1. Neonatal Diseases

2. common causes of respiratory distress in the neonate are : -
1. Hyaline Membrane Disease (HMD)
2. Meconium Aspiration Syndrome (MAS)
3. Transient Tachypnoea of the Newborn (TTNB)
4. Congenital or acquired pneumonia
5. Persistent Pulmonary Hypertension of the Newborn
(PPHN)
6. Air leaks

3. Cont.. 7. Congenital anomalies of upper airway (choanal
atresia), gut (tracheoesophageal fistula, congenital
diaphragmatic hernia) or lungs (lobar emphysema,
cysts)
8. Cardiac shock or Congenital Heart Disease (CHD).
9. Haematological causes (severe anaemia,
polycythaemia)
10. Neurological ( seizures )
11. Metabolic causes- metabolic acidosis

4. Clinical Examination
Clues to the likely aetiology on examination of the neonate :
1. A preterm baby weighing <1500 gms with retractions
and grunt is likely to have HMD.
2. A term baby born through meconium stained
amniotic fluid with an increase in the anteriorposterior
diameter of the chest (full chest) is likely
to be suffering from MAS.
3. A depressed baby with poor circulation is likely to
have neonatal sepsis with or without congenital
pneumonia.
4. A near term baby with no risk factors and mild
distress may have TTNB.
5. An asphyxiated baby may have PPHN.

5. Cont.. 6. A growth retarded baby with a plethoric look may
have polycythaemia.
7. A baby with respiratory distress should be checked
for an air leak by placing a cold light source over
the chest wall in a darkened room.
A baby presenting with tachypnoea and a cardiac
murmur may have a congenital heart disease.
9. Inability to pass catheter through the nostril
of a term baby is suggestive of choanal atresia.

6. Cont.. For babies presenting later with distress ask for :
a) Is the distress associated with feed refusal and lethargy? (sepsis, pneumonia)
b) Is there a family history of early neonatal deaths?
(CHD).

7. Respiratory Distress Syndrome (RDS) Synonym: hyaline membrane disease
Caused by the inadequate production of surfactant in the lungs.
produced by type II pneumocytes (reduce surface tension).
surfactant is produced after 30 weeks gestation.
Inadequate surfactant production causes air sacs to collapse on expiration and greatly increases the energy required for breathing.
The development of interstitial oedema makes the lung less compliant. This leads to hypoxia and retention of carbon dioxide.
Right-to-left shunting occurs: -
- in collapsed lung (intrapulmonary) or,
- if pulmonary hypertension is severe, across the ductus arteries and the foramen ovale (extrapulmonary).

8. Risk factors Premature delivery
Infants delivered via caesarian section without maternal labour.
Hypothermia
Perinatal asphyxia
Multiple pregnancy
Family history of RD

9. Clinical features . Usually preterm delivery. - tachypnoea,
expiratory grunting,
subcostal and intercostal retractions
diminished breath sounds,
cyanosis and
nasal flaring.
May rapidly progress to fatigue, apnoea and hypoxia

10. Investigations
Blood gases: respiratory and metabolic acidosis along with hypoxia.
Pulse oximetry should be maintained at 90-95%.
Chest x-ray (ground glass opacity )
Monitor full blood count, electrolytes, renal and liver function
Echocardiogram
diagnosing PDA
determine the direction and degree of shunting,
Cultures to rule out sepsis

12. Respiratory Distress Syndrome (RDS)
Also known as Hyaline Membrane Disease
(HMD)

13. Occurrence 1-2% of all births 10% of all premature births
Greatest occurrence is in the premature and low birth weight infant

14. Etiology & Predisposing Factors
Prematurity
Immature lung architecture and surfactant deficiency
Fetal asphyxia & hypoxia
Maternal diabetes
Increased chance of premature birth
Possible periods of reflex hypoglycemia in the fetus causing impaired surfactant production

15. The cycle continues until surfactant levels are adequate to stabilize the lung
Symptoms usually appear 2-6 hours after birth
Why not immediately?
Disease peaks at hours
Recovery usually occurs 5-7 days after birth

16. Clinical findings: Physical
Tachypnea (60 BPM or >)
Retractions
Nasal flaring
Expiratory grunting
Helps generate autoPEEP
Decreased breath sounds with crackles
Cyanosis on room air
Hypothermia
Hypotension

17. Clinical Findings: Lab
ABGs: initially respiratory alkalosis and hypoxemia that progresses to profound hypoxemia and combined acidosis
Increased Bilirubin
Hypoglycemia
Possibly decreased hematocrit

18. CXR: Normal

19. RDS CXR: Ground Glass Effect

20. RDS CXR: Air Bronchograms & Hilar Densities

21. Time constant is decreased since elastic resistance is so high
Increased elastic resistance means decreased compliance!

