Patent ductus arteriosus (PDA)

Published on 03/06/2015 by admin

Filed under Neonatal - Perinatal Medicine

Last modified 22/04/2025

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CHAPTER 7 Patent ductus arteriosus (PDA)

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.

Decision to treat

The decision to treat a PDA should be based on more than just finding it. Factors such as the baby’s age and gestational age, general condition, and degree of left-to-right shunting should be taken into account. Systematic reviews have not shown any significant benefit to treatment of asymptomatic nor symptomatic PDA. However, most neonatologists would have difficulty ignoring a symptomatic duct and many also choose to treat asymptomatic ducts under some circumstances.

Information that may be provided by the cardiologist or echocardiographer that would indicate a more significant or ‘troublesome’ duct includes:

• size of the duct

• direction of the shunt

• dilatation of the left heart — a left atrial : aortic root ratio >1.48 is significant

• absent or reversed diastolic flow in the descending aorta.

An assessment of left ventricle function (usually the fractional shortening) is also useful.

Treatment options

Treatment options include cyclo-oxygenase inhibitors or surgical ligation — this is discussed further below.

Indomethacin

Reasonably strong evidence is available to support the use of prophylactic indomethacin, where those at high risk of PDA are given treatment early — usually within 12 hours of birth. This has been shown to be quite safe and significantly reduces the incidence of PDA, the need for medical or surgical treatment of PDA, and grade 3 or 4 IVH.

As there are no proven long-term benefits (e.g. survival, neurosensory impairment), some neonatologists choose not to use prophylaxis.

• Treatment or prophylaxis usually consists of intravenous indomethacin (see page 81 for regimens). It should be given by infusion over at least 20 minutes.

• Enteral indomethacin should be avoided if possible.

• Contraindications to the use of indomethacin include duct-dependent congenital heart disease, significant renal disease, oliguria (<0.5 mL/kg/hr over 24 hours has been used in some trials), platelet count <50 × 10⁹/L, overt bleeding (other than pulmonary haemorrhage).

• Side effects include decreased urine output, oedema, hyponatraemia and gastrointestinal bleeding.

• Some use ibuprofen instead of indomethacin.

Fluid restriction

There is some evidence to suggest that babies managed with more restricted fluid intake in the first several days of life have lower risk of PDA than those whose fluid intake is more liberal.

Our preferred approach to fluid administration is regarded as being on the ‘restrictive’ end of the spectrum. This should be distinguished from fluid restriction as an approach to the management of PDA. In the presence of a large shunt and heart failure, it is sensible to use fluid restriction with or without diuretics. With asymptomatic or uncomplicated PDA, however, it is illogical to fluid-restrict, and doing so by 20–30 mL/kg/day (as is frequently done) probably achieves nothing other than denying important calories to the baby.

Surgical ligation

There is no good evidence to support the use of duct ligation as initial management of PDA under normal circumstances. Likewise, it is not clear whether those whose medical treatment has failed to close the duct benefit from ligation.

Ligation can be achieved via a number of approaches, which will be surgeon-dependent. Most babies who undergo ligation have a left lateral thoracotomy and the duct is either sutured or clipped.

Post-operative morbidity can include vocal cord paralysis, chylothorax, pneumothorax, exacerbation of chronic lung disease, thoracic scoliosis, infection and significant pain. Accidental ligation of the left pulmonary artery or aorta has been reported.

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