Valor de la duración del intervalo QRS para predecir la toxicidad por ropivacaína. Implicaciones en la práctica de la anestesia regional en Cirugía Mayor Ambulatoria / Value of QRS interval duration to predict ropivacaine toxicity. Implications in the practice of regional anesthesia in Major Ambulatory Surgery

Objetivo: La anestesia regional es ampliamente utilizada en Cirugía Mayor Ambulatoria (CMA), asociando innumerables ventajas y un mejor control del dolor postoperatorio. La ropivacaína surgió como una alternativa menos tóxica a la bupivacaína, sin embargo, se han descrito casos de arritmias o parada cardiorrespiratoria tras su administración. Las alteraciones electrocardiográficas en la intoxicación por anestésicos locales afectan a la conducción ventricular, prolongando el intervalo QRS del ECG. Nuestro objetivo fue evaluar si la prolongación del intervalo QRS se correlaciona con niveles elevados en sangre de ropivacaína, lo que podría alertar al clínico de una intoxicación grave. Material y métodos: El estudio se realizó en 4 cerdos minipig premedicados con ketamina intramuscular (20 mg/kg) que fueron anestesiados con tiopental sódico (5 mg/kg) y sevoflurano. Tras la instrumentalización y monitorización continua del ECG se administraron 5 mg/kg de ropivacaína intravenosa. Se realizaron determinaciones analíticas y mediciones de parámetros electrocardiográficos basales y a los 5, 15 y 30 minutos. Se evaluó la correlación entre los niveles plasmáticos de ropivacaína y la duración del intervalo QRS. Análisis estadístico: test de correlación de Spearman. Significación estadística: p < 0,05. Resultados: La ropivacaína indujo un aumento significativo del intervalo QRS a los 5, 15 y 30 minutos. Los intervalos PR, QT y QTc también aumentaron. El porcentaje de aumento máximo del QRS fue de un 51 % a los 5 minutos. Se observó una correlación positiva entre la duración del intervalo QRS y los niveles de ropivacaína, r = 0,8 (p < 0,0001). Conclusión: Nuestro modelo experimental ha permitido relacionar la duración del intervalo QRS con los niveles sanguíneos de ropivacaína. Su ensanchamiento instantáneo puede ser un marcador útil para detectar casos de intoxicación sistémica por ropivacaína, muy utilizada en anestesia regional en CMA (AU)

Objective: Regional anaesthesia is widely used in ambulatory surgery (AS) and is associated with numerous benefits and a better control of postoperative pain. Ropivacaine emerged as a less toxic alternative to bupivacaine, however, cases of arrhythmias or cardiorespiratory arrest have been reported following accidental administration. Electrocardiographic alterations in local anaesthetic intoxication affect ventricular conduction by prolonging the QRS interval of the EKG. Our aim was to assess whether QRS interval prolongation correlates with elevated blood levels of ropivacaine, which could alert the clinician to the presence of severe intoxication. Material and methods: The study was performed in 4 minipig pigs premedicated with intramuscular ketamine (20 mg/kg) and anaesthetized with sodium thiopental (5 mg/kg) and sevoflurane. After instrumentation and continuous ECG monitoring, 5 mg/kg of intravenous ropivacaine was administered. Analytical blood gas samples determinations and measurements of electrocardiographic parameters were performed at baseline and at 5, 15 and 30 minutes. Correla tion between plasmatic levels of ropivacaine and QRS interval duration was assessed. Statistical analysis: Spearman correlation test. Statistical significance: p < 0.05. Results: Ropivacaine induced a significant increase in the QRS interval at 5, 15 and 30 minutes. The PR, QT and QTc intervals also increased. The percentage of maximum QRS increase was 51 % at 5 minutes. A positive correlation was observed between QRS interval duration and ropivacaine levels, correlation coefficient r = 0.8 (p < 0.0001). Conclusion: our experimental model has allowed us to relate QRS interval duration to ropivacaine blood levels. Its instantaneous widening could be a useful marker to detect cases of systemic intoxication by ropivacaine, widely used in regional anesthesia in AS (AU)

Bupivacaine Toxicity Increases Transmural Dispersion of Repolarization, Developing of a Brugada-like Pattern and Ventricular Arrhythmias, Which is Reversed by Lipid Emulsion Administration. Study in an Experimental Porcine Model.

