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J Perinatol. 2006 May;26 Suppl 1:S14-8; discussion S22-3.

Patent ductus arteriosus: pathophysiology and management.

Author information

1
Drug Information Service, Robert Wood Johnson University Hospital, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, New Jersey, USA.

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.

PMID:
16625216
DOI:
10.1038/sj.jp.7211465
[Indexed for MEDLINE]

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