This document discusses respiratory disorders in newborns. It begins by defining respiratory distress and noting that it affects 4-7% of neonates and is responsible for 30-40% of NICU admissions, with higher rates in preterm infants. The main causes of respiratory distress are discussed as transient tachypnea of the newborn, respiratory distress syndrome, pneumonia, meconium aspiration syndrome and persistent pulmonary hypertension of the newborn. Diagnosis involves assessing respiratory rate, retractions, oxygen saturation and chest x-rays. Management involves supportive care, surfactant replacement therapy and managing complications.

1. Respiratory disorders in new
born
PRESENTERS- Dr Kumar Abhinav
Dr Renu Pilania
MODERATOR- Dr Bijoy Patra

2. Respiratory Distress
NNPD defines RD as any two of the following:-
a) RR >60,
b) Sub / inter-costal retractions,
c) Expiratory Grunt / groaning.
Prevelance
Effects 4-7% of all neonates and responsible for 30-40% of NICU
admission [Pre-term (30%) > Post-term (21%) > Term(4.2%)].

3. Etiology of RD in neonates

8. Initial Assesment
RD recognised
 Then Life threatening conditions are identified; e.g:-
a) Inadequate respiratory efforts - Apnea;
b) Obstructed Airway - Gasping, Choking, Stridor;
c) Circulatory collapse - bradycardia, hypotension, poor perfusion;
d) Cyanosis.
If such features are present emergency measures to be taken - e.g:-
a) Oxygen administration,
b) Bag and mask ventilation, or
c) Intubation.

9. Evaluation of RD in NB – Clinical History
Detailed birth history should be elicited
Antenatal History Most likely association
* Prematurity, IDMs * HMD
* PROM, maternal fever, * Pneumonia
Unclean vaginal exams,
UTI, diarrhoea
* Asphyxia/MSAF * Aspiration
* Caesarean delivery * TTN
* Polyhydramnios * TE fistula, CDH
* Oligohydramnios * Pulm. Hypoplasia
* H/o receiving steroids * RDS less
* Traumatic/breech delivery * ICH / Phrenic nerve paralysis

10. General examination
Inspection - Identify etiological clues:-
a) Dysmorphic features,
b) Anomalies,
c) Features of IUGR,
d) Single Umbilical artery,
e) Scaphoid abdomen,
f) Drooling of saliva.

11. Assesment of RD
Signs of RD are observed -
a) RR – Tachypnoea,
b) Symmetry of chest excursion,
c) Synchrony of Abdominal wall movement,
d) Colour of the neonate – pink / cyanosed,
e) Use of Pulse-Ox - Spo2,
f) Shape of chest wall - rounded thorax with increased A-P diameter
hyperinflation

12. Some important respiratory signs are described below :-
a) Tachypnea - improves minute volume,
b) Apnea or gasping - Pre-term neonates with immature resp. regulation,
Neonates due to CNS depression, those on verge of RF,
c) Nasal flaring,
d) Grunting – improves when neonate improving or going into
exhaustion,

13. e) Retractions,
3 types –
I. Intercostal retractions – parenchymal disease,
II. Suprasternal & supraclavicular retractions – airway obstruction.
III. Subcostal / Xiphoid
f) Stridor,
g) Stertor,
h) Wheezing.

14. RD scoring
- Preterm

15. Downe’s scoring – Term neonate

16. RESPIRATORY DISTRESS SYNDROME
• Acute illness of preterm infants
• presenting within 4-6 hours of delivery,
• characterised by Tachypnea
• respiratory distress with chest retractions and a characteristic grunt.
• Clinical equivalent of histopathological counterpart- Hyaline Membrane Disease (HMD).
• Commonest cause of respiratory failure in preterm babies

