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Anesth Analg 2003;97:1168-1172 © 2003 International Anesthesia Research Society
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Abstract |
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We sought to determine general anesthetic requirements to suppress skin vasomotor reflex (SVmR) and pupillary dilation (PD) in response to transcutaneous electrical stimulation (TES) during combined epidural-general anesthesia. Thirty-five patients undergoing lower abdominal surgery were randomly divided into 2 groups to epidurally receive 0.5% (Group 1) or 1% lidocaine (Group 2) with sevoflurane anesthesia. A bolus injection of either lidocaine was followed by the infusion of the same solution, and the central dermatomal level of loss of cold sensation (C) was determined. After the induction of general anesthesia with 5% sevoflurane and 67% nitrous oxide, nitrous oxide was discontinued, and sevoflurane concentration was decreased. TES was given at both site C and site three dermatomal segments (U) cephalad to C to determine the end-tidal sevoflurane concentration required to suppress SVmR and PD. End-tidal sevoflurane concentration that suppressed both responses was larger in Group 1 than in Group 2 at both sites and was larger at site U than at site C in both groups. We conclude that sevoflurane requirements to suppress SVmR and PD in response to TES during combined epidural-general anesthesia are different depending on the concentration of lidocaine and the site where surgical stimulation is applied.
IMPLICATIONS: We evaluated sevoflurane requirements to suppress skin vasomotor reflex and pupillary dilation in response to a transcutaneous electrical stimulation at the surgical site during combined epidural-general anesthesia. Our results indicate that when epidural anesthesia is combined, general anesthetic requirements decrease depending on the lidocaine concentration for epidural anesthesia and the site where surgical stimulation is applied.
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Introduction |
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A combined epidural-general anesthesia technique has been widely used in major abdominal and thoracic surgery for decades. Theoretically, epidural anesthesia blocks the nociceptive input originating from the surgical site to some degree and thus requires a smaller concentration of general anesthetic during surgery. However, in the literature, this reduction has not been quantified. Although a recent study by Hodgson et al. (1) demonstrated that lidocaine epidural anesthesia reduced the minimum anesthetic alveolar concentration (MAC) of sevoflurane, they assessed it by applying a tetanic electrical stimulation to the fifth cervical dermatome that was cephalad to the upper level of epidural anesthesia. Thus, the MAC obtained in their study did not reflect the general anesthetic requirements at the surgical site. In addition, quality of blockade should vary depending on concentrations of local anesthetic used for epidural anesthesia (2–4).
Several techniques have been proposed to assess the sensory blockade level under light general anesthesia. Larson et al. (5) demonstrated that pupillary dilation (PD) in response to electrical stimulation predicted the level of sensory blockade achieved during combined epidural-general anesthesia. Shimoda et al. (6), however, showed that skin vasomotor reflex (SVmR) testing to detect a transient reduction in skin blood flow was also a reliable method for evaluating a sympathetic nervous response to noxious stimulation and thus estimating the sensory level. However, it is presumable that the depth of general anesthesia, i.e., the concentration of volatile drugs, may affect the suppression of the above reflexes (7). If quality of epidural blockade varies from site to site, even in the area where blocking effects are expected, the use of different dosages of volatile drugs should result in variable sensory levels estimated. Conversely, the degree of epidural blockade may affect the general anesthetic requirements to suppress SVmR and PD in response to noxious stimulation at different surgical sites.
Accordingly, the current study was conducted to evaluate sevoflurane requirements to suppress SVmR and PD in response to a transcutaneous electrical stimulation (TES) at the surgical site during lidocaine epidural anesthesia. In addition, we tested the hypothesis that use of different concentrations of lidocaine for epidural anesthesia and use of different sites for TES change the values obtained.
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Methods |
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After IRB approval and written informed consent, we studied 41 patients classified as ASA physical status I or II who were scheduled for elective surgery on the lower abdomen. Patients who were taking regular medications or had a history of major back problems, coagulation abnormality, or neurologic disease were excluded. No patients had any sign of autonomic dysfunction or cardiovascular disease detected by routine clinical laboratory tests.
No patients received preanesthetic medication. On arrival at an operating room, an IV infusion of acetated Ringer’s lactate solution was initiated at a rate of 10 mL · kg-1 · h-1. The room temperature was adjusted to 24°C–25°C. Patients were placed in the left lateral decubitus position, and the skin, subcutaneous tissue, and supraspinous ligament were anesthetized with 2 mL of 1% mepivacaine. The epidural space was identified with a 17-gauge Tuohy needle with the bevel directed cephalad via the midline approach, and a catheter (Portex) was advanced 5 cm into the epidural space. Choice of vertebral level of epidural puncture was at the discretion of the anesthesiologist caring for the patient. The catheter was aspirated to exclude intrathecal or IV placement and then secured. The patient was then returned to the supine position.
