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Anesth Analg 2008; 107:708-721
© 2008 International Anesthesia Research Society
doi: 10.1213/ane.0b013e31817e7065
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ANALGESIA

Factors Affecting the Distribution of Neural Blockade by Local Anesthetics in Epidural Anesthesia and a Comparison of Lumbar Versus Thoracic Epidural Anesthesia

W. Anton Visser, MD, PhD*, Ruben A. Lee, BE(Hons){dagger}, and Mathieu J. M. Gielen, MD, PhD{ddagger}

From the *Department of Anesthesiology, Intensive Care and Pain Management, Amphia Hospital, Breda; {dagger}Department of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Technical University of Delft, Delft; and {ddagger}Department of Anesthesiology, University Medical Center Nijmegen, Nijmegen, The Netherlands.

Address correspondence to W. Anton Visser, MD, Department of Anesthesiology, Intensive Care and Pain Management, Amphia Hospital, PO Box 90157, 4800 RL Breda, The Netherlands. Address e-mail to avisser{at}amphia.nl.

Abstract

The spread of sensory blockade after epidural injection of a specific dose of local anesthetic (LA) differs considerably among individuals, and the factors affecting this distribution remain the subject of debate. Based on the results of recent investigations regarding the distribution of epidural neural blockade, specifically for thoracic epidural anesthesia, we noted that the total mass of LA appears to be the most important factor in determining the extent of sensory, sympathetic, and motor neural blockade, whereas the site of epidural needle/catheter placement governs the pattern of distribution of blockade relative to the injection site. Age may be positively correlated with the spread of sensory blockade, and the evidence is somewhat stronger for thoracic than for lumbar epidural anesthesia. Other patient characteristics and technical details, such as patient position, and mode and speed of injection, exert only a small effect on the distribution of sensory blockade, or their effects are equivocal. However, combinations of several patient and technical factors may aid in predicting LA dose requirements. Based on these results, we have also formulated suggested epidural insertion sites that may optimize both analgesia and sympathicolysis for various surgical indications.

The spread of sensory blockade after epidural injection of a specific dose of local anesthetic (LA) differs considerably among individuals, and the factors affecting this distribution remain the subject of debate. Reviews on the subject date back two decades or more.1,2 A systematic review of recent investigations may provide new insights into factors that affect the spread of epidural blockade, especially for thoracic epidural anesthesia, and may aid in delivering predictable and safe epidural anesthesia.

Although previous reviews have focused primarily on lumbar epidural anesthesia, the practice of thoracic epidural anesthesia has increased tremendously over the last decade.3,4 Differences in anatomy, physiology, and techniques to identify the epidural space make extrapolation of data for predicting spread of anesthesia gathered during lumbar epidural anesthesia to thoracic epidural anesthesia problematic. This article reviews recent investigations regarding the distribution of neural blockade, specifically for thoracic epidural anesthesia and, where possible, draws results from research regarding lumbar epidural anesthesia.

For the purpose of this review, we will consider C7–T2 as high-thoracic, T2–6 as mid-thoracic, and T6–L1 as low-thoracic. This classification reflects the different fields of surgery for which these epidural sites are typically used (cardiac, thoracic and abdominal surgery, respectively). In addition, most studies mentioned in this article have used either LA, or contrast medium, or both, to study the distribution of epidural anesthesia. However, it should be noted that the findings based on the use of contrast medium may not always be congruent to epidural spread of LA.1,5,6 Although this review will focus on distribution of sensory neural blockade, distribution of sympathetic and motor neural blockade will be briefly discussed.

A comprehensive description of epidural anatomy is beyond the scope of this article. The reader is referred to several excellent reviews.7–10 In addition, methods used to test sensory block have been reviewed elsewhere.11 These methods can be categorized as either qualitative (normal or abolished response to the application of stimuli such as cold or pinprick) or quantitative (e.g., pain on electrical stimulation with increasing current). It should be noted that studies mentioned in this review have used different modes of sensory testing, and that demonstration of blockade using qualitative testing does not guarantee adequate anesthesia. It should also be noted that, in general, surgical anesthesia has been the focus of investigations concerning bolus doses of LA, whereas postoperative analgesia has been the focus in evaluations regarding continuous infusions.

FACTORS AFFECTING THE DISTRIBUTION OF EPIDURAL NEURAL BLOCKADE

Patient Characteristics
Many studies have investigated patient characteristics to determine differences in spread of neural blockade in epidural anesthesia. Although different factors are examined separately in this review, multivariable analysis has shown that consideration of multiple patient characteristics may better reflect the cross-dependencies, and lead to a more accurate estimate of anesthetic requirements.12

Age
From the 1960s onward, the clinical impression that spread of epidural blockade may be greater in elderly patients has spawned a host of studies investigating this subject. In lumbar epidural anesthesia, Bromage was the first to report a strong correlation between patient age and the epidural segmental dose requirements.13 However, the validity of these findings has been questioned, as the assumption of linearity between LA dose and extent of anesthesia has later been proven to be a fallacy (see below).1 Nevertheless, since then, several authors have reported sensory blocks with maximum cephalad spread 3–8 segments higher in patients >60-yr old compared to patients <40-yr old after injection of the same epidural dose of LA.14–17 A linear relationship between age and spread of blockade is stronger when using volumes up to 10 mL compared to the 10–20 mL range14,18 and in patients younger than 40 yr, compared to patients over 40-yr old.12,14 In a study comparing the spread of sensory blockade in high-thoracic, mid-thoracic and lumbar epidural anesthesia, correlation coefficients of spread with age in these three regions were reported to be 0.58, 0.38, and 0.82, respectively.19 In contrast, other studies have reported either no effect of age on epidural spread,20–22 or statistically significant, but small correlation coefficients, with differences in spread of sensory blockade that may not be clinically important.18,23–26

In contrast with the conflicting reports on lumbar epidural anesthesia, the few studies investigating the effects of age on epidural spread in thoracic epidural anesthesia all suggest a positive correlation between age and spread of blockade. The epidural dose requirement in the elderly (60–79 yr) was demonstrated to be about 40% less than in young adults (20–39 yr).27 This study demonstrated a correlation coefficient between age and epidural dose requirement of –0.70 (Fig. 1). Low thoracic epidural test doses of lidocaine 2%, 5 and 8 mL, resulted in greater extent of blockade, smaller segmental dose requirements and an increased incidence of hemodynamic instability in patients aged 56–80 yr compared to patients aged 18–51 yr.28 Furthermore, positive correlation of thoracic epidural spread of contrast medium with the patient’s age has been reported.29,30


Figure 152
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  		Figure 1. Relationship between age and epidural dose requirement of 2% mepivacaine in thoracic (T9–10) epidural anesthesia (r = 0.70, P < 0.001, n = 62). D = Dermatome. 27

 

The mechanism for a positive correlation reported by several investigators between age and spread of blockade remains unclear. Although it has been suggested that this correlation could be explained by decreased leakage of LA through the intervertebral foramina in older patients,31–34 this has been refuted by others.30 Alternatively, compliance of the epidural space has been shown to increase with age, and it is positively correlated with spread of sensory blockade.35 This agrees with the fact that residual pressure after injection of LA is lower in older patients, which, in turn, is associated with wider spread of sensory block.19 Indeed, it has been demonstrated using epiduroscopy that the epidural space becomes more widely patent after injection of a given amount of air, and the fatty tissue in the epidural space diminishes with increasing age, which may promote the longitudinal spread of LAs in the elderly.36 Furthermore, with age, the dura becomes more permeable to LA owing to a progressive increase in size and number of arachnoid villi. This provides a large area through which LA can diffuse into the subarachnoid space.34 Finally, it has been proposed that a decrease in the number of myelinated nerve fibers in the nerve, and a general deterioration of the mucopolysaccharides of the ground substance, allows LA to more easily penetrate nerve roots in older patients.13,37

Height
It seems logical to assume that taller patients require more LA to establish a certain level of blockade than shorter subjects. This has been investigated in lumbar epidural anesthesia, again with conflicting results. Only weak correlation coefficients, ranging from –0.13 to –0.54 have been demonstrated.18,20,24,38 In thoracic epidural anesthesia, correlation coefficients from –0.2529 to –0.3730 have been found between the spread of epidurally injected contrast medium and patient height. To our knowledge, clinical trials evaluating the relationship between height and spread of blockade after epidural administration of LA are lacking in thoracic epidural anesthesia. Therefore, it is not possible to definitively draw conclusions on the significance of patient height in predicting the spread of blockade, except perhaps in extremely short or extremely tall individuals.

