673 - The Impact of Aminoglycoside Exposure on Patent Ductus Arteriosus Closure in Preterm Infants

Saturday, April 29, 2023

3:30 PM – 6:00 PM ET

Poster Number: 673
Publication Number: 673.241

Amy C. Hong, The University of Texas Health Science Center at San Antonio Joe R. and Teresa Lozano Long School of Medicine, San Antonio, TX, United States; Joseph B. Cantey, The University of Texas Health Science Center at San Antonio Joe R. and Teresa Lozano Long School of Medicine, SAN ANTONIO, TX, United States

Presenting Author(s)

Amy C. Hong, BS, MS (she/her/hers)

Medical Student
The University of Texas Health Science Center at San Antonio Joe R. and Teresa Lozano Long School of Medicine
Austin, Texas, United States

Background: Patent ductus arteriosus (PDA) is a major cause of morbidity among preterm infants. Incidence is inversely proportional to gestational age and affects ~20% of infants ≤32 weeks gestation. Aminoglycoside exposure causes PDA vasodilation in animal models, but clinical study of the association between aminoglycosides and PDA has yielded mixed results.

Objective: To investigate the association between aminoglycoside exposure and the incidence and management of PDA among preterm infants

Design/Methods: The study was a retrospective cohort of infants ≤32 weeks gestation admitted to a single level IV NICU during a 26-month period (7/1/20-8/18/22). Inclusion criteria were performance of at least one echocardiogram. Demographic, clinical, and outcome data were collected, including aminoglycoside exposure within 4 days of birth as well as total antibiotic exposure during NICU stay. PDA size, left atrium to aorta (LA:Ao) ratio, and medical or surgical closure of PDA were collected. Data were analyzed using STATA (StataCorp, College Station, TX).

Results:

129 infants were included; 9 infants were excluded due to participation in a blinded clinical trial of early antibiotic use. Median gestational age and birth weight were 27 weeks (IQR 25-30) and 930 g (710-1260). 60% were male and 87% received antenatal steroids.

72% (93/129) of infants received aminoglycosides (all gentamicin) within 4 days of birth, and 67% (86/129) had PDA on echocardiography. Median age at first echocardiogram was 8 days. In bivariate analysis, gestational age was the single best predictor of PDA; gentamicin exposure was not associated with the presence of PDA (p=0.10). Among infants with PDA, exposure to gentamicin was associated with larger PDA size (2.5 mm [IQR 2-3] vs. 1.75 [IQR 1-2.25]) and decreased rate of spontaneous closure (44% vs. 85%). These associations remained significant after controlling for gestational age. LA:Ao ratio was not different between gentamicin-exposed and -unexposed infants.

Conclusion(s): Aminoglycoside exposure was not associated with the presence of PDA among preterm infants. However, when PDA was present, aminoglycoside exposure was associated with increased size and increased rates of medical or surgical closure. Our findings support the proposed association between aminoglycoside exposure and PDA. Additional study is needed to determine the clinical significance of these findings.