Key Facts

RDS remains the most significant respiratory condition of the preterm neonate. The combination of antenatal steroids, postnatal CPAP, and surfactant replacement has transformed survival and outcomes over the past 40 years.

Epidemiology

RDS affects approximately 60-80% of infants born at <28 weeks, 15-30% at 32-36 weeks, and is rare at term. It is the most common cause of neonatal death from prematurity. Before surfactant therapy (introduced early 1990s), RDS mortality was approximately 50% in very preterm infants.

Aetiology

Primary surfactant deficiency:

• Prematurity (most common cause) — type II pneumocytes immature
• Risk increased by: Male sex, Caucasian ethnicity, maternal diabetes, caesarean section (reduced catecholamine surge), perinatal asphyxia

Secondary surfactant dysfunction:

• Meconium aspiration syndrome, pneumonia, pulmonary haemorrhage

Pathophysiology

Surfactant is a mixture of phospholipids (predominantly DPPC — dipalmitoylphosphatidylcholine) and surfactant proteins (SP-A, B, C, D) produced by type II alveolar pneumocytes. It reduces alveolar surface tension, preventing atelectasis at end-expiration and maintaining functional residual capacity (FRC). In surfactant deficiency, alveoli collapse with each expiration, requiring increased effort to re-expand them. This causes progressive atelectasis, intrapulmonary shunting, hypoxia, and acidosis. Protein-rich exudate forms hyaline membranes (hence the historical name 'hyaline membrane disease').

Clinical Features (Within First 4-6 Hours)

• Tachypnoea: RR >60/min
• Grunting: Expiratory — maintains positive end-expiratory pressure
• Nasal flaring: Accessory muscle use
• Intercostal/subcostal recession: Compliance mismatch (compliant chest wall, stiff lungs)
• Cyanosis: Worsening hypoxia
• Apnoeas: Especially in extremely preterm infants

Natural History

• Onset within 4-6 hours of birth
• Peaks at 48-72 hours
• Begins to improve after 72 hours (endogenous surfactant production increases)
• Without treatment: Progressive respiratory failure → death

Red Flags

• Worsening respiratory distress despite surfactant — consider complications (pneumothorax, pulmonary haemorrhage, sepsis)
• Sudden deterioration — tension pneumothorax until proven otherwise
• High O2 requirement (FiO2 >0.6) — consider repeat surfactant or intubation if on CPAP
• Persistent hypotension — may indicate PDA or sepsis

Bedside

• Continuous monitoring: SpO2 (pre-ductal), HR, RR, temperature
• Blood gas (capillary/arterial): pH, PaCO2, PaO2, base excess — guide respiratory support
• Blood glucose: Hypoglycaemia screening

Bloods

• FBC, CRP, blood culture: Rule out sepsis (clinical presentation overlaps)
• Blood gas: Serial — guide ventilation strategy

Imaging

• CXR: Ground-glass opacification (diffuse, bilateral), air bronchograms, reduced lung volumes, ETT position if intubated
• Serial CXR: If clinical deterioration — exclude pneumothorax, pulmonary haemorrhage

Special Tests

• Echocardiography: If persistent high O2 requirement — exclude CHD, assess PDA
• Transillumination: Rapid bedside test for pneumothorax (bright light through chest wall)

Antenatal Prevention

• Corticosteroids: Betamethasone 12mg IM ×2 doses 24h apart at 24-34 weeks — reduces RDS by ~50%, mortality, IVH, NEC

Delivery Room

• CPAP from birth: 5-8 cmH2O via T-piece or CPAP driver — establishes FRC, reduces need for intubation
• Surfactant: If FiO2 >0.3 on CPAP (or >0.4 — varies by unit); poractant alfa (Curosurf) 200mg/kg
• LISA technique: Thin catheter surfactant administration during CPAP — avoids intubation; reduced BPD risk

NICU Respiratory Support (Escalating)

1. CPAP (5-8 cmH2O): First-line; non-invasive; maintains FRC
2. NIPPV/BiPAP: Non-invasive; higher support than CPAP
3. Conventional mechanical ventilation (IPPV): If CPAP fails (persistent high FiO2, recurrent apnoeas, respiratory acidosis)
4. High-frequency oscillatory ventilation (HFOV): For refractory hypoxia or air leak

Pharmacological

• Surfactant: Poractant alfa 200mg/kg initial dose; can repeat 100mg/kg ×2 if ongoing high FiO2 requirement
• Caffeine citrate: Loading 20mg/kg IV; maintenance 5-10mg/kg OD — reduces apnoea of prematurity AND BPD (CAP trial)
• Analgesia/sedation: Morphine 10-20mcg/kg/hr if ventilated and distressed; minimise where possible

Supportive Care

• Thermoregulation: Incubator, plastic wrap (<28 weeks)
• Fluid management: Start at 60-80mL/kg/day; increase gradually; avoid fluid overload (worsens PDA, pulmonary oedema)
• Nutrition: Trophic feeds (breast milk) from day 1 if possible; TPN until full enteral feeds established
• Minimal handling: Clustered cares to reduce stress and energy expenditure

Referral Criteria

• All preterm infants with respiratory distress — neonatal team at delivery
• Persistent high FiO2 or respiratory failure despite surfactant — tertiary NICU if not already
• Air leak (pneumothorax) — chest drain; surgical team if needed
• Suspected CHD — cardiology/echocardiography

• With surfactant + CPAP: Survival >90% for infants >28 weeks with RDS
• Without surfactant: Mortality ~50% in very preterm RDS (historical)
• Surfactant NNT: ~6 to prevent 1 death in preterm RDS
• BPD (chronic lung disease): Defined as O2 requirement at 36 weeks CGA; affects ~30% of <28 weeks; most wean off O2 by 1-2 years
• CAP trial (caffeine): Reduced BPD from 47% to 36% AND improved 18-month neurodevelopmental outcome
• Long-term respiratory: Increased risk of asthma, reduced exercise tolerance, and abnormal lung function in childhood and adulthood

RDS vs TTN Comparison

Surfactant Preparations (UK)

Caffeine for Prematurity (CAP Trial)