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Acute Bronchiolitis

Paediatrics · Respiratory · lean revision notes

Acute Bronchiolitis

Acute bronchiolitis is the commonest lower respiratory tract infection of infancy, caused predominantly by Respiratory Syncytial Virus (RSV). It is a clinical diagnosis in a child under 2 years presenting with a viral prodrome followed by wheeze, crepitations and respiratory distress — and the management is essentially supportive, a fact tested relentlessly in NEET PG.


Definition & basic concept

Bronchiolitis is an acute inflammatory injury of the bronchioles (small airways, < 2 mm) in children younger than 2 years, characterised by oedema, necrosis of airway epithelium, increased mucus production and bronchospasm. The result is small-airway obstruction, air-trapping and hyperinflation.

  • Peak age: 2–6 months. Rare after 2 years (older children mount better immunity and have larger-calibre airways).
  • Seasonality: Winter and early spring epidemics (in India, also associated with the rainy/cold months).
  • Definition pearl: The first episode of wheezing associated with a viral URTI in an infant < 2 years is the classical operative definition used by examiners. Recurrent wheeze suggests viral-induced wheeze or early asthma rather than bronchiolitis.

High-yield: Bronchiolitis = disease of bronchioles (small airways). It affects infants < 2 years, peaks at 2–6 months, and the single most common cause is RSV.


Etiology

RSV is the dominant pathogen, but several viruses can produce an identical picture.

Organism Approx. contribution / notes
Respiratory Syncytial Virus (RSV) 50–80% — leading cause; type A more severe
Human Rhinovirus 2nd most common; associated with later asthma
Human Metapneumovirus (hMPV) Clinically indistinguishable from RSV
Parainfluenza virus Also causes croup
Influenza, Adenovirus Adenovirus → bronchiolitis obliterans
Mycoplasma pneumoniae Older children; atypical

High-yield: RSV is the single most common cause of bronchiolitis worldwide. RSV is also the commonest cause of viral pneumonia in infants and the commonest cause of hospitalisation for LRTI in infancy.

Risk factors for severe disease

  • Age < 3 months (especially < 6–12 weeks)
  • Prematurity (gestational age < 32–35 weeks)
  • Congenital heart disease (especially with pulmonary hypertension)
  • Chronic lung disease of prematurity (bronchopulmonary dysplasia)
  • Immunodeficiency
  • Neuromuscular disease
  • Low birth weight, passive smoke exposure, lack of breastfeeding, crowding

Pathophysiology

The virus infects and replicates in the respiratory epithelium of the terminal bronchioles, triggering:

  1. Necrosis and sloughing of ciliated epithelial cells.
  2. Submucosal oedema and peribronchiolar lymphocytic infiltration.
  3. Increased mucus secretion with plugs of cellular debris.
  4. Partial and complete obstruction of small airways.

Because airway resistance is inversely proportional to the fourth power of the radius (Poiseuille), even small-calibre infant bronchioles tolerate minimal narrowing.

Pathophysiological cascade:

Viral epithelial injury → mucosal oedema + mucus plugging + cellular debris → small-airway obstruction (worse on expiration due to dynamic airway collapse) → air-trapping & hyperinflation → ventilation–perfusion (V/Q) mismatch → hypoxaemia.

  • A ball-valve effect causes air to enter but not fully leave during expiration, producing the characteristic hyperinflation.
  • Complete obstruction → distal atelectasis (collapse).
  • The combination of hyperinflation and patchy atelectasis explains the chest X-ray appearance and the hypoxaemia.

High-yield: The earliest and most sensitive sign of severity is hypoxaemia (low SpO₂), not the degree of audible wheeze. Wheeze can paradoxically decrease in a tiring infant — a danger sign, not improvement.


Clinical features

A characteristic biphasic course:

  1. Prodrome (1–3 days): Coryza, low-grade fever, nasal congestion, mild cough, decreased feeding.
  2. Lower respiratory phase: Worsening cough, wheeze, tachypnoea, respiratory distress, feeding difficulty (because of tachypnoea), and irritability. Symptoms usually peak on days 3–5 and resolve over 1–2 weeks; cough may linger up to 3 weeks.

