• Roy Greengrass, MD

        INTRODUCTION WITH GENERAL CONSIDERATIONS & BRIEF HISTORY

Carl Koller, an ophthalmologist from Vienna, first described the use of topical cocaine for analgesia of the eye in 1884.¹ William Halsted and Richard Hall, surgeons at Roosevelt Hospital in New York City, took the idea of local anesthesia a step further by injecting cocaine into human tissues and nerves in order to produce anesthesia for surgery.² James Leonard Corning, a neurologist in New York City, described the use of cocaine for spinal anesthesia in 1885.³ Since Corning was a frequent observer at Roosevelt Hospital, the idea of using cocaine in the subarachnoid space may have come from observing Halsted and Hall performing cocaine injections. Corning first injected cocaine intrathecally into a dog and within a few minutes the dog had marked weakness in the hindquarters.⁴ Next, Corning injected cocaine into a man at the Tl1-T12 interspace into what he thought was the subarachnoid space. Since Corning did not notice any effect after 8 min, he repeated the injection. Ten minutes after the second injection, the patient complained of sleepiness in his legs, but was able to stand and walk. Because Corning made no mention of cerebrospinal fluid (CSF) efflux, most likely he inadvertently gave an epidural rather than a spinal injection to the patient.

        Durai puncture was described by Essex Wynter in 1891⁵ followed shortly by Heinrich Quincke 6 months later.⁶ Augustus Karl Gustav Bier, a German surgeon, used cocaine intrathecally on six patients for lower extremity surgery in 1898.^7,8 In true scientific fashion, Bier decided to experiment on himself and developed a postdural puncture headache (PDPH) for his efforts. His assistant, Dr. Otto Hildebrandt, volunteered to have the procedure performed after Bier was unable to continue due to the PDPH. After injection of spinal cocaine into Hildebrandt, Bier conducted experiments on the lower half of Hildebrandt’s body. Bier described needle pricks and cigar burns to the legs, incisions on the thighs, avulsion of pubic hairs, strong blows with an iron hammer to the shins, and torsion of the testicles. Hildebrandt reported minimal to no pain during the experiments; however, afterward he suffered nausea, vomiting, PDPH, and bruising and pain in his legs. Bier attributed the PDPH to loss of CSF and felt the use of small-gauge needles would help prevent the headache.⁹

        Dudley Tait and Guido Caglieri performed the first spinal anesthetic in the United States in San Francisco in 1899. Their studies included cadavers, animals, and live patients in order to determine the benefits of lumbar puncture, especially in the treatment of syphilis. Tait and Caglieri injected mercuric salts and iodides into the CSF, but worsened the condition of one patient with tertiary syphilis.¹⁰ Rudolph Matas, a vascular surgeon in New Orleans, described the use of spinal cocaine on patients and possibly was the first to use morphine in the subarachnoid space.^11,12 Matas also described the complication of death after lumbar puncture. Theodore Tuffier, a French surgeon in Paris, studied spinal anesthesia and reported on it in 1900. Tuffier felt that cocaine should not be injected until cerebrospinal fluid was recognized.¹³ Tuffier taught at the University of Paris at the same time that Tait was a medical student there and most likely was one of Tait’s mentors. Tuffier’s demonstrations in Paris helped popularize spinal anesthesia in Europe.

        Arthur Barker, a professor of surgery at the University of London, reported on the advancement of spinal techniques in 1907, including the use of a hyperbaric spinal local anesthetic, emphasis of sterility, and ease of midline over paramedian dural puncture.¹⁴ Advancement of sterility and the investigation of decreases in blood pressure after injection helped make spinal anesthesia safer and more popular. Gaston Labat was a strong proponent of spinal anesthesia in the United States and performed early studies on the effects of Trendelenburg position on blood pressure after spinal anesthesia.¹⁵ George Pitkin attempted to use a hypobaric local anesthetic to control the level of spinal block by mixing procaine with alcohol.¹⁶ Lincoln Sise, an anesthesiologist at the Lahey Clinic in Boston, used Barker’s technique of hyperbaric spinal anesthesia with both procaine and tetracaine.^17–19

        Spinal anesthesia became more popular as new developments occurred, including the introduction of saddle block anesthesia by Adriáni and Roman-Vega in 1946.²⁰ The height of spinal anesthesia’s popularity in the United States occurred in the 1940s, but fears of neurologic deficits and complications caused anesthesiologists to discontinue the use of spinal anesthesia. The development of novel intravenous anesthetic agents and neuromuscular blockers coincided with the decreased use of spinal anesthesia. In 1954 Dripps and Vandam described the safety of spinal anesthetics in more than 10,000 patients,²¹ and spinal anesthesia was revived.

        The early development of spinal needles paralleled the early development of spinal anesthesia. Corning chose a gold needle that had a short bevel point, flexible cannula, and set screw that fixed the needle to the depth of dural penetration. Corning also used an introducer for the needle, which was right-angled. Quincke used a beveled needle that was sharp and hollow. Bier developed his own sharp needle that did not require an introducer. The needle was larger bore (15-gauge or 17-gauge) with a long, cutting bevel. The main problems with Bier’s needle were pain on insertion and the loss of local anesthetic due to the large hole in the dura after dural puncture. Barker’s needle did not have an inner cannula, was made of nickel, and had a sharp, medium- length bevel with a matching stylet. Labat developed an unbreakable nickel needle that had a sharp, short-length bevel with a matching stylet. Labat believed that the short bevel minimized damage to the tissues when inserted into the back.

