The mechanism causing the symptoms, and even the clinical significance, of transient neurologic symptoms (TNSs) after spinal anesthesia is still unclear (1,2). Typically, the symptoms emerge after a pain-free interval of several hours and last up to 72 h. Fortunately, no persistent neurological findings or any late effects associated with TNSs have been documented.
Among the local anesthetics used in spinal anesthesia, lidocaine clearly enhances the risk of developing TNSs (1,2). The incidence of TNSs after lidocaine spinal anesthesia has varied from between 10% and 33%(3–6). The association between TNSs and lidocaine is peculiar because different doses, concentrations, and baricities do not seem to affect the occurrence of TNSs (5,7–10). Because of the potential neurotoxicity of large concentrations of lidocaine (11), it has been recommended that large doses or concentrations of lidocaine should not be used in spinal anesthesia (12).
Lithotomy position and knee arthroscopy have been considered risk factors for TNSs after lidocaine spinal anesthesia (5,13). The incidence of TNSs after knee arthroscopy has been reported to be 31% with 5% hyperbaric lidocaine (14) and 16%–22% with 2% isobaric lidocaine (5,8,15). Freedman et al. (13) also identified outpatient status as an important risk factor. In a study on inguinal herniorrhaphy patients, mobilization as soon as possible after spinal anesthesia with a large dose of lidocaine (100 mg) was associated with a similar incidence of TNSs (23%) as when staying in bed for 12 h or longer (16).
The purpose of the present study was to evaluate if the time of ambulation has any effect on the occurrence of TNSs after spinal anesthesia with 50 mg of 2% lidocaine.
After ethics committee approval and written informed consent, 120 ASA physical status 1 or 2 patients undergoing knee arthroscopy under spinal anesthesia were randomized to three groups of equal size by sealed envelope. Patients were excluded if they had received any analgesic medication within 8 h before the operation, had radicular pain or back pain of any type, had neurologic disease, or had a body mass index >35. The patients were allocated into early ambulation (Group E) with mobilization as early as possible after sensory and motor block regression, 6-h ambulation group (Group 6-h), or late mobilization group that was bedridden until next morning 18–24 h (Group L). The number of patients to be enrolled in this study (at least 35 patients per group) was determined by power analysis (power 80%; P < 0.05). The incidence of TNSs with 2% lidocaine for knee arthroscopy has been approximately 22% in our pilot studies with immediate ambulation and in the literature (15). We expected that the incidence of TNSs after overnight bed rest would conform to that associated with bupivacaine spinal anesthesia (TNSs incidence <3%).
Preoperatively, patients received a peripheral IV infusion with acetated Ringer’s solution. Patients were sedated pre- and intraoperatively with IV midazolam (Roche, Basel, Switzerland) in a mean dose of 4.1 mg (range, 2–5 mg) and alfentanil (Orionpharma, Espoo, Finland) in a mean dose of 0.65 mg (range, 0–1.75 mg) at the discretion of the attending anesthesiologist. Patients were monitored with the standard routine (electrocardiogram, automated noninvasive arterial blood pressure, and pulse oximetry). Subarachnoid puncture was performed at the L2-3 or L3-4 interspace with the patient in the lateral decubitus position using a 27-gauge or 26-gauge Yale spinal needle with needle bevel parallel to longitudinal axis of the spine (BD, Madrid, Spain). Either the midline or paramedian approach was applied according to the anesthesiologist’s preference.
Hypotension (systolic blood pressure decrease more than 30% from baseline) was treated with 10-mg increments of IV ephedrine. Bradycardia (heart rate <45 bpm) was treated with 0.5 mg IV atropine.
