Epidural Blockade

Epidural blockade is becoming one of the most useful and versatile procedures in modern anesthesiology. It is unique in that it can be placed at virtually any level of the spinal spine, allowing more flexibility in its application to clinical practice.

Epidural blockade is becoming one of the most useful and versatile procedures in modern anesthesiology. It is unique in that it can be placed at virtually any level of the spinal spine, allowing more flexibility in its application to clinical practice. It is more versatile than spinal anesthesia, giving the clinician the opportunity to provide anesthesia and analgesia, as well as enabling diagnosis and treatment of chronic disease syndromes. It can be used to supplement general anesthesia, decreasing the need for deep levels of general anesthesia, therefore providing a more hemodynamically stable operative course. It provides better postoperative pain control and more rapid recovery from surgery. When combined with spinal anesthesia in a technique called a CSE, or combined spinal epidural, benefits of both techniques can be combined and shortcomings of each avoided.

Numerous studies have demonstrated the benefits of epidural blockade. Epidural anesthesia or analgesia can reduce the adverse physiologic responses to surgery such as autonomic hyperactivity, cardiovascular stress, tissue breakdown, increased metabolic rate, pulmonary dysfunction, and immune system dysfunction. Thoracic epidural analgesia has been shown to decrease the incidence of myocardial infarction¹ postoperative pulmonary complications^2,3 and to promote the return of gastrointestinal motility without compromising fresh suture lines in the GI tract.⁴⁻⁶ Epidural anesthesia and analgesia reduces the incidence of hypercoagulability.^7,8 Well-conducted randomized trials have demonstrated the perioperative use of epidural anesthesia and analgesia reduces overal lmortality and morbidity by approximately 30% compared with general anesthesia using systemic opiods.⁹ This article aims to provide the information necessary to provide safe and effective epidural blockade. The reader is encouraged to review specific references in this text for a more detailed discussion on specialized topics such as local anesthetics, combined spinal-epidural anesthesia, obstetric anesthesia, and serious complications such as epidural hematomas.

Brief History

Two French physicians, Jean-Anthanase Sicard, a radiologist, and Ferdinand Cathelin have been credited with the intentional administration of caudal epidural anesthesia over a century ago in 1901. They found that injecting a dilute solution of cocaine through the sacral hiatus to be an effective treatment for severe sciatic pain and suggested the technique for surgical procedures.¹⁰ Nineteen years later, a Spanish military surgeon by the name of Fidel Pages Mirave, is credited with describing the lumbar approach to “peridural” anesthesia. Unfortunately he was killed in an accident at the early age of 37, and his work lay dormant for several years.¹¹ Then in 1931, an Italian surgeon, Archile Dogliotti, performed abdominal surgery using single-shot lumbar epidural anesthesia, popularizing the method of producing “segmental peridural anesthesia.” He noted that a sufficient length of spinal nerves needed to be blocked with an anesthetic solution of sufficient quantity to provide adequate anesthesia. He correctly identified the epidural space by describing the sudden loss of resistance noted after the needle had crossed the ligamentum flavum.¹²

Aburel, Hingson, and Edwards all devised methods for continuous but cumbersome epidural blockade; however, Cuban anesthesiologist, Manual Martinez Curbelo, is credited with making the technique more practical. On a visit to the Mayo Clinic in 1947, he watched Edward Tuohy perform continuous spinal blocks. Tuohy had replaced sharp spinal needles with a curved tip design developed by Ralph Huber. Tuohy modified the needle by adding a stylet to decrease the risk of skin plugging during insertion. Curbelo then used the Tuohy needle with a silk ureteral catheter to provide continuous segmental lumbar “peridural” anesthesia.¹³ Several modifications of the Tuohy–Huber epidural needle have been developed in the more recent past and are being utilized in modern anesthesia practice. The epidural catheters have undergone more major changes since the original 3.5 F silk catheter used by Curbelo. The silk catheters were difficult to sterilize and prone to causing serious infections. Polymers of nylon, Teflon, polyurethrane, and silicone are currently used by manufacturers to produce thin, kink-resistant catheters of appropriate tensile strength and stiffness.^10,14

Combining spinal with epidural anesthesia (CSE) began shortly after epidural anesthesia was reintroduced by Dogliotti. In 1939, Dr. A. L. Soresi presented a paper in which he and his colleagues provided a combination of spinal and epidural anesthesia safely to over 200 patients. He used one needle to first enter the epidural space, injected local anesthesia, then used the same needle to enter the subarachnoid space, dosing the patient with a smaller amount of local anesthetic. He demonstrated that he was able to provide anesthesia to his patients for 24 to 48 h.¹⁵ In 1979, a Swedish physician named Curelaru was the first to describe a combined technique using separate intervertebral injections. Then in 1982, Coates from England and Mumtaz from Sweden published reports of the popular needle-through-needle approach^16,17 for combined spinal-epidural anesthesia. Since that time, modifications of the CSE needle delivery systems as well as the creation of special trays for the procedure have been developed and are being utilized in the practice of modern anesthesiology.

Back to top

Indications

Epidural anesthesia has been typically limited to procedures involving the lower limbs, pelvis, perineum, and lower abdomen. As clinicians have become more experienced with its application, epidural anesthesia with or without sedation has been used as the sole anesthetic or in combination with general anesthesia for a larger variety of cases. Michalek reported the use of cervical epidural anesthesia at the C6–7 level for a total parathyroidectomy with parathyroid gland implantation into the forearm. He concluded that combined procedures involving the neck and upper limbs could be safely conducted under cervical epidural blockade.¹⁸ Several studies have described the use of high thoracic epidural anesthesia for off-pump coronary revascularization^19,20 and even for minimally invasive aortic valve replacement,²¹ although this has not become common practice in the United States. In patients in whom general anesthesia could lead to prolonged ventilatory care, such as those with diffuse interstitial lung disease, thoracic epidural anesthesia as the sole anesthetic has been described as a successful alternative.

Although it is intriguing to realize that epidural blockade can be performed for procedures that in the past were limited to general anesthesia, the decision about whether to use this form of neuraxial blockade should be determined by the needs of the patient. Physiologically, blocks above T5 have a far greater effect on patient hemodynamics than blocks at T10 or lower. However, if the benefits of epidural blockade outweigh the risks to the patient, and the sensory blockade needed for the particular procedure can be obtained, then it is indicated. This distinction is sometimes blurred in teaching institutions when the desire to “practice” overshadows the needs of the patient, or when impatient surgeons do not want to allow novice epiduralists the time to safely perform the procedure. By keeping the needs of the patient in the forefront, this should never be a problem in modern day clinical practice. Common applications for epidural blockade are listed in Table 1.

Contraindications

Absolute

Contraindications to epidural blockade have been historically divided into absolute, relative, and controversial (Table 2). Absolute contraindications include patient refusal, severe, uncorrected hypovolemia (sympathectomy with hypovolemia may cause profound circulatory collapse), increased intracranial pressure (may predispose patient to brainstem herniation if accidental dural puncture occurs or if a large volume of anesthetic is rapidly injected into the epidural space), and infection at the site of injection.²² True allergies to local anesthetics of both classes, although exceedingly rare, is also an absolute contraindication.