        Herbert Greene realized that loss of CSF was a major problem in spinal anesthesia and developed a smooth tip, smaller gauge needle that resulted in a lower incidence of PDPH.²² Barnett Greene described the use of a 26-gauge spinal needle in obstetrics with a decreased incidence of PDPH.²³ The Greene needle was very popular until the introduction of the Whitacre needle. Hart and Whitacre used a pencil-point needle to decrease PDPH from 5-10% to 2%.²⁴ Sprotte modified the Whitacre needle and published his trial of over 34,000 spinal anesthetics in 1987.²⁵ Modifications of the Sprotte needle occurred the 1990s to produce the needle that is in use today.²⁶

        Spinal anesthesia has progressed greatly since 1885 and has become standard technique in a number of different clinical situations. However, anatomy, choice of local anesthetic, physiologic effects of spinal anesthesia, patient positioning, and the approach to spinal anesthesia must all be considered. The patient should be educated about the possible side effects and complications that can occur from performing a spinal anesthetic in order to obtain informed consent before the procedure. Spinal anesthesia is an invaluable technique that all anesthesiologists should have in their armamentarium.

        CONTRAINDICATIONS TO SPINAL ANESTHESIA

There are absolute and relative contraindications to spinal anesthesia. The only absolute contraindications include patient refusal, infection at the site of injection, hypovolemia, indeterminate neurologic disease, severe coagulopathy, and increased intracranial pressure, except in cases of pseudotumor cerebri. Relative contraindications include sepsis distinct from the anatomic site of puncture (eg, chorioamnionitis or lower extremity infection) and unknown duration of surgery. In the former case, if the patient is treated with antibiotics and the vital signs are stable, spinal anesthesia may be considered.

        Prior to placing a spinal anesthetic, the anesthesiologist should examine the patient’s back to look for any signs of local skin infection, which may carry the risk of CNS infection. Preoperative hemodynamic instability or hypovolemia increase the risk of hypotension after placement of a spinal anesthetic. High intracranial pressure increases the risk of uncal herniation when CSF is lost through the needle. Coagulation abnormalities increase the risk of hematoma formation. It is also important to communicate with the surgeon to determine the amount of time needed to complete the operation before inducing spinal anesthesia. If the duration of surgery is unknown, the spinal anesthetic given may not last long enough to cover the surgery. Knowing the duration of surgery helps the anesthesiologist determine the local anesthetic that will be used, addition of additives such as epinephrine, and whether a spinal catheter will be necessary.

Clinical Pearls

        Performing spinal anesthesia in patients with neurologic diseases, such as multiple sclerosis, is controversial. In vitro experiments that suggest that demyelinated nerves are more susceptible to local anesthetic toxicity. However, no clinical study has convincingly demonstrated that spinal anesthesia worsens a preexisting neurologic disease. Indeed, perioperative pain, stress, fever, and fatigue can all exacerbate these diseases; therefore, a stress-free central neuraxial block may be preferred for surgery.^27–31 Significant cardiac disease when sensory levels above T6 are required may present a relative contraindication to spinal anesthesia.^32,33 Aortic stenosis, once considered to be an absolute contraindication for spinal anesthesia, does not always preclude a carefully conducted spinal anesthetic.^34–36 Severe deformities of the spinal column can increase the difficulty in placing a spinal anesthetic. Arthritis, kyphoscoliosis, and previous lumbar fusion surgery do not contraindicate a spinal anesthetic. It is essential to examine the patient’s back to determine any anatomic abnormality before attempting a spinal anesthetic.

        FUNCTIONAL ANATOMY OF SPINAL BLOCKADE

In reviewing the functional anatomy of spinal blockade, an intimate knowledge of the spinal column, spinal cord, and spinal nerves must be present. This chapter reviews briefly the curvature of the vertebral column, the ligaments of the spinal column, membranes and length of the spinal cord, and passage of the spinal nerves from the spinal cord.

        The vertebral column consists of 33 vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4 coccygeal segments. The vertebral column usually contains three curves. The cervical and lumbar curves are convex anteriorly, and the thoracic curve is convex posteriorly. The vertebral column curves, along with gravity, baricity of local anesthetic, and patient position, influence the spread of local anesthetics in the subarachnoid space. Figure 13-1 depicts the spinal column, vertebrae, and intervertebral discs and foramina.

        Five ligaments hold the spinal column together (Figure 13-2). The supraspinous ligaments connect the apices of the spinous processes from the seventh cervical vertebra (C7) to the sacrum. The supraspinous ligament is known as the ligamentum nuchae in the area above C7. The interspinous ligaments connect the spinous processes together. The ligamentum flavum, or yellow ligament, connects the laminae above and below together. Finally, the posterior and anterior longitudinal ligaments bind the vertebral bodies together.

