Patent ductus arteriosus: pathophysiology and management

Abstract

Patent ductus arteriosus (PDA) in preterm newborns prior to 28 weeks of gestation has led to many challenges regarding the type and timing of treatment regimens. A PDA results in increased pulmonary blood flow and redistribution of flow to other organs. Several co-morbidities (i.e., necrotizing enterocolitis, intracranial hemorrhage, pulmonary edema/hemorrhage, bronchopulmonary dysplasia, and retinopathy) are associated with the presence of a PDA, but whether or not a PDA is responsible for their development is still unclear. The prostaglandin inhibitor, indomethacin, is effective in the treatment of PDA. Questions regarding the optimal timing of the intervention – early prophylaxis or treatment, once signs and symptoms become evident – have challenged physicians for decades. Both evidence and experience are explored in this article. Comparative physiology between the full-term and preterm newborn and the barriers preventing the necessary cascade of events leading to permanent constriction of the PDA are reviewed.

DOI: 10.1038/sj.jp.7211465

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@article{HermesDeSantis2006PatentDA, title={Patent ductus arteriosus: pathophysiology and management}, author={Evelyn R Hermes-DeSantis and Ronald I. Clyman}, journal={Journal of Perinatology}, year={2006}, volume={26}, pages={S14-S18} }