Respiratory Distress Syndrome in Neonates

Surfactant is not produced in adequate amounts until relatively late in gestation (34 to 36 weeks); thus, risk of respiratory distress syndrome (RDS) increases with greater prematurity. Other risk factors include multifetal pregnancies, maternal diabetes, and being a White male.

Risk decreases with fetal growth restriction, preeclampsia or eclampsia, maternal hypertension, prolonged rupture of membranes, and maternal corticosteroid use.

Rare cases are hereditary, caused by mutations in surfactant protein (SP-B and SP-C) and ATP-binding cassette transporter A3 (ABCA3) genes.

Pulmonary surfactant is a mixture of phospholipids and lipoproteins secreted by type II pneumocytes (see Neonatal pulmonary function). It diminishes the surface tension of the water film that lines alveoli, thereby decreasing the tendency of alveoli to collapse and the work required to inflate them.

With surfactant deficiency, a greater pressure is needed to open the alveoli. Without adequate airway pressure, the lungs become diffusely atelectatic, triggering inflammation and pulmonary edema. Because blood passing through the atelectatic portions of lung is not oxygenated (forming a right-to-left intrapulmonary shunt), the infant becomes hypoxemic. Lung compliance is decreased, thereby increasing the work of breathing. In severe cases, the diaphragm and intercostal muscles fatigue, and CO2 retention and respiratory acidosis develop.

Symptoms and signs of RDS include rapid, labored, grunting respirations appearing immediately or within a few hours after delivery, with suprasternal and substernal retractions and flaring of the nasal alae. As atelectasis and respiratory failure progress, symptoms worsen, with cyanosis, lethargy, irregular breathing, and apnea, and may ultimately lead to cardiac failure if adequate lung expansion, ventilation, and oxygenation are not established.

Neonates weighing < 1000 g may have lungs so stiff that they are unable to initiate or sustain respirations in the delivery room.

On examination, breath sounds are decreased, and crackles may be heard.

• Clinical evaluation

• Arterial blood gases (hypoxemia and hypercapnia)

• Chest x-ray

• Blood, cerebrospinal fluid, and tracheal aspirate cultures

Diagnosis of RDS is by clinical presentation, including recognition of risk factors; arterial blood gases showing hypoxemia and hypercapnia; and chest x-ray. Chest x-ray shows diffuse atelectasis classically described as having a ground-glass appearance with visible air bronchograms and low lung expansion; appearance correlates loosely with clinical severity.

Differential diagnosis includes

• Group B streptococcal pneumonia and sepsis

• Transient tachypnea of the newborn

• Persistent pulmonary hypertension

• Aspiration

• Pulmonary edema

• Congenital cardiopulmonary anomalies

Neonates typically require cultures of blood. Cerebrospinal fluid cultures are not routinely done after birth because there is low incidence of meningitis associated with early-onset sepsis, but they may be done in certain cases (eg, blood cultures are positive for gram-negative bacilli, concern of late-onset sepsis) (1). Clinically, group B streptococcal pneumonia is extremely difficult to differentiate from RDS; thus, antibiotics should be started pending culture results.

• Intratracheal surfactant if indicated

• Supplementary oxygen as needed

• Mechanical ventilation as needed

Specific treatment of RDS is intratracheal surfactant therapy. This therapy requires endotracheal intubation, which also may be necessary to achieve adequate ventilation and oxygenation.

There is increasing evidence supporting use of less invasive ventilation techniques, such as nasal continuous positive airway pressure (CPAP), even in very preterm infants (1). Infants with RDS who are receiving nasal CPAP and who need an increasing fraction of inspired oxygen (FIO2) have been shown to benefit from brief intubation to deliver surfactant followed by immediate extubation (1). Administration of intratracheal surfactant via a thin catheter is a newer technique that has also been shown to be beneficial in reducing the risk of BPD. Both of these techniques show a trend toward fewer cases of BPD but not fewer days of mechanical ventilation (2, 3).

Surfactant hastens recovery and decreases risk of pneumothorax, interstitial emphysema, intraventricular hemorrhage, bronchopulmonary dysplasia, and neonatal mortality in the hospital and at 1 year. Options for surfactant replacement include

is a lipid bovine lung extract supplemented with proteins B and C, colfosceril palmitate, palmitic acid, and tripalmitin.

is a modified porcine-derived minced lung extract containing phospholipids, neutral lipids, fatty acids, and surfactant-associated proteins B and C.

is a calf lung extract containing phospholipids, neutral lipids, fatty acids, and surfactant-associated proteins B and C.

Lung compliance can improve rapidly after therapy. The ventilator peak inspiratory pressure may need to be lowered rapidly to reduce risk of a pulmonary air leak. Other ventilator parameters (eg, FIO2, rate) also may need to be reduced.

Prognosis with treatment is excellent; mortality is < 10%. With adequate ventilatory support alone, surfactant production eventually begins, and once production begins, RDS resolves within 4 or 5 days. However, in the meantime, severe hypoxemia can result in multiple organ failure and death.

Greater prematurity is associated with higher risk of chronic lung disease, bronchopulmonary dysplasia, or both.

Preterm Labor.)

Neonates who completed < 30 weeks gestation, especially those who were not exposed to antenatal corticosteroids, are at high risk of developing RDS. Giving prophylactic intratracheal surfactant therapy to these neonates has been shown to decrease risk of neonatal death and certain forms of pulmonary morbidity (eg, pneumothorax).