Handbook of Clinical Anesthesia

Chapter 37

Epidural and Spinal Anesthesia

Spinal anesthesia and epidural anesthesia have been shown to blunt the “stress response” to surgery, decrease intraoperative blood loss, lower the incidence of postoperative thromboembolic events, possibly decrease morbidity in high-risk surgical patients, and serve as a useful method to extend analgesia into the postoperative period (better analgesia than can be achieved with parenteral opioids) (Bernards CM: Epidural and spinal anesthesia. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 927–954).

  1. Anatomy
  2. Proficiency in spinal and epidural anesthesia requires a thorough understanding of the anatomy of the spine and spinal cord.
  3. Vertebrae
  4. The spine consists of 33 vertebrae (seven cervical, 12 thoracic, five lumbar, five fused sacral, and five fused coccygeal).
  5. With the exception of C1 (which lacks a body or spinous process), the vertebrae consist of a body anteriorly; two pedicles that project posteriorly from the body; and two lamina that connect the pedicles to form the vertebral canal, which contains the spinal cord, spinal nerves, and epidural space (Fig. 37-1).
  6. The laminae give rise to the transverse processes, which project laterally, and the spinous process, which projects posteriorly (see Fig. 37-1).
  7. The fifth sacral vertebra is not fused posteriorly, giving rise to a variably shaped opening known as the sacral hiatus (opening into the sacral canal, which is the caudal termination of the epidural space). The sacral cornu are bony prominences on either side to the hiatus and aid in identifying it.


  1. Identifying individual vertebrae is important for correctly locating the desired interspace for performance of epidural and spinal anesthesia (Table 37-1).

Figure 37-1. Anatomy of the vertebral column.

  1. Ligaments
  2. The vertebral bodies are stabilized by five ligaments that increase in size between the cervical and lumbar vertebrae (see Fig. 37-1).

Table 37-1 Landmarks for Vertebral Interspaces

Spinous process of C7

First prominent spinous process in the back of the neck

Spinous process of T1

Most prominent spinous process; immediately follows C7

Spinous process of T12

Palpate the 12th rib and trace back to its attachment of T12

Spinous process of L5

Line drawn between the iliac crests crosses the body of L5 or the L4–L5 interspace

  1. P.563
  2. The ligamentum flavumis thickest in the midline (3–5 mm at L2–L3) and also farthest from the spinal meninges in the midline (4–6 mm at L2–L3). As a result, midline insertion of an epidural needle is least likely to result in accidental meningeal puncture.
  3. Epidural Space
  4. The epidural space lies between the spinal meninges and the sides of the vertebral canal. It is bounded cranially by the foramen magnum, caudally by the sacrococcygeal ligament (sacral hiatus), and posteriorly by the ligamentum flavum and vertebral pedicles.
  5. The epidural space is not a closed space but communicates with the paravertebral space via the intervertebral foramina.
  6. The epidural space is composed of a series of discontinuous compartments, which become continuous when the potential space separating the compartments is opened up by injection of air or liquid.
  7. The most ubiquitous material in the epidural space is fat.
  8. Veins are present principally in the anterior and lateral portions of the epidural space with few, if any, veins present in the posterior epidural space (see Fig. 37-1). These veins anastomose freely with extradural veins (pelvic veins, azygous system, intracranial veins).
  9. Epidural fathas important effects on the pharmacology of epidurally and intrathecally administered opioids and local anesthetics.
  10. Lipid solubility results in opioid sequestration in epidural fat with associated decreases in bioavailability.
  11. Transfer of opioids from the epidural space to the intrathecal space is greatest with poorly lipid-soluble morphine and least for the highly lipid-soluble opioids fentanyl and sufentanil.
  12. Meninges
  13. Dura materis the outermost and thickest meningeal tissue that begins at the foramen magnum (fuses with the periosteum of the skull, forming the cephalad border of the epidural space) and ends at approximately S2, where it fuses with the filum terminale. The dura mater extends laterally along the spinal nerve roots and becomes continuous with the connective tissue of


the epineurium at approximately the level of the intervertebral foramina.