Relative

Coagulopathy, whether iatrogenic or idiopathic, previously an absolute contraindication, is now considered a relative contraindication.²³ Anticoagulants should be withheld based on the mechanism of action and duration of the drug. The greatest concern with anticoagulant therapy and anticoagulation is the risk of an epidural hematoma . According to the consensus statements by the American Society of Regional Anesthesia and Pain Medicine,²³ epidural block can be placed 4 h after the last dose of subcutaneous heparin, and 12 h after the last dose of low-molecular-weight heparin. NSAIDs, including aspirin, are not contraindications to epidural placement provided that catheter placement occurs after one or two attempts. Other relative contraindications include uncooperative patient (therefore exposing neural structures to an unacceptable risk of injury), fixed cardiac output states (inability to increase cardiac output in response to sympathectomy), anatomic abnormalities of the vertebral column (making placement technically impossible), and unstable neurologic disease (may mask exacerbation signs/symptoms).^24,25 Case reports have been published on patients undergoing epidural anesthesia safely with serious neurologic conditions such as neural tube defects, Guillain–Barr´e syndrome, and quadriplegia with autonomic hyperreflexia.²⁶⁻²⁸ Careful evaluation and documentation of the patient’s baseline neurologic status, a thorough discussion of risks as well as the benefits of epidural anesthesia and a multidisciplinary approach is required for these patients. The same approach should be taken with any patient with serious medical diseases prior to instituting epidural blockade.

Controversial

The more controversial contraindications to epidural anesthesia include inability to communicate with the patient (placing an epidural in an anesthetized patient)²⁹ tattoos (potential risk of pigment-containing tissue coring into the epidural space);³⁰ complicated surgeries with major blood loss,²⁵ and in surgical maneuvers in which respiration may be compromised or the airway will be difficult to manage.

Back to top

Figure 1. Anatomy of the vertebral column. Figure 2. Comparison of cervical, thoracic, and lumbar vertebrae. Figure 3. Arrangement of the vertebral ligaments.

The key to safe and effective administration of an epidural blockade begins with a thorough understanding of the anatomy of the vertebral column, ligaments, and blood supply, the epidural space, spinal canal, and associated structures. A three-dimensional mental picture of surface structures as they relate to internal structures helps the clinician troubleshoot difficult epidural placement.

Vertebral Column

General Appearance

The vertebral column consists of 7 cervical, 12 thoracic, and 5 lumbar vertebrae. At the caudal end, the 5 sacral vertebrae are fused to form the sacrum, and the 4 coccygeal vertebrae are fused to form the coccyx (Figure 1). The primary functions of the vertebral column are to maintain erect posture, to encase and protect the spinal cord, and to provide attachment sites for the muscles responsible for movements of the head and trunk.³¹ The normal spinal column is straight when viewed dorsally or ventrally.When viewed fromthe side, there are two ventrally convex curvatures in the cervical and lumbar regions, giving the spinal column the appearance of a double C.

Structure of Vertebrae

Each vertebra is composed of a vertebral body and a bony arch. The arch consists of two anterior pedicles and two posterior laminae. The transverse processes are located at the junction of the pedicles and lamina, and the spinous process is located at the junction of the laminae. The spinous processes vary in their angulation in the cervical, thoracic, and lumbar regions. The spinous processes are almost horizontal in the cervical, lower thoracic, and lumbar regions, but become significantly more sharply angled in the midthoracic region. The greatest degree of angulation is found between the T3 and T7 vertebrae, making insertion of an epidural needle in the midline more difficult.

The shape and size of the vertebrae differ from the cervical to the lumbar region secondary to function (Figure 2). The vertebral bodies are smaller in the cervical region an become progressively larger in the lumbar area where they support the greatest amount of weight.

Joints of the Vertebral Column

The vertebrae articulate at the intervertebral and facet joints. The intervertebral joints are located between adjacent vertebral bodies. They maintain the strength of attachment between vertebrae. The facet joints form between articular processes. The facet joints are heavily innervated by the medial branch of the dorsal ramus of the spinal nerves. This innervation serves to direct contraction of muscle that moves the vertebral column.

Ligaments

The vertebrae are joined together by a series of ligaments and disks. Anteriorly, the vertebral bodies are separated by the intervertebral disks. The ligament connecting them runs from the base of the skull to the sacrum and is called the anterior longitudinal ligament. The posterior surface of the vertebral bodies is connected by the posterior longitudinal ligament, which also forms the anterior wall of the vertebral canal. The other ligaments of importance (Figure 3):

• Intertransverse ligaments: connects transverse processes
• Supraspinous ligaments: attaches to the apices of the spinous processes, extends from sacrum to skull where it becomes the ligamentum nuchae
• Interspinous ligaments: connects spinous processes
• Ligamentum flavum: thick, elastic ligament, connects the laminae, composed of a right and left ligament that joins in the middle forming an acute angle; narrows toward the articular processes

Spinal Cord/Spinal Canal

The spinal canal is formed by adjacent vertebral foramina. The canal provides support and protection to the spinal cord and its nerve roots. The spinal cord extends from the foramen magnumto the L1-2 vertebral level in adults, and L3 vertebral level in children before becoming the conus medullaris.

Figure 4. Body dermatomes. Figure 5. Preganglionic fibers of the sympathetic nervous system.

From the spinal cord extends a series of dorsal and ventral roots that converge to form mixed spinal nerves. The mixed nerves contains motor, sensory, and in many cases, autonomic fibers. There are eight cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal pairs of spinal nerves. The roots inferior to the conus medullaris become the cauda equina before exiting through the lumbar and sacral foramina. After the spinal nerves leave the spinal canal through the intervertebral foramina, they divide into the anterior and posterior primary rami. The posterior primary rami innervate the skin and muscles of the back. The anterior rami supply the rest of the trunk and the limbs. Each spinal nerve supplies a specific region of skin referred to as a dermatome (Figure 4).

Figure 6. Surface landmarks for various dermatomal levels of epidural blockade.

There is overlap between adjacent segmental nerves. Loss of a single spinal nerve will produce an area of altered sensation, but won’t result in total sensory loss. For instance, destruction of at least three consecutive spinal nerves is required to produce a total sensory loss of the dermatome supplied by the middle nerve of the three.

Preganglionic fibers of the sympathetic nervous system originate from the spinal cord from T1 to L2. They travel with spinal nerves to form the sympathetic chain. This chain extends the entire length of the spinal column on the anterolateral aspects of the vertebral bodies. The chain gives rise to the stellate ganglion, splanchnic nerves, and the celiac plexus (Figure 5).

Simple surface landmarks can be used to indicate the level of dermatomal blockade, which correlates with the segmental spinal nerve (Figure 6). The degree and effect of sympathetic block depends on the height of the block (Table 3).

Meninges/Meningeal Spaces

Surrounding the spinal cord and its roots are three layers of membranes. The innermost layer is called the pia mater, which attaches intimately to the surface of the spinal cord and roots of the spinal nerves. As the roots of the spinal nerves extend distally, the pia mater transforms into the second layer called the arachnoid. The aranchoid detaches from the roots and reflects back across the pia, enclosing the spinal cord within a cavity called the subarachnoid space. The space is filled with cerebrospinal fluid and transmits blood vessels to and from the spinal cord. Superficial to the arachnoid is the thick dura mater. The space between the arachnoid and dura is called the subdural space. Because the arachnoid is pushed against the dura mater by the pressure of the CSF, the subdural space is negligible. It contains a small amount of serous fluid which allows the dura and arachnoid to move over each other.³² Because of its exceedingly small volume, it is referred to as a potential space.

