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Patent ductus arteriosus (PDA) in preterm neonates.


Review morbidities associated with a PDA; review risk factors for developing a PDA; identify PDA treatment options and their potential side effects and complications; identify a PDA treatment algorithm for preterm neonates.


The ductus arteriosus is a fetal blood vessel that connects the main pulmonary artery to the aorta. In utero, the ductus arteriosus shunts blood away from the lungs and to the systemic circulation. Postnatally, blood flow typically reverses across the ductus arteriosus due to decreasing pulmonary vascular resistance and increasing systemic vascular resistance. When the ductus arteriosus fails to close after birth it is referred to as a patent ductus arteriosus (PDA).

Factors which increase the risk of having a PDA include low gestational age, low birth weight, and sepsis, among others. Approximately 60% of neonates delivered at <28 weeks’ gestation are diagnosed with a PDA, with decreased rates observed with increased gestational age. Spontaneous PDA closure is ultimately likely to occur for preterm neonates of all gestational ages but is more likely to occur, and typically occurs sooner, with increased gestational age.

A physical examination is the first step in identifying a PDA. Examination findings consistent with a PDA include a systolic heart murmur, widened pulse pressure, bounding peripheral pulses, and a hyperdynamic precordium. A neonate may present with clinical signs or conditions that cannot otherwise be explained, including hypotension, pulmonary hemorrhage, and/or renal insufficiency. When a PDA is clinically suspected, an echocardiogram should be obtained to confirm clinical suspicion and to screen for ductal-dependent congenital cardiac lesions. In the setting where an echocardiogram cannot be obtained, one must use clinical judgment to weigh the risks and benefits of clinical diagnosis with empiric management versus transferring the preterm neonate to a referral hospital where subspecialty care is available.

A PDA is associated with, but has not been proven to be causative of, increased mortality and morbidity including chronic lung disease (CLD)/bronchopulmonary dysplasia (BPD), intraventricular hemorrhage (IVH), and necrotizing enterocolitis (NEC). It is pathophysiologically plausible that a sufficiently “hemodynamically significant” PDA may result in cardiopulmonary compromise, hypotension, and renal insufficiency due to increased pulmonary circulation and decreased systemic perfusion. However, there is no universally accepted and validated classification of PDA severity that correlates echocardiographic features or laboratory findings with clinical signs. The provider must determine to what extent, if any, a PDA is contributing to end-organ hypoperfusion and/or compromise. A “hemodynamically significant PDA” in this chapter is defined as a PDA with substantial left-to-right shunting of blood. In general, a ductus arteriosus diameter ≥1.5 mm, a left atrium/aortic root diameter ratio of ≥1.5:1, and reversed diastolic blood flow in the descending aorta and/or renal arteries indicate greater hemodynamic significance.


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