Journal of Dr. NTR University of Health Sciences

ORIGINAL ARTICLE
Year
: 2021  |  Volume : 10  |  Issue : 1  |  Page : 8--14

Dexmedetomidine with 0.5% lignocaine enhances postoperative analgesia in patients undergoing upper limb orthopedic surgeries under intravenous regional anesthesia


Neena Jain, Shilpi Tada, Surendra Kumar Sethi, Veena Patodi, Kavita Jain, Deepak Kumar Garg 
 Department of Anaesthesiology, J. L. N. Medical College and Hospital, Ajmer, Rajasthan, India

Correspondence Address:
Dr. Surendra Kumar Sethi
FLat No. 202, Shiv Enclave, Civil Lines, Ajmer, Rajasthan
India

Abstract

Background: Intravenous regional anesthesia (IVRA) is an effective technique to provide analgesia for upper limb surgeries of shorter duration. Various adjuvants are used with local anesthetics to prolong the duration of analgesia. This study was undertaken to establish the effect of dexmedetomidine with lignocaine for IVRA in upper limb orthopedic surgeries. Materials and Methods: Sixty patients aged 15 to 65 years of either sex belonging to the American Society of Anesthesiologists (ASA) physical status I and II undergoing upper limb orthopedic surgeries were enrolled. Group L (n = 30) received lignocaine 2%, 7.5 mL diluted to total volume of 30 mL using normal saline while Group LD (n = 30) received lignocaine 2%, 7.5 ml with dexmedetomidine 1 μg/kg dilu ted to total volume of 30 mL using normal saline in IVRA. The onset of sensory and motor block, recovery of sensory and motor block, duration of analgesia, hemodynamics, and adverse effects were noted. Results: The mean onset time of sensory block was significantly faster in Group LD (3.50 ± 0.41 min) than Group L (6.67 ± 0.65 min); P < 0.05. Group LD had significantly earlier motor blockade (8.83 ± 0.96 min vs 11.9 ± 0.75 min); P < 0.05. The recovery of sensory block was also significantly prolonged in Group LD (61.64 ± 5.18 min) when compared to Group L (12.76 ± 4.41 min); P < 0.05. The recovery of motor block was significantly prolonged in Group LD (67.40 ± 4.92 min vs 15.25 ± 4.44 min); P < 0.05. The duration of analgesia was significantly prolonged in Group LD (79.22 ± 4.84 min) as compared to Group L (22.07 ± 4.16 min); P < 0.05. No significant hemodynamic changes and side effects were noted; P > 0.05. Conclusion: Dexmedetomidine (1 μg/kg) in IVRA leads to faster onset of sensory and motor block, prolonged duration of analgesia with better hemodynamic stability and minimal side effects.



How to cite this article:
Jain N, Tada S, Sethi SK, Patodi V, Jain K, Garg DK. Dexmedetomidine with 0.5% lignocaine enhances postoperative analgesia in patients undergoing upper limb orthopedic surgeries under intravenous regional anesthesia.J NTR Univ Health Sci 2021;10:8-14


How to cite this URL:
Jain N, Tada S, Sethi SK, Patodi V, Jain K, Garg DK. Dexmedetomidine with 0.5% lignocaine enhances postoperative analgesia in patients undergoing upper limb orthopedic surgeries under intravenous regional anesthesia. J NTR Univ Health Sci [serial online] 2021 [cited 2021 Jun 23 ];10:8-14
Available from: https://www.jdrntruhs.org/text.asp?2021/10/1/8/316308


Full Text



 Introduction



Regional blocks like brachial plexus block are more common nowadays for upper limb surgeries, but this requires expert skills with good anatomical knowledge and recognition of surface landmarks. However, regional blocks have their own drawbacks such as the delayed onset of analgesia, failure of block, patchy or inadequate analgesia and moreover they can lead to complications such as pneumothorax, nerve injuries, or inadvertent arterial puncture.

