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Anesth Analg 2001;92:401-404
© 2001 International Anesthesia Research Society

OBSTETRIC ANESTHESIA

Does Pregnancy Protect Against Intrathecal Lidocaine-Induced Transient Neurologic Symptoms?

Marie T. Aouad, MD, Sahar S. Siddik, MD, FRCA, Maya I. Jalbout, MD, and Anis S. Baraka, MD, FRCA

Department of Anesthesiology, American University of Beirut, Beirut-Lebanon

Address correspondence and reprint requests to Anis Baraka, MD, FRCA, Professor and Chairman, Department of Anesthesiology, American University of Beirut, PO Box 113-6044, Beirut-Lebanon. Address e-mail to abaraka{at}aub.edu.lb


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
We investigated the incidence of transient neurologic symptoms (TNS) after the use of hyperbaric lidocaine as compared with hyperbaric bupivacaine in patients undergoing cesarean delivery under spinal anesthesia. Two hundred women scheduled for cesarean delivery were randomly allocated to receive spinal anesthesia with 75 mg hyperbaric lidocaine 5% (n = 100) or 12 mg hyperbaric bupivacaine 0.75% (n = 100). Spinal anesthesia was administered to all patients in the sitting position with a 25-gauge Whitacre needle. The level of sensory blockade, time to full recovery, and intraoperative hemodynamic profile were noted in all patients. The patients were interviewed postoperatively for three consecutive days to detect the occurrence of TNS. The incidence of TNS was zero (95% confidence interval 0%–3%) in both the Lidocaine and the Bupivacaine Groups. Our results indicate that the frequency of postoperative TNS does not exceed 3% in patients undergoing cesarean delivery at term using hyperbaric lidocaine 5% or hyperbaric bupivacaine 0.75%.

Implications: Transient neurologic symptom (TNS) can follow spinal anesthesia and manifests as back pain radiating to the legs, resolving spontaneously. Spinal anesthesia for cesarean delivery was performed with either hyperbaric lidocaine 5% (n = 100) or hyperbaric bupivacaine 0.75% (n = 100). TNS was not noted in any patient.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Intrathecal hyperbaric lidocaine, in contrast to hyperbaric bupivacaine, is associated with a relatively frequent incidence of transient neurologic symptoms (TNS), reaching up to 40% (1). The term "TNS" has been used to describe a symptom complex of acute onset low back pain with transient radiating pain into the lower extremities, the buttocks, or both corresponding to the L5-S1 distribution, occurring within 24 hours after spinal anesthesia. TNS is not accompanied by any serious motor or sphincter disturbances and starts after a latent period following the return of normal sensation (2).

Wong and Slavenas (3) found no TNS in obstetric patients who received either intrathecal hyperbaric lidocaine or bupivacaine for procedures performed during pregnancy, at term, or during the immediate postpartum period. However, in their report the lidocaine group included only 12 patients undergoing cesarean delivery (3).

The purpose of this study was to determine the incidence of TNS in parturients undergoing cesarean delivery using spinal anesthesia. Our report compares the incidence of TNS after the use of hyperbaric lidocaine versus hyperbaric bupivacaine in 200 patients undergoing elective cesarean section under spinal anesthesia.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After approval from the institution’s ethical committee and obtaining informed consent of the patients, 200 ASA physical status I and II women scheduled for elective cesarean delivery at term were enrolled. Patients with a history of acute or chronic back pain, preexisting neurological disease, or diabetes mellitus were excluded. Patients with a height <150 cm or more than 175 cm were also excluded. Patients were allocated randomly by sealed envelope to receive spinal anesthesia with either hyperbaric lidocaine 50 mg/mL (Group L) or hyperbaric bupivacaine 7.5 mg/mL (Group B). Patients were blinded as to the spinal anesthetic used. No epinephrine and no opioids were added to the spinal anesthetic. As per hospital routine, patients were premedicated with 0.5 mg atropine IM 30–40 min before surgery. Baseline arterial blood pressure was taken as the mean of three consecutive readings at 3-min intervals during which the systolic blood pressure did not vary by more than 10% from its average value. During the 10 min preceding the spinal block, subjects received 500 mL Hemaccel® (Polygeline; Hoechst Marion Roussel) via an 18-gauge IV cannula. Spinal anesthesia was performed at the L2-L3 or L3-L4 interspace with the patients in the sitting position via the midline approach, using a 25-gauge Whitacre needle through a 20-gauge introducer needle. All blocks were performed by an attending anesthesiologist or a chief resident. Once the correct needle position was identified by the free flow of cerebrospinal fluid (CSF), approximately 0.2 mL of CSF was aspirated, and the local anesthetic was injected with the aperture of the Whitacre needle facing cephalad. Group L received 75 mg of hyperbaric lidocaine 50 mg/mL solution in 7.5% glucose (AstraZeneca, Sodertalje, Sweden), whereas Group M received 12 mg of hyperbaric bupivacaine 7.5 mg/mL in dextrose 8.25% (Abbott Laboratories, North Chicago, IL). Thereafter, the patients in both groups were turned supine with left uterine displacement. Oxygen 5 L/min was administered by face mask.

