Spinal Anesthesia

Spinal anesthesia has progressed greatly since 1885 and is used successfully 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.

TABLE OF CONTENTS
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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 T11-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.

Dural puncture was described by Essex Wynter in 1891[5] 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 Adriani 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 is used successfully 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. If all of these factors are conducive for the patient to receive a spinal anesthetic, care must be taken to prevent complications. Learning how to perform spinal anesthesia is an invaluable skill 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, coagulopathy, and increased intracranial pressure, except in cases of pseudotumor cerebri. Relative contraindications include sepsis distinct from the anatomic site of puncture (e.g., chorioamnionitis or lower extremity infection) and unknown duration of surgery. In the latter case, if the patient is on 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 infection, which may increase the risk of meningitis. Preoperative shock or hypovolemia increases 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. If intracranial pressure rises after injection of the spinal anesthetic, brain herniation can occur. Coagulation abnormalities increase the risk of hematoma formation. It is 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 be long enough to cover the surgery. Knowing the duration of surgery helps the anesthesiologist determine the local anesthetic that will be used, addition of spinal adjuncts such as epinephrine, and whether a spinal catheter will be necessary.

Another consideration when performing spinal anesthesia is the site of surgery, since surgery above the umbilicus would be difficult to cover with a spinal as the sole technique. Performing spinal anesthesia in patients with neurologic diseases, such as multiple sclerosis, is controversial due to in vitro experiments that determine that demyelinated nerves are more susceptible to local anesthetic toxicity. However, no clinical study has convincingly demonstrated that spinal anesthesia worsens such neurologic diseases. Indeed, with the knowledge that pain, stress, fever, and fatigue exacerbate these diseases, a stress-free central neuraxial block may be preferred for surgery.[27–31] Cardiac disease when sensory levels above T6 are required is a relative contraindication to spinal anesthesia.[32,33] Certain cardiac diseases, such as aortic stenosis, once considered to be an absolute contraindication for spinal anesthesia, may now incorporate a carefully conducted spinal anesthetic into their anesthetic care.[34–36] Severe deformities of the spinal column can increase the difficulty in placing a spinal anesthetic. Arthritis, kyphoscoliosis, and previous lumbar fusion surgery all factor into the ability of the anesthesiologist to performa 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

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

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

Figure 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 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.

In reviewing the functional anatomy of spinal blockade, an intimate knowledge of the spinal column, spinal cord, and spinal nervesmust be present. This chapter reviews briefly the curves 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, alongwith gravity, baricity of local anesthetic, and patient position, influence the spread of local anesthetics in the subarachnoid space. Figure 1 depicts the spinal column, vertebrae, and intervertebral discs and foramina.

Five ligaments hold the spinal column together. 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. Figure 2 shows a cross section of the spinal canal with the ligaments, vertebral body, and spinous processes.

The three membranes that protect the spinal cord are the dura mater, arachnoid mater, and pia mater. The dura mater, or tough 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 3 depicts the spinal cord, dorsal root ganglia and ventral rootlets, spinal nerves, sympathetic trunk, rami communicantes, and pia, arachnoid, and dura mater.

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 applied, 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 L1 with 30% of people having a cord that ends at T12 and 10% at L3. Figure 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 cord can cause great damage and result in paralysis.[38]

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

Surface Anatomy

When preparing for spinal anesthetic blockade, it is important to find landmarks on the patient. The iliac crests usually mark the interspace between the fourth and fifth lumbar vertebrae, and 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 L1 to L2 level, it would not bewise to attempt spinal anesthesia at or above this level.

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 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 for common surgical procedures are listed in Table 1.

Figure 5. The dermatomes of the human body.

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 pKa also influence activity.[39]

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. 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 pKa 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 pKa, the faster the onset of action and vice versa.

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]

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

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. Figure 6 is a representation of the periarterial Virchow–Robin spaces around the spinal cord.

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, e.g., tetracaine increases cord flow but lidocaine and bupivacaine decrease it, which affects elimination of the local anesthetic.[47–49]

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 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 37â—¦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 3 compares the density, specific gravity, and baricity of different substances and local anesthetics.[50,51,53,59,60]

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 repositioning the patient after injection.

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 adult volume of 150 mL, 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. Predictability of CSF volume is difficult with weight being the main determinant on physical examination.

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] Higuchi found that CSF density 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 thewide 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 performed with lidocaine, bupivacaine, tetracaine, mepivacaine, and ropivacaine have been successful. Some of the more common local anesthetics used for spinal anesthesia will be discussed in this portion of the chapter. As the use of spinal anesthesia becomes more popular, there is more interest in medications that produce anesthesia and analgesia while limiting side effects. A variety of medications, including vasoconstrictors, opioids, α2-adrenergic agonists, and acetylcholinesterase inhibitors, have been added to spinal medications to assist in analgesia while reducing the amount of local anesthetics required for anesthesia.

Lidocaine was first used as a spinal anesthetic in 1945, and it has 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 should be used for short to intermediate length operating room cases, and the most common ampule is 5% lidocaine in 7.5% dextrose. One drawback of lidocaine has been the association with transient neurologic symptoms (TNS), which presents 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 intermediate-acting local anesthetics are being studied to see if their association with TNS may be less.

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 to 8 min with a duration of anesthesia that lasts from 210 to 240 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 inability to void. Bupivacaine has 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 210 to 240 min, and like bupivacaine, is used for cases that are intermediate to longer length. The package of 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 may play a role in the development of TNS.[71–73]

Mepivacaine is very 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 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 have been 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, 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, but most studies do 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 be associated with TNS.[73,91]

Epinephrine

Epinephrine is thought to work by decreasing local anesthetic uptake and thus prolonging the spinal blockade of some local anesthetics. Vasoconstrictors can cause ischemia, and there is 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]

Epinephrine comes packaged as 1mg in 1 mL, which is a 1:1000 solution. The dosage of epinephrine added to local anesthetics is 0.1 to 0.5mg, meaning 0.1mLto 0.5mLis added to the local anesthetic solution. Adding 0.1mLof 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] Epinephrine likely prolongs spinal blockade with both bupivacaine and lidocaine. 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]

Alpha-2-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 nitricoxide. 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. The next section reviews the cardiovascular, respiratory, and gastrointestinal consequences of spinal anesthesia. This portion of the chapter focuses on the hepatic and renal effects of spinal anesthesia.

Hepatic blood flow correlates to arterial blood flow. There is no autoregulation of hepatic blood flow, thus, as arterial blood flow decreases after spinal anesthesia, so does hepatic blood flow.[123] If the anesthesiologist maintains mean arterial pressure (MAP) after placing a spinal anesthetic, hepatic blood flow will 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.

Renal blood flow is autoregulated. The kidneys remain perfused when the MAP remains above 50mmHg. 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

Figure 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.