Epidural Space

Figure 7. Epidural space: 1. Anterior epidural space, 2. Posterior epidural space, 3. Ligamentum flavum, 4. Blood vessels in the epidural space, 5. Pedicles, 6. Nerve roots, 7. Transverse process, 8. Vertebral body, 9. Spinal cord. Figure 8. Blood vessels in the epidural space and their communication with systemic vessels.

The epidural space is smaller than the subarachnoid space, extends from the base of the skull to the sacral hiatus, and surrounds the dura mater anteriorly, laterally, and posteriorly. The epidural space is bound posteriorly by the ligamentum flavum and laterally by the pedicles and the intervertebral foramina. It is a space filled with the fat, areolar tissue, lymphatics, veins, and nerve roots that traverse it, but no free fluid (Figure 7). The volume of fat is greater in obese individuals and less in the elderly. It is postulated that the decrease in epidural fat explains the age-related changes in epidural dose requirements.^32,33

The epidural space is rich in blood vessels, including Batson’s venous plexus. Batson’s plexus is continuous with the iliac vessels in the pelvis and the azygos system in the abdominal and thoracic body walls (Figure 8). Because this plexus has no valves, blood from any of the connected systems can flow into the epidural vessels. This is especially important in obstetrics when compressed caval vessels can lead to engorgement of the epidural veins, increasing the risk of catheter entry into a vein. The engorgement is even greater at the intervertebral foramina where the vessels egress from the vertebral canal. Therefore, the incidence of penetrating a blood vessel with an “off-midline” needle insertion is more likely.

Controversies Regarding the Anatomy of the Epidural Space

Figure 9. Segmentation of the epidural space. The yellow areas indicate various segments that may be inconsistently connected.

Through endoscopic examination, computed tomography (CT), magnetic resonance imaging (MRI), and cryomicrotome sectioning of cadavers, the epidural space has been found to be more segmented and less uniform³⁴ than traditionally taught (Figure 9). In a cadaver study, Blomberg³⁵ identified a midline band that he attributed to septations in the epidural space. This was later suggested by Hogan[36] to actually be an artifact of the midline posterior epidural fat pad. Between the epidural segments, the dura is adjacent but not adherent to the periosteum of the vertebra, making this space a potential space that can be dilated by the injection of fluid. It has been postulated that these anatomic variations in the epidural space account for the unilateral block or unpredictable epidural drug spread that is occasionally seen.^32,36

Surface Anatomy, Structures Superficial to the Epidural Space

Surface structures assist the clinician in determining the level of entry into the epidural space. The spinous processes help define the location of the midline as they are usually midline structures. The cervical and lumbar spinous processes are horizontally directed whereas the T4 through T9 thoracic spinous processes have a sharp caudal angulation (Figure 10).

Figure 10. Needle angulation required to accomplish thoracic blockade in the high thoracic/low thoracic/lumbar regions. A: High thoracic region. B: Low thoracic region. C: Lumbar region.

The safest point of entry into the epidural space is below the level of the spinal cord. In adults, this corresponds to the lower border of the L1 vertebrae, and in children, at the lower border of the L3 vertebrae. Epidural insertion in adults is commonly introduced at either the L3-4 interspinous space or one higher, L2-3. A line drawn between the superior aspect of the iliac crests crosses either the spinous process of L4 or the L4-5 interspace. The interspinous space above this point (L3-4 interspinous space) or one higher (L2-3) can safely be chosen for needle entry into the epidural space of adults. Some research has challenged the accuracy of the iliac crest in assessing the level, but this is still a generally accepted surface landmark.³⁷⁻³⁹ By approximately the age of 8 years, the same interspaces can be chosen for children; however, under the age of 7, to avoid accidental cord injury the caudal approach to the epidural space is safer.

Anatomic landmarks used to identify vertebral levels prior to insertion of an epidural needle are summarized in Table 4.

Distance from Skin to Epidural Space

The last clinically salient anatomic feature of importance pertaining to the epidural space is the distance from the skin to the space. The depth varies depending on the body habitus. The distance is 4 cm in 50% of the population, and 4–6 cm in 80% of the population.^24,40,41 It is noteworthy that studies demonstrating skin-to-epidural space in extremes of weight have shown that in the thin patient, the distance can be less than 4 cm, and in the obese, greater than 8 cm.^24,42

Go to top

The primary site of action of local anesthetic solutions injected into the epidural space is the spinal nerve roots. The segmental nerve roots in the thoracic and lumbar regions are mixed nerves, containing somatic sensory, motor, and autonomic nerve fibers. Sensory blockade interrupts the transmission of both somatic and visceral painful stimuli, whereas motor blockade provides muscle relaxation with a varying degree of sympathetic blockade.²⁵ The injection site for epidural anesthesia should be close to the nerve roots of interest in order to obtain the best results with minimal amount of local anesthetic and decreased risk of side effects from systemic absorption of the local anesthetic (catheter/incisioncongruent).^25,43

Differential nerve block, an important concept for epidural anesthesia, refers to the phenomenon in which nerve fibers with different functions demonstrate a varying sensitivity to the effects of local anesthetics. Sympathetic fibers are usually blocked first followed by pain/temperature, then proprioception, followed by motor blockade. After an epidural block, sympathetic blockade (temperature) may vary from zero to four segments higher than the sensory block level (pain/light touch), which is two segments higher than motor blockade. Regression of the block occurs in reverse order.

The physiologic effects of epidural blockade on organ systems depends on the spinal level and the number of spinal segments blocked. In general, high thoracic epidural blocks and extensive epidural blocks are associated with more profound sympathetic block, resulting in a more profound physiologic effect in the cardiovascular system.

Cardiovascular

Block Below

The effect of epidural anesthesia on the cardiovascular system depends on the level and the degree of sympathetic blockade. Vasomotor tone is maintained by sympathetic fibers from T5 to L1 that innervate vascular smooth muscle. Blockade of these fibers cause venodilation with venous pooling as well as arterial vasodilation with decreased systemic vascular resistance. The venous pooling leads to a marked decrease in venous return, right atrial pressure, and subsequently, cardiac output. The decrease in venous return can then lead to an increase in cardiac vagal tone,⁴⁴ especially for blocks near the T5 level. Clinically, the patient can be hypotensive without a change or a decrease in heart rate.

The compensatory mechanism for the decrease in mean arterial pressure is a reflex increase in vasoconstriction above the level of the block as well as a release in catecholamines from the adrenal medulla. If normal cardiac output is maintained either by volume loading or by physiologic mechanisms, (i.e., physiologic release of catecholamines, vasoconstriction in unblocked area), the total peripheral vascular resistance will only decrease by approximately 15%, a value well tolerated by a healthy patient. In an elderly patient with cardiovascular disease, a more ominous decrease in blood pressure with significant hypotension can develop.

Block Above T4

The cardiovascular effects of a block above T4 are the result of a high sympathetic block. The cardiac sympathetic fibers arise from T1 to T4, and when blocked, profound hypotension (the result of a decrease in cardiac contractility) and bradycardia can occur. In addition to the cardiac effects, a high level of sympathetic blockade causes:^24,45

• Increased central venous pressure without an increase in stroke volume
  
• Vasoconstriction in the head, neck, and upper limbs
  
• Splanchnic nerve blockade with blockade of medullary secretion of catecholamines
  
• Blockade of vasoconstrictive effect on the capacitance vessels of the lower limbs

When a sympathetic block occurs at such a high level, the cardiovascular system may be left without its mechanisms for responding to low cardiac output states. This can be detrimental to a patient with limited cardiac reserve because profound hypotension with bradycardia and decreased contractility can result.⁴⁶ The anesthesiologist must be prepared to take over the control of the circulatory system until the block subsides and the patient stabilizes.

