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, MD
lu, MDDepartment of Anaesthesiology and Reanimation, Medical Faculty, Trakya University, Edirne, Turkey
Address correspondence and reprint requests to Alparslan Turan, MD, Trakya Üniversity T
p Fakültesi, Anesteziyoloji ve Reanimasyon AD, 22030 Edirne, Turkey. Address e-mail to alparslanturan{at}yahoo.com.
| Abstract |
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| Introduction |
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Parenteral magnesium has been used for many years on an empirical basis as an antidysrhythmic treatment for eclampsia and for intraoperative and postoperative analgesia (35). The mechanism of the analgesic effect of magnesium is not clear, but interference with calcium channels (4,6) and N-methyl-d-aspartate receptors seems to play an important role (7,8). The antinociceptive effects of calcium channel blockers have been demonstrated in animals (9). Magnesium has been shown to be successful in decreasing pain associated with injection of propofol (10) and rocuronium (11). Tramer and Glynn (12) used magnesium for the treatment of chronic limb pain in IVRA and demonstrated that the addition of magnesium to lidocaine improves the quality of the block, extends the analgesia, and reduces the overall failure rate. However, pain with injection of magnesium was the limitation of this technique, with similar results in other reports (10,11).
We designed this study to evaluate the effect of magnesium when added to lidocaine in IVRA for elective hand surgery. Our primary aim was to investigate tourniquet pain. The secondary aims were to investigate the onset of sensory and motor block and recovery time, quality of anesthesia, intraoperative and postoperative hemodynamic variables, postoperative pain, and sedation and to determine the effect of administering lidocaine with magnesium for magnesium-induced pain.
| Methods |
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Patients were premedicated with 0.07 mg/kg midazolam and 0.01 mg/kg atropine, which were administered IM 45 min before the surgical procedure. Patients were monitored (Cato PM 8040; Drager, Lübeck, Germany) for mean arterial blood pressure (MAP), oxygen saturation (Spo2), and heart rate (HR) in the operating room. Two cannulas were placed: one in a vein on the dorsum of the operative hand and the other in the opposite hand for crystalloid infusion. The operative arm was elevated for 2 min and was then exsanguinated with an Esmarch bandage; a pneumatic tourniquet was then placed around the upper arm, and the proximal cuff was inflated to 250 mm Hg. Circulatory isolation of the arm was verified by inspection, absence of a radial pulse, and a loss of the pulse oximetry tracing in the ipsilateral index finger. IVRA was achieved with 10 mL of saline plus 3 mg/kg lidocaine 0.5% (Aritmal; TEMS, Turkey) diluted with saline to a total of 40 mL in group C (n = 15) or with 10 mL of 15% magnesium sulfate (12.4 mmol; Biosel Ilaç San., Turkey) plus 3 mg/kg lidocaine 0.5% diluted with saline to a total of 40 mL in group M (n = 15). The solution was injected over 90 s by an anesthesiologist blinded to the injected drugs. The patients were observed and asked immediately whether they had pain in the arm, and the response was assessed by the following numeric scale: none (0), negative response to questioning; mild (1), pain reported in response to questioning only, without any behavioral signs; moderate (2), pain reported in response to questioning and accompanied by a behavioral sign, or pain reported spontaneously without questioning; severe (3), strong vocal response or response accompanied by facial grimacing, arm withdrawal, or tears.
Sensory block was assessed by pinprick with a 22-gauge short-beveled needle, every 30 s. Patient response was evaluated in the dermatomal sensory distribution of the medial and lateral antebrachial cutaneous, ulnar, median, and radial nerves. Motor function was assessed by asking the subject to flex and extend his/her wrist and fingers; complete motor block was noted when no voluntary movement was possible. Onset of sensory block was defined as the time elapsed from injection of the study drug to sensory block achieved in all dermatomes, and onset of motor block was defined as the time elapsed from injection of the study drug to complete motor block.
After sensory and motor block onset, the operative tourniquet (distal cuff) was inflated to 250 mm Hg, the proximal tourniquet was released, and surgery was started. MAP, HR, and Spo2 were monitored before and after tourniquet application; 5, 10, 15, 20, 30, 40, and 50 min after injection of an anesthetic; and after release of the tourniquet by an anesthesiology resident who did not know which medication was administered. Assessment of tourniquet pain scores was made on the basis of the visual analog scale (VAS) (0 = no pain and 10 = worst pain imaginable) measured before and after tourniquet application and 5, 10, 15, 20, 30, 40, and 50 min after study drug application. When tourniquet pain was
4 on the VAS, patients were given fentanyl 1 µg/kg, and the total administered dose and requirement time were noted. Treatment for bradycardia (25% decrease from baseline), hypotension (25% decrease from baseline), and decreased Spo2 (peripheral Spo2 more than 96%) was noted.
At the end of the operation, this resident was asked to qualify the operative conditions 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 that needed a supplemental analgesic; and unsuccessful (1), patient was given general anesthesia. At the end of the operation, the surgeon, who was blinded to group assignment, was asked to qualify the operative conditions and dryness of the operative field according to the following numeric scale: 0, unsuccessful; 1, poor; 2, acceptable; or 3, perfect.
The tourniquet was not deflated before 30 min and was not inflated for >2 h. At the end of surgery, the tourniquet was deflated by a cyclic deflation technique. Sensory recovery time was noted (the time elapsed from tourniquet deflation to recovery of sensation in all dermatomes, determined by pinprick test). Motor block recovery time was noted (the time elapsed from tourniquet deflation until movement of fingers). The first analgesic requirement time was also noted (the time elapsed from tourniquet release until first patient request for analgesic).
