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Anesth Analg 2004;98:1172-1177
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000108966.84797.72

REGIONAL ANESTHESIA

Tramadol Added to 1.5% Mepivacaine for Axillary Brachial Plexus Block Improves Postoperative Analgesia Dose-Dependently

Sébastien Robaux, MD*, Cornelia Blunt, FRCA*, Eric Viel, MD{dagger}, Philippe Cuvillon, MD{dagger}, Philippe Nouguier, MD*, Gilles Dautel, MD{ddagger}, Sylvie Boileau, MD*, Florence Girard, MD§, and Hervé Bouaziz, MD, PhD*

*Department of Anesthesiology and Critical Care Medicine, Hôpital Central, Nancy Cedex, the {dagger}Department of Anesthesiology and Pain Management, Hôpital Caremeau, Nimes Cedex 9, France, the {ddagger}Department of Plastic and Hand Surgery, Hôpital Jeanne d’Arc, Nancy, France, and the §Department of Clinical Epidemiology and Evaluation, Hôpital Marin, Nancy Cedex, France

Address correspondence and reprint requests to Hervé Bouaziz. Address email to h.bouaziz{at}chu-nancy.fr


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Adjuncts to local anesthetics for peripheral plexus blockade may enhance the quality and duration of anesthesia and postoperative analgesia. The analgesic, tramadol, has a unique mechanism of action that suggests efficacy as such an adjunct. It displays a central analgesic and peripheral local anesthetic effect. We designed a prospective, randomized, controlled and double-blind clinical trial to assess the effect of tramadol added to brachial plexus anesthesia. One-hundred patients scheduled for carpal tunnel release surgery under brachial plexus anesthesia were randomized into four groups. All patients received 1.5% mepivacaine 40 mL plus a study solution containing either isotonic sodium chloride (Group P, n = 17), tramadol 40 mg (Group T40, n = 22), tramadol 100 mg (Group T100, n = 20) or tramadol 200 mg (Group T200, n = 20). We evaluated the time of onset of anesthesia, duration of sensory and motor blockade, duration and quality of postoperative analgesia, and occurrence of adverse effects. Onset and duration of sensory and motor blocks were not different among groups. The number of patients requesting analgesia in the postoperative period was significantly less in the 3 tramadol groups compared with the placebo group (P = 0.02); this was also noted with the placebo and T40 groups compared with the T200 group. No statistical significance was demonstrated between the placebo and the T40 group or the T100 group and the T200 group. Furthermore, there was a significant trend effect among groups applying the Cochran-Armitage tendency test (P = 0.003), suggesting a dose-dependent decrease for additional postoperative analgesia requirements when tramadol was added. Side effects did not differ among groups, although they were more frequently recorded in the T groups. Our study suggests that tramadol added to 1.5% mepivacaine for brachial plexus block enhances in a dose-dependent manner the duration of analgesia with acceptable side effects. However, the safety of tramadol has to be investigated before allowing its use in clinical practice.

IMPLICATIONS: Tramadol’s unique mechanism of action suggests efficacy as a local anesthetic adjunct for peripheral plexus blockade. Our study demonstrates that tramadol, added to mepivacaine for brachial plexus anesthesia, extends the duration and improves the quality of postoperative analgesia in a dose dependent fashion with acceptable side effects.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Adjuncts to local anesthetics for peripheral plexus blockade have been proposed to enhance the quality and duration of anesthesia and postoperative analgesia. Clonidine, epinephrine, and opioids are such examples (1–3). Tramadol is a synthetic 4-phenyl-piperidine analog of codeine. Its mechanism of action has some characteristics in common with clonidine and opioids. Not only does tramadol display central analgesic effects as the result of its monoaminergic and mu-receptor agonistic activity, it also has peripheral local anesthetic properties (4–6) and has a small potential for serious adverse effects (7,8).

Clinical studies to determine the analgesic efficacy of neuraxial tramadol added into epidural anesthesia in adults have yielded contradictory results. Some studies have shown that perimedullary tramadol enhances the duration and quality of local anesthetics or is comparable to morphine and bupivacaine when administered as the sole drug (9). Other studies have not demonstrated these effects (10). Tramadol also exhibits a noncentral analgesic effect that has led to its use as an adjunct to local anesthetics in the peripheral nervous system. Thus, IV retained tramadol prevents injection pain caused by propofol (11). Tramadol may also modify the action of lidocaine providing a shorter onset time of sensory block for IV regional anesthesia (12).

