Bronchiolitis
Bronchiolitis is an acute viral lower respiratory tract infection, most commonly caused by respiratory syncytial virus (RSV), predominantly affecting infants and children under 2 years of age, characterized by inflammation and obstruction of the small airways (bronchioles) leading to wheezing, tachypnoea, and respiratory distress.
Acute Bronchiolitis in Paediatrics
Bronchiolitis is a clinical syndrome that occurs in children < 2 years of age, characterised by upper respiratory tract infection (URTI) symptoms followed by lower respiratory tract infection (LRTI) and inflammation, resulting in wheezing or crackles [1][2].
Let's break the word down:
- "Bronchio-" = bronchioles (the small airways, typically < 2 mm diameter)
- "-itis" = inflammation
So bronchiolitis literally means inflammation of the bronchioles — the terminal and respiratory bronchioles. This distinguishes it from bronchitis (larger airways) and pneumonia (alveolar parenchyma).
Why < 2 years?
Airway resistance (AR) ∝ 1/r⁴ (Poiseuille's law). Because the infant's airway lumen is already narrow, even a small reduction in cross-sectional area from mucosal oedema or mucus plugging causes an exponential increase in airway resistance and work of breathing [2]. Older children have larger airways and tolerate the same degree of mucosal swelling with far less clinical consequence — hence the same virus would more likely produce a simple URTI or "wheeze" rather than the bronchiolitis syndrome.
It is typically a viral infection, usually by respiratory syncytial virus (RSV), and occasionally a bacterial infection such as Mycoplasma pneumoniae or Bordetella pertussis [2].
It is usually a self-limited disease; most children do not require hospitalisation and recover by approximately 1 month [2].
2. Epidemiology
- Leading cause of hospitalisation in the first year of life [3][4]
- Approximately 100,000 hospital admissions annually in the United States; hospital charges exceeded US$1.7 billion in 2009 [3]
- Hospitalisation has a peak incidence between 2–6 months of age [2]
- The majority of cases occur in children aged 1–9 months [5]
- Seasonal peak principally during fall and winter season [2][3]. In Hong Kong, RSV peaks around spring-summer (March–June) with a smaller winter peak — note this may differ from temperate Northern Hemisphere patterns
- RSV bronchiolitis causes fewer than 500 deaths per year in the US, but globally accounts for significant morbidity in low-resource settings [3]
- Almost all children are infected with RSV by 2 years of age; approximately 40–50% develop LRTI during their first RSV infection
- RSV does NOT produce lasting immunity [6] — reinfection is common throughout life, although subsequent infections tend to be milder
- Boys appear to be at higher risk for severe illness than girls [3]. The exact mechanism is unclear, but it is hypothesised to relate to smaller airway calibre in males during infancy and potentially different immune responses
3.1 Risk Factors for Severe and Complicated Bronchiolitis
Clinicians should assess risk factors for severe disease, such as age < 12 weeks, a history of prematurity, underlying cardiopulmonary disease, or immunodeficiency, when making decisions about evaluation and management (AAP Key Action Statement 1b, Moderate recommendation, Level B evidence) [4]
Host factors:
| Risk Factor | Pathophysiological Basis |
|---|---|
| Age < 12 weeks (especially 1–3 months) | Protective maternal (transplacental IgG) antibodies wane; immature immune system; small airway calibre; obligate nose breathers [3] |
| Prematurity (especially < 29 weeks GA) | Miss the window of greatest transplacental transfer of maternal antibodies (mainly occurs in 3rd trimester); underdeveloped lungs with fewer alveoli; possible concurrent BPD [2][3] |
| Low birth weight | Correlates with reduced lung reserves and airway size [2] |
| Chronic lung disease of prematurity (Bronchopulmonary Dysplasia/BPD) | Baseline impaired gas exchange, airway hyperreactivity, and reduced pulmonary reserve [2][3] |
| Hemodynamically significant congenital heart disease (especially with pulmonary hypertension or CHF) | Pulmonary congestion impairs gas exchange; limited cardiac reserve to compensate for increased metabolic demands [2][3] |
| Immunodeficiency | Unable to mount effective antiviral response; prolonged viral shedding [2][4] |
| Trisomy 21 (Down syndrome) | Airway hypoplasia, relative macroglossia, hypotonia, and higher incidence of congenital heart disease [3] |
| Neuromuscular disorders | Impaired cough reflex and respiratory muscle weakness → poor airway clearance [3] |
| Anatomical defect of airways | Structural narrowing amplifies the effect of mucosal swelling [2] |
Environmental factors:
| Risk Factor | Mechanism |
|---|---|
| Cigarette smoke exposure (in utero and postnatal) | Impairs mucociliary clearance, increases airway inflammation, and alters immune function. In utero exposure was associated with increased ICU admission; postnatal exposure with increased odds of severe disease [3] |
| Air pollution (even at levels accepted as "safe") | Increases bronchiolitis risk, likely through airway epithelial damage and promotion of inflammatory mediators [3] |
| Crowded living conditions / daycare attendance | Increased viral transmission |
| Older siblings | Major source of viral transmission in the household |
| Lack of breastfeeding | Loss of protective secretory IgA and other immune factors |
4. Anatomy and Physiology of the Infant Airway
Understanding why bronchiolitis preferentially affects infants requires knowledge of the developmental anatomy:
| Feature | Infant | Older Child/Adult |
|---|---|---|
| Airway diameter | Small (bronchioles ~ 0.1–0.2 mm) | Larger |
| Cartilaginous support | Less developed → more collapsible | More rigid |
| Mucosal glands | Relatively more numerous → more mucus production | Proportionally fewer |
| Collateral ventilation (pores of Kohn, channels of Lambert) | Poorly developed → if a bronchiole is obstructed, there is no alternative route for ventilation | Well-developed |
| Rib cage compliance | Highly compliant → chest wall retractions with increased work of breathing | Less compliant |
| Diaphragm muscle fibre type | Fewer type I (fatigue-resistant) fibres → more susceptible to respiratory fatigue | More type I fibres |
The key equation is:
Resistance ∝ 1/r⁴
If an infant's bronchiole has a radius of 0.5 mm and mucosal oedema of just 0.25 mm reduces the radius to 0.25 mm, the resistance increases by a factor of 2⁴ = 16-fold. In contrast, an older child with a bronchiole radius of 2 mm losing 0.25 mm to oedema retains a radius of 1.75 mm, and resistance only increases by a factor of approximately 1.7-fold. This is why the same virus produces "just a cold" in an older child but respiratory distress in an infant.
Neonates and young infants (< 3–6 months) are obligate nasal breathers. Nasal congestion from the initial URTI phase alone can significantly increase work of breathing before the lower tract is even involved.
5. Aetiology
| Virus | Proportion | Key Features |
|---|---|---|
| Respiratory Syncytial Virus (RSV) | 50–80% (most commonly identified) | RNA virus, family Paramyxoviridae, genus Pneumovirus. Most common cause and often detected as sole pathogen. Most important cause of LRTI and rehospitalisation in preterm infants. Typically follows seasonal pattern causing winter epidemics (in temperate climates). Does NOT produce lasting immunity [2][3][5][6] |
| Rhinovirus | Second most common | Associated with bronchiolitis in spring and fall. Common cold is a more common presentation (30–50%) [2][6] |
| Human Metapneumovirus (HMPV) | Significant | Another Paramyxovirus; may co-infect with RSV |
| Parainfluenza virus | Variable | Type I and II can cause bronchiolitis but croup is the more common presentation. Type III is associated with bronchiolitis in spring and fall [2] |
| Influenza virus | Variable | Clinically indistinguishable from RSV and parainfluenza bronchiolitis. Unique in that it is vaccine-preventable [2] |
| Adenovirus | < 5% | Can cause LRTI including bronchiolitis. Pharyngitis and coryza are more common presentations. Notable for potentially causing bronchiolitis obliterans (permanent damage, rare) [2][5][6] |
| Coronavirus | Variable | Can cause LRTI including bronchiolitis. Common cold is a more common presentation [2] |
| Human Bocavirus | Emerging | Often detected as co-pathogen [2] |
High Yield: RSV Key Points
RSV is by far the most commonly identified virus, detected in up to 80% of patients [3]. Some data suggest RSV may be associated with a more severe illness course compared to other viruses [3]. Some studies point to greater disease severity in infants with co-infection by 2 or more viruses, although data are conflicting [3]. Despite the robust immune response, RSV infections occur throughout life, even in the absence of detectable antigenic change [3].
- Co-infection with 2 or more viruses is common (detected in 10–30% of cases in some studies)
- Some studies point to greater disease severity in infants with co-infection by 2 or more viruses, although data are conflicting [3]
- Secondary bacterial infection (e.g., otitis media, pneumonia) is a recognised complication rather than a primary cause
Adenovirus deserves special mention [6]:
- Respiratory infections: Pharyngitis, bronchiolitis, pneumonia
- Ocular infections: Conjunctivitis (follicular, self-limiting), keratoconjunctivitis (more severe, sight-threatening)
- GI infections: Gastroenteritis
- GU infections: Haemorrhagic cystitis (haematuria, dysuria, frequency with negative bacterial culture, sterile pyuria)
- Biochemical: Leukocytosis with neutrophilia (mimics bacterial infection)
- Radiological: Features more typical of bacterial disease including high fever, lobar infiltrates and parapneumonic effusions
- Rare but important: Bronchiolitis obliterans post-adenovirus infection — permanent small airway damage [5]
6. Pathophysiology
| Pathological Process | Consequence | Clinical Manifestation |
|---|---|---|
| Inflammation of bronchiolar epithelium | Mucosal oedema → narrowed lumen | Wheezing (turbulent flow through narrowed airways), tachypnoea |
| Peribronchial infiltration of WBCs | Further airway wall thickening | Increased resistance, crackles |
| Oedema of submucosa and adventitia | Airway narrowing (remember 1/r⁴) | SOB, retractions |
| Sloughed/necrotic epithelium + fibrin deposits | Intraluminal debris obstructing airways | Atelectasis (if complete), air trapping (if ball-valve mechanism) |
| Excessive mucus production | Further luminal narrowing/obstruction | Crackles, cough, desaturation |
| Impaired ciliary function | Unable to clear debris and mucus | Prolonged symptoms, risk of secondary infection |
| Distal air trapping | Hyperinflation | Barrel chest, hyperresonance, flattened diaphragms on CXR |
| Localised atelectasis | Collapse of alveoli distal to complete obstruction | Patchy opacities on CXR, V/Q mismatch → hypoxemia |
| V/Q mismatch | Perfusion of poorly ventilated lung units | Hypoxemia |
This is a key concept:
- During inspiration, the bronchioles dilate slightly (due to negative intrapleural pressure pulling them open), allowing some air past the partial obstruction
- During expiration, the bronchioles narrow (positive intrapleural pressure compresses them), and the already swollen/debris-laden lumen becomes completely obstructed
- Air gets trapped distally → progressive hyperinflation
- This is why expiratory wheeze is prominent and why the chest appears hyperinflated
Fever is not universal, occurring in approximately 50% of patients [3] (other sources cite ~70% [5]). It occurs because:
- Viral infection triggers innate immune cells (macrophages, dendritic cells) to release pyrogens (IL-1, IL-6, TNF-α, PGE₂)
- These act on the hypothalamic thermoregulatory centre to raise the temperature set-point
- Fever is part of the host defence, but can also increase metabolic demands and insensible fluid losses
Viral shedding may last up to 4 weeks, especially in very young or immunocompromised patients [3]. This has important infection control implications in hospitals.
7. Classification
There is no universally accepted severity scoring system, but most guidelines stratify into:
| Severity | Features |
|---|---|
| Mild | Coryza, mild cough, no/minimal respiratory distress, SpO₂ > 92–95%, feeding well |
| Moderate | Persistent cough, moderate tachypnoea, subcostal/intercostal recession, SpO₂ 90–92%, some difficulty feeding |
| Severe | Marked respiratory distress, grunting, nasal flaring, SpO₂ < 90% on room air, poor feeding/dehydration, apnoea, cyanosis, lethargy/exhaustion |
- RSV bronchiolitis (most common)
- Non-RSV bronchiolitis (rhinovirus, parainfluenza, etc.)
