Use of dexmedetomidine in treatment-refractory post-electroconvulsive therapy agitation

To the Editor

Post-electroconvulsive therapy (ECT) complications range from minor headaches to memory loss. The emergence of agitation, although not uncommon (1 in 10 patients) after an ECT session, is often mild and transient, requiring no specific intervention (Bryson et al., 2013). In some cases, agitation can be severe and require pharmacological interventions or lead to premature termination of the ECT course. We describe a case of severe post-ECT agitation which failed treatment with propofol and midazolam, but responded well to dexmedetomidine.

Ms T, a 19-year-old female with treatment-resistant depression, was referred for ECT. She underwent 10 treatments with right unilateral electrode placement (pulse width 1.0 ms) and a stimulus dose of 35% (approximately 176 mC). Anaesthesia consisted of propofol (80–90 mg induction dose), and succinylcholine (50–60 mg) was used as a paralytic agent. Upon awakening during the first eight treatments, Ms T experienced severe agitation with a Richmond Agitation–Sedation Scale (RASS) score of +3 (Very Agitated). The postictal agitation lasted up to 60 minutes and was clinically challenging and resource intensive to manage. Increasing doses of propofol (up to 420 mg) were administered postictally with minimal benefit. Midazolam was trialled with no effect. On the 9th and 10th treatments, 1µg/kg of dexmedetomidine over 10 minutes was administered immediately after stimulus dosing, reducing the requirement for propofol. During these treatments, Ms T was calm upon awakening with no agitation. Her RASS score improved from +3 previously to 0/−1 (Alert and Calm/Drowsy). ECT was clinically effective for Ms T, with her Montgomery–Åsberg Depression Rating Scale (MADRS) score improving from 32/60 pre-treatment to 4/60 post-treatment.

Dexmedetomidine, an α-2 agonist, is currently approved by the Food and Drug Administration for short-term sedation in intensive care units. Dexmedetomidine exhibits sedative and anxiolytic properties via activation of adrenergic receptors in the locus coeruleus, causing inhibition of adenylyl cyclase. This results in stimulation of parasympathetic outflow and inhibition of sympathetic outflow, overall causing a reduction in central nervous system excitation (Cohen and Stewart, 2013). In three separate case reports (Bryson et al., 2013; Cohen and Stewart, 2013; O’Brien et al., 2010), dexmedetomidine has been demonstrated to effectively decrease post-ECT agitation when administered postictally. Ms T’s response to dexmedetomidine was dramatic and allowed her to complete her course of ECT safely. Dexmedetomidine is emerging in the literature as another agent to manage severe post-ECT agitation. It should be considered in patients experiencing difficult-to-treat postictal agitation resultant from ECT especially when the option to cease ECT was not clinically viable as was the case of Ms T.