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Table of Contents  
Year : 2022  |  Volume : 16  |  Issue : 3  |  Page : 353-359  

Comparing efficacy of intravenous dexmedetomidine and lidocaine on perioperative analgesic consumption in patients undergoing laparoscopic surgery

Department of Anesthesiology, Shri Ram Murti Smarak Institute of Medical Sciences, Bareilly, Uttar Pradesh, India

Date of Submission27-Jul-2022
Date of Decision04-Sep-2022
Date of Acceptance13-Sep-2022
Date of Web Publication09-Dec-2022

Correspondence Address:
Dr. Ashita Mowar
D-02 Doctor's Residence, Shri Ram Murti Smarak Institute of Medical Sciences, Bareilly - 243 202, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aer.aer_121_22

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Background: Perioperative pain management is a major challenge for anaesthesiologists. IV lidocaine and dexmedetomidine have been utilised for peri-operative pain management. Aims and Objectives: To analyse the effects of intraoperative intravenous lignocaine/dexmedetomidine on pain relief, opioid consumption, peri-operative hemodynamic and side-effect profiles/ unique interactions in patients undergoing laparoscopic surgeries. Materials and Methods: Prospective, interventional, single-centric, double-blind, randomised, active-controlled, Helsinki protocol-compliant clinical study was conducted on 90 ASA I/II class patients aged 18-60 yrs. This Patients were block-randomised to Group-L (2% Lignocaine), Group-D (dexmedetomidine) and Group C (Control/Placebo/ 0.9% normal saline). Hemodynamic were noted at pre-defined time frames intra-/post-operatively. Post-operative VAS score and Richmond Agitation Sedation Score monitoring was done. Results: Demographic parameters of were comparable. Mean intra-operative fentanyl consumption amongst the three groups were 20.5 ± 20.05 mcg, 26.5 ± 17.57 mcg and 46.83 + 21.31 mcg (Group-L, Group-D, Group-C; P value Group-L vs Group-D:0.22, Group L/D vs Group C: <0.0001). Group-D exhibited the lower heart rates and MAP (P < 0.05). Extubation- First rescue analgesic phase was comparable for the Group-C and Group-L (59.17 ± 46.224 min vs 61.64 ± 53.819 min) and significantly greater in Group-D (136.07 + 55.350 min; P < 0.0001). Conclusion: Both Dexmedetomidine and lignocaine can be useful intra-operative pain relief adjuncts. Dexmedetomidine delayed First rescue analgesic and total analgesic consumption more than lignocaine. Dexmedetomidine patients exhibited bradycardia intraoperatively more than the other groups. we recommend, Dexmedetomidine in the intra-operative phase and lignocaine in the post-operative phase can be an alternative in patients who are poor candidates for post-operative opioids/sedation/ contraindicated regional anaesthesia regimes.

Keywords: Dexmedetomidine, enhanced recovery after surgery protocol, intravenous lignocaine, opioid consumption, postoperative analgesia

How to cite this article:
Singh V, Pahade A, Mowar A. Comparing efficacy of intravenous dexmedetomidine and lidocaine on perioperative analgesic consumption in patients undergoing laparoscopic surgery. Anesth Essays Res 2022;16:353-9

How to cite this URL:
Singh V, Pahade A, Mowar A. Comparing efficacy of intravenous dexmedetomidine and lidocaine on perioperative analgesic consumption in patients undergoing laparoscopic surgery. Anesth Essays Res [serial online] 2022 [cited 2023 Feb 3];16:353-9. Available from:

   Introduction Top

Perioperative pain management has been a major challenge for anesthesiologists, and there have been persistent efforts to bring out the best possible analgesic technique with the least side effects.[1]

The popularity of laparoscopic surgeries has grown manifold, owing to minimal surgical scars, short hospital stays, early ambulation, and rapid recovery.[2] The belief that minimally invasive surgeries result in lesser pain has been challenged.[3] Inadequate intraoperative and postoperative pain relief is associated with undesirable side effects resulting in chronic persistent pain, delayed recovery, and rarely opioid dependence.[4] Concern about opioid risks, especially in the postoperative period, has led to an increased interest in the use of nonopioid analgesic adjuncts.

