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Airway muscle in infants with congenital diaphragmatic hernia: response to treatment
A R Broughton1, D W Thibeault, S M Mabry
1Department of Pediatrics, University of Missouri-Kansas City School of Medicine, Children's Mercy Hospital, 64108, USA.
Insights
Congenital diaphragmatic hernia (CDH) infants develop increased airway muscle after treatment, especially with high ventilatory assistance. Acinar artery muscle mass also changes, with delayed postnatal decrease in CDH infants receiving high ventilatory support.
Area of Science:
- Pulmonary Medicine
- Pediatric Surgery
- Neonatology
Background:
- Congenital diaphragmatic hernia (CDH) is associated with airway hyperreactivity and chronic lung disease post-treatment.
- Understanding airway muscle development is crucial for managing long-term respiratory outcomes in CDH survivors.
Purpose of the Study:
- To quantify and compare airway smooth muscle and alveolar ductal artery muscle in infants with CDH.
- To investigate the impact of different treatment modalities, including ventilatory support and extracorporeal membrane oxygenation (ECMO), on airway muscle mass.
Main Methods:
- Postmortem lung tissue analysis from five groups: CDH with/without high ventilation/ECMO, and controls with/without high ventilation/bronchopulmonary dysplasia (BPD).
- Immunohistochemical staining for alpha-smooth muscle actin to quantify muscle in conducting airways and alveolar ductal arteries using computerized image analysis.
Main Results:
- CDH infants on low ventilatory assistance showed normal airway muscle quantity.
- Infants with CDH and prolonged high ventilatory assistance exhibited significantly increased airway muscle, similar to BPD infants.
- Acinar arteries in CDH infants presented with increased muscle at birth, reduced by ECMO but persisting with high ventilation.
Conclusions:
- Postnatal exposure to high ventilatory assistance in CDH infants leads to increased airway muscle in both lungs.
- The normal postnatal reduction in acinar artery muscle mass is delayed in CDH infants requiring high ventilatory support.
Background/Purpose:
Airway muscle hyperactivity and chronic lung disease frequently follow congenital diaphragmatic hernia (CDH) treatment. The aim of this study was to compare the quantity of airway muscle and alveolar ductal artery muscle in CDH infants after various treatments.
Methods:
Five groups were studied postmortem: CDH, died within 24 hours, without high ventilatory assistance (n = 3); CDH, various extracorporeal membrane oxgenation (ECMO) durations, without high ventilatory assistance (n = 4); CDH, various ECMO durations, with high ventilatory assistance (n = 7); no CDH, without high ventilatory assistance (n = 12); and no CDH, with high ventilatory assistance and bronchopulmonary dysplasia (BPD) (n = 5). Sections from standardized fixed lungs were immunohistochemically stained for alpha-smooth muscle actin. Muscle surrounding conducting airways from small preterminal bronchioles to bronchi was quantitated in both the ipsilateral and contralateral lungs with computerized image analysis. Similarly, muscle mass was quantitated in alveolar ductal arteries.
Results:
CDH infants with low ventilatory assistance, regardless of postnatal age, had the same quantity of airway muscle as low ventilatory assistance controls. Infants with CDH and prolonged high ventilatory assistance had significantly more muscle throughout the conducting airways, similar to BPD infants without CDH, even though the CDH infants had significantly less exposure to high ventilatory assistance. With both low and high ventilatory assistance, the quantity of muscle in both the ipsilateral and contralateral lungs was similar. In contrast, small acinar arteries in CDH infants have increased muscle mass at birth. This muscle is decreased by ECMO but persists in CDH infants with high ventilatory assistance.
Conclusions:
The authors show that postnatally, CDH infants acquire increased muscle quantity throughout the conducting airways, in both the ipsilateral and contralateral lungs, with relatively short exposure to high ventilatory assistance. The normal decrease in acinar arterial mass that occurs postnatally is delayed in CDH infants with high ventilatory assistance.