Respiratory

Epidural blockade to midthoracic levels have minimal effect on patientswith adequate lung function. Lung volumes (tidal volume, vital capacity), resting minute ventilation, and dead space are basically unchanged even with a higher thoracic epidural. Even with abdominal or intercostal muscle paralysis by a high thoracic block, major alteration in pulmonary function is not seen.

There is concern regarding the use of epidural blockade in patients with severe chronic lung disease dependent on accessory muscle function to maintain adequate ventilation, because paralysis of respiratory muscles and changes in bronchial tone from epidural analgesia can occur. In a study by Gruber and colleagues, thoracic epidurals were placed in patients with end-stage chronic obstructive pulmonary disease undergoing lung volume reduction surgery. Thoracic epidural analgesia with 0.25% bupivacaine did not adversely affect ventilatorymechanics, breathing pattern, gas exchange, and inspiratory muscle force generation in these patients⁴⁷ (Tables 5 and 6).

Rarely, respiratory arrest during high epidural blockade has been reported. Contrary to what may seem a logical explanation, the arrest is not due to the effects of sensory or motor blockade or any effect of the local anesthetic on the brain. The reported causes of rare instances of respiratory arrest is from the sympathetic block, leading to decreased cardiac output with subsequent reduced blood flow to the brain.

Gastrointestinal

The gastrointestinal effects of epidural anesthesia are largely the result of blockage of the sympathetic splanchnic fibers from the T5 through L1 level. Unopposed vagal dominance leads to an increase in secretions; peristalsis; and a small, contracted gut. Postoperatively, gastrointestinal motility returns more quickly when epidural analgesia with a local anesthetic is instituted. Several studies have been conducted demonstrating the positive effect of thoracic epidural anesthesia on visceral perfusion. Christopherson and colleagues used intramucosal pH measurements (pHi) as an indicator of stable visceral perfusion during abdominal surgery. They suggested that thoracic epidural anesthesia prevented the decrease of intramucosal pH during major abdominal surgery as an effect of stable visceral perfusion.⁴⁸ When thoracic epidural anesthesia is used as an adjunct to general anesthesia for major thoracic, cardiac, or abdominal surgery, a segmental block of T1 through T5 is typically the goal. Segmental sympatholysis creating an increase of sympathetic activity in segments below the block leading to impaired splanchnic blood flow has been a concern. In a study in awake and anesthetized dogs, an upper thoracic epidural block had no compromising effect on gastrointestinal perfusion.⁴⁹

Nausea is a common problem following neuraxial anesthesia. It has been reported to occur in up to 20% of patients undergoing neuraxial blocks. It is thought to be related to increased gastric peristalsis secondary to unopposed vagal activity. It can be prevented by promptly treating hypotension with a fluid bolus, ephedrine, or phenylephrine. (If a large dose of ephedrine is ineffective in treating the blood pressure, then 0.1 mcg of epinephrine is indicated). Atropine has been shown to be an effective treatment for nausea associated with a high thoracic block.^50,51

Renal/Genitourinary

Since renal blood flow is maintained through autoregulation, an epidural has very little effect on renal function. Neuraxial blockade at the lumbar level has been postulated to impair control of bladder function secondarily to blockage of the S2 to S4 segments. Urinary retention may occur until the block wears off. The clinician should avoid giving excessive intravenous crystalloids if a urinary catheter is not in place. If a continuous epidural is used, then urinary catheterization may be necessary. More recent studies have questioned the validity of this belief.^32,52

Neuroendocrine

Surgical stress produces a variety of changes in endocrine and metabolic function. Increased protein catabolism and oxygen consumption are common. Increased plasma concentrations of catecholamines, vasopressin, growth hormone, renin, angiotensin, cortisol, glucose, antidiuretic hormone, and thyroid-stimulating hormone have been documented and referred to as the surgical stress response. Intraoperative manifestations of the response is demonstrated as hypertension, tachycardia, hyperglycemia, suppressed immune function, and altered renal function. Afferent sensory information from the surgical site is thought to play a pivotal role in the response.⁵³ The response can be completely abolished by an appropriate level of sensory blockade produced by regional anesthesia. The inhibitory effect is greatest with lower abdominal and lower extremity surgery and slightly less effective in upper abdominal and thoracic surgery, probably because the epidural cannot completely block all nociceptive afferent pathways.⁵⁴

The most critical effect of neuroendocrine activation in the perioperative period is the increase in plasma norepinephrine, which peaks about 18 h after the surgical stimulus is initiated. The increase in plasma norepinephrine is associated with activation of nitric oxide in the endothelium of patients with atherosclerotic disease, producing paradoxic vasospasm.⁵⁵ Thus, in patients with significant atherosclerotic disease, the combination of paradoxic vasospasm and the hypercoagulable state may be the reason underlying the cardioprotective effects of thoracic epidural anesthesia and analgesia in patients with cardiac disease.

Back to top

To be successful with epidural blockade, the clinician must understand the physiology of nerve conduction and the pharmacology of the local anesthetics. Potency and duration of the drugs, their ability to preferentially block sensory and motor fibers, as well as the anticipated duration of surgery or need for postoperative analgesia are factors to be considered before instituting epidural blockade.

The principal site of action of local anesthetics after epidural injection is thought to be the spinal nerve roots, the spinal cord, and possibly the brain.⁵⁶ Nerve fibers with different features and function display varying sensitivity to local anesthetic blockade. For example, sympathetic fibers (thin, myelinated when entering the sympathetic trunk) tend to be blocked with the lowest concentration of drug, followed by pain, touch, and finally motor fibers.

Nerve Impulse Physiology

Nerve conduction involves the propagation of an electrical impulse created by the rapid movement of ions across the nerve cell membrane, creating an action potential. The principal ions involved in generating the action potential are sodium and potassium. The concentration of sodium is high extracellularly and low intracellularly. The opposite is true of potassium (high intracellularly, low extracellularly).

At rest, the cell is more permeable to the positively charged cation potassium. The leakage of a positively charged ion leaves the inside of the cell more negative than the outside of the cell, creating a negative resting membrane potential of –60 to –70 mV. The sodium–potassium pump actively transports sodium ions out of the cell and potassium into the cell to maintain the gradient at the resting level.

Once chemical, mechanical, or electrical excitation occurs, an impulse is conducted along the nerve axon, causing depolarization of the nerve cell membrane. If the depolarization exceeds the threshold level (membrane potential of–60 mV), ion channels in the cell membranes open, allowing a sudden influx of sodium. The rapid influx of positively charged sodium ions causes depolarization of the cell. The influx of positively charged ions alters the membrane potential to become positive (above +30 mV). When the membrane potential exceeds approximately −30 mV, the sodium channels close, abating the influx of sodium into the cell. Depolarization generates a current the causes further depolarization of adjacent segments of the nerve, allowing the action potential to spread along the entire length of the nerve. The cell attempts to return to its resting potential with the efflux of potassium, thereby making the membrane potential less positive (repolarization). Baseline concentration gradients are eventually reestablished by the sodium–potassium–ATP-ase pump.