Weight and Body Mass Index
Few studies report on the correlation between weight and spread of sensory blockade. In lumbar epidural anesthesia, no correlation was found,20,22 although a correlation coefficient of 0.41 was demonstrated for the association of body mass index (BMI) with height of sensory block.20 Weight was not correlated with epidural spread of contrast in thoracic epidural anesthesia.29

Apparently, changes that may occur with obesity, such as increased abdominal pressure or increased body fat, are not sufficient to affect the spread of epidural blockade. Indeed, while both weight and BMI are positively correlated with posterior subcutaneous body fat deposition, they are not or only poorly correlated with the amount of posterior epidural fat.39

Pregnancy
Due to the lack of studies involving thoracic epidural anesthesia during pregnancy, data on epidural anesthesia in pregnancy concern lumbar epidural anesthesia only. In general, less LA is required to produce a given level of epidural anesthesia in pregnant patients. Engorgement of epidural veins by increased intra-abdominal pressure has often been implied as the mechanism for this phenomenon. Furthermore, both animal40–42 and clinical studies43 have shown that during pregnancy, onset of blockade of nerve conduction by LA is faster and blockade is more intense. This may account for the appearance of increased spread of epidural blockade during early pregnancy (8–12 wk) when intra-abdominal pressure is probably still normal, which is similar to that found in pregnant women at term.44 In contrast, no difference in latency and density of motor and sensory blockade was found when tested with repeated electrical stimulation between pregnant and nonpregnant women receiving lumbar epidural anesthesia.45 Although cranial extension of blockade was higher in the pregnant group, onset of sensory block in the sacral segments was similar in both groups. In contrast to the general population (see above), epidural LA requirements are further reduced in obese parturients (BMI >30) compared to parturients with BMI ≤30.46

Dural Surface Area
It has been demonstrated that the surface area of the lumbosacral dura is correlated with the peak sensory block level in lumbar epidural anesthesia.47 Although this patient factor may not be clinically useful, future research in this area may further clarify the differences in epidural spread of LAs among patients.

Technical Factors
Choice of Epidural Insertion Site
The length of the lumbar section of the vertebral column is relatively short and the dimensions of the lumbar epidural space are fairly constant. Although statistically significant, only small differences in cranial spread of blockade have been demonstrated after injection of LA at three different lumbar interspaces.12 In contrast, the thoracic part of the spinal column encompasses more than half the length of the entire spine and adjoins many different anatomical structures and spaces, whereas the thoracic vertebrae and epidural space vary greatly in shape and size. Therefore, it may be speculated that the distribution of neural blockade may vary with the site of epidural injection.

It is alleged that dose requirements are larger in lumbar compared to thoracic epidural anesthesia. Interestingly, while this has also been suggested in several papers,1,2,18 surprisingly few studies have actually directly compared the differences in spread of blockade between lumbar and thoracic epidural anesthesia. No statistically significant differences in total numbers of segments blocked could be demonstrated after high-thoracic, mid-thoracic, low-thoracic or lumbar epidural injection of contrast medium (Fig. 2).29,48 Others have reported spread of blockade of 17.3 ± 0.6, 14.3 ± 0.4, and 13.3 ± 0.7 segments after injection of 15 mL of 2% mepivacaine in the cervical, thoracic and lumbar epidural space, respectively.19 Unfortunately, these data were not statistically analyzed.


Figure 252
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  		Figure 2. A: Extension of sensory blockade tested by pinprick after administration of 3 mL lidocaine 2% in the high (C7–T2), mid (T2–4) or low (T7–9) thoracic epidural space. Data represent means ± sd. Arrows indicate the level of epidural needle placement. 48 B: Mean contrast spread after injection of 5 mL iotrolan, 240 mg I/mL, in 90 patients. C = cervical segment; L = lumbar segment; S = sacral segment; T = thoracic segment. In this study, there was a strong correlation between radiographic and analgesic spread (r = 0.91–0.97).29 These figures illustrate two important issues in epidural anesthesia: First, in contrast to common teaching, no statistically significant differences in total number of segments blocked could be demonstrated between patients receiving cervical, high, mid-, or low-thoracic or lumbar epidural injections. Second, the intervertebral level of epidural injection is a statistically significant factor in the distribution of sensory blockade, either in the cranial or caudal direction relative to the injection site.

 

Different patterns of sensory blockade were found after a test dose of 3 mL of lidocaine 2% when injected at different sites in the thoracic epidural space. Spread of sensory blockade was primarily caudal after high-thoracic epidural injection, primarily cephalad after low-thoracic injection, and equally distributed caudal and cephalad after mid-thoracic injection (Fig. 2A).48 These patterns have been confirmed in a series of 90 patients receiving 5 mL of lidocaine 1.5% at vertebral levels ranging from C7 to L5 (Fig. 2B).29 Differences in epidural pressure (see below), and obstruction of spread of epidural LA by the larger relative volume of the spinal cord and the thecal sac in the cervical and high lumbar areas have been suggested as an explanation for this phenomenon.48 Also, epiduroscopy has shown that the mid-thoracic epidural space becomes more widely patent after injection of a given amount of air and that the amount of fatty and fibrous tissue is smaller compared to the upper lumbar epidural space.49 Greater cranial spread (up to C2–3) after epidural injection at the C7–T1 level has been reported when larger doses of LA are being used. However, even in this situation, caudal spread is more extensive than cranial spread.50–52 Despite the differences in spread of blockade in relation to the site of injection, no differences were found in the total number of segments blocked among different regions in the thoracic epidural space,29,48 indicating that it is safe to use the same initial dose of LA in high- thoracic, mid-thoracic and low-thoracic epidural anesthesia.

Patient Position and Gravity
In lumbar epidural anesthesia, epidural injection of LA with the patient in the lateral position produces sensory block levels approximately 0–3 segments greater on the dependent side compared to injection with the patient in the supine position.21,53–60 No differences have been reported in maximal cranial spread between groups receiving equal amounts of epidural LA in the sitting or supine position.21,22,61 Some of these studies report slightly faster onset times in the lateral or sitting positions compared to the supine position.22,53,54,60

Head down (Trendelenburg) position of 15° has been shown to result in higher sensory block levels with faster onset times after lumbar epidural injection of LA in pregnant women.62 There has been one case report in which a high epidural block was diagnosed in an elderly patient, which made mechanical ventilation necessary. This patient had received a continuous epidural infusion through a low-thoracic epidural catheter, while positioned in a 15° head down lithotomy position for 4.5 h.63

Once again, studies on the effects of patient position and gravity in thoracic epidural anesthesia are lacking. However, with regard to position only, it has recently been shown that high-thoracic (catheter tip at T1–2) epidural injection of contrast medium with the patient’s neck in extension or neutral position results in limited cranial spread, whereas significant cranial spread was observed in patients after injection with the neck flexed.64

Needle Direction and Catheter Position
Epidural injection through a Tuohy needle with the bevel oriented to one side1 or caudal65,66 has no or only minor effects on the spread of sensory blockade compared to injection directed cephalad. However, both in lumbar67,68 and cervical69 epidural anesthesia, threading an epidural catheter with the Tuohy needle rotated 45° toward the operative side has been shown to produce a preferential distribution of sensory and motor blockade toward this side. In pregnant women, insertion of an epidural catheter with the bevel of the Tuohy needle oriented laterally resulted in greater difficulty passing the catheter and, more frequently, paresthesia.70 In contrast with the reports mentioned above, no differences were noted in the incidence of asymmetric block.

Orienting the bevel of the Tuohy needle caudad or cranially does not reliably predict final lumbar71 nor thoracic48,72,73 epidural catheter position relative to the insertion site. Also, thoracic epidural catheters have been shown to progressively withdraw an average of 1 cm during the first 3 days after insertion.73 The optimal distance to advance a catheter into the lumbar epidural space is suggested to be 4–6 cm.74,75 Threading shorter or longer distances may result in inadequate analgesia or increased incidence of venous cannulation and frequency of paresthesias, respectively.74,75 Fortunately, computed tomography imaging and clinical experience demonstrate that a large variety of lumbar epidural catheter tip positions and solution distribution result in equally satisfactory epidural anesthesia.76

Injection Through Needle Versus Injection Through Catheter
Whether injection of LA through a Tuohy needle versus an epidural catheter yields differences in epidural spread remains controversial. Lumbar epidural bolus injection of LA via either a Tuohy needle or a catheter did not result in differences in epidural spread in patients undergoing cesarean delivery77 or lower extremity surgery.78 In contrast, injection of 14 mL lidocaine 2% through a lumbar epidural catheter resulted in a spread of sensory blockade four segments greater compared to injection at the same rate through a Tuohy needle.79 Another study comparing these two modes of injection in pregnant women reported better quality of anesthesia when LA was injected via an epidural catheter.80 However, injection times differed by a factor of three between groups, which may have affected the results. We are unaware of similar studies in thoracic epidural anesthesia.

Epidural Catheter Design
Epidural catheters may be categorized as either single-orifice or multiorifice designs. In vitro, using injection pressures derived from in vivo measurements, differential flow has been observed from multiorifice epidural catheters, i.e., the flow appears first at the proximal, then the middle, and finally the distal orifices.81 With low injection pressures, flow is largest from the proximal orifice, and no flow was observed from the distal orifice, rendering a multiorifice catheter effectively a single-orifice variant.

