An inadvertent subarachnoid injection reversed by cerebrospinal fluid lavage for the treatment of chronic low back pain: A case report.

RATIONALE: We present a case of high spinal anesthesia after inadvertent injection of local anesthetics and corticosteroids into the subarachnoid space during attempted epidural injection. Cerebrospinal fluid (CSF) lavage is a suitable method for treatment. PATIENT CONCERNS: A 45-year-old woman presented with posterior thigh, leg, and ankle pain for >6 months and was treated with epidural injection. Five minutes after the third time of epidural injection, the patient complained loss of sensation and muscle strength in the lower extremities and abdominal area. DIAGNOSES: A high spinal anesthesia was confirmed by the patient loss of sensation and muscle strength in the lower extremities and abdominal area. INTERVENTIONS: CSF lavage was performed for treatment. OUTCOMES: After CSF lavage, the patient gradually returns to normal sensory and motor functions of lower limbs. On the fourth day, the patient sensed her physical function restoring gradually and was discharged uneventfully. At 4-month follow-up, the patient could have normal activities without obvious subsequent complications and any pain. LESSONS: We conclude that CSF lavage could be a helpful maneuver to clear lidocaine and betamethasone and avoid potential nerve damage caused by an unintentional intrathecal injection during an epidural injection for the treatment of chronic low back pain.

Lidocaine concentration in cerebrospinal fluid after epidural administration: a comparison between epidural and combined spinal-epidural anesthesia.

BACKGROUND: In this study, lidocaine concentrations in cerebrospinal fluid (CSF) at different interspaces were measured with or without preceding spinal anesthesia, 10 min after epidural injection of lidocaine, to investigate the effects of preceding meningeal puncture on CSF concentrations of epidurally administered local anesthetic. METHODS: Sixty patients scheduled to receive combined spinal-epidural anesthesia were randomly allocated to receive either spinal anesthesia first (group CSEA) or epidural lidocaine first (group Epi). Each group was divided into three subgroups in which the site of epidural cannulation and spinal tap were separated by one, three, or five interspaces (sets I, II, and III, respectively). CSF was collected from the L4-L5 interspace 10 min after 10 ml lidocaine, 1%, was administered epidurally. In group Epi, CSF was collected after epidural administration of lidocaine and before spinal anesthesia. In group CSEA, spinal anesthesia was performed at the L3-L4 interspace after epidural cannulation and epidural lidocaine was administered postoperatively, after which CSF was sampled. RESULTS: Lidocaine concentrations in CSF were significantly higher with increasing proximity of epidural injection site to CSF collection site in both groups. There were no significant differences in CSF lidocaine concentrations between group CSEA and group Epi in set I, although lidocaine concentrations were significantly higher in group CSEA set II and III patients. CONCLUSION: Lidocaine concentration in CSF was similar with or without preceding meningeal puncture beneath the epidural administration site.

The relationship between the efficacy of epidural anesthesia and the concentration of lidocaine in cerebrospinal fluid.

BACKGROUND: Addition of bicarbonate to local anesthetics improves the efficacy of epidural anesthesia. We evaluated whether the addition of bicarbonate to lidocaine enhanced pain threshold in cesarean section. We speculated that bicarbonate would increase the concentration of lidocaine in cerebrospinal fluid (CSF). To examine this possibility, we evaluated the relationship between the lidocaine concentration in the CSF and the pain threshold. MATERIAL/METHODS: Twenty eight full-term parturients undergoing cesarean section under epidural anesthesia at L2-3 were divided into two groups: the first group (lidocaine group) received 17 mL of 2% lidocaine-epinephrine (1:200,000) and the second group (lidocaine-bicarbonate group) received the same concentration of lidocaine-epinephrine supplemented bicarbonate. Twenty min after administration of local anesthetics, we collected 1 mL samples of the CSF. The pain threshold after the repeated electrical stimulation was used to assess sensory blockade at the L2, S1, and S3 dermatomes. RESULTS: Demographic data were comparable between the groups. There were no differences in the pain threshold at all dermatomes and the lidocaine concentration between the groups. There was a significant correlation between the pain threshold and the lidocaine concentration at the combined S1 and S3 dermatomes in the lidocaine-bicarbonate group. CONCLUSIONS: We find neither bicarbonate caused a significant difference in the efficacy of epidural anesthesia nor it caused an increase of lidocaine concentration in the CSF. The result that we found a significant correlation between the lidocaine concentration in the CSF and the pain threshold at the sacral region in the lidocaine bicarbonate group suggests that, bicarbonate enhances the efficacy of anesthesia at outside of spinal canal.

