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Intravenous regional anaesthesia is a simple, safe and effective technique with good success rate for upper limb surgeries. The duration of postoperative analgesia is an important limitation of this technique. Various adjuvants have been used to overcome this drawback. In this study we evaluate the effect of dexmedetomidine 0.5 μgkg-1 as an adjuvant for lignocaine intravenous regional anaesthesia.
Sixty patients scheduled to undergo upper limb surgery were randomised to receive intravenous regional anaesthesia with lignocaine alone (Group L) or lignocaine with dexmedetomidine 0.5 μgkg-1 (Group LD). The quality of anaesthesia, onset of sensory and motor blocks and duration of postoperative analgesia were noted.
The onset of sensory and motor block was significantly rapid in group LD compared to group L (Group LD v/s Group L, sensory block: 2.5min ± 0.5v/s6.34min ± 0.7; motor block: 8.5min ± 1.05v/s14.78min ± 0.6; P < 0.001). The quality of anaesthesia was superior in group LD compared to group L and the duration of postoperative analgesia was also longer in group LD.
Dexmedetomidine 0.5 μkg-1 as an adjuvant to lignocaine for IVRA shortens the onset of sensory and motor blocks, improves the quality of anaesthesia and provides longer postoperative analgesia.
Brachial plexus block by supraclavicular approach is the more commonly employed regional anesthetic technique for surgeries on the upper limb. However, it requires technical skill, good anatomical knowledge, and precise recognition of surface landmarks. It is prone to delayed onset of analgesia, block failure, patchy or inadequate analgesia, as well as to complications such as pneumothorax, inadvertent intravascular injection, and rarely nerve injuries. Intravenous regional anesthesia (IVRA) is a simple, safe, and effective technique with a good success rate and can be a suitable alternative to brachial plexus block for upper limb surgeries of short duration. The greatest drawback of IVRA is its inability to provide postoperative analgesia when compared to peripheral nerve blocks.[2,3,4] To overcome this, adjuvants such as opioids (fentanyl, sufentanil, morphine, pethidine, and tramadol) and nonsteroidal anti-inflammatory drugs (ketorolac, tenoxicam, and aspirin) have been used along with local anesthetic to prolong post-tourniquet deflation analgesia as well as to hasten the onset of analgesia.[2,5] Addition of clonidine, the α2 adrenergic agonist, has shown to improve tourniquet pain tolerance, but has no effect on the onset or quality of analgesia. In addition, its effect of prolonging postoperative analgesia is controversial. Dexmedetomidine being more potent and selective adrenergic α2 agonist than clonidine may provide a better quality and longer duration of analgesia when used as an adjuvant for IVRA.
The primary outcome of the present study is to compare the quality of block, sensory and motor block characteristics, and duration of postoperative analgesia following IVRA with or without the use of dexmedetomidine. The secondary outcome is to assess the sedation and hemodynamic effects. We hypothesized that addition of dexmedetomidine to lidocaine for IVRA will provide a superior quality of block, better sensory and motor characteristics, and longer duration of postoperative analgesia.
Sixty participants of either sex aged 18–50 years and weighing 50–70 kg with physical status ASA classes I and II scheduled for elective hand or forearm surgeries lasting <90 min were included after obtaining written informed consent and ethical committee clearance. Patients with Raynaud's disease, peripheral vascular disease, skin disease on the operating hand, crush injury or open wound, allergy to study drugs, and psychiatric medications were excluded from the study. Study participants were randomized by sealed envelope technique into two groups (Group L and Group LD) of 30 each. Group L received 40 mL of 0.5% preservative-free lignocaine while Group LD received 40 mL of 0.5% preservative-free lignocaine with 0.5 μg/kg body weight dexmedetomidine. The solution was prepared by a personnel not involved in the study in an identical 50 mL syringe. All patients were premedicated with 0.015 mg/kg midazolam intravenously. In the operation room, minimal mandatory monitoring was instituted and baseline vitals were recorded. Before establishing the block two intravenous cannulae, one 22-gauge in a vein on the dorsum of the operative hand and another 20-gauge in the nonoperative hand were cited. The operative upper limb was elevated for 3 min, and then exsanguinated with esmarch bandage starting from the tip of the fingers till upper arm. A double-cuffed pneumatic tourniquet was placed around the upper arm, and the proximal cuff was inflated to 250 mmHg. Circulatory isolation of the upper limb was verified by the absence of radial pulse and loss of pulse oximetry tracing in the ipsilateral index finger. IVRA was induced with 40 mL of appropriate study solution, injected over 90 s by an anesthesiologist blinded to the study drug, as per the group allocation.
Sensory block was assessed by pin prick in the distribution of ulnar, median, radial, medial, and lateral antebrachial cutaneous nerves. Onset of sensory blockade was defined as time from the complete injection of drug till loss of pin prick sensation in all the dermatomes.
Motor function was assessed by asking the subject to flex and extend his/her wrist and fingers. Onset of motor block was defined as time from the complete injection of drug to no voluntary movement of wrist and fingers was possible.[4,6] After complete sensory block was achieved, the distal cuff was inflated to 250 mmHg and the proximal cuff was deflated, and the surgery was allowed to start.