Examination findings

  • Tachypnoea (most consistent sign) and prolonged expiration.
  • Subcostal, intercostal and suprasternal retractions; nasal flaring; head bobbing.
  • Hyperinflation — barrel chest, hyper-resonant percussion note, palpable liver and spleen edges pushed down (displaced, not enlarged).
  • Auscultation: widespread fine end-inspiratory crepitations + expiratory wheeze (rhonchi).
  • Apnoea — important in young (< 6 weeks) and preterm infants; may be the presenting feature even before respiratory signs.
  • Signs of dehydration from poor feeding and insensible losses.
Feature Bronchiolitis Childhood asthma
Typical age < 2 years (peak 2–6 mo) Usually > 2 years
Episode First/single episode Recurrent episodes
Crepitations Diffuse, prominent Usually absent
Family h/o atopy Variable Often positive
Response to bronchodilator Poor / inconsistent Good
Fever/coryza prodrome Typical Often trigger-related

Diagnosis & investigations

Bronchiolitis is a CLINICAL diagnosis. Routine investigations are NOT required and do not change management in a typical case — a heavily tested principle.

High-yield: No investigation is routinely needed to diagnose bronchiolitis. Do not order chest X-ray, CBC or viral panel in a typical, mild-to-moderate case.

  • Pulse oximetry (SpO₂): The single most useful bedside investigation; guides need for oxygen and admission.
  • Chest X-ray (only if diagnosis uncertain, severe, or atypical): hyperinflation (flattened diaphragm, horizontal ribs, increased intercostal spaces, hyperlucent lung fields), peribronchial cuffing, and patchy atelectasis. CXR tends to increase inappropriate antibiotic use, hence discouraged routinely.
  • Nasopharyngeal aspirate for RSV (rapid antigen / PCR / immunofluorescence): useful mainly for cohorting/isolation of admitted infants, not for management decisions.
  • ABG: only in impending respiratory failure — shows hypoxaemia ± hypercapnia (a rising CO₂ heralds fatigue).
  • Blood tests / cultures: reserved for suspected secondary bacterial infection or very young febrile infants.

High-yield: Investigation of choice for etiology = RSV detection on nasopharyngeal aspirate (PCR / rapid antigen / immunofluorescence) — but it is done for infection-control, NOT to make the diagnosis.


Management

The cornerstone is supportive care. There is no effective specific antiviral therapy for routine cases.

Stepwise approach:

Assess severity (SpO₂, work of breathing, feeding, hydration) → Maintain oxygenation → Maintain hydration/nutrition → Minimal handling & nasal suction → Decide admission → Supportive only; avoid unnecessary drugs.

What WORKS (supportive)

  1. Oxygen — give if SpO₂ < 90–92% (common cut-off used: keep SpO₂ ≥ 92%). Delivered by nasal prongs; heated humidified high-flow nasal cannula (HHFNC) or CPAP for severe distress/impending failure.
  2. Hydration & feeding — small frequent feeds; nasogastric or IV fluids if tachypnoea (> 60–70/min) precludes safe oral feeding (aspiration risk). Avoid overhydration (risk of SIADH).
  3. Nasal saline drops and gentle suctioning of secretions — improves feeding and comfort.
  4. Minimal handling, antipyretics (paracetamol) for fever, propped-up positioning.
  5. Monitoring for apnoea in young infants.

What does NOT work (do NOT use routinely)

High-yield: Bronchodilators (salbutamol), inhaled/systemic corticosteroids, adrenaline (nebulised), antibiotics, and antitussives are NOT recommended for routine bronchiolitis — none alter the natural course or reduce admission.

Therapy Evidence / recommendation
Salbutamol / ipratropium Not recommended — no consistent benefit
Nebulised adrenaline Not routine; possible transient effect in ED only
Corticosteroids (any route) Not recommended — no benefit
Antibiotics Only if proven/strongly suspected bacterial co-infection
Nebulised hypertonic (3%) saline May be considered in admitted patients; modest/uncertain
Ribavirin Not routine; rare use in severe immunocompromised RSV
Chest physiotherapy Not recommended
Montelukast Not recommended

Indications for hospitalisation

  • SpO₂ persistently < 90–92% / cyanosis / apnoea
  • Toxic appearance or severe respiratory distress (RR > 70/min, grunting, severe retractions)
  • Poor feeding (< 50% of normal intake) / dehydration
  • Age < 3 months or significant comorbidity (prematurity, CHD, chronic lung/immunodeficiency)
  • Unreliable home care / inability to follow up

High-yield: Persistent SpO₂ < 92%, apnoea, inability to feed, and severe distress are the classic admission criteria.


Prevention — Palivizumab & RSV products

  • Palivizumab is a humanised monoclonal antibody against the RSV F (fusion) protein. It provides passive immunisation and is given as monthly intramuscular injections (5 doses) through the RSV season.
  • It is prophylaxis, NOT treatment — useless once the infant is infected.
  • Indicated in high-risk infants: premature infants (< 29–35 weeks depending on guideline), chronic lung disease of prematurity, and haemodynamically significant congenital heart disease.
  • Newer agents (tested in recent updates): Nirsevimab (long-acting monoclonal, single dose covers a whole season) and the maternal RSV vaccine (RSVpreF) to confer transplacental antibody.
  • General prevention: hand hygiene, breastfeeding, avoiding tobacco smoke exposure, cohort isolation of admitted RSV cases. No active RSV vaccine for infants in routine use.

