This is the first report of dexmedetomidine to treat acute agitation during transport of an extubated pediatric patient. Dexmedetomidine does not depress the respiratory drive,5,7
making it a potential option for the transport of extubated patients. Although there are no reports of dexmedetomidine use in the out-of-hospital environment, there are several prospective trials evaluating its use for procedural sedation in spontaneously breathing children.8–11
In 4 trials, dexmedetomidine was given to a total of 180 children who ranged in age from 5 months to 16 years. Each child in these studies received an intravenous loading dose (0.5–2.0 µg/kg) followed by an infusion (0.5–1.0 µg/kg/h). In almost all cases, there was a statistically significant but not clinically important decrease in HR and BP. There were no clinically important affects on respiration in any patient. The degree of sedation required during procedural sedation is analogous to the depth necessary to ensure safe interhospital transport, creating a new potential application for dexmedetomidine.
At this time, there is no Food and Drug Administration (FDA) label for dexmedetomidine use in children. Dexmedetomidine is FDA approved for short-term sedation (<24 hours) in mechanically ventilated adults in the ICU. Despite the lack of FDA labeling in pediatrics, dexmedetomidine has become a widespread therapeutic option for children in the PICU and operating room settings.12
Multiple trials have examined dexmedetomidine to sedate mechanically ventilated children,13–16
to prevent emergence delirium after general anesthesia,17–20
and for both invasive21,22
Sedation with dexmedetomidine is achieved via α-adrenergic agonism, as with clonidine, but dexmedetomidine is much more potent owing to its higher specificity for the α2
Dexmedetomidine works via a G protein–regulated pathway that blunts the sympathetic response to create the desired clinical effects of sedation and anxiolysis.24
Even though dexmedetomidine does not affect respiratory drive, the ubiquity of α-receptors throughout the body leads to other end-organ effects. The most pronounced and often dose-limiting of these side effects are hypotension and bradycardia, which occur in adults at rates of 28% and 7%, respectively.25
In rare cases, sinus arrest has been reported.26,27
Hypotension and bradycardia appear to occur at lower rates in children. In 1 large trial of more than 1200 children, the reported incidence of hypotension was 2.2%, and in another trial of dexmedetomidine in 315 children with behavioral disorders, the incidence of hypotension and/or bradycardia was <3%. Although uncommon, hypotension and bradycardia, when they do occur, appear to be dose-related, and a 30% decrease in BP and HR after a load of 1 µg/kg given over 10 minutes has been reported.28,29
Other reported side effects include transient hypertension associated with a loading dose, nausea, and dry mouth.30
Our experience with dexmedetomidine, knowledge of the pediatric data, and the fact that this patient represented a threat to both himself and the medical air transport team, led to the decision to sedate this severely agitated and combative child with dexmedetomidine for transport. An alternative approach would have been to attempt to avoid intubation and mechanical ventilation by using the calming presence of a fam-ily member during ground transport; however, transport by ground in this circumstance would likely have been ineffective given the inability of the family to calm the patient for several hours in the referring ED. In this case, a prolonged ground transport (>3 hours), the persistent agitation despite family presence, and unclear trajectory of the child led to the decision to minimize out-of-hospital time by using air transport. By using dexmedetomidine, we were able to safely transport this child via air without intubation and mechanical ventilation.
Although this patient experienced transient hypotension, likely related to dexmedetomidine, the risk of additional intravenous fluids in this context seems minimal. As in this case, an adjunct (or alternative) to fluid resuscitation, is discontinuation of the dexmedetomidine infusion. An important consideration in this circumstance is that dexmedetomidine has a rapid distribution phase with a short distribution half-life (6 minutes), but a prolonged terminal elimination half-life of 2 hours. Vasoactive agents (eg, dopamine, epinephrine) are second-line therapy for treatment of dexmedetomidine-related hypotension, but should be used with caution during transport in a child without central vascular access.31
It is also important to note that hypotension may result during intubation, either from associated sedation administration or the transition to positive pressure ventilation. Although the risk of hypotension is a consideration with the use of dexmedetomidine, the risk between potential hemodynamic compromise versus intubation and ventilation must be carefully considered when faced with the need to transport an acutely agitated child with effective spontaneous breathing.
This patient’s overall hospital stay was likely shortened as a result of transport without intubation, as a longer period would have been necessary in the PICU for extubation and postextubation monitoring. In this case, he was able to be discharged within a day of arrival to our institution. This case demonstrates that with careful patient selection, dexmedetomidine may be safely used as a treatment of agitation in a spontaneously breathing child, but additional work remains to fully determine the clinical pharmacology and impact of dexmedetomidine in children. Dexmedetomidine may be applicable in select circumstances when the interhospital transport of agitated patients is necessary, with careful consideration of the risks and benefits of sedation, spontaneous respiration, and intubation/mechanical ventilation on a case-by-case basis.