Problems related to spinal punctures, such as multiple attempts, blood on insertion of the introducer needle or in the CSF or paresthesias, were noted. The segmental level of sensory blockade to pinprick was assessed at 10-min intervals for 30 min; maximum height of block was recorded. Motor block was assessed using a modified Bromage Scale (4) (0 = able to move hip, knee, and ankle, 1 = unable to move hip, able to move knee and ankle, 2 = unable to move hip and knee, able to move ankle, 3 = unable to move hip and knee and ankle) until the Bromage scale equaled 3. Duration of the block (time to Bromage scale = 0) was noted by the postanesthesia care unit nurse. The anesthesiologist who administered the spinal anesthetic and collected the data on sensory and motor blockade was not blinded as to the study groups. Blood pressure was measured with an automated blood pressure device (model 1094B; Hewlett Packard, Palo Alto, CA) every minute for 20 min and every 3 min thereafter. Minimal systolic arterial blood pressure was noted. Hypotension was defined as systolic arterial blood pressure <80% of baseline blood pressure and <100 mm Hg, and was treated with an IV bolus of 5 mg ephedrine and additional rapid infusion of lactated Ringer’s solution. Ephedrine treatment was repeated every 2 min if hypotension persisted or recurred.

All patients were interviewed on the first, second, and third postoperative days by an anesthesiologist who was unaware of the local anesthetic given. To ensure standardized data collection, a symptom checklist similar to that reported by Hampl et al. (5) was used. Patients were specifically asked about the presence of pain or strange sensation in locations other than the surgical site, including the site of lumbar puncture, low back, buttocks, and thighs.

The number of patients studied was determined based on a power analysis assuming a 3% incidence of TNS after lidocaine spinal anesthesia. This represents the least incidence reported in the large multicenter study of Freedman et al. (6). The 95% confidence interval was calculated using the "Rule of Three," i.e., the likelihood of an event occurring that was not detected in n patients is approximated with 95% confidence by 3/n (7). The mean values of quantitative data were compared using the Student’s t-test. The frequencies of occurrence were compared using the {chi}2 test. Statistical significance was considered at P < 0.05.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Demographic data did not differ significantly between the two groups concerning age, weight, height, parity, and gestational age ( Table 1). Complete recovery from the anesthetic was documented in all patients. Interviewing patients on three consecutive postoperative days concerning the acute onset of low back pain with transient radiating pain in the lower extremities, the buttocks, or both, corresponding to L5-S1 distribution or other dermatomal distribution, did not reveal any symptom suggestive of TNS in both groups.


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  		Table 1. Demographic Data
 
The incidence of pain at the site of puncture was significantly increased in the lidocaine group versus the bupivacaine group, whereas the incidence of blood on insertion of the introducer needle or in the CSF, paresthesias, postdural puncture headache, and multiple punctures was not significantly different between the two groups ( Table 2).


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  		Table 2. Details of Puncture of the Subarachnoid Space in Each Group
 
The relevant aspects of the surgical and anesthetic procedures are provided in Table 3. The number of patients with a block higher than T4 as well as the total dose of ephedrine required to treat hypotension were significantly larger in the lidocaine group. The duration of the block was significantly longer in the bupivacaine group.


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  		Table 3. Perioperative Characteristics and Details of Anesthesia
 

   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
TNS is common with intrathecal lidocaine occurring in up to 40% but is rare after intrathecal bupivacaine, with a reported incidence of 1.3% (1,6). Some authors consider TNS as a minor manifestation of the cauda equina syndrome that may follow administration of intrathecal lidocaine (8). Several studies have used desheathed peripheral nerve models designed to mimic unprotected nerve roots in the cauda equina; these models demonstrate that clinically used concentrations of 5% lidocaine cause irreversible conduction block, whereas 1.5% lidocaine or 0.75% bupivacaine do not, suggesting that lidocaine has an increased potential for neurotoxicity compared with bupivacaine at clinically relevant concentrations (9–11). Electrophysiologic neurotoxicity of lidocaine in these models is both time- and concentration-dependent (10).