17. EVENT POTENTIAL CONSEQUENCES
Alveolarization Reduced lung growth and lung surface area with
increased alveolar size; impaired pulmonary function
Type II cell differentiation RDS
Hydrophobic surfactant
proteins (SP-B, SP-C)
RDS
Hydrophilic surfactant
proteins (SP-A, SP-D)
Compromised host defense
Clara cell differentiation Impaired antioxidant and antimicrobial
defenses
Respiratory drive AOP
Fetal lung liquid Hypoplasia
PREMATURITY

18. Pulmonary surfactant
• Is a complex mixture of phospholipids, neutral lipids, and surfactant-specific proteins that is
synthesized, packaged, and secreted from alveolar type II cells of the lung.
• Production starts by 26th week - stored in lamellar bodies.
• Composition:
Lipids -90 -95 %
• Saturated phosphatidylcholine- 50 %
• Unsaturated phosphatidylcholine - 20 %
• Phosphatidylglycerol -8 %
• Neutral lipids -8 %
Proteins - 5-10 %
• Surfactant proteins- 5%
• Serum proteins -5%
• KEY component is SP-B

19. Surfactant

20. RESPIRATORY UNIT

21. SURFACE TENSION AND ITS EFFECTS
• SURFACE TENSION- molecular attractive forces in surface – avoids spreading
• Avoids bubbling inside water
LAPLACE LAW
P = 2T / r P – Pressure
T – Surface tension
r - radius
• Two interconnected bubbles of different sizes – smaller one will deflate into larger one

22. SURFACTANT AND SURFACE TENSION
• Surfactant reduces the surface
tension of the alveolar fluid
• Property – surface tension
reduces for smaller alveolus as
surfactant molecules come
closer
• In interconnected alveolus –
pressure will increase the size
of smaller alveoli into larger
one

23. Pressure volume relationship

24. Incidence
 Inversely related to gestational age and birth weight
 Occurs in 60–80% of infants < 28 wk
 15–30% of those between 32 - 36 wk
 About 5% > 37 wk
• In a report from the NICHD Neonatal Research Network, Fanaroff
reported
• 71% of infants b/w 500-750 g had RDS
• 54% b/w 751-1000 had RDS
• 36% b/w 1001-1250 g had RDS
• 22% b/w 1251-1500g had RDS

25. NNPD data
• Incidence of RDS varies from
• 6.8 to 14.1% in preterm live births in our country
• 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 overall
incidence of RDS in our country was 1.2 % of all live births

26. RISK OF DEVELOPING RDS
Increases with
 Prematurity
 Multiple Births
 Maternal Diabetes
 Asphyxia
 Precipitous Delivery
 History of previously
affected babies
 White race
 Male sex
Decreases with
 Antenatal Corticosteroid
prophylaxis
 Chronic or Pregnancy
associated Hypertension
 Prolonged rupture of
membranes
Respiratory Distress in the Preterm Infant
J. Craig Jackson, Avery’s textbook of neonatology, 9th e/2016

27. Genetic Predisposition to RDS
• Susceptibility to RDS is interaction between genetic, environmental
and constitutional factors
• Very preterm infants
• Common alleles predicts 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

28. Prematurity
Immature lung with underdeveloped and uninflated alveoli
Capillary damage
Hypoxaemia
Atelectasis
Fibrin ( Hyalin membrane )------- fall
in lung compliance, impaired gas
exchange
Co2 retention
Acidosis
Fibrinogen
Plasma leak
Decreased surfactant
Increased alveoli surface tension
Pulmonary vasoconstriction and hypo profusion

29. Diagnosis
The diagnosis of RDS by NNPD :
• 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

30. Radiographic evidence
• Atelectasis, low lung volumes
• Air bronchograms
• Diffuse reticular-granular infiltrates
• Severe bilateral opacity ( “whiteout”)
• Initial CXR may be normal with the typical pattern developing in 6-12 hr