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 bradycardia 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 about33%of the non-obstetric population.[134] Figure 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 vasodilation is not maximal after spinal blockade, and vascular smooth muscle continues to retain some autonomic tone after sympathetic denervation. Due to retention of autonomic 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 will be maximal, 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]

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]

Most patients do not experience a significant change in heart rate after spinal anesthesia, but in young (age < 50), healthy (ASA class 1) patients there is a higher risk of bradycardia. Beta-blocker use also increases the risk of bradycardia. 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] Even though 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

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

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 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. Combinedα- 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 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 cardio-inhibitory reflex and consists of the triad of symptoms, bradycardia, hypotension, and cardiovascular collapse, seen after intravenous injection of Veratrumalkaloids 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. With the dearth of data available, more research must be done before the BJR is named as the cause of bradycardia, hypotension, and circulatory collapse after spinal anesthesia.

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.

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]

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]

 

The Use Of Spinal Anesthesia In Obstetrics

In 1901, Kreis described the first spinal anesthetic for vaginal delivery.[159] Spinal anesthesia for labor and delivery has progressed greatly since that time. When contemplating induction of anesthesia in the pregnant patient, many factors play a role. The anesthesiologist must perform a complete preanesthetic evaluation, including past medical and surgical history, past reactions to anesthesia, any difficulties during the pregnancy, maternal airway and back anatomy, and fetal assessment. In addition, the anesthesiologist must obtain informed consent for both regional and general anesthesia. Before performing a spinal anesthetic on the labor floor, resuscitative equipment and emergency medication must be readily available. Although many arguments aremade against general anesthesia in the pregnant woman due to increased risk of aspiration and difficult intubation, the anesthesiologistmust be prepared to induce general anesthesia in the face of a failed or total spinal anesthetic.

Spinal anesthesia is useful in both elective and emergent cesarean sections. Non-cutting, pencil-point spinal needles are used for spinal obstetric anesthesia, which has resulted in a decreased incidence of PDPH. Most of the time, spinal obstetric anesthesia is administered as a single injection, and the rapid onset and dense neural block are of benefit. Because of the sympathetic blockade, hypotension may result, so it is prudent to monitor the blood pressure very carefully and frequently. The anesthesiologist should treat hypotension immediately with medications or fluid administration, or both.

Pregnant women require less local anesthetic to achieve the same level of anesthesia as non-pregnant women. This observation is likely due to both hormonal and mechanical factors. Procaine, tetracaine, lidocaine, bupivacaine, ropivacaine, and levobupivacaine have all been used for obstetric anesthesia, but the preferred local anesthetic is bupivacaine. Dosing is generally done either with a fixed amount of local anesthetic or changing the amount according to the height and weight of the patient. If hyperbaric bupivacaine is used, 12 mg is generally given, with a decreased dose for short patients and an increased dose if the spinal is given in the sitting position. Fentanyl 10–20 mcg is usually added to enhance the quality of the block. Prior to placement of a spinal anesthetic, the pregnant patient should receive 30 mL of 0.3 M sodium citrate orally to decrease the stomach acidity, and a bolus of Ringer’s lactate 15–20 mL/kg. Metoclopramide to improve gastric emptying can also be given prior to the spinal.

After the spinal anesthetic is given, the patient should be in the supine position with left uterine displacement. Fetal heart rate should be monitored by Doppler or fetal scalp electrocardiogram (ECG). Blood pressure and heart rate should be monitored every minute for at least 10 min, and immediate treatment should be given for decreases in blood pressure. A T4 level block is usually required for a cesarean section due to traction on the peritoneum and uterine exteriorization. Some patients complain of dyspnea due to abdominal and intercostal motor blockade, but if the patient is able to speak clearly, assurance and possible gentle bag- and mask-assisted ventilation is usually enough to calm the patient until delivery. Once the fetus is delivered, the uterus no longer causes up ward pressure on the diaphragm, and the patient is able to breathe more easily.

Factors Affecting Level Of Spinal Blockade

Many factors have been suggested as possible determinants of spinal blockade level.[50] The four main categories of factors are (1) characteristics of the local anesthetic solution, (2) patient characteristics, (3) technique of spinal blockade, and (4) diffusion. Characteristics of local anesthetic solution include baricity, local anesthetic dose, local anesthetic concentration, and volume injected. Patient characteristics include age, weight, height, gender, intra-abdominal pressure, anatomy of the spinal column, spinal fluid characteristics, and patient position.[160] Techniques of spinal blockade include site of injection, speed of injection, direction of needle bevel, force of injection, and addition of vasoconstrictors (see Table 1).

Although all these factors have been postulated as affecting spinal spread of anesthetic, not many have been shown to change the distribution of blockade when all other factors that affect blockade are kept constant. Site of injection, age, position of the patient during and after injection, dosage and volume of anesthetic solution injected, baricity of local anesthetic, anatomy of the spine, direction of the needle during injection, volume of CSF, and increased intraabdominal pressure can all influence the spread of spinal blockade.

Site of Injection

The site of injection of local anesthetics for spinal anesthesia can determine the level of blockade. In some studies, isobaric spinal 0.5% bupivacaine produces sensory blockade that is reduced by two dermatomes per interspace when injection at L2-3, L3-4, and L4-5 interspaces are compared.[161,162]

However, no difference in block height exists when hyperbaric bupivacaine or dibucaine is injected as a spinal anesthetic in different interspaces.[163–165]

Age

Some studies have reported changes in block height after spinal anesthesia in the elderly patient as compared with the young patient, but other studies have reported no difference in block height.[166–169] These studies were performed with both isobaric and hyperbaric 0.5% bupivacaine.

Isobaric bupivacaine appears to increase block height, and hyperbaric bupivacaine does not appear to change block height with increasing age. If there is a correlation between increasing age and spinal anesthesia height, it is not strong enough by itself to be a reliable predictor in the clinical setting.[170,171] Just as with site of injection, it appears that baricity plays a major role in determining block height after spinal anesthesia in older populations and age is not an independent factor.

Position

Positioning of the patient is very important for determining level of blockade after hyperbaric and hypobaric spinal anesthesia, but not for isobaric solutions. Sitting, Trendelenburg, and prone jackknife positions can greatly change the spread of the local anesthetic due to effect of gravity.[172–174] Gravity and baricity are interrelated when position is involved in determining spinal block height.

The combination of baricity of the local anesthetic solution and patient positioning determines spinal block height level.[175] Thesitting position in combination with a hyperbaric solution can produce analgesia in the perineum. Trendelenburg positioning will also affect spread of hyperbaric and hypobaric local anesthetics due to the effect of gravity.[151,176] Prone jackknife positioning is used for rectal, perineal, and lumbar procedures with a hypobaric local anesthetic.[59,177] This prevents rostral spread of the spinal blockade after injection.

Speed of Injection

Speed of injection has been reported to affect spinal block height, but the data available in the literature are conflicting.178

In studies using isobaric bupivacaine, there is no difference in spinal block height with different speeds of injection.[179–181] Even though spinal block height does not change with speed of injection, a smooth, slow injection should be used when giving a spinal anesthetic. If a forceful injection is given and the syringe is not connected tightly to the spinal needle, the local anesthetic might be aerosolized and lost to the atmosphere.

