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 Table of Contents  
ORIGINAL ARTICLE
Year : 2019  |  Volume : 6  |  Issue : 2  |  Page : 63-67

Effects of clonidine-bupivacaine combination on the onset and duration of brachial plexus block in upper extremities surgeries: a preliminary report


1 Department of Anaesthesia, University of Ilorin; University of Ilorin Teaching Hospital, Ilorin, Nigeria
2 University of Ilorin Teaching Hospital, Ilorin, Nigeria

Date of Web Publication04-Nov-2019

Correspondence Address:
Dr. Suleiman Zakari A
Department of Anaesthesia, University of Ilorin, Ilorin
Nigeria
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DOI: 10.4103/ssajm.ssajm_4_19

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  Abstract 


Objective Delayed onset of action and incomplete anaesthesia are often observed after brachial plexus block. Efforts have been made to hasten the onset of sensory and motor blocks as well as prolonging the duration of anaesthesia by combining several adjuvants to local anaesthetic agents for brachial plexus block. This study determined the onset of sensory and motor blocks and the duration of analgesia when clonidine was added to bupivacaine in patients who had upper extremities surgery under brachial plexus block.
Methods This prospective comparative single blind study involved randomization of 40 ASA I-II patients scheduled for upper extremities surgery under periclavicular brachial plexus blocks into two equal groups. Group CB received 1 mL of clonidine (100 µg) and 29 mL of 0.5% bupivacaine while group B received 1 mL of water for injection and 29 mL of 0.5% plain bupivacaine. The onset of sensory block, motor block, duration of analgesia, and first request to rescue analgesia were assessed in the two groups.
Results The onset of sensory and motor blocks was significantly faster in group CB compared with group B, 8.55 ± 3.0 versus 14.75 ± 5.7 min (P = 0.000) and 5.05 ± 1.1 versus 11.5 ± 4.6 (0.000), respectively. Similarly, the duration of sensory and motor blocks were 461 ± 94.2 versus 364 ± 39.1 min (P = 0.000) and 540 ± 81.3 versus 441.5 ± 41.5 min (P = 0.000), respectively. The time to request for rescue analgesia was longer in group CB in comparison with group B, 9.7 ± 2.3 versus 8.8 ± 2.5 hr but the difference was not statistically significant, P = 0.244.
Conclusion Brachial plexus block with bupivacaine/clonidine reduced the onset time of sensory and motor blocks and prolonged the duration of analgesia and time to request for rescue analgesia.

Keywords: Brachial plexus block, clonidine, bupivacaine, onset of block, duration of analgesia


How to cite this article:
SuleimanZ, KolawoleI, Abe O, AdegboyeK, Abdulrahman A. Effects of clonidine-bupivacaine combination on the onset and duration of brachial plexus block in upper extremities surgeries: a preliminary report. Sub-Saharan Afr J Med 2019;6:63-7

How to cite this URL:
SuleimanZ, KolawoleI, Abe O, AdegboyeK, Abdulrahman A. Effects of clonidine-bupivacaine combination on the onset and duration of brachial plexus block in upper extremities surgeries: a preliminary report. Sub-Saharan Afr J Med [serial online] 2019 [cited 2019 Nov 17];6:63-7. Available from: http://www.ssajm.org/text.asp?2019/6/2/63/270250




  Introduction Top


Brachial plexus block is a common regional technique for upper limb surgeries. It was first performed by Hall in 1884 through a direct application of cocaine to the upper limb nerves.[1] In recent times, the use of brachial plexus has been increasing in developing countries due to the growing expertise and confidence as well as improved access to nerve stimulators and other consumables.[2],[3],[4] The benefits of the technique include, among others, superior postoperative pain relief, reduced postoperative opioid consumption, and early discharge from the hospital.[5],[6] However, undesirable slow onset and poor quality of anaesthesia are frequently associated with the technique. Hence, adjuvants with proven peripheral nerve block property can be added to local anaesthetic to achieve quick, dense, and prolonged block. Several adjuvants have been used with successful outcomes.[7] However, due to their excessive sedation, depression of respiration, and psychomotor alterations, the use of drugs like morphine, fentanyl, pethidine, midazolam, and dexamethasone as adjuvants to bupivacaine for brachial plexus block are becoming less popular.