31. Grade 1 - Grade 2

33. Tests for fetal lung maturity
Lecithin- sphingomyelin ratio
• Lecithin increases with increasing gestational age and sphingomyelin
constant in 3rd trimester
• Correlates with the maturity of the fetal lung
• Ratio > 2 is used as cut-off
• Uses 3-4 ml amniotic fluid and TLC.
• Sensitivity – 50 -100% Specificity – 60 - 97%
Disadvantages :
• Time consuming
• Meconium and blood interferance
Clair CS, Norwitz ER et al. The probability of neonatal respiratory distress syndrome as a function of gestational age and lecithin/sphingomyelin ratio. Am J Perinat 2008

34. Foam stability test
SHAKE TEST
• Amniotic fluid plus equal volume of 95% ethanol followed by shaking and
• Observe meniscus for presence of a ring of bubbles
MODIFIED SHAKE TEST OR FSI
• Uses serial dilutions of ethanol and amniotic fluid.
GASTRIC ASPIRATE SHAKE TEST
• Recent entity
• Proven sensitivity of 80-90%

35. PHOSPHATIDYLGLYCEROL ESTIMATION
• Increases specificity when combined with LS ratio
• Useful in DM
LAMELLAR BODY COUNT
• Sensitivity – 83 – 100% Specificity – 50 – 100%
• More than 50000/μl
SURFACTANT : ALBUMIN RATIO (The TDx-FLM II )
• Fluroscent polarization method
• Rapid
• High sensitivity
• Value> 55mg/g suggests lung maturity

36. Investigations
• Sepsis screen and blood cultures
• Continuous pulse oximetry
• Arterial blood gas analysis
• Monitoring of sugar and electrolytes
• Echocardiography to r/o PDA, TAPVC,PPHN
• Gastric aspirate shake test
• Serial radiographs
• Lung ultrasound is still investigative*

37. • Establishing diagnosis
• Supportive therapy of a sick newborn
• Respiratory support
• Surfactant replacement therapy[SRT]
• Management of complications
• Long term follow up
Management

38. Role of Antenatal steroids
ACOG 2016 recommendations:
• A single course of corticosteroids between 24 and 33 6/7 weeks
• Single repeat course should be considered in women who are
• less than 34 0/7 weeks of gestation
• imminent preterm delivery within 7 days,
• prior course more than 14 days previously.
• May be considered at 23 0/7 weeks of gestation
• A single course between 34 0/7 weeks and 36 6/7 weeks of gestation at
risk of preterm birth within 7 days
Regularly scheduled repeat courses or serial courses (more than two) are
not currently recommended.
Antenatal Corticosteroid Therapy for Fetal Maturation, ACOG Committee Opinion, OCT 2016

39. What to administer ?
• Drug schedule
• Dexamethasone
• 6 mg intramuscular repeated every 12 hours x 4 doses
• Part of NHM protocol.
• Betamethasone
• 2 doses of 12 mg intramuscularly 24 hours apart
• Betamethasone versus dexamethasone
• conflicting evidence on individual superiority

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

41. Surfactant replacement therapy
• Prophylactically in preterm neonates < 25 weeks gestation
• Early rescue in preterm with clinical features consistent with RDS.
• Late rescue in Term with RDS
• SRT in secondary surfactant deficiency
• Pulmonary hemorrhage
• MAS
• CDH
• Severe pneumonia

42. Role of prophylactic SRT
• Prophylactic SRT reduces morbidity and neonatal mortality.
• Earlier meta-analysis had proved efficacy of SRT
• lower mortality rate [RR] 0.69; 95%
• decrease in the risk of air leak (RR 0.79)
• However in Indian settings issues arise due to
• Cost effectiveness
• Lack of ANS
• Relative lack of Level III facilities
• Easier availability of CPAP

43. RECENT ADVANCES IN SRT
• SRT refined with the increasing care for preterm infants born before
26 weeks' gestational age and the recent clinical focus on avoiding
mechanical ventilation
• Clinical evidence is evolving on :
 new types of surfactants
surfactant dosages
co-medication given before, with, or after surfactant replacement
mode of administration

44. Meconium Aspiration syndrome
• If meconium is present in the amniotic fluid, there is a chance that meconium may enter the
mouth of the fetus and be aspirated into the lungs k/a Meconium Aspiration syndrome.
Etiology
• Acute or chronic hypoxia and/or infection can result in the passage of meconium in utero.
• Gasping by the fetus or newly born infant can cause aspiration of amniotic fluid contaminated
by meconium.

