoea	In young infants	Also in young infants (pertussis can cause apnoea in neonates)
Vaccination history	Not relevant	Incomplete or absent pertussis vaccination is a major risk factor
WBC	Normal/mildly raised	Marked lymphocytosis (WBC can be > 50 × 10⁹/L in severe cases)

Why young infants are at risk: Maternal pertussis antibodies wane quickly, and the primary DTaP vaccination series is not complete until 6 months. Neonates and young infants may present with apnoea rather than the classic whoop — making the overlap with bronchiolitis very real.

Condition	Key Distinguishing Features	Why It's in the Differential
Bacterial tracheitis	Toxic-appearing child, high fever, stridor + productive cough, fails to respond to croup treatment; caused by S. aureus	Can present with both upper and lower airway signs
Anaphylaxis	Acute onset, exposure to allergen, urticaria, angioedema, wheeze, hypotension	Acute wheeze in a young child
Gastro-oesophageal reflux disease (GORD)	Chronic/recurrent wheeze, worse after feeds, wet burps, poor weight gain	Aspiration of refluxate causes recurrent lower airway inflammation
Tracheomalacia / Bronchomalacia	Chronic wheeze since birth, "noisy breathing," worsens with crying/feeding/URTI	Floppy airway that collapses dynamically; may worsen during a viral illness, mimicking bronchiolitis
Vascular ring / Pulmonary sling	Chronic stridor + wheeze from birth, dysphagia (difficulty with solids), barium swallow shows indentation	Aberrant vessels compressing the trachea and/or oesophagus externally
Cystic fibrosis (CF)	Recurrent respiratory infections, failure to thrive, steatorrhoea, meconium ileus history, salty sweat	Chronic airway disease presenting as "recurrent bronchiolitis"
Primary ciliary dyskinesia (PCD)	Neonatal respiratory distress, chronic wet cough, recurrent otitis media, situs inversus (50%)	Impaired mucociliary clearance → recurrent LRTI
Bronchiolitis obliterans ^[2]^[3]	History of severe adenovirus infection or post-transplant; persistent fixed airway obstruction not responding to bronchodilators; HRCT shows mosaic attenuation	Can present as chronic wheeze in a child with a history of severe previous bronchiolitis
Mediastinal mass	Progressive symptoms, superior vena cava syndrome, lymphadenopathy	Compresses airways externally → wheeze (typically monophonic)

When you're in the ED with a wheezy infant, ask yourself these critical questions:

Question	What It Helps You Distinguish
First episode or recurrent?	First → bronchiolitis; Recurrent → asthma, CF, CHD, immunodeficiency, anatomical
Coryzal prodrome?	Present → bronchiolitis, croup; Absent → foreign body, anaphylaxis, cardiac
Onset sudden or gradual?	Sudden → foreign body, anaphylaxis; Gradual → bronchiolitis, pneumonia
Bilateral or unilateral signs?	Bilateral → bronchiolitis, asthma; Unilateral → foreign body, lobar pneumonia
Wheeze or stridor or both?	Wheeze → lower airway (bronchiolitis, asthma); Stridor → upper airway (croup)
Feeding and growth normal?	Poor growth → CHD, CF, GORD; Acutely reduced → bronchiolitis
Cardiac murmur?	Present → CHD
Responds to bronchodilator?	Yes → asthma/reactive airways; No → bronchiolitis, structural
Vaccination status?	Incomplete → pertussis
Age-appropriate?	< 2 years typical for bronchiolitis; older = asthma more likely

In Hong Kong, the most commonly encountered differentials in clinical practice and exams are:

Bronchiolitis vs. Pneumonia — the most common overlap, especially viral pneumonia
Bronchiolitis vs. Early childhood asthma/viral-induced wheeze — particularly in children > 12 months with recurrent episodes
Bronchiolitis vs. Undiagnosed CHD — a high-yield exam topic; think of the infant with "recurrent bronchiolitis" who has an undiagnosed VSD or PDA
Foreign body aspiration — always consider in the right age group with acute onset and unilateral findings

High Yield Summary

Differential Diagnosis of Bronchiolitis — Must-Know Points:

The key differentials for a wheezy infant < 2 years are: bronchiolitis, pneumonia, asthma/viral-induced wheeze, foreign body aspiration, congenital heart disease, pertussis, and croup
Bronchiolitis = first/second episode of viral wheeze in infant < 2 years with coryzal prodrome → bilateral wheeze + crackles → minimal response to bronchodilators
Asthma/viral-induced wheeze: recurrent (≥ 3) episodes, family history of atopy, response to SABA, diurnal variation
Pneumonia: higher fever, focal crackles/bronchial breathing, consolidation on CXR, more systemic toxicity
Foreign body: sudden onset, choking history, unilateral wheeze — this is a dangerous miss
CHD with heart failure: failure to thrive, cardiac murmur, persistent/progressive symptoms, hepatomegaly, cardiomegaly on CXR — always consider in "recurrent bronchiolitis"
Pertussis: paroxysmal cough with whoop, post-tussive vomiting, prolonged course, lymphocytosis
Croup: stridor (NOT wheeze), barking cough, hoarseness → upper airway obstruction
Unilateral wheeze = foreign body until proven otherwise
"Recurrent bronchiolitis" = consider CHD, CF, immunodeficiency, or anatomical abnormality

Active Recall - Differential Diagnosis of Bronchiolitis

References

^[1] Lecture slides: GC 141. A child with cough acute and chronic cough in children.pdf (p15) ^[2] Senior notes: Adrian Lui Pediatrics.pdf (p163, Acute Bronchiolitis and Pneumonia sections) ^[3] Senior notes: Ryan Ho Respiratory.pdf (p97–98, Asthma Clinical Features and D/dx of wheeze) ^[4] Senior notes: Ryan Ho Respiratory.pdf (p110–111, D/dx of COPD including bronchiolitis obliterans) ^[5] Senior notes: Ryan Ho Respiratory.pdf (p63, Pneumonia differential diagnoses) ^[6] Senior notes: Adrian Lui Pediatrics.pdf (p161, Viral Laryngotracheobronchitis / Croup) ^[7] Senior notes: Ryan Ho Cardiology.pdf (p189, Patent Ductus Arteriosus) ^[8] Senior notes: Adrian Lui Pediatrics.pdf (p154, Pertussis)

Diagnosis of Bronchiolitis

This is the single most important concept to internalise: bronchiolitis is a clinical diagnosis ^[2]. There is no blood test, no CXR finding, and no viral PCR result that "makes" the diagnosis. You diagnose bronchiolitis at the bedside based on the history and examination.

The diagnostic criteria (as used in major guidelines — AAP 2014/reaffirmed 2023, NICE 2021, Australasian Bronchiolitis Guideline 2024) are:

Criterion	Detail
Age	Infant or young child < 2 years of age ^[2]
Clinical syndrome	URTI symptoms (coryzal prodrome) followed by LRTI ^[2]
Coryzal prodrome	Fever (~70%), nasal congestion, nasal discharge — typically 1–3 days before LRTI onset ^[2]
LRTI features	Cough, breathlessness (SOB), wheezing and/or crackles on auscultation ^[2]
± Respiratory distress	Tachypnoea, recession, nasal flaring, grunting, feeding difficulty ^[2]
Episode number	First or second episode of viral-induced wheeze (recurrent episodes → consider asthma)
Seasonality	Most common in winter ^[2] — supports but does not confirm the diagnosis

When Is Bronchiolitis NOT a Clinical Diagnosis?

You only need investigations when:

The diagnosis is uncertain (atypical features, unusual age, atypical course)
The disease is severe (need to assess for respiratory failure, guide oxygen therapy)
You suspect a complication (secondary bacterial infection, respiratory failure)
You need to guide infection control (cohorting in hospital — viral identification helps prevent nosocomial spread)

Investigation Modalities — What, When, Why, and Key Findings

Pulse oximetry is the single most important investigation in bronchiolitis ^[2].

