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Year : 2021  |  Volume : 15  |  Issue : 4  |  Page : 443-447  

A comparative study of effect of 0.25% levobupivacaine with dexmedetomidine versus 0.25% levobupivacaine in ultrasound-guided supraclavicular brachial plexus block

Department of Anaesthesiology, BMCRI, Bengaluru, Karnataka, India

Date of Submission19-Nov-2021
Date of Acceptance26-Jan-2022
Date of Web Publication30-Mar-2022

Correspondence Address:
Dr. H N Vijayakumar
2nd Floor, 326, 8th Main, 4th Cross, HRBR 1st Block, Kalyannagar, Bengaluru - 560 043, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aer.aer_145_21

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Context: Dexmedetomidine, an α2-agonist, has been studied widely as an adjuvant to local anesthetics in regional anesthesia techniques to enhance the quality and duration of analgesia (DOA). It was hypothesized that addition of dexmedetomidine 0.5‒1 to levobupivacaine would prolong the DOA. Aims: We aimed to evaluate the efficacy of dexmedetomidine as an adjuvant to levobupivacaine in supraclavicular brachial plexus block with respect to onset and duration of sensory and motor blockade, and duration of analgesia. Settings and Design: This was a prospective randomized double-blind study carried out at a tertiary hospital attached to medical college. Subjects and Methods: Sixty American Society of Anesthesiologists PS Class I and II patients aged between 18 and 60 years of either sex, undergoing elective upper-limb surgery lasting more than 30 min, were included in the study. They were randomly divided into two groups of thirty each to receive ultrasound-guided supraclavicular brachial plexus block. Group L was given nerve block with 20 mL of 0.25% levobupivacaine and 1 mL saline, and Group D received 20 mL of 0.25% levobupivacaine with 0.5‒1 of dexmedetomidine (diluted to volume of 1 mL). Onset time and duration of sensory and motor blockade, time to first rescue analgesia, and hemodynamic parameters were recorded. Statistical Analysis Used: Chi-square test for qualitative variables and Student's unpaired "t" test for continuous variables were used for statistical analysis. Results: The onset of sensory and motor blockade was 6.51 ± 0.77 min and 10.71 ± 0.34 min in Group D and 9.9 ± 0.45 and 15.93 ± 1.92 min in Group L, respectively (P < 0.005). DOA was 9.53 ± 0.29 h in Group D and 3.89 ± 0.30 h in Group L (P < 0.001). The duration of sensory and motor block was 9.14 ± 0.19 h and 8.55 ± 0.31 h in Group D and 6.15 ± 3.02 and 5.61 ± 2.98 h in Group L, respectively (P < 0.005). No adverse effects were observed in either of the groups. Conclusions: Addition of 0.5‒1 of dexmedetomidine to 20 mL 0.25% levobupivacaine in ultrasound guided (USG)-guided supraclavicular brachial plexus block shortens the onset time of sensory and motor blockade and prolongs duration of sensory and motor block and DOA.

Keywords: Adjuncts, brachial plexus, dexmedetomidine, local anesthetics, supraclavicular

How to cite this article:
Iyer LS, Bhat SS, Nethra H N, Vijayakumar H N, Sudheesh K, Ramachandriah. A comparative study of effect of 0.25% levobupivacaine with dexmedetomidine versus 0.25% levobupivacaine in ultrasound-guided supraclavicular brachial plexus block. Anesth Essays Res 2021;15:443-7

How to cite this URL:
Iyer LS, Bhat SS, Nethra H N, Vijayakumar H N, Sudheesh K, Ramachandriah. A comparative study of effect of 0.25% levobupivacaine with dexmedetomidine versus 0.25% levobupivacaine in ultrasound-guided supraclavicular brachial plexus block. Anesth Essays Res [serial online] 2021 [cited 2022 Nov 29];15:443-7. Available from:

   Introduction Top

With the introduction of ultrasonography, newer and safer local anesthetics, and adjuvants, regional anesthesia has become the most accepted and useful technique for upper-limb surgeries. Supraclavicular being the easier approach as the plexus lies more superficial above clavicle, and further, the use of ultrasound in supraclavicular brachial plexus block improved the success rate of block with excellent localization and improved safety margin.[1]

