Neonatal Respiratory Distress Syndrome (NRDS) is a condition in infants that occurs when the lungs are not fully developed. You may also hear it referred to as Hyaline Membrane Disease or Infant Respiratory Distress Syndrome.

This study guide was created to provide you with an overview of this topic. It contains practice questions for your benefit as well. So if you’re ready, let’s get started.

What is Neonatal Respiratory Distress Syndrome?

Neonatal Respiratory Distress Syndrome is a disease that is common in premature infants when they were born with lungs that aren’t fully developed.

The infant may show signs of respiratory distress, including:

  • Grunting
  • Retractions
  • Rapid, shallow breathing
  • Nasal flaring
  • Apnea
  • Tachycardia

Infant Respiratory Distress Syndrome is usually associated with decreased surfactant production at birth which results in severe hypoxemia. It should be treated with oxygen therapy, surfactant replacement therapy, and possibly mechanical ventilation.

Neonatal Respiratory Distress Syndrome Practice Questions:

1. What is characterized by the severe impairment of respiratory function?
Respiratory Distress Syndrome (RDS).

2. What is RDS caused by?
The underdevelopment of the lungs.

3. What is the reason for underdeveloped lungs?
The lack of surfactant.

4. In the early 20th century, RDS was characterized as what?
Hyaline membrane disease.

5. What is hyaline membrane disease?
It was a unique cellar character of the lung and thought to be a rare form of pneumonia.

6. What causes low alveolar compliance?
A decrease in surfactant.

7. What is the biggest problem with RDS?
Surfactant deficiency.

8. What causes difficulty in improving ventilation with poor maintenance of FRC?
Over ally compliant chest wall.

9. What worsens gas exchange along with a thick alveolar-capillary (A-C) membrane?
Increased distance between alveolar spaces and capillaries.

10. What is known as lung tissue underdevelopment?
Lung hypoplasia.

11. What is the primary cause of respiratory distress?
Lung hypoplasia.

12. What is a chemically complex agent whose main function is to stabilize the air-liquid interface of the alveoli and bronchiole and to lower surface tension?

13. What improves lung compliance?
Lower alveolar surface tension.

14. What will happen if you have improved lung compliance?
It will decrease the work of breathing.

15. What are surfactant molecules exerted and made of?
Alveolar type 2 cells.

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16. At what gestational week will surfactant appear?

17. Which cells in the alveoli produce surfactant?
Type II Pneumocytes.

18. What does surfactant do?
It decreases the alveolar surface tension. It increases lung compliance, and thus decreases the work of breathing.

19. What is the cause of Neonatal Respiratory Distress Syndrome?
Pathology is due to a lack of surfactant due to the immaturity of the neonate’s lungs. This leads to an increase in surface tension, decreased compliance, and increased work of breathing and alveolar collapse.

20. What will a Neonatal Respiratory Distress Syndrome chest x-ray show?
You will likely see diffuse interstitial infiltrates.

21. Who is at risk for neonatal respiratory distress syndrome?
Pre-term infants (born before <35 weeks).

22. What are some other risk factors for Neonatal Respiratory Distress Syndrome?
Maternal Diabetes and C-section.

23. During what stage of lung development do pneumocytes develop?
The saccular stage (week 26 to birth).

24. How do we test a pregnant mother to see if her baby’s lungs have reached maturity?
Look at the L:S ratio in the amniotic fluid. Both lecithin and sphingomyelin are lipids in surfactant- mostly lecithin that gives surfactant its qualities.

25. What lecithin molecule is most important in surfactant?
Dipalmitoyl phosphatidylcholine.

26. In NRDS, what is the Lecithin:Sphingomyelin ratio?
Less than 1.5. A ratio of greater than 2.0 indicates a low risk for NRDS.

27. What happens to the oxygen tension in NRDS?
Oxygen tension is decreased.

28. Persistently low oxygen tension within the blood can result in an increased risk for what cardiac complication?
Patent Ductus Arteriosus.

29. What is the risk of decreased oxygen tension?
Necrotizing enterocolitis.

30. When is poor survival likely in neonates?
Born before less than 24 weeks.

31. What are some interventions that can improve survival in neonates?
Administration of maternal steroids before birth to accelerate lung maturation, Administration of artificial and exogenous surfactant after birth, and CPAP/intubation with oxygen support.

