INTRODUCTION

Transient tachypnea of the newborn (TTN) is a parenchymal lung disorder characterized by pulmonary edema resulting from delayed resorption and clearance of fetal alveolar fluid [1]. TTN is a common cause of respiratory distress in the immediate newborn period. In a review of 33,289 term deliveries (37 to 42 weeks), the incidence of TTN was 5.7 per 1000 births [2]. Although thought to be a benign, self-limited condition, there are increasing data to suggest that TTN increases a newborn's risk for developing a wheezing syndrome early in life [3].

PATHOPHYSIOLOGY

The process of clearing fetal alveolar fluid begins before term birth and continues through labor and after delivery. During late gestation, in response to increased concentrations of catecholamines and other hormones, the mature lung epithelium switches from actively secreting chloride and liquid into the air spaces to actively reabsorbing sodium and liquid (figure 1) [4,5]. Increased oxygen tension at birth enhances the capacity of the epithelium to transport sodium and increases gene expression of the epithelial sodium channel [5]. Reduced gene expression of this channel contributes to the inability of immature lungs to switch from fluid secretion to absorption and can be upregulated by glucocorticoids [5].

Passive resorption of liquid also occurs after birth because of differences among the oncotic pressure of air spaces, interstitium, and blood vessels. The majority of water transport across the apical membrane is thought to occur through aquaporin 5 (AQP5) water channels [6].

Delayed resorption of fetal lung fluid is thought to be the underlying cause of TTN. Fluid fills the air spaces and moves into the interstitium, where it pools in perivascular tissues and interlobar fissures until it is eventually cleared by the lymphatics or absorbed into small blood vessels. The excess lung water in TTN results in decreased pulmonary compliance. Tachypnea develops to compensate for the increased work of breathing associated with reduced compliance. In addition, accumulation of fluid in the peribronchiolar lymphatics and interstitium promotes partial collapse of the bronchioles with subsequent air trapping. Continued perfusion of poorly ventilated alveoli leads to hypoxemia, and alveolar edema reduces ventilation, sometimes resulting in hypercapnia.

In one study, the expression of AQP5 was greater in patients with TTN than those with respiratory distress syndrome or controls. This finding suggests that upregulation of AQP5 increases reabsorption of postnatal lung fluid, which contributes to the quick resolution of symptoms in infants with TTN [6].