45. Incidence
 Occurrence approximately 10% to 15% of deliveries,
 Meconium staining diminishes with decreasing gestational age,
 It is rare before 34 weeks of gestation, whereas it is quite common >37 weeks,
 Approximately 3% to 4% of neonates born through MSAF develop meconium aspiration
syndrome (MAS),
 Approximately 30% to 50% of these require continuous positive airway pressure (CPAP) or
mechanical ventilation.

46. PATHOPHYSIOLOGY
Meconium is a sterile, thick, black-green odorless material that results from the accumulation
of debris in the fetal intestine starting in the third month of gestation,
Has phospholipase A2,
Post-term fetus with rising motilin levels and normal gastrointestinal function are more prone
to meconium passage,
Vagal stimulation produced by cord or head compression, or in utero fetal stress leads to its
passage,
Gasping leads to aspiration,

47. Pathophysiology of meconium aspiration.

48. Effects of meconium aspiration
I. It can also cause a reactive inflammatory process by releasing cytokines and vasoactive
substances,
II. Meconium can results in –
a) chemical pneumonitis,
b) mechanical obstruction of airways,
c) can result in a ball-valve obstruction of the airways causing gas trapping and pneumothorax,
III. Vasospasm, hypertrophy of the pulmonary arterial musculature, and pulmonary hypertension
leading to extrapulmonary right to left shunt through ductus arteriosus or foramen ovale.
a) Resulting in worsened V / Q mismatch and severe arterial hypoxemia.

49. b) 1/3rd infants with MAS develop persistent pulmonary hypertension of the newborn (PPHN),
IV. Aspirated meconium also inhibits surfactant function,
a) Several studies suggest that the enzymatic and sterol components of meconium disrupt the
surfactant phospholipids and limit the ability for surfactant to lower surface tension,
b) Thus rescue doses of surfactant can also be required in severe MAS.

54. C-X Ray
Classic roentgenographic findings are –
a) diffuse, asymmetric patchy infiltrates,
b) areas of consolidation, often worse on the right, and
c) hyperinflation.
d) pneumothorax and pneumomediastinum may be present .

56. Severity
• Mild :- in infants requiring <40% oxygen for <48 hours,
• Moderate :- in infants requiring >40% oxygen for >48 hours without air leak,
• Severe :-in infants who require assisted ventilation for >48 hours and is often associated with
PPHN.
Sequalae
• Term infants:- associated with an increased risk of perinatal and neonatal mortality, severe
acidemia, need for cesarean delivery, intensive care and oxygen administration, and adverse
neurologic outcome.
• Preterm infants:- with MAS have similar adverse effects as well as an increased incidence of
severe intraventricular hemorrhage, cystic periventricular leukomalacia, and cerebral palsy.

57. Prevention of MAS
Maternal risk factors
a) pre-eclampsia or increased blood pressure,
b) chronic respiratory or cardiovascular disease,
c) poor intrauterine fetal growth,
d) Post-term pregnancy, and
e) heavy smokers.
These women should be carefully monitored during pregnancy.
Amnioinfusion – help only in variable deceleration not after MSAF.
Timing & mode of delivery – induce early labour at 41 weeks in past due date pregnancy.

59. MANAGEMENT OF MECONIUM ASPIRATION SYNDROME
Oropharyngeal and nasopharyngeal suctioning on the perineum and routine tracheal
intubation and aspiration of meconium in vigorous infants are not effective in preventing
MAS.
If infant not improving with intubation and PPV, the trachea obstructed by thick secretions
or meconium.
The trachea suctioned using a suction catheter inserted through ET or directly suctioned
through the tube using a meconium aspirator attached to a suction source. The pressure of
80 to 100 mm Hg.

