Tzu-Cheg Kao

Back Pain after Epidural Anesthesia with Chloroprocaine

BackgroundChloroprocaine has been associated with severe back pain after epidural anesthesia. Factors proposed to contribute to this problem are: 1) the preservative disodium ethylenediaminetetraacetlc acid (EDTA), 2) large volumes of chloroprocaine, 3) low pH of chloroprocaine, and 4) local Infiltration with chloroprocaine. MethodsUsing a prospective, balanced, randomized study design, 100 patients aged 18–65 yr who were undergoing outpatient knee surgery during continuous epidural anesthesia received one of five local anesthetics (all containing epineph-rine 1:200,000). Group I received a bolus of 30 ml 2% lldocaine, followed by 10 ml every 45 min. Group II received 15 ml of 3% chloroprocaine (containing EDTA), plus 5 ml every 45 min. Group III received 30 ml of 3% chloroprocaine plus 10 ml every 45 min. Group IV received 30 ml of 3% chloroprocaine (containing metabisulfite as the preservative but no EDTA) plus 10 ml every 45 mln. Group V received 30 ml of 3% chloroprocaine with the pH adjusted to 7.3, plus 10 ml every 45 min. After the anesthesia dissipated and before any analgesic agents were given, the patients were asked to rank maximum knee and back pain on a visual analog scale (0–10) and to give a description of back pain. A telephone interview was conducted 24 h after surgery to determine if back pain returned. Back pain scoring was assessed using a verbal analog scale. ResultsAfter dissipation of anesthesia, the back pain reported by patients fell into two distinct categories. Type 1 pain was described commonly as superficial and localized to the site of needle insertion. There was no difference among groups in incidence of type 1 pain. Type 2 pain was described as deep, aching, burning, and poorly localized in the lumbar region (5% of the patients in group I,10% in groups II and IV, 50% in group III, and 25% in group V). The incidence of type 2 pain was significantly greater in group III than in groups I, II, or IV. Group III also had a significantly greater mean visual analog scale pain score (types 1 and 2) than all other groups. ConclusionsLarge doses (≤ 40 ml) of chloroprocaine containing EDTA resulted in a greater incidence of deep burning lumbar back pain. Using 25 ml or less of the same solution resulted in an incidence of both types 1 and 2 postepidural anesthesia back pain similar to that in the lldocalne control group.

The relative increase in skin temperature after stellate ganglion block is predictive of a complete sympathectomy of the hand

Background and Objectives. Although an increase in skin temperature of the hand implies sympathetic block after stellate ganglion block (SGB), it does not indicate complete sympathetic block unless accompanied by an absence of sweating because skin temperature may increase even with a partial sympathetic block. This study examined the efficacy of the SGB to block sweating in the hand and to determine if the magnitude of temperature change in the hand is predictive of a negative sweat test. Methods. Fifty‐nine SGBs were performed in 30 patients (15 women and 15 men) for diagnostic or therapeutic indications. Stellate ganglion block was performed via an anterior paratracheal approach at C6 using 15 mL 0.25% bupivacaine. Skin temperature was measured bilaterally on the index finger. A cobalt blue sweat test was performed bilaterally preand post‐SGB on the middle finger. Successful sympathetic block after SGB was considered present when: (a) (change in ipsilateral temperature (postblock‐preblock)] (Di)‐ [change in contralateral temperature] (Dc) ≥ 1.5°C; (b) Horners syndrome present; and (c) sweat test changed from positive to negative. Logistical regression was applied to determine what value of Di ‐ Dc could be used to predict a negative sweat test. Results. Thirty‐six percent (21/59) of blocks met all three criteria. Of the blocks where Di ‐ Dc ≥ 1.5°C, 72% (21/29) had a negative sweat test post‐SGB. Of the blocks where Di ‐ Dc < 1.5°C, 37% (11/30) had a negative sweat test postblock. If Di ‐ Dc ≥ 2.0°C, a negative sweat test could be predicted with 69 ± 12% sensitivity and 85 ± 10% specificity. Conclusions. Stellate ganglion block often fails to increase skin temperature in the ipsilateral more than the contralateral hand. A value of Di ‐ Dc ≥ 2.0°C was a good predictor of a sympathetic block, but was not sufficient to guarantee a complete sympathetic block of the hand after SGB in all cases. An apparently successful SGB as measured by “usual” clinical criteria may not result in a complete sympathectomy of the hand as is often assumed. Therefore, if obtaining a sympathectomy is important for diagnostic or therapeutic purposes, performing a sweat test provides important confirmatory evidence of the genuine success of the sympathetic block.

