π Key Learning
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Respiratory distress in neonates can be due to TTN, MAS, or RDS β distinguish based on timing, risk factors, and CXR findings
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TTN is most common and resolves with minimal intervention
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MAS is related to meconium-stained liquor and can cause significant pulmonary issues
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RDS occurs in preterm infants due to surfactant deficiency
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NEC is the most serious GI emergency in neonates, particularly in preterm, formula-fed babies β high risk of bowel necrosis and perforation
π¬οΈ Transient Tachypnoea of the Newborn (TTN)
𧬠Pathophysiology
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Delayed reabsorption of foetal lung fluid
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Leads to reduced lung compliance and impaired gas exchange
π Clinical Features
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Onset within first 4 hours after birth
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Tachypnoea
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Nasal flaring, grunting, subcostal/intercostal recession
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Fine crackles on auscultation
β οΈ Risk Factors
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Elective Caesarean section (no labour = less fluid clearance)
π§ͺ Investigations
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CXR:
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Hyperinflated lungs
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Perihilar streaking
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Fluid in horizontal fissures
π Management
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Supportive: Oβ as needed
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CPAP if respiratory effort increases
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Self-resolving within 48β72 hours
π© Meconium Aspiration Syndrome (MAS)
𧬠Pathophysiology
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Foetal distress β meconium passage in utero
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Gasping leads to aspiration of meconium-stained liquor
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Meconium causes:
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Surfactant inhibition
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Airway obstruction
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Chemical pneumonitis
π Clinical Features
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Respiratory distress immediately or very soon after birth
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Associated complications:
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Pulmonary air leaks (e.g. pneumothorax)
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Persistent pulmonary hypertension of the newborn (PPHN)
π§ͺ Investigations
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CXR:
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Hyperinflation
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Patchy collapse/consolidation
π Management
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Supportive: Oβ, CPAP, or ventilation
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May require surfactant therapy and inhaled nitric oxide for PPHN
π« Respiratory Distress Syndrome (RDS)
𧬠Pathophysiology
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Caused by surfactant deficiency
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Surfactant reduces surface tension β deficiency leads to alveolar collapse
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Type II pneumocytes begin producing surfactant from 24β28 weeks, typically sufficient by 34 weeks
β οΈ Risk Factors
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Prematurity is primary risk
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50% incidence in infants born 28β32 weeks
π‘οΈ Prevention
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Antenatal corticosteroids if preterm delivery is anticipated
π Clinical Features
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Respiratory distress at birth or within 4 hours
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Tachypnoea (>60 bpm)
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Nasal flaring, grunting
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Subcostal/sternal recession
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Cyanosis, low Oβ sats
π§ͺ Investigations
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CXR:
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Ground-glass appearance
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Air bronchograms
π Management
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Supportive: CPAP, Oβ
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Surfactant replacement via tracheal tube
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Mechanical ventilation if needed
π¦ Necrotising Enterocolitis (NEC)
𧬠Pathophysiology
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Multifactorial: ischaemia + infection + exaggerated immune response
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Inflammation β mucosal injury β necrosis and perforation
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Predominantly affects preterm, formula-fed neonates
π Clinical Features
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Occurs in 2ndβ3rd week of life
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Early signs:
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Vomiting
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Poor feeding
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Abdominal distension
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Late signs:
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Blood/mucus in stool
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Tender abdomen, peritonitis, perforation
π§ͺ Investigations
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AXR:
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Dilated bowel loops
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Thickened bowel wall
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Pneumatosis intestinalis (intramural gas)
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Gas in portal venous system
π Management
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NBM
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IV antibiotics
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Supportive care (fluids, ventilation if needed)
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Surgical review if perforation or failure to improve
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May require bowel resection
π Exam Clues & Clinchers
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C-section + tachypnoea <4 hrs β TTN
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Term infant + meconium-stained liquor + distress β MAS
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Preterm baby + ground-glass lungs on CXR β RDS
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Preterm formula-fed + distended tender abdomen in 2nd week β NEC