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Patent ductus arteriosus: pathophysiology and management


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.

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Correspondence to R I Clyman.

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Disclosure: No significant relationship to disclose.

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Hermes-DeSantis, E., Clyman, R. Patent ductus arteriosus: pathophysiology and management. J Perinatol 26 (Suppl 1), S14–S18 (2006).

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