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Original Article

Addition of dexmedetomidine to lidocaine for intravenous regional anaesthesia1

Esmaoglu, A.*; Mizrak, A.*; Akin, A.*; Turk, Y.; Boyaci, A.*

Author Information
European Journal of Anaesthesiology: June 2005 - Volume 22 - Issue 6 - p 447-451
doi: 10.1017/S0265021505000761

Abstract

Intravenous regional anaesthesia (IVRA) is a simple and reliable method of providing anaesthesia for hand surgery. The administration of IVRA only requires the skill necessary to perform a venipuncture, but IVRA occasionally does not provide effective anaesthesia and postoperative analgesia.

To improve the quality of IVRA and postoperative analgesia, addition of various drugs to local anaesthetics has been investigated with controversial results [1-5]. Studies investigating the addition of clonidine to local anaesthetic solution in IVRA have demonstrated reduced tourniquet pain and improved postoperative pain relief without adverse effects [6,7]. Dexmedetomidine, an imidazole compound, is the pharmacologically active dextroisomer of medetomidine. It is a potent α2-adrenoceptors agonist with eight times higher affinity for the α2-adrenoceptor than clonidine [8].

The aim of this study was to determine the quality of anaesthesia and postoperative analgesia by the addition of dexmedetomidine to local anaesthetic solution for IVRA.

Patients and methods

Forty patients scheduled for elective hand surgery by a single surgeon gave formal, written consent to participate in this prospective double-blind study, which was approved by our institutional review board. They were scheduled to undergo carpal tunnel release or tendon release. Patients with Raynaud's disease, sickle cell anaemia or a history of allergy to any drug used were excluded from the study.

Standard monitors including electrocardiography, noninvasive blood pressure (BP) measurement and pulse oximetry were used. Patients were allocated randomly into two groups according to a sealed envelope technique in a double-blind manner. Two intravenous (i.v.) cannulae were inserted, one in the hand to be operated on and the other in the contralateral hand for crystalloid infusion. A double tourniquet was positioned on the upper operative arm. The operative extremity was exsanguinated by elevating and wrapping it with a 10-cm Esmarch bandage. The proximal tourniquet was inflated to 100 mmHg more than systolic BP to a minimum of 250 mmHg and the Esmarch bandage was removed. Circulatory isolation of the operative arm was confirmed by inspection of the hand and by the absence of the radial pulse. IVRA was achieved using 3 mg kg−1 lidocaine diluted with saline to a total volume of 40 mL in the control group or 1 μg kg−1 of dexmedetomidine (Precedex® 200 μg/2 mL; Abbott) +3 mg kg−1 lidocaine diluted with saline to a total volume of 40 mL in the dexmedetomidine group. IVRA solutions were administered slowly via the cannula over 3 min.

Sensory block was assessed at 30 s intervals using a 25-G short beveled needle by a blinded observer. Sites used for sensory testing included the thenar eminence (median nerve), hypothenar eminence (ulnar nerve) and first web space (radial nerve). In addition, sensory regression was assessed at these same nerve sites at 30 s intervals after tourniquet deflation. Motor function was assessed by asking the patient to flex and extend his/her wrist and complete motor block was noted when no voluntary movement was possible.

After sensory and motor blocks were achieved, the distal tourniquet was inflated to 250 mmHg, the proximal tourniquet was released and surgery started. Mean arterial pressure and heart rate (HR) were recorded every 5 min. A 20% decrease of mean arterial pressure compared to the preoperative values was regarded as hypotension. HR lower than 55 beats min−1 were regarded as bradycardia.

At the end of the operation, the quality of anaesthesia was assessed according to the following numeric scale - excellent (4): no complaint from patient; good (3): minor complaint with no need for supplemental analgesics; moderate (2): complaint which required supplemental analgesics; unsuccessful (1): patient given general anaesthesia. Fentanyl® (fentanyl citrate; Abbott) was used to supplement analgesia if required.

At the end of the surgery, tourniquet deflation was performed by the cyclic deflation technique. Sensory and motor blocks regression time was noted. A blinded observer assessed the patient's pain and sedation levels 0 min (just after deflation), 15 min, 30min, 1 and 2 h after tourniquet deflation. Pain was assessed using a 10-cm visual analogue scale (VAS) (0: no pain to 10: the worst pain imaginable) and sedation on a numeric scale (0: alert; 1: arouses to voice; 2: arouses with gentle tactile stimulation; 3: arouses with vigorous tactile stimulation; 4: unrouseable).

An i.v. bolus of fentanyl 50 μg was administrated in the postanaesthesia care unit, whenever pain score exceeded 3. Intraoperative and postoperative fentanyl requirement was noted. These measurements were recorded by a resident who did not know which drug had been administered. Measurements in all patients were performed by the same resident. Any local or systemic complications were recorded during the study period.

Patient characteristic data, duration of surgery, tourniquet times, sensory and motor blocks onset and regression time, and analgesic requirement were analysed using t-test. Gender distribution was analysed with χ2-test. Qualities of anaesthesia, pain and sedation scores were analysed using the U-test. A P value <0.05 was accepted as statistically significant.

Results

There were no significant differences in age, weight, gender distribution, duration of surgery and tourniquet time (Table 1). There was no difference between two groups with respect to the sensory and motor blocks onset and regression time (P > 0.05, Table 2). Quality of anaesthesia was better in the dexmedetomidine group than the control group and this difference was statistically significant (P < 0.05, Table 3). Intraoperative and postoperative fentanyl requirements were lower in the dexmedetomidine group than the control group and this difference was statistically significant (P < 0.05, Table 3).