All patients received 50 mg of isobaric 2% lidocaine (Lidocard® 20 mg/mL inject, Orion Pharma, Espoo, Finland) for spinal anesthesia. The extent of anesthesia was assessed by the patient’s discrimination of warmth and cold using an alcohol swab. Motor block was assessed using modified Bromage scale (0 = movement in hip, knees, and ankles and 3 = no movement). The assessment was performed every 5 min until the sensory level and motor block had stabilized. The time from the injection of lidocaine until block resolution was checked. The time of block resolution was defined as the time the nurse could no longer detect discrimination of warmth and cold to the touch of an alcohol swab. Data on patient demographics, degree of difficulty for block placement (the number of attempts to puncture the subarachnoid space, paresthesias, etc.), adequacy of the block for surgery, duration of surgery, and tourniquet time were collected.
Five orthopedic surgeons performed the arthroscopies, and a thigh tourniquet was used in all patients. During arthroscopy, the leg was hanging down freely from the end of the operating table. The other limb was resting on the gynecologic holder in a slightly upward direction. The maneuver and positions of lower legs varied to some extent according the orthopedic surgeon.
All patients stayed in the hospital at least overnight. Postoperative pain medication consisted of oral diclofenac 50 mg or acetaminophen 1 g, supplemented with IM oxycodone 10 mg at patient’s request.
In Group E, time to ambulation was the time when the patient could detect discrimination of warmth and cold on the skin of the fifth toe on both sides and the motor function had recovered (movement in hips, knees, and ankles). The mobilization of the patients in Group E and Group 6-h was performed according to a standardized schedule consisting of walking tests. It consisted of at least four walks first in the room and later in the corridor at 30-min intervals. After that schedule, patients’ movement was not limited, but the activity was recorded. The patients in Group L were bedridden until the next morning. If the patients could not void in the lying position, they were taken in the bed to the restroom for voiding where they were allowed to void in a sitting position.
The patients filled in two structured follow-up questionnaires: the initial follow-up questionnaire on the first postoperative morning and the second one immediately after the seventh postoperative day.
The questionnaire requested detailed information about postoperative recovery, including pain, nausea, and satisfaction with anesthesia. In addition, questions were asked about any symptoms in the legs, buttocks, and back and about the nature of these symptoms. TNSs were defined as back pain or dysesthesia radiating bilaterally to the legs or buttocks after total recovery from spinal anesthesia and beginning within 24 h of surgery. The intensity of TNSs pain was assessed using a verbal rating scale where 0 = no pain, 1 = slight pain, 2 = moderate pain, and 3 = severe pain. A 100% documentation of patients’ follow-up was reached because all the patients were in military service and could be traced.
Data were analyzed using descriptive statistics. Continuous variables among groups were compared using analysis of variance. Categorical data among study groups were compared with the χ2 test and Yates correction. Continuous variables among patients with and without TNSs were compared using Student’s t-test or the Mann-Whitney test, as appropriate. Verbal rating scale values were compared with Kruskal-Wallis one-way analysis of variance on ranks. P < 0.05 was considered statistically significant.
Of the 120 patients enrolled in the study, one patient in Group 6-h was excluded because he refused to get up until the next morning. There were no significant differences among the groups with respect to ASA physical status and demographic or surgical data (Table 1).
The puncture was difficult in 5 of 119 cases. In 2 cases, the 27-gauge spinal needle was changed to a 26-gauge needle because of difficulty in obtaining cerebrospinal fluid (CSF). CSF was initially bloodstained in five patients. No paresthesias were reported. The midline approach for puncture was used in 90 patients and paramedian approach in the others. There was no statistical difference among the three groups concerning the above-mentioned spinal puncture, sensory block, or motor block (Table 1).
The spinal anesthesia was not adequate for surgery in 10 cases, and the patients complained of pain during the operation. In these cases, the spinal anesthesia was supplemented with IV alfentanil. In 4 of these cases, supplemental inhaled nitrous oxide was used as well, but no general anesthesia was required. Four patients were treated with ephedrine and atropine because of hypotension and bradycardia.
Complete recovery from the anesthetic was documented in all patients by the evening of surgery. The patients in Group E were mobilized on average 229 ± 21 min (range, 135–247 min) after spinal puncture, in Group 6-h after 355 ± 30 min (range, 301–378 min), and in Group L after 1300 ± 147 min (range, 1074–1402 min). There were no differences in the mobilization activity between Groups E and 6-h after standardized mobilization.