All patients were randomly divided into two groups according to a table of random numbers to receive 0.5% (Group 1) or 1% (Group 2) epidural lidocaine with sevoflurane general anesthesia. They received a bolus injection of 10 mL of either concentration of lidocaine followed by the same solution at a rate of 10 mL/h through the epidural catheter. Fifteen minutes after the injection, the level of sensory blockade was measured with an alcohol-soaked swab on the midclavicular line on both sides, and the central dermatomal level of loss of cold sensation (C) was determined. In case of asymmetry of the blockade, the site of the side that had larger number of segments blocked was chosen. Patients who displayed an asymmetry of the blockade of more than two dermatomes were excluded from the study, as well as patients whose upper level was higher than T3.
Besides our routine monitoring including noninvasive blood pressure, electrocardiography, and pulse oximetry, a plate-type probe of laser Doppler flowmeter (ALF2100; Advance, Tokyo, Japan) was attached to the palmar side of the left index finger tip to observe the peripheral skin blood flow. Bispectral index (BIS) was also monitored. General anesthesia was induced using tidal-breathing technique with 5% sevoflurane and 60% nitrous oxide (N2O) in oxygen. Endotracheal intubation was facilitated with vecuronium 0.15 mg/kg. The end-tidal concentrations of carbon dioxide (PETCO2) and sevoflurane (ETSevo) were continuously measured using an infrared multigas analyzer (Capnomac Ultima, Datex, Helsinki, Finland). Immediately after the endotracheal intubation, N2O was discontinued, and inspired sevoflurane concentration was reduced to 0.5%. The lungs were mechanically ventilated to maintain PETCO2 of 35–40 mm Hg. After ETSevo was kept stable at 0.5% for at least 15 min, we started to measure sevoflurane requirements to suppress SVmR and PD in response to noxious stimulation.
We applied a 5-s, 50-Hz, 60-mA TES from a nerve stimulator (NS252; Fisher & Paykel, Auckland, New Zealand) at site C and a site three dermatomal segments cephalad to site C on the ipsilateral side (U). A marked, transient reduction in the skin blood flow after the TES was recognized as the SVmR. To distinguish SVmR from basic wave, more than 20% reduction in the skin blood flow after the TES was considered a positive response. PD response was considered positive if a more than 1.0-mm increase in pupil size was detected immediately after the stimulus. Pupillary diameter was measured with a millimeter rule. If positive responses were detected with both tests, an inspired sevoflurane concentration was increased by approximately 0.20%, and then 10 min later, a TES was given again. We continued the procedure until a negative response was observed with both tests. If a positive response was not detected at approximately 0.50% with either test, the concentration was decreased by approximately 0.10%–0.30% until a positive response was observed. When the BIS value increased more than 60 during examination, we discontinued the measurements and excluded the patient from data analysis. Two independent investigators, who were blinded to the local anesthetic solution injected and the site of TES, participated in the assessment of SVmR and PD separately. Plasma samples were taken immediately before and after the above procedures for the measurement of lidocaine, which was determined by fluorescence polarization immunoassay (coefficient of variation was <5% with controls of 1.55, 3.03, and 7.55 µg/mL). Hypotension was treated with increasing fluid intake to 20 mL · kg-1 · h-1 and 5 mg of ephedrine IV if systolic arterial blood pressure decreased by >25% of the preanesthetic value. All the anesthetic procedures were conducted by an anesthesiologist who was also blinded to the study group.
Sevoflurane requirements were calculated as the average of the largest ETSevo at which a positive response occurred and the smallest ETSevo at which a negative response was observed. For example, if the SVmR to the TES was obtained at 0.90% ETSevo and no response was observed at 1.10%, sevoflurane requirement was considered 1.00%. Sample size was determined by a power analysis based on the variability observed in our pilot study using SVmR and the ability to detect a difference in ETSevo to suppress the reflex of 0.20% with ß set at 0.2 and 
set at 0.05. A minimal sample of 34 patients (17 in each group) met these criteria. Results are expressed as mean ± SD unless otherwise stated. Morphometric and anesthetic data in both groups were compared using Student’s t-test and 
2, as appropriate. ETSevo that suppress the responses were compared using Wilcoxon’s signed-rank test and Mann-Whitney rank-sum test for intra- and between groups assessment, respectively. Plasma concentrations of lidocaine were analyzed using Student’s t-test. P < 0.05 was considered significant.
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Results |
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Of the 41 patients enrolled in the study, one in each group had an upper level that was higher than T3 and was excluded from the study. An additional two patients were excluded from each group because they experienced BIS of more than 60 during the measurement of sevoflurane requirements. Thus, 35 patients consisting of 17 and 18 in Groups 1 and 2, respectively, completed the study.