Aspect	Detail
When	ALL cases — part of initial assessment and ongoing monitoring
Why	Hypoxaemia from V/Q mismatch is the primary physiological derangement; SpO₂ guides oxygen therapy decisions
How	Paediatric probe on finger or toe (or preductal in neonates); ensure good waveform and accurate reading
Key thresholds	SpO₂ ≥ 95%: reassuring; SpO₂ 90–94%: supplemental oxygen likely needed; SpO₂ < 92%: indication for hospitalisation and oxygen therapy ^[2]
Pitfalls	Motion artefact (fussy baby), poor peripheral perfusion (cold extremities), and nail polish can give false readings. Continuous monitoring preferred over intermittent spot checks in hospitalised infants

Why SpO₂ is so important: Remember from the pathophysiology that airway obstruction → air trapping + atelectasis → V/Q mismatch → hypoxaemia. SpO₂ tells you how well the lungs are gas-exchanging. An infant can have significant work of breathing but still maintain SpO₂ initially (compensating with tachypnoea); when SpO₂ drops, it means compensation is failing.

SpO₂ Threshold Debate

There is ongoing debate about whether to use SpO₂ < 90% or < 92% as the oxygen therapy threshold. NICE (2021) uses < 92% as the threshold for supplemental oxygen. AAP (2014) suggests considering < 90% as the threshold in otherwise stable infants to avoid overtreatment and prolonged hospitalisation. In Hong Kong / QMH practice, SpO₂ < 92% is generally used as the threshold for intervention ^[2]. For exams, know both cutoffs and state which guideline you are following.

NPA for common viruses ^[1] is the standard method for identifying the causative organism.

Aspect	Detail
When	Hospitalised patients — primarily for infection control (cohorting RSV-positive vs RSV-negative patients); NOT required to make the clinical diagnosis
Why	Viral identification allows: (1) cohorting to prevent nosocomial spread, (2) epidemiological surveillance, (3) guides prognosis (e.g., adenovirus → higher risk of bronchiolitis obliterans), (4) may avoid unnecessary antibiotics if viral aetiology confirmed
Method	NPA: gentle suction catheter into nasopharynx; NP swab: flocked swab inserted to nasopharynx
Tests performed	Rapid antigen detection (immunofluorescence or immunochromatographic rapid test) for RSV; PCR panel (multiplex respiratory viral PCR) for RSV, rhinovirus, HMPV, influenza, parainfluenza, adenovirus, coronavirus, bocavirus
Key findings	RSV positive in 50–80% of bronchiolitis cases ^[2]. Co-infection with ≥ 2 viruses found in 20–30%
Turnaround	Rapid antigen: ~30 minutes; PCR: 4–24 hours

Why not routinely test everyone? In a typical presentation during RSV season, the diagnosis is clinical and management is entirely supportive regardless of the specific virus. NPA results do not change treatment. The main value is infection control in hospital settings — RSV-positive infants should be cohorted together and isolated from RSV-negative patients to prevent nosocomial outbreaks on the paediatric ward.

CXR should be considered in the presence of lower respiratory tract signs, relentlessly progressive cough (past the 2-week point), or haemoptysis ^[1]. In bronchiolitis specifically:

CXR is NOT routinely indicated — it should only be performed if respiratory failure is suspected (± CXR/ABG if respiratory failure) ^[2] or if the diagnosis is uncertain (atypical features, possible pneumonia, possible foreign body, possible cardiac cause).

Aspect	Detail
When to order CXR	(1) Diagnostic uncertainty — atypical features, unilateral signs, possible pneumonia; (2) Respiratory failure ^[2] — to assess complications; (3) Failure to improve as expected; (4) Suspected complications (pneumothorax, bacterial superinfection)
When NOT to order	Typical bronchiolitis with clear clinical picture — routine CXR adds no value and may cause harm (unnecessary antibiotics for misinterpreted atelectasis, radiation exposure, distress to infant)

Key CXR findings in bronchiolitis:

Finding	Explanation (Pathophysiology)
Hyperinflation	Air trapping from ball-valve mechanism → increased lung volume → flattened diaphragms (> 8 posterior ribs visible), increased anteroposterior diameter, widened intercostal spaces
Peribronchial thickening ("dirty lung fields", "peribronchial cuffing")	Oedema and inflammation around the bronchioles → thickened bronchial walls seen as ring shadows (end-on) or tram-lines (longitudinal)
Patchy atelectasis / subsegmental collapse	Complete obstruction of small airways → absorption of trapped air → collapse of distal lung segments. Appears as linear or patchy opacities, often in the right upper or middle lobe
Flattened diaphragms	Consequence of hyperinflation pushing the diaphragms down
Normal or mildly increased perihilar markings	Mild vascular congestion from increased pulmonary blood flow in areas of compensatory ventilation

CXR Trap: Atelectasis vs Consolidation

The most common trap with CXR in bronchiolitis is misinterpreting patchy atelectasis as pneumonic consolidation, which then triggers unnecessary antibiotic use. Studies show that obtaining a CXR in typical bronchiolitis leads to a significant increase in antibiotic prescriptions without any improvement in outcomes. This is why current guidelines strongly advise AGAINST routine CXR in bronchiolitis ^[1]^[2].

How to distinguish: Atelectasis in bronchiolitis is typically bilateral, patchy, and subsegmental, occurring in the context of generalised hyperinflation. Lobar consolidation with air bronchograms suggests true bacterial pneumonia. But in practice, this distinction on CXR is often difficult, especially in infants.

ABG is indicated if respiratory failure is suspected ^[2].

Aspect	Detail
When	Severe respiratory distress, impending respiratory failure, SpO₂ < 90% despite supplemental O₂, apnoea, exhaustion, deteriorating consciousness
Why	Identifies Type 1 respiratory failure (hypoxaemia: PaO₂ < 8 kPa with normal/low PaCO₂) or Type 2 respiratory failure (hypoxaemia + hypercapnia: PaCO₂ > 6 kPa)
Method in infants	Capillary blood gas (CBG) is most commonly used in paediatrics (heel prick or finger); arterial sampling is painful and technically difficult in infants
Key findings	Early: respiratory alkalosis (hyperventilation → ↓PaCO₂ → ↑pH); Late/severe: respiratory acidosis (CO₂ retention → ↑PaCO₂ → ↓pH — indicates impending respiratory failure)

Interpretation guide:

Stage	PaO₂	PaCO₂	pH	Interpretation
Mild	Normal or slightly low	Low (hyperventilation)	High (alkalosis)	Compensating — increased RR blowing off CO₂
Moderate	Low	Normal	Normal	Tiring — cannot maintain hyperventilation
Severe	Very low	Elevated	Low (acidosis)	Respiratory failure — urgent escalation needed

Rising PaCO₂ = Danger

In a tachypnoeic infant with bronchiolitis, a normal or rising PaCO₂ is an ominous sign. It does NOT mean "all is well." It means the infant is tiring and can no longer hyperventilate to compensate. This infant needs immediate escalation of respiratory support (HFNC, CPAP, or intubation).

Blood tests are NOT routinely indicated in bronchiolitis. They are reserved for specific clinical scenarios:

Test	When to Order	Key Findings and Interpretation
CBC with differentials ^[1]	Suspected secondary bacterial infection; very unwell/toxic child; prolonged fever > 5 days	In typical bronchiolitis: normal WBC or mild lymphocytosis (viral pattern). Raised WBC with neutrophilia → suggests bacterial co-infection. Marked lymphocytosis (> 20 × 10⁹/L) → think pertussis
CRP / PCT	Suspected secondary bacterial infection	CRP typically low (< 20 mg/L) in uncomplicated bronchiolitis. CRP > 40–60 mg/L or procalcitonin > 0.5 ng/mL raises concern for bacterial infection
U&E (Urea, Electrolytes, Creatinine)	If requiring IV fluids — to guide fluid therapy and detect dehydration, SIADH	Bronchiolitis can cause SIADH (syndrome of inappropriate ADH secretion) → hyponatraemia. Also need to monitor electrolytes if on IV fluids
Blood culture	Suspected sepsis or bacterial pneumonia, especially in febrile neonates	Blood culture has a low detection rate even if bacterial aetiology ^[1]; still important in the septic-looking infant or neonate (where the pretest probability of bacterial infection is higher)
Blood glucose	Young infants (especially < 3 months), reduced feeding, lethargy	Infants have limited glycogen stores and are at risk of hypoglycaemia during illness with poor oral intake

Why SIADH occurs in bronchiolitis: The pathophysiology is multifactorial — positive pressure ventilation (if on CPAP), intrathoracic pressure changes from air trapping and respiratory distress, and inflammatory cytokines all stimulate ADH release. This leads to water retention and dilutional hyponatraemia. Always check Na⁺ before starting IV fluids in a bronchiolitis patient.

