Patent ductus arteriosus: an overview

Abstract

Patent ductus arteriosus (PDA) is one of the most common congenital heart defects, accounting for 5%-10% of all congenital heart disease in term infants. The occurrence of PDA is inversely related to gestational age and weight, with an even greater incidence in preterm infants. The maintenance of ductal patency is essential for the normal development of the fetus. In the neonate, however, persistent patency of the ductus arteriosus (DA) is associated with significant morbidity and mortality. Normally, at birth, the DA constricts, resulting in intraluminal ischemic hypoxia, which eventually leads to closure and remodeling of the ductus. PDA in term infants is usually associated with a functional defect, whereas in preterm infants it is associated with immaturity. Normal physiologic mechanisms contributing to closure - oxygen tension and decreased prostaglandins-are altered in prematurity. Clinical signs of ductal patency include murmur, tachycardia, bounding peripheral pulses, and congestive heart failure and associated symptoms. Symptoms are not always present; therefore, diagnostic imaging is critical if a PDA is suspected on clinical grounds. Three management strategies are currently available for PDA: fluid restriction and diuretics (as clinically appropriate), medical intervention, and surgical ligation. Pharmacologic closure can be achieved via administration of intravenous indomethacin or ibuprofen lysine. While both agents have shown similar efficacy, ibuprofen lysine has demonstrated an improved safety profile, particularly in terms of renal effects, compared to indomethacin.

Keywords: cyclooxygenase inhibitors; ibuprofen lysine; indomethacin; non-steroidal anti-inflammatory drugs; patent ductus arteriosus; prostaglandins.

Figure 1.

Left–The ductus arteriosus is an essential component of fetal circulation. It functions by shunting blood away from the nonfunctional fetal lung and into the systemic circulation through the aorta. Right–After birth, decreases in PGE₂ and oxygen tension contribute to the closure of the ductus Arteriosus, allowing gas exchange to occur in the newly functioning lungs rather than the now absent placenta. Blue = oxygen-poor blood; Red = oxygen-rich blood; LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. The paradoxical patent ductus arteriosus. J Clin Invest 166:2863–2866 by Ivey KN, and Srivastava D. Copyright 2006 by J Clin Invest. Reproduced with permission of J Clin Invest via Copyright Clearance Center.

Figure 2.

Comparison of fetal and both the premature and full-term newborn ductus arteriosus. The avascular zone in the preterm ductus (bottom row) does not sufficiently expand beyond the effective diffusion distance after birth (bottom right). Hermes-deSantis et al.16 Reprinted by permission from Macmillan Publishers Ltd: J Perinatol 26: s14–s18, copyright 2006.