Simultaneous determination of nikethamide and lidocaine in human blood and cerebrospinal fluid by high performance liquid chromatography.

Nikethamide and lidocaine are often requested to be quantified simultaneously in forensic toxicological analysis. A simple reversed-phase high performance liquid chromatography (RP-HPLC) method has been developed for their simultaneous determination in human blood and cerebrospinal fluid. The method involves simple protein precipitation sample treatment followed by quantification of analytes using HPLC at 263 nm. Analytes were separated on a 5 microm Zorbax Dikema C18 column (150 mm x 4.60 mm, i.d.) with a mobile phase of 22:78 (v/v) mixture of methanol and a diethylamine-acetic acid buffer, pH 4.0. The mean recoveries were between 69.8 and 94.4% for nikethamide and between 78.9 and 97.2% for lidocaine. Limits of detection (LODs) for nikethamide and lidocaine were 0.008 and 0.16 microg/ml in plasma and 0.007 and 0.14 microg/ml in cerebrospinal fluid, respectively. The mean intra-assay and inter-assay coefficients of variation (CVs) for both analytes were less than 9.2 and 10.8%, respectively. The developed method was applied to blood sample analyses in eight forensic cases, where blood concentrations of lidocaine ranged from 0.68 to 34.4 microg/ml and nikethamide ranged from 1.25 to 106.8 microg/ml. In six cases cerebrospinal fluid analysis was requested. The values ranged from 20.3 to 185.6 microg/ml of lidocaine and 8.0 to 72.4 microg/ml of nikethamide. The method is simple and sensitive enough to be used in toxicological analysis for simultaneous determination of nikethamide and lidocaine in blood and cerebrospinal fluid.

[The study on identification of lidocaine in blood and CSF by GC/MS].

OBJECTIVE: To establish a rapid and simple gas chromatographic-mass spectric method for qualitative and quantitative analysis of lidocaine in blood and cerebrospinal fluid(CSF). METHODS: Following an acidification of HCl, blood or CSF was alkalinized with NaOH (pH=9) and extracted with ether for two times. Evaporated in a water bath and with an air velocity of nitrogen gas, extract was dissolved with ethanol and analyzed by a gas chromatographic-mass spectrum method, lidocaine was analyzed qualitatively and quantitatively by GC/MS (SIM:86, 58, 72, 87). RESULTS: Linear range of lidocaine detected in blood or CSF by this method is 1.0-60.0 microg x mL(-1) (r=0.9999), the minimum detected concentration of lidocaine was 0.02 microg x mL(-1) (S/N=3), recovery is at 85%-103%. This method was used in the determination of lidocaine in dog model died of the anesthesia with lidocaine. CONCLUSION: This study provided a gas chromatographic-mass spectric analysis for lidocaine in blood and CSF. This method was more selective, little interferefering, more sensitivities and simpler. It could be used in the detection of lidocaine in biological fluids.

The study on identification of lidocaine in blood and CSF by GC/MS / 法医学杂志

OBJECTIVE@#To establish a rapid and simple gas chromatographic-mass spectric method for qualitative and quantitative analysis of lidocaine in blood and cerebrospinal fluid(CSF).@*METHODS@#Following an acidification of HCl, blood or CSF was alkalinized with NaOH (pH=9) and extracted with ether for two times. Evaporated in a water bath and with an air velocity of nitrogen gas, extract was dissolved with ethanol and analyzed by a gas chromatographic-mass spectrum method, lidocaine was analyzed qualitatively and quantitatively by GC/MS (SIM:86, 58, 72, 87).@*RESULTS@#Linear range of lidocaine detected in blood or CSF by this method is 1.0-60.0 microg x mL(-1) (r=0.9999), the minimum detected concentration of lidocaine was 0.02 microg x mL(-1) (S/N=3), recovery is at 85%-103%. This method was used in the determination of lidocaine in dog model died of the anesthesia with lidocaine.@*CONCLUSION@#This study provided a gas chromatographic-mass spectric analysis for lidocaine in blood and CSF. This method was more selective, little interferefering, more sensitivities and simpler. It could be used in the detection of lidocaine in biological fluids.

Spinal biopharmaceutics of bupivacaine and lidocaine by microdialysis after their simultaneous administration in rabbits.