Comparisons between these two catheter designs are commonly presented as differences in the quality of analgesia, rather than differences in spread of sensory blockade. In this regard, multiorifice catheters have been shown to be superior to single-orifice catheters in obstetric lumbar epidural anesthesia.82–84 In particular, unilateral analgesia and unblocked segments are reported to occur more frequently when a single-orifice catheter is placed.84 In contrast, one study did not find any differences in the quality of analgesia between single- and multiorifice catheters.85 Furthermore, injection of contrast medium resulted in a similar number of segments covered by dye above and below the injection site with both catheter designs.86 With newer soft-tipped single-orifice catheters, the lower incidence of paresthesias and venous cannulation during placement should be weighed against the higher incidence of inadequate or unilateral analgesia associated with this type of catheter.87,88 We are unaware of any studies comparing different designs of multiorifice catheters (e.g., longitudinal versus circumferential alignment of orifices).

Fractional Versus Single Bolus Injection
Administration of a specified dose of LA may result in different spread of blockade when injected as a single bolus compared to giving the same dose in smaller fractions.89 In low-thoracic epidural anesthesia, the effect of timing of fractionated doses of LA on the spread of sensory blockade has been investigated. Administration of two doses of 5 mL of LA with an interval of 5 min produced an epidural block of similar extent as a single injection of 10 mL of LA. However, with an interval of 10 min, the number of segments blocked was smaller compared to the two other modes of injection mentioned.89 The authors suggested that differences in residual epidural pressures (see below) may explain these differences. Also, prior injection of large volumes (5–10 mL) of saline, e.g., when the loss-of-resistance technique is used, may result in a greater spread of neural blockade after injecting LA.90 However, this phenomenon has only been observed using mepivacaine 1.5% and not when using mepivacaine 1%, indicating that dilution of the higher concentration by saline may also contribute.90 Also, this effect is exaggerated when the interval between both injections is short.91 We are unaware of similar studies in lumbar epidural anesthesia.

Speed of Injection
In lumbar epidural anesthesia, only one study has reported a positive correlation between speed of injection and cranial spread of blockade: Injection through a Tuohy needle of 14 mL lidocaine 2% at a rate of 1.2 mL/s resulted in a spread of sensory blockade four segments greater compared to injection at a rate of 0.24 mL/s.79 In contrast, rapid injection of mepivacaine 8 mL in 8 s versus 160 s resulted in the same number of dermatomes blocked after 15 min.92 However, onset of blockade was more rapid in the fast injection group. The number of patients with perineal blockade after 5 min was more than four times higher in the fast injection group compared to the slow injection group. A similar number of dermatomes blocked or maximum cranial level of blockade after 30 min with66,93 or without faster onset55 has also been reported by other investigators. Whether speed of injection may exert its effect on the spread of blockade through changes in epidural pressure remains controversial (see below).

Epidural Pressures and Pressures in Adjacent Body Cavities
Epidural Pressures
Pressure gradients within the epidural space, and between this space and adjacent body cavities may play a role in the distribution of LA injected in the thoracic epidural space.31,48 Since sensory block after both low-thoracic and high-thoracic epidural injection of lidocaine spreads from the site of injection toward the mid-thoracic epidural space,29,48,64,94 it has been suggested that the latter may harbor a lower pressure.48 This may facilitate spread of LA toward the mid-thoracic epidural space. Indeed, a small, but statistically significant, difference in epidural pressure has been demonstrated, with the mid-thoracic epidural pressure being slightly lower than the low-thoracic epidural pressure.95 Also, in this study, sub-atmospheric pressure was observed more frequently in the mid-thoracic compared to the low-thoracic epidural space. It is difficult to compare studies evaluating epidural pressures because of the many differences in study design, definition of epidural pressure, and lack of homogeneity in the populations studied. It should be noted that debate continues whether epidural pressure is positive or negative (with regard to atmosphere), and whether the pressures reported are true pressures or artifacts.96 Epidural pressure has been found to be positive by some authors,95,97–99 but slightly negative by others.31,96,100,101 In light of the pressures generated by epidural injection,102 it remains to be investigated whether pressure gradients within the epidural space are sufficient to influence spread of LA. Lumbar epidural pressure after epidural injection of LA may be correlated to the spread of sensory block. However, both positive19,31,35 and negative55,102,103 correlations have been reported.

Pressures in Adjacent Body Cavities
Since the epidural space is continuous (or contiguous) with many other body cavities, pressures in these cavities may also influence the spread of sensory blockade. The difference in patency after a given amount of injected air between the thoracic and lumbar epidural spaces, as seen by the epiduroscope, may be influenced by the negative intrapleural and positive intra-abdominal pressures.36 Increasing airway pressure using a continuous positive airway pressure (CPAP) device increases the number of segments blocked after a low-thoracic epidural injection of lidocaine by 57%, primarily through a more caudad spread of the block.104 Furthermore, a more cranial extension of sensory blockade was demonstrated after cervico-thoracic (C6–7 or C7–T1) epidural injection of lidocaine in patients breathing on CPAP.105 Therefore, when airway pressure is increased by the application of CPAP, the distal border of sensory blockade extends further away from the thorax, i.e., more cranially after high-thoracic injection,105 and more caudad after low-thoracic injection.104 Although speculative, a similar effect may occur during positive pressure ventilation in anesthetized patients.104

Alteration of epidural pressure by CPAP has not been confirmed.104 Although pneumoperitoneum during laparoscopic procedures106 and ventilation with positive end-expiratory pressure107 have been shown to increase epidural pressure, there are no studies that have investigated the effects of these maneuvers on the spread of epidural blockade.

Local Anesthetics
Total Dose, Concentration Versus Volume
Overall, the amount of LA injected influences the spread of epidural blockade. However, the notion that increasing the dose of LA results in a linear increase in the spread of blockade13 has often been questioned. Although there may be such a linear relationship in patients younger than 40 yr,14 in patients of 50 yr and older, the relationship between dose and number of segments blocked is dependent on the volume previously injected, i.e., the higher the volume already injected, the higher the dose requirement to block an additional segment (Fig. 3).14,21,23,108 Indeed, a linear relationship between subsequent segmental dose requirements and dose previously injected has been described.14,21,108 Given this complex relationship between LA dose and sensory blockade, formulas that have been proposed to predict segmental dose requirements of LA are equally complex.108 However, simpler formulas derived from cubic polynomial equations have been validated in clinical practice.109


Figure 352
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  		Figure 3. Scattergram and cubic polynomial fit between injected volume of 2% mepivacaine and number of anesthetized dermatomes. This figure illustrates the observation that the spread of epidural anesthesia changes proportionally more after a small volume of local anesthetic is administered than after a larger dose is given.122

 

Many studies have compared the effects of administering equal doses of LA, in solutions with different concentrations. The conclusion that the same total mass of drug given in different concentrations and volumes produces similar spread of sensory blockade and equally effective analgesia is widely supported in lumbar epidural anesthesia for bolus injections.2,20,110 In thoracic epidural anesthesia, this has been demonstrated both for single bolus injection48,111 and for continuous epidural infusion.112–115 However, some authors have reported cranial block levels 2–4 segments higher with low concentrations compared to higher concentrations of LA, without differences in quality of analgesia or incidence of motor block.116–119 Others have reported better analgesia with higher volumes of LA.120 Although administration of the same mass of LAs in different volumes results in similar spread of neural blockade, the intensity of blockade may vary with the concentration of LA. Differences in intensity of sensory blockade using cutaneous electrical stimulation between groups receiving equal amounts of LA in different volumes have both been confirmed121 and refuted.119 Most reports on perioperative epidural analgesia using bupivacaine have studied concentrations ranging from 0.1% to 0.5%. Since all studies mentioned above report equally satisfactory analgesia using different combinations of volume and concentration, the potential difference in intensity of blockade appears not to be clinically relevant.

It has been demonstrated that 2% lidocaine diluted with the same volume of saline produces less potent epidural blockade, in terms of number of segments blocked and achievement of perineal blockade, than commercially prepared 1% lidocaine.122 This may be explained by differences in the concentrations of sodium, chloride, hydroxide, and hydrogen ions.122

Additives to Local Anesthetics
Bicarbonate
An increase in pH by adding bicarbonate to a solution of LA results in an increase in the nonionized fraction of the LA and improved nerve penetration.123,124 Adding bicarbonate increases the pain threshold in blocked dermatomes,125–127 increases the depth of motor block,127 and reduces the time to onset of blockade of the first sacral segment.127 In contrast, spread of sensory blockade as evaluated by pinprick is not affected,126,127 however, the sample sizes in these studies were based on pain threshold data and may have been too small to demonstrate a difference in spread of blockade.

{alpha}2 Agonists and Opioids
Stimulation of {alpha}2 receptors located in the spinal cord produces antinociception.128 Both epinephrine and clonidine produce segmental hypoalgesia.129 The addition of {alpha}2 agonists to LA results in faster onset and longer duration of sensory and motor blockade,130 decreased plasma LA levels,131 and improved intraoperative anesthetic quality.131 However, spread of sensory block has been shown to be similar after injection of levobupivacaine alone, or with various amounts of epinephrine.131

Opioids exert their spinal analgesic effects at the level of the dorsal horn.132 Whether epidurally injected opioids produce analgesia through a spinal or supra-spinal mechanism or both,132,133 is beyond the scope of this article. However, it is clear that the synergistic action134,135 between these two types of drugs allows a reduction in the dose and side effects of both LA and opioid, while enhancing the degree of pain relief. Adding opioids to epidural LA has been shown to hasten the onset, but not affect the spread of sensory blockade.136 No difference in extent of sensory blockade was demonstrated between groups receiving epidural bupivacaine with sufentanil added epidurally versus IV,137 whereas consumption of sufentanil in the epidural group was half that of the IV group. However, since sample size was based on sufentanil consumption, this study may have been under-powered to demonstrate a difference in spread of blockade.

