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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionAppendix 1. Follow-up Interview...References |
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The syndrome of transient neurologic symptoms (TNS) after spinal lidocaine has been presumed to be a manifestation of local anesthetic neurotoxicity. Although TNS is not associated with either lidocaine concentration or dose, its incidence has never been examined with very small doses of spinal lidocaine. One hundred ten adult ASA physical status I and II patients presenting for arthroscopic surgery of the knee were randomly assigned to receive spinal anesthesia with either 1% hypobaric lidocaine 50 mg (Group L50) or 1% hypobaric lidocaine 20 mg + 25 µg fentanyl (Group L20/F25). Hemodynamic data, block height and regression, and time to first micturition and discharge were recorded. Follow-up phone calls were made by a blinded researcher at 48–72 h using a standardized questionnaire. Both groups had a median peak cephalad block level of T10. Lidocaine 50 mg was associated with a greater decrease in systolic blood pressure and a greater need for ephedrine. Time until block regression to the S2 dermatome (80 vs 110 min) and outpatient time to void (130 vs 162 min) and discharge (145 vs 180 min) were faster in the L20/F25 group. Complaints of TNS were found in 32.7% of the patients in the L50 group and in 3.6% of the patients in the L20/F25 group. We conclude that spinal anesthesia with lidocaine 20 mg + fentanyl 25 µg provided adequate anesthesia with greater hemodynamic stability and faster recovery than spinal anesthesia with lidocaine 50 mg. The incidence of TNS after spinal lidocaine 20 mg + fentanyl 25 µg was significantly less than that after spinal lidocaine 50 mg.
Implications: The use of a small-dose lidocaine plus fentanyl combination for spinal anesthesia provides greater hemodynamic stability, faster recovery, and a significantly reduced incidence of transient neurologic symptoms than a conventional dose (50 mg) of spinal lidocaine.
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1. Follow-up Interview...References |
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In 1991, there appeared several reports of cauda equina syndrome in association with the use of spinal lidocaine (1,2), reawakening concern as to the potential toxicity of intrathecal local anesthetics. There followed not long thereafter reports of transient neurologic symptoms (TNS) after the use of spinal lidocaine (3,4). This syndrome is characterized by postoperative development (within 24 h) of bilateral aching pain or dysesthesia in the buttocks with radiation into sacral dermatomes of the legs. Symptoms typically abate within a week, although they may persist for longer in up to 10% of patients, and are not associated with other neurologic findings. The syndrome has been repeatedly demonstrated to occur in 10%–20% of patients after spinal lidocaine, although it occurs only rarely with bupivacaine (5). Its incidence is greater when operations are performed in certain positions that cause a stretch of spinal nerve roots (e.g., lithotomy, arthroscopy) (5–7).
Although it remains unproven, many believe that the syndrome of TNS represents a mild and nonpermanent manifestation of neurotoxic injury. Laboratory data indicate the potential for lidocaine neurotoxicity (8) and a concentration dependence of local anesthetic neurotoxicity (9). Nevertheless, repeated study has not found a decreased incidence of TNS with spinal lidocaine dilutions to 2%, 1%, or even 0.5% solutions (5,10,11). Moreover, it is not certain that decreasing the dose of lidocaine will influence the incidence of TNS. Freedman et al. (6) reported no influence of lidocaine dose on the incidence of TNS. However, their definition of "small-dose" lidocaine was 50 mg or less. It remains unknown if substantially smaller doses would reduce the incidence of TNS.
The primary purpose of this study was to examine the incidence of TNS after spinal lidocaine in a dose range below that examined by Freedman et al. (6) as well as to explore the clinical potential for a small-dose lidocaine-fentanyl spinal anesthetic in outpatient surgery.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1. Follow-up Interview...References |
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This study was approved by the hospital ethics committee of both institutions in which it was conducted: Western Galilee Hospital, Nahariya, Israel (Hospital A) and Allegheny General Hospital, Pittsburgh, PA (Hospital B). The study was conducted after obtaining written, informed consent of the patients. The patients included 110 adult ASA physical status I and II patients presenting for arthroscopic surgery of the knee. They were randomly assigned to one of two groups (defined by the spinal injectate) by using a sealed envelope technique. Patient groups were as follows: Group L50 = spinal of 1% hypobaric lidocaine 50 mg and Group L20/F25 = spinal of 1% hypobaric lidocaine 20 mg + 25 µg fentanyl (final concentration of lidocaine was 0.8%). Exclusion criteria included peripheral vascular disease, major organ dysfunction, diabetes mellitus, and other endocrine/metabolic disorders, peripheral neuropathy, or other neurologic disease, or a current complaint of low back pain with associated radicular symptoms. The patient and surgeon were blinded as to group assignment. All recovery room data and postoperative follow-up data were obtained by a second blinded researcher.
