What is Respiratory Distress Syndrome (RDS)?

What is Respiratory Distress Syndrome (RDS)?

Respiratory Distress Syndrome is a respiratory disorder caused by surfactant deficiency that leads to alveolar collapse, impaired gas exchange, and characteristic clinical findings—occurring predominantly in preterm infants but also affecting term neonates under specific high-risk conditions. 1

Definition and Core Pathophysiology

RDS results from inadequate surfactant production, which causes widespread alveolar collapse at end-expiration. 1 The condition is further complicated by high alveolar-capillary permeability that allows serum proteins to leak into the airways, creating a vicious cycle that further inhibits any remaining surfactant function. 1

In adults and older patients, ARDS (Acute Respiratory Distress Syndrome) represents a different entity defined by acute arterial hypoxemia (PaO2/FiO2 ≤ 300 mmHg) with bilateral radiographic opacities occurring within 1 week of a known clinical insult, not fully explained by cardiac failure. 2

Population Most Affected

Preterm Infants (Primary Population)

• Highest incidence: Infants born at <30 weeks gestation and weighing <1,000g 1
• At 27 weeks gestation: 90-92% require surfactant therapy even after antenatal corticosteroid exposure 1
• Multiple gestation pregnancies increase risk 1
• Absence of antenatal corticosteroid administration is a major preventable risk factor 1

Term Infants (Secondary Population)

While less common (incidence 1.64% of term NICU admissions), term infant RDS has distinct characteristics: 3

• High-risk factors include: selective cesarean section (OR: 8.737), severe birth asphyxia (OR: 6.988), small for gestational age (OR: 6.222), maternal-fetal infection (OR: 5.337), premature rupture of membranes (OR: 3.380), male sex (OR: 2.641), and gestational diabetes (OR: 2.415) 4
• Earlier onset of symptoms (mean 3.11 hours after birth) compared to preterm RDS 5
• More likely to develop persistent pulmonary hypertension and multi-organ system failure 5
• Mortality rate of 3.2-5.1% in term infants, primarily from sepsis with multi-organ failure 5, 3

Clinical Presentation

Immediate onset at birth in preterm infants with: 6

• Severe respiratory distress with grunting, nasal flaring, and retractions 6
• Central cyanosis from impaired gas exchange 6
• Diffuse bilateral lung involvement without spared areas 6

Diagnostic Approach

Lung ultrasound is now preferred over chest X-ray for diagnosis, showing: 6

• Bilateral confluent B-lines throughout all lung fields 6
• Pleural line abnormalities 6
• Complete absence of A-lines and spared areas 6
• Diffuse "white lung" appearance 6

This distinguishes RDS from transient tachypnea of the newborn (TTN), which shows B-lines predominantly in dependent lower lung areas with normal-appearing upper fields. 6

Evidence-Based Management

Prevention

Antenatal corticosteroids are the most effective preventive intervention, working synergistically with postnatal surfactant to reduce mortality, RDS severity, and air leaks. 1

First-Line Treatment

Initiate CPAP at 5-6 cm H₂O immediately for all spontaneously breathing preterm infants with respiratory distress rather than routine intubation. 1, 6 CPAP prevents atelectasis by maintaining functional residual capacity and preventing alveolar collapse, and reduces the combined risk of death or bronchopulmonary dysplasia compared to immediate intubation. 1 Historical data confirms CPAP reduces failed treatment (death or need for assisted ventilation) with RR 0.70 and overall mortality with RR 0.52. 7

Surfactant Therapy

Administer early surfactant replacement therapy within 2 hours of birth for infants <30 weeks gestation. 1, 6 This intervention:

• Reduces mortality by 47% (RR 0.53, NNT=9) 1
• Decreases pneumothorax (RR 0.62, NNT=47) 1
• Reduces bronchopulmonary dysplasia or death (RR 0.85, NNT=24) 1

Critical Pitfall to Avoid

Never administer surfactant empirically without confirming RDS diagnosis—surfactant is contraindicated in transient tachypnea of the newborn and other non-surfactant-deficiency conditions and will not benefit pneumonia. 6, 8

Mechanical Ventilation When Needed

If CPAP fails and mechanical ventilation becomes necessary, use PEEP to prevent lung collapse at end-expiration and employ gentle ventilation strategies to minimize barotrauma and oxygen toxicity that contribute to bronchopulmonary dysplasia. 1

Long-Term Outcomes and Prognosis

RDS is the primary precursor to bronchopulmonary dysplasia (BPD), a chronic condition characterized by alveolar simplification in the modern era. 1 Survivors experience:

• Persistent airway obstruction and hyperreactivity into childhood 1
• Average FEV₁ approximately 80% of control subjects at 6-15 years of age 1
• Multisystem complications beyond respiratory issues are common 1

Adult ARDS Context

In mechanically ventilated ICU patients, approximately 25% develop ARDS with mortality rates of 35-40% that increase with hypoxemia severity. 2 Management focuses on low tidal volume ventilation, sufficient PEEP, and in severe cases, prone positioning, neuromuscular blocking agents, and ECMO to minimize ventilator-induced lung injury. 2