RDS

1. RESPIRATORY DISTRESS
SYNDROME
Moderator : Dr. NIRANJAN
Presenter : Dr. M.A. RAHEEM

2. Introduction
• Respiratory distress syndrome
(RDS) – the most common
respiratory disorder in preterm
neonates
• Once the major cause of mortality
in premature neonates
• The incidence and severity of RDS
is inversely related to the
gestational age and birth weight of
infant

3. • The Severity peaks at 24-
48 hours, resolution by 72-
96 hours (even without
surfactant therapy)
• HMD is the most common
cause of respiratory failure
during the first days after
birth

4. DEFINITION
• Acute lung disease of the
newborn caused by surfactant
deficiency
• RDS is the clinical expression
of surfactant deficiency and
its histologic counterpart,
hyaline membrane disease
(HMD)

5. INCIDENCE
• 60-80% of <28wk GA ; 15-30% of 32-36wk GA ;
5% of 37wk-term
• In a report from the NICHD Neonatal Research
Network, Fanaroff and coworkers reported that
71% of infants between 500 and 750 g had RDS
54% between 751and 1000 g,
36% between 1001 and 1250 g, and
22% between 1251 and 1500 g

6. • Incidence of RDS varies from 6.8 to 14.1%
in preterm live births in our country with
the incidence being about 58% in infants <
30 wks, 32% in infants b/w 30-32 wks and
10% in infants b/w 33-34 wks gestation
• 2003 report of National Neonatal Perinatal
Database (NNPD), the incidence of RDS
in our country was 1.2 % of all live births

7. DEVELOPMENT OF LUNG
• Typically lung development has been divided
into five stages:
• Embryonic (3.5-7 weeks)
• pseudoglandular (5-17 weeks )
• Canalicular (16-26 weeks )
• Saccular ( 24-38 weeks )
• alveolar period (32 weeks to 2years post
natally)
• The alveolar period has been split in two and a
sixth stage has been defined as the period of
microvascular maturation (birth to 3 years post
natally )

8. • The human lung originates as a
ventral endodermal pouch from the
primitive foregut during the fourth
week of embryonic life
• The endodermal bud will then
elongate, growing caudally, where it
will bifurcate into the primary left and
right lung buds

9. • The two lung buds (primary bronchi) will then
grow out in a posterior-ventral direction into the
splanchnic mesenchyme, where they will branch
again, with the left bronchi forming two
secondary bronchi and the right bronchi forming
three secondary bronchi
• Each of these secondary bronchi represents a
future lobe of the mature lung, and will undergo
further branching, thus expanding the major
airways within each lobe of the lung

11. LUNG MATURATION
• Lung maturation is a complex process requiring
establishment of highly branched tubes that lead
to a gas exchange area capable of supporting
respiration following birth
• By 24 weeks gestation during the canalicular-saccular
transition of lung morphogenesis,
respiratory epithelial cells in the lung periphery
begin to undergo differentiation marked by
accumulation and then utilization of glycogen
stores for lipid synthesis

12. • During the saccular stage of development,
structural and biochemical maturation of the lung
proceeds, associated with increasing
vascularization of peripheral airspaces and
thinning of the pulmonary mesenchyme
• Interactions between mesenchymal fibroblasts
and the epithelium result in the differentiation of
type II epithelial cells, with their characteristic
lamellar body inclusions, a storage granule for
pulmonary surfactant

13. • Type II cells differentiate to produce the highly
differentiated squamous type I epithelial cells
that form an increasing proportion of the
saccular-alveolar surface of the lung with
advancing gestation
• In the normal lung, differentiation of the type II
epithelial cell begins at 24–26 weeks gestation
and can be precociously induced by hormonal
stimulation with glucocorticoids

15. • Avery and Mead in 1959 were the first to
demonstrate that surfactant is deficient in the
lungs of infants dying of HMD
• Surfactant is identifiable in fetal lung as early as
16 weeks, though its proper secretion begins
after 24 weeks gestation and is synthesized
most abundantly after the 35th week of gestation
• Pulmonary Surfactants are phospholipids
synthesized in the type II cells lining the alveoli

