General pathology · Paediatric pathology
Neonatal respiratory distress syndrome: surfactant and hyaline membranes !
- Mechanism
The preterm lung lacks enough surfactant; the alveoli collapse on breathing out and the baby tires from the effort of breathing.
Updated 2026-11-01
What it is
Respiratory distress syndrome of the newborn (hyaline membrane disease) is caused by surfactant deficiency in an immature lung. It is the commonest cause of respiratory failure in the preterm infant and becomes more frequent the lower the gestational age. Antenatal corticosteroids and exogenous surfactant have changed its outlook.
Structure
- Gross: lungs of normal size but solid, airless and reddish-purple, liver-like; they sink in water.
- Microscopy: collapsed alveoli alternating with dilated alveolar ducts lined by eosinophilic hyaline membranes.
- The membranes are made of fibrin and debris of epithelial cells; neutrophils are scarce.
- If the baby survives several days, signs of repair appear and type II pneumocytes proliferate.
Step by step
- Without enough surfactant, surface tension in the alveolus is high.
- By Laplace's law, small alveoli collapse at the end of expiration (atelectasis).
- Each breath must reopen collapsed alveoli: the work of breathing rises and the baby tires.
- Hypoxaemia and acidosis follow; they injure alveolar endothelium and epithelium and further slow surfactant synthesis.
- A protein-rich, fibrin-rich exudate leaks from damaged capillaries and, with debris of necrotic cells, forms hyaline membranes.
- The membranes line ducts and alveoli and block gas exchange even further.
Clinical notes
- Minutes to hours after birth: tachypnoea, expiratory grunting, nasal flaring, retractions and cyanosis.
- Treatment is continuous positive airway pressure and, when needed, exogenous surfactant through the endotracheal tube.
In the lab
- Before birth, the lecithin/sphingomyelin ratio in amniotic fluid estimates lung maturity; a ratio of 2 or more suggests maturity.
- Phosphatidylglycerol in amniotic fluid also indicates lung maturity.
- Arterial blood gases: hypoxaemia with respiratory and metabolic acidosis.
Test yourself
Think of the answer, then tap the question to see it.
Which cells produce pulmonary surfactant?
Type II pneumocytes, which store it in lamellar bodies.
Why is the infant of a diabetic mother at higher risk of respiratory distress syndrome?
Because fetal hyperinsulinaemia inhibits surfactant synthesis and delays lung maturation.
What are hyaline membranes made of?
Fibrin and other plasma proteins mixed with debris of necrotic epithelial cells.
Which antenatal measure lowers the risk of this syndrome when preterm birth is expected?
Antenatal corticosteroids given to the mother, which speed up fetal lung maturation.
Related
- Prematurity and fetal growth restriction
- Necrotizing enterocolitis: why the premature gut is vulnerable
Related conditions
- Neonatal respiratory distress syndrome (hyaline membrane disease)
- Prematurity and its complications
- Bronchopulmonary dysplasia
- Retinopathy of prematurity
- Gestational diabetes mellitus
- Transient tachypnea of the newborn
- Patent ductus arteriosus
- Intraventricular haemorrhage of prematurity
- Meconium aspiration syndrome
Elsewhere in DurgiPedia
- Surface tension, surfactant and Laplace's law
- Lung and chest wall compliance
- Surfactant and fetal lung maturity
- Lung development: the five stages
- The alveolus: type I and II pneumocytes, surfactant, the blood–air barrier
In Pharmacology
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Neonatal respiratory distress syndrome: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Preterm birth (World Health Organization, 2026).
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Representative model, for educational purposes only.