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On-line version ISSN 1806-907X
Rev. Bras. Anestesiol. vol.56 no.5 Campinas Sept./Oct. 2006
LETTERS TO THE EDITOR
Effects of increasing spinal hyperbaric lidocaine concentrations of spinal cord and meninges. Experimental study in dogs
A study published recently in RBA on increasing doses of hyperbaric lidocaine (5%, 7.5%, and 10%, all in glucose 7.5% in water) demonstrated that the 5% concentration is safe to be used in subarachnoid anesthesia and that concentrations higher than 7.5% lead to histological changes in the spinal cord but not in the meninges 1. This experimental study corroborated my idea that 1.5% and 2% hyperbaric lidocaine is safe to be used in epidural anesthesia 2 and that it cannot be removed from the anesthesiologists' arsenal. Surgery has evolved; therefore, anesthesiology cannot afford the luxury of not having an anesthetic for short duration procedures, such as surgery for urinary incontinence, cystoscopy, curettage, anorectal procedures, and others.
An epidemiological study identified several risk factors for the development of transient neurological symptoms (TNS) with lidocaine, such as: outpatient surgery, obesity, and lithotomy position 3. Thirty patients, physical status ASA I and II, were randomized assigned to undergo subarachnoid anesthesia with 30 mg of 1.5% or 2% hyperbaric lidocaine, using a 27G Quicke tip needle, as outpatients, in the lithotomy position. Patients were evaluated regarding sensitive block, motor block, duration of the anesthesia, and the development of TNS 24, 48, and 72 hours after the procedure. There were no differences among latency, cephalic spread of the anesthetic, degree of motor anesthesia, and length of the surgical procedure, but the duration with the higher concentration of lidocaine (2%) was longer. There were no cases of TNS or permanent neurologic deficits.
Lidocaine is one of the most versatile anesthetics, being used for infiltration, peripheral nerve blocks, epidural anesthesia, and local anesthesia. Intravenous lidocaine is used as antiarrhythmic, analgesic, and cough suppressant. It is potent, with a fast onset of action, and moderate duration. Lidocaine was first used in subarachnoid anesthesia in 1948, at the 2% concentration with glucose, providing adequate anesthesia for cystoscopy and perineal surgical procedures 4. In 1954, the laboratory Astra introduced 5% hyperbaric lidocaine for subarachnoid anesthesia, which gained worldwide acceptance.
In 1991, four cases of cauda equina syndrome associated with 5% lidocaine, microcatheter, 1% tetracaine and epidural catheter were reported 5. Notice that the doses used extrapolate those normally used in clinical practice. In 1993, the first cases of TNS after subarachnoid anesthesia with 5% lidocaine were reported 6. Even though several studies reported the presence of TNS, its etiology has not been defined yet. Laboratory data indicate the neurotoxic potential of lidocaine 7, and this neurotoxicity is concentration-dependent 2,8. Several studies showed that the incidence of TNS does not decrease with 2%, 1%, or 0.5% concentrations 9-11, but that the limit of the total dose may be benefic 12. The incidence of TNS after low doses of lidocaine (20 mg) associated with fentanyl (25 mg) was significantly lower than with the conventional dose (50 mg) 12. Another study using 3% lidocaine with doses between 30 and 45 mg for anorectal surgeries confirmed the low incidence of those problems 13.
I have used 1.5% and 2% lidocaine with glucose 8% in since 1998 2. It was demonstrated, comparing 4 mL of 1.5% hyperbaric lidocaine (60 mg) with the same volume of 2% hyperbaric lidocaine (80 mg), that the spread and duration of the subarachnoid anesthesia depended more on the dose than on the concentration of the local anesthetic, and there were no cases of TNS or permanent neurologic deficits 2.
In this study, with only 30 patients, there were no cases of TNS with low doses of both concentrations of hyperbaric lidocaine with the patient in the lithotomy position and as an outpatient. It is necessary to perform randomized, double blind studies so we can use hyperbaric lidocaine with the same safety and peace of mind that we had in the past.
Luiz Eduardo Imbelloni, TSA, M.D.
Av. Epitácio Pessoa, 2356/203
22.411-070 Rio de Janeiro, RJ
01. Pires SRO, Ganem EM, Marques M et al. Efeitos de concentrações crescentes de lidocaína hiperbárica, administradas no espaço subaracnóideo, sobre a medula espinhal e as meninges. Estudo experimental em cães. Rev Bras Anestesiol, 2006;56:253-262.
02. Imbelloni LE, Carneiro ANG Estudo comparativo entre lidocaína a 1,5% e a 2% com glicose para raquianestesia. Rev Bras Anestesiol, 1999;49:9-13.
03. Freedman JM, Li DK, Drasner K et al. Transient neurologic symptoms after spinal anesthesia: an epidemiologic study of 1,863 patients. Anesthesiology 1998;89:633-641.