Unintentional administration of bupivacaine may be associated with electrocardiogram changes that promote the development cardiac arrhythmias. Ventricular repolarization markers (corrected QT, QT dispersion, Tpeak-Tend and Tpeak-Tend dispersion) are useful to predict cardiac arrhythmias. We aim to investigate the effects of bupivacaine on the transmural dispersion of repolarization and their reversion following intravenous lipid emulsion (ILE) administration. Fourteen pigs were anaesthetized with thiopental and sevoflurane and underwent tracheal intubation. After instrumentation, a 4 mg kg-bolus of bupivacaine was administrated followed by an infusion of 100 µg kg-1 min-1. QT interval, QTc:QT corrected by heart rate, Tpeak-to-Tend interval and QT and Tpeak-to-Tend dispersion were determined in a sequential fashion: after bupivacaine (at 1 min, 5 min and 10 min) and after ILE (1.5 mL kg-1 over 1 min followed by an infusion of 0.25 mL kg-1 min-1). Three additional animals received only ILE (control group). Bupivacaine significantly prolonged QT interval (∆:36%), QT dispersion (∆:68%), Tpeak-to-Tend (∆:163%) and Tpeak-to-Tend dispersion (∆:98%), from baseline to 10 min. Dispersion of repolarization was related to lethal arrhythmias [three events, including asystole, sustained ventricular tachycardia (VT)] and repeated non-sustained VT (4/14, 28%). A Brugada-like-ECG pattern was visualized at V1-4 leads in 5/14 pigs (35%). ILE significantly decreased the alterations induced by bupivacaine, with the termination of VT within 10 min. No ECG changes were observed in control group. Bupivacaine toxicity is associated with an increase of transmural dispersion of repolarization, the occurrence of a Brugada-like pattern and malignant VA. ILE reverses the changes in dispersion of repolarization, favouring the disappearance of the Brugada-like pattern and VT.

Desarrollo de un modelo experimental para el estudio de la toxicidad cardiaca inducida por bupivacaína, implicaciones para la anestesia en Cirugía Ambulatoria / Development of an experimental model for the study of bupivacaine induced cardiotoxicity, implications for anesthesia in Ambulatory Surger

Objetivo: Recientemente existe un renovado interés por las técnicas locorregionales, asistiendo a una gran demanda tanto por los pacientes como por los equipos quirúrgicos, especialmente en la cirugía ambulatoria. La descripción de casos clínicos graves asociados a intoxicación por bupivacaína es un evento infrecuente, sin embargo, para mejorar nuestro conocimiento y prevenir la toxicidad de los anestésicos locales es necesario el desarrollo de modelos animales. Los efectos adversos cursan con alteraciones electrocardiográficas relacionadas especialmente con la conducción ventricular y con prolongación del intervalo QRS. Poder detectar una intoxicación grave por anestésicos locales antes de que ocurra un colapso cardiovascular tendría importantes consideraciones clínicas. Nuestro objetivo fue desarrollar un modelo no letal de intoxicación aguda por bupivacaína y correlacionar los niveles del fármaco con el complejo QRS como marcador instantáneo de una intoxicación grave por anestésicos locales. Material y métodos: Se estudiaron 8 cerdos large-White premedicados con ketamina, 20 mg/kg, y anestesiados con tiopental sódico (19 ± 8 mg/kg-1) como inductor y sevoflurano 1 CAM (2,6 %) para el mantenimiento anestésico. Se canalizaron la arteria y vena femoral para la monitorización invasiva, determinaciones analíticas y de niveles de bupivacaína. Al finalizar la instrumentalización, se administró bupivacaína en dosis de 4 mg/kg-1. Se realizaron determinaciones analíticas antes y al 1, 5, 10 y 30 minutos de administración del fármaco. Se evaluó la correlación entre los niveles de bupivacaína en sangre y el intervalo QRS. Se consideró significativo una p < 0,05. Análisis estadístico: Test de correlación de Spearman. Resultados: Ningún animal falleció como resultado de la experiencia. El porcentaje medio de aumento del QRS fue de 185 ± 60 ms. Hubo una correlación estadísticamente significativa entre la duración del intervalo QRS y los niveles plasmáticos de bupivacaína, coeficiente de correlación de Spearman: 0,80; p < 0,0001. Conclusión: Nuestro modelo ha permitido el estudio de uno de los aspectos más relevantes de toxicidad de la bupivacaína. El ensanchamiento del intervalo QRS se ha relacionado positivamente con los niveles de bupivacaína. La modificación instantánea de este parámetro puede ser un marcador clínico instantáneo de gran utilidad en la práctica clínica diaria

