2. Respiratory Distress
• Presence of any two of the following features:
1. Respiratory rate >60/minute
2. Subcostal/intercostal recessions
3. Expiratory grunt/groaning
• In addition to the above features, presence of nasal flaring,
suprasternal retractions, decreased air entry on auscultation of
the chest also will indicate the presence of respiratory distress
• National Neonatal Perinatal Database (NNPD) definition
3. Respiratory Distress Syndrome
• Respiratory distress syndrome (RDS), a
disease affecting preterm infants, is
caused by insufficient pulmonary
surfactant.
• Formerly known as hyaline membrane disease (HMD)
4. Predisposing Risk Factors
• Prematurity
• Birth Asphyxia
• LSCS
Male sex
• Maternal Diabetes
• Caucasian race
• Rh Negative
• Second born twins
• < 28wk GA 60‐80%
• 32‐36wk GA 15‐30%
5. Pathogenesis
• Absent or insufficient surfactant due to
developmental immaturity of alveolar
type II cells or
• Spontaneous or inherited mutations of
surfactant-related genes, or
• Inactivation of surfactant due to
inflammation, chemical modification, or
lung injury, result in high surface tension
and atelectasis.
6. Pathogenesis
• Surfactant reduces surface tension at air-
fluid interface Improves lung compliance
• Surfactant deficiency = decreased
compliance
• Decreased compliance = alveolar collapse
and loss of FRC
• Loss of FRC = V/Q mismatch
• V/Q mismatch = desaturation, and
respiratory distress
7. Pathogenesis – Surfactant Composition
• SP-B and SP-C work
in concert to
facilitate rapid
adsorption and
spreading of DPPC as
a monolayer to lower
the surface tension
at the alveolar air-
fluid interface in vivo
during expiration,
thus preventing
atelectasis.
8. Clinical Features
• Respiratory Distress within 6 hrs of Life
(usually within minutes of birth)
• SCR, ICR, Grunting, Cyanosis, Ala nasi
Flaring*.
• Auscultation: ↓ air entry ± fine rales
• Shock
• Other features: Edema, ileus, & oliguria
• Apnea in extreme prematurity
9. Clinical Course
• Severe cases develop respiratory failure
needing ventilation / surfactant / CPAP – and
may tire and develop apnea / die if care not
offered
• Mild cases – can be managed with only
oxygen
• Symptoms progress to peak in 3 days
• Improvement thereafter (often heralded by
spontaneous diuresis)
10. Assessment of respiratory distress
A score greater than 7 indicates that the baby is in respiratory failure
12. Investigations
• Amniotic fluid – Lecithin to Sphingomyelin ratio
(L/S ratio)
> 2.5 = 0.5%,
> 2 =10% ,
1.5‐2 = 15‐20%,
< 1.5 = 60 % risk of developing RDS
– Blood & Meconium depress mature L/S ratio and may
elevate immature ratio
– Exceptions: IDM, Asphyxia‐ can develop RDS even if ratio ok
• Phosphatidylglycerol = present
• Saturated Phosphatidylcholine (SPC) > 500 ug/dl
13. Investigations contd…
Gastric Aspirate –
Shake Test
• Mix 0.5 ml of gastric
aspirate & 0.5 ml of
absolute alcohol
• Shake for 15
seconds & allow the
solution to settle for
15 seconds
• If no bubbles – 60 % chances of RDS
• Small bubbles to the extent of 1/3rd
of the circle of the test tube – 20%
chances of RDS
14. Investigations contd…
Lamellar body counts (phospholipid “packages”
produced by type 2 alveolar cells) in amniotic
fluid
– > 50,000 lamellar bodies/μL → lung maturity
15. Investigations: CXR
• Reticulo granular
pattern
• Air bronchogram
• Ground Glass
opacity
• White wash
appearance in
severe RDS
18. Prevention
• Induction of labour should preferably be delayed till lung
maturity
• Prevent fetal asphyxia by antenatal & intranatal
monitoring
• Antenatal Steroids (to Mother)
– Betamethasone 12 mg IM 2 doses in 24 hrs interval
(preferred)
– Dexamethasone 4 doses in 12 hrs interval
• Must be given to all mothers in preterm labor (<37 weeks)
• Decreases incidence of severe RDS, IVH, mortality by half
• Can be given even if mother has HTN, diabetes
20. Treatment – 1.Supportive care
• Maintenance of thermo-neutral environment
– Radiant warmer
• Ensuring normal blood glucose level
• Intravenous fluids
• Sepsis Rx – Antibiotics till infection is ruled out
• Developmental friendly nursing policy
21. Treatment – 2.Respiratory support
• Ensure adequate oxygenation and
ventilation, and thereby decrease the work
of breathing.
• Aim would be to maintain
– pH>7.25,
– pO2 50- 70 mm Hg,
– pCO2 <50 mmHg and
– SpO2 88%-93%.
22. Treatment – 2.Respiratory support
• Supplemental oxygen
• CPAP - via nasal prongs, nasal
mask, or face mask
• Mechanical ventilation
23. Treatment – 3.Monitoring for and
management of complications
• Monitored for
– worsening of the distress,
– hemodynamic instability,
– features of PPHN,
– acute kidney injury due to hypoxia and
– complications due to mechanical
ventilation etc.
24. Treatment- 4.Specific Therapy
• Types of surfactants:
– Natural – Bovine, Calf, Porcine
– Synthetic
• Timing of intervention:
– Prophylaxis (before onset of RD)
– Treatment (rescue – after onset of RD)
• Intubate surfactant and extubate (INSURE): intubation for
prophylactic or early rescue surfactant replacement
therapy, followed by extubation back to nCPAP
immediately once the infant is stable (usually within
minutes to <1 hr)
25. 4.Surfactant Therapy
• Given in to the trachea
• Produces immediate
improvement in lung
condition
• Relatively costly drug
• No serious side effects
in immediate period /
long term
26. Complications
• Acute
– Air leaks ‐ Pneumothorax, Pneumomediastinum, PIE,
Pneumopericardium, Air Embolism
– PDA – look for & treat aggressively
– Infection – NEC, GI perforation
– Intracranial hemorrhage
• Chronic
– Bronchopulmonary dysplasia
– Retinopathy of prematurity
– Neurologic impairment