RESPIARTORY DISTRESS SYNDROME

1. Respiratory Distress in Newborn

2. Flow of the presentation
• Introduction
• Definition of respiratory distress.
•

3. Introduction
• Respiratory distress is one of the most common reasons an
infant is admitted to the NICU.
• 15% of term infants and 29% of late preterm infants
admitted to the NICU develop significant respiratory
morbidity.
• Neonatal RDS is a frequent cause of increased morbidity
and mortality in neonates.
• Understanding the pathophysiology, clinical presentation,
diagnosis, prevention, and management of this condition
is vital to decreasing morbidity and mortality.

4. Definition of Respiratory Distress
Presence of any 2 of the following features:
1. R.R > 60/min
2. Subcostal/intercostal Recessions
3. Expiratory Grunt /Groaning
Signs should be assessed in context of Spo2,
colour, activity of the baby.

5. Incidence of RDS
• Incidence is inversely proportional to gestational age & birth
weight.
Worldwide data:
• <28 WOG – 60 to 80%
• 32-36WOG- 15 TO 30%
Indian data:
58% in <30 wog
32% b/w 30-32 wog
10% b/w 33-34 wog
• 37 WOG- Term – 5%
• 500-750 gm-54% (NICHD Neonatal Research Network,Fanaroff et.al)
• 751-1000gm- 36%
• 1251-1500gm-22%
• 6.8 to 14.1% of preterm live births in India
• 1.2% of all live births (NATIONAL NEONATAL PERINATAL DATA 2013 report)

6. Neonatal Respiratory Distress
Etiologies
Pulmonary
Transient tachypnea
of the newborn (TTN)
Pneumonia
Meconium aspiration
syndrome (MAS)
Air leak syndromes
Pulmonary
hemorrhage
Systemic
Metabolic (e.g.,
hypoglycemia, hypothermia
or hyperthermia)
metabolic acidosis
anemia, polycythemia
•
Cardiac
Congenital heart disease;
cyanotic or acyanotic
• Congestive heart failure
• Persistent pulmonary
hypertension of the newborn
(PPHN)
Neurological (e.g., prenatal
asphyxia, meningitis)
Anatomic
Upper airway
obstruction
Airway
malformation
Rib cage anomalies
Diaphragmatic
disorders
(e.g., congenital
diaphragmatic
hernia,
diaphragmatic
paralysis)

7. 
Neonatal Respiratory Distress
Signs and symptoms
o Tachypnea (RR > 60/min)
o Nasal flaring
o Retraction
o Grunting
o +/- Cyanosis
o +/- Desaturation
o Decreased air entry

8. Pathophysiology of RDS
RDS manifests histologically as HYALINE MEMBRANE
DISEASE.

9. Physiologic abnormalities
• Surfactant deficiency- increase in alveolar surface
tension.
• Lung compliance decreased to 10-20% of normal
• Atelectasis…areas not ventilated
• Decrease alveolar ventilation
• Reduce lung volume
• Areas not perfused

10. Normal Expiration
With Surfactant
Surfactant Function
Abnormal Respiration
Without Surfactant

11. Assessment of Respiratory Distress
Initial assessment: To find out life threatening
conditions requiring immediate management
1. Inadequate/Obstructed Airway:
Gasping ,Choking,Stridor.
2. Circulatory collapse: Bradycardia, Hypotension,
poor perfusion.
Intervention: Bag-Mask ventilation/intubation

12. Assessment of Severity: Silverman score

13. Downe’s score

14. Chest x-ray:findings can be graded according to the severity
Grade 1 (mild cases): the lungs show fine
homogenous ground glass shadowing
Grade 2: widespread air bronchogram become
visible
Grade 3: confluent alveolar shadowing
Grade 4: complete white lung fields with obscuring of
the cardiac shadow
Radiological