TNSs developed in 3 patients (7.5%) of Group E, in 11 patients (28%) of Group 6-h (P < 0.05 compared with Group E), and in 5 patients (13%) of Group L (Table 2). There were no significant differences between the characteristics of the patients who suffered from TNSs and those who did not (Table 3).
Two of the above-mentioned 5 patients in whom there had been puncture difficulties and CSF was slightly bloodstained developed TNSs.
Eighty-five percent of the patients used diclofenac 50 mg or acetaminophen 1 g for postoperative pain in the operated knee, and 18% required IM oxycodone as well. Ten of the 19 (53%) patients with TNSs received extra analgesics because of their painful neurologic symptoms.
One patient had problems in passing urine soon after the spinal anesthesia. Six patients suffered mild nausea on the day of operation. In the seventh-day questionnaire, 8 patients reported having experienced mild posture-dependent headache that was relieved with oral diclofenac, and 3 other patients had transiently slight visual or auditory disturbances.
Four patients reported dissatisfaction regarding their spinal anesthesia because of inadequate surgical anesthesia, but all the others (97%) were fully satisfied.
In the present study, early ambulation did not increase the risk of developing TNSs after spinal anesthesia. In fact, among our study groups, the smallest incidence of TNSs (7.5%) was recorded in the early mobilization group, i.e., in those starting to move about 135–247 minutes after lidocaine injection. The overall incidence of TNSs, 16%, was consistent with earlier studies using lidocaine spinal anesthesia for knee arthroscopy (5,15).
Lindh et al. (16) have shown that ambulation soon after the disappearance of lidocaine spinal block does not seem to increase the incidence of TNSs (23% in both early and late ambulation groups). There are some differences between their study and the present study. Their patients in the early ambulation group were mobilized one to three hours later than our patients, probably because they used a large lidocaine dose of 100 mg. Our smaller dose of lidocaine (50 mg) can be considered more suitable for ambulatory patients. Smaller doses of plain lidocaine may not be sufficient for arthroscopic knee surgery with a thigh tourniquet because in our study, four patients expressed their dissatisfaction because of inadequate analgesia during surgery. However, by using intrathecal opioid adjuvants, smaller doses of lidocaine have been found sufficient for ambulatory surgery (17,18). A direct comparison of our results to those of Lindh et al. (16) is also hampered by the fact that their patients were older and underwent inguinal herniorrhaphy. Our patients, undergoing knee arthroscopy, are regarded as patients at risk for TNSs (13).
We cannot explain why patients in the immediate-ambulation group had a less frequent incidence of TNSs than the patients in the six-hour ambulation group. To confirm this, more patients in the groups and, perhaps, other types of patient population would be required in future studies. In the literature, the effect of ambulation on the incidence of TNSs varies. The epidemiological study by Freedman et al. (13) found ambulatory status a risk factor for TNSs in contrast to 2 randomized studies, i.e., one by Lindh et al. (16) and the present one. In an epidemiological study, the variables are not as well controlled as in prospective randomized studies, and some confounding factors can explain the difference. The origin of TNSs remains unclear. Possible causes include local anesthetic toxicity, neural trauma, neural ischemia, patient positioning, pooling of the local anesthetic, muscle spasm, myofascial trigger points, or irritation of the dorsal root ganglion (2). Of these, early ambulation might exacerbate at least muscle spasm, myofascial pain, or dorsal root ganglion irritation.
An additional factor that may contribute to the development of TNSs is the type of surgery. Lithotomy position during the surgery or knee arthroscopy has been found to increase the risk of TNSs in several studies (3,5,7). The position and maneuvers of the knee in arthroscopic surgery may cause musculoskeletal strain and sciatic stretching. In our study, 5 different orthopedic surgeons operated on the patients. However, all patients had the same holder for the knee; otherwise, their position on the operating table was standardized. Trauma caused by the spinal needle may cause low back pain at the puncture level, which should be distinguishable from the TNSs, as defined above. There was no relationship between needle direction or the degree of difficulty of the subarachnoid puncture and the occurrence of TNSs.