61. 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.

62. 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.

63. 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 or persistent 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 to deteriorate.

64. Apnoea
Definition
• Apnea is defined as cessation of airflow.
• Has to differentiated from periodic breathing which is normal in neonates.
• Apnea in near term or term is almost always pathological.
• Apnea is pathologic (an apneic spell) when absent airflow is
a) >20 sec, or
b) accompanied by bradycardia (HR<100 bpm) or
c) hypoxemia detected clinically (cyanosis) or by oxygen saturation monitoring.

66. Types
1. Central apnea (40%)– complete cessation of inspiratory efforts without obstruction.
2. Obstructive apnea (10%) occurs when inspiratory efforts persist in the presence of
airway obstruction, usually at the pharyngeal level. Chest wall movements present.
3. Mixed apnea (50%) - occurs when airway obstruction with inspiratory efforts precedes
or follows central apnea.

68. • Temperature instability

69. Apnea of prematurity
• It is a diagnosis of exclusion.
Incidence
• Apneic spells occur frequently in premature infants.
• Essentially, all infants <28 weeks' gestational age have apnea & as many as
25% of all premature infants who weigh <1,800 g (34 weeks' gestational
age) have at least one apneic episode.
• It may be seen up to 42 weeks of postmenstrual age.

70. Pathogenesis of AOP
A. Developmental immaturity of central respiratory drive
Apnea may correlate with brainstem neural function.
The frequency of apnea decreases over a period as brainstem conduction time of the
auditory-evoked response shortens as gestational age increases.
B. Chemoreceptor response
In preterm hypoxia results in transient hyperventilation, f/b hypoventilation or sometimes
apnea, in contrast to the response in adults.
hypoxia makes the premature infant less responsive to increased levels of carbon dioxide
The ventilatory response to increased carbon dioxide is decreased in preterm infants.
C. Reflexes. stimulation of the posterior pharynx, lung inflation, fluid in the larynx, or
chest wall distortion can precipitate apnea in infants. vigorous use of suction catheters is
contraindicated.

71. D. Respiratory muscles. impaired coordination of the inspiratory muscles (diaphragm and
intercostal muscles) and the muscles of the upper airway (larynx and pharynx).
E. Many inhibitory neurotransmitters also play a role in the pathogenesis of apnea.
G. Inhibition of pharyngeal muscle tone during active sleep may contribute to upper airway
collapse and obstructive apnea.
H. Passive neck flexion, pressure on the lower rim of a face mask, and submental pressure (all
encountered during nursery procedures) can obstruct the airway and lead to apnea, especially
in premature infant.

72. MONITORING AND EVALUATION
All infants <35 weeks' gestational age – monitor for apneic spells for at least the first
week or until no significant apneic episode has been detected for at least 5 days.
Most apneic spells in preterm infants respond to tactile stimulation.
Infants who fail to respond to stimulation bag and mask, started with a fractional
concentration of inspired oxygen (FiO2) equal to the FiO2 used before the spell to avoid
marked elevations in arterial oxygen tension.
After the first apneic spell, the infant should be evaluated for a possible underlying cause

73. Treatment
• Specific measures
• Maintain temp.
• Avoid oral feeding and reflexes that trigger apnea
• Gentle cutaneous stimulation :mild and intermittent episodes
• Positioning – prone with 15-45 degree head tilting – improves EELV
• Immediate bag and mask ventilation : recurrent and prolonged apnea
• Oxygen
• Methylxanthines(theophylline or caffeine) enhance ventilation through a central
mechanism or by improving diaphragmatic strength.
loading dose of caffeine citrate (20 mg/kg) orally or intravenously >30 minutes,
followed by 24 hrs later maintenance doses of 5 -10 mg/kg OD.
Discontinued after 33- 34 wks of GA if no episode for 5-7 days.
• CPAP & HFNC

74. Bronchopulmonary Dysplasia
• Chronic lung disease (CLD) or bronchopulmonary dysplasia (BPD) usually occurs in
preterm infants who require mechanical ventilation and/or oxygen therapy for a primary
lung disorder in early neonatal period.
• Incidence of BPD has largely remained unchanged over the years, although better
treatment modalities are available now but the improved survival of more immature
infants has led to increased numbers of BPD.
• The definition, pathophysiology, and management of bronchopulmonary dysplasia (BPD)
has evolved significantly since first described by Northway almost 50 years ago.

