Transient Tachypnea of the Newborn


Stephen D Kicklighter, MD

Clinical Assistant Professor, Department of Pediatrics, Division of Neonatology, University of North Carolina at Raleigh and Wake Medical Center

Vol. 6, N. 2, Maggio 2008




Transient tachypnea of the newborn (TTN) is a disease common in infants throughout the world and has been encountered by all physicians who care for newborn infants. Infants with TNN present within the first few hours of birth with tachypnea, increased oxygen requirement, and occasional hypoxia noted on arterial blood gases without concomitant carbon dioxide retention. When managing an infant with TTN, it is important to observe for signs of clinical deterioration that may suggest other diagnoses and to observe closely for the development of fatigue.


Noninfectious acute respiratory disease develops in approximately 1% of all newborn infants and results in admission to a critical care unit. TTN is the result of a delay in clearance of fetal lung liquid. Respiratory distress typically was thought to be a problem of relative surfactant deficiency, but it 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 only develops the ability to actively reabsorb Na + during late gestation. At birth, the mature lung switches from active Cl - (fluid) secretion to active Na + (fluid) absorption in response to circulating catecholamines. 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, at least in large part, from an immaturity in the expression of ENaC, which can be upregulated by glucocorticoids.

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 TTN and respiratory distress syndrome (RDS) have defective amiloride-sensitive Na + transport.

These results suggest that infants with neonatal RDS have, in addition to a relative deficiency of surfactant, defective Na + transport, which plays a mechanistic role in the development of the disease. An infant born by cesarean delivery is at risk of having excessive pulmonary fluid as a result of having not experienced all of the stages of labor and subsequent low release of counter-regulatory hormones at the time of delivery.


In the US: Frequency is equivalent universally. 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 TTN. Of this 1%, approximately 33-50% is TTN.


TTN is generally a self-limited disorder without significant morbidity. TNN resolves over a 24- to 72-hour period.


No racial predilection exists.


Risk is equal in both males and females.


Clinically, TTN presents as respiratory distress in full-term or near-term infants.


Signs of respiratory distress (eg, tachypnea, nasal flaring, grunting, retractions, cyanosis in extreme cases) become evident shortly after birth. The disorder is indeed transient, with resolution occurring usually by age 72 hours.

Physical: Physical findings include tachypnea, with variable grunting, flaring, and retracting. Extreme cases also may exhibit cyanosis.

Causes: The disorder results from delayed absorption of fetal lung fluid following delivery. TNN commonly is observed following birth by cesarean delivery because infants do not receive the thoracic compression that accompanies vaginal delivery.

Other Problems to be Considered:

Cerebral hyperventilation
Metabolic acidosis

Lab Studies:

Imaging Studies:

Medical Care:


Infants with TTN occasionally may require consultation by a neonatologist. Consider this consultation if the fraction of inspired oxygen exceeds 40%, if metabolic or respiratory acidosis is present, if CPAP or mechanical ventilation is required, if the infant begins to display fatigue (periodic breathing or apnea), or if the infant fails to improve by age 48-72 hours.


Infants with TTN generally are supported by intravenous fluids or gavage feedings. Oral feedings are withheld until the respiratory rate is consistently normal (<60 bpm).


The use of medications for TTN is minimal. Aside from the use of antibiotics for a period of 36-48 hours after birth until sepsis has been ruled out, no further pharmacotherapy generally is prescribed. Diuretics have not been shown to be beneficial.

Drug Category: Antibiotics -- Used when sepsis is clinically suggested. Antibiotics generally consist of a penicillin (usually ampicillin) and an aminoglycoside (usually gentamicin) or a cephalosporin (usually cefotaxime). Choices are based on local flora and antibiotic sensitivities.

Further Inpatient Care:




Patient Education:

Inform parents that TTN is usually a self-limited disorder and is not life threatening.


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