Is dexmedetomidine the Jack of all perioperative trades?

Since it was first approved by the Food and Drug Administration in 1999 and in 2011 by the European Union, dexmedetomidine (DEX) has gained widespread use first in adults and later paediatric patients undergoing cardiac surgery. And considering this α₂-adrenoceptor agonist’s side-effect profile, it is no wonder its perioperative application continues to increase.

As an analgosedative that does not depress respiration, DEX’s beneficial properties extend from anaesthetic- and analgetic-sparing effects [1] enabling early extubation to delirium prophylaxis and overall faster recovery after surgery. Administering DEX is believed to reduce adverse neurocognitive outcomes in adults undergoing cardiovascular surgery [2]. Consistent with those findings, a recent meta-analysis on paediatric congenital heart surgery [3] reported reduced levels of S-100β and NSE, markers for postoperative cognitive function.

In this issue, Bourgoin et al. [4] describe the efficacy of intraoperative high-dose DEX, administration that resulted in an 8.8% reduction in postoperative tachyarrhythmias in neonates and infants undergoing congenital heart surgery. They also confirmed a sparing effect for other analgesics, and a tendency towards shorter intubation time.

How excited should we be? This research appears to be a breakthrough with huge implications for paediatric cardiac surgery. However, perioperative treatment with DEX mandates rigorous patient selection. These children are prone to vulnerable haemodynamics and thus hypotension and bradycardia, both possible and well-known side effects of DEX. In a multifactorial treatment setting such as a paediatric cardiac intensive care unit, any agent that is a potential iatrogenic source of cardiac depression should always be scrutinized, if not omitted altogether. Furthermore, certain procedures carry an inherently higher risk of arrhythmias, such as complete atrioventricular septal defect repair and arterial switch operations with ventricular septal defect closure [5, 6]. DEX therapy under these circumstances should be done with great caution, as it prolongs the atrioventriucular nodal refractory period [7], and in the absence of sinus rhythm, this medication should be avoided altogether due to the possible induction of atrioventricular block.

The promising implications of DEX should be understood with cautious enthusiasm and, guided by solid evidence from randomized controlled trials, lead the way to identifying those children with contraindications to this versatile drug. Especially in such a heterogeneous group as newborns and infants with congenital heart disease, multicentre studies are needed to ensure an adequate sample size enabling appropriate patient stratification. Furthermore, follow-up throughout the postoperative intensive care course would complete this scenario and should yield insightful data on how to ensure optimal practice when applying DEX in this most vulnerable group of children undergoing congenital heart surgery at an early age.

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