To the best of our knowledge, this is the first reported case of a pediatric patient with cannabinoid intoxication who was treated with dexmedetomidine. In the reported case, the use of dexmedetomidine allowed us to control the patient’s phases of agitation and aggressiveness without administering benzodiazepines or opioids, thereby avoiding any delirium or respiratory depression and thus the risk of intubation, mechanical ventilation and the need of further sedation. It was possible to evaluate the state of consciousness of the child and to move him out of our PICU only 24 hours after admission.

Dexmedetomidine was approved by the U.S. Food and Drug Administration in 1999 in the United States for use only as a short-term medication (<24 hours) for analgesia and sedation in the intensive care unit (ICU). Its unique properties render it suitable for sedation and analgesia during the whole peri-operative period: as a pre-medication, as an anesthetic adjunct for general and regional anesthesia and as a post-operative sedative and analgesic. It is widely used in the pediatric setting for sedation in ICU, as an analgesic after surgery, in burn patients who are inadequately sedated with opioids or benzodiazepines, for sedation in both non-invasive (i.e., infants diagnostic radiologic procedures) and invasive (i.e., placement of central venous lines, bronchoscopy, laryngoscopy, cardiac catheterization) procedures, in the post-anesthesia care unit to decrease the incidence of agitation, and to perform awake craniotomies [10].

Dexmedetomidine is an imidazole compound and a highly selective α₂-adrenergic receptor agonist. These receptors are pre- and post-synaptic. Through a negative feedback mechanism, pre-synaptic α₂-adrenergic receptors inhibit the release of norepinephrine, terminating the propagation of pain signals.

Dexmedetomidine has sedative and analgesic properties. Both supraspinal and spinal sites modulate the transmission of nociceptive signals in the central nervous system, and even peripheral α₂-adrenergic receptors may mediate anti-nociception. At the spinal level, dexmedetomidine produces its analgesic effects by acting on the α₂-adrenergic receptors in the dorsal horns of the spinal cord; thus, the drug inhibits the firing of nociceptive neurons and modulates the release of substance P. Dexmedetomidine acts even at a central level. The locus coeruleus is an important modulator of vigilance and nociceptive neurotransmission and has a high density of α₂-adrenergic receptors; therefore, the major sedative, anxiolytic and even anti-nociceptive effects of dexmedetomidine result primarily from its activity on this site.

The sedation produced by dexmedetomidine is different from that produced by GABAergic drugs (benzodiazepines and propofol). Patients receiving dexmedetomidine infusions have been described as being very easy to wake up and having the ability to follow commands and cooperate; undisturbed, patients were noted to fall asleep right away. This is called “cooperative sedation” [11]. Moreover, the α₂-adrenergic agonists also act through the endogenous sleep-promoting pathways to exert their sedative effect [12]. There is no respiratory depression and limited cardiovascular effects, providing wide safety margins.

The half-life of dexmedetomidine is around 2 hours, with a rapid distribution phase and a half-life of distribution of approximately 6 minutes. No significant sex- or age-based differences in the pharmacokinetic profile have been reported, even in patients with renal failure. Therefore, dexmedetomidine does not tend to accumulate, in contrast to other agents, such as benzodiazepines and opioids, which may have an unpredictable and prolonged duration of action, especially in critically ill patients [13].

Post-synaptic activation of α₂-adrenergic receptors in the central nervous system inhibits sympathetic activity and thus can cause bradycardia and hypotension. Usually, these temporary effects are successfully treated with atropine or ephedrine and volume infusions. Often, they occur during or briefly after the loading dose; thus, they can be reduced by omitting or reducing it. Additionally, hypertension may occur during the loading dose or with high infusion rates [14].

Several studies showed that dexmedetomidine might enhance patient safety and comfort in long-term sedation. It reduced the incidence of coma and delirium compared with lorazepam [15]; it reduced duration of mechanical ventilation and delirium; and, compared with midazolam and propofol, it improved patients’ ability to communicate about their pain [15].