RDS, TTN, MAS etc

1. RESPIRATORY DISEASES
OF THE NEWBORN
By: dr Ismah, Paeds department
1

2. 2
Respiratory diseases
of the newborn
Respiratory distress
syndrome - RDS
(hyaline membrane disease)
Transient tachypnea of the
newborn (TTN)
Meconium aspiration
syndrome (MAS)
Primary pulmonary
hypertension of the newborn
(PPHN)
Apnea of prematurity
Congenital pneumonia

3. 3
Preterm infant Term infant Both
• RDS
• Erythroblastosis
fetalis
• Nonimmune
hydrops
• Pulmonary
hemorrhage
• PPHN
• MAS
• Polycythemia
• Amniotic fluid
aspiration
• Bacterial sepsis e.g. GBS
• TTN
• Spontaneous pneumothorax
• Congenital anomalies e.g.
congenital lobar
emphysema, diaphragmatic
hernia
• Congenital heart disease
• Pulmonary hypoplasia
• Viral infection e.g. CMV,
herpes
• Inborn metabolic errors

4. 4
1. Respiratory distress
syndrome
- RDS
(hyaline membrane
disease)

5. Occurred after the onset of breathing
and is associated with an insufficiency
of pulmonary surfactant
 Incidence of RDS increase with decrease gestational
age
 RDS develops in 30-60% in infant 28-32 W
 Others risk factors: delivery of previous preterm infant
with RDS, maternal DM, male sex, 2nd born of twins, c
sec not in labor
 May develop immediately in extremely immature infant
or 3-4 hrs after birth in 34W infant 5

6. LUNG DEVELOPMENT
 Lining of alveolus consists 90% type 1 and 10% types
II cells
 The surfactant production depends on the fetal
cortisol, begins between 32-34 W of gestation
 Surfactant produced by type II cells sufficiently by 34-
36 W
6

7.  Contents of surfactant are 90% lipids (lecithin,
phosphatidylglycerol) and proteins SP-A, SP-B, SP-C
and SP-D
 Surfactant prevents atelectasis and contributes to the
lung recoil by manipulates the surface tension of the
lungs
 Lecithin/Sphingomyelin ratio 2:1 in amniotic fluid
usually indicate fetal lung maturity or the presence of
minor phospholipids e.g. phosphatidylglycerol
7

8. CLINICAL MANIFESTATION
 Tachypnea
 Nasal flaring
 Intercostal, sternal recession
 Grunting; closure of glottis during expiration
 Cyanosis
8

9. CXR
Shows air bronchograms
and reticulonodular
shadowing throughout
the lung fields (often
termed ‘ground glass’
appearance)
9

10. 10

11. PREVENTION AND TREATMENT
 Prevent preterm birth; treatment of infections, cervical
cerclage
 Prevention of neonatal cold stress, birth asphyxia,
hypovolemia reduces risk of RDS
 Administration of corticosteroid before delivery for lung
maturity
 Surfactant usage
 Aim SPO2 ≥ 90%, PaO2 60-70 mmHg, pH> 7.25
 Start antibiotic for 48-72 hrs (difficult to differentiate
sepsis, pneumonia from RDS)
11

12. SURFACTANT
Surfactant therapy reduces mortality rates most
effectively in infants <30 weeks and those of birth weight
<1250 gm
12

13. WHO TO GIVE?
 Depressed preterm infants who have no spontaneous respiration
after 30 seconds of ventilation that require positive pressure
ventilation (PPV)
 Preterm infants below 28 weeks gestation who are given only
CPAP from birth in delivery room, i.e. the infant has spontaneous
respiration and good tone at birth. Surfactant to be given within
30 minutes after birth
 Preterm infants between 28-32 weeks – to have CPAP from birth
in delivery room. To assess requirement for surfactant in NICU
based on oxygen requirement of FiO2 > 30% and respiratory
distress
 More mature or larger infants should also be given surfactant if
the RDS is severe 13

14. TIMING OF SURFACTANT
THERAPY
 The first dose has to be given as early as possible to the
preterm infants requiring mechanical ventilation for RDS but
not in 1st minute OL
 The repeat dose is given 4-6 hours later if FiO2 is still >
0.30 with optimal tidal volume settings for those below 32
weeks;
 And if FiO2 > 0.40 and CXR still shows moderate to severe
RDS (“white” CXR) for those infants > 32 weeks gestational
age.
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15. TYPES OF SURFACTANT
 Survanta , a natural surfactant, bovine derived
Dose : 4 ml/kg per dose.
 Curosurf , a natural surfactant, porcine derived
Dose: 1.25 mls/kg per dose.
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16. COMPLICATIONS
PDA
Pulmonary air
leaks
Bronchopulmonary
dysplasia
(chronic lung
disease)
ROP
16
RDS 
increased
pulmonary
pressure 
prevent
closure of
ductus
arteriosus
Associated
with
ventilation
that may
lead to
ruptured
alveolar
O2 dependent ≥
CGA 36W
Excessive
O2 
developing
blood
vessels of
premature
infant retina
 blindness

