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Neonatal respiratory distress syndrome

Why a premature newborn’s lungs lack surfactant, how collapsing alveoli and hyaline membranes cause shunt and exhausting breathing, how antenatal steroids, surfactant and CPAP act, and why complications reach the lungs, eyes and heart.

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  • 5 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Describe how type II pneumocytes make surfactant, when its production matures before birth and how the lecithin–sphingomyelin ratio reflected it.
  • Explain why prematurity, maternal diabetes and birth without labour leave a newborn short of surfactant.
  • Relate alveolar collapse, hyaline membranes and shunting to grunting, recession, cyanosis and the ground-glass X-ray with air bronchograms.
  • Explain how bronchopulmonary dysplasia, retinopathy of prematurity and a patent ductus arteriosus follow from immaturity and its treatment.
  • Tell neonatal RDS apart from transient tachypnoea, meconium aspiration and congenital pneumonia, and explain how antenatal glucocorticoids, surfactant and CPAP act on the mechanism.

What it is

Neonatal respiratory distress syndrome (RDS) is breathing failure in a newborn, usually premature, whose lungs make too little surfactant: alveoli collapse at the end of each breath, the injured lining forms hyaline membranes, and the baby works ever harder to breathe from minutes to hours after birth. Rarer forms in term babies follow maternal diabetes or inherited defects of surfactant.

3 types to tell apart
Surfactant deficiency of prematurity
By far the commonest: type II pneumocytes are too immature to make enough surfactant. It improves over days as they mature.
Inherited surfactant dysfunction
Rare variants in the genes for surfactant protein B or C, or for the lipid transporter ABCA3, in term babies: surfactant is made but does not work, so the disease does not resolve with maturation and can be severe and lasting.
Secondary surfactant inactivation
Surfactant that was adequate is inactivated after birth by meconium, blood, oedema fluid or pneumonia; the cause of the lung injury, not immaturity, drives the disease.

Normal function

Surfactant and the first breaths

Each is lined by a thin film of water whose surface tension pulls it inwards, and by the law of Laplace the pull matters most in the smallest alveoli. counter it with surfactant, a film made mostly of phospholipid, chiefly dipalmitoyl-phosphatidylcholine (a lecithin), with four surfactant proteins (SP-A to SP-D). The cells store it in lamellar bodies and release it onto the alveolar surface, where it lowers surface tension most as the alveolus shrinks. Alveoli therefore stay partly open at the end of breathing out, and the lung keeps a resting volume of air (the functional residual capacity).

Surfactant is one of the last things the fetal lung learns to make. Type II cells differentiate around 20 weeks and secrete a little; output rises through the third trimester and is usually enough only from about 34–36 weeks. Fetal cortisol, which surges late in pregnancy, is the main signal that speeds this maturation; thyroid hormones help, while high fetal insulin slows it. Fetal lung fluid flows out into the amniotic fluid, so the rising ratio of lecithin to sphingomyelin there (the L/S ratio) was once used to measure lung maturity.

Before birth the airspaces are full of fluid. Around labour, stress hormones switch the airway lining from secreting chloride to absorbing sodium through epithelial sodium channels, and water follows. The first breaths need a high pressure to push air into fluid-filled, closed airspaces; with enough surfactant the newly opened alveoli stay partly open after each breath, so the breaths that follow take far less effort.

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