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Pharmacologic Treatment of Patent Ductus Arteriosus in the Preterm Infant

P atent ductus arteriosus (PDA) is one of the most common clinical findings in preterm infants. Patent ductus arteriosus occurs when the ductus arteriosus fails to close following birth and is most often found in the setting of prematurity, affecting approximately 50% of all preterm infants. Patent ductus arteriosus with significant left-to-right shunts have been associated with increased morbidity in preterm infants for more than 50 years. Hemodynamically significant PDAs cause decreased renal blood flow, intestinal ischemia, and decreased cerebral artery blood flow. In addition, PDAs produce high pulmonary blood flow, often in the setting of surfactant deficiency and increased capillary permeability, which results in pulmonary edema and increased ventilation requirements. In extremely preterm infants, these alterations in vital organ blood flow may increase the risk of necrotizing enterocolitis, intraventricular hemorrhage, periventricular leukomalacia, and chronic lung disease (CLD). These morbidities are common complications of preterm birth and a causative link to PDA has not been proven. Care of the preterm infant with PDA in the neonatal intensive care unit is an ongoing challenge. Little consensus regarding treatment of PDA currently exists. Treatment requires careful consideration of the risks and benefits of available therapies, namely, surgical ligation and pharmacological interventions. While surgery typically results in reliable closure of the PDA, it is also associated with both shortand long-term surgical complications including infection and neurodevelopmental impairment. For this reason, surgical ligation of the PDA is usually considered only after medical treatment, which is focused primarily on a pharmacological approach to closing the PDA. Here, I briefly review both