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PEDIATRIC ANESTHESIA

Short Duration Large Dose Dexmedetomidine in a Pediatric Patient During Procedural Sedation

From the Department of Anesthesia and Pediatrics, Department of Anesthesiology, West Virginia University, Morgantown, West Virginia.

Address correspondence and reprint requests to David Rosen, MD, Department of Anesthesiology, West Virginia University, 3618 Hsc, PO box 9134, Morgantown, WV 26506-9134. Address e-mail to rosend{at}rcbhsc.wvu.edu.

	Abstract

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We describe an infusion of dexmedetomidine at 1.0 µg · kg^–1 · min^–1 for 10 min (total dose, 144 µg) sedation in a 3-yr-old child weighing 14 kg. The large dose of dexmedetomidine produced a hemodynamically stable patient who was deeply sedated for approximately 4 h after discontinuing the infusion.

	Introduction

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Dexmedetomidine is an alpha 2-adrenoceptor agonist approved for intensive care unit sedation of adult ventilated patients for <24 h. Compared with clonidine, dexmedetomidine is more specific for the 2 receptor and has a shorter half-life (1,2). It reduces anesthetic requirements, speeds recovery, and blunts the sympathetic nervous system (3). Experience in the pediatric patient is limited. Tobias et al. (2) and Finkel and Elrefai (4) reported success in the treatment of the clinical signs and symptoms of drug withdrawal and in the treatment of emergence delirium and postoperative shivering. Scher and Gitlin (5) used dexmedetomidine and small-dose ketamine for awake fiberoptic intubations. Moreover, Ibacache et al. (6) demonstrated that dexmedetomidine reduced agitation after sevoflurane anesthesia in children.

	CASE REPORT

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The patient was a 3-yr-old, 14-kg male scheduled for an outpatient magnetic resonance angiography to visualize a rapidly increasing intrathoracic vascular structure. The patient was born with Tetralogy of Fallot that was corrected at 9 mo of age. He was seizure-free and denied chest pain, syncope, cyanosis, palpitations, or respiratory difficulty. The only other significant finding was a recent upper respiratory infection.

The child presented extremely anxious. Oral premedication with midazolam (0.5 mg/kg) did little to make him more cooperative. The addition of intranasal dexmedetomidine (4 µg/kg) allowed for a mask induction of anesthesia. The patient underwent mask induction with halothane. His preoperative vital signs consisted of a heart rate of 89 bpm and arterial blood pressure (BP) 98/64. A 22-gauge IV was placed in the left hand and the dexmedetomidine infusion was started at 1.0 µg · kg^–1 · min^–1 instead of the desired initial dose of 1.0 µg/kg over 10 min. The halothane was discontinued and propofol was started at 200 µg · kg^–1 · min^–1 because of his elevated BP measurement. Additional time was spent outside of the magnetic resonance imaging chamber finding and placing a second 22-gauge IV in the right arm. The second IV was placed because of the incompatibility of propofol with inotropic drugs. The child was then taken into the magnetic resonance imaging chamber where he was positioned for the imaging study. At this time, it was noted that the dexmedetomidine syringe was empty. The patient was hemodynamically stable and the decision was made to proceed with only propofol at 200 µg · kg^–1 · min^–1. Ten minutes into the 25-min scan the propofol was stopped because it was felt the patient was adequately sedated and the elevated BP was the result of dexmedetomidine rather than light sedation. He tolerated the magnetic resonance angiography procedure well. His end-tidal carbon dioxide was stable in the upper 20 s and his arterial saturations were 100% on a 2 L nasal cannula throughout the study. His vital signs after the dexmedetomidine infusion and during the propofol infusion were HR 80 bpm and BP 135/75.

After the scan, the patient was taken to a recovery room. He was deeply sedated, responding minimally to a blood draw. His HR remained 80–90 bpm with a systolic blood pressure of 100 ± 5 mm Hg and saturations of 98%–100% in room air. After the dexmedetomidine had been discontinued for 1 h, the patient responded to significant stimulation with crying, thrashing movements, and disorientation. These symptoms lasted approximately 3–5 min, after which the child became somnolent again. This scenario was repeated every 30 min for the next 3 h. Three hours and 45 min after stopping the dexmedetomidine infusion, the child woke, could bear weight, and stay alert for approximately 90 s. After 4 h and 15 min, the child was fully awake, and was able to walk, speak, and drink; he was discharged home.

	DISCUSSION

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Characteristics of an ideal sedative for pediatric procedural sedation include a rapid onset, short duration of action, hemodynamic stability, and minimal respiratory depression. Additionally, the ability to deliver the drug via nonparenteral routes is desirable while IV access is secured.

