|Year : 2015 | Volume
| Issue : 4 | Page : 670-677
Anesthetic and analgesic efficacy, hemodynamic changes, and sedation following addition of dexmedetomidine to lignocaine in intravenous regional anesthesia for minor hand surgery
Nirvana Ahmed El-Shalakany1, Asmaa Mohamed Salah2
1 Head and Literature of Anesthesia, Faculty of Medicine, October Six University, Egypt
2 Literature of Anesthesia, Faculty of Medicine, October Six University, Egypt
|Date of Submission||21-Dec-2014|
|Date of Acceptance||15-Aug-2015|
|Date of Web Publication||29-Dec-2015|
Nirvana Ahmed El-Shalakany
Head and Literature of Anesthesia, Faculty of Medicine, October Six University, Compound Bayity Building A1 Villa 4, 6 October City, Giza
Source of Support: None, Conflict of Interest: None
Background and aims
Adding dexmedetomidine to local anesthetics in intravenous regional anesthesia has been found to produce effective anesthesia and analgesia for minor hand surgery. The aim of this study was to compare hemodynamic changes, adverse effects, patient satisfaction, and anesthetic, analgesic, and sedation qualities in patients who received lidocaine only versus those who received dexmedetomidine with lidocaine during minor hand surgery.
One hundred patients scheduled for minor hand surgery were randomly allocated into two equal groups: group L and group DL. Patients in group L received 3 mg/kg lidocaine 0.5% (maximum dose 200 mg), and patients in group DL received 3 mg/kg lidocaine 0.5% (maximum dose 200 mg) + 0.5 mg/kg dexmedetomidine; the total volume was diluted to 40 ml with normal saline 0.9% in both groups and injected at a rate of 20 ml/min. Anesthesia, analgesia, and sedation qualities, hemodynamic changes, patient satisfaction, and adverse effects were recorded.
The studied groups showed no significant difference in demographic data. In hemodynamics, mean arterial blood pressure and heart rate showed a statistically significant difference during and up to 30 min after tourniquet release (P < 0.001), and oxygen saturation showed no statistically significant difference during and after surgery (P > 0.05). There were statistically significant differences between the two groups (P < 0.05) as regards the quality of anesthesia, time of regression of sensory and motor blocks, and patient satisfaction. There were more patients who reported excellent satisfaction in the DL group (76%) compared with the L group (20%). Intraoperative and postoperative analgesic requirements were greater in the lidocaine group than in the dexmedetomidine group, and postoperative pain score (visual analog scale) was lower in the DL group compared with L group. Sedation score after release of tourniquet was significantly higher in the DL group compared with the L group except in the first 5 min.
On the basis of the results in this study we concluded that dexmedetomidine is a good adjuvant anesthetic, analgesic, and sedative agent in intravenous regional anesthesia.
Keywords: anaethesia and analgesia quality, dexmedetomidine, drug combinations, intravenous regional anesthesia, lidocaine, minor hand surgery
|How to cite this article:|
El-Shalakany NA, Salah AM. Anesthetic and analgesic efficacy, hemodynamic changes, and sedation following addition of dexmedetomidine to lignocaine in intravenous regional anesthesia for minor hand surgery
. Ain-Shams J Anaesthesiol 2015;8:670-7
|How to cite this URL:|
El-Shalakany NA, Salah AM. Anesthetic and analgesic efficacy, hemodynamic changes, and sedation following addition of dexmedetomidine to lignocaine in intravenous regional anesthesia for minor hand surgery
. Ain-Shams J Anaesthesiol [serial online] 2015 [cited 2019 Sep 15];8:670-7. Available from: http://www.asja.eg.net/text.asp?2015/8/4/670/172766
| Introduction|| |
Intravenous regional anesthesia (IVRA) is an effective method of providing anesthesia for procedures expected to last less than 1 h, and is widely used for minor operations in the extremities  . The technique includes applying a pneumatic tourniquet and injecting a local anesthetic distal to the tourniquet  for delivering the local anesthetic directly to the core of the major nerves through the vasa nervosa  .The major disadvantages of this technique are the occurrence of tourniquet pain, potential for local anesthetic toxicity, and minimal residual postoperative analgesia  . The development of compartment syndrome following IVRA has also been reported  .
