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*Clinique chirurgicale Bordeaux-Mérignac, Mérignac; and ISPED, Université Bordeaux 2, France
Address correspondence and reprint requests to Henri Iskandar, MD, Clinique chirurgicale Bordeaux-Mérignac, 9 rue Jean-Moulin, 33700 Mérignac, France. Address e-mail to henri.iskandar@ wanadoo.fr.
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Abstract |
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IMPLICATIONS: Clonidine administered via an interscalene catheter enhanced analgesia compared with systemic administration. Nevertheless, the adverse effect of clonidine at this dose limits its use for routine management for postoperative analgesia.
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Introduction |
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Methods |
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Patients did not receive any premedication. Arterial blood pressure, heart rate, and hemoglobin oxygen saturation were recorded during the entire study. Using a nerve stimulator, an interscalene catheter (Contiplex D, Braun, Sheffield, UK) was inserted by a single anesthesiologist experienced in the technique using a standard insertion procedure; the required position of the needle was determined when an output lower than 0.7 mA still produced a characteristic deltoid motor response. The catheter was advanced and secured with a transparent occlusive dressing. Paresthesias were not intentionally sought.
The patients were randomly divided into two groups. The interscalene group (n = 20) received clonidine 150 µg in 15 mL of saline through the catheter and 1 mL of subcutaneous saline. The systemic group (n = 20) received 15 mL of saline through the catheter and clonidine 150 µg (1 mL) subcutaneously. General anesthesia was induced with IV propofol 3 mg/kg and remifentanil and maintained with isoflurane and remifentanil with 50% N2O in O2 through an endotracheal tube.
On completion of arthroscopy, the patient was transferred to the postanesthesia care unit (PACU). Pain was evaluated for 24 h using a visual analog scale (VAS) by a nurse blinded to the analgesic technique used. The VAS, ranging from 0 mm (no pain) to 100 mm (worst imaginable pain), was assessed in the recovery room and 4, 8, 12, 16, and 24 h after surgery. Sensory block was evaluated using ice on the shoulder and scored as absent, diminished, or normal. Motor block was tested in the deltoid muscle and scored as absent, diminished, or normal.
All patients received patient-controlled analgesia via the interscalene catheter using 0.2% ropivacaine with an 8-mL bolus and a 1-h lockout interval. Additional postoperative analgesia was available with parenteral nalbuphine if required until VAS < 3. Analgesic duration was defined as the time from the end of surgery to the first requirement of an analgesic.
The postoperative analgesia protocol was initiated in the PACU and continued in the surgical ward. Data analysis was performed using SAS Software (version 8.2; SAS Institute Inc, Cary, NC). We defined analgesic duration as the primary outcome. Kaplan-Meier estimate was used to compare this outcome between the two groups. For this test, a P value <0.05 was considered to be statistically significant.
As a secondary analysis, we compared the groups according to ropivacaine and nalbuphine consumption and VAS scores measured at 0, 4, 8, 12, 16, and 24 h after surgery. For each of these variables, we found an equal variance between the two groups. VAS score at 0 h and ropivacaine and nalbuphine consumption had a normal distribution in both groups. A t-test was used to analyze these outcomes. VAS scores measured 4, 8, 12, 16, and 24 h after surgery did not have a normal distribution, thus we used Wilcoxon’s test for the statistical comparison of these variables in the two groups. For these secondary analyses, a P value <0.05 was considered to be statistically significant. Two-sided significance tests were used throughout.
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Results |
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Ropivacaine consumption was significantly less in the interscalene group than in the systemic group (P < 0.0001). Similarly, a significant difference was observed between the groups for nalbuphine consumption 7 (95% CI, 3.6–10.4) versus 14 (95% CI, 8.7–19.3; P < 0.05).
Analgesic duration was significantly longer in the interscalene group (P < 0.00001) (Fig. 1). Sensory and motor function were preserved in all patients.
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Discussion |
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The postoperative pain scores were significantly lower in the interscalene group only during PACU stay. However, the analgesic duration was significantly longer in the interscalene group, suggesting that interscalene clonidine enhanced the postoperative analgesia compared with subcutaneous clonidine. Nevertheless, the adverse effects of clonidine limit the advantages of this method, particularly in outpatient surgery, because residual orthostatic hypotension places the patient at risk of falling after discharge. Moreover, the analgesic effect of interscalene clonidine alone was not sufficient in all patients in the interscalene group who required use of supplemental analgesia (ropivacaine and nalbuphine).
Concerning the mechanism of action of clonidine on peripheral nerves, Eisenach et al. (7), after a clinical review, concluded that a peripheral action of clonidine was evident. The duration of anesthesia or analgesia was enhanced by clonidine added to the local anesthetic after plexus block (8,9) but not by subcutaneous and IM clonidine injections (10,11). In in vitro experiments, Butterworth and Strichartz (1) and Gaumann et al. (2) showed direct neuronal effects of clonidine. In an isolated rabbit vagus preparation, a very small dose of clonidine enhances the effects of lidocaine on C-fiber action potentials. Other investigators proposed that clonidine may exert a peripheral analgesic action by releasing enkephalin-like substances (12).
When used as the sole analgesic, clonidine produces analgesia after central (3,4) block and intraarticular administration (5). In a previous study, we demonstrated that by selectively applying clonidine with local anesthetics in the midhumeral block technique, it is possible to prolong the duration of sensory block in one or several trunks of the brachial plexus (13). Sia et al. (6) used clonidine as the sole analgesic for axillary block. The authors concluded that the administration of clonidine alone through an axillary catheter did not enhance postoperative analgesia after hand and forearm surgery and that clonidine must be added to a local anesthetic to produce improvement in postoperative analgesia. However, the absence of efficacy in their study may be explained by the inability of clonidine administered through the axillary catheter to spread uniformly through the axillary sheath because of septa separating the nerves (14). Therefore, there may have been an insufficient concentration of the drug at the level of the nerve fibers. Moreover, the difference of efficacy with the present study may be explained by the proximity from the exit of these nerve roots from the spinal cord where clonidine produces postoperative analgesia.
In conclusion, clonidine administered to the interscalene plexus enhanced analgesia compared with systemic administration. There was an increased time to first analgesic request and a decreased need for postoperative analgesics. Nevertheless, the adverse effect of clonidine and its insufficiency in producing alone a profound depth of analgesia limits its use as routine management for postoperative analgesia.
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References |
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2-adrenergic agonist clonidine and guanfacine produce tonic and phasic block of conduction in rat sciatic nerve fibers. Anesth Analg 1993; 76: 295–301.[Web of Science][Medline]
This article has been cited by other articles:
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  S. Blumenthal, M. Nadig, A. Borgeat, and I. Henri The Analgesic Effect of Interscalene Block Using Clonidine as an Analgesic for Shoulder Arthroscopy: Where Is the Catheter? * Response Anesth. Analg., September 1, 2003; 97(3): 928 - 928. [Full Text] [PDF]
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