1. Respiratory Distress in
New born
Presented by Dr. Ankit Agarwal
Guided by: Dr. J.P. Jain
Dept. of Pediatrics
NIMS, Jaipur

2. Overview
• General Considerations
– Epidemiology
– Definition and Clinical
Features
– Assessment of severity
– Causes
– Approach to a New born with
resp. distress
• Meconium Aspiration
Syndrome
– Epidemiology
– Etiopathogenesis
– Clinical Features
– Diagnosis
– Management
• Respiratory Distress Syndrome
– Epidemiology
– Etiopathogenesis
– Clinical Features
– Diagnosis
– Management
– Surfactant Therapy
– Complication
• Transient Tachypnea of
Newborn
– Epidemiology
– Etiopathogenesis
– Clinical Features
– Diagnosis
– Management

3. Epidemiology
• Commonest problem encountered within the
first few hours of life.
• It occurs in approximately 1%-6% of live
births
• Responsible for about 20% of neonatal
mortality
GeneralConsiderations

4. Definition and Clinical Features
Tachypnea
AND
Expiratory Grunt OR Inspiratory Retraction
Only Tachypnea is NOT Respiratory Distress
• Cyanosis
• Nasal Flaring
• Desaturation
• Lethargy/Poor feeding
• Pallor
• Decreased Breath Sounds
+- Rales or Ronchi
Other Features
GeneralConsiderations

5. GeneralConsiderations

6. Assessment of Severity
Downe’s Scoring System
Score 0 1 2
Respiratory Rate
(rate/min)
<60 60-80 >80
Cyanosis None in room air No cyanosis in
40% oxygen
Requiring more
than 40%
ambient oxygen
Retractions None Mild Moderate to
Severe
Grunting None Audible with
Stethoscope
Audible without
Stethoscope
Air Entry Good Decreased Barely Audible
GeneralConsiderations
Modified Downe’s Scoring System
No cyanosis with
oxygen support
Cyanosis in spite
oxygen support

7. Interpretation:
<4: No Respiratory Distress
4-7: Clinical Distress
>7: Impeding Respiratory Failure
Downe’s Score should be noted every 30mins-1
hour to monitor progression of respiratory
distress.
GeneralConsiderations

8. 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

9. 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

10. Causes
• Pulmonary
• Extra-pulmonary
GeneralConsiderations

11. Pulmonary Causes
1) Airway obstruction
A) Nasal – choanal atresia, nasal edema
B) Oral cavity – macroglossia, micrognathia, Glosoptosis
C) Laryngeal obstruction – laryngeal web, Subglottic
stenosis of larynx, Laryngomalacia, cord
paralysis
D) Neck obstruction – cystic hygroma, cong goitre
E) Tracheal obsruction – Tracheomalacia, TEF, Tracheal
stenosis
GeneralConsiderations

12. 2) Lung parenchyma
A. Aspiration syndrome (MAS)
B. Respiratory distress syndrome (HMD)
C. Transient Tachypnea of new born
D. Pneumonia
E. Pleural effusion
F. Pulmonary hemorrhage
G. Air leak – Pneumothorax, Pneumomediastinum
3) Developmental defects
A. Agenesis of lung
B. Hypoplasia of lung
C. Diaphragmatic hernia
D. Tracheal agenesis
E. TEF
F. Asphyxiating Thoracic dystrophy (Jeune Syndrome)
GeneralConsiderations

13. Extrapulmonary Causes
• CNS Trauma or Birth Asphyxia
• Cardiac Failure
• Metabolic acidosis
• Persistent pulmonary hypertension
• Diaphragmatic Hernia
• Intercostal muscle Paralysis
• Others: Hypothermia/Hyperthermia,
Hypoglycemia, Anemia/Polycythemia,
GeneralConsiderations