Method	Sensitivity	Speed	Cost	Use
Rapid antigen detection (immunochromatographic)	Moderate (80–90% for RSV)	~15–30 minutes	Low	Bedside / ED triage; rapid cohorting decision
Direct immunofluorescence (DIF)	Good (85–95%)	~2–4 hours	Moderate	NPA sample; good for multiple viruses simultaneously
Multiplex PCR	Excellent (> 95%)	4–24 hours	Higher	Gold standard for identification; detects multiple viruses including HMPV, bocavirus, rhinovirus
Viral culture	Variable	Days to weeks	High	Research / public health; rarely used clinically

These are NOT part of routine bronchiolitis workup but should be considered when the clinical picture is atypical or suggests an alternative/underlying diagnosis:

Investigation	When to Consider	What You're Looking For
Echocardiography	Murmur on examination, cardiomegaly on CXR, failure to thrive, "recurrent bronchiolitis" that doesn't resolve	Congenital heart disease (VSD, PDA, AVSD) causing heart failure mimicking bronchiolitis
Sweat test	Recurrent lower respiratory infections, failure to thrive, steatorrhoea, meconium ileus history	Cystic fibrosis (Cl⁻ > 60 mmol/L diagnostic)
HRCT chest ^[9]	Persistent symptoms beyond 4–6 weeks, suspected bronchiolitis obliterans (especially post-adenovirus)	Mosaic attenuation, air trapping, bronchial wall thickening in bronchiolitis obliterans ^[9]
Nasal NO / Cilia study ^[9]	Recurrent LRTI, chronic wet cough, neonatal respiratory distress, situs inversus	Primary ciliary dyskinesia (nasal NO low; abnormal ciliary motility on high-speed video microscopy)
Immunoglobulin pattern ^[9]	Recurrent severe infections	Primary immunodeficiency (low IgG, IgA, IgM → antibody deficiency syndromes)
pH probe / impedance study ^[9]	Recurrent wheeze worse after feeds, poor weight gain, chronic cough	Gastro-oesophageal reflux disease (GORD) with aspiration
Bronchoscopy with BAL ^[9]	Persistent lobar collapse, recurrent pneumonia in same location, suspected foreign body	Foreign body retrieval; BAL for culture (lipid-laden macrophages in aspiration); airway anatomy (tracheomalacia, vascular compression)
Peak flow / Lung function study ^[9]	Older children (typically > 5–6 years) with recurrent wheeze	Reversible airflow obstruction → asthma (if FEV₁ improves > 12% post-bronchodilator)
Mantoux test / IGRA ^[9]	TB exposure risk, chronic cough > 4 weeks, failure to thrive, immigrant from endemic area	Tuberculosis

The 'Chronic Cough' Investigation Panel

The lecture slides list a comprehensive panel for investigating chronic cough in children ^[9]: CXR, peak flow ± lung function, CBC with differentials, Mantoux/PPD or IGRA for TB, sputum/gastric aspirate for TB, HRCT, nasal NO/cilia study/sweat test, immunoglobulin pattern, pH probe, video fluoroscopy, bronchoscopy with BAL. You would work through these systematically in a child with atypical or prolonged symptoms, NOT in typical acute bronchiolitis.

Severity	Investigations Needed
Mild (home management)	Pulse oximetry only (± NPA if in ED for surveillance)
Moderate (hospitalised)	Pulse oximetry (continuous) + NPA for viral identification (infection control/cohorting) + assess hydration
Severe (PICU referral)	All of the above + CXR (assess for complications) + ABG/CBG (assess for respiratory failure) + U&E (guide IV fluids, check for SIADH) + Blood glucose + consider blood culture if toxic-looking
Atypical / not improving	All of the above + CXR (alternative diagnosis) + CBC with differentials + CRP + appropriate targeted investigations (echo, sweat test, HRCT, bronchoscopy etc.) depending on clinical suspicion

Red Flag	What to Investigate	Why
Age < 1 month or > 24 months	Full septic workup (neonate); consider asthma, foreign body (older child)	Age extremes are atypical for bronchiolitis
Recurrent episodes (≥ 3)	Echo, sweat test, immune workup, consider asthma	"Recurrent bronchiolitis" suggests an underlying structural, cardiac, immune, or chronic airway disease
Unilateral signs	CXR (inspiratory + expiratory), rigid bronchoscopy	Foreign body aspiration until proven otherwise
High fever (> 39°C) or toxic-looking	CBC, CRP, blood culture, CXR, urine culture	Bacterial co-infection or alternative bacterial diagnosis
Failure to improve by day 7–10	CXR, blood tests, consider echocardiography	Complication (secondary infection), wrong diagnosis (CHD, pertussis)
Failure to thrive / poor growth	Sweat test, echo, immune workup	CF, CHD, immunodeficiency
Cardiac murmur	Echocardiography	Congenital heart disease
Apnoea in neonate	Full septic screen, CBG, blood glucose, consider pertussis testing (NPA PCR for B. pertussis)	Neonatal bronchiolitis can present as apnoea, but so can sepsis, metabolic disease, and pertussis

High Yield Summary

Diagnosis of Bronchiolitis — Must-Know Points:

Bronchiolitis is a CLINICAL diagnosis ^[2] — made at the bedside from history + examination in an infant < 2 years with coryzal prodrome → wheeze/crackles ± respiratory distress
Pulse oximetry is the single most important investigation — performed in ALL cases ^[2]
CXR is NOT routinely indicated — only if respiratory failure, diagnostic uncertainty, or suspected complications ^[1]^[2]. Routine CXR leads to overdiagnosis of "pneumonia" and unnecessary antibiotics
NPA for viral identification is used for infection control (cohorting) in hospitalised patients, not to make the diagnosis ^[1]
ABG/CBG is reserved for suspected respiratory failure ^[2] — a normal or rising PaCO₂ in a tachypnoeic infant is an ominous sign
Blood tests are NOT routine — only if suspected bacterial co-infection, dehydration assessment, or SIADH screening ^[1]
Blood culture has a low detection rate even with bacterial aetiology ^[1]
In atypical or recurrent cases, think beyond bronchiolitis: order echo (CHD), sweat test (CF), immune workup, HRCT (bronchiolitis obliterans), or bronchoscopy (foreign body/structural) as appropriate
Key CXR findings (when performed): hyperinflation, peribronchial cuffing, patchy atelectasis (NOT consolidation), flattened diaphragms
Check Na⁺ before IV fluids — bronchiolitis can cause SIADH → hyponatraemia

Active Recall - Diagnosis and Investigations of Bronchiolitis

References

^[1] Lecture slides: GC 141. A child with cough acute and chronic cough in children.pdf (p14–15) ^[2] Senior notes: Adrian Lui Pediatrics.pdf (p163, Acute Bronchiolitis section) ^[9] Lecture slides: GC 141. A child with cough acute and chronic cough in children.pdf (p26, Investigations for chronic cough)

Management of Bronchiolitis

The following are indications for hospitalisation ^[2]:

Indication	Rationale
History of apnoea	Risk of recurrent apnoea → respiratory arrest; needs continuous monitoring
RR > 60	Significant tachypnoea indicates substantial respiratory compromise
Severe respiratory distress	Marked recession, grunting, nasal flaring, see-saw breathing — suggests impending failure
SpO₂ < 92% in room air	Hypoxaemia requiring supplemental oxygen therapy
Difficulty feeding	Cannot coordinate suck-swallow-breathe; risk of aspiration and dehydration
< 50% usual fluid intake in 24 hours	Dehydration risk; likely to need NG or IV fluids
Uncertain diagnosis	Need observation and investigation to exclude alternative diagnoses (cardiac, foreign body etc.)

