|Year : 2019 | Volume
| Issue : 3 | Page : 344-349
A comparative study on the effect of dexamethasone, dexmedetomidine, and lornoxicam as adjuncts to local anesthetic in intravenous regional anesthesia in forearm and hand surgery
Tamer Y Hamawy, John N Bestarous
Department of Anesthesia, Faculty of Medicine, Ain Shams University, Cairo, Egypt
|Date of Submission||09-Sep-2018|
|Date of Acceptance||08-May-2019|
|Date of Web Publication||29-Aug-2019|
MD Tamer Y Hamawy
Department of Anesthesia, Faculty of Medicine, Ain Shams University, Cairo, 11361
Source of Support: None, Conflict of Interest: None
Background Intravenous regional anesthesia (IVRA) is a simple and reliable technique. The ideal IVRA solution should be rapid in onset and offers prolonged analgesia. The aim of this study was to assess the effects of different additives to local anesthetic in IVRA to provide a successful operative anesthesia with minimal analgesic requirements.
Patients and Methods 80 patients ASA I–III scheduled for orthopedic and plastic surgeries in the forearm or the hand were randomly categorized into four groups, with 20 patients in each group. All groups received 30 ml of Lidocaine 1 % as IVRA solution in addition to the studied anesthetic adjunct.
Group I (LD) received 8 mg dexamethasone in 2 ml
Group II (LP) received 0.5 mcg/kg dexmedetomidine in 2 ml
Group III (LL) received 8 mg lornoxicam in 2 ml
Group IV (LS) received 2 ml normal saline 0.9%
Mean arterial pressure and heart rate changes in the four study group changes were noted. Motor and sensory block onset and recovery times (minutes) and postoperative analgesic (gram paracetamol) consumption in the four study groups were recorded. Incidence of tourniquet pain and operative conditions were also assessed.
Results The LP group showed a shorter time to onset of sensory block than the other three groups that was statistically significant with p<0.001. Both the LP and LL groups showed statistically significant longer time to recovery of sensory block (min) than the other groups (p<0.001). Both times to onset of motor block (min) and time to recovery of motor block (min) shows statistical insignificance regarding the relation between the 4 groups (p=0.073 and 0.794 respectively). Time to 1st postoperative analgesic request (min) was significantly late and the postoperative paracetamol consumption (gm) was significantly lower in the LP and LL groups than the other groups (p<0.001).
Conclusion On studying different additives to lidocaine in IVRA, we found that dexmedetomedine and lornoxicam provide the best patient outcome regarding the onset and recovery of sensory block and prolonged analgesia.
Keywords: dexamethasone, dexmedetomedine, intravenous regional anesthesia (IVRA), lornoxicam, regional anethesia
|How to cite this article:|
Hamawy TY, Bestarous JN. A comparative study on the effect of dexamethasone, dexmedetomidine, and lornoxicam as adjuncts to local anesthetic in intravenous regional anesthesia in forearm and hand surgery. Res Opin Anesth Intensive Care 2019;6:344-9
|How to cite this URL:|
Hamawy TY, Bestarous JN. A comparative study on the effect of dexamethasone, dexmedetomidine, and lornoxicam as adjuncts to local anesthetic in intravenous regional anesthesia in forearm and hand surgery. Res Opin Anesth Intensive Care [serial online] 2019 [cited 2019 Nov 21];6:344-9. Available from: http://www.roaic.eg.net/text.asp?2019/6/3/344/265727
| Introduction|| |
Intravenous regional anesthesia (IVRA) is a simple and reliable regional anesthesia. It was introduced by August Bier, in 1908. The popularization of Bier’s block is related to Holmes of Oxford, UK, 1963. He used lidocaine for the first time and introduced several modifications, including a second cuff and a subcutaneous band of local anesthetic (LA) to control tourniquet pain ,.
Disadvantages include concerns about LA toxicity, slow onset, poor muscle relaxation, tourniquet pain, and minimal postoperative pain relief. The ideal IVRA solution should have the following features: rapid onset, reduced dose of LA, reduced tourniquet pain, and prolonged postdeflation analgesia. At present, this may only be achieved by the addition of adjuncts to LA.
Lornoxicam is a NSAID of the oxicam class with analgesic, anti-inflammatory, and antipyretic properties which is available in oral and parenteral forms . It is rapidly eliminated, having a short plasma elimination half-life of 3–5 h, which suggests its suitability for short-term use in the postoperative period .