Intravenous regional anesthesia (IVRA) is a simple, safe, reliable, and effective technique to provide analgesia for upper limb surgeries with rapid onset and recovery, where no expertise or patient dependency is required so it seems to be safe and suitable for upper limb surgeries of shorter duration.[1] But IVRA has certain limitations such as very short postoperative analgesia and tourniquet pain with local anesthetics alone which causes discomfort to the patient. To overcome its limitations, adjuvants such as opioids (fentanyl, sufentanil, morphine, pethidine, and tramadol), nonsteroidal anti-inflammatory drugs (ketorolac, tenoxicam, and aspirin), and alpha-2 agonists (clonidine, dexmedetomidine) have been used in IVRA to hasten the onset and duration of analgesia.[2],[3],[4]

Lignocaine, an amide local anesthetic, prevents transmission of nerve impulses by inhibiting the passage of sodium ions through ion-selective sodium channels in the nerve membranes which slows the rate of depolarization such that the threshold potential is not reached; thus, the action potential is not propagated.[5] The ideal anesthetic agent for IVRA with low cardiovascular and central nervous system toxicity, lignocaine suits this criterion as bupivacaine in IVRA is associated with fatal cardiotoxicity,[6],[7],[8] whereas chloroprocaine in IVRA is not used after reports of hypersensitivity reactions and thrombophlebitis.[9] Although prilocaine also can be used in IVRA, lignocaine is most commonly used.[10]

Dexemedetomidine, an alpha-2 adrenoreceptor agonist, as an adjuvant to local anesthetics leads to a better quality of anesthesia with lesser intraoperative and postoperative analgesic requirements.[11] Dexmedetomidine with lignocaine has been associated with prolongation of the duration of the sensory blockade and postoperative analgesia.[12],[13],[14] Dexmedetomidine depresses nerve action potentials, especially in C fibers, by a mechanism independent of the stimulation of alpha-2 adrenergic receptors.

We hypothesized that dexmedetomidine (1 μg/kg) as an adjuvant to lignocaine in IVRA would provide a prolonged duration of analgesia with minimal hemodynamic changes and side effects. The present study was designed to evaluate the effects of adding dexmedetomidine with lignocaine on postoperative analgesia in IVRA as a primary objective while onset and recovery of sensory and motor block, hemodynamic changes, and side effects as secondary objectives.

 Materials and Methods



With due approval from institutional ethical committee, a prospective, double-blinded, randomized, controlled, comparative study was conducted on sixty adult patients of either sex, age between 15 and 65 years and weighing 35–60 kg belonging to American Society of Anesthesiologists (ASA) physical status I and II who were posted for various upper limb orthopedic surgeries. The patients who did not give consent, patients with an open wound, patients on analgesics, allergy to any of the study drugs, patients with a history of significant respiratory, cardiac, hepatic, renal, neurological, psychiatric, or neuromuscular disease, patients with any bleeding or thyroid disorder, sickle cell anemia, peripheral vascular disease were excluded from our study. [Figure 1]{Figure 1}

The patients were randomly allocated into two groups by computer-generated random number tables, and allocation concealment was done using the sequentially numbered closed opaque sealed envelope technique. Group L (n = 30) received lignocaine 2%, 7.5 mL diluted to total volume of 30 mL using normal saline and Group LD (n = 30) received lignocaine 2%, 7.5 mL with dexmedetomidine 1 μg/kg diluted to total volume of 30 mL using normal saline (final concentration of lignocaine 0.5%). To maintain double-blinding, the individual anesthesiologists who prepared the study drug, performed the procedure, and monitored the patient, as well as patient and surgeon, all, were unaware of group allocation.