16. Surfactant
• Phospholipid produced
by alveolar type II cells
• Lowers surface tension.
• As alveoli radius
decreases, surfactant’s
ability to lower surface
tension increases
• The half-life of surfactant
is 30 hours
Insert fig. 16.12
Figure 16.12

17. Production and release
Type ll cell
Alveolar air
space
Hypophase
Type I cell
Basal lamina
Capillary
endothelium
Alveolar gas
Monolayer
Hypophase
LMVB
Golgi
Tubular
myelin Lamellar
bodies
RER
DMVB
Type I
cell

18. Fig. 1. B, type II cells produce surfactant, which is stored in lamellar
bodies(1)and secreted into the alveolar space (2). The surfactant is
transformed (3) into tubular myelin (4),from which the monolayer (5) is
formed. After the surfactant is used, it is taken up again (6) by the type
II cells and reused (7).

20. Composition
1
DPPC - dipalmitoylphosphatidylcholine 50%*
• Reduces alveolar surface tension
2 3 4 5 6
7
PG - phosphatidylglycerol
7%*
• Promotes the spreading of
surfactant throughout the lungs
Apoproteins or surfactant
specific proteins 2%*
1. Serum proteins 8%*
2. Other lipids 5%*
3. Other phospholipids 3%*
4. Phosphatidylinositol 2%*
5. Sphingomyelin 2%*
6. Phosphatidylethanolamine
4%*
7. Unsaturated
Phosphatidylcholine 17%*
* By molecular weight

21. Endogenous Surfactant
composition and functions
• Major Lipids (~90%)
 Saturated Phosphatidylcholine DPPC (Lecithin) 60-80%
 Unsaturated Phosphospholipids
 Phosphatidylglycerol (PG) ~10%
• Proteins (~10%)
 SP-A
Hydrophilic, Host defence
Surfactant homeostasis
 SP-B
 Hydrophobic, Spreading,  surface tension
 SP-C
 Hydrophilic , Adsorption
 SP-D: ? Phagocytic function

23. SURFACTANT
Function of the Surfactant:-
 Decrease the surface tension
 To promote lung expansion during inspiration
 To prevent alveolar collapse and loss of lung volume at
the end of expiration

24. SURFACE TENSION
• The cohesive forces among liquid
molecules are responsible for
phenomenon of surface tension
• In the bulk of liquid each molecule is
pulled equally in every direction by
neighboring liquid molecules resulting in
net force of zero

25. • Molecules at the surface do not have
other molecules on all sides of them
and therefore are pulled inwards
• This creates some internal pressure
and forces liquid surfaces to contract
to minimal area

27. Surface Tension
Water has a VERY HIGH surface tension
Water will attempt to minimize its surface
area in contact with air

28. An air-filled sphere coated with water has a
tendency to collapse (reach a minimum
volume) due to the pulling force of water
surface tension

29. Alveoli are coated with lung surfactant in order
to reduce the surface tension of water, thus
preventing collapse (atelectasis) upon
exhalation and decreasing the force necessary
to expand the alveoli upon inhalation

30. Lipids form a monolayer at the air-water interface
Surface tension decreases as lipid monolayer is
compressed

31. Law of Laplace
• Pressure in alveoli is
directly proportional to
surface tension and
inversely proportional to
radius of alveoli
• Pressure in smaller
alveolus greater
Insert fig. 16.11
Figure 16.11

32. SURFACTANT
• Diminished surfactant :
Progressive Atelectasis
Loss of functional residual capacity
Alterations in ventilation perfusion ratios
Uneven distribution of ventilation

34. pathophysiology
• Instability of terminal airspaces due to
elevated surface forces at liquid-gas
interfaces
• Stable alveolar volume depends on a
balance between: 1)surface tension at the
liquid-gas interface, and 2) recoil of tissue
elasticity

35. Pathophysiology
• Reduced lung compliance (1/5th -1/10th)
• Poor lung perfusion ( 50-60% not perfused),
decreased capillary blood flow
• R--> L shunting ( 30-60% )
• Alveolar ventilation decreased
• Lung volume reduced
• Increased work of breathing
• Hypoxemia, hypercarbia, acidosis

36. Pathology
• Characteristic injury to terminal airways beginning
within the first few breaths
• Lungs are solid, congested, with destruction of
epithelium of terminal conducting airways
• Hyaline membranes: coagulum of sloughed cells
and exudate, plastered against epithelial
basement membrane

37. Gross : Lung firm, red, liverlike
• Photograph of an autopsy specimen demonstrates small atelectatic
lungs with focal hemorrhage (arrow) visible on the pleural surface.

