48 - Patent Ductus Arteriosus in the Preterm Infant

Abstract

In full-term infants, obliteration of the ductus arteriosus (DA) takes place through a process of vasoconstriction and anatomic remodeling after birth. In contrast, preterm newborn infants frequently fail to close their DA. Factors that play a prominent role in DA regulation involve those that promote constriction of the ductus (e.g., oxygen, endothelin, Ca2+ channels, catecholamines, and Rho kinase), those that oppose it (e.g., intraluminal pressure, prostaglandins, nitric oxide, carbon monoxide, potassium channels, and cyclic adenosine monophosphate [AMP] and cyclic guanosine monophosphate [GMP]), and those that regulate ductus smooth muscle hypoxia, neointimal mound formation, and smooth muscle cell death. The relative importance of each of these factors depends on the intrauterine and extrauterine environment, the degree of ductus maturation, and the genetic background and species being studied. The clinical consequences of a patent ductus arteriosus (PDA) are related to the magnitude of the left-to-right shunt through the PDA, the cardiac and vascular responses to the shunt, and the associated changes in blood flow to the lungs, kidneys, intestine, and brain. Controlled clinical trials demonstrate that a moderate-to-large PDA increases the incidence of severe pulmonary hemorrhage and systemic hypotension during the first week as well as the need for higher levels of ventilator support at the end of the first week. However, controversy exists about the consequences of exposure to a persistent moderate-to-large PDA shunt for greater than 1 week. Further investigations will be needed to determine which infants are likely to benefit from early PDA treatment and which infants might best be left untreated while awaiting spontaneous ductus closure.