Volume, Concentration, & Dose of Local Anesthetic

It is difficult to maintain volume, concentration, or dose of local anesthetic constant without changing any of the other variables, thus it is difficult to produce high-quality studies that investigate these variables singly. Axelsson and associates showed that volume of local anesthetic can affect spinal block height and duration when equivalent doses are used.[182]

Peng and coworkers showed that concentration of local anesthetic is directly related to dose when determining effective anesthesia.[183] However, dose of local anesthetic plays the greatest role in determining spinal block duration, as neither volume nor concentration of isobaric bupivacaine or tetracaine alter spinal block duration when the dose is held constant.[184,185] Studies have repeatedly shown that spinal block duration is longer when higher doses of local anesthetic are given.[54,61,182,186,187] When performing a spinal anesthetic, be cognizant of not only the dose of local anesthetic, but also the volume and concentration so as not to overdose or underdose the patient.

The use of hyperbaric solutions minimizes the importance of dose and volume except when doses of hyperbaric bupivacaine equal to or less than 10 mg are used. In those cases, there is less cephalad spread and a shorter duration of action.[173] A dose of hyperbaric bupivacaine between 10 and 20 mg results in similar block height.[163] When using hyperbaric solutions, it is important to note that patient positioning and baricity are the most influential factors on block height, except when low doses of hyperbaric bupivacaine are used.

 

Choice Of Local Anesthetic

The choice of local anesthetic determines the duration of the spinal blockade. The shortest acting local anesthetic for spinal use is preservative-free 2-chloroprocaine.[188] Procaine is the next shortest acting local anesthetic, followed by lidocaine. The long-acting local anesthetics include bupivacaine, ropivacaine, and tetracaine. Even though chloroprocaine is not currently approved by the FDA for the specific indication of intrathecal use, results from recent clinical trials have shown preservative-free 2-chloroprocaine to be safe, short-acting, and acceptable for outpatient surgery, with some episodes of flu-like symptoms and low back pain associated with the addition of epinephrine.[88] Chronic neurologic deficits have been reported in rabbits when sodium bisulfite is injected into the lumbar subarachnoid space, but when preservative-free 2-chloroprocaine was injected, no permanent neurologic sequelae were noted.[189] Onset time is very fast, and the duration is around 60 min for surgical anesthesia. The dose ranges from 20 to 60 mg, with 40 mg as a usual dose.

Procaine, commonly known as Novocain, is a short-acting ester local anesthetic. Procaine has an onset time of 3 to 5 min and a duration time of 50 to 60 min. However, there is a 14% incidence of block failure associated with procaine 10%.[190] A dose of 50 to 100 mg is suggested for perineal and lower extremity surgery. Concerns about the neurotoxicity of procaine have limited its use, but there appears to be less risk of TNS and transient radicular irritation (TRI).[191–193] Procaine can be used only for short cases.

Lidocaine, an amide local anesthetic, also provides an onset time of 3 to 5 min with a duration time of 60 to 90 min. As described previously, there is a strong association between lidocaine and TNS, which limits the usefulness of lidocaine.[65–67] For perineal surgery and saddle-block anesthesia, a dose of 25 to 50 mg is given. Lidocaine is also used for short operating room cases.

Tetracaine, another ester local anesthetic, provides anesthesia within 3 to 6 min and lasts 210 to 240 min. The duration of anesthesia is much longer than with the other ester anesthetics and also much longer than with lidocaine. The suggested dose is 5 mg for perineal and lower extremity surgery. Tetracaine is used for intermediate to long lasting cases.

Bupivacaine, another amide local anesthetic, has an onset time of 5 to 8 min with a duration time of 210 to 240 min, which is similar to tetracaine. The suggested dose is 8–10 mg for perineal and lower extremity surgery and 15–20mg for abdominal surgery. Bupivacaine is one of the most widely used local anesthetics for spinal anesthesia and provides adequate anesthesia and analgesia for intermediate to long duration operating room cases.

Number & Frequency of Local Anesthetic Injections

In the majority of cases, a single-shot injection of local anesthetic is given when a spinal anesthetic is performed. At times, a continuous spinal anesthetic is utilized with an infusion pump continuously providing medication though a spinal catheter or by giving boluses through a spinal catheter.

When a bolus of local anesthetic is given through a spinal catheter for surgical anesthesia, the onset time and efficacy of anesthesia are similar.[194] The level of neural blockade should be checked prior to giving a bolus through the catheter. When the spinal blockade level recedes lower than T10, half the initial dose of local anesthetic should be given through the catheter.

 

Equipment For Spinal Anesthesia

In the past, most institutions had reusable trays for spinal anesthesia. These trays required preparation by anesthesiologists or anesthesia personnel to ensure that bacterial and chemical contamination would not occur. The contents of the trays did not differ from those currently available commercially, but strict attention to sterility must be maintained to ensure patient safety while using the trays.

Figure 9. The contents of standard, commercially prepared spinal anesthesia tray.

Currently, commercially prepared, disposable spinal trays are available and are in use by most institutions. Most of these trays contain the same items: a paper towel, fenestrated drape, gauze sponges, prep solution well and sponges, medicine well, ampules of lidocaine 1% and epinephrine, standard or pencil-point needles, introducers, syringes and needles, a filter straw, povidone-iodine solution packet, needle block foam with holder, and an ampule of local anesthetic for spinal injection. These trays are portable, sterile, and easy to use. Familiarity with the contents of the spinal tray is essential to placing a spinal anesthetic quickly. Figure 9 shows the contents of standard, commercially prepared spinal anesthetic tray.

Resuscitation equipment must be available whenever a spinal anesthetic is performed. This includes medication for sedation and induction of general anesthesia (propofol, fentanyl, midazolam, succinylcholine), medication for support of cardiac function (ephedrine, epinephrine, atropine), an oropharyngeal airway, a laryngoscope with blade, an endotracheal tube with stylet and cuff syringe, tape for securing the endotracheal tube, a tongue depressor, a Yankauer suction tube, an oxygen source, and an Ambu bag and facemask. The patient must be monitored during the placement of the spinal anesthetic with a pulse oximeter, blood pressure cuff, and ECG. All of these precautions are necessary to provide the safest environment for performing a spinal anesthetic.

Needles

Figure 10. The different types of needles used for spinal anesthesia along with the type of point at the end of each type of needle.

Needles of different diameters and shapes have been developed for spinal anesthesia. The ones currently used have a close-fitting, removable stylet, which prevents skin and adipose tissue from plugging the needle and possibly entering the subarachnoid space. Figure 10 shows the different types of needles used along with the type of point at the end of the needle.