All patients had undergone a thorough preanesthetic evaluation before surgery including history, physical examination, and routine investigations. All patients were kept nil per oral at least 8 h before surgery. A written informed consent was obtained from all the patients before the procedure after explaining the anesthetic technique. All equipment and drugs necessary for resuscitation and general anesthesia were kept ready. After the arrival of the patient in the operating room, an intravenous (IV) line was secured using an 18G cannula, and ringer lactate was started. Standard ASA monitoring was applied including noninvasive blood pressure (NIBP), pulse oximetry (SpO2), and electrocardiogram (ECG). The baseline values of heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), respiratory rate (RR), SpO2, and sedation score were recorded. Another 22G IV cannula was secured on the dorsum of the hand of the arm to be anesthetized and was elevated for 5 min to exsanguinate, a pneumatic tourniquet was placed around the upper arm, a “double cuff” tourniquet to increase the reliability of the technique. Initially, the proximal cuff was inflated to 100 mm Hg above systolic blood pressure,[15] and the arm was inspected for the disappearance of both radial pulse and pulse oximetry readings in the ipsilateral index finger for complete circulatory isolation. Then, the study drug was injected as per group allocation at a rate of 0.5 mL/sec in the hand to be operated with constant monitoring of vital parameters including pulse rate, blood pressure, respiratory rate, SpO2, and signs and symptoms of local anesthetic toxicity.

Sensory block was assessed by pinprick with 22G short beveled needle every 30 s, and the response was evaluated in the dermatomal sensory distribution of medial and lateral brachial cutaneous, ulnar (little finger, hypothenar eminence), median (thenar eminence, index finger), and radial (forearm and first webspace) nerves. Sensory block was graded as Grade 4 - Excellent, no pain; Grade 3- Minor pain, with no need for supplemental analgesics; Grade 2 - Moderate pain, needed supplemental analgesics; Grade 1- Severe pain (General anesthesia needed). The patients who required general anesthesia were excluded. The onset of sensory block is considered when grade 4 is achieved. Recovery of sensory block was defined as the time elapsed from tourniquet deflation to the recovery of sensations in all dermatomes, as determined by the pinprick test.

Motor block was assessed by asking the patient to flex and extend his fingers and wrist.[16] The onset of motor block was defined as the time elapsed from the injection of a drug to complete motor block (Grade 4) up to 15 min.[17] Motor block was graded as Grade 4- No movement; Grade 3- Movement only at the interphalangeal joint; Grade 2- Movement at interphalangeal and wrist joint; Grade 1- Movement at the interphalangeal, wrist and elbow joint. The onset of motor block is considered when grade 4 is achieved. Recovery of motor block was defined as the time elapsed from the tourniquet deflation to the movement of fingers, hand, and forearm comparable to the opposite arm.

After the onset of sensory and motor block, surgery was allowed to start. HR, SBP, DBP, MAP, and SpO2 were noted at 5, 10, 15, 25, 35, 45 min after injection of anesthetic and postoperatively after the release of tourniquet till complete recovery of sensory and motor block. When the patient complained of pain in the proximal tourniquet during surgery, the distal tourniquet was inflated to 100 mm Hg above systolic blood pressure, and the proximal tourniquet was deflated. During the procedure, the patient was continuously observed for signs and symptoms of local anesthetic toxicity and tourniquet pressure on the pressure gauge.

The tourniquet was not deflated before 25 min and not kept inflated for more than 90 min. At the end of the surgery, the distal tourniquet was deflated by the cyclic deflation-inflation technique. The distal tourniquet was deflated initially for 1 min, then re-inflated for 1 min, and again deflated and then removed. After tourniquet deflation, patients were continuously monitored for arrhythmias (bradycardia), blood pressure changes (hypotension), CNS side effects like dizziness, tinnitus, lightheadedness, or presence of metallic taste and nausea or vomiting.

