|Year : 2020 | Volume
| Issue : 1 | Page : 23-32
Intraoperative lidocaine infusion reduces analgesic and anesthetic requirements in patients with high body mass index undergoing laparoscopic cholecystectomy
Praveen Benjamin Dennis1, Kirubakaran Davis2, Balaji Kuppuswamy2, Raj Sahajanandan2
1 Department of Paediatric Anaesthesia, GSMC and KEM Hospital, Mumbai, Maharashtra, India
2 Department of Anaesthesia, Christian Medical College Hospital, Vellore, Tamil Nadu, India
|Date of Submission||23-Aug-2019|
|Date of Decision||23-Sep-2019|
|Date of Acceptance||16-Oct-2019|
|Date of Web Publication||13-Feb-2020|
Dr. Kirubakaran Davis
Department of Anaesthesia, Christian Medical College Hospital, Vellore, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Background: Intravenous (IV) lidocaine has analgesic, antihyperalgesic, and anti-inflammatory properties. Intraoperative use of lidocaine infusion reduces the analgesic and anesthetic requirement during laparoscopic cholecystectomy surgeries.
Aims: Our study was designed to analyze the effect of intraoperative infusion of lidocaine, on perioperative opioid, anesthetic and neuromuscular agent requirements, and the incidence of side effects in patients with high body mass index undergoing laparoscopy cholecystectomy.
Methods: This is a randomized double-blinded prospective study conducted at a tertiary hospital. Of the 38 patients enrolled in the study, due to cancellation and conversion to open surgery, only 33 patients completed the study (16 in the control group [C] and 17 in the lidocaine group [L]). Patients from both the groups received the test drug (lidocaine or normal saline) as 2 mg/kg bolus during induction and continued as an infusion at a rate of 2 mg/kg/h throughout the surgery which was terminated 30 min after extubation. The patients were analyzed for perioperative analgesic, anesthetic, muscle relaxant requirement, and adverse effects.
Results: The mean visual analog scale (VAS) score in 1st and 2nd hour after surgery was less in the group receiving IV lidocaine infusion (7.5 ± 7.8* vs. 10.5 ± 11.8; 12.5 ± 8.1* vs. 23 ± 24.6 [* denotes lidocaine group]); compared to the control group the intraoperative opioid requirement decreased by 43% in the lidocaine group. There was a reduction of 13%–21% in the minimum alveolar concentration of isoflurane in the lidocaine group. The cumulative dose of rocuronium was found to be 53% lesser in the lidocaine group. There was no difference in the sedation scores and there were no adverse effects in either of the groups.
Conclusions: The study demonstrates the usefulness of IV lidocaine infusion as an adjunct to provide anesthesia with decreased requirements of opioid, inhalation, and neuromuscular-blocking agents.
Keywords: Isoflurane, laparoscopic cholecystectomy, lidocaine infusion, opioids, rocuronium
|How to cite this article:|
Dennis PB, Davis K, Kuppuswamy B, Sahajanandan R. Intraoperative lidocaine infusion reduces analgesic and anesthetic requirements in patients with high body mass index undergoing laparoscopic cholecystectomy. Indian Anaesth Forum 2020;21:23-32
|How to cite this URL:|
Dennis PB, Davis K, Kuppuswamy B, Sahajanandan R. Intraoperative lidocaine infusion reduces analgesic and anesthetic requirements in patients with high body mass index undergoing laparoscopic cholecystectomy. Indian Anaesth Forum [serial online] 2020 [cited 2020 Aug 14];21:23-32. Available from: http://www.theiaforum.org/text.asp?2020/21/1/23/278185
| Introduction|| |
High body mass index (BMI) is a well-established risk factor for the formation of gallstones and patients who require surgery for gallstone disease mostly fall into the overweight (BMI 25–29 kg/m2), obese (BMI 30–39 kg/m2) or morbidly obese (BMI ≥ 40 kg/m2) categories. As a result, a large proportion of patients who require a cholecystectomy for symptomatic cholelithiasis fall into these overweight, obese, or morbidly obese categories. Laparoscopic cholecystectomy has become the gold standard for the treatment of symptomatic gallstones, offering a shorter length of hospital stay and reduced postoperative pain.
Pain after laparoscopic cholecystectomy is complex in nature and has unique elements compared to other laparoscopic procedures. Intraoperative analgesia is generally provided by opioid analgesics. However, the use of opioids can be associated with an increased incidence of postoperative complications, such as respiratory depression, sedation, postoperative nausea and vomiting, ileus, and urinary retention Some of these side effects can delay recovery and prolonged hospital stay. It is, therefore, appropriate to minimize these side effects by using either multimodal analgesic techniques or adjuvant therapies to reduce the doses of opioids.