32. What are the complications of too much oxygen during the perinatal period?
Retinopathy which is more involved with O2 tension- once the O2 is removed, the relative hypoxia in the eye causes blood vessel overgrowth- which can result in blindness. Intraventricular Hemorrhage and Bronchopulmonary Dysplasia are also complications of too much oxygen.

33. Why does RDS happen?
It occurs because of a deficiency of alveolar surfactant, and is mainly seen in preemies. It leads to alveolar collapse and reinflation with each breath – exhausts the baby and causes respiratory failure.

34. What signs can result from hypoxia in RDS?
Reduced cardiac output, Hypotension, Acidosis, Renal failure, and Death.

35. What are the signs of RDS?
Respiratory distress shortly after birth (in the first 4 hours), and Tachypnoea (>60/min), grunting, nasal flaring, intercostal recession, cyanosis.

36. What would you see on a CXR in RDS?
Air bronchograms and Diffuse granular patterns (ground glass appearance).

37. What are the differentials for RDS?
Transient tachypnea of the Newborn (due to excess lung fluid, normally resolves after 24h), Meconium aspiration, Congenital pneumonia (group B strep), Tracheoesophageal fistula, suspect if respiratory problems after feeds, and Congenital lung abnormalities.

38. How to prevent RDS?
Betamethasone or dexamethasone to all women at risk of premature delivery from 23-35 weeks.

39. How to treat RDS?
Delay cord clamping by 3 minutes in order to promote placenta-fetal transfusion. Provide oxygen via the oxygen/air blender at the lowest possible concentration. If the infant is breathing spontaneously, stabilize with CPAP. Provide surfactant if needed.

40. How would you manage a baby born before 26 weeks in terms of RDS?
Intubate and provide prophylactic surfactant via the ET tube with ongoing doses if needed.

41. What are the poor prognostic signs in RDS?
Persistent pulmonary hypertension, Large right to left shunt via ductus, and Increased dead space fraction in lungs.

42. What is the prognosis if hypoxia worsens despite everything?
Death may occur for the infant. 

43. What is bronchopulmonary dysplasia?
It is a chronic lung disease in which premature infants are treated with supplemental oxygen and may require long-term oxygen therapy. It is more common in babies who are on prolonged mechanical ventilation for RDS. Due to prolonged high oxygen causing necrotizing bronchitis and alveolar septal injury with inflammation and scarring.

44. Which group at most risk of BPD?
Complicates ventilation for RDS in 40% of babies with birth weight less than 1kg.

45. What causes BPD?
Barotrauma and oxygen toxicity. It can also be surfactant related.

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46. What is seen while assessing for BPD?
CXR shows hyperinflation, rounded radiolucent areas, alternating with thin, denser lines.

47. What are early signs of BPD?
Reduced IQ, cerebral palsy, feeding problems, oxygen desaturation during feeds.

48. What are late signs of BPD?
By adolescence/early adulthood the main changes remaining are airways obstruction, airway hyperactivity, and hyperinflation.

49. How can BPD be prevented?
Steroids (ante and postnatally), Surfactant, and High-calorie feeding.

50. When do you suspect pulmonary hypoplasia?
All infants with persistent neonatal tachypnoea and feeding difficulties, especially if prenatal oligohydramnios. In a diaphragmatic hernia, it is due to an SOL. It can also be due to cystic adenomatoid malformations.

51. What is the number one reason for admission to the NICU?
Respiratory distress, pulmonary is the main cause, and non-pulmonary is CV.

52. What must we do before we determine the cause of respiratory distress?
Stabilize the infant. We don’t often know the cause because we treat all the babies the same.

53. What are the 4 most common causes of respiratory distress?
Respiratory distress syndrome (RDS)– like her case, Transient Tachypnea of the Newborn, Pneumonia/Aspiration syndromes, and Pneumothorax.

54. What is the most common pneumonia?
Perinatal pneumonia which is acquired in utero. Chlamydia pneumonia which is present later in life, 4-12 weeks, staccato cough, but no wheezing and fever, chest x-ray has bilateral infiltrates, eosinophilia, get macrolides for treatment.

