Respiratory distress in neonates can be caused by pulmonary issues like respiratory distress syndrome, pneumonia, or transient tachypnea of the newborn, or non-pulmonary issues like cardiac problems, hypoglycemia, or central nervous system conditions. Early recognition and prompt treatment is essential to improve outcomes. Respiratory distress is characterized by tachypnea, chest retractions, and/or grunting. Causes and management should be considered based on gestational age, time of onset, and associated clinical features.

1. E R I C M D 4
RESPIRATORY DISTRESS

2. Respiratory distress in the neonate is a common
problem
and it can be a serious neonatal emergency. Respiratory
distress is said to be present when tachypnea (RR >60
per
min) is accompanied by chest retractions and or grunt. It
can be due to respiratory and non-respiratory
Causes Early recognition and prompt
treatment is essential to improve outcomes

3. Approach
Respiratory distress in a neonate can be recognized by
the presence of varying combinations of tachypnea
(RR >60/min), chest retractions, grunting, flaring of ala
enasi and cyanosis. The gestation, age at onset, severity
of distress and presence of associated clinical features help
in arriving at diagnosis. It should be noted that chest
retractions are mild or absent in respiratory distress due
to non-respiratory causes. if a term baby born to a mother
with meconium stained liquor develops respiratory
distress within the first 24 hr, the most likely cause is
meconium aspiration syndrome (MAS). A term baby with
uncomplicated birth developing tachypnea in the first few
hours of birth is likely to have transient tachypnea of
newborn. Presence of suprasternal recessions with or
without stridor indicates upper airway obstruction.

4. Pulmonary causes of respiratory distress
Cause Time of onset Remarks
Respiratory distress
syndrome
Meconium aspiration
syndrome
Pneumonia
Transient tachypnea of
newborn
First 6 hr of life
First few hr of life
Any age
First 6 hr after birth
Common in preterm
neonates
Common in term, post-
term and small for date
babies; history
of meconium stained liquor
Often bacterial
Tachypnea with minimal
distress; lasts for 48-72 hr
Persistent pulmonary
hypertension
Pneumothorax
Tracheoesophageal fistula,
diaphragmatic hernia,
lobar
emphysema
Any age
Any age
Any age
Severe distress; cyanosis
Sudden deterioration;
usually during assisted
ventilation
May show associated
malformations;
polyhydramnios in
esophageal atresia

5. Non-pulmonary causes of rapid breathing
 Cardiac Congestive heart failure; congenital heart
 Disease
 Metabolic Hypothermia, hypoglycemia, metabolic
 Acidosis
 Central nervous System Asphyxia, cerebral edema,
hemorrhage
 Chest wall Asphyxiating thoracic dystrophy,
 Werdnig-Hoffman disease

6. Cardiac disease. Cardiac etiology for respiratory distress
should be suspected if a neonate with distress has cyanosis
or hepatomegaly. Congenital heart disease and
cardiomyopathies
or rhythm disorders can present as congestive
cardiac failure in the neonatal period. Transposition of
great vessels (TGV) and hypoplastic left heart syndrome
usually present on day one with progressive distress. Most
other cardiac conditions present after the first week of life.
A preterm neonate having a systolic murmur with
tachypnea
and hepatomegaly is likely to have patent ductus
arteriosus (PDA).

7. Neurological causes. Neonates with birth asphyxia,
cerebral
hemorrhage, or meningitis can present with tachypnea
and respiratory distress. These neonates are usually
lethargic with poor neonatal reflexes

8. Respiratory Distress Syndrome (RDS) or
Hyaline Membrane Disease (HMD)
RDS is common in preterm babies less than 34 weeks
of
gestation. The overall incidence is 10-15% but can be
as
high as 80% in neonates <28 weeks. In addition to
prematurity, asphyxia, acidosis, maternal diabetes and
cesarean section can increase the risk of RDS

9. Etiopathogenesis
In RDS, the basic abnormality is surfactant deficiency.
Surfactant is a lipoprotein containing phospholipids like
phosphatidylcholine and phosphatidylglycerol and
proteins. Surfactant is produced by type II alveolar cells
of lungs and helps reduce surface tension in the alveoli.
In the absence of surfactant, surface tension increases and
alveoli tend to collapse during expiration. During inspiration
more negative pressure is needed to keep alveoli
patent. There is inadequate oxygenation and increased
work of breathing. Hypoxernia and acidosis result in pulmonary
vasoconstriction and right to left shunting across
the forarnen ovale. This worsens the hypoxernia and the
neonate eventually goes into respiratory failure. Ischernic
damage to the alveoli causes transudation of proteins into
the alveoli that forms hyaline membrane. Surfactant production
starts around 20 weeks of life and peaks at 35 week
gestation. Therefore any neonate less than 35 week is prone
to develop RDS.