Intranasal dexmedetomidine was used in this patient as an adjuvant to sedation because the benzodiazepine had failed to calm him. Anttila et al. (7) documented the high bioavailability (73%–92%) when dexmedetomidine was given via the buccal route. The information regarding buccal availability was similar to the information used to predict whether midazolam, ketamine, or fentanyl could be successfully administered via the nasal route. Dexmedetomidine has a pKa of 7.1 and octanol:water partition coefficient of 2.89 at a pH of 7.4. Its pH of 4.5–7.0 would also support its effectiveness and relative comfort when being administered via this route. The total volume of 0.56 mL (100 µg/mL) was divided into each nare. The child did not complain of discomfort with installation. Though the child was less agitated, he resisted his mother slightly when she placed the halothane mask on his face 5 minutes later. Anttila et al. had found a lag time of 0.13 ± 0.04 hours after buccal administration with a peak concentration at 1.5 ± 0.2 hours, so that waiting additional time may have further reduced any resistance on the child's part. After securing IV access, the remaining 144 µg from the 200 µg vial was infused at a rate of 1 µg · kg^–1 · min^–1.

The patient's HR, oximetry, and end-tidal CO₂ remained stable throughout the procedure while BP increased from a preoperative value of 98/64 to the 130s/70s. After stopping the dexmedetomidine infusion, his BP returned to baseline over the next hour. At prescribed doses, dexmedetomidine typically decreases BP in adults. The increase in BP with large doses of dexmedetomidine parallels the work of Ebert et al. (8). They showed a biphasic hemodynamic response (low, then high) for BP and vascular resistances. Larger concentrations of dexmedetomidine resulted in systemic and pulmonary hypertension, increased sedation and analgesia, with minimal changes in respiration (8). A hypotensive period did not occur in our patient.

The optimal dosage strategy for dexmedetomidine in the pediatric population is still under development, and even adult doses listed in the package insert often exceed the upper limit of 0.7 µg · kg^–1 · min^–1 for 24 hours (9–11). Jorden et al. (12) reported three adult dexmedetomidine overdoses in patients concomitantly receiving opioids. Two patients received a 10-fold increase in dosage because of a decimal error, and one patient received a 60-fold increase secondary to dosing the drug per minute rather than per hour. Their patients had a deep level of sedation that corrected after discontinuation of the drug infusion.

The programming of the pump in µg · kg^–1 · min^–1 resulted in an excellent quality study and the patient with a recent upper respiratory infection did not have to be tracheally intubated. The time to return to baseline was similar to that reported when adults have received increased dosing (12). The agitation seen on early awakening resembled the symptoms that dexmedetomidine has been used to treat for patients wakening from sevoflurane anesthesia.

In conclusion, large-dose dexmedetomidine produced a hemodynamically stable patient who was deeply sedated and remained that way for approximately 4 hours after stopping the infusion. This case report confirms that more studies are needed on dexmedetomidine to determine the optimal dosing for this drug in pediatric patients, and to investigate the efficacy of non-IV administration of this drug.

	Footnotes

 
Accepted for publication February 1, 2006.

	REFERENCES

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1. Virtanen R, Savola JM, Saano V, et al. Characterization of selectivity, specificity and potency of dexmedetomidine as alpha-2-adrenoceptor agonist. Eur J Pharmacol 1988;150:9–14.[ISI][Medline]
2. Tobias JD, Berkenbosch JW, Russo P. Additional experience with dexmedetomidine in Pediatric Patients. South Med J 2003;96; 9:871–5.
3. Aantaa R, Kanto J, Scheinin M, et al. Dexmedetomidine, an alpha 2 adrenoceptor agonist, reduces anesthetic requirements for patients undergoing minor gynecologic surgery. Anesthesiology 1990;73:230–5.[ISI][Medline]
4. Finkel JC, Elrefai A. The use of dexmedetomidine to facilitate opioid and benzodiazapine detoxification in an infant. Anesth Analg 2004;98:1658–9.[Abstract/Free Full Text]
5. Scher CS, Gitlin MC. Dexmedetomidine and low-dose ketamine provide adequate sedation for awake fiberoptic intubation. Can J Anaesth 2003;50 6:607–10.
6. Ibacache ME, Munoz HR, Brandes V, Morales AL. Single–dose dexmedetomidine reduces agitation after sevoflurane anesthesia in children. Anesth Analg 2004;98:60–3.[Abstract/Free Full Text]
7. Anttila M, Penttila J, Helminen A, et al. Bioavailability of dexmedetomidine after extravascular doses in healthy subjects. Br J Clin Pharmacol 2003;56:691–93.[ISI][Medline]
8. Ebert TJ, Hall JE, Barney JA, et al. The effects of increasing plasma concentrations of dexmedetomidine in humans. Anesthesiology 2000;93:382–394.[ISI][Medline]
9. Berkenbosch JW, Wankum PC, Tobias JD. Prospective evaluation of dexmedetomidine for noninvasive procedural sedation in children. Pediatr Crit Care Med 2005; 6:435–9.[Medline]
10. Finkel JC, Johnson YJ, Quezado ZMN. The use of dexmedetomidine to facilitate acute discontinuation of opioids after cardiac transplantation in children. Crit Care Med 2005;33:2110–2.[Medline]
11. Precedex ® (dexmedetomidine) package insert. Abbott Park, IL: Abbott Laboratories; 2004.
12. Jorden VSB, Pousman RM, Sanford MM, et al. Dexmedetomidine overdose in the perioperative setting. Ann Pharm 2004;38:803–7.

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999