Clinical Pearls

        The three membranes that protect the spinal cord are the dura mater, arachnoid mater, and pia mater (Figure 13-3). The dura mater, or ttough mother”, is the outermost layer. The dural sac extends to the second sacral vertebra (S2). The arachnoid mater is the middle layer, and the subdural space lies between the dural mater and arachnoid mater. The arachnoid mater, or cobweb mother, also ends at S2, like the dural sac. The pia mater, or soft mother, clings to the surface of the spinal cord and ends in the filum terminale, which helps to hold the spinal cord to the sacrum. The space between the arachnoid and pia mater is known as the subarachnoid space, and spinal nerves run in this space, as does CSF. Figure 13-3 depicts the spinal cord, dorsal root ganglia and ventral rootlets, spinal nerves, sympathetic trunk, rami communicantes, and pia, arachnoid, and dura mater.

Figure 13-1. The spinal column is seen from a lateral view. All of the vertebrae, intervertebral discs, and intervertebral foraminae are shown.

        When performing a spinal anesthetic using the midline approach, the layers of anatomy that are traversed (from posterior to anterior) are skin, subcutaneous fat, supraspinous ligament, interspinous ligament, ligamentum flavum, dura mater, subdural space, arachnoid mater, and finally the subarachnoid space. When the paramedian technique is used, the spinal needle should traverse the skin, subcutaneous fat, ligamentum flavum, dura mater, subdural space, arachnoid mater, and then pass into the subarachnoid space.

        The length of the spinal cord varies according to age. In the first trimester, the spinal cord extends to the end of the spinal column, but as the fetus ages, the vertebral column lengthens more than the spinal cord. At birth, the spinal cord ends at approximately L3 and in the adult, the cord ends at approximately LI with 30% of people having a cord that ends at T12 and 10% at L3. Figure 13-4 shows a cross section of the lumbar vertebrae and spinal cord. The position of the conus medullaris, cauda equina, termination of the dural sac, and filum terminale are shown. A sacral spinal cord in an adult has been reported, though this is extremely rare.³⁷ The length of the spinal cord must always be kept in mind when a neuraxial anesthetic is performed, as injection into the spinal cord can result in severe neurologic complications or in paralysis.³⁸

Figure 13-2. A cross section of the spinal canal is shown with the ligaments, vertebral body, and spinous processes.

        Spinal nerves in the cervical region are named according to the upper cervical vertebral body from which they exit, with the exception of the eighth cervical nerve, which exits from below the seventh cervical vertebral body. This method of naming then continues in the thoracic and lumbar regions. The spinal nerve roots and spinal cord serve as the target sites for spinal anesthesia.

Figure 13-3. The spinal cord is shown along with the dorsal root ganglia and ventral rootlets, spinal nerves, sympathetic trunk, rami communicantes, and pia, arachnoid, and dura mater.

Figure 13-4. A cross section of the lumbar vertebrae and spinal cord. The position of the conus medullaris, cauda equina, termination of the dural sac, and filum terminale are shown.

Surface Anatomy

When preparing for spinal anesthetic blockade, it is important to accurately identify landmarks on the patient. The iliac crests usually mark the interspace between the fourth and fifth lumbar vertebrae; a line can be drawn between them to help locate this interspace. Care must be taken to feel for the soft area between the spinous processes to locate the interspace. Depending on the level of anesthesia necessary for the surgery and the ability to feel for the interspace, the L3-4 interspace or the L4-5 interspace can be used to introduce the spinal needle. Because the spinal cord ends at the LI to L2 level, spinal anesthesia at or above this level is usually not advised.

Clinical Pearls

        It would be incomplete to discuss surface anatomy without mentioning the dermatomes that are important for spinal anesthesia. A dermatome is an area of skin innervated

by sensory fibers from a single spinal nerve. The tenth thoracic (T10) dermatome corresponds to the umbilicus, the sixth thoracic (T6) dermatome the xiphoid, and the fourth thoracic (T4) dermatome the nipples. Figure 13-5 illustrates the dermatomes of the human body. To achieve surgical anesthesia for a given procedure, the extent of spinal anesthesia must reach a certain dermatomal level. Dermatomal levels of spinal anesthesia, required for common surgical procedures are listed in Table 13-1.

        PHARMACOLOGY

The choice of local anesthetic is based on potency of the agent, onset and duration of anesthesia, and side effects of the drug. Two distinct groups of local anesthetics are used in spinal anesthesia, esters and amides, which are characterized by the bond that connects the aromatic portion and the intermediate chain. Esters contain an ester link between the aromatic portion and the intermediate chain, and examples include procaine, chloroprocaine, and tetracaine. Amides contain an amide link between the aromatic portion and the intermediate chain, and examples include bupivacaine, ropivacaine, etidocaine, lidocaine, mepivacaine, and prilocaine. Although metabolism is important for determining activity of local anesthetics, lipid solubility, protein binding, and pK_a also influence activity.³⁹

Clinical Pearls

        Lipid solubility relates to the potency of local anesthetics. Low lipid solubility indicates that higher concentrations of local anesthesia must be given to obtain nerve blockade. Conversely, high lipid solubility produces anesthesia at low concentrations. Protein binding affects the duration of action of a local anesthetic. Higher protein binding results in longer duration of action. The pK_a of a local anesthetic is the pH at which ionized and nonionized forms are present equally in solution, which is important because the nonionized form allows the local anesthetic to diffuse across the lipophilic nerve sheath and reach the sodium channels in the nerve membrane. The onset of action relates to the amount of local anesthetic available in the base form. Most local anesthetics follow the rule that the lower the pK_a, the faster the onset of action and vice versa. Please refer to Chapter 6 (Clinical Pharmacology of Local Anesthetics) for more discussion of this topic.