Drugs of potential interest such as intravenous (i.v.) lignocaine and dexmedetomidine have been administered both intra and/or postoperatively to decrease perioperative pain and improve other outcomes.[5] Lignocaine has analgesic, anti inflammatory, and anti hyperalgesia properties.[6] Several studies have demonstrated that perioperative lidocaine infusion reduces postoperative pain intensity and opioid consumption.[2] Ease of availability, cost effectiveness, simplicity of administration, safety, and analgesic action make lignocaine an attractive option.[6] Dexmedetomidine is a highly selective and specific α2 adrenoceptor agonist with useful analgesic, sedative, anxiolytic, and sympatholytic properties.[7] I.V. dexmedetomidine has gained immense popularity owing to its efficacy as an analgesic adjuvant, translating into reduced opioid consumption.[8] Intraoperative dexmedetomidine and lignocaine also confirm the enhanced recovery after surgery protocol advocating the reduction/ elimination of opioid use.[9]

While numerous studies have analyzed i.v. lignocaine and dexmedetomidine versus placebo regarding postoperative analgesia and outcomes, researches and evidence in the context of minimally invasive surgeries regarding adverse effect profile, postoperative analgesic requirement, perioperative analgesia, anesthesia recovery, and opioid requirements are always welcome. Our study was conducted to analyze the effects of intraoperative i.v. lignocaine and dexmedetomidine on pain relief, intra- and postoperative analgesic (opioid) consumption, and effects of these infusions on intraoperative hemodynamic and to evaluate the side effect profiles/unique interactions with intraoperative conditions such as pneumoperitoneum in patients undergoing laparoscopic surgeries.

   Materials and Methods Top

This prospective, interventional, single-centric, double-blind, randomized, active-controlled, Helsinki protocol-compliant clinical study was registered with the Clinical Trials Registry of India (CTRI/2021/04/032968) and was conducted after written informed consent and approval from the Institutional Ethical Committee (SRMSIMS/ECC/2020-21/023). A total of 90 patients aged 18–60 years of either sex with the American Society of Anesthesiologists (ASA) physical status classes I and II undergoing elective laparoscopic surgeries were enrolled in the study. Exclusion criteria included patients refusal to be part of research, History of hypersensitivity to the drugs being evaluated, body mass index (BMI) more than 30 kg.m−2, parturient, significant/major comorbidities such as uncontrolled hypertension, congestive heart failure, myocardial infarction in the past 6 months, heart block, fixed cardiac output lesions, chronic liver/kidney illnesses, and chronic use of opioids/opioid addiction, steroids and inability to comprehend postoperatively the pain assessment scale/neuropsychiatric disorders.

Enrollment of patients commenced in May 2021 and completed in May 2022. Patients were block randomized (computer generated) to Group L (2% preservative-free lignocaine), Group D (dexmedetomidine), and Group C (control/placebo/0.9% normal saline). Concealment method comprised sequentially numbered, sealed, and opaque envelopes. The study was participant, outcome assessor blinded.

All patients were familiarized about 10-point Visual Analog Scale (VAS) during the preanesthetic visit. In the operating room, all standard monitors were applied and patients were premedicated with i.v. glycopyrrolate 4 μ−1 and midazolam 0.03−1. In Group D, dexmedetomidine loading dose (1 μ−1) was administered over 10 min followed by i.v. infusion at 0.5 μ−1 while Group L received 1.5−1 lidocaine hydrochloride 2% (400 mg/20 mL) slow bolus followed by i.v. infusion of 2−1 lidocaine. Infusions of study drugs were discontinued upon release of pneumoperitoneum. Subsequent to initial bolus, anesthetic induction with fentanyl (2 μ−1) and propofol (2−1) till the loss of verbal command was commenced. Endotracheal intubation (ETI) with vecuronium (0.1−1) was performed. Preemptive i.v. paracetamol 1000 mg was administered post-ETI and was continued 8th hourly. Anesthesia was maintained with oxygen/nitrous oxide/sevoflurane mixture and neuromuscular monitor-guided intermittent boluses of 0.001−1 of vecuronium to maintain neuromuscular blockade. Residual neuromuscular blockade was reversed with i.v. neostigmine 0.05−1 + glycopyrrolate 0.005−1. Following successful tracheal extubation, all patients were transferred to postanesthesia care unit (PACU).

