RESPIRATORY DISTRESS SYNDROME(RDS)

It is the one of the common complication of prematurity which ooccurs in about 24,000 infants born.
There’s increase incidence seen with white race, male gender, late preterm delivery, presence of maternal
diabetes, perinatal hypoxia, ischemia, delivery in the absence of labor, and decreased gestational age at
birth wherein it occurs 98% of babies born at 24 weeks, 5% of those born at 34 weeks and less than 1%
with those born at 37th weeks.

This happens due to surfactant deficiency as a result of under developed lungs. At 32 weeks AOG,
alveoli have not yet fully developed and thus decreases the area for the exchange for oxygen and lesser
surfactant is produced. The deficiency in surfactant increases the surface tension within the small airways
and alveoli, thereby reducing the compliance of the immature lung. Overdistension of the alveoli during
positive pressure ventilation leads to further damage and inflammation. Repeated atelectasis eventually
damages the respiratory epithelium, causing a cytokine-mediated inflammatory response resulting to
pulmonary edema increasing the amount of protein-rich fluid from the vascular space to leak into the
alveoli, which further inactivate surfactant, and thus oxidative stress. High oxygen tensions from
mechanical ventilation and inflammatory processes within the lung also promotes the conversion of
surfactant into an inactive form through protein oxidant damage and lipid peroxidation causing
hypoxemia through alveolar hyperventilation, diffusion abnormality, ventilation-perfusion mismatch,
intrapulmonary shunting, or a combination of these mechanisms. This hypoxemia and tissue
hypoperfusion ultimately lead to increased anaerobic metabolism at a cellular level with resultant lactic
acidemia.

MANIFESTATION:

Soon after birth, presence of tachypnea, prominent grunting, chest wall retractions, stridor, nasal
flaring, cyanosis, dyspnea, and wheezing are seen. Breath sounds may be normal or decreased with harsh
tubular quality and fine crackles can be observed with deep inspiration.

DIAGNOSIC TESTS:

1. Chest radiograph: Showing a characteristic “ground-glass” pattern or fine rectangular granularity

of parenchyma with low lung volumes and air bronchograms within the first 24 hours of life may
be present.
2. Arterial blood gas that may show hypoxemia, hypercarbia or/and metabolic acidosis
3. Blood Culture to check for bacteremia but results may take 48 hours
4. Blood Glucose to check for hypoglycemia that can cause or aggravate tachypnea
5. CBC with Differential
- Leukocytosis or bandemia indicates stress or infection
- Neutropenia correlates with bacterial infection
- Low hemoglobin levels show anemia
- High hemoglobin levels occur in polycythemia
6. Other tests include sepsis workup, 2D echocardiography to exclude possible cardiac pathology,
serum electrolytes levels to rule out other causes of respiratory distress
TREATMENT

Neonates with RDS are first given oxygen through either nasal cannula, CPAP (Continuous Positive
Airway Pressure) or by intubation and ventilatory support. Surfactants through the tube, IV fluids,
nutrition and medications such antibiotics with presence of infection can be given.

Prevention includes administration of corticosteroids to the mother (24 hours to 7 days before
delivery), antenatal steroids to prevent severity of RDS in preterm babies between 24 and 34 weeks of
gestation, and prophylactic administration of artificial surfactant into trachea of premature neonate.