The ductus arteriosus (DA) does one thing with its life, it constricts after birth in response to rising pO2, achieving functional closure often by 24 h. If it fails to constrict or close, it remains as a passive conduit with movement of blood determined by the relative pressure at each end. Constriction and closure in well preterm babies occurs in similar time frame to term babies but in the very immature or unwell preterm, this process can fail.
The early postnatal constriction of the preterm ductus predicts its subsequent behaviour with good constriction predicting closure and poor constriction predicting persisting patency. Because pulmonary pressures in preterm babies tend to be sub-systemic even early after birth, the dominant direction of shunting is left to right. In those where constriction fails, large movements of blood from the systemic to pulmonary circulation can occur. The haemodynamic impact of this can be much earlier than is widely appreciated with large PDA being a stronger predictor of low systemic blood flow early after birth than later and overload of the pulmonary circulation, apparent as pulmonary haemorrhage, within the first 24–36 hrs.
This pathophysiology suggests that early intervention will be needed to make a difference to DA related morbidity. The predictive properties of early DA constriction provides an opportunity to target early treatment. This has been tested in the pilot DETECT trial with a reduction in pulmonary haemorrhage. Larger RCTs that embrace the above physiology in their design are needed.