15. Grade 1
Grade 1 (mild cases): the lungs show fine homogenous ground
glass shadowing

16. General Management of Respiratory Distress
o Supplemental oxygen or MV, if needed.
o Continuously monitor with pulse oximeter.
o Obtain a chest radiograph.
o Correct metabolic abnormalities
(acidosis,hypoglycemia).
o Obtain a blood culture & begin an antibiotic
coverage (ampicillin + gentamicin)

17. Grade 2
Grade 2: widespread air bronchogram become visible

18. Grade 3
Grade 3: confluent alveolar shadowing

19. Grade 4
Grade 4: complete white lung fields with
obscuring of the cardiac shadow

20. Monitoring
Oxygenation and
Ventilation
Antenatal
corticosteroid
therapy
Assisted
Ventilation of the
Neonate
Exogenous
Surfactant
Therapy
Supportive Care
Management RDS

21. Management
• Lung maturity testing: lecithin/sphingomyelin (L/S) ratio:
(The normal L/S ratio is 2.0 to 2.5 and is significant for
appropriate fetal lung development. An L/S ratio of less
than 2.0 is significant for immature fetal lung
development)
• Tocolytics to inhibit premature labor. (Commonly used
tocolytic medications include β2 agonists, calcium channel
blockers, NSAIDs, and magnesium sulfate).

22. Antenatal corticosteroid therapy:
• They induce surfactant production and accelerate
fetal lung maturation.
• Are indicated in pregnant women 24-34 weeks'
gestation at high risk of preterm delivery within the
next 7 days.
• Optimal benefit begins 24 hrs after initiation of
therapy and lasts seven days.
Antenatal corticosteroid therapy consists of either :
• Betamethasone 12 mg/dose IM for 2 doses, 24 hrs apart,
or
• Dexamethasone 6 mg/dose IM for 4 doses, 12 hrs apart

23. Monitoring Oxygenation and Ventilation
T
arget SpO2
 <30 weeks or wt<1.250gm –88 to 92 %
 >30 weeks or wt >1.250gm-88 to 95%
ABG Monitoring: Frequent measurements during
acute stage, do ABG after 30 min of changes in
FiO2/ventilator setting Initiate CPAP as early as possible
In infants with mild RDS.
Start MV if respiratory acidosis (PaCO2 >60 mmHg, PaO2
<50 mmHg or SaO2 <90%) with an FiO2 >0.5, or severe
frequent apnea.
Specific management depends on the cause of distress.

24. Assisted Ventilation of the Neonate
The goals of assisted ventilation are to reduce atelectasis
by providing a constant distending positive airway
pressure.
CPAP /Bubble CPAP with selective surfactant
administration:
non-invasive modalities are preferred over invasive ventilation as they decrease
the risk of mortality, and bronchopulmonary dysplasia (BPD) compared to
invasive ventilation with or without surfactant. The goals of treatment
include keeping SpO2 between 90-95%, and PaCO2
between 45-65 mmHg.

25.  CPAP
🠶 Indication- In infants with RDS start CPAP as soon as possible.
🠶The most common cause of failed CPAP is???
🠶 Starting pressure 5 to 7 cm H2O, at flow of 5 to 10 L/min, FiO2
titrated to target SpO2.
🠶Use OG tube to decompress swallowed air.
🠶 As the infant improves, start tapering FiO2, when FiO2 requirement
is 0.3 bring CPAP to 5 cm H2O.
🠶 Discontinue CPAP if no distress and FiO2 remains <0.3.

26. Bubble CPAP

27. Assisted Ventilation of the Neonate
(Cont.)
Non-invasive Respiratory Support:
Nasal Intermittent Positive Pressure Ventilation (NIPPV) appears superior to CPAP alone for
decreasing extubation failure, the need for intubation in preterm infants, but the same in cost and
safety.
High Flow Nasal Canula: Heated humidified high-flow nasal cannulas (HFNC) are also used in some
centers as an alternative to CPAP to provide positive distending pressure ventilation to neonates with
RDS. As seen in a clinical trial by Roberts et al., HFNC was found to be inferior to CPAP.

