1Department of Anesthesiology, Shimane Medical University, Izumo City 693-8501, Japan. 2Department of Anesthesia, Miyoshi General Hospital, Miyoshi City, Japan*Corresponding author
Accepted for publication: August 3, 2001
![]() |
Abstract |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
Br J Anaesth 2002; 88: 1413
Keywords: anaesthetic techniques, combined subarachnoid and epidural; complications, neurological; anaesthetics local, amethocaine; anaesthetics local, hyperbaric; anaesthetics local, mepivacaine
![]() |
Introduction |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
Since Schneider and colleagues1 reported four patients in whom pain in the buttocks or lower extremities developed following recovery from spinal anaesthesia, it has been realized that such symptoms after uncomplicated spinal anaesthesia are not as rare as thought previously. However, the symptoms usually disappear within a week or two, and have been termed transient neurological symptoms (TNS). In addition, despite its name, pain is seldom accompanied by neurological deficits. In contrast, prolonged or persistent neurological symptoms, including cauda equina syndrome, have been associated with continuous spinal anaesthesia2 or intended epidural anaesthesia,3 and rarely with uneventful single shot spinal anaesthesia4 or combined spinal and epidural anaesthesia.5 Recently, we became aware of a patient who developed pain and persistent hypoaesthesia in the buttocks and legs after two consecutive Caesarean sections under uneventful combined spinal and epidural anaesthesia.
![]() |
Case report |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
Since an upper dermatomal level of block for pinprick discrimination 20 min after the injection was T-10 bilaterally, 10 ml of 1.5% mepivacaine was administered through the epidural catheter to obtain a more cephalad sensory level. The surgical procedure was uneventful and lasted 45 min. An additional 10 ml of 1.5% mepivacaine was administered immediately before the completion of surgery. The anaesthetic level was maintained at T-6 bilaterally and haemodynamic values remained stable throughout the intraoperative period. The epidural catheter was removed in the operating room and the immediate postoperative course was uneventful. Two days after surgery, the patient reported a sacral area of numbness and a moderate burning pain in the buttocks radiating to the dorsolateral sides of both thighs. There were no signs of bladder or bowel dysfunction. A diclofenac sodium suppository was administered to relieve pain. Although the painful sensation resolved within a week, the numbness continued for 5 months.
At age 31 yr, she was again admitted at term for her second Caesarean section because of the previous surgery. Preoperative neurological examination revealed no sensory-motor or muscle-tendon reflex abnormalities. Combined spinal and epidural anaesthesia was again performed using the same method. Intrathecally, 2 ml of 0.5% amethocaine in 10% glucose was injected over approximately 20 s, and a sensory block to pinprick was obtained at T-8 bilaterally. No paresthesias were elicited during the whole procedure. Since she complained of some pain immediately after the start of surgery, 9 ml of 2% mepivacaine was administered through the epidural catheter to obtain an upper sensory level of T-5 bilaterally. No clear fluid was aspirated from the epidural catheter before the injection. The surgical procedure was uneventful and lasted 30 min. An additional 10 ml of 1.5% mepivacaine was administered epidurally, immediately before the completion of surgery, and the continuous epidural infusion of 0.001% fentanyl and 0.2% bupivacaine was started thereafter at a rate of 2 ml h1 for 48 h postoperatively. Haemodynamic values remained stable throughout the intraoperative period.
Although the immediate postoperative course was uneventful, she again complained of numbness in the buttocks 12 h after surgery, when neurological examination revealed no motor disturbance but hypoaesthesia in the S3 dermatomal area. Next day, a tingling pain developed in the buttocks radiating to the dorsal area of the left thigh which became more intense after continuous epidural infusion was stopped. A diclofenac sodium suppository was administered to relieve pain, which lasted 11 days. The patient denied difficulty in voiding or defaecating. The numbness slowly decreased and disappeared 6 months later.
![]() |
Discussion |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
The characteristics of the pain on both occasions were remarkably similar to those of previous cases of TNS after the administration of a single injection of lidocaine,1 mepivacaine,6 amethocaine,7 and bupivacaine.8 One common feature of all these cases and the findings of prospective studies9 10 were moderate-to-severe pain in the buttock, lower back, and/or legs that appeared 124 h postoperatively after complete recovery from uneventful spinal anaesthesia. The pain was often characterized as dull, aching, cramping, sharp, or radiating. In most cases, the symptoms resolved fully within 1 or 2 weeks and neurological examination was normal.
Persistent neurological symptoms were initially reported after continuous spinal anaesthesia2 or intended epidural anaesthesia.3 Maldistribution, repeated injection, and relatively large doses of local anaesthetics have been implicated. However, Beardsley and colleagues11 recently described them after uncomplicated spinal anaesthesia. As part of their clinical investigation concerning epidural and spinal anaesthesia, one volunteer developed a minor sensory deficit lasting for 3 months in the sacral area after a slow injection of 2 ml of 5% lidocaine. Subsequently, Gerancher4 reported cauda equina syndrome, which involved bladder and/or bowel dysfunction, after an uneventful lidocaine spinal. Additionally, Auroy and colleagues12 performed a prospective multicentre study, in which two out of 40640 cases incurred permanent sensory deficits. These reports have suggested that even a recommended dose of local anaesthetic can cause neurological injury. Despite no direct evidence, many anaesthetists have proposed that persistent or permanent neurological symptoms are likely to result from a direct toxic effect of local anaesthetics.