14. Common Causes
Medical
• Transient Tachypnea
of new born
• RDS(HMD)
• Aspiration
syndromes
• Pneumonia/sepsis
• PPHN
• CCF
• Acidosis
Surgical
• Pneumothorax
• Diaphragmatic
hernia
• TEF
• Lobar emphysema
• Phrenic nerve
paralysis
GeneralConsiderations

15. New Born with Respiratory Distress
What to do???
GeneralConsiderations

16. History
What we need to know Why we need to know
Were there any risk factors in
the antepartum period or
evidence of fetal distress
prior to delivery?
Birth asphyxia or PPHN
Did the mother receive
antenatal steroids if it was a
preterm delivery?
Antenatal steroids
decrease the incidence of
HMD by 50%
Was there a history of
premature rupture of
membranes and fever?
Congenital pneumonia or
sepsis
Was there meconium stained
amniotic fluid?
MAS is a possibility
GeneralConsiderations

17. What we need to know. Why we need to know
Was resuscitation required
at birth?
Resuscitation trauma/
PPHN/ acidosis
Did the distress appear
immediately or a few hours
after birth?
HMD appears earlier than
pneumonia
Was it related to feeding or
frothing at the mouth?
Tracheo-esophageal fistula
or aspiration
Does the distress decrease
with crying
Choanal atresia
GeneralConsiderations

18. Signs-Will depend on cause
What we need to look for Why we need to look for
A preterm baby weighing
<1500 gms with retractions
and grunt
Likely to have HMD.
Meconium stained
amniotic fluid with an
increase in the anterio-
posterior diameter of the
chest (full chest)
Likely to be suffering from
MAS
A depressed baby with poor
circulation
Neonatal sepsis with or
without congenital
pneumonia.
GeneralConsiderations

19. What we need to look for Why we need to look for
A near term baby with no
risk factors and mild
distress.
May have TTNB
An asphyxiated baby May have PPHN/acidosis
A growth retarded baby with
a plethoric look
May have polycythaemia.
Check for an air leak by
placing a light source over
the chest wall in a darkened
room.
Air leak syndrome
Inability to pass an 5F
catheter through the nostril
of a term baby
Suggestive of choanal
atresia.
GeneralConsiderations

20. 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

21. Management
• Clear the airway, ensuring adequate breathing and circulation.
• Continuous pulse oximeter monitoring.
• Warm, humidified oxygen is given with a head box.
• Maintenance of correct temperature is essential.
• Fluid and electrolyte management: Electrolyte balance, fluids,
calcium and glucose homeostasis are all equally important.
• Maintenance of adequate hemoglobin: Any neonate with
respiratory distress should have a packed cell volume (PCV)
above 40% (but less than 75%).
• All preterm babies with respiratory distress should be started
on broad spectrum antibiotics. In term babies, decision to start
antibiotics would depend on the clinical situation, but the
threshold should be low.
GeneralConsiderations

22. Respiratory Support
Respiratory support is given in the form of continuous positive
airway pressure (CPAP) or intermittent mandatory ventilation
(IMV).
Depends upon condition and severity of distress.
0 1 2 3
PaO2
mmHg
>60 50-60 <50 <50
PaCO2
mmHg
<50 50-60 61-70 >70
pH >7.3 7.20-7.29 7.1-7.19 <7.1
ABG Scoring System
A score of >3 suggests ventilator/respiratory requirement
GeneralConsiderations

23. Indications for starting CPAP are
• Downes’ or Silvermann score of >6 at birth
• FiO2 requirement of >0.4 to maintain an acceptable
saturation on pulse oximeter.
• ABG score of more than 3.
CPAP is said to have failed when the FiO2 requirement is >0.6 or
the pressure required to maintain oxygenation exceeds 7-8 cm of
H2O.
Mechanical Ventilation: Time cycled pressure limited ventilation
is the modality of choice for ventilation. If patient triggered
ventilation is used it is given as synchronized intermittent
mandatory ventilation (SIMV).
Best outcome are seen in babies with impending respiratory failure
or failed CPAP rather than in complete respiratory failure.
GeneralConsiderations