Figure 13-5. The dermatomes of the human body.

Pharmacokinetics of Local Anesthetics in the Subarachnoid Space

Pharmacokinetics of local anesthetics includes uptake and elimination of the drug. Four factors play a role in the uptake of local anesthetics from the subarachnoid space into neuronal tissue, (1) concentration of local anesthetic in CSF, (2) surface area of nerve tissue exposed to CSF, (3) lipid content of nerve tissue, and (4) blood flow to nerve tissue.^40,41

        The uptake of local anesthetic is greatest at the site of highest concentration in the CSF and is decreased above and below this site. As discussed previously, uptake and spread of local anesthetics after spinal injection are determined by multiple factors including dose, volume, and baricity of local anesthetic and patient positioning.

        Both the nerve roots and the spinal cord take up local anesthetics after injection into the subarachnoid space. The more surface area of the nerve root exposed, the greater the uptake of local anesthetic.^42–45 The spinal cord has two mechanisms for uptake of local anesthetics. The first mechanism is by diffusion from the CSF to the pia mater and into the spinal cord, which is a slow process. Only the most superficial portion of the spinal cord is affected by diffusion of local anesthetics. The second method of local anesthetic uptake is by extension into the spaces of Virchow-Robin, which are the areas of pia mater that surround the blood vessels that penetrate the central nervous system. The spaces of Virchow-Robin connect with the perineuronal clefts that surround nerve cell bodies in the spinal cord and penetrate through to the deeper areas of the spinal cord.

Clinical Pearls

        Lipid content determines uptake of local anesthetics. Heavily myelinated tissues in the subarachnoid space contain higher concentrations of local anesthetics after injection. The higher the degree of myelination, the higher the concentration of local anesthetic, as there is a high lipid content in myelin. If an area of nerve root does not contain myelin, an increased risk of nerve damage occurs in that area.⁴⁶

        Blood flow determines the rate of removal of local anesthetics from spinal cord tissue. The faster the blood flow in the spinal cord, the more rapid the anesthetic is washed away. This may partly explain why the concentration of local anesthetics is greater in the posterior spinal cord than in the anterior spinal cord, even though the anterior cord is more readily accessed by the Virchow-Robin spaces. After a spinal anesthetic is administered, blood flow may be increased or decreased to the spinal cord, depending on the particular local anesthetic administered, eg, tetracaine increases cord flow but lidocaine and bupivacaine decrease it, which affects elimination of the local anesthetic.^47–49

Figure 13-6. A representation of the periarterial Virchow-Robin spaces around the spinal cord.

        Elimination of local anesthetic from the subarachnoid space is by vascular absorption in the epidural space and the subarachnoid space. Local anesthetics travel across the dura in both directions. In the epidural space, vascular absorption can occur, just as in the subarachnoid space. Vascular supply to the spinal cord consists of vessels located on the spinal cord and in the pia mater. Because vascular perfusion to the spinal cord varies, the rate of elimination of local anesthetics varies.⁴⁰

Distribution

The distribution and decrease in concentration of local anesthetics is based on the area of highest concentration, which can be independent of the injection site. Many factors affect the distribution of local anesthetics in the subarachnoid space. Table 13-2 lists some of these factors.⁵⁰

        The three most important factors for determining spread of local anesthesia in the subarachnoid space are baricity of the local anesthetic solution, position of the patient during and just after injection, and dose of the anesthetic injected.

        Baricity plays an important role in determining the spread of local anesthetic in the spinal space and is equal to the density of the local anesthetic divided by the density of the CSF at 37°C.^51–58 Local anesthetics can be hyperbaric, hypobaric, or isobaric when compared to CSF, and baricity is the main determinant of how the local anesthetic is distributed when injected into the CSF. Table 13-3 compares the density, specific gravity, and baricity of different substances and local anesthetics.^{50,51,53,59,60}

    CSF = cerebrospinal fluid.

        Hypobaric solutions are less dense than CSF and tend to rise against gravity. Isobaric solutions are as dense as CSF and tend to remain at the level at which they are injected. Hyperbaric solutions are more dense than CSF and tend to follow gravity after injection.

        Hypobaric solutions have a baricity of less than 1.0 relative to CSF and are usually made by adding distilled sterile water to the local anesthetic. Tetracaine, dibucaine, and bupivacaine have all been used as hypobaric solutions in spinal anesthesia. Patient positioning is important after injection of a hypobaric spinal anesthetic because it is the first few minutes that determine the spread of anesthesia. If the patient is in Trendelenburg position after injection, the anesthetic will spread in the caudal direction and if the patient is in reverse Trendelenburg position, the anesthetic will spread cephalad after injection. If a procedure were to be performed in the perineal or anal area in the prone, jackknife position, a hypobaric spinal anesthetic would be an excellent choice to avoid the need for waiting for the anesthetic to “set in” and repositioning the patient after injection.