Sympathetic Block
Over the last 10–15 yr, epidural sympathetic neural blockade has been recognized for its potential to improve outcome in cardiac138 and colorectal surgery.139 Sympathicolysis of the cardiac acceleration fibers (T1–4) may contribute to improved cardiac oxygen balance and decreased biochemical markers of perioperative cardiac ischemia,138 whereas blockade of the splanchnic sympathetic nerves (T6–L1) may protect against perioperative intestinal ischemia,140 and is associated with quicker return of bowel function and general recovery.139 Indeed, a future therapeutic role for low-thoracic epidural anesthesia has been suggested in the treatment of septic shock.140

Despite the possible presence of a small zone of differential block, spread of sympathetic blockade generally follows the same patterns as sensory blockade.141,142 Using changes in regional skin temperature in the lower extremities as an indirect indicator of diminished efferent sympathetic nerve activity, both animal143 and human144 studies have indicated that the sympathetic blockade associated with segmental high-thoracic epidural anesthesia may extend caudally beyond the area of sensory blockade. However, the change in foot skin temperature is much smaller compared to that induced by lumbar epidural anesthesia.144 Furthermore, direct techniques, such as muscle and skin sympathetic nerve activity measurements with microelectrodes, have shown no inhibition of resting sympathetic nerve activity to the lower extremities by thoracic epidural anesthesia limited to the upper thoracic dermatomes.145 Conversely, lumbar epidural anesthesia induces compensatory vasoconstriction146 and increased cardiac sympathetic nerve activity147 in unblocked segments. Therefore, when epidural anesthesia is to be used for both its analgesic and sympathicolytic effects, both these effects should be considered when selecting the site of epidural placement. This means, for example, that to provide complete blockade of the cardiac acceleration fibers, high-thoracic epidural anesthesia should be selected, and to block the splanchnic sympathetic system, low-thoracic epidural anesthesia should be used (Table 1).29,48


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  		Table 1. Recommendations for Epidural Catheter Insertion Site

 

Degrees of sympathetic blockade in clinical studies are most often derived from changes in hemodynamic variables, e.g., arterial blood pressure, heart rate or cardiac output. These cardiovascular sequelae of epidural anesthesia have been reviewed elsewhere.141 Specifically, factors that are positively correlated with the occurrence of hypotension and bradycardia during lumbar epidural anesthesia include increasing body weight, spread of sensory blockade, and the addition of fentanyl to the LA.148 In high-thoracic epidural anesthesia, no changes in hemodynamic variables were observed when comparing equal volumes of 0.25% bupivacaine to 0.375% in a crossover design.51

Motor Block
One of the attractive features of thoracic compared to lumbar epidural anesthesia is its lack of significant motor block of the lower extremities. However, motor block of the phrenic nerve and both upper and lower extremities can occur in thoracic epidural anesthesia, depending on the insertion site.

Phrenic Nerve Motor Block
Phrenic nerve function has been studied in patients receiving cervico-thoracic epidural anesthesia. Injection of 3105 or 15 mL52 of 2% lidocaine at the C7–T1 interspace resulted in only mild changes in pulmonary function as measured by forced expiratory volume in 1 min, forced vital capacity and maximum inspiratory pressure. In contrast, using the same variables and epidural catheters placed at the same interspace, a clinically important impairment of pulmonary function was observed in a concentration-dependent manner after injection of both bupivacaine 0.25% or 0.37550 and lidocaine 0.5%, 1% and 2%.149 In an older study, inspiratory capacity, vital capacity, total lung capacity, and forced expiratory volume in 1 min were reduced by thoracic epidural anesthesia using 10 mL of mepivacaine 2% at both the C7–T1 and T12–L1 levels.150 These changes were significantly greater with high-thoracic compared to low-thoracic epidural anesthesia. In contrast, functional residual capacity decreased after low-thoracic, but not after high-thoracic epidural anesthesia. Changes in Po2 and Pco2 were only minor. The authors concluded that motor block of both the diaphragm and the intercostal muscles may play a role in the ventilatory changes.

Upper Extremity Motor Block
A concentration-dependent decrease of hand strength has been demonstrated in cervico-thoracic epidural anesthesia.50 Mild hand weakness occurred in 16% of patients receiving continuous high-thoracic epidural anesthesia for cardiac surgery.151 Using a scoring scale for arm movements, decreased upper extremity motor function was demonstrated in 30% of patients with epidural catheters between C7 and T4.152 Indeed, this scale has been proposed to serve as a simple and reliable method for the early detection of cephalad spread of thoracic epidural anesthesia, before this affects phrenic nerve function.152

Lower Extremity Motor Block
Some degree of lower extremity motor block is common in lumbar epidural anesthesia. With continuous infusion of LA, increasing degrees of motor blockade have been reported with increasing infusion rates while the concentration of the LA is held constant,153 or when the concentration of LA is increased while the infusion rate is held constant.115,154 Therefore, similar to the spread of sensory blockade, total mass of LA appears to be the most important factor concerning the degree of lower extremity motor block. This has been confirmed in volunteers receiving different concentrations and volumes of equal doses of LA.119 Adding opioids to the LA accelerates the onset of motor blockade in lumbar epidural anesthesia.136 The intensity of motor block is not influenced by the speed of epidural injection,92 whereas it is increased when bicarbonate is added to the LA127 and in older patients.15,25,26,155 The decrease in conduction velocity in older patients affects motor nerves in particular,37 which may explain why there is less controversy on the effect of age on motor blockade compared to the effect of age on sensory blockade. Lumbar epidural injection in the lateral position results in more profound motor block on the dependent side.18,60 While not a clinically useful variable, posterior epidural fat volume is inversely correlated with the degree of motor block.47

In thoracic epidural anesthesia, lower extremity motor block can often be avoided, or is present in only mild degrees.113,114,116–118,156 A high concentration of LA in a low volume may cause less motor block to the lower extremities in thoracic epidural anesthesia,114 although this could not be confirmed in other studies by the same117 and other authors.156 Placement of catheters in proximity to lumbar spinal segments increases the risk of motor block when compared to a more cephalad placement.117,157,158 The severity of lower extremity motor block in thoracic epidural anesthesia may also be decreased by using patient-controlled epidural analgesia instead of continuous infusion of LA, as this results in smaller amounts of drugs used, while maintaining equally satisfactory levels of analgesia.113,156,159

CONCLUSION

Factors Affecting the Distribution of Epidural Block
Distribution of sensory blockade after epidural injection of LA varies widely among individuals, and may only be partially predicted based upon known factors. Based on this review, the total mass of LA appears to be most important factor in determining the extent of sensory, sympathetic, and motor neural blockade, while the site of epidural needle/catheter insertion governs the pattern of distribution of sensory blockade relative to the injection site. Age may be positively correlated with the spread of sensory blockade, although the evidence is somewhat stronger for thoracic than for lumbar epidural anesthesia. Other patient characteristics and technical details such as patient position and mode and speed of injection have all been shown to exert only a small effect on the distribution of sensory blockade, or their effects are controversial. However, combinations of several patient and technical factors may aid in predicting LA dose requirements. Also, maneuvers such as rapid injection, placing the patient in the lateral position, or adding bicarbonate to LA solutions may be applied to quicken the onset of blockade. The influence of the factors mentioned above may be summarized in a semi-quantitative fashion as presented in Table 2.


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  		Table 2. Summary of Factors Affecting the Spread of Epidural Neural Blockade

 

Selection of Epidural Insertion Site
It has been suggested that epidural catheters should be sited at an intervertebral space that represents the middle of the area of surgical incision.115 However, we feel this advice does not consider the different patterns of distribution after single injection or continuous infusion of LA. Also, with the recent recognition of the beneficial effects of sympathicolysis, sympathetic epidural blockade in a particular area of the body may be considered as important as satisfactory analgesia. Based on this review, we have formulated suggested epidural insertion sites for various surgical indications that may serve to accomplish both goals (Table 1).

ACKNOWLEDGMENTS

The authors thank Dr. André van Zundert and Dr. Quinn Hogan for critically reviewing and discussing earlier versions of the manuscript.

Footnotes

Reprints will not be available from the authors.

Accepted for publication April 18, 2008.

