The Cardiovascular Effects of Clonidine in Premature Infants Admitted to the Neonatal Intensive Care Unit: An Abstract from Akron Children’s Hospital Resident and Fellow Academic Day

Clonidine, an alpha-2 adrenergic receptor agonist, is used to treat pain and agitation in the neonatal intensive care unit (NICU). In older children and adults, clonidine is associated with hypotension and bradycardia. Additionally, upon discontinuation, clonidine can cause rebound hypertension and tachycardia. Clonidine use is increasing in preterm infants in the NICU in an attempt to reduce opiate exposure; however, a paucity of research exists about the cardiovascular effects of clonidine in this population. The objective of this study is to identify the effects of clonidine on heart rate (HR), systolic blood pressure (SBP), and diastolic blood pressure (DBP) after initiating and discontinuing clonidine in infants <32 weeks gestation admitted to the neonatal intensive care unit. This was a retrospective chart review from a tertiary care NICU at Akron Children's Hospital that included neonates <32 weeks gestation who received clonidine for analgesia from June 1, 2020, to August 1, 2025. This study was approved by the local Institutional Review Board. Data was extracted from the electronic medical records of qualifying infants. All HR values were averaged for all values over an 8-hour period, and BP over a 12-hour period. Clinical characteristics are presented as median and interquartile range (IQR). One-way repeated measures ANOVA was conducted to compare HR, SBP, and DBP for 48 hours after clonidine initiation and prior to discontinuation. A Spearman’s rank-order correlation was run to determine the relationship between dose and duration of clonidine and vital sign changes. 33 preterm infants were eligible for the study. The median gestational age (GA) at birth was 25 weeks (IQR 25-27), corrected gestational age (CGA) at time of clonidine initiation was 37.9 (IQR 31-45.3), max dose of clonidine was 4.9 mcg/kg/dose (IQR 3-7.6), and median duration of clonidine exposure was 59 days (IQR 17-106). All infants received clonidine via the enteral route at a dosing interval of every 6 hours. Ten infants were administered clonidine prior to a corrected gestational age of 34 weeks. The results of repeated measures one-way ANOVA indicated that clonidine was associated with a decrease in HR and SBP at 24 and 48 hours following initiation, p<0.001 for all. Clonidine was also associated with an increase in HR, SBP, and DBP at 24 and 48 hours following clonidine discontinuation, p<0.001 for all. The dose of clonidine was correlated with HR changes in the 24 h after starting and prior to stopping the medicine (r=0.8, p<0.01) but was not correlated with SBP or DBP. Duration of clonidine exposure did not correlate with any vital sign changes. Our study revealed that clonidine use is associated with changes in HR, SBP, and DBP upon initiation and discontinuation in the preterm population, which is important information for bedside physicians. Further research is needed to determine the clinical relevance of these vital sign changes. We are currently evaluating additional variables such as disease processes and medication exposures to assess confounding.