Surfactant deficiency in neonatal respiratory distress syndrome
In newborn respiratory distress syndrome the lungs make insufficient surfactant (a soapy mixture of phospholipids and proteins), so the alveoli collapse and the lungs stiffen.
Remember
A preterm baby, whose lung development is not finished, can make too little surfactant (the earlier the birth, the greater the risk), so the alveoli are hard to open and prone to collapse. Glucocorticoids (steroids) given to the mother before a preterm birth speed up surfactant production.
Memory aid
no surfactant means sticky sacs, like trying to blow up a wet balloon
Picture the alveoli as sticky sacs that are hard to inflate when surfactant is missing.
Each alveolus is lined by a thin film of water that pulls inwards. This effect is called surface tension, and it tends to make the air sac collapse and hard to inflate.
Surfactant is a soapy mixture of phospholipids (fats) and proteins. It is made by type II pneumocytes, the cells in the alveolar wall that secrete it. Surfactant breaks up the inward pull, so the alveoli stay open when a breath ends and take less pressure to inflate.
Lung development is not finished in a preterm baby. Surfactant production starts at around 24 to 28 weeks of pregnancy, but most babies do not make enough to breathe normally until about 34 weeks. The earlier a baby is born, the greater the risk of not having enough surfactant.
Without enough surfactant, the alveoli become stiff and sticky. Many collapse (atelectasis), a much higher pressure is needed to open them, and the baby has to work very hard to breathe. Blood passing the collapsed areas is not oxygenated, so oxygen levels fall. The baby shows fast breathing (tachypnoea), a grunting noise, recession (the skin between and below the ribs sucking in as the baby strains to breathe) and, if oxygen levels fall, blue discolouration (cyanosis).
If preterm birth is threatened, the mother may be given glucocorticoids (steroids). These stimulate surfactant production in the baby before birth and improve breathing afterwards. Artificial surfactant can also be given to the baby.
Key facts
- Cause
- immature type II pneumocytes make too little surfactant, so surface tension is high.
- Action of surfactant
- it lowers surface tension, so the alveoli stay open at the end of a breath and need less pressure to inflate.
- Timing
- surfactant production starts at around 24 to 28 weeks of pregnancy, but most babies do not make enough to breathe normally until about 34 weeks.
- Signs
- fast breathing, grunting and recession soon after birth.
- Steroids before birth
- glucocorticoids given to the mother before a preterm birth speed up surfactant production.
- Treatment
- artificial surfactant can be given to the baby.
Exam traps
- Mucus plugging of the small airways is a feature of conditions such as cystic fibrosis or asthma. It is not the main problem in newborn respiratory distress syndrome, where the air sacs are stiff and prone to collapse.
- Persistent pulmonary hypertension of the newborn keeps pulmonary vascular resistance (the resistance to blood flow through the lung's blood vessels) high and cuts blood flow through the lungs. It is a different condition, and in respiratory distress syndrome the low oxygen follows from collapsed alveoli.
- Delayed absorption of foetal lung fluid causes transient tachypnoea of the newborn (fast breathing that usually settles by itself over a few days). It is a separate condition from respiratory distress syndrome.
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