The pencil-point needles (Sprotte and Whitacre) have a rounded, noncutting bevel with a solid tip. The opening is located on the side of the needle 2–4 mm proximal to the tip of the needle. The needles with cutting bevels include the Quincke and Pitkin needles. The Quincke needle has a sharp point with a medium-length cutting needle, and the Pitkin has a sharp point and short bevel with cutting edges. Finally, the Greene spinal needle has a rounded point and rounded noncutting bevel. If a continuous spinal catheter is to be placed, a Tuohy needle can be used to find the subarachnoid space before placement of the catheter.

Pencil-point needles provide a better tactile sensation of the layers of ligament encountered but require more force to insert than bevel-tip needles. The bevel of the needle should be directed longitudinally to decrease the incidence of PDPH.[195]

Larger gauge needles and needles with rounded, noncutting bevels also decrease the incidence of PDPH, but are more easily deflected than smaller gauge needles.

Introducers have been designed to assist with the placement of spinal needles into the subarachnoid space due to the difficulty in directing needles of small bore through the tissues. Introducers also serve to prevent contamination of the CSF with small pieces of epidermis, which could lead to the formation of dermoid spinal cord tumors. The introducer is placed into the interspinous ligament in the intended direction of the spinal needle, and the spinal needle is then placed through the introducer.

Position Of The Patient

Proper positioning of the patient for spinal anesthesia is essential for a fast, successful block. Many factors come into play for positioning of the patient. Before beginning the procedure, both the patient and anesthesiologist should be comfortable. This includes a proper level of the operating room table, adequate blankets or covers for the patient, a functioning intravenous line, standard American Society of Anesthesiologists (ASA) monitors, administration of 100% oxygen, and sedation for the patient.

A trained assistant should be available to help optimize patient position. The patient should receive some sedation, but not too much, in order to be comfortable during the procedure. The patient should be able to cooperate before, during, and after administration of the spinal anesthetic. There are three main positions for administering a spinal anesthetic: the lateral decubitus, sitting, and prone position.

Lateral Decubitus Position

The most commonly used position for placing a spinal anesthetic is the lateral decubitus position. Ideal positioning consists of having the back of the patient parallel to the edge of the bed closest to the anesthesiologist, knees flexed to the abdomen, and neck flexed. Figure 11 shows a patient in the lateral decubitus position.

It is essential to have an assistant to help hold and encourage the patient to stay in this position. Depending on the operative site and operative position, a hypo-, iso-, or hyperbaric solution of local anesthetic can be injected.

Figure 11. A patient in the lateral decubitus position.

Sitting Position & ‘‘Saddle Block”

Strictly speaking, the sitting position is best utilized for low lumbar or sacral anesthesia and in instances when the patient is obese and there is difficulty in finding the midline in the lateral position. In practice, however, many anesthesiologists prefer the sitting position in all patient who can be positioned for the ease of identification of the landmarks. Using a stool for a footrest and a pillow for the patient to hold can be valuable in this position. The patient should have the neck flexed and push out the lower back to open up the lumbar vertebral space. Figure 12 depicts a patient in the sitting position and the L4-5 interspace is marked.

Figure 12. A patient in the sitting position with the L4/L5 interspace marked.

When performing a saddle block, the patient should remain in the sitting position for at least 5 min after a hyperbaric spinal anesthetic is placed to allow the spinal to settle into that region. If a higher level of blockade is necessary, the patient should be placed supine immediately after spinal placement and the table adjusted accordingly.

Prone Position

The prone position is utilized for spinal anesthesia if the patient needs to be in this position for the surgery, such as for rectal, perineal, or lumbar procedures. A hypobaric or isobaric solution of local anesthetic is preferred in the prone jackknife position for these procedures.

This allows the anesthetic to spread in the caudal direction and avoid rostral spread and the risk of high spinal anesthesia. Care should to be taken to keep the patient in the same position for at least 15 min after injection prior to moving so that the local anesthetic solution will not migrate to a level that it was not intended to be.

Another, less elegant solution is to inject a hyperbaric solution of local anesthetic with the patient in the sitting position and await until the spinal anesthesia “sets-in,” which is typically 15–20 min after injection. The patient is then positioned in the prone position with vigilant monitoring, including frequent verbal communication with the patient.

Technique of Lumbar Puncture

When performing a spinal anesthetic, appropriate monitors should be placed, and airway and resuscitation equipment should be readily available. All equipment for the spinal blockade should be ready for use, and all necessary medications should be drawn up prior to positioning the patient for spinal anesthesia. Adequate preparation for the spinal reduces the amount of time needed to perform the block and assists with making the patient comfortable.

Proper positioning is the key to making the spinal anesthetic quick and successful. Once the patient is correctly positioned, the midline should be palpated. The iliac crests are palpated, and a line is drawn between them in order to find the body of L4 or the L4-5 interspace. Other interspaces can be identified, depending on where the needle is to be inserted.

The skin should be cleaned with sterile cleaning solution, and the area should be draped in a sterile fashion. A small wheal of local anesthetic is injected into the skin at the site of insertion. More local anesthetic is then administered along the intended path of the spinal needle insertion to a depth of 1 to 2 in. This serves a dual purpose: additional anesthesia for the spinal needle insertion and identification of the correct path for spinal needle placement.

Midline Approach

If the midline approach is used, palpate the desired interspace and inject local anesthetic into the skin and subcutaneous tissue. The introducer needle is placed with a slight cephalad angle of 10 to 15 degrees. Next the spinal needle is passed through the introducer. The needle goes through the subcutaneous tissue, supraspinous ligament, interspinous ligament, ligamentum flavum, epidural space, dura mater, and subarachnoid mater in order to reach the subarachnoid space.

Resistance changes as the spinal needle passes through each level on the way to the subarachnoid space. Muscle has less resistance to the spinal needle than ligaments. When the spinal needle goes though the dura mater, a “pop” is often appreciated. Once this pop is felt, the stylet should be removed from the introducer to check for flow of CSF. For spinal needles of small gauge (26–29 gauge), this usually takes 5–10 sec, but in some patients, it can take a minute or longer. If there is no flow, the needle might be obstructed by and rotating it 90 degrees may be helpful. Debris can obstruct the orifice of the spinal needle and, if necessary, withdraw the needle and clear the orifice before attempting the spinal anesthetic again. Finally, the spinal needle may not be in the correct position if CSF does not flow freely and the needle should be repositioned.

Sometimes the needle hits bone when attempting a spinal anesthetic. When this occurs, note the depth of the needle at bone contact, and place the needle more cephalad. If bone is contacted on reinsertion of the needle, the depth should be compared. If the needle contacts bone deeper on reinsertion, then likely the inferior spinous process is being contacted and the needle should be inserted even more cephalad. If the bone contact is shallower, then likely the superior spinous process is being felt and the needle needs to be redirected in a caudal fashion. If the depth of bone contact is the same, then likely the vertebral lamina is being contacted and the needle is off the midline. Palpation and identification of the midline before reinsertion would be advisable.