Objective: Recently there has been an extraordinary advance in the techniques of regional anaesthesia, assisting to a great demand from the patients and the surgical team especially in day surgery. Reports of serious cardiac bupivacaine intoxication are fortunately unusual, however in order to improve our knowledge and prevention of local anaesthetic toxicity the development of animal models is needed. The adverse event comes along with important electrocardiographic alterations, especially those related to ventricular conduction such as the QRS interval widening. Detecting a severe intoxication with local anaesthetic before a cardiovascular collapse takes place involves important clinical considerations. We aimed to develop a non-lethal steady model of bupivacaine intoxication and correlate bupivacaine plasma levels with the QRS complex duration as an instantaneous marker of severe local anaesthetic intoxication. Material and methods: Eight mini-pigs were premedicated with ketamine and anesthetized with intravenous sodium thiopental 5 mg/kg. The anesthetic maintenance was performed with sevoflurane 1 CAM (2.6 %). Femoral artery and vein were canalized for invasive monitoring, analytical blood gas samples and bupivacaine levels determinations. After instrumentation and motorization, a bupivacaine bolus of 4 mg/kg-1 was administered. Electrocardiographic parameters were recorded and blood samples were taken before and 1, 5, 10 and 30 min after the drug administration. We correlated venous plasma concentration with the QRS widening observed. Statistical: Spearman rank correlation coefficient. A P-value < 0.05 was considered statistically significant. Results: No animal died as a result of the experience and hemodynamic data and blood gas analysis were maintained at physiological range. The mean maximal percent increase in QRS interval was 185 ± 60 ms. There was a statistically significant positive correlation between the QRS interval and bupivacaine plasmatic levels. (Correlation coefficient of r = 0,80 (p < 0,0001). Conclusions: This porcine model of bupivacaine intoxication has been steady, obtaining important electrocardiographic modifications and keeping alive all animals. The relevant QRS interval widening was positively correlated with bupivacaine plasmatic levels. The instantaneous modification of this electrocardiographic parameter could be a useful clinical marker of serious bupivacaine intoxication in a daily basis

Análisis de la regresión temporal en el ensanchamiento del intervalo QRS inducido por bupivacaína con la administración de Intralipid. Estudio en un modelo experimental porcino / Analysis of the temporal regression of the QRS widening induced by bupivacaine after Intralipid administration. Study in an experimental porcine model