Postoperative analgesia was assessed every 15 min according to the visual analog scale (VAS) in the first hour and later on every 1 h till the score was 4 or more. When VAS ≥4, tramadol 2 mg/kg was given IV slowly. Time elapsed from tourniquet release to the administration of the first rescue analgesia was considered as the duration of postoperative analgesia. Patients were followed up to 24 h postoperatively for the occurrence of side effects like edema, skin rash, hematoma, neurological injury and treated as needed. The time of starting of surgery (incision) and completion of surgery (skin closure) was noted. The duration of surgery was also noted.

Statistical analysis

The sample size calculation was based on the duration of postoperative analgesia in a previous study with a power of 80%. Using the table of tradeoffs for any combination of sample size (n) and power, a sample size of 10 in each group has the 80% power and 95% confidence interval. Hence, a sample size of 30 in each group was used in this study. The statistical analysis was carried out by Chi-square test for nominal categorical data such as gender and ordinal categorical data while unpaired student 'test/non parametric Mann-Whitney U test was used for intergroup comparison. The raw data were entered into a Microsoft Excel spreadsheet and were analyzed using standard statistical software SPSS statistical package version 18.0 (SPSS Inc., Chicago, IL, USA). P < 0.05 and < 0.0001 were taken as statistically significant and highly significant, respectively.

 Results



The demographic data including mean age, sex, weight, ASA physical status classification, and duration of surgery were comparable in both groups [Table 1].{Table 1}

The mean onset time of sensory block for Group L and LD were 6.67 ± 0.65 min and 3.50 ± 0.41 min, respectively, that was significantly earlier in Group LD as compared to Group L; (P < 0.0001). Similarly, the mean onset time of motor block for Group L and LD were 11.9 ± 0.75 min and 8.83 ± 0.96 min, respectively, that was also significantly earlier in Group LD as compared to Group L; (P < 0.0001) [Table 2].{Table 2}

The recovery of sensory block in Group L and LD were 12.76 ± 4.41 min and 61.64 ± 5.18 min, respectively, which was significantly prolonged in Group LD as compared to Group L; (P < 0.0001). Similarly, the recovery of motor block in Group L and LD were 15.25 ± 4.44 min and 67.40 ± 4.92 min, respectively, which was significantly prolonged in Group LD as compared to Group L (P < 0.0001). The mean duration of postoperative analgesia in Group L and LD were 22.07 ± 4.16 min and 79.22 ± 4.84 min, respectively i.e., significantly prolonged in Group LD as compared to Group L;(P < 0.0001) [Table 2].

No significant hemodynamic changes (HR, SBP, DBP, MAP) were noted in both groups; P > 0.05 [Figure 2],[Figure 3],[Figure 4],[Figure 5]. No significant adverse effects were observed in any of the patients in two groups during both intraoperative and postoperative periods except nausea or vomiting in 5 (16%) patients in Group L and 3 (10%) patients in Group LD; (P > 0.05) which were managed accordingly [Table 3].{Figure 2}{Figure 3}{Figure 4}{Figure 5}{Table 3}

 Discussion



The present study was designed with an aim to evaluate the effect of adding dexmedetomidine (1 μg/kg) to lignocaine (final concentration achieved was 0.5%) with a total volume of 30 mL in IVRA. We found satisfactory results regarding the efficacy of block and duration of analgesia in comparison with a similar study done by Jewlikar et al.,[18] who had used 30 mL of 0.5% lignocaine with or without 0.5 μg/kg dexmedetomidine.

In our study, the mean onset of sensory block was significantly shorter in the dexmedetomidine group when compared to the lignocaine alone group. Similarly, in Subramanya et al.[19] study, the onset of sensory block was around 2.5 min with dexmedetomidine, and when lignocaine alone was used the onset of sensory block was around 6 min. Slight early onset of the sensory blockade could be because of an increased volume of solution (40 mL) in their study in comparison to the volume used in our study. Gadre et al.[20] also found a significantly earlier onset of sensory block (4.73 ± 0.38 min) with dexmedetomidine in comparison to lignocaine alone (6.93 ± 0.86 min) when used in IVRA. Although they had used a total volume of 40 mL and found a significantly faster onset in the dexmedetomidine group, but the time of onset was slightly faster in our study which could be due to a lower dose (0.5 μg/kg) of dexmedetomidine used in their study.

