Patent Ductus Arteriosus



Patent Ductus Arteriosus


William M. DeCampli





FETAL CIRCULATION

In the fetus, the lungs are not ventilated and pulmonary resistance is high. The majority of relatively desaturated venous blood from the superior vena cava returning to the right ventricle passes through the ductus arteriosus into the descending aorta, whence some of it exits the fetal body through the umbilical artery to be oxygenated by the placenta. The ductus arteriosus is normally strategically positioned so that this desaturated blood does not travel to organs with the greatest oxygen metabolism (the brain and myocardium). After birth, pulmonary gas exchange commences and the circulation is “in series.” With the ductus arteriosus no longer essential, spontaneous closure normally occurs in hours to a few days after birth.


MECHANISMS OF SPONTANEOUS DUCTAL CLOSURE

Ductal closure occurs in two stages. The first is functional closure, occurring within the first 6 to 15 hours after birth. This stage results from medial smooth muscle constriction, promoted by four principal factors: (1) increase in arterial oxygen tension, (2) decrease in circulating prostaglandin E2 (PGE2), (3) decrease in mean ductal blood pressure, and (4) decline in the density of PGE2 receptors in the ductal wall. Part of the oxygen dependence is intrinsic to the specialized smooth muscle cells. The second stage (anatomic closure) is usually completed in a few days to weeks after birth and results from (1) subendothelial deposition of extracellular matrix, (2) resorption of the internal elastic lamina and elastin fibers in the media, and (3) migration of undifferentiated smooth muscle cells into the subendothelial space. The ductus closes from the pulmonary end toward the aortic end, often leaving a “ductal ampulla” seen on echocardiography. The resulting nonpatent ductus is then called the ligamentum arteriosum. The patent ductus arteriosus (PDA) is defined as persistent patency of the fetal ductus arteriosus beyond its normal time of spontaneous closure.


RISK FACTORS FOR PATENT DUCTUS ARTERIOSUS

Any pathology that alters the molecular mechanisms of normal ductal closure may result in PDA. By far, the most frequently encountered risk factor for PDA is prematurity. The incidence of PDA increases with lower birth weight and estimated gestational age (EGA), reaching 77% at EGA 28 weeks. Circulating PGE2 activity is greater in the preterm infant than in the full-term infant, promoting persistent ductal patency, presumably because PGE2 is completely metabolized with first pass through the mature lung but incompletely in the premature lung. The risk for PDA is further increased with infant respiratory distress syndrome (RDS). Ninety percent of babies with RDS and <32 weeks EGA have PDA.




NATURAL HISTORY


Premature Neonates

The natural history in this population is confounded by the coexisting morbidities of prematurity. No study clearly establishes PDA as a cause of death in this population. Spontaneous ductal closure continues to occur at least up to 1 year of age. In a study of 122 infants with birth weight <1,000 g, closure occurred within 3 days in 25, within 8 days in 42, and before hospital discharge in 46. Among infants with birth weight >1,000 g, the ductus closed without intervention in 67% by age 7 days and in 94% prior to discharge, at a median age of 7 days.


Children and Adults

The spontaneous closure rate in children >1-year old is about 0.6% per year. Among patients with significant sized PDA, the overall mortality in older patients with PDA at 0.49% per year (for age 2 to 19 years) and 1.8% per year (for age >20 years), 30% are dying from congestive heart failure. Patients with large, untreated PDAs that progress to severe PAH have survival curve typical for that of Eisenmenger’s syndrome. The risk of bacterial endocarditis is very low in the antibiotic era but not zero, even with a “silent ductus.”


Jun 15, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Patent Ductus Arteriosus

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