Patent Ductus Arteriosus.

Abstract

Patent ductus arteriosus (PDA) is a common congenital heart defect. PDA disproportionately affects low-birth-weight infants, resulting in an incidence of 21% among preterm births as compared to 0.05% in the general population. The ductus arteriosus remains patent in the fetus, allowing maternal blood to directly enter fetal systemic circulation, bypassing the fetal lungs. This is mediated through the mechanisms of nitric oxide and prostaglandins. At birth, increased partial pressure and decreased prostaglandin levels facilitate functional closure of the ductus arteriosus. Further migration of contractile smooth muscle cells and tissue remodeling results in fibrosis and anatomical closure of the ductus. Underdevelopment of contractile smooth muscle cells, the intimal layer in blood vessels, and vasa vasorum have been theorized as the mechanisms behind PDA in preterm-birth neonates. PDA creates a left-to-right shunt, sending oxygenated blood from the aorta to the lungs via the pulmonary artery, often manifesting with symptoms of pulmonary hypertension and edema. As the symptoms progress, the shunt is often reversed, resulting in cyanosis in a condition known as Eisenmenger syndrome. While most affected patients present with distinguishing clinical findings, many also remain asymptomatic, and the defect goes undetected for years.