Patient characteristics and surgical procedures performed did not differ between the two study groups (Table 1). Epidural anesthesia using both lidocaine solutions, which were injected at similar epidural sites, produced a demonstrable blockade with similar sites C (Table 2). Plasma lidocaine concentration was significantly larger in Group 2 than in Group 1 but similar between before and after the measurement of sevoflurane requirements in each group (Table 3).
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ETSevo that suppressed SVmR and PD was significantly larger at site U than at site C in both groups (Table 4). Group 2 required significantly less ETSevo that suppressed both responses than Group 1 at both sites. The ETSevo did not differ between the two responses in either group or at either site.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In the present study, we measured sevoflurane requirements that suppressed SVmR and PD in response to TES applied to the area blocked with epidural anesthesia. Three comparisons were made: (a) epidural anesthesia between 0.5% and 1% lidocaine, (b) dermatomal segments between the center and periphery of the blocked area, and (c) test of responses between SVmR and PD. First, the use of a smaller concentration of lidocaine required a larger concentration of sevoflurane to suppress the responses. Second, a larger concentration of sevoflurane was required to suppress the responses at the peripheral dermatomal segment than the central level of the block area. Finally, the two tests produced similar results.
This is the first study to measure sevoflurane requirements to block noxious stimulation that was applied to the area partially blocked by epidural anesthesia during general anesthesia. Previous researchers have succeeded in distinguishing the dermatomal segments blocked with epidural anesthesia from unblocked ones by using a small concentration (0.5%–0.8%) of isoflurane or sevoflurane (5,6). However, they did not change the concentration of volatile drugs to examine the effect on the sensory levels. In contrast, Hodgson et al. (1) changed the sevoflurane concentration to reveal that lidocaine epidural anesthesia reduced the MAC of sevoflurane from 1.18% to 0.52%, which they speculated was because of indirect central effects of spinal deafferentation. However, they assessed the MAC by applying a tetanic electrical stimulation only to the fifth cervical dermatome that was cephalad to the upper level of epidural anesthesia.
The reason for the difference observed between the two concentrations of lidocaine is probably a difference in intensity of the sensory blockade produced. The two groups differed in dosage and concentration of lidocaine, both of which have been demonstrated to affect the intensity of the epidural blockade (2–4). For example, Sakura et al. (3) compared the effects of 10 mL of 1% and 2% lidocaine on quality of epidural anesthesia by measuring cutaneous current perception thresholds, in which they found differences between the two solutions.
The concentrations of lidocaine used in the present study are rather small, even as a solution for epidural anesthesia in combination with general anesthesia. However, the present study was designed to measure the dosage of general anesthetic required to supplement epidural anesthesia that was insufficient by itself. If the epidural anesthesia produced had been potent enough to block the electric stimulation completely, no positive responses would have been obtained.
Sensory assessment of regional anesthesia has been performed mostly by qualitative methods using simple stimuli, such as touch, pinprick, or cold, and quantitative methods have rarely been used (8). Thus, although spread of epidural anesthesia has been assessed in an operating room every day and studied for a long time, the intensity of sensory blockade has not been explored adequately. Our clinical experience is that the intensity is not even but varies within the extent of epidural blockade. The results of the present study confirmed this with different sevoflurane requirements to block the electrical stimulation. The central dermatomes seemed to be blocked more profoundly than peripheral ones.
The mechanism of SVmR and PD is not fully understood. However, it seems that a TES to the skin that is conducted to the spinal cord via somatosensory nerve is partly mediated by sympathetic nerves and transferred to skin vessels and irises (9–11). Preganglionic sympathetic fibers to the upper extremities arise from the T2-7 spinal segments, and the efferent fibers to the dilator muscle of the iris originate from the first two thoracic segments (12,13). Thus, if efferent nerves from high thoracic levels are completely blocked, the SVmR and PD should be eliminated. In the present study, we excluded the patients who had an upper blocked level that was higher than T3 and found that the two tests can be used alternatively because the sevoflurane requirements to suppress both reflexes were similar.
