Bronchiolitis

Quick Answer

Bronchiolitis is an acute viral lower respiratory tract infection of the small airways (bronchioles) predominantly affecting infants under 12 months, with peak incidence at 2-6 months of age.

Key Clinical Features:

• Coryza prodrome (1-3 days) followed by cough, tachypnoea, wheeze, crackles
• Work of breathing: subcostal and intercostal recession, nasal flaring, grunting
• Hypoxia (SpO2 <92%) indicating need for oxygen
• Apnoea (especially infants <6 weeks) - a critical red flag

Emergency Management:

1. Supportive care: Oxygen for SpO2 <92%, ensure adequate hydration
2. Escalate respiratory support: High flow nasal cannula (HFNC) if deteriorating
3. Consider CPAP for HFNC failure; mechanical ventilation for CPAP failure

ICU Mortality: <1% in developed countries with appropriate supportive care

Must-Know Facts:

• RSV is causative in 60-80% of cases (peak in Australian winter: May-September)
• Management is supportive only - bronchodilators, steroids, antibiotics do NOT work
• HFNC is the preferred first-line escalation from low-flow oxygen
• Palivizumab is for prophylaxis in high-risk infants, not treatment
• Nirsevimab (2023) is a new single-dose monoclonal antibody for all infants

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CICM Exam Focus

What Examiners Expect

Second Part Written (SAQ):

Common SAQ stems (bronchiolitis is a very common exam topic):

• "A 3-month-old infant is admitted to PICU with bronchiolitis requiring HFNC at 2 L/kg/min. Despite this, work of breathing has increased. Describe your approach to escalation."
• "Discuss the evidence base for therapies in bronchiolitis. What interventions are NOT supported by evidence?"
• "Outline the pathophysiology of bronchiolitis and explain why bronchodilators are ineffective."
• "A 6-week-old premature infant (ex-28 weeks) presents with apnoea. List differential diagnoses and your immediate management."

Expected depth:

• Understanding of RSV pathophysiology (F and G surface proteins, small airway obstruction mechanism)
• Knowledge of what DOESN'T work (salbutamol, adrenaline, steroids, antibiotics, hypertonic saline)
• HFNC parameters (starting at 2 L/kg/min, weaning strategy)
• Mechanical ventilation strategy (low PEEP, long expiratory time, avoid auto-PEEP)
• Prevention strategies (palivizumab, nirsevimab, maternal vaccination)

Second Part Hot Case:

Typical presentations:

• Infant on HFNC with worsening work of breathing - "What are your escalation options?"
• Infant post-intubation Day 2 - "When would you attempt extubation?"
• Apnoeic infant requiring CPAP - "Discuss your management priorities"

Examiners assess:

• Systematic assessment of respiratory status
• Recognition of HFNC failure signs
• Safe decision-making around escalation
• Knowledge of ventilator settings for obstructive small airway disease
• Discussion of prognosis and parent communication

Second Part Viva:

Expected discussion areas:

• RSV immunobiology and pathophysiology
• Evidence for therapies (cite PARIS trial, Cochrane reviews)
• HFNC mechanics and PEEP effect
• Indigenous health disparities in bronchiolitis outcomes
• Prevention strategies and new monoclonal antibodies

Common Mistakes

• Prescribing bronchodilators/steroids "because the infant is wheezing" (wheeze is from edema and mucus, not bronchospasm)
• Using high PEEP in mechanical ventilation (worsens hyperinflation)
• Not recognizing apnoea as a presentation of bronchiolitis in young infants
• Forgetting to discuss Aboriginal and Torres Strait Islander health disparities
• Not knowing the PARIS trial findings

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Key Points

Must-Know Facts

1. RSV is the Major Pathogen: Respiratory syncytial virus causes 60-80% of bronchiolitis; other agents include rhinovirus, parainfluenza, human metapneumovirus, and adenovirus. [1]

2. Seasonal Pattern in Australia: Peak incidence occurs during winter months (May-September in temperate regions), though tropical regions may have year-round transmission. [2]

3. Age Group at Risk: Peak incidence at 2-6 months of age; 90% of cases occur in infants <12 months. Age <6 weeks is a major risk factor for severe disease and apnoea. [3]

4. Supportive Care is the Only Effective Treatment: No pharmacological intervention (bronchodilators, steroids, adrenaline, hypertonic saline, antibiotics) has been shown to improve clinically meaningful outcomes. [4, 5]

5. HFNC is First-Line Escalation: High flow nasal cannula reduces work of breathing and ICU admission rate. Start at 2 L/kg/min (maximum 20-25 L/min). [6]

6. Apnoea is a Critical Red Flag: Particularly in infants <6 weeks or ex-premature infants. May occur without significant respiratory distress. [7]

7. Mechanical Ventilation Strategy: Use low PEEP (4-6 cmH2O), long expiratory time (I:E ratio 1:3 to 1:4), and monitor for auto-PEEP. [8]

8. Prevention is Key: Palivizumab for high-risk infants; nirsevimab (2023) approved for all infants; maternal RSV vaccination now available. [9, 10]

9. Indigenous Health Disparity: Aboriginal and Torres Strait Islander infants have 3-5 times higher hospitalization rates for bronchiolitis. [11]

10. Self-Limiting Disease: Most cases resolve within 2-3 weeks; ICU mortality <1% with appropriate supportive care in developed countries. [12]

Memory Aids

Mnemonic "NO HELP": What Doesn't Work in Bronchiolitis

• N: No steroids (corticosteroids ineffective)
• O: Omit bronchodilators (salbutamol, adrenaline don't help)
• H: Hypertonic saline - no benefit for inpatients
• E: Exclude antibiotics (unless proven bacterial infection)
• L: Little benefit from chest physiotherapy
• P: Postpone routine CXR (clinical diagnosis)

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Definition & Epidemiology

Definition

Bronchiolitis is defined as the first episode of acute viral lower respiratory tract infection in children younger than 24 months, characterized by rhinitis, tachypnoea, wheeze, crackles, and increased work of breathing. [13]

The Australasian Bronchiolitis Guideline (2022) defines bronchiolitis as: "A clinical diagnosis based on typical history and findings in infants under 12 months with a viral prodrome followed by increased respiratory effort and wheeze/crackles on auscultation." [14]

Diagnostic Criteria (Clinical Diagnosis):

• Age <12-24 months (typically <12 months)
• Viral upper respiratory prodrome (1-3 days of coryza)
• Wheeze and/or crackles on auscultation
• Increased work of breathing (recession, nasal flaring, tachypnoea)
• First episode of wheezing illness

Severity Classification:

Epidemiology

International Data:

