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REGIONAL ANESTHESIA

Dexamethasone Added to Lidocaine Prolongs Axillary Brachial Plexus Blockade

Ali Movafegh, MD^*, Mehran Razazian, MD^*, Fatemeh Hajimaohamadi, MD^*, and Alipasha Meysamie, MD

*Department of Anesthesiology and Critical Care, Dr. Ali Shariati Hospital; and Department of Community Medicine, Tehran University of Medical Sciences, Tehran, Iran

Address correspondence and reprint requests to Ali Movafegh MD, Department of Anesthesiology and Critical Care, No: 57, 25^th Ave, Jahan Ara Street, Tehran 1438794811, Iran. Address e-mail to movafegh{at}sina.tums.ac.ir or ali{at}movafegh.com.

	Abstract

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Different additives have been used to prolong regional blockade. We designed a prospective, randomized, double-blind study to evaluate the effect of dexamethasone added to lidocaine on the onset and duration of axillary brachial plexus block. Sixty patients scheduled for elective hand and forearm surgery under axillary brachial plexus block were randomly allocated to receive either 34 mL lidocaine 1.5% with 2 mL of isotonic saline chloride (control group, n = 30) or 34 mL lidocaine 1.5% with 2 mL of dexamethasone (8 mg) (dexamethasone group, n = 30). Neither epinephrine nor bicarbonate was added to the treatment mixture. We used a nerve stimulator and multiple stimulations technique in all of the patients. After performance of the block, sensory and motor blockade of radial, median, musculocutaneous, and ulnar nerves were recorded at 5, 15, and 30 min. The onset time of the sensory and motor blockade was defined as the time between last injection and the total abolition of the pinprick response and complete paralysis. The duration of sensory and motor blocks were considered as the time interval between the administration of the local anesthetic and the first postoperative pain and complete recovery of motor functions. Sixteen patients were excluded because of unsuccessful blockade. The duration of surgery and the onset times of sensory and motor block were similar in the two groups. The duration of sensory (242 ± 76 versus 98 ± 33 min) and motor (310 ± 81 versus 130 ± 31 min) blockade were significantly longer in the dexamethasone than in the control group (P < 0.01). We conclude that the addition of dexamethasone to lidocaine 1.5% solution in axillary brachial plexus block prolongs the duration of sensory and motor blockade.

	Introduction

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Increasing the duration of local anesthetic action is often desirable because it prolongs surgical anesthesia and analgesia. Different additives have been used to prolong regional blockade. Vasoconstrictors can be used to vasoconstrict vessels, thereby reducing vascular absorption of the local anesthetic. Clonidine has also been studied in combination with local anesthetics (lidocaine, mepivacaine, bupivacaine) in axillary brachial plexus block (1). Some studies have demonstrated the analgesic effect of local spinal and systemic corticosteroids in combination with bupivacaine (2,3). Dexamethasone microspheres have been found to prolong the block duration in animal and human studies (4–6), and adding methylprednisolone to local anesthetic increases the duration of axillary brachial block (7). However, these findings must be verified in a randomized prospective clinical trial.

The present placebo-controlled clinical trial evaluates the effect of dexamethasone added to lidocaine on the onset and duration of axillary brachial plexus block.

	Methods

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After institutional approval and obtaining informed patient consent, 60 ASA physical status I-II patients aged 20–50 yr scheduled for elective short to moderate (<90 min) hand and forearm surgery under axillary brachial plexus block were included in the study. Patients with a history of peptic ulcer disease, diabetes mellitus, hepatic or renal failure, pregnant women, and those receiving any premedications (including opioids, benzodiazepines, and clonidine) were excluded from the study.

Patients were allocated into 2 groups in a controlled, randomized double-blind design using a computer-generated randomization list to receive either 34 mL lidocaine 1.5% with 2 mL of isotonic saline chloride (control group, n = 30) or 34 mL lidocaine 1.5% with 2 mL of dexamethasone (8 mg) (dexamethasone group, n = 30). Neither epinephrine nor bicarbonate were added to mixtures. All local anesthetic solutions and adjuvant drugs were prepared by an anesthesiologist not involved in the performance of brachial plexus block, patient care, or data collection.