  1. The inner edge of the dura mater is highly vascular, which likely results in the dura mater being an important route of drug clearance from both the epidural and subarachnoid space.
  2. The presence of a midline connective tissue band (plica medianis dorsalis) running from the dura mater to the ligamentum flavum is controversial but may be invoked as an explanation for unilateral epidural block.
  3. The subdural space is a potential space between the dura mater and arachnoid mater. Drug intended for either the epidural space or the subarachnoid space may be accidentally injected into this space.
  4. Arachnoid Mater
  5. The arachnoid mater is an avascular membrane that serves as the principal physiologic barrier for drugs moving between the epidural space and the subarachnoid space.
  6. The subarachnoid spacelies between the arachnoid mater and pia mater and contains cerebrospinal fluid (CSF). The spinal CSF is in continuity with the cranial CSF and provides an avenue for drugs in the spinal CSF to reach the brain. Spinal nerve roots and rootlets run in the subarachnoid space.
  7. Pia materis adherent to the spinal cord.
  8. CSF(100 to 160 mL in adults, produced at a rate of 20 to 25 mL/hr) is replaced roughly every 6 hours (removed by arachnoid villi).
  9. Contrary to a widely held view, CSF does not circulate through the subarachnoid space but rather oscillates in parallel with cerebral expansion and contraction during the cardiac cycle. (Net CSF movement is estimated to be 0.04% per oscillation.)
  10. CSF cannot be relied upon to distribute drugs in the subarachnoid space.
  11. The kinetic energy of the injection and baricity of the solution serve to distribute drug during a single-shot spinal.
  12. The lack of significant net CSF motion explains why drug distribution during slow infusions used for chronic intrathecal analgesia results in limited drug distribution.


  1. Spinal Cord
  2. In adults, the caudad tip of the spinal cord typically ends at the level of L1 (extends to L3 in 10% of adults).
  3. The spinal cord gives rise to 31 pairs of spinal nerves, each composed of an anterior motor root and a posterior sensory root.
  4. Dermatomeis the skin area innervated by a given spinal nerve (Fig. 37-2).
  5. The intermediolateral gray matter of T1–L12 contains the cell bodies of the preganglionic sympathetic neurons. These sympathetic neurons travel with the corresponding spinal nerve to a point just beyond the intervertebral foramen, where they exit to join the sympathetic chain ganglia.


  1. Because the spinal cord ends between L1 and L2, the thoracic, lumbar, and sacral nerve roots travel increasingly longer distances in the subarachnoid space (cauda equina) to reach the intervertebral foramen through which they exit.

Figure 37-2. Human sensory dermatomes.

  1. Technique
  2. Spinal and epidural anesthesia should be performed only after appropriate monitors are applied in a setting where equipment for airway management and resuscitation is immediately available.
  3. Needles
  4. Spinal and epidural needles are named for the design of their tips (“pencil point,” beveled tip with cutting edge) (Fig. 37-3).
  5. Epidural needles have a larger diameter than spinal needles, facilitating injection of air or fluid for the “loss of resistance” technique and passage of catheters.
  6. The outside diameters of spinal and epidural needles are used to determine their gauges. Large-gauge spinal needles (22–29 gauge) are often easier to insert if an introducer (inserted into the interspinous ligament) is used. Postdural puncture headache is less likely when small-gauge spinal needles are used.
  7. All spinal and epidural needles come with a tight-fitting stylet to prevent the needle from becoming plugged with skin or fat.
  8. Sedationbefore placement of the block is limited because patient cooperation (positioning, determination of level of sensory anesthesia, occurrence of paresthesias) is important. After the anesthesia is established, the patient may be sedated as deemed appropriate.

III. Spinal Anesthesia

  1. Position(Table 37-2)
  2. In the lateral decubitus position, the patient lies with the operative side down when hyperbaric solutions are being used. The patient's shoulders and hips are positioned perpendicular to the bed (preventing rotation of the spine), the knees are drawn up to the chest, the neck is flexed, and the patient is asked to


actively curve the back outward (which spreads the spinous processes apart).


Figure 37-3. Examples of commercially available spinal and epidural needles. Needles are distinguished by the design of their tips.


Table 37-2 Patient Position for Performance of Spinal Anesthesia

Lateral Decubitus Sitting
Easier to identify the midline in obese patients
Facilitates restriction of block to sacral segments
Prone (Jackknife)
Consider when surgery is to be performed in this position
Hypobaric solution produces sacral block for perirectal surgery

  1. Using the iliac crests as landmarks, the L2–3, L3–4, and L4–5 interspaces are identified and the desired interspace chosen.
  2. All antiseptic solutions are neurotoxic, and care must be taken not to contaminate spinal needles or local anesthetics. Chlorhexidine–alcohol antiseptic prevents colonization of percutaneous catheters better than 10% povidine–iodine and is the recommended prep for skin asepsis before regional anesthesia procedures.
  3. Midline Approach
  4. After infiltration of the selected needle insertion site with local anesthetic solution, the needle is advanced (subcutaneous tissue to supraspinous ligament to interspinous ligament to ligamentum flavum to epidural space to dura mater [“pop”] to arachnoid mater) until CSF is obtained (gentle aspiration may be helpful). The spinal meninges are typically at a depth of 4 to 6 cm.
  5. If bone is encountered, the depth should be noted and the needle withdrawn to subcutaneous tissue and redirected more cephalad (Fig. 37-4).
  6. If the patient experiences a paresthesia (which should be differentiated from discomfort caused by contacting bone), it is important to immediately stop advancing the needle and determine whether the needle tip has encountered a nerve root in the epidural space or in the subarachnoid space. (The presence of CSF confirms that the needle has encountered a cauda equina nerve root.)
  7. After completing the injection of local anesthetic solution, a small volume of CSF is again aspirated to confirm that the needle tip has remained in the subarachnoid space.