24. Specific Management depends on
the CAUSE of distress
GeneralConsiderations

25. 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

26. 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

27. 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

28. 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

29. 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

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

31. 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

32. 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

33. 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

34. Mec.Asp.Synd

35. 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

36. 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

37. Meconium stained umbilical cord
Mec.Asp.Synd

38. Meconium stained nails
Mec.Asp.Synd

39. • 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

40. 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

41. 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

42. Mec.Asp.Synd

43. Mec.Asp.Synd

44. Mec.Asp.Synd

45. Mec.Asp.Synd

46. 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

47. 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

48. 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

49. • 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

50. 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

51. Postnatal Management
Approach to the ill newborns:
1. Maintain temperature
2. O2 support by hood
3. 2/3rd restricted IV fluids
4. Look for and manage hypoglycemia/ hypocalcemia/
hypotension
5. ??? Antibiotics
6. Initiate CPAP/ventilation if indicated
7. ??? Surfactant therapy (Bolus/Trachebroncial Lavage) - should
be used in setups where ECMO facility is unavailable
8. iNO(Inhaled Nitric Oxide) – when PPHN complicates MAS
9. ECMO (Extra Corporeal Membrane Oxygenation)
10. Keep high suspicion for Air Leaks and PPHN
Mec.Asp.Synd

52. 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.

53. Risk Factors
Increased Risk Decreased Risk
• Maternal diabetes
• multiple births
• cesarean section
delivery
• perinatal asphyxia
• cold stress
• history of previously
affected infants
• Chronic or pregnancy-
associated
hypertension
• maternal heroin use
• prolonged rupture of
membranes
• antenatal
corticosteroid
prophylaxis
Resp.Dis.Syn.

54. Etiology & Pathophysiology
• Lack of surfactant due to immaturity of lungs
is the basic abnormality.
• Surface-Active-Agent (Surfactant) which is
produced by type II alveolar cells, reduces
surface tension and maintains alveolar stability
at low pressure so that end-expiratory alveolar
atelectasis does not occur.
• Surfactant production is also compromised in
birth asphyxia, acidosis, hypothermia, Rh
incompatibility, antepartum hemorrhage and
shock
Resp.Dis.Syn.

55. Resp.Dis.Syn.

56. Resp.Dis.Syn.

57. Surfactant deficiency
End-Expiratory Alveolar Atelectasis
Hypoventilation
Hypo-perfusion of lungs
Epithelial Necrosis
Transudation of Plasma
Formation of Hyaline Membrane
V/Q mismatch
Reduced Compliance
↓p02↑pCO2
↓ pHPPHN
Surfactant
deficiency
Resp.Dis.Syn.

58. Clinical Features
• Maternal Risk factors present in history
• Preterm Infant
• Features of respiratory distress usually appear
within few minutes of birth to upto 6 hours of
birth
• Breath sounds may be normal or diminished with
a harsh tubular quality
• Fine rales may be heard, especially posteriorly
over the lung bases
• Apnea and irregular respirations occur as
infants tire and are ominous signs requiring
immediate intervention
• Respiratory failure may occur in patients with
rapid progression of the condition
Resp.Dis.Syn.

59. • Patient may have a mixed respiratory-
metabolic acidosis, edema, ileus and oliguria.
• In most cases, the symptoms and signs reach a
peak within 3 days, after which improvement
is gradual
• Death is rare on the 1st day of illness, usually
occurs between days 2 and 7
– associated with alveolar air leaks (interstitial
emphysema, pneumothorax), pulmonary
hemorrhage, or IVH.
Resp.Dis.Syn.

60. Diagnosis
• 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.

61. • ABG initially shows hypoxemia and later worsening
of hypoxemia, hypercapnia and metabolic acidosis
• On X-Ray Chest
– Initial X-ray may be normal
– Typical pattern develop at 6-12 hours
– Grade 1 (mild cases): symmetrical reticulogranular
pattern due to scattered atelectasis
– Grade 2: widespread air bronchogram become visible
– Grade 3: reticulogranular pattern becomes
increasingly confluent leading to formation of ground
glass opacity due to marked underaeration
– Grade 4: complete white lung fields with obscuring
of the cardiac shadow due to global atelectasis
Resp.Dis.Syn.