Clinical Pearls

        The baricity of isobaric solutions is equal to 1.0. Tetracaine and bupivacaine have both been used with success for isobaric spinal anesthesia, and patient positioning does not affect spread of the local anesthetic, unlike the case with hyperbaric or hypobaric solutions. Injection can be made in any position, and then the patient can be placed into the position necessary for surgery. Gravity dose not play a role in the spread of isobaric solutions, unlike with hypo- or hyperbaric local anesthetics.

        Hyperbaric solutions in spinal anesthesia have baricity greater than 1.0. A local anesthetic solution can be made hyperbaric by adding dextrose or glucose. Bupivacaine, lidocaine and tetracaine have all been used as hyperbaric solutions in spinal anesthesia. Patient positioning affects the spread of the anesthetic. A patient in Trendelenburg position would have the anesthetic travel in a cephalad direction and vice versa.

        Dose and volume both play a role in the spread of local anesthetics after spinal injection, although dose has been shown to be more important than volume.⁶¹ Concentration of local anesthetic before injection has no bearing on distribution because after injection, due to the mixing of the CSF and local anesthetic, there is a new concentration.

Effects of the Volume of the Lumbar Cistern on Block Height

CSF is produced in the brain at 0.35 mL/min and fills the subarachnoid space. This clear, colorless fluid has an approximate volume of 150 mL in adults, half of which is in the cranium and half in the spinal canal. However, CSF volume varies considerably, and decreased CSF volume can result from obesity, pregnancy, or any other cause of increased abdominal pressure.⁶² This is partly due to compression of the intervertebral foramen, which displaces the CSF.

Clinical Pearls

        Multiple factors affect the distribution of local anesthesia after spinal blockade,⁵⁰ one being CSF volume. Carpenter showed that lumbosacral CSF volume correlated with peak sensory block height and duration of surgical anesthesia.⁶³ The density of CSF is related to peak sensory block level, and lumbosacral CSF volume correlates to peak sensory block level, and onset and duration of motor block.⁶⁴ However, due to the wide variability in CSF volume the ability to predict the level of the spinal blockade after local anesthetic injection is very poor, even if body mass index (BMI) is calculated and used.

Local Anesthetics

Cocaine was the first spinal anesthetic used, and procaine and tetracaine soon followed. Spinal anesthesia with lidocaine, bupivacaine, tetracaine, mepivacaine, and ropivacaine have also been introduced in clinical use over the last several decades. Some of the more common local anesthetics used for spinal anesthesia will be discussed in this portion of the chapter. In addition, there is a growing interest in medications that produce anesthesia and analgesia while limiting side effects. A variety of medications, including vasoconstrictors, opioids, ???-adrenergic agonists, and acetylcholinesterase inhibitors, have been added to spinal medications to enhance analgesia while reducing the motor blocade with local anesthetics.

        Lidocaine was first used as a spinal anesthetic in 1945, and it had been one of the most widely used spinal anesthetics since. Onset of anesthesia occurs in 3 to 5 min with a duration of anesthesia that lasts for 1 to 1.5 h. Lidocaine spinal anesthesia can be used for short to intermediate length operating room cases. One drawback of lidocaine has been the association with transient neurologic symptoms (TNS), which present as low back pain and lower extremity dysesthesias with radiation to the buttocks, thighs, and lower limbs after recovery from spinal anesthesia. TNS occurs in about 14% of patients receiving lidocaine spinal anesthesia.^65–67 Because of the risk of TNS associated with lidocaine, other intermediateacting local anesthetics with lower risk of TNS are being used instead of lidocaine in many practices.

    * Lidocaine has been less commonly used in the last decade due to the association with TNS.

Clinical Pearls

        Bupivacaine is a viable alternative to lidocaine for spinal anesthesia and has been used frequently with very little incidence of TNS.^68–70 Onset of anesthesia occurs in 5 to 8 min with a duration of anesthesia that lasts from 90 to 150 min; thus it is appropriate for intermediate to long operating room cases. For outpatient spinal anesthesia, small doses of bupivacaine are recommended to avoid prolonged discharge time due to offset of block. Bupivacaine has almost replaced lidocaine as the most commonly used spinal local anesthetic in the United States. Bupivacaine is often packaged as 0.75% in 8.25% dextrose. Other forms of spinal bupivacaine include 0.5% with or without dextrose and 0.75% without dextrose.

        Tetracaine has an onset of anesthesia within 3 to 5 min and a duration of 70 to 180 min, and like bupivacaine, is used for cases that are intermediate to longer duration. The 1% solution is. often mixed with 10% glucose in equal parts to form a hyperbaric spinal anesthetic that is used for perineal and abdominal surgery. With tetracaine, TNS occurs at a lower rate than with lidocaine spinal anesthesia. The addition of phenylephrine however, may play a role in the development of TNS.^71–73

        Mepivacaine is similar to lidocaine and has been used since the 1960s for spinal anesthesia. The incidence of TNS reported after mepivacaine spinal anesthesia varies widely, with rates from 0% to 30%.^74–76 Ropivacaine was introduced in 1996. For applications in spinal anesthesia, ropivacaine has been found to be less potent than spinal bupivacaine. Ropivacaine has significantly less risk of TNS than spinal lidocaine. Studies comparing ropivacaine to bupivacaine in spinal anesthesia are in progress.^77–79

