The pattern of chronic lung disease in infants born prematurely has changed considerably in the past decades, reflecting both better perinatal management and increasing lung immaturity with the survival of increasingly premature infants.14
However, the pathologic description of this new BPD is mostly based on autopsy specimens from the most severely ill infants.3
In infants with less severe BPD, little is known about the correlation between CT and lung function test findings and the neonatal history. We describe, for the first time, CT and lung function test findings before 2 years of life in infants with symptomatic BPD who benefited from optimised neonatal care and a high rate of administration of surfactant. Although our results are based on a selected population with persistent respiratory symptoms, and therefore do not constitute a global description of the respiratory outcome in very low birthweight infants, many findings of the present study are of interest. First, we have shown that multifocal hyperlucent areas, linear opacities and subpleural opacities are the prominent CT features. In contrast, no bronchial involvement was observed. Second, linear opacities and subpleural opacities, but not hyperlucent areas, correlated with FRC and neonatal management, suggesting different mechanisms for these CT findings.
All the infants had abnormal CT findings, although some CT scans showed only minor lesions. The cardinal CT features included multifocal hyperlucent areas, linear opacities and subpleural opacities. Many of our CT findings have been previously observed in children with “old” BPD.8
This is in agreement with many of the histopathological features of BPD described over the past 20 years, which are similar whether or not the infants benefited from optimised management.5
Thus, our CT findings strongly suggest that infants with BPD who have been treated with exogenous surfactant still show variable association between impaired alveolarisation, abnormal vascularisation and interstitial fibroproliferation. In previous CT studies, reticular opacities and multifocal areas of reduced density were routinely observed, and areas of architectural distortion,8
triangular subpleural opacities10
and a reduced bronchus‐to‐pulmonary artery diameter ratio9
were less frequent. These lesions may be induced by several mechanisms. Architectural distortions and reticular opacities are probably related mainly to fibrosis, which is the endpoint of abnormal lung repair. In our study, such lesions were still seen and we described them as linear opacities and triangular subpleural opacities. Areas of reduced density may be related to air trapping associated with bronchiolar obstruction. The airways are noticeably involved in classic BPD, and both bronchial wall thickening and decreased bronchial diameter have been observed in adulthood.9
We observed no such lesions in our population with new BPD, and the relative absence of bronchial involvement seems to confirm that reported in recent autopsy studies of infants having died of BPD.4
Furthermore, we found no relationship between the presence of areas of decreased density on CT and airway obstruction. These hyperlucent areas may therefore correspond mainly to abnormal alveolar development and reduced distal vascularisation, which constitute the key findings in new BPD.4
These features were present in nearly 90% of our infants and did not correlate with neonatal history, or with immaturity itself (reflected by low gestational age or birth weight), suggesting that prematurity per se interferes with alveolar development, as has been demonstrated in animal models.16
In contrast with hyperlucent areas, linear opacities and subpleural opacities correlated with neonatal insults such as oxygen supplementation and mechanical ventilation. Oxygen supplementation was the most consistent neonatal factor associated with these CT abnormalities. The number of triangular subpleural opacities had the strongest association with disease severity, as it was the unique finding that significantly differed between infants with mild BPD and those with moderate or severe disease. Aquino et al
similarly found in classic BPD a correlation with architectural distortion but not with areas of decreased density.8
However, the correlations we found between CT findings and oxygen exposure or mechanical ventilation do not imply a causal relationship. Oxygen supplementation may be the indicator of severe lung disease rather than the inducer of the lesions. Nevertheless, our results show that less aggressive care of very low birthweight neonates can still induce tissue injury and interfere with alveolar and pulmonary vascular development. Oxygen supplementation,17
have been all shown to inhibit alveolarisation.
Our lung function test findings are consistent with the above mentioned observations. The alterations in lung volume and airway flow were similar to those previously reported.7
However, only reduced FRC correlated with neonatal events. Similarly, Baraldi et al
did not find any relationship between VmaxFRC and the duration of supplemental oxygen exposure in premature infants evaluated at 16 months of age.6
The decreased values observed in our population of infants with symptoms may therefore reflect hyper‐reactive airway disease rather than oxygen‐induced airway sequelae. The absence of bronchial lesions on CT reinforces this hypothesis. However, in absence of measurement of hyper‐reactivity, we cannot exclude that a fixed, reduced airway calibre may have contributed to the low VmaxFRC values. In the absence of appreciable airway disease, low FRC may therefore be related to fibrotic pulmonary lesions and/or to reduced absolute lung volume due to arrested septation. This is consistent with the significant association that we found between FRC and the number of triangular subpleural opacities or linear opacities on CT.
Finally, CT and lung function abnormalities did not correlate with the severity of respiratory symptoms following discharge. This suggests that these lesions were mainly influenced by the neonatal insults in our population of very low birthweight infants, and are poor predictors of the severity of persistent symptoms after discharge. These results do not argue for considering CT or lung function tests as helpful in routine practice in the care of infants with symptomatic BPD.
In conclusion, CT lesions are illustrative of the pathologic mechanisms responsible for BPD: alveolar and vascular growth disorders, as well as abnormal tissue repair and fibrosis. Despite advances in neonatal care, many CT findings are similar to those observed in the pre‐surfactant era, and are still associated with duration of oxygen supplementation and mechanical ventilation. The absence of bronchial involvement was the most striking difference with previous studies, in agreement with autopsy data.