Treatment of bronchopulmonary dysplasia

Fundamental patient management goals

The logic of treatment is based on understanding the vulnerability of the immature lung. It is constantly exposed to damaging factors while undergoing continuous repair processes. There are four key vectors of therapy:

1. Tissue protection. Further pathological and iatrogenic damage to lung structures must be minimized.
2. Oxygenation control. Strict prevention of hypoxemia. This is critically important because hypoxia directly provokes pulmonary vasoconstriction, which exacerbates pulmonary hypertension.
3. Symptomatic control. Management of interstitial edema and elimination of bronchial obstruction.
4. Developmental support. Creating optimal conditions for lung tissue growth and adequate repair.

Pathogenetic rationale for interventions

Each therapeutic action has a strict pathophysiological target. They are conveniently grouped by the main links of pathogenesis:

• Respiratory support and gas exchange: In surfactant deficiency associated with respiratory distress syndrome (RDS), replacement therapy with exogenous surfactants is performed. To reduce the risk of barotrauma and volutrauma, exclusively gentle mechanical ventilation techniques are used. Hypoxia is corrected by oxygen supplementation and blood transfusions (to increase the oxygen-carrying capacity of the blood).
• Hemodynamics and fluid control: In patent ductus arteriosus (PDA), medical or surgical closure is indicated to reduce pulmonary overcirculation. Fluid retention and pulmonary edema require the use of diuretics. Pulmonary hypertension is corrected with oxygen therapy and inhaled nitric oxide (NO), which acts as a vasodilator.
• Inflammation and infection: Glucocorticoids and cromones are prescribed to suppress the inflammatory cascade. Oxidative stress requires the use of superoxide dismutase. When complicated by a bacterial infection, antibiotics are indicated, and for respiratory syncytial virus (RSV) infection, specific immunoglobulin and ribavirin are used.
• Trophics and structural changes: Bronchial obstruction is relieved by bronchodilators. To normalize cell differentiation in respiratory epithelial metaplasia, retinol (vitamin A) is prescribed. The deficit of structural building blocks in pulmonary hypoplasia is compensated by adequate nutritional support.

Discharge criteria and home oxygen therapy

Transfer of the child to the outpatient stage is possible only upon achieving complete respiratory stability. The ideal discharge criterion is that the child no longer requires supplemental oxygen, and their oxygen saturation (SaO2) stably remains above target values while breathing ambient air independently.

To confirm a stable state, the following are required:

• Adequate oxygenation: SaO2 $\ge$ 90% while breathing room air.
• Radiological findings: no negative dynamics.
• Somatic status: independent suckling and stable weight gain.
• Infection control: absence of markers of active infection.

If the patient does not meet these criteria, discharge is possible using an oxygen concentrator under strict pulse oximetry monitoring. The basic indication for home oxygen therapy is SaO2 < 90%. If the child has concomitant pulmonary hypertension, the threshold is higher — therapy is indicated at SaO2 < 92%.

Outpatient management, rehabilitation, and prognosis

The diagnosis of BPD is valid in pediatric practice until the child reaches 3 years of age. During this period, a comprehensive multidisciplinary approach is required, including strict monitoring of anthropometry and psychomotor development, as well as follow-up care by a pediatrician and pulmonologist.

Special attention is paid to infection safety: specific prophylaxis of RSV infection with monoclonal antibodies (palivizumab) and routine vaccination strictly according to the National Immunization Schedule are carried out. Rehabilitation is performed 1–2 times a year in rehabilitation departments (physiotherapy, exercise therapy, psychological and pedagogical support for the family). Upon reaching the age of three, the diagnosis is removed, and further follow-up by a pulmonologist is indicated only for children with established chronic bronchopulmonary pathology.

Predictors of poor prognosis:

• Prolonged need for mechanical ventilation (more than 6 months).
• Presence of intraventricular hemorrhages (IVH).
• Development of pulmonary hypertension and chronic cor pulmonale.
• Persistence of oxygen dependency past 1 year of age.

In the long term, severe forms of BPD can lead to structural changes (emphysema, bronchiolitis obliterans, local pneumosclerosis). A history of BPD is a proven risk factor for the early development of chronic obstructive pulmonary disease (COPD) in adults.

Class and exam questions

What else to study on this topic

• Pathogenesis of barotrauma and volutrauma during mechanical ventilation
• The link between patent ductus arteriosus and pulmonary hypervolemia
• Mechanisms of chronic cor pulmonale development in BPD
• Bronchiolitis obliterans and local pneumosclerosis as outcomes of BPD
• The link between a history of BPD and the risk of developing COPD in adults

Other topics in «Chapter 2. Neonatology»

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