38. • Microscopic : Diffuse atelectasis, pink
membrane lining alveoli & alveolar ducts.
Pulmonary arterioles with thick muscular
coat, small lumen. Distended lymphatics
• Electron microscopic : Damage / loss of
alveolar epithelial cells, disappearance of
lamellar inclusion bodies, swelling of
capillary endothelial cells

41. Lung Function in HMD
• Reduction in FRC from 30 ml/kg, to as low as 4-
5 ml/kg
• Caused by loss of volume and interstitial edema
• FRC mirrors changes in oxygenation
• Improvements can be due to distending
pressure, surfactant replacement, or clinical
resolution

42. • Lung Compliance is also reduced: from 1-2 to
0.2 -0.5 ml/cmH2O/kg
• Reduction due to decreased number of
ventilated alveoli, and increase in recoil pressure
of ventilated airspaces
• Lung resistance is significantly increased

43. Clinical presentation
• Signs usually develops before the neonate is 6
hours old and persist beyond 24 hours
• progressive worsening until day 2-3 and onset
of recovery by 72 hours
• Respiratory rate above 60/min
• Grunting expiration
• Indrawing of the chest, intercostals spaces and
lower ribs
• Cyanosis without oxygen

44. • The diagnosis of HMD by NNPD requires all of
the following three criteria:
 Preterm neonate
 Respiratory distress having onset within 6 hours
of birth
 Amniotic fluid L/S ratio of <1.5, or negative
gastric aspirate shake test, or X ray evidence
OR Autopsy evidence of HMD

45. • Risk factors:
• Prematurity
• Maternal diabetes, perinatal asphyxia, C-section
without labor
• White race, male sex
• Hypothermia, hypothyroidism
• Familial predisposition (AR)
• 2nd twin

46. Genetic Predisposition to RDS
• Susceptibility to RDS is interaction between genetic,
environmental and constitutional factors
• Very preterm infants
• Common allels preddicts RDS: SP- A 642, Sp-B121, Sp-
C 186 ASN.
• Near Term:
Rare alleles increase the risk: SP-A 643.
• Term Infants: Loss of function mutation of SP-B, SP-C,
ABCA3

47. • Protective factors
• STEROIDS
• Chronic PIH
• IUGR
• Maternal narcotic addiction
• PROM
• Sickle cell disease
• Chronic Renal disease
• Catecholemines, prolactin, thyroxine, estrogen

48. Antenatal Corticosteroid Effects on lung
and Surfactant production
• lung structure changes within 1 day – the
mesenchyme thins, the potential airspace
increases, and the epithelium is more resistant
to injury and the development of pulmonary
edema
• The corticosteroid-exposed preterm lung may be
surfactant-deficient and both therapies might
have additive effects to improve lung function

49. • The surfactant from the corticosteroid-treated
lambs is less sensitive to inhibition by plasma
proteins in vitro
• The clinical literature also supports the benefits
of antenatal corticosteroid treatment followed by
surfactant treatments for those infants with RDS
• Corticosteroids are indicated in all women in
preterm labour 24-34 week of gestation who are
likely to deliver a fetus within one week

50. • 2 doses of bethmethasone 12mg IM
seperated by 24hour interval or 4
doses of dexamethasone 6mg IM at
12 hourly intervals
• Repeated weekly doses of
betamethasone till 32 week gestation
may reduce neonatal morbidities

51. • Secondary surfactant deficiency may occur
in infants with the following:
 Pulmonary infections e.g. group B Strep
 Pulmonary hemorrhage
 Meconium aspiration pneumonia
 Oxygen toxicity; barotrauma or volutrauma to the lungs
 Congenital diaphragmatic hernia and pulmonary
hypoplasia

