RDS in newborn

1. RESPIRATORY DISTRESS
IN NEWBORN

2. • A 32 weeks preterm baby born to a GDM mother by
LSCS, developed distress, grunting, cyanosis soon after
birth. His SPO2 was 90%, hyperoxia test was positive.
Downe’s score was 7, silverman-anderson score 8.
Urgent CXR was done which showed :

3. RDS
3

4. Now what next ???
• Baby shifted to NICU and put on warmer. RBS was normal,
other blood samples taken. IV fluids were started, ABG was
done which showed acidosis.
• Baby was put on nasal CPAP, meanwhile survanta was arranged.
• Baby then put on venti, surfactant given at 4 hours of life.
• Now clinically better.

5. SIGNS AND SYMPTOMS
• Tachypnea (RR > 60/min)
• Nasal flaring
• Retraction
• Grunting
• +/- Cyanosis
• +/- Desaturation
• Decreased air entry

6. GeneralConsiderations

7. RD IN NB - Causes
• Pulmonary
- Parenchymal
- Extraparenchymal
• Non Pulmonary
- Heart
- Metabolic
- Brain
- Blood
- Abdominal

8. RD in Newborn– Causes
Pulmonary
Parenchymal Extraparenchymal
* RDS (HMD) * Upper airway obstruction
* TTN (RDS II) (Cloanal atresia, stenosis)
* Aspiration (Blood * Pneumothorax
meconium) * Pleural effusion
* PPHN * Cong. Diaph. hernia
* Pneumonia * Diaphragmatic paralysis
* Pulm. hemorrhage
* Pulm. hypoplasia

9. RD in Newborn– Causes
Extrapulmonary
Heart Metabolic Brain Blood Abdominal
- CCF - Met. Acidosis - Haemorrhage - Hypovolemia - NEC
- PDA - Hypoglycemia - Edema - Hyperviscosity - Pneumo
- CCHD - Hypothermia - Drugs - Acute blood peritonium
- Vascular - Sepsis - Pain loss - Large
mass

10. Surgical causes of respiratory distress
• Tracheo-esophageal fistula
• Diaphragmatic hernia
• Lobar emphysema
• Pierre -Robin syndrome
• Choanal atresia

11. Suspect surgical cause
• Obvious malformation
• Scaphoid abdomen
• Frothing
• History of aspiration

12. A progressively increasing O2 requirement to
maintain saturation is also a sensitive indicator
of the severity and progress of distress
>95% Term baby, pulmonary hypertension (PPHN)
88-94% 28-34 weeks preterm
85-92% Below 28 weeks gestational age
Guidelines for monitoring oxygen saturation levels
by pulse oximetry
MJAFI, Vol. 63, No. 3, 2007
GeneralConsiderations

13. Hyperoxia test
test Method result diagnosis
Hyperoxia 100 % fio2 5-10
min
Pao2 increases to
> 100 torr
Pao2 increases by
< 20 torr
Parenchymal
lung disease
PPHN / CCHD
Hyperoxia-
hypervetilation
MV 100 % fio2 &
VR 100-150 / min
Pao2 increases to
> 100 torr
w HV
Pao2 increases
at critical Pco2
No increase in
Pao2 with HV
Parenchymal
lung disease
PPHN
CCHD

14. Downe’s score

15. Silverman-Andersen Retraction Scoring
Interpretation
Score 0-3 = Mild respiratory distress
Score 4-6 = Moderate respiratory distress
Score > 6 = Impending respiratory failure
Score 10 = Severe Respiratory distress
GeneralConsiderations

16. Investigation
Complete Blood Count with a Peripheral blood smear
Sepsis screen including C-reactive protein and μ ESR
Arterial blood gas (ABG) analysis
Blood glucose, Serum calcium
Cultures: Blood , Surface swab (where indicated),
maternal vaginal swab
Chest radiograph with an oro-gastric tube in situ
GeneralConsiderations

17. Mathaissetal,MJAFI2007;63:269-272

18. RR
(bpm
Aspiration cong. Pneumonia, sev. HMD CDH
cardiac malformation
Approx. 6 Hours of age
Normal
60
Course of Neonatal Tachypnoea : Etiologic possibilities
Source : Baurn DJ, Birth Risks, Nastle Nutrition Workshop, 1993
TTNB
HMD

