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Respiratory Disorders of the Newborn

Michael A. Davis, MD

Respiratory distress is a common problem during the first few days of life. Respiratory distress may present with tachypnea, nasal flaring, sternal and intercostal retractions, cyanosis, and apnea. The most common respiratory disorders of the newborn are transient tachypnea of the newborn, respiratory distress syndrome, and bronchopulmonary dysplasia.

Transient Tachypnea of the Newborn

Transient tachypnea of the newborn (TTN) usually presents as early respiratory distress in term or preterm infants. It is caused by delayed reabsorption of fetal lung fluid.

TTN is a very common, and it is often seen following cesarean section because, compared with those born vaginally, babies born by cesarean section have delayed reabsorption of fetal lung fluid.

Symptoms of TTN include tachypnea, retractions, nasal flaring, grunting, and cyanosis.

Arterial blood gas reveals respiratory acidosis and mild to moderate hypoxemia.

Chest x-ray often reveals fluid in the interlobar fissures and perihilar streaking, which sometimes obscures the heart borders. Hyperaeration of the lungs and mild cardiomegaly may be seen; alveolar edema may appear as coarse, fluffy densities.

Delayed reabsorption of fetal lung fluid is seen in term or near-term infants as well as in small, preterm infants who may have respiratory distress syndrome (RDS). TTN initially may be difficult to distinguish from RDS or group B streptococcal pneumonia.

TTN usually resolves within12-24 hours. The chest radiograph appears normal in 2-3 days. The symptoms rarely last more than 72 hours.

Treatment of TTN consists of oxygen therapy. Infants will usually recover fully, without long-term pulmonary sequelae.

Respiratory Distress Syndrome

RDS is a lung disease caused by pulmonary surfactant deficiency. It occurs almost always in preterm infants who are born before the lungs are able to produce adequate amounts of surfactant.

Surfactant is produced by pneumocytes in the lung. It lowers the surface tension of the alveolus. The preterm neonate whose lungs are deficient in surfactant will develop diffuse atelectasis because of decreased lung compliance (stiff lungs).

Respiratory distress usually begins at, or soon after, delivery and tends to worsen over time. Infants will have tachypnea, nasal flaring, intercostal and sternal retractions, and expiratory grunting. Tiny preterm infants who lack pulmonary surfactant may fail to initiate ventilation in the delivery room and rapidly become hypoxic and apneic.

Chest radiography shows diffuse atelectasis, which appears as reduced lung volume, with homogeneous haziness or the "ground glass" appearance of lung fields, and air bronchograms. Positive pressure ventilation can reverse the radiographic findings of atelectasis.

RDS is diagnosed when a premature infant has respiratory distress and a characteristic chest radiograph. The differential diagnosis includes pneumonia, often caused by group B streptococci, which is more common in preterm infants and can mimic RDS, both clinically and radiographically.

Ventilatory Management

Continuous positive airway pressure (CPAP) improves oxygenation and survival. CPAP (about 5-7 cm H₂O pressure) is applied via nasal prongs, nasopharyngeal tube, or endotracheal tube. In some infants with milder disease, CPAP may prevent the need for mechanical ventilation.

For infants exhibiting respiratory acidosis, hypoxemia or apnea, intermittent positive pressure ventilation will be required in addition to positive end-expiratory pressure (PEEP), which stabilizes alveoli and improves lung volume and oxygenation.

An umbilical or radial arterial line is used to monitor blood gas levels and blood pressure in sicker infants.

Surfactant Replacement Therapy

Surfactant therapy reduces mortality by 30-50% and pneumothorax by 50%. However, there has not been a reduction in the rate of progression of RDS to bronchopulmonary dysplasia (BPD).

Survanta is a bovine lung surfactant extract and Exosurf is a synthetic surfactant preparation. Both natural and artificial surfactants appear to have comparable benefits.

Surfactant replacement therapy should be initiated as soon as respiratory distress has been clinically diagnosed. As long as the infant requires significant ventilatory support, including more than 30% oxygen, Survanta (every 6 hours for 4 doses) or Exosurf (every 12 hours for 2 doses) should be given.