Lidocaine is probably the most commonly chosen local anesthetic for IVRA, although it provides less effective blockage, is unable to provide effective postoperative analgesia, and causes tourniquet pain. Different additives have been combined with local anesthetics  , such as opioids, tramadol, NSAID, muscle relaxant, ketamine, and clonidine, to prolong postdeflation analgesia and reduce tourniquet pain, but their use is limited because of their side effects (e.g. mivacurium, which showed signs of local anesthetic toxicity  , and opioid  or limited efficacy (e.g. acetylsalicylate  .
Recently, a2-adrenergic receptor agonists have been the focus of interest for their sedative, analgesic, and perioperative sympatholytic and cardiovascular stabilizing effects in addition to their general anesthetic-sparing effect and their ability to prolong local anesthetic-induced analgesia when used in regional blocks , .
In clinical studies, clonidine-containing local anesthetic solutions have been shown to prolong and intensify analgesia, compared with plain solutions, when used for spinal, epidural, or peripheral nerve blocks  .
Dexmedetomidine is a selective, short-acting, agonist of the a2-adrenergic receptors  . In addition to sympatholytic effects, dexmedetomidine has antihypertensive, anxiolytic, sedative/hypnotic, and analgesic effects , . It has been used clinically as an adjunct to anesthesia, as an analgesic agent, and is useful in painful surgical procedures and intensive care unit sedation , .
This randomized, double-blinded, controlled study was designed to evaluate the effect of adding dexmedetomidine to lidocaine in IVRA for minor hand surgeries.
| Patient and methods|| |
After obtaining the approval of the medical ethics committee of October six university educational hospital, patients were informed of the protocol of the study and a written consent for the use of regional anesthesia was obtained from them. One hundred patients aged 20-60 years with American society of anesthesiologists physical status I or II undergoing minor hand surgeries (duration of surgery 60 min or less, such as carpal tunnel release, ganglion excision, trigger finger, tendon or nerve repair, and fracture finger or metacarpal bone) were enrolled in this study from October 2013 to May 2014. Patients who had a history of allergy to the drugs used, recent or chronic use of analgesics, uncontrolled hypertension, diabetic neuropathy, peripheral ischemia, sickle cell disease, or any psychological disturbances were excluded from the study.
Preoperative evaluation of the patients included medical history, physical examination, and laboratory investigations. Patients had to be in fasting state for at least 8 h before surgery, and the visual analog scale (VAS) (from 0 to 10: 0 = no pain up to 10 = severe pain) was explained to the patients to express their pain.
On arriving at the operating room, routine intraoperative monitors were applied, such as a noninvasive blood pressure monitor, a five-lead ECG, and a pulse oximeter. Two (20 G) venous cannulae were inserted, one in the dorsum of the operative hand and one in the other hand, for fluid infusion during surgery and for any intravenous medications.
All patients received 0.03 mg/kg midazolam before the block as premedication. A cotton pad was applied to the upper part of the operative arm and then a double-pneumatic tourniquet was positioned. The operative arm was elevated above the level of the heart for 3 min and exsanguinated using an Esmarch bandage. This was followed by inflation of the proximal tourniquet up to 100 mmHg above the systolic pressure and the circulatory isolation of the arm was confirmed by disappearance of radial artery pulsation and no pulse could be detected in the periphery by pulse oximetry placed in the ipsilateral index finger then placement of the upper extremity in horizontal position.
The patients were randomly allocated into two equal groups, with 50 patients in each group: group L and group LD. Patients in group L received 3 mg/kg lidocaine 0.5% (maximum dose 200 mg), with the volume diluted up to 40 ml with normal saline 0.9%. Patients in group LD received 3 mg/kg lidocaine 0.5% (maximum dose 200 mg)+0.5 mg/kg dexmedetomidine, with the total volume diluted to 40 ml with normal saline 0.9%. The solution was injected at a rate 20 ml/min by a blinded anesthetist. Assessment of sensory block time (time from injection of local anesthetic until complete loss of sensation) was made by means of the pin prick test using a 22 G needle every 60 s until complete sensory loss, and time of motor block (time from injection of local anesthetics until complete loss of motor power) was assessed by loss of voluntary movement of fingers and wrist joint.