55. How do we assess fetal lung maturity?
Amniocentesis (check the fluid in utero, only done in high risk), Lecithin, and phospholipid.

56. What is a more specific indicator of lung maturity in babies?
Saturated phosphatidylcholine or phosphatidylglycerol.

57. When are mature alveoli present?
36 weeks.

58. What helps the neonates to get a good first breath?
Vaginal delivery that causes intermittent compression of the thorax and helps with the removal of lung fluid. Surfactant helps to decrease surface tension which lowers the pressure needed to open the alveoli.

59. What are the 6 parts of the definition of respiratory distress?
Tachypnea (over 60 breaths/minute), grunting (stints alveoli open), nasal flaring, retractions,
Cyanosis, and decreased breath sounds.

60. What are the tests that must be done for respiratory distress?
Chest x-ray, serum glucose, blood gas, CBC with differential, CRP, blood culture, obtain maternal history (diabetes, premature, ultrasound abnormalities), details of labor and delivery (where was placenta).

61. What should you rule out with respiratory distress?
Cardiac disease; via murmurs, gallops, poor capillary refill, weak/delayed pulses, single heart sound, central cyanosis, hyperactive precordium.

62. What is respiratory distress syndrome formerly known as?
Hyaline membrane disease.

63. When do we most often see respiratory distress syndrome?
60-80% of babies less than 28 weeks.

64. What are the causes of respiratory distress syndrome?
Surfactant deficiency which causes an increase in surface tension and alveolar collapse, they cannot establish and maintain an FRC (functional residual capacity) and then the lungs become atelectatic. Classic chest x-ray appearance for respiratory distress syndrome ground glass appearance, diminished lung volume, air bronchograms.

65. Which disease has a ground glass appearance in the x-ray?
Respiratory distress syndrome.

66. What is the ABG of a child with respiratory distress syndrome?
Hypoxemia, hypercapnia, and metabolic acidosis.

67. When do symptoms of respiratory distress syndrome appear?
Within minutes of birth, worsens over time, if apnea and irregular breathing treat them.

68. How do we treat respiratory distress syndrome?
IV fluids and keep the temperature within the normal range, keep oxygen between 85% and 95%, CPAP, endotracheal intubation, and surfactant delivery.

69. What is surfactant replacement therapy?
It can have synthetic or natural, give as soon as you can after they are born and improves chest x-ray, give 3 doses usually.

70. How can we prevent respiratory distress syndrome?
Antenatal corticosteroids 24-34 weeks in preterm labor; speeds up fetal lung maturation
should also avoid c-section if unnecessary. Give prophylactic doses of surfactant to premature infants.

71. What is the biggest complication of respiratory distress syndrome?
Chronic lung disease (bronchopulmonary dysplasia).

72. What is the definition of bronchopulmonary dysplasia?
A breathing condition in infants where the lungs are not fully developed.

73. What are the risk factors of transient tachypnea of the newborn?
Male gender, C-section, perinatal asphyxia, umbilical cord prolapse, maternal asthma, diabetes, and anesthesia in delivery.

74. What is the transient tachypnea of the newborn pathogenesis?
Early-onset of tachypnea, occasional retractions, grunting, cyanosis; cyanosis fixed if given a bit of oxygen; chest clear, fixed in 1-5 days with minimal intervention.

75. What is the key x-ray finding with transient tachypnea of the newborn?
Fluid in the interlobar fissures, also increases interstitial markings.

76. What are the treatments for transient tachypnea of the newborn?
Supportive, sometimes CPAP, some oxygen, and NPO IV fluids.

77. What is meconium aspiration syndrome?
Respiratory distress in infants delivered through meconium-stained amniotic fluid, no other sources of distress.

78. Meconium passing is usually a sign of what?
Fetal distress, also often seen in post-term babies.

79. What is meconium?
It is the first stool produced by an infant and is toxic to the lungs.

80. What is a major problem with meconium?
It displaces surfactant; also activates complement which leads to inflammation.