75. Definition
• The earliest clinical definition of BPD was limited to oxygen requirement at 28 days with
consistent radiologic changes.(Northway et al in 1967 )
• These were originally modified to include continuing need for oxygen therapy at 36 weeks
corrected gestational age (CGA).
• One of the commonly used definitions of BPD is the NIH consensus definition by Jobe et al.,
which recommends diagnosing infants with BPD based on their oxygen exposure and
determines severity by assessing their respiratory support at 36 weeks postmenstrual age
(PMA).

77. Definition
A. For infants born at <32 weeks' gestation who received supplemental oxygen for their first 28
days, the NIH defined BPD at 36 weeks' postmenstrual age (PMA) as
1. Mild: no supplemental O2 requirement
2. Moderate: supplemental O2 requirement <30%
3. Severe: supplemental O2 requirement ≥30% and/or continuous positive airway pressure
(CPAP) or ventilator support.
B. For infants born at ≥32 weeks, the NIH defined BPD as supplemental O2 requirement for the
first 28 days with severity level based on O2 requirement at 56 days of life.

78. Physiologic definition of BPD
• The need for supplemental oxygen is based on oxygen saturation (SpO2) during a room air
challenge performed at 36 weeks' PMA (or 56 days for infants >32 weeks' PMA) or before
hospital discharge.
• Persistent SpO2 <90% is the cutoff below which supplemental O2 should be considered.

80. Limitations
 Fails to classify infants with respect to airway issues (including tracheal or bronchomalacia
and/or reactive airway disease) and pulmonary vascular disease.
 Infants who had intervals of off oxygen period in the first few weeks.
 Use of high-flow nasal cannula, is not addressed and can result in misclassification.
 Does not include morbidities in early infancy associated with BPD. i.e inability to diagnose
BPD in infants dying from severe respiratory failure before 36 weeks PMA.

81. Prevalence
• Incidence of BPD increases with decreasing gestational age at birth.
• Infants <28 weeks' gestation or <1,000 gm birth weight are most susceptible, with
incidence rates of 35% to 50%.
• Few reports are available from the centers in India; one study from Chandigarh found the
incidence of CLD (defined as need for oxygen at or beyond 28 days of life) to be 50%
and 9% in ELBW and VLBW infants respectively.
Narang A, Kumar P, Kumar R. Chronic Lung Disease in Neonates: Emerging problem in India. Indian Pediatr 2002; 39:
158-62
• relative risk is decreased in African Americans and females

82. ETIOLOGY AND PATHOGENESIS
1. Immature lung substrate -The lung is most susceptible before alveolar septation begins.
Injury lead to an arrest of alveolarization and simplified lung structures that are the
hallmark of new BPD.
2. Volutrauma and lung injury - from mechanical ventilation or bag-and mask ventilation
3. Oxygen toxicity - Insufficient production of the antioxidant enzymes superoxide
dismutase, catalase, glutathione peroxidase, and/or deficiency of free radical sinks such
as vitamin E, glutathione, and ceruloplasmin may predispose the lung to O2 toxicity
Similarly, inadequate antiprotease protection may predispose the lung to injury from the
unchecked proteases released by recruited inflammatory cells.
4. Genetic factors may contribute to BPD risk,
5. Excessive early iv fluid administration by contributing to pulmonary edema

83. 6. L R shunt through PDA.
7. Intrauterine or perinatal infection, with cytokine release
Ureaplasma urealyticum- in tracheal aspirate- has been associated with BPD in premature infants.
Intrauterine Chlamydia trachomatis and other viral infections have also been implicated.
8. IUGR linked to later development of BPD,
9. Increased inositol clearance may lead to diminished plasma inositol levels and decreased
surfactant synthesis or impaired surfactant metabolism.
10. An increase in vasopressin and a decrease in atrial natriuretic peptide release may alter
pulmonary and systemic fluid balance in the setting of obstructive lung disease.