• Bronchiolitis affects approximately 30% of infants in their first year of life [15]
• Hospitalization rate: 3-11% of infants with bronchiolitis [16]
• PICU admission rate: 2-6% of hospitalized infants (0.1-0.3% of all bronchiolitis cases) [17]
• Mechanical ventilation rate: 8-15% of PICU admissions for bronchiolitis [18]

Australian/NZ Data (ANZICS APD, PREDICT Network):

• Annual bronchiolitis hospitalizations: Approximately 15,000 children in Australia [19]
• Peak hospitalization rate: 35-55 per 1,000 infants aged 0-2 months [20]
• PICU admission rate in Australia: 3-5% of hospitalized bronchiolitis cases [21]
• Seasonal variation: June-August peak in temperate Australia, year-round in tropical regions [22]

Risk Factors for Severe Disease:

Non-modifiable:

• Age <6 weeks (OR 4.2 for PICU admission) [23]
• Prematurity <37 weeks, especially <32 weeks (OR 2.5-4.0) [24]
• Male sex (slight increased risk)
• Indigenous ethnicity (Aboriginal, Torres Strait Islander, Māori)

Comorbidities:

• Congenital heart disease (especially cyanotic or hemodynamically significant) [25]
• Chronic lung disease/bronchopulmonary dysplasia [26]
• Immunodeficiency (primary or acquired) [27]
• Neuromuscular disorders affecting respiratory function
• Down syndrome (3-4x higher hospitalization) [28]

Environmental:

• Passive smoke exposure (OR 1.5-2.0) [29]
• Lack of breastfeeding
• Overcrowded living conditions
• Daycare attendance
• Older siblings in household

High-Risk Populations:

• Aboriginal and Torres Strait Islander infants: 3-5x higher hospitalization rates for bronchiolitis [30]
• Māori infants: 2-3x higher hospitalization rates [31]
• Remote/rural populations: Higher severity at presentation due to delayed access to care
• Pacific Islander infants: Higher hospitalization rates

Outcomes:

• ICU mortality: <1% in developed countries with appropriate care [32]
• Hospital mortality: <0.5% [33]
• Length of stay: Median 3-5 days (PICU), 2-3 days (ward)
• Long-term: 40-50% develop recurrent wheeze/asthma in first 5 years [34]

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Applied Basic Sciences

Virology

Respiratory Syncytial Virus (RSV):

RSV is a single-stranded, negative-sense RNA virus of the family Pneumoviridae (formerly Paramyxoviridae). It is the most common cause of bronchiolitis worldwide. [35]

RSV Structure and Surface Proteins:

Two critical surface glycoproteins determine pathogenicity:

1. F (Fusion) Protein:

   • Mediates viral entry by fusing viral and host cell membranes
   • Essential for syncytium formation (multinucleated giant cells)
   • Highly conserved between RSV subtypes A and B
   • Target for palivizumab and nirsevimab monoclonal antibodies [36]

2. G (Attachment) Protein:

   • Mediates initial viral attachment to host cell receptors
   • Highly variable between RSV subtypes (antigenically diverse)
   • Contributes to immune evasion
   • Associated with modulation of host immune response [37]

RSV Subtypes:

• RSV-A: Generally causes more severe disease
• RSV-B: Co-circulates with RSV-A; historically considered less virulent
• Both subtypes circulate annually; predominant subtype varies by season

Other Causative Pathogens (in order of frequency):

• Rhinovirus (10-25%)
• Human metapneumovirus (5-15%)
• Parainfluenza virus types 1, 2, 3 (5-10%)
• Influenza A and B (3-5%)
• Adenovirus (3-5%)
• Coronavirus (including pre-pandemic strains)
• Co-infection occurs in 10-30% of cases [38]

Pathophysiology

Sequence of Events:

1. Viral Entry and Initial Infection:

   • RSV enters via nasopharyngeal mucosa
   • Initial replication in upper respiratory epithelium
   • Spreads to lower respiratory tract over 1-3 days (coryza phase)

2. Bronchiolar Infection:

   • RSV preferentially infects small airway epithelial cells (bronchioles <2mm diameter)
   • Direct cytopathic effect causes epithelial necrosis
   • Formation of syncytia (fused cells) contributes to tissue damage

3. Inflammatory Response:

   • Primarily T-cell mediated immune response [39]
   • CD8+ cytotoxic T cells are critical for viral clearance but also cause tissue damage
   • Th2-dominant response in severe cases (IL-4, IL-5, IL-13)
   • Neutrophil and eosinophil infiltration of airways
   • Limited antibody response (explains reinfection susceptibility)

4. Airway Obstruction Mechanism:

Three Components of Small Airway Obstruction (crucial for understanding why bronchodilators don't work):

This explains why bronchodilators are ineffective: the obstruction is primarily from edema and debris, NOT smooth muscle constriction. [40]

5. Pathophysiological Consequences:

Ball-Valve Effect:

• Small airways collapse more during expiration (dynamic compression)
• Air trapping and hyperinflation result
• FRC increases, work of breathing increases
• V/Q mismatch leads to hypoxemia

Gas Exchange Abnormalities:

• Atelectasis (from mucus plugging and surfactant dysfunction)
• V/Q mismatch (hypoxemia with normal or low PaCO2 initially)
• Shunt physiology in severe cases
• Hypercapnia indicates respiratory failure

Apnoea Mechanism (especially young infants):

• Immature respiratory control center
• RSV may directly affect brainstem respiratory neurons
• Reflex apnoea from upper airway stimulation
• May occur with minimal lower respiratory signs [41]

Anatomy

Infant Airways - Critical Differences from Adults:

Surface Area to Volume Ratio:

• Infants have relatively larger airways per body mass but absolute size is smaller
• Same volume of edema/mucus causes proportionally greater obstruction

Pharmacology

Medications That Do NOT Work (Evidence-Based):

1. Bronchodilators (Salbutamol/Albuterol):

• Mechanism: Beta-2 agonist causing bronchial smooth muscle relaxation
• Why Ineffective: Bronchiolitis obstruction is NOT from bronchospasm
• Evidence: Cochrane review (30 RCTs, n=1,992): No improvement in oxygen saturations, hospital admission, or length of stay. [42]
• Recommendation: NOT recommended (Australasian Guideline Grade A)

2. Adrenaline (Nebulized):

• Mechanism: Alpha and beta-adrenergic effects; theoretically reduces mucosal edema
• Evidence: Cochrane review: No benefit on hospital admission or length of stay. May provide transient improvement but not clinically meaningful. [43]
• Recommendation: NOT recommended routinely

3. Corticosteroids (Oral or IV):

• Mechanism: Anti-inflammatory, reduces airway edema
• Why Ineffective: Inflammation is predominantly neutrophilic/T-cell mediated; steroids less effective than in eosinophilic asthma
• Evidence: Cochrane review (17 RCTs, n=2,596): No reduction in hospital admission, length of stay, or clinical scores. [44]
• Recommendation: NOT recommended (Grade A)