The aim of the present study was to determine the intrathecal bioavailability of a mixture of lidocaine and bupivacaine in a rabbit model of spinal anesthesia by using the microdialysis technique. Catheter and microdialysis probe were inserted under control of the view either in the epidural or in the intrathecal space. First, the epidural disposition of the mixture of bupivacaine and lidocaine was studied after epidural administration. Then, the intrathecal and plasma dispositions of bupivacaine and lidocaine were investigated following intrathecal or epidural administration. The epidural clearance of bupivacaine was higher than that of lidocaine, suggesting a more significant uptake of bupivacaine into the systemic circulation and/or into the CSF. The intrathecal bioavailability of bupivacaine and lidocaine was 12.3 and 17.9%, respectively, while it was 5.5 and 17.7% following the separate administration of each agent [Clément, R., Malinovsky, J.M., Le Corre, P., Dollo, G., Chevanne, F., Le Verge, R., 1999. Cerebrospinal fluid bioavailability and pharmacokinetics of bupivacaine and lidocaine following intrathecal and epidural administrations in rabbits using microdialysis. J. Pharmacol. Exp. Ther. 289, 1015-21]. After intrathecal administration, a decrease in C(max) and AUC values was observed for bupivacaine in comparison with the separate administration. Moreover, after epidural administration, the systemic resorption was slower and lower, especially for bupivacaine. Such a reduction in the systemic absorption of bupivacaine might increase its intrathecal bioavailability, resulting from a vasoconstrictor effect of lidocaine reducing the systemic absorption of bupivacaine from the epidural space leading to an increase of its extent of absorption through meninges into CSF although its absorption rate was not modified.

Cerebrospinal fluid bioavailability and pharmacokinetics of bupivacaine and lidocaine after intrathecal and epidural administrations in rabbits using microdialysis.

The aim of this work was to study the cerebrospinal fluid (CSF) bioavailability and pharmacokinetics of bupivacaine (BUP) and lidocaine (LID) administered separately in rabbits using microdialysis with retrodialysis calibration. Microdialysis probe and catheters were inserted under control of the view in the intrathecal or epidural spaces. The epidural disposition of BUP and LID after epidural administration of low (0.69 microM) and high (6.9 microM) doses was studied. Then, the intrathecal and plasma dispositions after separate intrathecal (0.2 microM) and epidural administration (6.9 microM) were investigated. The CSF binding of BUP and LID was linear in a range from 50 to 500 micrograms/ml, and the mean unbound CSF fraction at a concentration of 100 micrograms/ml was 39. 3 +/- 2.3% for BUP and 75.8 +/- 7.7% for LID. Epidural and intrathecal disposition of BUP and LID showed a biexponential decline. After epidural administration, the CSF concentrations of BUP and LID were much higher than those in plasma. After intrathecal administration, the plasma concentrations were below the limit of quantitation. Although the absorption rate of BUP appeared higher than that of LID, the mean CSF bioavailability of epidural BUP and LID was 5.5 and 17.7%, respectively. The unexpectedly higher CSF bioavailability of LID, the less lipophilic drug, may result from the difference in the processes competing for drug epidural removal.

Addition of opioids alters the density and spread of intrathecal local anesthetics? An in vitro study.

PURPOSE: To determine whether the addition of opioids alters the density and spread of intrathecal local anesthetics in vitro. METHODS: In Part I, the densities of hyperbaric bupivacaine 0.75% (HB), hyperbaric lidocaine 5% (HL) and isobaric bupivacaine 0.5% (IB) with and without morphine (M), and fentanyl (F) were measured at 22 degrees C. In Part II a model was constructed utilizing a column containing a solution similar in composition to cerebrospinal fluid (CSF) at 37 degrees C. The various local anesthetic-opioid solutions, coloured with crystalline methylene blue dye, were injected at 22 degrees C into the column at a controlled rate through a spinal needle. The direction and extent of spread of the injectates were compared. RESULTS: The relative densities of the five solutions were: HB = HL > IB > M > F. The addition of fentanyl to IB reduced the density of the final solution (P < 0.05). In the model, IB alone and IB with morphine showed mainly downward spread, with the addition of fentanyl to IB resulting in upward movement (P = 0.004). The hyperbaric local anesthetics moved downward with or without opioids. CONCLUSION: The addition of fentanyl reduces the density of IB in vitro and alters its movement in simulated CSF. This may prove to be important in predicting the level of spinal block in clinical practice.