62. Resp.Dis.Syn.

63. Prevention
• Suppress Premature labor to gain gestational
maturity
• Delay induction of labour till pulmonary
maturity is assured by L/S ratio
• Antenatal Steroids to mother
– Betamethasone (12mg IM every 24 hr for 2 doses)
– Dexamethasone(6mg IM every 12 hr for 4 doses)
Resp.Dis.Syn.

64. Management
1. Shift to NICU setup with respiratory support
facilities available
2. Close monitoring for Respiratory distress.
3. Maintain temperature
4. O2 support by hood
5. 2/3rd restricted IV fluids
6. Look for and manage hypoglycemia/
hypocalcemia/ hypotension
7. ???Antibiotics
8. Initiate CPAP/ventilation if indicated
9. Surfactant therapy if indicated
10.Vitamin E
11.???Post natal steroids
Resp.Dis.Syn.

65. Surfactant
• Surfactant reduces surface tension, improves lung compliance, and
stabilizes lung volumes at a lower transpulmonary pressure
• Surfactant’s secondary function is to enhance macrophage activity
and mucociliary clearance, and to reduce inflammation.
• Types of Surfactant
– Natural or Synthetic
• Indications
– Prophylactic
• Premature infants at high risk of developing RDS secondary to
surfactant deficiency (eg 32 weeks or low birth weight 1, 300 g)
• Infants in whom there is laboratory evidence of surfactant
deficiency such as lecithin/sphingomyelin ratio 2:1 or the
absence of phosphatidylglycerol
Resp.Dis.Syn.surf

66. • Indication
– Rescue or therapeutic administration is indicated in
preterm or full-term infants who are suspected of having
surfactant deficiency by inactivation and
• who require endotracheal intubation and mechanical
ventilation secondary to respiratory failure
OR
• who require an FiO2 ≥ 40% or a PEEP of ≥7 to maintain
adequate PaO2 and SpO2 and have Clinical and radiographic
evidence of neonatal RDS or MAS.
– Surfactants may be used as a vehicle to deliver other
drugs such as antibiotics, anti-inflammatory agents, and
bronchodilators.
Resp.Dis.Syn.surf

67. • Indication
– Postoperative development of ARDS following cardiac
surgery. Reduces time on ventilation and ICU and hospital
stay.
– Porcine surfactant in RSV induced respiratory failure may
improve gas exchange and respiratory mechanics and
shorten the duration of ventilation and hospital stay.
• Contraindication
– Presence of congenital anomalies incompatible with life
beyond the neonatal period
– Respiratory distress in infants with laboratory evidence of
lung maturity
– Diagnosis of congenital diaphragmatic hernia. Studies
have shown that early use of surfactant increases mortality.
– Patient hemodynamically unstable
– Active pulmonary hemorrhage
Resp.Dis.Syn.surf

68. • Frequency
– Multiple doses of surfactant to infants with ongoing
respiratory insufficiency appears to be the most effective
treatment regimen
– It has resulted in greater improvements in oxygenation and
ventilatory requirements, a decreased risk of necrotizing
enterocolitis, and decreased mortality.
– Additional doses of surfactant, given at 6–24-hour intervals,
may be indicated in infants who experience increasing
ventilator requirements or whose conditions fail to improve
after the initial dose
Name Type Dose
Calfactant Bovine 105 mg/kg/dose (3 mL/kg)
Beractant Bovine 100 mg/kg/dose (4 mL/kg)
Poractant alfa Porcine
100–200 mg/kg/dose
(1.25–2.5 mL/kg)
Lucinactant Synthetic 5.8 mL/kg
• Availability
Resp.Dis.Syn.surf

