Anatomic Alterations of the Lungs

Transient tachypnea of the newborn (TTN) (also called type II respiratory distress syndrome and “wet lung” syndrome) was first described in the literature in 1965. Within the first 4 to 6 hours after birth, TTN produces clinical signs very similar to those associated with the early stages of respiratory distress syndrome (see Chapter 34). However, the anatomic alterations of the lungs associated with TTN are much different from the pulmonary pathology seen in respiratory distress syndrome.

As shown in Figure 33-1, the infant with TTN has a delay in the pulmonary fluid absorption by the lymphatic system and pulmonary capillaries. It is thought that this condition results, in part, from the infant’s hypoxemia and inadequate inspiratory effort, producing a delay in clearance of pulmonary fluid. As this condition worsens, the infant develops pulmonary capillary congestion, interstitial edema, decreased lung compliance, decreased tidal volume, and increased dead space. Because the swallowing and cough efforts of infants with TTN are commonly depressed, the clearance of bronchial secretions is compromised. This condition often leads to air trapping and alveolar hyperinflation.

In severe cases, the excessive fluid accumulation throughout the alveolar-capillary interstitial tissue may also compress the bronchial airways. As a general rule, however, the abnormal anatomic alterations of the lungs associated with TTN usually begin to resolve about 48 to 72 hours after birth.

The major pathologic or structural changes associated with TTN are as follows:

Etiology and Epidemiology

TTN affects 1% to 2% of all newborns. Classically, TNN is most often seen in full-term infants. Risk factors include elective cesarean section, excessive administration of fluids to the mother during labor, male gender, and macrosomia (a newborn with excessive birth weight). The infant’s history often includes maternal analgesia or anesthesia during labor and delivery or episodes of intrauterine hypoxia. TTN is also commonly associated with maternal bleeding, maternal diabetes, and prolapsed cord. TTN is occasionally seen in very small infants.

Although the precise mechanism is not known, it is believed that TTN results from a delayed absorption of fetal lung fluid. The delayed absorption of lung fluid is thought to be caused by any condition that increases the central venous pressure, which in turn slows the clearance of lung fluid by the lymphatic system. Infants with TTN are often lethargic at birth, resulting in a depressed cough effort and accumulation of airway secretions and mucus. The typical baby with TTN usually has good Apgar scores at birth. During the next few hours, however, signs of respiratory distress develop. Early clinical manifestations include tachypnea, retractions nasal flaring, grunting, and cyanosis. It is common to see respiratory rates of 80 to 120 breaths/minute. In fact, the rapid and shallow breathing pattern often is considered a hallmark clinical manifestation of TTN. In addition, the infant may demonstrate a barrel chest and coarse breath sounds. Within 24 to 48 hours, the clinical manifestations of respiratory distress usually disappear.