Neonatal Respiratory Distress Syndrome (NRDS)

Neonatal Respiratory Distress Syndrome (NRDS)

Neonatal respiratory distress syndrome (NRDS) is the most common cause of respiratory distress in preterm neonates. Diagnosis is by clinical presentation and Chest X-ray. Use of antenatal steroids reduces RDS by an average of 40%.

Affects 5% (1 in 20) of babies born btw 35-36 weeks of gestation and 50% of babies born btw 26-28 weeks. M>F.

• Predisposing factors
  • Prematurity (< 34 weeks gestation, especially < 28 weeks)
  • Maternal diabetes (delayed surfactant due to fetal hyperinsulinism)
  • Perinatal asphyxia (hypoxia impairs surfactant production)
  • Caesarean section OR precipitous delivery (lack os stress-induced steroid surge)
  • Multiple gestation (particularly the second twin)
  • Cold stress
  • History of NRDS in a sibling
  • Male sex
• Pathophysiology
  • Surfactant is produced by type II pneumocytes. Production begins at 20 – 24 weeks and mature levels are reached at 35 weeks of gestation. Corticosteroids increase surfactant production
  • Surfactant helps to reduce alveolar surface tension and prevent atelectasis
  • In preterms < 34 weeks surfactant synthesis is insufficient. This causes increased surface tension and atelectasis during exhalation
  • Persistent atelectasis causes endothelial damage causing fibrin and proteins to leak into the alveoli and form a hyaline membrane
  • Atelectasis and hyaline membrane formation causes ventilation-perfusion (V/Q) mismatch which leads to hypoxemia and cyanosis
  • Pulmonary vasoconstriction from hypoxia can worsen ventilation-perfusion mismatch
• Signs and symptoms
  • Respiratory distress (tachypnea, intercostal indrawing, grunting, cyanosis, flaring of nasal alae)
  • On auscultation
    • Diminished air entry
    • Basal fine crepitations
• Antenatal investigations
  • Lecithin/sphingomyelin ratio
    • 2.5 = Mature lungs
    • 1.5-2 = Transitional lung with increased risk of RDS
    • < 1.5 = Immature lung with risk of severe RDS
  • Saturated phosphatidylcholine
    • <500 μg/dL = Immature lung with high risk of RDS
    • 500 μg/dL = Mature lung
• Post-natal investigations
  • Chest X-ray:
    • Diffuse bilateral reticulonodular infiltrates (diffuse ground glass appearance),
    • Air bronchograms (contrast of aerated airways vs collapsed airways),
    • Small lung volumes
    • Severe RDS shows opacification of both lungs
  • Arterial blood gases:
    • Hypoxemia
    • Hypercapnia
    • Respiratory and metabolic acidosis
  • U/E/Cs:
    • hyponatremia due to fluid retention
  • CBC + CRP: evaluate the possibility of early-onset NNS in a preterm baby (clinically indistinguishable from RDS)
  • Shake test : Done within one hour of life to determine amount of surfactant present. 0.5ml of gastric aspirate + 4ml of Normal saline + 0.5ml of alcohol are mixed and shaken; check for presence of bubbles
    • Absence of bubbles – absent surfactant hence high risk of RDS
    • Incomplete bubbles – intermediate risk of surfactant
    • Double row of bubbles or more – no risk of RDS
• Prevention
  • Antenatal prophylaxis: administer betamethasone to mother in preterm labor (at least 24 hrs before deliver). Accelerates surfactant production.
  • Avoid risk factors
• Supportive treatment
  • Supplemental O2 via nasal CPAP for mild cases
  • Mechanical intubation for severe cases
  • Incubator care
  • Frequent vital monitoring
  • Adequate fluids and feeds
• Definitive treatment
  • Intubation for exogenous surfactant administration: definitive treatment. 3-5ml per kg per dose given at 6-12 hour intervals
  • Prophylactic exogenous surfactant for all neonates born ≤ 27 weeks
  • Empiric antibiotics (Benzylpenicillin/Ampicillin + Gentamicin) should be given as RDS is hard to differentiate from congenital pneumonia
• Indications for surfactant therapy
  • FiO2 required >30%
  • Recent intubation
  • SAS score <4

Differentiating TTN from NRDS