Rom A. Stevens

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.