4. Hypertonic Saline (3%):

• Mechanism: Osmotic effect to reduce mucosal edema, improve mucociliary clearance
• Evidence: Initial studies showed benefit in ED/outpatient settings; subsequent large RCTs (including SABRE trial, n=317) showed no benefit for inpatients. [45]
• Recommendation: NOT recommended for inpatients (may consider in ED)

5. Antibiotics:

• Mechanism: Treat bacterial infection
• Why Ineffective: Bronchiolitis is a viral disease; bacterial co-infection is rare (<5%)
• Evidence: Cochrane review confirms no benefit; risk of adverse effects and resistance [46]
• Recommendation: NOT recommended unless proven bacterial infection

6. Chest Physiotherapy:

• Evidence: Cochrane review (12 RCTs): No improvement in severity, oxygen requirement, or length of stay
• Recommendation: NOT recommended routinely

Medications Used for Supportive Care:

Oxygen Therapy:

• Target SpO2 ≥92% (some guidelines accept ≥90%)
• Low-flow oxygen: Start at 0.5-2 L/min via nasal cannula
• HFNC when low-flow insufficient

Antipyretics:

• Paracetamol 15 mg/kg Q4-6H PRN for fever
• Ibuprofen 10 mg/kg Q6-8H for infants >3 months

Sedation (if intubated):

• Morphine 10-40 mcg/kg/hr infusion
• Midazolam 1-4 mcg/kg/min infusion
• Dexmedetomidine 0.2-0.7 mcg/kg/hr (preserves respiratory drive)

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Clinical Presentation

ICU Admission Scenarios

Typical Presentations:

Scenario 1: Progressive Respiratory Failure

• History: 4-month-old, 3 days of coryza, then progressive cough and wheeze, reduced feeding over 24 hours
• Examination: RR 65, HR 165, SpO2 88% on room air, moderate subcostal recession, diffuse wheeze and crackles
• Severity: Severe - requires PICU for HFNC

Scenario 2: Apnoea in Young Infant

• History: 5-week-old ex-34 week preterm, brief cough and coryza, then witnessed apnoeic episode with cyanosis
• Examination: RR 50, mild recession, minimal wheeze, but witnessed desaturation to 75%
• Severity: Severe - PICU for apnoea monitoring and respiratory support

Scenario 3: High-Risk Infant with Moderate Disease

• History: 6-month-old with known VSD, 2 days coryza, increased WOB
• Examination: RR 55, HR 150, SpO2 91% on 2L O2, moderate recession, hepatomegaly
• Severity: Moderate-severe - PICU for cardiac comorbidity and close monitoring

Symptoms & Signs

History:

Coryza Prodrome (1-3 days):

• Clear rhinorrhoea
• Sneezing
• Low-grade fever (38-38.5°C)
• Mild cough

Lower Respiratory Phase:

• Chief complaint: Increased work of breathing, poor feeding
• Cough: Persistent, often paroxysmal
• Wheeze: Audible wheeze
• Feeding: Reduced oral intake (tachypnoea interferes with coordination)
• Time course: Peak severity Day 3-5, recovery over 2-3 weeks

Past Medical History (critical risk factors):

• Prematurity (<37 weeks, especially <32 weeks)
• Chronic lung disease/BPD
• Congenital heart disease
• Immunodeficiency
• Neuromuscular disease

Examination:

General:

• Appearance: Irritable or lethargic (exhaustion = danger sign)
• Hydration: Assess for dehydration from poor feeding
• Colour: Pallor or cyanosis

Vital Signs:

A - Airway:

• Usually patent
• Nasal congestion common
• Assess for stridor (consider croup, foreign body)

B - Breathing:

Work of Breathing Assessment:

• Nasal flaring: Indicates accessory muscle use
• Tracheal tug: Visible in-drawing of trachea on inspiration
• Subcostal recession: Most common sign of increased WOB
• Intercostal recession: Moderate-severe disease
• Head bobbing: Severe - using sternocleidomastoid as accessory muscle
• Grunting: Ominous - creating auto-PEEP to maintain alveolar patency

Auscultation:

• Inspiratory crackles (from secretions, small airway closure)
• Expiratory wheeze (from airway narrowing)
• Prolonged expiratory phase
• Decreased air entry in severe cases (silent chest = danger)

C - Circulation:

• Tachycardia (normal response to hypoxia and distress)
• Assess perfusion: CRT, peripheral warmth
• Check for hepatomegaly (may indicate cardiac comorbidity or hyperinflation pushing liver down)

D - Disability/Neurology:

• Alert or irritable (normal); lethargy is concerning
• Assess for encephalopathy (rare, consider pertussis, adenovirus)
• Document any apnoeic episodes

E - Exposure/Everything Else:

• Temperature: Low-grade fever typical; high fever consider bacterial superinfection
• Skin: Check for eczema (atopy association)
• Weight: Calculate hydration status

Severity Scoring

Australasian Bronchiolitis Severity Assessment (Clinical Assessment):

PICU Admission Criteria:

• SpO2 <90% despite low-flow O2
• HFNC failure (increasing WOB, rising FiO2)
• Apnoea requiring monitoring/stimulation
• Respiratory failure (rising PaCO2 >60 mmHg)
• Exhaustion
• High-risk comorbidities with moderate-severe disease

Differential Diagnosis

Key Differentials:

1. Viral Pneumonia: More focal findings on examination, CXR consolidation, higher fever
2. Pertussis: Paroxysmal cough with whoop, apnoea more prominent, lymphocytosis
3. Congenital Heart Disease: Hepatomegaly, cardiac murmur, failure to thrive
4. Croup: Stridor (inspiratory), barking cough, minimal lower respiratory signs
5. Aspiration: Recurrent episodes, association with feeds, neurological impairment
6. Foreign Body Aspiration: Sudden onset, unilateral wheeze, history of choking
7. Cystic Fibrosis: Failure to thrive, recurrent infections, meconium ileus history
8. Asthma/Viral-Induced Wheeze: Recurrent episodes, family history, responds to bronchodilators (older infants)

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Investigations

Laboratory Investigations

Bedside Tests:

Arterial/Capillary Blood Gas (for moderate-severe disease):

Interpretation: Initially respiratory alkalosis (tachypnoea); respiratory acidosis with rising PaCO2 indicates impending failure

Blood Tests:

FBC:

• WCC: Usually normal or mildly elevated (viral lymphocytosis)
• Marked leukocytosis (>15-20 × 10⁹/L) suggests bacterial superinfection or pertussis
• Thrombocytosis common in viral infections

UEC:

• Usually normal
• Assess for dehydration (elevated urea)
• Hyponatremia may occur with inappropriate ADH secretion