On arrival to the operating room, standard monitoring was established (pulse oximetry, electrocardiography, and noninvasive arterial blood pressure monitoring) and oxygen was delivered via a Venturi facemask at a rate of 3 L/min. After insertion of a 20-gauge IV catheter in a peripheral vein in the contralateral arm and administration of 1 µg/kg IV fentanyl, axillary block was performed with the patient in the supine position and the upper arm abducted 90° and the elbow flexed at 110°. A nerve stimulator (Polymedic®) with a 24-gauge 7 cm Sprotte needle was used for precise localization of each nerve. The stimulation frequency was set at 3 Hz, the duration of stimulation at 0.1 ms, and the intensity of the stimulating current was initially set to deliver 3 mA and was then gradually decreased. The position of the needle was considered to be acceptable when an output current <0.7 mA still elicited a slight distal motor response in each of the nerve distributions (thumb opposition for median, thumb abduction for radial, thumb adduction or ulnar deviation of the hand for ulnar, and flexion of forearm on the arm for musculocutaneous nerves). We used multiple stimulations technique in all of the patients. Increments of anesthetic mixture (8 mL/nerve in total) were injected through a stationary needle after identifying the 4 nerves in each patient in the following order: median, radial, ulnar, and musculocutaneous. The remaining 4 mL was injected subcutaneously as the needle was withdrawn to block the intercostobrachial nerve. In case of blockade failure in any of the nerve distributions (i.e., if the patient did not achieve satisfactory levels of anesthesia) or in any of the nerve distributions that complete sensory (zero in verbal analog scale) or motor (zero in Levvott rating scale) block did not reach, the patients were excluded from the study and replaced on the randomization list, even when the block was adequate for surgery.

Sensory and motor blockade of radial, median, musculocutaneous and ulnar nerves were recorded after 5, 15, and 30 min and every 10 min after the end of the surgery. Sensory blockade of each nerve was assessed by pinprick and compared with the same stimulation on the contralateral hand. Sensory blockade of each nerve was rated by the patient on a verbal analog scale from 100% (normal sensations) to 0% (no sensation). Motor block was evaluated by thumb abduction (radial nerve), thumb adduction (ulnar nerve), flexion of the elbow in supination and pronation of the forearm (musculocutaneous), and thumb opposition (median nerve). Measurements were performed using a modification of the Lovett rating scale from 6 (normal muscular force) to 0 (complete paralysis) (1). The onset time of the sensory and motor blockade was defined as the time between the end of last injection and the total abolition of the pinprick response and complete paralysis in all of the nerve distributions. The duration of sensory block was considered as the time interval between the administration of the local anesthetic and the first postoperative pain, and the duration of motor block was defined as the time interval between the local anesthetic administration and complete recovery of motor functions. The patients and the anesthesiologist who evaluated the sensory and motor blockades were blinded as to the mixture used.

In the absence of historical data, the necessary sample size was estimated based on a pilot study of 10 patients. Dexamethasone added to lidocaine prolonged the duration of the axillary brachial plexus sensory block from 100 ± 45 min to 165 ± 73 min compared with placebo. It was estimated that a minimum of 27 patients in each group would be required to have an 80% power of detecting a 35-min difference at a significance level of 0.05. Statistical analysis was performed with SPSS for Windows (SPSS Inc., Chicago, IL), version 11.5. For statistical analysis of demographic data and for comparison of groups, ², Kruskal-Wallis test, Mann-Whitney U-test, and independent Student's t-test analyses were performed.

	Results

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Sixteen patients were excluded from study because of unsuccessful blockade (Table 1). The mean patient age, weight, and height and the duration of surgery were similar in the two groups (Table 1). There was no significant difference in the onset time of the sensory (14 ± 5 min in dexamethasone group versus 11 ± 4 min in control group) and motor (26 ± 7 min in dexamethasone group versus 22 ± 8 min in control group) block between groups. The duration of sensory (242 ± 76 min in dexamethasone group versus 98 ± 33 min in control group) and motor (310 ± 817 min in dexamethasone group versus 130 ± 31 min in control group) blockade were significantly longer in the dexamethasone than in the control group (P < 0.01). The sensory and motor blockade of axillary block of each nerve distribution at the 5-, 15-, and 30-min points is presented in Table 2; there was no statistical difference between groups (Table 2).

	Discussion

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The present study indicates that the addition of 8 mg dexamethasone to 34 mL lidocaine 1.5% for axillary brachial plexus block results in a significant increase in duration of sensory and motor blocks but that the onset time of sensory and motor blockade is similar.

In our study, duration of axillary brachial plexus block with lidocaine (98 ± 33 minutes and 130 ± 31 minutes for sensory and motor blockade) is moderately shorter than other works (8).

Ten patients in the control group and 6 patients in the dexamethasone group (approximately 21% of the patients in this study) failed to achieve satisfactory levels of anesthesia and required induction of general anesthesia. The 21% incidence of failure may be frequent (9), but this is comparable to an incidence that has been reported in some previous studies on various local anesthetics (8,10–12). Also, the incidence of block failure did not differ significantly between groups.

