respiratory difficulty commonly in a preterm neonate and is due to deficiency of pulmonary surfactant. It was formerly known as Hyaline Membrane Disease (HMD). presented by Dr. Taher

1. RESPIRATORY DISTRESS
SYNDROME (RDS)

2. DEFINITION:
•Respiratory Distress Syndrome is
defined as respiratory difficulty shortly
after birth, commonly in a preterm
neonate and is due to deficiency of
pulmonary surfactant.
•It was formerly known as Hyaline
Membrane Disease (HMD).

3. INCIDENCE:
•Its incidence is inversely related to
gestational age and birth weight.
•It occurs in 60-80% of infants <28 wk of
gestational age, in 15-30% of those
between 32 and 36 wk of gestational age,
and rarely in those>37 wk of gestational
age.

4. FACTORS INCREASING THE INCIDENCE OF RDS:
•Preterm male or white infants. (Highest)
•Perinatal asphyxia in preterm.
•Precipitous delivery.
•Multiple births.
•Maternal diabetes.

5. FACTORS INCREASING THE INCIDENCE OF RDS:
•Maternal history of previously affected
infants.
•Thoracic malformation (Diaphragmatic
hernia).
•Elective caesarean section without labor.
•Second twin.

6. FACTORS DECREASING THE INCIDENCE OF RDS:
•Intrauterine Growth Retardation.
•Pregnancies with chronic or pregnancy-
associated hypertension.
•Prolonged rupture of membranes.
•Antenatal corticosteroid prophylaxis.
•Maternal heroin use.

7. ETIOLOGY ANDPATHOPHYSIOLOGY:
Surfactant deficiency (decreased
production and secretion)is the primary
cause of RDS.
The failure to attain an adequate FRC and
the tendency of affected lungs to become
atelectatic correlate with high surface
tension and the absence of pulmonary
surfactant.

8. The major constituents of surfactant are:
• Dipalmitoyl phosphatidylcholine(lecithin).
• Phosphatidylglycerol.
• Apoproteins.
• Cholesterol.
With advancing gestational age, increasing
amount of phospholipids are synthesized
and stored in type-II alveolar cells. These
surface-

9. active agents are released into the alveoli,
where they reduce surface tension and help
maintain alveolar stability by preventing the
collapse of small air-spaces at end-expiration.
Surfactant is present in high conc. in fetal lung
by 20 wk of gestation. It appears in amniotic
fluid between 28 and 32 wk of gestation.
Mature levels of pulmonary surfactant are
present usually after 35 wk of gestation.

10. •Deficiency of pulmonary surfactant leads to
alveolar atelactasis, edema and cell injury.
Subsequently, serum proteins that inhibit
surfactant function leak into the alveoli.
•Macroscopically, there are eosinophilic
membranes in collapsed alveoli (so is the
name Hyaline Membrane Disease) and
sometimes pulmonary hemorrhage and
interstitial emphysema.

11. CLINICAL MANIFESTATIONS:
Signs of RDS usually appear minutes of birth,
although they may not be recognized for
several hours in larger premature infants until
rapid, shallow respirations become more
obvious.
•Tachypnoea.
•Expiratory grunting (Often audible).
•Intercostal and subcostal retractions.
•Cyanosis.

14. CLINICAL MANIFESATIONS:
•Breath sound may be normal or
diminished with a harsh tubuler
quality.
•Fine inspiratory crackles.
•Untreated patients may have mixed
respiratory-metabolic acidosis,
edema, ileus and oliguria.

15. SCORING SYSTEMTO EVALUATE SEVERITYOF
RESPIRATORYDISTRESS:
Clinical sign Score
0 1 2
Respiratory
rate/min
<60 60-80 >80
Cyanosis Absent Absent with up to
40% oxygen
Require >40%
oxygen
Retractions Absent Mild Moderate-severe
Grunting Absent Audible Audible with
stethoscope
Breath sounds Good Decreased Barely audible

16. •Mild: 0-3
•Moderate: 4-6 (need CPAP)
•Severe: 7-10 (need Assisted
Ventilation)

17. DIAGNOSTIC CRITERIAFOR RDS:
EARLY SIGNSOF RDS(AFTERTHE 1ST HOUR OF LIFE):
• Tachypnea (>60/min).
• Expiratory grunting (by closure of glottis).
• Sternal and intercostal recession.
• Cyanosis in room air.
These signs must develop before the neonate is 4
hours old and persist beyond 24 hours of age.
Diagnosis: At least 2 of the above signs plus typical
chest x-ray.

18. DIFFERENTIAL DIAGNOSIS:
•Early –onset sepsis.
•Pneumonia
•Cyanotic heart disease (Particularly,
Total Anomalous Pulmonary Venous
Return).
•Transient tachypnoea of newborn.
•Meconium aspiration syndrome.
•Diaphragmatic hernia.

19. INVESTIGATIONS:
Chest x-ray alone almost confirms the diagnosis.
The typical x-ray findings (develop during the 1st
6 hours) are-
•low lung volumes.
•A generalized haziness or reticulogranular
“ground glass” appearance of lung fields,
and when severe, obscuring heart borders.
• An air bronchogram, due to air in the major
bronchi being highlighted against the white
opacified lung.

25. Laboratory studies:
Bloodgas sampling:
Essential in the management of RDS.
pH, Po2, Pco2, HCo3-
(Mixed respiratory-metabolic acidosis)
Sepsis workup:
CBC and Blood culture
(to exclude Early onset neonatal sepsis).