Few studies have investigated the effect of tramadol added to peripheral plexus blockade. All have concluded that the addition of 100 mg tramadol to brachial plexus anesthesia prolongs the duration of the sensory and motor block significantly (13–15). Kapral et al. (13) included a control group receiving 100 mg tramadol IV to exclude that the effect is central as a result of systemic absorption. Significantly increased duration of anesthesia in this study could only be demonstrated when tramadol was added to the brachial plexus. Antonucci (14) and Sarihasan et al. (15) also showed that the duration of postoperative analgesia is markedly prolonged. Antonucci demonstrated that tramadol provided similar prolongation of anesthesia and analgesia compared with sufentanil or clonidine but with a better side effect profile.

In summary, all three studies have shown that 100 mg tramadol as adjunct to brachial plexus anesthesia exerts a beneficial effect. Yet, the potential for doses of tramadol less than or more than 100 mg to provide maximum analgesia with minimal side effects is unknown. We decided to undertake a prospective, randomized and double-blind clinical trial to study the dose-effect relationship and determine the optimal dose of tramadol added to brachial plexus anesthesia for carpal tunnel release surgery.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Approval from the regional ethics committee and written consent from each patient was obtained. We performed a prospective, controlled, double-blind study with 100 ASA physical status I–II patients scheduled for carpal tunnel release surgery under axillary brachial plexus block. Patients receiving clonidine, opioids, or ß-blockers were excluded.

We allocated patients into 1 of 4 groups, each comprising 25 subjects, by envelope randomization. The anesthetic mixture contained 1.5% mepivacaine 40 mL plus 4 mL of the study solution containing isotonic sodium chloride (Group P), tramadol 40 mg (Group T40), tramadol 100 mg (Group T100), or tramadol 200 mg (Group T200).

Routine monitoring was applied and IV access secured for each patient. An experienced anesthesiologist performed axillary brachial plexus blockade inserting a 50-mm 22-gauge insulated short bevel needle (Stimuplex®; B. Braun, Melsungen, Germany) with the help of a peripheral nerve stimulator (Stimuplex® HNS 11; B. Braun).

Needle position was considered adequate when monostimulation of the median nerve at a current of <0.6 mA and duration of 0.1 ms triggered pronation or flexion at the wrist or flexion of the second and third fingers. The entire volume was slowly injected with a single injection technique after ensuring that twitches ceased immediately with the injection of 1 mL of the anesthetic solution.

Blockade of the musculocutaneous, radial, ulnar, median, and medial cutaneous nerves of the arm and forearm were evaluated at 5, 10, 20, and 30 min thereafter, at the end of surgery, and before discharge from the day case unit. Sensation in each dermatome was compared in the anesthetized and contralateral arm by light touch perception on a 3-point ordinate scale (0 = none, 1 = reduced, 2 = normal). Motor block was evaluated by thumb abduction (radial nerve), thumb adduction (ulnar nerve), thumb opposition (median nerve), and flexion at the elbow (musculocutaneous nerve) on a 3-point scale for motor function (0 = complete motor block, 1 = reduced motor strength but able to move fingers, 2 = normal motor function). Anesthesia was deemed sufficient for surgery when complete sensory blockade was obtained in the regions innervated by the ulnar and median nerve. Patients who did not achieve satisfactory levels of anesthesia and needed supplementation of any nerve block were excluded.

The time of onset of anesthesia was defined as the interval between the end of injection and maximum sensory blockade. The duration of sensory and motor block respectively was taken as the time interval between the maximum sensory or motor blockade and reappearance of paresthesia or complete recovery of motor function. Duration of analgesia was defined as the time elapsed between drug injection and the first request for analgesia. The severity of pain at that time was rated using a Visual Analog Scale (VAS, 0 = no pain and 10 = worst pain imaginable). Heart rate, arterial blood pressure, oxygen saturation, nausea, vomiting, pruritus, and the presence of any degree of sedation (not sedated = wide awake, sedated = not wide awake) were charted at the end of surgery, at the point of complete recovery of the sensory and motor blockade, and at the first request for analgesia. The recorded adverse events comprised hypotension (mean arterial blood pressure of <55 mm Hg), bradycardia (heart rate of <45 beats per minute), hypoxemia (oxygen saturation of <90%), nausea, vomiting, and pruritus (no = not present, yes = present).

