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Print version ISSN 0034-7094
Rev. Bras. Anestesiol. vol.54 no.1 Campinas Jan./Feb. 2004
Transient neurological symptoms after spinal anesthesia*
Síntomas neurológicos transitorios después de raquianestesia
Pedro Paulo Tanaka, TSA, M.D.I; Maria Aparecida Almeida Tanaka, M.D.II
IProfessor Adjunto da Disciplina de
Anestesiologia da Universidade Federal do Paraná. Co-responsável
CET do Hospital de Clínicas da UFPr
IIAnestesiologista do Hospital de Clínicas da UFPr
BACKGROUND AND OBJECTIVES: Transient neurological
symptoms have been described in patients submitted to spinal anesthesia without
other complications, after total spinal block recovery. This study aimed at
reviewing this subject.
CONTENTS: Transient neurological symptoms history, incidence, possible etiologies, risk factors and treatment are presented.
CONCLUSIONS: Spinal anesthesia is a very safe procedure with a low incidence of these symptoms, not justifying abandoning the technique as well as lidocaine.
Key Words: ANESTHETICS, Local: lidocaine; ANESTHETIC TECHNIQUES; Regional: spinal block; COMPLICATIONS: transient neurologic symptoms
JUSTIFICATIVA Y OBJETIVOS: Los síntomas
neurológicos transitorios han sido descritos en pacientes sometidos a
raquianestesia sin más complicaciones, después de la completa
recuperación del bloqueo espinal. Este estudio tiene por objetivo presentar
una revisión sobre el asunto.
CONTENIDO: Son presentados la historia, incidencia, posibles etiologías, factores de riesgo y tratamiento de los síntomas neurológicos transitorios.
CONCLUSIONES: La raquianestesia es bastante segura y la incidencia de estos síntomas es relativamente baja, no justificando el abandono de la técnica anestésica, bien como el uso de la lidocaína.
Recent publications 1,2 have brought to light some questions about spinal lidocaine. Although this anesthetic technique is already 100 years old 3, and notwithstanding its safety and quality, some complications have been reported 4, among them transient neurological symptoms 5, characterized by post-anesthetic lower limb pain or dysesthesia and tingling. This study aimed at describing major transient neurological symptoms.
Post spinal anesthesia neurological complications are major anesthesiologists' concerns; so much so that, in the past, the safety of the technique has been object of several studies. In Brazil, in the early 1960s, Fortuna 6 has published his experience with 1259 patients submitted to spinal anesthesia, where more than 50% of patients received lidocaine as local anesthetic agent. Phillips et al. 7 have evaluated more than 9000 patients receiving lidocaine during spinal anesthesia. Out of them, 284 have referred low back pain and 8 patients had neurological symptoms (e.g.: abducent nerve paresis), resolved before hospital discharge. Both articles have concluded that lidocaine was a safe anesthetic drug.
At one edge of complications one may highlight cauda equina syndrome (CES), characterized by limited injury evidenced by lumbar arachnoiditis starting in the immediate postoperative period. Symptoms are in general below L2 with perineal analgesia, followed by vesical and rectal dysfunction. Some reports 8,9 have related microcatheters and lidocaine to this neurological injury. The combination of poor local anesthetic distribution and high doses would result in neurological damage. Continuous spinal anesthesia had its advocates also in Brazil. Cunto et al. 10 have evaluated 56 patients with epidural catheters submitted to different surgical procedures. More recently, a new catheter has been described for the technique 11. There has been a case report 12 of cauda equina syndrome, where the patient was submitted to two spinal punctures with 15 mg bupivacaine in the first puncture followed by 100 mg lidocaine. Patient evolved to perineal hypoesthesia followed by vesical retention and anal incontinence which were resolved within 6 months.
Schneider et al. 13, in 1993, have reported 4 cases of patients submitted to spinal anesthesia who presented pain and tingling in breeches and lower extremities. These symptoms were initially called transient radicular irritation. This term was further changed to transient neurological symptoms (TNS) for better reflecting symptoms and the lack of permanent etiology. So, the scientific community started studying the subject and at least 30 randomized studies comparing the most different local anesthetics and the incidence of TNS were published 14-16. Mean incidence is 16.9% for lidocaine and 1.1% for bupivacaine. In Brazil, Palmieri et al. 17 have evaluated C-section patients and found 7.6% TNS in the lidocaine group.
In an attempt to explain the origin of TNS and its variable incidence, some factors were listed, among them: local anesthetics (lidocaine); early ambulation; toxicity; neural ischemia; trauma lesion; abnormal distribution; concentration.
