Patent ductus arteriosus medical therapy in preterm infants

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Priyamvada Singh, M.B.B.S. [2], Cafer Zorkun, M.D., Ph.D. [3]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [4]

Prostaglandin E2 plays a key role in maintaining the patency of ductus arteriosus before birth. Thus, prostaglandin E2 inhibitors are used as a therapeutic options to close the patent ductus arteriosus.

In term infants the ductus closure occur by 24 hours of birth in 50% of babies, by 48 hours in 90% of babies and by 72 hours in most of them. However, the ductal closure is delayed in preterm infants.

Ductal constriction occurs after birth due to the following reasons

• The increased oxygen tension after birth with the onset of breathing.
• Decreased prostaglandin E2 due to removal of placenta.
• Increased removal of prostaglandin E2 from lung.

• Prostaglandin E2 has been found to play a key role in maintaining the patency of ductus arterisus (DA) in the fetal life. Thus, the use of inhibitors of prostaglandin synthesis (e.g, indomethacin and ibuprofen) have been found to be effective in the treatment of PDA. These drugs were also found to be useful in ductus closure if given antenatally. Patients with cases involving the transposition of the great vessels (TGV) may need the ductus arteriosus kept open with prostaglandin E1 (PGE1).
• Steroids like hydrocortisone have been found to decrease the sensitivity of ductus to PGE2. Thus, facilitating ductal constriction.
• Nitric oxide synthesized from endothelial cells have been shown to cause ductus constriction in animal studies.