General Supportive Care

Sepsis and pneumonia are part of the differential diagnosis of RDS. Presumptive treatment with ampicillin plus gentamicin or cefotaxime usually is given until blood and CSF cultures are reported to be negative.

A decrease in lung compliance due to pulmonary edema increases the need for ventilatory support and the risk for BPD. Hence, restricting intravenous fluid in infants who have RDS lowers the risk for development of BPD.

Systemic blood pressure should be maintained in the normal range with dopamine (3-20 mg/Kg/min IV) or dobutamine (2.5-15.0 mg/kg/min IV based on response).

Bronchopulmonary Dysplasia

Bronchopulmonary dysplasia (BPD) is a chronic lung disease characterized by hypoxia, hypercarbia, and oxygen dependence that persists beyond 1 month of age. The chest radiograph shows hyperexpansion and focal hyperlucency, alternating with strands of opacification.

BPD is extremely common among infants who have severe RDS treated with mechanical ventilation. The incidence of BPD is inversely proportional to birthweight. Virtually all babies who develop BPD have had mechanical ventilation, suggesting an important role for barotrauma and oxygen toxicity.

The combination of pulmonary immaturity, positive pressure ventilation, oxygen therapy, and increased lung water cause BPD in the susceptible neonate.

RDS is the most common pulmonary disease causing BPD. Other neonatal diseases requiring oxygen and mechanical ventilation may also cause BPD, including immature lungs, meconium aspiration syndrome, congenital heart disease, neonatal pneumonia, and aspiration pneumonia.

Signs of BPD include tachypnea and retractions, after extubation. Blood gas measurements show respiratory acidosis with elevated PaVCO₂; increased HCO₃ indicates metabolic compensation. Higher inspired oxygen concentration is required to maintain normal oxygenation.

Management of BPD consists of minimizing barotrauma. Adjustments in peak pressure should deliver adequate, but not excessive, tidal volume; acceptable minute ventilation can be maintained by monitoring the PaCO₂. A moderate degree of respiratory acidosis should be allowed in order to decrease the amount of ventilatory assistance needed, thus reducing the barotrauma. Supplemental oxygen therapy should maintain the PaO₂ in the 60-80 mm Hg range. This often can be achieved by maintaining an oxygen saturation >90% with pulse oximetry and occasionally measuring blood gases. FIO₂ should be lowered slowly, 1- 2% at a time, and not more often than every 1-7 days, as tolerated.

Nutrition. Nutrition is crucial in promoting repair and growth of lung tissue. Infants who have BPD may not tolerate even normal fluid intakes. Total fluid intake should be limited to approximately 120 mL/kg/day. Adding supplemental fat or carbohydrate to 24 kcal/oz of formula increases caloric intake and minimizes fluid intake. These infants may need up to 150 kcal/kg/day for optimal growth.

Antibiotics. Intubated infants who have BPD are susceptible to pneumonia. Close observation for pneumonia and prompt treatment with antibiotics, when pneumonia is suspected, are recommended.

Chest physiotherapy, with chest percussion, postural drainage and suctioning should be performed as needed.

Diuretic Therapy

Furosemide (1 mg/kg q 24 h IV or PO) may be used. Milder diuretics such as chlorothiazide (10-20 mg/kg per dose q12h PO) and spironolactone (1-2 mg/kg per dose q12h PO) may help reduce airway resistance and improve pulmonary compliance.

If diuretics are used over the long term, especially furosemide, the patient should be monitored for metabolic alkalosis, hypokalemia, hypochloremia, hyponatremia, hypercalciuria, nephrolithiasis, and nephrocalcinosis.

Bronchodilators

Aminophylline (5-7 mg/kg loading dose, followed by 2 mg/kg q6-12h IV) decreases airway resistance and increases lung compliance.

Inhaled albuterol, 0.15 mg/kg q 8 h, has been shown to benefit pulmonary function.

Corticosteroid Therapy. Dexamethasone (0.25 mg/kg q 12 h PO or IV for 3 days, followed by a tapering course over 2-6 weeks) has been shown to improve pulmonary function rapidly and allow earlier extubation.

Home oxygen therapy should be considered for infants who are receiving supplemental oxygen therapy. Most infants who have BPD show improvement in lung function over a variable period of time. §