Intraoperative opioid requirement was recorded. Heart rate (HR) and mean arterial pressure (MAP) were noted at baseline, induction, tracheal intubation, before pneumoperitoneum, at 15 minute intervals thereafter till end of surgery. Hypotension (20% MAP fall below baseline) was managed with crystalloid boluses and mephentermine 3–6 mg. Bradycardia (HR <50 beats/min) was managed with i.v. atropine 0.6 mg. For >20% rise in HR or MAP above baseline intraoperatively, rescue analgesic (i.v. fentanyl: 0.5 μ−1) was given and if nonresponding i.v. esmolol (0.5−1) bolus was given.

The time from skin incision to completion of skin closure was noted and the duration of surgery was calculated in minutes. The total duration of anesthesia from the time of commencement of infusion till tracheal extubation was calculated in minutes (min).

Postoperatively; pulse oximetry, HR, mean blood pressure along with VAS score monitoring and sedation assessment via “Richmond Agitation Sedation Score (RASS)” monitoring was done. VAS (0–10 scale with no pain [VAS = 0], mild [VAS = 1–3], moderate [VAS = 4–7], and severe [VAS = 7–9]) and RASS assessment for the patients was assessed immediately following extubation and in PACU. In PACU, the assessment was done on arrival and at 15 min, 30 min, and 1 h followed by assessment hourly till 4 h after surgery and then at 8 h, 12 h, and 24 h postoperatively. Tramadol 1.5−1 slow i.v. was given as a rescue analgesic if the VAS exceeded 4. The time to first rescue analgesic and the total number and cumulative dosage of rescue analgesics received by the patient over 24 h were noted.

Statistical analysis

Sample size calculation was estimated on a mean value of a study by Cho et al.[8] The authors reported that the mean ± standard deviation (SD) of VAS score in the control group was 7 ± 2 and the dexmedetomidine group was 5 ± 3. Twenty-five subjects in each group were required with P = 0.05 and a power of 80%, but considering dropout/cancellations and intraoperative changes in surgical plan, the sample size was determined to be 30 subjects per group. The formula used for sample size calculation was N = (r + 1) (Z1−α/2 + Z1−β)2 σ2/rΔ2. In this formula r = sample size ratio of two groups, Z1−α/2 = two sided Z value (e.g., Z = 1.96 for 95% confidence interval), Z1−β = power, σ= standard deviation and Δ= difference between the two means. Data were expressed as mean ± SD or as number unless otherwise indicated. Statistical analyses were performed with SAS 9.2 (SAS Institute, USA) and Epi Info software. A repeated measures analysis of variance was performed to compare VAS pain scores, HR, SBP, DBP, and recovery profiles. One-way analysis of variance was used to compare quantitative parameters whereas Fischer's exact test was used to compare qualitative parameters.

   Results Top

Ninety ASA physical status classes I and II patients aged 18–60 years undergoing laparoscopic surgery were enrolled in the study. The CONSORT flow diagram [Figure 1] depicts the flow of participants among the three groups. Demographic variables reveal that both the groups were comparable with respect to age, height, weight, BMI, ASA PS classification, and sex composition [Table 1].
Figure 1: CONSORT diagram

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Table 1: Demographic profile

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Intraoperative fentanyl consumption (apart from the initial bolus) was analyzed among the three groups. The mean intraoperative fentanyl consumption was 20.5 ± 20.05 μg, 26.5 ± 17.57 μg, and 46.83 ± 21.31 μg for lignocaine, dexmedetomidine, and control groups. While the difference between the lignocaine and dexmedetomidine groups was not significant statistically (P = 0.22), lignocaine/dexmedetomidine versus control indicated a highly significant difference (P < 0.0001).