Inflammatory Markers:

• CRP: Usually normal or mildly elevated (<30 mg/L)
• Procalcitonin: May help distinguish viral from bacterial if diagnostic uncertainty

Specific Tests:

Viral PCR/Detection (Nasopharyngeal Aspirate or Swab):

• NOT required for diagnosis (clinical diagnosis)
• Indicated for: Cohorting purposes (infection control), atypical presentations, research
• RSV rapid antigen test: Sensitivity 80-90%, specificity 90-95%
• Multiplex viral PCR: RSV, rhinovirus, influenza, parainfluenza, metapneumovirus, adenovirus

Blood Culture: Only if bacterial superinfection suspected (high fever, toxic appearance)

Imaging

Chest X-Ray:

Routine CXR is NOT Recommended [47]

Reasons:

• Does not change management
• Leads to unnecessary antibiotic use (overinterpretation of atelectasis as consolidation)
• Radiation exposure

When to Consider CXR:

• Atypical clinical features
• Suspected complication (pneumothorax, significant atelectasis)
• Failure to improve as expected
• Pre-existing cardiorespiratory disease
• To confirm ETT position post-intubation

Typical CXR Findings (if obtained):

Misinterpretation Pitfall: Atelectasis is commonly misread as consolidation, leading to inappropriate antibiotics

Ultrasound:

• Lung ultrasound: May show B-lines (interstitial syndrome), subpleural consolidations
• Cardiac echo: If cardiac comorbidity suspected

Physiological Monitoring

Non-Invasive Monitoring:

• Continuous SpO2: Target ≥92%
• Continuous ECG: Detect arrhythmia (rare)
• Temperature: Q4H
• Respiratory rate: Trend monitoring (decreasing RR may indicate fatigue)
• Work of breathing: Clinical assessment Q1-2H

HFNC-Specific Monitoring:

• FiO2 requirement: Titrate to SpO2 92-98%
• Flow rate: Document L/kg/min
• Work of breathing: Key indicator of HFNC failure

Invasive Monitoring (if intubated):

• Arterial line: Continuous BP, ABG sampling
• ETT: Confirm position, monitor cuff (if cuffed)
• Ventilator waveforms: Detect auto-PEEP, dyssynchrony

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ICU Management

Initial Resuscitation (First Hour)

A - Airway:

Assessment:

• Usually patent in bronchiolitis
• Nasal congestion may require gentle suctioning
• Assess for stridor (suggests alternative diagnosis)

Intervention:

• Gentle nasal suction PRN (avoid deep/aggressive suctioning - causes reflex apnoea)
• Intubation only for respiratory failure (rarely needed <5%)

Indications for Intubation:

• Apnoea requiring more than stimulation
• Exhaustion with decreasing respiratory effort
• PaCO2 >60-70 mmHg with rising trend
• SpO2 <88% despite maximal non-invasive support
• Impaired consciousness

RSI Drug Choices (if intubation required):

• Induction: Propofol 2-3 mg/kg or ketamine 1-2 mg/kg (preserves respiratory drive)
• Paralysis: Rocuronium 1 mg/kg
• Avoid suxamethonium in known neuromuscular disease
• ETT size: (Age/4) + 3.5 for cuffed tube

B - Breathing:

Oxygen Therapy Ladder:

High Flow Nasal Cannula (HFNC) - Detailed Protocol:

Starting Parameters:

• Flow rate: 2 L/kg/min (range 1-2.5 L/kg/min)
• Maximum flow: 20-25 L/min (depends on equipment)
• Starting FiO2: Titrate to SpO2 92-98%
• Humidification: Mandatory (37°C, 100% relative humidity)

HFNC Mechanism of Action:

• Washout of nasopharyngeal dead space (reduces CO2 rebreathing)
• Generation of low-level PEEP (2-5 cmH2O at 2 L/kg/min)
• Reduces inspiratory resistance (warm, humidified gas)
• Reduces metabolic cost of gas conditioning
• May reduce airway oedema (warm humidified gas)

HFNC Failure Criteria (escalate to CPAP or intubation):

Critical Alert: HFNC Failure - When to Escalate:

• FiO2 requirement >0.6 to maintain SpO2 ≥92%
• Increasing work of breathing despite HFNC
• Apnoea requiring intervention
• Rising PaCO2 >60 mmHg
• Exhaustion
• Clinical deterioration

Predict HFNC Failure Early (within 60-90 minutes of starting):

• Failure to reduce respiratory rate by >20% from baseline
• Failure to reduce work of breathing
• Rising heart rate

CPAP (if HFNC fails):

• Starting pressure: 6-8 cmH2O
• Interface: Nasal prongs, nasal mask, or full-face mask
• FiO2: Titrate to SpO2 92-98%
• Monitor for gastric distension (insert NG tube)

C - Circulation:

Fluid Management:

• Assess hydration status (reduced oral intake common)
• IV/NG fluids if feeding unsafe (SpO2 <92% during feeds, marked tachypnoea)
• Maintenance fluids: 80-100% maintenance initially
• Avoid fluid overload (worsens respiratory mechanics)

D - Disability:

• GCS assessment age-appropriate
• Apnoea monitoring (cardiorespiratory monitor with apnoea alarm)
• Caffeine citrate 10 mg/kg loading, 5 mg/kg daily if recurrent apnoea [48]

E - Everything Else:

• Temperature: Target normothermia
• Nutrition: NGT feeding when safe; hold oral feeds if significant respiratory distress

Definitive Management (First 24-48 Hours)

What Works - Supportive Care:

1. Supplemental Oxygen: Target SpO2 ≥92%
2. Respiratory Support Escalation: HFNC → CPAP → MV as needed
3. Hydration: IV/NG fluids to maintain euvolemia
4. Minimal Handling: Cluster cares, reduce stimulation (reduces oxygen consumption)
5. Thermoregulation: Maintain normothermia

What DOESN'T Work - Evidence-Based "No" List:

Surfactant Therapy:

• Rationale: RSV may cause surfactant dysfunction
• Evidence: Limited RCTs show possible benefit but not definitive
• Recommendation: Not routine; may consider in refractory cases as rescue therapy [49]

Heliox:

• Rationale: Lower density gas reduces work of breathing in turbulent flow
• Evidence: Limited; some studies show short-term benefit
• Recommendation: Not routine; may consider in severe disease as bridge [50]

Mechanical Ventilation Strategy

When Mechanical Ventilation is Required (8-15% of PICU admissions):

Key Principles:

• Bronchiolitis = small airway obstructive disease
• Main issue = hyperinflation and air trapping
• Strategy: Avoid worsening hyperinflation

Initial Ventilator Settings:

Critical Alert: Avoid Auto-PEEP (Intrinsic PEEP):