Additional risk factors that lower the threshold for admission (even if the above criteria are not met):

Age < 6 weeks (higher risk of apnoea)
Prematurity (< 37 weeks, especially < 32 weeks)
Known comorbidity: CHD, CLD/BPD, immunodeficiency, neuromuscular disease, Down syndrome
Social factors: distance from hospital, parental ability to monitor, language barriers
Inadequate caregiver understanding of safety-net advice

Treatment Modalities — Detailed Breakdown

Fluid support is a critical component of management ^[2].

There is a higher fluid requirement due to fever, tachypnoea, reduced oral intake, and vomiting ^[2].

Modality	When	How	Why
Small, frequent oral feeds	Mild disease; infant still able to feed	Offer breast/bottle feeds more frequently in smaller volumes	Tachypnoeic infants fatigue quickly during feeds; smaller volumes reduce aspiration risk and are easier to manage
Nasogastric (NG) feeds	Moderate disease; unable to take sufficient oral feeds but gut functioning	Insert NG tube; give breast milk or formula as bolus or continuous feeds	Preserves gut function (enteral feeding preferred over IV), reduces IV cannula-related complications. Use breast milk if breastfeeding to maintain supply
Intravenous (IV) fluids	Severe disease; unable to tolerate enteral feeds; significant dehydration; PICU setting	Isotonic fluids (0.9% NaCl + 5% dextrose) at 2/3 to 3/4 maintenance rate	Full maintenance may cause fluid overload (SIADH risk). Use isotonic fluids to avoid worsening any existing hyponatraemia from SIADH

Why restrict fluids to 2/3–3/4 maintenance? Bronchiolitis is associated with SIADH (syndrome of inappropriate ADH secretion) — ADH is released due to intrathoracic pressure changes from air trapping, positive pressure ventilation, and inflammatory cytokines. SIADH causes water retention → dilutional hyponatraemia. Full maintenance fluids would exacerbate this. Always check serum Na⁺ before starting IV fluids and monitor 12–24-hourly.

Fluid Choice in Paediatrics

Never use hypotonic fluids (e.g., 0.18% NaCl, "one-fifth normal saline") as maintenance fluids in sick children. The risk of iatrogenic hyponatraemia is significant, especially with SIADH. Current paediatric guidelines (NICE, APLS) recommend isotonic maintenance fluids (0.9% NaCl ± dextrose) for ALL hospitalised children requiring IV fluids. This applies to bronchiolitis as much as any other condition.

Oxygen support is provided as a stepwise escalation — you start with the least invasive and escalate only if needed ^[2]:

High flow O₂ ± CPAP, BiPAP ^[2]

Level	Device	Flow / Settings	When to Use	Mechanism
Step 1: Low-flow nasal prong O₂	Nasal prongs/cannulae	0.5–2 L/min (in infants)	SpO₂ < 92% on room air; mild-moderate hypoxaemia	Increases FiO₂ in inspired gas to overcome V/Q mismatch
Step 2: High-flow nasal cannula (HFNC)	Optiflow / Fisher & Paykel system	2 L/kg/min (typical starting flow; max ~8 L/min for infants)	Persistent hypoxaemia or significant work of breathing despite low-flow O₂; moderate-severe disease	Delivers heated, humidified O₂ at high flow → provides a degree of positive airway pressure (washout of dead space, small amount of CPAP effect), reduces work of breathing, improves mucociliary function via humidification
Step 3: CPAP	Nasal CPAP via prongs or mask	5–8 cmH₂O, FiO₂ titrated to target SpO₂	Failure of HFNC; significant respiratory distress; recurrent apnoea; SpO₂ < 92% on HFNC	Continuous positive airway pressure → splints open the small airways, prevents collapse during expiration, recruits atelectatic alveoli, reduces work of breathing
Step 4: BiPAP	Nasal BiPAP	IPAP 8–12 cmH₂O, EPAP 5–6 cmH₂O	Failure of CPAP; rising PaCO₂ with respiratory acidosis; need for additional ventilatory support	Bilevel pressure → EPAP keeps airways open (like CPAP) + IPAP assists inspiration → augments tidal volume and reduces work of breathing
Step 5: Intubation + Mechanical ventilation	Endotracheal tube + ventilator	Age-appropriate ETT size and ventilator settings	Respiratory failure despite non-invasive support; recurrent/prolonged apnoea; exhaustion; loss of consciousness	Full ventilatory support. Use low-tidal-volume, longer expiratory time strategy to avoid worsening air trapping

HFNC — Why it has transformed bronchiolitis management: HFNC has become the most important respiratory support tool in moderate-severe bronchiolitis. The mechanisms are:

Dead space washout: High-flow gas flushes expired CO₂ from the nasopharynx, reducing rebreathing
Low-level CPAP effect: The high flow generates ~2–5 cmH₂O of positive pressure, keeping small airways open
Humidification: Heated humidified gas improves mucociliary clearance and reduces airway drying
Reduced metabolic cost: Less energy spent heating and humidifying inspired air
Better tolerated than CPAP/BiPAP in infants (nasal prongs rather than a tight mask)

Multiple RCTs (including the landmark PARIS trial 2017) have shown HFNC reduces the need for CPAP/ICU escalation and is now first-line respiratory support for moderate bronchiolitis in most paediatric units globally, including Hong Kong.

Target SpO₂ in bronchiolitis:

≥ 92% is the standard target in Hong Kong / NICE guidelines ^[2]
AAP suggests ≥ 90% may be acceptable in otherwise well infants (to avoid over-monitoring and prolonged hospitalisation)
Do not aim for 100% — this leads to unnecessary oxygen administration and delayed discharge

When to wean oxygen:

Trial off oxygen when SpO₂ consistently ≥ 92–95% for ≥ 4 hours (including during sleep and feeds)
Monitor for 12–24 hours off oxygen before discharge

Nebulised 3% hypertonic saline: 1st line treatment in QMH, shown in meta-analysis to decrease hospitalisation rate ^[2]

Aspect	Detail
Dose	4 mL of 3% NaCl nebulised over 15–20 minutes, every 4–8 hours
Mechanism	(1) Osmotic effect: draws water into the airway lumen from the submucosa → thins mucus and rehydrates the airway surface liquid → makes secretions easier to clear. (2) Improves mucociliary clearance by enhancing ciliary beat frequency. (3) Reduces mucosal oedema by osmotic dehydration of the swollen submucosal tissue. (4) May disrupt ionic bonds in the mucus gel layer, reducing its viscosity
Evidence	Cochrane meta-analysis (Zhang et al. 2017) showed reduced length of hospitalisation by ~1 day in inpatients. Less clear benefit in ED-only use
Indication	Hospitalised infants with bronchiolitis — 1st line treatment at QMH ^[2]
Contraindications/Cautions	May cause transient bronchospasm (consider pre-treatment with salbutamol or administering with salbutamol in high-risk patients); avoid in very severe cases where nebuliser mask may worsen distress
Not recommended	As sole treatment in ED for immediate discharge; not a substitute for supportive care

Why Hypertonic Saline and Not Normal Saline?

Normal saline (0.9%) is isotonic — it does not create an osmotic gradient. Hypertonic (3%) saline creates an osmotic gradient that draws water into the airway lumen, thinning secretions and pulling fluid out of the oedematous mucosa. Think of it as "de-swelling" the airway wall while simultaneously making the mucus easier to cough out. This is the same principle behind hypertonic saline use in CF patients.