- This distinction may have prognostic relevance: rhinovirus bronchiolitis may be more strongly associated with later development of recurrent wheezing/asthma
- Uncomplicated (majority)
- Complicated (apnoea, respiratory failure, secondary bacterial infection)
8. Clinical Features
The illness typically begins with a URTI prodrome for 2–3 days, followed by LRTI symptoms presenting with respiratory distress and increased work of breathing [2].
An uncomplicated illness may last 1 to 3 weeks before all symptoms are completely resolved [3].
Most recover within 2 weeks, but 50% have recurrent episodes [5].
Symptoms are worst on Day 2–3 (Adrian Lui notes) [5] or peaks on Day 3–5 (Felix Lai notes) [2] — the key point is that there is a predictable peak around day 3–5, after which gradual improvement occurs. If symptoms worsen after this point, consider complications (secondary bacterial infection, respiratory failure).
| Symptom | Timing | Pathophysiological Basis |
|---|---|---|
| Rhinorrhoea (runny nose) | URTI prodrome (Day 1–3) | Viral replication in nasal epithelium → mucosal inflammation → increased secretions |
| Nasal congestion | URTI prodrome | Submucosal oedema and excess secretions in narrow nasal passages; especially distressing in obligate nose-breathing infants |
| Fever (~50–70%) | URTI prodrome into LRTI phase | Pyrogenic cytokines (IL-1, IL-6, TNF-α) acting on hypothalamic thermoregulatory centre; typically low-grade (< 39°C); very high fever should prompt consideration of bacterial superinfection |
| Cough | Begins in URTI phase, worsens in LRTI phase | Initially from postnasal drip and pharyngeal irritation; later from bronchiolar inflammation stimulating cough receptors (vagal afferents in airway epithelium) |
| Difficulty breathing / Shortness of breath (SOB) | LRTI phase (Day 3–5 peak) | Airway obstruction → increased resistance → increased work of breathing |
| Wheeze (often audible) | LRTI phase | Turbulent airflow through narrowed bronchioles; predominantly expiratory due to ball-valve mechanism |
| Poor feeding / Reduced oral intake | LRTI phase | Tachypnoea makes coordinating suck-swallow-breathe difficult; nasal congestion (obligate nose breathers feed inefficiently); general malaise |
| Vomiting | LRTI phase | Mucus swallowing → gastric irritation; post-tussive vomiting; increased gastric air from mouth breathing |
| Irritability | Throughout | Hypoxaemia, general discomfort, difficulty feeding |
| Apnoea (alarming) | Can be presenting symptom | Particularly in preterm infants and infants younger than 2 months of age [2]. Mechanism not fully understood — likely central (immature brainstem respiratory centres) plus reflex (laryngeal chemoreceptor stimulation) |
Apnoea as a Presenting Feature
Bronchiolitis may be complicated by apnoea, particularly in preterm infants and infants younger than 2 months of age. Presenting with apnoea is a risk factor for respiratory failure and need for mechanical ventilation [2]. A young infant presenting with apnoea may have no obvious wheeze or cough yet — RSV infection should be considered in the differential. Don't dismiss apnoea in a neonate during RSV season as "just a blue spell."
| Sign | Pathophysiological Basis |
|---|---|
| Tachypnoea (RR > 60 in neonates, > 50 in infants 1–12m, > 40 in 1–5y) | Compensatory mechanism to maintain minute ventilation despite increased dead space from air trapping and reduced tidal volume from obstruction |
| Tachycardia | Sympathetic response to hypoxaemia, fever, and increased work of breathing; also catecholamine-mediated compensation |
| Intercostal and subcostal retractions | Highly compliant infant chest wall "sucks in" when strong inspiratory effort is generated against obstructed lower airways |
| Nasal flaring | Activation of alae nasi muscles to maximise nasal airway diameter and reduce nasal resistance — a sign of significant increased work of breathing |
| Grunting | Partial closure of glottis during early expiration to generate "auto-PEEP" (positive end-expiratory pressure), maintaining functional residual capacity and preventing alveolar collapse. A sign of severe disease |
| Head bobbing | Accessory muscle use (sternocleidomastoid) in young infants who cannot effectively recruit intercostal muscles; a sign of severe respiratory distress |
| Hyperinflated chest (barrel-shaped) | Air trapping distal to partially obstructed bronchioles; bilateral hyperinflation |
| Hyperresonance to percussion | Air trapping → hyperinflation |
| Wheezing (expiratory > inspiratory) | High-pitched sound from turbulent airflow through narrowed bronchioles. Predominantly expiratory because airways narrow further during expiration (ball-valve mechanism). Generalised and bilateral (distinguishes from foreign body aspiration which causes localised unilateral wheeze) [2][7] |
| Crackles (fine inspiratory) | Opening of previously collapsed small airways and alveoli during inspiration; fluid/mucus in small airways crackling with airflow |
| Prolonged expiratory phase | Increased time needed to exhale through narrowed airways (increased time constant = resistance × compliance) |
| Cyanosis | Severe hypoxaemia (SpO₂ typically < 85%); occurs when deoxyhaemoglobin > 5 g/dL |
| Low SpO₂ | V/Q mismatch and diffusion impairment from mucus plugging and atelectasis |
| Signs of dehydration | Reduced oral intake + increased insensible losses from fever and tachypnoea. Check for: dry mucous membranes, reduced urine output, sunken fontanelle, poor skin turgor, prolonged CRT |
| Hepatomegaly (apparent) | Not true hepatomegaly — hyperinflated lungs push the diaphragm down, causing the liver edge to be palpable below the costal margin |
- Auscultation findings can change rapidly: initially may hear just crackles, then wheeze predominates, then if airways become completely obstructed → silent chest (ominous sign of impending respiratory failure)
- Assess hydration carefully: weigh the infant (compare to recent known weight), count wet nappies, check fontanelle
- Check ears: otitis media is a common concurrent finding, especially with RSV (virus spreads via Eustachian tube)
- Assess feeding: the ability to take ≥ 50–75% of normal feeds is often used as a threshold for safe discharge
| Age | Normal RR (breaths/min) |
|---|---|
| Neonate (0–28 days) | 30–60 |
| 1–12 months | 25–50 |
| 1–5 years | 20–30 |
Differential Diagnosis Clues from the Wheeze Pattern
Generalised wheeze → Bronchiolitis (children), COPD, bronchiectasis, bronchiolitis obliterans [7]
Localised wheeze → Tumour, foreign body [7]
This is a classic GC lecture point. If a child presents with unilateral localised wheeze, think foreign body aspiration and get an expiratory CXR (the side with the foreign body will show air trapping/hyperinflation that is more apparent on the expiratory film) [2].
- Most recover within 2 weeks [5]
- 50% have recurrent episodes of wheezing [5]
- Post-bronchiolitis wheezing: many infants develop recurrent viral-triggered wheeze in the first few years of life. This is thought to be due to a combination of:
- Residual airway inflammation and remodelling
- Immune priming (Th2-biased immune response)
- Pre-existing smaller airway calibre
- Some may have permanent damage (e.g., bronchiolitis obliterans) after adenovirus infection (rare) [5]
- The relationship between bronchiolitis and subsequent asthma is complex: rhinovirus bronchiolitis appears more predictive of later asthma than RSV bronchiolitis
Differential diagnosis of acute bronchiolitis [2]:
| Differential | Key Distinguishing Feature |
|---|---|
| Asthma | Recurrent episodes, response to bronchodilators, family history of atopy, age usually > 12 months |
| Pneumonia | Higher fever, focal crackles, consolidation on CXR |
| Foreign body aspiration | Localised unilateral wheeze, sudden onset, age typically 1–3 years |
| GORD | Chronic, recurrent, related to feeds |
| Bronchopulmonary dysplasia (BPD) | History of prematurity and prolonged ventilation |
| Primary ciliary dyskinesia | Chronic, recurrent, situs inversus, neonatal respiratory distress |
| Cystic fibrosis | Chronic, failure to thrive, steatorrhoea, recurrent infections |
| Congestive heart failure (with pulmonary venous congestion) | Hepatomegaly, murmur, cardiomegaly on CXR, poor weight gain |
Prevention [5]:
- Palivizumab: monoclonal antibody against RSV glycoprotein (F protein)
- Route: IM injection every month (Q1m) during RSV season
- Efficacy: shown to decrease hospitalisation rate, but limited use due to cost and multiple injections required
- Nirsevimab (Beyfortus®, 2023–): a long-acting monoclonal antibody requiring only a single dose per RSV season. Now recommended by AAP (2023) for all infants < 8 months entering their first RSV season and for high-risk children 8–19 months. This represents a paradigm shift from the older palivizumab approach
- RSV vaccines (Abrysvo®, Arexvy®): maternal RSV vaccination in pregnancy now approved (2023) to provide passive protection to the newborn
- Infection control: hand hygiene, contact precautions, cohorting in hospital
High Yield Summary
-
Definition: Clinical syndrome in children < 2 years; URTI prodrome → LRTI with wheezing/crackles. Usually RSV.
-
Why infants?: Airway resistance ∝ 1/r⁴ — small airways mean exponential increase in resistance with even minor oedema.
-
Peak age: 2–6 months; peak season: winter (temperate) / spring-summer (HK for RSV).
-
Most common pathogen: RSV (50–80%); second is rhinovirus.
-
Risk factors for severe disease: Age < 12 weeks, prematurity (< 29 wk GA), BPD, haemodynamically significant CHD, immunodeficiency, Trisomy 21, neuromuscular disease, smoke exposure.
-
Pathophysiology: Viral replication → bronchiolar mucosal oedema + necrotic epithelium + mucus + fibrin → airway obstruction → air trapping → hyperinflation + atelectasis → V/Q mismatch → hypoxaemia.
-
Clinical course: URTI prodrome (2–3 days) → LRTI phase peaking Day 3–5 → gradual resolution over 1–3 weeks.
-
Key signs: Tachypnoea, retractions, nasal flaring, wheeze (generalised, bilateral), crackles, hyperinflated chest.
-
Red flags: Apnoea (especially < 2 months / preterm), grunting, cyanosis, poor feeding, exhaustion/listlessness.
-
Diagnosis: Clinical — history and physical examination. Routine lab/imaging NOT recommended (AAP).
-
Generalised wheeze (think bronchiolitis, COPD, bronchiectasis) vs Localised wheeze (think foreign body, tumour).
-
Adenovirus can cause bronchiolitis obliterans (permanent damage).
-
Prevention: Palivizumab (monthly IM), Nirsevimab (single dose, new standard), maternal RSV vaccine, hand hygiene.
Active Recall - Bronchiolitis (Definition, Epidemiology, Risk Factors, Aetiology, Pathophysiology, Clinical Features)
[1] GC 040. Cough and wheezing_asthma and allergic lung diseases.pdf (p25) [2] MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p148–150) [3] Paediatrics in Review - Bronchiolitis.pdf (p2–4) [4] Paediatrics in Review - Bronchiolitis.pdf (p2, Table 1 — AAP Guidelines) [5] Adrian Lui Pediatrics Notes.pdf (p163) [6] MBBS Final MB (Medicine) (Felix PY Lai).pdf (p118, p146) [7] GC 040. Cough and wheezing_asthma and allergic lung diseases.pdf (p25)
Differential Diagnosis of Acute Bronchiolitis
A wheezing, tachypnoeic infant under 2 years is one of the most common presentations to a paediatric emergency department. While acute viral bronchiolitis accounts for the vast majority, the clinician must systematically consider and exclude mimics — some benign, some life-threatening. The differential revolves around two clinical questions:
- Is this truly lower airway obstruction (wheezing)? — or is the sound actually stridor (upper airway)?
- If it is lower airway obstruction, what is the cause? — infection, structural, allergic, cardiac, or other?
GC High Yield — Wheeze Pattern
Differential diagnosis of cough and wheeze [7]:
Generalised wheeze: chronic obstructive lung disease, bronchiectasis, bronchiolitis obliterans, viral bronchiolitis (children)
Localised wheeze: tumour, foreign body
This distinction is the single most important first-pass filter. In an infant, bilateral generalised wheeze points toward bronchiolitis or reactive airway disease; unilateral/localised wheeze is foreign body aspiration until proven otherwise.
