Patent ductus arteriosus (PDA) is a congenital condition in which the ductus arteriosus, a normal fetal blood vessel connecting the aorta and the pulmonary artery, fails to close after birth. During fetal development, the ductus arteriosus diverts blood away from the non-functioning lungs. Normally, the rise in oxygen levels at birth triggers closure of the ductus within the first days to weeks of life. When it remains open (patent), it creates an abnormal connection between the two great arteries.
Under normal circumstances, blood pressure is higher in the aorta than in the pulmonary artery, so blood shunts from the aorta to the pulmonary circulation, increasing blood flow to the lungs and volume load on the left heart. A small PDA may cause no symptoms; a large PDA causes breathlessness, poor growth in infants, and a classic ‘machinery’ murmur on auscultation. If untreated over years it can lead to irreversible pulmonary hypertension.
PDA is more common in premature infants, in whom spontaneous closure is less reliable. In premature babies, indomethacin or ibuprofen can be used to promote closure. When medical treatment fails or in older patients, closure can be achieved by a catheter-based transcatheter occlusion device or by surgical ligation.
In adults with an unrepaired or previously repaired PDA, follow-up in adult congenital heart disease services is recommended. Residual PDAs in adults are usually treated when haemodynamically significant, due to the long-term risk of pulmonary hypertension and left heart volume overload.
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