Transient Tachypnea of the Newborn (TTN)


  • TTN is a self-limited disorder characterized by tachypnea and other signs of mild respiratory distress such as retractions and cyanosis.
  • Occurs secondary to a delayed clearance of fetal lung liquid, which leads to airway compression, bronchiolar collapse, and air trapping.

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Risk Factors

Clinical Manifestation

Differential Diagnosis



  • Prematurity
  • Precipitous delivery
  • C-section delivery without labor

  • Presentation within 6 h of birth
  • Tachypnea, typically 60–120 breaths/min + mild-to-moderate respiratory distress
  • Physical examination: good air entry ± crackles
  • Symptoms tend to last 12–72 h

  • Pneumonia
  • Sepsis
  • RDS (may complicate TTN, especially if infant is premature)
  • Cyanotic heart disease
  • Meconium aspiration
  • Persistent pulmonary hypertension

  • ABG: may see mild hypoxemia with mild respiratory acidosis
  • CXR: prominent perihilar streaking and mild-to-moderate cardiomegaly
  • May also see hyperinflation, pleural effusions, and widened fissures

  • Supportive with supplemental O2, as TTN is a self-limited disease
  • May need CPAP for lung recruitment (may increase the risk of air leak)
  • May offer PO feeding when RR <70 breaths/min and weaned to room air
  • Diuretics have not been shown to improve symptoms or shorten course and are contraindicated

Respiratory Distress Syndrome (RDS)


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Risk Factors

Clinical Manifestation



  • Prematurity
  • Male sex
  • Caucasian race
  • Maternal diabetes
  • Perinatal asphyxia
  • C-section without labor
  • Thoracic malformations
  • Genetic disorders of surfactant production


  • Tachypnea, grunting, and retractions
  • O2 requirement tends to increase over the first 48 h if not treated

Laboratory/radiographic findings:

  • CXR: diffuse, fine granular densities that develop during the first few hours of life

  • Hypotension (treat as appropriate)
  • A PDA can lead to poor recovery from RDS, and closure should be considered if patient is 3–4 d old with hemodynamic compromise or continued RDS with poor weaning from mechanical ventilation

Surfactant therapy:

  • Many centers start CPAP and do not give “prophylactic” surfactant therapy.
  • Many formulations are available. Check with your institution to determine the appropriate dosage/interval/number of doses.
  • Consider prophylactic surfactant therapy as soon as clinically feasible for infants <27 wk gestation who require intubation.
  • For all other infants, early rescue surfactant (within 1–2 h after birth) is indicated for worsening respiratory distress on exam or increasing Fio2 requirement above 30%–40%.

  • Lack of antenatal corticosteroid therapy in infants 24–34 wk gestation

  • ABG: hypoxia, hypercarbia, mild metabolic acidosis, ± elevated lactate

Monitoring/supportive therapy:

  • ABG: should be checked within 30–60 min of surfactant therapy or with changes in ventilator settings
  • Temperature: neutral thermal environment should be maintained
  • Antibiotics: RDS is difficult to distinguish from pneumonia and sepsis; consider appropriate cultures and initiate broad-spectrum antibiotics (ie, ampicillin and gentamicin) for 48 h

  • Ensure appropriate ETT position and equal lung inflation prior to giving surfactant.
  • Dosage: 4 mL/kg (Survanta dosing) per ETT q4–6h for up to four doses.
  • Pulmonary hemorrhage can be seen after surfactant therapy; this is thought to result from rapid change in lung compliance.


  • O2 saturations alarms should be 85%–97% if ≥1250 g and 85%–93% if <1250 g to limit exposure to high Fio2 (these are oximetry alarm limits, not targets; targets are ≥88%).


  • Early NCPAP administration may ↓ need for mechanical ventilation.
  • Indicated in infants with mild respiratory distress; Fio2 requirement <40% and Paco2 <55–60 mm Hg.
  • Start with 5–6 cm H2O, and increase as required by 1–2 cm increments to a max of 8–10 cm H2O.
  • Place an NG tube to decompress gastric air.
  • Monitor via CXR for lung overdistention leading to decreased tidal volume and hypercarbia.

