Features

The ductus arteriosus usually closes functionally by 48 hours and anatomically by 3 weeks of age in well, term babies. Closure may take longer in preterm or unwell babies.

PDA is associated with increased risk of death, intraventricular haemorrhage (IVH), chronic lung disease, necrotising enterocolitis and impaired renal function; although a causal relationship has not been proved. Most PDAs are asymptomatic and there is no uniformity in the approach to management of PDA. Many will eventually close spontaneously without any specific intervention. Only a small number will cause heart failure. Complications of PDA are related, at least theoretically, to shunting through the duct, circulatory overload and the ‘diastolic steal’ phenomenon.

Ductal reopening after closure is uncommon.

Diagnosis

The diagnosis of PDA is best done using echocardiography. Clinical signs of a PDA often lag behind the echocardiographic findings by several days, consistent with findings that clinical diagnosis has very low sensitivity. The specificity of many clinical features is also low, as is the inter-observer agreement of the presence of signs. Classical signs that may be sought include:

• systolic or continuous murmur

• wide pulse pressure and bounding pulses

• active precordium

• hepatomegaly

• chest X-ray changes — increased heart size, increased vascularity.

A chest X-ray has been found to add very little to the other clinical signs in the diagnosis of PDA. In high-risk babies, most but certainly not all systolic murmurs will indicate the presence of a duct. Remember also that some babies (including preterm ones) will have a duct-dependent cardiac lesion.