Kulenkampff in Germany performed the first percutaneous supraclavicular block in 1911, reportedly on himself which was later modified as Winnie block.[2] Currently, levobupivacaine with favorable clinical profile and lesser cardiotoxicity when compared with racemic bupivacaine is being favored local anesthetic for regional block. Adjuvant drugs are often added to local anesthetics for several reasons.[2],[3] The α2-receptor agonist dexmedetomidine was found to fasten the onset time, prolong the duration of action of local anesthetics, and increase the quality of analgesia in a regional block.[4],[5],[6] Dexmedetomidine is being used for intravenous (i.v.) regional anesthesia (Bier's block),[6],[7] i.v. sedation, and analgesia for intubated and mechanically ventilated patients in intensive care units.[8],[9],[10] Its usage as an adjuvant in central neuraxial blocks has also been mentioned.[11],[12],[13],[14] Its use in peripheral nerve blocks has recently been described.[15],[16],[17] However, the reports of its use in supraclavicular brachial plexus block is limited.[18] Hence, this study was designed to explore the effects of low-dose dexmedetomidine as adjuvant to levobupivacaine in USG-guided supraclavicular brachial plexus block for elective upper-limb surgeries. It was hypothesized that addition of dexmedetomidine 0.5‒1 to levobupivacaine will improve the onset and duration of supraclavicular brachial plexus block.

   Subjects and Methods Top

Study design

This double-blind, randomized prospective clinical study was conducted in a tertiary care hospital attached to medical college, from February 2018 to June 2019, following ethical committee approval (BMC/PGs/303/2017-18) and registered with ISRCTN registry (ISRCTN55964940) and after obtaining written informed consent from all patients included in the study, and the data were used for research purpose only. The process of patient inclusion, procedures, and data collection were followed as per Helsinki Declaration 2013.

Inclusion criteria

Sixty patients aged 18–60 years with body mass index 18.55-29.99, belonging to American Society of Anesthesiologists (ASA) Physical status 1 and 2 who gave informed written consent, were included in the study. SPSS- Statistical Package for the social statistics package version 17.0 2009 Chicago Ill., USA.

Exclusion criteria

Patient refusal and those who had hypertension, uncontrolled diabetes mellitus, arrhythmia, heart failure, renal failure, liver failure, epilepsy or bleeding tendencies, pregnant, preexisting peripheral neuropathy, known hypersensitivity to local anesthetics, and those whose BMI was >30 were excluded from the study.

   Methodology Top

Sixty patients were randomly divided into two groups D (n = 30) and L (n = 30) using random sequence generated from a website –

Preanesthetic evaluation was done and Patients were kept nil per oral for 6–8 h prior to surgery. All patients received alprazolam 0.5 mg, and pantoprazole 40 mg orally, the previous night of surgery. On the day of surgery, patient was shifted to operating room and standard anesthetic monitoring (noninvasive blood pressure, electrocardiogram, pulse oximetry) was established and basal heart rate (HR), blood pressure and peripheral oxygen saturation (SpO2) were recorded. (i.v.) fluid infusion was started after securing an (i.v.) line. All patients received midazolam 1 mg intravenously. Under all aseptic conditions, the brachial plexus located using ultrasound guidance. A linear high frequency ultrasound probe was placed above and parallel to the clavicle and the brachial plexus was identified as a bunch of hyperechoic structures lying posterosuperior to the subclavian artery. The probe position was altered by sliding and rotation to get a good view of artery and plexus. A 20-gauge block needle was passed from lateral to medial side by an in-plane approach, and the drug solution was injected around the brachial plexus and the spread of the drug around the plexus confirmed by ultrasound. Group D had received 21 mL of solution containing 20 mL 0.25% levobupivacaine with dexmedetomidine 0.5‒1 diluted to 1 mL, and Group L received 21 mL solution containing 20 mL 0.25% levobupivacaine and 1 mL of saline. The random sequence number was written on a piece of paper and kept in an opaque envelope, to ensure random allocation concealment, and was opened just before preparation of drug solution. An anesthesiologist not involved in the study opened the envelope and then prepared the drug solution as per group allocation. The anesthesiologist performing the block followed up the patient and recorded the study parameters. The patient and the anesthesiologist were unaware of the group allocation. Sensory block was assessed by atraumatic pinprick test using a 3-point scale: 0 – normal sensation, 1 – loss of sensation of pinprick (analgesia), and 2 – loss of sensation of touch (anesthesia).[18] Motor block was assessed by using modified Bromage 3-point scale: Grade 0: normal motor function, Grade 1: decreased motor strength with ability to move the fingers only, and Grade 2: complete motor block.[18] Sensory and motor block was assessed at 2-min intervals till there was complete sensory and motor block. Sedation score was assessed by the Ramsay Sedation Scale. This has scoring from 1 to 6. Score 1 – patient is anxious and agitated or restless or both; 2 – patient is cooperative, oriented, and tranquil; 3 – patient responds to commands only; 4 – patient exhibits brisk response to light glabellar tap or loud auditory stimulus; 5 – patient exhibits a sluggish response to light glabellar tap or loud auditory stimulus; and 6 – patient exhibits no response.[9] Hemodynamic parameters were assessed at 5-min intervals from the time of shifting to operation theater till the end of surgery. Onset of sensory block was defined as time from administration of block to loss of pain sensation to pinprick, whereas onset of motor block was considered from the time of administration of block to onset of Grade 1 motor blockade. If there was no complete analgesia even at the end of 30 min following administration of block, it was considered as failure and patient received general anesthesia and patient was excluded from statistical analysis of outcome measures. If patient complained of pain intraoperatively, it was managed with fentanyl 2‒1bolus, and if not sufficient, general anesthesia was instituted. Postoperatively, parameters were assessed every 15 min for 2 h and then 30 min till block effect has resolved. Pain was assessed using the Visual Analog Scale (VAS) 0–10, and injection tramadol 50 mg i.v. was administered when VAS ≥ 3 (rescue analgesia). The time interval between the administration of block and the first analgesic request was recorded as duration of analgesia (DOA). Incidence of side effects such as pneumothorax, neuropraxia, and hemodynamic disturbances if any was noted.

