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?

Although some may consider this to be semantics, the difference between a PDA and a haemodynamically significant ductus arteriosus (HSDA) has not been emphasised clearly enough in the literature, so the two terms have been used synonymously. It must be remembered that “patent ductus” does not necessarily imply there are physiological effects leading to haemodynamic instability or indeed any clinical problem. The PDA may represent normal physiological adaptation, where it has an important role in supporting pulmonary blood flow in the transitioning lung.12 The decision to intervene should be based on the echocardiographic documentation of an important left‐to‐right transductal shunt, with measurable haemodynamic effects, leading to clinical instability.

Although an HSDA has been linked to important neonatal morbidities such as CLD and NEC,18,19,20 there remains little evidence that treatment improves either short‐term or long‐term outcomes. A recent study in premature baboons showed altered pulmonary mechanics and arrested alveolarisation after 14 days of exposure to a moderate‐sized ductus21; Pharmacological intervention led to improvement in lung mechanics and increased alveolarisation. Why therefore have the benefits of ductal closure seen in animal models not been translated into improved outcomes for human neonates?

The effects of the HSDA on acute physiological change and short‐term clinical outcomes are also variable. These effects of the HSDA are usually related to altered pulmonary (Qp) to systemic (Qs) blood flow, leading to pulmonary overcirculation and systemic hypoperfusion. Although improved lung function, coinciding with ductal closure, has been shown with both indometacin treatment and surgical ligation,25,26 others have found no difference in compliance in neonates with respiratory distress syndrome.27 Oftentimes, the primary presenting problem of the HSDA may be early systolic and diastolic hypotension.28 Inadvertently these babies are commonly treated with cardiotropic agents, such as dopamine or dobutamine, in an attempt to increase the blood pressure.29 These agents may be of benefit if there is coexisting myocardial dysfunction, however, they may also promote left‐to‐right ductal shunting by increasing systemic vascular resistance.

The trials conducted to date, although not designed to assess harm, do provide some useful information on adverse effects of non‐steroidal treatment. Transient alterations in cerebral perfusion6 during indometacin administration have been shown, but prophylactic treatment is more likely to decrease the incidence of periventricular leucomalacia10 and led to improved long‐term outcome at 4.5 and 8 years.33 In addition, any renal impairment during medical treatment is entirely reversible.7 These studies do not provide any plausible rationale for complete avoidance of medical intervention. The adverse effects of PDA ligation are well recognised and include both reversible complications, such as pneumothorax, infection or haemorrhage, and irreversible complications, including chylothorax and vocal cord paralysis,34 which may lead to major patient morbidity and even mortality. Not uncommonly the postoperative course is characterised by a post‐ligation cardiac syndrome consisting of oxygenation failure due to pulmonary oedema, systolic hypotension and the need for cardiotropic support, which typically occur 8–12 hours after the procedure.35 Previously we have shown that surgical intervention was associated with myocardial dysfunction secondary to increased left ventricular afterload coinciding with the clinical deterioration. Kabra et al have recently highlighted an association between PDA ligation and an increased risk of bronchopulmonary dysplasia, severe retinopathy of prematurity and neurosensory impairment.36 It is impossible to determine whether this relationship reflects causality or whether need for PDA ligation is merely a marker for illness severity. Unfortunately their study did not consider the heterogeneity of clinical and echocardiographic changes that may occur with varying severity of ductal disease.