High-yield: Palivizumab = anti-RSV-F-protein monoclonal, given IM monthly for passive prophylaxis in high-risk preterm/CHD/CLD infants. It does NOT treat established disease.


Complications

  • Respiratory failure — leading cause needing ventilation.
  • Apnoea — especially in young/preterm infants.
  • Dehydration and feeding failure.
  • Secondary bacterial infection / pneumonia.
  • Atelectasis and air-leak (pneumothorax, rarely).
  • SIADH with hyponatraemia (from positive-pressure / lung disease + iatrogenic over-hydration).
  • Bronchiolitis obliterans — chronic small-airway fibrosis, classically post-adenovirus.
  • Recurrent wheeze / later asthma — particularly after rhinovirus and severe RSV bronchiolitis.

Key differentials

Condition Distinguishing clue
Viral-induced wheeze / asthma Recurrent episodes, older child, bronchodilator-responsive
Pneumonia (bacterial) High fever, focal crepitations, lobar consolidation, toxic
Foreign body aspiration Sudden onset, choking, unilateral wheeze/decreased air entry
Congestive cardiac failure Murmur, cardiomegaly, hepatomegaly, failure to thrive
Pertussis (whooping cough) Paroxysmal cough, whoop, post-tussive vomiting, lymphocytosis
GERD / aspiration Feed-related, recurrent
Cystic fibrosis Failure to thrive, steatorrhoea, recurrent infections

High-yield: Unilateral wheeze or focal decreased breath sounds in a previously well infant → think foreign body aspiration, not bronchiolitis.


Mnemonics & memory aids

  • "RSV"Really Sick Viral bronchiolitis; Respiratory Syncytial Virus — the same letters keep the cause anchored.
  • Management = "Don't just do something, stand there" — emphasising supportive care over drugs.
  • "O-H-S-A" supportive bundle: Oxygen, Hydration, Suction (saline), Assess/monitor — what actually helps.
  • "No SABA, No Steroid, No Antibiotic" — the three big "Nos" of bronchiolitis.

Recently asked / exam angle

  • "Most common cause of bronchiolitis"RSV (perennial single-best answer).
  • "Drug NOT useful in bronchiolitis" → bronchodilators / corticosteroids / antibiotics — recognising that management is supportive.
  • "Best/earliest indicator of severity"hypoxaemia (pulse oximetry SpO₂).
  • Palivizumab questions: mechanism (anti-F protein monoclonal antibody), route (IM, monthly), purpose (prophylaxis in high-risk preterm infants), and that it is NOT therapeutic.
  • CXR findinghyperinflation with patchy atelectasis.
  • Bronchiolitis obliterans linked to adenovirus.
  • Apnoea as a presenting feature in young/preterm infants — favourite trap.
  • Newer additions: Nirsevimab and maternal RSVpreF vaccine for prevention.
  • Image-based: hyperinflated chest X-ray, infant with subcostal retractions.

High-yield: If a question stem gives an infant < 2 years with coryza → wheeze → hyperinflation and asks for management, the answer is almost always oxygen + supportive care, NOT nebulised salbutamol or steroids.


Rapid revision

  1. Bronchiolitis = inflammation of bronchioles in infants < 2 years; peak 2–6 months.
  2. RSV is the single most common cause (50–80%); rhinovirus is second.
  3. Course: coryza/prodrome → wheeze + crepitations + distress, peaking on days 3–5.
  4. Hallmark signs: tachypnoea, hyperinflation, subcostal retractions, diffuse crepitations + wheeze.
  5. Apnoea may be the first sign in young/preterm infants.
  6. Diagnosis is clinical — no routine CXR, CBC or viral testing.
  7. SpO₂ (pulse oximetry) is the key investigation and best severity marker.
  8. CXR (if done): hyperinflation + patchy atelectasis.
  9. Management = supportive: oxygen (SpO₂ < 92%), hydration, nasal suction, minimal handling.
  10. No role for bronchodilators, steroids, antibiotics, or chest physio routinely.
  11. Admit for SpO₂ < 92%, apnoea, poor feeding/dehydration, severe distress, age < 3 months.
  12. Palivizumab = anti-RSV-F monoclonal, monthly IM prophylaxis for high-risk preterm/CHD/CLD infants; nirsevimab and maternal RSVpreF vaccine are newer preventives.