I. Anatomy. The reader is referred to Chapter 6 (Spinal Anesthesia) for an in-depth discussion of neuraxial anatomy. For epidural blocks, one needs to remember certain key facts:

A. Surface landmarks can be used to estimate spinal levels and to select the optimal insertion site for continuous epidural blocks. For instance, the scapular spine, the inferior angle of the scapula, and the intercristal line correspond to the T3 level, T8 level, and L4-L5 intervertebral space, respectively (Fig. 7.1). However, significant interindividual variation exists. Thus, correlation between surface landmark and spinal level is approximate at best.

B. Spinous processes are almost horizontal in the cervical and lumbar levels. In contrast, they possess a moderate caudal angulation in the upper and lower thoracic levels. In the midthoracic spine, spinous processes display a notoriously sharp caudal angulation (Fig. 7.2). To further compound the technical challenge, the interlaminar spaces can be narrow, and laminae can sometimes overlap between T4 and T7.

C. The interspinous ligament, which connects adjacent spinous processes, displays a high incidence of age-related cysts.

D. Midline gaps can often be found in ligamenta flava in the cervical, thoracic, and lumbar levels.

E. The epidural space contains loose connective tissues, fat, arterial vessels, a plexus of veins, as well as nerve roots. Pockets of epidural adipose tissue are commonly found in the posterior and anterolateral epidural spaces (Fig. 7.3). Their pharmacokinetic importance stems from the fact that they act as a reservoir for lipophilic (opioid) drugs, thereby slowing the latter’s onset and/or increasing their duration of action. Epidural veins are usually confined to the anterior epidural space and rarely does one find a prominent vein posterior to the intervertebral foramen. The distance between ligamentum flavum and dura (i.e., the width of the epidural space) varies between 2 and 25 mm, with an average of 7 mm. The epidural space is largest at the lumbar level and progressively narrows as it ascends rostrally.

F. The dura mater is composed of multiple layers of collagen and elastic fibers. The latter do not display any specific orientation. The dura is closely adherent to the arachnoid mater, a 5- to 6-cell-thick layer whose fibers run parallel to the spinal axis. Contrary to popular belief, the arachnoid mater (and not the dura) is responsible for containing the cerebrospinal fluid inside the intrathecal space.

II. Pharmacology

A. Site of action. Although local anesthetics can penetrate the spinal meninges to reach the cerebrospinal fluid, spinal cord transmission remains intact, thus indicating that the spinal cord itself is not the primary site of action. Instead, animal studies suggest that epidural blocks target the extradural spinal nerves (which traverse the epidural space) as well as the spinal nerve rootlets (within the subarachnoid space).

B. Local anesthetic agents. Only preservative-free local anesthetic solutions should be used in the epidural space. Local anesthetics are commonly classified according to their duration of action. The latter can be defined in terms of “two-dermatome regression” (i.e., the time it takes a block to recede by two dermatomes from its maximum extent), which estimates the duration of effective surgical block, or “complete resolution,” which approximates the time required for outpatient discharge (Table 7.1).

1. Short duration. Chloroprocaine (2% or 3%) provides the fastest onset and the shortest duration for epidural blockade (Fig. 7.4). Large doses of preservative-free chloroprocaine have been associated with back pain, whereas lower doses (900 mg) may result in mild back pain. The latter usually appears immediately unlike the back pain associated with Transient Neurologic Symptoms. For reasons unknown, epidural chloroprocaine decreases the efficacy of subsequently administered epidural morphine and clonidine.

2. Intermediate duration. These agents provide an onset that is comparable to that of chloroprocaine. However, their slower rate of resolution may delay outpatient discharge. Lidocaine
(1.5% or 2.0%) provides excellent anesthesia for 60 to 90 minutes (as a single injection) but can result in tachyphylaxis (i.e., decreasing duration with repeated injection) when (repeatedly) administered through an epidural catheter. The mechanism behind tachyphylaxis remains poorly understood, but may stem from changes in drug distribution/elimination from the epidural space. Mepivacaine (1% or 1.5%) can produce a slightly longer block than lidocaine.

