ANESTH ANALG

817

1991;72:817-9

Case Reports Cauda Equina Syndrome and Continuous Spinal Anesthesia Donald H. Lambert,

PhD, MD,

and Ronald J. Hurley,

Key Words: ANESTHETIC TECHNIQUES, SPINAL. ANESTHETICS, LOCAL-lidocaine, bupivacaine. COMPLICATIONS, NEUROLOGIC4aUda equina syndrome. TOXICITY, NEUROTOXICITY. Recently, Kendall Health Care Products Company issued a precaution concerning continuous spinal anesthesia using the Cospan spinal catheter after receiving reports of neurologic deficits associated with continuous spinal anesthesia characterized by perineal sensory loss and changes in sphincter function. Similarities in these reports include (a) the use of 5% lidocaine in 7.5% dextrose (50 mg/mL); (b) less than the expected anesthetic effect for a given dose; (c) an initial lidocaine dose of 100 mg or more to establish the spinal anesthetic; and (d) a total lidocaine dose exceeding 100 mg. Because of these similarities, the company recommended that (a) the spinal catheter not be threaded more than 2 cm beyond the tip of the needle; (b) the amount of 5% lidocaine in 7.5% dextrose be limited to 100 mg in establishing the initial block; (c) less concentrated local anesthetic be used; and (d) the total dose of drug administered be limited in a manner consistent with the duration of the operation. Normally, 5% lidocaine solution for spinal anesthesia is given by single injection and doses greater than 100 mg are rarely used. However, with a spinal catheter, there is a temptation to inject more 5% lidocaine solution when spinal anesthesia is inadequate. We speculate that spinal anesthesia doses of 5% lidocaine in 7.5% dextrose exceeding 200 mg may cause cauda equina syndrome. A possible mechanism for these neurologic deficits is maldistribution of 5% lidocaine in 7.5% dextrose. In Received from the Departments of Anesthesia, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts. Accepted for publication February 5, 1991. Address correspondence to Dr. Lambert, Department of Anesthesia, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115. 01991 by the International Anesthesia Research Society 0003-2999/91/$3.50

MD

fact, we commented on this problem in our earlier report concerning continuous spinal anesthesia with a microcatheter (1). We suggested that nonuniform distribution of the local anesthetic was due to a slow flow rate as the local anesthetic leaves the catheter tip owing to high resistance to injection when microcatheters are used. We further suggested that when inadequate anesthesia occurs, a solution of different density be used and the patient’s position be altered to ”direct” the local anesthetic to the poorly blocked nerves. In this report, we present pictures produced with a spinal canal model to demonstrate how neural damage might occur with continuous spinal anesthesia. The hypothesis is based on the fact that nerves exposed to large volumes of 5% lidocaine solution may be damaged (2,3). Apparently, all deficits reported to the Kendall Company involve the cauda equina. Nerves in the cauda equina are devoid of protective sheaths as they pass through the distal end of the dural sac, and neural damage may occur when they are exposed to large volumes of hyperbaric 5% lidocaine solutions. This is analogous to the neural toxicity that can occur if large volumes of chloroprocaine containing sodium bisulfite intended for epidural anesthesia are injected into the cerebrospinal fluid (CSF) (4). The spinal canal model we used consists of venous tubing used during open heart operations cut to the length of the dural sac and filled with lactated Ringer’s solution (specific gravity [SG] = 1.005), which has essentially the same SG (1.006) as CSF. (All specific gravities in this study were measured using an American Optical TS Meter at 20°C.) Injections can be made to mimic spinal anesthesia. Local anesthetics are colored with methylene blue dye to aid in visualizing the distribution of the local anesthetic in the model. Figure 1 shows the injection of 1 mL (50 mg) of 5% lidocaine in 7.5% dextrose through a Kendall Cospan 28-gauge catheter inserted at the peak of the lumbar

