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© 1999 International Anesthesia Research Society
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Abstract |
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The reinforcement of anesthesia by an epidural "top-up" in combined spinal-epidural anesthesia may be explained by a dual mechanism: a volume effect compressing the dural sac and a local anesthetic effect. The purpose of our study was to investigate the relative importance of each of these factors. Fifty patients scheduled for lower limb orthopedic surgery under combined spinal-epidural anesthesia were randomly allocated to one of five groups comprising 10 patients each. Using a needle-through-needle technique, all patients received a subarachnoid injection of 10 mg of plain bupivacaine and an epidural catheter. After the maximal level of sensory blockade as a result of the subarachnoid injection had been established, an epidural top-up was given according to the randomization code. Patients in Group 1 received 10 mL of bupivacaine 0.25%; patients in Group 2 received 10 mL of saline; patients in Group 3 received 5 mL of bupivacaine 0.5%; patients in Group 4 received 5 mL of saline; and patients in Group 5 received no epidural top-up. The maximal level of sensory blockade was then assessed for an additional 30 min. In Groups 1–4, the maximal level of sensory blockade increased significantly, whereas there was no significant increase in Group 5. There was no significant difference in the increase in the maximal level of sensory blockade among Groups 1–4. We conclude that, under the conditions of our study, there is no difference between 5 and 10 mL with regard to the volume effect of an epidural top-up in combined spinal-epidural anesthesia and that to produce an additional local anesthetic effect with bupivacaine, the dose must be larger than 25 mg.
Implications: In combined spinal-epidural anesthesia, an epidural "top-up" may increase the maximal level of sensory blockade by means of a volume effect and a local anesthetic effect. In this study, volumes of 5 and 10 mL produced a similar increase, and 25 mg of bupivacaine was insufficient to produce an additional local anesthetic effect.
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Introduction |
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Combined spinal-epidural anesthesia (CSE) is becoming increasingly popular, especially in obstetrics and orthopedic surgery. CSE combines the rapid onset and intensity of subarachnoid blockade and the flexibility of an epidural catheter, allowing intraoperative extension of anesthesia and postoperative epidural analgesia.
The mechanism by which an epidural "top-up" reinforces anesthesia in CSE has not been fully elucidated. Previous studies have demonstrated that the increase in the maximal level of sensory blockade after an epidural top-up can be partly attributed to a volume effect, as the volume of the local anesthetic in the epidural space compresses the dural sac and causes cephalad spread of local anesthetic already present within the subarachnoid space (1,2). Another factor that may contribute to the extension of sensory blockade after an epidural top-up is the dose of the local anesthetic (2). We designed the present study to investigate the relative contribution of each of these factors.
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Methods |
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We studied 50 patients (18–80 yr, ASA physical status I–III) scheduled for lower limb surgery under CSE after obtaining local ethics committee approval and informed consent. The study design was double-blinded and prospective. The patients were randomly allocated to one of five groups of 10 patients each. Randomization was achieved using a randomization table: codes were stored in sealed envelopes numbered 1 to 50 that were only available to the anesthesiologist administering the local anesthetic. Each envelope contained the designated epidural top-up to be given: 10 mL of plain bupivacaine 0.25% (Group 1), 10 mL of saline (Group 2), 5 mL of plain bupivacaine 0.5% (Group 3), 5 mL of saline (Group 4), or nothing (Group 5). Premedication consisted of midazolam 5–7.5 mg orally 1 h before regional anesthesia was started. All patients were prehydrated with 500 mL of isotonic saline IV. Standard monitoring was applied with blood pressure measurements at 5-min intervals throughout the study.
A 16-gauge Tuohy needle was introduced at the fourth lumbar interspace with the patient in the sitting position. In all patients, a paramedian approach was used, and the epidural space was identified using loss of resistance to saline. Care was taken to limit the injection of saline on entry into the epidural space. Using the needle-through-needle technique, a long 27-gauge Whitacre needle was introduced into the subarachnoid space. After obtaining a free flow of cerebrospinal fluid (CSF), 10 mg of plain bupivacaine 0.5% was administered into the subarachnoid space (start of the spinal phase), and the spinal needle was then withdrawn. An 18-gauge lateral eye catheter was introduced 5 cm into the epidural space via the epidural needle, which was subsequently removed. The patient was then placed in the supine horizontal position for the entire study period.
During the spinal phase, the level of sensory blockade was measured every 5 min by an independent blinded observer by determining the loss of temperature sensation in the anterior axillary line using an ice cube. The highest segment at which the patient was not capable of determining the temperature of the ice cube was recorded. Establishment of the maximal level of sensory blockade was defined as no further increase during three consecutive measurements and >20 min after subarachnoid injection. The onset time to maximal sensory blockade was defined as the time from subarachnoid injection to the time when the maximal level of sensory blockade was first recorded. After achieving maximal sensory blockade during the initial spinal phase, the observer assessing sensory blockade left the room. After careful aspiration of the epidural catheter, the designated epidural top-up was administered to patients in Groups 1–4 and was simulated in patients in Group 5. Patients in Groups 1–4 were blinded to the epidural injection given. Patients in Group 5 were told that an epidural injection was made while the epidural catheter was manipulated. After completing the simulated or real epidural injection, time was designated as t0. The observer measuring sensory blockade returned to continue assessing sensory blockade at 5-min intervals during a further 30 min (epidural phase). The onset time of maximal sensory blockade during this phase was defined as the time from t0 until the next maximal level of sensory blockade was first recorded. The study was concluded at the end of this observation period, and the epidural catheter was used for intraoperative top-ups and/or postoperative analgesia as deemed necessary by the attending anesthesiologist.
