A premature infant is born with a patent ductus arteriosus. Its closure can be stimulated by administration of –

Management of PDA After birth ductus arieriosus constricts within a few hours producing functional closure. Permanent anatomic closure follows in the next 10-21 days due to extensive intimal thickening. The mechanism producing the initial constriction is not completely understood, but the increase in arterial 02 tension plays an important role. One more factor which helps in closure of the ductus arteriosus is the decrease in concentration of prostaglandins at the time of birth In the intrauterine period the concentration of prostaglandin PGF2 a is very high. This prostaglandin has a vasodilatory effect which keeps the ductus open. The synthesis of these vasodilator is inhibited at birth by the inhibition of the enzyme cycloxygenase at birth. Cycloxygenase is an important enzyme in the synthetic pathway of prostaglandin. In many premature infants the ductus fail to close spontaneously. In these cases the closure can be produced by infusion of drugs that inhibit cyclooxygenase. Indomethacin is a potent inhibitor of prostaglandin synthesis. It inhibits prostaglandin synthesis by inhibiting the enzyme cyclooxygenase. Indomethacin is routinely used to close the PI A in premature infants, it does not close the P I.A of full term  infants or children. The success of indomethacin therapy is as high as 80-90% in premature infants with birth  weight over 1200 g. If indomethacin is not successful and the ductus remains hemodynamically significant, surgical ligation should be performed without hesitation. Recent studies from Europe indicate that ibuprofen may be as effective as indomethacin for the medical closure of pretenn PDA.