The syndrome known as transient neurologic symptoms (TNS) often occurs after spinal anesthesia administration with lidocaine, but relatively infrequently with bupivacaine or tetracaine (1). TNS has not been described after epidural analgesia with bupivacaine, but the following two case reports indicate that such an occurrence is possible.
Patient 1, a 22-yr-old, gravida 3, para 2, Hispanic parturient who was in active labor when she requested epidural analgesia gave a history of two uncomplicated pregnancies followed by uneventful labor and delivery without the need for epidural anesthesia. She had no history of back or lower extremity pain. When seen by the anesthesiologist, the patient had been in active labor for 4 h, and her cervix was dilated 4 cm. After the usual preparation and draping of the back, an 18-gauge Tuohy needle was placed in the L3-4 interspace with the patient in the sitting position. The needle was advanced using the loss of resistance to air technique until the epidural space was identified. An epidural catheter was inserted without difficulty and secured to the skin at 10 cm. No pain, bleeding, or paresthesias occurred during the placement of the needle or insertion of the catheter. After a 3-mL test dose of 1.5% lidocaine with epinephrine 1:200,000, which was negative for intrathecal or intravascular injection, 5 mL of 0.25% bupivacaine was injected, resulting in a T10 level of analgesia. After 2.5 h, complete cervical dilation occurred, and during the 20 min of the second stage of labor, the patient proceeded to deliver a 3750-g infant by normal spontaneous delivery without the use of forceps. One hour after the delivery, when the patient had completely recovered from the anesthetic, the epidural catheter was removed intact.
Twenty-five hours after the delivery, the patient complained of pain in her lower back, buttocks and legs. The pain was described as burning, was bilateral, and extended from her lower buttocks to the posterior and lateral aspects of the thighs and inferiorly to below the calves. Palpation of the areas exacerbated the pain, as did walking, and she could lie only on her side to avoid extreme discomfort. She did not complain of bowel or bladder dysfunction. On examination, there was hyperalgesia of the skin over the affected areas, all of which were equally sensitive. No motor or reflex abnormalities were noted, nor did the pain follow any peripheral nerve or vascular distribution. She was treated only with acetaminophen with codeine, and her symptoms were completely resolved over the next 24 h.
Patient 2, a 37-yr-old, gravida 3, para 1, Asian female, was at gestational term and in active labor when she requested management of her labor pain. Other than one previous uncomplicated pregnancy and one miscarriage, her medical history was unremarkable. She had no history of lower back or extremity pain, nor had she received epidural analgesia during her previous delivery. The only medication she took during her pregnancy was a vitamin preparation. After the IV administration of 500 mL of crystalloid solution, the patient was placed in the sitting position, and after the usual preparation and draping of the skin, an 18-gauge Tuohy needle was inserted in the L3-4 interspace and advanced 6.5 cm, at which point the epidural space was identified on the first attempt by using a loss of resistance to air technique. An epidural catheter was placed without difficulty, and taped at 10 cm at the skin. No pain, bleeding or paresthesias were elicited at any time. After a 3-mL test dose of 1.5% lidocaine with 1:200,000 epinephrine injected through the catheter resulted in no signs of intrathecal or intravascular injection, two 5-mL boluses and a 3-mL bolus of 0.25% bupivacaine were given sequentially over 20 min, resulting in a T10 level of analgesia. An epidural infusion of 0.125% bupivacaine was then administered at 5 mL/h for 4 h and 40 min, when the second stage of labor commenced. The second stage of labor lasted 17 min, after which the patient delivered a 3239-g infant by normal spontaneous delivery without the use of forceps. The patient first complained of low back pain approximately 1 h after the delivery, stating that the pain radiated bilaterally to the lower buttocks, posteriorly as far as the lower gluteal fold. She described the pain as “a deep ache of a burning nature” with a visual analog score of 7 of 10. She also complained of dysesthesia in the affected area, but no motor or reflex abnormalities. Again, the patient was treated only with acetaminophen with codeine, and her symptoms also disappeared the next day.
Local anesthetics were first implicated as potentially neurotoxic drugs in 1991, when Rigler et al. (2) reported four cases of cauda equina syndrome after continuous spinal anesthesia using microbore spinal catheters. Similar cases of cauda equina syndrome were subsequently reported; in May of 1992, the Food and Drug Administration issued a safety alert (3) warning practitioners about the association of cauda equina syndrome with continuous spinal anesthesia. At the time, the concept that clinically used concentrations of local anesthetics might be neurotoxic, especially lidocaine, with its long history of safety, was new to most anesthesiologists, although several earlier animal studies had indicated such a possibility (4–7). Then, only a year after the Food and Drug Administration warning, Schneider et al. (8) reported a new syndrome of possible transient neurologic toxicity, a syndrome currently referred to as TNS. It was postulated by the authors that the stretching of the cauda equina by the lithotomy position stretched some of the nerve fibers within the cauda equina, rendering them vulnerable to toxic potential of a 5% solution of lidocaine.
Although most anesthesiologists considered this to represent a new syndrome, it may in fact have been described earlier but not recognized as such. For example, almost a decade earlier Flaatten and Raeder (9) reported that 15 of 51 patients (29%) who received spinal anesthesia for vasectomy described an unusual form of back pain that radiated to the lower extremities and lasted 3–10 days.