When complete sensory and motor block was achieved, the surgery was started. Vital data [heart rate (HR), blood pressure, and oxygen saturation] of the patients were monitored 5 min before induction and every 5 min after inflation of tourniquet and during the surgery, and for 60 min after the surgery. Fifteen minutes after administration of the drug, the distal tourniquet was inflated up to 250 mmHg and the proximal one was deflated.
Fentanyl at 1 mg/kg intravenously was used for intraoperative analgesia when needed if there was any pain (VAS > 4; that is, moderate pain). Intraoperative hypotension (systolic blood pressure <90 mmHg) was treated with intravenous 5 mg ephedrine; intraoperative bradycardia (HR <60 beats/min) was treated with intravenous 0.5 mg atropine; nausea and vomiting was treated with 4 mg of intravenous ondansetron; and hypoxemia (decrease in oxygen saturation <90%) was treated with an oxygen face mask.
After completion of surgery the distal tourniquet was deflated by cyclic technique at 10 second interval for least 45 min from local anesthetic injection and not inflated more than 1.5 hour, then the patients. The patients were then transported to the postanesthesia care unit where they were monitored closely every 30 min for any sign of local anesthetic toxicity, any hemodynamic disturbances, or any complications such as headache, nausea, vomiting, hypotension, and bradycardia.
Motor recovery time, defined as the time from proximal tourniquet deflation until return of voluntary movement in the fingers, and sensory recovery time, defined as the time from proximal tourniquet deflation to return of sensation as assessed by the pin prick test, were assessed.
Assessment of onset of tourniquet pain, time of first analgesic requirement intraoperaively and postoperatively, and total analgesia consumption intraoperatively and postoperatively were recorded.
After completion of surgery patient satisfaction was recorded by using the numeric scale as follows: excellent (4): no complaint; good (3): patient complaint of minor pain but no need for analgesia; fair (2): patient complaint of moderate pain and required analgesics; failed (1): patient could not tolerate IVRA and required general anesthesia.
Postoperative sedation was assessed with the following sedation scores: 1 = completely awake; 2 = awake but drowsy; 3 = asleep but responsive to verbal commands; 4 = asleep but responsive to tactile stimulus; and 5 = asleep and not responsive to any stimulus.
All drugs were injected by anesthesiologists blinded to our study, and data were read and recorded by another anesthesiologist blinded to the study.
Statistical presentation and analysis of the present study was conducted, using the mean, standard error, unpaired student t-test and chi-square tests by SPSS V17. Unpaired Student T-test was used to compare between two groups in quantitative data. Chi-square the hypothesis that the row and column variables are independent, without indicating strength or direction of the relationship. Pearson chi-square and likelihood-ratio chi-square. Fisher's exact test and Yates' corrected chi-square are computed for 2 ΄ 2 tables. Sedation score was analyzed using Mann-Whitney test. P value<0.05 was accepted to be statistically significant. A sample of 100 patients (50 in each group) was calculated to detect no reduction with power of 90% (power of test) with type I error 0.05 (Alfa).
| Results|| |
One hundred patients undergoing hand surgery during the period from October 2013 to May 2014 in October six university hospital were divided into two equal groups. All 100 patients completed the study.
The groups were compared by age, weight, height, sex, duration of surgery, and tourniquet time [Table 1]. There was no significant difference between the two groups as regards their demographic data (P > 0.05).