Patients received no premedication before arrival in the operating room. An IV infusion of lactated Ringer’s solution was begun on arrival in the operating room, but no fluid loading was used before spinal anesthesia. Patients received midazolam 0.03–0.04 mg/kg + fentanyl 0.75–1.0 µg/kg IV several minutes before positioning for lumbar puncture. Standard monitoring included continuous electrocardiogram and pulse oximetry. Noninvasive automated blood pressure measurements were recorded before any medication and at 5-min intervals thereafter. Lumbar puncture was performed in the sitting position with the patient immediately returned to supine on completion of the spinal. Lumbar punctures were made with 25- or 26-gauge pencil point needles positioned midline at the L3-4 interspace with the orifice directed cephalad. Injections were made over 10 to 15 s.
Patients received no more than a total of 1000 mL lactated Ringer’s solution perioperatively. Inadequate anesthesia (patient complaint of pain) was to be treated with an additional bolus of IV fentanyl 0.75–1.0 µg/kg, with a second bolus allowable. The protocol allowed for conversion to general anesthesia as deemed necessary by the anesthesiologist. Patients were to be treated for hypotension with IV ephedrine (5- to 10-mg boluses) when systolic blood pressure decreased by 33% or more.
Pinprick testing in the midline every 2 min was used to establish onset and peak level of sensory blockade. Postoperatively pinprick testing was done every 10 min until regression to S2 was established. Time from block placement to first urination was recorded. Patients at Hospital A (n = 60) were hospitalized overnight, whereas patients at Hospital B (n = 50) were discharged home from an ambulatory surgery center facility. Hospital B patients were discharged home only after micturition, and the times of this were recorded by the blinded researcher. Hospital A patients were discharged to the hospital ward without micturition. Their time to first urination was recorded on the chart by ward nursing staff. Follow-up phone calls were made at 48–72 h by using a standardized questionnaire (Appendix 1). Calls were made by a blinded researcher.
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Statistical analysis was conducted by using Statview 5 (SAS Institute, Cary, NC). Data were analyzed by using the Mann-Whitney U-test, analysis of variance,
2, or Fisher’s exact tests as appropriate. Results were considered significant at a P value of 0.05. |
Results |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1. Follow-up Interview...References |
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There were no significant differences in age (46 ± 15 vs 44 ± 17), weight (83 ± 15 vs 83 ± 17 kg), height (172 ± 8 vs 173 ± 10 cm), sex (38:17 vs 35:20, male:female), or operating room times (46 ± 8 vs 48 ± 10 min) between the two groups. Sixty patients were studied at Hospital A, and 50 patients were studied at Hospital B. At each institution, there was an even distribution between the two study groups.
Although the median peak cephalad block for both groups was similar (T10) there was a nonnormal distribution of the data that yielded a statistically higher level of block in the L50 Group (Table 1). Group L50 also required ephedrine significantly more frequently and incurred a significantly greater decrease in systolic blood pressure. There was no difference in the decrease in diastolic blood pressure. There were several patients in both groups who required IV fentanyl supplementation for pain, but no patient in the study required a second fentanyl dose or conversion to general anesthesia. Spinal block regression to S2 occurred 30 min faster in Group L20/F25 (80 ± 21 vs 110 ± 25 min, P < 0.0001). Time to voiding was significantly greater in the inpatients than in the outpatients. When the outpatients were looked at specifically, Group L20/F25 had a significantly faster time to void (130 ± 34 vs 162 ± 35 min, P = 0.002) and to discharge (145 ± 38 vs 180 ± 31 min, P = 0.002) than did Group L50.
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On the basis of the follow-up interview TNS was diagnosed in 32.7% of the Group L50 patients as opposed to 3.6% of the Group L20/F25 patients (P < 0.0001; Table 2). There was no difference in the incidence of TNS in the inpatient versus the outpatient groups. Symptoms were typically a burning or aching pain radiating into the buttocks, coccyx, or thighs and frequently associated with back pain. In some patients the pain was associated with persistent numbness in the buttocks and legs. Because further follow-up calls were not made, there are no data available as to the duration of patients’ symptoms, although a number of patients felt the symptoms had improved by the time of the follow-up phone call. There was no difference in average block height or block duration for the patients with TNS when compared with the patients who did not have it.