Clonidine, an imidazoline, α-2 adrenergic receptor agonist has been proven to provide better analgesia and minimal side effects when a dose of up to 150 µg was added to bupivacaine.[8],[9] It is an extensively studied drug as an adjuvant to local anaesthetic agent in peripheral nerve block.[10],[11],[12],[13],[14] The present study compared the onset of block and duration of postoperative analgesia when clonidine was added to bupivacaine for brachial plexus block in upper extremities surgeries.


  Materials and method Top


The study was approved by the Ethical Review Committee of the University of Ilorin Teaching Hospital. Forty patients ASA I-III, age ranged 18–63 years with upper limb injuries, were enrolled into the study from May 2015 to December 2016. All the patients were assessed preoperatively and written informed consent was obtained. Details of the anaesthetic procedure and study protocols were also fully explained to patients; and they were fasted according to the standard fasting guidelines. The patients were divided into two groups of 20 each. The bupivacaine-clonidine group received 29 mL of 0.5% plain bupivacaine and clonidine (100 µg) 1 ml, total of 30 mls. Similarly, the bupivacaine-only group received 29 ml of 5% plain bupivacaine and 1 ml of water for injection (30 mL solution). Patients’ refusal, presence of coagulopathy, cardiac, respiratory, hepatic and/or renal disorders, and pregnancy constituted the exclusion criteria. Patients with known allergy to clonidine or local anaesthetics, hypertension, peripheral neuropathy, and local infections at the site of block were also excluded from the study.

On arrival to the operating suite, the multiparameter patient monitor probes were attached to the patient. Baseline non-invasive blood pressure, pulse rate, and arterial oxygen saturation (SpO2) were measured and recorded. Intravenous access was secured with 18G cannula on the forearm of non-operated limb and infusion of normal saline was commenced. Under aseptic precautions, brachial plexus block was established in supine position with head turned to the opposite side and forearm on the epigastric area. Periclavicular, supraclavicular (in 6 patients), or infraclavicular (in 34 patients) approaches were used. Plexus localization was achieved with a peripheral nerve stimulator (Life-Tech EZ stim II peripheral nerve locator/stimulator model ES400, Stafford, TX, USA), connected to size 22G insulated (Teflon-coated) short-beveled, 60 mm long stimulating needle with active 0.5 mm tip (Stimuplex D; B. Braun Melsungen, Melsungen, Germany). Stimulation frequency was set at 2 Hz, and the position of the needle was adjudged accurate when a slight distal motor response was achieved with an output current of 0.5 mA. After negative aspiration, the drug solution was injected. Sensory and motor blocks were assessed every 5 min for the first 30 min after the completion of drug administration. Sensory block, assessed by pinprick discrimination using size 22G hypodermic needle, was graded as Grade 0 = no sensation felt, Grade 1 = dull sensation felt, Grade 2 = sharp pain felt. Motor block was assessed using a modified Bromage scale[12] (3 = extension of elbow against gravity, 2 = flexion of wrist against gravity, 1 = finger movement, and 0 = no movement).

The time to surgical anaesthesia was defined as the time from the end of injection of anaesthetic agent to loss of pinprick sensation along the distribution of the ulnar and radial nerves along with inability to circumrotate the thumb of the concerned limb. When surgical anaesthesia was not achieved in a patient even after 30 min from the time of anaesthetic injection, the block was considered as failed and such patient was excluded from the study.

The duration of sensory block was considered as the time interval from complete sensory block till first complaint of postoperative pain. The duration of motor block was defined as the time interval between the complete paralysis and complete recovery of motor function.

Postoperative pain intensity was assessed with numeric pain rating (NPR) scale from 0 (no pain) to 10 (worst pain ever). Rescue analgesia was provided with intramuscular administration of tramadol 100 mg when patients complained of pain. The time to first request of analgesic was noted. The time between the end of local anaesthetic administration and the first analgesic request was recorded as the duration of analgesia. Hypotension (defined as a 20% decrease in systolic blood pressure from baseline value), hypertension (defined as a 20% increase in systolic blood pressure above the baseline value), bradycardia (HR < 50 beats/min), hypoxemia (SpO2 < 90%), or nausea and vomiting were the adverse effects sought for in this study.

