Lidocaine administered intrathecally for spinal anesthesia, on the one hand, is considered by many the prototypical drug for spinals, especially for same-day surgery and short-stay procedures while, on the other hand, it is the source of apparently continued controversy over postulated potential risks of this classic application of a classic medication. No sooner were spinal microbore catheters pulled off the market in 1992 than reports of “Transient Radicular Irritation” (TRI) after single-dose hyperbaric lidocaine intrathecal injection began to appear.
[Editor’s Note: This has been a popular topic in the pages of this Newsletter: Blitt C. Safety of 5% Lidocaine Heavily Defended, 10:24, Summer 1995; Blitt C. Package Insert Has Last Word on Lidocaine Risk, 10:33, Fall 1995; Lambert L&D. 5% Lidocaine Safety Debate Continues, 11:22, Summer 1996.]
The suggested TRI syndrome clearly differs from common positional local backache in that pain radiates into buttocks, legs, or both–often so intensely as to require opioid analgesia. As this radicular pain doesn’t come on till several hours after spinal anesthesia has worn off–by which time the patient having same-day surgery has long been discharged home– its prevalence was not appreciated till recently.
All well and good, but why should it have taken nearly 50 years for this neurologic event to manifest; didn’t the grand masters decades ago pronounce spinal anesthesia safe from major neurologic sequelae? That is correct, but they noted transient (“minor”) neurologic complications as well; in fact, the term “spinal irritation” for postspinal transient leg dysesthesias was coined in 1954. Just before intrathecal lidocaine came on the scene, the incidence of TRI (after spinal tetracaine, procaine, or both) was 0.9%–not much different from recent Mayo Clinic data. Nevertheless, with some fifty million lidocaine spinals given the past 50 years without reference to TRI, one has to wonder whether drug formulation, patient population, clinical practice or vigilance have changed this decade.
In June 1994, the FDA reconvened its Advisory Committee to relook at safety issues because concern had mounted that intrathecal lidocaine was linked to TRI. The consensus developed that 5% hyperbaric lidocaine irritated bare spinal roots and should be weakened by adding an equal volume of saline or spinal fluid before intrathecal injection. The package insert was altered accordingly, and circularized with a “Dear Doctor” letter to the anesthesia community.
Tranquility was short-lived, however, for prospective studies of spinal anesthesia revealed that TRI followed even 2.5% or 2% lidocaine–but never bupivacaine or tetracaine. Further, stretching lumbosacral rootlets (as with lithotomy positioning or leg manipulation) makes nerve tissue more susceptible to chemical damage by lidocaine–as demonstrated by a severalfold greater incidence of TRI after GYN/GU or knee arthroscopy, as compared with supine herniorrhaphy.[4,5]
Still, how could lidocaine neurotoxicity have gone undetected for nearly half a century, only to become a contentious issue in the past few years? Neither the drug manufacturing process nor dosage formulation have changed within memory. Clinical practice has changed some over the years with the switch to thinner non-coring spinal needles… but that’s old news. As best I see it, our vigilance for any neurologic sequelae has been heightened by the unfortunate rash of incidents following microbore catheter spinal anesthesia; sharpened further by expanding measures of continued quality improvement and patient satisfaction followup. That is, nowadays we routinely probe sooner and deeper into adverse post-anesthetic events and also know better what questions to ask.
I venture that TRI was just as common a problem before the 1990’s, but rather was written off as just myoskeletal discomfort secondary to contortioned positioning…for no functional damage was done and pain cleared soon after the patient was up and about. Be that as it may, are we really uncovering the new phenomenon of lidocaine neurotoxicity, or are we just crying wolf over transient back and leg ache from the unaccustomed stretching of muscles and twisting of joints aided, so it is claimed, by profound muscle relaxation from spinal lidocaine?
My response to that rather disingenuous assertion is twofold. First, were it nothing but myoskeletal back and leg pain, TRI should occur just as often with bupivacaine or tetracaine as with lidocaine spinal anesthesia. Truth is, it doesn’t.[3-5] The implication that lidocaine causes more intense relaxation of back muscles than other local anesthetics is both unproved and deceptive. And, even were it correct, bypass the needless burden of back pain altogether… select a local anesthetic more benign than lidocaine. Why risk both a pain in the head and a pain in the butt?
Second, and of considerably graver implication, is that transient radicular pain and florid cauda equina syndrome are but the low and high extremes, respectively, of a continuous dose-effect curve representing actual lidocaine neurotoxicity. Points on such a dose-effect curve intermediate between these two extremes have now been identified: patchy groin numbness, persistent isolated myotomal weakness, or sensory cauda equina syndrome. Should such lidocaine exposure-neurotoxicity correlation exist… as I fear it does…a rare but finite probability exists that some day an unusually vulnerable patient may emerge from spinal lidocaine block with a not-quite-so-transient radiculopathy.
To sum up: the incidence of transient leg, buttock, and back pain is distressingly high after spinal block with lidocaine; the time required for a neural inflammatory reaction to build up to pain threshold accounts for the several hours interval between drug injection and first onset of pain. Lumbo-sacral radicular pain is as common after 2.5% (or even 2%) as it is after 5% hyperbaric lidocaine; whereas it is not seen at all with either bupivacaine or tetracaine. Transient radicular irritation (TRI) is aggravated by positional stretching of lumbo-sacral dorsal roots–as occurs in lithotomy positioning or other leg manipulation. TRI could well be an early warning sign of ominous dose-time related lidocaine neurotoxicity. Whatever the cause, TRI appears to me causally linked to single-dose lidocaine spinal anesthesia; should you select lidocaine for spinal anesthetic administration, do inform the patient of this potential entity as part of a thorough informed-consent discussion in order to help avoid any possible later misunderstanding and grief.
Dr. deJong, a long-recognized authority and widely published author and editor on local anesthetics and their use, is Professor of Anesthesiology at the University of South Carolina, Columbia, SC.
1. Dripps RD, Vandam LD: Long-term follow-up of patients who received 10,098 spinal anesthetics: Failure to discover major neurological sequelae. J Am Med Assn 156:1486-1491,1954.
2. Horlocker TT, McGregor DG, Matsushige DK, et al: A retrospective review of 4767 consecutive spinal anesthetics: Central nervous system complications. Anesth Analg 84:578-584,1997.
3. Pollock JE, Neal JM, Stephenson CA, Wiley CE: Prospective study of the incidence of transient radicular irritation in patients undergoing spinal anesthesia. Anesthesiology 84:1361-1367,1996.
4. Hampl KF, Schneider MC, Pargger H, et al: A similar incidence of transient neurologic symptoms after spinal anesthesia with 2% and 5% lidocaine. Anesth Analg 83:1051-1054,1996.
5. Freedman J, Li D, Jaskela M, et al: Risk factors for transient neurologic symptoms after spinal anesthesia. Anesthesiology 85:A741,1996. [abstract]
6. Hartrick CT: Transient radicular irritation: A misnomer? Anesth Analg 84:13921393,1997. [letter]
7. Pollock JE, de Jong RH: Hyperbaric lidocaine for spinal anesthesia? Am J Anesthesiol 24:161-165,1997.