52. Investigations
• CBC WITH BLOOD CULTURE
• GRBS
• CHEST X RAY
• ABG
• Gastric aspirate
• To confirm diagnosis:
• Shake test on gastric aspirate
• Amniotic fluid : L / S ratio, SPC, PG

53. • The X-ray appearances depend on
the severity of the disorder, with
poorly inflated lungs being the
cardinal feature

54. Grade 1 - mild disease, the lungs show fine homogeneous
reticulogranular pattern

56. Grade 2 - more severe, widespread air bronchograms
become visible

59. Grade 3 - development of confluent alveolar shadowing

60. Grade 4 - severe case, complete white-out of the lung fields
with obscuring of the cardiac border

63. • L/S ratio
 Separates lecithin (PC) and sphingomyelin from
amniotic fluid by TLC
 L/S > 2 indicates mature lung
>2.5 = 0.5%, >2 =10% ,
1.5-2 = 15-20%, <1.5 = 60% risk
• Blood & meconium depress mature L/S ratio and may
elevate immature ratio
• Exceptions : IDM ( L/S>3.5 ), Asphyxia, Hydrops, IUGR,
Abruptio, Toxemia
• Saturated Phosphatidylcholine (SPC) > 500 ug/dl
(latex agglutination)

64. • Fluorescence polarization(TDx) measures
surfactant – albumin ratio ; >45mg/dl – mature
lungs
• Lamellar body count – packages of phospholipids
produced by type II alveolar cells, no. ↑ with
gestational age
>50,000 lamellar bodies/μlit – lung maturity
• Shake test on gastric aspirates – 0.5ml of NS + 1ml
of 95% ethyl alcohol + 0.5ml gastric aspirate in a
test tube, shake for 15 min & allow to stand for
15min
 Bubbles < 1/3rd – 60% risk
 >2/3rd – mature lungs, risk < 1%

65. Differential Diagnosis
• Bacterial pneumonia
• TTNB
• Congenital anomalies
• Massive pulmonary haemorrhage
• Aspiration syndrome e.g. Meconium
• Pulmonary air leaks e.g. Pneumothorax
• Diaphragmatic hernia
• Cardiac anomalies

66. Differential Diagnosis
• Pulmonary hypoplasia
• PPHN
• Birth asphyxia
• Primary neurological or muscle disease
• Hypothermia

67. Management
• Concepts
• Respiratory
• Prevent hypoxia and acidosis
• Prevent worsening atelectasis, edema
• Minimize barotrauma and hyperoxia
• Supportive management
• Optimize fluid and nutrition management
• Perfusion, Infection, Temperature control

68. • Respiratory management
• Surfactant replacement therapy
• Ventilatory Assistance
Oxygen therapy
• CPAP ( Nasal, ET, Face-mask )
• Positive pressure ventilation
• High-frequency ventilation
•ECMO
• Liquid ventilation

69. Initial Care
• Maintain warmth- cold stress will mimic other
causes of distress
• Monitor blood glucose levels- assure they are
normal
• Provide enough oxygen to keep the baby pink

70. Temperature Control
• Body Temperature that is too high or too low will
increase metabolic demands
• Servo controlled warmers are very helpful

71. Initial Care
Ensure adequate hydration:
• Start fluids at 80 ml/kg/day 10% glucose solution
• Smaller babies may need more fluid
• Add electrolytes by the 3rd day
• On day 3-4 watch for diuresis as spontaneous diuresis
occurs preceding improvement in pulmonary function

72. Surfactant replacement therapy
• Fujiwara in 1980 reported the 1st successful clinical
trial of tracheal applications of surfactant in infants
with RDS ,showing that surfactant replacement
therapy improved oxygenation, ventilatory
requirements, x-ray abnormalities, acidosis and
hypotension in 10 preterm infants with RDS
• Commercial preparations of surfactant were
subsequently approved by the FDA in the USA in
1989

73. Surfactant replacement therapy
• When: Prophylaxis (prevention) vs. Treatment (rescue) ;
Early vs. Late
• What: Synthetic preparation (Exosurf) vs. Natural
(Survanta)
• How: Administration : Indications, Dosage, Technique

