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© 1999 International Anesthesia Research Society
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Abstract |
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We evaluated the effect of 1, 20, and 40 mL of epidural saline flush on recovery from lidocaine epidural anesthesia. Eight volunteers were studied for three study periods, each separated by 72 h. The volume of saline was randomized, and a new catheter was inserted for each study period. A standardized dose of 20 mL of 2% plain lidocaine was injected for 10 min, followed by an epidural saline flush 30 min later. Sensory block was assessed by pinprick and transcutaneous electrical stimulation and motor block by a modified Bromage scale and isometric maximal force contraction. Times to void and ambulate independently before discharge were recorded. Peak plasma lidocaine concentrations and time to peak concentration were determined. Results from six volunteers showed that epidural saline, 40 mL, significantly altered anesthetic resolution, accelerating the time of complete sensory and motor block regression (P < 0.05). Median peak levels of sensory and motor block and times to void and ambulate were similar among treatment groups. Peak plasma lidocaine concentrations were similar in all treatment groups. Our data suggest that a 40-mL epidural saline injection 30 min after the induction facilitates regression of epidural lidocaine anesthesia, but a 20-mL bolus does not. Epidural saline injection does not affect vascular absorption of epidural lidocaine.
Implications: Epidural catheter flushing with 40 mL of saline, after establishment of epidural lidocaine anesthesia, can facilitate sensory and motor block recovery. However, this does not affect vascular absorption of epidural lidocaine.
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Introduction |
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Local anesthetic in the epidural space maintains nerve conduction blockade as a result of the net drug concentration effect on the spinal nerve roots and spinal cord. Redistribution of local anesthetic away from neural tissues that are already blocked determines the resolution of epidural anesthesia. In theory, redistribution can be enhanced, directly, by decreasing the concentration of residual local anesthetic in the epidural compartment, or, indirectly, by increasing the extent of local anesthetic absorption into the epidural vasculature. Preliminary data suggest that an epidural injection of 20–45 mL of saline can speed resolution of anesthesia by 40%–50% (1–3). Still lacking, however, is information regarding the optimal saline volume, optimal timing of saline injection relative to the last dose of local anesthetic, and the effect of saline injection on local anesthetic vascular absorption.
Any therapeutic intervention that can enhance the resolution of epidural anesthesia is desirable, especially after ambulatory surgery. Our study was undertaken to evaluate the effect of different volumes of epidural saline flush on the resolution of lidocaine epidural anesthesia and on vascular absorption of local anesthetic. We used a cross-over study design, with the goal of minimizing interindividual variability in block resolution.
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Methods |
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After obtaining institutional review board approval and informed consent, we studied eight healthy ASA physical status I volunteers (23–37 yr old, 152–182 cm, 52–97 kg, 5 men and 3 women). Each volunteer participated in three separate study periods, which differed only in the volume of saline flush to the epidural catheter. Study periods were separated by at least 72 h to ensure no carryover effects. The administered volume of saline was randomized across study periods, but the dose of epidural lidocaine was standardized. A new epidural catheter was inserted for each study.
Epidural Anesthesia
After an overnight fast of at least 8 h and voiding immediately before the study, each volunteer received an IV cannula, through which normal saline was infused, initially at 6 mL/kg for a period of 15 min, then at 8 mL · kg-1 · hr-1 for 1 h, and 2 mL · kg-1 · hr-1 thereafter. With the volunteer lying laterally decubitus, epidural anesthesia was induced in a sterile fashion by advancing a 17-gauge Tuohy needle at the midline of the L2-3 or L3-4 interspace, until reaching the epidural space, as indicated by a loss of air resistance. A 20-gauge multi-orifice catheter was then inserted until 3–5 cm of catheter lay within the epidural space. The needle was then removed, the externalized section of catheter was taped in place, and the volunteer was positioned horizontally supine and remained so for the duration of the study period. A test dose of 3 mL of 1.5% lidocaine with 1:200,000 epinephrine was administered epidurally to eliminate inadvertent IV or subarachnoid injection. After waiting 3 min, a total of 20 mL of 2% plain lidocaine was injected for 10 min, at a rate of 4 mL every 2 min. No further local anesthetic was given. The time at the end of lidocaine injection was considered time 0.
Saline Flush Protocol
Saline flush of the epidural catheter began 30 min after injection of lidocaine. Using a cross-over design, each volunteer was randomly assigned to receive a bolus of 1, 20, or 40 mL of sterile saline at a rate of 10 mL/min during the three study periods. To ensure proper blinding of both volunteers and investigators, the saline syringes were masked by a towel during injection.