REFERENCES

  1. Park WY. Factors influencing distribution of local anesthetics in the epidural space. Reg Anesth 1988;13:49–57[Web of Science]
  2. Bromage PR. Mechanism of action of extradural analgesia. Br J Anaesth 1975;47:199–211[Web of Science][Medline]
  3. Wheatly RG, Schug SA, Watson D. Safety and efficacy of postoperative epidural analgesia. Br J Anaesth 2001;87:47–61[Abstract/Free Full Text]
  4. Pennefather SH, Gilby S, Danecki A, Russell GN. The changing practice of thoracic epidural analgesia in the United Kingdom: 1997–2004. Anaesthesia 2006;61:363–9[Web of Science][Medline]
  5. Marret E, Gibert S, Bonnet F. Can epidurography help to predict the extent of epidural blockade? Anesthesiology 2005;102:478–9[Web of Science][Medline]
  6. Slappendel R, Gielen MJM, Hasenbos MAWM, Heystraten FMJ. Spread of radiopaque dye in the thoracic epidural space. Anaesthesia 1988;43:939–42[Web of Science][Medline]
  7. Reina MA, De Andrés JA, Maches F, Lopez A. Anatomy of the epidural space and new insights. Highlights in regional anaesthesia and pain therapy. Proceedings of the 25th Annual Meeting of the Eur Society of Regional Anaesthesia (ESRA), 2006
  8. Elizaga AM, ed. Illustrated notes in regional anesthesia. 1997. Available at http://depts.washington.edu/anesth/regional/Page1.html
  9. Hogan QH. Epidural anatomy: new observations. Can J Anaesth 1998;45:R40–R44[Web of Science][Medline]
  10. Hogan QH. Lumbar epidural anatomy: a new look by cryomicrotome section. Anesthesiology 1991;75:767–75[Web of Science][Medline]
  11. Curatolo M, Petersen-Felix S, Arendt-Nielsen L. Assessment of regional analgesia in humans: a review of methods and applications. Anesthesiology 2000;93:1517–30[Web of Science][Medline]
  12. Curatolo M, Orlando A, Zbinden AM, Scaramozzino P, Venuti FS. A multifactorial analysis of the spread of epidural analgesia. Acta Anesthesiol Scand 1994;38:646–52[Web of Science][Medline]
  13. Bromage PR. Exaggerated spread of epidural analgesia in arteriosclerotic patients: dosage in relation to biological and chronological ageing. BMJ 1962;2:1634–8[Free Full Text]
  14. Sharrock NE. Epidural anesthetic dose response in patients 20 to 80 years old. Anesthesiology 1978;49:425–8[Web of Science][Medline]
  15. Nydahl PA, Philipson L, Axelsson K, Johansson JE. Epidural anesthesia with 0.5% bupivacaine: influence of age on sensory and motor blockade. Anesth Analg 1991;73:780–6[Abstract/Free Full Text]
  16. Simon MJ, Veering BT, Stienstra R, van Kleef JW, Burm AG. The effect of age on neural blockade and hemodynamic changes after epidural anesthesia with ropivacaine. Anesth Analg 2002;94:1325–30[Abstract/Free Full Text]
  17. Finucane BT, Hammonds WD, Welch MB. Influence of age on vascular absorption of lidocaine from the epidural space. Anesth Analg 1987;66:843–6[Abstract/Free Full Text]
  18. Grundy EM, Ramamurthy S, Patel KP, Mani M, Winnie AP. Extradural analgesia revisited: a statistical study. Br J Anaesth 1978;50:805–9[Abstract/Free Full Text]
  19. Hirabayashi Y, Matsuda I, Sohzaburoh I, Shimizu R. Spread of epidural analgesia following a constant pressure injection-an investigation of relationships between locus of injection, epidural pressure and spread of analgesia. J Anesth 1987;1:44–50[Medline]
  20. Duggan J, Bowler GM, McClure JH, Wildsmith JA. Extradural block with bupivacaine: influence of dose, volume, concentration and patient characteristics. Br J Anaesth 1988;61:324–31[Abstract/Free Full Text]
  21. Andersen S, Cold GE. Dose response studies in elderly patients subjected to epidural analgesia. Acta Anaesthesiol Scand 1981;25:279–81[Web of Science][Medline]
  22. Whalley DG, D’Amico JA, Rybicki LA, Gottlieb A, Ryckman JV, Schoenwald PK, Bedocs NM. The effect of posture on the induction of epidural anesthesia for peripheral vascular surgery. Reg Anesth 1995;20:407–11[Web of Science][Medline]
  23. Park WY, Hagins FM, Rivat EL, Macnamara TE. Age and epidural dose response in adult men. Anesthesiology 1982;56:318–20[Web of Science][Medline]
  24. Park WY, Massengale MD, Kim SI, Poon KC, Macnamara TE. Age and the spread of local anesthetic solutions in the epidural space. Anesth Analg 1980;59:768–71[Abstract/Free Full Text]
  25. Veering BT, Burm AG, van Kleef JW, Hennis PJ, Spierdijk J. Epidural anesthesia with bupivacaine: effects of age on neural blockade and pharmacokinetics. Anesth Analg 1987;66:589–93[Abstract/Free Full Text]
  26. Veering BT, Burm AGL, Vletter AA, van den Heuvel RP, Onkenhout W, Spierdijk J. The effect of age on the systemic absorption, disposition and pharmacodynamics of bupivacaine after epidural administration. Clin Pharmacokinet 1992;22:75–84[Web of Science][Medline]
  27. Hirabayashi Y, Shimizu R. Effect of age on extradural dose requirement in thoracic extradural anaesthesia. Br J Anaesth 1993;71:445–6[Abstract/Free Full Text]
  28. Holman SJ, Bosco RR, Kao TC, Mazzilli MA, Dietrich KJ, Rolain RA, Stevens RA. What constitutes an effective but safe initial dose of lidocaine to test a thoracic epidural catheter? Anesth Analg 2001;93:749–54[Abstract/Free Full Text]
  29. Yokoyama M, Hanazaki M, Fujii H, Mizobuchi S, Nakatsuka H, Takahashi T, Matsumi M, Takeuchi M, Morita K. Correlation between the distribution of contrast medium and the extent of blockade during epidural anesthesia. Anesthesiology 2004;100:1504–10[Web of Science][Medline]
  30. Saitoh K, Hirabayashi Y, Shimizu R, Mitsuhata H, Fukuda H. Extensive extradural spread in the elderly may not relate to decreased leakage through intervertebral foramina. Br J Anaesth 1995;75:688–91[Abstract/Free Full Text]
  31. Usubiaga JE, Wikinski JA, Usubiaga LE. Epidural pressure and its relation to spread of anesthetic solutions in the epidural space. Anesth Analg 1967;46:440–6[Free Full Text]
  32. Burn JM, Gruyer PB, Langdon L. The spread of solutions injected into the epidural space: a study using epidurograms in patients with the lumbosciatic syndrome. Br J Anaesth 1973;45:338–45[Abstract/Free Full Text]
  33. Bromage PR. Tissue space connections. In: Bromage PR, ed. Epidural analgesia. Philadelphia: WB Saunders, 1978:31–2
  34. Shanta TR, Evans JA. The relationship of epidural anesthesia to neural membranes and arachnoid villi. Anesthesiology 1972;37:543–57[Web of Science][Medline]
  35. Hirabayashi Y, Shimizu R, Matsuda I, Inowe S. Effect of extradural compliance and resistance on spread of extradural analgesia. Br J Anaesth 1990;65:508–13[Abstract/Free Full Text]
  36. Igarashi T, Hirabayashi Y, Shimizu R, Saitoh K, Fukuda H, Mitsuhata H. The lumbar extradural structure changes with increasing age. Br J Anaesth 1997;78:149–52[Abstract/Free Full Text]
  37. Dorfman LJ, Bosley TM. Age-related changes in peripheral and central nerve conduction in man. Neurology 1979;29:38–44[Abstract/Free Full Text]
  38. Bromage PR. Spread of analgesic solutions in the epidural space and their site of action: a statistical study. Br J Anaesth 1962;34:161–78[Free Full Text]
  39. Wu HT, Schweitzer ME, Parker L. Is epidural fat associated with body habitus? J Comput Assist Tomogr 2005;29:99–102[Web of Science][Medline]
  40. Datta S, Lambert DH, Gregus J, Gissen AJ, Covino BG. Differential sensitivities of mammalian nerve fibers during pregnancy. Anesth Analg 1983;62:1070–2[Abstract/Free Full Text]
  41. Kaneko M, Saito Y, Kirihara Y, Kosaka Y. Pregnancy enhances the antinociceptive effects of extradural lignocaine in the rat. Br J Anaesth 1994;72:657–61[Abstract/Free Full Text]
  42. Flanagan HL, Datta S, Lambert DH, Gissen AJ, Covino BG. Effect of pregnancy on bupivacaine-induced conduction blockade in the isolated rabbit vagus nerve. Anesth Analg 1987;66:123–6[Web of Science][Medline]
  43. Butterworth JF, Walker FO, Lysak SZ. Pregnancy increases median nerve susceptibility to lidocaine. Anesthesiology 1990;72:962–5[Web of Science][Medline]
  44. Fagraeus L, Urban BJ, Bromage PR. Spread of epidural analgesia in early pregnancy. Anesthesiology 1983;58:184–7[Web of Science][Medline]