When the spinal needle needs to be reinserted, it is important to withdraw the needle back to the skin without removing it before redirection. Only make small changes in the angle of direction when reinserting the spinal needle as even small changes at the surface can lead to large changes in direction when the needle reaches the meninges. Bowing and curving of the spinal needle when inserting through the skin can steer the needle off course when attempting to contact the subarachnoid space.

Paresthesias may be elicited when passing a spinal needle. If the needle tip encounters a nerve root, the patient may feel a paresthesia. The stylet should be removed from the spinal needle, and if CSF is seen and the paresthesia no longer present, it is safe to inject the local anesthetic. Most likely a cauda equina nerve root was encountered. If there is no CSF flow, most likely the spinal needle has contacted a spinal nerve root traversing the epidural space. The needle should be removed and redirected toward the side opposite the paresthesia. Sometimes, needle contact with bone can be interpreted as a paresthesia and in this case, the spinal needle should be redirected.

After free flow of CSF is established, inject the local anesthetic smoothly and slowly at a speed of less than 0.5 mL/sec. Additional aspiration of CSF at the midpoint and end of injection should be attempted to confirm continued subarachnoid administration but may not always be possible when small needles are used. Once local anesthetic injection is complete, the introducer and spinal needle are removed as one unit from the back of the patient. The patient should then be positioned according to the surgical procedure and baricity of local anesthetic given. The table can be tilted either in the Trendelenburg or reverse Trendelenburg position as needed to adjust the height of the block after testing the sensory level. The anesthesiologist should carefully monitor and support vital signs.

Paramedian (Lateral) Approach

If the patient has a heavily calcified interspinous ligament or difficulty in flexing the spine, a paramedian approach to achieve spinal anesthesia can be utilized. The patient can be in any position for this approach: sitting, lateral, or even prone jackknife. After identifying the correct level for spinal anesthesia placement, the spinous process is palpated. The needle should be inserted 1 cm lateral to this point and directed toward the middle of the interspace. The ligamentum flavum is usually the first resistance identified, but sometimes the lamina is contacted. If this is the case, redirection of the needle should be performed.

Another method is to insert the needle 1 cm lateral and 1 cm inferior to the interspace and contact the lamina. After the bone is contacted, the needle should be walked off the lamina and into the subarachnoid space. Figure 13 shows the landmarks used for a paramedian approach to spinal anesthesia. Figure 14 depicts successful performance of a paramedian spinal anesthetic.

	Figure 13. The landmarks used for a paramedian approach to spinal anesthesia. The patient is in the right lateral decubitus position and the spinous processes are marked.
	Figure 14. Successful performance of a paramedian spinal anesthetic. The needle is inserted 1 cm lateral to the spinous process and directed toward the middle of the interspace.

Taylor Approach

The Taylor, or lumbosacral, approach to spinal anesthesia is a paramedian approach directed toward the L5-S1 interspace. Due to the fact that this is the largest interspace, the Taylor approach can be used when other approaches are not successful or cannot be performed. As with the paramedian approach, the patient can be in any position for this approach: sitting, lateral, or prone.

The needle should be inserted at a point 1 cm medial and inferior to the posterior superior iliac spine, then angled cephalad 45–55 degrees. This should be medial enough to reach the midline at the L5 spinous process. After needle insertion, the first significant resistance felt is the ligamentum flavum, and then the dura mater is punctured to allow free flow of CSF as the subarachnoid space is entered. Figure 15 shows the Taylor approach to spinal anesthesia.

Figure 15. The Taylor approach to spinal anesthesia. The needle is inserted 1 cm medial and inferior to the posterior superior iliac spine, then angled cephalad 45–55 degrees.

Continuous Catheter Techniques

Sometimes a catheter is placed for continuous spinal anesthesia. Local anesthetics can be dosed repeatedly through the catheter and the level and duration of anesthesia adjusted as necessary for the surgical procedure. Placement of a continuous spinal catheter occurs in a similar fashion as a regular spinal anesthetic except that a larger gauge needle, such as a Tuohy, is used to enable the passage of the catheter. After insertion of the Tuohy needle, the subarachnoid space is found and the spinal catheter is passed 2–3 cm into the subarachnoid space. If there is difficulty in passing the catheter, attempt to rotate the Tuohy needle 180 degrees. Never withdraw the catheter back into the needle shaft because there is a risk of shearing the catheter and leaving a piece of it in the subarachnoid space. If the catheter needs to be withdrawn, withdraw the catheter and needle together, and attempt the continuous spinal at another interspace.

Since the needle used to pass the spinal catheter is a large-bore needle, there is a much higher risk of PDPH, especially in young female patients. Cauda equina syndrome can occur with small spinal catheters, so the FDA has advised against using catheters smaller than 24 gauge for continuous spinal anesthetics.[196–199]

Intraoperative & Postoperative Management

Depending on the baricity of the local anesthetic solution injected, the level of the spinal anesthetic may be adjusted in the first few minutes, i.e., if a hypobaric or hyperbaric solution is used. After injection of the spinal anesthetic, assess the cardiovascular status of the patient, as changes can occur up to 20 min after spinal anesthesia injection. Continued monitoring of the heart rate and frequent readings of the blood pressure are recommended to detect hypotension so that corrections can be made early and quickly.

Intraoperative management of spinal anesthesia is much like intraoperative management with other forms of regional anesthesia. The patient may not feel operative pain but may still be uncomfortable. Supplemental benzodiazepines or opioids can be given intravenously. Comforting words from a caring, empathetic anesthesiologist also go a long way toward putting the patient at ease. Many factors come into play about whether to administer additional intravenous medications.

Elderly patients can become confused with benzodiazepines. Propofol can be given as an infusion to assist with making the patient more comfortable, and opioids can assist with pain from an unanesthetized portion of the body. Oxygen should always be administered via facemask or nasal cannula. Postoperatively the anesthesiologist must continue to monitor the patient until the spinal anesthetic recedes. In most circumstances the patient should void prior to being discharged from the postanesthesia care unit. Since the voiding mechanism is innervated by sacral autonomic fibers, which are the last to return to preoperative function, voiding may be delayed. The risk of discharging a patient from the recovery room prior to voiding includes complications involving a distended or ruptured bladder. Hypotension from continued blood volume redistribution as well as surgical bleeding should be monitored postoperatively.

Complications

Complications of spinal blockade include local anesthetic neurotoxicity and neurologic injury, PDPH, high spinal blockade, and cardiovascular collapse. Neurotoxicity studies performed in animal models producing neurologic deficits and changes in spinal cord histology are not seen in clinically useful concentrations of tetracaine, lidocaine, bupivacaine, or chloroprocaine in humans. High concentration tetracaine and lidocaine causes histopathologic changes and neurologic deficits in animal models.[200–202] Spinal cord blood flow is increased, and vasodilation occurs with intrathecal bupivacaine, lidocaine, mepivacaine, and tetracaine, but ropivacaine causes vasoconstriction and decreased spinal blood flow in a dose-dependent fashion. TNS may occur with spinal anesthesia, usually with lidocaine.

