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Transient tachypnea of the newborn (TTN) is a self-limited disease commonly seen in neonatesthroughout the world and is encountered by all physicians who take care of newborn infants. Infantswith transient tachypnea of the newborn present within the first few hours of life with tachypnea andother signs of respiratory distress, increased oxygen requirement, and ABGs that do not reflectcarbon dioxide retention. When managing transient tachypnea of the newborn, it is imminent toobserve for development of respiratory fatigue and signs of clinical deterioration that may suggest

some other diagnoses. See the image below.

 A supine anteroposterior chest radiograph of an infant with transient tachypneaof the newborn (TTN). Note the reticular appearance of the film with mild cardiomegaly and obvious interstitial fluid. 

Pathophysiology

Noninfectious acute respiratory disease develops in approximately 1% of all newborn infants andresults in admission to a critical care unit. Transient tachypnea of the newborn is the result of a delayin clearance of fetal lung liquid. In the past, respiratory distress was thought to be a problem ofrelative surfactant deficiency but is now characterized by an airspace-fluid burden secondary to theinability to absorb fetal lung liquid.

In vivo experiments have demonstrated that lung epithelium secretes Cl- and fluid throughoutgestation but develops the ability to actively reabsorb Na+ only during late gestation. At birth, themature lung switches from active Cl- (fluid) secretion to active Na+ (fluid) absorption in response tocirculating catecholamines; evidence suggests glucocorticoids play a role in this switch. Changes inoxygen 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 switchfrom fluid secretion to fluid absorption results, mainly because of immaturity in the expression ofENaC, which can be up-regulated by glucocorticoids.[1] Glucocorticoids induce lung Na+ reabsorptionmost likely through the fetal lung alveolar ENaC channel in late gestational age.[2] 

Both pharmacologic blockade of the lung's ENaC channel and genetic knockout experiments usingmice deficient in the ENaC pore-forming subunit have demonstrated the critical physiologicimportance of lung Na+ transport at birth. When Na+ transport is ineffective, newborn animals developrespiratory distress; hypoxemia; fetal lung liquid retention; and, in the case of the ENaC knockoutmice, death. Bioelectrical studies of human infants' nasal epithelia demonstrate that both transienttachypnea 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 andlung epithelial systems. Transient tachypnea of the newborn occurs in mature newborns with maturesurfactant pathways and poorly developed respiratory epithelial Na+ transport, whereas neonatal RDSoccurs 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 andassociation with prolonged tachypnea of newborns.[5] 

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 around35% is cleared postnatally during active crying and breathing. An infant born by cesarean delivery isat risk of having excessive pulmonary fluid as a result of not having experienced all of the stages oflabor and subsequent lack of appropriate catecholamine surge, which results in low release ofcounter-regulatory hormones at delivery. The result is alveoli with retained fluid that inhibit gasexchange.

Epidemiology

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Frequency

United States Approximately 1% of infants have some form of respiratory distress that is not associated withinfection. Respiratory distress includes both RDS (ie, hyaline membrane disease) and transienttachypnea of the newborn. Of this 1%, approximately 33-50% have transient tachypnea of thenewborn.

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

Male neonates are more affected than females.

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