69. • DELIVERY TECHNIQUES
– INSURE (Intubation, Surfactant, Extubation)
• This technique features early surfactant replacement therapy
with prompt extubation to nasal CPAP. The technique is
associated with less need for mechanical ventilation, lower
incidence of BPD, and fewer air leak syndromes.
– Selective surfactant replacement therapy with mechanical
ventilation followed by extubation from lower ventilator
settings
• This technique is initiated upon clinical evidence of RDS,
such as radiological findings, increased FIO2 requirement,
and/or increased work of breathing.
– Pharyngeal instillation before first breath
• There have been no randomized controlled trials in humans
to validate this technique. Animal studies have confirmed
improvement of lung expansion and better survival rates.
Resp.Dis.Syn.surf

70. – Laryngeal mask airway (LMA) administration
• In an animal studies on surfactant delivery, it was reported that
surfactant delivery could be accomplished sooner in the LMA
group than ETT with equivalent efficacy. While far from
conclusive, this method holds hope for areas in which ETT
intubation skills are lacking.
– Bronchoalveolar lavage
• Bronchoalveolar lavage has shown promise in the treatment of
MAS. Studies have demonstrated that surfactant lavage is a
safe and effective alternative treatment for MAS.
• In animal studies, it is shown that distribution of intratracheally
instilled surfactant has been largely determined by gravity, and
unaffected by the position of the chest. Therefore, leaving the chest
in a horizontal position may result in the most even distribution of
surfactant to the lungs.
Resp.Dis.Syn.surf

71. Complication of Surfactant Therapy
Procedural complications Physiologic complications
• Plugging of endotracheal tube
(ETT) by
• surfactant
• Hemoglobin desaturation and
increased need for supplemental
O2
• Bradycardia due to hypoxia
• Tachycardia due to agitation, with
reflux of surfactant into the ETT
• Pharyngeal deposition of
surfactant
• Administration of surfactant to
only one lung (ie, right mainstem
intubation)
• Administration of suboptimal dose
• Apnea
• Pulmonary hemorrhage from right
to left shunting
• Increased necessity for treatment
for patent ductus arteriosus
• Marginal increase in retinopathy of
prematurity
• Volutrauma resulting from increase
in lung compliance failure to
change ventilator settings
accordingly
• Hyperventilation or
hypoventilation, both of which can
alter blood flow to the brain,
leading to further complications
Complication can be prevented by slow administration of surfactant
and by decreasing Fio2 and mean airway pressure after administration

72. Complication of RDS
• Intraventricular Hemorrhage
• Air Leaks
• Pulmonary Infection
• Pulmonary Hemorrage
• Hypoglycemia
• DIC
• Cardiac Failure
• Metabolic alterations
Resp.Dis.Syn.

73. 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

74. 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

75. 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

76. • 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

77. Tran.Tachy.Newborn

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

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

80. Management
• Continuous Monitoring of distress.
• Supportive Management
• O2 by hood if required
• Provide adequate nutrition
• ???Furosemide
• ???Antibiotics
Usually a self limited condition and no active
management is required
Tran.Tachy.Newborn

81. Bibliography
1. Alok Kumar, B. Vishnu Bhat Epidemiology of respiratory distress of newborns The
Indian Journal of Pediatrics January–February 1996, Volume 63, Issue 1, pp 93-98
2. Antonowiez I, Schwachman H. Meconium in health and disease. Adv Paediatr 1979;
26:275-92.
3. Basu S, Kumar A, Bhatia BD. Role of antibiotics in meconium aspiration syndrome.
Ann Trop Paediatr. 2007 Jun;27(2):107-13.
4. Brian K Walsh, Brandon Daigle, Robert M DiBlasi, and Ruben D Restrepo AARC
Clinical Practice Guideline. Surfactant Replacement Therapy: 2013Respir
Care, February 2013 58:2 367-375
5. Canadian Pediatric Society, “Recommendation for neonatal surfactant
therapy,” Paediatrics and Child Health, vol. 2, no. 10, pp. 109–116, 2004.
6. Carbine DN. Meconium aspiration. Paediatr Rev 2008; 29: 212-3
7. Clark P, Doff P. Inhibition of neutrophil oxidative burst and phagocytosis by
meconium.Am J Obstet Gynecol 1995; 173:1301-5.
8. Fanaroff AA. Meconium aspiration syndrome: historical aspects. J Perinatol. 2008
Dec;28 Suppl 3:S3-7
9. I. El Shahed, P. Dargaville, A. Ohlsson, and R. F. Soll, “Surfactant for meconium
aspiration syndrome in full term/near term infants,” Cochrane Database of Systematic
Reviews, no. 3, Article ID CD002054, 2007.

