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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.
A supine anteroposterior chest radiograph of an infant with transient tachypnea
of 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 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.
[1]
Glucocorticoids induce lung Na
+
reabsorption
most 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 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.
[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 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.
Epidemiology
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
Male neonates are more affected than females.
Age
Clinically, transient tachypnea of the newborn presents as respiratory distress in full-term or near-term
infants.

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