Permanent Neurologic Injury

Permanent neurologic injury is a devastating complication after spinal anesthesia. In a large, prospective survey in France, Auroy and colleagues reported 12 neurologic complications when a series of 35,439 spinal anesthetics were reviewed.[203] Nine peripheral neuropathies and three cases of cauda equina were seen, which correlates to a 0.03% neurologic complication rate. Moen and coworkers reported similar complication rates after spinal anesthesia.[204] Neurologic injury can occur after needle introduction into the spinal cord or nerves, spinal cord ischemia, bacterial contamination of the subarachnoid space, or hematoma formation. Although the elicitation of paresthesias during spinal anesthesia has been implicated as a risk factor for persistent neurologic injury, it is not known whether injection of the local anesthetic solution after a paresthesia is elicited should be stopped.[205] It is also unknown as to whether the actual injection of local anesthesia after paresthesia is elicited causes permanent neurologic damage, similar to what happens in peripheral nerves when an injection is associated with high pressures during injection of local anesthetic solution.[206,207] It is possible that when paresthesia occurs, that a spinal nerve has been penetrated by the spinal needle; consequently– injection of local anesthetic into the spinal nerve causes permanent neurologic damage.

Cauda Equina Syndrome

Cauda equina syndrome is associated with the use of continuous spinal microcatheters.[196–199] The use of hyperbaric 5% lidocaine for spinal anesthesia is also associated with an increased incidence of cauda equina syndrome,[208–210] although other local anesthetics have been found to cause it.[204,211–213] Other risk factors for cauda equina syndrome include repeated dosing of local anesthetic solution through continuous spinal catheters or multiple single-shot spinal anesthetics. Current suggestions for prevention of cauda equina syndrome from spinal anesthesia include aspiration of CSF before and after local anesthetic injection, and if CSF cannot be aspirated after injection, do not inject a full dose of local anesthetic. Evaluation of sacral blockade after spinal injection is important so that distribution of local anesthetic can be documented. Limiting the amount of local anesthetic given in the subarachnoid space, and if a spinal anesthetic has to be repeated, use of a different local anesthetic also may help preventing cauda equina syndrome.

Arachnoiditis

Arachnoiditis can occur after spinal injection of local anesthetic solution, but is also known to occur after intrathecal steroid injection.[214–217] Causes of arachnoiditis include infection, myelograms from oil-based dyes, blood in the intrathecal space, neuroirritant, neurotoxic or neurolytic substances, surgical interventions in the spine, intrathecal corticosteroids, and trauma. In regard to spinal anesthesia, arachnoiditis has resulted from traumatic dural puncture, local anesthetics, detergents, antiseptics or other substances unintentionally injected into the spinal canal.[218]

Spinal Hematoma Formation

Spinal hematoma formation is rare complication after spinal anesthesia and infrequently occurs in the absence of trauma or anticoagulant therapy. Major spontaneous hemorrhagic complications have been reported after antithrombotic and thrombolytic therapy.[219] Risk factors for spinal hematoma formation include the intensity of the anticoagulant effect, increased age, female gender, history of gastrointestinal bleeding, concomitant aspirin use, and length of therapy.[220] Although most spinal hematomas occur in the epidural space due to the prominent epidural venous plexus, very few reports have mentioned subarachnoid bleeding as causing neurologic deficits because of the lack of major blood vessels in this area. The source of the bleeding can be from either an injured artery or vein. If new or progressive neurologic symptoms develop, an immediate neurosurgery consult should be obtained and a magnetic resonance image (MRI) of the spine should be performed as soon as possible.

A recent study from Sweden showed that over a 10-year period from 1990 to 1999, out of 1,260,000 spinal anesthetics, eight spinal hematomas occurred, for an incidence of 0.00063%. Seven of the hematomas formed after single-shot spinal anesthesia and one formed after a continuous spinal blockade. A total of 33 spinal hematomas were noted in the study after both epidural and spinal blockade, and of these, 11 patients had evidence of coagulopathy or thromboprophylaxis administered soon before or after the central neuraxial blockade. In 10 patients who had spinal hematoma formation, difficulty in placing the epidural or spinal was noted, and in 5 patients symptoms of spinal hematoma appeared in the immediate postoperative period or shortly after removal of epidural catheter. Fourteen patients had symptoms of spinal hematoma appear from 6 h to 3 days after central neuraxial block was performed, and in one patient, pain and paraparesis appeared 2 weeks after difficult spinal anesthetic placement. Of the 33 patients, 6 had full recovery, but 27 suffered permanent neurologic damage. Five of the six patients that had full recovery were treated conservatively, but one underwent laminectomy. Eleven of the patients who did not recover underwent laminectomy, and in a further six cases, laminectomy was considered, but, due to delay in diagnosis, was not performed. Thirteen patients suffered paraparesis, three had cauda equina syndrome, three were left with sensory deficit, three died, and five were reported only to have lack of recovery without more information.[204]

Meningitis

Meningitis, either bacterial or aseptic, can occur after spinal anesthesia is performed.[221] Sources of infection include contaminated spinal trays and medication, patient infection, and oral flora from anyone behind the patient without a facemask on. Povidone-iodine solution is most commonly chosen for skin antisepsis before initiation of epidural and spinal anesthesia, and single-use containers are suggested. Most cases of meningitis after spinal anesthesia in the first half of the twentieth century were aseptic and could be traced to chemical contamination and detergents.[222,223] Marinac showed that causes of drug- and chemical-induced meningitis include the nonsteroidal antiinflammatory drugs, certain antibiotics, radiographic agents, and muromonab-CD3. There also appears to be an association between the occurrence of the hypersensitivity-type reactions and underlying collagen vascular or rheumatologic disease.[224] Carp and Bailey performed lumbar puncture (LP) in bacteremic rats, and only those with a circulating Escherichia coli count of greater than 50 CFU/mL at the time of LP developed meningitis.[225] Although meningitis after LP also been described in bacteremic children,[226] the incidence of meningitis after diagnostic LP is not significantly different in bacteremic patients compared with spontaneous incidence of meningitis.[227] Oral flora can contaminate the CSF when a spinal anesthetic is being performed. Streptococcus salivarius, S. viridans, Staphylococcus aureus, Pseudomonas aeruginosa, Acinetobacter, and Mycobacterium tuberculosis have all been isolated in cases of bacterial meningitis after spinal anesthesia or LP.[228–231] It is of utmost importance to use a strict aseptic technique when performing spinal anesthesia. Anyone behind the patient during spinal anesthetic administration must wear a cap and facemask to prevent seeding of the patient’s CSF with oropharyngeal flora.