Does spinal anesthesia result in a more complete sympathetic block than that from epidural anesthesia

Background: Spinal and epidural injection of local anesthetics are used to produce sympathetic block to diagnose and treat certain chronic pain syndromes. It is not clear whether either form of regional anesthesia produces a complete sympathetic block. Spinal anesthesia using tetracaine has been reported to produce a decrease in plasma catecholamine concentrations. This has not been demonstrated for epidural anesthesia in humans with level of anesthesia below C8. One possible explanation is that spinal anesthesia results in a more complete sympathetic block than epidural anesthesia. To examine this question, a cross-over study was performed in young, healthy volunteers. Methods: Ten subjects underwent both spinal and epidural anesthesia with lidocaine (plain) on the same day with complete recovery between blocks. By random assignment, spinal anesthesia and epidural anesthesia were induced via lumbar injection. Before and 30 min after local anesthetic injection, a cold pressor test (CPT) was performed. Blood was obtained to determine epinephrine and norepinephrine plasma concentrations at four stages: (1) 20 min after placing peripheral catheters, (2) at the end of a 2-min CPT (before conduction block), (3) 30 min after injection of epidural or spinal lidocaine, and (4) at the end of a second CPT (during anesthesia). Mean arterial pressure, heart rate, noninvasive cardiac index, and analgesia to pin-prick were monitored. Results: Neither spinal nor epidural anesthesia changed baseline resting values of catecholamines or any hemodynamic variable, except heart rate, which was slightly decreased during spinal anesthesia. Median level of analgesia was T4 during spinal and T3 during epidural anesthesia. CPT before conduction block reliably increased heart rate, mean arterial pressure, cardiac index, epinephrine, and norepinephrine. Conduction block attenuated the increase in response to CPT only in mean arterial pressure (spinal and epidural) and cardiac index (spinal only). Neither technique blocked the increase in heart rate, norepinephrine, or epinephrine to CPT. Conclusions: Spinal anesthesia did not result in a more complete attenuation of the sympathetic response to a CPT than did epidural anesthesia. In response to the CPT, spinal anesthesia blocked the increase in cardiac index, and epidural anesthesia resulted in a decrease in total peripheral resistance compared to the pre-anesthesia state. The differences betweenthe techniques are not significant and are of uncertain clinical implications

time Course of the Effects of Cervical Epidural Anesthesia on Pulmonary Function

Background and Objectives. During cervical epidural anesthesia the C4, C5, and sometimes C3 nerve roots are anesthetized. One might therefore expect pulmonary compromise due to the block of the phrenic nerve if anesthesia extends to C3. This study was conducted to measure the effects of cervical epidural anesthesia using 2% lidocaine on pulmonary function, with specific attention given to the time course of pulmonary changes in relation to spread of analgesia. Methods. Fifteen adult patients without preexisting lung disease undergoing carotid endarterectomy, breast surgery, or cervical epidural steroid injection were enrolled. Cervical epidural anesthesia was performed at the C7‐T1 interspace using 300 mg lidocaine with epinephrine. Pulmonary function, including forced expiratory volume in one second (FEV1), forced vital capacity (FVC), maximum inspiratory pressure (MIP), and SpO2 while breathing room air were measured prior to and 5, 10, 20, and 40 minutes after lidocaine injection. Results. Analgesia to pinprick reached median dermatomes of C3 to T8 (range: C2‐T12) by 20 minutes after lidocaine injection. FEV1 and FVC decreased approximately 12‐16% between 20 and 40 minutes after injection. Maximum inspiratory pressure and SpO2 did not significantly change. Conclusions. Cervical epidural anesthesia using 300 mg lidocaine results in measurable reduction in bedside pulmonary functions concomitant with the spread of analgesia to the C3 dermatome. These changes were complete 20 minutes after lidocaine injection. In patients without preexisting lung disease, these changes were not clinically significant, except in one patient. We conclude that motor block of the phrenic nerve is incomplete under the conditions of this study.