Figure 37-4. Midline approach to the subarachnoid space. The spinal needle is inserted with a slight cephalad angulation and advanced in the midline (B). If bone is contacted, it may be either the caudad (A) or cephalad (C) spinous process. The needle should be redirected slightly, and if bone is encountered at a shallower depth, then the needle is likely walking up the cephalad spinous process. If bone is encountered at a deeper depth, then the needle is likely walking down the inferior spinous process. If bone is repeatedly contacted at the same depth, then the needle is likely off the midline and walking along the lamina.

  1. After the block has been placed, strict attention must be directed to the patient's hemodynamic status with blood pressure and heart rate supported as necessary.
  2. The level of anesthesia should be assessed by pinprick or temperature sensation. If the anesthesia is not rising high enough, the table may be tilted to influence spread of a hyperbaric or hypobaric local anesthetic.
  3. The paramedian approachis used when the patient cannot flex the spine or heavily calcified interspinous ligaments. The needle is inserted 1 cm lateral to the desired interspace with advancement toward the midline. (The first significant resistance is the ligamentum flavum as the interspinous ligament is bypassed.)
  4. The lumbosacral approachis a paramedian approach directed at the L5–S1 interspace.


  1. Continuous Spinal Anesthesia
  2. The technique is similar to that used for a single-shot spinal anesthesia except that a needle large enough to accommodate the desired catheter must be inserted. (The catheter is inserted 2 to 3 cm into the subarachnoid space.)
  3. Although smaller catheters decrease the risk of postdural puncture headache, they have been associated with reports of neurologic injury. (The recommendation is to avoid using a catheter smaller than 24 gauge.)
  4. Epidural Anesthesia
  5. Patient preparation and positioning, the use of monitors, and the needle approaches for epidural anesthesia are the same as for spinal anesthesia. However, unlike spinal anesthesia, epidural anesthesia may be performed at any intervertebral space.
  6. Using the midline approach, the epidural needle is inserted into the interspinous ligament (“gritty” feel) and then advanced slowly until the ligamentum flavum is contacted (increased resistance).
  7. The epidural needle must traverse the ligamentum flavum and stop in the epidural space (“loss of resistance”) before encountering the spinal meninges.
  8. A glass syringe containing 2 to 3 mL of saline and 0.1 to 0.3 mL of air is attached to the epidural needle, and the plunger is pressed. If the needle is properly placed in the ligamentum flavum, it will be possible to compress the air bubble without injecting the saline. If the air bubble cannot be compressed without injecting fluid, then the needle tip is most likely not in the ligamentum flavum but instead in the interspinous ligament or off midline in the paraspinous muscles.
  9. After the ligamentum flavum is identified, the needle is slowly advanced with the nondominant hand while the dominant hand maintains constant pressure on the syringe plunger (Fig. 37-5).
  10. As the needle enters the epidural space, there will be a sudden and dramatic loss of resistance as the saline is rapidly injected (the patient should be warned of possible pain). If the needle is advancing obliquely through the ligamentum flavum, it is


possible to enter into the paraspinous muscles instead of the epidural space (loss of resistance is less dramatic).


Figure 37-5. Proper hand position when using the loss of resistance technique to locate the epidural space. After placing the tip of the needle in the ligamentum flavum, a syringe containing 2 to 3 mL of saline and an air bubble is attached. The dominant hand maintains constant pressure on the syringe plunger while the nondominant hand rests against the patient's back and is used to slowly advance the needle. If the needle is properly placed in the ligamentum flavum, it will be possible to compress the air bubble without injecting the saline. As the needle tip enters the epidural space, there will be a sudden loss of resistance, and the saline will be easily ejected from the syringe.

  1. When the syringe is disconnected from the needle, it is common to have a small amount of fluid flow from the needle hub (usually saline, which is at room temperature in contrast to CSF).
  2. A test dose of local anesthetic solution is injected to help detect unrecognized intravenous (IV) or subarachnoid placement of the needle. After a negative test dose, the desired volume of local anesthetic solution should be administered in 5-mL increments (this decreases the risk of pain during injection and allows early detection of adverse reactions).
  3. Continuous Epidural Anesthesia
  4. Use of a catheter for epidural anesthesia affords greater flexibility than the single-shot technique but introduces the risk of catheter migration (subarachnoid space,


intervertebral foramen) and increases the likelihood of a unilateral epidural block.

