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From the Second Department of Anesthesiology, Toho University School of Medicine, Tokyo, Japan.
Address correspondence to: Dr. Masayuki Arakawa, Second Department of Anesthesiology, Toho University School of Medicine, 2-17-6 Ohashi, Meguro-ward, Tokyo 153-8515, Japan. Phone: +81-03-3468-1251; Fax: +81-03-3481-7336; E-mail: atruth{at}oha.toho-u.ac.jp
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Abstract |
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Methods: Forty-four patients undergoing epidural anesthesia with 17 mL of 2% lidocaine containing 1:200,000 epinephrine at L4–5 or L5–S1 were randomly divided into four groups. Lidocaine was administrated via epidural catheter [lidocaine catheter (LC) group] or Tuohy needle (lidocaine bolus group), lidocaine-bicarbonate was administrated via catheter (lidocaine-bicarbonate catheter group) or needle [lidocaine-bicarbonate bolus (LBB) group]. Pain threshold after repeated electrical stimulation was performed at L2 and S1 regions. Motor blockade was evaluated using the Bromage scale. Sympathetic blockade was assessed with plethysmographic waveforms from the toe.
Results: The pain threshold of the S1 dermatome in LBB group was significantly higher than in the lidocaine only groups, however, differences in the pain threshold at the L2 dermatome among the groups were insignificant. The onset of sensory blockade in the S1 dermatome in the LBB group was significantly shorter than in the LC group. Significantly greater motor blockade was achieved in the lidocaine-bicarbonate groups than in the lidocaine-only groups. The amplitude of plethysmographic waveforms significantly increased within each group.
Conclusion: Epidural bolus injection of lidocaine-bicarbonate with epinephrine improves the pain threshold and speeds the onset of the blockade of the first sacral region.
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Introduction |
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We compared the clinical efficacy (analgesia, motor block, and sympathetic block) of sodium bicarbonate and epinephrine added to lidocaine with that of epinephrine added to lidocaine (administered either by epidural bolus or catheter) in lumbar epidural anesthesia. Repeated electrical stimulation enables a quantification of analgesia, and the induction of temporal summation may render this test closer to clinical pain.2,6 Temporal summation occurs when the repetition of a peripheral stimulus causes increased and prolonged firing of dorsal horn neurons (central sensitization).
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= 0.05 and 1 – ß = 0.8). After obtaining informed consent, 44 patients with ASA physical status I–II undergoing epidural anesthesia at L4–5 or L5–S1 were randomly divided into four groups according to the type of anesthetic solution and mode of administration. The epinephrine (1:200,000) was freshly added at the time of administration in all groups. The solutions were as follows: lidocaine [20 mL of 2% xylocaine; (Astra Zeneca, Osaka, Japan) plus 2 mL of saline 0.9%] and lidocaine-bicarbonate (20 mL of 2% xylocaine plus 2 mL of sodium bicarbonate 8.4% added immediately before injection). Lidocaine was administrated via the epidural catheter; lidocaine catheter (LC) group or via the Tuohy needle; lidocaine bolus (LB) group. Lidocaine-bicarbonate was administrated via catheter; lidocaine-bicarbonate catheter (LBC) group or needle; lidocaine-bicarbonate bolus (LBB) group.
A pulse oximeter probe was applied to a big toe. Plethysmographic waveforms were recorded before and after epidural injection (Datex AS/3TM, Helsinki, Finland). The increment of pulse amplitude is an objective detector of early effects during epidural anesthesia.7 After 3 mL of 2% lidocaine were administrated as a test dose, 14 mL of the anesthetic solutions were injected through the catheter or the needle. The time at which the study drug injection ended was termed "time zero" for the purpose of subsequent patient assessment. The pH of lidocaine was determined by a pH meter (Shimadzu, Kyoto, Japan).
It has been reported that a train-of-five pulses at 2 Hz evoke temporal summation,6 as do two pulses at 0.5 Hz or three pulses at 1 Hz.8 Based on these findings, it is possible to use a train-of-four pulses to assess pain threshold. In this study, we used four stimuli at 2 Hz delivered by the TOF GUARDTM (Biometer International, Odense, Denmark), designed originally to evaluate neuromuscular blockade. Bipolar surface Ag-AgCl electrodes were placed at the S1 dermatome (the lateral malleolus) as an index of caudal spread and L2 (the ventral femoral region) as an index of cephalad spread. A 200 µsec square wave impulse was used as a single stimulus. To determine the threshold for temporal summation, the single stimulus was repeated four times at 2 Hz, and current intensity was increased from 5 mA in steps of 1–5 mA until summation (perception of the last stimulus was perceived as painful) was observed, or a maximum current of 60 mA was reached. The test was repeated at the dermatomes L2 and S1 at zero, five, ten, 15, and 20 min.