The rapid influx of sodium that leads to depolarization of the nerve occurs through specific channels in the cell membrane. The sodium channel is a path that changes the nerve from nonconductive to conductive of an action potential (referred to as gated channels). If the change in conductance is created by electrical changes, the channel is called a voltage-gated channel. The voltage-gated sodium channel in the nerve is considered to be the site of action for local anesthetics.⁵⁷

Action of Local Anesthetics

Local anesthetic binds to sodium channels, primarily in the inactivated state, preventing further channel activation. Sodium ion movement into the cell is prevented, effectively blocking the development of the action potential. The resulting resting membrane potential is unaffected by further nerve stimulation, referred to as membrane stabilization of local anesthetics.

Mechanism of Action of Local Anesthetics in Neural Blockade

Within the dorsal horn, local anesthetics can block both sodium and potassium ion channels in the dorsal horn neurons, inhibiting the generation and propagation of pain signals (nociceptive electrical activity). Motor blockade occurs from a similar action on the ventral horn neurons. Blockade of calcium ion channels in the spinal cord leads to resistance of electrical stimulation from nociceptive afferent nerves, creating an intense analgesic action seen in centrally administered local anesthetics.⁵⁸

In addition to ion channel alterations in the central neuraxis, epidurally administered local anesthetics indirectly inhibit the release of substance P and other neurotransmitters involved in pain signal processing. Substance P is involved in pain transmission from the presynaptic terminals of dorsal root ganglionic cells. The putative effects of centrally administered local anesthetics on substance P and these other transmitters is linked to the presynaptic blockade of the voltage-gated calcium channel.^59,60 When calcium entry is blocked at the presynaptic level, release of these neurotransmitters (glutamate, substance P, calcitonin gene-related peptide [CGRP], neurokini-1 and -2 [NK1, NK2]) at the presynaptic level does not occur. Therefore, epidurally administered local anesthetics can indirectly inhibit pain signal transmission.

Choice of Local Anesthetics

Drugs used for epidural blockade can be categorized into short-, intermediate-, and long-acting local anesthetics. Onset of epidural blockade in the dermatomes immediately surrounding the site of injection can usually be detected within 5 or 10 min of injection of any of the local anesthetics. The time to peak effect varies with the type of local anesthetic chosen. Table 7 summarizes the characteristics of the most commonly used local anesthetics for epidural anesthesia.The shortest acting local anesthetic for neuraxial blockade is chloroprocaine (an ester). In the past, it was associated with adhesive arachnoiditis when large volumes were administered into the subarachnoid space.⁶¹ When volumes greater than 25 mL were used in the epidural space, severe back pain most likely secondary to localized hypocalcemia introduced by the preservatives, ethylenediaminetetraacetic acid (EDTA) and bisulfites, in the solution. As of 1996, preservative-free chloroprocaine has been available and has not been associated with either neurotoxic effects or back pain. In ambulatory settings, utilizing the favorable characteristics of chloroprocaine with epidural catheter insertion provides excellent surgical anesthesia without delaying recovery room discharge.

The most commonly used intermediate-acting local anesthetic for surgical anesthesia via the epidural route is 2% lidocaine. When epinephrine is added to the solution (1:200,000), it prolongs the duration of action by 40 to 60%. However, the incidence of hypotension is increased in patients receiving lumbar epidural analgesia due to the beta effect of epinephrine-containing solutions that leads to peripheral vasodilation.

Long-acting local anesthetics used for epidural blockade are 0.5% bupivacaine, 0.5% levobupivacaine, and 0.5% ropivacaine. Of these, the most commonly used agent for epidural blockade is bupivacaine. Dilute concentrations can be used for analgesia, with more concentrated solutions employed for surgical anesthesia. Epinephrine added to the solution can prolong its duration of action, but this is less consistent with the shorter acting agents. Accidental intravascular injection of bupivacaine has produced severe cardiotoxic reactions (hypotension, atrioventricular block, ventricular fibrillation) refractory to usual resuscitation methods. The rationale for the resistance to resuscitative measures lies in its high degree of protein binding and more pronounced effect on cardiac sodium channel blockade.^62,63 Levobupivacaine, the S-enantiomer of bupivacaine, has nearly an identical profile to bupivacaine but without the systemic cardiac toxic effects of bupivacaine. Ropivacaine, amepivacaine analog, also has a similar profile of action to bupivacaine. In most studies, ropivacaine has demonstrated a slightly shorter duration of action than bupivacaine, with a less dense motor block when comparing equivalent doses. The major deterrent to ropivacaine in clinical practice is cost.^64,65

Etidocaine, another long-acting amide local anesthetic, is infrequently used for epidural anesthesia. It produces a profound motor block that unfortunately can outlast the sensory block,⁶⁶ making it an undesirable choice for epidural anesthesia (see Table 7).

Onset/Duration of Local Anesthetics

Several investigators have attempted to find methods to speed up the onset or increase the duration of epidural blockade. Adding epinephrine to the local anesthetic can substantially increase the duration of action of some local anesthetics by decreasing the vascular absorption. The effect is greatest with 2-chloroprocaine, lidocaine, and mepivacaine, and less effective with the longer acting agents. Other vasoconstrictors, such as phenylephrine, have not been as effective in reducing the peak blood levels of local anesthetics as epinephrine.⁶⁷

Alkalinization of the local anesthetic solution has been used to increase the speed of onset of local anesthetics. By increasing the concentration of the nonionic form of the drug, more drug is available to penetrate the lipid nerve cell membranes to produce more rapid intraneural diffusion. Adding sodium bicarbonate (1 mEq/10 mL of local anesthetic) immediately before injection of lidocaine, mepivacaine, or chloroprocaine produces a clinically significant faster onset of anesthesia and may provide a more complete block.^68,69 Ropivacaine and bupivacaine will precipitate with the addition of bicarbonate unless a low concentration (0.1 mEq/10mLof local anesthetics) is used. Combining long-and short-acting drugs to obtain a rapid onset aswell as prolonged sensory block has not proven to be an effective means of providing anesthesia. For example, mixing 2-chloroprocaine with bupivacaine for the rapid onset of the former and long duration of the latter resulted in shortening the duration and effectiveness of the bupivacaine.⁷⁰ Utilizing the additives currently available and using continuous techniques of drug administration rather than single-shot techniques obviates the need for mixing local anesthetics.

Novel Additives to Local Anesthetics in the Epidural Space

A variety of other classes of drugs have been studied more recently to try to improve the quality of neuraxial blockade, both in the epidural space and in the subarachnoid space. In addition to a variety of opioids (e.g., fentanyl, sufentanil, and preparations of morphine), α-adrenergic agonists, cholinesterase inhibitors, semisynthetic opioid agonist–antagonists, ketamine, and midazolam have been studied with varied results.