Auto-PEEP occurs when the next breath starts before complete exhalation. This worsens hyperinflation and can cause:

• Barotrauma (pneumothorax)
• Hemodynamic compromise (increased intrathoracic pressure → reduced venous return)
• Breath stacking

How to Detect Auto-PEEP:

• Flow waveform: Flow doesn't return to zero before next breath
• Expiratory hold: Measure intrinsic PEEP
• Clinical: Palpable end-expiratory wheeze, hypotension

How to Manage Auto-PEEP:

• Reduce respiratory rate
• Shorten inspiratory time
• Lower tidal volume
• Increase I:E ratio (1:4 or 1:5)
• Disconnect briefly (1-2 sec) to allow complete exhalation if severe

Why LOW PEEP in Bronchiolitis:

• Unlike ARDS, the problem is air trapping NOT atelectasis
• High PEEP worsens hyperinflation
• Start at 4-6 cmH2O, only increase if atelectasis predominates

Permissive Hypercapnia:

• Accept PaCO2 55-65 mmHg if pH >7.25
• Avoid aggressive ventilation to normalize PaCO2

Sedation and Analgesia in Mechanically Ventilated Patient:

• Morphine 10-40 mcg/kg/hr infusion
• Midazolam 1-4 mcg/kg/min infusion
• Consider dexmedetomidine 0.2-0.7 mcg/kg/hr
• Neuromuscular blockade if severe dyssynchrony (rocuronium)

Weaning and Extubation:

• Wean FiO2 to <0.4, PEEP to 4-5 cmH2O
• Reduce rate, consider pressure support trial
• Extubate when: Minimal secretions, alert, cough present, stable on minimal settings
• Post-extubation: HFNC commonly used to support transition

Australian-Specific Protocols

Australasian Bronchiolitis Guideline (2022):

• Developed by the PREDICT network (Paediatric Research in Emergency Departments International Collaborative)
• Key recommendations align with above (supportive care only)
• Emphasizes clinical assessment over investigations

ANZICS Paediatric Study Group:

• Bronchiolitis is one of the most common PICU admissions
• Focus on non-invasive support where possible
• HFNC has significantly reduced intubation rates

State-Based Protocols:

• NSW: HFNC-first approach for moderate-severe bronchiolitis
• Victoria: Children's Health Network bronchiolitis pathway
• Queensland: CHQ bronchiolitis clinical practice guideline

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Monitoring & Complications

ICU-Specific Monitoring

Daily Parameters:

• Vital signs: Continuous SpO2, HR, RR; Q1H documented
• Fluid balance: Strict I/O, daily weight
• Feeding tolerance: NG/oral intake
• Work of breathing assessment: Clinical scoring Q4H

Trend Monitoring:

• Respiratory rate trend: Improving or worsening
• FiO2 requirement: Escalating need suggests deterioration
• Blood gas: Q6-12H if on HFNC/CPAP; more frequent if intubated

Safety Monitoring:

• HFNC prong position: Ensure <50% nares occluded
• ETT position: CXR post-intubation, document depth
• Skin integrity: Nasal septum (pressure injury from HFNC/CPAP)

Complications

Early Complications (First 24-48 hours):

1. Apnoea:

• Incidence: 2-5% overall; 10-20% in infants <6 weeks
• Risk factors: Age <6 weeks, prematurity, first 24 hours of illness
• Management: Caffeine citrate, continuous monitoring, may need intubation
• Prevention: Low threshold for PICU admission in high-risk infants

2. Respiratory Failure Requiring Intubation:

• Incidence: 8-15% of PICU admissions
• Risk factors: Age <6 weeks, prematurity, CHD, high initial FiO2 requirement
• Management: See mechanical ventilation strategy above

3. Acute Deterioration (Mucus Plug):

• Presentation: Sudden desaturation, unilateral decreased air entry
• Management: Suction, consider bronchoscopy if refractory

Late Complications (Beyond 48 hours):

4. Secondary Bacterial Infection:

• Incidence: <5% of hospitalized cases
• Pathogens: S. pneumoniae, H. influenzae, S. aureus
• Clues: High fever >39°C, rising CRP/WCC, focal consolidation
• Management: Blood culture, consider antibiotics if strong clinical suspicion

5. Pneumothorax:

• Incidence: <1% overall; higher if intubated with high pressures
• Risk factors: Aggressive ventilation, high PEEP
• Management: Needle decompression if tension; intercostal catheter

6. Feeding Difficulties:

• Cause: Tachypnoea interferes with suck-swallow-breathe coordination
• Management: NG feeding, small frequent feeds when ready to oral

ICU-Acquired Complications:

• Skin breakdown: Nasal septum (HFNC/CPAP interface)
• Nosocomial infection: Strict infection control
• Dehydration/overhydration: Monitor fluid balance

---

Prognosis & Outcome Measures

Mortality

Short-Term Outcomes:

• ICU mortality: <1% in developed countries [51]
• Hospital mortality: <0.5%
• Deaths occur primarily in high-risk groups (CHD, immunodeficiency, extreme prematurity)

Long-Term Outcomes:

• Recurrent wheeze: 40-50% within 5 years [52]
• Childhood asthma: Increased risk (OR 1.5-2.0), but causation vs association debated
• Most children recover completely with no long-term respiratory sequelae

Morbidity

Short-Term:

• Median PICU LOS: 3-5 days
• Median hospital LOS: 4-7 days
• Oxygen requirement may persist 1-2 weeks

Long-Term:

• Post-viral bronchial hyperreactivity (viral-induced wheeze)
• No significant impact on lung function at school age in most
• High-risk groups may have prolonged respiratory morbidity

Prognostic Factors

Good Prognostic Factors:

• Age >6 weeks at presentation
• Term infant, no comorbidities
• SpO2 >92% on room air at presentation
• Feeding maintained >50%

Poor Prognostic Factors:

• Age <6 weeks
• Prematurity <32 weeks
• Congenital heart disease (especially cyanotic)
• Immunodeficiency
• Chronic lung disease/BPD
• Apnoea at presentation
• Requiring HFNC/CPAP on arrival

Australian/NZ Outcome Data

ANZICS APD Data:

• Bronchiolitis accounts for 5-10% of PICU admissions in winter months
• Overall PICU mortality <1%
• Mechanical ventilation rate decreasing with increased HFNC use

Indigenous Health Outcomes:

• Aboriginal and Torres Strait Islander infants: 3-5x higher hospitalization
• Higher PICU admission rates
• Contributing factors: Overcrowding, smoke exposure, later presentation, comorbidities
• Solutions: Community outreach, early intervention, culturally safe care

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Prevention Strategies

RSV Prophylaxis

Palivizumab (Synagis):

Palivizumab is a humanized monoclonal antibody targeting the RSV F protein. It is used for prophylaxis (NOT treatment) in high-risk infants.