Hemodynamic change in both groups [Figure 1] [Figure 2] [Figure 3]
|Figure 1: Mean arterial blood pressure in the lidocaine group (L) versus the lidocaine and dexmedetomidine group (DL). Data are expressed as mean ± SD. There was a statistically signifi cant difference as MAB decrease by 5 -10 mmHg below normal (70 mm Hg) in DL group at 30 min to 60 min|
Click here to view
|Figure 2: Heart rate in the lidocaine group (L) versus the lidocaine and dexmedetomidine group (DL). Data are expressed as mean ± SD. There is a statistically significant difference as HR decreased in the DL group with release of tourniquet and for 30 min after its release (P < 0.05). HR, he art rate|
Click here to view
|Figure 3: Oxygen saturation in the lidocaine group (L) versus the lidocaine and dexmedetomidine group (DL). Data are expressed as mean ± SD. There was no statistically significant difference (P > 0.05) during and after the procedure|
Click here to view
With regard to hemodynamic changes during and after surgery, mean arterial blood pressure and HR [Figure 1] and [Figure 2], respectively) showed statistically significant difference as it decreased more in the DL group compared with the L group with release of tourniquet, and for up to 30 min after its release (P < 0.05). Before and after release of the tourniquet there was no statistically significant difference (P > 0.05). O 2 saturation showed no statistically significant difference (P > 0.05) during and after the procedure (Fig 3).
There was no statistically significant difference between the two groups with respect to time of onset of sensory and motor blocks (P > 0.05) [Table 2], but regression times were significantly longer in the DL group (P < 0.05).
The number of patients with excellent quality of anesthesia was higher in the DL group compared with the L group (25 vs. 11, respectively). There was a statistically significant difference between the two groups (P < 0.05) regarding quality of anesthesia, onset of tourniquet pain (which was longer in the DL group), time of first analgesic requirement intraoperatively and postoperatively (delayed in the DL group), and total analgesic consumption intraoperatively and postoperatively (low consumption in the DL group) [Table 3].
Postoperative pain score (VAS) after 5, 15, 30, 60, 90, 120, 150, and 180 min was lower in the DL group compared with the L group. Eighty-eight percent of patients in the DL group compared with 60% in the L group scored the analgesic quality as excellent [Table 4].
Patient satisfaction score was considerably different between the two groups. There was a higher number of patients with excellent satisfaction in the DL group (76%) compared with the L group (20%) [Figure 4].
Sedation score after release of tourniquet at 15, 30, 60, 90, 120, 150, and 180 min was higher in the DL group compared with the L group [Table 5], with a statistically significant difference (P < 0.05), except in the first 5 min when there was no statistically significant difference (P > 0.05).
There were minimum adverse effects throughout the intraoperative and postoperative period in both groups. Bradycardia (HR <60) was transiently resolved without treatment and experienced in two patients only in the DL group. Other adverse effects such as hypotension (mean arterial blood pressure <60), nausea, vomiting, and desaturation were not recorded in either group.
| Discussion|| |
The outcome of this study demonstrated that the addition of dexmedetomidine to lidocaine in IVRA for minor hand surgeries prolongs sensory and motor block recovery times, and improves the quality of anesthesia, reduces tourniquet pain, prolongs first analgesic requirement time, decreases the total amount of analgesic consumption, and provides good sedation without any side effects.
Many researchers have been aiming to overlap the disadvantages of this type of block, including tourniquet pain and insufficient postoperative pain relief, by using adjuvant drugs to potentiate local anesthetics  .
Our study depends on the fact that dexmedetomidine is a selective a2-adrenergic receptor agonist  with a dose-dependent a-2 selectivity that is approximately seven- to eight-fold greater than that of clonidine  . The interactions with the central nervous system and spinal cord a2-adrenergic receptors mediate dexmedetomidine's primary physiologic effects by stimulating the parasympathetic outflow and inhibiting the sympathetic outflow  . It has a unique mechanism of action, providing sedation and anxiolysis through receptors within the locus ceruleus and primary analgesic effects and potentiation of opioid-induced analgesia results through the activation of a2-adrenergic receptors in the dorsal horn of the spinal cord and the inhibition of substance P release, and attenuation of the stress response with no significant respiratory depression , . Dexmedetomidine is a selective a2-adrenoceptor agonist that can be given in relatively high doses for sedation and analgesia without the unwanted vascular side effects from activation of a-1 receptors. These properties make dexmedetomidine suitable for sedation and analgesia as premedication, and as an anesthetic adjunct for general and regional anesthesia, and as postoperative sedative and analgesic  .
