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[Pulmonary dysplasia in infancy. Pathogenesis, pneumologic course studies and therapy possibilities]
Insights
Broncho-pulmonary dysplasia (BPD) in newborns involves damage to airways from respiratory support. This damage can lead to chronic lung issues, but some lung function may improve over time.
Area of Science:
- Neonatal respiratory medicine
- Pediatric pulmonology
- Pathology of the respiratory system
Context:
- Broncho-pulmonary dysplasia (BPD) is a common complication in newborns requiring respiratory support.
- Intermittent positive airway pressure (IPPV) and high oxygen concentrations are often necessary for treating respiratory distress syndrome.
- Radiographic and electron microscopic findings reveal characteristic airway damage in BPD.
Purpose:
- To describe the characteristic damage of bronchi and bronchioles in BPD.
- To categorize radiographic findings into four progressive stages.
- To investigate the potential long-term consequences of airway injury in BPD.
Summary:
- BPD involves airway damage (bronchi, bronchioles) in newborns treated with IPPV and high oxygen.
- Radiographic stages range from granularity to emphysema, atelectasis, and fibrosis.
- Electron microscopy shows ciliary damage, goblet cell hyperplasia, and epithelial metaplasia, potentially leading to chronic obstructive airway disease.
Impact:
- Understanding BPD's airway pathology is crucial for managing chronic respiratory conditions in infants.
- Identifying risk factors like IPPV, oxygen, fluid intake, and PDA is key for prevention.
- Therapeutic strategies include symptomatic treatment and preventive measures focusing on ventilation and fluid management.
Abstract:
Some premature and mature newborns who require intermittent positive airway pressure (IPPV) and high oxygen concentrations for respiratory distress syndrome develop characteristic damage of bronchi and bronchioles termed broncho-pulmonary dysplasia (BPD). According to the radiographic findings the changes are categorized into four progressive stages. Stage 1 describes a radiographic feature with a pattern of fine, faint granularity as it is characteristic for the hyaline-membrane-syndrome. Stages 2 to 4 represent diffuse interstitial emphysema, a bubbly appearance of the lung, atelectasis and a progressive fibrosis. Electronmicroscopic investigations of bronchial imprints could demonstrate a rarefication of the cilia and a ciliary damage which took the form of compound cilia. In addition, a marked increase of goblet cells in the bronchial mucosa as well as a metaplasia of the epithelial cells was present. These findings may be a prerequisite for chronic infections, and perpetuate a cycle which may result in chronic obstructive airway disease. The significance of bronchial and bronchiolar injury in children with BPD is said to be due to IPPV, high inspiratory oxygen concentrations, high fluid intake, vitamin E deficiency or an increased intrapulmonary pressure secondary to a patent ductus arteriosus. When pulmonary mechanics were measured in a baby-body-plethysmograph a high pulmonary resistance and a low dynamic compliance occurred at the first investigation after IPPV or oxygen administration. On re-examination there was a strong tendency to normalisation of x-ray findings and pulmonary mechanics, depending upon the time which elapsed between ventilation and re-examination. Current therapy has to be symptomatic and may include secretolytics, glucocorticoids and bronchodilators. The preventive interventions have to take into consideration ventilation techniques, restrictions in O2 and fluid intake.