An alternative approach to reduce perioperative analgesic requirements and to facilitate earlier postoperative recovery is administration of intravenous (IV) lidocaine, which has analgesic, antihyperalgesic, and anti-inflammatory properties. Furthermore, nontoxic plasma lidocaine concentrations reduce requirements for various volatile anesthetics in several animal species. In addition, IV lidocaine is inexpensive, easy to administer, and relatively safe. It is thus an attractive intervention with wide potential applicability.
We, therefore, tested the hypothesis that systemic lidocaine infusion reduces the perioperative analgesic and anesthetic requirement during laparoscopic cholecystectomy surgeries. Our present prospective, randomized controlled trial was designed to analyze the effect of intraoperative infusion of lidocaine, on perioperative opioid, anesthetic and neuromuscular agents' requirements, and the incidence of side effects in patients with high BMI undergoing laparoscopy cholecystectomy.
| Methods|| |
With approval of the Institutional Ethics Committee and written informed consent from each patient, we enrolled 38 American Society of Anesthesiologists (ASA) Physical Status I–II patients aged between 18 and 65 years with BMI >25 kg/m2 scheduled to undergo elective laparoscopic cholecystectomy for nonmalignant disease at a tertiary medical center in India. Exclusion criteria were patients with ASA Physical Status III and greater; history of hepatic, renal, or cardiac failure; organ transplant; seizure disorder; pregnant and lactating mothers; allergy to local anesthetics; or inability to comprehend pain assessment.
Of the 38 patients enrolled in the study, three patients were excluded as the surgery was cancelled. Thirty-five patients were randomized into two groups (17 in the control group [C] and 18 in the lidocaine group [L]). One patient in each group was eliminated as the laparoscopy was converted to open surgery. Thirty-three patients completed the study (16 in the control group and 17 in the lidocaine group); data from these patients were used in the analysis [Figure 1].
During the preanesthetic checkup visit, all patients were explained and familiarized about the study, including the use of visual analog scale (0–100 mm) for pain assessment (0 as “no pain” to 100 as “worst imaginable pain”) and the use of incentive spirometry.
All the patients were premedicated with oral diazepam 0.2 mg/kg given the night before and 2 h prior to surgery. On arrival in the operation theater, on the day of surgery, peripheral venous access was secured in all the patients with 16G or 18G IV cannula on the dorsum of the left hand. Patients were connected to the patient monitor for monitoring ECG, pulse rate, noninvasive blood pressure (NIBP), bispectral index (BIS), and pulse oximetry.
Patients were randomly allocated to two groups based on computer-generated codes that were maintained in sequentially numbered opaque envelopes. Allocation envelopes were opened by the primary investigator who then prepared either preservative-free 2% lidocaine (LoxicardR 2%, Neon, India) or saline in 50-ml syringes coded as “TEST drug.” The anesthesiologist in charge of the case was unaware of the patient's group assignment; the study was thus fully double-blinded.
Since the participants enrolled in the trial have a BMI >25 kg/m2, the drug doses are calculated based on ideal and adjusted body weight (ABW) to avoid overdosing as recommended in the literature. The bolus dose of lidocaine and all the doses of fentanyl were calculated using ABW. Ideal body weight (IBW) was used in the calculation of all the remaining drugs for boluses and infusions.,
In all the patients, anesthesia was induced with injection propofol 2.0 mg/kg, fentanyl 2.0 μg/kg, followed by rocuronium 0.6 mg/kg intravenously to facilitate the laryngoscopy and orotracheal intubation. A bolus of 2 mg/kg of the test drug was administered 30 s after administration of rocuronium. Intubation was done 90 s after the test drug bolus, the patients were mask ventilated till then. After tracheal intubation, anesthesia was maintained with isoflurane, the minimum alveolar concentration (MAC) of which was titrated for BIS values of 40–60 and the heart rate and mean blood pressure within ± 20% of respective baseline values.