  1. Epidural catheters are usually inserted through a curved-tip needle to help direct the catheter away from the dura mater. The catheter typically encounters resistance as it reaches the curve of the needle, but using steady pressure usually results in its passage into the epidural space. One explanation for the inability to thread an epidural catheter is that the tip of the epidural needle was bent during bony contact and now partially occludes the needle lumen.
  2. The catheter should be advanced only 3 to 5 cm into the epidural space. (This minimizes the risk of forming a knot, entering a vein, puncturing dura mater, exiting via an intervertebral foramen, and wrapping around a nerve root.)
  3. After the catheter is appropriately positioned, the needle is slowly withdrawn with one hand as the catheter is stabilized with the other. The length of the catheter in the epidural space is confirmed because this distance is important when trying to determine if a catheter used in the postoperative period has been dislodged.
  4. A test dose of the local anesthetic solution is injected before the initial injection and any subsequent “top-up dose” (typically 50% of the initial dose at an interval equal to two thirds the expected duration of the block).

VII. Epidural Test Dose

  1. The most common test dose is 3 mL of local anesthetic solution containing 5 µg/mL of epinephrine (1:200,000).
  2. This dose is sufficient to produce evidence of spinal anesthesia if accidental subarachnoid injection occurs.
  3. IV injection of the epinephrine dose typically increases the heart rate an average of 30 bpm.
  4. Reflex bradycardia may occur in patients being treated with α-blockers. (A increase in systolic blood pressure of 20 mm Hg or more may be a more reliable indicator of intravascular injection in these patients.)
  5. The sensitivity of epinephrine as a test dose in parturients is questionable because maternal heart rate increases during contractions are often as large as those produced by epinephrine.


  1. Aspirating the catheter or needle to check for blood or CSF is helpful if positive, but the incidence of false-negative aspirations is too high to rely on this technique alone.

VIII. Combined Spinal–Epidural Anesthesia

  1. This technique combines the rapid onset and dense block of spinal anesthesia with the flexibility afforded by an epidural catheter.
  2. After the peak spinal block height has been established, the injection of saline or a local anesthetic solution into the epidural space causes the block height to increase, presumably reflecting compression of the spinal meninges forcing CSF cephalad as well as a local anesthetic effect.
  3. A potential risk of this technique is that the meningeal hole made by the spinal needle may allow high concentrations of subsequently administered epidural drugs to reach the subarachnoid space.
  4. Pharmacology
  5. Interindividual variability makes it difficult to reliably predict the height and duration of central neuraxial block that will result from a particular local anesthetic dose (Table 37-3).
  6. Spinal Anesthesia
  7. Block Height(Table 37-4)
  8. Baricity and Patient Position.Of the factors that exert significant influence on local anesthetic spread, the baricity of the local anesthetic solution relative to patient position is probably the most important.
  9. Hyperbaric solutions(more dense than CSF) are typically prepared by mixing the local anesthetic solution with 5% to 8% dextrose. Gravity causes hyperbaric solutions to flow downward in the CSF to the most dependent regions of the spinal column. Spinal anesthesia can be restricted to the sacral and lower lumbar dermatomes (“saddle block”) by administering a hyperbaric local anesthetic solution with the patient in the sitting position.
  10. Hyperbaric solutionscan be used to advantage for unilateral surgical procedures performed in



the supine position if the operative site is dependent during drug injection and the patient is left in the lateral position for at least 6 minutes.

Table 37-3 Representative Surgical Procedures Appropriate for Spinal Anesthesia

Surgical Procedure

Block Height

Suggested Technique




Hyperbaric solution or sitting position

Patients must remain in relative head-up or head-down position when using hypobaric and hyperbaric solutions to maintain restricted spread during the procedure



Hypobaric solution or jackknife position
Isobaric solution or horizontal position


Lower extremity


Isobaric solution

Hypobaric and hyperbaric solutions are also suitable but may produce higher blocks than necessary

Transurethral resection of the prostate
Vaginal or cervical



Hyperbaric solution or horizontal position

Isobaric solutions injected at the L2–L3 interspace may also be suitable

Pelvic procedures



Hyperbaric solution or horizontal position

Upper abdominal procedures usually require concomitant general anesthesia to prevent vagal reflexes and pain from traction on the diaphragm and esophagus



  1. When the patient is turned supine after hyperbaric drug injection in the lateral position, the normal


spinal curvature influences subsequent movement of the injected solution. Hyperbaric solutions injected at the height of the lumbar lordosis tend to flow cephalad to pool in the thoracic kyphosis and caudad to pool in the sacrum (Fig. 37-6).