Lidocaine concentrations in plasma and cerebrospinal fluid after systemic bolus administration in humans.

UNLABELLED: Preclinical studies suggest that systemic lidocaine acts at the level of the spinal dorsal horn to inhibit hyperalgesia resulting from nerve injury, yet no clinical data are available to support this view. Therefore, we sought to characterize the time course of lidocaine in the plasma and cerebrospinal fluid (CSF) after an IV bolus injection of lidocaine 2 mg/kg in patients scheduled for surgery involving spinal anesthesia. Sixty-five patients were randomly allocated to one of five study groups (n = 13 per group) receiving IV lidocaine before CSF/ plasma sampling at 5, 10, 15, 30, or 60 min. Gas chromatographic analysis of these samples revealed a fast but transient peak (5-15 min) in lidocaine plasma levels (1.7+/-0.16 microg/mL), which declined rapidly thereafter. Only small concentrations of IV lidocaine were found in the CSF (6%- 8% of plasma concentration), but this fraction remained stable from 15 min until termination of the experiment. No statistical correlation was observed between plasma and CSF lidocaine levels. These data suggest that because of the prolonged availability of lidocaine at the spinal dorsal horn level, systemic administration of lidocaine suppresses central sensitization within the spinal cord after nerve injury in humans. IMPLICATIONS: Cerebrospinal fluid concentrations of lidocaine after its systemic bolus delivery in humans indicate that the spinal cord may be the major site of antinociceptive action by this route of drug administration.

Auditory evoked responses under total spinal anesthesia in rats.

In order to investigate the function of the auditory pathway from the cochlea to the brain stem under total spinal anesthesia, the auditory brain stem response (ABR), compound action potential of the cochlear nerve (CAP), and cochlear microphonics (CM) were simultaneously recorded in rats. Total spinal anesthesia was induced by infusion of 2% lidocaine hydrochloride at a constant rate of 0.10 mL/min into the cerebrospinal fluid through the rats' skulls. The ABR completely disappeared within 1.5 to 4 minutes. After cessation of the injection, the ABR reappeared, starting from wave I and progressing through waves II and III to wave IV. The latency change of the CAP throughout the recording period was quite similar to that of wave I of the ABR. A reduction in amplitude of the CM was observed, but the CM did not disappear during the recording period. Disappearance of the ABR was due, not to loss of cochlear function, but to anesthetic effects on the acoustic nerve and the brain stem. Monitoring of the ABR provided information on the level of neural activity in the brain stem under total spinal anesthesia.

Spinal anesthesia. Volume or concentration--what matters?

BACKGROUND AND OBJECTIVES: An investigation was made of the effects of volume and concentration of a constant dose of subarachnoid lidocaine on the extent and duration of sensory and motor anesthesia produced, as well as of the lidocaine concentration of the cerebrospinal fluid (CSF) as a function of time. METHODS: In a prospective study, 40 American Society of Anesthesiologists (ASA) status 2 or 3 patients were assigned to one of five groups, who received a 70-mg subarachnoid dose of lidocaine hydrochloride as a 0.5, 1, 2, 5, or 10% solution. Dural puncture was performed at the L3-L4 interspace with a 19.5-gauge Periquick needle (Pajunk, Germany), and a 24-gauge catheter was inserted 3-4 cm into the subarachnoid space. The patient remained in the lateral position during injection of the local anesthetic and was then turned to the supine horizontal position. The level of anesthesia and the motor block were measured at 5, 10, 15, 20, 30, 40, 50, and 60 minutes and then at 15-minute intervals until the effect of the anesthesia had ceased. Samples of CSF were collected at the same times that the pinprick and motor block measurements were made. RESULTS: Five minutes after injection, a median sensory block height of T4 or T5 was observed in all groups. The range of mean total times to complete recovery of the sensory blocks was 139-152 minutes, while that for the motor blocks of the lower extremities was 100-122 minutes. The values were similar in all groups (P > .05). The motor block was complete in all patients 10 minutes after the lidocaine injection. Five minutes after injection, the mean CSF lidocaine concentration was highest in the 10% group (P < .001 vs. the other four groups). At 15 minutes, the only statistical difference was found between the 0.5% and the 10% group (P = .026). At 20 minutes, the CSF lidocaine concentrations were similar in all groups (P > .05). CONCLUSIONS: A constant 70-mg dose of subarachnoid lidocaine produced the same pinprick level of analgesia, degree of motor block, and duration of spinal anesthesia in spite of being injected over an extremely broad range of concentrations and volumes. Despite the fact that all patients received the same dose of lidocaine, the CSF concentrations at 5, 10, and 15 minutes were different and directly related to the concentration of the solution injected. at 20 minutes, the CSF concentrations were similar in all groups. These results indicate a relatively uniform distribution of lidocaine in the CSF for all solutions tested.