Inhaled SABA: may provide modest short-term improvement but no change in overall outcome ^[2]

Aspect	Detail
Drug	Salbutamol (albuterol)
Paediatric dose	Nebulised: 2.5 mg (< 5 years) via nebuliser; MDI + spacer: 2–6 puffs via spacer with face mask
Mechanism	β₂-adrenergic receptor agonist → relaxes bronchial smooth muscle → bronchodilation
Why it doesn't work well in bronchiolitis	The predominant mechanism of obstruction is mucosal oedema, mucus plugging, and epithelial debris, NOT smooth muscle bronchospasm. Smooth muscle contraction is a minor component in bronchiolitis (unlike in asthma). Therefore, relaxing smooth muscle provides, at best, modest and transient improvement
Evidence	Multiple Cochrane reviews show no significant improvement in hospitalisation rates, length of stay, or clinically meaningful outcomes. May produce short-term improvement in clinical scores in some infants
Current recommendations	NOT routinely recommended by AAP (2014), NICE (2021), or Australasian guidelines (2024). May consider a single therapeutic trial in moderate-severe cases — if no objective improvement (assessed by SpO₂, RR, work of breathing), discontinue
Side effects	Tachycardia, tremor, hypokalaemia (rare at standard doses)

The 'Therapeutic Trial' Approach

Some guidelines allow a single trial dose of salbutamol in hospitalised infants with moderate-severe bronchiolitis. The rationale: a small subset of infants (especially those > 6 months, those with family history of atopy, those with recurrent wheeze) may have a component of bronchospasm that responds. If the infant objectively improves (reduced RR, improved SpO₂, reduced work of breathing within 20 minutes), you can continue. If there is no improvement, stop. Do not continue salbutamol "just because."

This is just as important as knowing what TO do — knowing what NOT to do prevents harm and scores marks:

Treatment	Why NOT Recommended	Explanation
Systemic corticosteroids (oral prednisolone, IV dexamethasone)	No benefit proven; potential harm	Unlike asthma (where eosinophilic inflammation responds to steroids), bronchiolitis inflammation is neutrophil-predominant and involves epithelial necrosis — steroids do not help. Multiple large RCTs (including CANADIAN AVERY trial) show NO reduction in hospitalisation, length of stay, or clinical improvement. Steroids also have side effects (immunosuppression, hyperglycaemia)
Inhaled corticosteroids	No benefit in acute bronchiolitis or prevention of recurrent wheeze	Same reasoning as systemic steroids; the inflammatory profile does not respond to steroids
Nebulised adrenaline (epinephrine)	May provide transient improvement but no sustained benefit	α-adrenergic effect causes mucosal vasoconstriction → reduces oedema. Some short-term improvement in clinical scores, but no change in hospitalisation or length of stay. Not routinely recommended; may be considered in very severe cases as a rescue measure
Antibiotics	Only indicated if suspect secondary bacterial infection (e.g., pneumonia, otitis media, sinusitis) ^[2]	Bronchiolitis is VIRAL. Antibiotics have no antiviral activity. Routine antibiotic use in bronchiolitis drives antimicrobial resistance and adds cost and side effects without benefit
Chest physiotherapy	No benefit; may worsen distress	Vibration and percussion techniques do not improve mucus clearance in bronchiolitis and can agitate the infant, increasing oxygen demand. May be considered in specific situations (e.g., pre-existing neuromuscular disease with secretion retention) but NOT as routine
Antitussives / mucolytics	No evidence of benefit; potential harm	Cough is a protective mechanism for airway clearance. Suppressing it can worsen secretion retention. Mucolytics (e.g., acetylcysteine) are not proven effective and can cause bronchospasm
Oral/nasal decongestants	No benefit; potential harm in infants	Pseudoephedrine, phenylephrine etc. have no proven efficacy and carry risks of tachycardia, irritability, and seizures in young infants

The 'Don't Do' List

For exams, you MUST know that the following are NOT recommended in bronchiolitis:

❌ Systemic or inhaled corticosteroids
❌ Routine antibiotics (only if bacterial co-infection suspected)
❌ Routine bronchodilators (only a single trial if moderate-severe)
❌ Chest physiotherapy
❌ Antitussives / mucolytics / decongestants
❌ Nebulised adrenaline (not routine)

The evidence base for this is strong and is tested repeatedly in exams.

Measure	Detail	Why
Minimal handling	Limit examinations and interventions; cluster cares	Agitation increases oxygen demand, heart rate, and respiratory distress. A sleeping baby with SpO₂ 93% is better than a screaming baby with SpO₂ 88%
Position of comfort	Head slightly elevated (15–30°); allow the child to find their own comfortable position, usually in the parent's arms	Reduces work of breathing; mild elevation reduces gastro-oesophageal reflux and improves diaphragmatic excursion
Nasal suctioning	Gentle bulb suction or suction catheter to clear nasal secretions BEFORE feeds and oxygen assessment	Infants are obligate nasal breathers (up to ~4–6 months). Nasal obstruction from secretions directly impairs breathing and feeding. Keep it gentle — overly aggressive or deep suctioning can cause mucosal oedema and worsen obstruction
Nasal saline drops	1–2 drops of normal saline in each nostril before suctioning	Loosens thick secretions, making suctioning more effective
Antipyretics	Paracetamol 15 mg/kg/dose Q4–6H (max 4 doses/day) or ibuprofen 5–10 mg/kg/dose Q6–8H (> 3 months age and > 5 kg)	Fever increases metabolic demand and oxygen consumption. Treating fever reduces energy expenditure and improves comfort. Note: antipyretics are for comfort, not to treat the underlying disease
Infection control	Contact precautions: gown, gloves, hand hygiene. RSV-positive cohorted together. Strict hand hygiene for all contacts	RSV survives on surfaces for hours and is transmitted via droplets and fomites. Nosocomial RSV outbreaks on paediatric wards are well-documented and devastating
Monitoring	Continuous SpO₂, HR, RR. Regular clinical assessment of work of breathing, feeding, hydration	Disease peaks on day 2–3 ^[2] — an infant admitted on day 1 may deteriorate before improving. Regular reassessment is essential

Consider PICU referral when:

Criterion	Rationale
Recurrent or prolonged apnoea	Risk of respiratory arrest; needs continuous monitoring and possible intubation
SpO₂ < 92% despite HFNC/CPAP	Refractory hypoxaemia despite non-invasive support
Rising PaCO₂ > 6–7 kPa with respiratory acidosis	Impending Type 2 respiratory failure; may need intubation
Exhaustion — decreasing respiratory effort, lethargy	Respiratory muscle fatigue → sudden decompensation
Need for intubation and mechanical ventilation	By definition requires PICU-level care
Cardiovascular instability	Tachycardia, poor perfusion, hypotension — rare but serious

Palivizumab: monoclonal antibody against RSV glycoprotein ^[2]

Aspect	Detail
Drug class	Humanised monoclonal antibody targeting the F (fusion) protein of RSV
Name breakdown	"palivi-" (derived from the target — RSV), "-zu-" (humanised antibody), "-mab" (monoclonal antibody)
Route	IM injection ^[2]
Dosing	Once monthly (Q1 month) during RSV season — typically 5 monthly doses ^[2]
Dose	15 mg/kg IM per dose
Efficacy	Shown to decrease hospitalisation rate ^[2] — reduces RSV hospitalisation by ~50% in high-risk infants (IMpact trial)
Limitations	Limited use due to cost and multiple injections required ^[2]
Indications	High-risk infants: (1) Preterm < 29 weeks (< 12 months old at start of RSV season); (2) Chronic lung disease of prematurity (< 2 years); (3) Haemodynamically significant CHD (< 2 years); (4) Severe immunodeficiency

Nirsevimab (Beyfortus) — The Game-Changer (2023–2025)

This is a newer monoclonal antibody approved by the FDA (2023) and EMA (2023) that has transformed RSV prevention:

Aspect	Detail
Drug class	Long-acting monoclonal antibody targeting RSV F protein (same target as palivizumab but extended half-life)
Name breakdown	"nirsevu-" (RSV target), "-mab" (monoclonal antibody)
Route	Single IM injection
Dosing	ONE dose before the RSV season (cf. palivizumab's 5 monthly doses)
Efficacy	~75–80% reduction in RSV-related LRTI hospitalisation; ~80% efficacy against RSV bronchiolitis
Advantage over palivizumab	Single dose vs. monthly injections; lower cost per course; can be given to ALL infants (not just high-risk)
Current status	Approved in EU, US, and several Asian countries. Being evaluated for inclusion in Hong Kong's HA programme. The AAP (2023–2024) now recommends nirsevimab for all infants in their first RSV season and for high-risk children in their second season

