|Year : 2019 | Volume
| Issue : 1 | Page : 31-34
Dexmedetomidine with 0.375% bupivacaine for prolongation of postoperative analgesia in supraclavicular brachial plexus block
Jaya Lalwani, Rashmi Naik Bhuaarya, Nasir Ali, Pratibha Jain Shah
Department of Anaesthesiology and Critical Care, Pt. J. N. M. Medical College, Raipur, Chhattisgarh, India
|Date of Web Publication||9-Apr-2019|
Dr. Rashmi Naik Bhuaarya
Department of Anaesthesiology and Critical Care, Pt. J. N. M. Medical College, Raipur, Chhattisgarh
Source of Support: None, Conflict of Interest: None
Background: Regional anesthesia is the recommended technique for upper-limb surgeries with better postoperative profile. Various agents have been used as adjuvants to prolong the duration of action and improve the efficacy of local anesthetic agents, α2-agonists being the most recent ones. We evaluated the effect of dexmedetomidine with bupivacaine for prolongation of the duration of analgesia in supraclavicular brachial plexus block. Materials and Methods: After Institutional Ethics and Scientific Committee approval and written informed consent, this prospective, observational study was carried out on 64 ASA Grade I and II patients of either sex, aged 18–60 years who underwent upper-limb surgery under brachial plexus block. Patients received either bupivacaine or bupivacaine with dexmedetomidine and were randomly divided into two groups. The primary outcome was duration of analgesia, and the secondary outcome was onset and duration of sensory and motor blockade, Ramsay sedation score, and side effects, if any observed at scheduled intervals. Results: Duration of analgesia in Group B was 391.46 ± 30.66 min and in Group BD was 810 ± 39.52 min (P < 0.0001), onset of sensory block in Group B was 7.9 ± 1.33 min and in Group BD was 5.65 ± 0.68 min (P < 0.0001), onset of motor block in Group B was 15.65 ± 1.66 min and in Group BD was 8.93 ± 0.788 min (P < 0.0001), duration of sensory block in Group B was 236.43 ± 17.52 min and in Group BD was 479.68 ± 40.50 min (P < 0.0001), duration of motor block in Group B was 206.09 ± 24.26 min and in Group BD was 447.81 ± 41.88 min, and slightly higher Ramsay sedation score was seen in Group BD as compared to Group B. The side effects were found to be insignificant and incidental. Only two cases of bradycardia(6.25%) and one case(3.12%) of hypotension were noticed in group BD. Conclusion: Addition of dexmedetomidine to bupivacaine was associated with prolonged analgesia, prolonged sensory and motor blockades with mild sedation.
Keywords: Adjuvant, dexmedetomedine, supraclavicular brachial plexus block
|How to cite this article:|
Lalwani J, Bhuaarya RN, Ali N, Shah PJ. Dexmedetomidine with 0.375% bupivacaine for prolongation of postoperative analgesia in supraclavicular brachial plexus block. Indian J Pain 2019;33:31-4
|How to cite this URL:|
Lalwani J, Bhuaarya RN, Ali N, Shah PJ. Dexmedetomidine with 0.375% bupivacaine for prolongation of postoperative analgesia in supraclavicular brachial plexus block. Indian J Pain [serial online] 2019 [cited 2019 Nov 16];33:31-4. Available from: http://www.indianjpain.org/text.asp?2019/33/1/31/255718
| Introduction|| |
Supraclavicular brachial plexus block is a very popular anesthesia technique for various upper-limb surgeries due to its versatility, effectiveness in terms of cost and performance, margin of safety, and good postoperative analgesia. Many drugs have been used as adjuvants to local anesthetic agents to prolong the duration of peripheral nerve blocks and decrease the time of onset such as opioids, ketamine, dexamethasone, tramadol, clonidine, butorphanol tartrate, buprenorphine, verapamil, methylprednisolone, dexmedetomidine, etc.,,
There has always been a search for adjuvants to the regional nerve block with drugs that prolong the duration of analgesia but with lesser adverse effects. We used the new α2-adrenergic agonist, dexmedetomidine, which is more selective toward α2-adrenoreceptors. Dexmedetomidine is a highly selective α2-agonist, provides anxiolysis and sedation without respiratory depression, and has organ-protective effects against ischemic and hypoxic injury, including cardioprotection, neuroprotection, and renoprotection. In this study, we assessed the effect of dexmedetomidine as an adjuvant to bupivacaine in supraclavicular brachial plexus block in terms of duration of postoperative analgesia and complications, if any.
The aim of our study was to assess the postoperative analgesic efficacy of dexmedetomidine for brachial plexus blockade along with bupivacaine.