In contrast, the aetiology of TNS has been controversial, since neurological deficits have rarely been associated with pain. For example, Freedman and colleagues9 demonstrated in their recent epidemiological study that 118 out of 1864 patients who had spinal anaesthesia developed TNS and, out of 118, only four patients reported neurological symptoms such as lower extremity weakness, numbness, and/or paraesthesia lasting less than 1 month. We10 previously showed in our prospective study that only one out of 11 patients who developed TNS after amethocaine spinal anaesthesia had numbness, which lasted for only 3 days.
Although our patient did not incur bladder or bowel dysfunction, the duration of numbness in the sacral area (>5 months) makes the symptoms worthy of note. The similarity in location between pain and hypoaesthesia in our patient suggests that both TNS and neurological injury may share a common mechanism and that TNS may be related to a direct neurotoxic effect of local anaesthetic solutions.
Although the similarity in symptoms on the two occasions suggests that the repeated events may have resulted from the same mechanism, it is not clear which procedure was responsible for the symptoms; spinal anaesthesia, epidural anaesthesia, and/or postoperative epidural analgesia. It has been demonstrated that TNS can follow amethocaine spinal anaesthesia although the incidence is lower compared with lidocaine.10 In addition, Freedman and colleagues9 demonstrated in their clinical study that one patient developed TNS accompanied by numbness in the lower extremity after spinal amethocaine. Epidural anaesthesia alone has been associated with TNS,13 but not persistent neurological symptoms, as long as the catheter is inside the epidural space. In our patient, although the proper positioning of the epidural catheter was not confirmed on both occasions, the catheter was probably kept in the epidural space because there was no aspiration of cerebrospinal fluid and there was a complete and rapid motor recovery after surgery. Another possible explanation involves diffusion of the local anaesthetic from the epidural into the intrathecal space through the dural hole made by the 25-gauge spinal needle. Since a top-up with mepivacaine had to be given twice and once on the first and second occasions, respectively, the cauda equina incurred a relatively large exposure to mepivacaine. Finally, it is possible that postoperative epidural analgesia was responsible for the symptoms. However, the postoperative pain management described has been used in our institution without causing similar neurological symptoms or muscle weakness.14 Moreover, many other researchers 1518 have recommended using similar dosage of bupivacaine.
![]() |
Acknowledgement |
---|
![]() |
References |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
2 Rigler ML, Drasner K, Krejcie TC, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 1991; 72: 27581
3 Drasner K, Rigler ML, Sessler DI, Stoller ML. Cauda equina syndrome following intended epidural anesthesia. Anesthesiology 1992; 77: 5825
4 Gerancher JC. Cauda equina syndrome following a single spinal administration of 5% hyperbaric lidocaine through a 25-gauge Whitacre Needle. Anesthesiology 1997; 87: 6879
5 Kubina P, Gupta A, Oscarsson A, Axelsson K, Bengtsson M. Two cases of cauda equina syndrome following spinal-epidural anesthesia. Reg Anesth 1997; 22: 44750
6 Lynch J, zur Nieden M, Kasper S-M, Radbruch L. Transient radicular irritation after spinal anesthesia with hyperbaric 4% mepivacaine. Anesth Analg 1997; 85: 8723
7 Sumi M, Sakura S, Kosaka Y. Intrathecal hyperbaric 0.5% tetracaine as a possible cause of transient neurologic toxicity. Anesth Analg 1996; 82: 10767
8 Casati A, Fanelli G, Aldegheri G, Berti M, Leoni A, Torri G. A transient neurological deficit following intrathecal injection of 1% hyperbaric bupivacaine for unilateral spinal anaesthesia. Eur J Anaesthesiol 1998; 15: 1123
9 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: 63341
10 Sakura S, Sumi M, Sakaguchi Y, Saito Y, Kosaka Y, Drasner K. The addition of phenylephrine contributes to the development of transient neurologic symptoms after spinal anesthesia with 0.5% tetracaine. Anesthesiology 1997; 87: 7718
11 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: 31420
12 Auroy Y, Narchi P, Messiah A, Litt L, Rouvier B, Samii K. Serious complications related to regional anesthesia: results of a prospective survey in France. Anesthesiology 1997; 87: 47986
13 Markey JR, Naseer OR, Bird DJ, Rabito SF, Winnie AP. Transient neurologic symptoms after epidural analgesia. Anesth Analg 2000; 90: 4379
14 Sakaguchi Y, Sakura S, Shinzawa M, Saito Y. Does adrenaline improve epidural bupivacaine and fentanyl analgesia after abdominal surgery? Anaesth Intens Care 2000; 28: 5226
15 Hobbs GJ, Roberts FL. Epidural infusion of bupivacaine and diamorphine for postoperative analgesia: use on general surgical wards. Anaesthesia 1992; 47: 5862
16 Leith S, Wheatley RG, Jackson IJB, Madej TH, Hunter D. Extradural infusion analgesia for postoperative pain relief. Br J Anaesth 1994; 73: 5528
17 Niemi G, Breivik H. Adrenaline markedly improves thoracic epidural analgesia produced by a low-dose infusion of bupivacaine, fentanyl and adrenaline after major surgery: a randomised, double-blind, cross-over study with and without adrenaline. Acta Anaesthesiol Scand 1998; 42: 897909
18 Andersen G, Rasmussen H, Rosenstock C, et al. Postoperative pain control by epidural analgesia after transabdominal surgery: efficacy and problems encountered in daily routine. Acta Anaesthesiol Scand 2000; 44: 296301