19. EvaluationofRD inNB–ClinicalHistory
Antenatal History Most likely association
* Prematurity, IDMs * HMD
* PROM, maternal fever, * Pneumonia
Unclean vaginal exams,
UTI, diarrhoea
* Asphyxia/MSAF * Aspiration
* Caesarean delivery * TTN
* Polyhydramnios * Pulm. Hypoplasia
* Oligohydramnios * TE fistula, CDH
* H/o receiving steroids * RDS less
* Traumatic/breech delivery * ICH / Phrenic nerve paralysis

20. HMD/RDS

21. Respiratory Distress Syndrome (RDS)
• Also known as Hyaline Membrane Disease (HMD)
• Commonest cause of preterm neonatal mortality
• RDS occurs primarily in premature infants; its incidence is
inversely related to gestational age and birth weight
Nelson Textbook of Pediatrics, 18th Ed.
Gestational age Percentages
Less than 28 wks 60-80%
32-36 wks 15-30%
37-39 wk 5%
Term Rare
Resp.Dis.Syn.

22. ETIOLOGYAND PATHOPHYSIOLOGY.
• Surfactant deficiency is the 1O cause of RDS.
• Low levels of surfactant cause high surface tension
• High surface tension makes it hard to expand the alveoli.
• Tendency of affected lungs to become atelectatic at end-expiration
when alveolar pressures are too low to maintain alveoli in
expansion
• Leads to failure to attain an adequate lung inflation and therefore
reduced gaseous exchange

23. • With advancing gestational age, increasing amounts of
phospholipids are synthesized and stored in type II alveolar
cells .
• Wk 20: start of surfactant production and storage. Does not
reach lung surface until later
• Wk 28-32: maximal production of surfactant and appears in
amniotic fluid
• Wk 34-35; mature levels of surfactant in lungs
• Quality : The amounts produced or released may be insufficient
to meet postnatal demands because of immaturity.
• Surfactant inactivating states eg maternal DM may lead to
surfactant of lower quality/ immature

24. • Rare genetic disorders may cause fatal respiratory distress
syndrome eg.
• Abnormalities in surfactant protein B and C genes
• gene responsible for transporting surfactant across membranes
(ABC transporter 3 [ABCA3]) are associated with severe and often
lethal familial respiratory disease

25. Clinical manifestation
• Tachypnea
• Nasal flaring
• Intercostal, sternal recession
• Grunting; closure of glottis during expiration
• Cyanosis
25

26. Risk factors
• Prematurity
• Maternal diabetes
• Multiple births
• Elective cesarean section without labor
• Perinatal asphyxia
• Cold stress
• Genetic disorders

27. Decreased risk
•Chronic intrauterine stress
•Prolonged rupture of membranes
•Antenatal steroid prophylaxis

28. Structure of lung surfactant
major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin),
phosphatidylglycerol, apoproteins (surfactant proteins SP-A, -B, -C, -D), cholesterol

29. Resp.Dis.Syn.

30. Resp.Dis.Syn.

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

33. Respiratory distress - Management
•Monitoring
•Supportive
- IV fluid
- Maintain vital signs
- Oxygen therapy
- Respiratory support
•Specific

34. 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

35. Is a Clinical diagnosis: respiratory distress occurring soon after birth.
Pay attention to risk factors! Pulse Oximetry: aim for SPO2 >85%.
ROUTINE!
Full blood count and Cultures to check for sepsis: rem culture only
positive 40-50% of the time!! gastic aspirates/ buffy smears for GBS
Chest radiograph: air bronchogram, reticular/ ground-glass appearance
after 6-12 hrs to full opacity later on.
Blood gases: hypoxia, hypercapnia, acidosis. Signs of RESP FAILURE
determine mgmt eg CPAP vs ventilation etc
 Electrolytes, glucose, renal and liver function
 Echocardiogram: diagnosing PDA, determine the direction and degree
of shunting, making the diagnosis of pulmonary hypertension and
excluding structural cyanotic heart disease

36. cxr
36
Shows air bronchograms
and reticulonodular
shadowing throughout
the lung fields (often
termed ‘ground glass’
appearance)

37. 37

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

40. BubbleCPAP

41. • Avery and Mead in 1959 were the first to demonstrate
that surfactant is deficient in the lungs of infants dying
of HMD
• Fujiwara in 1980 reported the 1st successful clinical
trial of tracheal applications of surfactant in infants
with RDS
• Commercial preparations of surfactant were
subsequently approved by the FDA in the USA in 1989
• Pulmonary Surfactants are phospholipids synthesized
in the type II cells lining the alveoli