Sympathetic block during spinal anesthesia in volunteers using lidocaine, tetracaine, and bupivacaine

Background and Objectives. Spinal anesthesia to high thoracic dermatomes is alleged to result in almost complete block of all sympathetic efferent nerves. To examine the degree of sympathectomy during spinal anesthesia, the sympathetic response to a cold pressor test (CPT) applied to unblocked dermatomes before and during spinal anesthesia was measured with use of three different local anesthetics. Methods. Twelve healthy volunteers were studied in a randomized and double‐blind fashion on three separate occasions. In random order, each volunteer received approximately equipotent spinal doses of tetracaine 15 mg, bupivacaine 15 mg, and lidocaine 100 mg in hyperbaric solutions. Prior to and 30 minutes after spinal injection of local anesthetic, a CPT was applied for 2 minutes, and changes from baseline resting conditions in five physiologic variables were measured. Results. The CPT 1 given before anesthetic administration resulted in an increase in heart rate, mean arterial pressure, cardiac index, and plasma concentrations of norepinephrine and epinephrine. Spinal anesthesia to a median level of T3 resulted in a decrease in mean arterial pressure by 10‐12% but did not significantly decrease the other variables. Spinal anesthesia did not change the increase in heart rate or cardiac index in response to the second CPT, but the increase in mean arterial pressure was attenuated compared to the CPT before anesthesia. No increase in norepinephrine or epinephrine concentration was observed during the CPT given during spinal anesthesia. There was no significant relationship between level of analgesia and sympathetic response to stress. Conclusions. Spinal anesthesia with hyperbaric solutions of tetracaine 15 mg, bupivacaine 15 mg, and lidocaine 100 mg attenuated sympathetic function but did not produce complete sympathectomy. The effects were independent of the local anesthetic used.

Does the Choice of Local Anesthetic Affect the Catecholamine Response to Stress during Epidural Anesthesia

BackgroundPrevious work has established that 2-chloro-procaine epidural anesthesia has no effect on circulating plasma epinephrine concentrations in young, healthy, resting volunteers, and results in a decrease in norepinephrine concentration only when a level of analgesia to pinprick of C-8 is reached. The current study was performed to evaluate the possibility that this finding is unique to 2-chloroprocaine. MethodsNine healthy volunteers were studied on three occasions at least 48 h apart; each received three local anesthetics (0.75% bupivacaine, 2% lidocaine, and 3% 2-chloroprocaine, all without epinephrine). After placement of lumbar epidural and central venous catheters, blood samples were drawn from the central venous catheter at the following stages: (1) 20 min after catheter placement (baseline), (2) during the first cold pressor test (CPT; hand held in an ice water bath for 90 s), (3) 20 min after reaching epidural analgesia to T-1 level of analgesia, and (4) during a second CPT (epidural analgesia to T-1). Monitoring consisted of noninvasive cardiac output (impedance), noninvasive blood pressure, and EKG. ResultsExtensive epidural block (stage 3) altered measured variables only minimally with respect to resting baseline state. During stage 2 (first CPT), mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), epinephrine, and norepinephrine increased. During stage 4 (second CPT), Increases in HR and CI were not attenuated by any of the three local anesthetics. Increases in MAP were attenuated by epidural anesthesia with all three local anesthetics. Bupivacaine and 2-chloroprocaine epidural anesthesia significantly attenuated increases in plasma catecholamines, but lidocaine epidural anesthesia did not. ConclusionsEpidural anesthesia with all three local anesthetic agents tested resulted in an Incomplete sympathectomy in the resting state in healthy young men, judged by plasma catecholamine concentrations and cardiovascular variables minimally changed from resting baseline. Lidocaine epidural anesthesia did not attenuate the catecholamine response to CPT, indicating decreased blockade of sympathetic efferent neural traffic compared with bupivacaine and chloroprocaine epidural anesthesia.

