πŸ”‘ Key Learning

  • Respiratory distress in neonates can be due to TTN, MAS, or RDS β€” distinguish based on timing, risk factors, and CXR findings
  • TTN is most common and resolves with minimal intervention
  • MAS is related to meconium-stained liquor and can cause significant pulmonary issues
  • RDS occurs in preterm infants due to surfactant deficiency
  • NEC is the most serious GI emergency in neonates, particularly in preterm, formula-fed babies β€” high risk of bowel necrosis and perforation

🌬️ Transient Tachypnoea of the Newborn (TTN)

🧬 Pathophysiology

  • Delayed reabsorption of foetal lung fluid
  • Leads to reduced lung compliance and impaired gas exchange

πŸ‘€ Clinical Features

  • Onset within first 4 hours after birth
  • Tachypnoea
  • Nasal flaring, grunting, subcostal/intercostal recession
  • Fine crackles on auscultation

⚠️ Risk Factors

  • Elective Caesarean section (no labour = less fluid clearance)

πŸ§ͺ Investigations

  • CXR:
    • Hyperinflated lungs
    • Perihilar streaking
    • Fluid in horizontal fissures

πŸ’Š Management

  • Supportive: Oβ‚‚ as needed
  • CPAP if respiratory effort increases
  • Self-resolving within 48–72 hours

πŸ’© Meconium Aspiration Syndrome (MAS)

🧬 Pathophysiology

  • Foetal distress β†’ meconium passage in utero
  • Gasping leads to aspiration of meconium-stained liquor
  • Meconium causes:
    • Surfactant inhibition
    • Airway obstruction
    • Chemical pneumonitis

πŸ‘€ Clinical Features

  • Respiratory distress immediately or very soon after birth
  • Associated complications:
    • Pulmonary air leaks (e.g. pneumothorax)
    • Persistent pulmonary hypertension of the newborn (PPHN)

πŸ§ͺ Investigations

  • CXR:
    • Hyperinflation
    • Patchy collapse/consolidation

πŸ’Š Management

  • Supportive: Oβ‚‚, CPAP, or ventilation
  • May require surfactant therapy and inhaled nitric oxide for PPHN

🫁 Respiratory Distress Syndrome (RDS)

🧬 Pathophysiology

  • Caused by surfactant deficiency
  • Surfactant reduces surface tension β†’ deficiency leads to alveolar collapse
  • Type II pneumocytes begin producing surfactant from 24–28 weeks, typically sufficient by 34 weeks

⚠️ Risk Factors

  • Prematurity is primary risk
    • 50% incidence in infants born 28–32 weeks

πŸ›‘οΈ Prevention

  • Antenatal corticosteroids if preterm delivery is anticipated

πŸ‘€ Clinical Features

  • Respiratory distress at birth or within 4 hours
    • Tachypnoea (>60 bpm)
    • Nasal flaring, grunting
    • Subcostal/sternal recession
    • Cyanosis, low Oβ‚‚ sats

πŸ§ͺ Investigations

  • CXR:
    • Ground-glass appearance
    • Air bronchograms

πŸ’Š Management

  • Supportive: CPAP, Oβ‚‚
  • Surfactant replacement via tracheal tube
  • Mechanical ventilation if needed

🦠 Necrotising Enterocolitis (NEC)

🧬 Pathophysiology

  • Multifactorial: ischaemia + infection + exaggerated immune response
  • Inflammation β†’ mucosal injury β†’ necrosis and perforation
  • Predominantly affects preterm, formula-fed neonates

πŸ‘€ Clinical Features

  • Occurs in 2nd–3rd week of life
  • Early signs:
    • Vomiting
    • Poor feeding
    • Abdominal distension
  • Late signs:
    • Blood/mucus in stool
    • Tender abdomen, peritonitis, perforation

πŸ§ͺ Investigations

  • AXR:
    • Dilated bowel loops
    • Thickened bowel wall
    • Pneumatosis intestinalis (intramural gas)
    • Gas in portal venous system

πŸ’Š Management

  • NBM
  • IV antibiotics
  • Supportive care (fluids, ventilation if needed)
  • Surgical review if perforation or failure to improve
    • May require bowel resection

πŸ“ Exam Clues & Clinchers

  • C-section + tachypnoea <4 hrs β†’ TTN
  • Term infant + meconium-stained liquor + distress β†’ MAS
  • Preterm baby + ground-glass lungs on CXR β†’ RDS
  • Preterm formula-fed + distended tender abdomen in 2nd week β†’ NEC