The differentials below are listed in order of clinical relevance for a paediatric setting, with the pathophysiological reason each condition mimics bronchiolitis and the key distinguishing features [2][5][8][9].
| Differential | Why It Mimics Bronchiolitis | Key Distinguishing Features |
|---|---|---|
| Asthma | Wheeze, cough, SOB in a young child; both involve small-airway obstruction | Recurrent episodic attacks with symptom-free intervals; diurnal variation (worse at night/early morning); response to bronchodilators; personal/family history of atopy (eczema, allergic rhinitis); typically age > 12 months (though "infant wheeze" overlaps); triggers include exercise, allergens, cold air; spirometry shows reversible airflow obstruction [5][8][9] |
| Pneumonia | Fever, cough, tachypnoea, respiratory distress overlap | Higher/more persistent fever; focal crackles (not generalised wheeze); consolidation on CXR (lobar or bronchopneumonic pattern with air bronchograms); toxic appearance; productive/purulent sputum in older children; neutrophilia/raised CRP [2][5][10] |
| Foreign body aspiration ± aspiration pneumonia | Sudden-onset wheeze, cough, respiratory distress in a toddler | Localised unilateral wheeze instead of generalised wheeze; sudden onset without preceding URTI prodrome; age typically 1–3 years (mobile child, exploring with mouth); history of choking episode (may not be witnessed); expiratory CXR should be taken — unilateral hyperinflation more apparent on expiratory film [2][5][7][8] |
| Viral croup (Laryngotracheobronchitis) | Viral URTI prodrome in a young child with respiratory distress | Inspiratory stridor (not expiratory wheeze); barking "sea-lion" cough; hoarseness; age typically 6 months – 6 years (peak 2 years); caused by parainfluenza virus (mainly); worse at night; steeple sign on neck XR [11] |
| Pertussis (Whooping Cough) | Paroxysmal cough in a young infant; can cause apnoea | Paroxysmal cough with inspiratory "whoop"; post-tussive vomiting; apnoea in young infants (< 3 months); classically afebrile during paroxysmal phase; marked lymphocytosis on CBC; under-immunised or incompletely immunised infant [6][10] |
| Gastroesophageal reflux disease (GERD) | Recurrent wheeze, cough, apnoea in infants | Temporal relationship to feeds (worse post-prandially, when supine); recurrent vomiting/regurgitation; chronic rather than acute; may cause recurrent aspiration → chemical pneumonitis; failure to thrive; does not follow a "URTI prodrome → LRTI" pattern [2][5] |
| Congestive heart failure (CHF) with pulmonary venous congestion | Tachypnoea, wheeze ("cardiac wheeze"), hepatomegaly, poor feeding in infant | Murmur on auscultation; cardiomegaly on CXR; hepatomegaly (true — not pseudo-hepatomegaly from hyperinflated lungs); poor weight gain/FTT; gallop rhythm; diaphoresis with feeds; no URTI prodrome; echocardiography confirms structural heart disease [2][5] |
| Bronchopulmonary dysplasia (BPD) | Chronic wheeze, tachypnoea, oxygen dependence in infant | History of prematurity and prolonged mechanical ventilation/oxygen; oxygen dependence at 36 weeks corrected GA; chronic course rather than acute; CXR shows chronic changes (hyperinflation, fibrosis, cystic changes) [2][5][8] |
| Cystic fibrosis (CF) | Recurrent wheeze, chronic cough with sputum in infant/child | Chronic productive cough; failure to thrive; steatorrhoea/malabsorption (pancreatic insufficiency); rectal prolapse; meconium ileus (neonatal); salty taste of skin; finger clubbing; ethnicity (more common in Caucasians, rare in Chinese); sweat chloride test diagnostic [2][5][8] |
| Primary ciliary dyskinesia (PCD) | Recurrent wheeze, chronic cough, recurrent LRTI | Neonatal respiratory distress (unexplained); chronic wet cough from birth; recurrent sinopulmonary infections; situs inversus or heterotaxy (in ~50%); nasal NO markedly low; recurrent otitis media; electron microscopy of cilia shows ultrastructural defects [2][5][8] |
| Bronchiolitis obliterans (BO) | Fixed wheeze, air trapping | History of preceding severe lower airway injury (adenovirus infection, post-transplant, toxic inhalation); persistent wheeze not responsive to bronchodilators (irreversible obstruction); HRCT shows mosaic attenuation and air trapping; PFT shows fixed obstructive pattern; not an acute presentation [5][7][8][12] |
| Vascular ring / airway compression | Stridor ± wheeze, feeding difficulties in infancy | Biphasic stridor (not purely expiratory wheeze); dysphagia/feeding difficulties; symptoms from birth or very early infancy (not seasonal); barium swallow shows posterior oesophageal indentation; CT angiography or MRA diagnostic [9] |
| Tracheo-/bronchomalacia | Expiratory wheeze, recurrent "noisy breathing" | Symptoms from birth; wheeze worsens with crying/feeding/exertion (increased airflow collapses floppy airway); improves with prone positioning; does not follow viral prodrome pattern; flexible bronchoscopy shows dynamic airway collapse [9] |
The following flowchart summarises the thought process when an infant or young child presents with wheeze and/or respiratory distress:
Key Distinguishing Principles — Explained from First Principles
This is arguably the most common diagnostic challenge. Both cause wheeze in young children.
- Bronchiolitis = a single acute episode of virus-triggered lower airway inflammation in a child < 2 years, with URTI prodrome
- Asthma = a chronic inflammatory airway disease with recurrent episodic attacks characterised by variable airflow obstruction that is reversible (spontaneously or with treatment) [8][9]
Why the confusion? Many viruses that cause bronchiolitis (especially rhinovirus) also trigger asthma exacerbations. In a child under 12 months having their first wheeze episode preceded by coryzal symptoms → call it bronchiolitis. In a child with recurrent episodes, family/personal history of atopy, and response to bronchodilators → think asthma [2][8].
Practically: A first episode of virus-triggered wheeze in a child < 12 months = bronchiolitis. If ≥ 3 episodes of wheezing, or age > 2 years, or clear atopic background → consider asthma.
- Both are viral LRTIs and can overlap (bronchopneumonia)
- Pneumonia primarily involves the alveolar parenchyma (filled with pus/exudate → consolidation), while bronchiolitis involves the small airways (mucosal oedema, mucus, debris → airflow obstruction and air trapping) [2][10]
- Clinically: pneumonia → focal crackles, high fever, toxic-looking, consolidation on CXR; bronchiolitis → bilateral wheeze + crackles, hyperinflation on CXR [2]
Foreign body aspiration typically presents with localised unilateral wheeze instead of generalised wheeze [2][7]. The history may include a witnessed choking event, but up to 40% of cases have no witnessed aspiration. Think of it in any toddler (1–3 years) with sudden-onset unilateral wheeze.
Expiratory CXR should be taken when foreign body aspiration is suspected since the unilateral hyperinflation may be more apparent on the expiratory film [2][8]. On the expiratory film, the normal lung deflates while the obstructed side remains hyperinflated — this asymmetry is the key radiological finding. If the child is too young to cooperate with an expiratory film, bilateral lateral decubitus films can demonstrate the same principle (the dependent lung should normally deflate; if it doesn't, suspect FB on that side).
Infants with hemodynamically significant congenital heart disease (e.g., large VSD, AVSD, PDA) can present with tachypnoea and wheeze that mimics bronchiolitis [2][5]. The mechanism: left-to-right shunt → pulmonary overcirculation → pulmonary oedema → fluid in the peribronchiolar interstitium compresses small airways → "cardiac wheeze." Key clues: murmur, hepatomegaly, cardiomegaly on CXR, failure to thrive, diaphoresis with feeds. An echocardiogram is diagnostic.
Bordetella pertussis can present with paroxysmal cough and apnoea in young infants, mimicking severe bronchiolitis (especially in under-immunised or incompletely immunised infants) [2][10]. The paroxysmal phase is typically afebrile, and there is a characteristic marked lymphocytosis (WBC often > 20 × 10⁹/L with > 60% lymphocytes). NPA for Bordetella PCR is the confirmatory test. This matters because pertussis requires specific treatment (macrolides) and contact prophylaxis.
These congenital structural anomalies cause chronic noisy breathing and wheeze from birth — they do not follow a viral prodrome pattern. A vascular ring (e.g., double aortic arch, right aortic arch with aberrant left subclavian and ligamentum arteriosum) externally compresses the trachea and/or oesophagus. Tracheobronchomalacia involves excessive collapsibility of the airway wall due to cartilage immaturity. Both can be misdiagnosed as "recurrent bronchiolitis" if not specifically considered [9].
A quick mnemonic to recall the bronchiolitis differentials:
| Letter | Differential |
|---|---|
| B | BPD (Bronchopulmonary Dysplasia) |
| A | Asthma |
| D | Default — Bronchiolitis itself (most common) |
| B | Bronchiolitis Obliterans |
| F | Foreign Body Aspiration |
| C | Cystic Fibrosis / Congenital Heart Disease (CHF) |
| G | GERD |
| P | Pneumonia |
| P | Pertussis / Primary Ciliary Dyskinesia |
| V | Vascular ring / airway malacia |
High Yield Summary — DDx of Bronchiolitis
-
Generalised bilateral wheeze in an infant with URTI prodrome → most likely bronchiolitis. Localised unilateral wheeze → think foreign body (get expiratory CXR).
-
The hardest DDx is asthma vs bronchiolitis: first episode + age < 12 months + viral prodrome = bronchiolitis; recurrent episodes + atopy + bronchodilator response = asthma.
-
Pneumonia has higher/persistent fever, focal signs, consolidation on CXR.
-
CHF mimics bronchiolitis but look for murmur, hepatomegaly, cardiomegaly, FTT, diaphoresis with feeds.
-
Pertussis: afebrile paroxysmal cough, apnoea, marked lymphocytosis, under-immunised infant.
-
Chronic/recurrent wheeze from birth without clear viral triggers → structural (vascular ring, malacia, BPD) or genetic (CF, PCD).
-
Always assess for red flags: unilateral wheeze (FB), FTT + steatorrhoea (CF), situs inversus (PCD), murmur (CHD), ex-premature + O₂-dependent (BPD).
Active Recall - Differential Diagnosis of Bronchiolitis
References
[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p148–151) [3] Lecture slides: Paediatrics in Review - Bronchiolitis.pdf (p3–4) [5] Senior notes: Adrian Lui Pediatrics Notes.pdf (p163) [6] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p118–122) [7] Lecture slides: GC 040. Cough and wheezing_asthma and allergic lung diseases.pdf (p25) [8] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p176) [9] Lecture slides: Evaluation of wheezing in infants and children - UpToDate.pdf (p9) [10] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p139, p146) [11] Senior notes: Adrian Lui Pediatrics Notes.pdf (p161) [12] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p191, p220, p233)
Diagnostic Criteria, Diagnostic Algorithm, and Investigations for Acute Bronchiolitis
This is the single most important concept to internalise:
Clinicians should diagnose bronchiolitis and assess disease severity on the basis of history and physical examination findings (AAP Key Action Statement 1a, Strong recommendation, Level B evidence) [4]
When clinicians diagnose bronchiolitis on the basis of history and physical examination findings, radiographic or laboratory studies should not be obtained routinely (AAP Key Action Statement 1c, Strong recommendation, Level B evidence) [4]
Why? Because bronchiolitis has a characteristic clinical pattern that is highly recognisable, and routine investigations:
- Do not change management in uncomplicated cases
- May lead to harm (e.g., abnormal CXR findings → unnecessary antibiotic use; blood draws → pain and distress in infants) [3]
- Add cost without improving outcomes
That said, investigations become important when you need to: (a) confirm severity, (b) rule out differentials, (c) guide specific therapies (e.g., antivirals for influenza), or (d) manage complications.
