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Comparison of dexmedetomidinepropofol vs. fentanylpropofol for laryngeal mask insertion

Uzümcügil, F.1; Canbay, O.1; Celebi, N.1; Karagoz, A. H.1; Ozgen, S.1

Author Information
European Journal of Anaesthesiology: August 2008 - Volume 25 - Issue 8 - p 675-680
doi: 10.1017/S0265021508004213



The laryngeal mask (LM) is a device with a lumen that provides a seal around the laryngeal inlet. It allows spontaneous ventilation, as well as positive pressure ventilation with an airway pressure <15 cm H2O [1]. An LM can be used safely in operations allowing spontaneous ventilation, instead of a face mask [2]. It has been shown that insertion of LM requires lighter anaesthesia levels than endotracheal intubation [1,3]. LM insertion requires adequate mouth opening and minimal upper airway reflexes such as coughing, gagging or laryngospasm [4,5]. Because of these reasons, there have been many studies to find the optimum anaesthetics to provide excellent conditions for LM insertion.

Since the time required for LM insertion was reported to be longer with inhalational anaesthetics, intravenous (i.v.) agents have been preferred [5,6]. Also patient satisfaction was found better with i.v. anaesthetics [7]. Among the i.v. agents, propofol has been preferred the most because of its potential suppressor effects on upper airway reflexes [3]. When used alone without premedication, propofol provides conditions for LM insertion that is far from satisfactory [5,8,9] and causes cardiorespiratory depression [8,10]. In order to decrease the adverse effects of propofol, opioids or muscular relaxants were added to reduce the propofol dose requirement [11-14]. Muscle relaxants were not found to be effective [15] and even found to increase the risk of aspiration [8]. Fentanyl and remifentanil were studied. Unfortunately, these medications increased the incidence and duration of apnoea [9,16].

Dexmedetomidine, a highly selective α2-adrenoceptor agonist, was shown to have sedative and analgesic properties. α2-adrenoceptors have many locations in the central nervous system (CNS). α2-adrenoceptor agonists were reported to exert their sedative effects via the receptors in locus coeruleus, known to have a role in respiratory control and function as an alarm system. Hsu and colleagues [17] reported dexmedetomidine, even when used at supramaximal plasma levels, to be clinically safe for respiration. Dexmedetomidine was also shown to diminish airway and circulatory responses during intubation and extubation [18-20].

In this study, we aimed to provide successful LM insertion conditions by using dexmedetomidine with propofol and to compare its effect with fentanyl combined with propofol.