Results from a large multicenter epidemiological study suggest that lithotomy position and early ambulation after outpatient surgery are major cofactors predisposing to TNS (6). The lithotomy position may increase the vulnerability of nerve fibers exposed to 5% lidocaine by stretching lumbo-sacral nerve roots. Pollock et al. (12) indicated that patient position may be an important contributing factor to TNS based on the increased incidence of TNS in patients undergoing arthroscopy compared with those having inguinal hernia. Other predisposing factors include needle trauma, neural ischemia (13), pooling of local anesthetics around certain nerve roots secondary to maldistribution (14), muscle spasm, and myofascial pain, as well as excessive muscle relaxation resulting in facet joint irritation (15,16).

In contrast to the relatively frequent incidence of TNS in the general population, a previous prospective randomized clinical study in obstetric patients demonstrated a zero incidence of TNS (95% confidence interval 0%–4.5%) after hyperbaric intrathecal lidocaine anesthesia performed during pregnancy, labor, or the immediate postpartum period (3). However, that study was not randomized to patient group or type of surgery. The present study, which was randomized to the anesthetic drug used for spinal anesthesia, found that no parturient undergoing cesarean delivery at term using spinal anesthesia developed TNS whether lidocaine or bupivacaine was used.

The zero incidence of TNS (95% confidence interval 0%–3%) in our patients, in contrast to the relatively frequent incidence in the general population, which includes both males and nonobstetrical females, may be related to the absence of predisposing factors. Data of Freedman et al.’s (6) study indicates a spectrum of risk for TNS after lidocaine ranging from 3.1% for inpatients having surgery in positions other than lithotomy to 24.3% for outpatients operated in the lithotomy position. All patients included in our study had surgery as inpatients and in the supine position. Also, our patients were young females; Martinez-Bourio et al. (17) found that patients with TNS were significantly older than patients without TNS (mean age 58 vs 48 years, P < 0.05).

The zero incidence of TNS (95% confidence interval 0%–3%) after intrathecal lidocaine in our patients undergoing elective cesarean delivery at term, as well as in the obstetrical population in general (3), may also be attributed to factors associated with pregnancy. During pregnancy, the engorgement of epidural veins, as well as the downward shift and exaggerated lumbar lordosis, favor a more cephalad spread of the local anesthetic, as evidenced by the higher level of analgesia after intrathecal administration of local anesthetics during pregnancy (18). Therefore, it is probable that intrathecal lidocaine in pregnant women is less likely to pool toward the L5-S1 roots involved in the pain distribution of TNS. Also, endogenous analgesic neuropeptides, such as endorphins and enkephalins, are increased in the plasma and CSF of pregnant women and in the brain of pregnant experimental animals (19,20). The increased endogenous analgesic neuropeptides, as well as the hormonal changes that accompany pregnancy, such as the increased progesterone levels, may result in an increase in the threshold of pain, and hence may protect against the development of TNS in the obstetrical population. As TNS may be myofascial pain, the already increased elasticity of the musculoskeletal system during pregnancy by the hormone relaxin and the biochemical strain on the ligaments and skeleton (21), may be another potentially protective factor for TNS. The hormonal factors reach their maximal effect at term, which may explain the very infrequent incidence of TNS encountered in our patients undergoing cesarean delivery at term.

The use of intrathecal hyperbaric lidocaine in our study was associated with a larger number of patients with a sensory block >T4 (42 in lidocaine group versus 14 in bupivacaine group, P < 0.05). This may be attributed to a greater cephalad spread of lidocaine secondary to its smaller glucose content and hence its lower baricity as compared with bupivacaine (lidocaine in 7.5% glucose versus bupivacaine in 8.25% glucose). The higher level of sensory blockade in the lidocaine group and its more rapid onset of action may also explain the larger total ephedrine dose required for management of hypotension in the lidocaine group (27 ± 22.48 mg in lidocaine group versus 19 ± 18.8 mg in bupivacaine group). The frequent incidence of pain at the site of puncture in the lidocaine group may be related to the multiple attempts of puncture rather than to the type of the anesthetic used.

Because of the higher sensory blockade achieved by spinal lidocaine, the increased ephedrine requirement, as well as its shorter duration of action, the use of bupivacaine instead of lidocaine for cesarean delivery may be advantageous.