In our study, it was noticed that dexmedetomidine did not affect the onset of sensory or motor block but instead prolonged sensory and motor block duration. Studies performed by Calasans-Maia et al.  and Kaya et al.  suggested that the duration of motor block induced by spinal injection of levobupivacaine could be prolonged by intrathecal or intraperitoneal administration of dexmedetomidine in guinea pigs. Another study by Kanazi et al.  showed that the combination of 12 mg of intrathecal bupivacaine with a low dose (3 mg) of dexmedetomidine significantly prolonged both motor and sensory block when compared with bupivacaine alone. A study by Memis et al.  found that sensory and motor block recovery times were also statistically prolonged on adding dexmedetomidine 0.5 mg/kg to lidocaine. Other studies investigated the effect of dexmedetomidine on the action of the local anesthetic - for example, studies by Gandhi et al.  (brachial plexus block), Marhofer et al.  (peripheral nerve block), Abdallah et al.  (spinal block), Abdallah and Brull  (neuraxial and peripheral nerve blocks), and Gupta et al.  (IVRA) supported our results as regards prolongation of sensory and motor block recovery times.
In contrast to our study, Esmaoglu et al.  observed that addition of dexmedetomidine to lignocaine in IVRA anesthesia has no effect on the sensory and motor block onset and regression times as they used a high dose of dexmedetomidine (1 mg/kg) compared with our study.
In our study, it was noticed that addition of dexmedetomidine to lidocaine in IVRA decreases pain scores (VAS) intraoperatively and postoperatively, improves anesthesia quality, delays the onset of tourniquet pain, and decreases analgesic requirement intraoperatively and in the first 24 h postoperatively.
A study by Memis et al.  documented that adding dexmedetomidine to the local anesthetic delayed the onset of tourniquet pain and reduced total analgesic consumption intraoperatively and postoperatively. Also, a study by Mizrak et al.  showed that addition of dexmedetomidine 0.5 mg/kg to lidocaine in IVRA improves the quality of anesthesia and perioperative analgesia without severe side effects. These results are in accordance with our study's result.
Hunter et al.  reported that in transgenic mice the sedative and analgesic properties of dexmedetomidine rely on the presence of the a-2A adenoreceptor subtype.
A study by Abosedira  concluded that a dexmedetomidine-lidocaine mixture provided better quality of anesthesia and tourniquet tolerance, and provided longer postdeflation analgesia with reduction of intraoperative and early postoperative analgesic consumption. This study supported our study results.
Kol et al.  demonstrated that addition of dexmedetomidine to prilocaine in IVRA decreases pain scores, improves anesthesia quality, decreases analgesic requirement, and prolongs sensory block recovery time. A study by Esmaoglu et al.  proved that addition of dexmedetomidine to lignocaine in IVRA improves the quality of anesthesia and decreases the analgesic requirements. Another study by Kumar et al.  demonstrated that the addition of dexmedetomidine at a dose of 1 mg/kg to lignocaine for IVRA improves the quality of anesthesia and postoperative analgesia without causing significant side effects, which supports our study results.
Addition of dexmedetomidine to a local anesthetic is associated with hypotension and bradycardia, both of which usually resolve without intervention  . Further, dexmedetomidine causes a dose-dependent decrease in blood pressure and HR associated with decreased concentration of plasma norepinephrine  .
Regarding side effects, only two patients suffered from bradycardia, which resolved without treatment in the dexmedetomidine group; this finding is in agreement with the results of Memis et al.  .
Esmaoglu et al.  using 1 mg/kg dexmedetomidine did not observe any side effects such as hypotension or bradycardia that required treatment when compared with the dose used in our study (0.5 mg/kg).
Patient satisfaction was found to be higher in the dexmedetomidine group, which may be due to increase in intraoperative and postoperative analgesia and sedation. Our results are commensurate with the results of Hall et al.  and Gupta et al.  . In contrast, in the study by Memis et al.  there was no sedation on using dexmedetomidine in IVRA.