The TEST drug infusion was continued at a rate of 2 mg/kg/h throughout the surgery and terminated 30 min after extubation. Supplemental analgesia was achieved with IV boluses of fentanyl up to a maximum of 5 μg/kg or morphine up to a maximum of 0.2 mg/kg and neuromuscular blockade with rocuronium whenever needed in either group during maintenance of anesthesia. The patient's lungs were mechanically ventilated with a mixture of air in oxygen with minute ventilation adjusted to maintain normocarbia (CO2 between 35 and 40 mmHg).Intraoperative normothermia was maintained with forced-air warming blankets positioned overexposed parts of the body. Nasopharyngeal temperature was monitored throughout surgery. Soon after intubation, 30 mg/kg of paracetamol administered as an infusion over 15 min, 0.05 mg/kg bolus of morphine, and 0.1 mg/kg of dexamethasone were given intravenously. Episodes of intraoperative hypotension (mean arterial blood pressure <60 mmHg) are treated with IV boluses of 5 mg ephedrine or 50–100 μg of phenylephrine. Isoflurane was discontinued after the last skin suture, and after completion of the surgery, the residual neuromuscular blockade was antagonized with the mixture of injection neostigmine 0.05 mg/kg and glycopyrrolate 0.01 mg/kg IV. The trachea was extubated once the patient regained consciousness, and the patients were transferred to the postanesthesia care unit (PACU) where the infusion was continued for further 30 min. In the PACU blood pressure, pulse, respiration, and temperature were monitored and recorded by nurses who were blinded to the randomization sequence. The patient was evaluated in the PACU and in the surgical ward by the investigator who was unaware about the study medication given. Intensity of pain and features of possible systemic toxicity of lidocaine was monitored at the interval of 15 min for 2 h in the immediate postoperative period. The intensity of pain was assessed by asking the patient to indicate on the 0–100 mm Visual Analog Scale at the point that corresponded to the level of pain intensity they felt.
The primary outcome was perioperative analgesia, of which intraoperative analgesia assessed by changes in hemodynamic parameters such as heart rate, blood pressure during various periods of stimuli, and postoperative analgesia measured using a 0–100 mm-Horizontal Visual Analog Scale.
Secondary outcome measures were as follows:
- Depth of anesthesia measured by BIS.
- Concentration of inhalational agent as measured by MAC. Perioperative requirement of anesthetic agents, analgesic drugs, and neuromuscular blocking agents.
- Volumes generated on the Incentive spirometry.
- Postoperative recovery assessed by Modified Aldrete Score (MAS).
- Complications documented at any point when they occur.
The sample size estimation was based on primary outcome measure, namely the VAS score. Based on prior study, a minimum of 15 patients in each arm will be required to obtain a mean difference of 8.6 units in visual analog scores (VAS) between the intervention (lidocaine) arm and control (saline) arm.
This would provide a standard deviation of 7 units in the control group, a power of 80% and a significance level of 5%.
The sample size was calculated using the following formula:
(Noninferiority-Two Groups-Parallel-Two proportions–Equal Allocation).
The primary outcome was to assess perioperative pain.
Intraoperative pain was assessed using hemodynamic parameters as surrogates. A two-sample t-test was applied to calculate the significance between the hemodynamic parameters of the two arms.
Posoperative pain was assessed using the 0–100 visual analog score. Two-sample Wilcoxon rank-sum (Mann–Whitney) test was used to check for statistical significance. The median values and interquartile range was used, as the data did not follow normal distribution but was skewed.
Volumes generated by Incentive Spirometer were analyzed using Pearson Chi-squared test. Depth of anesthesia parameters: Two-sample Wilcoxon rank-sum (Mann–Whitney) test was used to check for statistical significance. The median values and interquartile range was used, as the data did not follow normal distribution but was skewed.
| Results|| |
Comparison of the general characteristics of the study population of both the groups is given in [Table 1]. No statistical difference was observed in their age, BMI, IBW, ASA physical status and sex ratio, mean duration of surgery, baseline heart rate, and mean blood pressure between the groups.
Following the induction of anesthesia and intubation of the patient as described in the methodology, the hemodynamic and depth of anesthesia variables were obtained and analyzed. These variables were collected during different time frames.
Heart rate and blood pressure
The heart rate and mean blood pressure were recorded at different intraoperative time frames [Table 2]. The recordings were done (a) before induction (baseline), (b) following intubation, (c) following insufflations of the peritoneum with carbon dioxide, (d) in the period between insufflation and exsufflation, (e) during extubation, and (f) postextubation. The mean overall heart rate and mean blood pressure in both the groups during various intraoperative events were similar and not statistically significant except following intubation (87 ± 12 vs. 100 ± 23, P = 0.049) and following insufflations (79.8 ± 8.3 vs. 93.9 ± 13.5, P = 0.001) when the mean blood pressure in the lidocaine group was lower and significant statistically than that in the saline group.
