RDS

Respiratory distress syndrome (RDS), also called hyaline membrane disease, is the most common respiratory disorder of premature infants. Symptoms of RDS may be seen immediately after birth and are usually present before 6 hours of age. RDS is common in pre-term infants and it almost invariably in those born before 28 weeks gestation however older infants may also have delayed lung maturation.

In 1959 Avery and Mead (AMA J Dis Child 1959; 97: 517-23) demonstrated that in infants dying of RDS, surfactant deficiency has a key role in the pathogenesis of this disease.

The alveolar collapse and the decreased surfactant production cause a reduced lung compliance. This subsequently results in decreased functional residual capacity and increased dead space that leads to atelectasis.

The atelectatic areas of the lung often have preserved perfusion but are poorly ventilated resulting in alveolar hypoventilation, with severe hypoxemia and hypercarbia, anaerobic metabolism and lactic acidosis. If severe pulmonary hypertension occurs with right to left shunting at level of foramen ovale and ductus arteriousus further worsening the respiratory failure. Perhaps a bigger problem is a left to right shunting through the ductus arteriosus that often is patent in these babies, hence contributing to congested lungs and impaired gas exchange.

Artificial Ventilation and oxygen supplementation are often needed. Surfactant therapy modifies the course of RDS. The degree of modification is dependent not only on gestational age but also the timing of treatment.

Very early in the disease process inflammatory mediators are released causing more endothelial and epithelial injury; reduced surfactant synthesis and function as well as increased endothelial permeability. This leakage of proteins into alveolar space determines surfactant inactivation. (see figure)

If severe asphyxia occurs (especially around the time of birth) lung perfusion falls and ischemic damage to pulmonary capillaries occurs. After recovery there is pulmonary hyperperfusion and protein-rich fluid leaks out of the damaged capillaries. This inhibits surfactant activity, and can worsen RDS.

Histological findings show alveolar epithelial cell necrosis develops within 30 mins of birth. The airways become congested with fluid and exudate from leaky capillaries. The epithelial cells become detached from the basement membrane and the hyaline membrane (a fibrinous matrix of materials from blood and cellular debris) lines the visible airspaces that constitute dilated terminal bronchioles and alveolar ducts.