In conclusion, early ambulation was not found to be a risk factor for TNSs after spinal anesthesia for knee arthroscopy with 50 mg of 2% lidocaine. Despite using 2% lidocaine for spinal anesthesia, the incidence of TNSs was disturbingly frequent. Therefore, the role of lidocaine in the mechanism of TNSs after spinal anesthesia remains to be solved.
1. Eberhart LH, Morin AM, Kranke P, et al. Transiente neurologische symptome nach spinalanästhesie: eine quantitative systematische übersichte (Metaanalyse) randomisierter kontrollierter studien (Abstract in English). Anaesthesist 2002; 51: 539–46.
2. Pollock JE. Transient neurologic symptoms: etiology, risk factors, and management. Reg Anesth 2002; 27; 581–6.
3. Hampl KF, Schneider MC. Hyperosmolarity does not contribute to transient radicular irritation after spinal anesthesia with hyperbaric 5% lidocaine. Reg Anesth 1995; 20: 363–8.
4. Tarkkila P, Huhtala J, Tuominen M. Transient radicular irritation after spinal anaesthesia with hyperbaric 5% lidocaine. Br J Anaesth 1995; 74: 328–9.
5. Pollock JE, Neal JM, Stephenson CA, Wiley CE. Prospective study of the incidence of transient radicular irritation in patients undergoing spinal anesthesia. Anesthesiology 1996; 84: 1361–7.
6. Hiller A, Karjalainen K, Balk M, Rosenberg PH. Transient neurological symptoms after spinal anaesthesia with hyperbaric 5% lidocaine or general anaesthesia. Br J Anaesth 1999; 82: 575–9.
7. Hampl KF, Schneider MC, 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.
8. 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.
9. Alley EA, Pollock JE. Transient neurologic syndrome in a patient receiving hypobaric lidocaine in the prone jack-knife position. Anesth Analg 2002; 95: 757–9.
10. Tong D, Wong J, Chung F, et al. Prospective study on incidence and functional impact of transient neurologic symptoms associated with 1% versus 5% hyperbaric lidocaine in short urologic procedures. Anesthesiology 2003; 98: 485–94.
11. Lambert LA, Lambert DH, Strichartz GR. Irreversible conduction block in isolated nerve by high concentrations of local anesthetics. Anesthesiology 1994; 80: 1082–93.
12. Beardsley D, Holman S, Gantt R, et al. Transient neurologic deficit after spinal anesthesia: local anesthetic maldistribution with pencil point needles? Anesth Analg 1995; 81: 314–20.
13. Freedman JM, Li D-K, Drasner K, et al. Transient neurologic symptoms after spinal anesthesia: an epidemiologic study of 1,863 patients. Anesthesiology 1998; 89: 633–41.
14. Hodgson PS, Liu SS, Batra MS, et al. Procaine compared with lidocaine for incidence of transient neurologic symptoms. Reg Anesth Pain Med 2000; 25: 218–22.
15. Liguori GA, Zayas VM, Chrisholm MF. Transient neurologic symptoms after spinal anesthesia with mepivacaine and lidocaine. Anesthesiology 1998; 23: 511–5.
16. Lindh A, Andersson A-S, Westman L. Is transient lumbar pain after spinal anaesthesia with lidocaine influenced by early mobilisation? Acta Anaesthesiol Scand 2001; 45: 290–3.
17. Ben-David B, DeMeo PJ, Lucyk C, Solosko D. Minidose lidocaine-fentanyl spinal anesthesia in ambulatory surgery: prophylactic nalbuphine versus nalbuphine plus droperidol. Anesth Analg 2002; 95: 1596–600.
18. Lennox PH, Vaghadia H, Henderson C, et al. Small-dose selective spinal anesthesia for short-duration outpatient laparoscopy: recovery characteristics compared with desflurane anesthesia. Anesth Analg 2002; 94: 346–50.