17.  Tachypnea, mild retraction, hypoxia, occasional
grunting, rarely cyanosis  which may persist for up to
48 hrs
 Caused by retained lung fluid or slow resorption of
lung fluid
 Associated in larger premature infant or term infant in
precipitate delivery (not in labor), infant DM mother or
use of analgesia intrapartum
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2. TTN

18. PATHOPHYSIOLOGY
The lungs in utero are constantly secreting fluid to aid lung
growth and development
However the rate of lung fluid production and volume of foetal
lung lumen decreases before birth, most during labour
The mechanism for fluid absorption is triggered by
neuroendocrine hormones, which cause lymphatic vessel
dilatation
As the lung pulmonary circulation increases following the first
breath, the fluid in the lungs is cleared thus interruption of this
process of clearing fluid from the lungs may result in
respiratory distress.
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19. 19

20. MANAGEMENT
 It is often managed conservatively by a period of close
observation on the postnatal ward or in the neonatal unit
but must be weighed against other differential diagnoses
including RDS and pneumonia which may progress rapidly
in newborn infants
 Oxygen therapy
 Antibiotics may be used if persistent (consider other
associated condition e.g. sepsis)
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21. 3. MAS
 Term and post term delivery
 Tachypnea, hypoxia, hypercapnia, small airway obstruction,
air trapping, overdistention and extra alveolar air leaks
 Meconium stained liquor suggest utero distress with
asphyxia, hypoxia and acidosis
21

22.  The inhaled meconium can cause:
• Mechanical obstruction of the airways leading to
mismatched ventilation/ perfusion
• Chemical pneumonitis (in 24-48 hrs)
• Infection which inhibit surfactant function and leads to
inflammation and swelling, which also can obstruct small
airways
• The combination of ventilation/perfusion mismatch and
pulmonary inflammatory can trigger vasoconstriction of
the pulmonary vasculature leading to PPHN
22

23. MANAGEMENT
 Mostly supportive therapy
 Most cases of MAS will recover within 2–3 days
 However, some infants will progress to develop severe
MAS requiring intubation and ventilation
 Start on antibiotic in view of distinguishing MAS from
pneumonia can be difficult
• The initial chest radiograph is often similar to findings
associated with pneumonia with bilateral patchy infiltrates and
possible pleural effusion
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24. CXR
24
Bilateral diffuse
grossly patchy
opacities

25. 4. PPHN
 Term, post term
 Defined as a failure of normal pulmonary vasculature
relaxation at or shortly after birth, resulting in
impedance to pulmonary blood flow which exceeds
systemic vascular resistance, such that unoxygenated
blood is shunted to the systemic circulation
25

26.  PPHN can be:
• Idiopathic - 20%
• Associated with a variety of lung diseases:
Meconium aspiration syndrome (50%)
Pneumonia/sepsis (20%)
RDS (5%)
Congenital diaphragmatic hernia (CDH)
Others: Asphyxia, Maternal diabetes, Polycythemia
26

27. DIAGNOSIS
 History
- Precipitating factors during antenatal, intrapartum, postnatal
periods
 Respiratory signs
- Signs of respiratory distress
- Onset at birth or within the first 4 to 8 hours of life
- Marked lability in pulse oximetry
 Cardiac signs
- Central cyanosis
- Prominent precordial impulse
- Murmur
27

28.  Radiography
- Lung fields: normal, parenchymal lesions if lung disease is
present, or oligaemia
- Cardiac shadow: normal sized-heart, or cardiomegaly (usually
right atrial or ventricular enlargement)
 Echocardiography
- Exclude congenital heart disease
- To look for pulmonary artery pressure
- Define the presence, degree, direction of shunt through the
duct / foramen ovale
- Define the ventricular output.
28

29. Differentiate PPHN from Congenital
Cyanotic Cardiac diseases.
Differentiating points between the two are:
• Infants with PPHN usually had some perinatal hypoxia
• Bradycardia is almost always due to hypoxia, not a
primary cardiac problem
• Babies with congenital cyanotic heart diseases are
seldom critically ill at delivery
• Infants with cyanotic lesions usually do not have
respiratory distress
• The cyanosed cardiac baby is usually pretty happy, but
blue
29

30. MANAGEMENT
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• Preventing and treating; hypothermia,
hypoglycaemia, hypocalcaemia,
hypovolemia, anaemia
General
measures
• Morphine, midazolamSedation
Ventilation