82. 10. Jones CA. Early production of pro inflamatory cytokines in the pathogenesis of
neonatal ARDS associated with meconium aspiration.Pediatr Res 1994; 35:339.
11. Kamala Swarnam, Amuchou S. Soraisham, and Sindhu Sivanandan, “Advances in
the Management of Meconium Aspiration Syndrome,” International Journal of
Pediatrics, vol. 2012, Article ID 359571, 7 pages, 2012. doi:10.1155/2012/359571
12. Mechanical Ventilation in Neonatal Medicine zuhair aldajani
13. National Neonatal-Perinatal Database Report 2002-2003
14. Nelson Textbook of pediatrics 18th edition SAUNDERS
15. Nelson Textbook of pediatrics 19th edition SAUNDERS
16. Neonatal morbidity and mortality. Report of the national neonatal perinatal
database. Indian Pediatrics 1997; 34: 1039-42
17. Neonatal resuscitation: 2010 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Kattwinkel
J, Perlman JM, Aziz K, Colby C, Fairchild K, GallagherJ, Hazinski MF, Halamek
LP, Kumar P, Little G, McGowan JE, Nightengale B, Ramirez MM, Ringer S,
Simon WM, Weiner GM, Wyckoff M, ZaichkinJ. Circulation. 2010;122:S909 –
S919.
18. Sankhyan Naveen, Sharma Vijay Kumar, Sarin Ritu, Pathania Kushla. Predictors
of meconium stained amniotic fluid : a possible strategy to reduce neonatal
morbidity and mortality J Obstet Gynecol India Vol. 56, No. 6
:November/December 2006

83. 19. Soll RF, Blanco F. Natural surfactant extract versus synthetic surfactant for
neonatal respiratory distress syndrome. Cochrane Database Syst Rev
2001(2):CD000144.
20. Surg Cdr SS Mathai , Col U Raju , Col M Kanitkar. Management of Respiratory
Distress in the Newborn Medical Journal Armed Forces India 2007; 63 : 269-272
21. Text book on Care of Newborn 8th edition,Meharban Singh, CPS publication
22. U Raju, Maj V Sondhi, Maj SK Patnaik. Meconium Aspiration Syndrome : An
Insight Medical Journal Armed Forces India, Vol. 66, No. 2, 2010
23. Vain NE, Szyld EG, Prudent LM, Wiswell TE, Aguilar AM, Vivas NI.
Oropharyngeal and nasopharyngeal suctioning of meconium-stained neonates
before delivery of their shoulders: multicentre, randomised controlled trial.
Lancet. 2004;364:597– 602.
24. W. P. Kanto Jr.v, “A decade of experience with neonatal extracorporeal membrane
oxygenation,”Journal of Pediatrics, vol. 124, no. 3, pp. 335–347, 1994
25. Wiswell TE, Gannon CM, Jacob J, Goldsmith L, Szyld E, Weiss K, Schutzman D,
Cleary GM, Filipov P, Kurlat I, Caballero CL, Abassi S, Sprague D, Oltorf C,
Padula M. Delivery room management of the apparently vigorous meconium-
stained neonate: results of the multicenter, international collaborative trial.
Pediatrics. 2000;105(1 Pt 1)