Mechanical ventilation:

  • Indications for mechanical ventilation include respiratory acidosis (Paco2 >55–60 mm Hg), FiO2 >40%, or severe apnea.
  • Initial ventilator settings: SIMV rate 20–40; PIP 20–25; PEEP 4–6; Ti 0.3–0.35; Fio2 adjusted for desired saturations.
  • After intubation, rescue surfactant therapy as above.
  • The ventilator should be weaned (sometimes very rapidly after surfactant administration) as tolerated to avoid lung injury from volutrauma and barotrauma.

Pulmonary Hemorrhage



  • Pathologic: presence of red blood cells in the alveoli
  • Clinical: presence of hemorrhagic fluid in the trachea along with need for increased respiratory support secondary to respiratory decompensation and CXR changes
  • Occurs in 1–12/1,000 live births


  • Occurs secondary to hemorrhagic pulmonary edema, as opposed to direct hemorrhage into the lungs.
  • Hypoxia and acidosis or left-to-right shunt through a PDA can lead to left ventricular failure → increased pulmonary venous and capillary pressure → transudation and rupture of alveolar blood vessels.

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Risk Factors



  • RDS, IUGR, infection, oxygen toxicity, CHD, and intrauterine asphyxia.
  • PDA with left-to-right shunting causes increased pulmonary flow and can lead to poor LV function.
  • Surfactant therapy has been a debatable risk factor.

  • Clinical diagnosis is made in the setting of respiratory compromise with hemorrhagic fluid in the respiratory tract (eg, bloody ETT secretions).
  • CXR may show diffuse opacification with air bronchograms.

  • Treatment is generally supportive, including suctioning of hemorrhagic fluid and adjusting ventilator strategies to correct for the accompanying respiratory decompensation.
  • Correct any hemodynamic instability with volume resuscitation.
  • Correct any contributing factors such as coagulopathy, sepsis, and hemodynamically significant PDA.
  • Increase PEEP to 6–8 to help decrease the interstitial fluid, or switch to HFOV if higher airway pressure is needed.
  • Additional surfactant therapy is controversial.

Pulmonary Air Leak



Risk Factors

  • Term infants: mechanical ventilation, meconium aspiration, pneumonia, and congenital lung or chest wall malformation
  • Preterm infants: mechanical ventilation, RDS, pneumonia, sepsis


  • Increased pulmonary pressures can damage the respiratory epithelium → alveolar rupture → allows air to enter the pulmonary interstitium → PIE.
  • If elevated pressure continues, air can dissect toward the pleura.
  • Rupture of the pleura leads to pneumothorax and can dissect toward the mediastinum, pericardium, or retroperitoneum.
  • Retroperitoneal air can rupture into the peritoneum or dissect to the scrotal/labial folds.


  • Spontaneous pneumothorax can be found in 0.07%–2% of healthy term infants.
  • Lung disease increases the rate of pneumothorax to 5%–10%.

Pulmonary Air-Leak Syndromes: Pneumothorax, Pulmonary Interstitial Emphysema, Pneumomediastinum, Pneumopericardium


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  • Physical examination:

    • Vitals: tachycardia or bradycardia, ↑ blood pressure (can be ↓ if tension pneumothorax → decreased venous return and CO), tachypnea, apnea, desaturation, cyanosis.

  • Observation:

    • If the pneumothorax is found incidentally and if patient is in no respiratory distress, has no underlying lung disease, and is not mechanically ventilated, the patient may be closely observed.

  • Ventilatory and circulatory compromise can lead to progressive acidosis (respiratory and metabolic) and death if untreated.