Bispectral Index and minimum alveolar concentration values
Thirty seconds after intubation
BIS value 30 s after intubation was 50.5 and 57.3 in the intervention (lidocaine) group and control (saline) group, respectively. The difference in BIS values 30 s after intubation was 6.8 units significantly higher in the control group which was statistically significant [Table 3]. This decrease in BIS may be explained by the fact that lidocaine can independently reduce BIS values. Although the median BIS values were <60, there were six patients in the control group versus two patients in the intervention (lidocaine) group who had transient increase in BIS values >60, needing a bolus of propofol to increase the depth of anesthesia postintubation.
The overall median MAC value of isoflurane, 30 s following intubation in the control (saline) and intervention (lidocaine) was 0.8 and 0.7, respectively, which was statistically significant (P = 0.028) [Table 4].
Combining the interpretation of the MAC and BIS value 30 s after intubation, it is seen that, although the MAC values are higher in the control group (saline), the BIS values are unexpectedly higher as well.
Thirty seconds after insufflations of the peritoneum
The BIS values recorded 30 s after insufflations of peritoneum [Table 3] were 48.5 and 45.6 in the intervention (lidocaine) group and the control (saline) group, respectively, but were not statistically significant. The MAC of agent to maintain BIS < 60 during insufflation was 0.74 and 0.86 in the intervention (lidocaine) and control (saline) arml respectively [Table 4]. This was statistically significant (P = 0.005).
Insufflation to extubation
The BIS values during the intraoperative period from insufflations to extubation were 48.5 in the intervention (lidocaine) group as compared to 47.5 the control (saline) group [Table 3]. There is almost no difference in the BIS value between the two groups.
The MAC of isoflurane required to maintain adequate depth of anesthesia titrated to BIS values between 40 and 60 during the intraoperative period from insufflations to extubation was compared [Table 4]. The MAC was 0.67 in the intervention group and 0.83 in the control group. This is statistically significant finding (P = 0.0001). Clinically, this translates to lesser quantity of inhalational anesthetics required for maintaining anesthesia.
The age-adjusted MAC of inhalation agent when the patient was extubated was 0.22 across both the control and intervention group [Table 4]. Concerns regarding delayed awakening were not significant since the patients in both the arms were extubated at same MAC of isoflurane.
The pain intensity scores estimated using the 0–100 mm Visual Analog Scale (VAS) in the 1st hour postextubation in the intervention (lidocaine) and control (saline) group were 7.5 and 10.5, respectively, and 12.5 and 23 in the 2nd hour of postextubation, which were not statistically significant [Table 5].
Incentive spirometer was used to a similar extent in both the groups. Most (76.5%) of the participants in the lidocaine group could generate 600–900 ml and 23.5%, of participants could generate more than 900 ml [Table 6]. In the control arm, 56.2% of the patients could generate more than 900 ml, while 37.5% could generate 600–900 ml. P = 0.065, hence, probably not statistically significant.
The drugs fentanyl, morphine, propofol, rocuronium, ephedrine, and phenylephrine, used during the surgery were documented at four-time points.
- From induction to insufflation of peritoneum with carbon dioxide
- Insufflation of peritoneum with carbon dioxide to extubation
- Through 2 h after extubation (except rocuronium).
The drugs dosages administered were divided by the duration of the surgery and analyzed as well, because longer surgeries may require higher quantities of anesthetic drugs and may imply a greater surgical difficulty and greater pain.
The total fentanyl administered in the intervention group (lidocaine) and control (saline) was 133.8 and 208.4 μg, respectively, which was statistically significant (P = 0.000). The total fentanyl administered per minute of surgery obtained by dividing the total dose of fentanyl by the duration of the surgery was 0.79 and 1.3 μg/min, respectively, which was statistically significant (P = 0.000). The total morphine administered in the intervention group (lidocaine) versus control (saline) was 3.1 and 7.9 mg, respectively, which was statistically significant (P = 0.000). The total morphine administered per minute of surgery in the intervention group (lidocaine) versus control (saline) was 20 and 50 μg/min, respectively, which was statistically significant (P = 0.000). The time weighted total opioid administered per minute of surgery was obtained by dividing the total dose of fentanyl by the potency conversion factor of 7.5 and summing it to the total dose of morphine and dividing the whole by the duration of the surgery [Table 7]. The intervention group (lidocaine) versus control (saline) received 17.9 and 27.8/min, respectively, which was statistically significant (P = 0.000).