3. Long duration. Bupivacaine (0.5% or 0.75%), which is supplied as a racemic mixture of the levo- and dextrorotatory optical isomers, produces a denser sensory than motor block. This property explains its popularity (in dilute concentrations) for continuous epidural blocks. Bupivacaine displays a slower uptake from the epidural space than intermediate-duration local anesthetics, and thus has less potential for systemic toxicity caused by local anesthetic absorption. However, because of its inherent cardiotoxicity, bupivacaine should not be used
in high doses, and inadvertent intravascular injection should be avoided by using a test dose and incremental injection. Ropivacaine, a single optical isomer, is less cardiotoxic but also 40% less potent than bupivacaine in the epidural space. If one accounts for this difference in potency, contrary to popular belief, it does not have greater “motor sparing” effects than bupivacaine despite its increased cost.

C. Adjuvants. The duration of sensory and/or motor block produced by local anesthetic agents can be “fine-tuned” with various adjuvants.

1. Epinephrine. A 5 µg/mL concentration of epinephrine prolongs the duration of sensorimotor block produced by short- and intermediate-duration local anesthetics, but not by long-duration drugs. In addition to this pharmacokinetic effect, epinephrine also displays α₂-adrenergic agonistic properties and may decrease pain transmission in the spinal cord. Compared to plain local anesthetic agents, the addition of epinephrine results in a greater decrease in the mean arterial pressure (MAP) (Fig. 7.5). The lower MAP is caused by a reduction in systemic vascular resistance (SVR), which seems to be mediated by the vasodilatory β₂-adrenergic properties of low-dose epinephrine. The decrease in SVR also leads to a significantly higher cardiac output and a modestly elevated heart rate. Animal studies reveal that the presence
of epinephrine in the local anesthetic solution does not decrease cardiovascular toxicity in the event of accidental intravascular injection. However, epinephrine will decrease the plasmatic levels of local anesthetics (through its α₁-vasoconstrictive properties) and provide a marker for intravascular injection (through its β₁-chronotropic properties).

2. Opioids. The addition of opioids to epidural local anesthetics increases the duration of sensory, but not motor block. The magnitude (and duration) of sensory prolongation depends on the dose administered and the opioid chosen. For instance, hydrophilic opioids (e.g., morphine) provide a greater effect than their hydrophobic counterparts (e.g., fentanyl). Moreover, they display greater rostral spread in the epidural space.

3. Clonidine. Epidural clonidine (150 to 300 µg) prolongs sensory, but not motor block. Unlike epinephrine, its effect occurs with long-acting local anesthetic agents. Epidural clonidine can result in sedation as well as a decrease in blood pressure. Unlike epinephrine, epidural clonidine is associated with a modest decrease in heart rate.

4. Bicarbonate. Addition of sodium bicarbonate (0.1 mEq/mL) to local anesthetic agents has been historically advocated to hasten the onset of epidural block. This effect is unreliable at best.

D. Dose. Within the epidural space, local anesthetic solutions spread cephalad and caudad from the initial injection site (Fig. 7.6). Unfortunately, it is impossible to predict with certainty the dose required to produce a given extent of epidural blockade. Consequently, clinicians must be cognizant of the major and minor factors that determine the spread of epidural blocks (Table 7.2).

1. Dose, volume, and concentration. Dose and volume constitute independent predictors of the spread of epidural blockade. In other words, increasing the dose while keeping the volume constant (i.e., increasing the drug concentration) and increasing the drug volume while keeping the dose constant (i.e., decreasing concentration) will both increase the extent of epidural blockade. Unfortunately, the relationship is not linear: as the dose is increased, the spread per milliliter injected decreases so the net increase in spread is only a few dermatomes.

2. Technique. Because local anesthetic can spread cephalad and caudad from the injection site, the latter becomes an important determinant of dermatomes blocked. With mid- to high thoracic epidural blocks, local anesthetic molecules tend to diffuse in a caudal direction, whereas lower epidural blocks display a predominantly cephalad local anesthetic spread. Because the volume of the epidural space increases as one moves caudad, a greater local anesthetic dose is required to anesthetize the same number of dermatomes in the lumbar/caudal level compared to the thoracic level. Gravity, needle angulation, direction of needle aperture, and speed of injection confer negligible effects on the spread of epidural blocks.

3. Patient factors. The influence of pregnancy on the spread of epidural blockade is controversial. Interestingly, pregnant women are more sensitive to the effects of local anesthetics. In theory, increasing age, short stature, and obesity contribute to increase the spread of epidural blocks. However, the effect is small, and considerable interindividual variability exists.