Table 37-4 Factors That May Influence the Spread of Local Anesthetic Solutions in the Subarachnoid Space

Characteristics of the Local Anesthetic Solution
Baricity relative to patient position (most important of all factors)
Local anesthetic dose (little effect with isobaric solutions)
Local anesthetic concentration
Volume injected
Patient Characteristics
Age, weight, and height (poor predictors of extent of sensory blockade)
Site of injection
Speed of injection
Direction of needle bevel
Addition of vasoconstrictors


Figure 37-6. In the supine position, hyperbaric local anesthetic solutions injected at the height of the lumbar lordosis (circle) flow down the lumbar lordosis to pool in the sacrum and in the thoracic kyphosis. Pooling in the thoracic kyphosis is thought to explain the fact that hyperbaric solutions produce blocks with an average sensory level of T4–T6.

  1. Gravity influences the distribution of hyperbaric and hypobaric solutions only until they are sufficiently diluted in CSF so that they become isobaric (solution no longer moves in response to changes in position).
  2. Dose, Volume, and Concentration.Drug dose and volume appear to be relatively unimportant in predicting the spread of hyperbaric local anesthetic solutions injected in the horizontal plane (reflecting the predominate effect of baricity and patient position).
  3. Injection siteis the same as for drug dose and volume.
  4. Patient Characteristics.The most important variable governing block height may be the patient's lumbosacral CSF volume. The patient's age, weight, and height have not been proven to be important predictors of block height.
  5. The onsetof spinal anesthesia is within a few minutes regardless of the drug used, although time to reach peak block is different among drugs (e.g., lidocaine sooner than bupivacaine).
  6. The durationof spinal anesthesia is characterized by gradual waning of the block beginning with the most cephalad dermatome.
  7. When speaking about duration of block, it is necessary to distinguish between duration at the surgical


site and the time required for anesthesia to completely resolve (which influences discharge time) (Table 37-5).

Table 37-5 Dose and Duration of Local Anesthetics Used for Spinal Anesthesia


Dose (mg)

Two-Dermatome Regression (min)

Complete Resolution (min)

Prolongation by Adrenergic Agonists (%)





Not recommended
















  1. A thorough understanding of the factors that govern the duration of anesthesia is necessary for the anesthesiologist to choose techniques that result in an appropriate duration (Table 37-6). Intrathecal epinephrine decreases blood flow in the dura mater without altering spinal cord blood flow, which is consistent with decreased drug clearance via the dural vasculature.
  2. Epidural Anesthesia
  3. Any procedure that can be performed under spinal anesthesia can also be performed under epidural anesthesia and requires the same block height (see Table 37-3). As with spinal anesthesia, there is a great


interindividual variability in the spread and duration of epidural anesthesia (Table 37-7).

Table 37-6 Factors That May Influence the Duration of Sensory Blockade Produced by Spinal Anesthesia

Local anesthetic drug (principal determinant of duration)
Drug dose
Block height (higher blocks regress faster as cephalad spread results in relatively lower drug concentration in CSF)
Adrenergic agonists (effectiveness depends on local anesthetic with which they are combined; tetracaine > bupivacaine)
   Epinephrine 0.2–0.3 mg
   Phenylephrine 2–5 mg
   Clonidine 75–150 µg

CSF = cerebrospinal fluid.

Table 37-7 Local Anesthetics Used for Surgical Epidural Anesthesia


Two-Dermatome Regression (min)

Complete Resolution (min)

Prolongation by Epinephrine (%)

Chloroprocaine 3%








Mepivacaine 2%




Ropivacaine 0.5%–1%




Etidocaine 1%–1.5%




Bupivacaine 0.5%–0.75%




  1. Block Spread.To choose the most appropriate local anesthetic and dose for a particular clinical situation, the anesthesiologist must be familiar with the variables that affect the spread and duration of epidural anesthesia (Table 37-8).

Table 37-8 Factors That May Influence the Spread of Local Anesthetic Solutions in the Epidural Space

Injection site (unlike spinal anesthesia, epidural anesthesia produces a segmental block that spreads both caudally and cranially from the site of injection)
Drug volume (increasing the volume results in greater spread and density of block; increases cephalad distribution)
Drug dose (important with volume in determining spread and density of block)
Drug concentration (relatively unimportant in determining block spread)
Position (does not seem to have a clinically important effect on the spread of the block from side to side)
Patient characteristics
   Age (greater spread in elderly perhaps because of less compliant epidural space and decreased likelihood of local anesthetic solution to escape via intervertebral foramina)
   Height and weight (weak correlation except at extremes)
   Pregnancy (conflicting data)
   Atherosclerosis (relationship not confirmed)