In conclusion, addition of dexmedetomidine to lidocaine in IVRA prolongs sensory and motor block recovery times, and improves the quality of anesthesia, reduces tourniquet pain, prolongs first analgesic requirement time, decreases the total amount of analgesic, and provides good sedation without any side effects.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Jankovic RJ, Visnjic MM, Milic DJ, Stojanovic MP, Djordjevic DR, Pavlovic MS. Does the addition of ketorolac and dexamethasone to lidocaine intravenous regional anesthesia improve postoperative analgesia and tourniquet tolerance for ambulatory hand surgery?. Minerva Anestesiol 2008; 74:521-527.
Niemi TT, Kuitunen AH, Vahtera EM, Rosenberg PH. Haemostatic changes caused by i.v. regional anaesthesia with lignocaine. Br J Anaesth 1996; 76:822-828.
Casey WF. Intravenous regional anesthesia (Bier's block). Update anesthesia 1992; 1:1-3.
Turan A, White PF, Karamanlioglu B, Pamukcu Z. Premedication with gabapentin: the effect on tourniquet pain and quality of intravenous regional anesthesia. Anesth Analg 2007; 104:97-101.
Ramadhyani U, Park JL, Carollo DS, Waterman RS, Nossaman BD. Dexmedetomidine: clinical application as an adjuvant for intravenous regional anesthesia. Anesthesiol Clin 2010; 28:709-722.
Torrance JM, Lewer BM, Galletly DC. Low-dose mivacurium supplementation of prilocaine i.v. regional anaesthesia. Br J Anaesth 1997; 78:222-223.
Choyce A, Peng P. A systemic review of adjuncts for intravenous regional anesthesia for surgical procedures. Can J Anaesth 2002; 49:32-45.
Corpataux JB, Van Gessel EF, Donald FA, Forster A, Gamulin Z. Effect on postoperative analgesia of small-dose lysine acetylsalicylate added to prilocaine during intravenous regional anesthesia. Anesth Analg 1997; 84:1081-1085.
Murphy DB, McCartney CJ, Chan VW. Novel analgesic adjuncts for brachial plexus block: a systematic review. Anesth Analg 2000; 90:1122-1128.
Kamibayashi T, Maze M. Clinical uses of alpha2-adrenergic agonists. Anesthesiology 2000; 93:1345-1349.
Coursin DB, Coursin DB, Maccioli GA. Dexmedetomidine. Curr Opin Crit Care 2001; 7:221-226.
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.
Lao HC, Tsai PS, Su JY, Kwok TG, Huang CJ. Dexmedetomidine attenuates tourniquet-induced hyperdynamic response in patients undergoing lower limb surgeries: a randomized controlled study. J Surg Res 2013; 179:e99-e106.
Gurbet A, Basagan-Mogol E, Turker G, Ugun F, Kaya FN, Ozcan B. Intraoperative infusion of dexmedetomidine reduces perioperative analgesic requirements. Can J Anaesth 2006; 53:646-652.
Khan ZP, Ferguson CN, Jones RM. Alpha-2 and imidazoline receptor agonists. Their pharmacology and therapeutic role. Anaesthesia 1999; 54:146-165.
Nasr YM, Waly SH. Lidocaine-tramadol versus lidocaine-dexmedetomidine for intravenous regional anesthesia. Egypt J Anaesth 2012; 28:37-42.
Bhana N, Goa KL, McClellan KJ. Dexmedetomidine. Drugs 2000; 59:263-268
Murthy TVSP, Singh R. Alpha 2-adrenoceptor agonist-dexmedetomidine role in anaesthesia and intensive care: a clinical review. J Anaesthesiol Clin Pharmacol 2009; 25:267-272.
Correa-Sales C, Nacif-Coelho C, Reid K, et al
. Inhibition of adenylate cyclase in the locus ceruleus mediates the hypnotic response to an alpha2 agonist in the rat. J Pharmacol Exp Ther 1992; 263:1046-1050.
Ricker RR, Shehabi Y, Bokesch PM, et al
. Dexmedetomidine versus midazolam for sedation of critically ill patients: A randomized trial. JAMA 2009; 301:489-499.
Mittal NP, Goyal M. Dexmedetomidine: a potential agent for use in procedural dental sedation. Indian J Dent 2013; 3:1-7.