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In both groups, 18.9% of the remaining patients reported localized pain at the site of the spinal injection. The denominator used for this calculation was the number of patients in each group who had not had TNS insofar as it was impossible to know if a patient with TNS had a contribution to the back pain from a localized irritation. One patient in each group had a spinal headache diagnosed, but in both cases, it was mild and did not require medical intervention.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1. Follow-up Interview...References |
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The most important finding of this study is the reduction of the incidence of TNS after lidocaine spinal anesthesia. The incidence of 3.6% TNS in the L20/F25 group, it will be recalled, was despite this being a high risk group for the development of TNS (arthroscopy positioning). The association of TNS with positioning (5–7) remains unexplained, but it has been suggested that stretching of the nerve roots may reduce blood flow of the vasa nervorum and increase vulnerability to the toxic effects of local anesthetics. Whether the smaller incidence of TNS in the L20/F25 group is the result of the smaller dose of lidocaine or of either a protective or obscuring effect of the fentanyl cannot be determined from this study, although in a previous report, the use or nonuse of intrathecal fentanyl was found not to correlate with TNS (6).
Our findings are thus consistent with (but not conclusive of) the concept that TNS represents a neurotoxic effect of intrathecal lidocaine. The laboratory evidence for lidocaine neurotoxicity (8,9) is supported by clinical reports (1,2) and epidemiologic data (12). Until now, however, the failure to link postlidocaine spinal TNS with either concentration (5,10,11) or dose (6) of the injected lidocaine has suggested the possibility of some other etiology. In retrospect, it is perhaps not surprising that no effect was found in the dilution studies. Patients in the various groups in those studies received comparable doses (typically 50 mg) of lidocaine. Because local anesthetic distributes within the CSF fairly rapidly (13), it seems likely that similar cerebrospinal fluid (CSF) concentrations of lidocaine would have been reached quickly, regardless of the injectate lidocaine concentration.
The primary determinants of local anesthetic concentration reached within the CSF ought be the total dose of local anesthetic and the CSF volume, not the injectate’s local anesthetic concentration or volume (which is substantially less than the CSF volume). The only two certain ways to decrease CSF concentration of the local anesthetic would be to (a) use very large injectate volumes to increase CSF volume or (b) use smaller than conventional doses of local anesthetic. The problem with the former may be that it unduly increases intracranial pressure by a sudden drastic increase in CSF volume. The problem with the latter may be an inadequate block. However, with the addition of a small intrathecal dose of lipophilic opioid, such as fentanyl or sufentanil, this problem can be overcome. Whereas a small dose of intrathecal lidocaine may not, of itself, provide adequate anesthesia, opioids and local anesthetics administered together intrathecally have a potent synergistic analgesic effect (14–16). Intrathecal opioids greatly enhance subtherapeutic doses of local anesthetic (16,17) and make it possible to achieve successful spinal anesthesia by using otherwise inadequate doses of local anesthetic (18).
Carpenter et al. (19) showed a large interpatient variability of lumbosacral CSF volume and a correlation between CSF volume and cephalad spread of the spinal block (19). A correlation between block height (i.e., CSF volume) and TNS might be suggestive of a dose-response relationship. Freedman et al. (6) found no difference in the incidence of TNS in patients with a block height < T10 versus > T10. Our study also failed to show such a correlation. Patients who suffered TNS did not differ from the remainder of the patients for either block height or duration.
That there was a significant difference of peak block height (L50 higher) between groups despite the identical median levels of T10 implies a nonnormal distribution of the data. In this case, it is doubtful that statistical significance translates into clinical significance. Furthermore, higher block levels are readily achievable with hypobaric spinal anesthesia by leaving the patient in a sitting position after completion of the spinal injection. This technique for attaining a higher level of spinal block has been used successfully with similar hypobaric spinal anesthesia mixtures (20). Certainly it is evident that surgical anesthesia can be provided by this small-dose lidocaine-fentanyl combination.
The addition of fentanyl to the 1% lidocaine did produce a 0.8% solution in the L20/F25 group, which was different from the 1% solution of the L50 group. It is unlikely that this difference affected outcomes because concentrations as small as 0.5% do not decrease the incidence of TNS (11). Because inpatients may have a smaller incidence of TNS than ambulatory patients, the combination of both is a potential confounding factor which might have weakened the study. Despite this, the results were highly significant (P < 0.0001). Moreover, our results do not support previous findings of a different incidence between inpatients and outpatients. What is unique about our study’s comparison of inpatients and outpatients is that it was neither patient nor surgical factors that determined the choice of pathway but rather differences in the health care systems (Israel, United States).