Moreover, wound infiltration with a combination of LA plus lornoxicam improved postoperative pain control and patient comfort and decreased the need for opioid as compared with the use of either drug alone suggesting a local effect .
α-2-Adrenergic receptor (adrenoceptor) agonists have been of interest as they have sedative, analgesic, and perioperative sympatholytic and cardiovascular stabilizing effects, with reduced anesthetic requirements .
Dexmedetomidine is more selective for α-2 receptors than clonidine, which accounts for its preferential sedative over hemodynamic effects. It improves postoperative analgesia and may shorten sensory block onset time . Its sedative and analgesic properties have been shown to decrease anesthetic requirements by up to 90% .
Acute inflammation induced by tissue injury plays a significant role in the genesis of surgical pain, and dexamethasone should theoretically be beneficial in the management of acute surgical pain as a result of its potent anti-inflammatory effect . It has been reported that bupivacaine combined with dexamethasone prolongs the duration of analgesia in nerve blocks .
The aim of this study was to assess the effects of different additives to LA in IVRA, which provide successful operative anesthesia and have minimal requirement of postoperative analgesia.
| Patients and methods|| |
After ethical committee approval and obtaining an informed written consent from all patients, this prospective double-blind study was carried out on 80 patients of both sexes, with their ages ranging from 18 to 60 years of ASA I–III with average body weight between 60 and 90 kg scheduled for orthopedic and plastic surgeries in the forearm or the hand with expected operative time less than 1 h.
Patients with Raynaud’s disease, scleroderma, sickle cell anemia, myasthenia gravis, decompensated cardiac disease, diabetes mellitus, peptic ulcer, gastritis, and coagulation disorders; psychiatric, apprehensive, or uncooperative patients; those with liver or renal insufficiency; and those with prolonged operative time were excluded from the study.
Preoperative investigations were done as appropriate (in the form of complete blood picture, coagulation profile, metabolic profile, ECG, and chest radiograph).
After establishing basic monitors [ECG, pulse oximeter, and nom-invasive blood pressure (NIBP)], two venous cannulas were inserted: the first one in a vein on the dorsum of the operative hand (22-G) and the other in the opposite hand for crystalloid infusion. All patients of both groups were pre-medicated with midazolam in a dose of 0.01 mg/kg, intravenous, with 10 mg metoclopramide and 150 mg ranitidine 15 min before the start of anesthesia.
The selected cases were randomly categorized into four groups, with 20 patients in each group.
- Group I (LD) (n=20): it received 30 ml of lidocaine (Lidocaine, Lidocaine HCl, Debocaine 2%, DBK Pharma, Cairo, Egypt) 1%+8 mg dexamethasone in 2 ml (Fortecortin; Merck, Darmstadt, Germany).
- Group II (LP) (n=20): it received 30 ml of lidocaine 1%+0.5 mcg/kg dexmedetomidine in 2 ml (Precedex; Hospira, Hospira, Lake Forest, Illinois, United States).
- Group III (LL) (n=20): it received 30 ml of lidocaine 1%+8 mg lornoxicam in 2 ml (Xefo; Nycomed, Zurich, Switzerland).
- Group IV (LS) (n=20): it received 30 ml of lidocaine 1%+2 ml normal saline 0.9%.
The operative arm was elevated for 2 min and by using an Esmarch bandage, the venous capacitance of the arm was emptied. Then, a double-pneumatic tourniquet was applied and the proximal tourniquet was inflated to a pressure of 250 mmHg. After the Esmarch bandage was released, patients in each group received the IVRA which was administered at a rate of 0.5 ml/s.
After anesthesia was obtained, the distal tourniquet was inflated to 250 mmHg pressure, and the proximal tourniquet was deflated. The times for tourniquet and drug administration were recorded. After administration of drug, motor and sensory block were assessed every minute till achieving adequate motor and sensory block.
Drugs were prepared and concealed by a resident not involved in any other part of the study. An anesthesiology resident blinded to the group and drug allocation applied the concealed syringes and recorded all the data.
All evaluations were performed by an anesthesia resident blinded to the study. The time to first analgesic requirement (the time elapsed after tourniquet release to first patient request of analgesic) was also noted. Patients were questioned and monitored about adverse effects during the first 2 h in the postanesthesia care unit and later in the ward every 2 h by an anesthesia resident who was blinded to the study.
