JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (15) Citing Articles via Google Scholar Google Scholar Articles by Koroglu, A. Articles by Ersoy, O. M. Search for Related Content PubMed PubMed Citation Articles by Koroglu, A. Articles by Ersoy, O. M.

---

PEDIATRIC ANESTHESIA

A Comparison of the Sedative, Hemodynamic, and Respiratory Effects of Dexmedetomidine and Propofol in Children Undergoing Magnetic Resonance Imaging

Ahmet Koroglu, MD^*, Huseyin Teksan, MD, Ozlem Sagr, MD^*, Aytaç Yucel, MD^*, Huseyin I. Toprak, MD^*, and Ozcan M. Ersoy, MD^*

From the *Department of Anesthesiology and Reanimation, Inonu University, Medical Faculty, Malatya, Turkey; Group of Vatan's Hospital, Clinic of Anesthesiology, Karabuk, Turkey.

Address correspondence and reprint requests to Ahmet Koroglu, Inonu University, Faculty of Med, Department of Anesthesiology and Reanimation, 44315 Malatya, Turkey. Address e-mail to akoroglu{at}inonu.edu.tr.

	Abstract

Top Abstract Introduction METHODS RESULTS DISCUSSION REFERENCES

 
We compared the sedative, hemodynamic, and respiratory effects of dexmedetomidine and propofol in children undergoing magnetic resonance imaging procedures. Sixty children were randomly distributed into two groups: The dexmedetomidine (D) group received 1 µg/kg initial dose followed by continuous infusion of 0.5 µg · kg^–1 · h^–1 and a propofol group (P) received 3 mg/kg initial dose followed by a continuous infusion of 100 µg · kg^–1 · min^–1. Inadequate sedation was defined as difficulty in completing the procedure because of the child's movement during magnetic resonance imaging. Mean arterial pressure (MAP), heart rate, peripheral oxygen saturation, and respiratory rate (RR) were recorded during the study. The onset of sedation, recovery, and discharge time were significantly shorter in group P than in group D. MAP, heart rate, and RR decreased during sedation from the baseline values in both groups. MAP and RR were significantly lower in group P than in group D during sedation. Desaturation was observed in four children of group P. Dexmedetomidine and propofol provided adequate sedation in most of the children. We conclude that although propofol provided faster anesthetic induction and recovery times, it caused hypotension and desaturation. Thus, dexmedetomidine could be an alternative reliable sedative drug to propofol in selected patients.

	Introduction

Top Abstract Introduction METHODS RESULTS DISCUSSION REFERENCES

 
Sedation is frequently necessary for children 1 to 7 yr of age undergoing magnetic resonance imaging (MRI) to ensure examinations that are of diagnostic quality. Because procedural sedation is unable to guarantee patient compliance in these cases, a deeper level of sedation is required (1,2). The success of sedation for MRI has typically been measured by two factors: the safety of the sedation procedure (lack of adverse events) and the effectiveness of the procedure (successful completion of the diagnostic examination) (3). Sedation of children for MRI is usually associated with inadequate or failed sedation because of difficulty in having patients motionless while maintaining hemodynamic and respiratory stability. Also, limited access to the patient may pose a safety risk during MRI examination (1,4). Therefore, appropriate drugs need to be selected, administered, and titrated to achieve these objectives (5).

Dexmedetomidine is a potent, highly selective ₂ adrenoreceptor agonist having a distribution half-life of approximately 8 min and a terminal half-life of 3.5 h (6,7). At therapeutic doses, dexmedetomidine provides profound levels of sedation without affecting cardiovascular and respiratory stability (7–9). There is significant interest in the use of propofol for sedation in children in the MRI setting because of its predictability, rapid onset, and offset of action (2,10,11). There is no study comparing dexmedetomidine and propofol sedation for use in children undergoing MRI.

The aim of this prospective study was to compare the sedative, hemodynamic, and respiratory effects of dexmedetomidine and propofol in children undergoing MRI examination.

