Transient Tachypnea of the Newborn (TTN)

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 TTN present within the first few hours of life with tachypnea, increased oxygen requirement, and arterial blood gases that do not reflect carbon dioxide retention. When managing TTN, observing for signs of clinical deterioration that may suggest other diagnoses and for the development of respiratory fatigue is important.

Transient tachypnea of the newborn appears soon after birth. It may be accompanied by chest retractions, by expiratory grunting, or by cyanosis. (This last manifestation can be relieved with minimal oxygen.) Recovery usually is complete within 3 days.

Radiologically, this syndrome frequently is termed wet lung disease. In the medical literature, discussions concerning transient tachypnea of the newborn also can be found under the following names: retained fetal lung liquid, retention of fetal lung fluid, respiratory distress syndrome type II, transient respiratory distress of the newborn, and neonatal retained fluid syndrome.

In a case-control study, infants delivered vaginally at 37 weeks or later, from 2005 through 2007, were analyzed to identify factors associated with transient tachypnea of the newborn. The incidence of transient tachypnea was found to be significantly associated with nulliparity; a history of infertility therapy, such as in vitro fertilization; augmentation of labor; nonreassuring fetal status; vacuum/forceps delivery; and a low Apgar score (<7) at 1 and 5 minutes. The factor most strongly associated with the incidence of transient tachypnea of the newborn was a low Apgar score at 1 minute.

Pathophysiology

During fetal life, the lungs are expanded with an ultrafiltrate of the fetal serum. In the course of neonatal transition, this ultrafiltrate must be removed and replaced with air. The classic explanation for how this occurs was that passage through the birth canal would, by squeezing the thorax, help eliminate the liquid in the lungs, with the remaining fluid being removed by pulmonary capillaries and the lymphatics. Currently, however, the bulk of this clearance is thought to be mediated by transepithelial sodium reabsorption through sodium channels in the alveolar epithelial cells, with only a limited contribution from mechanical factors and Starling forces. Changes in the hormonal milieu of the fetus and its mother, brought about mainly by the onset of spontaneous labor, prepare the fetus for the neonatal transition to air breathing.

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. In the past, respiratory distress 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 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. 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.

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) involve defective amiloride-sensitive Na+ transport. Mature newborns who have normal transitions from fetal to postnatal life have mature surfactant and epithelial systems. TTN occurs in mature newborns with mature surfactant pathways and poorly developed respiratory epithelial Na+ transport, while 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.

Causes

The disorder results from delayed absorption of fetal lung fluid following delivery. Transient tachypnea of the newborn (TTN) 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. 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
    • In a recent study, Demissie et al performed a historical cohort analysis on singleton live deliveries in New Jersey hospitals from 1989-1992. After controlling for confounding effects of important variables, infants of mothers with asthma were more likely to exhibit TTN 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. Both groups had normal pulmonary function test results and were matched for age and smoking status. TTN 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 TTN risk factors were observed.
  • Other factors: Excessive maternal sedation, perinatal asphyxia, and elective cesarean delivery without preceding labor are frequently associated with TTN.

Differential Diagnoses

Treatment

Medical Care

  • Medical care is supportive. As the retained lung fluid is absorbed by the infant’s lymphatic system, the pulmonary status improves.
  • Supportive care includes intravenous fluids and gavage feedings until the respiratory rate has decreased enough to allow oral feedings. Supplemental oxygen to maintain adequate arterial oxygen saturation, maintenance of thermoneutrality, and an environment of minimal stimulation are the therapies necessary in these infants. ABG assessments should be periodically repeated, especially if the infant’s condition worsens. Similarly, chest radiography should be repeated if clinical decompensation is observed.
  • As transient tachypnea of the newborn (TTN) resolves, the infant’s tachypnea improves, oxygen requirement decreases, and chest radiography shows resolution of the perihilar streaking.
  • Infants with TTN may have signs that last from a few hours to several days. Rarely, an infant develops a worsening picture of respiratory distress after several days. This may require more aggressive support including the use of continuous positive airway pressure (CPAP) or mechanical ventilation.

Consultations

  • 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.

Diet

  • Infants with TTN generally are supported by intravenous fluids or gavage feedings. Infants with significant distress have poor bowel motility and require intravenous therapy. Oral feedings are withheld until the respiration has improved.

Medication

  • The use of medications in transient tachypnea of the newborn (TTN) is minimal. Empiric antibiotics are often used for 48 hours after birth, until sepsis has been ruled out. Diuretics have not been shown to be beneficial.

Antibiotics

  • These agents are used when sepsis is clinically suggested. Antibiotics generally consist of a penicillin (usually ampicillin) and an aminoglycoside (usually gentamicin). Choices are based on local flora and antibiotic sensitivities. Dosage amounts and intervals are based on postmenstrual age (PMA), measured in weeks, and postnatal age, measured in days.

source : emedicine

read more :

  1. Transient Tachypnea of the Newborn (TTN)

  2. Transient Tachypnea of the Newborn (TTN)

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