LOCAL ANESTHETICS AND EARLY AMBULATION
In an epidemiological study published by Freedman et al. 18, who have evaluated more than 1800 patients, a higher TNS incidence was observed in patients submitted to outpatient procedures. There has been significant association between lidocaine and early ambulation, and TNS. The hypothesis was that it would be a radicular irritation caused by the blood going down the spinal canal and suffering hemolysis, promoting nervous roots irritation. A different study 19, involving inguinal herniorrhaphy patients, has observed that early ambulation does not interfere with TNS. In this study, patients were divided in two groups receiving 100 mg lidocaine. One group was allowed to walk 5 hours after surgery and the other has remained at rest for at least 12 hours.
TOXICITY AND NEURAL ISCHEMIA
Lab tests have proven local anesthetics neurological effects. High lidocaine concentrations (32%) have promoted neurological injuries in rabbits 20. However, a recent study 21 has observed axonal degeneration with lower lidocaine concentrations. Some aspects were unfolded by Eisenach et al. 22, suggesting that 300 thousand patients would be necessary to clinically observe this phenomenon. Researchers have increased local anesthetic dose or exposure time to be able to observe the phenomenon.
Pollack et al. 23 have evaluated 12 healthy volunteers previously submitted to electromyography, conduction and somatosensory evoked potential studies. Patients were submitted to spinal anesthesia with 50 mg lidocaine. TNS was observed in 5 volunteers who had no postoperative electrophysiologic studies changes. It has been recently shown 24 that lidocaine had neurological effects in a human model established to study drug-induced neuronal apoptosis. Results were consistent with clinical lidocaine neurotoxic effects. These effects may be produced by more than one mechanism.
Some investigators have looked for lidocaine alternatives. Although with some methodological problems, Martinz-Bourio et al. 25 have not shown significant clinical differences between patients receiving spinal lidocaine or prilocaine. Other authors 26 however have shown a higher incidence of TNS in the lidocaine group as compared to prilocaine, in patients in lythotomy position. It has been suggested that lumbar and sacral nervous roots stretching would decrease blood flow, favoring lidocaine's toxic action. In a study with rats 27, Japanese investigators considering the equivalence of lidocaine and prilocaine potencies, have suggested that both local anesthetics have similar therapeutic indices in terms of neurological damage.
In the search for TNS etiology, a report 28 has suggested that the combination of lidocaine, surgical position and legs manipulation during surgery could have a major effect on its genesis.
Another hypothesis would be direct nervous roots injury. Two French studies 29,30 involving more than 80 thousand patients have reported 24 TNS or Cauda Equina Syndrome cases, however paresthesia was described in 3 patients only who remained with neurological sequela for at least 6 months. They have shown that paresthesia during puncture is not a significant factor for TNS.
A different proposed etiology was abnormal local anesthetic distribution. As a consequence, an anesthetic-like solution spread was studied 31 in an in vitro model of the spine. Different types of needles, injection rate and bevel orientation (caudal or cephalad) were used. It has been shown that in slow injections with Whitacre needles (25G or 27G) in the caudal direction there has been abnormal distribution with approximately 2% concentration in simulations with lidocaine. The same was not reported with Quincke needles. In an epidemiological study, Freeman et al. 18 have reported that bevel orientation and needle type were not related to TNS.
Another object of research was lidocaine concentration. In a report 32 where fixed spinal 1 mg.kg-1 lidocaine doses were used, the incidence of TNS was similar for 2% and 5% solutions. A proposed alternative was to decrease local anesthetic concentration. Faced to this fact, a group of investigators 33 has used up to 0.5% concentrations (fixed 50 mg doses), but was unable to decrease the incidence of TNS.
TNS is characterized by breeches or legs pain or damping after spinal block recovery. Most often pain is moderate and lasts 2 to 3 days. One should have in mind the differential diagnoses. Among them, one may highlight cauda equina syndrome, abscess or even spinal hematoma. Lower limbs muscle weakness should raise the suspicion of some medullary compression process, being recommended an immediate MRI evaluation. The characteristics of each one are well described and established in a review article 34.
Prevention is the best management, through careful patients selection, preventing risk situations. Therapy with anti-inflammatory and myorelaxant drugs is indicated for patients with muscle spasm. Opioids are of moderate efficacy for these situations. Symptomatic therapy with local heat may be applied for symptoms relief.
Neurological symptoms are associated to several factors and the abandonment of spinal lidocaine should not by all means be recommended.
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Dr. Pedro Paulo Tanaka
Address: Rua Justiniano de Mello e Silva, 355
ZIP: 82350-150 City: Curitiba, Brazil
Submitted for publication March 12, 2003
Accepted for publication May 14, 2003
* Received from CET/SBA do Hospital de Clínicas da Universidade Federal do Paraná, PR