Continuing Education Activity

Transient tachypnea of the newborn (TTN) is a benign, self-limited condition that can present in infants of any gestational age shortly after birth. It is caused by a delay in the clearance of fetal lung fluid after birth, which leads to ineffective gas exchange, respiratory distress, and tachypnea. It often poses a significant, diagnostic dilemma in the care of newborn babies with respiratory distress. This activity reviews the evaluation and management of transient tachypnea of the newborn and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance outcomes for affected patients.

Objectives:

• Describe the risk factors for transient tachypnea of the newborn.
• Describe the presentation of an infant with transient tachypnea of the newborn.
• Describe the management of transient tachypnea of the newborn.
• Explain the importance of improving coordination amongst the interprofessional team to enhance care for patients affected by transient tachypnea of the newborn.

Introduction

Transient tachypnea of the newborn (TTN) is a benign, self-limited condition that can present in infants of any gestational age, shortly after birth. It is caused due to delay in clearance of fetal lung fluid after birth which leads to ineffective gas exchange, respiratory distress, and tachypnea. In the nursery, it often poses a significant, diagnostic dilemma in the care of newborn babies with respiratory distress.

Etiology

Maternal risk factors include delivery before completion of 39 weeks gestation, a cesarean section without labor, gestational diabetes, and maternal asthma.[1][2]

Fetal risk factors include male gender, perinatal asphyxia, prematurity, small for gestational age, and large for gestational age infants.[3]

Epidemiology

Incidence is inversely proportional to gestation age and affects approximately 10% of infants delivered between 33 and 34 weeks, approximately 5% between 35 and 36 weeks, and less than 1% in term infants.[4][5][6]

Pathophysiology

Fetal Lung

• The fetal pulmonary epithelium secretes alveolar fluid at around 6 weeks of gestation.[7]
• Chloride ions in the interstitium enter the pulmonary epithelial cell through the active transport of sodium, potassium, and chloride into cells (Na-K-2Cl transporter) which, in turn, are secreted into the alveolus through various chloride channels.
• Sodium follows the chloride ions through para-cellular pathways, and water is transported across the cells via aquaporin.[8][9]
• Volume of fetal lung is maintained by the larynx, which acts as a one-way valve, allowing only outflow of fluid.

Neonatal Lung

• Passive movement of sodium through epithelial sodium channels (ENaC) is believed to be the principle mechanism of reabsorption of fetal lung fluid with starling forces and thoracic squeeze playing a minor role in clearance.
• With the onset of labor, maternal epinephrine,[10] and glucocorticoids activate the ENaC on the apical membranes of type II pneumocytes.
• Sodium in the alveolus is transported passively across the ENaC proteins which in turn is actively transported back to the interstitium by the Na+/K+-ATPase pump.[11]
• An osmotic gradient is created which allows chloride and water to follow and be absorbed into pulmonary circulation and lymphatics.

History and Physical

The condition presents within the first few minutes to hours after birth.

Physical exam findings usually include signs of respiratory distress:

• Tachypnea (respiratory rate greater than 60 per minute)
• Nasal flaring
• Grunting[12]
• Intercostal/subcostal/suprasternal retractions
• Crackles, diminished or normal breath sounds on auscultation

Other occasional exam findings:

• Tachycardia
• Cyanosis
• Barrel-shaped chest because of hyperinflation

Evaluation

Duration of respiratory distress is the principal determinant for diagnosis of TTN. If distress resolves within the first few hours of birth, it can be labeled as "delayed transition." Six hours is an arbitrary cutoff between "delayed transition" and TTN because by this time baby might develop issues with feeding and might require further interventions. TTN is usually a diagnosis of exclusion and hence any tachypnea lasting over 6 hours requires workup to rule out other causes of respiratory distress.

The workup usually includes:

• Preductal and postductal saturations: to rule out differential cyanosis
• Complete blood count (CBC), blood culture,  C-reactive protein (CRP), lactate to rule out neonatal sepsis
• ABG analysis may show hypoxemia and hypocapnia due to tachypnea; hypercapnia is a sign of fatigue or air leak.
• Chest x-ray: May show hyperinflation, prominent perihilar vascular markings, edema of interlobar septae or fluid in the fissures.[13][14]

Other workups to consider:

• Ammonia level in the setting of lethargy and metabolic acidosis to rule out inborn errors of metabolism
• Echocardiography to rule out congenital cardiac defects in patients with differential cyanosis or persistent tachypnea for over 4 to 5 days

Treatment / Management

Given TTN is a self-limited condition, supportive care is the mainstay of treatment.