        Table 13-4 shows some of the local anesthetics used for spinal anesthesia and dosage duration, and concentration for different levels of spinal blockade/^79–88

Additives to Local Anesthesia

Vasoconstrictors are often added to local anesthetics, and both epinephrine and phenylephrine have been studied. Anesthesia is intensified and prolonged with smaller doses of local anesthetics when epinephrine or phenylephrine is added. Tissue vasoconstriction is produced, thus limiting the systemic reabsorption of the local anesthetic and prolonging the duration of action by keeping the local anesthetic in contact with the nerve fibers. However, ischemic complications can occur after the use of vasoconstrictors in spinal anesthesia. In some studies, epinephrine was implicated as the cause of cauda equina syndrome because of anterior spinal artery ischemia. Regardless, most studies did not demonstrate an association between the use of vasoconstrictors for spinal anesthesia and the incidence of cauda equina.^89,90 Phenylephrine has been shown to increase the risk of TNS.^73,91

        Epinephrine is thought to work by decreasing local anesthetic uptake and thus prolonging the spinal blockade of local anesthetics. However, vasoconstrictors can cause ischemia, and there is a theoretical concern of spinal cord ischemia when epinephrine is added to spinal anesthetics. Animal models have not shown any decrease in spinal cord blood flow or increase in spinal cord ischemia when epinephrine is given for spinal blockade, even though some neurologic complications associated with the addition of epinephrine exist.⁴⁷·^49,92,93

Clinical Pearls

        Epinephrine comes packaged as 1 mg in 1 mL, which is a 1:1000 solution. The dosage of epinephrine added to local anesthetics is 0.1 to 0.5 mg, meaning 0.1 mL to 0.5 mL is added to the local anesthetic solution. Adding 0.1 mL of epinephrine to 10 mL of local anesthetic yields a 1:100,000 concentration of epinephrine. Adding 0.1 mL of epinephrine to 20 mL of local anesthetic yields a 1:200,000 concentration, and so on (0.1 mL in 30 mL = 1:300,000). Calculation of epinephrine concentration does not need to be complex if this simple formula is remembered.

        Epinephrine prolongs the duration of spinal anesthesia.^94–96 In the past, it was thought that epinephrine had no effect on hyperbaric spinal bupivacaine using two-segment regression to test neural blockade.⁹⁷ However, a recent study showed that epinephrine prolongs the duration of hyperbaric spinal bupivacaine when pinprick, transcutaneous electrical nerve stimulation (TENS) equivalent to surgical stimulation (at umbilicus, pubis, knee, and ankle), and tolerance of a pneumatic thigh tourniquet were used to determine neural blockade.⁹⁸ Currently there is controversy regarding prolongation of spinal bupivacaine neural blockade when epinephrine is added.^99–102 The same controversy exists about the prolongation of spinal lidocaine with epinephrine.^103–107

        All three types of opioid receptors are found in the dorsal horn of the spinal cord and serve as the target for intrathecal opioid injection. Receptors are located on spinal cord neurons and terminals of afferents originating in the dorsal root ganglion. Fentanyl, sufentanil, meperidine, and morphine have all been used intrathecally. Side effects that may be seen include pruritus, nausea and vomiting, and respiratory depression.^108–112

        Alpha₂-adrenergic agonists can be added to spinal injections of local anesthetics in order to enhance pain relief and prolong sensory block and motor block. Enhanced postoperative analgesia has been demonstrated in cesarean deliveries, fixation of femoral fractures, and knee arthroscopies when clonidine was added to the local anesthetic solution. Clonidine prolongs the sensory and motor blockade of a local anesthetic after spinal injection.^113–115 Sensory blockade is thought to be mediated by both presynaptic and postsynaptic mechanisms. Clonidine induces hyperpolarization at the ventral horn of the spinal cord and facilitates the action of the local anesthetic, thus prolonging motor blockade when used as an additive. However, when used alone in intrathecal injections, clonidine does not cause motor block or weakness.¹¹⁶ Side effects can occur with the use of spinal clonidine, and include hypotension, bradycardia, and sedation. Currently, neuraxial clonidine is approved by the Food and Drug Administration (FDA) for intractable neuropathic pain.^117,118

        Acetylcholinesterase inhibitors prevent the breakdown of acetylcholine and produce analgesia when injected intrathecally. The antinociceptive effects are due to increased acetylcholine and generation of nitric oxide. It has been shown in a rat model that diabetic neuropathy can be alleviated after intrathecal neostigmine injection.¹¹⁹ Side effects of intrathecal neostigmine include nausea and vomiting, bradycardia requiring atropine, anxiety, agitation, restlessness, and lower extremity weakness.^120–122 Although spinal neostigmine provides extended pain control, the side effects that occur do not allow its widespread use.

        PHARMACODYNAMICS OF SPINAL ANESTHESIA

The pharmacodynamics of spinal injection of local anesthesia are wide-ranging.