Maternal RSV Vaccine (Abrysvo — RSVpreF)

Aspect	Detail
What	Bivalent RSV prefusion F protein vaccine given to pregnant women
Timing	Single dose at 32–36 weeks gestation
Mechanism	Stimulates maternal RSV antibodies → transplacental transfer to fetus → passive immunity in the newborn for first ~6 months
Efficacy	~57% efficacy against severe RSV LRTI in infants up to 6 months
Status	FDA-approved (September 2023); recommended as an alternative to nirsevimab (not both)

Other preventive measures:

Hand hygiene — the single most effective infection control measure
Avoiding exposure to sick contacts during RSV season
Breastfeeding — provides secretory IgA and other immune factors
Avoiding tobacco smoke exposure
Avoiding crowded settings during peak RSV season for high-risk infants

Palivizumab vs Nirsevimab

For exams in 2025–2026, know BOTH:

Palivizumab: IM Q1 month × 5 doses; only for high-risk infants; shown to decrease hospitalisation; limited by cost and need for multiple injections ^[2]
Nirsevimab: Single IM dose; for ALL infants entering first RSV season; superior convenience and wider applicability; now the preferred agent in AAP 2024 guidelines

The key conceptual difference: palivizumab is passive immunoprophylaxis requiring repeated dosing because of its shorter half-life; nirsevimab has an engineered extended half-life allowing single-dose protection for an entire RSV season.

Discharge Criteria and Safety-Net Advice

Intervention	Recommendation	Evidence Level
Supportive care (oxygen, fluids, monitoring)	✅ RECOMMENDED — MAINSTAY	Strong
Nebulised 3% hypertonic saline	✅ Recommended (inpatient) — QMH 1st line	Moderate (meta-analysis shows ↓LOS)
HFNC	✅ First-line respiratory support for moderate-severe	Strong (PARIS trial 2017)
CPAP/BiPAP	✅ If HFNC fails	Moderate
Inhaled SABA	⚠️ Consider single trial; discontinue if no response	Weak (no overall outcome benefit)
Nebulised adrenaline	⚠️ Not routine; may consider in severe cases	Weak
Systemic corticosteroids	❌ NOT recommended	Strong (no benefit, potential harm)
Antibiotics	❌ NOT routine; only if suspect 2° bacterial infection	Strong
Chest physiotherapy	❌ NOT recommended	Strong (no benefit)
Antitussives / mucolytics	❌ NOT recommended	Strong (no benefit, potential harm)

High Yield Summary

Management of Bronchiolitis — Key Exam Points:

Supportive care is the MAINSTAY ^[2]: fluids + oxygen + monitoring
Fluid support ^[2]: Higher fluid requirement due to fever, tachypnoea, reduced oral intake, vomiting. Use NG feeds before IV. If IV needed, use isotonic fluids at 2/3–3/4 maintenance. Check Na⁺ (risk of SIADH)
Oxygen support ^[2]: High flow O₂ ± CPAP, BiPAP. Escalation ladder: nasal prongs → HFNC → CPAP → BiPAP → intubation. Target SpO₂ ≥ 92%
Nebulised 3% hypertonic saline ^[2]: 1st line treatment in QMH; meta-analysis shows decreased hospitalisation rate. Works by osmotic effect — thins mucus, reduces mucosal oedema
Inhaled SABA ^[2]: May provide modest short-term improvement but no change in overall outcome. Not routine; consider single trial only
Antibiotics ^[2]: ONLY indicated if suspect secondary bacterial infection (e.g., pneumonia, otitis media, sinusitis). NOT routine
NOT recommended: systemic/inhaled steroids, routine antibiotics, chest physiotherapy, antitussives, mucolytics, decongestants
Palivizumab ^[2]: Monoclonal Ab against RSV glycoprotein; IM injection Q1 month; shown to decrease hospitalisation; limited by cost and multiple injections
Nirsevimab (2023): Single IM dose; for ALL infants; extended half-life; now preferred agent in AAP 2024
Hospitalisation criteria ^[2]: apnoea, RR > 60, severe respiratory distress, SpO₂ < 92%, difficulty feeding, < 50% usual fluid intake, uncertain diagnosis
Disease peaks day 2–3; most recover within 2 weeks; 50% have recurrent episodes ^[2]

Active Recall - Management of Bronchiolitis

References

^[1] Lecture slides: GC 141. A child with cough acute and chronic cough in children.pdf (p14–15) ^[2] Senior notes: Adrian Lui Pediatrics.pdf (p163, Acute Bronchiolitis section)

Complications of Bronchiolitis

Acute Complications

Aspect	Detail
Incidence	~2–5% of hospitalised bronchiolitis cases; higher in high-risk infants
Mechanism	Progressive small airway obstruction → worsening V/Q mismatch → initially compensated by tachypnoea (Type 1: hypoxaemia with low/normal PaCO₂). As respiratory muscles fatigue → inability to maintain minute ventilation → CO₂ retention → Type 2 respiratory failure (hypoxaemia + hypercapnia + respiratory acidosis)
Risk factors	Age < 6 weeks, prematurity, pre-existing lung disease (BPD), CHD, neuromuscular disease, immunodeficiency
Clinical signs	Rising PaCO₂ (> 6–7 kPa), falling pH (< 7.30), persistent SpO₂ < 92% despite supplemental O₂, exhaustion, decreasing respiratory effort (paradoxically may look "calmer" as they tire), grunting, see-saw breathing, apnoea
Management	Escalation of respiratory support: HFNC → CPAP → BiPAP → intubation and mechanical ventilation. PICU referral mandatory

Why respiratory failure occurs more readily in infants than adults: Infants have (1) smaller airway calibre (Poiseuille's law — resistance ∝ 1/r⁴), (2) higher chest wall compliance (floppy ribs collapse inward instead of expanding), (3) limited respiratory muscle reserve (diaphragm has fewer type I slow-twitch fatigue-resistant fibres compared to adults), (4) higher baseline metabolic rate and O₂ consumption, (5) fewer collateral ventilation channels. All of these mean they have less reserve before decompensating.

The Deceptively Quiet Baby

A tachypnoeic, wheezy infant who suddenly becomes quiet and appears "settled" may NOT be improving. They may be exhausting — the respiratory muscles are failing and can no longer generate the high airway pressures needed to wheeze. A quiet chest with rising PaCO₂ is an emergency. Always correlate clinical appearance with gas exchange (SpO₂, blood gas).

Aspect	Detail
Incidence	~1–24% of hospitalised infants (higher in youngest and most premature)
Definition	Cessation of breathing for ≥ 20 seconds, or < 20 seconds if accompanied by bradycardia (HR < 100 in infants) or desaturation (SpO₂ < 90%)
Mechanism	Multifactorial: (1) Central apnoea — immature brainstem respiratory centres, particularly in premature infants and neonates, are depressed by the viral infection (possibly mediated by inflammatory cytokines affecting the medullary respiratory centre); (2) Reflex apnoea — vagally-mediated reflex triggered by nasopharyngeal secretions or laryngeal chemoreceptor stimulation; (3) Obstructive apnoea — mucus plugging and oedema can intermittently completely obstruct airways
Risk factors	Age < 2 months (especially < 6 weeks), history of prematurity, history of apnoea of prematurity, low birth weight
Importance	Apnoea may be the presenting feature of bronchiolitis in very young infants — even before wheeze or respiratory distress develop. It is also a direct risk factor for sudden respiratory arrest
Management	Continuous cardiorespiratory monitoring, caffeine citrate (if central apnoea — particularly in ex-premature infants; loading 20 mg/kg then maintenance 5–10 mg/kg/day), CPAP (provides a continuous pneumatic splint to keep airways open), and intubation if apnoea is recurrent/prolonged

