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Neonatal respiratory distress syndrome (RDS) is a problem most often seen in preterm infants due to a developmental deficiency in pulmonary surfactant. However, infants of mothers with gestational diabetes may develop RDS even born near term. Surfactant production by type 2 alveolar pneumocytes occurs predominantly after 32 weeks of gestation. If surfactant is inadequate, hyaline membranes form in the distal bronchioles and alveoli, leading to respiratory insufficiency. The severity of RDS depends upon with the degree of pulmonary immaturity of the lungs and may be worsened by concomitant factors such as infection or oligohydramnios.


The cardiopulmonary system of the neonate is driven by the need to deliver sufficient oxygen to maintain a high metabolic rate. The normal oxygen consumption of a neonate is approximately 5–8 mL/kg/min, which is about three times that of an adult. Due to this high oxygen consumption, the neonate will suffer from rapid decreases in arterial oxygen partial pressure (PaO2) during periods of inadequate ventilation.

Surfactant is a phospholipid that coats the surface of alveoli and reduces its tension. Loss of pulmonary surfactant leads to progressive alveolar collapse because of the higher inspiratory pressures required to overcome the stiffer alveoli (Figure 143-1). In accordance with the law of Laplace (P = 2T/R), the increased surface tension means that greater pressure is need to keep the alveolus open, especially at end-expiration when the radius is small. Atelectasis in neonates may also be caused by anatomic forces that decrease lung volume. The relatively large abdomen in a neonate displaces the diaphragm in a cephalad direction which further increases the work of breathing. Neonates with RDS also develop pulmonary edema when plasma proteins cross into the alveoli followed by intravascular water.

FIGURE 143-1

Pressure–volume relationships for inflation and deflation of surfactant-deficient and surfactant-treated preterm rabbit lungs. (Reproduced with permission from Jobe AH. The developmental biology of the lung. In: Fanaroff AA, Martin RJ, eds. Neonatal–Perinatal Medicine: Diseases of the Fetus and Infant. 6th ed. Mosby, 1997.)

As a result of these changes, pulmonary compliance decreases, airway resistance increases, and atelectasis results. Ultimately, the shunting of blood through the atelectatic, nonventilated lung leads to systemic hypoxemia, reduced tissue oxygen delivery, and acidosis. Poor peripheral circulation and systemic hypotension may also be evident.


The differential diagnosis for respiratory insufficiency in the newborn includes RDS, sepsis, pneumonia, meconium aspiration, pneumothorax, persistent fetal circulation, heart failure, and malformations involving thoracic structures such as diaphragmatic hernia.

Signs and Symptoms at Birth

  • Hypoxemia

  • Labored breathing

  • Grunting (prevents end-expiratory alveolar collapse)

  • Nasal flaring

  • Chest retractions

  • Tachypnea

  • Poor peripheral circulation

Chest Radiograph

  • Decreased ...

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