• Rule of 2 hours: Two hours after onset of respiratory distress, if an infant’s condition has not improved or has worsened or if FiO2 required is more than 0.4 or chest x-ray is abnormal, consider transferring infant to a center with a higher level of neonatal care. [15]
• Routine NICU care including continuous cardiopulmonary monitoring, maintenance of neutral thermal environment, securing intravenous (IV) access, blood glucose checks, and observation for sepsis should be provided.

Respiratory

• Oxygen support may be required if pulse oximetry or ABG suggest hypoxemia.
• An oxygen hood is the preferred initial method; however, nasal cannula, CPAP can also be used.
• Concentration should be adjusted to maintain oxygen saturation in low 90s.
• Endotracheal intubation and requirement of ECMO support is usually uncommon but should always be considered in patients with declining respiratory status.
• Arterial blood gas (ABG) analysis should be repeated, and pulse oximetry monitoring should be continued until signs of respiratory distress have resolved.

Nutrition

• Neonates’ respiratory status is the usual determinant for the degree of nutritional support required.
• Tachypnea of over 80 breaths per minute with associated increased work of breathing often makes it unsafe for the infant to receive oral feeds.
• Such infants should be kept nil per oral (NPO), and intravenous (IV) fluids should be started at 60 to 80 ml per kg per day.
• If respiratory distress is resolving, diagnosis is certain and respiratory rate is less than 80 breaths per minute; enteral feeds can be started.
• Enteral feeds should always be started slowly with progressive increments in volume of feeds until tachypnea has completely resolved

Infectious

• Since TTN may be difficult to distinguish from early neonatal sepsis and pneumonia, empiric antibiotic therapy with ampicillin and gentamicin should always be considered.

Medications

• Randomized control trials studying the efficacy of furosemide[16] or racemic epinephrine[17] in TTN showed no significant difference in duration of tachypnea or length of hospital stay compared with controls
• Salbutamol (inhaled beta2-agonist) has been shown to decrease the duration of symptoms and hospital stay; however, more evidence-based studies are needed to confirm its efficacy and safety.[18][19]

Differential Diagnosis

• Pneumonia
• Respiratory distress syndrome
• Aspiration syndromes: meconium, blood or amniotic fluid
• Pneumothorax
• Left-to-right cardiac shunt defects with failure
• Persistent pulmonary hypertension
• Central nervous system (CNS) irritation or disease: Subarachnoid hemorrhage, hypoxic-ischemic encephalopathy
• Inborn errors of metabolism
• Congenital malformations: Congenital diaphragmatic hernia, cystic adenomatoid malformations

Prognosis

Overall prognosis is excellent with most of the symptoms resolving within 48 hours of onset.

In some case reports, malignant TTN has been reported in which affected newborns develop persistent pulmonary hypertension due to a possible elevation of pulmonary vascular resistance due to retained lung fluid.[20]

Complications

Air leaks and pneumothoraces are other rare complications.

Longitudinal studies have shown an association between TTN and subsequent development of asthma.[21][22]

Pearls and Other Issues

What is transient tachypnea of the newborn? 

Transient tachypnea of the newborn (TTN) is a condition that causes breathing problems in newborn babies. Babies have fluid in their lungs before birth. The fluid normally goes away when a baby is born. In some babies, the fluid does not go away as quickly as it should. This causes TTN.

A mother who has diabetes, asthma, or a C-section without labor is more likely to have a baby with TTN.

What are the symptoms of TTN? 

• Fast breathing of more than 60 breaths a minute
• Hard breathing: Nostrils that open wide when the baby takes a breath, skin, and muscles that look like they are caving in; grunting  

How is TTN treated? 

TTN usually goes away by the time a baby is 3 days old. Until that happens, doctors can help the baby get enough oxygen and nutrition if he or she needs it. Treatments might include:

• Extra oxygen
• An intravenous (IV) feeding tube
• Antibiotics

Enhancing Healthcare Team Outcomes

Transient tachypnea of the newborn is a common condition seen in newborn babies. Healthcare workers including intensive care nurses need to know that the cause is due to fluid accumulation in the lungs. The condition is usually managed by an interprofessional team as there are many disorders which can present with similar symptoms. The condition, once diagnosed, is treated conservatively with oxygen, antibiotics, and sometimes with the use of a diuretic. The prognosis for most infants is excellent.