Clonidine, the prototypical α2-adrenoceptor agonist used in neuraxial blocks, has been studied extensively in combination with local anesthetics, as a primary agent, and in combination with a variety of other drugs. Clonidine is an α-adrenoreceptor agonist with selectivity for α2-adrenoreceptors. The mechanism by which clonidine prolongs neuraxial anesthesia is unclear. Animal studies have shown that clonidine reduces regional spinal cord blood flow, therefore, slowing the rate of drug elimination.⁷¹ Kroin and colleagues demonstrated that the mechanism by which clonidine prolongs the duration of a block when mixed with local anesthetics is not mediated by an α-adrenergic mechanism but is more likely related to the hyperpolarization-activated cation current (Ih).⁷²

Some of the benefits of the administration of clonidine in the epidural space include

1. Prolongs and intensifies the effects of epidural local anesthetics without increasing the degree of hypotension for epidural anesthesia and analgesia
   
2. Reduces the dose requirements of local anesthetics for labor epidural analgesia^73,74
   
3. Produces analgesia without motor impairment and prolongs the duration of the local anesthetic analgesic effect⁷¹
   
4. Has a synergist effect when combined with opioids and opioid agonist–antagonists, allowing reduced doses and therefore side effects of both
   
5. Modulates the immune stress response to thoracic surgery⁷⁵
   
6. Is superior in preserving preoperative lung function for thoracotomy patients⁷⁶
   
7. May reduce cytokine response, therefore further reducing pain sensitivity⁷⁷
   
8. Has possible antibacterial activity against Staphylococcus aureus/epidermidis

 

Side effects that are commonly associated with epidural clonidine include a dose-independent hypotension, bradycardia, sedation, and dry mouth. Combination of clonidine with other agents such as opioids, anticholinergics, opioid agonist–antagonists, and ketamine have been studied to enhance the beneficial effects of these drugs while limiting the adverse side effects.^78,79

Neostigmine, a cholinesterase inhibitor, is a more recent addition to the list of epidural additives for selective analgesia. The mechanism of action for the analgesic effect of neostigmine appears to be the inhibition of the breakdown of acetylcholine and the indirect stimulation of muscarinic and nicotinic receptors into the spinal cord, inducing analgesia. By administering it via the epidural route, the gastrointestinal side effects (nausea/vomiting) noted with subaranchoid administration are eliminated. It has been reported to provide postoperative pain relief without inducing respiratory depression, motor impairment, or hypotension.⁷⁸ When combined with other opioids, clonidine, and local anesthetics, it may provide benefits similar to clonidine without the side effect profile of any of the drugs given alone.⁸⁰⁻⁸²

Other agents such as ketamine, tramadol, droperidol, and midazolam have been studied with various effectiveness in epidural analgesia. Considerable controversy surrounds the use of midazolam intrathecally. Despite multiple publications recommending its use intrathecally,⁸³⁻⁸⁵ recent studies have demonstrated that even a single dose of intrathecal midazolam may have neurotoxic effects on the neurons and myelinated axons.⁸⁶ Until its safety profile can be ensured in human subjects, it is not recommended for use intrathecally or epidurally at this time.⁸⁷

One agent showing promise is a new formulation of one of the oldest opioids, morphine. Epidural morphine has proven analgesic efficacy without the bothersome side effects of intravenous dosing. Pain relief with single epidural injection lasts less than 24 h, requiring the institution of alternate methods to provide pain relief. Depodur, the brand name for extended-release epidural morphine, uses a drug-release delivery system called Depofoam. Depofoam is composed of microscopic lipid-based particles with internal vesicles that contain the active drug and slowly release it. Recent studies of Depofoam have demonstrated effective pain relief with minimal side effects for up to 48 h.⁸⁸⁻⁹⁰

Other Factors Affecting Epidural Blockade

Injection Site

The epidural blockade is most effective when the block or the catheter is inserted in a location that corresponds to the dermatomes covered by the surgical incision. The most rapid onset and the densest block occurs at the site of injection. By inserting the catheter closer to the surgical site, a lower dose of drug can be given, thereby reducing drug-related side effects.^91,92 This concept is especially important when thoracic epidurals are used for postoperative analgesia.

After lumbar injection, analgesia–anesthesia spreads caudally and, to a greater degree, cranially. There is a delay at the L5 to S1 segments secondarily to the larger size of these nerve roots.⁹³ With thoracic injection, the local anesthetic spreads evenly from the site of injection, but because of the larger nerve roots, there is greater resistance to blockade. By controlling the dose in the thoracic region, a true segmental block can be placed, affecting only the thoracic region. Lumbar and sacral regions will be spared, therefore, avoiding more extensive sympathetic blockade and subsequent associated hypotension and bladder dysfunction.

Dose, Volume, and Concentration

The dose of local anesthetics necessary for analgesia or anesthesia is a function of the concentration of the solution and the volume injected. Concentration of the drug affects the density of the block. The higher the concentration, the more profound the motor and sensory block. Lower concentrations can produce a more selective sensory block.⁹⁴

Volume is the variable that affects the degree of distribution of the block. A larger volume will block a greater number of segments. A generally accepted guideline for dosing an epidural in adults is 1–2 mL per segment to be blocked. This guideline should be adjusted for shorter patients or for the very tall. For example, to achieve a T10 sensory level from an L3-4 injection, approximately 9–18 mL of local anesthetic should be administered. Below concentrations of the equivalent of 1% lidocaine, motor block is minimal, regardless of the volume of the local anesthetic injected, unless doses are given at repeating intervals.⁵⁷

Repeat doses of local anesthetics depend on the duration of the drug. Doses are administered before the block regresses to the point where the patient experiences pain, commonly referred to as “time to two-segment regression.” This is defined as the time it takes for the sensory block to regress by two dermatome levels.When two-segment regression has occurred, one-third to one-half of the initial loading dose can safely be administered to maintain the block. For example, the time to two-segment regression of lidocaine is 60–140 min²⁵ (Table 8).

Patient Position

The patient may be placed in either the lateral or sitting position depending on the patient’s body habitus and medical conditions. The midline of the spine is easier to palpate when the patient is sitting, especially in the obese patient, therefore making the block technically easier.Whether the patient is sitting or in the lateral position, there is no significant difference in block height.⁹⁵ It has been suggested in a study by Seow and associates, that there is slightly faster onset time, duration, and density of motor block on the dependent side when the epidural in placed with the patient in the lateral position.⁹⁶

Characteristics of the Patient: Age, Weight, Height, Pregnancy

With advancing age, the dose required to achieve the same level of block is reduced. The difference in block height with a fixed volume and concentration of local anesthetic in patients older than age 50 was between one to three segments higher (not considered clinically significant).^97,98 Greater spread in the elderly is theorized to be related to reduced size of the intervertebral foramina, therefore limiting the local anesthetic from leaving the epidural space; decreased epidural fat, allowing more of the drug to bathe the nervous tissue; and changes in the compliance of the epidural space, leading to enhanced cephalad spread has also been suggested⁹⁹ (Table 9).

There is little correlation between the spread of analgesia and the weight of the patient. However, in morbidly obese patients, there may be compression of the epidural space secondarily to increased intraabdominal pressure, creating a higher block for a given dose of local anesthetic. Just as in the pregnant patient, venous engorgement in the epidural veins increases the risk of entry into a vessel.^94,100

The correlation with height is usually not clinically significant. For short patients (less than or equal to 5 ft 2 in.), the common practice has been to reduce the dose to 1 mL per segment to be blocked instead of 2 mL per segment. Bromage suggested a more precise dosing regime of increasing the dose of local anesthetic by 0.1 mL per segment for each 2 in. over 5 ft of height.¹⁰¹ The safest practice is to use incremental dosing and monitor the effect to avoid excessively high anesthetic levels.

Pregnancy causes an increased sensitivity to both regional and general anesthetics, although the studies regarding the causes have been conflicting. The most recent studies attribute the sensitivity of pregnant women to regional and general anesthetics to levels of progesterone or increased concentrations of endorphins, causing an increase in the pain threshold.^102,103

Intermittent vs Continuous Epidural Block

Whether the clinician chooses to use intermittent dosing after the initial activation dose or a continuous infusion, safe and effective epidural anesthesia can be provided. Advantages of continuous infusion include greater cardiovascular stability, less labor intensive, decreased incidence of tachyphylaxis, decreased frequency and severity of side effects related to bolus injections, less rostral spread, less potential risk of contamination, and the ability to achieve a steady-state of anesthesia. The advantages of intermittent bolus dosing is that it is simple and doesn’t require additional equipment (infusion devices).

