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The clinical syndrome of transient tachypnea of the newborn (TTN) is caused by persistence of fetal lung fluid in the neonate. Other terms for this syndrome include wet lung disease, transient respiratory distress of the newborn, and neonatal retained fluid syndrome. Transient tachypnea is the most common of the various causes of respiratory distress in term newborns (Table 2-1).1 Factors that are associated with an increased risk for transient tachypnea include prolonged labor, cesarean section, narcotic depression, maternal asthma, and maternal diabetes.2,3 Typically, the infant is clinically normal immediately after delivery, but becomes tachypneic over the next few hours. Despite the signs of mild to moderate respiratory distress, there is usually normal oxygenation. As the name indicates, TTN is typically a self-limited process.

Table 2–1.Causes of Tachypnea in the Neonate

In the fetus, lung fluid is produced by type II pneumocytes. This fluid is cleared from the neonatal lung by capillary resorption, lymphatic resorption, and expulsion via the airways. The pathophysiology of transient tachypnea involves compromised clearance of fetal lung fluid.4 The association with cesarean section delivery presumably relates to the lack of normal physiological expulsion of fluid from the lungs by the extrinsic compression that occurs during vaginal delivery. These infants may also have a diminished catecholamine surge – a result of lack of exposure to all stages of labor. There is evidence that diminished β-adrenergic responsiveness may be a factor in some affected neonates. Proper function of the β-adrenergic response system is important for the successful transition of the neonate from fetal life to breathing air. Other conditions that result in diminished clearance of lung fluid in the newborn are hypoalbuminemia, elevated pulmonary venous pressure, diminished respiratory drive (sedation), endothelial cell damage (oxygen toxicity), and bronchial obstruction.5

The clinical findings in neonates with transient tachypnea include a rapid respiratory rate, mild retractions, and expiratory grunting. Occasionally, there is mild cyanosis that is promptly relieved by supplemental oxygen administration. The tachypnea develops within the first several hours of life. The respiratory rate is usually normal for the first hour, with gradual subsequent increase. In most affected infants, the tachypnea peaks between 6 and 36 hours after birth and then slowly returns to normal by the third or fourth day. Pneumothorax can complicate the clinical course (Figure 2-1). Physical examination may reveal an overexpanded chest; the lungs are typically clear to auscultation. Unlike respiratory distress syndrome, there are no substantial abnormalities on blood gas ...

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