Patent ductus arteriosus: pathophysiology and management

J Perinatol. 2006 May;26 Suppl 1:S14-8; discussion S22-3. doi: 10.1038/sj.jp.7211465.

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.

Publication types

  • Review

MeSH terms

  • Cardiac Surgical Procedures
  • Cardiovascular Agents / therapeutic use
  • Comorbidity
  • Ductus Arteriosus, Patent / drug therapy
  • Ductus Arteriosus, Patent / physiopathology*
  • Ductus Arteriosus, Patent / surgery
  • Ductus Arteriosus, Patent / therapy*
  • Gestational Age
  • Humans
  • Indomethacin / therapeutic use
  • Infant, Newborn
  • Infant, Premature*
  • Treatment Outcome

Substances

  • Cardiovascular Agents
  • Indomethacin