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Key Concepts


  • Epidemiology

    • The ductus arteriosus is a normal fetal structure, that arises from the left sixth aortic arch, and connects the proximal left main pulmonary artery to the upper descending thoracic aorta. Persistent patency beyond the neonatal period occurs in approximately 1 in 2500 term live births, with a male-to-female ratio of 2:1. Patent ductus arteriosus (PDA) accounts for 5 to 10 percent of all congenital heart defects, with up to 30 percent of cases observed in preterm infants.

  • Pathophysiology

    • The presence of a large, nonrestrictive PDA leads to left-to-right shunting with pulmonary overcirculation, subsequent left atrial dilatation, left ventricular volume overload, and congestive heart failure; if left untreated, irreversible pulmonary hypertension and Eisenmenger physiology with right-to-left shunting and cyanosis ultimately ensue.

  • Clinical features

    • Presentation may range from absence of symptoms to the presence of a “machinery-like” murmur with poor feeding, failure to thrive, tachypnea, and recurrent respiratory infections.

  • Diagnosis

    • Chest x-ray typically discloses increased pulmonary vascular markings, pulmonary edema, and cardiomegaly. Transthoracic echocardiography demonstrates the ductal anatomy and any coexisting defects.

  • Treatment

    • Treatment strategies include pharmacologic closure with indomethacin in premature infants, catheter-based closure with coil occlusion in older children and adults, video-assisted thoracoscopic (VATS) closure, and conventional thoracotomy and ligation. Whereas operative outcomes in premature newborns are heavily dependent on associated comorbidities, morbidity and mortality from surgical or percutaneous closure in infants and children are almost negligible.




The ductus arteriosus is a normal vascular connection between the pulmonary arterial trunk and the proximal descending thoracic aorta, and is an essential component of the fetal circulation. During fetal life, it allows right-to-left shunting of maternally-derived oxygenated placental blood to the systemic circulation, bypassing the high-resistance pulmonary bed. Following birth, increases in oxygen tension and a drop in pulmonary vascular resistance trigger spontaneous closure (contraction and subsequent fibrosis) of the ductus. Patent ductus arteriosus (PDA) is the persistence of the ductus as a vascular structure (rather than a ligamentous connection) beyond the early neonatal period, leading to unabated left-to-right shunting between the aorta and pulmonary artery with subsequent pulmonary overcirculation.


With an incidence of 1 in 2500 to 5000 births, PDA is the second most common congenital cardiac malformation.1 Although recognition of the presence of the ductus arteriosus during fetal circulation dates to Galen, it was not until 1907 that John Monro first suggested surgical ligation of PDA in an address to the Philadelphia Academy of Surgery.2 Thirty-one years later, in 1938, the first operation was attempted by Graybiel and Stieder in a 22-year-old woman with bacterial endocarditis involving the arterial duct.3 Although the PDA was successfully ligated, the patient succumbed to infection and gastrointestinal complications a week later. Although primacy is still disputed, Robert Gross is credited, later in that same year, with the first ligation of a PDA in a 7-year-old child with severe heart failure.4 Although a PDA can today be interrupted through interventional ...

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