10. Clinical Features
Respiratory distress usually occurs within the first 6 hr of
life. Clinical features include tachypnea, retractions,
grunting, cyanosis and decreased air entry. Diagnosis can
be confirmed by chest X-ray. Radiological features include
reticulogranular pattern, ground glass opacity, low lung
volume, air bronchograrn and white out lungs
in severe disease.

11. Moderate to severe hyaline membrane disease. Note
homogenous opacification of lungs obscuring heart borders and
presence of air bronchogram (arrows)

12. Management
Neonates suspected to have RDS need to be cared for in
neonatal intensive care unit with IV fluids and oxygen.
Mild to moderate RDS can be managed with continuous
positive airway pressure (CPAP). CPAP is a non invasive
modality of support where a continuous distending
pressure (5-7 cm of water) is applied at nostril level to
keep the alveoli open in a spontaneously breathing baby

13. This is an excellent modality of respiratory
support which minimizes lung injury and other
complications
such as air leak and sepsis. Preterm babies
developing severe RDS often require mechanical
ventilation. Preterm babies are at risk of lung injury by
excessive pressure and high oxygen. High saturations of
oxygen (above 95%) can produce retinopathy of
prematurity
(ROP) which can blind the infant.

14. Since surfactant deficiency is the basis of RDS,
exogenous surfactant is recommended as the treatment
of choice in neonates with RDS. Surfactant is indicated in
all neonates with moderate to severe RDS. The route of
administration is intra tracheal. It can be given as a rescue
treatment (when RDS actually develops) or prophylactically
(all neonates less than 28 weeks irrespective of
presence or absence of RDS). Surfactant decreases duration and level of
support of ventilation in neonates and
therefore improves outcome. Many babies can be
INtubated, given SURfactant and rapidly Extubated
(lnSurE approach) to CPAP. This avoids the
need for mechanical ventilation in many neonates.
RDS has generally a good prognosis if managed
appropriately. Survival is as high as 90% in very low birth
weight babies (<1500 g). In the absence of ventilatory
support, most neonates with severe disease will die

15. Continuous positive airway pressure being provided to a
preterm baby

16. Prevention of RDS
Administration of antenatal steroids to mothers in
preterm
labor ( <35 week) has been a major breakthrough in
management of preterm infants. Antenatal steroids
reduces RDS, intraventricular hemorrhage and
mortality
in preterm neonates

17.  Benefits of administering antenatal
glucocortlcoids
 Reduction in neonatal mortality by 40%
 Reduction in respiratory distress by 50%
 Reduction in intraventricular hemorrhage by 50%
 Reduction in occurrence of patent ductus arteriosus,
 necrotizing enterocolitis, hemodynamic instability

18. Pneumonia
Pneumonia is a common cause of respiratory distress in
both term and preterm babies and is caused by bacteria
such E. coli, S. aureus and K. pneumoniae. Neonatal
pneumonia may be due to aspiration or occasionally due
to viral or fungal infection. Though group B streptococcal
pneumonia is common in the West, it is uncommonly
reported in India.

19. Pneumonia
Pneumonia is a common cause of respiratory distress in
both term and preterm babies and is caused by bacteria
such E. coli, S. aureus and K. pneumoniae. Neonatal
pneumonia may be due to aspiration or occasionally due
to viral or fungal infection. Though group B streptococcal
pneumonia is common in the West, it is uncommonly
reported in India.
The neonate has features suggestive of sepsis in addition
to respiratory distress. Chest X-ray shows
pneumonia8.46), blood counts are raised and blood
culture may
be positive.

20. Pneumonia. Note heterogeneous opacities in both the lung
fields

21. Treatment includes supportive care and
specific antibiotic therapy. Ampicillin or cloxacillin
with
gentamicin is usually used. If the pneumonia is due to
hospital acquired infection, antibiotics like
cephalosporins
with amikacin may have to be used.

22. Transient Tachypnea of Newborn (TTN)
Transient tachypnea of the newborn is a benign
selflimiting
disease occurring usually in term neonates and
is due to delayed clearance of lung fluid. These babies
have tachypnea with minimal or no respiratory
distress.
Chest X-ray may show hyperexpanded lung fields,
prominent vascular marking and prominent interlobar
fissure Oxygen treatment is often adequate.
Prognosis is excellent.