Back to top

Patient Evaluation

As with any neuraxial blockade, the risks and benefits of epidural placement need to be discussed with the patient. These should be explained in a thorough but appropriate manner in order to provide informed consent. The inability of the patient to speak English should not be a barrier to providing epidural placement as long as there is a mechanism in place for obtaining informed consent either through translation services in the hospital or through telephone systems.

Patients (particularly older patients) occasionally have misconceptions about epidural placement, such as:

• Permanent paralysis from the block
  
• Being awake during the operation
  
• Big needles puncturing the back while awake
  
• Epidural injection leads to back pain

 

These issues as well as any other concerns of the patient should be discussed prior to premedication. The level of awareness during the epidural placement and during the operation can usually be tailored to the patient’s desires. The patient as well as the surgical staff need to understand that the patient will have absent or reduced motor function after the block is placed until the block resolves.

The patient’s medical history and medications should be evaluated to determine the presence of any condition that may increase the risks involved with epidural placement (i.e., clotting abnormalities, platelet count, recent administration of anticoagulants).²³ Drug therapy that may influence the patient’s physiologic response to epidural blockade should be noted to prepare the clinician for altered or exaggerated responses to dosing or test dosing (e.g., beta-blockers, alpha-blockers). Medical conditions that may become more severe with reducing afterload or preload should be evaluated (e.g., severe aortic stenosis, mitral stenosis, hypertrophic cardiomyopathy, congenital conditions requiring stable systemic vascular resistance such as ventricular septal defects). Other medical conditions that may become more severe with motor blockade (e.g., myasthenia gravis, pulmonary fibrosis, severe chronic obstructive disease) require careful review of the patient’s history, prior medical evaluations and testing, as well as a thorough physical examination. History of sensitivity to local anesthetics, adverse drug reactions, or prior history of complications related to epidural placement should be reviewed. Rather than eliminate these patients from receiving epidural anesthesia, a well-planned procedure with controlled initiation of the block can provide excellent anesthesia.

Physical examination should include an evaluation of the spine for evidence of scoliosis, focal infection or pain, scars, severely limited range of motion, or other findings that may make epidural placement more challenging or impossible. Obesity, especially central obesity, may obscure physical landmarks, making placement more difficult.

Baseline laboratory assessment of the patient’s coagulation status and platelet count should be obtained when the patient has a history of coagulopathy or has recently received anticoagulants or any medications known to influence platelet quality or function. This includes an internationalized ration (INR) (or prothrombin time), activated partial thromboplastin time (aPTT), platelet count, and bleeding time (only if there is a specific concern). Many clinicians choose to obtain a hematocrit at the same time, especially when appreciable blood loss is expected.

The final consideration before placing the epidural is to determine the goal of the block. Epidural placement can be used for surgical anesthesia, as an adjunct to general anesthesia, or for postoperative analgesia. The advantage of epidural placement is the ability to provide segmental blockade, meaning that the block can cover as many or as few dermatomal levels as is clinically desired to meet the needs of the patient. Once the decision has been made as to the purpose and levels to be blocked, patient preparation can be initiated (Table 10).

Patient Preparation

The key to providing safe epidural anesthesia is preparation. Intravenous access with a catheter large enough to administer fluids or emergency drugs should be in place (i.e., 18- to 20-gauge). Reversible conditions such as severe hypovolemia should be managed prior to block placement. However, preloading nondehydrated patients with a balanced salt solution has been questioned and may prove to be harmful in patients with decreased serum colloid oncotic pressure (e.g., those with burns, preeclamptic patients, patients on tocolytic therapy).^104,105 The type of monitoring and resuscitative equipment available depends on the purpose of the epidural block. Epidural blocks for analgesia, such as for labor or postoperative analgesia, require blood pressure and pulse oximetry at a minimum. Drugs and equipment for life support, including airway management,must be readily available if the block is to be performed for surgical anesthesia or as an adjunct to general anesthesia (ASA Standard Monitors).

Controversies about placing the epidural block while the patient is awake or asleep continue to be addressed in the literature. The advantages to having the patient sedated or asleep are avoiding movement that could lead to injury to the spinal cord or neural tissue and alleviating the stress response associated with fear of pain or needles. The disadvantages are similar in that the patient is unable to verbalize when neural structures are encountered. For years, neuraxial blocks have been placed in children with heavy sedation or under general anesthesia without a preponderance of case reports on neural structure damage. Horlocker and colleagues at the Mayo Clinic recently published a report of over 4000 patients undergoing lumbar epidural placement under general anesthesia without any neurologic complications.¹⁰⁶ Sedating the patient with a benzodiazepam (i.e., midazolam) and a narcotic (i.e., alfentanil/fentanyl) allows the clinician to safely place the epidural catheter without undue stress to the patient. The choice of drugs for sedation depends on the patient’s overall medical condition and age. An exception to the use of sedation is in the pregnant patient (potential of harming the fetus).

Communication with Surgical Staff

A discussion with the surgical staff to understand the operative approach, the desired positioning of the patient, and an estimated length of the surgical procedure is important for the anesthesiologist to determine the best choice of anesthetic. The anesthesiologist can decide if a simple epidural or a combined spinal-epidural with an initial more intense motor block is indicated. Postoperative analgesia can be determined at the same time. Communicating with the nursing staff leads to better cooperation and assistance with the epidural block. If feasible, turnover time can be reduced by bringing the patient into the operating room and placing the epidural block while the nursing staff is still setting up. Cooperation with the surgical staff improves when delays are not attributed to “anesthetic procedures.”

Equipment

Commercially prepared, sterile disposable epidural trays are available and used by most institutions (Figure 11). All of the drugs included in the tray are preservative-free. A standard kit includes the following:

• Figure 11. Prepared epidural tray. 1. Solution of antiseptic 2. Syringe/needle for skin localization 3. Epidural needle 4. Glass syringe, 5. Epidural catheter, 6. Luer Lok attachment, 7. Glass filter, 8. Dosing syringe, 9. Local anesthetic, 10. Saline.

  Drapes:
  • Paper towel
  • fenestrated plastic drape
  • one paper drape
• Small tray with prep sponges, 4 × 4 gauze sponges, packet of povidone-iodine solution
  
• Drugs:
  • 10-mL ampule of 0.9% sodium chloride
  • 5-mL ampule of 1.5% lidocaine with epinephrine 1:200,000
  • 5-ml ampule of 1% lidocaine
  • 1-mL ampule of epinephrine 1:1000
    
• One filter straw
  
• Needles/Syringes:
  • 25-gauge 1.5-in. needle
  • 18-gauge 1.5-in. needle
  • 18-gauge 3.5-in. Tuohy epidural needle with stylet
  • 3 mL/20 mL plastic syringes
  • 5-mL glass Luer Lok syringe
• 20-gauge calibrated epidural catheter

 

Figure 12. Common designs of epidural needles. A: Hustead 17-gauge, B: Hustead 18-gauge, C: Crawford, D: Tuohy.

