197 - Hemodynamic Effects of Low-Dose Dexamethasone on Patent Ductus Arteriosus in Preterm Neonates

Publication Number: 197.5450

Ahmed Elkordy, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada; Renjini Lalitha, The University of Western Ontario - Schulich School of Medicine & Dentistry, London, ON, Canada; Michael Miller, The University of Western Ontario - Schulich School of Medicine & Dentistry, London, ON, Canada; Soume Bhattacharya, Western University, London, ON, Canada

Background: Patent ductus arteriosus (PDA) is a common cardiovascular morbidity in preterm neonates. Pharmacological treatment of PDA works primarily by inhibiting prostaglandins leading to ductal constriction. Anecdotal reports suggest that steroids may cause suppression of prostaglandin levels or decrease the sensitivity of ductal muscles to prostaglandin thereby promoting PDA constriction. Low dose dexamethasone (Dex) is a steroid that is commonly used for prevention and treatment of Bronchopulmonary dysplasia (BPD) in preterm neonates, but its effects on PDA closure and associated hemodynamic changes in preterm infants remains underexplored.

Objective: To investigate the effects of Dex on PDA hemodynamics and explore its dose dependent effect on PDA hemodynamic scores.

Design/Methods: This was a secondary analysis of a prospective cohort study that investigated the cardiac effects of low dose Dex for prevention of BPD in neonates < 29weeks gestational age (GA), at a level III neonatal intensive care unit between April 2019 and July 2022 using serial echocardiography. For this study, PDA related echocardiographic parameters prior to initiation of Dex and after completion of Dex were analyzed. Two Dex dosing regimens were used during the study period— < 1mg/kg and >1mg/kg cumulative dose- which were compared to determine any dose-response effects. Institutional ethical approval was obtained (WREM124259)

Results: Out of 30 neonates included in the original cohort, 15 neonates with mean GA(SD) of 24.5(1.06) weeks and mean birth weight (SD) 637.33(96.03) grams, had a PDA prior to Dex initiation (Table 1). PDA presence decreased to 66.7% after Dex completion. There was a significant decrease in both mean PDA size (SD) from 1.57(0.51) mm to 1.01(0.78)mm (p=0.010), and the hemodynamic significance score(SD) from 9.4(3.78) to 6.13(6.19) (p=0.021) respectively (Table 2). In a subset analysis, 50% of infants treated with lower-dose Dex experienced PDA closure, compared to 14.3% in the higher-dose group, although the difference was not statistically significant (p=0.282) (Table 3).

Conclusion(s): Echocardiographic assessment before and after dexamethasone therapy demonstrated smaller ductal size and lower PDA hemodynamic significance score post treatment. Higher dose did not potentiate the effect in this cohort Whether this is a causal or temporal relationship remains to be seen in larger prospective cohorts.

Table1. Baseline demographic and clinical characteristics of cohort
Table 1 Baseline clinical and demographic characteristics of cohort.pdf

Table 2 Clinical and PDA related echocardiographic changes before and after dexamethasone
Table 2 Clnical and PDA related echocardiographic changes before and after dexamethasone.pdf

Table 3 Exploring Dose Response Relationship Between Dex and PDA
Table 3 Exploring Dose Response Relationship between Dex and PDA.pdf