All data were recorded on a data sheet, after collection. The data, expressed as means and standard deviations, were then analysed with SPSS version 20.0 for windows and statistical significance was tested using independent Student’s ‘t’ test, ANOVA, chi- squared test or Fisher’s exact test as appropriate. A P-value < 0.05 was considered statistically significant.


  Results Top


There was no difference in the demographic parameters between the two groups, ([Table 1]). Though all the blocks were successful in the two groups, the onset time of sensory and motor blocks were faster in the bupivacaine/clonidine group compared with the bupivacaine only group and the differences were statistically significant ([Table 2]). In this study, the block was used tendon repair wound debridement and construction of arterio-venous fistula
Table 1 Demographic data of patients in the two groups

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Table 2 Characteristics of blocks in the two groups

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The durations of sensory and motor blocks were prolonged in the bupivacaine/clonidine group compared with bupivacaine-only group; 461 ± 94.2 versus 364.39.1 (P = 0.000) and 540 ± 81.3 versus 441.5 ± 41.5 (P = 0.000), respectively ([Table 2]). Similarly, the duration of analgesia was prolonged in the bupivacaine/clonidine group compared with bupivacaine-only group but the difference was statistically insignificant (P = 0.244). However, the duration of surgery was 109 ± 37.05 min. The pain scores at 8 hr, 16 hr, and 24 hr after the surgery were lower in the bupivacaine/clonidine group compared with bupivacaine-only group, though the differences were statistically insignificant, P-values were 0.353, 0.573, and 0.64, respectively ([Table 3]).
Table 3 Comparison of postoperative pain scores in the two groups

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There was no reported episode of nausea, vomiting, drowsiness, or hypoxaemia but three patients in the bupivacaine/clonidine group experienced hypotension which responded to increased fluid therapy.


  Discussion Top


This study shows that the onset of anaesthesia was shorter and duration of sensory and motor blocks was prolonged when 100 µg clonidine was added to bupivacaine for brachial plexus block in upper limb surgeries. However, the pain scores in the bupivacaine/clonidine group were comparable with bupivacaine/saline group at various time intervals in the postoperative period.

The results of this study agree with the findings of the previous studies.[12],[13],[15],[16],[17] Chakraborty and colleagues[15] reported a prolonged duration of analgesia and motor block in patients who had brachial plexus block with small dose of clonidine (30 µg) added to 0.5% bupivacaine; this agrees with our finding. The two studies used peripheral nerve stimulator to locate the plexus which might have contributed to high success rate of the block in both studies. Similar prolongation of the duration of analgesia and improved quality of anaesthesia was reported by Eledjam and associates[13] and Ahmed et al.[16] While we compared clonidine-bupivacaine with bupivacaine alone they compared clonidine-bupivacaine with fentanyl-bupivacaine[13] and epinephrine-bupivacaine,[16] respectively. In contrast to our study, higher dose of clonidine (150 µg) and lower concentration of bupivacaine (0.25%) were used by the researchers. The higher dose of clonidine used by Ahmed et al. may explain a more prolonged duration of analgesia observed in their patients compared with our findings where 100 µg was used, 14.4 ±1.3 hr versus 9.7 ± 2.3, respectively.

In our study, although not statistically significant, the pain score 16 hr postoperatively was comparatively lower in the clonidine-bupivacaine group compared with the control group as was observed in the study by Ahmed and coworkers.[16] The choice of 100 µg clonidine in our study was based on previous report in which prolongation of duration of analgesia and anaesthesia and shorter onset of sensory and motor blocks was observed when a dose as low as 0.5 µg/kg clonidine was added to mepivacaine for axillary plexus by Singelyn and coworkers[17] and Bernard and colleagues.[18] Furthermore, our findings of increased duration of analgesia and anaesthesia are consistent with the findings of El Saied and colleagues who evaluated the effects of addition of clonidine to ropivacaine for axillary plexus block.[12] The similarity in the pharmacokinetic profiles of both ropivacaine and bupivacaine could be responsible for the comparable results. The published work of Singh and Aggarwal[10] also agrees with our findings despite the sole use of supraclavicular approach to brachial plexus block by the researchers. Though both supraclavicular and infraclavicular approaches were used in our study, the two periclavicular approaches targeted the plexus at the level of its trunks where all the nerves that supply the upper extremity seem to have intertwined together.