The HR and MAP were recorded at baseline, induction, tracheal intubation, immediately prior and subsequent to pneumoperitoneum, 15 min, 30 min, 45 min, 60 min, 75 min, 90 min, 105 min, 120 min and post-extubation [Figure 2] and [Figure 3]. All subjects had comparable baseline HR and MAP (P = 0.565, 0.231). The dexmedetomidine group showed the lowest HR at all time points and significant intergroup difference existed (P < 0.05). The dexmedetomidine group also exhibited significantly lower MAP compared to the control group in all time frames (P = 0.02, <0.0001, 0.0018, 0.0147, 0.0071, 0.02, 0.02, 0.0094, 0.0018, 0.0167). No significant difference was observed between the lignocaine and dexmedetomidine groups and the lignocaine-control group in majority of the time frames (P > 0.05). Intragroup trends were also analyzed. While the control group exhibited a response to laryngoscopy/intubation, this response was not significant in the lignocaine/dexmedetomidine group. There was no significant inter-group difference in terms of blood SpO2.
Figure 2: Heart rate trends between the study groups

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Figure 3: Mean arterial trends between the groups

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Subsequently, the patients of all the three groups were monitored postoperatively and were analyzed in terms of total analgesic (tramadol) requirement guided by the individual VAS scores at various endpoints over the next 24 h, extubation-first rescue analgesic time (EFRD) requirement interval, and level of sedation/residual sedation in the postoperative phase guided by the RASS. EFRD phase was comparable for the control and lidocaine groups (59.17 ± 46.224 vs. 61.64 ± 53.819 min) while the EFRD phase was significantly greater in the dexmedetomidine group (136.07 ± 55.350 min) (P < 0.0001). The total rescue tramadol consumption in the first 24-h postoperative period was significantly lower in the dexmedetomidine group (122.52 ± 57.827 mg) versus the control/lignocaine group (178 ± 79.449 mg/173.25 ± 65.459) (P = 0.017) [Table 2].
Table 2: Total rescue analgesic (tramadol) consumption in 24 postoperative hours (mg)

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VAS was analysed at predefined endpoints i.e. at extubation, In PACU, at 15 min, 30 min, 1 h, 2 h, 3 h, 4 h, 8 h, 12 h, and 24 h. Although VAS scores of all patients were sub-4 till 2 h; patients of the dexmedetomidine group exhibited significantly low mean VAS scores compared to the lignocaine/control group (P value at VAS-extubation, PACU, 15 min, 30 min, 1 h: <0.0001/0.0166, <0.0001/0.0012, <0.0001/0.0029, <0.0001/0.0001, 0.0004/0.001). The P values are not a ratio but instead indicate values at mentioned time points in lignocaine and control group and have been exhibited in this manner for sake of better comparison. Subsequently at no time point, the P value between the three groups was significant (P > 0.05) [Figure 4].
Figure 4: Mean VAS score trends among the groups. VAS: Visual Analog Scale

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Residual sedation was evaluated via RASS and was assessed at the same time frame as VAS evaluation. Number of patients with sub-0 RASS; immediately post-extubation, in PACU and at 15 min, 30 min, and 1 h were 39, 17, 10, 03, and 01, respectively, with predominant contributor being the dexmedetomidine group (20/39, 11/17, 6/10, 03/03, and 01/01). None of the patients exhibited a below-0 RASS from 2-h monitoring frame onward.

While most patients were free of any significant side effects, the most common adverse effect observed was bradycardia in nine patients (dexmedetomidine [7/9], lidocaine (1/9) and control (1/9)). Three of these nine patients responded to a single dose of atropine with no further intervention required, rest (6/9) of patients responded to lowering insufflation pressure. Next most common side-effect was postoperative nausea-vomiting in 5 patients of the control group. A single patient of the lignocaine group exhibited intraoperative premature ventricular complexes which did not require any intervention (resolved by reduction of insufflation pressure).

   Discussion Top

Approximately 13 million minimally invasive surgeries are performed worldwide.[10] The preferences come in the light of multitude of advantages offered, namely better cosmesis, early and enhanced postoperative recovery, reduced blood loss, and fewer complications.[11] Patients undergoing laparoscopic surgeries may experience severe pain with pain scores drifting rightward on the pain measurement scales translating into a sizeable requirement of NSAIDs and opioid analgesics, which have been the mainstays in perioperative pain regimes. Regional anesthetic techniques have provided a much-needed relief to the pain physicians. However, not all patients are candidates for the regional analgesic pain models resulting in renewed interest in perioperative usage of drugs with notable analgesic potency such as lignocaine, dexmedetomidine, and pregabalin in allaying the perioperative pain while simultaneously reducing the use of narcotics and realize the long-cherished dream of an opioid-free anesthesia world with enhanced and early recovery after surgery.