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ANESTH ANALG 1991;72:817-9

Figure 1 . The distribution of 1 mL (50 mg) of 5% lidocaine in 7.5% dextrose when injected through a 28-gauge catheter into a model of the subarachnoid space. (The model is in the supine horizontal position.) The catheter enters the model as seen in the lower panel (right arrowhead) and extends to the left for 3 cm (the catheter is not visible inside the model). The upper and middle photographs were taken during injection of the lidocaine. The lower photograph, taken immediately after injection, shows the dye clearly pooled at the distal end of the tube (left arrowhead). (See text for further details.)

lordosis and directed caudally a distance of 3 cm. Injection was made with a 1-mL tuberculin Luer lock syringe with the spinal model in the supine horizontal position. The stream of local anesthetic was visible to the observers during the injection but is not detectable in the photographs. However, the stream (localized to the area between the arrowheads shown in the upper panel of Figure 1) flowed distally and rolled along the lower portion of the spinal curve to pool in the sacral end of the model (middle panel, arrowhead). Immediately after injection, the dye was clearly pooled at the distal end of the tube (lower panel, arrowhead). Figure 2 shows the effect of injecting additional 1-mL (50 mg) volumes of 5% lidocaine in 7.5% dextrose. As shown in Figure 2, the total amount of 5% lidocaine solution injected into the model is as follows: upper panel, 2 mL (100 mg); middle panel, 3 mL (150 mg); lower panel, 4 mL (200 mg). The time that elapsed between these additional injections was approximately 5-10 min. Accumulation of large volumes of 5% lidocaine in 7.5% dextrose, as shown in the model (Figure 2), may prove to be neurotoxic to the cauda equina nerves as they pass through the pooled local anesthetic en route to their destination. The small amount of 5% lidocaine solution normally used for single-injection spinal anesthesia does not produce neurotoxicity because it is rapidly diluted out by the CSF into which it is injected; and it is further decreased in concentration by vascular absorption, uptake into nervous tissue, and diffusion across the dura into the epidural space. However, during continuous spinal anesthe-

CASE REPORTS

Figure 2 . Photographs taken immediately after injection showing the effect of injecting additional 1-mL volumes of 5% lidocaine in 7.5%' dextrose after injection of 1 mL of 5% lidocaine (Figure 1). (See text for further details).

sia, it is possible to inject volumes of 5% lidocaine solution so great that they displace the CSF, thus preventing their dilution by CSF. Although a large volume of 5% lidocaine in 7.5% dextrose may displace CSF and prevent its dilution, this does not mean that the concentration of lidocaine shown in the figures can ever increase and exceed 5%. Figure 3 shows an alternative approach to injection of local anesthetic solutions during continuous spinal anesthesia. The upper panel shows the injection of 2% plain lidocaine (1 mL, 20 mg). This solution, though reported to be isobaric (5), is in fact slightly hyperbaric (SG = 1.014) but much less so than 5% lidocaine in 7.5% dextrose (SG > 1.035). The 2% plain lidocaine solution distributes itself more uniformly than the heavier 5% lidocaine in 7.5% dextrose. The middle panel shows the injection of an additional 1mL of 2% plain lidocaine solution (total volume now 2 mL). At this point, the model contains only 40 mg of lidocaine but the distribution appears equivalent to that which occurred with 3 - 4 mL of 5% lidocaine in 7.5% dextrose (Figure 2). In the event that 40 mg (2 mL) of 2% lidocaine solution injected in this way does not produce adequate anesthesia, we suggest injecting a hypobaric solution, for example, 1 mL of 0.37570 bupivacaine made hypobaric by addition of an equal volume of distilled water to 0.75% plain bupivacaine. This solution is clearly hypobaric (SG = 1.004), as shown in the lower panel of Figure 3. Figure 4 upper panel shows the injection of an additional milliliter of 0.375% hypobaric bupivacaine solution. Now the spinal canal (in the supine horizontal position) is nearly uniformly filled with local anesthetic from the peak of the lumbar lordosis distally. Yet, the amounts of local anesthetic are only 40 mg of lidocaine and 7.5 mg of bupivacaine. The photograph in the lower panel of Figure 4, taken 5

