ADMINISTRATION OF LOCAL ANESTHETIC into the subarachnoid space results in a reliable and rapid onset of dense surgical anesthesia. Despite the technical simplicity of spinal blocks, the anesthesiologist should possess a thorough understanding of the anatomy of the lumbosacral spine, the determinants of subarachnoid local anesthetic distribution, and the factors that influence block duration. Furthermore, knowledge of the physiologic effects and potential complications related to spinal anesthesia is paramount to ensure patient safety.
I. Anatomy
A. Vertebral column. The vertebral column is composed of 33 vertebrae and 5 ligaments. Together, they form a protective exoskeleton around the spinal cord.
1. There are
7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4 coccygeal vertebral segments (
Fig. 6.1). Spinal anesthesia is typically performed in
the lower lumbar region. The lumbar vertebra is composed of an anterior vertebral body and posterior bony elements. The latter include two pedicles, which project posteriorly from the vertebral body, and two flattened laminae, which connect the pedicles to form the vertebral arch. The anterior and posterior bony elements combine to delineate the
vertebral foramen (
Fig. 6.2). Vertebral foramina of adjoining vertebrae form the longitudinal spinal canal, which houses the spinal cord. The adjoining paired pedicles of each vertebra display superior and inferior notches. The latter form the
intervertebral foramina through which the paired segmental spinal nerves exit the spinal canal (
Fig. 6.2). A single
spinous process projects posteriorly (and slightly caudally) from the posterior aspect of the vertebral arch at the midline junction of the paired laminae. The bony elements provide sites for muscular and ligamentous attachments
2. Five ligaments anchor the vertebral column (
Fig. 6.3). The
supraspinous ligament connects the tips of the spinous processes from the seventh cervical vertebra to the sacrum. The
interspinous ligament connects adjoining spinous processes. The laminae of adjacent vertebral arches are connected by the tough, wedge-shaped
ligamentum flavum, which is composed primarily of elastin. The ligamentum flavum binds the paired laminae of adjoining vertebrae together, thereby forming the
posterior wall of the vertebral spinal canal. It is this posterior ligamentous “opening” (i.e., the intervertebral or interlaminar space) that a spinal needle traverses to reach the subarachnoid space. Anatomic studies demonstrate a 9% to11% incidence of gaps in the midline of the ligamenta flava.
3. The vertebral column displays
characteristic curvatures in the lumbar and thoracic regions (
Figs. 6.1 and
6.4). Local anesthetic solution injected at the peak height of the lumbar anterior convexity (lumbar lordosis) will distribute both caudad and cephalad to varying degrees depending on the baricity of the solution. The cephalad spread of hyperbaric local anesthetic solutions is typically limited to the mid-to-upper thoracic dermatomes because of pooling within the thoracic concavity (thoracic kyphosis).
B.
Meninges. The spinal meninges consist of
three membranes (the
dura mater, arachnoid mater, and
pia mater). In conjunction with the cerebrospinal fluid (CSF), the meninges cushion the spinal cord and nerve roots in the subarachnoid space (
Fig. 6.5).
1. The
dura mater (“tough mother”), the outermost and thickest meningeal membrane, is composed primarily of collagen fibrils, interspersed with elastic fibers and ground substance in an anatomic arrangement that allows ready passage of drugs (
1). Historically, the dura was (incorrectly) assumed to be the primary barrier for drug diffusion from the epidural to the subarachnoid space. The dura mater forms the
dural sac, which consists of a long tubular sheath contained within the surrounding spinal canal, which extends from the foramen magnum to the lower border of the second sacral vertebra. At this level, the dural sac fuses with the filum terminale. The dura mater also extends laterally along the spinal nerve roots, becoming continuous with the epineurium of spinal nerves at the level of intervertebral foramina.
2. The
arachnoid mater, which is closely adherent to the inner surface of the dura mater, is composed of overlapping layers of flattened epithelial-like cells that are connected by frequent tight and occluding junctions (
2). The arachnoid is not directly attached to the dura
but is held against its inner surface (dura-arachnoid interface) by the pressure of the
CSF. During spinal anesthesia, the needle penetrates the dura and arachnoid simultaneously. Functionally, the arachnoid mater accounts for the resistance to drug diffusion through spinal meninges.