42. Prophylactic therapy
Extremely preterm <28 wks
<1000 gm
Not routine in India
Rescue therapy
Any neonate diagnosed to have RDS
Surfactant therapy - Issues
Dose 100mg/kg phospholipid Intra tracheal

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

44. SURFACTANT
Surfactant therapy reduces mortality rates most effectively in
infants <30 weeks and those of birth weight <1250 gm
44

45. Insure technique
• Intubation-
• surfactant-
• extubation to CPAP

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

47. Management
Prevention:
• Tocolytics to inhibit premature labor.
• 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.

48. Diagnosis of lung maturity
• Amniotic Fluid Lecithin/Sphingomyelin Ratio
• ≥2 suggests lung maturity.
• ≤1.5 associated with HMD
• Phosphatidyl Glycerol estimation
• More specific than L/S ratio
• Absence is invariably associated with HMD
• Gastric Aspirate Shake Test
• Unreliable if gastric aspirate is contaminated with blood
or meconium
• Serial tests can be done to assess maturity of lungs
during course of disease
Resp.Dis.Syn.

49. Shake test
• Take a test tube
• Mix 0.5 ml gastric aspirate +
0.5 ml absolute alcohol
• Shake for 15 seconds
• Allow to stand 15 minutes for
interpretation of result

50. • NATURAL COURSE
• Usually illness peaks in 3 days, then gradual
improvement
• Improvement is often heralded by spontaneous
diuresis and the ability to oxygenate the infant at
lower inspired oxygen levels or lower ventilator
pressures
• Death may occur esp from day2-3

51. MORTALITY
• Death is rare on the 1st day,
• usually occurs between days 2 and 7
• causes are:
• alveolar air leaks (interstitial emphysema, pneumothorax),
• pulmonary hemorrhage
• Intracranial hemorrhage
• Late mortality from bronchopulmonary dysplasia

52. COMLICATIONS
acute
Apnea
Air leak
infection
ICH
PDA & foramen
ovale
End-organ hypoxic
injury
chronic
ROP
PPH &
BPD
Neurodevep.
impairment

53. MAS

54. Meconium Aspiration Syndrome
Definition
MAS is defined as respiratory distress in
an infant born through meconium-
stained amniotic fluid (MSAF) whose
symptoms cannot be otherwise
explained
J Perinatol. 2008 Dec
Mec.Asp.Synd

55. Epidemiology
•Most common cause of respiratory
distress in term and post-term infants.
•MSAF observed in 5-25% of all births out
of which 10% develop MAS.
•One third require ventilator support
•10% develop air leaks
•5-10% of them have a fatal outcome
Mec.Asp.Synd

56. What is meconium?
• The term was coined by Aristotle from the Greek word
“meconium arion” meaning “opium like”
• Consists of gastrointestinal, hepatic and pancreatic secretions,
cellular debris, swallowed amniotic fluid, lanugo, vernix
caseosa and blood
• Appear in the fetal intestines by the 10th week of life gradually
increasing in amount to reach 200gms at birth
Mec.Asp.Synd

57. Cause of MSAF
• The passage of meconium from the fetus into amnion is
prevented by lack of peristalsis(low motilin level) , tonic
contraction of the anal sphincter, terminal cap of viscous
meconium.
• Vagal Stimulation due to in utero hypoxia, acidosis, cord or
head compression cause increased peristalsis and a relaxed
anal sphincter.
• Fetal maturation (post term) causes high motilin level 
increased peristalsis
Mec.Asp.Synd

58. Risk factors for MAS
• Post term pregnancy
• Primigravida
• Maternal Anemia
• Chorioamnionitis
• Prolonged Labour
• Fetal Distress
• IUGR
• Maternal Age >30yrs
• Maternal DM
• Maternal heavy cigarette
smoking
• Pre-eclampsia / eclampsia
• Oligohydramnios
• Antepartum Hemorrhage
Mec.Asp.Synd

59. Pathophysiology
1. Mechanical obstruction of airways
2. Chemical Pneumonitis
3. Surfactant Inactivation
Mec.Asp.Synd

60. Mechanical obstruction of airways
• With onset of respiration – meconium migrates from central to
peripheral airways.
• Thick particulate and viscous meconium lead to complete or
partial airway obstruction.
• Complete obstruction  Atelectasis  Ventilation-Perfusion
(V-Q) mismatch
• Partial obstruction Ball-valve – air trapping  Obstructive
Emphysema  Risk of pneumothorax (15 – 33%)
Mec.Asp.Synd

