2. Is the commonest neonatal respiratory disease
RDS due to 1. Deficiency of surfactant in the
infants lungs.
2. immature lungs
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3. RDS – is an acute illness – usually of preterm
infants characterised by:
a respiratory rate > 60/min
dsypnoea (intercostal, subcostal recession and
sternal retraction)
Predominantly diaphragmatic breathing
pattern
Expiratory grunt
Must be present within 4 – 6 hours of delivery
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4. Prematurity commonest predisposing factor to
RDS
RDS common in infants < 30 weeks gestation
but can occur up to 34 weeks.
Occurs invariably in infants < 28 weeks
gestation
Can also occur in Term infants: e.g. Infants
born of a diabetic mother
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5. Perinatal asphyxia: Predisposes to RDS in
various ways:-
Hypoxia: reduces surfactant synthesis
Acidosis: also reduces surfactant synthesis
Asphyxia damages the pulmonary vasculature,
allowing protein rich fluid to leak onto alveolar
surface where it inhibits surfactant activity
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6. The protein rich substance forms a hyaline
membrane on the surface of the alveolar
Lungs become atelectic and non-compliant
If child survives the first 2-3 days, there is an
increase in surfactant activity.
Hyaline membrane subsequently absorbed
inflammatory cells e.g. macrophages
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7. However, sometimes organisation and fibrous
tissue formation occurs in the healing process,
especially in over ventilated children
This causes chronic lung disease called
broncho-pulmonary dysplasia and eventual
death
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8. Maternal diabetes: is associated with an
increase in RDS.
Cause is partly due to – early delivery (C/S)
- and due to delay in
maturation of surfactant.
Allowing delivery to be delayed to 38-40 weeks
gestation with good diabetic control almost
eliminates problem
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9. Caesarean section
Caesarean section carried out before labour
starts in women beyond 32 weeks gestation
removes the B-adrenergic mediated surfactant
release
Thus less surfactant is released
Also interferes with removal of fluid from the
lungs during labour predisposing to transient
tachypnoea of the newborn
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10. Other predisposing factors include:
Anti-partum haemorrhage
Second twin
Male: boys are more likely to die from the disease
and develop RDS. In boys maturation of RDS
delayed
Shock
Incidence higher amongst Caucasian infants than
black infants
Assisted ventilation prolongs recovery from RDS
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11. Surfactant is an agent which reduces surface
tension in lungs
Is produced by mature lung: thus surfactant
starts to appear in lungs at 20 weeks gestation
but is only sufficient after 34 weeks gestation
The alveolus has two cell types: an alveolar cell
with thin protein containing cell wall –
pneumocyte type I and the thicker protein
containing cell wall - type II pneumocyte.
Type II pneumocytes produce and release
surfactant into the alveolar lumen
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12. Surfactant is a protein containing dipalmitoyl
lecithin
The dipalmitoyl lecithin is a phospoholipid
composed of lecithin and sphingomyelin
Forms a film around the alveolar cells keeping
the alveolar open
RDS occurs if lecithin:sphingomyelin ratio is
<2:1
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14. Avoid predisposing factors
Administration of steroids antenatally to
mother
Prophylactic administration of surfactant to
baby at resuscitation
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15. In order to prevent RDS in a baby being born
before 34 weeks of gestation steroid are given.
The steroids include betamethasone and
glucortiocoids such as dexamethasone.
The steroids have several effects:-
They induce the enzyme for surfactant
synthesis and increase amount of surfactant
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16. They improve quality of surfactant produced
They mature the non-surfactant producing
tissues of the lung
They reduce the leakage of proteins out of
capillaries onto alveolar surface in asphyxia
They promote postnatal closoure of patent
ductus arteriosus(PDA)
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17. A combination of steroids (Betamethasone)
and Thyroid releasing hormone (TRH) given to
the mother causes greater release of surfactant
as TRH crosses the placenta and stimulates
production of fetal thyroid hormones which
also promote surfactant maturation
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18. In newborn infant born before 34 weeks
gestation surfactant is given – within first few
minutes of birth through an intubation tube.
More than one dose may be needed.
Further doses are given at 1 hour and 24 hours
after birth
There are different types of surfactant
preparation
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19. Asphyxiated babies must be immediately
intubated and oxygenated either via ambubag
or intermittent positive pressure ventilation.
If no intubation tubes are available, patient
must still be ambubagged, holding up the chin
and neck appropriately.
This eliminates acidosis, hypoxia and improves
ventilation, perfusion thereby reducing the
incidence of RDS
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20. This resuscitation causes adequate surfactant
release
Thus resuscitation must be prompt and
vigorous
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21. Avoiding the above predisposing factors
Administration of steroids antenatally
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22. During birth, fluid is squeezed out of infant’s
lungs by compression of chest as baby passes
through birth canal
At first breath, baby makes large inspiratory
effort to expand lungs with air
New born lung is stiff and will collapse if
surfactant is not present or is inadequate
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23. Due to inadequate surfactant, the alveoli
collapse and the lungs become very stiff. This
causes the following changes in pulmonary
physiology:
Lung compliance falls to about 25% of normal
There is increased work of breathing
There is increase intra pulmonary shunting and
severe hypoxemia
There is hypoventilation which causes a
respiratory acidosis
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24. Features which occur secondary to hypoxia
include
High right sided heart pressure and high
pulmonary pressure causing a right to left
shunt through a Patent Ductus Arteriosus
(PDA)
Vascular damage causing transudation no fluid
onto alveolar surface and into subcutaneous
tissue
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25. Hypotension
Severe metabolic acidosis due to lactic acidosis
accumulation after anaerobic respiration
Decreased perfusion and oxygenation of other
tissues predisposing to Necrotising
enterocolitis (NEC), renal failure
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26. Exudation of plasma into alveoli and airway
occurs further compromising surfactant
function
This forms a hyaline membrane which lies the
respiratory bronchioles and alveolar ducts
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27. Earliest changes are interstitial oedema and
congestion of the alveolar walls leading to
desquamation of type II alveolar epithelial cells
Alveolar ducts dilate but alveoli become
atelectatic because of surfactant deficiency
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28. RDS presents within 4 hours of birth with:-
Sternal retraction, intercostal and subcostal
recession
An expiratory grunt
Tachypnoea above 60/min
Signs and symptoms should be present before
four hours of age, should still be there at 4
hours of age and persist beyond 4 hours of age
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29. Child may be cyanosed
Examination of the lungs reveals reduced air
entry and there may be a few crepitations.
Baby is inactive. Tends to lie in frog position
Blood pressure is 20-25% lower than normal for
gestation
The patient has moderate generalised
subcutaneous oedema owing to capillary
leakiness
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30. Patient passes small amounts of urine
Has an ileus
May not pass meconium until 3rd – 4th day
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31. In uncomplicated RDS, surfactant begins to
reappear in lungs at about 36 – 48 hours of age.
Illness initially gets worse over the first 24 – 36
hours and infant tires
Subsequently his condition stabilizes and there
is a steady improvement form 60 – 72 hours of
age
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32. By end of week 1, patient has usually recovered
However if assisted ventilation has been used,
recovery takes longer
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33. Investigations: Cxr shows ground glass
appearance
Treatment:
Ventilate: maintain adequate arterial
oxygenation or give additional Oxygen to
maintain partial pressure of oxygen at 9.2 to 12
kPa.
Give surfactant if available
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34. If infant breathing spontaneously, give oxygen
by face mask or nasal prongs or head box
oxygen
Indications for continuous positive airway
pressure:-
Apnoea
Hypercapnea
Progressive hypoxia (IPPV must be used –
intermittent positive pressure ventilation)
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