Aspect	Detail
Mechanism	Higher fluid requirement due to fever, tachypnoea, reduced oral intake, and vomiting ^[2]. Infants are obligate nasal breathers — nasal congestion prevents them from coordinating suck-swallow-breathe during feeding. Tachypnoea further disrupts this coordination. The combined effect is dramatically reduced oral intake
Clinical features	Reduced wet nappies (< 50% of normal), dry mucous membranes, sunken fontanelle, poor skin turgor, lethargy
Management	NG or IV fluid support (isotonic fluids at 2/3–3/4 maintenance due to SIADH risk). Always check serum Na⁺

Aspect	Detail
Incidence	Reported in up to 30–40% of hospitalised bronchiolitis cases (often subclinical)
Mechanism	Intrathoracic pressure changes from air trapping and hyperinflation → reduced venous return → perceived hypovolaemia by baroreceptors → ADH release. Also: inflammatory cytokines (IL-6) directly stimulate ADH release from the posterior pituitary. If the infant is on CPAP/HFNC, the positive intrathoracic pressure further stimulates ADH secretion
Consequence	Water retention → dilutional hyponatraemia (serum Na⁺ < 135 mmol/L). If severe (< 125 mmol/L) → cerebral oedema → seizures, altered consciousness
Diagnosis	Serum Na⁺ < 135, serum osmolality < 280 mOsm/kg, urine osmolality > 100 mOsm/kg (inappropriately concentrated), urine Na⁺ > 30 mmol/L, euvolaemic clinical status
Management	Fluid restriction (2/3–3/4 maintenance); use isotonic IV fluids (0.9% NaCl + dextrose); monitor Na⁺ 12–24-hourly; treat underlying cause (the SIADH resolves as bronchiolitis improves)

Antibiotics are only indicated if you suspect secondary bacterial infection (e.g., pneumonia, otitis media, sinusitis) ^[2].

Site	How It Happens	Clinical Clues
Bacterial pneumonia	Damaged bronchiolar epithelium and impaired mucociliary clearance create a fertile environment for bacterial superinfection. Common organisms: S. pneumoniae, H. influenzae, S. aureus	New-onset high fever (> 39°C) after initial improvement ("second spike"), focal consolidation on CXR, rising CRP/WBC with neutrophilia, purulent secretions
Acute otitis media (AOM)	RSV infection causes Eustachian tube oedema and dysfunction → middle ear fluid accumulation → secondary bacterial colonisation	Ear pulling, irritability, bulging/red tympanic membrane on otoscopy
Sinusitis	Mucosal oedema of the paranasal sinuses disrupts normal drainage → bacterial overgrowth	Persistent nasal discharge (> 10 days), facial pain/pressure (difficult to assess in infants)

The "double sickening" pattern: A child with bronchiolitis who initially improves around day 3–5 and then deteriorates again with new high fever and focal signs should raise suspicion for secondary bacterial infection. This is the classic biphasic course of a viral illness complicated by bacterial superinfection.

Complication	Mechanism	Clinical Significance
Atelectasis	Complete small airway obstruction (mucus plug + debris) → absorption of trapped air distal to the obstruction → alveolar collapse. Most common in right upper and middle lobes (anatomy of the bronchial tree — right middle lobe bronchus is narrower and branches at a sharper angle)	Usually subsegmental and resolves spontaneously as the airway clears. Can be mistaken for consolidation on CXR (leading to unnecessary antibiotics). Rarely causes significant clinical deterioration
Pneumothorax	Air trapping and hyperinflation → overdistension of alveoli → alveolar rupture → air leak into the pleural space. More common in mechanically ventilated infants (barotrauma/volutrauma)	Sudden deterioration with desaturation, unilateral reduced air entry, hyperresonance. Rare in non-ventilated bronchiolitis. Requires urgent decompression if tension pneumothorax
Pneumomediastinum	Same mechanism as pneumothorax — air dissects along perivascular sheaths towards the mediastinum rather than the pleural space	Usually self-limiting. Subcutaneous emphysema may be palpable. Rarely requires intervention

Long-Term Complications

Aspect	Detail
Incidence	50% have recurrent wheezing episodes ^[2] following bronchiolitis
Mechanism	Debated and likely multifactorial: (1) Epithelial damage from RSV may alter airway remodelling, making the airways more susceptible to subsequent viral triggers; (2) Neurogenic inflammation — RSV infection upregulates substance P and neurokinin receptors in airway nerves, lowering the threshold for bronchoconstriction; (3) Immunological priming — RSV infection may skew the immune response towards a Th2 phenotype (the "allergic" pathway), promoting airway hyperreactivity; (4) Shared genetic susceptibility — children who are genetically predisposed to atopy and asthma may also be more susceptible to severe RSV bronchiolitis, meaning bronchiolitis and asthma may be parallel outcomes of a common genetic/immunological predisposition rather than bronchiolitis causing asthma
Clinical significance	Parents should be counselled that wheezing may recur with future viral infections. This does NOT necessarily mean the child has "asthma" — many outgrow episodic viral-induced wheeze by age 5–6 years. However, children with severe RSV bronchiolitis in infancy do have a 2–3-fold increased risk of developing childhood asthma
Which virus matters	Rhinovirus bronchiolitis appears to carry a higher risk of subsequent asthma than RSV bronchiolitis, possibly because rhinovirus-associated wheeze is more strongly linked to atopic predisposition

Does RSV Cause Asthma?

This is a classic exam discussion question. The honest answer: we don't know for certain whether RSV causes asthma or whether the two share common risk factors (genetic predisposition, atopy). The association is clear (50% recurrent wheeze, increased asthma risk), but causation is unproven. The best way to frame it is: RSV bronchiolitis in infancy is an independent risk factor for recurrent wheeze and asthma, but it may be a marker rather than a cause.

Some may have permanent damage (e.g., bronchiolitis obliterans) after adenovirus infection (rare) ^[2].

Aspect	Detail
Definition	"Obliterans" = obliterating/destroying. A chronic condition where severe inflammatory injury to the bronchiolar epithelium leads to fibrotic obliteration of the bronchiolar lumen → permanent fixed airflow obstruction
Aetiology in children	Most commonly following severe adenovirus bronchiolitis ^[2] (especially serotypes 3, 7, 21). Also reported after influenza, measles, Mycoplasma pneumoniae infection, and post-lung/bone marrow transplantation ^[10]
Pathogenesis	Initial insult → injury to bronchiolar epithelium → repair can result in complete recovery or characterised by excessive proliferation of granulation tissue → narrowing or obliteration of airway lumen ^[10]
Clinical features	Slowly progressive dyspnoea and cough developing over weeks to months after the initial acute infection ^[10]. Persistent wheeze that does NOT respond to bronchodilators. Exercise intolerance. Recurrent LRTI. Failure to thrive
Investigations	PFT: obstructive pattern without bronchodilator reversibility ^[10]. HRCT: mosaic attenuation, air trapping on inspiratory and expiratory views, bronchial wall thickening, centrilobular nodules ^[10]. CXR: hyperinflation, unilateral hyperlucent lung (Swyer-James syndrome)
Swyer-James syndrome	A specific form of post-infectious bronchiolitis obliterans → hypoplastic lung with pulmonary hyperlucency due to overly distended alveoli and reduced arterial flow ^[11]. Results from bronchiolitis in infancy (RSV, adenovirus, Mycoplasma, staphylococcal infection). The affected lung fails to grow normally → unilateral small, hyperlucent lung on CXR
Management	No cure. Supportive: bronchodilators (limited benefit), inhaled corticosteroids (limited evidence), pulmonary rehabilitation, nutritional support, vaccination to prevent further respiratory infections. Severe cases may require long-term oxygen or lung transplantation
Prognosis	Permanent lung damage. Some children stabilise and compensate; others have progressive decline. Quality of life depends on the extent of lung involvement

Bronchiolitis Obliterans in the Paediatric Exam

BO is the most important long-term complication of bronchiolitis and is specifically linked to adenovirus ^[2]. When you're asked about long-term sequelae of bronchiolitis, this is the answer. Key exam facts: (1) Most commonly post-adenoviral, (2) Permanent fibrotic obliteration of bronchioles, (3) Fixed airflow obstruction without bronchodilator reversibility, (4) HRCT shows mosaic attenuation and air trapping, (5) Rare but devastating.