Statistical analysis

Sample size was estimated based on findings of pilot study involving ten patients. Considering DOA as primary outcome objective, assuming an effect size of 30 min and standard deviation of 60 min, a minimum of 26 patients would be required in each group to attain a power of 80% at an alpha error of 5%. We included thirty patients in each group to compensate for possible dropouts.

Data were entered and tabulated in an Excel sheet. Qualitative data are expressed as numbers and percentages, whereas continuous data are analyzed for normal distribution using Shapiro–Wilk test and represented as mean with standard deviation or median with interquartile range as per distribution. Qualitative data are analyzed with Chi-square/Fisher's exact test, and continuous data are analyzed using Student's t-test/Mann–Whitney U-test. P < 0.05 was considered statistically significant. Analysis was carried out using Statistical Package for the social statistics package version 17.0 2009 (SPSS Inc., Chicago, Ill, USA).

   Results Top

Sixty patients were enrolled in the study, all of them completed the study, and there were no dropouts [Figure 1]. The demographic data, BMI, body weight, ASA PS class, and duration of surgery were comparable in both the groups [Table 1]. There was a clinically and statistically significant decrease in HR in Group D compared to Group L, however, the blood pressures were comparable intraoperatively [Figure 2] and [Figure 3]. Onset time for sensory and motor block was shorter while duration of sensory and motor blockade was longer in Group D than in Group L and difference was clinically and statistically significant [Table 2]. There was a significant difference in mean duration of sensory block, motor block, and DOA between the two groups [Table 2].
Figure 1: Consort diagram showing number of patients included and analyzed

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Figure 2: Comparison of mean intraoperative and postoperative heart rate trends between two groups. There was significant difference in heart rate from 5th min intraoperative till the end of surgery

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Figure 3: Comparison of mean intraoperative and postoperative mean arterial pressure in both groups

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Table 1: Demographic characters

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Table 2: Mean onset of sensory and motor block duration of sensory block, motor block, and analgesia comparison between two groups

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The maximum mean intraoperative sedation score in Group D was 2.4 ± 0.5 noted at 140 min and in Group L was 2.37±0.49 noted at 130 min (P = –0.78). The mean postoperative VAS score was lower in Group D compared to Group L after 2 h of postoperative period [Figure 4].
Figure 4: Mean comparison of Visual Analog Scale score between two groups

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   Discussion Top

In the present study, it was observed that addition of dexmedetomidine hastened the onset and prolonged the duration of sensory and motor blockade and DOA. Among the various adjuvants studied, dexmedetomidine prolongs the duration of sensory and motor blockade as well as DOA. The mechanism by which alpha2-adrenergic receptor agonists produce analgesia and sedation is not fully understood that it is likely to be multifactorial.[19] Peripherally, alpha2-agonists produce analgesia by reducing release of norepinephrine and causing alpha2-receptor-independent inhibitory effects on nerve fiber action potentials.[20] Centrally, alpha2-agonists produce analgesia and sedation by inhibiting substance P release in the nociceptive pathway at the level of dorsal root neuron and by activating alpha2-adrenoceptors in the locus ceruleus.[20]

In our study, we used 20 mL of 0.25% levobupivacaine as the local anesthetic with 0.5‒1 of dexmedetomidine. Previous studies reported that the use of 50 ug dexmedetomidine with local anesthetic prolonged the duration motor and sensory blockade. In the present study, we tried to explore if further reduction in dose would achieve the desired result. The use of dexmedetomidine as an adjuvant and administration under USG guidance helped in reducing the volume of anesthetic drug and so improved the safety profile. Edel Duggan et al conducted a study to find out minimum effective volume of local anaesthetic and observed that the minimum volumes required were 23ml and 42 ml in 50% and95% of patients respectively.

In our study, we found that the mean onset of sensory block was earlier in the dexmedetomidine group, compared with control group, matches with observations of study conducted by Haramprit Kaur et al. the addition of dexmedetomidine to varying concentration of levobupivacaine hastened onset of action of sensory block.