Our research revealed a significant reduction in intraoperative fentanyl requirement with IV lignocaine/dexmedetomidine over placebo (20.5 ± 20.05 mcg, 26.5 ± 17.57 mcg, and 46.83 ± 21.31 mcg for the lignocaine, dexmedetomidine, and control groups, respectively). EFRD duration was similar in the patients of the control and lignocaine groups (59.17 ± 46.224 min vs. 61.64 ± 53.819 min). A significantly longer EFRD was observed in patients receiving dexmedetomidine (136.07 ± 55.350 min) (P < 0.0001). Reduction in the intraoperative analgesic requirement is due to the fact that i.v. lignocaine possesses analgesic, antihyperalgesic, and anti-inflammatory properties. Lignocaine exhibits a significant reduction in sensitivity and activity of spinal cord neurons (central sensitization) while bringing down N-methyl-D-aspartate receptor-mediated postsynaptic depolarization while alpha-2 adrenergic receptor agonist activity at spinal and supraspinal level (dorsal horn and locus coeruleus) accounts for the analgesic and sympatholytic activity of dexmedetomidine.[12],[13]

Ghimire et al. compared i.v. lignocaine versus placebo and confirmed opioid-sparing qualities of lignocaine in patients undergoing laparoscopic surgeries. The time for first perception of pain was more in the lignocaine group (15–30 min) over placebo.[4] Staikou et al. compared intraoperative i.v. lidocaine versus placebo and concluded i.v. lignocaine offered no benefit over placebo in postoperative analgesia.[14] Both these studies had similar findings as ours where while lignocaine offered some degree of analgesia in the postoperative period, it was not significant compared to placebo/saline. Anis et al. compared intraoperative lignocaine versus dexmedetomidine to conclude higher sedation score and higher/comparable pain scores and analgesic requirements in the dexmedetomidine group.[6] We attribute the longer EFRD interval in dexmedetomidine and comparable EFRD interval in lignocaine and placebo to the elimination of half-lives of i.v. lignocaine and dexmedetomidine. While the elimination half-life in healthy adults is 2.1–3.1 h in dexmedetomidine, the corresponding value in lignocaine is less ranging from 6 min after a bolus till up to 90–120 min after infusions <12 h. Relatively, similar EFRD duration in the control group was possibly due to higher (almost double) intraoperative administration of Fentanyl.[15],[16],[17],[18]

VAS was analysed at predefined endpoints. Of the three groups, the dexmedetomidine group had a significantly lower mean VAS score (P < 0.5) compared to the other two groups on extubation, in PACU, 15 min, 30 min, 45 min, and 1 h post-extubation. The initial lower pain scores in the control group can be attributed possibly to the residual fentanyl effect and the variability in the extent of tissue damage and degree of inflammatory response. Equivalent VAS scores post 2 h can be attributed to the context-sensitive half-life of dexmedetomidine (20, 50, and 55 min after an infusion of 1, 2, and 3 h infusion with a ceiling effect beyond 3-h infusion period). This may account for lower total 24-h tramadol consumption in the dexmedetomidine group over the lignocaine or control group (122.52 ± 57.827 mg vs. 178 ± 79.449 mg/173.25 + 65.459) (P = 0.017), despite comparability in terms of the number of tramadol doses administered (dexmedetomidine vs. lignocaine vs. control: 1.60 ± 0.70 vs. 2.06 ± 0.68 vs. 2.10 ± 0.738; P = 0.063). These findings of ours corroborate with Staikou et al. whose research proposed no significant difference in pain scores on coughing/movement but only at rest and Martin et al. who revealed no significant difference in pain scores at rest or movement between the control and lignocaine groups in total hip replacement patients who received intraoperative lignocaine at 24 h, 48 h, or 3 months.[14],[19] Insler et al. found no effect of lignocaine infusion in patients undergoing coronary artery bypass graft surgery in terms of pain scores. However, all the mentioned studies do indicate a reduction in opioid consumption in the postoperative period.[20]

These findings reveal the shorter residual analgesic action of i.v. lignocaine and lesser potency of i.v. lignocaine as an analgesic.

