• 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

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

Clinical:

• 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.

Oxygen:

• 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%).

NCPAP:

• 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.

• 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.

Pneumothorax

• 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).

Pneumomediastinum

• 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.

Pneumopericardium

• 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)