In our study, the mean onset time of motor block was significantly shortened in the dexmedetomidine group. Our study results are comparable with Jewlikar et al.[18] study in which onset of motor block (15.33 ± 2.25 min) was significantly earlier in lignocaine with dexmedetomidine group. Similarly, Shilpashri et al.[21] found a significantly faster onset of motor block in dexmedetomidine group (13.63 ± 1.54 min) when compared to lignocaine only group (18.07 ± 1.26 min); however, we have observed faster onset of motor block in our study that could be explained on the basis of dexmedetomidine's drug dosage used.

The mean recovery time of both sensory and motor block was significantly prolonged in the dexmedetomidine group. Jewlikar et al.[18] reported a significantly prolonged recovery of sensory block and motor block (22.27 ± 6.66 min and 27.10 ± 6.79 min) in lignocaine with dexmedetomidine (0.5 μg/kg) group. Again, dexemedetomidine in a higher dose (1 μg/kg) resulted in more delayed recovery to around 60 min in our study which could be beneficial in certain situations.

The mean duration of postoperative analgesia was significantly prolonged in Group LD as compared to Group L. Jewlikar et al.[18] found the significantly prolonged duration of postoperative analgesia in lignocaine with dexmedetomidine group (38.43 ± 13.85 min) which concurs with our study. Subramanya et al.[19] also reported that IVRA with lignocaine after adding dexmedetomidine (0.5 μg/kg) results in prolonged postoperative analgesia (30.16 ± 4.04 min) in our study. Shilpashri et al.[21] and Gadre et al.[20] also found a prolonged duration of postoperative analgesia after using dexmedetomidine with lignocaine supporting our study. A higher dose of dexmedetomidine (1 μg/kg) justifies our more prolonged duration of postoperative analgesia (79.22 ± 4.84 min). Dexmedetomidine depresses nerve action potentials, especially in C fibers, by a mechanism independent of the stimulation of alpha-2 adrenergic receptors. This mechanism accounts for the strengthening of the local anesthetic block achieved by perineural administration of the drug and could be the reason for the effect observed in our study. Also, alpha-2 receptors located at nerve endings may have a role in the analgesic effects of the drug by preventing norepinephrine release.[11],[12],[13],[14]

As far as hemodynamic parameters are concerned, intraoperative mean HR, SBP, DBP, and MAP were not significantly different in Group LD and Group L at different time intervals. Similar trends of hemodynamic parameters were found in studies carried out by Jewlikar et al.[18] and Shilpashri et al.[21] No significant side effects were observed in any patient of both groups except only a few cases of nausea and vomiting. Dexmedetomidine at a dose of 1 μg/kg with lignocaine in IVRA had no bradycardia, hypotension, and respiratory depression which favors its use as an adjuvant in terms of better hemodynamic stability with minimal side effects.

The main limitations of our study was tourniquet pain, surgeries performed under IVRA were not versatile, could not perform open wound surgery in IVRA, patients with ASA physical status III and above were not taken in our study, and patients with sickle cell anemia in whom tourniquet use is prohibited were not studied.

