Blitt on Lidocaine…

Laura A. Lambert, B.A;Donald H. Lambert, Ph.D., M.D.

To the Editor

We found Dr. Casey Blitt’s letters regarding the use of 5% lidocaine for single injection spinal anesthesia provocative.(1,2) However, Dr. Blitt ignores data that prompted this reply. Clearly, 5% lidocaine can cause cauda equina syndrome.(3,4) In vitro and in vivo amphibian (5,6) and mammalian (7,9) experiments show also that 5% lidocaine can be neurotoxic. Worrisome are the case reports of painful lower extremity dysesthesias that occur after single injection 5% lidocaine spinal anesthesia.(10-12) These can last as long as three days and the literature suggests an incidence of 15-34%.(12,13)

We and others reported that certain concentrations of lidocaine cause irreversible conduction block in isolated amphibian nerve.(5,6) Similar phenomena occur in in vivo mammalian preparations.(7,9) We believe the nerve injuries in patients result from direct contact of lidocaine with the cauda equina nerves. We think the painful dysesthesias seen after single injection 5% lidocaine spinal anesthesia result also from the lidocaine damaging or irritating the cauda equina fibers. With time (? days), these damaged or irritated fibers die or recover and anesthesiologists perceive the dysesthesias as self-limited and therefore inconsequential.(12) Yet, it is possible that the patient has suffered neurological injury that becomes subliminal or the patient recovers from the injury. Does any physician deny that pain (dysesthesia) is a sign that something is wrong? We express our concern here because until the physiological mechanism causing the painful dysesthesias is known, we think that patients given 5% lidocaine for spinal anesthesia run the risk of nerve injury.

Why do anesthesiologists use the highest concentration of local anesthetic for spinal anesthesia – the nerve block that has the least barriers to diffusion of the local anesthetic to the target tissue? With other nerve blocks (epidural, axillary nerve, etc.) the volume of local anesthetic needed to produce anesthesia necessitates injecting lower concentrations to avoid systemic toxicity. Nonetheless, lower concentrations of local anesthetic produce adequate anesthesia even in nerve blocks, where there are formidable diffusion barriers. Thus, the need to use 5% lidocaine for spinal anesthesia, where the diffusion barriers are fewest, is illogical and unnecessary. Astra Pharmaceuticals sells a 1.5% lidocaine solution that contains 7.5% dextrose (1995 PDR, page 583), which is made specifically for spinal anesthesia. The 1.5% lidocaine solution is adequate for spinal anesthesia14 and it is an alternate that might eliminate the painful dysesthesias and potential for nerve injury seen with the 5% solution. We caution, nonetheless, on the basis of isolated nerve data, (5,6) that even the 1.5% concentration may be too high if there is poor mixing of this solution with the cerebrospinal fluid. However, should poor mixing occur, the l.5% might cause less neural injury or irritation than the 5% solution.

Dr. Blitt complains, “The Swiss study,(10) while interesting, must be viewed as a clinical aberration with questionable implications for subarachnoid anesthesia.” In rebuttal, he cites his own non-peer-reviewed ” database of 3,372 administrations of single dose 5% lidocaine, without known neurologic sequelae.” Yet, a personal database does not qualify as rigorous statistics. Dr. Blitt’s statement that “experienced investigators should prospectively evaluate the issue of neurotoxicity owing to single injection 5% hyperbaric lidocaine” is harsh. At least, the Swiss study was peer-reviewed.

Dr. Blitt complains further, “Our specialty has been plagued by fingerpointing at the wrong variable (such as the suggestion that isoflurane causes cancer).” While this might be true, it is also true that some anesthesiologists pointed their finger at halothane as a cause of hepatitis in certain patients – and in that case they were right. Actually, there are some interesting parallels between the old halothane controversy and the current lidocaine argument. Both drugs rarely cause serious injury (massive hepatic necrosis in the case of halothane and cauda equina syndrome in the case of lidocaine). Both cause more frequent minor tissue injury (transient serum transaminase elevations in the case of halothane and transient dysesthesias in the case of lidocaine). Just prior to its falling out of favor, the number of halothane anesthetics administered (like 5% hyperbaric lidocaine) was very large and it too had ” stood the test of time,” according to its advocates. Yet, today, anesthesia residents finish training without having given a halothane anesthetic, except perhaps to children. Halothane hardly enjoys the popularity it once did and, as a result of fingerpointing, some patients no longer develop transaminemia or hepatitis from it. We agree with Dr. Blitt that lidocaine spinal anesthesia has advantages. We believe also that the recent literature suggests that using lower concentrations of lidocaine might be safer for patients.

Laura A. Lambert, B.A, Student, Harvard Medical School. Donald H. Lambert, Ph.D., M.D., West Roxbury VA Medical Center and Associate Professor of Anaesthesia, Harvard Medical School, Boston, MA

References

  1. Blitt, C. Package insert has last word on lidocaine risk [letter]. Anesthesia Patient Safety Foundation Newsletter, 1995; 10:33.
  2. Blitt, C. Safety of 5% lidocaine heavily defended [letter]. Anesthesia Patient Safety Foundation Newsletter, 1995; 10:24.
  3. Rigler, ML, Drasner, K, Krejcie, TC, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg, 1991; 72:275-281.
  4. Schell, R, Brauer, F, Cole, D, et al. Persistent sacral nerve root deficits after continuous spinal anaesthesia. Can J Anaesth, 1991; 38:908-11.
  5. Lambert, LA, Lambert, DH, Strichartz, GR. Irreversible conduction block in isolated nerve by high concentrations of local anesthetics. Anesthesiology, 1994; 80:1082-93.
  6. Bainton, CR, Strichartz, GR. Concentration dependence of lidocaine-induced irreversible conduction loss in frog nerve. Anesthesiology, 1994; 81 :657-67.
  7. Sakura, S, Chan, VW, Ciriales, R, et al. The addition of 7.5% glucose does not alter the neurotoxicity of 5% lidocaine administered intrathecally in the rat. Anesthesiology, 1995; 82:236-40.
  8. Steele, S, Montine, T, Dentz, M, et al. Histopathological changes of cauda equina syndrome in a canine continuous spinal anesthesia model. Anesthesiology, 1993; 79:A850.
  9. Steele, S, Dentz, M, Dickens, C, et al. The correlation of motor evoked potentials and cauda equina syndrome in a canine continuous spinal anesthesia model. Anesthesiology, 1993; 79:A829.
  10. Schneider, M, Ettlin, T, Kaufmann, M, et al. Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine. Anesth Analg, 1993; 76:1154 ll57.
  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; SI:314-20.
  12. Pollock, J, Mulroy, M, Stephenson, C. Spinal anesthetics and the incidence of transient radicular irritation. Anesthesiology, 1994; 81:A1029.
  13. Pollack, J. Hyperbaric lidocaine for spinal anesthesia. Pro: ASRA News, 1995; November 13 14.
  14. Manica, VS, Bader, AM, Fragneto, R, et al. Anesthesia for in vitro fertilization: a comparison of 1.5% and 5% spinal lidocaine for ultrasonically guided oocyte retrieval. Anesth Analg, 1993; 77:453-6.