Treatment of Respiratory Distress Syndrome in Newborns

Extrapulmonary causes of respiratory disorders

In addition to primary lung tissue damage, the clinical presentation of respiratory distress syndrome can be triggered by internal organ malformations and neurological pathologies.

The most common extrapulmonary cause is perinatal nervous system injury (PNSI). Severe hypoxia and ischemia damage the brainstem structures (medulla oblongata and pons), leading to persistent disruption of central respiratory control.

The second significant cause is spinal cord injury or spinal cord damage, the clinical manifestations of which depend on the level of the lesion:

• $C_1–C_4$ level: injury to the spinal respiratory center.
• $Th_1–Th_2$ level: impairment of respiratory muscle innervation and, consequently, their function.

Basic therapy and monitoring

Treatment begins with establishing a protective care environment. To maintain normothermia, humidity, and oxygenation, infants are placed in incubators or open radiant warmers.

Postural therapy Proper positioning is critical for the prevention of pressure ulcers, improvement of bronchial drainage, and optimization of hemodynamics (especially in the pulmonary circulation).

• The infant's head should be slightly extended to maintain patent airways. To achieve this, a 3–4 cm thick bolster is placed under the upper chest.
• The body position must be changed every 2–3 hours following a "supine — prone — side" cycle.
• Special instructions: if a preterm infant is born with asphyxia, airway suctioning and endotracheal intubation are performed immediately in the delivery room.

Laboratory and instrumental monitoring The main goal of therapy is to correct hypoxia, acidosis, and signs of cardiopulmonary failure. This requires rigorous monitoring:

• Acid-base balance (ABB) and arterialized capillary blood gases ($p_aO_2$, $p_aCO_2$).
• Complete blood count and biochemical panel (hemoglobin, hematocrit, electrolytes, glucose).
• Chest X-ray.

Infusion and nutritional support

During the first 2–3 days of life, an enteral fast is prescribed — feeding via the gastrointestinal tract is completely discontinued.

Intravenous therapy is initiated within 40–60 minutes after birth. A 5–10% dextrose (glucose) solution is used as the base fluid. The fluid volume is calculated based on the day of life:

• Day 1: 50–60 mL/kg.
• On each subsequent day, the volume is increased by 20 mL/kg (up to the 7th day of life).

Once the enteral fast ends, maternal milk or specialized formulas for preterm infants become the priority substrate. Feeding is dosed every 3 hours and administered primarily via a nasoesophageal tube. This is done to minimize physical exertion and energy expenditure in an infant with respiratory failure.

Step-by-step respiratory support

The respiratory support strategy is chosen based on blood gas parameters and disease severity.

1. Oxygen therapy. A basic requirement to relieve hypoxia. Administered via oxygen hoods, incubators, masks, or nasal cannula.
2. CPAP (continuous positive airway pressure). Indicated for mild-to-moderate RDS, as well as when $p_aO_2$ drops < 50 mmHg and $p_aCO_2$ rises > 60 mmHg. This method recruits hypoventilated alveoli, improving the ventilation-perfusion ratio and reducing hypoxemia.
3. Mechanical ventilation (MV). Indicated for decompensated acidosis (pH < 7.2) and frequent apnea episodes with progressive cyanosis and hemodynamic instability.

Pharmacotherapy and surfactant therapy

Surfactant replacement therapy (natural porcine/bovine or synthetic preparations) is used for extremely preterm infants with endogenous surfactant deficiency. The "golden hour" rule applies here: administration within the first minutes of life yields maximum efficacy. By 6–8 hours, the therapeutic window closes.

Concomitant pharmacotherapy:

• Antibiotics: prescribed parenterally as a preventive measure (usually a combination of two drugs) due to the high risk of infection. In severe cases, intravenous immunoglobulins are added.
• Retinol (Vitamin A): administered before the start of enteral feeding to reduce the risk of necrotizing enterocolitis and bronchopulmonary dysplasia.
• Tocopherol (Vitamin E): mandatory during oxygen therapy (intramuscularly 10 mg/kg/day). Acts as an antioxidant and prevents retinopathy of prematurity.
• Glucocorticoids: not used routinely; indicated only for laboratory-confirmed adrenal insufficiency.

Class and exam questions

What else to study on this topic

• Pathophysiology of hypoxic-ischemic brainstem injury
• Mechanism of retinopathy of prematurity associated with hyperoxia
• Bronchopulmonary dysplasia: risk factors and outcomes
• Necrotizing enterocolitis in extremely preterm infants
• Principles of acid-base balance (ABB) calculation in newborns

Other topics in «Chapter 2. Neonatology»

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