 Conclusion



We concluded that dexmedetomidine (1 μg/kg) significantly improved the duration of postoperative analgesia when used as an adjuvant to lignocaine in IVRA. In addition, dexmedetomidine also leads to significantly faster onset of sensory as well as motor block, prolonged recovery of both sensory and motor block with better hemodynamic stability, and minimal side effects which favors its use as a safe and effective adjuvant with lignocaine in IVRA.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Brown EM, McGriff JT, Malinowski RW. Intravenous regional anaesthesia (Bier block): Review of 20 years' experience. Can J Anaesth 1989;36:307-10.
2Johnson CN. Intravenous regional anesthesia: New approaches to an old technique. CRNA 2000;11:57-61.
3Choyce A, Peng P. A systematic review of adjuncts for intravenous regional anesthesia for surgical procedures. Can J Anaesth 2002;49:32-45.
4Chatrath V, Sharan R, Soni S, Kansal C. Comparative evaluation of adding clonidine v/s dexmedetomidine during Bier's block in upper limb orthopaedic surgeries. Int J Med Res Prof 2015;1;1-7.
5Raj PP, Garcia CE, Burleson JW, Jenkins MT. The site of action of intravenous regional anesthesia. Anesth Analg 1972;51:776-86.
6Davies JAH, Gill SS, Weber JCP. Intravenous regional anaesthesia using bupivacaine. Anesthesia 1981;36:1059-60.
7Heath ML. Deaths after intravenous regional anaesthesia. Br Med J 1982;285:913-4.
8Albright GA. Cardiac arrest following regional anaesthesia with etidocaine or bupivacaine. Anesthesiology 1979;51:285-7.
9Pitkanen MT, Suzuki N, Rosenberg PH. Intravenous regional anaesthesia with 0.5% prilocaine or 0.5% chloroprocaine. A double-blind comparison in volunteers. Anaesthesia 1992;47:618-9.
10Bader AM, Concepcion M, Hurley RJ, Arthur GR. Comparison of lidocaine and prilocaine for intravenous regional anesthesia. Anesthesiology 1988;69:409-12.
11Abdallah FW, Brull R. Facilitatory effects of perineural dexmedetomidine on neuraxial and peripheral nerve block: A systematic review and meta-analysis. Br J Anaesth 2013;110:915-25.
12Memis D, Turan A, Karamanloglu B, Pamukçu Z, Kurt I. Adding dexmedetomidine to lidocaine for intravenous regional anesthesia. Anesth Analg 2004;98:835-40.
13Mizrak 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;164:242-7.
14Nilekani E, Menezes Y, D'souza SA. A study on the efficacy of the addition of low dose dexmedetomidine as an adjuvant to lignocaine in intravenous regional anaesthesia (IVRA). J Clin Diag Res 2016;10:UC01-5.
15Atanassoff PG, Ocampo CA, Bande MC, Hartmannsgruber MW, Halaszynski TM. Ropivacaine 0.2% and lidocaine 0.5% for intravenous regional anesthesia in outpatient surgery. Anesthesiology 2001;95:627-31.
16Sardesai SP, Patil KN, Sarkar A. Comparison of clonidine and dexmedetomidine as adjuncts to intravenous regional anaesthesia. Indian J Anaesth 2015;59:733-8.
17Peng PW, Coleman MM, McCartney CJ, Krone S, Chan VW, Kaszas Z, et al. Comparision of anesthetic effect between 0.375% ropivacaine versus 0.5% lidocaine in forearm intravenous regional anesthesia. Reg Anesth Pain Med 2002;27:595-9.
18Jewlikar S, Suryawanshi A. Comparative study of 0.5% lignocaine with dexmedetomidine and 0.5% lignocaine in intravenous regional anesthesia. MedPulse Int J Anesth 2017;3:66-70.
19Subramanya V, Kapinigowda ST, Math AT, Chennaiah VB. Dexmedetomidine as an adjuvant for intravenous regional anesthesia in upper limb surgeries. Anesth Essays Res 2017;11:661-4.
20Gadre SP, Gulzar U. Comparison of effects of lignocaine versus lignocaine with dexmedetomidine in Bier's block: A prospective double blinded study. Indian J Res 2017;6:612-5.
21Shilpashri AM, Kavya KG, Choudhury PR. Dexmedetomidine as an adjunct to 0.5% lignocaine for intravenous regional anaesthesia for upper limb surgeries. J Evid Based Med Healthcare 2015;2:5171-8.