Neonatal Respiratory Distress Syndrome

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Neonatal respiratory distress syndrome (hyaline membrane disease)
The neonatal respiratory distress syndrome (NRDS) is due to deficiency of surfactant in the lungs. It is primarily a disease affecting premature infants, but is also seen in infants born to diabetic mothers, as excess production of insulin by the fetus suppresses surfactant production.

A very common condition, the incidence of NRDS increases with increasing prematurity (20% incidence at 32-36 weeks' gestation; 60% incidence at <28 weeks' gestation).
With development of disease, the chest radiograph shows a 'ground glass' opacity in the lung fields.
The mortality from NRDS is 50% in infants weighing under 1000 g.
The lungs from infants who die from the condition appear airless, dark red and dense.
Depending on the stage of disease, atelectasis, epithelial necrosis, hyaline membranes, and organization may be seen histologically.

There are four main risk factors for development of NRDS.
The immature or damaged lung is unable to make enough surfactant, the lecithin-rich surface-active lipid secreted by Type II pneumocytes.
Normally this reduces surface tension in alveoli and keeps alveoli open. In NRDS, lack of surfactant means that alveoli collapse with microatelectasis.

Hypoxia leads to damage of alveolar lining cells, hypoxia and pulmonary arterial constriction.
Endothelial damage causes plasma to leak into alveoli, being deposited as fibrin.
The fibrin appears as bright, pink-stained membranes lining alveoli, hence the name hyaline membrane disease. The presence of fibrin further impairs gas exchange and makes hypoxia worse.
The process is similar to that in diffuse alveolar damage.
Later, regenerative changes in the lung lead to organization of hyaline membranes and fibrosis.
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