	METHODS

Top Abstract Introduction METHODS RESULTS DISCUSSION REFERENCES

 
After local Institutional Ethics Committee approval and written parental consent, ASA physical status I-II children aged between 1–7 yrs undergoing MRI were included in this randomized and prospective study. Patients with known heart, lung, and neurological disease, central nervous system or extremity trauma, and airway abnormalities were excluded from the study. Patients with known allergies to the study drugs or patients having received any study drug in the last 30 days were also excluded. Children older than 3 yr of age were NPO for solids and milk for at least 8 h and children 1–3 yr of age were NPO for solids and milk for 6 h. All the children were allowed to take clear liquids up until 2 h before the beginning of the sedation. To facilitate IV drug administration, EMLA cream was applied on the dorsum of both hands 1 h before transfer to the preparation room. Presedation behavior was assessed on a 4-point scale, by a person (Anesthesiologist 1) who did not know which drug would be administered, 1 = calm, cooperative; 2 = anxious but reassurable; 3 = anxious and not reassurable; 4 = crying or resisting. Categories 1 and 2 were called "undistressed behavior," and categories 3 and 4 were defined as "distressed behavior." Baseline values were recorded upon the arrival of the unpremedicated children to the preparation room before the 22-gauge or 24-gauge venous cannula was inserted into the dorsum of the hand. Children were allocated according to a random number table to receive either dexmedetomidine (group D, n = 30) or propofol (group P, n = 30). Solutions of dexmedetomidine (Precedex®, Abbott Laboratories, North Chicago, IL), 1 mL at a concentration of 100 µg/mL, was diluted with 49 mL normal saline to a concentration of 2 µg/mL. The initial dose of the study drugs were administered for 10 min (dexmedetomidine 1 µg/kg or propofol [propofol 1% Fresenius®, Fresenius kabi, Bad Homburg, Germany] 3 mg/kg), followed by continuous infusion (dexmedetomidine 0.5 µg · kg^–1 · h^–1 or propofol 100 µg · kg^–1 · min^–1). To reduce propofol injection pain, 1 mL of 1% lidocaine (Aritmal® 2%, Biosel, Istanbul, Turkey) was administered IV before propofol administration.

The sedation level of the children was measured by the anesthesiologist using the Ramsay sedation scale every 10 min. The Ramsay scale assigns a score of 1–6 based on the clinical assessment of the level of sedation as follows: 1 = anxious, agitated, restless; 2 = awake, but cooperative, tranquil, orientated; 3 = responds to verbal commands only. Scores 4–6 are used for sleeping patients and are graded according to the response to loud noises or glabellar taps as follows: 4 = brisk response; 5 = sluggish response; 6 = no response. Score 3 was accepted as procedural sedation and 5 was accepted as deep sedation. Children were transferred and positioned on the scanning table with a shoulder roll under the neck (either a rolled up towel or sheet) after both a Ramsay score of 5 was achieved and hemodynamic and respiratory stability was ensured. If a Ramsay score of 5 was not achieved after infusion of the study drug for 25 min, the infusion rate of the study drugs was increased to 0.7 µg · kg^–1 · h^–1 in group D and to 150 µg · kg^–1 · min^–1 in group P for 5 min by anesthesiologist 2. If a Ramsay score of 5 was not achieved after 25 + 5 min of study drug infusion IV a supplementary bolus dose of midazolam (0.05 mg/kg) in group D or 1 mg/kg propofol in group P was given. If patient movements were observed during the imaging process, an additional supplementary bolus dose of midazolam 0.05 mg/kg in group D or propofol 1 mg/kg in group P was administered, and the continuous infusion dose of the study drug was increased to 0.7 µg · kg^–1 · h^–1 in group D and to 150 µg · kg^–1 · min^–1 in group P. Inadequate sedation was defined as difficulty in completing the procedure as a result of the child's movement during MRI examination.

Mean arterial blood pressure (MAP), heart rate (HR), peripheral oxygen saturation (Spo₂), and respiratory rate (RR) were monitored continuously and recorded at 5-min intervals during the study period by anesthesiologist 1. Patients were allowed to breathe spontaneously without an artificial airway throughout the procedure. Ventilatory function was assessed by observation of respiratory activity by anesthesiologist 1. If the Spo₂ level decreased below 93% for 30 s the imaging process would be interrupted and the patient would be taken out of the MRI tunnel. After airway patency was assessed, the neck was extended slightly and oxygen was administered via facemask, and the study drug infusion was discontinued temporarily.

Quality of the MRI was evaluated by a radiologist using a three-point scale (1 = no motion; 2 = minor movement; 3 = major movement necessitating another scan). At the end of the MRI, the drug infusion was discontinued and the children were then transferred to the recovery room.

The onset of sedation time was defined as the period of time between the beginning of study drug infusion and reaching a Ramsay score of 5. Recovery time was accepted as the period of time between discontinuation of study drug infusion and reaching a Ramsay score of 2. Discharge time was defined as the period of time between discontinuation of drug infusion and the discharge of the children from the hospital. The criterion of the discharge was the return of vital signs and level of consciousness to baseline, and the ability to maintain a patent airway. Side effects (e.g., nausea, vomiting, dysphoria) occurred during and after sedation were recorded.