22. RDS Treatment: Primarily supportive until lung stabilizes
Maintain perfusion, maintain ventilation and oxygenation
O2 therapy, CPAP or mechanical ventilation
May require inverse I:E ratios if oxygenation can not be achieved with normal I:E ratio
Surfactant instillation!!!
May cause a sudden drop in elastic resistance!

23. Prognosis/Complications
Prognosis is good once infant makes it past the peak (48-72 hours)
Complications possible are:
Intracranial Bleed
BPD (Bronchopulmonary Dysplasia)
PDA (Patent Ductus Arteriosus)

24. Meconium Aspiration Syndrome -MAS-
Syndrome of respiratory distress that occurs when meconium is aspirated prior to or during birth

25. Occurrence 10-20% of ALL births show meconium staining
10-50% of stained babies may be symptomatic
More common in term and post-term babies

26. Etiology & Predisposing Factors
Intra-uterine hypoxic or asphyxic episode
Post-term
Cord compression

27. Pathophysiology: Check Valve Effect
Causes gas trapping (obstruction)
If complete obstruction, then eventually atelectasis occurs
Irritating to airways, so edema and bronchospasm
Good culture ground for bacteria, so pneumonia possible

28. Pathophysiology (cont.)
V/Q mismatch leads to hypoxia and acidosis which increases PVR
TC increases because it increases airway resistance
Meconium is usually absorbed in hours; there are still many possible complications

29. Clinical Signs Respiratory depression or distress at birth
Hyperinflation
Pallor
Meconium stained body
Possible cyanosis on room air
Moist crackles
ABGs – hypoxemia with combined acidosis
CXR – coarse, patchy infiltrates with areas of atelectasis and areas of hyperinflation
May see flattened diaphragms if obstruction is severe

30. Management Surfactant replacement therapy (endotracheal tube).
Oxygen: infants with mild RDS.
Continuous positive airway pressure (CPAP).
CPAP may be administered via an endotracheal tube, nasal prongs, or nasopharyngeal tubes.
Assisted ventilation at fast rates (more than 40 breaths per minute)

31. Supportive therapy includes the following :.
. Temperature regulation:
prevent hypothermia.
Fluids, metabolism, and nutrition:
monitor and maintain blood glucose, electrolytes, acid balance, renal function, and hydration.
Once the infant is stable, intravenous nutrition with amino acids and lipid.
After the respiratory status is stable, initiate small volume gastric feeds (preferably breast milk) via a tube to initially stimulate gut development.

32. Cont.. Circulation and anaemia:
monitor heart rate, peripheral perfusion, and blood pressure. Blood or volume expanders may be required.
Antibiotics:
start antibiotics in all infants who present with respiratory distress at birth after obtaining blood cultures. Discontinue antibiotics after three to five days if blood cultures are negative.
Support of parents and family:
keep the parents well informed. Encourage parents to frequently visit and stay with their baby.

33. Treatment schedule
Inj. Betamethasone 12 mg IM every 24 hours , 2 doses
Inj. Dexamethasone 6 mg IM every 12hours , 4 doses
Timing of effect :
Opitimal effect occurs after 24 hours of initiating treatment
Effect of one course lasts for 7 days.

34. Prevention
Antenatal corticosteroids (dexamethasone) accelerate foetal surfactant production and lung maturation. They have been shown to reduce respiratory distress syndrome, intraventricular haemorrhage and mortality by 40%.
Delaying premature birth. Tocolytics, e.g.nifedipine or ritodrine, may delay delivery by 48 hours and therefore enable time for antenatal corticosteroids to be given.
Avoid hypothermia in the neonate.

35. M.A.S. Treatment NaHCO3 if severe metabolic acidosis
Broad spectrum antibiotics
Bronchial hygiene
May need mechanical ventilation
Slow rates and wide I:E ratios because of increased TC
Low level of PEEP may help prevent check valve effect
May need HFO
Amnioinfusion – artificial amniotic fluid infused into uterus to dilute meconium Proper resuscitation at birth(clear meconium from trachea before stimulating respiration) Oro-gastric tube NTE O2

36. Prognosis & Complications
Good prognosis if there are no complications
Complications:
Pneumonia
Pulmonary baro/volutrauma
Persistent Pulmonary Hypertension (PPHN)

37. CXR: Pneumothorax