In this study, we assessed the effect of dexmedetomidine as an adjuvant to bupivacaine in supraclavicular brachial plexus block in terms of:
- Postoperative analgesia
- Onset and duration of sensory and motor blockades
- Complications/side effects if any.
| Materials and Methods|| |
The present study was conducted in the Department of Anesthesiology and Critical Care, Pt. J. N. M. Medical College and Dr. Bhim Rao Ambedkar Memorial Hospital, Raipur, Chhattisgarh, from June 2016 to July 2017 after approval from Institutional Ethics and Scientific Committee. Sixty-four patients of age 18–60 years, body mass index 18.5–22.9, and American Society of Anesthesiologists Grades I and II who underwent upper-limb surgery under brachial plexus block, received either bupivacaine or bupivacaine with dexmedetomidine, were randomly divided into two groups, Group B and Group BD, during data analysis. Group B (n = 32) received 29 ml of 0.375% of bupivacaine with 1-ml normal saline and Group BD (n = 32) received 29 ml of 0.375% of bupivacaine with 1μg/kg body weight dexmedetomidine (diluted to 1 ml). Patient refusal and patients with a history of bleeding disorders, local infection at the site of block, documented neuromuscular disorders, known respiratory compromise, and known allergy to local anesthetic drugs were excluded.
After routine preanesthetic checkup, informed and written consent was taken and patients were shifted to Operation Theatre. Multipara monitor (Philips MP 30) was attached and baseline vital parameters were recorded. In the operating room, intravenous (IV) catheter was inserted in the contralateral limb, and Ringer's lactate at the rate of 10 ml/kg/h was started. Lignocaine sensitivity test was performed on all patients. All the patients were premedicated with ranitidine 50 mg IV and ondansetron 4 mg IV. Patients were placed in supine position with the head turned laterally away from the site of the block, and the arms were placed along the side of the body. After explaining the procedure to the patient, under all aseptic precautions, brachial plexus was approached through supraclavicular route and was identified by ultrasonography machine Mindray M7. Once plexus was localized by its characteristic honeycomb appearance, then 30 ml of drug was given. Vital parameters such as pulse rate (PR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP), respiratory rate (RR), and peripheral capillary oxygen saturation of all patients were recorded after administration of drug at every 5min interval up to 30 min. Thereafter vital parameters were rercoded at every 15 min interval up to 60 min and then at 120, 240, 360 min. Patients were monitored postoperatively to assess duration of sensory and motor blocks, postoperative analgesia and adverse effects such as nausea, vomiting, hypotension, bradycardia, pneumothorax, diaphragmatic paralysis, and Horner's syndrome. The onset time of sensory block was defined as the time interval between the end of local anesthetic administration and complete sensory block (score 2 for all nerves). Sensory block was assessed by 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). The onset time of motor block was defined as the time interval between the end of local anesthetic administration and complete motor block Grade 2. Motor block was assessed 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. Duration of sensory blockade was time taken from onset of sensory blockade to complete recovery of all the sensations in all the four dermatomes. Duration of motor blockade was the time taken from the onset of motor blockade to complete recovery of motor function. Duration of analgesia was defined as the time from completion of block to first rescue analgesia required. Sedation score was assessed by Ramsay sedation scale (1–4): score 1 – fully awake and oriented and follows verbal command; score 2 – drowsy, eyes closed but arousable only to commands; score 3 – eyes closed but arousable to mild physical stimulation; and score 4 – eyes closed and unarousable to mild physical stimulation.
Statistical analysis was performed using “unpaired Student's t-test.”For the calculation of sample size, data from the study of Gandhi et al was taken and calculated using G power software. P < 0.05 was taken as significant and P < 0.001 was taken as highly significant.
| Result|| |
Both the groups were comparable in terms of age, sex, height, and weight [Table 1].
Mean onset time of sensory and motor blocks was faster in Group BD (5.65 ± 0.68 and 8.93 ± 0.78 min, respectively) as compared to Group B (7.9 ± 1.33 and 15.65 ± 1.66 min, respectively) (P < 0.0001). Duration of sensory and motor blocks was significantly longer in Group BD as compared to Group B (P < 0.0001). Mean duration of analgesia in Group B was 391.46 ± 30.66 min and in Group BD was 810 ± 39.52 min. Duration of analgesia was prolonged in Group BD, and this difference was statistically highly significant (P < 0.0001) [Table 2]. Mean PR and blood pressure were lower in Group BD as compared to Group B (P < 0.05) at all time intervals [Graph 1],[Graph 2],[Graph 3]. However, active intervention was not required in any patient. Only two cases of bradycardia (6.25%) and one case (3.12%) of hypotension were noticed in dexmedetomidine group, but no treatment was required. Higher sedation score was observed in patients belonging to Group BD than those of Group B, but all patients were arousable, and none of them required assistance for airway maintenance. None of the patients had mean sedation score 3 or 4 in Group B which was observed in Group BD (13 and 3 patients, respectively), and the difference among the groups was statistically highly significant (P < 0.01) [Graph 4].