81. When do the meconium aspiration syndrome kids present?
First 12 hours of life, from thick particulate meconium aspirated into the lungs, on the first breath or in utero.

82. What do you hear on auscultation with meconium aspiration syndrome?
Crackles and rhonchi.

83. What is the specific symptom of meconium aspiration syndrome?
Barrel chest from overdistension and obstruction.

84. What is the chest x-ray meconium aspiration syndrome?
Patchy atelectasis, areas of over inflation which severe can have total white out of the lungs.

85. What is the treatment for meconium aspiration syndrome?
Supportive care get surfactant to overcome the surfactant displacement. Sometimes get ECMO, inhaled nitric oxide.

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86. What is the purpose of inhaled nitric oxide with meconium aspiration syndrome?
Vasodilates the pulmonary capillaries to help alleviate pulmonary hypertension, causes an improved ventilation-perfusion match and decreases the need for ECMO

87. When do we use ECMO?
If a kid has meconium aspiration syndrome that fails inhaled nitric oxide.

88. What is used in the prevention of meconium aspiration syndrome?
Prompt delivery is the key. Now, it is not required to intubate if meconium is present, we treat them like other babies and check.

89. What is a major complication of meconium aspiration syndrome?
Persistent pulmonary hypertension of the newborn.

90. What is the persistent pulmonary hypertension of the newborn?
inadequate ventilation that leads to impaired pulmonary transition; causes the release of pulmonary vasoconstrictors and this leads to pulmonary hypertension.

91. What is the cause of respiratory distress syndrome?
Surfactant deficiency.

92. What is the cause of transient tachypnea of the newborn?
Retained renal fluid.

93. What causes meconium aspiration syndrome?
Toxic properties of meconium on the lungs.

94. A radiograph that reveals increased interstitial markings with fluid in the interlobar fissures in an infant who has respiratory distress is most likely to represent?
Transient tachypnea of the newborn

95. The most likely diagnosis associated with the radiographic findings of a diffuse ground-glass appearance of the parenchyma in an infant who has respiratory distress is:
Hyaline membrane disease/RDS.

96. What is sudden infant death syndrome?
Sudden unexplained death before 1 year of age, usually occurs in a previously healthy infant and the cause of death remains unexplained.

97. SIDS is more likely to occur in which infants?
Male infants.

98. What are the types of surfactant?
Survanta, Curosurf, and Infasurf.

99. Can a high-flow nasal cannula be used to treat Infant Respiratory Distress Syndrome?
Yes, at 1-6 L/min.

100. Should PEEP be used to treat Infant Respiratory Distress Syndrome?
Yes, PEEP will likely be necessary when severe hypoxemia is present.

Final Thoughts

So there you have it. That wraps up our study guide on Neonatal Respiratory Distress Syndrome. When an infant is born with low surfactant production and underdeveloped lungs, this is a very serious condition.

As a Respiratory Therapist, it’s important to know and understand the proper treatment modalities. Hopefully, this study guide can help you learn the information that you need to know. Thanks for reading and as always, breathe easy my friend.

Medical Disclaimer: This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Please consult with your physician with any questions that you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you read in this article.


The following are the sources that were used while doing research for this article:

  • Faarc, Kacmarek Robert PhD Rrt, et al. Egan’s Fundamentals of Respiratory Care. 12th ed., Mosby, 2020. [Link]
  • Rrt, Des Terry Jardins MEd, and Burton George Md Facp Fccp Faarc. Clinical Manifestations and Assessment of Respiratory Disease. 8th ed., Mosby, 2019. [Link]
  • Faarc, Walsh Brian PhD Rrt-Nps Rrt-Accs Rpft. Neonatal and Pediatric Respiratory Care. 5th ed., Saunders, 2018. [Link]
  • “Neonatal Respiratory Distress Syndrome: Tackling A Worldwide Problem.” National Center for Biotechnology Information, Jan. 2019,
  • “Respiratory Distress in the Newborn.” National Center for Biotechnology Information, Oct. 2014,
  • “Respiratory Distress in the Neonate: Case Definition & Guidelines for Data Collection, Analysis, and Presentation of Maternal Immunization Safety Data.” National Center for Biotechnology Information, 4 Dec. 2017,

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