Respiratory distress in neonates can be identified by tachypnea, chest indrawing, and other signs. It can be caused by pulmonary issues like respiratory distress syndrome, meconium aspiration syndrome, or transient tachypnea of the newborn. Non-pulmonary causes include perinatal asphyxia, hypothermia, and congenital heart disease. Transient tachypnea of the newborn involves defective sodium transport leading to retained lung fluid and is often seen in babies delivered by c-section. It typically resolves within a few days with supportive care like oxygen and feeding assistance. Persistent pulmonary hypertension of the newborn results when normal postnatal pulmonary pressure reduction fails and presents a serious

1. RESPIRATORY DISTRESS IN
NEONATES

2. definition
Identified with the presence of tachypnea
(respiration rate more than 60 breaths/min)
Chest indrawing ( subcostal, substernal,
intercostal retractions) and expiratory grunting.
Cyanosis, nasal flaring along with alteration of
air entry may also found in this problem.

3. Common Causes
PULMONARY CAUSES:
RDS/HMD: due to surfactant deficiency.
MAS
TTNB
PPHN
PNEUMONIA
MILKASPIRATION, PNEUMOTHORAX, PLEURAL
EFFUSION
SURGICAL CAUSES: TEF, EA, CDH, BILATERAL
CHOANAL ATRESIA

4. Contd.
 NONPULMONARY CAUSES:
 Perinatal asphyxia
 Hypothermia
 Hypoglysemia
 Metabolic acidosis
 Cerebral edema
 Neurological disorders
 Congenital heart disease
 Congestive heart failure
 Haemorrhage
 Severe anemia etc.

5. TTNB( Transient tachypnea of
newborn)
• What is transient tachypnea of the newborn?
Transient tachypnea (tak-ip-nee-ah) of the
newborn, or TTN, is temporary fast breathing.
It is sometimes called “wet lungs.”

6. RISK FACTORS
• Elective c-section,
• Pre-term
• Maternal diabetes
• Male gender
INCIDENCE:
5in 1000 neonates.

7. Pathophysiology
NORMALLY:
• During Gestation: Lung epithelium secretes Cl- and
fluid.
• Late Gestation: Na+ reabsorption ability starts in lung
epithelium.
• At birth: Mature lung switches from active Cl- (fluid)
secretion to active Na+ (fluid) absorption in response to
circulating catecholamines; with the help of
glucocorticoids.
• Changes in oxygen tension augment the Na+ -
transporting capacity of the epithelium and increase
gene expression for the epithelial Na+ channel (ENaC).

8. Pathophysiology in TTNB
• Bioelectrical studies of human infants' nasal
epithelia demonstrate that both transient
tachypnea of the newborn and respiratory
distress syndrome (RDS) involve defective
amiloride-sensitive Na+ transport.
• Transient tachypnea of the newborn occurs in
mature newborns with mature surfactant
pathways and poorly developed respiratory
epithelial Na+ transport.

9. Why mostly in Cs babies?
• Fetal lung fluid clears by 35% a few days prior to birth,
owing to changes in the ENaC
• by around 30% during active labour owing to mechanical
transpulmonary forces and catecholamine surge
• 35% is cleared postnataly during active crying and
breathing.
• An infant born by caesarean delivery is at risk of having
excessive pulmonary fluid as a result of not having
experienced all of the stages of labour and subsequent lack
of appropriate catecholamine surge, which results in low
release of counter-regulatory hormones at delivery. The
result is alveoli with retained fluid that inhibit gas
exchange.

10. Sign and symptoms
• Rapid breathing
• Flaring of the nostrils when breathing in
• Sharp pulling in of the chest muscles during
breathing (retraction)
• Bluish skin colour (cyanosis) around the nose
and mouth.

11. Diagnostic evaluations
• evaluation of respiratory distress by
SilvermanWAchart.
• Chest X-rays to look for fluid in the lungs
• Blood tests to look for infection
• Constant monitoring of the baby’s oxygen
level, breathing rate, and heart rate
The diagnosis of TTN is often made after ruling
out other causes.

12. Treatment
• Extra oxygen – usually given through a nose tube
or mask
• Help feeding – rapid breathing can make feeding
hard. baby may be given fluid and nutrients through
an IV or a feeding tube until breathing is easier.
• Antibiotics – until infection can be ruled out
• CPAP (continuous positive airway pressure) – a
treatment that uses mild pressurized air to keep the
lungs open
• Mechanical ventilator (in rare cases)

13. Prognosis
TTN usually goes away on its own within a few
days of birth.
In most cases, there are no long-term problems
due to TTN.

14. PPHN (Persistent Pulmonary
Hypertension of the Newborn)
• Definition:
PPHN is persistence after birth of the high
pulmonary arterial pressure (PPA), often
suprasystemic, that is characteristic of the fetal
circulation. PPHN may occur with or without
apparent pulmonary disease.

15. Pathophysiology
• NORMALLY:
 In fetal life: pulmonary blood flow (Qp) is low (5-10% of
cardiac output [CO]) due to high pulmonary vascular
resistance (PVR) and shunts (i.e., foramen ovale, ductus
arteriosus) which permit blood to bypass the
pulmonary vascular bed.
 At birth, PVR normally falls dramatically (due to lung
inflation and oxygenation), Qp increases to 100% of CO
and, by 24 hours after birth, PPA ( pulmonary Arterial
Pressure) falls to about 50% of systemic arterial
pressure.

16. pathophysiology
• When this normal transition fails, PVR and PPA
remain elevated, Qp stays low, right to left
shunting occurs at the foramen ovale and ductus
arteriosus, and hypoxemia results.
• Clinical scenarios associated with PPHN include: -
Abnormal pulmonary vascular development
Pulmonary hypoplasia with associated hypoplasia
of pulmonary vasculature
Postnatal elevation in pulmonary vasoconstrictors
Congenital heart disease

17. Clinical presentation
• Term or post-term infant
• Onset at birth or within a few hours
• History or clinical findings consistent with
condition associated with PPHN
• Cyanosis, often with pre-ductal (right upper
extremity) O2 saturation >post-ductal
• Respiratory distress is common
• Chest radiograph clear (idiopathic PPHN) or
abnormal due to associated condition

18. Diagnostic evaluation
• Blood culture
• Chest radiograph
• Pre-ductal and post-ductal pulse O2 saturation
(SpO2) monitors (to detect R → L shunting at
ductus arteriosus). A difference of ≥10%
suggests marked pulmonary hypertension.
• Cardiology consultation and echocardiogram
to detect congenital heart disease.

19. Treatment
• The primary therapy is supplemental oxygen.High
inspired oxygen concentration. Start with 100%
O2. Maintain pre-ductal PaO2 at 90 to 100
mmHg.
• Consider intubation and mechanical ventilation in
infants who have significant respiratory distress
or CO2 retention
• Correct metabolic & respiratory acidosis. Do not
administer alkali unless the patient is receiving
adequate assisted ventilation.

20. Contd.
• Assisted ventilation. Use lowest mean airway pressure, in
infants without significant parenchymal disease. High
frequency ventilation may be effective in those with severe
lung disease.
• Inhaled nitric oxide (iNO): dose is 20ppm
• Maintain adequate systemic blood pressure.
• Use dopamine; begin at dose of 5 mcg/kg per min IV and
increase as necessary.
• Adequate sedation & Minimize handling.
• ECMO (Extracorporeal membrane oxygenation) - for those
in whom less invasive therapy is not effective in
maintaining oxygenation, normal acid-base status or
hemodynamic stability.

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