        Hepatic blood flow correlates to arterial blood flow. There is no auto regulation of hepatic blood flow, thus, as arterial blood flow decreases after spinal anesthesia, so does hepatic blood flow.¹²³ If the mean arterial pressure (MAP) after placing a spinal anesthetic, is maintained hepatic blood flow will also be maintained. Patients with hepatic disease must be carefully monitored and their blood pressure must be controlled during anesthesia to maintain hepatic perfusion. No studies have conclusively shown the superiority of regional or general anesthesia in patients with liver disease.^124–128 In patients with liver disease either regional or general anesthesia can be given, as long as the MAP is kept close to baseline.

Clinical Pearls

        Renal blood flow is autoregulated. The kidneys remain perfused when the MAP remains above 50 mm Hg. Transient decreases in renal blood flow may occur when MAP is less than 50 mm Hg, but even after long decreases in MAP, renal function returns to normal when blood pressure returns to normal. Again, attention to blood pressure is important after placing a spinal anesthetic, and the MAP should be as close to baseline as possible. Spinal anesthesia does not affect autoregulation of renal blood flow. It has been shown in sheep that renal perfusion changed very little after spinal anesthesia.^129–132

Cardiovascular Effects of Spinal Anesthesia

The sympathectomy produced by spinal anesthesia induces hemodynamic changes. The block height determines the extent of sympathetic blockade, which determines the amount of change in cardiovascular parameters. However, this relationship cannot be predicted. Hypotension and bradycar-dia are the most common side effects seen with sympathetic denervation.¹³³ Risk factors associated with hypotension include hypovolemia, preoperative hypertension, high sensory block height, age older than 40 years, obesity, combined general and spinal anesthesia, and addition of phenylephrine to the local anesthetic.^134–136 Chronic alcohol consumption, history of hypertension, elevated BMI, high level of sensory block height, and urgency of surgery all increase the likelihood of hypotension after spinal anesthesia.¹³⁷ Hypotension occurs in about 33% of the nonobstetric population.¹³⁴ Figure 13-7 depicts changes in blood pressure and heart rate after injection of hyperbaric bupivacaine and tetracaine.¹³⁸

        Arterial and venodilation both occur in spinal anesthesia and combine to produce hypotension. Arterial vasodi-lation is not maximal after spinal blockade, and vascular smooth muscle continues to retain some autonomie tone after sympathetic denervation. Due to retention of autonomie tone, total peripheral vascular resistance (TPVR) decreases only by 15% to 18%, thus MAP decreases by 15% to 18% if cardiac output is not decreased. In patients with coronary artery disease, systemic vascular resistance can be decreased by up to 33% after spinal anesthesia.¹³⁹ However after spinal anesthesia, venodilation, is significant depending on the location of the veins. If the veins lie below the right atrium, gravity will cause pooling of the blood peripherally, and if the veins are above, there is back-flow of the blood into the heart. Venous return to the heart, or preload, therefore depends on patient positioning during spinal anesthesia.¹⁴⁰

Clinical Pearls

Because preload determines cardiac output and patient positioning is a major factor in determining preload, as long as a euvolemic patient is positioned with the legs elevated above the heart, there should be no significant changes in cardiac output after spinal anesthesia. The reverse Trendelenburg position, however, leads to large decreases in preload and thus large decreases in cardiac output.^141,142

Figure 13-7. A graph depicting changes in blood pressure and heart rate after injection of hyperbaric bupivacaine and tetracaine. Blood pressure is shown in the upper graph and heart rate is shown in the lower graph with the mean ± SD. Time 0 is the time before spinal anesthetic placement and time 5 is 5 minutes after spinal anesthetic placement. Reproduced with permission from Nishiyama T, Komatsu K, Hanaoka K.: Comparison of hemodynamic and anesthetic effects of hyperbaric bupivacaine and tetracaine in spinal anesthesia. J Anesth., 17:219,2003.

        Most patients do not experience a significant change in heart rate after spinal anesthesia, but in young (age 1 < 50), healthy (ASA class 1) patients there is a higher risk of brady-cardia. Beta-blocker use also increases the risk of brady-cardia. The incidence of bradycardia in the nonpregnant population is about 13%.¹³⁴ The sympathetic cardiac accelerator fibers emerge from the T1 to T4 spinal segments, and blockade of these fibers is proposed as the cause of bradycardia. Decreased venous return may also cause bradycardia, due to a fall in filling pressures. This triggers the intracardiac stretch receptors to lower the heart rate. Even though both of these mechanisms are proposed to cause bradycardia, other as yet undetermined factors may contribute to the bradycardia seen with spinal anesthesia.¹⁴³ Although bradycardia is usually well tolerated, asystole and second- and third-degree heart block can occur, so it is wise to be vigilant when monitoring a patient after spinal anesthesia and treat promptly and aggressively.¹⁴⁴ Hypotension occurs in about 33% of the nonobstetric population.¹³⁴

Treatment of Hypotension After Spinal Anesthesia

To effectively treat hypotension, the cause of the hypotension must be corrected. Decreased cardiac output and venous return must be treated, and a bolus of crystalloid is often used to enhance venous volume. The practice of prehydration with 500 to 1500 mL of crystalloid has been shown to decrease hypotension in some studies, but not in others.^145–147 No reliable method to prevent hypotension after spinal blockade exists. Treatment of hypotension, however, remains essential so that the myocardium and brain remain perfused. If a patient without major target organ disease is asymptomatic, decreases in blood pressure up to 33% need not be treated. Careful monitoring of blood pressure as well as supplemental oxygen should be implemented when performing spinal anesthesia. Fluid bolus should be carefully monitored as excess fluid may cause patients to go into congestive heart failure, pulmonary edema, or both, and also may necessitate bladder catheterization after surgery. Bladder catheterization can lead to its own set of problems, including urinary tract infections.