The quality of block was assessed on a numeric scale of 1–4: 4 (excellent) = no complaint from patient, 3 (good) = minor complaint with no need for supplemental analgesics, 2 (moderate) = complaint that required supplemental analgesics, and 1 (unsuccessful) = patient given general anesthesia. Tourniquet pain was assessed by visual analog score (VAS) on a scale of 0–10. If VAS >4, 25 μg fentanyl was administered iv. Hemodynamic variables were recorded at 5, 10, 15, 20, and 40 min intervals. Degree of sedation (scale 1–5, 1 = completely awake, 2 = awake but drowsy, 3 = asleep but responsive to verbal commands, 4 = asleep but responsive to tactile stimulus, and 5 = asleep and not responsive to any stimulus) was noted at 5, 10, 15, 20, and 40 min intervals. Postoperatively, diclofenac 75 mg was administered when VAS was >5. Duration of postoperative analgesia was the time from deflation of tourniquet to the first dose of diclofenac injection. Total amount of diclofenac consumption over first 24 h after surgery was noted.
At the end of surgery, tourniquet was deflated by cyclic deflation technique. If surgery was completed with 20 min after the injection of the drug, tourniquet was kept inflated for a minimum of 20 min. After tourniquet deflation, hemodynamic variables and pain and sedation scores were noted at 30 min and 2, 4, 6, 12, and 24 h. Hypotension (30% decrease from baseline) was treated with ephedrine 3–6 mg bolus; bradycardia (heart rate [HR] <50 bpm) was treated with atropine 0.5 mg.
The sample size was estimated from data of previous studies, using alpha level of 0.05 and beta level of 0.9 to establish a desired power of 90% using two-sample means test assuming unequal variance. Enrollment of at least 28 patients in each group was required. We decided to recruit thirty cases in each group to overcome any loss during follow-up. The result of the study was analyzed by following statistical methods, contingency coefficient analysis, t-test from independent samples, t-test from paired samples, and repeated measure ANOVA using SPSS Statistics for windows, version 16.0 (SPSS Inc., Chicago, IL, USA) software.
There were no significant differences among the two groups for demographic data, duration of surgery, and tourniquet time [Table 1]. The sensory and motor block onset times in Group LD was compared to Group L (P < 0.001) [Table 2]. The majority of patients in Group LD had excellent quality of block as compared to Group L, in whom most of them had moderate quality of block requiring intraoperative supplemental fentanyl analgesia [Table 2]. The duration of postoperative analgesia was longer in patients in Group LD compared to Group L (P < 0.001) [Table 2]. The hemodynamic variables (HR and mean arterial pressure) were comparable between the two groups during the entire study period. An increase in HR and a fall in mean arterial pressure were noted transiently following tourniquet deflation in both groups.
The VAS scores for tourniquet pain intraoperatively and the postoperative pain for the first 6 h after tourniquet deflation were significantly less in Group LD compared Group L (P < 0.001) [Figure 1]. Sedation scores were comparable between the two groups at all time periods except for the first 2 h post-tourniquet deflation, during which participants in Group LD were more sedated than Group L (P < 0.001) [Figure 2]. Two patients in Group LD developed bradycardia requiring atropine administration. None of the patients in any group developed hypotension or hypoxemia during surgery or during the first 24 h postoperatively.
The present study demonstrates that the use of dexmedetomidine 0.5 μg/kg as adjuvant to lignocaine for IVRA provides better quality of block, leads to earlier onset of sensory and motor block, and prolongs the duration of postoperative analgesia without any significant side effect. These improvements were associated with more sedation, which was short-lived.
This result of this study is similar to the other studies[4,6,7,8] which demonstrated improved quality of anesthesia and longer postoperative analgesia with dexmedetomidine. Sardesai et al. and Esmaoglu et al. employed dexmedetomidine in the dose of 1 μg/kg whereas Memis et al. used it in the dose of 0.5 μg/kg. Dexmedetomidine was effective in both doses. However, Gupta et al. who compared two different doses of dexmedetomidine found it to be superior in terms of onset of sensory, onset of motor block, and duration of analgesia when dexmedetomidine was used in the dose of 1 μg/kg when compared to 0.5 μg/kg. Studies comparing 0.5 μg/kg dexmedetomidine as adjuvant of IVRA have found it to be superior to lornoxicam, but similar to magnesium sulfate.
Tourniquet pain, which is a dull aching sensation, is a well-known problem with IVRA. This was also found to be significantly less in the present study with the use of dexmedetomidine as demonstrated by lower VAS scores and less fentanyl requirement in the intraoperative period.
α2-adrenergic receptors at the nerve endings are thought to play a role in the analgesic effect of the drug by preventing norepinephrine release.[11,12] The actions of dexmedetomidine as found to be mediated via postsynaptic α2-adrenoceptors activate G-proteins, thereby increasing conductance through potassium channels. Studies in mice have demonstrated that the α2A-adrenoceptor subtype is responsible for relaying the sedative and analgesic properties of dexmedetomidine.[11,12,13] Thus, α2-agonists are an attractive option as an adjuvant in pain management because of their potentiation at central and peripheral sites.
Following deflation of tourniquet, two patients in dexmedetomidine had bradycardia requiring atropine administration and the patients in dexmedetomidine group had higher sedation scores for the first 2 h. Tourniquet deflation can lead to an abrupt introduction of dexmedetomidine into the systemic circulation. Acute intravenous administration of dexmedetomidine is known to produce hypotension, bradycardia, and also sedation.[15,16]
Dexmedetomidine 0.5 μg/kg as an adjuvant to lignocaine for IVRA shortens the onset of sensory and motor blocks, improves the quality of anesthesia, and provides longer postoperative analgesia.
There are no conflicts of interest.