04. Gordh T Xylocaine. A new local analgesia. Anaesthesia, 1949;4:4.
05. Rigler ML, Drasner K, Krejcie TC et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg, 1991;72:275-281.
06. Schneider M, Ettlin T, Kaufmann M et al. Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 55 lidocaine. Anesth Analg, 1993;76:1154-1157.
07. Drasner K, Sakura S, Chan V et al. Persistent sacral sensory deficit induced by intrathecal local anesthetic infusion in the rat. Anesthesiology, 1994;80:847-852.
08. Bainton C, Strichartz G Concentration dependence of lidocaine-induced irreversible conduction loss in frog nerve. Anesthesiology, 1994;81:657-667.
09. Pollock JE, Neal JM, Stephenson CA et al. Prospective study of the incidence of transient radicular irritation in patients undergoing spinal anesthesia. Anesthesiology, 1996;84:1361-1367.
10. Pollock JE, Liu SS, Neal JM et al. Dilution of spinal lidocaine does not alter the incidence of transient neurologic symptoms. Anesthesiology, 1999;90:445-450.
11. Tong D, Wong J, Chung F et al. Prospective study on incidence and functional impact of transient neurologic symptoms associated with 1% versus 5% hyperbaric lidocaine in short urologic procedures. Anesthesiology, 2003;98:485-494.
12. Ben-David B, Maryanovsky M, Gurevitch A et al. A comparison of minidose lidocaine-fentanyl and conventional-dose lidocaine spinal anesthesia. Anesth Analg, 2000;91:865-870.
13. Morisaki H, Masuda J, Kaneko S et al. Transient neurologic syndrome in one thousand forty-five patients after 3% lidocaine spinal anesthesia. Anesth Analg, 1998;86:1023-1026.
Regarding Dr. Imbelloni's observations, I would like to emphasize that:
- In this experimental model in dogs, 5% hyperbaric lidocaine did not cause nervous tissue injury because the local anesthetic was administered rapidly, in 10 seconds 1, which favored its spread in the CSF. However, in another study with the same experimental model in which 5% hyperbaric lidocaine was introduced slowly in the subarachnoid space of dogs (60 seconds) to hinder its spread in the CSF, 25% of the animals sustained nervous tissue injury 2;
- It is well established that 5% hyperbaric lidocaine should not be used in situations that favor its accumulation or hinders its spread because it can trigger cauda equina syndrome, as described after the slow 5 subarachnoid administration of this drug with a microcatheter 3,4 and pencil-point needles 5,6;
- The possible etiologic factors capable of triggering neurotoxicity (high doses and concentration of the local anesthetic) are not the same that cause the transient neurologic symptoms (TNS). The evaluation of the conduction of nerve impulses shows that it is irreversibly changed when there is neurotoxicity 7 and that it is normal in patients with TNS 8. It is believed that TNS is associated with lidocaine because this drug causes severe neuromuscular block, allowing for musculoskeletal stretching when the patient is in the lithotomy position, therefore causing the clinical picture of TNS 9,10.
Eliana Marisa Ganem, TSA, M.D.
Anesthesiology Department of FMB de Botucatu
01. Pires SRO, Ganem EM, marques M et al Efeitos de concentrações crescentes de lidocaína hiperbárica, administradas no espaço subaracnóideo, sobre a medula espinhal e as meninges. Estudo experimental em cães. Rev Bras Anestesiol, 2006;56:253-262.
02. Silva DM, Ganem EM, Marques M Lidocaína hiperbárica a 5% administrada pela via subaracnóidea com agulha de Quincke em diferentes velocidades de injeção. Efeitos sobre a medula e meninges. Rev Bras Anestesiol, 2004;54:(Suppl):249A.
03. Rigler ML, Drasner K, Krejcie TC et al Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg, 1991;72:275-281.
04. Schell RM, Brauer FS, Cole DJ et al Persistent sacral nerve root deficits after continuous spinal anaesthesia. Can J Anaesth, 1991;38:908-911.
05. Beardsley D, Holman S, Gantt R et al Transient neurologic deficit after spinal anesthesia: local anesthetic mal distribution with pencil point needles? Anesth Analg, 1995;81:314-320.
06. Gerancher JC Cauda equina syndrome following a single spinal administration of 5% hyperbaric lidocaine through a 25-gauge Whitacre needle. Anesthesiology, 1997;87:687-689.
07. Vianna PT, Resende LA, Ganem EM et al Cauda equina syndrome after spinal tetracaine: electromyografic evaluation 20 years follow-up. Anesthesiology, 2001;95:1290-1291.
08. Pollock JE, Burkhead D, Neal JM et al Spinal nerve function in five volunteers experiencing transient neurologic symptoms after lidocaine subarachnoid anesthesia. Anesth Analg, 2000;90:658-665.
09. Hampl KF, Heinzmann-Wiedmer S, Luginbuehl I et al Transient neurological symptoms after spinal anesthesia: a lower incidence with prilocaine and bupivacaine than with lidocaine. Anesthesiology, 1998;88:529-633.
10. Pollock LE, de Jong RH Hyperbaric lidocaine for spinal anesthesia? Am J Anesthesiol, 1997;24:161-165.