Statistical analyses were made with SPSS® 10.0 (SPSS Inc., Chicago, IL). Results are presented as mean (sd) or their confidence interval (CI). Analysis of variance for repeated measures was performed on hemodynamic and respiratory variables, with compensation for post hoc comparisons using the Bonferroni correction. Intergroup statistical analyses were performed using Student's t-test, and nonparametric data were analyzed using ² test. Statistical significance was considered at P < 0.05. The power of the study was calculated based on the onset of sedation time. Setting a significance level of P = 0.05, it was calculated that a group size of 30 patients allowed detection of a difference of 4 min between groups with a power of 100%.

	RESULTS

Top Abstract Introduction METHODS RESULTS DISCUSSION REFERENCES

 
The patients' demographics, presedation behavior score, and the duration, type, and quality of MRI procedure were not statistically different between groups (Table 1).

Adequate sedation, as defined by quality of the examination, was obtained in 25 children from group D (83%, 95% CI, 0.65–0.94) and in 27 children from group P (90%, 95% CI, 0.73–0.97). Although, deep sedation (Ramsay score of 5) was obtained with the dexmedetomidine or propofol infusion before MRI examination, inadequate sedation was observed in 5 children from group D and in 3 children of group P during MRI. MRI examination was successfully completed in all of these children with supplementary bolus doses of midazolam in group D and propofol in group P. In group P, the onset of sedation, recovery, and discharge time were significantly shorter than in group D (P < 0.05). The level of consciousness was the same in both groups at the time of discharge. The duration of drug infusion was not different between groups (P > 0.05) (Table 2).

MAP, HR, and RR were not statistically different between groups before sedation. MAP and HR decreased significantly from baseline during sedation in both groups (P < 0.001). HR at 10, 20, 25 min was significantly more rapid in group P than in group D, and MAP at 10, 15, 20, 35 and 50 was lower in group P than group D; however, these differences were not clinically significant. MAP in group P decreased below 20% from baseline only at 50 min. The RR was statistically significantly less in group P than group D but these differences were not clinically significant. Bradycardia was not observed in any child. The maximum decreases in MAP during sedation in groups D and P were 17% and 21%, where the maximum decreases in HR during sedation were 15% and 17%, respectively, and the maximum decreases in RR during sedation in groups D and P were 8% and 17%, respectively (Table 3).

No side effects such as nausea, vomiting, or dysphoria were observed in either group during or after sedation. However, desaturation was observed in 4 children of group P in whom Spo₂ decreased below 93% (average Spo₂, 89%) during MRI examination. In these children, oxygen desaturation was treated with chin lift, temporary cessation of the propofol infusion, and oxygen supplementation via facemask.

	DISCUSSION

Top Abstract Introduction METHODS RESULTS DISCUSSION REFERENCES

 
Our results indicate that although both drugs prevented undesired movement in most of the children, propofol provided more rapid rates of induction, recovery, and discharge but dexmedetomidine better preserved MAP and RR and did not cause any desaturations. The ideal pediatric sedative drug should maintain a patient's ventilation, provide hemodynamic stability, provide patient immobility, and allow easy drug titration. Ideal pediatric sedative drugs should also ensure rapid anesthetic induction and recovery while producing minimal side effects such as nausea, vomiting, dysphoria, or pain (10).

Inadequate sedation is the most common adverse event (5%–15%) resulting in failure (3.7%) of MRI procedures. Inadequate sedation was more frequent in hyperactive, uncooperative, and older children (3,4,12). Previous studies indicate that infusion doses of dexmedetomidine (0.1–0.7 µg · kg^–1 · h^–1) have provided effective sedation (13–16). Various studies (2,10,11) demonstrated that infusion of propofol at a rate of 100–150 µg · kg^–1 · min^–1 effectively prevents at least 90% of children from moving during elective MRI. These doses are similar to our propofol doses, and our results were consistent with these studies. The inadequate sedation rate observed with dexmedetomidine and propofol in our study was similar to that previously reported. In our study, propofol's onset, discharge, and recovery times were compatible with previously published studies (2,9,11,17). Adequate sedation was obtained with dexmedetomidine and propofol in most of the children.

In a previous study (9), we noted that the onset of sedation time was 19 minutes for dexmedetomidine in MRI sedation. In this study, the faster onset of sedation time could be explained by the fact that we accepted the Ramsay score of 5 as the time to onset of sedation as opposed to the accepted Ramsay score in our previous study. In our study, propofol provided faster onset of sedation, recovery, and discharge times than dexmedetomidine.

