Bronchopulmonary Dysplasia Workup

Updated: Jan 13, 2020
  • Author: Namasivayam Ambalavanan, MD, MBBS; Chief Editor: Muhammad Aslam, MD  more...
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Workup

Laboratory Studies

Arterial blood gas (ABG) assessment in patients with bronchopulmonary dysplasia (BPD) may reveal acidosis, hypercarbia, and hypoxia (with increased oxygen requirements).

Continuously monitor oxygenation by using pulse oximeter because of frequent desaturations.

Transcutaneous or end-tidal carbon dioxide monitoring may be helpful in evaluating trends, especially if the results are correlated with ABG levels. A transcutaneous monitor may injure the fragile skin of the very preterm infant. Endotracheal carbon dioxide monitors may increase dead space or become blocked with secretions.

Changes in pulmonary mechanics include increased airway resistance, decreased lung compliance, increased airway reactivity, and increased airway obstruction. Increased resistance and airway hyperactivity may be evident in the early stages of bronchopulmonary dysplasia. With worsening severity, airway obstruction can become clinically significant, with expiratory flow limitation.

In the early and mild stages of bronchopulmonary dysplasia, functional residual capacity can be increased. However, increases in functional residual capacity are noted in severe bronchopulmonary dysplasia secondary to air trapping and hyperinflation. Airway hyperresponsiveness is also increased (with an increased incidence of respiratory syncytial virus [RSV] infections and asthma) in infants in both presurfactant and postsurfactant eras. Lung compliance is reduced in infants with bronchopulmonary dysplasia.

Changes on pulmonary function tests appear to be correlated with radiographic findings. Serial pulmonary function testing may help in assessing therapeutic modalities used to treat bronchopulmonary dysplasia. However, variability related to excessive chest-wall distortion and the location where measurements are made can be problematic. Pulmonary function can slowly improve over time, but abnormalities can persist into late childhood and adolescence.

Structural changes in the lung vasculature contribute to high pulmonary vascular resistance due to narrowing of the vessel diameter and decreased angiogenesis. In addition to these structural changes, the pulmonary circulation is characterized by abnormal vasoreactivity, which also increases pulmonary vascular resistance.

Overall, injury to the pulmonary circulation can lead to pulmonary hypertension and cor pulmonale, which substantially contribute to the morbidity and mortality associated with severe bronchopulmonary dysplasia. Persistent right ventricular hypertrophy or fixed pulmonary hypertension unresponsive to oxygen supplementation on cardiac catheterization portends a poor prognosis.

Infants with bronchopulmonary dysplasia can also develop systemic hypertension; therefore, their blood pressures should be routinely monitored.

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Imaging Studies

Echocardiography

Echocardiographic assessment is an extremely valuable tool in confirming these diagnoses. Prospective studies based on echocardiography findings indicated that pulmonary hypertension is relatively common, affecting at least 1 in 6 extremely low birth weight infants, and persists to discharge in most survivors. [19] However, qualitative variables of pulmonary hypertension are not consistently provided in echo reports, even though the inter-rater reliability of cardiologists is high, especially at 36 weeks postmenstrual age. [20] Recent recommendations for the evaluation and management of pulmonary hypertension in children with BPD have been published. [21] In current practice, the role of brain natriuretic peptide in monitoring pulmonary hypertension and response to therapy in these infants has not been adequately described.

Chest radiography

Chest radiography is helpful in determining the severity of bronchopulmonary dysplasia and in differentiating bronchopulmonary dysplasia from atelectasis, pneumonia, and air leak syndrome. Chest radiographs may demonstrate decreased lung volumes, areas of atelectasis and hyperinflation, pulmonary edema (PE), and pulmonary interstitial emphysema (PIE). Hyperinflation or interstitial abnormalities on chest radiograph appears to be correlated with the development of airway obstruction later in life.

More recently, CT and MRI studies of infants with bronchopulmonary dysplasia have provided detailed images of the lung. High-resolution CT may detect radiographic abnormalities not readily identified with routine chest radiography.

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Other Tests

Members of families with a strong history of atopy and asthma may be at increased risk for bronchopulmonary dysplasia and severe bronchopulmonary dysplasia. A review of monozygotic preterm twins revealed concordance of bronchopulmonary dysplasia compared with dizygotic twins.

Polymorphisms in surfactant protein B are associated with bronchopulmonary dysplasia.

Variations in proinflammatory mediators, such as tumor necrosis factor-alpha, are associated with a heightened risk of bronchopulmonary dysplasia.

Future DNA array studies of patients in large multicenter trials may reveal genetic loci specific for abnormal alveolar, pulmonary vascular, and elastin development. Animal studies of the overexpression or underexpression of these genotypes could further elucidate the complex process of pulmonary development.

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Histologic Findings

Four distinct pathologic stages of bronchopulmonary dysplasia are generally described: acute lung injury, exudative bronchiolitis, proliferative bronchiolitis, and obliterative fibroproliferative bronchiolitis.

At present, pathologic examination of extremely low birth weight infants with bronchopulmonary dysplasia reveal greatly reduced total numbers of alveoli and septa. This condition is commonly referred to as the "new" bronchopulmonary dysplasia. [22, 23, 24] A striking arrest in pulmonary alveolar and vascular development is noted, in association with abnormalities in vascular endothelial growth factor and other signaling molecules important for the migration and development of endothelial cells.

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