eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Transient Tachypnea of the Newborn

Author: KN Siva Subramanian, MD, Professor of Pediatrics and Obstetrics/Gynecology, Chief of Neonatal Perinatal Medicine, Director of Nurseries, Georgetown University Hospital
Coauthor(s): Monisha Bahri, MBBS, MD, Fellow in Neonatal/Perinatal Medicine, Department of Neonatology, Georgetown University Hospital; Stephen D Kicklighter, MD, Clinical Assistant Professor, Department of Pediatrics, Division of Neonatology, University of North Carolina at Raleigh and Wake Medical Center
Contributor Information and Disclosures

Updated: Sep 16, 2009

Introduction

Background

Transient tachypnea of the newborn (TTN) is a self-limited disease common in infants throughout the world and is encountered by all physicians who care for newborn infants. Infants with transient tachypnea of the newborn present within the first few hours of life with tachypnea, increased oxygen requirement, and ABGs that do not reflect carbon dioxide retention. When managing transient tachypnea of the newborn, observing for signs of clinical deterioration that may suggest other diagnoses and for the development of respiratory fatigue is important.

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; more recently, evidence suggests glucocorticoids play a role in this switch.¹ 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, in large part, from an immaturity in the expression of ENaC, which can be up-regulated by glucocorticoids. Glucocorticoids induce lung Na⁺ reabsorption most likely through the EnaC channel in late gestational age fetal lung alveolar epithelia.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.

Mature newborns who have normal transitions from fetal to postnatal life have mature surfactant and 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.

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 end result is alveoli with retained fluid that inhibit gas exchange.

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

Risk is equal in both males and females.

Age

Clinically, transient tachypnea of the newborn presents as respiratory distress in full-term or near-term infants.

Clinical

History

• The maternal history in transient tachypnea of the newborn (TTN) consists of caesarian delivery without labor or precipitous delivery.
• 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 usually occurring within 72 hours after birth.

Physical

• Physical findings include tachypnea with variable grunting, flaring, and retracting.
• The infant is often described as having "quiet" tachypnea.
• Extreme cases may exhibit cyanosis.
• A study investigating the risk factors for duration of tachypnea in patients with transient tachypnea of the newborn reported that peak respiratory rate of more than 90 breaths per minute during the first 36 hours of life was associated with prolonged tachypnea lasting more than 72 hours.³

Causes

The disorder results from delayed absorption of fetal lung fluid following delivery. Transient tachypnea of the newborn is commonly observed following birth by cesarean delivery.

• Cesarean delivery
  • Studies using lung mechanic measurements were performed in infants born by either cesarean or vaginal delivery. Milner et al noted that the mean thoracic gas volume was 32.7 mL/kg in infants born vaginally and 19.7 mL/kg in infants born via cesarean delivery.⁴ Importantly, chest circumferences were the same. Milner et al noted that the infants born via cesarean delivery had higher volumes of interstitial and alveolar fluid compared with those born vaginally, even though the overall thoracic volumes were within the reference range.
  • Epinephrine release during labor affects fetal lung fluid. In the face of elevated epinephrine levels, the chloride pump responsible for lung liquid secretion is inhibited, and the sodium channels that absorb liquid are stimulated. As a result, net movement of fluid from the lung into the interstitium occurs. Therefore, caesarian delivery without labor and the subsequent lack of this normal surge in counter-regulatory hormones limits the excursion of pulmonary fluid.
• Maternal asthma and smoking
  • Demissie et al performed a historical cohort analysis on singleton live deliveries in New Jersey hospitals from 1989-1992.⁵ After controlling for confounding effects of important variables, infants of mothers with asthma were more likely to exhibit transient tachypnea of the newborn than infants of mothers in the control group.
  • Schatz et al studied a group of 294 pregnant women with asthma and a group of 294 pregnant women without asthma.⁶ Both groups had normal pulmonary function test results and were matched for age and smoking status. transient tachypnea of the newborn was found in 11 infants (3.7%) of mothers with asthma and in 1 infant (0.3%) of a mother from the control group. No significant differences between asthmatic and matched control subjects in other transient tachypnea of the newborn risk factors were observed.
• Male sex and macrosomia: These have also been associated with increased risk of transient tachypnea of the newborn.
• Other factors: Excessive maternal sedation, perinatal asphyxia, and elective cesarean delivery without preceding labor are frequently associated with transient tachypnea of the newborn.

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