Assessment of postoperative pain was made on the basis of the VAS. MAP, HR, VAS, and degree of sedation were recorded at 1, 2, 4, 6, 12, and 24 h. Patients were instructed to receive 75 mg of IM diclofenac when VAS was >4, and total diclofenac consumption was recorded. All evaluations were performed by an anesthesiology resident not involved in the study. Nausea, vomiting, skin rash, tachycardia, bradycardia, hypotension, hypertension, headache, dizziness, tinnitus, hypoxemia, sedation, and other side effects were noted if encountered through 24 postoperative hours in the ward.
A reduction in the tourniquet pain score (VAS) of 15% compared with the lidocaine group would be clinically significant. On the basis of these estimates, we calculated that a sample size of 15 patients would be sufficient to permit a Type I error of
= 0.05 and a power of 80% (13). Independent samples Students t-tests were used for evaluation of the demographic data, intraoperative and postoperative hemodynamic data, the time of the onset and recovery of sensory and motor block, the duration of the operation and tourniquet, the duration of analgesia, and intraoperative and postoperative analgesic use. The Mann-Whitney U-test was used for intraoperative and postoperative VAS and sedation scores and the quality of anesthesia. Significance was determined at P < 0.05.
| Results |
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There was no statistical difference between groups for MAP, HR, or Spo2 at any time. Sensory and motor block onset times were statistically shorter in group M (P < 0.05). Sensory and motor block recovery times were also statistically prolonged in this group (P < 0.05) (Table 1). There was a statistically significant difference in VAS scores for tourniquet pain at 15, 20, 30, 40, and 50 min after tourniquet inflation (P < 0.001); VAS scores were lower in group M. The fentanyl requirement time was significantly prolonged (P < 0.001) in group M (35 ± 11 min) compared with group C (22 ± 10 min). Additional fentanyl requirements were significantly less in group M compared with group C (P < 0.05). Anesthesia quality, as determined by the anesthesiologist and the surgeon, was statistically better in group M (P < 0.05) (Table 2).
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The time to first postoperative analgesic request in group C was 95 ± 29 min and in group M was 155 ± 38 min; this was statistically significant (P < 0.05). Postoperative VAS scores were significantly higher for the first postoperative 6 h in group C compared with group M (P < 0.05) (Table 3). Diclofenac consumption was statistically significantly less in group M (50 ± 35 mg) compared with group C (130 ± 55 mg) (P < 0.05). No adverse effect was seen through the 24-h postoperative period in either group; only four patients in group M and three patients in group C had nausea that required treatment.
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| Discussion |
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The mechanism of action of magnesium as an adjunct to IVRA is obviously multifactorial. The different possible mechanisms of action of magnesium (other than those mentioned in the introduction) have been discussed. Studies have reported that magnesium has an endothelium-derived nitric oxide-induced vasodilatory effect (14,15). Nitric oxide causes an activation of guanyl cyclase and an increase in cyclic guanine monophosphate, which mediates the relaxation of vascular smooth muscles (16,17). Nitric oxide is also a potent inhibitor of neutrophil adhesion to vascular endothelium (16). Magnesium, even at doses often used for the treatment of preeclampsia, is associated with limited passage across the blood-brain barrier (18). With IVRA, local anesthetics and adjuvants are injected close to the surgical site. The pneumatic tourniquet causes ischemia, which distorts nerve penetration by oxidative stress and affects the blood-nerve barrier (19). Nitric oxide donors have also been shown to protect vascular endothelium from ischemia/reperfusion-mediated endothelial dysfunction (16). Protective effects of magnesium administration on ischemia/reperfusion injury of the spinal cord (20) have also been demonstrated. All these mechanisms or their combination may have played a role in our results. The findings concerning the actions of magnesium during IVRA in our study could also be used to evaluate other peripheral actions of magnesium not mediated by central effects.
Caution should be exercised in administering magnesium to patients with compromised renal function, bradycardia, and atrioventricular conduction abnormalities, and if the patient is going to be anesthetized, precautions must be taken for enhancing the effects on neuromuscular block.
In conclusion, the addition of magnesium to lidocaine in IVRA demonstrated decreased intraoperative fentanyl consumption and pain associated with the tourniquet. It also shortened sensory and motor block onset times, prolonged sensory and motor block recovery times, and improved the quality of anesthesia while prolonging the time to the first postoperative analgesic requirement. The side effect seen with magnesium is injection pain; however, it was diminished with the lidocaine dose and concentration we used. The addition of magnesium to a local anesthetic in IVRA is effective; however, further studies must be performed with experimental models, other peripheral techniques, and different doses to determine a relevant conclusion before its routine use.
| Footnotes |
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| References |
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LT, French JH. Magnesium: nature's physiologic calcium blocker [editorial]. Am Heart J 1984;108:18894.[ISI][Medline]
oglu B, et al. The prevention of pain from injection of rocuronium by magnesium sulfate, lignocaine, sodium bicarbonate and alfentanil. Anaesth Intensive Care 2003;31:27781.[ISI][Medline]
y
k F, Aakar I. Ischaemia-reperfusion injury of the peripheral nerve: an experimental study. Microsurgery 1999;19:37480.[ISI][Medline]
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