        If pharmacologic treatment of hypotension is indicated, vasopressors remain the mainstay of treatment. Combined α- and β -adrenergic agonists may be better than pure α-agonists for treating blood pressure depression, and ephedrine is currently the drug of choice.^148,149 Cardiac output and peripheral vascular resistance are increased by ephedrine, which restores blood pressure. However, physiologic treatment of hypotension centers on restoration of preload. The most effective and simple way to achieve this is by positioning the patient in the Trendelenburg, or head down, position.¹⁵⁰ This position should not exceed 20 degrees because extreme Trendelenburg can lead to a decrease in cerebral perfusion and blood flow due to increases in jugular venous pressure. If the level of spinal anesthesia is not fixed, the Trendelenburg position can alter the level of spinal anesthesia and cause a high level of spinal anesthesia in patients receiving hyperbaric local anesthetic solutions.¹⁵¹ This can be minimized by raising the upper part of the body with a pillow under the shoulders while keeping the lower part of the body elevated above heart level. Figure 13-8 shows an algorithm for the treatment of hypotension after spinal anesthesia.

The Bezold-Jarisch Reflex

The Bezold-Jarisch reflex (BJR) has been implicated as a cause of bradycardia, hypotension, and cardiovascular collapse after central neuraxial anesthesia, and. in particular spinal anesthesia.^152,153 The BJR is a cardioinhibitory reflex and consists of the triad of symptoms, bradycardia, hypotension, and cardiovascular collapse, seen after intravenous injection of Veratrum alkaloids in animals.¹⁵⁴ The BJR is usually not a dominant reflex and the association with spinal anesthesia is probably weak.^154,155 Blood pressure regulation is multimodal and complex, and while the BJR likely plays a role in this regulation, the dominant reflex in regulation of blood pressure is the baroreceptor reflex. The BJR is also not a vasovagal reflex, although BJR has been blamed for bradycardia after spinal anesthesia, especially after hemorrhage.¹⁵⁶ No studies have yet defined this relationship. The definitive role of BJR as the cause of bradycardia, hypotension, and circulatory collapse after spinal anesthesia has not been fully established.

Respiratory Effects of Spinal Anesthesia

In patients with normal lung physiology, spinal anesthesia has very little effect on pulmonary function.¹⁵⁷ Lung volumes, resting minute ventilation, dead space, arterial blood gas tensions, and shunt fraction show minimal change after spinal anesthesia. The main respiratory effect of spinal anesthesia occurs during high spinal blockade when active exhalation is affected due to paralysis of abdominal and intercostal muscles. During high spinal blockade, expiratory reserve volume, peak expiratory flow, and maximum minute ventilation are reduced. Patients with obstructive pulmonary disease that rely on accessory muscle use for adequate ventilation should be monitored carefully after spinal blockade. Patients with normal pulmonary function and a high spinal block may complain of dyspnea, but if they are able to speak clearly in a normal voice, ventilation is usually normal. The dyspnea is usually due to the inability to feel the chest wall move during respiration, and simple assurance is usually effective in allaying the patient’s distress.

Clinical Pearls

        Arterial blood gas measurements do not change during high spinal anesthesia in patients who are spontaneously breathing room air. The main effect of high spinal anesthesia is on expiration, as the muscles of exhalation are impaired. Since a high spinal usually does not affect the cervical area, sparing of the phrenic nerve and normal diaphragmatic function occurs, and inspiration is minimally affected. Although Steinbrook and colleagues found that spinal anesthesia was not associated with significant changes in vital capacity, maximal inspiratory pressure, or resting end-tidal Pco₂, an increased ventilatory responsiveness to CO₂ with bupivacaine spinal anesthesia was seen.¹⁵⁸

Figure 13-8. Treatment of hypotension after spinal anesthesia. CVA = ardiovascular accident, CNS = central nervous system, BP = blood pressure, HR = heart rate, bpm = beats per minute.

Gastrointestinal Effects of Spinal Anesthesia

The sympathetic innervation to the abdominal organs arises from T6 to L2. Due to sympathetic blockade and unopposed parasympathetic activity after spinal blockade, secretions increase, sphincters relax, and the bowel becomes constricted. Nausea and vomiting occur after spinal anesthesia approximately 20% of the time, and risk factors include blocks higher than T5, hypotension, opioid administration, and a history of motion sickness.¹³⁴ Increased vagal activity after sympathetic block causes increased peristalsis of the gastrointestinal tract, which leads to nausea. Accordingly, atropine is useful for treating nausea after high spinal blockade.¹⁴⁹

Clinical Pearls

Related posts:

Regional Anesthesia in the Patient with Preexisting Neurologic Disease. The History of Local Anesthesia. Stimulating Catheters. Ultrasound-Assisted Nerve Blocks in Adults. Cutaneous Blocks for the Upper Extremity. Cervical Plexus Block.

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