Patent Ductus Arteriosus (PDA)

Last updated 2015 - Written by Dr. Benjamin Marsh

Definition

The ductus arteriosis, derived from the 6th embryologic arch, connects the left PA to the descending aorta. Its patency is normal in the fetal period but is abnormal beyond a few days postnatal. Incidence is near 0.8/1000 live births and 5-10% of full-term infants with CHD have PDA. Term and preterm present and are treated very differently. In preterm infants <1750g,  45% will have clinical evidence of PDA. This increases to 80% of premature infants less than 1200 g.

PDA can lead to pHTN and pulmonary vascular obstructive disease eventually leading to R->L shunt, cyanosis and CHF.

Clinical Manifestations

• Presentation: asymptomatic if the duct is small, but CHF, recurrent PNA may develop if it is large.
• Preterm infants present with episodes of apnea, bradycardia or delayed weaning from ventilation.
• PE: a grade 1 to 4/6 continuous (machinery) murmur best audible at the ULSB or left infraclavicular area is pathoneumonic. In early neonatal period a SEM ULSB may be heard. A large PDA may have an apical diastolic rumble, bounding pulses with wide pulse pressure

• There are a number abnormalities that mimic this continuous murmur including venous hum (benign and disappears when supine), various fistula, collaterals, VSD with AR, truncus arterious, AP window, PPS, valsalva aneurysm and TAPVR.
• ECG: WNL or LVH . A large PDA may have BVH. If long standing RVH indicates PVOD
• CXR: cardiomegaly and increased PVM may be present in a large PDA. Normal heart size and prominent MPA and hilar vessels are present in PVOD
• Echo is diagnostic.

Management

In term infants spontaneous closure of PDA usually does not occur nor is indomethacin effective.

If the PDA is <4 mm in diameter it can be closed with a catheter placed coil.  If the PDA is 4-10mm an Amplatzer PDA device can be used with a near 100% closure rates.

Complications may include residual leaks, coil embolization to PA, hemolysis, left PA stenosis, aortic occlusion with the Amplatzer device, and femoral vessel occlusion.

If the PDA is larger than 10mm than surgery is an option. Surgery is often used in very small infants where trans-catheter delivery is not possible. Ligation and division is done through a left posterolateral thoracotomyor VATS without bypass.

Asymptomatic preterm infants with a small PDAF can be followed for 6mo as >30% will close spontaneously.

In a preterm infant with hyaline membrane disease a PDA will increase the need for ventilator support and may lead to chronic lung disease and pulmonary hypertention.

Symptomatic preterm infants are managed with fluid restriction to 108 mL/kg per day, chlorothiazid, PEEP, and maintain HCT 35-40%. Indomethacin Q12h x3 can be used to close the PDA. Contraindications include BUN>25 or creatinine>1.8, and platelets <80,000, ICH, NEC and high bili. If medical treatment is unsuccessful or contraindicated, surgical ligation of the ductus can be performed in the NICU. It is typically well tolerated and mortality is 0% to 3%.

Post op

No restriction of activity is indicated unless pHTN is present.

Sources: Park Ch 3, Nadas’ Ch 35, Nelsons