Gupta A, Mahobia M, Narang N, Mahendra R. A comparative study of two different doses of dexmedetomidine as adjunct to lignocaine in intravenous regional anaesthesia of upper limb surgeries. Int J Sci Study 2014; 2:53-62.
Calasans-Maia JA, Zapata-Sudo G, Sudo RT. Dexmedetomidine prolongs spinal anaesthesia induced by levobupivacaine 0.5% in guinea-pigs. J Pharm Pharmacol 2005; 57:1415-1420.
Kaya FN, Yavascaoglu B, Turker G, Yildirim A, Gurbet A, Mogol EB, Ozcan B. Intravenous dexmedetomidine, not midazolam, prolongs bupivacaine spinal anesthesia. Can J Anesth 2010; 57:39-45.
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; 50:222-227.
Memis D, Turan A, Karamanlioglu B, Pamukcu Z, Kurt I. Adding dexmedetomidine to lidocaine for intravenous regional anesthesia. Anesth Analg 2004; 98:835-840.
Gandhi R, Shah A, Patel I. Use of dexmedetomidine along with bupivacaine for brachial plexus block. Nat J Med Res 2012; 2:67-69.
Marhofer D, Kettner SC, Marhofer P, Pils S, Weber M, Zeitlinger M. Dexmedetomidine as an adjuvant to ropivacaine prolongs peripheral nerve block: a volunteer study. Br J Anaesth 2013; 110:438-442.
Abdallah FW, Abrishami A, Brull R. Facilitatory effects of intravenous dexmedetomidine on duration of spinal anesthesia: a systemic review and metaanalysis. Anesth Analg 2013; 117:271-278.
Abdallah FW, Brull R. Facilitatory effects of perineural dexmedetomidine on neuraxial and peripheral nerve block: a systemic review and meta-analysis. Br J Anaesth 2013; 110:915-925.
Esmaoglu A, Mizrak A, Akin A, Turk Y, Boyaci A. Addition of dexmedetomidine to lidocaine for intravenous regional anaesthesia. Eur J Anaesthesiol 2005; 22:447-451.
Mizrak A, Gul R, Erkutlu I, Alptekin M, Oner U. Premedication with dexmedetomidine alone or together with 0.5% lidocaine for IVRA. J Surg Res 2010; 164:242-247.
Hunter JC, Fontana DG, Hedley LR, Jasper JR, Lewis R, Link RE, et al
. Assessment of the role of alpha 2-adenoreceptor subtypes in the anti-nociceptive, sedative and hypothermic action of dexmedetomidine in transgenic mice. Br J Pharmacol 1997; 122:1339-1344.
Abosedira MA. Adding clonidine or dexmedetomidine to lidocaine during Bier's block: a comparative study. J Med Sci 2008; 8:660-664.
Kol IO, Ozturk H, Kaygusuz K, Gursoy S, Comert B, Mimaroglu C. Addition of dexmedetomidine or lornoxicam to prilocaine in intravenous regional anaesthesia for hand or forearm surgery: a randomized controlled study. Clin Drug Investig 2009; 29:121-129.
Kumar A, Sharma DK, Datta B. Addition of ketamine or dexmedetomidine to lignocaine in intravenous regional anesthesia: a randomized controlled study. J Anesthesiol Clin Pharmacol 2012; 28:501-504.
Hoy SM, Keating GM. Dexmedetomidine: a review of its use for sedation in mechanically ventilated patients in an intensive care setting and for procedural sedation. Drugs 2011; 71:1481-1501.
Kallio A, Scheinin M, Koulu M, Ponkilainen R, Ruskoaho H, Viinamäki O, Scheinin H. Effects of dexmedetomidine, a selective alpha 2-adrenoceptor agonist, on hemodynamic control mechanisms. Clin Pharmacol Ther 1989; 46:33-42.
Hall JE, Uhrich TD, Barney JA, Arain SR, Ebert TJ. Sedative, amnesic and analgesic properties of small-dose dexmedetomidine infusions. Anesth Analg 2000; 90:699-705.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]