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  1. Condition: patent ductus arteriosus

    1. Definition: The ductus arteriosus (DA) is a vascular connection between the aorta and the main pulmonary artery that shunts blood away from the lungs and to the body during fetal development. After birth, the ductus usually closes; however, postnatal failure of ductal closure results in a patent ductus arteriosus (PDA).

    2. Incidence: A PDA is more common in premature infants and has been reported in 30% of very low birthweight infants (birthweight less than 1500 g) and in 65% of those born at less than 28 weeks' gestational age.

    3. Pathophysiology

      1. In utero the DA is approximately the same diameter as the aorta and 85% to 90% of the blood ejected from the right ventricle shunts from the pulmonary circulation to the systemic circulation across the DA.

      2. After birth, lung ventilation and increased pulmonary arterial oxygenation cause a drop in pulmonary vascular resistance. Concomitantly, elimination of the placental circulation increases systemic vascular resistance. The change in the relative resistances causes reversal of the shunt across the PDA from a right-to-left shunt to a left-to-right shunt.

      3. Consequently, the PDA results in increased pulmonary blood flow and diastolic steal from the systemic circulation. These physiologic alterations account for many of the clinical features.

      4. Two factors determine postnatal DA closure.

        • Increased arterial oxygen concentration typically seen with transition from fetal circulation.

        • Decreased circulating prostaglandin E2 (PGE2). Circulating PGE2 levels decrease after birth due to a decrease in placental production and increased clearance by the lungs as they receive more blood flow. Neonatal levels of circulating PGE2 are close to maternal levels within hours of birth with the exception of severely ill neonates, especially those with respiratory distress syndrome.

    4. Risk factors

      1. Prematurity: The incidence of PDA increases as the gestational age decreases. This occurs because preterm neonates have a higher circulating level of PGE2 than do full-term neonates.

      2. Genetics: Genes that regulate prostaglandin activity and/or smooth muscle development and contraction have been associated with the PDA. Numerous congenital syndromes have an increased incidence of PDA including trisomy 13, trisomy 18, Char syndrome, Holt-Oram syndrome, DiGeorge syndrome, Noonan syndrome, and others.

      3. Respiratory distress syndrome (RDS): RDS disrupts the normal physiological processes that result in ductal closure, particularly for neonates born prior to 30 weeks' gestational age.

      4. Surfactant administration: Administration of artificial surfactant within 30 minutes of delivery has been linked to an increase in ductal size and increased left-to-right flow. An increase in the left-to-right shunt can partially be explained with surfactant causing a decrease in pulmonary vascular resistance; however, the apparent vasodilation of the ductus after surfactant administration is not understood.

      5. Asphyxia: Any neonate who has had a perinatal event consistent with asphyxia is at increased risk of having a PDA. In some situations, hypoxia from the event can lead to increased pulmonary resistance, which can cause a persistent right-to-left shunt across the PDA.

      6. High altitude: There is a higher rate of PDAs in infants born at high altitudes compared to those ...

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