The sensory block was assessed by an ice bag every 60 s. A patient’s response was evaluated in the dermatomal sensory distribution of the medial and lateral antebrachial cutaneous, ulnar, median, and radial nerves. Motor function was assessed by asking the patient to flex and extend his/her wrist and fingers, and complete motor block was noted when no voluntary movement was possible.
Sensory block onset time was noted as the time elapsed from injection of the study drug to sensory block achieved in all dermatomes, and motor block onset time was the time elapsed from injection of study drug to complete motor block.
After sensory block and motor block were achieved, intraoperatively, boluses of 0.5 μg/kg fentanyl (Fentanyl; Janssen Cilag, Beerse, Belgium) were provided for treatment of tourniquet pain when required [when visual analog scale (VAS) was>3], and the total fentanyl consumption was recorded.
At the end of operation, the anesthesia resident was asked to qualify the operative conditions according to the following numeric scale: 4 (excellent)=no complaint from patient, 3 (good)=minor complaint with no need for supplemental analgesics, 2 (moderate)=complaint that required supplemental analgesics, and 1 (unsuccessful).
The tourniquet was not deflated before 30 min and was not inflated for more than 1.5 h. At the end of surgery, tourniquet deflation was performed using the cyclic deflation technique. Sensory recovery time (time elapsed after tourniquet deflation to recovery of pain in all dermatomes determined by pinprick test) was noted. Motor block recovery time (the time after tourniquet deflation to movement of fingers) was noted.
Arterial blood pressure, heart rate, and peripheral oxygen saturation were recorded preoperatively, after inflation of the tourniquet, every 5 min after administration of drug, and after tourniquet release. During the operation, tourniquet pain, and after surgery, pain at the operative site were assessed by VAS (0 cm=no pain and 10 cm=worst pain imaginable) and a verbal pain score (0=no pain, 1=light pain, 2=moderate pain, 3=severe pain, and 4=most severe pain).
For supplemental analgesia intraoperatively fentanyl 0.5 μg/kg and postoperatively 500 mg acetaminophen were used when VAS was more than 3 and verbal pain score was more than 2. Time to first request of analgesic was recorded. Patients were telephoned 24 h after surgery, and a resident not involved in the study asked about pain after discharge from hospital and amount of acetaminophen consumed. The total analgesic consumption during 24 h was recorded.
The patients were questioned about complications such as allergic reaction, nausea, vomiting, tinnitus, cooling, tremor, arrhythmia, and metallic taste.
Statistical analysis was done using the statistical package for the social sciences, version 17 (SPSS; SPSS Inc., Chicago, Illinois, USA).
The Shapiro–Wilk test was used to examine the normality of numerical variables. Numerical variables were presented as mean (SD), and differences among the groups were compared using one-way analysis of variance with application of Tukey’s honestly significant difference test for post-hoc pairwise comparisons.
Categorical variables were presented as number (%), and intergroup differences were compared using Fisher’s exact test.
P value less than 0.05 was considered statistically significant.
| Results|| |
Both heart rate and blood pressure were comparable in the baseline reading, immediately after tourniquet inflation, immediately before surgical incision, and 3 min after tourniquet release readings, except in the dexmedetomidine group ([Table 1] and [Table 2]), where the heart rate shows significantly lower heart rate and mean arterial pressure than the three other groups in the 3 min after tourniquet release reading. No patients needed treatment for hypotension or bradycardia.
|Table 2 Comparison of mean arterial pressure changes in the four study groups|
Click here to view
Regarding time to onset of sensory block (min), the dexmedetomidine group showed a shorter time to onset of sensory block than the other three groups, which was statistically significant, with P value less than 0.001, whereas the lornoxicam group showed shorter time than the dexamethasone and saline groups.
Both the dexmedetomidine and lornoxicam groups showed statistically significant longer time to recovery of sensory block (min) than both the dexamethasone and saline groups.
Both time to onset of motor block (min) and time to recovery of motor block (min) show statistical insignificance regarding the relation among the four groups ([Table 3]).
|Table 3 Block onset and recovery times and postoperative analgesic consumption in the four study groups|
Click here to view
Time to first postoperative analgesic request (min) was significantly late and the postoperative paracetamol consumption (g) was significantly lower in the dexmedetomidine and lornoxicam groups than the dexamethasone and saline groups.