61. Chemical pneumonitis
• Meconium in the airways initiates an inflammatory reaction
• Meconium inhibits oxidative burst and phagocytosis by
neutrophil  increased risk of infection
• Meconium induces production of inflammatory cytokines 
Injury of parenchyma and vascular leakage  injury similar to
ARDS
Mec.Asp.Synd

62. Surfactant inactivation
• Bilirubin, fatty acid, triglycerides, cholesterol and proteins
present in meconium alter phospholipid structure of surfactant
 reduced surfactant function
• Bile has cytotoxic effect on Type II Pneumocytes  Reduced
surfactant production.
Mec.Asp.Synd

63. Mec.Asp.Synd

64. Clinical Features
History
• Maternal risk factors present
• Term or Post term Infants
• Meconium Stained Amniotic fluid (Thick 
pea soup/Thin)
• IUGR.
• Many babies are depressed at birth.(in utero
aspiration)
Mec.Asp.Synd

65. Physical examination
• Evidence of postmaturity: peeling skin, long fingernails, and
decreased vernix.
• The vernix, umbilical cord, and nails may be meconium-stained,
depending upon how long the infant has been exposed in
utero.
• In general, nails will become stained after 6 hours and vernix
after 12 to 14 hours of exposure .
• umbilical cord staining (thick-15min, thin-1hour)
Mec.Asp.Synd

66. Meconium stained umbilical cord
Mec.Asp.Synd

67. Meconium stained nails
Mec.Asp.Synd

68. • Features of respiratory distress within first few hours of birth
• The chest typically appears barrel-shaped, with an increased
anterior-posterior diameter caused by over inflation.
• Auscultation reveals rales and rhonchi -immediately after birth.
• Some patients are asymptomatic at birth and develop
worsening signs of respiratory distress as the meconium moves
from the large airways into the lower tracheobronchial tree.
• In case of massive meconium aspiration, meconium pigments
may be absorbed from lungs excreted in urine. Urine may
appear dark brown in colour.
Mec.Asp.Synd

69. Diagnosis
MAS must be considered in any infant
born through MSAF who develops
symptoms of Respiratory Distress with
typical chest x ray findings
Mec.Asp.Synd

70. Diagnosis
• A chest radiographs is characterized by hyperinflation of the
lung field and coarse nodular opacities due to areas of
atelectasis and consolidation.
• There are coarse irregular patchy infiltrates
• A pneumothorax and pneumomediastinum may be present .
Mec.Asp.Synd

71. Mec.Asp.Synd

72. Mec.Asp.Synd

73. Mec.Asp.Synd

74. Mec.Asp.Synd

75. Diagnosis
• Arterial blood gas measurements typically show hypoxemia and
hypercarbia.
• Infants with pulmonary hypertension and right-to-left shunting
may have a gradient in oxygenation between preductal and
postductal samples.
• Echocardiogram for evaluation of Persistent Pulmonary
Hypertension.
Mec.Asp.Synd

76. Management
• Prenatal management: Key management lies in prevention during
prenatal period.
• Identification of high risk pregnancies and close monitoring.
Pregnancy that continue past due date, induction as early as 41
weeks may help prevent meconium aspiration.
• If there is sign of fetal distress corrective measure should be
undertaken or infant should be delivered in timely manner.
• Amnioinfusion has no role.
Mec.Asp.Synd

77. Delivery Room Management
Baby delivered through MSAF
Intrapartum Suctioning
Assess the baby after 10-15 sec
Vigorous
• HR > 100/min
• Spontaneous Respiration
• Crying
• Reasonable tone
No intervention
Non Vigorous
• Intubate
• Tracheal Suction
Mec.Asp.Synd

78. • When the infant is not vigorous:
1. Place under radiant warmer but delay
stimulation.
2. Clear airways as quickly as possible.
3. Intubation and then suction directly to the ET
tube.  repeat until either ‘‘little meconium
is recovered, or until the baby’s heart rate
indicates that resuscitation must proceed
without delay’’.
4. May also require saline lavage to remove
thick particles.
5. After all meconium is sucked out, ventilate
the baby with bag and mask.
Mec.Asp.Synd

