Transient neurological symptoms after spinal anaesthesia with hyperbaric 5% lidocaine or general anaesthesia

British Journal of Anaesthesia 82 (4): 575–9 (1999)

Transient neurological symptoms after spinal anaesthesia with hyperbaric 5% lidocaine or general anaesthesia† A. Hiller1*, K. Karjalainen2, M. Balk3 and P. H. Rosenberg4 1Department

of Anaesthesia, Helsinki University Central Hospital, Otolaryngological Hospital, Haartmaninkatu 4E, FIN-00290 Helsinki, Finland. 2Department of Anaesthesia, Kuusankoski District Hospital, FIN-45750 Sairaalama¨ki, Finland. 3Department of Anaesthesia, Pa¨ija¨t-Ha¨me Central Hospital, Keskussairaalankatu 7, FIN-15850 Lahti, Finland. 4Department of Anaesthesiology, Helsinki University Central Hospital, FIN-00290 Helsinki, Finland *To whom correspondence should be addressed Transient neurotoxicity of concentrated local anaesthetics has been thought to be the main reason for transient neurological symptoms after spinal anaesthesia. Profound musculoligamental relaxation by high doses of local anaesthetics may contribute to the development of postoperative musculoskeletal pain. In order to evaluate the role of the loss of strength of the supportive structures of the spine in the development of transient neurological symptoms, 60 patients (ASA I–II) undergoing minor orthopaedic, varicose vein or inguinal hernia operations were allocated randomly to receive spinal anaesthesia with hyperbaric lidocaine 50 mg ml–1 (85–100 mg) or balanced general anaesthesia with neuromuscular block. Patients were interviewed 24 h later and after 1 week they returned a written questionnaire. Transient neurological symptoms, consisting of pain in the buttocks or pain radiating symmetrically to the lower extremities, occurred in eight patients (27%) receiving spinal anaesthesia and in one patient (3%) receiving general anaesthesia (P,0.05). We conclude that a transient neurotoxic effect of hyperbaric lidocaine 50 mg ml–1 is probably the main reason for transient neurological symptoms after spinal anaesthesia but musculoligamental relaxation may contribute to the development of low back or leg pain after both anaesthetic techniques. Br J Anaesth 1999; 82: 575–9 Keywords: anaesthetic techniques, subarachnoid; anaesthetics local, lidocaine; complications, neurological Accepted for publication: November 12, 1998

Transient neurological symptoms, defined as symmetrical bilateral pain in the back or buttocks or pain radiating to the lower extremities after recovery from anaesthesia, have been reported after spinal anaesthesia with all local anaesthetics, but most commonly after hyperbaric lidocaine 50 mg ml–1,1–6 plain7 or hyperbaric lidocaine 20 mg ml–1 8 9 and hyperbaric mepivacaine 40 mg ml–1.6 10 11 To some extent, the mechanisms of action of spinal anaesthesiaassociated transient neurological symptoms can be explained by a neurotoxic action of high concentrations of local anaesthetics.12 13 The similarity of the radiating back and leg symptoms to those caused by positional deformities or diseases of the spine has raised speculations regarding the possible contribution of musculoskeletal (stretching/ relaxation) mechanisms for transient neurological symptoms after spinal anaesthesia. Typically, transient neurological symptoms have been seen rarely after spinal blocks with bupivacaine 5 mg ml–1,3 4 6 10 which produces a weaker motor block compared with the above-mentioned concentrated solutions.6 10

In order to elucidate further the role of the loss of strength of the supportive structures of the spine and local anaesthetic neurotoxicity in the development of radiating back and leg pain after anaesthesia and surgery, we have compared spinal anaesthesia (hyperbaric lidocaine 50 mg ml–1) with general anaesthesia in patients undergoing similar types of surgery. Hyperbaric lidocaine 50 mg ml–1 (glucose 7.5 mg ml–1) was chosen because, in spite of reports of the occurrence of transient neurological symptoms after its use,1 4 it has a remarkable safety record in routine use in our country for more than 40 yr.