Objetivo: La toxicidad cardiaca inducida por la bupivacaína (B) se relaciona con el bloqueo de los canales de sodio, que se traduce por un ensanchamiento del intervalo QRS. Estudios experimentales recientes, sugieren que el Intralipid (IL) es eficaz en revertir la toxicidad cardiaca de la B. Nuestro objetivo fue analizar la evolución temporal del ensanchamiento del QRS inducido por la B con la administración de IL. Material y método: Doce cerdos fueron anestesiados con tiopental sódico, 5 mg kg−1, y sevoflurano a concentración alveolar mínima de 2,6%. Tras la instrumentalización se administró un bolo de B de 4-6 mg kg−1 con el objetivo de inducir un aumento de 150% en la duración del QRS. El grupo IL recibió 1,5 mL kg−1 de IL seguido de 0,25 mL kg min−1; el grupo control (C) recibió salino. Se registraron los parámetros electrocardiográficos tras la infusión de B y a 1, 5,10 y 30 min de la administración de Intralipid/salino. Resultados: La administración de B (4,33°æ 0,81 mg/kg en el grupo IL y 4,66°æ 1,15 mg/kg en el grupo C) indujo cambios electrocardiográficos similares en ambos grupos; el porcentaje medio de incremento máximo en el QRS fue de 184°æ 62% en el grupo IL, y de 230°æ 56% en el grupo C. El IL revirtió el ensanchamiento del QRS inducido por la B, a los 10 min de su administración el intervalo QRS disminuyó 132°æ 56% vs. 15°æ 76%, en relación al máximo incremento inducido por la B, en el grupo IL y grupo C respectivamente. Conclusión: El IL revirtió eficazmente el ensanchamiento del intervalo QRS inducido por la B. El tiempo hasta la normalización de los parámetros electrocardiográficos puede prolongarse más de 10 min. Mientras persistan los fenómenos de toxicidad cardíaca, las medidas de resucitación y monitorización deben continuarse hasta que los parámetros de conducción cardíaca se hayan restaurado de forma adecuada (AU)

Objective: The principal mechanism of cardiac toxicity of bupivacaine relates to the blockade of myocardial sodium channels, which leads to an increase in the QRS duration. Recently, experimental studies suggest that lipid emulsion is effective in reversing bupivacaine cardiac toxicity. We aimed to evaluate the temporal evolution of the QRS widening induced by bupivacaine with the administration of Intralipid. Material and methods: Twelve pigs were anesthetized with intravenous sodium thiopental 5 mg kg−1 and sevoflurane 1 MAC (2.6%). Femoral artery and vein were canalized for invasive monitoring, analysis of blood gases and determination of bupivacaine levels. After instrumentation and monitoring, a bupivacaine bolus of 4-6 mg kg−1 was administered in order to induce a 150% increase in QRS duration (defined as the toxic point). The pigs were randomized into two groups of six individuals. Intralipid group (IL) received 1.5 mL kg−1of IL over one minute, followed by an infusion of 0.25 mL kg min−1. Control group (C) received the same volume of a saline solution. The electrocardiographic parameters were recorded, and blood samples were taken after bupivacaine and 1, 5, 10 and 30 minutes after Intralipid/saline administration. Results: Bupivacaine (4.33°æ 0.81 mg/kg in IL group and 4.66°æ 1.15 mg/kg in C group) induced similar electrocardiographic changes in both groups; mean maximal percent increase in QRS interval was 184°æ 62% in IL group, and 230°æ 56% in control group (NS). Lipid administration reversed the QRS widening previously impaired by bupivacaine. After ten minutes of the administration of IL, the mean QRS interval decreased to 132°æ 56% vs. 15°æ 76% relative to the maximum widening induced by bupivacaine, in IL and C group, respectively. Conclusion: Intralipid reversed the lengthening of QRS interval induced by the injection of bupivacaine. Time to normalization of electrocardiographic parameters can last more than 10 minutes. While the phenomena of cardiac toxicity persist, resuscitation measures and adequate monitoring should be continued until adequate heart conduction parameters are restored (AU)

Analysis of the temporal regression of the QRS widening induced by bupivacaine after Intralipid administration. Study in an experimental porcine model.