Although the advantage of dexmedetomidine was hemodynamic stability, there are contradictory results related to its hemodynamic effects in the literature (7–9, 16, 18–20). Hypotension and bradycardia have been reported, particularly with large bolus dosing regimens, in patients with preexisting cardiac problems and in patients administered an initial dose in <10 minutes (6,21). Hypotension and bradycardia are observed occasionally when propofol infusion, used as a single drug, is titrated to achieve adequate sedation (5,11,22,23). It has been reported that the decrease in MAP and HR after propofol induction was 15%–31% and 17%–24%, respectively (2,17,22). In our study, an initial dose of propofol was administered for 10 minutes both to allow for equivalent modes of dexmedetomidine and propofol administration and to minimize cardiovascular and respiratory depression related to the initial dose. In our study, although MAP and HR decreased significantly after dexmedetomidine and propofol infusion, the decrease in MAP was larger with propofol infusion. These decreases could have been exaggerated because the patients were not premedicated and the baseline values may have been high and not reflective of a time baseline value. Because decreases in MAP and HR with dexmedetomidine infusion were <20% of baseline and no bradycardia or hypotension occurred in any child, these decreases in MAP and HR were considered clinically insignificant. Although at most time points the decrease in MAP in the propofol group was more than with dexmedetomidine, only the decrease at 50 minutes was more than 20% of baseline.

Respiratory events make up a large proportion (5.5%) of the complications of the sedation in children (4). Some authors have reported that dexmedetomidine did not affect RR, Spo₂, and ETco₂ (13,24). However, some respiratory complications have been reported with large and rapid initial loading doses (6,20,25). When a dexmedetomidine initial dose was administered rapidly (2 minutes), it caused irregular respiration, apnea, slight hypoxemia, and hypercapnia (19). Propofol may depress ventilation, suppress pharyngeal and laryngeal reflexes, and cause transient apnea (5,10,22). However, this is not a consistent finding (2,11). In this current study, the clinically insignificant decrease in RR during dexmedetomidine or propofol infusion may have been a result of high baseline values. Although RR decreased more with propofol than dexmedetomidine during sedation, and propofol was associated with more respiratory events (desaturations), dexmedetomidine may provide more respiratory stability.

In conclusion, dexmedetomidine and propofol provided adequate sedation in most of the children aged between 1–7 years. Although propofol provided more rapid rates of anesthetic induction and recovery, dexmedetomidine better preserved MAP and RR. Thus, dexmedetomidine could be an alternative sedative drug to propofol in selected patients.

	Footnotes

 
Accepted for publication February 9, 2006.

	REFERENCES

Top Abstract Introduction METHODS RESULTS DISCUSSION REFERENCES

 