There is no single universally accepted set of "diagnostic criteria" with a point score (unlike, say, the Jones criteria for rheumatic fever). Instead, the diagnosis rests on the combination of clinical features within the correct clinical context [2][4][5]:
| Criterion | Detail |
|---|---|
| Age | Child < 2 years of age (by definition) [2] |
| URTI prodrome | 2–3 days of preceding coryzal symptoms: rhinorrhoea, nasal congestion ± low-grade fever [2][5] |
| Followed by LRTI features | Wheezing and/or crackles on auscultation, cough, tachypnoea, signs of increased work of breathing (retractions, nasal flaring, grunting) [2][4] |
| Appropriate seasonality and exposure | Winter/spring epidemic in temperate climates; known circulating RSV/other respiratory viruses; contact with sick individuals |
| First or early episode | First episode is most typical; recurrent wheeze pushes toward asthma |
| No alternative explanation | No clinical features suggesting a more serious or alternative diagnosis (e.g., no murmur suggesting CHD, no unilateral wheeze suggesting FB) |
2. Physical Examination — Systematic Approach
The physical examination serves both to confirm the diagnosis and to assess disease severity [2][3]:
| Parameter | What to Look For | Why |
|---|---|---|
| Assessment of respiratory distress | Tachypnoea, nasal flaring, grunting, intercostal or subcostal retractions [2] | Quantifies work of breathing; grunting = generating auto-PEEP to prevent alveolar collapse (severe sign) |
| Hypoxaemia | Cyanosis, hypoxemia on pulse oximeter [2] | V/Q mismatch from atelectasis and mucus plugging |
| Assessment of hydration status [2] | Sunken fontanelle, dry mucous membranes, poor skin turgor, delayed capillary refill, reduced wet nappies | Tachypnoea + fever → ↑ insensible losses; poor feeding → ↓ intake |
| System | Findings | Significance |
|---|---|---|
| ENT examination | Conjunctivitis, otitis media, pharyngitis [2] | Concurrent viral involvement of upper aerodigestive tract; otitis media is a common co-infection |
| Respiratory examination | Hyperexpanded lungs, wheezing ± coarse or fine crepitations, prolonged expiratory phase [2] | Hyperexpansion = air trapping; wheeze = turbulent flow through narrowed bronchioles; crackles = fluid/mucus in small airways opening during inspiration |
| General | Lethargy, irritability, feeding behaviour | Exhaustion / listlessness = impending respiratory failure |
Physical examination findings may vary from moment to moment, so often-repeated observations are helpful to truly assess clinical severity [3]. The nature of inherent variability in children with bronchiolitis has made it difficult for a single clinical severity scoring system to be widely accepted [3].
| Feature | Mild | Moderate | Severe |
|---|---|---|---|
| Respiratory rate | Mildly ↑ for age | Moderately ↑ | Markedly ↑ or ↓ (ominous) |
| SpO₂ on room air | > 92% | 90–92% | < 90% |
| Retractions | None–mild | Moderate | Severe, ± grunting |
| Feeding | Taking > 75% normal | 50–75% | < 50% or unable to feed |
| Behaviour | Alert, playful | Irritable | Lethargic / exhausted |
| Apnoea | Nil | Nil | Present |
The following flowchart represents the systematic clinical approach from presentation to diagnosis and disposition:
4. Investigation Modalities — When, Why, and How to Interpret
The philosophy is: investigate only when the result will change your management. Below is a systematic breakdown of each investigation modality.
Pulse oximetry is the single most important bedside investigation [5].
| Aspect | Detail |
|---|---|
| What it measures | Estimates arterial oxygen saturation (SpO₂) by measuring differential absorption of two wavelengths of infrared light by oxyhaemoglobin vs deoxyhaemoglobin (Beer-Lambert law) [13] |
| Why it matters | Hypoxaemia (from V/Q mismatch due to mucus plugging and atelectasis) is the major physiological derangement in bronchiolitis; SpO₂ guides need for supplemental O₂ |
| Key threshold | AAP: clinicians may choose not to administer supplemental oxygen if the oxyhemoglobin saturation exceeds 90% [4]. Most UK/Australasian guidelines use 92% as threshold. NICE (2021) uses ≤ 92% as criterion for O₂ therapy |
| Continuous vs intermittent | Clinicians may choose not to use continuous pulse oximetry (AAP KAS 6b, Weak recommendation, Level C) [4]. Continuous monitoring can lead to unnecessary intervention for transient desaturations and prolong hospital stay |
| Pitfalls | Errors: dark skin, nail varnish, poor peripheral perfusion (check HR matches ECG), abnormal Hb (COHb → falsely high, metHb → falsely high or low) [13]. In infants, sensors are typically placed on the foot (especially neonates) |
High Yield — SpO₂ Interpretation
Normal SpO₂ does NOT equal normal ventilation [13]. The oxyhaemoglobin dissociation curve is sigmoid: SpO₂ remains > 90% until PaO₂ drops to approximately 60 mmHg (the "cliff edge"). Below this, SpO₂ falls precipitously. Also, SpO₂ tells you nothing about CO₂ — a child can have normal SpO₂ but be hypercapnic (type 2 respiratory failure). If ventilatory failure is suspected, you need an ABG.
Radiographic studies are NOT necessary to make the diagnosis of bronchiolitis and should not be routinely performed [2]
The AAP clinical practice guideline specifically recommends against the routine use of chest radiography for the evaluation of bronchiolitis [3]
Why not? Most patients with bronchiolitis have chest radiographs with hyperinflation, possibly with atelectasis or infiltrates, which often do not correlate with disease severity or aid with management [3]. Abnormal findings may lead to increased use of antibiotics without true underlying bacterial pneumonia, increasing both potential harms to the patient and health-care costs [3].
When to get a CXR:
- Suspected respiratory failure (need to assess degree of air trapping, atelectasis, or rule out pneumothorax)
- Atypical presentation (e.g., very high fever with focal signs → query pneumonia)
- Clinical deterioration despite appropriate supportive care
- To rule out alternative diagnoses (cardiomegaly → CHD/CHF; unilateral hyperinflation → FB)
CXR findings in bronchiolitis — variable and non-specific [2]:
| Finding | Pathophysiological Basis | Appearance |
|---|---|---|
| Hyperinflation of lungs (hallmark) [2] | Air trapping distal to partially obstructed bronchioles (ball-valve mechanism) | > 6 anterior ribs visible above the diaphragm on PA view; flattened diaphragms; increased AP diameter on lateral; hyperlucent lung fields |
| Peribronchial thickening ("peribronchial cuffing") [2] | Inflammation and oedema around bronchiolar walls | Ring-like or "doughnut" opacities around bronchi seen end-on; "tram-track" lines along bronchi seen longitudinally |
| Patchy infiltrates [2] | Atelectasis from mucus plugging; may mimic consolidation | Patchy opacities, often bilateral; commonly right upper lobe and right middle lobe (due to anatomy — more vertical right main bronchus → more debris deposition) |
| Atelectasis [2] | Complete bronchiolar obstruction → distal alveolar absorption collapse | Sub-segmental or segmental opacification; volume loss with mediastinal shift toward the affected side |
CXR Misinterpretation Trap
Patchy atelectasis in bronchiolitis is frequently misinterpreted as pneumonic consolidation, leading to unnecessary antibiotic prescriptions. The key differentiator: consolidation in bacterial pneumonia tends to be lobar and dense with air bronchograms, while bronchiolitis atelectasis is patchy, shifting, and associated with generalised hyperinflation. If you see hyperinflation + patchy opacities in an infant with bilateral wheeze → it's almost certainly bronchiolitis-related atelectasis, NOT pneumonia [3].
CXR can also appear on the GC radiology slide as part of diffuse lung lesions — bronchiectasis and bronchiolitis are listed as causes of diffuse lung shadow patterns alongside ILD, infections, and emphysema [14].
CXR interpretation — plain radiograph also provides:
- Assessment of cardiac silhouette (cardiomegaly → CHD/CHF)
- Assessment for pleural effusion (parapneumonic or cardiac)
- Assessment of the mediastinum (lymphadenopathy, vascular ring appearance)
± ABG if respiratory failure [5]
| Aspect | Detail |
|---|---|
| When | Suspected respiratory failure: recurrent apnoea, signs of exhaustion, cyanosis, SpO₂ < 90% despite supplemental O₂ |
| What you expect | Type 1 respiratory failure (early/moderate): hypoxaemia (PaO₂ < 60 mmHg) with normal/low PaCO₂ (hyperventilation compensating). Type 2 respiratory failure (late/severe): hypoxaemia + hypercapnia (PaCO₂ > 50 mmHg) ± respiratory acidosis (pH < 7.35) — indicates respiratory muscle fatigue and impending need for ventilatory support |
| Why capillary is often preferred | In infants, arterial puncture is technically difficult and distressing; capillary blood gas (from warmed heel prick) gives adequate estimation of pH and pCO₂, though pO₂ is less reliable. Venous blood gas can estimate pH and pCO₂ but significantly underestimates PaO₂ |
| Normal infant values | pH 7.35–7.45; PaCO₂ 35–45 mmHg (4.7–6.0 kPa); PaO₂ 60–80 mmHg in neonates, 80–100 in older infants |
4.4 Laboratory Studies (Blood Tests)
Laboratory studies are NOT necessary to make the diagnosis of bronchiolitis and should not be routinely performed [2]
CBC has not been established to be clinically useful in most patients with bronchiolitis [2]. WBC does not appear to predict bacteremia in febrile children with LRTI due to RSV [2].
Why not useful? RSV bronchiolitis can produce a normal or mildly elevated WBC. There is no consistent pattern (unlike pertussis where marked lymphocytosis is a clue). A high WBC may prompt unnecessary antibiotics.
When to consider: If clinical features suggest secondary bacterial infection (persistently high fever, toxic appearance, focal signs) or if the child is very young (< 90 days — see below).
NOT routinely indicated in infants and children hospitalised with LRTI due to RSV [2].
Why? The rate of concurrent bacteraemia in RSV-positive infants is very low (< 1% in most studies). Blood cultures are only cost-effective when pre-test probability of bacteraemia is sufficient, which is not the case in typical bronchiolitis.
When to consider: Toxic-appearing infant, suspected sepsis, young infant < 28 days with fever (applying neonatal fever workup rules).
Consider urinalysis in infants < 90 days old hospitalised with LRTI due to RSV to screen for serious secondary bacterial infection such as urinary tract infection (UTI) [2].
Why? Positive urine culture found in 5.4% of febrile infants < 60 days with RSV infection [2]. In very young infants, the presence of RSV does not "rule out" concurrent serious bacterial infection (especially UTI), because their immature immune system can harbour both.
NPA for respiratory virus (RV) panel [2]:
- Methods: RT-PCR, rapid antigen detection, immunofluorescence (IF), viral culture
- Panel components (typical Hong Kong HA panel): RSV Ag, Human metapneumovirus Ag, Adenovirus Ag, Influenza A and B Ag/IF, Parainfluenza 1,2,3 Ag [2]
- Note: The panel does not contain rhinovirus and enterovirus [2] — these require separate multiplex PCR
The AAP clinical practice guideline recommends against routine viral testing given that identification of a given virus does not alter management [3]
Then when IS viral testing indicated? Testing is indicated if the results will alter management of the patient, including [2]:
| Indication | How It Changes Management |
|---|---|
| Initiation/discontinuation of antibiotics or anti-influenza therapy | If influenza is detected → oseltamivir may be started. If RSV is confirmed → antibiotics less justified |
| Discontinuation of palivizumab prophylaxis | Determination of breakthrough RSV infection in patients receiving prophylaxis — if RSV is confirmed, palivizumab is stopped for the remainder of that season |
| Isolation or cohorting of hospitalised patients | RSV-positive infants can be cohorted together; prevents nosocomial cross-infection. This is particularly important in Hong Kong HA hospitals during winter surges |
Practical Point — NPA in Hong Kong Hospitals
In practice at QMH and other HA hospitals, NPA for respiratory virus panel is frequently performed on admitted infants — even though it doesn't change bronchiolitis treatment per se — because it guides infection control decisions (cohorting, isolation), informs palivizumab decisions, and identifies influenza (which is treatable with oseltamivir). So while the AAP says "don't routinely test," the real-world Hong Kong practice is to test most admissions. Understand the principle (don't test if it won't change management) but know the practical caveats.