  1. P.579
  2. The onsetof epidural anesthesia can usually be detected within 5 minutes in the dermatomes immediately surrounding the injection site.
  3. The time to peak effect is 15 to 20 minutes with shorter acting drugs and 20 to 25 minutes with longer acting drugs.
  4. Increasing the dose of local anesthetic speeds the onset of both motor and sensory block.
  5. Duration(Table 37-9)
  6. Physiology
  7. Neurophysiology
  8. The site of actionof spinal and epidural anesthesia is not precisely known but can potentially occur at any or all points along the neural pathways extending from the site of drug administration to the interior of the spinal cord.
  9. Differential neural blockrefers to the clinically important phenomenon in which nerve fibers subserving different functions display varying sensitivity to local anesthetic blockade.
  10. Sympathetic nervous system nerve fibers appear to be blocked by the lowest concentration of local anesthetic followed in order by fibers responsible for pain, touch, and motor function.
  11. Although the mechanism for differential block in spinal and epidural anesthesia is not known, it is clear that fiber diameter is not the only, nor


perhaps even the most important, factor contributing to differential blockade.

Table 37-9 Factors That Influence the Duration of Sensory Blockade Produced by Epidural Anesthesia

Local anesthetic drug (principal determinant of duration)
Dose (increasing dose results in increased duration and density)
Age (conflicting results)
Adrenergic agonists (epinephrine 1:200,000)
   Prolongs duration of lidocaine and mepivacaine > bupivacaine and etidocaine
   Mechanism may reflect decreased absorption from epidural space or direct inhibitory effect of epinephrine on sensory and motor neurons

  1. During spinal and epidural anesthesia, differential block is manifested as a spatial separation in the modalities blocked. (Sympathetic block may extend two to six dermatomes higher than sensory block, which is two to three dermatomes higher than motor block.) This spatial separation is believed to result from a gradual decrease in local anesthetic concentration within the CSF as a function of distance from the site of injection.
  2. An occasional patient has intact touch and proprioception at the surgical site despite adequate blockade of pain sensation.
  3. Central neuraxial block produces sedation, potentiates the effects of sedative drugs, and markedly decreases the anesthetic requirements.
  4. Cardiovascular Physiology
  5. Understanding the homeostatic mechanisms responsible for control of blood pressure and heart rate is essential for understanding and treating the cardiovascular changes associated with spinal and epidural anesthesia (Fig. 37-7).
  6. Spinal Anesthesia.Blockade of sympathetic nervous system efferent fibers is the principal mechanism by which spinal anesthesia produces cardiovascular derangements.
  7. The incidence of significant hypotension or bradycardia is generally related to the extent of sympathetic nervous system blockade, which in turn parallels block height.
  8. Hypotension during spinal anesthesia is the result of arterial (decreased systemic vascular resistance) and venous (decrease preload responsible for decreased cardiac output) dilation. An intact renin–angiotensin system helps to offset the hypotensive effects of sympathetic block. (Caution should be exercised when administering central neuraxial block to patients taking antihypertensives that impair the angiotensin system.)
  9. Heart rate slows significantly in 10% to 15% of patients (because of blockade of sympathetic cardioaccelerator fibers or diminished venous return and the associated decreased stretch of intracardiac stretch receptors). Patients with unexplained severe


bradycardia and asystole during spinal and epidural anesthesia may require aggressive intervention with epinephrine.


Figure 37-7. The cardiovascular effects of spinal and epidural anesthesia in volunteers with T5 sensory blocks. The effects of spinal anesthesia and epidural anesthesia without epinephrine were generally comparable and are both qualitatively and quantitatively different from the effects of epidural anesthesia with epinephrine added to the local anesthetic solution.

  1. Spinal anesthesia can also produce second- and third-degree heart block. Pre-existing first-degree heart block may be a risk factor for progression to higher grade heart block during spinal anesthesia.
  2. Epidural Anesthesia.The hemodynamic changes produced by epidural anesthesia are largely dependent on whether or not epinephrine is added to the local anesthetic solution (see Fig. 37-7).


  1. Hemodynamic changes of high epidural anesthesia without epinephrine in the local anesthetic solution resemble the changes seen with spinal anesthesia, although the magnitude is usually less than that seen with comparable levels of spinal block.
  2. When epinephrine is added to the local anesthetic solution, the resulting β2-mediated vasodilation leads to a greater decrease in blood pressure than occurs in the absence of epinephrine.
  3. Treating Hemodynamic Changes(Table 37-10)
  4. Respiratory Physiology
  5. Spinal and epidural anesthesia to midthoracic levels have little effect on pulmonary function in patients without pre-existing disease. (Drugs used for sedation may have a greater effect.)
  6. The adverse impact of high blocks on active exhalation suggests that caution should be exercised when using spinal or epidural anesthesia in patients with chronic obstructive pulmonary disease and those who rely on the accessory muscles of respiration to maintain adequate ventilation.
  7. Patients with high spinal or epidural anesthesia may complain of dyspnea (loss of ability to feel the chest


move while breathing, which is usually adequately treated by reassurance). A normal speaking voice suggests that ventilation is normal (with an excessively high block, the patient will have a faint, gasping whisper).

