Last edited 03/2021 and last reviewed 05/2022

Because the shunt is initially left to right there is normally no cyanosis.

With time, pulmonary hypertension and pulmonary vascular disease may develop, resulting in reversal of the flow, causing right ventricular hypertrophy, cyanosis, clubbing and polycythaemia.

Because the ductus joins the aorta distal to the left subclavian artery, the cyanosis does not affect the head and arms.

If the shunt is small and the pulmonary pressure is normal then if is possible for there to be survival, without symptoms, into adult life. However the chronic overloading of the left ventricle, as a result of flow from the aorta to pulmonary artery, may lead to cardiac failure.

Although systolic blood pressure may be sustained despite a left-to-right ductal shunt, the drop in diastolic blood pressure and localized vasoconstriction are believed to contribute to the clinical consequences of PDA (1,2,3)

  • a significant left-to-right shunt secondary to the ductus has been associated with complications that include increased rates of bronchopulmonary dysplasia, intraventricular hemorrhage (IVH), necrotizing enterocolitis, decreased middle cerebral artery blood flow, worsening RDS, and death
  • note though that a precise causal link between these associations has not been demonstrated (3)


  • Clyman RI. Ibuprofen and patent ductus arteriosus. New England Journal of Medicine 2000;343(10):728-30.
  • Dice JE, Bhatia J. Patent ductus arteriosus: an overview. Journal of Pediatric Pharmacology and Therapeutics 2007;12(3):138-46.
  • Benitz WE. Treatment of persistent patent ductus arteriosus in preterm infants: time to accept the null hypothesis? Journal of Perinatology 2010;30(4):241-52.