3. The
pia mater, which closely invests the surface of the spinal cord and nerve roots, is composed of three to six layers of cells (
3). The
subarachnoid space, which lies between the arachnoid mater and the pia mater and contains the CSF, constitutes the target compartment for spinal anesthesia. The pia mater extends to the conus medullaris, where it becomes the filum terminale. The latter anchors the spinal cord to the sacrum (
Fig. 6.5).
C. Spinal cord
1. The spinal cord is a
cylindrical structure that gives rise to 31 pairs of spinal nerves. In turn, each spinal cord segment gives rise to paired
ventral motor and dorsal sensory roots. Motor and sensory roots cross the subarachnoid space separately before joining together (close to the intervertebral foramina) to form the mixed spinal nerves. Although larger than their ventral counterparts, dorsal nerve roots commonly divide into two or three separate bundles upon exiting the spinal cord. In contrast, most ventral roots exit as a single bundle (
4). Moreover, as dorsal nerve root bundles course further laterally, they further subdivide into as many as 10 fascicles before the dorsal root becomes the dorsal root ganglion (
5). Therefore, the larger multifilamentous dorsal nerve roots offer a substantially larger surface area for local anesthetic uptake compared to the smaller, unitary ventral roots. This partially explains the faster onset of sensory versus motor blockade.
2. The skin area supplied by a spinal nerve (and its corresponding spinal cord segment) is called a
dermatome (
Fig. 6.6). Dermatomal assessment for the loss of sensory functions (such as temperature, pinprick, and touch) provides a surrogate marker for the segmental distribution of surgical anesthesia.
3. In adults, the
spinal cord is shorter than the vertebral column. The caudal extent of the spinal cord (known as the
conus medullaris [
Fig. 6.5]) usually extends to the
lower third of the first lumbar vertebral body, but may occasionally reach the upper third of the third lumbar vertebral body (
6) and rarely the L4 level. Therefore, attempting spinal anesthesia at or above the L2-L3 intervertebral space (IVS) could result in mechanical trauma to the spinal cord in a small number of patients.
4. The discrepancy in length between spinal cord and vertebral column results in a
progressive obliquity of the lower thoracic, lumbar, and sacral spinal nerve roots. The collection of spinal nerve roots caudal to the conus medullaris is known as the
cauda equina (
Fig. 6.5). The enlargement of the subarachnoid space containing the cauda equina is termed the
lumbar cistern. Local anesthetics are deposited within the latter during the performance of spinal anesthesia.
D. Surface anatomy
1. Accurate identification of
IVS levels is paramount for successful spinal anesthesia. The desired level is determined by the palpation of surface landmarks. A
line connecting the iliac crests (i.e., the intercristal or Tuffier’s line) most commonly intersects the vertebral column at the L4-L5 IVS (
Fig. 6.7) (
6). However, the intercristal line may intersect the vertebral column as cephalad as the L3-L4 IVS and as caudad as the L5-S1 IVS (
Fig. 6.8). Even
experienced anesthesiologists incorrectly identify the IVS 70% of the time (
7). Thus, inexperienced operators should preferentially
attempt spinal anesthesia at a lower lumbar (L3-L4 or L4-L5) IVS to minimize the potential risk for spinal cord injury (
8,
9). Fortunately, lumbar flexion, which is commonly used to improves access to the intervertebral-interlaminar space, does not alter the position of the intercristal line (
10).
II. Indications and contraindications
A.
The injection of local anesthetics into the subarachnoid space results in (afferent) sensory block as well as varying degrees of (efferent) motor block. The
cephalad extent of spinal anesthesia depends on the baricity of the local anesthetic solution as well as the patient’s position during the spinal block and the surgical procedure. The CSF concentration of local anesthetic decreases as the distance from the injection site starts to increase. This results in a gradient of afferent and efferent conduction block, which stems from the differential sensitivity of spinal nerve fibers to local anesthetic agents (
Table 6.1). For instance,
preganglionic efferent fibers are the most sensitive to local anesthetic conduction block and are commonly anesthetized
two to six dermatome segments more cephalad than afferent sensory block. In turn, sensory block can be
two to three dermatomes higher than efferent motor block (
11). Although sensory block can be used as a surrogate marker for surgical anesthesia, tolerance to transcutaneous electrical stimulation of 10-mA, 50-Hz continuous square wave for 5 seconds constitutes a more
reliable predictor of tolerance to surgical stimulation (
12).
B.