Incidence of tourniquet pain and operative conditions shows statistically insignificant results regarding the four groups ([Table 4]).
| Discussion|| |
Our study demonstrated that the addition of 0.5 μg/kg of dexmedetomidine and lornoxicam to lidocaine in IVRA improved the quality of anesthesia in terms of rapid onset, prolonged duration of the block, and postoperative analgesia in forearm and hand surgeries with minimal adverse effects compared with dexamethasone, which in turn is better than lidocaine 1% only. Tourniquet pain is a common problem complicating the use of a pneumatic tourniquet during surgical procedures involving the upper or lower limb. The mechanism of tourniquet pain remains unclear despite the role of A fibers and unmyelinated C fibers . Clonidine has been reported to depress nerve action potentials, especially in C fibers, by a mechanism independent of the stimulation of α-2-adrenergic receptors [12,. Dexmedetomidine is approximately eight times more selective toward the α-2-adrenoceptors than clonidine . Therefore, we expect that dexmedetomidine may be even more effective in IVRA. Dexmedetomidine intravenous administration produces abrupt hypertension and bradycardia until the central sympatholytic effect dominates, resulting in moderate decreases in both mean arterial pressure and heart rate from baseline, and it also has a sedative effect . Its sedative, proanesthetic, and proanalgesic effects stem mainly from its ability to blunt the central sympathetic response. It also minimizes opioid-induced muscle rigidity, lessens postoperative shivering, causes minimal respiratory depression, and has hemodynamic stabilizing effects . At the level of the dorsal root neuron, α-2 agonists inhibit substance P release in the nociceptive pathway. α-2-Adrenergic agonists produce sedation, and the electroencephalographic studies confirm the increase in stage I and II sleep. Hypnosis is probably induced by activation of α-2-adrenoceptors in the locus coeruleus, which are coupled via G protein (pertussis toxin-sensitive), changing ion channel conduction . In addition, α-2-adrenergic receptors located at nerve endings may have a role in the analgesic effect of the drug by preventing norepinephrine release . Perioperative dexmedetomidine administration decreased the requirements for opioid or nonopioid analgesics both intraoperatively and postoperatively . In a previous study, Memis et al.  demonstrated that the addition of 0.5 μg/kg of dexmedetomidine to lidocaine for IVRA improved quality of anesthesia and postoperative analgesia. However, they failed to assess dexmedetomidine’s systemic effect through parenteral administration.
Sen et al.  have reached a similar conclusion to our study that the addition of lornoxicam to lidocaine in IVRA shortens sensory and motor block onset times, prolongs sensory and motor block recovery times, and improves tourniquet pain; in addition, it prolongs first analgesic requirement time and decreases total amount of analgesic requirements. The mechanism is not yet fully proved, but Reuben and Duprat  also explained that NSAIDs decrease the synthesis of inflammatory mediators and afferent nociceptive signals arising from the site of surgery. So, the effect of NSAID is assumed to be owing to COX-2 inhibition which is an inducible molecule . Furthermore, the pKa of lidocaine is 7.8 and the pH of the lidocaine solution alone is 6.7 but the pH of lornoxicam–lidocaine mixture is 7.6 . It is possible that alkalinization of lidocaine with lornoxicam (pH is 8.7) might increase the percentage of free base and thus improve the nerve penetration and thus explain the faster rate of onset of both motor and sensory blockade in the lornoxicam group. Lornoxicam might also produce a peripheral analgesic effect via NO–cGMP pathway and mediate the opening of K+ channels. Buritova and Besson  also suggested that lornoxicam shows antinociceptive effect in predominantly peripheral site.Many studies discussed the addition of 8 mg dexamethasone to lidocaine for IVRA prolonged the sensory and motor block recovery times after the tourniquet release and improved the quality of anesthesia while decreasing postoperative analgesic requirements. These are based on that the local application of corticosteroids block transmission in the nonmyelinated C fibers .
In this study, we observed that adding 8 mg dexamethasone to an IVRA solution provides better postoperative analgesia. In the local dexamethasone group, the mean analgesic consumption and the number of patients requesting analgesics were significantly less when compared with the lidocaine-only group.
| Conclusion|| |
On studying different additives to lidocaine in IVRA we found that dexmedetomidine and lornoxicam provide the best patient outcome regarding the onset and recovery of sensory and motor block also provide decrease in patients’ needs for analgesia than dexamethasone, which in turn is better than lidocaine alone.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Brill S, Middelton W, Brill G, Fisher A. Bier’s block; 100 years old and still going strong!. Acta Anesthesiol Scand 2004; 48:117–122.
Collins VJ. Principles of anesthesiology. 3rd edition. Philadelphia, PA: Lea & Febiger 1993. pp. 794–808.
