Patent ductus arteriosus (PDA) is common problem, with rates of 40–55% in babies born less than 29 weeks’ gestation,1 2 yet decisions related to management remain highly controversial. Despite numerous studies on the topic there remains uncertainty with respect to diagnosis, assignment of clinical importance, whether treatment is indicated and if so the preferred treatment modality. The most fundamental question remains unanswered: does a PDA cause acute physiological or clinical change that either acutely or chronically leads to organ damage, which further leads to important neonatal morbidities? Put simply is the PDA an “innocent bystander” or is it pathological to the extent that early detection and intervention is warranted to prevent neonatal morbidity?

It is physiologically plausible that a major systemic to pulmonary (left-to-right) shunt can lead to considerable postnatal morbidities in extremely low birthweight (ELBW) infants, either from pulmonary overcirculation (eg, chronic lung disease (CLD)) and/or systemic hypoperfusion (eg, necrotising enterocolitis (NEC), acute renal impairment).3 The lack of evidence supporting causality,4 5 failure of medical treatment in some cases1 and the inherent risks of medical6 7 or surgical treatment options8 has led some investigators to question whether intervention is necessary. In contrast, studies of prophylactic indometacin show reduced rates of PDA ligation, early major pulmonary haemorrhage and serious (grades III–IV) intracranial haemorrhage.9 10 This strategy does, however, expose 40% of babies, in whom spontaneous PDA closure would have occurred, to any adverse effects of treatment.

The medical community is becoming increasingly divided on the question of treatment of the PDA. Laughon and Bose highlight some important gaps in our knowledge with respect to therapeutic intervention.11 They emphasise that recent trials of non-steroidal anti-inflammatory agents have not led to any …