Table 1
Table 1:
Patient characteristic data (mean ± SD).
Table 2
Table 2:
Sensory and motor blocks onset and regression time (min).
Table 3
Table 3:
Quality of anaesthesia and fentanyl requirement.

Baseline mean arterial pressure and HR values were comparable. Mean arterial pressure in the dexmedetomidine group was lower than the control group at 45, 60 min and this difference was statistically significant (P < 0.05, Fig. 1). The variations of BP did not increase more than 20% of basal values in any patient. HR was similar in both groups at all time points (P > 0.05, Fig. 2). According to the baseline assessment, differences in mean arterial pressure and HR during the intraoperative and postoperative period were not statistically significant in both groups.

Figure 1.
Figure 1.:
Mean arterial pressure.
Figure 2.
Figure 2.:
Heart rate.

Postoperative pain score in the dexmedetomidine group was lower than the control group and the difference was statistically significant at 0, 15, 30 and 60 min (Table 4). Sedation score values at 0, 15, 30, 60, 120 min were higher for the dexmedetomidine group than the control group (Table 5). There were no adverse effects throughout the intraoperative and postoperative period in either group. No patient experienced hypotension, bradycardia or hypoxaemia.

Table 4
Table 4:
Postoperative pain score (VAS 0-10).
Table 5
Table 5:
Postoperative sedation score.

Discussion

Our study demonstrated that the addition of 1 μg kg−1 dexmedetomidine to lidocaine for IVRA improved quality of anaesthesia and postoperative analgesia, without causing side-effects.

Dexmedetomidine is a potent α2-adrenoceptor agonist with eight times higher affinity for the α2-adrenoceptors than clonidine. Clonidine induces analgesia mainly through stimulation of α2-adrenegic receptors in the dorsal horn of the spinal cord. It also depresses nerve fibre action potentials especially in small, unmyelinated C fibres [9]. In previous clinical studies clonidine has been used as an adjuvant for IVRA [6,7]. Gentili and colleagues [7] showed that clonidine 150 μg produced a significant increase in tourniquet tolerance in patients undergoing IVRA. Lurie and colleagues [10] reported the efficacy of 1 μg kg−1 clonidine added to IVRA lidocaine in decreasing the onset of severe tourniquet pain and found that it delayed the onset time. Reuben and colleagues [6] demonstrated lower pain scores and lower analgesic consumption in patients who received clonidine and lidocaine for IVRA.

Dexmedetomidine produces sedation, analgesia and anxiolysis [8]. Reports of animal studies showed that dexmedetomidine reduced anaesthetic and analgesic requirements in rats [11] and dogs [12]. Previous clinical studies with dexmedetomidine have demonstrated reduced anaesthetic requirements. A previous human study showed that dexmedetomidine decreased the minimum alveolar concentration (MAC) of isoflurane by up to 47% depending on its dose [13]. Dexmedetomidine 0.7 ng mL−1 decreased the MAC of sevoflurane by 17% [14]. The anaesthetic requirement of dexmedetomidine-treated patients undergoing abdominal hysterectomy was significantly reduced when compared with placebo in a double-blind placebo-controlled trial [15].

Dexmedetomidine also has analgesic effect, which may have clinical implications. Dexmedetomidine also significantly reduced rescue analgesic requirements compared with placebo in postsurgical patients. Aho and colleagues [16] concluded that i.v. administered dexmedetomidine relieved pain and reduced opioid requirement after laparoscopic tubal ligation. However, patients who received dexmedetomidine were more sedated than other patients in the study.

α2-adrenergic receptors located at nerve endings may play a role in the analgesic effect of the drug by preventing norepinephrine release [17,18]. The actions of dexmedetomidine are suggested to be mediated through postsynaptic α2-adrenoceptors which activate pertussis toxin-sensitive-G proteins thereby increasing conductance through potassium ion channels. Studies in transgenic mice have demonstrated that the α2A-adrenoceptor subtype is responsible for relaying the sedative and analgesic properties of dexmedetomidine [8,17,18]. The use of an α2-agonist as an adjunct in pain management is attractive because of the potentiation that occurs through their action at the central and peripheral sites [19].

A recent study by Memis and colleagues [20] found that the addition of dexmedetomidine 0.5 μg kg−1 to lidocaine for IVRA leads to significant decreases in sensory and motor blocks onset time compared with a control group. In contrast to their study, we documented the sensory and motor blocks onset times to be similar as were sensory and motor blocks regression times, although we used 1 μg kg−1 of dexmedetomidine.

In this study, we observed that dexmedetomidine increased the quality of anaesthesia and decreased the postoperative analgesic requirements. Increased quality of anaesthesia may be explained by the peripheral effect of dexmedetomidine in IVRA. Less analgesic requirements and occurrence of sedation after tourniquet release in the dexmedetomidine group may be explained by the central effect of dexmedetomidine.

Dexmedetomidine causes a dose-dependent decrease in BP and HR associated with decreased concentration of plasma norepinephrine [21]. We preferred to use dexmedetomidine at a dose of 1 μg kg−1, and at this dose we did not observe any side-effect such as hypotension or bradycardia which required treatment.

In conclusion, the addition of 1 μg kg−1 dexmedetomidine to lidocaine for IVRA improves quality of anaesthesia and postoperative analgesia without causing side-effects, but it does not shorten onset time of sensory and motor blocks.

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1Presented at Euroanaesthesia Lisbon, 5-8 June 2004.

Keywords:

ANAESTHESIA CONDUCTION; intravenous regional block; ANAESTHETICS LOCAL; lidocaine; DEXMEDETOMIDINE

© 2005 European Society of Anaesthesiology