1. NEONATAL RESPIRATORY
DISEASES
BY
Dr.(Mrs) P. O. OBIAJUNWA

2. Introduction
• Respiratory diseases usually present as
respiratory distress in the neonate. It has
four main clinical features.
• Tachypnoea; resp rate >60c/min.
• Recessions; indrawing of the sternum and
intercostals and subcostal regions.
• Grunting.
• Cyanosis.
• All four symptoms may not be present in
every case, but the presence of 2 or more
symptoms qualifies for respiratory distress.

3. • Causes of Neonatal Respiratory distress
include;
• Respiratory distress syndrome (hyaline
membrane disease),
• Pneumonias, Pneumothorax, aspiration
syndrome (meconium, milk, blood, Amniotic
squames), Congenital diaphragmatic hernia,
Transient tachypnoea of the newborn,
Tracheo-eosophageal fistula, cardiac failure,
Pulmonary hypoplasia, Persistent fetal
circulation (Primary pulmonary hypertension),
Broncho-pulmonary dysplasia, chronic
pulmonary insufficiency of prematurity,

4. • Respiratory distress syndrome (Hyaline membrane
diseases)
• This is due to lack of Surfactant, which is a
phospholipids that lowers the surface tension within
the terminal airway. Surfactant is secreted by the
type 2 pneumocytes situated within the alveolar
membrane. They are present by 22 weeks of
gestation but become functionally active by full
term. Surfactant production can be switched on by
stress, premature rupture of membrane, and
exogenous steroid given to mother. Maternal
diabetes suppresses development of surfactant so
that their babies may have RDS even when term.

5. • The birth process squeezes out fluid from the lungs by
compression of the chest wall. The infant’s first breath
expands the alveoli. In the presence of surfactant, the
alveoli remain expanded, but if absent, the alveoli collapse
down to their foetal state, and the baby’s next breath is
another massive one to re-expand the terminal airways.
Surfactant molecules form a monolayer on the inside of the
alveolar membrane. They are poorly compressible and
maintain the alveolus in an expanded state. In RDS, each
breath is like the first breath in effort, respiratory distress
results and baby gets tired.
• About 1% of newborns infant have RDS. It is closely related
to immaturity; 60-70% of infants born at<28 weeks and 20%
of those born less than 34weeks have it.
• Risk factors for RDS are diadetes in mother, 2nd twin, ante
partum haemorrhage, shock, maleness.

6. Pathology:
Hyaline membranes are seen within the
alveoli of dead babies dying of RDS, and are
part of the inflammatory response to the
condition. The infant shows signs of
respiratory distress soon after birth,
progressing over the first day, peaks at 48
hours. The infant may be oliguric initially,and
may become oedematous, diuresis occurring
as the infant starts to recover.

7. Diagnosis
• Chest –ray Ground glass appearance
showing airless alveoli with an air
bronchogram, air-filled eosophagus may be
seen too.
• Measuring directly or indirectly the amount
of surfactant in the amniotic fluid or gastric
aspirate. The lecithin: sphingomyelin (L:S)
ratio reflects surfactant activity and a ratio of
<1.5 predicts a high risk for RDS.

8. Management
• It is self-limiting. The baby’s lungs recover
with endogenous production of surfactant.
Management is directed towards supporting
the infant during respiratory distress.
• In mild disease, give humidified oxygen
supplements by headbox to maintain normal
arterial blood oxygen tension.
• In more severe cases continuous positive
airway pressure (CPAP) is used to provide
constant positive pressure during expiration
which limits collapse of the alveoli.

9. Management (contd)
• Mechanical ventilation is indicated when
there is hypoxia, and there is hypercapnoae
with a rising Pco2 >8 kpa(60mmHg with
falling pH( <7.25) or there is apnoea.
• General supportive treatment are chest
physiotherapy, early infection treatment,
blood pressure monitoring, optimal
environmental temperature.
• Exogenous surfactant replacement therapy
can be given.

10. Complications of respiratory distress
syndrome.
Pulmonary:
• Air leak including Pneumothorax,
• Pulmonary interstitial emphysema,
• Pneumonia, atelectasis, Lobar collapse,
chronic lung disease.
Extrapulmonary ones are;
Patent doctus arteriosus, Intraventricular
haemorrhage, Retinopathy of prematurity,
Subglottic stenosis.

