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Postnatal ductal closure is stimulated by rising oxygen tension and withdrawal of vasodilatory mediators (prostaglandins, nitric oxide, adenosine) and by vasoconstrictors (endothelin-1, catecholamines, contractile prostanoids), ion channels, calcium flux, platelets, morphologic maturity, and a favorable genetic predisposition. A persistently patent ductus arteriosus (PDA) in preterm infants can have clinical consequences. Decreasing pulmonary vascular resistance, especially in extremely low gestational age newborns, increases left-to-right shunting through the ductus and increases pulmonary blood flow further, leading to interstitial pulmonary edema and volume load to the left heart. Potential consequences of left-to-right shunting via a hemodynamically significant patent ductus arteriosus (hsPDA) include increased risk for prolonged ventilation, bronchopulmonary dysplasia, necrotizing enterocolitis or focal intestinal perforation, intraventricular hemorrhage, and death. In the last decade, there has been a trend toward less aggressive treatment of PDA in preterm infants. However, there is a subgroup of infants who will likely benefit from intervention, be it pharmacologic, interventional, or surgical: (1) prophylactic intravenous indomethacin in highly selected extremely low gestational age newborns with PDA (<26 1 0/ 7 weeks' gestation, <750 g birth weight), (2) early targeted therapy of PDA in selected preterm infants at particular high risk for PDA-associated complications, and (3) PDA ligation, catheter intervention, or oral paracetamol may be considered as rescue options for hsPDA closure. The impact of catheter-based closure of hsPDA on clinical outcomes should be determined in future prospective studies. Finally, we provide a novel treatment algorithm for PDA in preterm infants that integrates the several treatment modalities in a staged approach. [ABSTRACT FROM AUTHOR]

A persistently patent ductus arteriosus (PDA) in preterm infants can have significant clinical consequences, particularly during the recovery period from respiratory distress syndrome. With improvement of ventilation and oxygenation, the pulmonary vascular resistance decreases early and rapidly, especially in very immature infants with extremely low birth weight (<1000 >). Subsequently, the left-to-right shunt through the ductus arteriosus (DA) is augmented, thereby increasing pulmonary blood flow, which leads to pulmonary edema and overall worsening of cardiopulmonary status. Prolonged ventilation, with the potential risks of volutrauma, barotrauma, and hyperoxygenation, is strongly associated with the development and severity of bronchopulmonary dysplasia/chronic lung disease. Substantial left-to-right shunting through the ductus may also increase the risk of intraventricular hemorrhage, necrotizing enterocolitis, and death. Postnatal ductal closure is regulated by exposure to oxygen and vasodilators; the ensuing vascular responses, mediated by potassium channels, voltage-gated calcium channels, mitochondrial-derived reactive oxygen species, and endothelin 1, depend on gestational age. Platelets are recruited to the luminal aspect of the DA during closure and probably promote thrombotic sealing of the constricted DA. Currently, it is unclear whether and when a conservative, pharmacologic, or surgical approach for PDA closure may be advantageous. Furthermore, it is unknown if prophylactic and/or symptomatic PDA therapy will cause substantive improvements in outcome. In this article we review the mechanisms underlying DA closure, risk factors and comorbidities of significant DA shunting, and current clinical evidence and areas of uncertainty in the diagnosis and treatment of PDA of the preterm infant. [ABSTRACT FROM AUTHOR]