Aspect	Detail
Mechanism	Severe or recurrent bronchiolitis causes chronic bronchiolar inflammation → damage to bronchial wall elastic tissue and cartilage → irreversible bronchial dilatation → impaired mucociliary clearance → cycle of obstruction, infection, and further destruction (the "vicious cycle" of bronchiectasis) ^[11]
Risk factors	Severe adenoviral bronchiolitis, recurrent infections in immunodeficient children, underlying ciliary dyskinesia or cystic fibrosis
Clinical features	Chronic productive cough with daily purulent sputum, recurrent respiratory infections, clubbing (late), haemoptysis
Investigation	HRCT: bronchial dilatation ("signet ring sign" — bronchus larger than accompanying pulmonary artery), bronchial wall thickening, "tram-line" appearance
Hong Kong relevance	Bronchiectasis secondary to childhood LRTI is still encountered in Hong Kong, particularly in children with underlying conditions

Complication	Mechanism	Prevention
Nosocomial RSV transmission	RSV survives on surfaces for hours; transmitted via large droplets and fomites. On paediatric wards, an RSV-positive infant can infect vulnerable neonates and immunocompromised children	Strict contact precautions, hand hygiene, cohorting of RSV-positive patients, NPA testing for infection control purposes
Hospital-acquired infections	Prolonged hospitalisation → exposure to nosocomial pathogens; IV cannulae → phlebitis/line infection	Minimise duration of hospitalisation; early transition to oral feeds; remove IV access when no longer needed

Category	Complication	Frequency	Key Points
Acute	Respiratory failure	2–5% of hospitalised	Type 1 → Type 2; PICU referral
	Apnoea	1–24%	Presenting feature in neonates; monitor closely
	Dehydration	Common	Higher fluid requirement from fever, tachypnoea, poor intake ^[2]
	SIADH	Up to 30–40% (subclinical)	Hyponatraemia; fluid restrict; check Na⁺
	Secondary bacterial infection	~5–10%	Pneumonia, otitis media, sinusitis ^[2]; "double sickening"
	Atelectasis	Common (usually mild)	Often mistaken for pneumonia on CXR
	Pneumothorax	Rare	More common if mechanically ventilated
Long-term	Recurrent wheezing	50% ^[2]	May outgrow by age 5–6; associated with asthma risk
	Bronchiolitis obliterans	Rare ^[2]	Post-adenovirus; permanent damage
	Bronchiectasis	Rare	Post-severe or recurrent infections
	Impaired lung function	Variable	Reduced FEV₁ trajectories in severe RSV bronchiolitis

High Yield Summary

Complications of Bronchiolitis — Key Exam Points:

Most children recover within 2 weeks — bronchiolitis is generally a self-limiting illness ^[2]
50% have recurrent wheezing episodes ^[2] — this is the most common long-term consequence. Whether RSV "causes" asthma or is a marker of shared susceptibility remains debated
Bronchiolitis obliterans is the most important long-term complication: permanent damage after adenovirus infection (rare) ^[2]. Pathology: fibrotic obliteration of bronchiolar lumen ^[10]. HRCT: mosaic attenuation, air trapping ^[10]. Irreversible
Acute complications to know: respiratory failure (Type 1 → Type 2), apnoea (especially neonates and ex-prems), dehydration, SIADH (hyponatraemia), secondary bacterial infection (pneumonia, AOM, sinusitis), atelectasis (commonly misread as consolidation on CXR), pneumothorax (rare, mostly in ventilated infants)
Secondary bacterial infection is the reason antibiotics are sometimes needed — but only when suspected, NOT routine ^[2]
SIADH: check Na⁺ before IV fluids; use isotonic fluids at 2/3–3/4 maintenance; hyponatraemia can cause seizures
Swyer-James syndrome: unilateral hyperlucent lung from post-infectious bronchiolitis obliterans in infancy ^[11]
Prevention of complications: supportive care, appropriate oxygen therapy, early recognition of deterioration, infection control to prevent nosocomial spread

Active Recall - Complications of Bronchiolitis

References

^[2] Senior notes: Adrian Lui Pediatrics.pdf (p163, Acute Bronchiolitis — Prognosis section) ^[10] Senior notes: Ryan Ho Respiratory.pdf (p115–117, Bronchiolitis Obliterans Syndrome) ^[11] Senior notes: Ryan Ho Respiratory.pdf (p127–129, Bronchiectasis and Swyer-James syndrome)

Bronchiolitis

Definition

Epidemiology

Age Distribution

Seasonality

Incidence and Burden

Hong Kong Context

Risk Factors

Anatomy and Function: Why Small Airways Matter

Airway Anatomy

Poiseuille's Law — The Key Physics

Why Infants Are Particularly Vulnerable

Aetiology (Microbiology)

Causative Organisms

About RSV

Pathophysiology

Step 1: Viral Inoculation and Spread

Step 2: Epithelial Damage and Inflammation

Step 3: Airway Obstruction

Step 4: Downstream Consequences

Ball-Valve Mechanism (Partial Obstruction)

Complete Obstruction

V/Q Mismatch

Classification

By Severity

By Aetiology

Special Types

Clinical Features

Natural History and Timeline

Symptoms (What the Parent Reports)

Signs (What You Find on Examination)

Auscultation Findings — What You'll Hear

Examination Checklist for Bronchiolitis

Age-Specific Considerations

Summary of Pathophysiology → Clinical Features Correlation

Active Recall - Bronchiolitis (Definition, Epidemiology, Aetiology, Pathophysiology, Clinical Features)

References

Clinical Approach to the Wheezy/Tachypnoeic Infant

Differential Diagnosis — Systematic Breakdown

Detailed Differential Diagnoses

1. Viral-Induced Wheeze / Recurrent Wheezing / Early Childhood Asthma

2. Pneumonia (Viral or Bacterial)

3. Croup (Viral Laryngotracheobronchitis)

4. Foreign Body Aspiration

5. Congenital Heart Disease (Especially Left-to-Right Shunts)

6. Pertussis (Whooping Cough)

7. Other Important Differentials

Approach to Differentiating — Key Discriminating Features

Hong Kong Context

Active Recall - Differential Diagnosis of Bronchiolitis

Diagnostic Criteria — A Clinical Diagnosis

Why a Clinical Diagnosis? — Reasoning from First Principles

Diagnostic Algorithm

Investigation Modalities — What, When, Why, and Key Findings

1. Pulse Oximetry (SpO₂)

2. Nasopharyngeal Aspirate (NPA) / Nasopharyngeal Swab

3. Chest X-Ray (CXR)

4. Blood Gas Analysis (ABG / CBG / VBG)

5. Blood Tests (CBC, CRP, U&E, Blood Culture)

6. Viral Testing — Methods Compared

7. Other Investigations — Reserved for Atypical Cases

Summary: Investigation Strategy by Severity

When to Suspect This Is NOT Bronchiolitis — Red Flags Prompting Investigation

Active Recall - Diagnosis and Investigations of Bronchiolitis

Core Principle: Supportive Care Is the Mainstay

Management Algorithm

Indications for Hospitalisation

Treatment Modalities — Detailed Breakdown

1. Fluid Support

2. Oxygen Support — The Escalation Ladder

3. Nebulised 3% Hypertonic Saline

4. Inhaled Short-Acting Beta-Agonists (SABA)

5. Treatments that are NOT Recommended

6. Supportive Measures — The Practical Details

7. PICU Referral / Escalation Criteria

8. Prevention

Discharge Criteria and Safety-Net Advice

Discharge Criteria (from hospital)

Safety-Net Advice (for parents)

Summary Table: Evidence-Based Management of Bronchiolitis