Clinical Findings

HISTORY

The typical child with a PDA is asymptomatic.
  • A history of premature birth, perinatal distress, or perinatal hypoxia may be present.

  • Some series have suggested that children born at extreme altitude have an increased incidence of a persistent PDA.

  • Occasionally, a history of feeding difficulties and poor growth during infancy, described as failure to thrive, is found. However, frank symptoms of congestive heart failure are rare.

  • In the low birthweight premature infant, diagnosing a PDA on auscultation may be difficult. Babies that have a more severe clinical course of hyaline membrane disease may have a higher prevalence of PDA. The exact reason for this is unclear.


PHYSICAL

As many as one third of children with PDA are small for their age. In the presence of significant pulmonary overcirculation, tachypnea, tachycardia, and a widened pulse pressure may be found.
  • Findings upon cardiac examination include the following:

    • If the left-to-right shunt is large, precordial activity is increased, with the magnitude of increased activity related to the magnitude of left-to-right shunt.

    • The apical impulse is laterally displaced. A thrill may be present in the suprasternal notch or in the left infraclavicular region.

    • The first heart sound (S1) is typically normal. The second heart sound (S2) often is obscured by the murmur. Phonocardiographic data from the past suggested the occurrence of paradoxical splitting of S2 related to premature closure of the pulmonary valve and a prolonged ejection period across the aortic valve.

    • In 1898, Gibson described the classic murmur. Subsequently, the classic PDA murmur has been referred to as a machinery murmur, which is continuous. The murmur may be systolically accentuated. It is typically loudest at the left upper chest. If the pulmonary-to-systemic blood ratio approaches or exceeds 2:1, an apical flow rumble, caused by high flow across the mitral valve into the left ventricle, frequently is present. Also, since flow through the left ventricle into the aorta is increased, an aortic ejection murmur may be present. If the PDA is small, the amplitude of the murmur may increase with inspiration as pulmonary impedance drops.

  • The peripheral pulses often are referred to as bounding. This is related to the high left ventricular stroke volume, which may cause systolic hypertension. The phenomenon of bounding pulses also is caused by the low diastolic pressure in the systemic circulation as blood runs off from the aorta into the pulmonary circulation.

  • In the low birthweight premature infant, the classic signs of a PDA are usually absent. The classic continuous murmur rarely is heard. A rough systolic murmur may be present along the left sternal border, but a small baby with a large PDA and significant pulmonary overcirculation may have no murmur. In that case, typically, precordial activity is increased and peripheral pulses are bounding. The increased precordial activity is caused by the large left ventricular stroke volume. The bounding pulses are caused by the relatively low systemic arterial blood pressure due to the continuous runoff of blood from the aorta into the pulmonary artery.


CAUSES
  • Familial cases of PDA have been recorded, but a genetic cause has not been determined.

  • Several chromosomal abnormalities are associated with persistent patency of the ductus arteriosus. Implicated teratogens include congenital rubella (associated with PDA and pulmonary artery branch stenosis), fetal alcohol syndrome, maternal amphetamine use, and maternal phenytoin use.