I wrote about this trial after last year’s PAS meeting, mentioning that it looked like a potential significant improvement in respiratory care of the preterm The full publication confirms that is a real possibility. McEvoy CT, et al. Extended Continuous Positive Airway Pressure in Preterm Infants Increases Lung Growth at 6 Months: A Randomized Controlled Trial. Am J Respir Crit Care Med. 2025;211(4):610-8.

The trial enrolled 100 preterm infants (24 to 32 weeks GA) who had at least 24 hours of CPAP and were considered ready to have the CPAP stopped (5 cmH2O, 21% O2, without tachypnoea or retractions or frequent apnoea, and tolerating breaks from CPAP during care procedures). They had to satisfy these criteria for 12 hours to be considered “stable”. (The pilot trial published previously used a pressure of 4-5 cmH2O, with the same criteria). They randomized the babies to their usual care, which was stopping the CPAP, or to remain on CPAP for a further 2 weeks. Neither this publication, nor the pilot, nor the registration documents, states what pressure was used for this extended CPAP treatment. Which I think is critical, did they use 4 or 8 cmH2O? or something in between?

Babies averaged about 30 weeks GA, and were eligible for the trial at a mean 32.4 weeks PMA, a minority in each group had required surfactant (25% vs 37%). Occasional infants paused the extended CPAP because of local nasal trauma, and occasional controls had to have their CPAP restarted.

Short term results confirmed the increase in FRC with prolonged CPAP, as demonstrated in the pilot, when measured just after the intervention period. At 6 months the infants had lung function testing, which showed improved Alveolar volume, improved DLCO, and better Forced Expiratory Flows.

FEF is, of course, a measure of small airways function, and is frequently impacted by preterm delivery, this result is reassuring that the increase in alveolar volume is not just because the alveoli are distended, but probably lung growth overall is increased, including small airways. That would be consistent with findings from animal models; prolonged CPAP does not simply distend the lungs, it seems to promote lung growth, and, in a couple of models, decreases airway reactivity.

Parents were questioned about wheezing, and bronchodilator use. The questionnaire also asked about hospitalisations, and respiratory hospitalisations, but those data are not reported. Babies in the extended CPAP group were less likely to have wheeze, 43% vs 56%, but this is within the confidence intervals of no difference.

The major limitation of this trial, in terms of impact on clinical practice, is that these are babies with very little lung disease, only about 7% in each group had BPD, (Oxygen at 36 weeks). Although even such relatively minor lung disease of prematurity is known to lead to long term impacts on pulmonary health, whether the intervention would be equally as effective among infants with sicker lungs is unknown.

Routinely extending every baby’s CPAP by 2 weeks would have major impacts on resource utilisation, so we really need robust data. It also could have adverse impacts on oral feeding, especially breast feeding, during the time period when orality is also developing. Most of the babies in this study finished the intervention between 34 and 35 weeks, so the interference with developing breast feeding may have been small, but if babies who become eligible later (in terms of PMA) are treated with extended CPAP, the progression of breast feeding might be a major issue.

I hope that further trials, including infants requiring oxygen supplementation, and with more extensive analysis of outcomes of direct interest to parents, are planned. I also hope that the possible impact on breast feeding is investigated. If every very preterm baby, who is otherwise clinically ready to have their CPAP discontinued, will have that treatment extended for 2 weeks, we need to be very sure that the benefits justify the extra resources, and that there are no balancing negative effects.