| Investigation | When to Consider | What You're Looking For |
|---|---|---|
| Echocardiography | Murmur, cardiomegaly on CXR, hepatomegaly, failure to thrive, diaphoresis with feeds | Structural heart disease (VSD, ASD, PDA, AVSD), pulmonary hypertension, ventricular function |
| Sweat chloride test | FTT, steatorrhoea, recurrent infections, meconium ileus history, family history | Sweat chloride ≥ 60 mmol/L → diagnostic for CF |
| Nasal nitric oxide (nNO) | Chronic wet cough from birth, situs inversus, recurrent otitis media | Markedly low nNO → primary ciliary dyskinesia |
| CT thorax (HRCT) | Suspected bronchiolitis obliterans (persistent wheeze post-severe adenovirus infection or post-transplant) | Mosaic attenuation, air trapping on expiratory views, bronchial wall thickening [15] |
| Flexible bronchoscopy | Suspected airway malacia, foreign body not seen on imaging, recurrent unexplained wheeze | Dynamic airway collapse (malacia); retained FB; structural anomaly |
| pH probe / impedance | Suspected GERD causing recurrent aspiration and wheeze | Acid and non-acid reflux episodes correlating with respiratory events |
| Pulmonary function tests | Older cooperative children (usually > 5–6 years) with recurrent wheeze — NOT applicable in acute bronchiolitis in infants | Obstructive pattern with bronchodilator reversibility → asthma [16] |
| Investigation | Routine? | Key Indication | Key Finding |
|---|---|---|---|
| Pulse oximetry | YES — always | Assess oxygenation | SpO₂ < 90% → give O₂ |
| CXR | NO — not routine | Respiratory failure, atypical features, exclude DDx | Hyperinflation (hallmark), peribronchial thickening, atelectasis, patchy infiltrates [2] |
| ABG / CBG | NO — not routine | Suspected respiratory failure | Type 1 → hypoxaemia; Type 2 → hypoxaemia + hypercapnia |
| CBC | NO — not routine | Suspected 2° bacterial infection, young infant | Non-specific; does not predict bacteraemia [2] |
| Blood culture | NO — not routine | Toxic infant, suspected sepsis | Bacteraemia (rare in RSV) |
| Urinalysis | Consider if < 90 days | Screen for concurrent UTI in young febrile infants | 5.4% positive urine culture in febrile infants < 60 days with RSV [2] |
| NPA viral panel | Not routine per AAP; commonly done in HK | Cohorting, influenza treatment, palivizumab decisions | RSV, HMPV, adenovirus, influenza, parainfluenza antigen/PCR |
High Yield Summary — Diagnosis of Bronchiolitis
-
Clinical diagnosis — history + physical examination. No lab or imaging required routinely (AAP Strong recommendation).
-
Diagnostic triad: Age < 2 years + URTI prodrome (2–3 days) + LRTI features (bilateral wheeze/crackles, tachypnoea, respiratory distress).
-
Pulse oximetry is the only "routine" investigation — guides O₂ therapy (threshold: SpO₂ ≤ 90% per AAP, ≤ 92% per NICE/Australasian guidelines).
-
CXR NOT routine — hallmark finding is hyperinflation; patchy atelectasis is often misread as pneumonia → unnecessary antibiotics.
-
Blood tests NOT routine — CBC doesn't predict bacteraemia; blood culture not indicated unless toxic/septic.
-
Urinalysis: consider in febrile infants < 90 days to screen for concurrent UTI (5.4% positive rate).
-
NPA viral panel: not routine per AAP but commonly done in Hong Kong for infection control (cohorting), influenza treatment decisions, and palivizumab breakthrough confirmation.
-
ABG/CBG: only if respiratory failure suspected (recurrent apnoea, exhaustion, cyanosis, SpO₂ < 90% despite O₂).
-
Severity is assessed clinically — repeated observations are key; no single scoring system is universally accepted.
Active Recall - Diagnosis and Investigations of Bronchiolitis
References
[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p148, p151) [3] Lecture slides: Paediatrics in Review - Bronchiolitis.pdf (p1–5) [4] Lecture slides: Paediatrics in Review - Bronchiolitis.pdf (p2, Table 1 — AAP Guidelines) [5] Senior notes: Adrian Lui Pediatrics Notes.pdf (p163) [13] Senior notes: Maksim Medicine Notes.pdf (p280–282) [14] Lecture slides: GC 012. Abnormal lung shadow on chest radiograph CXR, CT.pdf (p39) [15] Senior notes: Ryan Ho Respiratory.pdf (p115–117) [16] Lecture slides: Evaluation of wheezing in infants and children - UpToDate.pdf (p8)
Management of Acute Bronchiolitis
Although bronchiolitis is a condition commonly encountered in paediatrics, there is no single effective therapeutic agent; therefore, clinicians should be aware that the main treatment plan for bronchiolitis is supportive care [3]
This is one of the most frequently tested concepts. The vast majority of pharmacological interventions studied — bronchodilators, corticosteroids, antibiotics, chest physio — have been shown to NOT improve outcomes. The mainstay is keeping the infant oxygenated and hydrated until the self-limiting illness resolves.
Any of the following features should lead to further review and referral for hospital admission [2]:
| Criterion | Pathophysiological Rationale |
|---|---|
| History of apnoea | Central apnoea is a risk factor for respiratory failure and need for mechanical ventilation; especially concerning in infants < 2 months or ex-premature |
| Respiratory rate > 60 breaths per minute | Tachypnoea beyond the upper normal range for neonates indicates significant increased work of breathing; infants have limited respiratory reserve |
| Severe respiratory distress with accessory muscle use or grunting | Grunting = auto-PEEP generation to prevent alveolar collapse — indicates severe disease approaching respiratory failure |
| SpO₂ < 92% in room air | Significant V/Q mismatch requiring supplemental oxygen; below this threshold, the infant is on the steep part of the oxyhaemoglobin dissociation curve |
| Difficulty feeding / taken < 50% of usual fluid intake in preceding 24 hours | Inability to coordinate suck-swallow-breathe due to tachypnoea and nasal obstruction → risk of dehydration → requires supported feeding (NG or IV) |
| Diagnostic uncertainty | If you're not sure it's bronchiolitis, admit to observe and investigate |
Additional social considerations for admission:
- Young infant < 6 weeks (very limited reserve; high apnoea risk)
- High-risk infant (ex-premature, CHD, BPD, immunodeficiency)
- Unreliable follow-up / caregiver unable to monitor at home
- Long travel distance to nearest hospital
3. Supportive Care — The Cornerstone
The management of bronchiolitis is largely supportive; despite numerous trials of various medical therapeutic interventions, no clear single therapy has been found to be significantly beneficial [3]
There is a higher fluid requirement due to fever, tachypnoea, reduced oral intake and vomiting [5].
| Modality | When to Use | Key Points |
|---|---|---|
| Oral feeds (breast milk or formula) | Mild-moderate; infant can coordinate suck-swallow-breathe | Offer frequent small volumes rather than large infrequent feeds; breastfed infants should continue breastfeeding |
| Nasogastric (NG) feeds | Too tachypnoeic to feed safely orally but not in severe respiratory failure | Preferred over IV in many centres because it maintains gut integrity and provides calories; bolus or continuous drip |
| Intravenous (IV) fluids | Diet as tolerated (DAT) or NPO with IV fluid if in respiratory distress [2]; GCS reduced; active vomiting; imminent intubation | Severe bronchiolitis may be associated with greater potential for hyponatraemia [3], and management with hypotonic fluids may also be associated with less favourable outcomes [3] → use isotonic fluids (e.g., 0.9% NaCl with appropriate dextrose, or Plasma-Lyte) |
Why Isotonic IV Fluids?
Sick infants with bronchiolitis have elevated ADH (SIADH-like state) from lung disease, stress, and positive-pressure ventilation. ADH causes free water retention. If you give hypotonic fluids (e.g., 0.45% NaCl) on top of this, you exacerbate dilutional hyponatraemia, which can cause seizures. Hence, use isotonic fluids [3]. Maintenance rate is calculated using the Holliday-Segar formula, but restrict to 2/3 maintenance if there is evidence of fluid retention or SIADH.
Nasal O₂ supplementation to keep SpO₂ > 92% [2] (note: AAP threshold is > 90% [4]; local practice at QMH and most HA hospitals targets > 92%).
Hypoxaemia may be intermittent or variable due to the intermittent nature of plugging of bronchioles by mucus resulting in ventilation-perfusion mismatch [3].
Escalation ladder for respiratory support:
| Level | Device | Flow Rate / Settings | Mechanism | When to Use |
|---|---|---|---|---|
| 1. Low-flow nasal cannula | Nasal cannula [2] | 0.5–2 L/min (age-dependent) | Simple supplemental FiO₂ increase; no positive pressure | SpO₂ < 92% on room air; mild-moderate disease |
| 2. Face mask / Head box | Face mask, head box [2] | Variable FiO₂ | Higher FiO₂ delivery; cannot precisely titrate | If higher FiO₂ needed but not yet requiring pressure support |
| 3. Humidified High-Flow Nasal Cannula (HFNC) | Humidified high-flow nasal cannula (HFNC) [2] | Typically 2 L/kg/min (max ~8–10 L/min in infants) | Delivers heated humidified high-flow gas; generates modest CPAP effect (2–5 cmH₂O); washes out dead space → improves CO₂ clearance; reduces work of breathing | Moderate-severe; not responding to low-flow O₂; increasing work of breathing but not yet requiring formal CPAP |
| 4. Nasal CPAP (nCPAP) / BiPAP | CPAP, BiPAP [2][5] | CPAP 5–8 cmH₂O; BiPAP IPAP 8–12 / EPAP 5–6 | Constant positive pressure (CPAP) splints airways open → recruits collapsed alveoli → ↓ atelectasis → ↑ FRC → ↓ V/Q mismatch. BiPAP adds inspiratory support to augment tidal volume | Moderate-severe disease failing HFNC; persistent hypoxaemia; increasing pCO₂ |
| 5. Intubation + Mechanical Ventilation | ETT + IPPV | Ventilator settings individualised | Full ventilatory support when respiratory muscles have failed | Recurrent apnoea, signs of exhaustion (listlessness, decreased respiratory effort), failure to maintain adequate SpO₂ despite O₂ [2] |
HFNC — The Modern Workhorse
Heated humidified high-flow nasal cannula oxygen is a treatment modality that has more recently gained popularity in use for the treatment of infants with bronchiolitis [3]. Data suggest it may decrease respiratory effort and work of breathing, as well as some potential evidence of decreasing need for escalation of care [3]. All studies suggest that HFNC is a safe treatment modality [3]. It has become the de facto first escalation step above simple nasal cannula in most Hong Kong and international units.
Relieves nasal obstruction. Consider in children with respiratory distress or apnoea or feeding difficulties due to upper airway secretions [2].
Why it helps: infants < 6 months are obligate nasal breathers. Thick nasal secretions from the URTI prodrome dramatically increase upper airway resistance. Gentle bulb or catheter suctioning clears the nasal passages, immediately reducing total airway resistance and improving feeding ability.
Technique: instil 1–2 drops of normal saline per nostril → gentle suction with bulb syringe or low-pressure catheter suction. Avoid deep aggressive suctioning which can cause mucosal oedema and bleeding, paradoxically worsening obstruction.
Agitation increases oxygen consumption and can worsen desaturation. Handle the infant as little as necessary — cluster cares, avoid unnecessary blood draws, allow parents to hold and comfort the child (family-centred care).
AR/RR Q 1–4 H and SpO₂ monitoring [2].
Clinicians may choose not to use continuous pulse oximetry (AAP KAS 6b) [4]. Continuous monitoring can lead to unnecessary intervention for transient desaturations (e.g., brief dips during sleep) and prolong hospitalisation. Intermittent spot checks may be adequate for a stable, feeding infant.
4. Pharmacological Therapies
Nebulised 3% hypertonic saline: 1st line treatment in QMH, shown in meta-analysis to decrease hospitalisation rate [5]. Considered in hospitalised infants and children with bronchiolitis [2].
| Aspect | Detail |
|---|---|
| Mechanism | Osmotic effect draws water into the airway lumen → rehydrates airway surface liquid and mucus → ↓ mucus viscosity → improved mucociliary clearance. Also induces cough (which helps clear secretions) and may reduce mucosal oedema through osmotic "dehydration" of swollen tissue |
| Dose | 4 mL of 3% NaCl nebulised over ~15 min; can repeat Q4–8H |
| Evidence | 2018 meta-analysis of RCT shows reduced rate of hospitalisation among children with bronchiolitis when administered in the emergency department [2]. However, more recent analyses, particularly in US populations, lean toward recommending against its use for routine treatment [3] |
| AAP position | Nebulised hypertonic saline should not be administered to infants with a diagnosis of bronchiolitis in the emergency department (KAS 4a, Moderate, Level B) [4]. Clinicians may administer nebulised hypertonic saline to infants and children hospitalised for bronchiolitis (KAS 4b, Weak, Level B) [4] |
| HK practice | 1st line treatment at QMH [2][5]. Local protocol may differ from AAP — know both |
| Side effects | Bronchospasm (can pre-treat with bronchodilator if concerns); cough (generally therapeutic) |
Hypertonic Saline — Exam Nuance
The AAP says do not use in ED but may use in hospitalised patients. QMH uses it as 1st line. In exams, frame your answer: "Per AAP guidelines, not recommended routinely in ED. However, there is evidence supporting use in hospitalised patients, and it is used as 1st line at QMH." This shows you know both the guideline and the local practice [4][5].