Mechanism:

• Binds RSV F protein → prevents viral fusion with host cell membrane
• Does NOT cross blood-brain barrier (no CNS protection)

Indications (Australian PBS-subsidized):

• Infants born ≤28 weeks gestation (first RSV season)
• Infants with chronic lung disease (oxygen requirement at 36 weeks corrected)
• Infants with hemodynamically significant CHD (<24 months)
• Immunodeficiency in first 2 years of life

Dosing:

• 15 mg/kg IM monthly during RSV season (typically April-September in Australia)
• Maximum 5 doses per season

Efficacy:

• 45-55% reduction in RSV hospitalization in high-risk groups [53]
• NNT ~17 to prevent one hospitalization

Limitations:

• Expensive (~$1,500 per dose)
• Monthly injections required
• Only for prophylaxis in high-risk groups
• Does not prevent infection, reduces severity

New RSV Prevention Strategies

Nirsevimab (Beyfortus) - 2023 Approval:

Nirsevimab is a long-acting monoclonal antibody (also targeting F protein) with extended half-life.

Key Advantages over Palivizumab:

• Single dose provides protection for entire RSV season (5 months)
• Approved for ALL infants (not just high-risk)
• Simpler administration

Dosing:

• <5 kg: 50 mg IM single dose
• ≥5 kg: 100 mg IM single dose
• Given before or during first RSV season

Efficacy:

• 70-80% reduction in RSV hospitalization in clinical trials [54]
• MELODY trial: 74.5% reduction in RSV LRTI requiring medical attention

Australian Status (2024-2025):

• TGA approved November 2023
• NIP (National Immunisation Program) inclusion under consideration
• Likely to transform bronchiolitis prevention

Maternal RSV Vaccination (RSVpreF - Abrysvo):

Maternal vaccination during pregnancy transfers protective antibodies to infant.

Mechanism:

• Recombinant RSV prefusion F protein vaccine
• Given during pregnancy (32-36 weeks gestation)
• Transplacental antibody transfer protects infant for first 6 months

Efficacy:

• 69% reduction in severe RSV LRTI in first 180 days of life [55]
• 57% reduction in RSV hospitalization

Australian Status:

• TGA approved 2024
• Expected to be offered during pregnancy alongside pertussis and influenza vaccines

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Indigenous Health Considerations

Aboriginal and Torres Strait Islander Infants

Epidemiology:

• Hospitalization rate: 3-5x higher than non-Indigenous infants
• PICU admission rate: 2-3x higher
• Higher rates of mechanical ventilation
• More likely to present with severe disease

Contributing Factors:

• Housing: Overcrowding increases RSV transmission
• Smoke exposure: Higher rates of household smoking
• Comorbidities: Higher rates of prematurity, low birth weight
• Access: Geographic isolation, delayed presentation
• Socioeconomic: Poverty, food insecurity

Culturally Safe Care in PICU:

Critical Alert: Cultural Safety Considerations:

1. Family Involvement:

   • Extended family may wish to be present
   • Decision-making often involves broader family/community
   • Allow flexibility in visiting

2. Aboriginal Health Workers (AHWs) / Aboriginal Liaison Officers (ALOs):

   • Involve early in admission
   • Assist with communication, interpretation
   • Support family in navigating hospital system

3. Communication:

   • Use interpreters if English is second language
   • Explain procedures clearly, check understanding
   • Avoid medical jargon

4. Cultural Practices:

   • Be aware of Sorry Business (bereavement customs)
   • Men's/women's business considerations
   • Ceremonial obligations

5. Discharge Planning:

   • Community health nurse follow-up
   • Ensure family has access to follow-up care
   • Education on when to seek help

Māori Health (New Zealand)

Epidemiology:

• 2-3x higher bronchiolitis hospitalization rates
• Higher rates of severe disease

Culturally Safe Care:

• Whānau (family) involvement in care decisions
• Māori Health Workers involvement
• Respect for tikanga (customs)
• Consider manaakitanga (hospitality, care)

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SAQ Practice

SAQ 1: HFNC Failure and Escalation

Time Allocation: 10 minutes Total Marks: 20

Stem: A 4-month-old male infant is admitted to PICU with bronchiolitis. He was born at term with no significant past medical history. He presented with 3 days of coryza followed by increasing work of breathing and poor feeding.

Current Status:

• On HFNC at 2 L/kg/min (12 L/min), FiO2 0.55
• Weight: 6 kg
• HR: 175, RR: 72, SpO2: 91%, Temp: 37.8°C
• Marked subcostal and intercostal recession, nasal flaring, head bobbing
• Chest: Bilateral wheeze and crackles, prolonged expiration
• Capillary blood gas: pH 7.28, pCO2 58, HCO3 24, BE -3, Lactate 1.8

He has been on HFNC for 90 minutes with no improvement in work of breathing.

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Question 1.1 (8 marks)

List the clinical features that indicate HFNC failure in this patient and outline your immediate management plan.

Question 1.2 (6 marks)

The infant fails a trial of CPAP and requires intubation. Describe appropriate ventilator settings for this patient and explain the rationale for each setting.

Question 1.3 (6 marks)

The infant's parents ask why you are not giving "puffers" like other children with wheezing get. Explain the pathophysiology of bronchiolitis and why bronchodilators are not effective.

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Model Answer

Question 1.1 (8 marks)

Clinical Features of HFNC Failure (4 marks):

1. High FiO2 requirement (0.55 >0.5 threshold) with SpO2 still below target (1 mark)
2. Persistent/worsening work of breathing (marked recession, nasal flaring, head bobbing) (1 mark)
3. Rising PaCO2 (58 mmHg with respiratory acidosis pH 7.28) indicating ventilatory failure (1 mark)
4. 90 minutes without improvement - failure to improve within 60-90 minutes predicts HFNC failure (1 mark)

Immediate Management Plan (4 marks):

1. Escalate to CPAP - Start at 6-8 cmH2O, FiO2 titrated to SpO2 ≥92%; Insert NG tube for gastric decompression (1 mark)
2. Prepare for intubation - Alert senior, prepare drugs (ketamine or propofol + rocuronium), prepare airway equipment (cuffed ETT 4.0mm) (1 mark)
3. Optimize supportive care - Ensure adequate IV access, check hydration, minimal handling (1 mark)
4. Inform parents - Explain deterioration, potential need for intubation, prognosis (1 mark)

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Question 1.2 (6 marks)

Ventilator Settings for Bronchiolitis (3 marks):

Rationale Explanation (3 marks):

