Bronchopulmonary dysplasia

Bronchopulmonary dysplasia is a chronic lung injury in premature babies caused by oxygen and prolonged mechanical ventilation.

Bronchopulmonary dysplasia is considered if the infant continues to require supplemental oxygen in premature infants at 36 weeks gestation who have no other conditions requiring oxygen (pneumonia, congenital heart disease). Bronchopulmonary dysplasia is caused by high inspired oxygen concentrations, usually in patients on prolonged mechanical ventilation. The incidence increases with the degree of prematurity; additional risk factors include pulmonary interstitial emphysema, high peak inspiratory pressure, increased airway resistance, and high pulmonary artery pressure, as well as male sex. Bronchopulmonary dysplasia is usually suspected when the infant cannot be weaned from oxygen therapy, mechanical ventilation, or both. Patients develop increasing hypoxemia, hypercapnia, and increasing oxygen requirements. Chest radiography initially shows diffuse opacities due to exudate accumulation; the appearance then becomes multicystic or sponge-like, with emphysema, scarring, and atelectasis developing in the affected areas. Desquamation of the alveolar epithelium may be noted, and macrophages, neutrophils, and inflammatory mediators may be detected in the tracheal aspirate.

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Treatment of bronchopulmonary dysplasia

Treatment of bronchopulmonary dysplasia is supportive and includes nutritional support, fluid restriction, diuretics, and possibly inhaled bronchodilators. Respiratory infections should be identified early and treated aggressively. Weaning the child from mechanical ventilation and oxygen support should be done as early as possible.

More than 120 kcal/(kg per day) should be supplied with food; calorie requirements are increased, since the work spent on breathing is increased, and energy is also required by the lungs for recovery and development.

Because pulmonary congestion and edema may develop, daily fluid intake is often limited to about 120 ml/(kg day). Diuretics are sometimes used: chlorothiazide 10-20 mg/kg orally twice daily plus spironolactone 1-3 mg/kg once daily or in 2 divided doses. Furosemide (1-2 mg/kg intravenously or intramuscularly or 1-4 mg/kg orally every 12-24 hours for neonates and every 8 hours for older children) may be used for a short period, but long-term use causes hypercalciuria and, as a result, osteoporosis, fractures, and kidney stones. Fluid and electrolyte balance should be monitored during diuretic therapy.

In severe forms of bronchopulmonary dysplasia, weeks or months of additional mechanical ventilation and/or oxygen supplementation may be required. The pressure and fraction of inspired oxygen (FiO2) should be reduced as rapidly as the child can tolerate, but the child should not be allowed to become hypoxemic. Arterial oxygenation should be continuously monitored with a pulse oximeter and maintained at greater than or equal to 88% of saturation. Respiratory acidosis may develop during weaning from mechanical ventilation; however, it can be treated without returning to the previous mechanical ventilation regimen if the pH remains above 7.25 and the child does not have severe respiratory distress.

Passive immunoprophylaxis with palivizumab, a monoclonal antibody to respiratory syncytial virus (RSV), reduces RSV-related hospitalizations and intensive care unit stays, but is expensive and is reserved for high-risk children. During the RSV season (November through April), children receive 15 mg/kg of the antiviral drug every 30 days until 6 months after treatment for acute illness. Children over 6 months of age should also be vaccinated against influenza.

How is bronchopulmonary dysplasia prevented?

Bronchopulmonary dysplasia is prevented by reducing mechanical ventilation parameters as rapidly as possible to the minimum tolerable level and then by completely eliminating mechanical ventilation; early use of aminophylline as a respiratory stimulant may help premature infants to wean off intermittent mechanical ventilation. Prenatal administration of glucocorticoids, prophylactic surfactant in extremely low birth weight infants, early correction of patent ductus arteriosus, and avoidance of large volumes of fluid also reduce the incidence and severity of bronchopulmonary dysplasia. If the infant cannot be weaned off mechanical ventilation within the expected time, possible underlying causes such as patent ductus arteriosus and nosocomial pneumonia should be excluded.

What is the prognosis for bronchopulmonary dysplasia?

The prognosis varies depending on the severity. Infants who are still ventilator dependent at 36 weeks of gestation have a mortality rate of 20-30% in the first year of life. Infants with bronchopulmonary dysplasia have a 3-4 times higher incidence of growth retardation and neurodevelopmental delay. For several years, children are at increased risk of lower respiratory tract infections (especially viral), and they can rapidly develop respiratory decompensation if an infectious process occurs in the lung tissue. Indications for hospitalization should be broader if signs of respiratory infection or respiratory failure appear.