OBJECTIVE: The principal mechanism of cardiac toxicity of bupivacaine relates to the blockade of myocardial sodium channels, which leads to an increase in the QRS duration. Recently, experimental studies suggest that lipid emulsion is effective in reversing bupivacaine cardiac toxicity. We aimed to evaluate the temporal evolution of the QRS widening induced by bupivacaine with the administration of Intralipid. MATERIAL AND METHODS: Twelve pigs were anesthetized with intravenous sodium thiopental 5mg kg(-1) and sevoflurane 1 MAC (2.6%). Femoral artery and vein were canalized for invasive monitoring, analysis of blood gases and determination of bupivacaine levels. After instrumentation and monitoring, a bupivacaine bolus of 4-6 mg kg(-1) was administered in order to induce a 150% increase in QRS duration (defined as the toxic point). The pigs were randomized into two groups of six individuals. Intralipid group (IL) received 1.5 mL kg(-1)of IL over one minute, followed by an infusion of 0.25 mL kg min(-1). Control group (C) received the same volume of a saline solution. The electrocardiographic parameters were recorded, and blood samples were taken after bupivacaine and 1, 5, 10 and 30 minutes after Intralipid/saline administration. RESULTS: Bupivacaine (4.33±0.81 mg/kg in IL group and 4.66±1.15 mg/kg in C group) induced similar electrocardiographic changes in both groups; mean maximal percent increase in QRS interval was 184±62% in IL group, and 230±56% in control group (NS). Lipid administration reversed the QRS widening previously impaired by bupivacaine. After ten minutes of the administration of IL, the mean QRS interval decreased to 132±56% vs. 15±76% relative to the maximum widening induced by bupivacaine, in IL and C group, respectively. CONCLUSION: Intralipid reversed the lengthening of QRS interval induced by the injection of bupivacaine. Time to normalization of electrocardiographic parameters can last more than 10 minutes. While the phenomena of cardiac toxicity persist, resuscitation measures and adequate monitoring should be continued until adequate heart conduction parameters are restored.

LC-MS/MS method for the determination of nine antidepressants and some of their main metabolites in oral fluid and plasma. Study of correlation between venlafaxine concentrations in both matrices.

In this paper, a fast, sensitive and selective LC-MS/MS method is described for the simultaneous determination of amitriptyline, imipramine, clomipramine, fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram and venlafaxine, as well as some of their main metabolites (nortriptyline, desipramine, norclomipramine and norfluoxetine), in oral fluid and plasma. The sample (0.2 mL) was extracted with an automated solid-phase extraction system (ASPEC XL), using mixed mode OASIS MCX cartridges. Chromatographic separation was performed in a Sunfire C18 IS column (20 mmx2.1 mm, 3.5 microm), using a gradient of acetonitrile and ammonium formate (pH 3; 2 mM) as mobile phase, which allowed the elution of all the compounds in less than 5 min. The method has been fully validated in both specimens. This method was initially applied to the analysis of oral fluid and plasma samples from patients on antidepressant treatment in order to assess for which compounds it was likely to find a good correlation between both matrices. The best results were obtained for venlafaxine, so the study was extended for this compound, comparing the ratio between oral fluid and plasma concentrations (ROF/PL) in five patients on venlafaxine treatment when both samples were collected simultaneously on four different occasions. An important inter and intraindividual variability was found in oral fluid concentrations for 150 mg dose (mean=287.5 ng/m, range 58.8-531.2 ng/mL) and for 75 mg dose (mean=186.3 ng/mL, range=82.1-289.2 ng/mL). R(OF/PL) was calculated for each patient on the four different occasions, showing also a high variability (CV=24.2-69.6%).

Determination of methadone, 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine and alprazolam in human plasma by liquid chromatography-electrospray ionization mass spectrometry.

A fast liquid chromatographic assay with mass spectrometric detection (LC/MS) has been developed and validated for the simultaneous determination of methadone (MT), its primary metabolite, 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) and alprazolam, in human plasma. The extraction procedure was performed with automatic solid phase extraction, and the compounds were separated with a Sunfire column using a gradient mode. Deuterated analogues for all of the analytes of interest were used for quantitation. Limits of detection (LOD) were established between 0.5 and 1 ng/ml. Linearity was obtained over a range of 2-2,000 ng/ml with an average correlation coefficient (R(2)) of >0.99. Intra- and inter-batch coefficients of variation and relative mean errors were less than 10% for all analytes and concentrations. The recoveries were higher than 50.0% in all cases. The method proved to be suitable for evaluation of plasma obtained from patients enrolled in a MT-maintenance program who are frequently treated with alprazolam as a sedative.

