Conditions · Pediatrics and neonatology
Neonatal respiratory distress syndrome (hyaline membrane disease) !
A breathing problem of premature newborns whose lungs lack surfactant, so the air sacs collapse. It starts within hours of birth.
Updated 2026-11-01
Structures involved
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- Right lower lobe
- Left lower lobe
- Right upper lobe
- Left upper lobe
- Trachea
- Main bronchi
- Pleura
- Ligamentum arteriosum
In embryology
- Fetal lung, kidney and brain maturation: what preterm birth interrupts
- Patent ductus arteriosus
- Lung development: the five stages
- Surfactant and fetal lung maturity
- Maternal diabetes and obesity as teratogens
In the clinical exam
Why it happens
- Neonatal respiratory distress syndrome: surfactant and hyaline membranes
- Prematurity and fetal growth restriction
- Surface tension, surfactant and Laplace's law
- Lung and chest wall compliance
- The alveolus: type I and II pneumocytes, surfactant, the blood–air barrier
What it is
Acute respiratory failure of the newborn, mainly the preterm infant, caused by a deficiency of pulmonary surfactant that lets the alveoli collapse at the end of each breath. It is the most common cause of respiratory distress in premature babies.
Who gets it
Its frequency rises sharply as gestational age falls: it affects most infants born before about 28 weeks and is uncommon at term. In Colombia and Latin America it is a leading reason for neonatal intensive care admission, and access to antenatal corticosteroids, surfactant and non-invasive ventilation shapes outcomes.
Causes
- Deficient production of surfactant by immature type II pneumocytes
- Structural immaturity of the lungs (few alveoli, thick air–blood barrier)
- Less often, inactivation of surfactant or genetic surfactant protein defects in term infants
Risk factors
- Preterm birth, especially before 32 weeks
- Infant of a diabetic mother (insulin delays surfactant maturation)
- Male sex and white ethnicity
- Caesarean delivery without labour and second-born twin
- Perinatal asphyxia and hypothermia
- No antenatal corticosteroids before a preterm birth
Pathophysiology
Without surfactant, surface tension in the alveoli is high, so they collapse on expiration (diffuse atelectasis) and lung compliance falls. Collapsed alveoli are perfused but not ventilated, causing intrapulmonary shunting, hypoxaemia and hypercapnia. Injured epithelium leaks protein-rich fluid that forms eosinophilic hyaline membranes lining the airspaces.
Classification
- Mild: oxygen or non-invasive support (CPAP) is enough
- Moderate to severe: rising oxygen need on CPAP, needing surfactant and often mechanical ventilation
Symptoms and signs
- Onset within minutes to hours after birth
- Tachypnoea (fast breathing)
- Expiratory grunting
- Nasal flaring and intercostal and subcostal retractions
- Cyanosis in room air
- Diminished breath sounds; worsening over the first one to two days, then gradual improvement
Diagnosis
- Clinical
- A preterm infant with respiratory distress starting soon after birth; severity is followed with breathing effort and the oxygen needed to keep target saturation.
- Tests
- Pulse oximetry and blood gases (hypoxaemia, hypercapnia, respiratory or mixed acidosis). Blood culture and inflammatory markers to look for sepsis. Glucose and temperature monitoring.
- Imaging
- Chest X-ray: low lung volumes with a diffuse fine reticulogranular (ground-glass) pattern and air bronchograms; in severe cases a «white-out». Lung ultrasound is increasingly used at the bedside.
Differential diagnosis
- Transient tachypnoea of the newborn (term, after caesarean, quick recovery)
- Neonatal pneumonia or early-onset sepsis (often group B streptococcus)
- Meconium aspiration syndrome (term or post-term, meconium-stained fluid)
- Pneumothorax
- Cyanotic congenital heart disease and persistent pulmonary hypertension of the newborn
Goal of treatment
Keep the alveoli open and oxygenation and ventilation in a safe range with the least invasive support, while supporting temperature, fluids and nutrition until the lungs make their own surfactant.
Treatment
- Acute
- Early continuous positive airway pressure (CPAP) from the delivery room is the first-line respiratory support; oxygen is titrated to target saturations to avoid both hypoxia and hyperoxia.
- Medical
- Exogenous surfactant given into the trachea, by intubation or less invasive techniques, when oxygen needs rise on CPAP; mechanical ventilation if CPAP fails. Antibiotics are often started until sepsis is excluded.
- Follow-up
- Nursing care: continuous oximetry and heart rate, blood gases, thermoneutral environment, minimal handling, careful fluids and glucose, nasal and skin care around the interface, and watching for pneumothorax.
- Medical
- Prevention before birth: antenatal corticosteroids to the mother at risk of preterm delivery speed lung maturation and reduce the incidence and severity of RDS.
Complications
- Air leaks: pneumothorax and pulmonary interstitial emphysema
- Bronchopulmonary dysplasia (chronic lung disease of prematurity)
- Intraventricular haemorrhage
- Patent ductus arteriosus
- Retinopathy of prematurity linked to oxygen exposure
Prognosis
With antenatal corticosteroids, CPAP and surfactant most infants recover within days; risk of death and chronic lung disease is highest in the most premature babies.
Prevention
- Antenatal corticosteroids when preterm birth is expected
- Prevention of preterm birth through good prenatal care
- Good glycaemic control in pregnant women with diabetes
- Avoiding elective caesarean before 39 weeks without a medical reason
Test yourself
Think of the answer, then tap the question to see it.
What is the basic defect in neonatal respiratory distress syndrome?
Deficiency of pulmonary surfactant from immature type II pneumocytes, so alveoli collapse at end-expiration.
What is the classic chest X-ray of neonatal RDS?
Low lung volumes with a diffuse reticulogranular (ground-glass) pattern and air bronchograms.
Which antenatal measure reduces the risk of RDS in an expected preterm birth?
Corticosteroids given to the mother before delivery to accelerate fetal lung maturation.
Why does an infant of a diabetic mother have higher risk of RDS?
Fetal hyperinsulinaemia delays surfactant production even at later gestational ages.
What is the first-line respiratory support for a preterm infant with RDS?
Early CPAP, with surfactant added if oxygen needs rise.
Related conditions
- Prematurity and its complications
- Neonatal sepsis
- Pneumothorax
- Patent ductus arteriosus
- Neonatal hypoglycaemia (including infant of a diabetic mother)
- Acute respiratory distress syndrome (ARDS)
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Neonatal respiratory distress syndrome (MedlinePlus (U.S. National Library of Medicine), 2024).
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Representative model, for educational purposes only.