Independent of the volume of saline administered, the investigator flushing the catheter remained with the volunteer for at least 4 min.
Monitoring and Measurements
Epidural anesthesia was conducted per standard clinical practice. Volunteers were monitored using electrocardiography, noninvasive automatic blood pressure measurement, and pulse oximetry. Measurements were obtained before induction of anesthesia (baseline), at 5-min intervals for 1 h, then at 10-min intervals until complete recovery from blockade, by an observer blinded to the volume of saline administered for epidural flush.
The segmental level of sensory anesthesia was determined by response to pinprick and transcutaneous electrical stimulation (TCS). Response to pinprick was assessed bilaterally at 5-min intervals, using a 23-gauge needle, beginning immediately after epidural lidocaine injection (time 0) and continuing until complete resolution of anesthesia to the S2 dermatome. TCS was performed using a peripheral nerve stimulator (Life-Tech, Inc., Houston, TX), applied to the midline of the T10 and T12 dermatomes and bilaterally at the L2-3 dermatome (medial aspect above the knee) and the L5-S1 dermatome (lateral aspect above the ankle). At each site, a 5-s stimulus of 50-Hz tetanus was delivered in 10-mA increments until the subject reported the stimulus as a "tingling" sensation or we delivered a total of 60 mA, equivalent to a noxious surgical stimulus (4). Tolerance to electrical stimulation was assessed before induction of anesthesia (baseline), after lidocaine injection at 5-min intervals for 30 min, and at 10-min intervals thereafter, moving systematically from proximal (T10) to distal (L5-S1) dermatomes, until recovery to baseline stimulation level.
Motor block of the lower extremities was evaluated by a modified Bromage scale (0 = no block, 1 = hip movement block, 2 = hip and knee block, 3 = complete block in hip, knee, and ankle) at 10-min intervals until complete block resolution. An isometric force dynamometer (Micro FET; Hoggan Health Industries, Draper, UT) was used to assess 5-s isometric maximal force contraction of the quadriceps and gastrocnemius muscles bilaterally every 10 min after lidocaine injection, until return of function to at least 90% of baseline. Isometric muscle strength was measured in triplicate, and the values were averaged. Also recorded were the times to void and to ambulate independently (i.e., walk in tandem unassisted) before discharge from the study center. Postoperative follow-up was accomplished by telephone interview during the course of 3 days after discharge, during which postanesthetic complications were recorded.
To evaluate the extent of vascular absorption, before and after saline flush, plasma lidocaine concentration was determined serially by withdrawing blood samples in 5-mL aliquots from an 18-gauge angiocatheter placed in a peripheral arm vein. Venous samples were obtained immediately before administration of the lidocaine test dose and at 5, 15, 30, 40, 50, 60, 70, 80, 90, 120, 180, and 240 min after epidural injection of 2% lidocaine. A total of 65 mL of blood was collected during each of the three study periods, from which we determined the peak plasma lidocaine concentration and the time to reach peak concentration. Plasma samples were centrifuged, immediately frozen, and stored at -20°C. Lidocaine concentration in plasma was determined by gas chromatography, with the limit of detection set at 0.02 mg/L.
Statistical analysis was performed using SPSS (Chicago, IL) statistics program. Differences in the time of onset, duration, and regression of sensory anesthesia and motor blockade after 1-, 20-, and 40-mL saline flush were determined using nonparametric repeated-measures analysis of variance and intergroup comparison using Wilcoxon’s signed rank test. The level of sensory block during regression was compared using the Friedman test. The times to void and ambulate were compared using t tests. Values are reported as the median (range) for discrete variables and mean ± SD for continuous variables. Statistical significance was accepted at P < 0.05.
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Results |
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Eight volunteers were studied for all three study periods. Data of two volunteers were excluded from analysis, because these individuals developed patchy sensory and negligible motor block 30 min after induction of epidural lidocaine anesthesia during the second or third study period. This represents a failure to establish a baseline block level comparable to that in other study periods. Data from the remaining six volunteers showed that saline flush of the epidural catheter influenced the rate of resolution of epidural anesthesia.
Sensory Anesthesia
After injection of the same dose of epidural lidocaine, the median peak dermatomal level of sensory anesthesia was similar in all three study periods. The peak sensory level was T7 (range, C5-T10), T6 (range, T2-10), and T6 (range, T3-10) occurring at 31, 33, and 37 min in the 1-, 20-, and 40-mL groups, respectively (Fig. 1).