Apart from the advantage of a reduced incidence of TNS the small-dose local anesthetic-fentanyl combination has been shown to provide a more stable hemodynamic course (20–23). Our results concur with previous findings, but we recognize that the blood pressure changes in this study may have been exaggerated by our having taken baseline blood pressure readings before administration of any sedative.
In addition to the more stable hemodynamic response, the small-dose lidocaine-fentanyl spinal also provided for a significantly more rapid regression of blockade and a more rapid return of the ability to void spontaneously. We chose to evaluate the inpatient and outpatient groups separately with regard to micturition for several reasons. First, the outpatients were held in a recovery area and were closely followed through the time of discharge, whereas the inpatients were discharged to a hospital ward on achieving regression of the block to S2. Therefore, the data gathered on the outpatients was more likely to be accurate. Second, patient management in an outpatient stage 2 recovery area is quite different from that of a hospital ward. Because our interest in this matter pertains to ambulatory surgery, it seems germane to focus our attention on this subset of patients. Whereas others have found a rapid return in the ability to void on achieving S2 block regression (24,25), our patients exhibited a delay of 50 minutes in both groups. This may represent differences in nursing management, such as the rapidity with which patients are placed in a chair or allowed to ambulate.
The use of a dilute solution of spinal lidocaine provided for both more accurate dosing and a more rapid recovery than would a more concentrated solution (22,25). It is unlikely that the addition of fentanyl prolonged recovery because fentanyl added to a lidocaine spinal prolongs sensory anesthesia without prolonging recovery (24). Liu et al. (25) have shown a more rapid recovery with use of a hyperbaric spinal solution as opposed to a dextrose-free one. Therefore it is possible that the small-dose group’s recovery times would have been shorter still had we used a dextrose-containing solution. Lastly, patient discharge could also be speeded by eliminating the requirement that patients void before discharge. This requirement may not be necessary with a minidose lidocaine-fentanyl spinal.
The 1.8% incidence of spinal headache and the 18.9% incidence of localized back pain are consistent with the literature. These complaints were mild in degree and required no medical interventions. The similar incidence of back pain between groups suggests that there was not a problem of misdiagnosis or confusing these cases with cases of TNS.
Problems of delayed discharge after ambulatory surgery and the high incidence of TNS have resulted in controversy concerning the continued use of spinal lidocaine. The use of minidose lidocaine + fentanyl spinal anesthesia appears to offer multiple advantages, particularly in the ambulatory setting: faster recovery, hemodynamic stability, and a reduced risk of TNS.
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Appendix 1. Follow-up Interview Questionnaire |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1. Follow-up Interview...References |
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Appendix 1
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References |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1. Follow-up Interview...References |
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Rigler ML, Drasner K, Krejcie TC, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 1991; 72: 275–81.
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Lambert DH, Hurley RJ. Cauda equina syndrome and continuous spinal anesthesia. Anesth Analg 1991; 72: 817–9.
[Free Full Text] - Hampl K, Schneider M, Ummenhofer W, et al. Transient neurologic symptoms after spinal anesthesia. Anesth Analg 1995; 81: 1148–53.[Abstract]
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Schneider M, Ettlin T, Kaufmann M, et al. Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine. Anesth Analg 1993; 76: 1154–7.
[Free Full Text] - Pollock J, Neal J, Stephenson C, Wiley C. Prospective study of the incidence of transient radicular irritation in patients undergoing spinal anesthesia. Anesthesiology 1996; 84: 361–7.
- Freedman JM, Li D-K, Drasner K, et al. Transient neurologic symptoms after spinal anesthesia. Anesthesiology 1998; 89: 633–41.[Web of Science][Medline]
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- Hampl K, Schneider M, Pargger H, et al. A similar incidence of transient neurologic symptoms after spinal anesthesia with 2% and 5% lidocaine. Anesth Analg 1996; 83: 1051–4.[Abstract]
- Pollock JE, Liu SS, Neal JM, Stephenson CA. Dilution of spinal lidocaine does not alter the incidence of transient neurologic symptoms. Anesthesiology 1999; 90: 445–50.[Web of Science][Medline]
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