79. Postnatal Management
• Shift to NICU setup with respiratory support facilities available
• Gastric wash with normal saline to reduce gastritis and
aspiration of meconium stained products.
• Close monitoring for Respiratory distress.
• Most infants who develop symptoms will do so in the first 12
hours of life.
Mec.Asp.Synd

80. Management
• Consider CPAP, if FiO2 requirements >0.4; however CPAP
mayaggravate air trapping and must be used cautiously.
• Mechanical ventilation: in severe cases (paCO2 >60 mmHg
orpersistent hypoxemia (paO2 <50 mmHg).
• Correct systemic hypotension (hypovolemia, myocardial
dysfunction).
• Manage PPHN, if present
• Manage seizures or renal problems, if present.
• Surfactant therapy in infants whose clinical status continue
todeteriorate.

81. TTNB

82. Transient Tachypnea of Newborn
• Also called Wet Lung Syndrome or Type II Respiratory Distress
Syndrome
• The most common cause of neonatal respiratory distress
constituting more than 40 percent of cases
• 11 per 1,000 live births.
• Represents a milder form of HMD or due to failure of drainage
of alveolar fluids resulting in pulmonary edema  decreased
compliance and increased airway resistance  Respiratory
Distress
Tran.Tachy.Newborn

83. Risk Factors
• Term or Near Term Babies
• Male Child
• Cesarean Section
• Delayed cord clamping or cord milking
• Macrosomia
• Maternal Sedation
• Large amount of IV Fluids to mother during labor
• Maternal Asthma
• Maternal Diabetes
Tran.Tachy.Newborn

84. Clinical Features
• Tachypnea immediately after birth or within 6hrs after delivery
with mild to moderate respiratory distress.
• These manifestations usually persist for 12-24hrs, but can last
up to 72hrs
• Auscultation usually reveals good air entry with or without
crackles
• Usually maintain good color and are alert.
Tran.Tachy.Newborn

85. • X-Ray Chest
• Hyperinflation of the lungs
• Linear streaking at hila due to dilated lymphatics
• Interlobar Fluid
• Mild Cardiomegaly
• Chest x-ray usually shows evidence of clearing by 12-18 hrs
with complete resolution by 48-72 hrs
Tran.Tachy.Newborn

86. Tran.Tachy.Newborn

87. Fluid in the inter lobar fissure
Tran.Tachy.Newborn

88. chestX-ray:Transient Tachypneaof Newborn
Fluid in the
fissure

89. TTN is a clinical diagnosis
of exclusion
Tran.Tachy.Newborn

90. General Management
• Provide an adequate nutrion. Infants with sustained
RR >60 breaths/min should not be fed orally &
should be maintained on gavage feedings for RR 60-
80 breaths/min, and NPO with IV fluids or TPN for
more severe tachypnea

91. Results from slow absorption of
lung fluid
Term born by LSCS/IDM /maternal
asthma
Mild respiratory distress
Peaks at about 36 hours of life
Resolve spontaneously
SUMMARY : Transient Tachypnea of
the Newborn

92. OTHERS

93. Air Leak Syndromes
Risk Factors:
• MV,MAS, surfactant therapy without
decreasing pressure support in ventilated
infants
• vigorous resuscitation,
• prematurity
• pneumonia

94. Chest x-ray: Right-sided pneumothorax

95. Left-sidedpneumothoraxundertension.

96. Others
Pneumomediastinum
• It can occur with aggressive ETT insertion, Ryle's feeding tube
insertion, lung disease, MV, or chest surgery (e.g., TEF).
Pneumopericardium
Pneumoperitoneum
Subcutaneous emphysema
Systemic air embolism

97. Chest x-ray with Pneumomediastinum

98. Chest x-ray with pneumopericardium

99. Pneumopericardium
99

100. Management
• Conservative therapy: close observation of the
degree of respiratory distress as well as oxygen
saturation, without any other intervention aiming at
spontaneous resolution and absorption of air.
• Needle aspiration should be done for suspected
cases of pneumothorax with deteriorating general
condition until intercostal tube is inserted.
• Decompression of air leak according to the type
(intercostal tube insertion in case of pneumothorax).

101. Ground glass opacity

102. X-ray - RDS

103. X-ray - MAS

104. MAS
104

105. X-ray - Pneumothorax

106. Pneumothorax
106

107. • Right lateral decubitus view of pneumothorax
107

108. Left Congenital Diaphragmatic
Hernia
108