The propofol administered from induction to insufflation of peritoneum with carbon dioxide in the intervention group (lidocaine) versus control (saline) was 52.5 and 86.9 mg, respectively, which was statistically significant (P = 0.000). The total propofol administered in the intervention group (lidocaine) versus control (saline) was 108 and 173.8 mg, respectively, which was statistically significant (P = 0.000). The total propofol administered per minute of surgery was obtained by dividing the total dose of propofol by the duration of the surgery [Table 8]. The intervention group (lidocaine) versus control (saline) received 0.63 and 0.86 mg/min, respectively, which was statistically significant.
The total median rocuronium administered in the intervention group (lidocaine) versus control (saline) was 35 and 62 mg, respectively, which was statistically significant [Table 9]. The total rocuronium administered per minute of surgery was obtained by dividing the total dose of rocuronium by the duration of the surgery. The intervention group (lidocaine) versus control (saline) received 0.21 and 0.37 mg/min, respectively, which was statistically significant (P = 0.000). Rocuronium used in micrograms per kilogram per minute during the surgery was 0.41 and 0.71 in the lidocaine and saline group, respectively. This result is statistically significant (P = 0.000). The dose of rocuronium administered was 53% lesser in the lidocaine group.
Intraoperative hypotensive episodes were treated with boluses of either ephedrine or phenylephrine [Table 10]. The vasopressor requirements in both the groups were comparable and similar, but there was no statistical significance.
| Discussion|| |
This study demonstrated that perioperative IV infusion of nontoxic doses of lidocaine improved postoperative analgesia, reduced perioperative opioid, and anesthetic requirements without any significant adverse effects in patients with high BMI undergoing laparoscopic cholecystectomy. Perioperative pain management has always been challenging in patients with high BMI due to their altered physiology and pharmacokinetics., With the higher incidence of comorbidities in this patient population, traditional opioid-centric pain management can often result in opioid-induced ventilatory impairment and increased morbidity and/or mortality. Multimodal analgesia strategies based on opioid-sparing approach can improve patient safety and outcome; perioperative administration of lidocaine infusion has become an attractive option in reducing perioperative analgesic requirements. Lidocaine infused intravenously has analgesic, anti-hyperalgesic, and anti-inflammatory properties,,, and it also reduces intra- and post-operative analgesic requirements These properties are mediated by a variety of mechanisms, including sodium channel blockade, as well as inhibition of G protein-coupled receptors, and N-methyl-D-aspartate receptors. IV lidocaine also depresses spike activity, amplitude, and conduction time in both myelinated A and unmyelinated C fibers., Lidocaine's anti-inflammatory activity may be another potential mechanism in improving perioperative pain by reducing cytokines release and neutrophil activation. The effect of systemic lidocaine infusion on the MAC of volatile anesthetics is partially explained. The anesthetic agents suppress central nervous system (CNS) Na+ channels in a voltage-dependent manner. Lidocaine action on both peripheral and CNSs also involves blockade of Na+ channels. Hence, both inhalant anesthetics and lidocaine act on voltage-gated Na+ channels in the CNS, and thus, their effects during general anesthesia could be additive. Lidocaine ensures pain relief on the spinal level, which correlates with a reduction in MAC and decreases the volatile agents demand. Finally, lidocaine is capable of blocking brain cell excitability, and this could explain both its analgesic and MAC-reducing properties., These observations have been demonstrated in many animal studies.,
Our results are consistent with previous reports, in which IV lidocaine infusion was found to reduce intraoperative opioid use. In our study, we were able to demonstrate an opioid sparing effect in the intraoperative period in the lidocaine group from the decrease in opioid (fentanyl and morphine) requirement by 43%. In the study by Saadawy et al. on patients undergoing laparoscopic cholecystectomy, the total fentanyl consumption was found to be significantly lower by 34% in the lidocaine group.(242 ± 48.5 μg vs. 323 ± 70.8 μg). Kaba et al. found that the total dose of sufentanil given to patients during laparoscopic colectomy in the lidocaine group was significantly lower by 22% than in the control group (13.0 ± 3.7 μg vs. 16.3 ± 3.6 μg). A similar result was obtained in ambulatory surgery where lidocaine use yielded a 30% reduction in intraoperative opioid use.
Participants in our study had BMI >25 kg/m2, and these patients may be sensitive to the respiratory depressant effects of opioids. De Oliveira et al. has shown that in patients undergoing bariatric surgery, lidocaine infusion reduced 24-h opioid consumption by 10 mg morphine equivalents compared to placebo, which correlated with improved quality of recovery scores.