1. Bronchiolitis is an obstructive disease with air trapping - the key issue is hyperinflation, NOT atelectasis (1 mark)
2. Long expiratory time - allows complete exhalation; prevents auto-PEEP which worsens hyperinflation and causes hemodynamic compromise (1 mark)
3. Low PEEP - high PEEP would worsen hyperinflation; we accept some atelectasis to avoid air trapping; permissive hypercapnia acceptable (PaCO2 55-65 if pH >7.25) (1 mark)

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Question 1.3 (6 marks)

Pathophysiology Explanation (3 marks):

1. Bronchiolitis is a viral infection of small airways (bronchioles <2mm) caused primarily by RSV (1 mark)
2. Mechanism of airway obstruction:
   • Mucosal and submucosal edema (40-50% of obstruction)
   • Mucus plugging with necrotic epithelial debris (30-40%)
   • Bronchospasm is a minor component (<20%) (1 mark)
3. Immune response is T-cell mediated, not the eosinophilic inflammation seen in asthma (1 mark)

Why Bronchodilators Don't Work (3 marks):

1. Bronchodilators (salbutamol/albuterol) work by relaxing bronchial smooth muscle to relieve bronchospasm (1 mark)
2. In bronchiolitis, obstruction is primarily from edema and mucus, NOT smooth muscle constriction - therefore bronchodilators have no target (1 mark)
3. Multiple large RCTs and Cochrane reviews confirm no improvement in oxygen saturation, hospitalization, or length of stay with bronchodilators (1 mark)

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SAQ 2: Differential Diagnosis and Risk Factors

Time Allocation: 10 minutes Total Marks: 20

Stem: A 6-week-old female infant is brought to the Emergency Department by her parents with a 2-day history of poor feeding and a witnessed apnoeic episode at home. She was born at 35 weeks gestation (now corrected age 1 week) and was in the NICU for 2 weeks for feeding issues. She has been unwell for 3 days with nasal congestion and occasional cough.

On examination:

• HR: 145, RR: 48, SpO2: 96% on room air, Temp: 37.2°C
• Mild subcostal recession
• Occasional wheeze and crackles bilaterally
• Alert, feeding 60% of normal

---

Question 2.1 (6 marks)

List the differential diagnoses for this presentation and identify the most likely diagnosis. Justify your answer.

Question 2.2 (8 marks)

Identify ALL risk factors for severe bronchiolitis in this patient and explain why each increases risk.

Question 2.3 (6 marks)

Outline your disposition decision and explain why this infant requires PICU admission despite relatively mild respiratory signs.

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Model Answer

Question 2.1 (6 marks)

Differential Diagnoses (4 marks, 0.5 marks each):

1. Bronchiolitis (most likely) - viral prodrome, wheeze, crackles, seasonal
2. Pertussis - apnoea prominent, paroxysmal cough, may have minimal respiratory signs
3. Viral pneumonia - overlapping features, may have more focal signs
4. Sepsis/meningitis - young infant, may present with apnoea
5. Congenital heart disease presenting - may present with poor feeding, respiratory distress
6. Aspiration - recurrent episodes, feeding history
7. Brief resolved unexplained event (BRUE) - previously "ALTE"
8. Inborn error of metabolism - young infant with feeding issues

Most Likely Diagnosis and Justification (2 marks):

• Bronchiolitis is most likely given:
  • Classic viral prodrome (nasal congestion, cough) preceding respiratory signs (1 mark)
  • Age-appropriate presentation (peak 2-6 months, this infant corrected 1 week)
  • Apnoea is a recognized presentation in young infants with bronchiolitis, especially premature (1 mark)

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Question 2.2 (8 marks, 2 marks per risk factor)

Risk Factor 1: Age <6 weeks

• This infant is 6 weeks chronological age (corrected age 1 week) (1 mark)
• Young infants have immature respiratory control and are at high risk of apnoea; immune system is immature; brainstem respiratory centers susceptible to RSV (1 mark)

Risk Factor 2: Prematurity

• Born at 35 weeks gestation (1 mark)
• Premature infants have smaller airways, reduced surfactant, immature immune systems, and reduced respiratory reserve (1 mark)

Risk Factor 3: Previous NICU Admission with Feeding Issues

• May indicate underlying feeding coordination problems or prior respiratory compromise (1 mark)
• Suggests potential for chronic lung disease or ongoing respiratory vulnerability (1 mark)

Risk Factor 4: Apnoea at Presentation

• Witnessed apnoeic episode at home is a critical red flag (1 mark)
• Indicates central respiratory involvement; may recur and be life-threatening; requires monitoring in high-acuity setting (1 mark)

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Question 2.3 (6 marks)

Disposition Decision: PICU admission required (2 marks for clear decision)

Reasons for PICU despite Mild Respiratory Signs (4 marks):

1. Apnoea is a critical red flag - The witnessed apnoeic episode mandates continuous cardiorespiratory monitoring with apnoea detection. Apnoea may be the predominant presentation in young infants before significant lower respiratory signs develop. (1 mark)

2. Age <6 weeks - Young infants are at highest risk for sudden deterioration. The peak of apnoea risk is in the first 24-48 hours of illness. General ward may not provide adequate monitoring intensity. (1 mark)

3. Prematurity - Preterm infants have lower respiratory reserve and may deteriorate rapidly. The combination of prematurity + age <6 weeks + apnoea identifies a very high-risk patient. (1 mark)

4. Unpredictable deterioration - Even with currently mild respiratory signs, infants in this risk category may deteriorate rapidly without warning. PICU allows immediate escalation (HFNC, CPAP, intubation) if needed. (1 mark)

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Viva Scenarios

Viva 1: Evidence for Treatments in Bronchiolitis

Stem: "A colleague asks you about the evidence base for bronchiolitis treatments. They have read about various nebulized therapies and want to discuss the literature."

Duration: 12 minutes (2 min reading + 10 min discussion)

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Opening Question:

"What is the evidence for bronchodilator use in bronchiolitis?"

Expected Answer (2-3 minutes):

Multiple high-quality studies demonstrate no benefit from bronchodilators:

1. Cochrane Review (Gadomski & Scondra, 2014) - 30 RCTs, n=1,992:

   • No improvement in oxygen saturation, hospital admission, or length of stay
   • Inhaled bronchodilators do NOT support routine use [42]

2. Pathophysiological basis:

   • Bronchiolitis obstruction is from edema and mucus plugging, NOT bronchospasm
   • Bronchodilators have no physiological target

3. Guideline recommendations:

   • Australasian Bronchiolitis Guideline: Do NOT recommend (Grade A)
   • AAP Clinical Practice Guideline: "Should not use" (Strong recommendation)
   • NICE NG9: "Do not use salbutamol"

---

Follow-up Question 1:

"What about nebulized adrenaline? Some guidelines suggest a trial."

Expected Answer:

Nebulized adrenaline has theoretical benefit due to alpha-adrenergic effects causing mucosal vasoconstriction and reduced edema.

