Dexmedetomidine Infusion Associated with Transient Adrenal Insufficiency in a Pediatric Patient: A Case Report

Dexmedetomidine is a highly selective α2-adrenoceptor agonist used for sedation due to its anxiolytic and analgesic properties without respiratory compromise. Due to its structural similarity to etomidate, there has been concern that dexmedetomidine may cause adrenal insufficiency. This concern was initially supported by animal studies, but subsequent human studies demonstrated mixed results. We describe the case of transient adrenal insufficiency in a 1-year-old male who presented with 24% total body surface 2nd degree burns. He required sedation with a prolonged, high-dose dexmedetomidine infusion with a peak infusion dose of 2.7？mcg/kg/hr and duration of 6.5 days. The patient developed lethargy and hypotension four days after discontinuation of his infusion. He had a random cortisol level which was low at 0.4？mcg/dL, and the concern for adrenal suppression was confirmed with an ACTH stimulation test with the baseline cortisol of 0.4？mcg/dL and inappropriate 60 minute post-ACTH stimulation cortisol of 7.8？mcg/dL. While further studies will be needed to clarify the risk of adrenal suppression secondary to dexmedetomidine, this case suggests that caution should be taken when administering dexmedetomidine to pediatric patients and highlights the need for future studies to look at appropriate dosing and duration of dexmedetomidine infusions. 1. Introduction Dexmedetomidine is a highly selective α2-adrenoceptor agonist whose use in pediatrics has increased since its approval by the Food and Drug Administration (FDA) for sedation in adults [1]. Unlike other sedative medications that act on the γ-amino butyric acid (GABA) receptor, it works to provide sedation resembling natural sleep, anxiolysis, analgesia, reduced delirium, sympatholysis, and antishivering properties without respiratory depression [2–7]. The presumed safety of dexmedetomidine has translated to its use in several settings: in pediatric and adult intensive care units for sedation and sedative weaning, in operating rooms to attenuate the cardiovascular and neuroendocrine responses to surgery by decreasing sympathetic activity, and in outpatient radiologic centers for imaging sedation with low risk of respiratory compromise [1, 2, 4–7]. Because of dexmedetomidine’s structural similarity to etomidate, there has been concern that dexmedetomidine could cause adrenal insufficiency [8]. Etomidate is known to cause adrenal insufficiency by inhibiting 11β-hydroxylase and side chain cleavage enzymes, thereby inhibiting adrenal steroidogenesis [9]. The mechanism of this enzyme inhibition is dependent