In our study, the postoperative pain during the first and 2nd hour following extubation as measured with Visual Analog Scale (VAS) was higher in the saline group by 3 and 10.5 points, respectively. Although these findings may be clinically significant, they were not statistically significant, probably due to the smaller size and the higher requirement of opioid in the saline group to provide analgesia and thus reducing the pain scores.
In addition to opioid sparing effect, there was a reduction of 13%–21% in the MAC of isoflurane required to maintain hemodynamic stability and BIS values between 40 and 60 during surgery. This observation is in agreement with other studies which report a reduction in the concentration of inhalational agents with concurrent infusion of lidocaine.,,,
Altermatt et al. found that the administration of IV lidocaine resulted in a significant reduction in propofol requirements during the maintenance phase of TIVA for elective laparoscopic cholecystectomies. In the present study, we used propofol as a rescue agent to increase depth of anesthesia during episodes when BIS was >60 and the intraoperative requirement was significantly higher (45% more) in the control (saline) group.
Cumulative dose of rocuronium used intraoperatively in our study was found to be 53% lesser in the lidocaine group than in the control group in comparison to Omar study which showed only 15% lesser requirement of rocuronium in the lidocaine group. The probable explanation of decreased needs of rocuronium in lidocaine group is the ability of lidocaine to blunt the cough airway's reflexes to endotracheal tube. The results of this study may be encouraging to use lidocaine infusion in general anesthesia to decrease NMBD doses in places lacking quantitative neuromuscular monitors. However, this conservative use of NMBD might be inappropriate in surgeries that necessitate deep muscle relaxation. Cardoso et al. has shown that IV lidocaine administered before rocuronium was unable to shorten its onset, but prolonged its pharmacological duration without prolonging total neuromuscular function recovery.
Attenuation of the sympathetic response during laryngoscopy and endotracheal intubation with the use of Lidocaine has been well described., In our study, the heart rate and Mean blood pressures during intubation, insufflation, and during the surgery were higher in the saline group. This reflects the lidocaine ability to control the hemodynamic response not only during intubation but also during pneumoperitoneum and surgery. In addition, a statistically significant difference was observed during peritoneal insufflations where the MAP in the lidocaine group was lower than that in the control group (79.8 ± 8.3 vs. 93.9 ± 13.5, P = 0.001). Weinberg et al. have reported the effects of intraoperative lidocaine infusion on hemodynamic changes in patients undergoing open radical prostatectomy.
In our study, we administered lidocaine 2 mg/kg as slow IV bolus injection followed by a continuous infusion of 2 mg/kg/h throughout the surgery and terminated 30 min after extubation. Since we continued lidocaine infusion up to 30-min postoperatively, we could not ascertain whether prolonging the lidocaine infusion would have improved analgesia further.
Although accumulation of lidocaine is a concern with continuous infusion, at doses used in the previous studies, plasma concentrations remain well below the toxic level (5 μg/ml) even after 24 h., Toxicity from perioperative lidocaine infusion is exceedingly rare, but may present with symptoms of tinnitus, perioral numbness, and cardiac dysrhythmias. In our study, we did not have any adverse effects in either of the groups. Monitoring plasma lidocaine levels may be considered in patients at increased risk for lidocaine toxicity such as those with abnormal liver or kidney function.
Postoperative recovery as measured by MAS showed the lidocaine group had a slightly lesser score (0.8) in the first 30 min after extubation. This was not statistically significant, and this may be due to sedative effect of lidocaine which as well could have contributed to the relatively better Peak expiratory flow rate (PEFR) volume generated in 56.2% of control group patients who were able to generate >900 ml, as PEFR is an effort-dependent maneuver.
There are reports of patients who receive perioperative lidocaine appear to be more sleepy during emergence from anesthesia. Wallin et al. have found that the apparent delayed awakening results from patients being less responsive to the endotracheal tube as lidocaine has shown to blunt sympathetic responses to tracheal extubation.
There are some limitations in our study which are as follows.
The smaller sample is of critical limitation in our study. Rather, a larger sample size would have provided greater statistical significance and greater insight into the secondary objectives.
The hemodynamic parameters and depth of anesthesia were recorded only every 30 min during the maintenance phase of anesthesia, but the hemodynamic perturbations were adequately treated.
Neuromuscular monitoring before giving additional doses of rocuronium would have given a better picture of the direct action of lidocaine on the neuronal conduction.
PEFR was measured only during the postoperative period, and the values could have been affected by the sedative effect of lidocaine as well as by the higher opioid consumption in the saline group.
