Dexmedetomidine: What's New for Pediatrics? A Narrative Review

Abstract

Over the past few years, despite the lack of approved pediatric labelling, dexmedetomidine's (DEX) use has become more prevalent in pediatric clinical practice as well as in research trials. Its respiratory-sparing effects and bioavailability by various routes are only some of the valued features of DEX. In recent years the potential organ-protective effects of DEX, with the possibility for preserving neurocognitive function, has put it in the forefront of clinical and bench research. This comprehensive review focused on the pediatric literature but presents relevant, supporting adult and animal studies in order to detail the recent growing body of literature around the pharmacology, end-organ effects, organ-protective effects, alternative routes of administration, synergetic effects, and clinical applications, with considerations for the future.

Keywords: anesthesia; neuroprotection; neurotoxicity; pediatric; pharmacology; sedation; side effects.

Figure 1

Final population pharmacokinetic (PK) model diagnostic plots: observed versus population prediction (A) and individual prediction (B), conditional weighted residuals versus population predictions (C), and time after last dose (D). The solid line in (A,B) is the line of identity. The solid line in (C,D) is a reference line at y = 0. The dashed lines in (A–D) are smooth lines.

Figure 2

Schematic illustration that surgical trauma triggers perioperative stress, systemic inflammation, and immune suppression, all of which are negated by dexmedetomidine (DEX). HPA, hypothalamic-pituitary-adrenal; SNS, sympathetic nervous system [36].

Figure 3

Topographic electroencephalogram maps detailing group-averaged global coherence for each electroencephalogram frequency of interest. (A) Dexmedetomidine is associated with increased occipital theta global coherence. (B) Dexmedetomidine is associated with a shift in the globally coherent occipital awake alpha to frontal regions. (C) Dexmedetomidine is associated with globally coherent fronto-central spindle oscillations [14].

Figure 4

Contrast images showing regions where functional connectivity is higher during dexmedetomidine- than propofol-induced unresponsiveness (dexmedetomidine > propofol), dexmedetomidine than N3 sleep (dexmedetomidine > sleep), N3 sleep than propofol (sleep > propofol), N3 sleep than dexmedetomidine (sleep > dexmedetomidine), propofol than N3 sleep (propofol > sleep), or propofol than dexmedetomidine (propofol > dexmedetomidine). Only those contrasts where significant differences (false discovery rate-corrected p < 0.05) were found are shown, as was the case for connectivity with the thalamus (thalamus), within the default mode network (DMN), the right executive control network (right ECN), the auditory network (auditory resting state network RSN (Auditory resting state network)), and the visual network (visual RSN). Contrast images are superimposed on a canonical three-dimensional brain representation providing a left, right, and sagittal view of the brain. A left or right view of the internal face of the brain was chosen as a function of the presence of significant clusters or not. When no significant clusters were visible on one view, the other one was chosen [15].