  • Respiratory: grunting, flaring, retractions, chest asymmetry, decreased breath sounds on affected side.
  • Cardiac: shift in PMI.
  • GI: abdominal distention from displacement of the diaphragm.
  • CXR:

    • AP view—hyperlucent hemithorax, flattened diaphragm, mediastinal shift if tension pneumothorax.
    • Cross-table lateral—may allow for visualization of small collections of intrapleural air not seen on AP view.
    • ABG—may see ↓ Pao2 and ↑ Paco2.

  • Transillumination:

    • • May be able to illuminate pneumothorax by placement of a high-intensity light source directly on the skin.
    • • ↓ sensitivity if severe PIE, chest wall edema, full-term, very small infants, or infants with dark skin.

  • Needle aspiration:

    • If the patient is rapidly decompensating, needle aspiration can be diagnostic and therapeutic.

  • Observation:

    • If the pneumothorax is found incidentally and if patient is in no respiratory distress, has no underlying lung disease, and is not mechanically ventilated, the patient may be closely observed.
    • Although some infants may require an increase in their FiO2, routine treatment with 100% O2is not recommended.

  • Needle aspiration:

    • Should be performed in all patients who are rapidly deteriorating.
    • Can be a temporizing measure in patients who are mechanically ventilated and may be definitive treatment for patients not receiving mechanical ventilation.

  • Pigtail catheter/chest tube:

    • Often required for patients who develop pneumothorax who are receiving mechanical ventilation.
    • Consider removal of the catheter or chest tube after no air has been drained for 24–48 h; Some centers will first place the chest tube to water seal and/or clamp, with a follow-up CXR to evaluate for reaccumulation before removal.

  • IVH is thought to result secondary to hypercapnia, hypoxia, and fluctuating cerebrovascular pressures.
  • SIADH may occur.

Pulmonary Interstitial Emphysema

  • PIE can occur in mechanically ventilated infants during the first 48 h of life.
  • Risk factors include extreme prematurity, RDS, and sepsis.
  • Vitals: hypotension, bradycardia.

  • Ventilator strategies

    • ↓ mean airway pressure by ↓ PEEP and Ti and ↑ respiratory rate.
    • Consider HFOV to avoid swings in lung volume.

  • Positioning: Place affected lung in a dependent position.

  • PIE can lead to pneumothorax, pneumopericardium, and air embolus.

  • CXR: linear lucencies radiating from the hilum and occasionally cyst-like blebs.
  • ABG: acidosis, hypercarbia, hypoxia.

  • Avoid suctioning and bag ventilation.
  • In very severe cases, selective bronchial intubation or surgical resection may be considered (although no proven benefit).


  • PE: Muffled heart sounds.
  • CXR: Air is best seen on the lateral view.

  • Pneumomediastinum is usually of little clinical significance and rarely needs treatment.
  • Rare cardiorespiratory effects can occur if the air is under tension and will require mediastinotomy drainage.

  • Can lead to pneumothorax.


  • Vitals: initial tachycardia followed by bradycardia, hypotension, cyanosis.
  • PE: Muffled and distant heart sounds; may hear a pericardial knock or millwheel-like murmur.
  • Labs/imaging:

    • CXR: AP view demonstrates air surrounding the heart. It is most often seen at the inferior aspect of the heart.
    • EKG: Decreased voltages throughout.

  • Transillumination: Illumination may occur in the substernal region. Flickering with cardiac cycle is sometimes seen and can help to differentiate from pneumomediastinum.

  • Observation:

    • If the patient is asymptomatic and is not receiving mechanical ventilation, the patient can be observed carefully with close monitoring of vital signs.
    • Serial CXRs should be monitored until the pneumopericardium resolves.

  • Needle aspiration:

    • Pericardiocentesis should be performed immediately if cardiac tamponade develops.
    • This is best accomplished under US guidance to avoid puncturing the myocardium.

  • Continuous pericardial drainage:

    • If recurrence of cardiac tamponade occurs, a pericardial tube will need to be placed.

  • Cardiac tamponade
  • Tension pneumomediastinum
  • Mediastinitis (if resulting from esophageal perforation)

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Jan 9, 2019 | Posted by in PEDIATRICS | Comments Off on Pulmonology
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