|Table 2: Onset time and duration of motor and sensory blocks and duration of analgesia|
Click here to view
| Discussion|| |
Brachial plexus block today has become anesthesia of choice for upper-limb surgeries. It offers several advantages over general anesthesia. It is suitable for day care anaesthesia, patients with full stomach and patients in whom general anaesthesia cannot be administered due to systemic diseases. It provides not only good quality anesthesia but is also beneficial for postoperative analgesia.
Onset of sensory and motor blockades is earlier, and duration is prolonged in our study as compared to studies done by Gandhi et al. and Annapurna et al. which can be explained by higher dose of dexmedetomidine (1-μg/kg body weight) used in our study as against 30-μg dexmedetomidine in their studies. In our study, earlier onset and prolonged duration of sensory and motor blocks as compared to Kalyanam et al., More et al., Waindeskar et al., might be due to higher concentration of bupivacaine (0.375%) in our study. Kalyanam et al. and More et al. used 0.25% whereas Waindeskar et al., used 0.325% bupivacaine in their study.. Bupivacaine was used in lower concentration in our study (0.375% vs. 0.5%) as compared to studies of Singh et al., Meena et al., Hegazy et al., and Modh et al., and still, the block resulted in earlier onset of sensory and motor blockades. Since we used ultrasound for localization and identification of brachial plexus, the local anesthetic could be deposited in close vicinity of brachial plexus.
Dexmedetomidine prolongs the duration of block and the duration of postoperative analgesia. This may be because peripheral α2-agonists produce analgesia by decreasing, release of norepinephrine, leading to α2-receptor-independent inhibitory effect on nerve fiber action potentials. Centrally α2-agonists produce analgesia and sedation by inhibition of substance P release in the nociceptive pathway at the level of the dorsal root neuron and by activation of ά2-adrenoreceptor in the locus coeruleus.
Higher dose of dexmedetomidine (1-μg/kg body weight) used in our study as compared to Gandhi et al. and Annapurna et al. (30 μg) explains the prolonged duration of analgesia. Prolonged duration of analgesia in our study as compared to Swami et al. (0.25%), Kalyanam et al. (0.25%), More et al. (0.25%), Munshi et al. (0.25%), and Waindeskar et al. (0.325%) can be explained by higher concentration of bupivacaine (0.375%) used in our study and and brachial plexus block was guided by ultra sound machine. This also explains shorter duration of analgesia in studies of Bhaskarbabu et al. (despite using 0.5% 20-ml bupivacaine + lignocaine 2% with adrenaline 20 ml + dexmedetomidine 50 μg), Hegazy et al. (0.5%), Meena et al. (0.5%), and Modh et al. (0.5%).
Patients in Group BD were comfortable throughout the surgery with arousable sedative effects. This can be explained on the basis of systemic absorption of drug which could be present. As ά2-agonists produce sedation by central action, they produce inhibition of substance P release in the nociceptive pathway at the level of the dorsal root neuron and by activation of ά2-adrenoceptor in the locus coeruleus.
Effects of dexmedetomidine on blood pressure is biphasic with an initial transient rise with a reflex fall in heart rate (HR) brought about by stimulation of α2B-subtypes of receptors present in vascular smooth muscles. This is followed by fall in blood pressure and HR due to inhibition of central sympathetic outflow with stimulation of presynaptic α2-receptors leading to decreased release of noradrenaline leading to further fall in the blood pressure., Baroreceptor reflex is well preserved with the use of dexmedetomidine, and bradycardia is easily treatable conferring hemodynamic stability. In our study, hemodynamic parameters such as HR, SBP, DBP, and MBP were significantly lower in Group BD than Group B (P < 0.001). Our result was in accordance with Swami et al., Singh et al., Bhaskarbabu et al., and More et al. In the studies of Annapurna et al. and Gandhi et al., the stable hemodynamic parameters might be due to lower dose of dexmedetomidine (30 μg).
| Conclusion|| |
In the present study, dexmedetomidine as an adjuvant to bupivacaine 0.375% was studied in terms of onset of sensory and motor blockades, duration of sensory and motor blockades, duration of analgesia, and side effects in patient undergoing arm and forearm surgeries, and it was found that dexmedetomidine is a good adjuvant to local anesthetic agents as its addition to bupivacaine, hastens the onset, and prolongs duration of sensory and motor blockades with prolonged postoperative analgesia without any adverse effects.