Evidence:

1. Cochrane Review (Hartling et al, 2011) - 19 RCTs:

   • May provide transient improvement in clinical scores
   • No benefit on hospitalization rate or length of stay
   • Does NOT change clinically important outcomes [43]

2. Australasian Guideline position:

   • Do NOT recommend routine use
   • Single trial in ED reasonable but do not continue if no response

3. My practice:

   • I do not routinely use nebulized adrenaline
   • Supportive care with oxygen and HFNC is the evidence-based approach

---

Follow-up Question 2:

"What is the evidence for HFNC in bronchiolitis?"

Expected Answer:

HFNC is the major advance in bronchiolitis management over the past decade.

Key Evidence:

1. Franklin et al (2018) - PARIS Trial - NEJM, PMID: 29576494:

   • Multicenter RCT, n=1,472 infants with bronchiolitis
   • HFNC vs standard low-flow oxygen therapy
   • Primary outcome: Treatment failure requiring escalation
   • Result: 12% failure with HFNC vs 23% with standard oxygen (p<0.001)
   • HFNC reduced escalation to higher levels of care [6]

2. Mechanism of benefit:

   • Nasopharyngeal dead space washout
   • Low-level PEEP generation (2-5 cmH2O)
   • Reduced work of breathing
   • Warm humidified gas delivery

3. Current recommendation:

   • HFNC is first-line escalation from low-flow oxygen
   • Start at 2 L/kg/min, maximum 20-25 L/min
   • Monitor for failure criteria (FiO2 >0.6, worsening WOB)

---

Follow-up Question 3:

"How do you identify HFNC failure early?"

Expected Answer:

Early identification of HFNC failure allows timely escalation.

Predictors of HFNC Failure (within 60-90 minutes):

1. Respiratory rate not improving - Failure to reduce RR by >20% from baseline suggests inadequate response

2. Persistent or worsening work of breathing - Head bobbing, marked recession despite HFNC indicates failure

3. Rising FiO2 requirement - Needing FiO2 >0.5-0.6 to maintain SpO2 ≥92%

4. Rising PaCO2 - Serial blood gases showing upward trend

PARIS 2 Trial (Ramnarayan et al, 2022) - PMID: 35320666:

• Investigated early HFNC vs late HFNC in bronchiolitis
• Early HFNC (at admission) did not reduce treatment failure compared to starting at deterioration
• However, confirmed HFNC is effective rescue therapy

My approach:

• Reassess at 60-90 minutes
• If no improvement in RR or WOB, escalate to CPAP or prepare for intubation
• Do not persist with failing therapy

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Viva 2: RSV Prevention Strategies

Stem: "The parents of a premature infant (born 30 weeks, now 4 months old) ask about preventing bronchiolitis. They have heard about new vaccines and want to understand their options."

---

Opening Question:

"What prevention strategies are available for RSV in high-risk infants?"

Expected Answer (2-3 minutes):

Three strategies are now available:

1. Palivizumab (Synagis) - established prophylaxis for high-risk infants
2. Nirsevimab (Beyfortus) - new long-acting monoclonal antibody for all infants
3. Maternal RSV vaccination - new option for pregnant women

Palivizumab:

• Humanized monoclonal antibody against RSV F protein
• 15 mg/kg IM monthly during RSV season
• PBS-subsidized for: Prematurity ≤28 weeks, chronic lung disease, significant CHD
• 45-55% reduction in RSV hospitalization (NNT ~17) [53]
• This infant (ex-30 weeks) may qualify depending on criteria

---

Follow-up Question 1:

"Tell me about nirsevimab. How is it different from palivizumab?"

Expected Answer:

Nirsevimab (Beyfortus) - approved 2023:

Mechanism:

• Long-acting monoclonal antibody targeting RSV prefusion F protein
• Extended half-life through Fc modification (YTE mutations)

Key Advantages:

1. Single dose provides protection for 5 months (entire RSV season)
2. For ALL infants - not restricted to high-risk groups
3. Simpler administration - one injection vs monthly palivizumab

Dosing:

• <5 kg: 50 mg IM single dose
• ≥5 kg: 100 mg IM single dose
• Given before first RSV season (or early in season)

Efficacy:

• MELODY Trial: 74.5% reduction in RSV LRTI requiring medical attention
• 70-80% reduction in RSV hospitalization [54]
• Superior efficacy data compared to palivizumab

Australian Status:

• TGA approved November 2023
• Under consideration for National Immunisation Program
• May become standard of care for all infants

---

Follow-up Question 2:

"What about maternal vaccination? How does that work?"

Expected Answer:

Maternal RSV Vaccination (RSVpreF - Abrysvo):

Mechanism:

• Recombinant RSV prefusion F protein vaccine
• Given during pregnancy at 32-36 weeks gestation
• Transplacental transfer of maternal IgG antibodies to fetus
• Protects infant for first 6 months of life

Efficacy (MATISSE Trial) - PMID: 37018464:

• 69% reduction in severe RSV LRTI in first 180 days of life
• 57% reduction in RSV hospitalization [55]
• Protection highest in first 3 months

Advantages:

• Single injection during pregnancy (no infant injections)
• Protects infant from birth (immediate protection)
• Combined with existing antenatal vaccines (Tdap, influenza)

Australian Status:

• TGA approved 2024
• Expected to be offered during pregnancy

Complementary Strategy:

• For this preterm infant, maternal vaccination would have been given at 32-36 weeks
• However, preterm delivery may have reduced antibody transfer
• Nirsevimab or palivizumab would provide additional protection

---

Follow-up Question 3:

"How would you counsel these parents about their options?"

Expected Answer:

Counselling Approach:

1. Acknowledge their concern - RSV bronchiolitis is common and can be severe in premature infants. Their concern is appropriate.

2. Explain their child's risk:

   • Ex-30 weeks premature = higher risk of severe bronchiolitis
   • First RSV season (usually winter) is highest risk period
   • May need hospitalization and respiratory support if infected

3. Review options:

Palivizumab:

• May be eligible for PBS-subsidized treatment (check criteria)
• Monthly injections during RSV season
• Well-established safety and efficacy

Nirsevimab:

• Single injection, likely superior efficacy
• Not yet on NIP - may need private purchase (cost ~$700-1000)
• Recommended if accessible

4. Non-pharmacological prevention:

• Hand hygiene (most important)
• Avoid sick contacts
• Avoid crowded places during RSV season
• No smoking in household
• Breastfeeding if possible (some protective effect)

5. Summarize recommendation:

• "Given your son's prematurity, I would recommend RSV prophylaxis. Palivizumab may be covered by PBS; nirsevimab is a newer option requiring single dose. Either would reduce his risk of severe bronchiolitis by 50-75%."