There are possible criticisms in the study design. First, there is a possibility of change in spread of epidural anesthesia during the course of measurements. The sites C and U were determined by the evaluation of sensory level 15 minutes after the bolus injection of epidural lidocaine and thus might not have represented accurate sites when the sevoflurane requirements were measured. However, in a preliminary study, we found that the sensory level of continuous epidural infusion of 2% lidocaine at a rate of 10 mL/h was kept constant at least during the first hour. Second, the dosage of lidocaine administered in the two groups differed. As expected, plasma lidocaine concentrations between the two groups were different. Thus, the differences in effects between the groups might have been associated with a difference in the systemic effects of lidocaine. However, the results of a study by Hodgson and Liu (14) showed that systemic effects of lidocaine did not affect MAC of sevoflurane to obtain a BIS value of <50 by comparing a group of patients receiving IV lidocaine with those receiving only general anesthesia. The plasma lidocaine concentration in their patients was 1.9 µg/mL and similar to that in a group of patients given 1% lidocaine in the present study. In addition, Larson et al. (15) showed that lidocaine, at plasma concentrations near 5 µg/mL, did not alter the pupillary response to electrical stimulation. Thus, it is unlikely that the addition of IV lidocaine to a group of patients given 0.5% epidural lidocaine would have led to different conclusions. Finally, unlike many other studies (16), we did not use the conventional up-down methodology, with which the quantal response to a stimulus is assessed only once for each individual (17). However, the present study was designed to measure more than one variable in each patient and thus would have made the methodology more complicated and required a large number of patients. Instead, to decrease the effect of previous measurements on subsequent ones that used different concentrations of sevoflurane, we waited for more than 10 minutes to evaluate the responses after changing the concentration.
In conclusion, we evaluated sevoflurane requirements to suppress SVmR and PD in response to TES during combined epidural-general anesthesia. The present results indicate that when epidural anesthesia is combined, general anesthetic requirements are reduced, but the reduction depends on the concentration of lidocaine for epidural anesthesia and the site where surgical stimulation is applied.
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References |
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- Hodgson PS, Liu SS, Gras TW. Does epidural anesthesia have general anesthetic effects: a prospective, randomized, double-blind, placebo-controlled trial. Anesthesiology 1999; 91: 1687–92.[Web of Science][Medline]
- Liu SS, Ware PD, Rajendran S. Effects of concentration and volume of 2-chloroprocaine on epidural anesthesia in volunteers. Anesthesiology 1997; 86: 1288–93.[Web of Science][Medline]
- Sakura S, Sumi M, Yamada Y, et al. Quantitative and selective assessment of sensory block during lumbar epidural anaesthesia with 1% or 2% lidocaine. Br J Anaesth 1998; 81: 718–22.
[Abstract/Free Full Text] - Sakura S, Sumi M, Kushizaki H, et al. Concentration of lidocaine affects intensity of sensory block during lumbar epidural anesthesia. Anesth Analg 1999; 88: 123–7.
[Abstract/Free Full Text] - Larson MD, Sessler DI, Ozaki M, et al. Pupillary assessment of sensory block level during combined epidural/general anesthesia. Anesthesiology 1993; 79: 42–8.[Web of Science][Medline]
- Shimoda O, Ikuta Y, Terasaki H. Assessing the level of regional blockade under general anesthesia using the skin vasomotor reflex test. Anesth Analg 1998; 87: 83–7.
[Abstract/Free Full Text] - Kano T, Shimoda O, Higashi K, Sadanaga M. Effects of neural blockade and general anesthesia on the laser-Doppler skin blood flow waves recorded from the finger or toe. J Auton Nerv Syst 1994; 48: 257–66.[Medline]
- Curatolo M, Petersen-Felix S, Arendt-Nielsen L. Sensory assessment of regional analgesia in humans: a review of methods and applications. Anesthesiology 2000; 93: 1517–30.[Web of Science][Medline]
- Iwase S, Mano T, Sugenoya J, et al. Relationship among skin sympathetic nerve activity, sweating, and skin blood flow. Environ Med 1988; 32: 55–67.
- Khan F, Struthers AD, Spence VA. The effect of prazosin on skin microcirculation as assessed by laser Doppler flowmetry. Br J Clin Pharmacol 1988; 26: 267–72.[Web of Science][Medline]
- Larson MD, Sessler DI, Washington DE, et al. Pupillary response to noxious stimulation during isoflurane and propofol anesthesia. Anesth Analg 1993; 76: 1072–8.
[Abstract/Free Full Text] - Duke-Elder S, Scott GI. Direct pupillary anomalies. In: Duke-Elder S, ed. Neuro-ophthalmology. London: Henry Kimpton, 1971: 595–639.
- Pick J. The autonomic nervous system: morphological, comparative, clinical and surgical aspects. Philadelphia: Lippincott, 1970: 341–9.
- Hodgson PS, Liu SS. Epidural lidocaine decreases sevoflurane requirement for adequate depth of anesthesia as measured by the bispectral index monitor. Anesthesiology 2001; 94: 799–803.[Web of Science][Medline]
- Larson MD, Kurz A, Sessler DI, et al. Lidocaine does not depress reflex dilation of the pupil. Reg Anesth 1997; 22: 461–5.[Medline]
- Paul M, Fisher D. Are estimates of MAC reliable? Anesthesiology 2001; 95: 1362–70.[Web of Science][Medline]
- Dixon WJ. Efficient analysis of experimental observations. Annu Rev Pharmacol Toxicol 1980; 20: 441–62.[Web of Science][Medline]
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