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 3–5 days. Synonymous terms include wet lung, type II respiratory distress syndrome (type II RDS), transient respiratory distress syndrome, retained fetal lung liquid 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:
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) are released and the lung switches from active chloride and fluid secretion to active sodium absorption. However, when during labor sodium channels are inactivated or ineffective, this will result in a larger volume of lung liquid at birth, leading to a 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 before birth.
Whatever mechanism is responsible for the liquid remaining in the lung, at birth the transpulmonary pressure created during inspiration is for a major part 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 to temporarily positive pressure in the interstitium. The role of the activated Na 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. When the sodium channels are immature or ineffective, liquid will fill the air spaces, leading to a decrease in compliance and diffusion problems, and respiratory distress will occur.
Uterine contractions. Infants delivered by elective cesarean 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 first goes through the birth canal, which increases abdominal pressure, elevates the diaphragm, and increases transpulmonary pressure, thereby forcing liquid out via the nose and mouth.
Pulmonary immaturity. One study noted that a mild degree of pulmonary immaturity is a central factor in ...
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