Patients and methods We studied 60 ASA I or II patients undergoing minor orthopaedic, varicose vein, urological or inguinal hernia operations in the supine position in a randomized, open †Presented in part to Esra XVII Annual Congress, Geneva, September 1998

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Table 1 Patient characteristics (median (range) or number)

n Sex (M/F) Age (yr) Height (cm) Weight (kg) Duration of operation (min)

Spinal anaesthesia

General anaesthesia

30 14/16 47 (23–61) 171 (156–187) 72 (53–98) 43 (13–104)

30 14/16 43 (21–60) 169 (153–186) 75 (48–96) 43 (5–90)

study (Table 1). Patients with a history of acute or chronic back pain, pre-existing neurological disease or diabetes mellitus were excluded. The study was approved by the Hospital Ethics Committee and written informed consent was obtained from patients. The number of patients enrolled was determined by power analysis, anticipating transient neurological symptoms in 30% of patients in our hospitals after spinal anaesthesia with both hyperbaric lidocaine 50 mg ml–1,5 6 and mepivacaine 40 mg ml–1, 6 10 and 0% transient neurological symptoms after general anaesthesia with 95% confidence limits. On the day before operation, patients were allocated randomly by sealed envelope to receive either spinal anaesthesia with lidocaine 50 mg ml–1 or general anaesthesia. All patients received midazolam 7.5 mg orally, approximately 1 h before operation, or midazolam 1–2 mg i.v. immediately before induction of anaesthesia. A peripheral i.v. infusion with acetated Ringer’s solution was started before surgery in both groups. All patients were monitored with electrocardiography, automated arterial pressure and pulse oximetry. End-tidal carbon dioxide was monitored in patients receiving general anaesthesia. For spinal anaesthesia, patients received hyperbaric lidocaine 50 mg ml–1 (Lidocain pond 50 mg ml–1, Orion, Espoo, Finland). The dose of lidocaine was 100 mg for inguinal hernia operations and 85–100 mg for other operations. The skin was disinfected with a 0.5% solution of chlorohexidine (Klorhexol, Unimedic ab, Sweden). After drying, the skin at the puncture site was re-scrubbed with a saline-soaked swab. Spinal anaesthesia was performed at the L3–4 or L2–3 interspace with the patient in the lateral position using a 27- or 25-gauge Quincke-type needle. Free flow of cerebrospinal fluid was verified before and after injection of local anaesthetic. Immediately after intrathecal injection, the patient was turned to the supine position with the operating table in a slight head-up tilt position. During spinal anaesthesia, hypotension (systolic arterial pressure ,90 mm Hg or .30% decrease from baseline) was treated with 200-µg increments of phenylephrine. Bradycardia (heart rate ,50 beat min–1) was treated with atropine 0.5 mg. Testing of sensory block (cold swab) and motor block was performed at 3, 5, 10, 15 and 60 min and thereafter at 30-min intervals. A modified Bromage scale was used for testing motor block: 05no paralysis (full flexion of the knees and feet), 15inability to flex the extended leg (just able to move the knees), 25inability to flex the knee (able to move the feet only), 35inability to

flex the ankle joint (unable to move the feet or knees). Patients were discharged from the recovery room when recovery of motor block was complete (score50). Nurses on the ward recorded the time when patients reported they had normal sensation in the buttocks and feet and the first time to void. For general anaesthesia a standardized technique was used comprising glycopyrrolate 0.2 mg i.v., thiopental 4–6 mg kg–1, fentanyl 0.1 mg for induction and isoflurane and 70% nitrous oxide in oxygen for maintenance of anaesthesia. The trachea was intubated after administration of rocuronium 0.5 mg kg–1 and neuromuscular block maintained (using a peripheral nerve stimulator) with rocuronium 0.15 mg kg–1 as needed. Fentanyl 0.05–0.1 mg was given before skin incision and during anaesthesia to maintain arterial pressure and heart rate within 30% of pre-anaesthetic measurements. At the end of anaesthesia neuromuscular block was antagonized with neostigmine 2.5 mg preceded by glycopyrrolate 0.5 mg. Before the end of surgery all patients, after both anaesthesia techniques, received ketoprofen 100 mg i.v. All inpatients were interviewed on the first postoperative morning by an anaesthetist unaware of the anaesthetic technique used. They were asked if they had experienced any of the symptoms on the following standardized symptom checklist: headache, backache, pain not associated with surgery, sensory disturbances, change in muscle strength, or difficulties in voiding or hearing. Special attention was paid to lower extremity symptoms, type of pain and radiation of pain. Patients were requested to return a mailed questionnaire 1 week after anaesthesia. They were asked to mention symptoms which they particularly associated with anaesthesia. Enquiries concerning symptoms and their duration included headache, backache, pain in the operation area and pain in the thighs, buttocks, calves or elsewhere. Patients were also asked to assess the degree of satisfaction with their type of anaesthesia.

Statistical analyses Results are expressed as median (range). Categorical variables were analysed using Fisher’s exact test and continuous variables with the Student’s t test. P,0.05 was considered significant. All data were analysed using the Systat System.