28. Mechanical Ventilation:
The goals of mechanical ventilation include providing adequate respiratory
support while balancing the risks of barotrauma, volutrauma, and oxygen
toxicity.
neonates who do not respond to CPAP, develop respiratory acidosis (PH < 7.2
and PaCo2 > 60-65 mm of Hg), hypoxemia (PaO2 < 50 mm of Hg or Fio2 > 0.40 on
CPAP), or severe apnea are managed with endotracheal intubation and
mechanical ventilation.
Time-cycled pressure limited ventilation is the preferred initial mode of
ventilation in preterm infants with RDS.
High-frequency oscillatory ventilation (HFOV) and high-frequency jet ventilation
(HFJV) are often used as rescue modalities when requiring high conventional
ventilator support or concerns for pulmonary air leaks.

29. 30
Exogenous Surfactant Therapy
The targeted treatment for surfactant deficiency is
intratracheal surfactant replacement therapy via an
endotracheal tube.
 Improvement in compliance, functional residual
capacity, and oxygenation
 Reduces incidence of air leaks
 Decreases mortality
 Surfactant administered within 30 to 60 minutes of the birth of a premature
neonate is found to be beneficial

30. Types of Surfactant
Natural Surfactants: contain appoproteins SP-B & SP-C
o Curosurf (extract of pig lung mince)
o Survanta (extract of cow lung mince)
o Infasurf (extract of calf lung)
Synthetic Surfactants:do not contain proteins
o Exocerf
o ALEC
o Lucinactant (Surfaxin)

31. However, neonates who receive surfactant for established
RDS, have an increased risk of apnea of prematurity.
According to European census guidelines, the surfactant is
administered to immature babies with FiO2 > 0.3, and
mature babies with FiO2 > 0.4. Currently, there are no
clinically significant advantages of using one type over
another when used in similar doses:Beractant: This is a
modified natural surfactant prepared from minced bovine
lungs with the additives
Poractant alfa: This is a modified natural surfactant
derived from minced porcine lung extract
Calfactant: This is a natural surfactant obtained from
lavaging calf lung alveoli and contains 80%

32. death, and need for mechanical ventilation compared to surfactant
administration through endotracheal intubation.[38] Still, further
investigations are required to prefer the LISA technique as the
standard technique of surfactant administration in place of
endotracheal intubation. If the neonates maintain adequate
respiratory drive with FiO2 <0.3, it should be planned to stop
surfactant and switch to CPAP. Oxygen saturation (>90%),
thermoregulation (36.5 to 37.5 C), and fluid and nutrition
status should be monitored.

33. 1. warmth - radiant warmer/ incubator
2. maintain hydration
3. nutrition
b) initially d5w or d10w (with protein, if possible) npo if rr >
60 or moderate/severe 8.
work of breathing
c)gavage feeds if stable, conider parteral feed
if entreal feed is deleyed.
4. antibiotics if at riskfor pneumonia/sepsis
5. supplemental oxygen
6. spo2 monitoring, with appropriate target for infantsat
riskfor rop.

34. Mode of administration of Surfactant
 Dosing may be
divided into 2
alliquots and
adminitered via
a 5-Fr catheter
passed in the
ET

35. Insure technique
Intubation-
surfactant-
extubation to CPAP

36. Complications of
RDS
ACUTE :
1. Air leak
2. ETT/ nasal cannulation complications
3. Infections
4. Intracranial haemorrhage
5. PDA
LONG TERM:
1. BPD,PPHN
2. ROP
3. PVL,IVH
4.AKI (d/t acidosis)

37. PROGNOSIS
Prognosis of infants managed with
antenatal steroids, respiratory support,
and exogenous surfactant therapy is
excellent. Mortality is less than 10%,
with some studies showing survival rates
of up to 98% with advanced care.