31. 31
• Aim MAP>50 mmHg
• Inotropes to increase CO
Circulatory
• Inhaled NOVasodilators
• Extracorporeal membrane
oxygenationECMO

32. 5. APNEA OF PREMATURITY
 Defined as sudden cessation of breathing that lasts for
at least 20 seconds or is accompanied by bradycardia
or oxygen desaturation (cyanosis) in an infant less
than 37 weeks’ gestational age
 Incidence increase with decrease gestational age
32

33. CLASSIFICATION
 Central
Complete cessation of airflow and respiratory efforts with
no chest wall movement with no evidence of obstruction
 Obstructive
Absence of noticeable airflow but with continuation of
chest wall movement
 Mixed apnea – most common
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34. ETIOLOGY
 Symptomatic of underlying problems, commoner ones
of which are:
• Respiratory conditions (RDS, pulmonary haemorrhage,
pneumothorax,
upper airway obstruction, respiratory depression due to drugs).
• Sepsis
• Hypoxemia
• Hypothermia
• CNS abnormality (e.g. IVH, asphyxia, increased ICP, seizures)
• Metabolic disturbances (hypoglycaemia, hyponatraemia,
hypocalcaemia)
• Cardiac failure, congenital heart disease, anaemia
• Aspiration/ Gastro-oesophageal reflux
• Vagal reflex: Nasogastric tube insertion, suctioning, feeding
34

35. Differentiate from Periodic
breathing
 Regular sequence of respiratory pauses of 10-20 sec
interspersed with periods of hyperventilation (4-15 sec) and
occurring at least 3x/ minute, not associated with cyanosis
or bradycardia
 Benign respiratory pattern for which no treatment is
required
 Respiratory pauses appear self-limited, and ventilation
continues cyclically
 Periodic breathing typically does not occur in neonates in 35

36. MANAGEMENT
 Immediate resuscitation.
36
Pediatrics Protocol 3rd ed

37. Review possible underlying causes and institute specific
therapy, e.g. septic workup if sepsis suspected and
commence antibiotics
Remember to check blood glucose via glucometer
Management to prevent recurrence
- Nurse baby in thermoneutral environment
- Nursing prone can improve thoraco-abdominal wall synchrony and
reduce apnoea
Monitoring:
- Pulse Oximeter, cardio-respiratory monitor
37

38.  Drug therapy
- Methylxanthine compounds:
Caffeine citrate (preferred if available)
IV Aminophylline or Theophylline
• Start methylxanthines prophylactically for babies < 32
weeks gestation
• For those > 32 weeks of gestation, give methylxanthines if
babies have apnoea
• To stop methylxanthines if
- Gestation > 34 weeks
- Apnoea free for 1 week when the patient is no longer on CPAP
- Monitor for at least 1 week once the methylxanthines are stopped
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39.  After discharge, parents should be given advice
- Supine sleep position
- Elimination of exposure to tobacco smoke
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40. 6. CONGENITAL PNEUMONIA
 Acquired through the birth passages especially after
prolonged rupture of membranes
 Pneumonia in newborn infants is often difficult to
diagnose and often difficult to distinguish from other
causes of respiratory distress including RDS and TTN
 Investigations including blood white cell counts, blood
cultures, C-reactive protein, CXR
40

41. PATHOPHYSIOLOGY
Pneumonia may be acquired due to ascending
infection especially when chorioamnionitis is
present
Common pathogens include
• Bacteria, such as group B Streptococci (GBS), Streptococcus
pneumonia, Staphylococcus aureus, Listeria and gram-
negative enteric rods (e.g. E.Coli)
• Viruses, such as Herpes simplex virus, Respiratory syncytial
virus and Influenza A & B viruses
• Atypical organisms such as chlamydia
• Fungi such as Candida albicans.
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42. RISK FACTORS
Prolonged rupture of membranes (PROM)
Prematurity
Maternal infection (maternal fever or raised
white cell count) e.g. GBS
42

43. MANAGEMENT
 Blood gases and pulse oximetry monitoring will guide
the respiratory support required by the infant
 Antibiotic; Penicillin and gentamicin
 Supportive care such as oxygen, thermoregulation,
prevention of hypoglycaemia and parenteral nutrition
or nasogastric tube feeding
43

44. CXR
A chest radiograph may
show bilateral patchy
shadowing with or without
pleural effusion.
44

45. TAKE HOME MESSAGE
Gestation age
Risk factors
Recognize signs of respiratory distress
Early intervention, consultation and close
monitoring
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46. THANK YOU
Ref:
1. Nelson Essential of Pediatrics 6th ed
2. Pediatrics Protocol 3rd ed
3. http://www.learningradiology.com
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