After the study was approved by the Institutional Ethics Commitee, informed consent was obtained from each patient. In all, 52 patients, aged 26–65 yr, ASA physical status I–II, scheduled to have minor urological procedures, were randomized into two groups. Patients with gastroesophageal reflux, allergy or sensitivity to volatile anaesthetics or propofol, asthma, dysrhythmia, congestive heart failure and any pathology of CNS and respiratory tract were excluded from the study. On arrival in the operating room without any premedication, each patient was monitored with electrocardiogram (ECG), pulse-oximeter and non-invasive blood pressure (BP). An i.v. line was inserted and an infusion of normal saline (NS) was started. After 3 min of preoxygenation, Group F received 1 μg kg−1 fentanyl diluted in 10 mL NS and Group D received 1 μg kg−1 dexmedetomidine diluted in 10 mL NS over a 2 min duration. Thirty seconds later, after injection of 3 mL prilocaine 2% for propofol pain, each patient was given 1.5 mg kg−1 propofol for induction, without any neuromuscular blocking agent. For the maintenance of anaesthesia, we used 50% N2O and 1.5% sevoflurane in oxygen with a fresh gas flow (FGF) of 4 L min−1, in order to provide a minimum alveolar concentration (MAC) of 1. At the end of 90 s after the completion of propofol bolus, the first attempt was made to insert an LM. During this 90-s period of time, patients received volatile anaesthetic and N2O in oxygen. Patients were ventilated via a face mask manually with assisted ventilation allowing spontaneous ventilation. A size of 3 LM was selected for women and 4 for men. After lubricating with a water-soluble gel, we inserted the LM and first inflated the cuff with the recommended volumes, then connected it to the breathing circuit. In order to confirm correct placement, we monitored the absence of any air leakage with manual ventilation and the end-tidal carbon dioxide (etCO2). We recorded apnoea time (from the last spontaneous breath after propofol administration to the first spontaneous breath), respiratory rates, haemodynamic variables (BP, heart rate (HR)) immediately before insertion of LM, 1 min, 3 min and 5 min after insertion, and at 5-min intervals during the operation, as well as the baseline haemodynamic variables and respiratory rates. In order to assess the tolerance of LM insertion, we used a scoring system, modified from Muzi and colleagues [21]. According to this scoring system, we observed the patients for jaw mobility (1: fully relaxed, 2: mild resistance, 3: tight but opens, 4: closed), coughing or movement (1: none, 2: one or two coughs, 3: three or more coughs, 4: bucking/movement) and other events such as spontaneous ventilation, breath holding, expiratory stridor and lacrimation. In each category scores < 2 were defined as acceptable for LM insertion. If any movement occurred before LM insertion or after LM insertion, we added 0.5 mg kg−1 propofol and waited for 30 s before the next attempt. HR < 45 beats min−1 was accepted to be a bradycardia and we administered atropine (0.01 mg kg−1). The additional propofol requirement and administration of atropine were also recorded. Five minutes after LM insertion, Group F received NS and Group D received dexmedetomidine as an infusion at a rate of 1 μg kg−1 h−1. The investigator administering the drugs was also blinded to these infusions as well as to the boluses. The drugs were prepared by another investigator apart from the one inserting the LM and recording the measurements. LMs were inserted by the same anaesthesiologist. The responses were assessed by the same three anaesthesiologists, one of whom was out of the study. Basal respiratory rates were counted by auscultation by the same anaesthesiologist.

The sample size required for the study was calculated based on the primary outcome variable, i.e. Muzi Score System. Power analysis identified 52 patients (26 per group) as the total sample size required to detect a 33% difference between Group F and Group D with a power of 80% at the 5% significance level. The difference of 33% was taken from both pilot study and clinical experience.

Data analysis was performed using SPSS for Windows, v. 11.5 (SAS Institute Inc., Cary, NC, USA). Data were shown as mean ± SD or median (range) for continuous variables, where appropriate. Categorical variables were presented as percentages. Means were compared using Student's t-test or the U-test. Haemodynamic parameters were evaluated using Repeated Measures ANOVA or Friedman test. When the P value from the Variance Analysis and Friedman test statistics were statistically significant, multiple comparison tests were used to determine which measurement differed from the others. The Bonferroni correction was applied for comparisons of repeated measures between groups. For categorical comparisons χ2-test or Fisher's exact test were used, where appropriate. P < 0.05 was considered statistically significant.


Two groups were similar in terms of gender distribution, age, weight and durations of surgical procedures (Table 1). The number of patients developing apnoea was greater in Group F (24 patients) than in Group D (11 patients) (P < 0.01). The apnoea times were shorter in Group D than in Group F (P < 0.01) (Table 1). Baseline respiratory rates in Group F were 14.9 ± 1.02 and 16.0 ± 1.82 in Group D. In Group D, the respiratory rates increased compared to the baseline. The 3 min and 5 min measurements were similar but significantly different from the first three measurements (Fig. 1).

Table 1
Table 1:
Patient characteristics, duration of surgery and incidence of apnoea.
Figure 1.
Figure 1.:
Respiratory rate at different times (breaths min−1). *Statistically significant difference compared to the baseline measurements (P < 0.001). **Statistically significant difference compared to the measurements before laryngeal mask (LM) insertion (P < 0.001). §Statistically significant difference compared to the measurements 1 min after LM insertion (P < 0.001). †Statistically significant difference between groups (P < 0.001).