23. Transient tachypnea of newborn. Note hyperinflated lungs,
prominent bronchovascular markings and horizontal fissure (arrow

24. Surgical Problems
Tracheoesophageal fistula (TEF) should be suspected in
any neonate with excessive frothing. Diagnosis can be
confirmed by a plain X-ray with a red rubber catheter (not
infant feeding tube, it is soft and gets coiled up) inserted
in stomach; the catheter generally stops at 10th thoracic
vertebrae in presence of esophageal atresia. Presence of
gastric bubble suggest concomitant TEF.
Diaphragmatic hernia should be suspected in any
neonates who has severe respiratory distress and has a
scaphoid abdomen. This condition can be detected during
antenatal ultrasonography. Chest X-ray shows presence
of bowel loops in the thoracic cavity.

25. Bronchopulmonary Dysplasla (BPD)
CLD occurs because of barotrauma and oxygen toxicity
that causes damage to the alveolar cells, interstitium and
blood vessels. Inflammatory mediators are released and
there is increased permeability causing leakage of water
and protein. In later stages, there is fibrosis and cellular
hyperplasia. Severe lung damage leads to respiratory
failure. These babies continue to require prolonged oxygen
therapy or ventilatory support.

26. Pneumothorax
Presence of air in the pleural cavity (pneumothorax) is
most common in babies with meconium aspiration
syndrome and those being ventilated (Fig. 8.48).
Transillumination of the chest can help in diagnosis.
Needle aspiration or chest tube drainage is a life saving
procedure in this situation

27. Apnea
Apnea is defined as cessation of respiration for 20 seconds
with or without bradycardia and cyanosis or for shorter
periods if it is associated with cyanosis or bradycardia.
Apnea is a common problem in preterm neonates. It could
be central, obstructive or mixed.
Apnea of prematurity occurs in preterm neonates
between the second to fifth days of life and is because of
the immaturity of the developing brain. Central apnea can
also occur because of pathological causes like sepsis,
metabolic problems (hypoglycemia, hypocalcemia), temperature
instability, respiratory distress, anemia and
polycythemia. Obstructive apnea can occur because of
block to the airway by secretion or improper neck
positioning.

28. Treatment is supportive and involves correction of
underlying cause. Apnea of prematurity is treated with
aminophylline or caffeine. Prognosis is good in apnea
of
prematurity. In other cases it depends on the
underlying

29. Meconium Aspiratrion Syndrome (MAS)
Meconiurn staining of amniotic fluid (MSAF) occur in
10%-14% of pregnancies. Neonates born through MSAF
can aspirate the meconium into the lungs and develop
respiratory distress (meconium aspiration syndrome;
MAS). Aspirated meconium can block the large and small
airway causing areas of atelectasis and emphysema which
can progress to develop air leak syndromes like
pneumothorax.
Presence of atelectasis and emphysema can cause
ventilation perfusion mismatch in these babies that can
progress to respiratory failure. Meconium also induces
chemical pneumonitis.

30. Clinical Features and Course
MAS usually occurs in term or post term babies and small
for dates babies. Infants usually develops respiratory
distress in the first few hours of life that often
deteriorates
in subsequent 24-48 hr. If untreated, distress can progress
to respiratory failure. Complications include
pneumothorax,
other air leak syndromes (pneumopericardiurn,
pneumomediastinurn) and persistent pulmonary
hypertension.
Chest X-ray shows bilateral heterogeneous
opacities, areas of hyperexpansion and atelectesis and air
leak

31. Meconium aspiration syndrome. Note hyperexpansion of
lungs and heterogeneous opacities in right lung

32. Management
Clinical course in these babies can be complicated by
severe pulmonary hypertension. A good supportive care
in terms of maintenance of normal body temperature,
blood glucose and calcium levels, ensuring analgesia and
avoiding unnecessary fiddling pay good dividends.
Oxygenation and ventilation is maintained by judicious
use of oxygen and mechanical ventilation. With ventilatory
support, 60-70% neonates survive, but in the absence of
ventilatory support, mortality is high in severe disease

33. Persistent Pulmonary Hypertension (PPHN)
It is caused by a persistent elevation in pulmonary vascular
resistance resulting in right to left shunt across the
forarnen
ovale and/ or ductus. The disease is more common in term
and post-term babies and occurs as a result of persistent
hypoxia and acidosis. Hypoxia and hypercarbia cause
pulmonary vasoconstriction. This increases pulmonary
vascular pressure and results in right to left shunting

34. Common causes include asphyxia, respiratory distress
due to MAS, RDS, diaphragmatic hernia, etc. Primary
pulmonary hypertension can also occur because of an
abnormal pulmonary vasculature secondary to chronic
intrauterine hypoxia.
The neonate usually presents with severe respiratory
distress and cyanosis. It is often difficult to differentiate
PPHN from cyanotic congenital heart disease.
Echocardiography
helps in ruling out congenital heart disease
and may demonstrate right to left shunt across the forarnen
ovale. Ventilatory support is mandatory. Nitric oxide, a
selective pulmonary vasodilator is an effective therapy.