Transient tachypnea of the newborn (TTN) is an elevated respiratory rate in the newborn due to retention of fetal lung fluid following delivery.

The fetal lungs in utero are filled with fluid due to active secretion of chloride ions by type II pneumocytes. During labor, elevation in maternal epinephrine and glucocorticoids activate amiloride-sensitive epithelial sodium channels (ENaC) in fetal type II pneumocytes that leads to a net resorptive state in the lungs. The lung fluid is then reabsorbed into the pulmonary circulation and lymphatics. The pathophysiology of TTN is when alveolar fluid is incompletely resorbed following delivery, leading to respiratory distress and tachypnea.

TTN is one of the most common causes of neonatal respiratory distress. It is associated with lower gestational age, with an incidence of 10% in infants delivered at 33-34 weeks, 5% at 35-36 weeks, and less than 1% at term. Other risk factors include cesarean delivery (especially without labor), gestational diabetes, maternal asthma, newborn of male sex, and newborn who is small or large for gestational age. Studies have identified a significant reduction in respiratory morbidity with elective cesarean deliveries scheduled after 39 weeks of gestation.

TTN typically presents within minutes to hours after birth. Signs include tachypnea (respiratory rate > 60 breaths/min), nasal flaring, grunting, intercostal / subcostal / suprasternal retractions, and crackles or diminished breath sounds on auscultation. Additionally, tachycardia, cyanosis, and hyperinflated chest may be present. Occasionally, infants with TTN may have hypoxemia and require supplemental oxygen or additional respiratory support. Chest radiograph will show perihilar vascular markings, edema, and fluid in interlobar fissures, consistent with retained fetal lung fluid.

Tachypnea due to TTN is transient and will typically resolve within 72 hours. Nearly all cases resolve within the first postnatal week.