Background Closure of the ductus arteriosus (DA) is complete in 99% of term neonates by 96 h postnatal. In neonates < 1500 g there is an inverse relationship between persistent patent ductus arteriosus (PDA) and BW and gestational age (EGA). It is unclear in neonates ≤ 1000 g birth weight (BW) when the DA spontaneously closes postnatally, how often closure is permanent, and how frequently these neonates fail medical therapy with indocin.
Objective To prospectively determine in in-born neonates ≤ 1000 g BW the time of spontaneous DA closure, prevalence of persistent PDA, and failure rate following indocin therapy.
Methods Neonates ≤ 1000 g BW born at Parkland Hospital between 2/16/01 and 12/21/03 were eligible for study. Exclusion criteria included congenital cardiac disease (CHD) or death < 10 d postnatal. Serial echocardiograms were obtained 48-72 h after birth to assess anatomy and DA patency and every 48 h until 10 d to assess DA patency and size. If DA closure occurred < 10 d postnatal, examinations ceased and an echocardiogram was obtained at 10 d. Echocardiograms were provided clinical care teams when PDA was clinically evident. Data were collected from maternal, delivery, and neonatal records. Informed consent was obtained.
Results 139 consecutive neonates were enrolled; 10 were excluded due to death < 10 d and 7 with CHD, 6 with VSD, and 1 ASD. BW ranged from 470-990 g, EGA 23-31 wks, and 43% were female. The population was 72% Hispanic, 22% African-American, and 3% Caucasian. Spontaneous permanent DA closure occurred in only 42/122 (34%) at 4.3 ± 2.2 (SD) d postnatal with 100% closure occurring at 8 d. 67% (28/42) of neonates with spontaneous permanent closure did not receive antenatal steroids and their EGA did not differ from those that did, 26 ± 2.1 vs 26 ± 1.5 wks. 56% (68/122) received indocin at 6.2 ± 4.1 d postnatal for persistent PDA. Treatment failure was EGA-dependent (p = .001) and occurred in 28/68 (41%) neonates, resulting in subsequent surgical ligation.
Conclusion This is the first prospective study in neonates ≤ 1000 g BW demonstrating that spontaneous permanent DA closure is generally delayed to ≥ 4 d postnatal, occurs in only 1/3 of these neonates, is more likely to occur in the absence of antenatal steroid exposure, and that indocin therapy fails in > 40% with persistent PDA. These data will be used to characterize neonates at risk of a persistent PDA and to determine which of these neonates will be at risk of failing medical therapy.