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Chronic lung disease of prematurity: clinical and pathophysiological correlates
1Department of Child Health, University of Leicester, Leicester LE2 7LX, United Kingdom.
Insights
Chronic lung disease of prematurity (CLD) affects preterm infants needing mechanical ventilation. This condition involves lung structural abnormalities, leading to breathing difficulties and potential long-term respiratory issues.
Area of Science:
- Neonatology
- Pediatric Pulmonology
- Respiratory Medicine
Background:
- Chronic lung disease of prematurity (CLD) primarily affects preterm infants requiring mechanical ventilation.
- Development is linked to preterm birth, pulmonary inflammation, oxidative stress, ventilator-induced barotrauma, and infections.
Purpose of the Study:
- To describe the pathological and clinical characteristics of CLD.
- To outline current management strategies and concerns for long-term outcomes.
Main Methods:
- Review of pathological findings in infants with established CLD.
- Analysis of clinical manifestations and contributing factors.
Main Results:
- Pathology reveals airway wall thickening, smooth muscle hypertrophy, alveolar hypoplasia, and pulmonary vascular remodeling.
- These structural changes correlate with hypoxemia, hypercapnia, tachypnea, wheezing, and reduced exercise tolerance.
Conclusions:
- CLD involves significant structural lung abnormalities in preterm infants.
- Management focuses on symptom control and growth, but long-term respiratory failure risk remains a concern.
Abstract:
Chronic lung disease of prematurity (CLD) is largely confined to preterm infants who require mechanical ventilation in the newborn period. Its development is associated with preterm labour and pulmonary inflammation secondary to oxidant stress, barotrauma of mechanical ventilation and antenatally--or postnatally--acquired respiratory tract infection. Pathological studies have shown that infants dying of established CLD have airway wall thickening secondary to increased airway wall smooth muscle mass, alveolar hypoplasia and pulmonary vascular re-modelling. These structural abnormalities are likely to account for the clinical problems of arterial hypoxemia and hypercapnia, tachypnea, recurrent wheezing and decreased exercise tolerance. Severity of the structural components may account for the clinical variation that is observed in a particular child. Management of CLD is aimed at decreasing the effects of hypoxemia and in maximising somatic, and by implication lung, growth. Low flow domiciliary oxygen and bronchodilators are used for arterial hypoxemia and recurrent wheezing. Systemic and inhaled corticosteroids may be beneficial but it is unclear if such treatment alters the natural history of CLD in the developing lung. Gastro-esophageal reflux should be sought in these infants and they should receive immunizations or immunoprophylaxis against respiratory tract pathogens. There is considerable concern that survivors of CLD may develop respiratory failure in early--or late--middle age.