Clinicians should not administer albuterol (or salbutamol) to infants and children with a diagnosis of bronchiolitis (AAP KAS 2, Strong recommendation, Level B) [4]
Clinicians should not administer epinephrine to infants and children with a diagnosis of bronchiolitis (AAP KAS 3, Strong recommendation, Level B) [4]
| Agent | Mechanism | Evidence in Bronchiolitis | Senior Notes / HK Practice |
|---|---|---|---|
| Salbutamol (albuterol) — SABA | β₂-agonist → relaxes bronchial smooth muscle → bronchodilation | Bronchodilator may provide modest short-term clinical improvement but do not affect overall outcome (reduce hospital admission, reduce duration of hospitalisation or time to resolution of illness) [2] | Inhaled SABA: may provide modest short-term improvement but no change in overall outcome [5]. Trial of SABA is reasonable but should be continued ONLY in those who showed clinical improvement [2] |
| Epinephrine (adrenaline) | α₁ + β₂ effects → vasoconstriction (↓ mucosal oedema) + bronchodilation | Not superior to placebo in RCTs for clinically meaningful outcomes | Not recommended [4] |
Why don't bronchodilators work well in bronchiolitis? The obstruction in bronchiolitis is NOT primarily due to smooth muscle bronchospasm (which is the asthma mechanism). Instead, the obstruction comes from:
- Mucosal oedema (inflammatory)
- Luminal debris (sloughed epithelium, fibrin, mucus)
- Impaired mucociliary clearance
β₂-agonists relax smooth muscle but don't address oedema, debris, or mucus. That's why they provide at best a modest and transient improvement. The small improvement seen in some infants may indicate an underlying reactive airway component (early asthma phenotype), which is why a trial is reasonable — but continue ONLY if there is a clinical response [2].
Practical approach ("bronchodilator trial"):
- Give nebulised salbutamol 2.5 mg (< 5 years)
- Observe for 15–20 minutes
- If clear improvement (reduced retractions, improved air entry, reduced RR) → continue
- Absence of response is expected in acute bronchiolitis [2] → discontinue if no benefit
Clinicians should not administer systemic corticosteroids to infants with a diagnosis of bronchiolitis in any setting (AAP KAS 5, Strong recommendation, Level A evidence) [4]
Systemic steroid is NOT recommended [2].
Why not? Multiple large RCTs and meta-analyses show NO benefit of systemic corticosteroids (oral prednisolone, IV dexamethasone, IV hydrocortisone) in bronchiolitis — no reduction in hospitalisation, length of stay, or disease severity. The inflammatory process in bronchiolitis is driven by direct viral cytopathic effects and neutrophilic inflammation rather than the eosinophilic / Th2-mediated inflammation seen in asthma (where steroids are effective). Steroids carry risks: immunosuppression, hyperglycaemia, adrenal suppression — all risk with no benefit.
Antibiotics: only indicated if suspect secondary bacterial infection (e.g., pneumonia, otitis media, sinusitis) [5].
Should not be routinely administered in treatment of bronchiolitis which is almost always caused by virus [2].
Antibiotic drug therapy is not recommended for the treatment of bronchiolitis unless an identified concomitant bacterial infection is confirmed or suspected [3].
| When to Give | What to Cover | Example |
|---|---|---|
| Concurrent AOM | Typical AOM pathogens (S. pneumoniae, H. influenzae, M. catarrhalis) | Amoxicillin 80–90 mg/kg/day in 2 divided doses |
| Secondary bacterial pneumonia | Community-acquired pneumonia pathogens | Amoxicillin PO or IV ampicillin depending on severity |
| UTI (especially in < 90-day-old febrile infant) | E. coli, Klebsiella | Cephalosporin (e.g., cefotaxime IV or cephalexin PO) |
| Suspected sepsis | Broad-spectrum | Ampicillin + gentamicin (neonatal) or ceftriaxone + ampicillin |
Occasionally concomitant or secondary bacterial infection should be treated in the same manner as it would be treated in the absence of bronchiolitis [2].
Ribavirin is NOT recommended although may have a place in children post-transplant [2].
| Agent | Status | Notes |
|---|---|---|
| Ribavirin (inhaled nucleoside analogue) | NOT recommended for routine use [2] | May be considered for use in selected patients with documented, potentially life-threatening RSV infection [2]. Antivirals may play a role in immunocompromised patients with severe bronchiolitis [2]. Teratogenic — requires negative-pressure room, impractical |
| Oseltamivir (neuraminidase inhibitor) | Consider if influenza confirmed | Antiviral drug therapy is not recommended unless specifically in the setting of influenza infection [3]. Dose for infants: 3 mg/kg/dose BD × 5 days |
Clinicians should not use chest physiotherapy for infants and children with a diagnosis of bronchiolitis (AAP KAS 7, Moderate recommendation, Level B) [4]
NO chest physiotherapy in the acute stage [2]. Not used routinely since it does not reduce severity of disease or time to recovery and is discouraged because it may increase distress and irritability of ill infants [2].
Exception: May be warranted in children with comorbidities associated with difficulty in clearing respiratory secretions (e.g., spinal muscular atrophy, neuromuscular disorders, severe tracheomalacia, cystic fibrosis) [2]. In these children, the underlying condition impairs their ability to cough and clear secretions, so physiotherapy provides a benefit that outweighs the distress.
| KAS | Statement | Strength | Evidence |
|---|---|---|---|
| 2 | Should NOT administer albuterol (salbutamol) | Strong | B |
| 3 | Should NOT administer epinephrine | Strong | B |
| 4a | Should NOT administer nebulised hypertonic saline in ED | Moderate | B |
| 4b | MAY administer nebulised hypertonic saline in hospitalised patients | Weak | B |
| 5 | Should NOT administer systemic corticosteroids in any setting | Strong | A |
| 6a | May choose NOT to give O₂ if SpO₂ > 90% | Weak | D |
| 6b | May choose NOT to use continuous pulse oximetry | Weak | C |
| 7 | Should NOT use chest physiotherapy | Moderate | B |
6. Prevention
6.1 Passive Immunoprophylaxis
Palivizumab: humanised monoclonal antibody against the RSV glycoprotein (F protein) [2][5].
| Aspect | Detail |
|---|---|
| Mechanism | Binds to the F (fusion) protein on the RSV surface → prevents viral entry into respiratory epithelial cells |
| Route and frequency | IM monthly injection (max 5 doses recommended) for prevention during RSV season [2] |
| Efficacy | Decreases the risk of hospitalisation due to severe RSV illness [2]. IMpact-RSV trial: 55% reduction in RSV hospitalisation in premature infants |
| Limitations | Limited use due to cost and multiple injections required [5]. Indications for prophylaxis have become increasingly restricted, driven in part by the high cost associated with monthly administration [2] |
| Indications [2] | Premature infants < 34 weeks without comorbidities; Infants with chronic lung disease (BPD) who require home O₂ and medical treatment on discharge; Infants with haemodynamically significant congenital heart disease including cyanotic heart disease, acyanotic heart disease receiving medications to control heart failure and requiring cardiac surgery, and moderate to severe pulmonary hypertension |
| Aspect | Detail |
|---|---|
| Mechanism | Long-acting monoclonal antibody against RSV F protein (extended half-life via Fc modification) |
| Route and frequency | Single IM injection per RSV season (paradigm shift from monthly palivizumab) |
| Indication | All infants < 8 months entering their first RSV season; high-risk children 8–19 months entering second RSV season (per 2023 AAP/CDC recommendations). Availability in Hong Kong may vary |
| Advantages | Single dose = better compliance, lower cost per season compared to 5 monthly palivizumab injections |
- Abrysvo® (RSVpreF): Approved for administration to pregnant women at 32–36 weeks GA during RSV season
- Mechanism: stimulates maternal anti-F protein IgG → transplacental transfer → passive protection of newborn for first ~6 months
- Studies show ~57% reduction in RSV-associated LRTI in the first 90 days and ~51% reduction through 180 days
Clinicians should educate and counsel families about bronchiolitis and ways to minimise risk [3][4]:
| Measure | Detail |
|---|---|
| Hand hygiene | Using alcohol-based hand rubs or, when not available, soap and water [3] |
| Decrease exposure of young infants to those who are ill | Limit visitors during RSV season; avoid crowded indoor settings |
| Tobacco smoke exposure | Clinicians should inquire about exposure and counsel caregivers about environmental tobacco smoke and smoking cessation (AAP KAS 12a/12b) [4] |
| Breastfeeding | Clinicians should encourage exclusive breastfeeding for ≥ 6 months to decrease the morbidity of respiratory infections (AAP KAS 13, Moderate, Level B) [4]. Breast milk provides secretory IgA, lactoferrin, and oligosaccharides |
| Hospital infection control | Contact precautions, gowns and gloves, cohorting of RSV-positive patients |
The infant can be considered for discharge when:
- SpO₂ consistently > 92% on room air for ≥ 4 hours (including during sleep)
- Feeding adequately (taking > 75% of normal intake)
- No/minimal respiratory distress (no retractions, RR appropriate for age)
- Caregivers confident and have received safety-net advice
- Follow-up arranged within 24–48 hours (GP or paediatric clinic)
Safety-net advice for parents:
- Watch for: worsening breathing difficulty, poor feeding (< 50% usual intake), apnoea/colour change, decreased wet nappies, lethargy
- How to clear nasal secretions (saline drops + bulb suction)
- When to return to ED immediately
- Reassure that cough may persist for 2–3 weeks (this is normal)
High Yield Summary — Management of Bronchiolitis
-
Supportive care is the cornerstone — oxygenation + hydration + nasal suctioning + minimal handling.
-
Admission criteria: Apnoea, RR > 60, severe distress/grunting, SpO₂ < 92%, poor feeding (< 50% intake), diagnostic uncertainty.
-
O₂ therapy: Target SpO₂ > 92% (HK) / > 90% (AAP). Escalation: nasal cannula → HFNC → nCPAP/BiPAP → intubation.
-
IV fluids: Use isotonic fluids (risk of hyponatraemia with hypotonic fluids due to SIADH-like state).
-
Hypertonic saline 3%: 1st line at QMH; AAP says not in ED but may use in inpatients. Know both.
-
DO NOT routinely use: bronchodilators (SABA/epinephrine), systemic steroids (Strong, Level A), antibiotics, ribavirin, chest physiotherapy.
-
Bronchodilator trial: Reasonable to try; continue only if clinical improvement observed.
-
Antibiotics: Only for secondary bacterial infection (AOM, pneumonia, UTI).
-
Prevention: Palivizumab (monthly IM, high-risk infants), Nirsevimab (single dose, all infants — new standard), maternal RSV vaccine, hand hygiene, breastfeeding, smoke avoidance.
-
HFNC: Safe, increasingly used as first-line escalation; may reduce work of breathing.
-
Discharge: SpO₂ > 92% on room air for ≥ 4 hours, adequate feeding, confident caregivers with safety-net advice.
Active Recall - Management of Bronchiolitis
References
[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p152–153) [3] Lecture slides: Paediatrics in Review - Bronchiolitis.pdf (p1, p5–7) [4] Lecture slides: Paediatrics in Review - Bronchiolitis.pdf (p2, Table 1 — AAP Guidelines) [5] Senior notes: Adrian Lui Pediatrics Notes.pdf (p163)
Complications of Acute Bronchiolitis
By nature, bronchiolitis is a self-limited disease with a relatively good prognosis [3]. Overall prognosis for infants and children with bronchiolitis is good because it is a self-limited illness [3]. Most recover within 2 weeks, but 50% have recurrent episodes [5].
However, a subset of infants — particularly those with risk factors (age < 12 weeks, prematurity, CHD, BPD, immunodeficiency) — can develop serious acute complications. Additionally, there are important medium- and long-term sequelae that families should be counselled about.