74. Indications
• 3 main indications for surfactant administration in newborns
1. Prophylactic therapy
a. Neonates with gestation < 30 weeks of gestation
b. Surfactant given within 15 minutes of birth before a
diagnosis of RDS is made
2. Early Rescue therapy
a. Neonate with RDS (confirmed clinically & radiologically).
b. Surfactant given within first 2 hours of life
3. Late Rescue therapy
a. Neonate with RDS and requiring ventilation with a MAP of
at least 8 cms of water and/or an FiO2 > 30% ( or a/A ratio
< 0.22) Or PEEP > 7
b. Surfactant given after 2 hours of birth

75. Timing of surfactant
• Surfactant may be given as:
 Prophylactic therapy
 Early rescue therapy
 Late rescue therapy
• In reference to decreasing the incidence of air leaks and
mortality, prophylactic therapy is better than early rescue
which in turn is better than late rescue

76. Nomenclature
At risk baby born
Surfactant given at < 15
min age before
respiratory distress=
“Prophylactic”
Signs of RDS
develop
Nevertheless, if
baby develops
signs of RDS
Multiple doses
Described as part of
“prophylaxis” regime
Surfactant given at
<2 hrs, after resp
distress starts but
before obvious
HMD =
“Early rescue”
Surfactant given at
>2 hrs, after
obvious HMD =
“Late rescue” or
“Selective”
If baby continues to have
signs of RDS
Multiple doses
Described as part of “rescue” regime

77. Is early rescue better than late?
Early rescue
reduces
Pneumothorax
PIE
BPD
Neonatal mortality
Give surfactant within 2 hours of birth;
the earlier the better
Benefit much more in  29 wks

78. INSURE
Intubation,Surfactant
administration, Extubation
• Continued post-surfactant intubation and
ventilation are risk factors for BPD
• Early surfactant administration with brief mechanical
ventilation (< 1 hour) was followed by extubation to
nasal CPAP

79. INSURE reduces
Need for mechanical
ventilation
BPD
Number of surfactant
doses/patient
Air leak syndromes

80. Repeat doses
• 2nd or subsequent doses of surfactant are
given if the infant with RDS is requiring
ventilation and has a FiO2 requirement of
> 30%
• A minimum duration of 6 hours is
recommended between any 2 doses of
surfactant. Surfactant is usually not
continued beyond 3 days of life (72 hours)

81. Benefits of multiple doses
Multiple doses
reduce
Pneumothorax
Mortality

82. How many doses & how often?
• Current guidelines
• If extubated or on FiO2 <0.4, no more doses
• If improved after 1st dose but worsened again, give
repeat dose irrespective of time gap
• Generally no more than 2 doses required
• Rarely 3, never 4
• Have lower threshold for re-treatment if complicated by
asphyxia or sepsis

83. Surfactant preparations are of basically 3 types:
• Natural surfactant (animal derived by either
lung mince extract or by lung lavage extract)–
phospholipids with surfactant proteins
• Synthetic surfactant – only phospholipds
• Newer surfactant –synthetic surfactants with
synthetic peptides modelled on surfactant
proteins, Aerosolized surfactants

84. Exogenous Surfactants
• Natural
• Natural: from animal
lungs
• Examples:
• Bovine (beractant):
SURVANTA, NEOSURF
• Porcine (poractant):
CUROSURF
• Animal lung extract +
extra DPPC + palmitate
• Has natural SP-B &
SP-C
• Synthetic
• DPPC + hexadecanol
+ tyloxapol
• Examples:
• Without proteins
(colfosceril):
EXOSURF, SURFACT
• With proteins
(lucinactant): SURFAXI

85. Naturals Vs Synthetics
Survanta Vs Exosurf
Survanta reduces
Pneumothorax
BPD
ROP
Death

86. Brand Source Vol Conc Dose MRP (Rs)
Curosurf Porcine
minced
1.5 ml 1 ml= 80 mg 200 & 100
mg/k (1st &
2nd resp.)
[2.5 & 1.25
ml/kg]
10,680
Neosurf Bovine
lavage
3 ml & 5 ml 1 ml= 27mg 135 mg/kg
(5 ml/kg)
3 ml= 4,900
5 ml= 8,000
Survanta Bovine
minced
4 ml & 8 ml 1 ml= 25 mg 100 mg/kg
(4 ml/kg)
4 ml= 7,260
8 ml= 12,000