CASE REPORTS

Figure 3. Spinal canal model (see text for details) showing alternative approach to injecting local anesthetic solutions during continuous spinal anesthesia when inadequate spinal anesthesia occurs. Upper panel, immediately after injection of 1mL of 2% plain lidocaine (20 mg). Middle panel, approximately 2 min after injection of another milliliter of 2% lidocaine (40 mg total). Lower panel, immediately after injection of 1 mL of hypobaric 0.375% bupivacaine (3.75 mg).

Figure 4. Spinal canal model showing the effect of injecting an additional 1 mL of hypobaric 0.375% bupivacaine (7.5 mg total). Loiver panel, same as upper panel but 5 min after injection. The spinal canal is nearly uniformly filled with local anesthetic from the peak of the lumbar lordosis and distally.

min after the second bupivacaine injection, shows that the solutions remain fixed because of their density and the shape of the model. Should the level of anesthesia at this time still not be sufficient, the patient can be repositioned for a short period of time to direct the hypobaric bupivacaine solution in a cephalad direction (Figure 5). After the solution has achieved the desired level, repositioning in the supine horizontal position prevents further spread of the hypobaric solution (Figure 5, middle and lower panels). We would like to emphasize that the validity of this model is based on an assumption that is not entirely valid. What happens to the concentration and localization of local anesthetics injected into the model does not accurately represent what happens in vivo in patients because the model assumes that there is no change in concentration of local anesthetic after

ANESTH ANALG 1991;72:817-9

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Figure 5 . Spinal canal model (see text for details) illustrating the effect of position on the distribution of hypobaric bupivacaine. Upper panel, head-up posture for 30 s. Middle panel, further spread in the cephalad direction is prevented by returning the model to the supine horizontal position. Lower panel, 2 min after returning the model to the supine horizontal position, the hypobaric bupivacaine has migrated back toward the peak of the lumbar lordosis.

injection. This is, of course, not correct, as the concentration and the amount of local anesthetic in the CSF after injection decrease rapidly for three reasons: (a) uptake into neural tissue, (b) vascular absorption, and (c) diffusion from the CSF through the dura into the epidural space. However, this loss of local anesthetic under clinical conditions after injection into the subarachnoid space does not necessarily invalidate the use of the model as used in this report. We hope these figures provide anesthesiologsts with appreciation of the distribution of local anesthetics within the spinal subarachnoid space when continuous spinal anesthesia is given. Using low-concentration solutions of lidocaine and bupivacaine may prevent the development of cauda equina syndrome.

References 1. Hurley RJ, Lambert DH. Continuous spinal anesthesia with a microcatheter technique: preliminary experience. Anesth Analg 1990;7097-102. 2. Li DF, Bahar M, Cole G, et al. Neurological toxicity of the subarachnoid infusion of bupivacaine, lignocaine or Z-chloroprocaine in the rat. Br J Anaesth 1985;57:424-29. 3. Ready LB, Plummer MH, Haschke RH, et al. Neurotoxicity of intrathecal local anesthetics in rabbits. Anesthesiology 1985;63: 36470. 4. Gissen AJ, Datta S, Lambert DH. The chloroprocaine controversy. 11. Is chloroprocaine neurotoxic. Reg Anaesth 1984;9: 135-45. 5. Lawrence VS, Rich CR, Magitsky L, et al. Spinal anesthesia with isobaric lidocaine 2% and the effect of phenylephrine. Reg Anaesth 1984;9:17-21.

Cauda equina syndrome and continuous spinal anesthesia.

ANESTH ANALG 817 1991;72:817-9 Case Reports Cauda Equina Syndrome and Continuous Spinal Anesthesia Donald H. Lambert, PhD, MD, and Ronald J. Hurl...
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