  45. Arakawa M. Does pregnancy increase the efficacy of lumbar epidural anesthesia? Int J Obstet Anesth 2004;13:86–90[Web of Science][Medline]
  46. Panni MK, Columb MO. Obese parturients have lower epidural local anaesthetic requirements for analgesia in labour. Br J Anaesth 2006;96:106–10[Abstract/Free Full Text]
  47. Higuchi H, Adachi Y, Kazama T. Factors affecting the spread and duration of epidural anesthesia with ropivacaine. Anesthesiology 2004;101:451–60[Web of Science][Medline]
  48. Visser WA, Liem TH, van Egmond J, Gielen MJM. Extension of sensory blockade after thoracic administration of a test dose of lidocaine at three different levels. Anesth Analg 1998;86:332–5[Abstract]
  49. Igarashi T, Hirabayashi Y, Shimizu R, Saitoh K, Fukuda H. Thoracic and lumbar extradural structure examined by extraduroscope. Br J Anaesth 1998;81:121–5[Abstract/Free Full Text]
  50. Capdevila X, Biboulet P, Rubenovitch J, Serre-Cousine O, Peray P, Deschodt J, d’Athis F. The effects of cervical epidural anesthesia with bupivacaine on pulmonary function in conscious patients. Anesth Analg 1998;86:1033–8[Abstract]
  51. Biboulet P, Deschodt J, Capdevila X, Landreau L, Aubas P, du Cailar J, d’Athis F. Hemodynamic effects of 0.375% versus 0.25% bupivacaine during cervical epidural anesthesia for hand surgery. Reg Anesth 1995;20:33–40[Web of Science][Medline]
  52. Stevens RA, Frey K, Sheikh T, Kao TC, Mikat-Stevens M, Morales M. Time course of the effects of cervical epidural anesthesia on pulmonary function. Reg Anesth Pain Med 1998;23:20–4[Web of Science][Medline]
  53. Grundy EM, Rao LN, Winnie AP. Epidural anesthesia and the lateral position. Anesth Analg 1978;57:95–7[Abstract/Free Full Text]
  54. Apostolou GA, Zarmakoupis PK, Mastrokostopoulos GT. Spread of epidural anesthesia and the lateral position. Anesth Analg 1981;60:584–6[Abstract/Free Full Text]
  55. Husemeyer RP, White DC. Lumbar extradural injection pressures in pregnant women: an investigation of relationships between rate of injection, injection pressures, and extent of analgesia. Br J Anaesth 1980;52:55–60[Abstract/Free Full Text]
  56. Park WY, Hagins FM, Macnamara TE. Lateral position and epidural anesthetic spread. Anesth Analg 1983;62:278–9
  57. Preston R, Crosby ET, Kotarba D, Dudas H, Elliott RD. Maternal positioning affects fetal heart rate changes after epidural analgesia for labour. Can J Anaesth 1993;40:1136–41[Web of Science][Medline]
  58. Soetens FM, Meeuwis HC, van der Donck AG, de Vel MA, Schijven MP, van Zundert AA. Influence of maternal position during epidural labor analgesia. Int J Obstet Anesth 2003;12:98–101[Web of Science][Medline]
  59. Shapiro A, Fredman B, Zohar E, Olsfanger D, Abu-Ras H, Jedeikin R. Alternating patient position following the induction of obstetric epidural analgesia does not affect local anaesthetic spread. Int J Obstet Anesth 1998;7:153–6[Web of Science][Medline]
  60. Seow LT, Lips FJ, Cousins MJ. Effect of lateral posture on epidural blockade for surgery. Anaesth Intensive Care 1983;11:97–102[Web of Science][Medline]
  61. Park WY, Hagins FM, Massengale MD, Macnamara TE. The sitting position and anesthetic spread in the epidural space. Anesth Analg 1984;63:863–4[Free Full Text]
  62. Setayesh AR, Kholdebarin AR, Saber Moghadam M, Setayesh HR. The Trendelenburg position increases the spread and accelerates the onset of epidural anesthesia for cesarean section. Can J Anaesth 2001;48:890–3[Web of Science][Medline]
  63. White N. Cephalad spread of epidural blockade in a 15-degree head-down position. Anaesthesia 1999;54:1007–8[Web of Science][Medline]
  64. Lee CJ, Jeon Y, Lim YJ, Bahk JH, Kim YC, Lee SC, Kim CS. The influence of neck flexion and extension on the distribution of contrast medium in the high thoracic epidural space. Anesth Analg 2007;104:1583–6[Abstract/Free Full Text]
  65. Park WY, Poon KC, Massengale MD, Macnamara TE. Direction of the needle bevel and epidural spread. Anesthesiology 1982;57:327–8[Web of Science][Medline]
  66. Rosenberg PH, Saramies L, Alila A. Lumbar epidural anaesthesia with bupivacaine in old patients: effect of speed and direction of injection. Acta Anaesthesiol Scand 1981;25:270–4[Web of Science][Medline]
  67. Borghi B, Agnoletti V, Ricci A, van Oven H, Montone N, Casati A. A prospective, randomized evaluation of the effects of epidural needle rotation on the distribution of epidural block. Anesth Analg 2004;98:1473–8[Abstract/Free Full Text]
  68. Dauri M, Sidiropoulou, Fabbi E, Mariani PP, Sabato AF. Intentional lateral epidural catheter placement for anterior cruciate ligament reconstruction. Acta Anaesthesiol Scand 2005;49:671–6[Web of Science][Medline]
  69. Buchheit T, Crews JC. Lateral cervical epidural catheter placement for continuous unilateral upper extremity analgesia and sympathetic block. Reg Anesth Pain Med 2000;25:313–7[Web of Science][Medline]
  70. Richardson MG, Wissler RN. The effects of needle bevel orientation during epidural catheter insertion in laboring parturients. Anesth Analg 1999;88:352–6[Abstract/Free Full Text]
  71. Tiso RL, Thomas PS, Macadaeg K. Epidural catheter direction and local anesthetic dose. Reg Anesth 1993;18:308–11[Web of Science][Medline]
  72. Choi DH, Lee SM, Cho HS, Ahn HJ. Relationship between the bevel of the Tuohy needle and catheter direction in thoracic epidural anesthesia. Reg Anesth Pain Med 2006;31:105–12[Web of Science][Medline]
  73. Hendriks GW, Hasenbos MA, Gielen MJ, van Egmond J, Barentz JO. Evaluation of thoracic epidural catheter position and migration using radio-opaque catheters. Anaesthesia 1997;52:457–9[Web of Science][Medline]
  74. Beilin Y, Bernstein HH, Zucker-Pinchoff B. The optimal distance that a multiorifice epidural catheter should be threaded into the epidural space. Anesth Analg 1995;81:301–4[Abstract]
  75. D’Angelo R, Berkebile B, Gerancher JC. Prospective examination of epidural catheter insertion. Anesthesiology 1996;84: 88–93[Web of Science][Medline]
  76. Hogan Q. Epidural catheter tip position and distribution of injectate evaluated by computed tomography. Anesthesiology 1999;90:964–70[Web of Science][Medline]
  77. Husain FJ, Herman NL, Karuparthy VR, Knape KG, Downing JW. A comparison of catheter vs needle injection of local anesthetic for induction of epidural anesthesia for cesarean section. Int J Obstet Anesth 1997;6:101–6[Web of Science][Medline]
  78. Yun MJ, Kim YC, Lim YJ, Choi GH, Ha M, Lee JY, Ham BM. The differential flow of epidural local anaesthetic via needle or catheter: a prospective randomized double-blind study. Anaesth Intensive Care 2004;32:377–82[Web of Science][Medline]
  79. Omote K, Namiki A, Iwasaki H. Epidural administration and analgesic spread: comparison of injection with catheters and needles. J Anesth 1992;6:289–93[Medline]
  80. Crochetière CT, Trépanier CA, Cotè JJ. Epidural anaesthesia for caesarean section: comparison of two injection techniques. Can J Anaesth 1989;36:133–6[Web of Science][Medline]
  81. Power I, Thorburn J. Differential flow from multihole epidural catheters. Anaesthesia 1988;43:876–8[Web of Science][Medline]
  82. Segal S, Eappen S, Datta S. Superiority of multi-orifice over single-orifice epidural catheters for labor analgesia and cesarean section. J Clin Anesth 1997;9:109–12[Web of Science][Medline]
  83. D’Angelo R, Foss ML, Livesay CH. A comparison of multiport and uniport epidural catheters in laboring patients. Anesth Analg 1997;84:1276–9[Abstract]
  84. Michael S, Richmond MN, Livesay CH. A comparison between open end (single hole) and closed end (three lateral holes) epidural catheters. Anaesthesia 1988;44:78–80[Web of Science]
  85. Morrison LM, Buchan AS. Comparison of complications associated with single-holed and multi-holed extradural catheters. Br J Anaesth 1990;64:183–5[Abstract/Free Full Text]
  86. Magides AD, Sprigg A, Richmond MN. Lumbar epidurography with multi-orifice and single-orifice catheters. Anaesthesia 1996;51:757–63[Web of Science][Medline]