Data on patient characteristics and the time to onset of maximal sensory blockade are expressed as mean ± SD. Data on the maximal level of sensory blockade and segmental increase are presented as median (range). Comparisons among the groups regarding continuous variables were performed by using one-way analysis of variance and Tukey-Kramer multiple comparisons tests when appropriate. Statistical analysis comparing the increase in maximal sensory blockade after epidural top-up within each group was performed by using the Wilcoxon signed rank test. Comparisons among the groups regarding ordinal data was performed with the Kruskal-Wallis test and Dunn’s multiple comparisons test when appropriate. P < 0.05 was considered statistically significant.
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Results |
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All patients enrolled completed the study successfully. The volume of saline injected into the epidural space on entry of the Tuohy needle was <1 mL in all patients. In all patients, the characteristic feeling of the Whitacre needle passing through the dura was felt, and a free flow of CSF obtained. Epidural catheter insertion was easy in all patients, and all patients were placed in the supine horizontal position within 3 min after subarachnoid injection. There were no significant differences among the five groups regarding age, height, or weight (Table 1). The maximal levels of sensory blockade and the onset times during the spinal phase were comparable (Table 2). In Groups 1–4, the epidural top-up resulted in a significant increase in the maximal level of sensory blockade. In Group 1, the maximal level of sensory blockade increased in nine patients, whereas in one patient there was no change; the median increase in Group 1 (calculations including all patients) was 2.5 (0–7) segments. In Group 2, the maximal level of sensory blockade increased in eight patients and remained the same in two patients; the median increase (calculations including all patients) was 2 (0–5) segments. In Group 3, the maximal level of sensory blockade increased in six patients and did not change in the remaining four patients, resulting in a median increase (calculations including all patients) of 1 (0–7) segment. In Group 4, the maximal level of sensory blockade increased in seven patients and did not change in the remaining three patients; the median increase (calculations including all patients) was 1.5 (0–6) segments. In Group 5, the maximal level of sensory blockade increased one segment in three patients and remained unchanged in seven patients; this resulted in a median increase of 0 (0–1) segments (calculations including all patients; not significant versus spinal phase). Intergroup comparison among Groups 1–4 showed that there were no statistically significant differences in the increase in the maximal level of sensory blockade during the epidural phase. Data on the maximal level of sensory blockade are summarized in Table 2. A graphical representation of the changes in the maximal level of sensory blockade of each individual patient is shown in Figure 1. Figure 2 represents the change in the maximal level of sensory blockade during the epidural phase versus time.
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) and epidural (
) phases. The horizontal axis represents individual patients and the vertical axis represents the dermatomal level.
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) = epidural top-up with 10 mL of saline; Group 3 (
) = epidural top-up with 5 mL of bupivacaine 0.5%; Group 4 (Onset times to the maximal level of sensory blockade during the epidural phase (calculations for patients who showed an increase) were 15.0 ± 7.1 min (Group 1), 13.1 ± 10.3 min (Group 2), 14.1 ± 10.7 min (Group 3), and 7.1 ± 2.7 min (Group 4); the differences in the onset times during the epidural phase among Groups 1–4 were not statistically significant.
Analgesia during surgery was excellent in all patients. None of the patients developed postdural puncture headache.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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When studying the mechanism of action of an epidural top-up in CSE, one must consider two anesthetic techniques, each with a different mode of action. A local anesthetic injected into the subarachnoid space is immediately in close contact with spinal nerves and the spinal cord, causing neural blockade in a relatively short timespan. In the epidural space, things are more complicated and subject to debate. A local anesthetic injected into the epidural space is thought to cause neural blockade in several ways, the most important being passage from local anesthetic through the dural sleeves, the extensions of dura mater covering the spinal nerves in the epidural space (3,4). By diffusing through the dural sleeves, the local anesthetic will block the spinal nerves intradurally; this mode of action explains the relatively slow onset of epidural versus spinal neural blockade. Diffusion of the local anesthetic through the dura also results in the appearance of local anesthetic in the CSF. This probably plays a minor role in establishing initial neural blockade resulting from the first epidural injection; however, the presence of local anesthetic in the subarachnoid space would explain the intensifying effect on sensory and motor blockade when an epidural top-up is given (4).