In general, to reduce neurologic complications after spinal anesthesia, some safety rules should be followed. Maintain strict sterility throughout the spinal block procedure. Anyone behind the patient during spinal anesthetic placement must wear a cap and facemask. Check laboratory values of the patient and make sure coagulation parameters are within normal limits. Follow the second ASRA consensus conference guidelines on neuraxial anesthesia and anticoagulation.[232] When giving a spinal anesthetic, use the lowest efficient dose of local anesthetic solution. Incomplete neural blockade should not necessarily lead to another spinal injection of local anesthetic solution, reevaluate and attempt to change the level of the spinal block prior to repeat injection. Avoid large volumes and repeated injections of hyperbaric lidocaine. Never inject preservative-containing solutions into the subarachnoid space. The administration of new compounds in the subarachnoid space must be supported by data of spinal neuropharmacology and the lack of neurotoxicity must have been previously checked with animal studies.[233]

Postdural Puncture Headache

PDPH was first described by Dr. August Bier in 1898, after experimenting on himself. The incidence of PDPH is up to 25% after spinal anesthesia, and the main morbidity after PDPH is restriction of activities of daily living. The headache is characteristically worse when the head is elevated and becomes milder or completely relieved when the patient is supine. PDPH is due to loss of CSF. The subsequent low CSF pressure causes traction on nerve roots and intracranial structures when the patient stands upright. Pain after dural puncture is probably due to increase in cerebral blood flow (CBF). As CSF pressure decreases, CBF increases in order to maintain a constant intracranial volume. Cranial nerve symptoms such as diplopia and tinnitus may occur along with nausea and vomiting. Incidence of PDPH decreases with increasing age and use of small-diameter needles with noncutting, pencil-point needles.[234–236] Although most patients can be treated conservatively with fluids, caffeine, bed rest, analgesics, and sumatriptan, it can take anywhere from 1 to 6 weeks for symptoms to resolve spontaneously. Epidural blood patch remains the mainstay of invasive treatment for PDPH.[237] Effectiveness of blood patching ranges from 64% in obstetrical patients to 95% in the nonpregnant population. The proposed mechanism of action of blood patching is believed to be clot formation over the meningeal hole, preventing further leakage of CSF while the dural puncture heals. Symptoms usually resolve within 1 to 24 h. In patients who do not have symptomatic relief after the first epidural blood patch, a second epidural blood patch is effective 90% of the time. Complications may also arise after epidural blood patch. Reports of back pain, neck pain, lower extremity pain, transient temperature elevation, cranial nerve palsies, nerve root irritation, seizures, acute mental deterioration, subdural hematoma, permanent paresthesias, and cauda equina syndrome have been noted after an epidural blood patch was performed. The most common complication is back pain, which can occur in up to 35% of patients. However, an epidural blood patch is well tolerated if performed with attention to asepsis.[238] If any acute mental changes occur or a second blood patch fails to produce relief, a neurology consult should be immediately obtained.

Intravenous injection of 500 mg of caffeine results in better relief of PDPH than placebo.[234,239,240] One to two doses intravenously should be adequate. Three hundred milligrams of oral caffeine has also been shown to be better than placebo in relieving PDPH.[241] A cup of 150 mL of coffee contains 150 mg of caffeine. Because caffeine is a cerebral vasoconstrictor and a CNS stimulant, complications may occur after administration, including seizures and transient atrial fibrillation. Sumatriptan is a serotonin agonist and causes cerebral vasoconstriction. Sumatriptan is used for the treatment of migraines; however, there are conflicting reports on the value of sumatriptan for PDPH.[242–244] Caution should be used for patients with coronary artery disease or Prinzmetal angina as sumatriptan can cause coronary artery vasospasm. Since sumatriptan is injected subcutaneously, pain at the injection site may occur. More studies need to be performed to determine the usefulness of sumatriptan in treating PDPH.

High Spinal Anesthesia

High spinal anesthesia can result in profound respiratory impairment, most likely due to brainstem ischemia. If the blood pressure and cardiac output become too low due to vasodilation, cerebral blood flow can be impaired. This leads to ischemia of the medullary respiratory center. If blood pressure and cardiac output are restored quickly, spontaneous respiration can return almost immediately. This illustrates the importance of monitoring the vital signs closely and acting quickly to correct them.

Cardiovascular Collapse

Cardiovascular collapse can occur after spinal anesthesia, although it is a rare event. Auroy and coworkers reported only 9 cardiac arrests in 35,439 spinal anesthetics performed.[203] Bradycardia usually precedes cardiac arrest,[143,153,245–247] and early, aggressive treatment of bradycardia is warranted. Treatment of bradycardia includes intravenous atropine, ephedrine, and epinephrine. In cases of cardiac arrest after spinal anesthesia, epinephrine should be used early, and the Advanced Cardiac Life Support (ACLS) protocol should be initiated.[248] There are a few theories as to why spinal anesthesia results in cardiac arrest. Respiratory depression, excessive sedation, and decrease in preload have all been implicated in the past, but they have all been disputed. Hyperventilation, not hypoventilation occurs with spinal block levels up to T4.[249] Cardiac arrest after spinal anesthesia can occur with an oxygen saturation above 95%, and hypoxemia cannot be blamed as the sole cause of cardiac arrest.[153,250] Excessive sedation has also been proposed as a reason for cardiac arrest, but with the use of pulse oximeters, it is unlikely that either excessive sedation or hypoxemia is a cause.[248] A decrease in preload likely leads to increased parasympathetic response that results in bradycardia.[248,251] Activation of three types of receptors have been proposed to cause bradycardia: the low-pressure baroreceptors in the right atrium, the receptors in the myocardial pacemaker, and the mechanoreceptors in the left atrium.[153] Other factors that can lead to more severe bradycardia after spinal anesthesia include high sympathetic blockade from the spinal anesthetic, hypercarbia, hypoxemia, excess sedation from medications given, and chronic medications that cause suppression of the sympathetic nervous system.

Several treatments have been advocated to decrease the incidence of and improve the survival after cardiac arrest due to spinal anesthesia. Prevention of a decrease in preload by volume loading prior to placement of the spinal and prompt replacement of fluid losses are key to lowering the risk of bradycardia and cardiac arrest. Treating even mild decreases in heart rate with atropine and adding a vasopressor for aggressive vagolytic treatment can be lifesaving.[245,246] Epinephrine should be administered early in cases of profound bradycardia or full cardiac arrest after spinal anesthesia. Cardiopulmonary resuscitation (CPR) can be ineffective after spinal anesthesia because of vasodilation, and successful CPR requires a coronary perfusion pressure gradient of 15 to 20 mm Hg. This amount of coronary perfusion pressure can be achieved with epinephrine 0.01–0.02 mg/kg IV initially with an increase to 0.1 mg/kg IV. IF these measures are unsuccessful, a larger dose of epinephrinemay be needed or open chest CPR may need to be instituted.[252]

Outpatient Spinal Anesthesia

Each year the number of surgeries increase and more are performed on an outpatient basis. As anesthesiologists,we are always looking for new ways to provide efficient anesthetic care that is safe, controls pain, allows the patient to be discharged home in a timely fashion as per postanesthesia care unit protocol, and is easily performed and reproducible in multiple patients. Spinal anesthesia fits very well into the outpatient surgery model,[253] and techniques and medications from the past are being used again.

