Transient tachypnea of the newborn (TTN) is a self-limited disease commonly seen in neonates throughout the world and is encountered by all physicians who take care of newborn infants. Infants with transient tachypnea of the newborn present within the first few hours of life with tachypnea and other signs of respiratory distress, increased oxygen requirement, and ABGs that do not reflect carbon dioxide retention. When managing transient tachypnea of the newborn, it is imminent to observe for development of respiratory fatigue and signs of clinical deterioration that may suggest some other diagnoses. See the image below.
Noninfectious acute respiratory disease develops in approximately 1% of all newborn infants and results in admission to a critical care unit. Transient tachypnea of the newborn is the result of a delay in clearance of fetal lung liquid. In the past, respiratory distress was thought to be a problem of relative surfactant deficiency but is now characterized by an airspace-fluid burden secondary to the inability to absorb fetal lung liquid.
In vivo experiments have demonstrated that lung epithelium secretes Cl- and fluid throughout gestation but develops the ability to actively reabsorb Na+ only during late gestation. At birth, the mature lung switches from active Cl- (fluid) secretion to active Na+ (fluid) absorption in response to circulating catecholamines; evidence suggests glucocorticoids play a role in this switch. Changes in oxygen tension augment the Na+ -transporting capacity of the epithelium and increase gene expression for the epithelial Na+ channel (ENaC). The inability of the immature fetal lung to switch from fluid secretion to fluid absorption results, mainly because of immaturity in the expression of ENaC, which can be up-regulated by glucocorticoids.  Glucocorticoids induce lung Na+ reabsorption most likely through the fetal lung alveolar ENaC channel in late gestational age. 
Both pharmacologic blockade of the lung's ENaC channel and genetic knockout experiments using mice deficient in the ENaC pore-forming subunit have demonstrated the critical physiologic importance of lung Na+ transport at birth. When Na+ transport is ineffective, newborn animals develop respiratory distress; hypoxemia; fetal lung liquid retention; and, in the case of the ENaC knockout mice, death. Bioelectrical studies of human infants' nasal epithelia demonstrate that both transient tachypnea of the newborn and respiratory distress syndrome (RDS) involve defective amiloride-sensitive Na+ transport. [3, 4]
Mature newborns who have normal transitions from fetal to postnatal life have mature surfactant and lung epithelial systems. Transient tachypnea of the newborn occurs in mature newborns with mature surfactant pathways and poorly developed respiratory epithelial Na+ transport, whereas neonatal RDS occurs in infants with both premature surfactant pathways and immature Na+ transport. Although, full-term neonates may have lower lamellar body counts, suggesting diminished surfactant function and association with prolonged tachypnea of newborns. 
Fetal lung fluid clears by 35% a few days prior to birth, owing to changes in the ENaC; by around 30% during active labor owing to mechanical transpulmonary forces and catecholamine surge; and around 35% is cleared postnatally during active crying and breathing. An infant born by cesarean delivery is at risk of having excessive pulmonary fluid as a result of not having experienced all of the stages of labor and subsequent lack of appropriate catecholamine surge, which results in low release of counter-regulatory hormones at delivery. The result is alveoli with retained fluid that inhibit gas exchange.
Approximately 1% of infants have some form of respiratory distress that is not associated with infection. Respiratory distress includes both RDS (ie, hyaline membrane disease) and transient tachypnea of the newborn. Of this 1%, approximately 33-50% have transient tachypnea of the newborn.
Transient tachypnea of the newborn is generally a self-resolving disorder with excellent prognosis. It frequently resolves over a 24-hour to 72-hour period.
However, this condition has been associated with subsequent respiratory morbidity, with a significantly increased risk of a wheezing disorder in childhood.
No racial predilection has been reported.
Male neonates are more affected than females.
Clinically, transient tachypnea of the newborn presents as respiratory distress in full-term or near-term infants.
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