Results Patient characteristics are summarized in Table 1. All patients were expected to be inpatients but five patients (three who received spinal anaesthesia and two who received general anaesthesia) wanted to be discharged from hospital on the same evening. Details of the spinal anaesthesia procedure are presented in Table 2. The mean dose of lidocaine was 97 (range 85–100) mg. Motor block was complete (inability to move legs) in all patients who received spinal anaesthesia. Mean time to void after spinal

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Transient neurological symptoms after anaesthesia

Table 2 Details of the spinal anaesthetic procedures (median (range) or number)

n Sex (M/F) Age (yr) Height (cm) Time to total recovery of motor block (min) Surgery Orthopaedic Varicose veins Hernia Needle size 25-gauge 27-gauge Attempt at dural puncture 1 2–3 .3 Paraesthesia during dural puncture Median maximum height of block (range)

All patients

Patients with transient neurological symptoms

30 14/16 47 (23–61) 171 (156–187) 111 (60–150)

8 3/5 49 (35–60) 169 (156–183) 112 (60–120)

7 12 11

0 3 5

11 19

3 5

27 1 2

7 0 1

2

1

T4 (T3–T12)

T4–5 (T4–T12)

Table 3 Incidence of transient neurological symptoms (TNS) after spinal anaesthesia with 5% lidocaine or general anaesthesia. *P , 0.05

n TNS All patients Non-TNS back pain All patients

Spinal anaesthesia

General anaesthesia

30

30

8 (27%)* 10 (30%)

1 (3%) 6 (20%)

anaesthesia was 331 (176–585) min and after general anaesthesia 576 (120–1260 ) min (P50.001). All patients except one in the spinal anaesthesia group returned the questionnaire. One patient in both groups was not satisfied with the anaesthetic. Transient neurological symptoms occurred in eight patients (27%) who received spinal anaesthesia with hyperbaric lidocaine 50 mg ml–1 and in one patient (3%) who received general anaesthesia (P50.026) (Tables 3, 4). The patient who experienced transient neurological symptoms after general anaesthesia was a 21-yr old man (ASA class I) undergoing surgery for inguinal hernia repair. Peripherally radiating pain started 72 h after anaesthesia and lasted for 3 days. The pain was moderate and he took NSAID to relieve the pain in his legs. No patient had sensory disturbances, change in muscle strength or difficulties in voiding on the first postoperative morning. Ten patients (33%) in the spinal anaesthesia group and six patients (20%) in the general anaesthesia group had lower back pain that was not radiating to the buttocks or lower extremities (non-transient neurological back pain). After spinal anaesthesia, lower back pain started in most of cases during the first postoperative night whereas after general anaesthesia pain started soon after recovery from anaesthesia or later that evening. Two patients in the spinal anaesthesia group and one in the general anaesthesia group

Table 4 Nature of pain and analgesic requirements in patients with transient neurological symptoms after spinal anaesthesia with 5% lidocaine (NSAID 5 non-steroidal anti-inflammatory drug). *P , 0.05

n Location of pain Buttocks Buttocks and thighs Buttocks, thighs and legs Legs Severity of pain Severe Moderate Not known Onset of pain after recovery of block 1st postop. day 2nd postop. day 3rd postop. day Duration of pain (h) ,12 48 72–84 Needed analgesia Yes NSAID No

Spinal anaesthesia

General anaesthesia

8*

1

5 2 1 1 2 5 1

1

6 2 0

1

4 3 1

1

6 6 2

1 1

needed NSAID for this type of postoperative low back pain. The latter patient was a 50-yr-old woman who developed back pain 3 h after the end of a varicose vein operation. In four patients, turning to the lateral position or standing up and walking relieved the pain. In spite of these symptoms, all patients with transient neurological symptoms were satisfied with spinal anaesthesia and would like to have spinal anaesthesia for a similar type of surgery in the future. One patient was not satisfied after spinal anaesthesia because of extensive spread of block (T4) during operation. All symptoms reported in the questionnaire were transient and had disappeared within 1 week. Six patients (20%) in the spinal anaesthesia group had transient headache at home, one for 2 days and two for 1 week. In three, the pain had started in hospital. The nature of the headache could not be analysed from the questionnaire. However, none of the patients needed an epidural blood patch. After general anaesthesia, seven patients (23%) suffered headache in hospital and four at home. One patient who received spinal anaesthesia and two who received general anaesthesia reported transient deterioration in hearing after anaesthesia and one patient had aching in the ear after spinal anaesthesia. Two patients reported bad dreams for 2 nights after general anaesthesia. One patient was not satisfied with general anaesthesia because of vomiting and would not want to have general anaesthesia for a similar type of surgery in the future.