26. Serumglucose: May be high or low.
Serumelectrolytes and calcium:
Should be monitored every 12-24 hours.
Echocardiography:
It is used to confirm the diagnosis of PDA.

27. MANAGEMENT:
Prevention:
• Avoidance of unnecessary or poorly timed early
caesarean section (<39 wk) or induction of labor.
• Appropriate management of high-risk pregnancy
and labor (including administration of antenatal
corticosteroids).
Maternal corticosteroid therapy:
Administration of antenatal corticosteroids to women
before 34 wk of gestation significantly reduces incidence
and mortality of RDS as well as overall neonatal
mortality.

28. It is recommended for all women in preterm
labor who are likely to deliver a fetus within 1
wk.
• Assessment of fetal lungs maturity before
delivery by amniotic fluid indices:
L/S ratio, PG concentration.
• 1st dose of surfactant into the trachea of
symptomatic premature infants immediately after
birth (prophylactic) or during the 1st few hr of life
(early rescue) showed reduced air leak and
mortality from RDS.

29. TREATMENT:
Treatment of infants with RDS is best
carried out in neonatal ICU.
Regulation of temperature:
Scheduled “touch times” to avoid hypothermia
and minimize oxygen consumption.
The infant should be placed in an incubator or
radiant warmer & core temp. maintained
between 36.5 and 37*C.

30. TREATMENT:
Nutritional support:
For the 1st 24 hr, 10% glucose solution with
additional amino acids in extremely premature
infants, should be infused through a peripheral
vein at a rate of 65-75ml/kg/day.

31. TREATMENT:
Oxygentherapy:
Warm humidified oxygen should be provided at a
conc. initially sufficient to keep arterial O2
pressure between 50-70mmHg (91-95%
saturation) in order to maintain normal tissue
oxygenation while minimizing the risk of O2
toxicity.
Oxygen therapy by-
Nasal Cannulae (1-2L/min).
Face Mask (5L/min).

32. TREATMENT:
IndicationOf continuous positive airway pressure(CPAP):
If O2 saturation <85%,
FiO2: 40-70% or greater.
PaO2: <50mmHg.
Continuous Positive Airway Pressure(CPAP)
reduces collapse of surfactant-deficient
alveoli and improves both FRC and
ventilation-perfusion matching.

34. TREATMENT:
 indication ofAssisted mechanical ventilation:
If infant with RDS undergoing CPAP cann’t
keep O2 saturation >90% while breathing 40-
70% O2.
pH: <7.20
PCO2: >60mmHg.
CPAP: 5-10 cm H2O.
Persistent apnea.

37. The goal of mechanical ventilation is to improve
oxygenation and elimination of CO2 without
causing pulmonary injury or oxygen toxicity.
Complication of Mechanical Ventilation:
Pneumothorax and other air leaks.
Asphyxia from obstruction or dislodgement of the
tube.
Bradycardia during intubation or suctioning.
Subsequent development of subglottic stenosis.
Bleeding from trauma during intubation.

38. Surfactant replacement therapy:
Early administration of exogenous surfactant via
endotracheal tube to premature infants
significantly reduces severity of RDS.
It can either be given as rescue treatment in
preterm babies with an evidence of RDS or
prophylactically within 15 minutes of birth to
almost all infants <26 wks of gestation.
Even those babies who have been given
surfactants will need ventilatory support.

39. Surfactantreplacement therapy:
There are 2 types of surfactant:
 Natural Surfactant:
 Beractant (Survanta): (25mg/ml)
Bovine lung extract.
Dose: 4 ml/kg via endotracheal tube q 6 hours; 4 doses.

40. Poractant alfa (Curosurf): (120mg/1.5ml)
Porcine lung extract.
Dose: 2.5 ml/kg via endotracheal tube q 12
hours; 1-2 doses.

41. Natural surfactant preparations are better than
synthetic at reducing pulmonary air leaks.
Natural surfactants are therefore treatment of
choice.
Synthetic Surfactant:
Colfosceril Palmitate (Exosurf) (67.5mg/5ml):
5 ml/kg via endotracheal tube q 12 hours; 2-4
doses.

44. Antibiotictherapy:
Antibiotic coverage with ampicillin and an
aminoglycoside or cefotaxime should be provided.
Correctionof metabolicacidosis
by NaHCO3.
Sedation:
Commonly used to control ventilation in these sick
infants.Morphine, fentanyl or lorazepam may be
used for anagesia as well as sedation.

45. PHARMACOLOGIC THERAPIES-BEYOND SURFACTANT:
Nitric oxide (NO):
Inhaled nitric oxide-a selective pulmonary
vasodilator improves oxygenation in preterm
infants with severe RDS.
Nitric oxide may be a signaling molecule in
parenchymal lung growth and may reduce
lung injury and chronic lung injury.

46. COMPLICATIONS:
Pulmonary:
Air leaks (Pneumothorax,
Pneumomediastinum, Interstitial
emphysema).
Aspiration pneumonia.
Bronchopulmonary dysplasia.
Cardiac:
PDA.
Pneumopericardium.

47. Complications of mechanical
ventilation.
Infection: Septicaemia.
Neurological:
Intraventricular haemorrhage
Retinopathy of prematurity

48. OUTCOME:
Improvement:
Spontaneous diuresis.
Improved blood gas values at lower inspired
oxygen levels and/or lower ventilator support.
Death:
Severe impairment of gas exchange.
Alveolar air leaks (interstitial emphysema,
pneumothorax).
Pulmonary hemorrhage.
IVH.