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Neonatal respiratory distress syndrome is the most common cause of respiratory failure in the first days after birth, occurring in 1% to 2% of newborn infants. Until about 25 years ago, approximately 50% of infants with this condition died.1 Over the last three decades, improved methods of treatment have markedly reduced mortality, and the majority now survive.

Hyaline membrane disease (HMD) occurs mainly in prematurely born infants and is more common in whites than in blacks. It develops when an infant attempts to ventilate an immature lung with small respiratory units that inflate with difficulty and do not remain gas-filled between respiratory efforts. This behavior is due to rudimentary alveolarization of the lung and an inadequate amount of pulmonary surface-active material or surfactant. When surfactant is absent, the surface tension at the interface between alveolar gas and the alveolar wall is high, and the lung tends to become progressively atelectatic. This causes increasingly labored breathing and cyanosis as the volume of the lung decreases and the infant hypoventilates.

It appears to take only 1 to 2 days following birth for an immature lung to mature as it responds to the surge of glucocorticoids and β-adrenergic compounds released by the stress of delivery. Glucocorticoids increase surfactant synthesis, and β-adrenergic stimulation promotes its secretion. Also, in 1 to 2 days, structural changes occur in the lung. Thin-walled respiratory units develop, and the number of capillaries increases. With these changes, the signs and symptoms of respiratory distress subside. However, during this brief interval, lung damage may occur from the combined effects of pulmonary edema, ischemia, pulmonary air leaks, oxygen toxicity, and injury from barotrauma if high pressures are used to mechanically assist ventilation. As a consequence, HMD can result in chronic lung disease that may persist for weeks or months.

At postmortem examination, the lungs from infants with neonatal respiratory distress are firm and airless. Atelectasis is striking on gross inspection; when the lungs are fixed in inflation, only the airways and a few alveolar ducts are air filled (Fig. 54-1). Diffuse atelectasis and dilated terminal bronchioles and alveolar ducts lined with a homogenous hyaline-staining material characterize the microscopic picture (Fig. 54-2). The hyaline membranes are plasma clots containing fibrin, other plasma constituents, and cellular debris. The small pulmonary arterioles appear constricted. There is congestion of pulmonary capillaries and veins and an increase in pulmonary water with dilation of the lymphatics.

Figure 54-1.

A. Longitudinal section of the left lung of a 1560-g infant, born at 30 weeks’ gestation, who died at 2.5 days of age from neonatal respiratory distress syndrome. The lung was expanded with air to a pressure of 40 cm H2O, then deflated to 10 cm H2O and fixed with the bronchus clamped. The airways are distended, and a few of the respiratory bronchioles are overinflated. ...

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