The duration of analgesia was the primary outcome variable on which sample size estimation was based. To detect a 10% effect of intervention with an {alpha} risk of 5% and a power of 80%, an adequate sample size of 25 patients per group was calculated. Statistical analysis was performed using SAS® software version 6.18 (SAS Institute Inc, Cary, NC). Data were expressed as mean ± SD. The 4 groups were compared using the Mann-Whitney U-test for quantitative variables and {chi}2 tests for qualitative variables. For comparison of parametric data two-way analysis of variance was applied, and for nonparametric data Kruskal-Wallis analysis was followed by a Mann-Whitney U-test for two groups. Duration of analgesia was compared by a log-rank test. To evaluate a trend effect between groups the Cochran-Armitage tendency test was performed. A P value < 0.05 was considered significant.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
One-hundred patients were enrolled; 21 were excluded because they required additional nerve blocks for the surgical procedure. None of the remaining 79 patients required sedation or analgesia during the surgical procedure. Demographic data and technical anesthetic variables such as intensity of nerve stimulation and quality and extent of sensory and motor block were not significantly different among the 4 groups (Table 1).


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  		Table 1. Demographic Data
 
The onset time for median and ulnar nerve blockade as well as the duration of sensory and motor blockade was similar in each group, as shown in Table 2. The duration of analgesia demonstrated in Figure 1 was significantly longer in the groups where tramadol was added compared with the placebo group (P = 0.02). Duration of postoperative analgesia was shorter in the placebo and T40 group compared with the T200 group (P < 0.05).


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  		Table 2. Quality of Analgesia and Block Characteristics
 


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  		Figure 1. Duration of analgesia.

 
The number of patients requesting analgesia in the postoperative period was significantly less in the 3 tramadol groups compared with the placebo group (P = 0.02) (Table 2); this was also noted with the placebo and T40 groups compared with the T200 group. No statistical significance was demonstrated between the placebo and the T40 group or the T100 group and the T200 group. Furthermore, there was a significant trend effect among groups applying the Cochran-Armitage tendency test (P = 0.003), suggesting a dose-dependent decrease for additional postoperative analgesia requirements when tramadol was added.

The mean VAS scores were generally low and only showed a statistically significant difference among groups when measured at first analgesia request. At this point of the data collection the mean VAS scores were significantly reduced in all 3 tramadol groups together when compared with the placebo group (P = 0.01) and when singled out only between the placebo and the T200 groups. A significant result was not achieved among any of the other groups such as the placebo versus T40 or T100 groups, the T40 versus the T100 or T200 groups, or the T100 versus the T200 group (Table 2).

Although nausea/vomiting and sedation were more frequently recorded in the tramadol groups, neither a statistical difference nor a significant trend effect was seen among the groups (Table 3). Episodes of hypotension, bradycardia, or hypoxemia as defined previously were not observed in any group throughout the study.


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  		Table 3. Adverse Effects Observed Throughout the Study
 

   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The central and peripheral analgesic effects of tramadol have not been fully explained (4,5). The actions of the two enantiomers contained in the racemic mixture are complementary and synergistic. (+)-tramadol is a selective agonist of mu-receptors that is 6000 times weaker than morphine. Its analgesic properties can be reversed by the opioid antagonist naloxone, which preferentially inhibits serotonin (5-HT, 5-hydroxytryptamine) and noradrenalin uptake whereas tramadol mainly inhibits noradrenaline uptake. Tramadol also promotes serotonin and noradrenaline release. The monoaminergic activity of tramadol enhances the inhibitory activity of the descending pain pathways, resulting in a suppression of nociceptive transmission at the spinal level. This effect is partially reversed by the antagonists ritanserin and yohimbine at {alpha}-2-receptors and also by the competitive antagonist ondansetron at serotonin subtype 3(5-HT3) receptors (16).

