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LETTERS TO THE EDITOR

Troubling Incidence of Lidocaine Radiculotoxicity (TNS) in Volunteers

University of South Carolina, Columbia, SC, dejong@nuvox.net

To the Editor:

In their landmark studies of intrathecal chloroprocaine (2-chlorprocaine; 2-CP), Virginia Mason Clinic investigators documented, in sequential papers (1,2), the safety and efficacy of 2-CP as a serious contender for drug of choice in short-acting spinal anesthesia. In the process of dethroning lidocaine, the reigning title holder, the authors convincingly demonstrated that intrathecal chloroprocaine lacked the troubling transient postspinal radicular pain symptom complex (TRI; TNS) that has plagued lidocaine in ambulatory anesthesia practice (Table 1). Whether one considers the radiating lumbosacral pain to be a fleeting expression of lidocaine radiculotoxicity (TRI), or of a more benign sciatic nerve stretching secondary to myoskeletal relaxation (TNS), its iatrogenic origin and postoperative manifestation detract from overall patient and surgeon satisfaction with ambulatory spinal anesthesia.

Telling—as this faculty group (3) has long championed a myoskeletal cause for post-lidocaine radicular pain under the banner of "Transient Neurologic Symptoms"—is their painstaking differentiation between localized posttraumatic low back pain, encountered rarely after 2-CP administration (1), and radiating (i.e., radicular) low back and leg pain occurring frequently in subjects given lidocaine (1) or chloroprocaine with added epinephrine (2). Even so, old habits die hard, for the authors (1) relapsed in the article’s Introduction to characterizing post-lidocaine radicular pain as a "... syndrome of myoskeletal pain [emphasis mine] radiating to the buttocks or lower extremities."

All in all, Dr. Kopacz and his team of faculty and resident volunteers have earned the profession’s gratitude for their painstaking studies to establish the clinical safety (as well as efficacy) of 2-CP, notwithstanding doubts raised about experimental neurotoxicity (4,5). With that in mind, the distressingly high incidence of post-lidocaine radiculopathy warrants a concerted effort to replace that local anesthetic with a more benign intrathecal anesthetic.

References

1. Kouri ME, Kopacz DJ. Spinal 2-chloroprocaine: a comparison with lidocaine in volunteers. Anesth Analg 2004; 98: 75–80.[Abstract/Free Full Text]
2. Smith KN, Kopacz DJ, McDonald SB. Spinal 2-chloroprocaine: a dose-ranging study and the effect of added epinephrine. Anesth Analg 2004; 98: 81–8.[Abstract/Free Full Text]
3. Pollock JE. Transient neurologic symptoms: etiology, risk factors, and management. Reg Anesth Pain Med 2002; 27: 581–6.[Web of Science][Medline]
4. Gissen AJ, Datta S, Lambert D. The chloroprocaine controversy: II. Is chloroprocaine neurotoxic? Reg Anesth 1984; 9: 135–45.
5. Taniguchi M, Bollen AW, Drasner K. Sodium bisulfite: scapegoat for chloroprocaine neurotoxicity? Anesthesiology 2004; 100: 85–91.[Web of Science][Medline]

Response

Department of Anesthesiology, Virginia Mason Medical Center, Seattle, WA

In Response:

We would like to thank Dr. deJong for his encouraging and congratulatory remarks. Dr. deJong correctly points out our institutional bias in describing the syndrome of postspinal transient neurologic symptoms (TNS) as myoskeletal pain. In this series of studies investigating spinal 2-chloroprocaine, we were simply attempting to describe TNS without speculating on its cause. The pathophysiology of TNS remains unknown. Because TNS is a syndrome of subjective symptoms, no animal model exists to investigate its etiology. The only human study that we are aware of failed to demonstrate a neurologic mechanism, as assessed by EMG, nerve conduction studies, or SSEPs, in volunteers with TNS after spinal lidocaine (1). As these electrophysiologic tests may not be sensitive enough to detect minor changes in spinal nerves, they do not exclude a possible neurotoxic mechanism. However, they certainly do not confirm it either. In our opinion, the current series of spinal 2-CP studies neither add nor remove supporting evidence to any of the proposed mechanisms of TNS.

Interestingly, Dr. deJong introduces a different bias when he states "knee arthroscopy or lithotomy position intensifies lidocaine’s threshold neurotoxicity [emphasis ours]." This study observed a significant difference in postspinal TNS between subjects receiving equal doses of spinal 2-CP and lidocaine, but cannot be construed as proof that inherent neurotoxicity of the local anesthetic is the source of this result.

While we feel this series of studies is a very significant step in finding a possible solution to the dilemma of TNS, we do not claim to have established the safety 2-CP for spinal anesthesia. This is a crossover study in 8 subject volunteers, designed solely to investigate the efficacy of spinal anesthesia with 2-CP as compared with lidocaine, and using doses that are reasonable for outpatient anesthesia. It clearly does not have sufficient power to observe rare complications. We leave that to the growing body of evidence, which currently includes over surgical 800 patients who have received intrathecal 2-CP without apparent neurotoxic effects (2–4), to determine if this drug is appropriate for widespread spinal use.

References

1. Pollock JE, Burkhead D, Neal J, et al. Spinal nerve function in five volunteers experiencing transient neurologic symptoms after lidocaine subarachnoid anesthesia. Anesth Analg 2000; 90: 658–65.[Abstract/Free Full Text]
2. Foldes F, McNall P. 2-chloroprocaine: a new local anesthetic agent. Anesthesiology 1952; 13: 287–96.[Web of Science][Medline]
3. Yoos J, Kopacz D. Spinal 2-chloroprocaine for surgery: an initial 10-month experience. Anesth Analg. In press.
4. Palas T. 1% chloroprocaine for spinal anesthesia [abstract]. Reg Anesth Pain Med 2003; 28: A52.

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