To the Editor
I write because I believe many patients are still receiving spinal anesthesia that is associated with transient radicular irritation (TRI, also known as transient neurologic syndrome or TNS). Dr. Marcus Schneider first described TRI in 1993.1 TRI is a constellation of low back, buttock, and lower extremity pain that occurs usually within 24 hours of spinal anesthesia and persists for as long as 4 to 5 days. Lidocaine and mepivacaine are more likely to cause TRI than other anesthetics. Bupivacaine and prilocaine rarely cause TRI, and procaine and tetracaine are intermediate in causing this disorder.2
Some anesthesiologists believe that lidocaine-induced TRI is possibly benign because it is poorly understood and because of its transience,3,4 and they argue that lidocaine’s “long safety record” and the “lack of a suitable short duration substitute” is a reason to continue using lidocaine for spinal anesthesia.5,6 This is not a reasonable argument to continue a practice that is harmful to patients.
The true cause of TRI remains unknown. I have argued that TRI is likely toxicity that is clinically undetectable after the symptoms of TRI resolve.7 Others have argued that it is not toxicity.3,5 We may never know if TRI is due to local anesthetic toxicity because studies of toxicity involving patients are unethical and because we do not have an animal model that adequately duplicates TRI. Nonetheless, it is my opinion that anesthesiologists should avoid local anesthetics in spinal anesthesia that:
- Cause pain that can last from 2 to 5 days.
- Cause pain that is often worse than the pain associated with the operation for which the spinal was used.
- Cause pain that can rate as high as a 6 on a 10-point VAS.
- Cause patients to visit the emergency room out of fear that something is wrong.
- Sometimes result in CT or MRI scans to rule out serious neurologic injury.2
Anesthesiologists should prevent and treat pain, not cause it. We may not know what TRI is, but we know how to avoid it. It can be avoided by using drugs that do not cause it. Procaine and bupivacaine are two approved local anesthetics that can substitute for lidocaine.8,9 Procaine has been downplayed because of a perceived poor quality of anesthesia and high incidence of nausea and vomiting.9 It is argued that bupivacaine results in a prolonged motor block that is unacceptable in this day of “fast-tracking” anesthesia in outpatients.10 On the other hand, is it reasonable to continue to use lidocaine to save an hour of PACU time, only to have some patients returning to the emergency room for the reasons outlined above?
Chloroprocaine is a drug that has recently been tested in volunteers.11 If it is similar to procaine, it may cause less TRI than lidocaine, and it may have a duration that would make it useful for outpatient anesthesia. Similarly, ropivacaine should be evaluated both in terms of toxicity and its TRI potential. Unlike bupivacaine, it produces less motor block and could have a recovery profile that would also make it useful for outpatient operations.
Eight years ago, one anesthesiologist wrote in the APSF Newsletter that lidocaine was safe and that it was used in 500,000 to 1,000,000 spinal anesthetics annually.5 Just this year, others argued, “Since spinal lidocaine has been used previously for approximately 50 million spinal anesthetics, it seems hard to imagine that the use of lidocaine should be limited or abandoned.”12 Because of the reports of cauda equina syndrome and TRI owing to lidocaine spinal anesthesia, lidocaine is probably used much less frequently today. Nonetheless, even if it is used only one-tenth as often today, then 50,000 to 100,000 lidocaine spinal anesthetics are still being given. That means that as few as 2,500 or as many as 10,000 patients are suffering from TRI after the lowest risk operations (operations performed in the supine position =5% incidence of TRI).
Those numbers rise to 17,500 to 70,000 for patients having lower extremity arthroscopy or operations performed in the lithotomy position (35% incidence of TRI). Even if it does not result in permanent injury, we should eliminate the pain and suffering caused by TRI. In keeping with the APSF mission, that no patient shall be harmed by [or suffer from] anesthesia, we can eliminate TRI simply by not using the local anesthetics that cause it.
Donald H. Lambert, PhD, MD Boston, MA
1. Schneider M, Ettlin T, Kaufmann M, et al. Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine. Anesth Analg 1993;76:1154-7.
2. Pollock JE. Transient neurologic symptoms: etiology, risk factors, and management. Reg Anesth Pain Med 2002;27:581-6.
3. Moore D, Thompson G. Commentary: neurotoxicity of local anesthethics—an issue or a scapegoat? Reg Anesth Pain Med 1998;23:605-10.
4. Neal J, Pollock J. Can scapegoats stand on shifting sands? Reg Anesth Pain Med 1998;23:533-7.
5. Blitt C. Safety of 5% lidocaine heavily defended. APSF Newsletter 1995;10:24.
6. Pollock JE. TNS: Is it clear that lidocaine is the culprit (reply). Reg Anesth Pain Med 2003;28:151-2.
7. Lambert DH. Continuous spinal anesthesia redux. Anesthesiology 2003;98:797-8.
8. Lambert DH. Limiting transient radicular irritation. Reg Anesth Pain Med 2001;26:177-8.
9. Hodgson PS, Liu SS, Batra MS, et al. Procaine compared with lidocaine for incidence of transient neurologic symptoms. Reg Anesth Pain Med 2000;25:218-22.
10. Pollock JE, Neal JM, Stephenson CA, et al. Prospective study of the incidence of transient radicular irritation in patients undergoing spinal anesthesia. Anesthesiology 1996;84:1361-7.
11. Smith KN, Kopacz DJ, McDonald SB. Spinal chloroprocaine. Anesth Analg 2003;96:S285.
12. Pollock JE, Alley E. Virginia Mason Medical Center’s promotion of outpatient lidocaine spinal anesthesia questioned (reply). Anesth Analg 2003;96:1237-8.