In terms of hemodynamics (HR and MAP), dexmedetomidine and lignocaine blunted the sympathetic response to laryngoscopy and intubation which was not abolished in the control group. Approximately 8/30 patients who were administered dexmedetomidine exhibited a rise in the MAP after initial bolus administration that can be accounted by the stimulation of the postsynaptic alpha-2 receptors in vascular smooth muscles that resulted in vasoconstriction.[21]

Subsequent to creation of the pneumoperitoneum, while no difference was seen between the three groups in terms of MAP, the dexmedetomidine group exhibited a significantly lower HR. The effect of dexmedetomidine on hemodynamics is due to the stimulation of the presynaptic alpha-2 receptors resulting in cessation of the noradrenaline from the peripheral nerve endings.[21]

Large doses/rapid administration/young volunteers with a high vagal tone may exhibit bradycardia upon administration or while the initiation of pneumoperitoneum.[13] This was the most common adverse event seen in our research, and the major contributors to this were patients from the dexmedetomidine group (7/9). This is due to the combined effect of attenuation of catecholamine release following sympatholysis by dexmedetomidine and sudden stretch while insufflation. All these patients were administered a single dose of atropine, and the procedure continued uneventfully. This highlights the need for caution and awareness while administering dexmedetomidine in laparoscopic surgeries

Residual sedation following extubation was graded according to RASS at pre-defined end-points (immediately after extubation, in PACU, at 15, 30 min, 1 h, 2 h, 3 h, 4 h, 8 h, 12 h, and 24 h post-extubation). Patients from the dexmedetomidine group were the major contributors to the sub-0 RASS community. Even though these patients were sedated, none of them had respiratory depression. While most studies report an earlier emergence and no delay in awakening, the mean awakening time in our study was significantly higher in the dexmedetomidine group as compared to the lidocaine/control group (13.74 ± 3.70 vs. 5.76 ± 2.88 vs. 8.2 ± 4.77 min). Despite a prolonged time to awaken exhibited by patients of dexmedetomidine group, it cannot be termed as delayed awakening as per accepted definition of delayed awakening. It is proposed that dexmedetomidine-induced sedation resembles normal, arousable sleep and is termed cooperative sedation. However, the authors believe this can be hazardous in patients who are poor candidates for postoperative sedation and in conditions where postoperative monitoring facilities are not up to the acceptable standards, especially in resource-limited settings. Similar findings were reported by Menshawi and Fahim.[13] Tufanogullari et al. and Kang et al. reported an earlier emergence and decreased PACU stay in the dexmedetomidine group. Patel et al. reported significant sedation at 30-min postextubation.[22],[23],[24]


The limitations of this study were small sample size, single-centric study, and inability to measure plasma levels of individual drugs. Furthermore, our study was conducted primarily in ASA physical status classes I and II patients, and further research is needed in patients with higher ASA class so that true and universal assessment of the two study drugs can be done.