At the first attempt to insert the LM in Group F, five patients had a score >2; three moved extremities and two had >3 coughs. In Group D, two patients had a score >2; one moved upper extremities and the other one had gagging. These patients received additional 0.5 mg kg−1 propofol and tolerated an LM at the second attempt. In both groups, the adverse events during LM insertion (Group F: 19.2%, Group D: 7.7% patient) were similar (Table 2).

Table 2
Table 2:
Observed parameters for laryngeal mask (LM) insertion conditions and the number of patients who had adverse events. (Muzi and colleagues [21]).

Baseline systolic BP (SBP) and mean BP (MBP) were similar. In both groups, SBP and MBP showed statistically significant reductions from baseline. The reduction rates in terms of percentage for both SBP and MBP from baseline to immediately before LM insertion (approximately 90 s after induction) were greater in Group F than Group D (Table 3). SBP and MBP (except MBP before LM insertion) at different time intervals were similar between groups. The maximum and minimum SBP and MBP during procedures were also similar between groups (Table 3).

Table 3
Table 3:
Maximum and minimum systolic (SBP) and mean blood pressures (MBP) and percentage changes.

Baseline HRs were similar. In Group F, HR at 1 min, 3 min and 5 min after LM insertion were similar, but less than HR at baseline and immediately before LM insertion. In Group D, the HRs at different time intervals were similar but significantly different from the baseline. The HR immediately before LM insertion was significantly lower in Group D than Group F. The HR was similar between the groups 1 min after LM insertion. In Group F, one patient and in Group D, two patients had a bradycardia and responded well to 0.01 mg kg−1 atropine.

The emergence time, the time needed for the patients to respond to verbal stimulus, was 81–385 s (mean: 253.5 s) in Group F and 85–992 s (mean: 397.5 s) in Group D (P < 0.001).


This study of 52 patients undergoing minor urological procedures suggests that 1 μg kg−1 dexmedetomidine with 1.5 mg kg−1 propofol provides satisfactory LM insertion conditions comparable to 1 μg kg−1 fentanyl with 1.5 mg kg−1 propofol. Dexmedetomidine was reported to be effective both in sedation for awake intubation with topical anaesthetics [18,22] and in reducing the airway and circulatory responses to intubation [23,24] and extubation [18,19]. Our study has shown that dexmedetomidine (1 μg kg−1), co-administered with propofol (1.5 mg kg−1), provides successful LM insertion comparable to the combination of fentanyl (1 μg kg−1) and propofol (1.5 mg kg−1).

The respiratory depression in Group F was greater than in Group D, when compared in terms of numbers of patients developing apnoea and their apnoea times. Dexmedetomidine caused apnoea in fewer patients than fentanyl (P < 0.001). These patients developing apnoea had shorter apnoea times than patients receiving fentanyl (P < 0.001). Our data support the results of the study by Hsu and colleagues [17] with respect to respiration although we combined its bolus with propofol. Among the patients receiving dexmedetomidine, the ones developing apnoea were probably affected by the depressant effect of propofol. However, since this effect was not potentiated by the fentanyl the apnoea times were significantly shorter than fentanyl.

Hsu and colleagues [17] and Ebert and colleagues [25] reported a statistically significant increase in respiratory rate while using infusions of dexmedetomidine. However, Bellville and colleagues [26] used a bolus injection of dexmedetomidine and found a slight decrease in respiratory rates. Lawrence and colleagues [23] found no change in respiratory rate after 2 μg kg−1 bolus injection of dexmedetomidine. Our results supports the data found by Hsu and colleagues [17] and Ebert and colleagues [25] although we used a bolus injection. The increase became significant at 3 min after LM insertion and this time period was approximately 5.5 min after dexmedetomidine bolus.

