Transient Tachypnea of the Newborn 

Transient tachypnea of the newborn (TTN) is a self-limited disease common in infants throughout the world and is encountered by all physicians who care for newborn infants. Infants with transient tachypnea of the newborn present within the first few hours of life with tachypnea, increased oxygen requirement, and ABGs that do not reflect carbon dioxide retention. When managing transient tachypnea of the newborn, observing for signs of clinical deterioration that may suggest other diagnoses and for the development of respiratory fatigue is important.

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; more recently, evidence suggests glucocorticoids play a role in this switch.^[1] 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, in large part, from an immaturity in the expression of ENaC, which can be up-regulated by glucocorticoids. Glucocorticoids induce lung Na⁺ reabsorption most likely through the EnaC channel in late gestational age fetal lung alveolar epithelia.^[2]

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.

Mature newborns who have normal transitions from fetal to postnatal life have mature surfactant and 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.

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 end result is alveoli with retained fluid that inhibit gas exchange.

Frequency

United States

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.

Mortality/Morbidity

Transient tachypnea of the newborn is generally a self-limited disorder without significant morbidity. Transient tachypnea of the newborn resolves over a 24-hour to 72-hour period.

Race

No racial predilection has been reported.

Sex

Risk is equal in both males and females.

Age

Clinically, transient tachypnea of the newborn presents as respiratory distress in full-term or near-term infants.