To the Editor: Dexmedetomidine has been used to treat agitation and delirium in the intensive care units (ICUs). 1 However, there is very little literature reporting agitation following use of dexmedetomidine. A 45-year-old male weighing...
moreTo the Editor: Dexmedetomidine has been used to treat agitation and delirium in the intensive care units (ICUs). 1 However, there is very little literature reporting agitation following use of dexmedetomidine. A 45-year-old male weighing 72 kg presented to our pain clinic with sharp and lancinating pain on the right side of face and forehead for one year. The pain was not relieved by different medications and remained within the distribution of V1 and V2 divisions of the trigeminal nerve. His past history and physical examination were unremarkable. Radiofrequency ablation of the respective divisions under sedation was planned. In the operating, routine monitors such as ECG, noninvasive blood pressure (BP), SpO 2 , EtCO 2 (via nasal prongs) were attached, baseline vitals recorded, and an intravenous (IV) access was secured. Oxygen was administered via nasal prongs at 2 L/minute and a loading dose of dexmedetomidine (1 lg/kg over 10 minutes) was started with an infusion pump. Five minutes later (35 lg dexmedetomidine infused), the patient displayed signs of agitation, disorientation, flailing of arms, and irritable behavior. His heart rate was 96/min, BP 130/84 mmHg, and SpO 2 100%. Dexmedetomidine was presumed to be the possible cause of agitation, and hence, the infusion was stopped; the patient was kept under observation. His behavior became normal after 15 minutes, and he had no recall of the event. Although the patient requested to proceed with the procedure, it was decided to postpone it to a later date. A week later, he underwent the procedure, uneventfully, under sedation with midazolam 2 mg and fentanyl 100 lg IV; there was no sign of agitation. The pain relief was complete, and there was no recurrence of agitation at 1-month follow-up. Dexmedetomidine is known to reduce emergence agitation during the postoperative period. 1 It is also used to reduce agitation and delirium in ICU as it has sedative and analgesic properties without respiratory depression. 2 These effects are attributed to selective central presynaptic a-2 agonist properties, which inhibits the action of norepinephrine and epinephrine centrally and peripherally by inhibiting presynaptic as well as postsynaptic a-2 receptors. 3 The reduction in central sympathetic activity which inhibits nociception is mainly responsible for reducing agitation. 4 However, the presence of agitation during infusion in this case points toward the possibility of increase in central sympathetic activities. Agitation has been reported with the use of dexmedetomidine for prolonged ICU sedation (more than 24 hours), with an incidence of 2%. 5 However, this is the first report of agitation with infusion of dexmedetomidine during procedural sedation, observed at a small dose of 0.5 lg/kg. We believe that dexmedetomidine may have some degree of unknown central postsynaptic a-receptor activity increasing sympathetic surge which may result in agitation. Caution must therefore be exercised, and possible occurrence of agitation may be anticipated during infusion of dexmedetomidine for procedural sedation.