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Regression of sensory anesthesia, as measured by response to pinprick, was significantly faster after the 40-mL saline flush than the 1-mL flush, in the time to complete resolution from the time of peak sensory level (Table 1). When the sensory level (median) returned to baseline at 65 min in the 40-mL group, persistent block remained in the other two groups (P < 0.05, Fig. 1). However, although the data show a trend of earlier recovery in 2-segment regression, regression to L1 and toleration to transcutaneous tetanic stimulation in the 40-mL group, the differences are not statistically significant (Table 1). TCS tolerance over the T10, T12, or L5-S1 dermatomes was not consistently detected in all volunteers; therefore, recovery data were not reported.
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Motor Block
Complete and near-complete motor block (a modified Bromage score of 2–3) were obtained in 5 of 6 volunteers in all three study periods. The time to complete the resolution of motor block from maximal block level was significantly shorter after the 40-mL flush than the 1-mL flush (P < 0.04, Table 1). Recovery of muscle strength to 90% of baseline in the quadriceps muscles, as quantified by isometric muscle testing, also occurred earlier after 40-mL flush (P < 0.05, Table 1). Motor block in the gastrocnemius muscle group was not consistently achieved, precluding meaningful data analysis.
There were no significant differences in the speed of sensory and motor recovery between the 1- and 20-mL groups, despite the trend suggesting earlier recovery in the 20-mL group. Likewise, the differences in recovery data between the 20- and 40-mL groups were not significant (Table 1). The time to void and the time to ambulate were similar in all treatment groups (voiding: 186.8 ± 42.4 vs 185.5 ± 28.7 vs 178.8 ± 54.6 min for 1, 20, and 40 mL, respectively; ambulation: 189.8 ± 21.1 vs 181.4 ± 25.9 vs 175.4 ± 54.3 min for 1, 20, and 40 mL, respectively). There was no significant change in heart rate, blood pressure, or oxygen saturation in any volunteer throughout study. Telephone interview follow-up indicated no postanesthetic complications in any volunteer.
Vascular Absorption
Independent of volume, saline flush had no demonstrable effect on vascular absorption of lidocaine from the epidural space. Similar peak plasma lidocaine concentrations (2.31 ± 0.40 vs 2.31 ± 0.51 vs 2.39 ± 0.59 µg/mL for 1, 20, and 40 mL, respectively) were noted in all treatment groups at 56–58 min after epidural lidocaine injection (Fig. 2).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Our data suggest that 30 minutes after the induction of epidural lidocaine anesthesia in volunteers, when anesthesia is well established, administration of a 40-mL bolus of sterile saline epidurally can facilitate regression of both sensory and motor block, but a 20-mL bolus does not.
Flushing the epidural catheter with saline can hasten recovery from epidural anesthesia, possibly by several mechanisms. First, a washout effect of saline may dilute residual unbound local anesthetic in the epidural space, thereby quickly decreasing local anesthetic concentration and reversing the concentration gradient required to penetrate the neural tissues. In vitro studies have shown that neural blockade can be readily reversed by washout of local anesthetic from neural tissue using crystalloid solutions (5,6). Alternatively, saline flush might reduce the epidural concentration by displacing local anesthetic through the intervertebral foramina into the paravertebral space. Second, saline injection into the epidural space reportedly augments both secretion and clearance of cerebrospinal fluid (7), thus enhancing local anesthetic elimination from the subarachnoid space. Finally, injection of saline into the epidural space could wash out some of the local anesthetic bound to neural tissues, making it available for vascular absorption or binding to nonneural structures, such as fat or lymphatics. However, our results, showing similar peak serum lidocaine level after epidural saline flush with 1 and 40 mL, give no evidence to support that an increase in local anesthetic vascular absorption is the mechanism of enhanced epidural block recovery.