Explanations for the local anesthetic action of tramadol remain hypothetical (16–18). 5-HT3 receptors are expressed on the peripheral and spinal terminal of the nociceptive primary afferent fibers (PAF) as well as on the superficial laminae of the dorsal horn, but serotonin agonists at the presynaptic level, in regard to the PAF, mediate a pro-nociceptive action. Mert et al. (19) have shown a definitive local anesthetic effect of tramadol in experiments on frog sciatic nerves. In their animal study, the nerve conduction block of tramadol was 3–6 times weaker than that of lidocaine. Interestingly, adding calcium to the test solution decreased the local anesthetic effect of lidocaine but enhanced that of tramadol. Therefore, the blocking mechanism of the two drugs is likely to be different. Although lidocaine inhibits Na channels, it has been suggested that tramadol inhibits K channels. Animal studies have also been done to investigate the anesthetic properties of the tricyclic antidepressant amitriptyline and its derivative N-methyl amitriptyline (20). Like tramadol they are inhibitors of noradrenaline and 5-HT uptake. In addition, they show potent spinal and sciatic nerve anesthesia as the result of Na+ channel blockade.

Three publications state that tramadol modifies peripheral plexus anesthesia (13–15). Kapral et al. (15) were the only group to choose the local anesthetic mepivacaine but at the weaker concentration of 1% compared with our study. They concluded that 100 mg tramadol significantly prolongs the motor and sensory blockade, a result we did not observe. One possible explanation is the discrepancy of definition for these terms between the two studies. We set the starting point of the duration of anesthesia as the maximum sensory or motor blockade respectively and the end-point of sensory blockade as reappearance of paresthesia. Kapral et al. defined these points as the time of injection and the offset of paresthesia. Sensation was assessed by method of light touch perception in our study and pinprick perception in Kapral et al.’s study. Furthermore, the primary outcome variable in Kapral et al.’s study was duration of anesthesia, whereas we based our sample size calculation on the duration of analgesia. Kapral et al. were the only researchers to also include a control group receiving 100 mg tramadol IV. The additional anesthetic effect was observed when adding tramadol to the brachial plexus but not in the control groups. Therefore, it is unlikely that the prolonged duration of anesthesia was a result of systemic absorption. Antonucci (14) and Sarihasan et al. (15) added tramadol to the longer acting local anesthetics ropivacaine 0.75% and bupivacaine 0.25% respectively. Therefore, direct comparison to our study is of limited value. Antonucci compared different adjuncts (100 mg tramadol, 1.5 µg/kg clonidine, 20 µg sufentanil) to brachial plexus anesthesia against a control group. This study showed that all three substances reduced the onset time of brachial plexus blockade and prolonged the duration of anesthesia and postoperative analgesia significantly to the same extent. Sarihasan et al. concluded that 100 mg tramadol as adjunct to supraclavicular plexus blocks improved the quality of anesthesia and extended the duration of postoperative analgesia. These three studies found no difference to the placebo group when investigating the occurrence of adverse effects of 100 mg tramadol added to the brachial plexus, and our study confirmed these results. Antonucci found that in comparison with tramadol the adjuncts clonidine and sufentanil resulted in an increase in both sedation score and incidence of respiratory depression with SaO2 <90%. In addition, clonidine caused hypotension and bradycardia. Clonidine as an adjunct to enhance anesthesia and analgesia, as well as for adverse effects, is dose-dependent. The effective dose is as small as 0.5 µg/kg, one-third of the amount used in Antonucci’s study.

The lack of preclinical trials to prove the safety of tramadol for use in a peripheral nerve sheath may raise concern. Whether there is evidence of neurotoxicity has been the focus of only one study. Tsai et al. (21) measured spinal somatosensory evoked potentials (SSEP) after tramadol application to the sciatic nerve in rats. The amplitude and conduction velocity of the SSEPs was reduced dose-dependently when compared with the baseline data. Changes were only temporary and there was no evidence of irreversible conduction blockade indicative of direct neural toxicity. Clinical trials with tramadol applied via the perimedullary route have been published since 1990 and experience is mounting. Localized neural toxicity of the central nervous system has not been reported. Presently, there is no evidence that tramadol causes damage to the peripheral system.

The value of tramadol as an adjunct to peripheral plexus block with local anesthetics is uncertain. Our study provides additional evidence of benefit.

We conclude that, when added to brachial plexus anesthesia, tramadol extends the duration and improves the quality of postoperative analgesia in a dose-dependent fashion. The incidence of adverse effects also increases with larger doses, but the side effect profile remained acceptable up to 200 mg tramadol in our study.


   References
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 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication November 6, 2003.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press