1. Lawson GR. Sedation of children for magnetic resonance imaging. Arch Dis Child 2000;82:150–2.[Free Full Text]
2. Hasan RA, Shayevitz JR, Patel V. Deep sedation with propofol for children undergoing ambulatory magnetic resonance imaging of the brain: Experience from a pediatric intensive care unit. Pediatr Crit Care Med 2003;4:454–8.[Medline]
3. Bluemke DA, Breiter SN. Sedation procedures in MR imaging: safety, effectiveness, and nursing effect on examinations. Radiology 2000;216:645–52.[Abstract/Free Full Text]
4. Malviya S, Voepel LT, Eldevik OP, et al. Sedation and general anaesthesia in children undergoing MRI and CT: adverse events and outcomes. Br J Anaesth 2000;84:743–8.[Abstract/Free Full Text]
5. Dial S, Silver P, Bock K, Sagy M. Pediatric sedation for procedures titrated to desired degree of immobility results in unpredictable depth of sedation. Pediatr Emerg Care 2001;17:414–20.[Web of Science][Medline]
6. Bhana KNL, McClellan GJ, McClellan KJ. Dexmedetomidine. Drugs 2000;59:263–8.[Web of Science][Medline]
7. Shelly MP. Dexmedetomidine: a real innovation or more of the same? Br J Anaesth 2001;87:677–8.[Free Full Text]
8. Nelson LE, Lu J, Guo T, et al. The alpha2-adrenoceptor agonist dexmedetomidine converges on an endogenous sleep-promoting pathway to exert its sedative effects. Anesthesiology 2003;98:428–36.[Web of Science][Medline]
9. Koroglu A, Demirbilek S, Teksan H, et al. Sedative, hemodynamic and respiratory effects of dexmedetomidine in children undergoing magnetic resonance imaging examination: preliminary results. Br J Anaesth 2005;94:821–4.[Abstract/Free Full Text]
10. Frankville DD, Spear RM, Dyck JB. The dose of propofol required to prevent children from moving during magnetic resonance imaging. Anesthesiology 1993;79:953–8.[Web of Science][Medline]
11. Usher GA, Kearney RA, Tsui BCH. Propofol total intravenous anesthesia for MRI in children. Paediatr Anaesth 2005;15:23–8.[Medline]
12. Voepel LT, Malviya S, Prochaska G, Tait RA. Sedation failures in children undergoing MRI and CT: is temperament a factor? Paediatr Anaesth 2000;10:319–23.[Web of Science][Medline]
13. Hall JE, Ulrich TD, Barney JA, et al. Sedative, amnestic and analgesic properties of small-dose dexmedetomidine infusions. Anesth Analg 2000;90:699–705.[Abstract/Free Full Text]
14. Tobias JD, Berkenbosch JW. Initial experience with dexmedetomidine in paediatric-aged patients. Paediatr Anaesth 2002;12:171–5.[Web of Science][Medline]
15. Tobias JD, Berkenbosch JW, Russo P. Additional experience with dexmedetomidine in pediatric patients. South Med J 2003;96:871–5.[Web of Science][Medline]
16. Triltsch AE, Welte M, Von Homeyer P, et al. Bispectral index-guided sedation with dexmedetomidine in intensive care: randomized, double blind, placebo-controlled phase II study. Crit Care Med 2002;30:1007–14.[Web of Science][Medline]
17. Bloomfield EL, Masaryk TJ, Caplin A, et al. Intravenous sedation for MR imaging of the brain and spine in children: pentobarbital versus propofol. Pediatr Radiol 1993;186:93–7.
18. Venn RM, Bradshaw CJ, Spencer R, et al. Preliminary UK experience of dexmedetomidine, a novel agent for postoperative sedation in the intensive care unit. Anaesthesia 1999;54:1136–42.[Web of Science][Medline]
19. Ebert TJ, Hall JE, Barney JA, et al. The effects of increasing plasma concentrations of dexmedetomidine in humans. Anesthesiology 2000;93:382–94.[Web of Science][Medline]
20. Venn RM, Karol MD, Grounds RM. Pharmacokinetics of dexmedetomidine infusions for sedation of postoperative patients requiring intensive care. Br J Anaesth 2002;88:669–75.[Abstract/Free Full Text]
21. Kallio A, Scheinin M, Koulu M, et al. Effects of dexmedetomidine, a selective alpha2-adrenoceptor agonist, on hemodynamic control mechanisms. Clin Pharmacol Ther 1989;49:33–42.
22. Aun CS. New i.v. agents. Br J Anaesth 1999;83:29–41.[Free Full Text]
23. Tramer MR, Moore RA, McQuay HJ. Propofol and bradycardia: causation, frequency and severity. Br J Anaesth 1997;78:642–51.[Abstract/Free Full Text]
24. Venn RM, Hell J, Grounds RM. Respiratory effects of dexmedetomidine in the surgical patient requiring intensive care. Crit Care 2000;4:302–8.[Web of Science][Medline]
25. Belleville JP, Wards DS, Bloor BC, Maze M. Effects of intravenous dexmedetomidine in human: sedation, ventilation and metabolic rate. Anesthesiology 1992;77:1125–33.[Web of Science][Medline]

This article has been cited by other articles:

				M. Munkwitz Dexmedetomidine vs Midazolam in Critically Ill Patients: a RCT AAP Grand Rounds, July 1, 2009; 22(1): 7 - 7. [Full Text] [PDF]

				C. Heard, F. Burrows, K. Johnson, P. Joshi, J. Houck, and J. Lerman A Comparison of Dexmedetomidine-Midazolam with Propofol for Maintenance of Anesthesia in Children Undergoing Magnetic Resonance Imaging Anesth. Analg., December 1, 2008; 107(6): 1832 - 1839. [Abstract] [Full Text] [PDF]

				S. L. Shafer Anesthesia & Analgesia's Policy on Off-Label Drug Administration in Clinical Trials Anesth. Analg., July 1, 2007; 105(1): 13 - 15. [Full Text] [PDF]

				A. T Gerlach and J. F Dasta Dexmedetomidine: An Updated Review Ann. Pharmacother., February 1, 2007; 41(2): 245 - 252. [Abstract] [Full Text] [PDF]

				P. M. Bokesch Untying the gordian knot. Anesth. Analg., July 1, 2006; 103(1): 249 - 250. [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (15) Citing Articles via Google Scholar Google Scholar Articles by Koroglu, A. Articles by Ersoy, O. M. Search for Related Content PubMed PubMed Citation Articles by Koroglu, A. Articles by Ersoy, O. M.

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