What constitutes an effective but safe initial dose of lidocaine to test a thoracic epidural catheter

To investigate the effects of age and dose on the spread of thoracic epidural anesthesia, we placed thoracic epidural catheters in 50 surgical patients divided into groups by age (Group I [young], 18–51 yr; Group II [old], 56–80 yr) and randomly assigned patients to receive either 5 mL (A) or 9 mL (B) of 2% lidocaine (plain) injected via the epidural catheter. Hemodynamic variables were measured (heart rate, mean arterial blood pressure, noninvasive impedance cardiac index) at baseline and every 5 min for 30 min. Detectable blockade occurred within 8 min after injection of 3 + 2 mL or 3 + 6 mL in 48 of 50 patients. Maximum spread of analgesia to pinprick occurred 15–23 min after completion of local anesthetic injection and was significantly different between age and volume groups by two-way analysis of variance (Group IA [young 5], 10.9 ± 4.0 dermatomes; Group IIB [young 9], 13.9 ± 4.5 dermatomes; Group IIA [old 5], 14.1 ± 5.6 dermatomes; and Group IIB [old 9], 17.4 ± 5.1dermatomes). Minor decreases in mean arterial blood pressure (8%–17%) and heart rate (4%–11%) were noted. Two patients in the Old 9 group required IV ephedrine or ephedrine/atropine to treat hypotension and bradycardia. We conclude that given the rapid onset (3–8 min), extensive spread (11–14 dermatomal segments), and consistent hemodynamic stability, thoracic epidural anesthesia should be initiated with lidocaine 100 mg (5 mL 2% lidocaine) to establish proper location of the catheter in the epidural space in both younger and older patients.

Differential sensory block: spinalvs epidural with lidocaine

PurposeIn this study we sought to determine if and when a difference exists with regards to differential sensory blockade between spinal and epidural anaesthesia using lidocaine.MethodsTen healthy volunteers were randomly assigned to receive both spinal and epidural anaesthesia. Nonepinephrine containing solutions of lidocaine, 100 mg lidocaine 5% with 7.5% dextrose (spinal) and 600 mg lidocaine 2% (epidural), were used to establish sensory blockade. At five minute intervals, for a total of 65 min, the following sensory modalities were tested: anaesthesia (complete loss of sensation to pinprick), analgesia (loss of an equally sharp sensation to pinprick compared with that at an unblocked dermatome), cold sensation (complete loss of cold temperature discrimination).ResultsAt all times, except at time = 0 during spinal anaesthesia, the levels of analgesia and cold sensation were more cephalad than the level of anaesthesia for both spinal and epidural anaesthesia. Multiple comparison testing among the three dermatomal response levels showed that, during epidural anaesthesia, the level of analgesia was more cephalad than the level of cold sensation at the following times: 25 min, 30 min, and from 40 to 60 min. In contrast, the level of analgesia was not different from the level of cold sensation during spinal anaesthesia.ConclusionsSpinal and epidural anaesthesia with lidocaine produce a similar degree of differential sensory blockade. Epidural anaesthesia produces a detectable difference between the level of analgesia and cold sensation at various times, whereas spinal anaesthesia did not reliably do so in this study.RésuméObjectifNous avons tenté de déterminer dans cette étude si une différence existe, et à quel moment elle se manifeste, entre une anesthésie rachidienne et une anesthésie péridurale avec de la lidocaïne, en ce qui concerne le blocage sensitif différentiel.MéthodeDix volontaires, en bonne santé, ont été désignés de façon aléatoire pour recevoir une anesthésie rachidienne et péridurale. Des solutions de lidocaïne sans épinéphrine, 100 mg de lidocaïne 5 % avec 7,5 % de dextrose (rachidienne) et 600 mg le lidocaïne 2 % (péridurale), ont été utilisées pour provoquer le blocage sensitif. À des intervalles de cinq minutes, pendant 60 min, les modalités sensitives suivantes ont été étudiées : anesthésie (perte de sensibilité complète à la piqûre), analgésie (perte de sensibilité équivalente à la piqûre à partir d’une comparaison avec celle d’un dermatome non touché), sensibilité au froid (perte complète de la discrimination de la température froide).RésultatsPendant l’anesthésie, les degrés d’analgésie et de sensibilité au froid étaient toujours, sauf au temps = 0 de l’anesthésie rachidienne, plus grands que le degré d’anesthésie autant pour une anesthésie rachidienne que péridurale. Les épreuves de comparaisons multiples parmi les trois niveaux de réponses segmentaires ont montré que, pendant l’anesthésie péridurale, le degré d’analgésie était plus grand que le degré de sensibilité au froid aux temps suivants : 25 min, 30 min, et de 40 à 60 min. En comparaison, le degré d’analgésie n’était pas différent de celui de la sensibilité au froid pendant l’anesthésie rachidienne.ConclusionLanesthésie rachidienne et péridurale avec de la lidocaïne produit un degré similaire de blocage sensitif différentiel. Selon cette étude, l’anesthésie péridurale produit une différence détectable entre le degré d’analgésie et de sensibilité au froid à différents moments, pendant que l’anesthésie rachidienne ne fournit pas de données prévisibles en ce sens.