In the past, spinal administration of 2-choloroprocaine was associated with chronic neurologic deficits that were believed to be due to sodium bisulfite, an antioxidant used to prolong the shelf life of chloroprocaine.[189,200,254] Trials of spinal 2-chloroprocaine are being performed with new formulations that do not include sodium bisulfite.[186,188,255–260] Forty milligrams of spinal 2-chloroprocaine produces a peak block height of T7, tourniquet tolerance of 46 min, and discharge within 104 min. Forty milligrams of 2% isobaric lidocaine produces a peak block height of T8, tourniquet tolerance of 38 min, and discharge within 134 min. Slightly hyperbaric bupivacaine (1.00100; 7.5 mg) produces a peak block height of T9, tourniquet tolerance of 46 min, and ambulation within 191 min. Table 5 lists various choices of local anesthetics for spinal anesthesia, peak block height level and the duration of anesthesia.

Common Clinical Problems & Dilemmas In Practice Of Spinal Anesthesia

As with any other form of anesthesia, spinal anesthesia can present clinical problems. This includes inability to locate the subarachnoid space due to difficulties with patient positioning, a lower level of spinal blockade than required for surgery, and the use of spinal anesthesia for outpatient surgery.

Whenever there are problems with placing a spinal anesthetic, the anesthesiologist should check the position of the patient. In order to maximize the chances of success, optimal positioning of the patient should be sought. If the patient is in the sitting position, the shoulders should be placed in a down position, arms should be in front of the patient, neck should be flexed, and the lower back should be pushed out posteriorly so that the interspace can be maximally exposed to the anesthesiologist. A member of the operating room personnel who is trained to assist with patient positioning should be used. If the proposed interspace cannot be found by the midline technique, the paramedian technique can be attempted. The interspace above or below the original site of spinal injection can be attempted with adjustment to the local anesthetic that is injected.

Positioning of the patient can also be enhanced with commercially available positioning devices. These devices can help maintain spinal flexion and create a stable support for the personnel are available to assist with positioning. When the sitting position cannot be used or is unsuccessful, the lateral decubitus position can be used. Either the midline or lateral paramedian technique can be attempted. The largest interlaminar space is at L5, and this can be sought via Taylor’s approach, which is described previously in this article. Sometimes an insufficient dose of local anesthetic is injected into the subarachnoid space and the level of anesthesia is inadequate for surgery. A repeat injection of local anesthetic could lead to excess spinal blockade and possibly cause high or total spinal anesthesia. The alternatives include general anesthesia, peripheral nerve blockade, or infiltration of local anesthesia at the surgical site by the surgeon along with sedation. Every case can offer different options depending on the health status of the patient, the surgery being performed, use of a tourniquet, and other issues pertaining to the case. It is important to think through what will be best for the patient before choosing another plan of action.

In the past, spinal anesthesia was used sparingly in outpatient surgical procedures because of prolonged recovery room stays after a long-acting local anesthetic was given. Currently, spinal anesthesia is an accepted and sometimes preferred method of providing outpatient anesthesia. Short-acting local anesthetics, such as preservative-free 2-chloroprocaine, have been used with success for surgical procedures lasting an hour or less with no reports of TNS after surgery.[255]

Recent Developments In Spinal Anesthesia

Use of a unilateral spinal block for elderly patients and outpatient surgery has recently come into vogue. Unilateral spinal anesthesia was described in 1950 by Ruben and Kamsler. They reported 116 patients for surgical reduction of hip fracture performed under unilateral spinal blockade.[261] No deaths were reported and no increase in the hazard of operation was found. Recently, attention has returned to the use of unilateral spinal anesthesia in elderly patients[262] and for outpatient surgery.[263]

Elderly patients frequently present with femoral neck fractures and changes in blood pressure can be deleterious. Use of unilateral spinal anesthesia has shown no significant changes in systolic, mean and diastolic pressures, or oxygen saturation in elderly trauma patients. It is recommended that a fascia iliaca block be performed, keeping the operative side up and using a hypobaric spinal solution in low dose for these cases.

Outpatient surgery using hyperbaric 0.5% bupivacaine takes about 16 minutes for surgical anesthesia from time of injection for unilateral spinal anesthesia and 13 minutes with traditional bilateral spinal anesthesia. Less hemodynamic changes are found in the unilateral spinal anesthesia group with quicker regression of the block and equal time to discharge home.[264]

In performing a unilateral spinal anesthesia, use of a Whitacre 25-gauge or 27-gauge needle with the bevel opening directed at the operative side is suggested. Low-dose bupivacaine should be used, with hyperbaric bupivacaine in outpatient surgery and hypobaric bupivacaine in the elderly trauma patient.[265] A slow injection rate should be used to produce laminar flow that will assist in producing a unilateral blockade. There is little evidence that keeping a patient in the lateral position for more than 15 min is helpful.

As the population of older patients increases, novel methods of preventing deep venous thrombosis (DVT) and keeping these patients anticoagulated have been developed. Reports of spontaneous spinal and epidural hematoma formation were noted in the cardiology and neurosurgery literature in patients who were anticoagulated.[266–270] As spinal anesthesia was found to be useful in controlling pain postoperatively, such as in lower leg amputations, concern arose over complications occurring in such patients who may have been on concomitant anticoagulant therapy.[271–275]

The concerns of performing central neuraxial block on anticoagulated patients led to the second ASRA consensus conference on neuraxial anesthesia and anticoagulation.[232] There is a very limited risk of spinal hematoma when performing spinal anesthesia while a patient is on subcutaneous heparin. After LMWH administration, spinal anesthesia should be delayed 10–12 h. If blood is noted during needle placement, LMWH therapy should be delayed 24 h. In cases of continuous spinal anesthesia and accidental LMWH therapy, the catheter should be removed 10–12 h after the last dose of LMWH. Spinal anesthesia should not be performed for 14 days after the last dose of ticlopidine and 7 days after clopidogrel. Patients should not receive glycoprotein IIb/IIIa inhibitors for 4weeks after surgery, and spinal anesthesia should not be attempted until platelet function returns to normal. Many patients ingest herbal medications, and currently there are no specific concerns regarding spinal anesthesia in these patients.

Summary

Ever since the introduction of local anesthetics, physicians have investigated different methods of using them. Spinal anesthesia has enjoyed a long and successful history since the late nineteenth century and is currently more popular than ever. Mastery of spinal anesthesia comes with practice; diligence; and knowledge of physiology, pharmacology, and anatomy. Patient safety must always be at the forefront when considering performing a spinal anesthetic. The ease of performance and versatility of spinal anesthesia will continue to result in its widespread popularity in both hospital and ambulatory surgical applications.

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