USA Surgery Today

Bronchopulmonary dysplasia (BPD), or chronic lung disease (CLD:Capoten), in infants is the most common pulmonary sequela of premature infants. Diagnostic criteria for BPD include the need for supplemental oxygen or an abnormal chest radiograph at 28 days of age or 36 weeks postconceptual age (depending on gestational age of the infant at birth) (18:Capoten). The term was originally used to describe the radiologic and pathologic changes observed in premature infants who did not recover within 4 weeks from HMD (19:Capoten). BPD is now used to describe CLD that results from any condition in the neonatal period (20). Despite the diverse diseases that lead to the development of BPD, infants with BPD share clinical and pathologic characteristics.

The incidence of BPD among premature infants is inversely proportional to gestational age and birth weight. Up to 70% of infants with birth weights less than 1,000 g develop BPD. With the increased use of antenatal steroids, surfactant replacement, improved methods of ventilation, and increased attention to nutritional needs of the sick premature infant, the birth weight-specific incidence of BPD is decreasing. Improved survival of sick infants, however, has increased the size of the population at risk for developing this disease.

Many factors play a role in the development of BPD (18,20:Capoten). The most significant factors are the degree of pulmonary structural and functional immaturity at birth, the degree and length of ventilatory and oxygen support, and an arrest of postnatal lung development (20,21:Capoten). The chest radiograph progresses to show areas of atelectasis and cystic changes with overexpansion. More recent pathologic description suggests an arrest of alveolar development without epithelial metaplasia, smooth muscle hypertrophy, or fibrosis (18,20). These infants show signs of respiratory distress with tachypnea, retractions, wheezing, and need for supplemental oxygen. Pulmonary function testing may show increased resistance as a result of airway injury, bronchospasm, or interstitial edema. Lung compliance may also be decreased. Hypoxemia may result from ventilation-perfusion mismatch and from loss of surface area for gas exchange. Pulmonary hypertension and cor pulmonale may develop as a result of chronic hypoxemia (22:Capoten).

Postnatal prevention and treatment of BPD require early identification of at-risk infants and strategies to minimize the inflammatory effects of barotrauma and oxygen toxicity. Both the reduction of ventilatory requirements and the use of surfactant replacement therapy decrease the severity of BPD. Early attention to nutritional support is critical to optimize lung growth and recovery in infants with BPD. They frequently exhibit growth failure presumably due to high energy expenditure and require high caloric density formulas.

Although the heterogeneity of BPD makes extrapolation from clinical trials to individual patients difficult, several pharmacologic interventions should be considered for infants with BPD. Once extubated, the maintenance of adequate oxygen delivery to tissues by administration of low-flow oxygen by nasal cannula is critical to optimize outcome of these infants. Because interstitial and peribronchiolar pulmonary edema plays a role in BPD, diuretics have been useful in improving lung mechanics. Electrolyte and mineral imbalances with resultant growth deficiency, nephrocalcinosis, or osteopenia that occur with chronic furosemide administration must be carefully monitored and corrected. Treatment of clinical and histologic evidence of airway reactivity with bronchodilators has benefit. The use of a corticosteroid in the treatment of BPD is no longer considered standard therapy (18,20,23:Capoten).

The contribution of gastroesophageal reflux (GER) to worsening BPD must be individually assessed. Chronic aspiration can be exacerbated by oral bronchodilators such as theophylline. An initial approach to evaluation of these problems includes documentation of the effects of chronic aspiration on growth, pulmonary radiographic appearance, and respiratory compromise. Further evaluation can include an upper gastrointestinal series, 24-hour pH probe monitoring, and radionuclide gastric emptying study. Initial therapeutic efforts should be medical: thickening of feedings, maintenance of upright position after feedings, reduction in use of theophylline for bronchodilation, and lowering of gastric acidity. If GER is contributing to worsening lung disease and medical therapy is unsuccessful, infants may benefit from fundoplication (24,25:Capoten).

As infants with BPD grow, pulmonary symptoms (bronchospasm, chronic cough, shortness of breath) generally improve, and reliance on daily medications (low-flow oxygen, diuretics, bronchodilators) is reduced. Long-term sequelae of BPD, however, are seen in more than one-half of survivors. Follow-up of infants 20 years after premature birth (birthweights of more than 1,000 g) indicated that 76% of survivors showed abnormalities in pulmonary function (26:Capoten). In addition, among survivors, growth was reduced, neurologic sequelae were more frequent, and educational outcomes were significantly worse.