However, the results of our study are at variance with the outcomes of the study by Duma et al.[19] who concluded that the addition of clonidine 0.5 µg/kg to a local anaesthetic for axillary block had no analgesic-prolonging effect. The dissimilarity in the outcomes of the two studies could not be explained by the types of local anaesthetic agents since both used bupivacaine. Rather, the differences in the approaches to brachial plexus block may be responsible, resulting in disproportional spread of the local anaesthetic agents. A few other researchers also reported no effect when clonidine was added to local anaesthetic agents.[20],[21],[22],[23]

While the use of clonidine in regional anaesthesia has been shown to be associated with no side effects,[17] some trials reported occurrence of hypotension and bradycardia when it is combined with local anaesthetic agent for perineural block.[18],[24] Unlike in our study where no patient was sedated despite the use of larger dose of clonidine (100 µg), sedation was the only adverse effect observed in the Chakraborty et al. study.[15] It is worthy of note that intravenous midazolam was given to all their patients after the block was established; and this could be partially responsible for the observed sedation. Contrary to 0% observed in the present study, the incidence of sedation was reported to be 10% by Ahmed and colleagues. Clonidine induces sedation through centrally mediated sympatholysis due its stimulatory action on the post-synaptic α-2 adrenoceptors.[25] Thus the sedative effect of clonidine might be dose-dependent.In our study, hypotension and hypertension were observed in three patients (15%) each in the clonidine-bupivacaine and bupivacaine-only groups. The observed hypotension in the present study is consistent with the outcomes of some previous studies[18],[26],[27] that reported hypotension and bradycardia. The hypotension responded to rapid fluid infusion.

The mechanism by which α-2 adrenergic receptor agonists such as clonidine and dexmedetomidine prolong the duration of anaesthesia and analgesia when added to local anaesthetic agents for nerve blocks involves a number of credible postulations. One of such mechanisms is through the enhancement of sodium channel-blocking action of local anaesthetic agents which results into the opening up of potassium channels and consequent membrane hyperpolarization.[28] It also mediates analgesia centrally, through a direct action on peripheral nerve and by reduction of release of norepinephrine.[29] The findings in our study further confirm the enhancement of analgesic effect of local anaesthetic agents by clonidine, in addition to its other reported clinical benefits, thereby touting it as one of the most versatile adjuvants in the anaesthesia practice.


  Conclusion Top


This study showed that addition of 100 µg of clonidine to 0.5% plain bupivacaine for brachial plexus block significantly shortened the onset of sensory and motor blockades as well as prolonged the duration of analgesia in patients who had upper extremities surgery. Our patients were not excessively sedated and the hypotensive side effects resolved with increased fluid therapy.

Acknowledgement

We would like to thank Dr AA Nasir of Department of Surgery, University of Ilorin, for his assistance with the analysis of the study.

Financial support and sponsorship

There was no external funding for this study.

Conflicts of interest

None was declared.



 
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Hall RJ. Hydro chlorate of cocaine. NY Med J 1884;40:643-646.  Back to cited text no. 1
    
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Singh S, Aggarwal A. A randomized controlled double-blinded prospective study of the efficacy of clonidine added to bupivacaine as compared with bupivacaine alone used in supraclavicular brachial plexus block for upper limb surgeries. Indian J Anaesth 2010;54:552-557.  Back to cited text no. 10
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El Saied AH, Steyn MP, Ansermino JM. Clonidine prolongs the effect of ropivacaine for axillary brachial plexus blockade. Can J Anaesth 2000; 47:962-967.  Back to cited text no. 12
    
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Eledjam JJ, Deschodt J, Viel EJ, Lubrano JF, Charavel P, d’Athis F et al. Brachial plexus block with bupivacaine: effects of added alpha-adrenergic agonists: comparison between clonidine and epinephrine. Can J Anaesth 1991;38:870-875.  Back to cited text no. 13
    
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