Reducing the potential morbidity of an unintentional spinal anaesthetic by aspirating cerebrospinal fluid.

We describe two cases where we attempted to reduce the adverse effects of inadvertent spinal anaesthesia by aspirating local anaesthetic-contaminated cerebrospinal fluid (CSF). Analysis of this CSF for its local anaesthetic concentration revealed that we were able to recover 51% and 39% of the administered lignocaine. It is suggested that such aspiration may be a helpful additional measure to the supportive management of this complication.

Transient neurologic deficit after spinal anesthesia: local anesthetic maldistribution with pencil point needles?

Recent reports of transient neurologic deficits have raised concern about the potential toxicity of single-dose spinal 5% lidocaine in 7.5% dextrose. Two cases of volunteers who experienced minor local sensory deficits after slow (60 s) injections of 2 mL 5% lidocaine via Whitacre needles are described. One case was a result of a double injection because of a "failed" block. It seemed possible that the neurologic deficit in these cases resulted from neurotoxicity associated with maldistribution of local anesthetic. Using an in vitro spinal model, we investigated drug distribution resulting from injections through side-port spinal needles to determine whether the use of these needles could result in high local concentrations of hyperbaric solutions. A spinal canal model was fabricated using human magnetic resonance measurements. The model was placed in a surgical supine position and filled with lactated Ringer's solution to simulate the specific gravity of cerebral spinal fluid at 22 degrees C. A hyperbaric solution of phthalocyanine blue dye and dextrose (SG 1.042), simulating the anesthetic, was injected through three different needles (27-gauge 4 11/16-in. Whitacre, 25-gauge 3 1/2-in. Whitacre, 25-gauge 3 1/2-in. Quincke). Triplicate injections were done at rapid (2 mL/10 s) and slow (2 mL/60 s) rates, with needle side ports oriented in a sacral and cephalad direction. At slow rates of injection, using 27- or 25-gauge sacrally directed Whitacre needles, injections showed evidence of maldistribution with extrapolated peak sacral lidocaine concentrations reaching 2.0%. In contrast, distribution after slow injection through sacrally directed Quincke needles was uniform.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of adrenalin on the pharmacokinetics of interpleurally administered lidocaine in patients with pancreatic neoplasia.

The influence of adrenalin on the pharmacokinetics of lidocaine given interpleurally to 10 patients with pancreatic neoplasia was studied. Five patients received an interpleural dose of lidocaine (200 mg; control group), and 5 patients received an interpleural dose of lidocaine (200 mg) plus adrenalin (1:200,000). Plasma and cerebrospinal fluid (CSF) levels of lidocaine were measured before and at specified times (up to 8 hours) after the dose. The analytical technique was radioimmunoassay; and plasma and CSF data were assessed using noncompartmental analysis. The drug was quickly absorbed into the plasma in the control group (Cmax = 2.76 +/- 0.10 microgram/mL at 0.33 +/- 0.14 hours after administration); whereas drug access to CSF was decreased and occurred slowly (Cmax = 0.32 +/- 0.07 microgram/mL at 1.66 +/- 1.35 hours). The drug was eliminated more quickly from plasma than from CSF, with half-lives of 1.71 +/- 0.43 hours and 3.86 +/- 1.27 hours, respectively. The simultaneous administration of adrenalin delayed absorption (tmax = 0.91 +/- 0.52 hours). The drug elimination half-lives in plasma and CSF of this group increased to 3.22 +/- 1.22 hours and 8.71 +/- 3.28 hours, respectively. The duration of the analgesia, evaluated as the time until the patient needed another dose, increased from 8.2 +/- 1.5 hours in the control group to 9.7 +/- 1.3 hours in the group that received adrenalin. From these results the levels that would be reached on a multiple-dose regimen (D = 200 mg, tau = 8 hours) were predicted.(ABSTRACT TRUNCATED AT 250 WORDS)