Discussion In this study, the incidence of transient neurological symptoms was greater after spinal anaesthesia with hyperbaric lidocaine 50 mg ml–1 (27%) than after general anaesthesia

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(3%). From the description of symptoms by the patient who experienced transient neurological symptoms after general anaesthesia, it was not possible to distinguish this case from spinal anaesthesia-associated transient neurological symptoms. Musculoligamental relaxation could explain the symptoms as the patient was on his back during anaesthesia and surgery, and received a non-depolarizing neuromuscular blocking agent. It may be speculated that the reason why radiating pain symptoms were not reported more in the general anaesthesia group could be because fentanyl and ketoprofen were administered during anaesthesia and that the dose of rocuronium did not cause complete (100%) motor block of the muscles which support the spine. A longer lasting and potent motor block action of the spinal local anaesthetic may weaken the supportive structures of the spine and cause flattening of the lordotic curve. This could give rise to radiating symptoms in the back, buttocks and legs. Comparing lidocaine 50 mg ml–1 or mepivacaine 40 mg ml–1 with bupivacaine 5 mg ml–1, it can be assumed that there is a relationship between potent motor block by the former two agents and the occurrence of transient neurological symptoms.6 10 Non-radiating low back pain, probably as a result of the supine position on the operating table, occurred in 20% of patients in the general anaesthesia group. This seems to be in accordance with earlier observations where postoperative backache has been noted in approximately 20% of patients receiving general, spinal or epidural anaesthesia for surgery.14 Except for one patient, this was easily distinguishable from typical transient neurological symptoms in both groups, because analgesics are usually not required for such post-anaesthetic low back pain. In only one patient in the general anaesthesia group was an NSAID administered for non-transient neurological low back pain which, in addition to active mobilization, relieved the pain. The incidence of transient neurological symptoms after spinal anaesthesia with hyperbaric lidocaine 50 mg ml–1 (27%) was similar to that observed by us after spinal anaesthesia with hyperbaric mepivacaine 40 mg ml–1 10 and similar to that of several other published studies where patients were in the lithotomy position during operation.3 5 6 8 15 Lithotomy position with flexion of the hips and knees,1 5 6 15 and knee arthroscopy,7 16 which also involves repeated passive hip and knee flexion, have been suggested to contribute to the development of transient neurological symptoms after spinal anaesthesia. This observation is not supported by our study as none of those patients who experienced transient neurological symptoms was operated on in the lithotomy position or with the hips flexed. However, the influence of surgical position and movement of the lower extremities cannot be a major determinant as transient neurological symptoms after similar types of surgery under spinal anaesthesia with 0.5% bupivacaine are rare.10 17 Recently, Martinez-Bourio and colleagues reported a 4% incidence of transient neurological symptoms after spinal anaesthesia in patients operated on in the supine

position.18 When comparing our study with these data,18 we note that they used smaller doses of lidocaine (mean 67 mg vs 97 mg), another type of spinal needle (pencilpoint vs cutting) and the majority of their patients were sitting (vs lateral decubitus) during puncture and intrathecal injection. To what extent these differences can explain the low incidence of transient neurological symptoms remains speculative.18 The high incidence of transient neurological symptoms after lidocaine spinal anaesthesia in our patients is surprising, because ketoprofen was administered to all patients during anaesthesia and six of eight patients reported transient neurological symptoms during the first 24 h after block. One explanation for the relatively high incidence of transient neurological symptoms in our study may be the follow-up method used. Patients interviewed on the ward are probably more likely to report minor symptoms than those interviewed by telephone. Interestingly, except for having been operated on in the lithotomy position, those patients receiving spinal anaesthesia with 5% hyperbaric lidocaine and who experienced a higher incidence of transient neurological symptoms were interviewed on the first postoperative morning.3 5 6 8 9 In contrast, patients operated on in the supine position with a lower incidence of transient neurological symptoms were interviewed on the third postoperative day by telephone7 15 18 or after 1 week by letter or telephone.4 The power of the study for evaluation of differences in the occurrence of other expected (registered) side effects after spinal compared with general anaesthesia is not sufficient. Mild headache occurred at a similar frequency in both groups. Interestingly, transient deterioration of hearing, which has been considered a variant or an additional symptom of postural puncture headache,19 20 was also reported spontaneously by two patients in the general anaesthesia group. In summary, in this study, hyperbaric lidocaine 50 mg ml–1 was associated with a significantly greater incidence of transient neurological symptoms compared with general anaesthesia. The transient neurotoxic effect of hyperbaric lidocaine 50 mg ml–1 is probably the main reason for transient neurological symptoms after spinal anaesthesia. Supine position on a relatively hard operating table with concomitant musculoligamental relaxation may be a contributing factor in the origin of transient low back pain (transient neurological symptoms and non-transient neurological symptoms) after anaesthesia and surgery.

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