Subsequent to the report by Schneider et al. (8), there have been many reports of TNS after spinal anesthesia, but in 1996, Wong et al. (10) reported the first case of TNS after epidural anesthesia. In that case, although the patient’s epidural anesthetic administration was for a very short (30 minutes) laparoscopic procedure with the patient in the lithotomy position, after a test dose of 3-mL of 1.5% lidocaine with epinephrine 1:100,000, the patient received a total of 600 mg of 2% lidocaine (over a period of 20 minutes), to provide a level of T7. Resolution of the sensory and motor block was complete within 2 hours after surgery, but 12 hours postoperatively, the patient developed TNS that persisted three days. Although it occurred after an epidural anesthetic, in view of the large-dose of local anesthetic injected (645 mg) and the large concentration used, the transdural transfer of lidocaine would have resulted in a fairly large concentration of the anesthetic, probably sufficient to cause TNS by a mechanism similar to that produced by 0.5% lidocaine injected intrathecally, especially when administered for surgery performed on patients in the lithotomy position (11).
In the two patients we presented, it could be argued that the symptoms were simply caused by the trauma of the delivery. However, this is unlikely, because neither patient experienced a prolonged first or second stage of labor, and neither had symptoms of nerve compression, which typically results in both motor and sensory deficits. These two patients had symptoms which were entirely sensory in nature. It is also unlikely that the TNS was caused by the inadvertent intrathecal injection of local anesthetic, because neither patient experienced hypotension or even a significant motor block at any time. However, both patients were delivered of the infants in the lithotomy position, a factor associated with an increased risk of TNS in patients receiving intrathecal lidocaine (1).
The cases we present here differ significantly from the previously reported case in that lidocaine was not the primary local anesthetic used. Instead, both patients received bupivacaine as their primary local anesthetic, with each patient receiving a total bupivacaine dose of 12.5 mg in the case of Patient 1 and 62 mg in the case of Patient 2. The only lidocaine (45 mg) both patients received was with the epidural test dose from which they developed no significant motor block or hypotension, making the possibility of an intrathecal injection extremely unlikely.
Whether the TNS after epidural analgesia in our two patients were caused by the lidocaine solution used in the test dose or by the low doses of bupivacaine, is unclear. However, several factors in combination could make these symptoms possible:
- 1. Local anesthetics injected in the epidural space are known to diffuse into the subarachnoid space, resulting in cerebrospinal fluid concentrations that are, however, lower than those after intrathecal injection (12).
- 2. In the majority of epidural analgesic or anesthetic procedures performed in obstetric patients, the injection of local anesthetic is performed at the level of the cauda equina.
- 3. The nerves in the cauda equina are devoid of the connective tissue sheaths that protect peripheral nerves, increasing the exposure of the nerve fibers to local anesthetics.
- 4. Furthermore, the nerves of the pregnant patient are known to be more sensitive to the toxic effects of the local anesthetics than the nerves of the nonpregnant patient (13).
- 5. As stated previously, dilute concentrations of local anesthetics administered intrathecally are also associated with a high incidence of TNS (11).
- 6. And, finally, as stated in 1 above, because it is well established that much of the local anesthetics injected into the epidural space undergoes transmeningeal transfer into the cerebrospinal fluid (12), mostly via the arachnoid villi in the dural cuff region (14,15), but also across the meninges proper (16), it stands to reason that repeated injections will result in elevated intrathecal concentrations of local anesthetics in the spinal fluid.
All of these factors, combined with the fact that most deliveries are performed with the parturient in the lithotomy position, could result in TNS after epidural injections of local anesthetics for delivery, especially if a catheter technique, which allows for repeat injections, is used.
1. Freedman JM, De-Kun L, Drasner K, et al. Transient neurologic symptoms after spinal anesthesia. Anesthesiology 1998; 89:633–41.
2. Rigler ML, Drasner K, Krejcie TC, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 1991; 72:275–81.
3. FDA Safety Alert. Cauda equina syndrome associated with the use of small-bore catheters in continuous spinal anesthesia. Washington DC: Food and Drug Administration, 1992.
4. Adams HJ, Mastri AR, Eicholzer, Kilpatrick G. Morphologic effects of intrathecal etidocaine and tetracaine on the rabbit spinal cord. Anesth Analg 1974; 53:904–8.
5. Kalichman MW, Powell HC, Myers RR. Quantitative histologic analysis of local anesthetic-induced injury to rat sciatic nerve. J Pharmacol Exp Ther 1989; 250:406–13.
6. Ready LB, Plumer MH, Haschke RH, et al. Neurotoxicity of intrathecal local anesthetics in rabbits. Anesthesiology 1985; 63:364–70.
7. Nicholson MJ, Eversole UH. Neurologic complications of spinal anesthesia. JAMA 1946; 132:679–85.
8. Schneider M, Ettlin T, Kaufmann M, et al. Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine. Anesth Analg 1993; 76:1154–7.
9. Flaatten H, Raeder J. Spinal anaesthesia for outpatient surgery. Anaesthesia 1985; 40:1108–11.
10. Wong CA, Benzon H, Kim C. Bilateral radicular pain after epidural lidocaine. Reg Anesth 1996; 21:600–1.
11. 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.
12. Frumin MJ, Schwartz H, Burns JJ, et al. Sites of sensory blockade during segmental spinal and segmental peridural anesthesia in man. Anesthesiology 1953; 14:576–83.
13. Datta S, Lambert DH, Covino BG. Differential sensitivities of mammalian nerve fibers during pregnancy. Anesth Analg 1983; 62:1070–2.
14. Shantha TR, Evans JA. The relationship of epidural anesthesia to neural membranes and arachnoid villi. Anesthesiology 1972; 37:543–57.
15. Shantha TR. Spinal nerve root is one of the preferred routes for transfer of drugs to the nerve roots and spinal cord from the epidural space. Anesthesiology 1992; 77:750–6.
16. Bernard CM, Hill HF. The spinal nerve root sleeve is not a preferred route for redistribution of drugs from the epidural space to the spinal cord. Anesthesiology 1991; 75:827–32.