Problem of patent ductus arteriosus in premature infants

Postanatal closure of the ductus arteriosus depends on the level of O2 to which it is exposed. Certain vasoactive substances may also play a role in this constriction. The response to O2 is not as well developed in immature fetal animals and this probably explains the high incidence of patent ductus arteriosus (PDA) in premature human infants. The magnitude of shunting through a PDA depends on its size and the relationship between the pulmonary and systemic vascular resistances. Factors affecting the pulmonary vascular resistance (such as hypoxia) will therefore affect the shunt. The ability of the infant to handle the volume overload also depends on maturity of the infant since myocardial development may not be complete even at term. The clinical manifestations and management of PDA with and without pulmonary disease are described. Recent attempts at pharmacological closure of the PDA are presented.