87. Cost at diff wt groups
Brand 750 gm 1 kg 1.25 kg 1.5 kg
Curosurf: 1st
2nd
21,360
10,680
21,360
10,680
31,740
10,680
31,740
21,360
Neosurf 8,000 8,000 13,000 13,000
Survanta 7,260 7,260 12,000 12,000

88. What does surfactant not
achieve?
Surfactant generally does not reduce
• ROP
• Severe IVH
• NEC
• Sepsis

89. Dose
• Survanta 100mg/kg for the first and subsequent
doses.
• Curosurf 200mg/kg for the first dose and 100mg/kg
for the subsequent doses or 100 mg/kg for all the
doses.
Administration of surfactant
• Technique of administering intratracheal surfactant
vary from preparation to preparation
• Entire dose is administered in a single instillation or
aliquots through a feeding tube that is cut to a
length just slightly longer than that of the
endotracheal tube

90. • Multiple aliquots could be administered
through a feeding tube or side adapter
• A more uniform distribution has been
reported if the aliquots are restricted to 4
and they are administered in the supine
position with interposed ventilations
between aliquots

91. What to Monitor?
• Before administration
• ETT position
• During administration
• Ventilator settings
• Surfactant reflux
• Chest wall movements
• Vitals
• After
administration
–ABG
–CXR
– Vitals
– Ventilator
settings
–BP

92. Contraindications to
surfactant
• Major malformations
• HIE III
• B/L Grade 4 IVH
• Lab evidence of lung maturity
• Pulmonary haemorrhage.(??)

93. POOR RESPONSE TO
SURFACTANT THERAPY
• Delayed administration
• Leakage of proteinaceous materials into the
alveolar space
• High FiO2 or PIP at entry
• High MAP
• Additional neonatal pulmonary conditions like
pneumonia and perinatal asphyxia

94. COMPLICATIONS OF
SURFACTANTS
• Transient hypoxia, bradycardia and fluctuating BP
• Rapid changes in lung compliance leading to
barotrauma if not monitored
• Pulmonary hemorrhage - more with natural(5-6%)as
compared to synthetic(1-3%)
• Theoretical risk of immunological reactions to foreign
proteins
• Theoretical risk of transmission of infective agents such
as prions and virions

95. Additional Support
• Oxygen
• Continuous Positive Airway Pressure
• Mechanical Ventilation
• Bag and mask / endotracheal tube
• Ventilator if available

96. • First used by mask in 1936 for acute
insufficiency in ventilation
• First used in 1940s in high altitude flying
• Introduced in treatment of Adult
Respiratory Distress Syndrome in 1967
• First applied to infants with HMD in 1971

97. CPAP
• Indication: Significant respiratory distress, FiO2 >
0.40
• INSURE therapy
• Start with Nasal prong CPAP, 5 cm H2O pressure,
flow 5-10 lpm, FiO2 0.40-0.60

98. - Mechanism of action
• CPAP prevents collapse of unstable alveoli upon
expiration
• Facilitates recruitment of unventilated alveoli
• Reduces right to left shunting across foramen
ovale
• Reduces left to right shunting across the Ductus
Arteriosus, improving cardiac output and blood
pressure

99. CPAP
Concept:
Prevents atelectasis
Reduces pulmonary edema
Improving Functional residual capacity
Correcting ventilation-perfusion abnormalities
Reducing intrapulmonary shunting
Problems:
• High CPAP may decrease venous return
• High CPAP may decrease minute ventilation
• Abdominal distension

100. CPAP Delivery
• Endotracheal tube: simple and efficient, but
increased work of breathing
• Face mask: Easy to apply, inexpensive, but
difficult to regulate, causes abdominal distention
• Nasopharyngeal prongs
• Nasal cannulae
• Nasal Prongs: Simple to apply and use, minimal
cost, mouth leaks hampers efficacy. Usually the
preferred method