Regarding the extension of sensory blockade by an epidural top-up in CSE, several mechanisms have been implied. Rawal and et al. (5) suggested the possibility of transfer of local anesthetic through the hole in the dura mater made by the spinal needle. In an analogy of Bromage’s earlier observations regarding epidural anesthesia, Carrie (6) suggested the existence of "subclinical" analgesia as a result of low concentrations of local anesthetic in the CSF above the upper level of sensory block after subarachnoid injection, expanding rapidly into sensory blockade after a relatively small dose of epidurally administered local anesthetic. Blumgart et al. (1) postulated that the extension of sensory blockade is caused by an epidural volume effect, in which the dural sac is compressed by the injectate, resulting in a cephalad shift of CSF containing local anesthetic. This claim has been confirmed in a myelographic study, which showed that 10 mL of saline given as an epidural top-up reduced the volume of the subarachnoid space to 25% (7).
In a previous study, we found that the epidural injection of 10 mL of saline or 50 mg of bupivacaine in a volume of 10 mL after the maximal level of sensory blockade had been established resulted in a significant increase in the maximal level of sensory blockade (2). However, in that study, the increase observed in the group receiving 50 mg of bupivacaine was significantly greater compared with the increase in the saline group, which indicates that the increase in the maximal level of sensory blockade may be attributed partly to a volume effect and partly to a local anesthetic effect.
In the present study, there was no significant difference in the extent of the increase of the maximal level of sensory blockade among the four groups receiving an epidural top-up. In Groups 1–4, a number of patients did not respond to the epidural top-up. This may be the result of catheter malposition; however, we consider this unlikely because in all patients in whom the epidural catheter was used after the study, the epidural catheters functioned properly. It therefore seems that, under the conditions of our study, not all patients respond to an epidural top-up. If the nonresponders in each group had been excluded, the differences among Groups 1–4 regarding the average increase in the maximal level of sensory blockade would have been even smaller. These findings indicate that the increase in the maximal level of sensory blockade as a result of a volume effect is independent of the volume used (5 or 10 mL) and that a dose of 25 mg of bupivacaine is insufficient to cause an additional increase in the maximal level of sensory blockade. However, given the relatively small sample size of our groups, the possibility of a type II error must be kept in mind, and studies using more individuals per group are needed to substantiate these conclusions.
A number of authors have reported difficulties in reaching the subarachnoid space when using the needle-through-needle technique in CSE: failure rates as high as 16% (8) and 24.5% (9) have been reported. Interestingly, we did not encounter such problems. Lumbar puncture through the epidural needle and subsequent epidural catheter placement was easily accomplished in all patients. Whether this has to do with the fact that we routinely use the paramedian approach is speculative.
In conclusion, extension of the maximal level of sensory blockade in CSE may be achieved by an epidural top-up. We found no difference between epidural top-up volumes of 5 and 10 mL, and 25 mg of bupivacaine was insufficient to produce an additional effect. We conclude that, under the conditions of our study, when administering an epidural top-up in CSE, the injected volume (5 or 10 mL) is not critical with regard to the extent of the increase in the maximal level of sensory blockade. To obtain an additional local anesthetic effect, the dose of bupivacaine has to be larger than 25 mg.
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Footnotes |
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This work was presented in part at the 23rd annual meeting of the American Society of Regional Anesthesia, Seattle, WA, May 1998.
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References |
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Blumgart CH, Ryell D, Dennison B, Thompson-Hill LM. Mechanism of extension of spinal anaesthesia by extradural injection of local anaesthetic. Br J Anaesth 1992;69:457–60.
[Abstract/Free Full Text] - Stienstra R, Dahan A, Alhadi BZR, et al. Mechanism of action of an epidural top-up in combined spinal epidural anesthesia. Analg 1996;83:382–6.[Abstract]
- Bromage PR. Mechanism of action of extradural analgesia. Br J Anaesth 1975;47:199–212.
- Bromage PR. Mechanism of action. In: Bromage PR, ed. Epidural analgesia. Philadelphia:WB Saunders, 1978:119–59.
- Rawal N, Schollin J, Wesström G. Epidural versus combined spinal epidural block for cesarean section. Acta Anaesthesiol Scand 1988;32:61–6.[Web of Science][Medline]
- Carrie LES. Epidural versus combined spinal epidural block for cesarean section. Acta Anaesthesiol Scand 1988;32:595–6.[Web of Science][Medline]
- Takiguchi T, Okano T, Egawa H, et al. The effect of epidural saline injection on analgesic level during combined spinal and epidural anesthesia assessed clinically and myelographically. Anesth Analg 1997;85:1097–100.[Abstract]
- Lyons G, MacDonald R, Mikl B. Combined epidural/spinal anaesthesia for caesarean section. Through needle or in separate spaces? Anaesthesia 1992;47:199–201.[Web of Science][Medline]
- Urmey WF, Stanton J, Peterson M, Sharrock NE. Combined spinal-epidural anesthesia for outpatient surgery. dose-response characteristics of intrathecal disobaric lidocaine using a 27-gauge Whitacre spinal needle. Anesthesiology 1995;83:528–34.[Web of Science][Medline]
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