We wish to thank the orthopedic department for their cooperation.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Duma A, Urbanek B, Sitzwohl C, Kreiger A, Zimpfer M, Kapral S, et al.
Clonidine as an adjuvant to local anaesthetic axillary brachial plexus block: A randomized, controlled study. Br J Anaesth 2005;94:112-6.
Patki YS, Bengali R, Patil T. Efficacy of dexmedetomidine as an adjuvant to 0.5% ropivacaine in supraclavicular brachial plexus block for postoperative analgesia. Int J Sci Res 2015;4:2345.
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.
Prielipp RC, Wall MH, Tobin JR, Groban L, Cannon MA, Fahey FH, et al.
Dexmedetomidine-induced sedation in volunteers decreases regional and global cerebral blood flow. Anesth Analg 2002;95:1052-9.
Gandhi R, Shah A, Ila P. Use of dexmedetomidine along with bupivacaine for brachial plexus block. Nat J Med Res 2012;2:67-9.
Annapurna B, Sundari M, Suman VJ, Rao M. Low dose dexmedetomidine as an adjuvant to bupivacaine in supraclavicular brachial plexus block. IOSR J Dent Med Sci 2015;14:104.
Kalyanam P, Julakanti M, Shyam B, Kiran M, Raghuram CG. A prospective randomized study to compare dexmedetomidine with clonidine as an adjuvant to bupivacaine in supraclavicular brachial plexus block. J Evol Med Dent Sci 2015;4:15289-97.
More P, Basavaraja, Laheri V. Comparison of dexmedetomidine and clonidine as an adjuvant to local anaesthesia in supraclavicular brachial plexus block for upper limb surgeries. JMR 2015;1:142-7.
Waindeskar V, Jain A, Pandey JK, Songir S. Dexmedetomidine as an adjuvant to bupivacaine ultrasound guided supraclavicular brachial plexus block. Int J Med Dent Sci 2016;4:1184.
Singh R, Bisoi P, Mohanty SN, Debata PC. Study on effect of dexmedetomidine when added to bupivacaine on the onset time and duration of block in supraclavicular brachial plexus block. Pharm Biomed Sci 2015;5:338-43.
Meena R, Loha S, Pandey A, Meena K, Paswan A, Chaudhary L, et al
. Dexmedetomidine as an adjuvant to bupivacaine in supraclavicular brachial plexus block. J Anesth Clin Res 2016;7:10.
Hegazy AA, Ali M, Ali A, Ahmed S, Alaa M. Dexmedetomidine versus tramadol as an adjuvant to bupivacaine in ultrasound guided supraclavicular brachial plexus blockade for upper limb surgeries. ESRAPMJ. 2016;1.
Modh DB, Parmar M, Solanki S. Effect of dexmedetomidine as adjuvant in supraclavicular block for upper limb orthopedic surgeries. Int Surg J 2017;4:1510-5.
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.
] [Full text]
Munshi FA, Bano F, Khan A, Saleem B, Rather M. Comparison of dexmedetomidine and clonidine as an adjuvant to bupivacaine in supraclavicular brachial plexus block: A randomised double – Blind prospective study. J Evol Med Dent Sci 2015;4:7263-8.
Bhaskarbabu BD, Kiran AV, Jajee PR. Dexmedetomidine an adjuvant to local anaesthetics in supraclavicular brachial plexus block a comparative study. J Chem Pharm Res 2015;7:421-4.
Bloor BC, Ward DS, Belleville JP, Maze M. Effects of intravenous dexmedetomidine in humans. II. Hemodynamic changes. Anesthesiology 1992;77:1134-42.
Hall JE, Uhrich TD, Barney JA, Arain SR, Ebert TJ. Sedative, amnestic, and analgesic properties of small-dose dexmedetomidine infusions. Anesth Analg 2000;90:699-705.
Snapir A, Posti J, Kentala E, Koskenvuo J, Sundell J, Tuunanen H, et al.
Effects of low and high plasma concentrations of dexmedetomidine on myocardial perfusion and cardiac function in healthy male subjects. Anesthesiology 2006;105:902-10.
Singh S, Nanda HS. A comparitive study of clonidine and dexmedetomidine as adjuvant to 0.25% bupivacaine in supraclavicular brachial plexus block for duration of action and haemodynamic changes. J Evol Med Dent Sci 2014;3:11648-55.
[Table 1], [Table 2]