Previous works demonstrated that the addition of corticosteroid microspheres to local anesthetic prolonged duration of blockade of the peripheral nerves (4–6). In one study, a prolonged percutaneous blockade of sciatic nerve in rat using bupivacaine-dexamethasone microspheres was demonstrated (4). In another study, incorporation of dexamethasone into bupivacaine microspheres significantly prolonged intercostal nerve block in sheep (5). It has been reported that the intercostal injection of dexamethasone-containing bupivacaine microcapsules produces a prolonged duration of anesthesia and analgesia (6). These authors believe that there is a causative relationship between the suppression of inflammation and the remarkably longer duration of effect (5). In our study, however, the prolongation of blocks by adding dexamethasone could have been caused by a completely different mechanism.

Other preliminary data suggest that methylprednisolone can increase the duration of sensory and motor block. In this study (7), patients were divided into 2 groups to receive solutions containing 20 mL mepivacaine, 20 mL bupivacaine, 0.2 mL epinephrine, and, in one group, 40 mg methylprednisolone was added to this solution. The authors found that the duration of sensory analgesia (23 hours versus 16 hours; P < 0.01) and motor block (19 hours versus 13 hours; P < 0.001) were significantly longer in the steroid group. The authors believed that the applicability of these findings to clinical practice should be verified in a randomized prospective clinical trial.

Although corticosteroids have been used successfully for postoperative pain relief in oral, general, and orthopedic surgery (13,14), other studies have not corroborated these reports (15,16).

The mechanism of the analgesia induced by corticosteroids is not fully understood. This effect is suspected to be mediated by their antiinflammatory or immune-suppressive effects (17,18). The use of corticosteroids as an adjuvant to local anesthetic for peripheral nerve blocks rarely has been described, and its mechanism of action is not clearly understood. Corticosteroids cause skin vasoconstriction on topical application. The vasoconstriction effects of topical steroids are mediated by occupancy of classical glucocorticoid receptors rather than by nonspecific pharmacological mechanisms (19,20). According to the traditional theory of steroid action, steroids bind to intracellular receptors and modulate nuclear transcription. In our study, dexamethasone produced a relatively rapid effect which cannot be explained by the above mechanism (21). Therefore, vasoconstriction, the presumed mechanism of action for epinephrine's adjunctive effect on local anesthetics, is probably not responsible for block prolongation by dexamethasone. Corticosteroids may have a local effect on the nerve; the dexamethasone effect may be related to this action (22).

One possibility is that prolongation of local anesthetic block occurs because of systemic effects of dexamethasone. Some authors believe that analgesic properties of corticosteroids are the result of their systemic effect (13,14). Unfortunately, a control group receiving parenteral administration of the same dose of dexamethasone was not considered when this study was designed. It was not the aim of this study, however, to elucidate the mechanism of action of dexamethasone. Because of our positive results, the question of whether these results were attributable to a local or systemic effect warrants further investigation.

The safety of dexamethasone use in a nerve sheath may raise some concerns. In animal experiments, repeated intrathecal injections of small-dose betamethasone (23) and triamecilonon acetate (24) did not induce spinal neurotoxicity. In one study, after approximately 2000 intrathecal injections of dexamethasone (8 mg) in 200 patients for treatment of posttraumatic visual disturbance, no neurological disorders were found at 1-month follow up (25). Nerve injury is a rare complication of dexamethasone injection, and it usually occurs in the context of needle trauma (26,27).

The use of dexamethasone as an adjuvant to local anesthetics for peripheral nerve block has not been described; we used a dose of 8 mg because administration of this dose seems to be safe in adults. Adverse effects with a single dose of dexamethasone are probably extremely rare and minor in nature, and previous studies have demonstrated that short-term (<24 hours) use of dexamethasone was safe (16,28).

Adding a steroid to local anesthetic solution may not be indicated for all patients. For example, diabetic patients may experience hyperglycemia and patients with a continuing infectious process may be detrimentally affected by the antiinflammatory effects of steroids. The use of dexamethasone to increase the duration of action of local anesthetics is not an indication of this drug. This study led us to hypothesize that it may be useful in situations in which epinephrine must be used with caution (e.g., hypertension, ischemic heart disease).

In our center, lidocaine is routinely used for regional block procedures, which is why we chose lidocaine for this study. Considering cardiovascular toxicity, lidocaine is safer than bupivacaine. However, repetition of this study could be done with longer-acting drugs, such as bupivacaine or ropivacaine, to assess the effect of dexamethasone on duration of sensory and motor blockade.

In conclusion, the addition of dexamethasone to lidocaine 1.5% solution in axillary brachial plexus block prolongs the duration of sensory and motor blockade. Further studies are needed to evaluate the optimal dose of dexamethasone to be used for prolonged brachial plexus block as well as the mechanism of this effect.

	Footnotes

 
Accepted for publication August 24, 2005.

The authors have no financial or proprietary interest in the instrumentation used.

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Movafegh, A. Articles by Meysamie, A. Search for Related Content PubMed PubMed Citation Articles by Movafegh, A. Articles by Meysamie, A.