Both dexmedetomidine and fentanyl, when used 30 s before a propofol bolus, provided optimum jaw relaxation and mouth opening 90 s after propofol injection. The predetermined periods of 30 s and 90 s were used as suggested by Goyagi and colleagues [16] and Tanaka and colleagues [11]. In our study, the dose of propofol used (1.5 mg kg−1) with 1 μg kg−1 fentanyl was adequate for LM insertion in most of the patients (80.8%) and less than the doses used in the study of Goh and colleagues [8] (2.5 mg kg−1), supporting the data of the studies of Tanaka and colleagues [11] (1 μg kg−1 fentanyl with 1.42 (0.26) mg kg−1 propofol) and Goyagi and colleagues [16] (2 μg kg−1 fentanyl with 1.17 mg kg−1 propofol). Adverse events during LM insertion were similar for both agents.

Our results showed that both fentanyl (1 μg kg−1) and dexmedetomidine (1 μg kg−1) provide similar BPs when used with propofol (1.5 mg kg−1); however, it should be kept in mind that the reduction in BPs from baseline may become clinically important for the elderly. HRs decreased significantly in both groups when compared to baseline. In Group F, the reduction stabilized at 1 min after LM insertion and 1 min, 3 min and 5 min were similar, but different from HR immediately before LM insertion. In Group D, the HR did not change after the measurement immediately before LM insertion, which was lower than Group F; however, it was clinically insignificant. Turan and colleagues [27] used propofol (2.5 mg kg−1) and fentanyl (1.5 μg kg−1) with mivacurium (0.2 mg kg−1) to insert an LM and reported that the large dose of propofol might have blunted the increases in BP and HR induced by placement of the LM. In our study, we used propofol (1.5 mg kg−1) and fentanyl (1 μg kg−1) for induction and sevoflurane for manual ventilation for 90 s before LM insertion.

Emergence times were significantly longer in patients receiving dexmedetomidine (P < 0.001). Güler and colleagues [20] reported that dexmedetomidine when given before extubation prolongs emergence time by 2 min. In our study, dexmedetomidine prolonged emergence time by approximately 2.4 min. This time difference may be due to the infusion of dexmedetomidine in Group D. During this time period, all the patients were spontaneously breathing without desaturation.

As a limitation of our study we did not include a control group in which propofol was used alone. We thought that it would be unethical because propofol was reported, several times, to be inadequate for LM insertion when used alone and the doses increased to make it adequate were reported to be unsafe for haemodynamics and respiration. Another limitation may have been the respiratory rates. The baseline respiratory rates were not similar statistically, but the difference (Group F: 14.9 ± 1.02 and Group D: 16.0 ± 1.82) was clinically insignificant for us. To demonstrate the increase in respiratory rates in homogeneous groups would have been more convenient. However, the increase in respiratory rates in Group D was significant when compared to baseline. We think that this may provide a guide for further studies. In our study, we used prilocaine in order to eliminate pain related to propofol injection before induction, and sevoflurane for manual ventilation during 90 s before LM insertion. We used them in both groups to standardize the conditions; however, the LM tolerance may have been affected by these drugs and therefore lead to underestimation of the drug requirements in both groups. During the procedures, 5 min after LM insertion, we started an infusion of NS in Group F and dexmedetomidine in Group D. We chose this time in order to compare the effects of single doses of fentanyl and dexmedetomidine on LM insertion conditions and responses. Since dexmedetomidine was reported to be used as a maintenance after loading dose in several studies, we preferred to use an infusion but this may be omitted in further studies to compare the effects of single doses on both haemodynamics and emergence time. In order to make the investigator blind to the infusions, we used a NS infusion for the fentanyl group.

In conclusion, 1 μg kg−1 dexmedetomidine when used 30 s before 1.5 mg kg−1 propofol induction, provides successful LM insertion and is comparable to 1 μg kg−1 fentanyl with 1.5 mg kg−1 propofol, while preserving respiratory functions more than fentanyl. So, dexmedetomidine may be an alternative to fentanyl, to co-administer with propofol for LM insertion. Our study was not a dose ranging study, but our aim was to compare the effect of dexmedetomidine on LM insertion conditions with fentanyl. Our results may lead to further studies for dose ranging.


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