Transient tachypnea of the newborn (TTN) is a benign self-limited respiratory distress syndrome of term and late preterm infants related to delayed clearance of lung liquid. The distress appears shortly after birth and usually resolves within 3 to 5 days. Synonymous terms include wet lung syndrome, type II respiratory distress syndrome (RDS), transient RDS, neonatal retained fluid syndrome, and benign unexplained respiratory distress in the newborn.
It is the most common perinatal respiratory disorder, responsible for 40% of respiratory distress after birth. Incidence varies in the literature from 4 to 11 cases per 1000 singleton live births.
A delayed resorption of liquid from the lungs is believed to be the central mechanism for TTN. The lung liquid inhibits gas exchange, leading to an increased work of breathing. Tachypnea develops to compensate for that. Hypoxia develops because of poorly ventilated alveoli. The following factors are involved:
Elevated airway liquid volumes
Inactivated/immature amiloride-sensitive sodium channels. During gestation, the pulmonary epithelium actively secretes fluid and chloride into the air spaces. During labor, a surge of fetal catecholamines (adrenaline, glucocorticoids) is released, and the lung switches from active chloride and fluid secretion to active sodium absorption. However, when sodium channels are inactivated or ineffective during labor, this will result in a larger volume of lung liquid at birth, leading to reduced postnatal respiratory function. Infants born by elective cesarean section have a higher risk of TTN as they are not exposed to the stress (catecholamines) during labor.
Whatever mechanism is responsible for the liquid remaining in the lung, at birth, the transpulmonary pressure created during inspiration is largely responsible for the direct lung aeration and clearance of lung liquid (seconds). The pressure moves the column of liquid distally toward the alveolus, where it is transferred passively through the membrane into the interstitium. Then the liquid in the interstitium is slowly absorbed by the lymph and blood vessels (hours), leading temporarily to positive pressure in the interstitium. The role of the activated sodium transport from alveolus to interstitium after birth is to prevent the liquid from going back into the alveolus as a consequence of the positive pressure in the interstitium.
Uterine contractions. Infants delivered by elective cesarean section miss the lung liquid efflux via the trachea by high transpulmonary pressures caused by uterine contractions. Infants delivered by cesarean and breech deliveries miss the fetal trunk flexion when the head goes through the birth canal first, which increases abdominal pressure, elevates the diaphragm, and increases transpulmonary pressure, thereby forcing liquid out via the nose and mouth.
Both mechanisms will lead to larger airway liquid volumes at birth that must be accommodated within the lung tissue following lung aeration, resulting in higher interstitial pressures and a greater likelihood of liquid flooding back into the airways when the lungs are at functional residual capacity ...