Liquid chromatography-electrospray ionisation mass spectrometry for the determination of nine selected benzodiazepines in human plasma and oral fluid.

A new simple and rapid liquid chromatographic-mass spectrometric technique was designed for the determination of nine benzodiazepines in plasma and oral fluid. Benzodiazepines were extracted from alkalinised spiked and clinical plasma and oral fluid samples using a single step, liquid-liquid extraction procedure with diethyl ether. The chromatographic separation was performed with a Xterra RP18, 5 microm (150 x 2.1 mm i.d.) reversed-phase column using deuterated analogues of the analytes as internal standard. The recovery ranged from 70.3 to 86.9% for plasma and 63.9 to 77.2% for oral fluid. The limits of detection ranged from 0.5 to 1 ng/ml in plasma and 0.1 to 0.2 ng/ml for oral fluid. The method was validated for all the compounds, including linearity and the main precision parameters. The procedure, showed to be sensitive and specific, was applied to real plasma and oral fluid samples. The method is especially useful to analyse saliva samples from drivers undergoing roadside drug controls.

Development and validation of a method for the quantitation of Delta9tetrahydrocannabinol in oral fluid by liquid chromatography electrospray-mass-spectrometry.

Analysis of Delta(9)tetrahydrocannabinol (Delta(9)THC) and its metabolites in biological samples is of great relevance for forensic purposes. In the case of oral fluid (OF), the analysis should determine Delta(9)THC, whereas in urine, it detects the inactive metabolite tetrahydrocannabinol carboxylic acid (THC-COOH). Most laboratories analyze Delta(9)THC in such samples using GC-MS methods, but these procedures are time-consuming and involve unavoidable previous extraction and derivatization. No data is yet available on the application of liquid chromatography-mass-spectrometry to detect Delta(9)THC in oral fluid. We report a validation method in which the Delta(9)THC is isolated from oral fluid by a simple liquid-liquid extraction with hexane and subsequently analyzed by liquid chromatography-mass-spectrometry. The method here reported for the determination of Delta(9)THC in oral fluid only requires 200 microl of sample and achieves limits of detection of 2 ng/ml, and has been used to analyze oral fluid samples collected from current drug users.

Vitreous humour as a complementary sample to blood for the detection/confirmation of diazepam: ante-mortem and post-mortem studies in an animal model.

The quantification of medical or toxic substances in vitreous humour (VH) could be very useful in forensic toxicology when blood sample determinations are impossible due to absence or deterioration. However, few studies have been made in this area and even fewer have tried to find a relationship between drug levels in both samples. To determine a correlation ratio between blood and VH diazepam (DZ) levels, we performed an experimental study using rabbits administered with a sub-toxic dose of DZ under known and controlled conditions. Blood and VH samples were collected 0.5, 1, 2, 3 and 6 hours after the drug administration in order to determine DZ and its main active metabolite, desmethyldiazepam (DMD). In addition, we have studied an animal group sacrificed 2 hours after intramuscular (i.m.) drug administration with blood and VH collection 24 hours later, to evaluate the existence of possible post-mortem changes. After DZ administration, a fast absorption phase was observed with a plasma Cmax value 1 hour after, followed by a rapid concentration decrease, with a half-life of 1 hour, indicating that, besides elimination, a fast distribution to other organs and tissues and/or hepatic metabolism occurred. Diazepam Cmax value in VH was achieved between 1 and 2 hours, when plasma concentrations had already decreased to half the value. The plasma/VH DZ ratio calculated at this time was 10. In the post-mortem study, while plasma DZ concentration at 24 hours was smaller, DMD levels were higher than those at the time of death. In the VH, both DZ and DMD concentrations at 24 hours were higher than those obtained at the time of death. That is, in both fluids DZ and DMD concentrations were different from those at the time of death and post-mortem distribution and redistribution phenomena occurred. The combination of ante-mortem and post-mortem studies has allowed the determination of a correlation ratio for DZ in the rabbit of 6 x, comparing the concentrations in VH collected 24 hours after death with the concentrations detected in plasma at the time of death. This study opens new perspectives for the use of VH as a complementary sample to blood for DZ detection and confirmation. The putative relevance of the correlation ratio obtained, for forensic toxicology practice with medical substances, namely benzodiazepines, recommends further studies in humans.

