Rapid onset and prolonged analgesia and motor block without adverse effects highlighted an ideal local block. Hence many various drugs have been added to topical anesthetic drugs as an adjuvant. In prior studies, clonidine has been used as an α2 agonist with ropivacaine in the axillary block [24]. In recent studies, Intravenous administration of dexmedetomidine has been described as an effective drug in increasing the time of spinal anesthesia [25, 26]
Dexmedetomidine is an active D-isomer of medetomidine and a specific agonist of the α2 adrenoceptor. Dexmedetomidine is similarly related to clonidine, but dexmedetomidine has an (α-2: α-1) selectivity 1620:1 compared with Clonidine that has a specificity of 220: 1 (α-2: α-1) [25, 27]. The activation of the presynaptic receptor in the central nervous system prevents the nor-epinephrine releases and pain signals. It also prevents sympathetic activity by postsynaptic effects and reduces heart rate and blood pressure. Dexmedetomidine produces a natural sleep for the patient with an effect on the Locus coeruleus [28, 29].
Dexmedetomidine has been used without nerve damage. In the Brummet et al. study that had been done on rats, After 24 hours and 14 months, axons and myelin have been reported as no damage [30].
In the Rachana G et al. study in 2012 that it was conducted on 70 patients, the onset time of sensory block was lower in the bupivacaine group compared to bupivacaine with dexmedetomidine and also in the control group the onset of motor block was less than dexmedetomidine group and duration of sensory and motor block was prolonged in dexmedetomidine group. Mean arterial pressure and heart rate variations were similar between the two groups and the duration of analgesia in the control group was less than the intervention group (dexmedetomidine) [31]. The results of this study are consistent with our finding.
In this study, the rapid onset of motor block compared to sensory block indicated the existence of motor fibers in the outer layers of the nerve versus central sensory fibers have been mentioned and in Winnie et al. study has been explained [32]. In the study that had done on 50 patients in 2014 by Saudlyer A et al. the onset time of sensory block and limb immobilization in the group that they had received dexmedetomidine with bupivacaine was less than of bupivacaine singly and it also the duration of sensory and motor block in group who had received dexmedetomidine was more. The duration of analgesia in the dexmedetomidine group was prolonged than the control group. The results of this study are consistent with our study, however; the dose of the drug used in the two studies is different.
In a study by Neerja Bharti et al was conducted on 60 patients in two groups were divided into control (Ropivacaine and lidocaine with adrenaline) and intervention (Dexmedetomidine 1 µg / kg plus other drugs) groups, the onset of sensory block was similar in the two groups. The onset of immobility was less in the receiving dexmedetomidine group and the duration of sensory block and immobility was higher in the dexmedetomidine group that had reduced postoperative pain and need for analgesia in patients in the intervention group. [33] In the present study, the onset of sensory block was less in the dexmedetomidine group and this difference was statistically significant. In other measured parameters, the results of the two studies were not different. It seems, no difference in the onset time of sensory block in two groups Due to used the low dose of dexmedetomidine combined with the high volume of other drugs that have reduced the effective dose of local dexmedetomidine.
In a recent meta-analysis that performed by Abdallah Brull, the adding of dexmedetomidine to other drugs has been reported to prolong the motor block of the brachial plexus and prolonged the postoperative analgesia [34]. The results of this study are consistent with our study findings.
In separate studies conducted by Saumya B and Suncet Katarina et al., Dexmedetomidine with ropivacaine had improved the onset of sensory and motor block and the duration of sensory block and motor block compared with ropivacaine[35].
In our study, dexmedetomidine reduced the onset time of sensory and motor block and had increased the duration of sensory and motor block. This was similar to previous studies. The decrease of the onset time of sensory and motor block in present study and the inconsistent results of previous studies, it’s due to the use of multiple drugs at the same time and there was a difference in definition of the onset of sensory and motor block however in Rachana Gandhi's study did not provide a precise definition of the onset time of sensory and motor block [31].
In explaining the mechanism of dexmedetomidine effect in previous studies that conducted on rat, Cationic hyperpolarization block and maintaining of nerve stimulus mode has been attributed to the prolonged sensory and motor blocks [36]. In a study that performed by Kosung et al. on α2 agonist, the intravenous dose required for nerve block have reported more than 1000 times of topical dose and they have reported the effect of dexmedetomidine with local anesthetic is through vasoconstriction and delayed in local anesthetic uptake and as well as nerve conduction direct block[37].
In another study conducted by Fritsch G et al. in 2014, they have reported the use of dexmedetomidine with ropivacaine in intrascalen block, decreases postoperative pain and prolonged block time [38]. Also in our study, postoperative pain reduction was more prominent in the dexmedetomidine group.
Postoperative pain score in all hours of the present study in the intervention group was lesser than the control group. In Bharti N et al study, pain score was comparable among groups except at 8 and 10 hours, and pain scores were lower in the dexmedetomidine group versus the control group [33]. The results of this study are consistent with our study findings. In Gyu Choi et al. in their study that used the MgSO4 with Bupivacaine they illustrated there were no differences in VAS scores between the two groups [12].
Hypotension and bradycardia are the most common side effect observed with α2 agonists. In a study that Esmaglu and his colleagues had done, adding 100 μg of dexmedetomidine to levobupivacaine had caused bradycardia in 7 of the 30 patients [39]. In Youngsuk Kwon et al. study heart rate and mean arterial pressure in the dexmedetomidine group had decreased significantly [40]. Whereas in our study, this decrease occurred in mean arterial pressure and mean heart rate, and it was not statistically significant.
In our study, bradycardia was observed in 4 of the 30 patients in the intervention group, which seems to be due to the low dose of dexmedetomidine. Hypotensions in 3 patients have occurred in both groups and this difference was not statistically significant. However, in previously conducted studies, the use of dexmedetomidine was not associated with hypotension and bradycardia [41, 42].
Finally, the use of dexmedetomidine with bupivacaine in the supraclavicular block was effective in reducing the onset time of sensory and motor blocks and increasing the duration of sensory and motor blocks without considerable side effects such as hypotension and bradycardia. Besides, dexmedetomidine significantly reduced postoperative pain in the dexmedetomidine with the bupivacaine group.
Limitations of our study included:
The limitations of our study were the no measurement of dexmedetomidine serum dose during surgery that would make unpredictable the evaluation of the systemic effect of this drug after local absorption and evaluation of another group of patients with receiving intravenous dexmedetomidine in future studies will be resolved this restriction.
Increased duration of surgery and the needs for general anesthesia were other limitations of the present study that led to the exclusion of these cases.