  87. Jaime F, Mandell GL, Vallejo MC, Ramanathan S. Uniport soft-tip, open-ended catheters versus multiport firm-tipped close-ended catheters for epidural labor analgesia: a quality assurance study. J Clin Anesth 2000;12:89–93[Web of Science][Medline]
  88. Banwell BR, Morley-Forster P, Krause R. Decreased incidence of complications in parturients with the Arrow (Flex Tip Plus) epidural catheter. Can J Anaesth 1998;45:370–2[Web of Science][Medline]
  89. Okutomi T, Hashiba MM, Hashiba S, Masubuchi A, Morishima HO. The effects of single and fractionated doses of mepivacaine on the extent of thoracic epidural block. Reg Anesth Pain Med 2001;26:450–5[Web of Science][Medline]
  90. Okutomi T, Minakawa M, Hoka S. Saline volume and local anesthetic concentration modify the spread of epidural anesthesia. Can J Anaesth 1999;46:930–4[Web of Science][Medline]
  91. Okutomi T, Hoka S. Saline-anesthetic interval and the spread of epidural anesthesia. Can J Anaesth 1999;46:935–8[Web of Science][Medline]
  92. Kanai A, Suzuki A, Hoka S. Rapid injection of epidural mepivacaine speeds the onset of nerve blockade. Can J Anaesth 2005;52:281–4[Web of Science][Medline]
  93. Griffiths RB, Horton WA, Jones IG, Blake D. Speed of injection and spread of bupivacaine in the epidural space. Anaesthesia 1987;42:160–3[Web of Science][Medline]
  94. Hirabayashi Y, Matsuda I, Inoue S, Shimizu R. Epidural pressure and its relation to spread of epidural analgesia. J Anesth 1987;1:168–72[Medline]
  95. Visser WA, Gielen MJM, Giele JL, Scheffer GJ. Comparison of epidural pressures and incidence of true subatmospheric pressure between the mid-thoracic and low-thoracic epidural space. Anesth Analg 2006;103:1318–21[Abstract/Free Full Text]
  96. Bengis RG, Guyton AC. Some pressure and fluid dynamic characteristics of the canine epidural space. Am J Physiol 1977;232:H255–H259[Web of Science][Medline]
  97. Shah JL. Influence of cerebrospinal fluid on epidural pressure. Anaesthesia 1981;36:627–31[Web of Science][Medline]
  98. Telford RJ, Hollway TE. Observations on deliberate dural puncture with a Tuohy needle: pressure measurements. Anaesthesia 1991;46:725–7[Web of Science][Medline]
  99. Okutomi T, Watanabe S, Goto F. Time course in thoracic epidural pressure measurement. Can J Anaesth 1993;40:1044–8[Web of Science][Medline]
  100. Zarzur E. Genesis of the ‘true’ negative pressure in the lumbar epidural space. Anaesthesia 1984;39:1101–4[Web of Science][Medline]
  101. Usubiaga JE, Moya F, Usubiaga LE. Effect of thoracic and abdominal pressure changes on the epidural space pressure. Br J Anaesth 1967;39:612–8[Abstract/Free Full Text]
  102. Cardoso MM, Carvalho JC. Epidural pressures and spread of 2% lidocaine in the epidural space: influence of volume and speed of injection of the local anesthetic solution. Reg Anesth Pain Med 1998;23:14–9[Web of Science][Medline]
  103. Paul DL, Wildsmith JAW. Extradural pressure following the injection of two volumes of bupivacaine. Br J Anaesth 1989;62:368–72[Abstract/Free Full Text]
  104. Visser WA, Gielen MJM, Giele JLP. Continuous positive airway pressure breathing increases spread of sensory blockade after low-thoracic injection of lidocaine. Anesth Analg 2006;102:268–71[Abstract/Free Full Text]
  105. Visser WA, van Eerd MJPG, van Seventer R, Gielen MJM, Giele JL, Scheffer GJ. Continuous positive airway pressure breathing increases cranial spread of sensory blockade after cervico-thoracic injection of lidocaine. Anesth Analg 2007;105:868–71[Abstract/Free Full Text]
  106. Ogura A, Yoshikawa T, Ikeda K, Inoue T. Time course of epidural pressure change under intraperitoneal insufflation during laparoscopic surgery. Masui 1997;46:484–91[Medline]
  107. Iwama H, Ohmori S. Continuous monitoring of lower thoracic epidural pressure. J Crit Care 2000;15:60–3[Web of Science][Medline]
  108. Kaneko T, Iwama H. The association between injected volume of local anesthetic and spread of epidural anesthesia: a hypothesis. Reg Anesth Pain Med 1999;24:153–7[Web of Science][Medline]
  109. Iwama H, Ohmizo H, Kaneko T. Estimation of spread of lumbar or lower thoracic epidural anesthesia by a simple equation. J Anesth 2000;14:224–5[Medline]
  110. Nakayama M, Yamamoto J, Ichinose H, Yamamoto S, Kanaya N, Namiki A. Effects of volume and concentration of lidocaine on epidural anaesthesia in pregnant females. Eur J Anaesthesiol 2002;19:808–11[Web of Science][Medline]
  111. Renck H, Edstrom H, Kinnberger B, Brandt G. Thoracic epidural analgesia-II: prolongation in the early postoperative period by continuous injection of 1% bupivacaine. Acta Anaesthesiol Scand 1976;20:47–56[Web of Science][Medline]
  112. Laveaux MM, Hasenbos MA, Harbers JB, Liem T. Thoracic epidural bupivacaine plus sufentanil: high concentration/low volume versus low concentration/high volume. Reg Anesth 1993;18:30–43[Web of Science][Medline]
  113. Dernedde M, Stadler M, Bardiau F, Seidel L, Boogaerts JG. Low vs. high concentration of levobupivacaine for postoperative epidural analgesia: influence of mode of delivery. Acta Anaesthesiol Scand 2006;50:613–21[Web of Science][Medline]
  114. Dernedde M, Stadler M, Bardiau F, Boogaerts JG. Continuous epidural infusion of large concentration/small volume versus small concentration/large volume of levobupivacaine for postoperative analgesia. Anesth Analg 2003;96:796–801[Abstract/Free Full Text]
  115. Scott DA, Chamley DM, Mooney PH, Deam RK, Mark AH, Häglöff B. Epidural ropivacaine infusion for postoperative analgesia after major lower abdominal surgery–a dose finding study. Anesth Analg 1995;81:982–6[Abstract]
  116. Dernedde M, Nuyens V, Stadler M, Boogaerts JG. Comparison of two concentrations of levobupivacaine for postoperative continuous epidural analgesia. Anesthesiology 2006;105:A93
  117. Dernedde M, Stadler M, Bardiau F, Boogaerts JG. Comparison of different concentrations of levobupivacaine for post-operative epidural analgesia. Acta Anaesthesiol Scand 2003;47:884–90[Web of Science][Medline]
  118. Pittoni G, Mangano A, Arcidiacono S, Aiello L, Perona J. Post-operative analgesia: effectiveness of different concentrations of epidural levobupivacaine. Anesthesiology 2006; 105:A1631
  119. Liu SS, Ware PD, Rajendran S. Effects of concentration and volume of 2-chloroprocaine on epidural anesthesia in volunteers. Anesthesiology 1997;86:1288–93[Web of Science][Medline]
  120. Snijdelaar DG, Hasenbos MA, van Egmond J, Wolff AP, Liem TH. High thoracic epidural sufentanil with bupivacaine: continuous infusion of high volume versus low volume. Anesth Analg 1994;78:490–4[Abstract/Free Full Text]
  121. Sakura S, Sumi M, Kushizaki H, Saito Y, Kosaka Y. Concentration of lidocaine affects intensity of sensory block during lumbar epidural anesthesia. Anesth Analg 1999;88:123–7[Abstract/Free Full Text]
  122. Kanai A, Hoka S. A comparison of epidural blockade produced by plain 1% lidocaine and 1% lidocaine prepared by dilution of 2% lidocaine with the same volume of saline. Anesth Analg 2006;102:1851–5[Abstract/Free Full Text]
  123. Strobel GE, Bianchi CP. The effects of pH gradients on the action of procaine and lidocaine in intact and desheathed sciatic nerves. J Pharmacol Exp Ther 1970;172:1–17[Abstract/Free Full Text]
  124. Strobel GE, Bianchi CP. The effects of pH gradients on the uptake and distribution of C14-procaine and lidocaine in intact and desheathed sciatic nerve trunks. J Pharmacol Exp Ther 1970;172:18–32[Abstract/Free Full Text]
  125. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Lauber R, Högström H, Scaramozzino P, Luginbühl M, Sieber TJ, Zbinden AM. Adding sodium bicarbonate to lidocaine enhances the depth of epidural blockade. Anesth Analg 1998;86:341–7[Abstract]
  126. Arakawa M, Aoyama Y, Ohe Y. Block of the sacral segments in lumbar epidural anaesthesia. Br J Anaesth 2003;90:173–8[Abstract/Free Full Text]
  127. Arakawa M, Aoyama Y, Ohe Y. Epidural bolus injection with alkalinized lidocaine improves blockade of the first sacral segment-a brief report. Can J Anaesth 2002;49:566–70[Web of Science][Medline]