Knowledge of dermatomal projections is paramount to determine whether the sensory block is adequate for the planned surgical procedure, and to evaluate regression of the spinal block. For example, the
fourth thoracic dermatome corresponds to the nipples, the
sixth thoracic dermatome to the
xyphoid process, and the
tenth thoracic dermatome to the
umbilicus (
Table 6.2 and
Fig. 6.6). It is also essential to remember that viscera are innervated differently and that anesthesia of an overlying cutaneous region does not inherently confer surgical anesthesia on an underlying visceral organ (
Table 6.3).
C.
There exist absolute and relative contraindications to spinal anesthesia. Absolute contraindications include
patient refusal, infection at the puncture site, severe untreated hypovolemia, coagulopathy, and
increased intracranial pressure. Performance of spinal anesthesia in patients with
preexisting neurologic deficits such as radicular or peripheral neuropathies (
14,
15) and demyelinating diseases (e.g., multiple sclerosis) (
16) remains
controversial. This issue is discussed in the chapter pertaining to complications of regional anesthesia (
Chapter 14).
Aortic stenosis, once considered an absolute contraindication to spinal anesthesia, does not necessarily preclude a carefully conducted spinal anesthetic (
17). Although spinal blocks should not be performed in patients with untreated systemic infection, subjects with evidence of
systemic infection may safely undergo spinal anesthesia if appropriate antibiotic therapy has been initiated before dural puncture and response to therapy (e.g., decrease in fever and granulocytosis) demonstrated (
18).
III. Determinants of local anesthetic distribution and duration of action
A.
The clinical pharmacology of local anesthetics and adjuvants is addressed in Chapters 1 and 2. This section will discuss only the determinants of local anesthetic distribution and duration
for spinal anesthesia. From a pharmacodynamic standpoint, subarachnoid
distribution of local anesthetic agents determines the extent of sensorimotor and sympathetic block.
Uptake of local anesthetics dictates the neuronal functions most affected by the spinal block.
Elimination of local anesthetics from the subarachnoid space determines the duration of action.
B.
Determinants of subarachnoid local anesthetic distribution. Many factors have been proposed to explain the distribution of local anesthetic solutions in the subarachnoid space (
19,
20). After their injection, local anesthetics will initially spread by simple
bulk flow. Subsequently, the most important determinant of distribution is the
baricity of the local anesthetic solution. Other relevant factors include the
total dose, the IVS selected for injection, and several patient characteristics.
1. Baricity. Baricity is defined as the ratio of the density of the local anesthetic solution to the CSF density at 37°C. Local anesthetic solutions that possess the same density as CSF are termed
isobaric. Local anesthetic solutions that have a greater density than CSF are classified as
hyperbaric, whereas solutions with a lower density than CSF are termed
hypobaric. Hyperbaric solutions will sink to the most dependent areas, whereas hypobaric solutions will rise to the nondependent areas of the subarachnoid space. The effects of gravity are determined by the choice of patient position as well as by the natural curvatures of the spine. The mean density of CSF varies significantly among different patient subpopulations (
Table 6.4). Thus, local anesthetics (e.g., plain bupivacaine 0.5% and plain lidocaine 2.0%) commonly classified as “isobaric” may in fact behave in a hypobaric manner.
Table 6.4 lists the density range and classification of commonly used local anesthetics.
a. Hyperbaric spinal anesthesia. Hyperbaric solutions are commonly prepared by mixing the local anesthetic with
dextrose. When the patient is placed in the supine position after the injection of a hyperbaric solution, the latter will distribute toward the
lowest points of the thoracic (T6-T7) and sacral (S2) curvatures (
Fig. 6.4) (
21). In fact, pooling of hyperbaric local anesthetic solutions within the thoracic kyphosis has been postulated to explain its peak sensory block height in the midthoracic region (
22).
(1) Injection of hyperbaric local anesthetic solutions with the patient in the sitting position (for 5 to 10 minutes) has been (mistakenly) advocated to restrict distribution to the lumbosacral dermatomes, producing a so-called
“saddle block” (
Fig. 6.9). Unfortunately, clinical studies have demonstrated that a hyperbaric spinal anesthetic
block initially restricted to the lumbosacral dermatomes will eventually distribute to a peak thoracic height equivalent to that which would have been achieved had the patient been immediately placed in the supine position (
23).
Only gold members can continue reading.
Log In or
Register to continue
Related
Full access? Get Clinical Tree