101. CPAP delivery systems

104. Complications of CPAP
• Pulmonary air leaks - over distension of the
lungs caused by inappropriately high pressures
• Decreased cardiac output due to reduction in the
venous return, decreased right ventricular stroke
volume
• Impedance of pulmonary blood flow with
increased pulmonary vascular resistance
• Gastric distension and ‘CPAP belly syndrome’
• Nasal irritation, damage to the septal mucosa, or
skin damage and necrosis from the fixing
devices

105. Failure
• Worsening respiratory distress
• Hypoxemia (PaO2 <50mmHg) /
hypercarbia (PaCO2 >60mmHg)
despite CPAP pressure of 7-8 cm
H2O and FiO2 of 0.8
• Recurrent episodes of apnea

106. Mechanical Ventilation
• Indications:
• ABG criteria - respiratory acidosis with a pH of <7.20
to7.25 or severe hypoxemia with a PaO2 < 50 to 60
despite a highFiO2 (0.6 to 0.7)
• Clinical criteria - respiratory distress on CPAP, severe
respiratory distress with shock or severe apnea
• Severe apnea
• Decreasing “work of breathing”
• To give surfactant therapy

107. • Initial settings
• Continuous flow, pressure-limited,
ventilator conventional
• PIP 20-25 , PEEP 4-5 cm H2O
• Frequency 40-60/min
• Ti 0.3-0.5 sec
• FiO2 50-60%

108. • Rapid ventilator rates and short Ti are
recommended because of the low pulmonary
compliance and short time constant in neonatal
RDS
• A/w a lower incidence of air leaks
• Following surfactant administration, oxygenation
improves rapidly because of an increase in
functional residual capacity and is followed by a
slower improvement in compliance
• Permissive hypercapnia, permissive hypoxemia,
minimal peak pressures, rapid rates, early
therapeutic CPAP, and rapid extubation help
reduce ventilation induced lung injury (VILI) and
possibly reduce BPD

109. • High Frequency vs. Conventional Ventilation
• Initial HiFi study disappointing - no reduction in BPD.
Increased IVH, PVL
• Subsequently,
• HFOV may decrease incidence of air leak
• HFOV does not increase BPD or IVH
• HFJV and HFFI similar to CMV: Mortality,
BPD, air leak incidence similar
• Use: Air leaks, Hypercapnia, ? R->L shunting

110. • Liquid Ventilation
• CONCEPT
• 1) Eliminate air-fluid surface tension by
converting alveoli to fluid filled structures.
• 2) Use fluid as a carrier for resp. gases.
• PFCs ( PerFluoroChemicals /
PerFluoroCarbons ) have O2 solubility 50-
53 ml gas / 100 ml liquid and CO2 solubility
140-210 ml gas / 100 ml liquid
• Undergoing trials, still experimental, very promising

111. Pharmacotherapy – beyond surfactant
• Nitric oxide
• Inhaled nitric oxide (iNO)– a selective pulmonary
vasodilator improves oxygenation in preterm
infants with severe RDS.
• Nitric oxide may be a signaling molecule in
parenchymal lung growth & may reduce lung
injury and chronic lung disease

112. Complications
• Acute complications
• Air leak : Pneumothorax, PIE, Pneumomediastinum :
deterioration with hypotension, bradycardia, apnea,
acidosis
• ET complications : Blocked / dislodged ETT
• Infection : culture and treat rapidly
• Intracranial hemorrhage : monitor USG
• PDA : look for and treat aggressively

113. Complications & Outcome
• Long-term complications
• Bronchopulmonary dysplasia (BPD)
5-30%
• Retinopathy of prematurity (ROP)
7% of <1250 g
• Neurologic impairment
10-15% of survivors of RDS - associated with PVL, IVH,
degree of prematurity

114. • A meta-analysis of 13 RCTs to review neuro-developmental
outcome at 1 and 2 years of age following surfactant therapy
documented improved survival without an increase in
subsequent morbidity at 1 and 2 years of age
• Survival in RDS has varied from 25 to 84% in
different centers in India.
• RDS contributes to 13.5% of neonatal mortality in India
• High initial FiO2 >0.6, gestational age <34 weeks, birth weight
<1500 g, air leak syndromes have been a/w higher
mortality

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