  128. Yaksh TL. Pharmacology of spinal adrenergic systems which modulate spinal nociceptive processing. Pharmacol Biochem Behav 1985;22:845–58[Web of Science][Medline]
  129. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Fischer M, Zbinden AM. Epidural epinephrine and clonidine. Segmental analgesia and effects on different pain modalities. Anesthesiology 1997;87:785–94[Web of Science][Medline]
  130. Murphy TM, Mather LE, Stanton-Hicks M D’A, Bonica JJ, Tucker GT. The effects of adding adrenaline to etidocaine and lignocaine in extradural anaesthesia I: block characteristics and cardiovascular effects. Br J Anaesth 1976;48:893–8[Abstract/Free Full Text]
  131. Kopacz DJ, Helman JD, Nussbaum CE, Hsiang JNK, Nora PC, Allen HW. A comparison of epidural levobupivacaine 0.5% with or without epinephrine for lumbar spine surgery. Anesth Analg 2001;93:755–60[Abstract/Free Full Text]
  132. De Leon-Casasola OA, Lema MJ. Postoperative epidural opioids: what are the choices? Anesth Analg 1996;83:867–75[Abstract]
  133. Ginosar Y, Riley ET, Angst MS. The site of action of epidural fentanyl in humans: the difference between infusion and bolus administration. Anesth Analg 2003;97:1428–38[Abstract/Free Full Text]
  134. Kaneko M, Saito Y, Kirihara Y, Collins JG, Kosaka Y. Synergistic antinociceptive interaction after epidural coadministration of morphine and lidocaine in rats. Anesthesiology 1994;80:137–50[Web of Science][Medline]
  135. Vercauteren M, Meert TF. Isobolographic analysis of the interaction between epidural sufentanil and bupivacaine in rats. Pharmacol Biochem Behav 1997;58:237–42[Web of Science][Medline]
  136. Cherng CH, Yang CP, Wong CS. Epidural fentanyl speeds the onset of sensory and motor blocks during epidural ropivacaine anesthesia. Anesth Analg 2005;101:1834–7[Abstract/Free Full Text]
  137. Joris JL, Jacob EA, Sessler DI, Deleuse J-FJ, Kaba A, Lamy ML. Spinal mechanisms contribute to analgesia produced by epidural sufentanil combined with bupivacaine for postoperative analgesia. Anesth Analg 2003;97:1446–51[Abstract/Free Full Text]
  138. Williams JP. Thoracic epidural anesthesia for cardiac surgery. Can J Anaesth 2002;49:R1–R6
  139. Carli F, Kehlet H. Continuous epidural analgesia for colonic surgery–but what about the future? Reg Anesth Pain Med 2005;30:140–2[Web of Science][Medline]
  140. Sielenkämper AW, van Aken H. Thoracic epidural anesthesia, more than just anesthesia/analgesia. Anesthesiology 2003; 99:523–5[Web of Science][Medline]
  141. Veering BT, Cousins MJ. Cardiovascular and pulmonary effects of epidural anaesthesia. Anaesth Intensive Care 2000; 28:620–35[Web of Science][Medline]
  142. Brull SJ, Greene NM. Zones of differential sensory block during extradural anaesthesia. Br J Anaesth 1991;66:651–5[Abstract/Free Full Text]
  143. Peters J, Kousulis L, Arndt J. Effects of segmental thoracic extradural analgesia on sympathetic block in conscious dogs. Br J Anaesth 1989;63:470–6[Abstract/Free Full Text]
  144. Hopf H-B, Weiszbach B, Peters J. High thoracic segmental epidural anesthesia diminishes sympathetic outflow to the legs, despite restriction of sensory blockade to the upper thorax. Anesthesiology 1990;73:882–9[Web of Science][Medline]
  145. Magnusdottir H, Kirnö K, Ricksten S-E, Elam M. High thoracic epidural anesthesia does not inhibit sympathetic nerve activity in the lower extremities. Anesthesiology 1999;91:1299–304[Web of Science][Medline]
  146. Baron J-F, Payen D, Coriat P, Edouard A, Viars P. Forearm vascular tone and reactivity during lumbar epidural anesthesia. Anesth Analg 1988;67:1065–70[Web of Science][Medline]
  147. Tanaka M, Goyagi T, Kimura T, Nishikawa T. The effects of cervical and lumbar epidural anesthesia on heart rate variability and spontaneous sequence baroreflex sensitivity. Anesth Analg 2004;99:924–9[Abstract/Free Full Text]
  148. Curatolo M, Scaramozzino P, Venuti FS, Orlando A, Zbinden AM. Factors associated with hypotension and bradycardia after epidural blockade. Anesth Analg 1996;83:1033–40[Abstract]
  149. Kushizaki H, Doi K, Sakura S, Saito Y. High thoracic epidural anesthesia with lidocaine, concentration and effect on pulmonary function. Anesthesiology 2005;103:A969[Web of Science][Medline]
  150. Takasaki M, Takahashi T. Respiratory function during cervical and thoracic epidural analgesia in patients with normal lungs. Br J Anaesth 1980;52:1271–6[Abstract/Free Full Text]
  151. Barrington MJ, Kluger R, Watson R, Scott DA, Harris KJ. Epidural anesthesia for coronary artery bypass surgery compared with general anesthesia alone does not reduce biochemical markers of myocardial damage. Anesth Analg 2005; 100:921–8[Abstract/Free Full Text]
  152. Abd Elrazek E, Scott NB, Vohra A. An epidural scoring scale for arm movements (ESSAM) in patients receiving high thoracic epidural analgesia for coronary artery bypass grafting. Anaesthesia 1999;54:1097–109[Web of Science][Medline]
  153. Etches RC, Writer WDR, Ansley D, Nydahl PA, Ong BY, Lui A, Badner N, Kawolski S, Muir H, Shukla R, Beattie WS. Continuous epidural ropivacaine 0.2% for analgesia after lower abdominal surgery. Anesth Analg 1997;84:784–90[Abstract]
  154. Murdoch JAC, Dickson UK, Wilson PA, Berman JS, Gad-Elrab RR, Scott NB. The efficacy and safety of three concentrations of levobupivacaine administered as a continuous epidural infusion in patients undergoing orthopedic surgery. Anesth Analg 2002;94:438–44[Abstract/Free Full Text]
  155. Li Y, Zhu S, Bao F, Xu J, Yan X, Jin X. The effects of age on the median effective concentration of ropivacaine for motor blockade after epidural anesthesia with ropivacaine. Anesth Analg 2006;102:1847–50[Abstract/Free Full Text]
  156. Liu SS, Moore JM, Luo AM, Trautman WJ, Carpenter RL. Comparison of three solutions of ropivacaine-fentanyl for postoperative patient controlled epidural analgesia. Anesthesiology 1999;90:727–33[Web of Science][Medline]
  157. Liu SS, Allen HW, Olsson GL. Patient-controlled epidural analgesia with bupivacaine and fentanyl on hospital wards: prospective experience with 1030 surgical patients. Anesthesiology 1998;88:688–95[Web of Science][Medline]
  158. Schug SA, Scott DA, Payne J, Mooney PH, Hägglöf B. Postoperative analgesia by continuous extradural infusion of ropivacaine after upper abdominal surgery. Br J Anaesth 1996; 76:487–91[Abstract/Free Full Text]
  159. Standl T, Burmeister M-A, Ohnesorge H, Wilhelm S, Striepke M, Gottschalk A, Horn EP, Schulte Am Esch J. Patient-controlled epidural analgesia reduces analgesic requirements compared to continuous epidural infusion after major abdominal surgery. Can J Anaesth 2003;50:258–64[Web of Science][Medline]
  160. Salvi L, Sisillo E, Brambillasca C, Juliano G, Salis S, Marino MR. High thoracic epidural anesthesia for off-pump coronary artery bypass surgery. J Cardiothorac Vasc Anesth 2004;18:256–62[Web of Science][Medline]
  161. Liem TH, Booij LHDJ, Hasenbos MAWM, Gielen MJM. Coronary artery bypass grafting using two different anesthetic techniques: part I: hemodynamic results. J Cardiothorac Vasc Anesth 1992;6:148–55[Medline]
  162. Goertz AW, Seeling W, Heinrich H, Lindner KH, Schirmer U. Influence of high thoracic epidural anesthesia on left ventricular contractility assessed using the end-systolic pressure-length relationship. Acta Anaesthesiol Scand 1993;37:38–44[Web of Science][Medline]
  163. Licker M, Spiliopoulos A, Tschopp JM. Influence of thoracic epidural analgesia on cardiovascular autonomic control after thoracic surgery. Br J Anaesth 2003;91:525–31[Abstract/Free Full Text]
  164. Senard M, Joris JL, Ledoux D, Toussaint PJ, Lahaye-Goffart B, Lamy ML. A comparison of 0.1% and 0.2% ropivacaine and bupivacaine combined with morphine for patient-controlled epidural analgesia after major abdominal surgery. Anesth Analg 2002;95:444–9[Abstract/Free Full Text]




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