Complications can be categorised into:
- Acute complications (during the illness)
- Medium-term sequelae (weeks to months after)
- Long-term sequelae (months to years after)
1. Acute Complications
Bronchiolitis may be complicated by apnoea, particularly in preterm infants and infants younger than 2 months of age [2].
Presenting with apnoea is a risk factor for respiratory failure and need for mechanical ventilation [2].
| Aspect | Detail |
|---|---|
| Definition | Cessation of breathing for ≥ 20 seconds, or any pause accompanied by bradycardia, cyanosis, or desaturation |
| Incidence | Risk of apnoea in young infants varies in studies from less than 1% to 24% [3] |
| Who is at risk | Preterm infants (especially < 32 weeks GA); infants < 2 months of age; apnoea may even be the presenting feature of bronchiolitis before other respiratory signs are obvious |
| Mechanism | Not fully understood, but likely multifactorial: (a) Central — immature brainstem respiratory centres in young/preterm infants are more susceptible to suppression by viral inflammatory mediators and hypoxia; (b) Reflex — viral stimulation of laryngeal chemoreceptors (superior laryngeal nerve) triggers a protective reflex that inhibits breathing; (c) Obstructive — thick nasal secretions in an obligate nose-breathing infant can cause obstructive pauses |
| Why it matters | Apnoea is an independent predictor of clinical deterioration → respiratory failure → need for intubation and mechanical ventilation. Any history of apnoea is an absolute indication for hospital admission with cardiorespiratory monitoring [2] |
| Management | Continuous cardiorespiratory monitoring (SpO₂ + heart rate + respiratory rate); caffeine citrate may be considered in ex-premature infants with central apnoea (loading dose 20 mg/kg IV, maintenance 5 mg/kg/day); escalation to CPAP or intubation if recurrent |
Suspect respiratory failure when there are [2]:
- Recurrent apnoea
- Signs of exhaustion such as listlessness or decreased respiratory effort
- Failure to maintain adequate oxygen saturation despite O₂ supplementation
| Type | Mechanism in Bronchiolitis | Blood Gas Pattern |
|---|---|---|
| Type 1 (hypoxaemic) — early | Hypoxaemia associated with mucus plugging and atelectasis [2] → V/Q mismatch. Perfused but poorly ventilated lung segments shunt deoxygenated blood into the systemic circulation | PaO₂ < 60 mmHg; PaCO₂ normal or low (compensatory hyperventilation) |
| Type 2 (hypercapnic) — late | Hypercapnia associated with respiratory fatigue [2]. The infant's diaphragm (with fewer type I fatigue-resistant fibres) tires → minute ventilation falls → CO₂ accumulates. Also, severe air trapping increases dead space ventilation | PaO₂ < 60 mmHg; PaCO₂ > 50 mmHg (> 6.7 kPa); pH < 7.35 (respiratory acidosis) |
Why respiratory failure occurs more easily in infants (from first principles):
- Small airways (1/r⁴ law) → exponential resistance with minor oedema
- Fewer type I (slow-twitch, fatigue-resistant) diaphragm muscle fibres → diaphragm tires quickly
- Highly compliant chest wall → retracts inward rather than expanding the lungs efficiently
- Poorly developed collateral ventilation (no pores of Kohn / channels of Lambert) → if a bronchiole is plugged, there's no alternative ventilation pathway → rapid atelectasis
- Higher baseline metabolic rate and O₂ consumption per kg → smaller reserve
Hypercapnia associated with respiratory fatigue requires additional respiratory support such as intubation and mechanical ventilation [2].
Clinical Pearl — The Quiet Baby
A critically important sign of impending respiratory failure is the baby who becomes quiet and still after a period of obvious respiratory distress. Parents may say "they seem to be getting better." In reality, decreased respiratory effort with listlessness indicates exhaustion, not improvement. The respiratory rate may even decrease (paradoxically). This is the most dangerous moment — the infant is running out of reserve and needs immediate escalation.
Infants with bronchiolitis have difficulty maintaining adequate hydration because of increased fluid needs related to fever and tachypnoea, decreased oral intake or vomiting [2].
| Contributing Factor | Mechanism |
|---|---|
| Increased insensible losses | Fever increases metabolic rate → ↑ evaporative losses; tachypnoea increases respiratory water losses (warm humidified air exhaled at rates up to 80 breaths/min) |
| Decreased oral intake | Nasal congestion → difficulty coordinating suck-swallow-breathe (obligate nose breathers); tachypnoea → too breathless to pause and feed; general malaise → poor appetite |
| Vomiting | Post-tussive vomiting; mucus swallowing → gastric irritation; increased gastric air from mouth breathing |
| Increased secretions | Copious nasal and bronchial secretions represent a fluid loss |
Assessment: weight loss compared to recent known weight, decreased wet nappies (< 4 per day), sunken fontanelle, dry mucous membranes, delayed capillary refill ( > 2 seconds), tachycardia, reduced skin turgor.
Parenteral or nasogastric fluid administration may be necessary [2]. As discussed in the management section, use isotonic IV fluids due to risk of SIADH-like hyponatraemia.
Severe bronchiolitis may be associated with greater potential for hyponatraemia [3].
Mechanism: Syndrome of Inappropriate ADH secretion (SIADH) is common in sick infants with pulmonary disease. The triggers include:
- Positive-pressure ventilation (stimulates thoracic baroreceptors → ADH release)
- Hypoxia and hypercapnia (stimulate ADH release)
- Stress, pain, nausea (hypothalamic-pituitary axis activation)
- Medications (if any are used)
ADH causes free water retention → dilutional hyponatraemia. If serum Na⁺ drops below ~125 mmol/L, the infant is at risk of hyponatraemic seizures and cerebral oedema.
Management with hypotonic fluids may also be associated with less favourable outcomes [3] — hence the emphasis on using isotonic maintenance fluids.
Antibiotics: only indicated if suspect secondary bacterial infection (e.g., pneumonia, otitis media, sinusitis) [5].
| Site | Pathogenesis | Usual Organisms | Clinical Clue |
|---|---|---|---|
| Acute otitis media (AOM) | Viral inflammation and oedema of the Eustachian tube → impaired middle ear drainage → stasis of secretions → secondary bacterial colonisation | S. pneumoniae, H. influenzae, M. catarrhalis | Ear pulling, irritability, otoscopic findings (bulging, erythematous TM with loss of light reflex) |
| Bacterial pneumonia | Viral damage to bronchiolar epithelium → impaired mucociliary clearance + sloughed epithelial debris provides a nidus for bacterial growth → secondary pneumonia | S. pneumoniae, S. aureus, H. influenzae | New/persistent high fever after day 3–5 (when viral illness should be improving); focal crackles/signs; lobar consolidation on CXR; rising CRP/procalcitonin |
| Bacterial sinusitis | Same mechanism as AOM — viral inflammation of sinus ostia → impaired drainage → secondary bacterial infection | S. pneumoniae, H. influenzae, M. catarrhalis | Persistent purulent nasal discharge > 10 days without improvement; facial pain (rare in infants) |
| UTI | Not a direct complication of bronchiolitis per se, but febrile infants < 90 days with RSV may harbour concurrent UTI (5.4% positive urine culture in febrile infants < 60 days with RSV infection [2]) | E. coli, Klebsiella | Persistent fever, irritability; screen with urinalysis in young febrile infants |
When to Suspect Secondary Bacterial Infection
The classic "double sickening" pattern: the infant initially improves around day 3–5 (as expected), then develops new-onset or escalating fever, worsening respiratory distress, focal lung signs, or toxic appearance. This should prompt CXR, blood culture, CBC with differential, CRP, and consideration of antibiotics [5].
Mechanism: Complete obstruction of a bronchiole by mucus plug + sloughed epithelium + fibrin → air distal to the obstruction is absorbed into the pulmonary capillary blood → alveolar collapse. This is absorption atelectasis.
Clinical relevance:
- Atelectasis is common and usually sub-segmental → seen as patchy opacities on CXR (often misinterpreted as pneumonia)
- Worsens V/Q mismatch → contributes to hypoxaemia
- Usually resolves spontaneously as the bronchiolitis improves and mucus clears
- Significant right upper lobe or right middle lobe collapse may occur (more vertical right main bronchus → preferential mucus deposition)
Mechanism: Severe air trapping → distal alveolar hyperinflation → if distending pressure exceeds alveolar wall tensile strength → alveolar rupture → air dissects along perivascular sheaths into the mediastinum (pneumomediastinum) or into the pleural space (pneumothorax).
Risk: Highest in ventilated infants (barotrauma/volutrauma) but can occur spontaneously in severe air trapping.
Signs: Sudden deterioration, asymmetric chest movement, decreased air entry on one side, tracheal deviation, haemodynamic compromise (tension pneumothorax).
2. Medium-Term Sequelae (Weeks to Months)
Many infants continue to cough and wheeze intermittently for 4–8 weeks after the acute illness. This relates to:
- Ongoing airway epithelial repair (ciliary regeneration takes weeks)
- Residual airway inflammation and hyperreactivity
- Incomplete clearance of mucus and debris
Parents should be reassured that this is expected and does not necessarily indicate asthma. However, persistence beyond 8 weeks or recurrence with subsequent viral infections should prompt reassessment.
50% have recurrent episodes of wheezing [5]. This so-called "post-bronchiolitis wheeze" or "episodic viral wheeze" is characterised by:
- Wheeze episodes triggered by subsequent viral URTIs
- Symptom-free intervals between episodes
- Tends to diminish with age as airways grow larger (remember 1/r⁴ → larger airways = less impact of minor oedema)
- Most children outgrow this pattern by age 5–6 years
3. Long-Term Sequelae (Months to Years)
The most common sequela attributed to bronchiolitis is the development of reactive airway disease or asthma later in childhood [3].
Although the reported risk varies from 20% to 60%, infants with severe bronchiolitis, such as those requiring hospitalisation (particularly infants < 6 months of age), have a higher risk of developing asthma later in life [3].
Asthma may occur with increased frequency in infants with a personal or family history of atopy [3].
| Factor | Association with Later Asthma |
|---|---|
| Severity of bronchiolitis | Hospitalised infants, especially < 6 months, have higher risk |
| Causative virus | Rhinovirus bronchiolitis appears to be a stronger predictor of later asthma than RSV bronchiolitis (some studies) |
| Atopic background | Personal eczema, food allergy, or family history of atopy amplifies risk |
| Environmental exposures | Tobacco smoke exposure increases risk of both severe bronchiolitis and later asthma |
Mechanism (debated — two main hypotheses):
- Causal hypothesis: The bronchiolitis itself damages the developing airways and alters immune programming (Th2 skewing), predisposing to subsequent airway hyperreactivity
- Susceptibility hypothesis: Infants who develop severe bronchiolitis were already predisposed to airway reactivity (smaller airways, atopic tendency) — the bronchiolitis episode simply uncovers a pre-existing susceptibility
The truth is likely a combination of both.
Counselling to all families after the initial episode of bronchiolitis should include advice to be attentive to the potential for wheezing or increased respiratory distress if the child develops another viral respiratory illness in the future [3].
Providers and caregivers should remain vigilant for future signs and symptoms consistent with asthma [3].
Some may have permanent damage (e.g., bronchiolitis obliterans) after adenovirus infection (rare) [5].
This is a rare but devastating complication that warrants understanding:
| Aspect | Detail |
|---|---|
| Definition | Bronchiolitis obliterans: a rare disease caused by epithelial injury to the lower respiratory tract that results in obstruction and obliteration of the distal airways [17] |
| Name breakdown | "Bronchiolitis" = inflammation of bronchioles; "obliterans" = obliterating/destroying → the bronchioles are literally destroyed and scarred shut |
| Pathogenesis | Initial insult → injury to bronchiolar epithelium → repair characterised by excessive proliferation of granulation tissue → narrowing or obliteration of airway lumen [15]. This is an aberrant wound-healing response — instead of regenerating normal epithelium, fibroblasts proliferate and lay down collagen within and around the bronchiolar lumen, permanently occluding it |
| Causes in children | Postviral bronchiolar damage is the most common cause of BO in the nontransplant population [17]. Adenovirus is the most likely virus to cause BO, but other pathogens, including influenza, measles, and Mycoplasma, have also been identified [17]. Also seen post-lung/bone marrow transplant (chronic graft-versus-host disease) [15][17] |
| Clinical presentation | Patients with BO usually present with tachypnoea, dyspnoea, persistent cough, and wheezing that is unresponsive to bronchodilator therapy [17]. Hypoxaemia is present in more severe cases, either at rest or only with exercise and/or during sleep [17]. Slowly progressive over weeks to months |
| HRCT findings | Mosaic attenuation, air trapping on inspiratory and expiratory views, bronchial wall thickening, centrilobular nodules [15] |
| PFT | Normal or obstructive pattern without bronchodilator reversibility [15] — this distinguishes it from asthma (which IS reversible) |
| Prognosis | Irreversible airway obstruction. Some children stabilise with supportive care; others progressively deteriorate. No proven disease-modifying therapy; systemic corticosteroids and azithromycin are sometimes tried |
Swyer-James-MacLeod Syndrome
A specific entity within the BO spectrum relevant to paediatrics: post-infectious bronchiolitis obliterans after childhood/infantile infections leading to hypoplastic lung with pulmonary hyperlucency due to overly distended alveoli and reduced arterial flow [15]. Causes include RSV, Mycoplasma, influenza, staphylococcal and streptococcal infections. On CXR, the affected lung appears unilaterally hyperlucent (darker/more radiolucent) with reduced vascular markings, and the affected hemithorax may be smaller. This is often an incidental finding on CXR in later life.