Corpataux J-B, 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.
Rosenow DE, Albrechtsen M, Stolke D. A comparison of patient controlled analgesia with lornoxicarn versus morphine in patients undergoing lumbar disk surgery. Anesth Analg 1998; 86:1045–1050.
Karamanlioglu B, Turan A, Memis D, Kaya G, Ozata S, Ture M. Infiltration with ropivacaine plus lornoxicam reduces postoperative pain and opioid consumption. Can J Anaesth 2005; 52:1047–1053.
Kamibayashi T, Maze M. Clinical uses of alpha2-adrenergic agonists. Anesthesiology 2000; 93:1345–1349.
Sardesai SP, Patil KN, Sarkar A. Comparison of clonidine and dexmedetomidine as adjuncts to intravenous regional anesthesia. Indian J Anaesth 2015; 59:733–738.
] [Full text]
Bigat Z, Karsli B, Boztug N, Cete N, Ertok E. Comparison of the effect of low-dose ropivacaine and lidocaine in intravenous regional anesthesia: a randomized, double-blind clinical study. Clin Drug Investig 2005; 25:209–214.
Liu K, Hsu CC, Chia YY. Effect of dexamethasone on postoperative emesis and pain. Br J Anaesth 1998; 80:85–86.
Kopacz DJ, Lacouture PG, Wu D, Nandy P, Swanton R, Landau C et al.
The dose response and effects of dexamethasone on bupivacaine microcapsules for intercostal blockade (T9 to T11) in healthy volunteers. Anesth Analg 2003; 96:576–582.
Crews JC, Hilgenhurst G, Leavitt B, Denson DD, Bridenbaugh PO, Stuebing RC et al.
Tourniquet pain: the response to the maintenance of tourniquet inflation on the upper extremity in volunteers. Reg Anesth 1991; 16:314–317.
Gaumann DE, Brunet P, Jirounek P. Clonidine enhances the effects of lidocaine on C-fiber action potential. Anesth Analg 1992; 74:719–725.
Kalso EA, Pöyhiä R, Rosenberg PH. Spinal antinociception by dexmedetomidine, a highly selective α2-adrenergic agonist. Pharmacol Toxicol 1991; 68:140–143.
Dyck JB, Shafer SL. Dexmedetomidine pharmacokinetics and pharmacodynamics. Anaesth Pharmacol Rev 1993; 1:238–245.
Weinbroum AA, Ben-Abraham R. Dextromethorphan and dexmedetomidine: new agents for the control of perioperative pain. Eur J Surg 2001; 167:563–569.
Maze M, Regan JW. Role of signal transduction in anesthetic action: α2-adrenergic agonists. Ann N Y Acad Sci 1991; 625:409–422.
Sato J, Perl ER. Adrenergic excitation of cutaneous pain receptors induced by peripheral nerve injury. Science 1991; 251:1608–1610.
Scheinin H, Jaakola ML, Sjövall S, Ali-melkkila T, kaukinen S, Turunen J, kanto J. Intramuscular dexmedetomidine as premedication for general anesthesia. Anesthesiology 1993; 78:1065–1075.
Memiş D, Turan A, Karamanlioğlu B, Pamukcu Z, Kurt I. Adding dexmedetomidine to lidocaine for intravenous regional anesthesia. Anesth Analg 2004; 98:835–840.
Sen S, Ugur B, Aydın ON, Ogurlu M, Gezer E, Savk O. The analgesic effect of lornoxicam when added to lidocaine for intravenous regional anesthesia. Br J Anaesth 2006; 3:408–413.
Reuben SS, Duprat KM. Comparison of wound infiltration with ketorolac versus intravenous regional anesthesia with ketorolac for postoperative analgesia following ambulatory hand surgery. Reg Anesth 1996; 21:565–568.
Samad TA, Moore KA, Sapirstein A, Billet S, Allchome A, Poole S et al.
Interleukin-1 beta mediated induction of Cox-2 in the CNS contributes to inflammatory pain hypersensitivity. Nature 2001; 410:471–475.
Buritova J, Besson JM. Dose-related anti-inflammatory/analgesic effects of lornoxicam: a spinal c-Fos protein study in the rat. Inflamm Res 1998; 47:18–25.
Johansson A, Hao J, Sjölund B. Local corticosteroid application blocks transmission in normal nociceptive C-fibers. Acta Anaesthesiol Scand 1990; 34:335–338.
[Table 1], [Table 2], [Table 3], [Table 4]