The pinprick test was repeated at the dermatomes L2 and S1 at five, ten, 15, and 20 min. The level of anesthesia was assessed at 20 min by loss of cold sensation. Both pinprick test and cold sensitivity were defined as abolished discrimination. Motor blockade was recorded with the Bromage scale (0 = full flexion of feet and knees, 1 = just able to move knees, 2 = able to move feet only, and 3 = unable to move feet or knees) at five, ten, 15, and 20 min. The onset of sensory blockade was defined as the time between "time zero" and the abolition of the pinprick response.
Differences among the groups were analyzed with one way analysis of variance (ANOVA) or Kruskal-Wallis test as appropriate. The paired t test was used for differences of hemodynamic data and amplitude of plethysmographic waveforms within the groups. Pain threshold and amplitude of plethysmographic waveforms among the groups were compared by repeated measures of ANOVA. Bromage scale was compared by the Kruskal-Wallis test. Bonferroni adjustment was made for multiple comparisons. Analysis for the onset of sensory blockade was performed by survival analysis. The log rank test was used for comparisons among the groups. Results are expressed as means and SD were considered significant when P < 0.05.
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Results |
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). The pH of lidocaine in the LBC and LBB groups was significantly higher than in the LC and LB groups (Table I). Mean arterial blood pressure decreased and heart rate increased within each group after 20 min (Table II). The pain threshold in the S1 dermatome in the LBB group was significantly higher than in the LC and LB groups (Figure 1-B). Motor blockade assessed by the Bromage scale was significantly higher in the LBC and LBB groups than in the LC and LB groups (Figure 1-C).
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). There were no differences in the amplitude of the plethysmographic waveforms between the groups, however they increased significantly within each group after five minutes (Table II
).
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Discussion |
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Why bolus injection with alkalinized lidocaine was superior to the other three lidocaine administration techniques is not clear. Epidural catheter inserted 3 cm into the lumber spinal canal from a skin puncture most commonly travels to a site in the lateral epidural space by computed tomography.11 In case of epidural catheter insertion, there is a possibility that a variety of catheter tip locations could affect the quality of epidural blockade. If we accept the possibility that local anesthetics spread more cephalad than caudally after a bolus injection compared with injection via a catheter because the threshold in S1 dermatome was the lowest in the lidocaine bolus group, we suppose that bolus injection caused more local anesthetic to accumulate at L2 (cephalad) in the epidural space. More alkalinized local anesthetic diffused across the meninges and blocked S1 nerve roots in a shorter time.
Temporal summation is not blocked by 0.5% bupivacaine epidural anesthesia,12 contrary to spinal anesthesia with plain bupivacaine 0.5% where the pain response to repeated stimulation disappeared at the sural nerve.13 Our results suggest that epidural anesthesia with alkalinized 2% lidocaine and epinephrine may inhibit temporal summation also. Protection of sensory neurons against central sensitization may offer relief from pain occurring after injury or surgery.14 Thus, our results suggest that alkalinization, by enhancing the quality of the block, may contribute to preemptive analgesia.
Bicarbonate was added to the lidocaine solution immediately prior to injection and precipitation was not a problem. However, precipitation has been reported ten minutes after the addition of 2 mL of sodium bicarbonate to 20 mL of lidocaine.15 The significance of this finding in the clinical context remains unclear but warrants further attention.
We conclude that bolus injection of lidocaine with added bicarbonate and 1: 200,000 epinephrine increases the pain threshold, improves analgesia and reduces the onset of blockade of the first sacral segment. Further studies on the most appropriate dose of bicarbonate will be necessary.
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Acknowledgments |
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Revision received March 18, 2002. Accepted for publication January 14, 2002.
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References |
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2 Curatolo M, Petersen-Felix S, Arendt-Nielsen L, et al. Adding sodium bicarbonate to lidocaine enhances the depth of epidural blockade. Anesth Analg 1998; 86: 341–7.[Abstract]
3
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Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Fischer M, Zbinden AM. Temporal summation during extradural anaesthesia. Br J Anaesth 1995; 75: 634–5.
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Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Zbinden AM. Spinal anaesthesia inhibits central temporal summation. Br J Anaesth 1997; 78: 88–9.
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P < 0.01 compared with LC group. +P < 0.05, ++P < 0.01 compared with LB group. #P < 0.05, ##P < 0.01 compared with LB group. Values are mean ± SD.