   Conclusion Top

Both dexmedetomidine and lignocaine can be useful adjuncts to opioids in patients undergoing laparoscopic surgeries. Dexmedetomidine extends its opioid-sparing effect than lignocaine in the postoperative period in terms of delayed first rescue analgesic and total analgesic consumption. However, awareness should be exercised by the anesthesiologist when dexmedetomidine is administered in laparoscopic surgeries, owing to the tendency of bradycardia intraoperatively and in patients who are poor candidates for postoperative sedation or in resource-limited settings where monitoring facilities are deficient. In such patients, dexmedetomidine in the intraoperative phase and lignocaine in the postoperative phase can be an alternative.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Shaikh SI, Dattatri R. Dexmedetomidine as an adjuvant to hyperbaric spinal bupivacaine for infra-umbilical procedures: A dose related study. Anaesth Pain Intensive Care 2014;18:180-5.  Back to cited text no. 1
Li J, Wang G, Xu W, Ding M, Yu W. Efficacy of intravenous lidocaine on pain relief in patients undergoing laparoscopic cholecystectomy: A meta-analysis from randomized controlled trials. Int J Surg 2018;50:137-45.  Back to cited text no. 2
Ekstein P, Szold A, Sagie B, Werbin N, Klausner JM, Weinbroum AA. Laparoscopic surgery may be associated with severe pain and high analgesia requirements in the immediate postoperative period. Ann Surg 2006;243:41-6.  Back to cited text no. 3
Ghimire A, Subedi A, Bhattarai B, Sah BP. The effect of intraoperative lidocaine infusion on opioid consumption and pain after totally extraperitoneal laparoscopic inguinal hernioplasty: A randomized controlled trial. BMC Anesthesiol 2020;20:137.  Back to cited text no. 4
Ventham NT, Kennedy ED, Brady RR, Paterson HM, Speake D, Foo I, et al. Efficacy of intravenous lidocaine for postoperative analgesia following laparoscopic surgery: A meta-analysis. World J Surg 2015;39:2220-34.  Back to cited text no. 5
Anis SG, Samir GM, ElSerwi HB. Lidocaine versus dexmedetomidine infusion in diagnostic laparoscopic gynecologic surgery: A comparative study. Ain Shams J Anaesthesiol 2016;9:508-16.  Back to cited text no. 6
Gupta M, Gupta P, Singh DK. Effect of 3 different doses of intrathecal dexmedetomidine (2.5 μg, 5 μg, and 10 μg) on subarachnoid block characteristics: A prospective randomized double blind dose-response trial. Pain Physician 2016;19:E411-20.  Back to cited text no. 7
Cho K, Lee JH, Kim MH, Lee W, Lim SH, Lee KM, et al. Effect of perioperative infusion of lidocaine versus dexmedetomidine on reduced consumption of postoperative analgesics after laparoscopic cholecystectomy. Anesth Pain Med 2014;9:185-92.  Back to cited text no. 8
Kaye AD, Chernobylsky DJ, Thakur P, Siddaiah H, Kaye RJ, Eng LK, et al. Dexmedetomidine in enhanced recovery after surgery (ERAS) protocols for postoperative pain. Curr Pain Headache Rep 2020;24:21.  Back to cited text no. 9
iData Research. Over 13 Million Laparoscopic Procedures Are Performed Globally Every Year. Available from: y-every-year. [Last accessed on 2022 Jul 23].  Back to cited text no. 10
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Menshawi MA, Fahim HM. Dexmedetomidine versus lidocaine as an adjuvant to general anesthesia for elective abdominal gynecological surgeries. Ain Shams J Anesthesiol 2019;11:12.  Back to cited text no. 13
Staikou C, Avramidou A, Ayiomamitis GD, Vrakas S, Argyra E. Effects of intravenous versus epidural lidocaine infusion on pain intensity and bowel function after major large bowel surgery: A double-blind randomized controlled trial. J Gastrointest Surg 2014;18:2155-62.  Back to cited text no. 14
Bennett PN, Aarons LJ, Bending MR, Steiner JA, Rowland M. Pharmacokinetics of lidocaine and its deethylated metabolite: Dose and time dependency studies in man. J Pharmacokinet Biopharm 1982;10:265-81.  Back to cited text no. 15
Weinberg L, Peake B, Tan C, Nikfarjam M. Pharmacokinetics and pharmacodynamics of lignocaine: A review. World J Anesthesiol 2015;4:17-29.  Back to cited text no. 16
Iirola T, Aantaa R, Laitio R, Kentala E, Lahtinen M, Wighton A, et al. Pharmacokinetics of prolonged infusion of high-dose dexmedetomidine in critically ill patients. Crit Care 2011;15:R257.  Back to cited text no. 17
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Martin F, Cherif K, Gentili ME, Enel D, Abe E, Alvarez JC, et al. Lack of impact of intravenous lidocaine on analgesia, functional recovery, and nociceptive pain threshold after total hip arthroplasty. Anesthesiology 2008;109:118-23.  Back to cited text no. 19
Insler SR, O'Connor M, Samonte AF, Bazaral MG. Lidocaine and the inhibition of postoperative pain in coronary artery bypass patients. J Cardiothorac Vasc Anesth 1995;9:541-6.  Back to cited text no. 20
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