11. Pneumonias
• Neonatal pneumonia could be early, within
24 hours of birth intrapartum that is through
the birth canal, or later.
• Early onset pneumonia is said to be mainly
caused by Group B beta haemolytic
Stretococcus acquired from mother (10% of
women are carriers.) It causes pneumonia or
meningitis. Presents as respiratory distress
or apnoae. The child could have septicaemia
and shock.

12. Chest X-ray may be similar to RDS.
• Management includes respiratory support with
oxygen supplement, mechanical ventilation,
presumptive antibiotic management (ampicillin with
gentamicin, 3rd generation cephalosporin). Change
antibiotic according to sensitivity pattern.
• Later onset pneumonias could be due to damaged
lungs in ventilated babies, or acquired from those
around the babies. Causative germs include
Pseudomonas, Staph aureus. E-coli, Klebsiella,
Mycoplasma, Chlamydia, unusually candida or
viruses.
• X-ray shows patchy opacities.

13. • Treatment is with appropriates antibiotics,
oxygen if needed.
• Manage congestive cardiac failure if present.
• Vigorous physiotherapy.
• Air leak from the alveoli can occur. If the
leakage is into lung interstium it is called
pulmonary interstitial emphysema. Air can
track along the perivascular spaces and
rupture into the mediastinum causing
Pneumomediastinum, into the pleural space
resulting in Pneumothorax, and when air
leaks into the pericardial space, it is
pneumopericardium.

14. • Pneumothorax may be spontaneous, but mostly
following resuscitation especially with bag and
mask.Risk afctors include RDS, meconium
aspiration, and lung hypoplasiain conjuction with
diaphragmatic hernia.
• Diagnosis-suspect when there is a sudden
deterioration in infant’s condition. There is a
reduction of breath sounds over the affected lung.
Left-sided tension pneumothorax may displace the
heart to the right side with heart sounds.
• Confirm by chest x-ray which shows a hyperlucency
of the side affected with no air bronchogram.
Treament involves placing a tube in the2nd
intercostal space at the mid-clavicular line. Place the
other end of the tube into a container of water below
the infant.

15. • Meconium aspiration syndrome. Intrapartum
asphyxia may cause the foetus to pass meconium
which baby can aspirate into the small bronchi when
gasping. During resuscitation at birth, the meconium
is further driven into terminal airway. Meconium is
very irritant and causes an inflammatory reaction,
Meconium plugs some airways causing a “ball
valve” effect of the with some hyperinflation, and air
leak. An intense inflammatory exudates develop
and secondary bacterial infection occurs.
Ventillation/ perfusion inequality develops causing
the infant to become more hypoxic and in severe
cases pulmonary hypertension commonly develops.

16. • Diagnosis is suggested when there is the
presence of meconium in the liquor, in the
airway with respiratory distress.
• Chest X-ray shows hyperinflation with diffuse
patchy opacities throughout the lung fields.
• Management involves the use of Oxygen,
antibiotics, and steroids.
• Prevention; careful evaluation of the child
with meconium-stained liquor and sucking it
out from mouth. If meconium is seen below
the vocal cords, remove it and lavage the
• Trachea with normal saline through an
endotracheal tube.

17. • Milk aspiration is common in infants
with gastro-eosophageal reflux,
those with apnoae and tetanus
patients. Naso-duodenal feeding
may be useful in these. Total
parenteral nutrition may be
considered.

18. Congenital diaphragmatic hernia.
• Occurs I 1 in 2500 births. There is a defect in the
postero-lateral part of the diaphragm in 80% of
cases. Severity depends on the defect size, amount
of bowel in chest and timing of herniation. Bowel in
the chest causes lung compression and hypolasia.
Large bilateral defects is not compartible with life.
development.
• Their severe respiratory distress present from birth
in severe cases.
• Suggestive features are scaphoid abdomen, and
apparent dextrocardia if defect is left-sided.
Diagnosis is confirmed by chest x-ray showing
loops of bowel in the thorax.

19. Management:
Patient can be delayed a few days to stabilize
before surgery. The bowel is returned to the
abdomen and defect is repaired.
• Medical treatment: adequate ventilation, shock
treatment, calories.
• Prognosis depends on lung hypoplasia. Mortality
of 60-70% in early presentation <6 hours.
• Transient tachypnoae of new born is diagnosed in
retrospect and is due to delayed clearance of fluid
from the lungs in term infants especially born by
C/S soon after birth.
• X-ray shows streakiness due to interstitial fluid and
fluid in horizontal fissure.