Table 37-10 Treating Hemodynamic Changes Secondary to Spinal and Epidural Anesthesia

Ephedrine (5–10 mg IV treats causes of hypotension by increasing cardiac output [venous return] and systemic vascular resistance)
Dopamine (long-term infusion because tachyphylaxis can develop to repeated doses of ephedrine)
Phenylephrine (increase blood pressure by increasing systemic vascular resistance, which may decrease cardiac output; this may be specific treatment for hypotension during epidural anesthesia provided by epinephrine-containing local anesthetic solutions)
Fluid Administration
Prehydration with 500–1500 mL of crystalloid solution (cannot be relied on to prevent hypotension); 6% hetastarch (500 mL) may be an alternative to crystalloids

  1. Gastrointestinal Physiology
  2. Unopposed parasympathetic nervous system activity results in increased secretions, relaxation of sphincters, and constriction of the bowel.
  3. Nausea is a common complication of spinal and epidural anesthesia. (The cause unknown but is often associated with blocks higher than T5, hypotension, and opioid administration).
  4. Endocrine–Metabolic Physiology.Spinal anesthesia and epidural anesthesia inhibit many of the changes associated with the stress response to surgery (presumed to reflect blockade of afferent sensory information).
  5. Complications
  6. Backache
  7. Postoperative backache occurs after general anesthesia but is more common after spinal (11%) or epidural anesthesia (30%).
  8. Possible explanations for backache include needle trauma, local anesthetic irritation, and ligamentous strain secondary to muscle relaxation.
  9. Postdural Puncture Headache
  10. Headache is characteristically mild or absent when the patient is in the supine position, but head elevation results in fronto-occipital headache. Occasionally, cranial nerve symptoms (diplopia, tinnitus) and nausea and vomiting are present.
  11. Headache is believed to result from the loss of CSF through the meningeal needle hole, resulting in decreased buoyant support for the brain.
  12. In the upright position, the brain sags in the cranial vault, putting traction on pain-sensitive structures and possibly cranial nerves.
  13. The incidence of postdural puncture headache decreases with increasing age and with the use of small-diameter spinal needles with noncutting tips.
  14. Inserting cutting needles with the bevel aligned parallel to the long axis of the meninges results in


a meningeal opening that is likely to be pulled closed by the longitudinal tension present on the dura mater.

  1. Up to 50% of young patients develop postdural puncture headache after accidental meningeal puncture with a large epidural needle.
  2. If age is considered, there does not seem to be a gender difference in the incidence of postdural puncture headache.
  3. Remaining supine does not decrease the incidence of postdural puncture headache.
  4. Use of fluid rather than air for determining loss of resistance during attempted location of the epidural space decreases the risk of developing postdural puncture headache in the event of an accidental meningeal puncture.
  5. Postdural puncture headache usually resolves spontaneously in a few days with conservative therapy (bed rest, analgesics, and caffeine).
  6. Epidural blood patch(10–20 mL of autologous blood is aseptically injected into the epidural space near the interspace where the meningeal puncture occurred) produces relief in 85% to 95% of patients within 1 to 24 hours. (It is presumed to form a clot over the meningeal hole.)
  7. The most common side effects of blood patch are backache and radicular pain.
  8. Use of a prophylactic blood patch is effective in preventing postdural puncture headache in patients in whom the meninges are accidentally punctured during attempted epidural anesthesia.
  9. Epidural administered fibrin glue (meningeal patch) is an effective alternative to a blood patch for treatment of postdural puncture headache.
  10. Transient hearing loss(lasting 1–3 days) is common after spinal anesthesia, especially in female patients.
  11. Systemic toxicitymanifests as central nervous system (CNS) and cardiovascular toxicity during epidural anesthesia (drug doses are too low during spinal anesthesia).
  12. CNS toxicity may result from intravascular absorption from the epidural space but is more commonly caused by accidental IV injection of the local anesthetic solution.