In conclusion, the present report shows that the frequency of TNS does not exceed 3% in patients undergoing cesarean delivery at term using hyperbaric lidocaine 5% or hyperbaric bupivacaine 0.75%. Further study comparing pregnant and nonpregnant patients is warranted.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Hampl KF, Schneider MC. Pragger H, et al. A similar incidence of transient neurologic symptoms after spinal anesthesia with 2%and 5% lidocaine. Anesth Analg 1996; 83: 1051–4.[Abstract]
  2. Corbey MP, Bach AB. Transient radicular irritation (TRI) after spinal anaesthesia in day-care surgery. Acta Anaesthesiol Scand 1998; 42: 425–9.[Web of Science][Medline]
  3. Wong CA, Slavenas P. The incidence of transient radicular irritation after spinal anesthesia in obstetric patients. Reg Anesth Pain Med 1999; 24: 55–8.[Web of Science][Medline]
  4. Bromage PR. A comparison of the hydrochloride and carbon dioxide salts of lidocaine and prilocaine in epidural analgesia. Acta Anesthesiol Scand 1965; 16: 55–69.
  5. Hampl KF, Schneider MC, Ummenhofer W, Drewe J. Transient neurologic symptoms after spinal anesthesia. Anesth Analg 1995; 81: 1148–53.[Abstract]
  6. Freedman JM, De-Kun Li, Drasner K, et al. Transient neurologic symptoms after spinal anesthesia: an epidemiologic study of 1,863 patients. Anesthesiology 1998; 89: 633–41.[Web of Science][Medline]
  7. Hanley JA, Lippman-Hand A. If nothing goes wrong, is everything all right? Interpreting zero numerators. JAMA 1983; 249: 1743–5.[Abstract/Free Full Text]
  8. Gisvold SE. Lidocaine may still be an excellent drug for spinal anesthesia. Acta Anesthesiol Scand 1999; 43: 369–70.[Web of Science][Medline]
  9. Bainton C, Strichartz G. Concentration dependence of lidocaine-induced irreversible conduction loss in frog nerve. Anesthesiology 1994; 81: 657–67.[Web of Science][Medline]
  10. Kanai T, Katsuki H, Takasake M. Graded. Irreversible changes in crayfish giant axon as manifestations of lidocaine neurotoxicity in vitro. Anesth Analg 1998; 86: 569–73.[Abstract]
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  12. Pollock JE, Neal JM, Stephenson CA, Wiley CE. Prospective study of the incidence of transient radicular irritation in patients undergoing spinal anesthesia. Anesthesiology 1996; 84: 1361–7.[Web of Science][Medline]
  13. Salmela L, Cozanitis DA. Leg and back pain after spinal anesthesia involving hyperbaric 5% lignocaine. Anaesthesia 1996; 51: 391–3.[Web of Science][Medline]
  14. Beardsley D, Holma S, Gantt R, et al. Transient neurological deficit after spinal anesthesia: local anesthetics maldistribution with pencil point needles? Anesth Analg 1995; 81: 314–20.[Abstract]
  15. Hartrick CT. Transient radicular irritation: a misnomer? Anesth Analg 1997; 84: 1392–3.
  16. Naveira FA, Copeland S, Anderson M, et al. Transient neurologic toxicity after spinal anesthesia, or is it myofascial pain? 2 case reports. Anesthesiology 1998; 88: 268–70.[Web of Science][Medline]
  17. Martinez-Bourio R, Arzuaga M, Quintana J, et al. Incidence of transient neurologic symptoms after hyperbaric subarachnoid anesthesia with 5% lidocaine and 5% prilocaine. Anesthesiology 1998; 88: 624–8.[Web of Science][Medline]
  18. Brown DL. Spinal, epidural and caudal anesthesia: anatomy, physiology and technique. In: Chestnut DH, ed. Obstetric anesthesia: principles and practice. St. Louis: Mosby, 1999: 187–208.
  19. Abboud TK, Sarkis F, Hung TT, et al. Effects of epidural anesthesia during labor on maternal plasma beta-endorphin levels. Anesthesiology 1983; 59: 1–5.[Web of Science][Medline]
  20. Wardlaw SL, Frantz AG. Brain beta-endorphin during pregnancy, parturition, and post-partum period. Endocrinology 1983; 113: 1664–8.[Abstract/Free Full Text]
  21. Berg G, Hammar M, Moller-Nielson J, et al. Low back pain during pregnancy. Obstet Gynecol 1988; 71: 71–5.[Web of Science][Medline]
Accepted for publication September 26, 2000.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press