Even without frank BO, some studies show that children who had severe bronchiolitis (especially RSV) in infancy may have mildly reduced lung function (lower FEV₁, increased airway resistance) when tested years later. This is likely related to subtle airway remodelling during a critical window of lung development. The clinical significance varies — many are asymptomatic, while others may have exercise intolerance or increased susceptibility to wheeze with viral infections.
| Complication | Timing | Mechanism | Key Features |
|---|---|---|---|
| Apnoea | Acute | Central (immature brainstem) + reflex (laryngeal chemoreceptors) | Preterm and < 2 months; risk factor for respiratory failure |
| Respiratory failure | Acute | V/Q mismatch (Type 1) → respiratory fatigue (Type 2) | Recurrent apnoea, exhaustion, SpO₂ < 90% despite O₂, hypercapnia |
| Dehydration | Acute | ↑ insensible losses + ↓ oral intake + vomiting | Sunken fontanelle, dry mucous membranes, ↓ urine output |
| Hyponatraemia | Acute | SIADH-like state → dilutional | Risk of seizures if Na⁺ < 125; use isotonic IV fluids |
| Secondary bacterial infection | Acute | Damaged epithelium → impaired clearance → bacterial superinfection | AOM, pneumonia, sinusitis; "double sickening" pattern |
| Atelectasis | Acute | Complete mucus plugging → absorption collapse | Patchy CXR opacities; contributes to hypoxaemia |
| Pneumothorax | Acute (rare) | Air trapping → alveolar rupture | Sudden deterioration; more common if ventilated |
| Recurrent viral wheeze | Medium-term | Residual airway inflammation + hyperreactivity | 50% have recurrent episodes; most outgrow by 5–6 years |
| Asthma | Long-term | Airway remodelling + immune priming ± pre-existing susceptibility | 20–60% risk; higher if severe, RSV/rhinovirus, atopic background |
| Bronchiolitis obliterans | Long-term (rare) | Aberrant fibroproliferative repair → permanent small airway obliteration | Post-adenovirus mainly; irreversible obstruction; HRCT: mosaic attenuation |
| Reduced lung function | Long-term | Subtle airway remodelling during critical development window | Reduced FEV₁; may be subclinical |
High Yield Summary — Complications of Bronchiolitis
-
Bronchiolitis is self-limited with good prognosis in healthy infants; mortality < 100/year in the US.
-
Acute complications: Apnoea (preterm, < 2 months), respiratory failure (Type 1 → Type 2), dehydration (↑ losses + ↓ intake), hyponatraemia (SIADH → use isotonic fluids), secondary bacterial infection (AOM, pneumonia — "double sickening"), atelectasis, and rarely pneumothorax.
-
Apnoea is a risk factor for respiratory failure and mechanical ventilation — any history of apnoea = admit and monitor.
-
The quiet baby is the dangerous baby — decreased respiratory effort with listlessness = exhaustion, not improvement.
-
50% have recurrent wheezing episodes — most outgrow by 5–6 years.
-
20–60% risk of asthma later in childhood, especially if severe (hospitalised < 6 months), atopic background, or rhinovirus aetiology. Counsel families to watch for recurrent wheeze.
-
Bronchiolitis obliterans: rare, irreversible, mainly post-adenovirus; persistent wheeze unresponsive to bronchodilators; HRCT shows mosaic attenuation and air trapping.
-
Swyer-James-MacLeod syndrome: unilateral hyperlucent lung on CXR after childhood BO.
-
Prevention counselling at follow-up: hand hygiene, breastfeeding, smoke avoidance, watch for recurrent wheeze.
Active Recall - Complications of Bronchiolitis
References
[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p149–153) [3] Lecture slides: Paediatrics in Review - Bronchiolitis.pdf (p1, p3–4, p7, p9) [5] Senior notes: Adrian Lui Pediatrics Notes.pdf (p163) [15] Senior notes: Ryan Ho Respiratory.pdf (p115–117, p127–129) [17] Lecture slides: Evaluation of wheezing in infants and children - UpToDate.pdf (p5)
High Yield Summary
-
Definition: Clinical syndrome in children < 2 years; URTI prodrome → LRTI with wheezing/crackles. Usually RSV.
-
Why infants?: Airway resistance ∝ 1/r⁴ — small airways mean exponential increase in resistance with even minor oedema.
-
Peak age: 2–6 months; peak season: winter (temperate) / spring-summer (HK for RSV).
-
Most common pathogen: RSV (50–80%); second is rhinovirus.
-
Risk factors for severe disease: Age < 12 weeks, prematurity (< 29 wk GA), BPD, haemodynamically significant CHD, immunodeficiency, Trisomy 21, neuromuscular disease, smoke exposure.
-
Pathophysiology: Viral replication → bronchiolar mucosal oedema + necrotic epithelium + mucus + fibrin → airway obstruction → air trapping → hyperinflation + atelectasis → V/Q mismatch → hypoxaemia.
-
Clinical course: URTI prodrome (2–3 days) → LRTI phase peaking Day 3–5 → gradual resolution over 1–3 weeks.
-
Key signs: Tachypnoea, retractions, nasal flaring, wheeze (generalised, bilateral), crackles, hyperinflated chest.
-
Red flags: Apnoea (especially < 2 months / preterm), grunting, cyanosis, poor feeding, exhaustion/listlessness.
-
Diagnosis: Clinical — history and physical examination. Routine lab/imaging NOT recommended (AAP).
-
Generalised wheeze (think bronchiolitis, COPD, bronchiectasis) vs Localised wheeze (think foreign body, tumour).
-
Adenovirus can cause bronchiolitis obliterans (permanent damage).
-
Prevention: Palivizumab (monthly IM), Nirsevimab (single dose, new standard), maternal RSV vaccine, hand hygiene.
High Yield Summary — DDx of Bronchiolitis
-
Generalised bilateral wheeze in an infant with URTI prodrome → most likely bronchiolitis. Localised unilateral wheeze → think foreign body (get expiratory CXR).
-
The hardest DDx is asthma vs bronchiolitis: first episode + age < 12 months + viral prodrome = bronchiolitis; recurrent episodes + atopy + bronchodilator response = asthma.
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Pneumonia has higher/persistent fever, focal signs, consolidation on CXR.
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CHF mimics bronchiolitis but look for murmur, hepatomegaly, cardiomegaly, FTT, diaphoresis with feeds.
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Pertussis: afebrile paroxysmal cough, apnoea, marked lymphocytosis, under-immunised infant.
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Chronic/recurrent wheeze from birth without clear viral triggers → structural (vascular ring, malacia, BPD) or genetic (CF, PCD).
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Always assess for red flags: unilateral wheeze (FB), FTT + steatorrhoea (CF), situs inversus (PCD), murmur (CHD), ex-premature + O₂-dependent (BPD).
High Yield Summary — Diagnosis of Bronchiolitis
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Clinical diagnosis — history + physical examination. No lab or imaging required routinely (AAP Strong recommendation).
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Diagnostic triad: Age < 2 years + URTI prodrome (2–3 days) + LRTI features (bilateral wheeze/crackles, tachypnoea, respiratory distress).
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Pulse oximetry is the only "routine" investigation — guides O₂ therapy (threshold: SpO₂ ≤ 90% per AAP, ≤ 92% per NICE/Australasian guidelines).
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CXR NOT routine — hallmark finding is hyperinflation; patchy atelectasis is often misread as pneumonia → unnecessary antibiotics.
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Blood tests NOT routine — CBC doesn't predict bacteraemia; blood culture not indicated unless toxic/septic.
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Urinalysis: consider in febrile infants < 90 days to screen for concurrent UTI (5.4% positive rate).
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NPA viral panel: not routine per AAP but commonly done in Hong Kong for infection control (cohorting), influenza treatment decisions, and palivizumab breakthrough confirmation.
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ABG/CBG: only if respiratory failure suspected (recurrent apnoea, exhaustion, cyanosis, SpO₂ < 90% despite O₂).
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Severity is assessed clinically — repeated observations are key; no single scoring system is universally accepted.
High Yield Summary — Management of Bronchiolitis
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Supportive care is the cornerstone — oxygenation + hydration + nasal suctioning + minimal handling.
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Admission criteria: Apnoea, RR > 60, severe distress/grunting, SpO₂ < 92%, poor feeding (< 50% intake), diagnostic uncertainty.
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O₂ therapy: Target SpO₂ > 92% (HK) / > 90% (AAP). Escalation: nasal cannula → HFNC → nCPAP/BiPAP → intubation.
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IV fluids: Use isotonic fluids (risk of hyponatraemia with hypotonic fluids due to SIADH-like state).
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Hypertonic saline 3%: 1st line at QMH; AAP says not in ED but may use in inpatients. Know both.
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DO NOT routinely use: bronchodilators (SABA/epinephrine), systemic steroids (Strong, Level A), antibiotics, ribavirin, chest physiotherapy.
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Bronchodilator trial: Reasonable to try; continue only if clinical improvement observed.
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Antibiotics: Only for secondary bacterial infection (AOM, pneumonia, UTI).
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Prevention: Palivizumab (monthly IM, high-risk infants), Nirsevimab (single dose, all infants — new standard), maternal RSV vaccine, hand hygiene, breastfeeding, smoke avoidance.
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HFNC: Safe, increasingly used as first-line escalation; may reduce work of breathing.
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Discharge: SpO₂ > 92% on room air for ≥ 4 hours, adequate feeding, confident caregivers with safety-net advice.
High Yield Summary — Complications of Bronchiolitis
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Bronchiolitis is self-limited with good prognosis in healthy infants; mortality < 100/year in the US.
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Acute complications: Apnoea (preterm, < 2 months), respiratory failure (Type 1 → Type 2), dehydration (↑ losses + ↓ intake), hyponatraemia (SIADH → use isotonic fluids), secondary bacterial infection (AOM, pneumonia — "double sickening"), atelectasis, and rarely pneumothorax.
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Apnoea is a risk factor for respiratory failure and mechanical ventilation — any history of apnoea = admit and monitor.
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The quiet baby is the dangerous baby — decreased respiratory effort with listlessness = exhaustion, not improvement.
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50% have recurrent wheezing episodes — most outgrow by 5–6 years.
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20–60% risk of asthma later in childhood, especially if severe (hospitalised < 6 months), atopic background, or rhinovirus aetiology. Counsel families to watch for recurrent wheeze.
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Bronchiolitis obliterans: rare, irreversible, mainly post-adenovirus; persistent wheeze unresponsive to bronchodilators; HRCT shows mosaic attenuation and air trapping.
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Swyer-James-MacLeod syndrome: unilateral hyperlucent lung on CXR after childhood BO.
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Prevention counselling at follow-up: hand hygiene, breastfeeding, smoke avoidance, watch for recurrent wheeze.
Asthma
Asthma is a chronic inflammatory airway disease characterized by reversible bronchoconstriction, bronchial hyperresponsiveness, and mucus hypersecretion leading to episodic wheezing, dyspnea, and cough.
Primary Immunodeficiency
Primary immunodeficiency comprises a group of inherited disorders, typically presenting in infancy or early childhood, in which one or more components of the immune system are absent or dysfunctional, leading to increased susceptibility to recurrent, severe, or unusual infections.