  1. Because plasma concentrations of local anesthetic required to produce cardiovascular toxicity are high, this complication likely results only from accidental IV injection of the local anesthetic solution.
  2. An adequate test dose and incremental injection of the local anesthetic solution are the most important methods for preventing systemic toxicity during epidural anesthesia.
  3. Total Spinal Anesthesia
  4. Total spinal anesthesia occurs when the local anesthetic solution spreads high enough to block the entire spinal cord and occasionally the brainstem during either spinal or epidural anesthesia.
  5. Profound hypotension and bradycardia may occur secondary to sympathetic nervous system blockade. Apnea may occur as a result of respiratory muscle dysfunction or depression of brainstem control centers.
  6. Management includes administration of vasopressors, atropine, fluids, and oxygen plus controlled ventilation of the lungs. If the cardiovascular and ventilatory consequences are managed appropriately, total spinal block will resolve without sequelae.
  7. Neurologic Injury
  8. Neurologic injury occurs in approximately 0.03% to 0.1% of all spinal and epidural anesthesia. (Persistent paresthesias and limited motor weakness are the most common injuries.)
  9. Hyperbaric 5% lidocaine has been implicated as a cause of cauda equina syndrome after subarachnoid injection through small-bore (high-resistance) catheters during continuous spinal anesthesia. (Injection through these high-resistance catheters produces little turbulence, and undiluted local anesthetic solution tends to pool around dependent cauda equina nerve roots.)
  10. Transient neurologic symptoms(TNS) or transient radicular irritation (TRI) is defined as pain or dysesthesia in the buttocks or legs after spinal anesthesia (Table 37-11).
  11. Use of a double-orifice pencil-point needle may reduce the risk of TNS compared with the use of a single-orifice needle.
  12. Pain usually resolves spontaneously in 72 hours.


Table 37-11 Transient Neurologic Symptoms

Risk Factors

Not Risk Factors


Lidocaine dose

Addition of phenylephrine to 0.5% tetracaine

Addition of epinephrine to lidocaine

Lithotomy position

Presence of dextrose

Leg flexed (as for menisectomy)

Paresthesia or blood-tinged CSF

Outpatient status


CSF = cerebrospinal fluid.

  1. The mechanism responsible for TRI is unknown but it is not simply a milder form of cauda equina syndrome.
  2. Chloroprocaine(preservative free) is a short-acting spinal anesthetic and does not seem to be associated with TNS.
  3. Spinal hematomais a rare (estimated to occur in fewer than one in 150,000 patients) complication of spinal or epidural anesthesia manifesting as lower extremity numbness or weakness. Detection is difficult in patients receiving perioperative spinal local anesthetic solution pain control.
  4. Early detection is critical because a delay of more than 8 hours in decompressing the spinal cord decreases the likelihood of neurologic recovery.
  5. Coagulation defects are the principal risk factor for development of an epidural hematoma.
  6. Patients receiving nonsteroidal anti-inflammatory drugs (NSAIDs) with antiplatelet effects or subcutaneous unfractionated heparin for deep thrombosis prophylaxis are not considered to be at increased risk for development of a spinal hematoma.
  7. Patients taking antiplatelet drugs (thienopyridine derivatives such as ticlopidine and clopidogrel; glycoprotein IIb/IIIa antagonists such as abciximab) should generally not receive a neuraxial block.
  8. Patients receiving fractionated low-molecular-weight heparin (LMWH; enoxaparin, dalteparin, tinzaparin) are considered to be at increased risk for development of a spinal hematoma. Patients receiving drugs preoperatively at thromboprophylactic


doses should have the drug held for 10 to 12 hours before central neuraxial block.

Table 37-12 Conditions That May Increase the Risk of Spinal or Epidural Anesthesia

Increased intracranial pressure
Coagulopathy or thrombocytopenia (epidural hematoma)
Sepsis (increased risk of meningitis)
Infection at the puncture site
Pre-existing neurologic disease (there is no evidence that epidural or spinal anesthesia alters the course)
Patient refusal (absolute contraindication)

  1. For patients in whom LMWH is begun after surgery, single-shot neuraxial blocks are not contraindicated provided the first dose of heparin is not administered until 24 hours after surgery using twice-daily dosing regimens (or 6 to 8 hours if using once-daily dosing regimens).
  2. If an indwelling central neuraxial catheter is in place, it should not be removed until 10 to 12 hours after the last dose of LMWH, and subsequent doses should not be administered until at least 2 hours after catheter removal.
  3. Patients who are fully anticoagulated (prolonged prothrombin time and plasma thromboplastin


time) at the time of block placement or removal of the epidural catheter are considered to be at increased risk for the development of a spinal hematoma.

Table 37-13 Choice of Spinal or Epidural Anesthesia

Spinal Anesthesia
Less time to perform
More rapid onset
Better quality sensory and motor block
Less pain during surgery
Epidural Anesthesia
Less risk of postdural puncture headache
Less hypotension if epinephrine is not added to local anesthetic solution
Ability to prolong or extend block via an indwelling catheter
Option of using an epidural catheter to provide postoperative analgesia

  1. The risk of spinal hematoma during removal of an epidural catheter is nearly as great as with placement of the catheter. The timing for removal of the epidural catheter and the degree of anticoagulation need to be coordinated.
  2. Drugs or regimens not considered to increase the risk of neuraxial bleeding when used alone (minidose unfractionated heparin, NSAIDs) may increase the risk when combined.

XII. Contraindications

(Table 37-12)

XIII. Choice of Spinal or Epidural Anesthesia

(Table 37-13)

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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