Surgical and anesthetic experiences were not factored into the study due to heterogeneous surgical anesthetic team involved. Previous abdominal surgeries which would increase the surgical technical difficulty and greater pain scores were not factored into the study as well.
We followed the patients only for 2 h after the surgery, if the patients had been followed up for longer, additional information such as onset of bowel movement and requirement for further analgesia and time to mobility and discharge could have been analyzed.
| Conclusions|| |
IV Lidocaine infusion is a useful adjunct to provide anesthesia, and at the doses used for the study rarely cause side effects. The sparing effect of systemic lidocaine on opioid, inhalation anesthetic, and neuromuscular-blocking agent requirements is of considerable importance in patients with a BMI >25, as it provides better postoperative lung function and better airway patency, decreased chance of residual neuromuscular blockade, and most importantly, decreased perioperative pain, all leading to decreased morbidity and shorter length of hospital stay.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Tandon A, Sunderland G, Nunes QM, Misra N, Shrotri M. Day case laparoscopic cholecystectomy in patients with high BMI: Experience from a UK centre. Ann R Coll Surg Engl 2016;98:329-33.
Wills VL, Hunt DR. Pain after laparoscopic cholecystectomy. Br J Surg 2000;87:273-84.
Kehlet H, Rung GW, Callesen T. Postoperative opioid analgesia: Time for a reconsideration? J Clin Anesth 1996;8:441-5.
Bisgaard T. Analgesic treatment after laparoscopic cholecystectomy: A critical assessment of the evidence. Anesthesiology 2006;104:835-46.
Hollmann MW, Durieux ME. Local anesthetics and the inflammatory response: A new therapeutic indication? Anesthesiology 2000;93:858-75.
Barras M, Legg A. Drug dosing in obese adults. Aust Prescr 2017;40:189-93.
Ingrande J, Lemmens HJ. Dose adjustment of anaesthetics in the morbidly obese. Br J Anaesth 2010;105 Suppl 1:i16-23.
Kaba A, Laurent SR, Detroz BJ, Sessler DI, Durieux ME, Lamy ML, et al.
Intravenous lidocaine infusion facilitates acute rehabilitation after laparoscopic colectomy. Anesthesiology 2007;106:11-8.
De Baerdemaeker LE, Mortier EP, Struys MM. Pharmacokinetics in obese patients. Contin Educ Anaesth Crit Care Pain 2004;4:152-5.
Casati A, Putzu M. Anesthesia in the obese patient: Pharmacokinetic considerations. J Clin Anesth 2005;17:134-45.
Groudine SB, Fisher HA, Kaufman RP Jr., Patel MK, Wilkins LJ, Mehta SA, et al.
Intravenous lidocaine speeds the return of bowel function, decreases postoperative pain, and shortens hospital stay in patients undergoing radical retropubic prostatectomy. Anesth Analg 1998;86:235-9.
Koppert W, Weigand M, Neumann F, Sittl R, Schuettler J, Schmelz M, et al.
Perioperative intravenous lidocaine has preventive effects on postoperative pain and morphine consumption after major abdominal surgery. Anesth Analg 2004;98:1050-5.
Koppert W, Ostermeier N, Sittl R, Weidner C, Schmelz M. Low-dose lidocaine reduces secondary hyperalgesia by a central mode of action. Pain 2000;85:217-24.
Hollmann MW, Strumper D, Herroeder S, Durieux ME. Receptors, G proteins, and their interactions. Anesthesiology 2005;103:1066-78.
Sugimoto M, Uchida I, Mashimo T. Local anaesthetics have different mechanisms and sites of action at the recombinant N-methyl-D-aspartate (NMDA) receptors. Br J Pharmacol 2003;138:876-82.
De Oliveira CM, Issy AM, Sakata RK. Intraoperative intravenous lidocaine. Rev Bras Anestesiol 2010;60:325-33.
Nakhli MS, Kahloul M, Guizani T, Zedini C, Chaouch A, Naija W. Intravenous lidocaine as adjuvant to general anesthesia in renal surgery. Libyan J Med 2018;13:1433418.
Herroeder S, Pecher S, Schönherr ME, Kaulitz G, Hahnenkamp K, Friess H, et al.
Systemic lidocaine shortens length of hospital stay after colorectal surgery: A double-blinded, randomized, placebo-controlled trial. Ann Surg 2007;246:192-200.
Herold KF, Hemmings HC Jr. Sodium channels as targets for volatile anesthetics. Front Pharmacol 2012;3:50.