Epidural washout with high volumes of saline to accelerate recovery from epidural anaesthesia.

BACKGROUND: Prolonged postoperative blockade can follow neuraxial blocks for short surgical procedures. We investigated whether washout with a high volume of saline through an epidural catheter could provide a faster recovery after epidural anaesthesia. METHODS: Thirty patients were randomly assigned to a control group (no washout), to group 2x (epidural washout with twice the volume of 2% mepivacaine) and group 4x (epidural washout with four times that volume). RESULTS: Recovery times from sensory blockade at L2 were 151+/-24, 122+/-29 and 116+/-24 min for control, 2x and 4x groups respectively. Significant differences were found in both saline groups when compared with control group, but not between group 2x and group 4x. No differences were found concerning motor blockade. One patient in group 4x demonstrated signs of intracranial hypertension. Mepivacaine plasma concentrations were increased by saline washout in group 4x. CONCLUSIONS: Epidural washout with a high volume of saline can not be recommended since no clinically significant reduction in the recovery time can be achieved without risk.

High doses of mepivacaine for brachial plexus block in patients with end-stage chronic renal failure. A pilot study.

BACKGROUND AND OBJECTIVE: Patients with end-stage chronic renal failure are at risk of developing several serious postanaesthetic complications. Many anaesthesiologists perform brachial plexus anaesthesia with high doses of local anaesthetic in order to achieve an extensive blockade of the upper limb. Brachial plexus block is a suitable technique for anaesthesia for creation, repair or removal of vascular access for haemodialysis. The aim of this study was to measure mepivacaine plasma concentrations after axillary block with 650 mg plain mepivacaine in patients with end-stage chronic renal failure. METHODS: Mepivacaine plasma concentrations were assessed throughout a 150-min period, in 10 patients after axillary block with 650 mg plain mepivacaine (600 mg for axillary block and 50 mg for supplementation). RESULTS: Mepivacaine plasma concentrations expressed in microg mL(-1) as medians and their ranges were: 1.69 (1.23--7.78) at 5 min, 5.61 (4.36--8.19) at 30 min, 8.28 (3.83--11.21) at 60 min, 7.93 (5.63--11.1) at 90 min and 6.49 (5.56--8.35) at 150 min without any symptoms of toxicity. CONCLUSIONS: Brachial plexus anaesthesia with 650 mg plain mepivacaine did not result in serious systemic toxicity in these patients despite the high mepivacaine plasma concentrations found.

Evaluation of cocaine, amphetamines and cannabis use in university students through hair analysis: preliminary results.

The evaluation of drug abuse in a defined population was performed through toxicological hair analysis. Hair samples from university students ranging from 18 to 25 years of age were anonymously collected and screened for cocaine, amphetamines and cannabinoids by radioimmunoassay (RIA). Positive results (cut-off values adopted were 2 ng/mg for cocaine and amphetamines and 0.5 ng/mg for cannabinoids) were confirmed by GC/MS. Preliminary results showed 19% of positive results for cocaine on 200 samples analysed. No confirmed positive results were obtained for amphetamine analysis. RIA technique demonstrated its unsuitability for cannabinoids preliminary screening on hair, giving a high percent of false positive results.