In our study, we found that onset of motor blockade to be significantly faster with dexmedetomidine and this observation augurs well with study by Srinivas Rao et al., In our study, the mean duration of sensory and motor blockade was similar to that observed by Sowmya Biswas et al., who evaluated the effect of combining higher dose of dexmedetomidine (100 ug ) with 35 mL 0.5% levobupivacaine. similarly duration of analgesia was comparable with observations by Waindeskar et al. who used higher dose of levobupivacaine.

By reducing the volume and dose of levobupivacaine and dexmedetomidine, we could reduce the side effects without affecting the efficacy. The adverse effects were not reported in both the groups in this study and hemodynamic parameters were well maintained within normal range and we could not follow-up cases for if any long-term adverse effects of dexmedetomidine on nerves.

   Conclusions Top

Addition of dexmedetomidine 0.5‒1 added to levobupivacaine hastened the onset of sensory and motor block and prolonged the DOA and sensory and motor blockade.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Horlocker TT, Kopp SL, Wedel DJ. Peripheral nerve block. In: Miller RD, Cohen NH, Eriksson LI, Fleisher LA, Kronish JP, Young WL, et al., editors. Millar's Anesthesia. 8th ed. Philadelphia: Elsevier; 2015. p. 1723-62.  Back to cited text no. 1
Singelyn FJ, Dangoisse M, Bartholomée S, Gouverneur JM. Adding clonidine to mepivacaine prolongs the duration of anesthesia and analgesia after axillary brachial plexus block. Reg Anesth 1992;17:148-50.  Back to cited text no. 2
Duma A, Urbanek B, Sitzwohl C, Kreiger A, Zimpfer M, Kapral S. Clonidine as an adjuvant to local anaesthetic axillary brachial plexus block: A randomized, controlled study. Br J Anaesth 2005;94:112-6.  Back to cited text no. 3
Pöpping DM, Elia N, Marret E, Wenk M, Tramèr MR. Clonidine as an adjuvant to local anesthetics for peripheral nerve and plexus blocks: A meta-analysis of randomized trials. Anesthesiology 2009;111:406-15.  Back to cited text no. 4
Virtanen R, Savola JM, Saano V, Nyman L. Characterization of the selectivity, specificity and potency of medetomidine as an alpha 2-adrenoceptor agonist. Eur J Pharmacol 1988;150:9-14.  Back to cited text no. 5
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Esmaoglu A, Mizrak A, Akin A, Turk Y, Boyaci A. Addition of dexmedetomidine to lidocaine for intravenous regional anaesthesia. Eur J Anaesthesiol 2005;22:447-51.  Back to cited text no. 7
Mantz J, Singer M. Importance of patient orientation and reusability as components of Intensive Care Unit sedation. In: Maze M, Marrison P, editors. Redefining Sedation. London: The Royal Society of Medicine Press Ltd.; 1998. p. 23-9.  Back to cited text no. 8
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Shukry M, Miller JA. Update on dexmedetomidine: Use in nonintubated patients requiring sedation for surgical procedures. Ther Clin Risk Manag 2010;6:111-21.  Back to cited text no. 10
Kanazi GE, Aouad MT, Jabbour-Khoury SI, Al Jazzar MD, Alameddine MM, Al-Yaman R, et al. Effect of low-dose dexmedetomidine or clonidine on the characteristics of bupivacaine spinal block. Acta Anaesthesiol Scand 2006;50:222-7.  Back to cited text no. 11
Konakci S, Adanir T, Yilmaz G, Rezanko T. The efficacy and neurotoxicity of dexmedetomidine administered via the epidural route. Eur J Anaesthesiol 2008;25:403-9.  Back to cited text no. 12
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Obayah GM, Refaie A, Aboushanab O, Ibraheem N, Abdelazees M. Addition of dexmedetomidine to bupivacaine for greater palatine nerve block prolongs postoperative analgesia after cleft palate repair. Eur J Anaesthesiol 2010;27:280-4.  Back to cited text no. 16
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Swami SS, Keniya VM, Ladi SD, Rao R. Comparison of dexmedetomidine and clonidine (α2 agonist drugs) as an adjuvant to local anaesthesia in supraclavicular brachial plexus block: A randomised double-blind prospective study. Indian J Anaesth 2012;56:243-9.  Back to cited text no. 18
[PUBMED]  [Full text]  
Williams SR, Chouinard P, Arcand G, Harris P, Ruel M, Boudreault D, et al. Ultrasound guidance speeds execution and improves the quality of supraclavicular block. Anesth Analg 2003;97:1518-23.  Back to cited text no. 19
Correa-Sales C, Nacif-Coelho C, Reid K, Maze M. Inhibition of adenylate cyclase in the locus coeruleus mediates the hypnotic response to an alpha 2 agonist in the rat. J Pharmacol Exp Ther 1992;263:1046-9.  Back to cited text no. 20


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2]


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