Rehberg B, Xiao YH, Duch DS. Central nervous system sodium channels are significantly suppressed at clinical concentrations of volatile anesthetics. Anesthesiology 1996;84:1223-33.
Bach FW, Jensen TS, Kastrup J, Stigsby B, Dejgård A. The effect of intravenous lidocaine on nociceptive processing in diabetic neuropathy. Pain 1990;40:29-34.
Pypendop BH, Ilkiw JE. The effects of intravenous lidocaine administration on the minimum alveolar concentration of isoflurane in cats. Anesth Analg 2005;100:97-101.
Butterworth J, Cole L, Marlow G. Inhibition of brain cell excitability by lidocaine, QX 314, and tetrodotoxin: A mechanism for analgesia from infused local anesthetics? Acta Anaesthesiol Scand 1993;37:516-23.
Zhang Y, Laster MJ, Eger EI 2nd
, Sharma M, Sonner JM. Lidocaine, MK-801, and MAC. Anesth Analg 2007;104:1098-102.
Saadawy IM, Kaki AM, Abd El Latif AA, Abd-Elmaksoud AM, Tolba OM. Lidocaine vs. magnesium: Effect on analgesia after a laparoscopic cholecystectomy. Acta Anaesthesiol Scand 2010;54:549-56.
McKay A, Gottschalk A, Ploppa A, Durieux ME, Groves DS. Systemic lidocaine decreased the perioperative opioid analgesic requirements but failed to reduce discharge time after ambulatory surgery. Anesth Analg 2009;109:1805-8.
De Oliveira GS Jr., Duncan K, Fitzgerald P, Nader A, Gould RW, McCarthy RJ. Systemic lidocaine to improve quality of recovery after laparoscopic bariatric surgery: A randomized double-blinded placebo-controlled trial. Obes Surg 2014;24:212-8.
Lauwick S, Kim DJ, Michelagnoli G, Mistraletti G, Feldman L, Fried G, et al.
Intraoperative infusion of lidocaine reduces postoperative fentanyl requirements in patients undergoing laparoscopic cholecystectomy. Can J Anaesth 2008;55:754-60.
Omar AM, Aboushanab OH. Effect of intravenous lidocaine infusion on sevoflurane requirements as monitored by bispectral index: A randomized double-blinded controlled study. Egypt J Anaesth 2013;29:235-9.
Altermatt FR, Bugedo DA, Delfino AE, Solari S, Guerra I, Muñoz HR, et al.
Evaluation of the effect of intravenous lidocaine on propofol requirements during total intravenous anaesthesia as measured by bispectral index. Br J Anaesth 2012;108:979-83.
Omar AM. Effect of systemic lidocaine infusion on train-of-four ratios during recovery from general anesthesia. Egypt J Anaesth 2012;28:281-6.
Cardoso LS, Martins CR, Tardelli MA. Effects of intravenous lidocaine on the pharmacodynamics of rocuronium. Rev Bras Anestesiol 2005;55:371-80.
Gurulingappa, Aleem MA, Awati MN, Adarsh S. Attenuation of cardiovascular responses to direct laryngoscopy and intubation-A comparative study between iv bolus fentanyl, lignocaine and placebo (NS). J Clin Diagn Res 2012;6:1749-52.
Baral BK, Bhattarai BK, Rahman TR, Singh SN, Regmi R. Perioperative intravenous lidocaine infusion on postoperative pain relief in patients undergoing upper abdominal surgery. Nepal Med Coll J 2010;12:215-20.
Weinberg L, Jang J, Rachbuch C, Tan C, Hu R, McNicol L. The effects of intravenous lignocaine on depth of anaesthesia and intraoperative haemodynamics during open radical prostatectomy. BMC Res Notes 2017;10:248.
Vigneault L, Turgeon AF, Côté D, Lauzier F, Zarychanski R, Moore L, et al.
Perioperative intravenous lidocaine infusion for postoperative pain control: A meta-analysis of randomized controlled trials. Can J Anaesth 2011;58:22-37.
McCarthy GC, Megalla SA, Habib AS. Impact of intravenous lidocaine infusion on postoperative analgesia and recovery from surgery: A systematic review of randomized controlled trials. Drugs 2010;70:1149-63.
Wallin G, Cassuto J, Högström S, Lindén I, Faxén A, Rimbäck G, et al.
Effects of lidocaine infusion on the sympathetic response to abdominal surgery. Anesth Analg 1987;66:1008-13.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10]