84. Note :
• Inflammation plays a vital role in pathogenesis but only corticosteroids have shown benefit in
BPD other inflammatory modulators were not shown to benefit in trials.

85. Stages of lung development
 Embryonic stage (week: 8)
 Pseudoglandular (weeks: 8-16)
 Canalicular (weeks: 16-24)
 Saccular (weeks:24-near term)
 Alveolar (weeks: 34 weeks to postnatal period)
 The specific timing and duration of exposures influences the pattern of pulmonary damage

87. Pathogenesis
• The etiology of BPD is clearly multifactorial and involves:-
• Derangements in multiple aspects of lung function -
a) Surfactant production,
b) Repair from injury (e.g., elastin deposition) and
c) Growth and development (e.g., alveologenesis).
 The phenotype seen with BPD is the end result of a complex multifactorial process in which
various pre- and postnatal factors compromise normal development in the immature lung.
 Susceptible host with immature lung structure,
 Developmental deficiencies of factors crucial to lung development and function such as
surfactant, nitric oxide, innate immune defense, and antioxidant capability
 Inadequate nutrition,resulting in postnatal growth failure,

89. Clinical and Radiological features
• Respiratory signs in infants with CLD include fast breathing, retractions, and paradoxical
breathing. Rales and coarse rhonchi are usually heard on auscultation.
 Radiographic features of ‘old’ and ‘new’ BPD are quite different.
 New BPD shows haziness reflecting diffuse loss of lung volume. Occasionally they have dense
areas of segmental or lobar atelectasis or pneumonic infiltrates, but they do not show severe
overinflation.
 ‘Old’ BPD, as originally described by Northway, had four distinct stages.

93. Prevention of BPD
• Management strategies are aimed at protecting against lung injury and the development of
BPD.
• As the pathogenesis of disease is multifactorial, diverse approaches have been adopted
including both ventilation and medical strategies.

94. Antenatal Steroids
 The effect of antenatal glucocorticoids on the incidence of BPD among
survivors has been inconsistent.
 Some studies have demonstrated a benefit (Gagliardi et al,2007; Van Marter et
al, 1990).
 The inconsistent effect of antenatal steroids on BPD may be due to increased
survival of less mature preterm infants.
 Antenatal steroids less RDS/HMD  less BPD
 but more survival of less mature preterms increased BPD

96. Ventilatory- Strategies:
 Minimizing ventilatory support
 Prefer non invasive ventilation, whenever it is possible
 CPAP/HHHFNC
 If invasive ventilation used:
 Volume targeted ventilation
 Patient triggered ventilation (SIMV)
 Low tidal volume (3-6 ml/kg)
 Moderate PEEP (4-5 cm H2o)
 Slightly high Ti (0.4-0.45)
• Permissive hypercapnea (PaCO2 >55 mm Hg provided pH >7.25)

97. Continuous positive airway pressure (CPAP):
• Non invasive ventilation is always better than
invasive modalities.
Patient-triggered ventilation (PTV):
• Patient triggered modes (SIMV, assist-control, and pressure support ventilation) improve the
infant-ventilator asynchrony and reduce the risk of Ventilator induced lung injury.
• The Cochrane review concluded that though PTV is associated with shorter duration of
ventilation, it does not reduce the incidence of BPD.
High-frequency ventilation:
• A recent meta-analysis that included 17 RCTs of conventional versus high frequency
ventilation found no significant difference in the incidence of BPD. Therefore, elective use of
HFV cannot be recommended for preterm infants with RDS at present.

98. Heated humidified high flow nasal cannula
• Similar efficacy to CPAP

100. THANK YOU