Patent Ductus Arteriosus of the Preterm Infant

Abstract

A persistently patent ductus arteriosus (PDA) in preterm infants can have significant clinical consequences, particularly during the recovery period from respiratory distress syndrome. With improvement of ventilation and oxygenation, the pulmonary vascular resistance decreases early and rapidly, especially in very immature infants with extremely low birth weight (<1000 g). Subsequently, the left-to-right shunt through the ductus arteriosus (DA) is augmented, thereby increasing pulmonary blood flow, which leads to pulmonary edema and overall worsening of cardiopulmonary status. Prolonged ventilation, with the potential risks of volutrauma, barotrauma, and hyperoxygenation, is strongly associated with the development and severity of bronchopulmonary dysplasia/chronic lung disease. Substantial left-to-right shunting through the ductus may also increase the risk of intraventricular hemorrhage, necrotizing enterocolitis, and death. Postnatal ductal closure is regulated by exposure to oxygen and vasodilators; the ensuing vascular responses, mediated by potassium channels, voltage-gated calcium channels, mitochondrial-derived reactive oxygen species, and endothelin 1, depend on gestational age. Platelets are recruited to the luminal aspect of the DA during closure and probably promote thrombotic sealing of the constricted DA. Currently, it is unclear whether and when a conservative, pharmacologic, or surgical approach for PDA closure may be advantageous. Furthermore, it is unknown if prophylactic and/or symptomatic PDA therapy will cause substantive improvements in outcome. In this article we review the mechanisms underlying DA closure, risk factors and comorbidities of significant DA shunting, and current clinical evidence and areas of uncertainty in the diagnosis and treatment of PDA of the preterm infant.

Persistent Ductus Arteriosus in Critically Ill Preterm Infants

“…As in other studies the current data showed a significant association between PDA and BPD (p=0.002) (Table 4) [6,9,15,20,21,25,41,42,47,[66][67][68][69]. An almost similar risk was reported by Marshall et al in VLBW infants (BW <1500 g) [69].…”

“…A link between PDA and IVH has been reported in many studies, as in the current report where there was an increased risk for IVH in Group 1 compared to Group 2 [20,40,46,47,68] (Table 4).…”

“…In preterm infants, PDA is diagnosed significantly more often than in term infants, 40-60% according to gestational age in preterm infants [17,18,49] versus 57/10.000 live births in term infants [7,20], and is associated with considerably increased morbidity and mortality [14]. Functional closure of DA in preterm infants with GA≥30 weeks gestation occurs towards the fourth day of life, while in those with GA<30 weeks or with RDS the incidence of PDA is about 65% [5,19,51].…”

“…Sometimes PDA accompanies congenital ductal-dependent heart defects and closure of the PDA soon after birth may precipitate clinical deterioration [12]. In premature infants, PDA incidence is inversely associated with gestational age (GA) and birth weight (BW), the incidence varying between 20-70% in very low birth weight infants (VLBW) [3,6,8,[13][14][15][16][17][18][19][20].…”

“…In the short term, PDA is associated with decreased blood pressure [5,8], decreased renal function [5], cardiac congestive failure [18,37,38], pulmonary haemorrhage [8,39], apnea and ventilator-dependency [6,38], bronchopulmonary dysplasia (BPD) [5,14,20,21,25,34,41,42], necrotizing enterocolitis (NEC) [8,9,11,19,20,34,39,43,44], intraventricular hemorrhage (IVH) [5,19,20,39,42,45,46], periventricular leukomalacia (PVL) [5], retinopathy of prematurity (ROP), cerebral palsy [24], delayed growth [11], and increased mortality rate [6,34,45,[47][48][49][50].…”