Studies examining the impact of epidural saline flush on the resolution of epidural anesthesia show beneficial effects. Johnson et al. (1) report that epidural administration of 45 mL of saline or lactated Ringer’s solution (15 mL given three times) during a period of 30 minutes hastened the resolution of motor block by approximately 2-fold after epidural bupivacaine anesthesia for cesarean delivery (mean, 70–84 vs 178 min for the control group). Regression of sensory block was unaffected, however. In contrast, our data show a smaller impact of saline flush on the rate of resolution of motor block (40 vs 65 min for the control group), but sensory block regression is enhanced. The difference in the magnitude of effect of epidural saline flush in the two studies is perhaps caused by the administration of a smaller volume of saline in our study (40 vs 45 mL), an earlier time of flush (30 vs 60 min), and the use of a shorter acting local anesthetic (lidocaine versus bupivacaine). In another study, Difazio et al. (2) compared the effects of 30 and 15 mL of saline flush on the time with recovery from epidural lidocaine anesthesia. In agreement with this study, we also demonstrated that the larger saline dose reduced the time to recovery from both sensory and motor block (2), whereas the lower dose did not. Finally, an epidural injection of 20 mL of saline after epidural lidocaine anesthesia for knee arthroscopy reportedly decreases motor block recovery and the time to reach postanesthesia care unit discharge criteria (83 vs 110 minutes for the control) (3). In our study, the effect of a 20-mL saline flush on block regression time was not significant. This difference in effect may be associated with the difference in timing of epidural saline flush in the two studies, i.e., 30 minutes after establishing epidural anesthesia in our study versus the end of surgery in the study by Brock-Utne et al. (3).
The data of two volunteers are not included for analysis. Quite unexpectedly, with our cross-over design, we observed remarkable intraindividual variability in the level of sensory and motor block. In these two volunteers, despite injection of the same dose of epidural during each study period and consistent conditions of epidural catheter placement, i.e., insertion site between L2-3 and L3-4 and catheter indwelling segment between 3–5 cm, anesthesia was much less than expected, with patchy sensory anesthesia and incomplete motor block after 20 mL of epidural lidocaine injection. This happened during the second study period in one volunteer and during the third study period in the other. In both cases, 1 mL was used for flushing. As a result, this made it impossible to detect an effect of saline flush on the resolution of anesthesia. We do not have a good explanation for the lack of anesthetic effect after repeated epidural lidocaine injection in the second and third study period, but perhaps this is a tachyphylaxis phenomenon.
Our study fails to show an earlier time to void and ambulation after the 40-mL saline flush. This is likely a result of our monitoring frequency and criteria, which were not vigorous enough to detect a difference. Furthermore, the difference in time to complete motor block recovery is only 15 minutes between the 1- and 40-mL groups (Table 1).
In summary, epidural saline flush with 40 mL injected 30 minutes after the induction of epidural lidocaine anesthesia can accelerate the regression of pinprick sensory anesthesia and motor block. Vascular absorption of epidural lidocaine, as indicated by peak plasma lidocaine concentration and the time to peak, is not affected by epidural saline flushing. An epidural saline flush should be considered in clinical practice if quicker epidural anesthetic recovery is desired.
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Acknowledgments |
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The authors thank Winnifred von Ehrenberg for her excellent editorial assistance.
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Footnotes |
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Research supported by The SAMBA Research Grant Award.
Presented in part at the annual meeting of the Society of Ambulatory Anesthesia, Orlando, FL, 1997.
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References |
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Johnson MD, Burger GA, Mushlin PS, et al. Reversal of bupivacaine epidural anesthesia by intermittent epidural injections of crystalloid solutions. Anesth Analg 1990;70:395–9.
[Abstract/Free Full Text] - DiFazio CA, Sitzman TB, Playfair PA, et al. Reversal of dense lidocaine epidural block with epidural saline washout [abstract]. Reg Anesth 1997;22:S4.
- Brock-Utne JG, Macario A, Dillingham MF, Fanton GS. Postoperative epidural injection of saline can shorten postanesthesia care unit time for knee arthroscopy patients. Reg Anesth Pain Med 1998;23:247–51.[Medline]
- Petersen-Felix S, Zbinden AM, Fischer M, Thomson DA. Isoflurane minimum alveolar concentration decreases during anesthesia and surgery. Anesthesiology 1993;79:959–65.[Web of Science][Medline]
- Gissen AJ, Covino BG, Gregus J. Differential sensitivities of mammalian nerve fibers to local anesthetic agents. Anesthesiology 1980;53:467–74.[Web of Science][Medline]
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Benzon HT, Gissen AJ, Strichartz GR, et al. The effect of polyethylene glycol on mammalian nerve impulses. Anesth Analg 1987;66:553–9.
[Abstract/Free Full Text] - Cousins M, Bridenbaugh P. Neuronal blockade. 2nd ed. New York:JB Lippincott, 1988:306.
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  A. Kanai and S. Hoka A comparison of epidural blockade produced by plain 1% lidocaine and 1% lidocaine prepared by dilution of 2% lidocaine with the same volume of saline. Anesth. Analg., June 1, 2006; 102(6): 1851 - 1855. [Abstract] [Full Text] [PDF]
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