The efficacy of epinephrine test doses during spinal anesthesia in volunteers : Implications for combined spinal-epidural anesthesia

Epinephrine test doses may be administered during combined spinal-epidural anesthesia to determine intravascular placement of epidural catheters. This study was designed to determine systolic blood pressure (SBP) and heart rate (HR) responses to intravenous injection of epinephrine (15 micro g) during spinal anesthesia. Twelve volunteers received three spinal anesthetics (lidocaine 100 mg, tetracaine 15 mg, and bupivacaine 15 mg) in a randomized, double blind, cross-over fashion. Epinephrine was administered prior to spinal anesthesia (control), 30 min after injection of spinal anesthesia, and at regression of sensory block to T-10. SBP was measured with a radial arterial catheter and HR with an electrocardiogram. Positive responses were defined as peak increase in SBP >or=to 15 mm Hg or HR >or=to 20 bpm after injection of epinephrine. Compared with control, peak SBP responses decreased by a mean of 12 mm Hg during spinal anesthesia with tetracaine and bupivacaine (P < 0.05). Peak HR responses decreased by 11 bpm during all three spinal anesthetics (P < 0.05). Incidences of detection of intravenous injection by positive SBP and HR responses ranged from 50% to 100% and were not significantly affected by spinal anesthesia. Spinal anesthesia reduces hemodynamic responses to intravenous epinephrine injection but is unlikely to reduce detection by positive SBP and HR criteria. (Anesth Analg 1997;84:780-3)

Differential Sensory Block: Spinal vs. Epidural With Lidocaine

Purpose: In this study we sought to determine if and when a difference exists with regards to differential sensory blockade between spinal and epidural anaesthesia using lidocaine. Methods : Ten healthy volunteers were randomly assigned to receive both spinal and epidural anaesthesia. Nonepinephrine containing solutions of lidocaine, 100 mg lidocaine 5% with 7.5% dextrose (spinal) and 600 mg lidocaine 2% (epidural), were used to establish sensory blockade. At five minute intervals, for a total of 65 min, the following sensory modalities were tested: anaesthesia (complete loss of sensation to pinprick), analgesia (loss of an equally sharp sensation to pinprick compared with that at an unblocked dermatome), cold sensation (complete loss of cold temperature discrimination). Results: At all times, except at time = 0 during spinal anaesthesia, the levels of analgesia and cold sensation were more cephalad than the level of anaesthesia for both spinal and epidural anaesthesia. Multiple comparison testing among the three dermatomal response levels showed that, during epidural anaesthesia, the level of analgesia was more cephalad than the level of cold sensation at the following times: 25 min, 30 rain, and from 40 to 60 min. In contrast, the level of analgesia was not different from the level of cold sensation during spinal anaesthesia. Conclusions: Spinal and epidural anaesthesia with lidocaine produce a similar degree of differential sensory blockade. Epidural anaesthesia produces a detectable difference between the level of analgesia and cold sensation at various times, whereas spinal anaesthesia did not reliably do so in this study.