A styletted Tuohy epidural needle is typically 16 to 18 gauge, 8 cm in length,with surface markings at 1-cm intervals. It has a 15- to 30-degree curve at the tip with a blunt bevel. The curved Huber tip is designed to prevent accidental dural puncture and to facilitate passage of the epidural catheter (Figure 12). At the junction of the needle shaft and hub are wings to allow better control as the needle is passed through tissue. Longer needles up to 10 cm in length are available for obese patients. A variety of needles are used for single-shot epidurals, but this practice is less common in modern anesthesia because of the inability to redose if the initial block wears off.

Epidural catheters made of a durable, flexible plastic are designed to pass through the lumen of the Tuohy needle. They have either a single end hole or a number of side holes at the distal end. The 20-gauge catheters are calibrated for ease of determining the depth on insertion. The calibration markings, openings, and the flexibility of the catheter depend on the manufacturer. A more flexible catheter is designed to prevent forcing the catheter into a space other than the epidural space, but it can be more difficult to handle. The stiffer catheter is easier to pass, but can be forced into spaces other than the epidural space. Some catheters include a reinforced, spring-loaded tip to prevent kinking. It is prudent for the clinician to become familiar with all of the trays and catheters used by the institution in the event that one particular tray is not available.

The only additional equipment needed for placement is a dressing for the puncture site and tape to secure the catheter on the patient’s back. Usually a large OpSite dressing with silk or cloth adhesive tape is sufficient to prevent catheter dislodgement and to keep the site clean. The tray should be prepared while an assistant is positioning the patient or prior to positioning out of sight of the patient to prevent increased anxiety especially for needle-phobic patients. The prep solution should not contaminate the epidural needles to prevent the rare possibility of chemical arachnoiditis.^107,108

Patient Positioning

Careful attention to the patient’s position is essential to successful placement of the epidural needle and catheter. Depending on the patient’s medical status, weight, and ability to cooperate, the sitting or lateral decubitus position can be used. In general, it is technically easier to identify the midline in an obese patient in the sitting position, but this requires the assistance of a trained assistant to maintain the correct posture. Improper positioning can turn an otherwise easy epidural placement into a needlessly challenging one.

Monitoring equipment and oxygen can be attached to the patient before or after the patient is positioned. The operating table should be at a comfortable height for the clinician, blankets or covers should be available for the patient’s comfort and privacy, a stool for the patient’s feet to rest on (if sitting), and an assistant to support the patient in the correct posture should be ready prior to beginning the block. Intravenous sedation should be given to alleviate anxiety early in the preparation for the block. It is our practice to provide the patient with 2 mg of midazolam and 100 mcg of fentanyl IV for sedation purposes just prior to catheter insertion (Exception: pregnant mothers for labor and delivery or caesarian section). Since the great majority of patients will develop hypoxemia, we always administer oxygen via a face mask at 8 L/min in all of our patients. Likewise, we implement pulse oximetry and capnography during the insertion of the catheter.

Sitting Position

Figure 13. Patient in sitting position in preparation for epidural placement.Note the outward back-curving leg flexion and feet resting on the stool. Figure 14. Patient positioning in lateral decubitus position and common problems accompanying this positioning.

If the sitting position is chosen, the patient should be assisted to sit on the edge of the table or bed with feet resting on a stool (or touching the floor if very tall). The patient should lean forward with elbows resting on a pillow or on the thighs. The back should be maximally flexed to open up the lumbar vertebral spaces. Flexing the neck will help the patient to flex the lower spine (Figure 13). The assistant should help the patient to hold this position during the entire procedure.

Lateral Decubitus Position

In the lateral decubitus position, the patient is placed on her side with the back at the edge of the operating table that is closest to the anesthesiologist. The spinous processes should be oriented parallel to the floor to prevent rotation of the spine. The thighs should be flexed on the abdomen with the knees drawn to the chest and the neck flexed so that the chin rests on the chest. Asking the patient to “assume the fetal position” or “touch your kneeswith your chin”may help with positioning during lumbar epidural placement. In contrast, it is not useful for thoracic epidural placement because the facet joints in the thoracic spine have very limited flexion and extension function. An assistant should be available to help with both positioning and maintenance of the proper position. Benefits of the lateral decubitus position are that sedation can be more liberally used, and that dependence on a well-trained assistant is not as important as for the sitting position.³² Successful block placement depends on keeping the spine parallel to the floor (Figure 14). Obese patients or those with larger hips may require additional pillows to maintain proper alignment of the spine.

Technique

The level of insertion and dosing of the epidural needle or catheter depends on the purpose of the epidural block. In pediatric cases, a single-shot caudal block is sometimes used, but in most adult cases, a catheter is placed so that either bolus dosing or a continuous infusion can be instituted. Preparation of the epidural tray and medications to be administered should be completed prior to positioning the patient. For epidural anesthesia, the same monitors required for general anesthesia should be applied. Oxygen by nasal cannula or mask should be in place prior to sedation. For epidural analgesia, blood pressure and pulse oximetry monitoring are the minimum requirements. There is a wide variation in practice with regard to the extent of aseptic precautions prior to epidural placement.Most clinicians agree that at a minimum, head covering, mask, and sterile gloves should be in place.^109−111

Approach

Four common approaches to the epidural space are possible: midline, paramedian, Taylor (modified paramedian), and caudal. Each will be described in the following paragraphs. Clinical expertise in each of these techniques gives the anesthesiologist more flexibility when using an epidural block.

MIDLINE APPROACH

This approach is most commonly used for lumbar or low thoracic epidural placement in the sitting position. After appropriate monitors are attached and the patient is positioned, the lumbar spine is prepped and draped in a sterile fashion (Figure 15A)

1. A fully prepared epidural tray should be placed to anesthesiologist’s right for right-handed, left for left-handed clinician
   
2. Identify the vertebral level to be entered by surface landmarks (e.g., crest of iliac spines L4 to L5, entry level usually L2-3 or L3-4).
   
3. Infiltrate skin with local anesthetic using 25-gauge 1 1/2 -in. needle at midpoint between two adjacent vertebrae to raise a large skin wheel (Figure 15B).
   
4. Without removing needle, infiltrate deeper tissues to alleviate pain and to assist with locating midline.
   
5. Insert epidural needle with stylet through same skin puncture. The dorsum of the anesthesiologist’s noninjecting hand rests on the patient’s back with the thumb and index finger holding the hub of the epidural needle (Bromage grip).¹¹²
   
6. Advance the needle through the supraspinous ligament and into the interspinous ligament (approximately 3 cm depth) at which point the needle should sit firmly in the midline (see Figure 15C).
   
7. After the ligaments are penetrated, it is no longer possible to change the direction of the needle tip.¹¹³
   
8. Remove the stylet and attach the glass syringe to the hub of the needle. Lock it on firmly so that a false loss of resistance is not encountered (Figure 15D).

Figure 15A. Lumbar epidural block through the midline approach: Positioning and draping for midline approach.			Figure 15B. Lumbar epidural block through the midline approach: Administration of local anesthesia to reduce pain during consequent epidural needle entry through the skin and subcutaneous tissues.
Figure 15C. Lumbar epidural block through the midline approach: Tuohy needle lodged in the interspinous ligament.			Figure 15D. Lumbar epidural block through the midline approach: Tuohy needle with glass syringe attached for testing the loss of resistance to air.

As a review, there are three alternative techniques to identify the epidural space: loss of resistance (LOR), hanging drop, and ultrasonography. Dogliotti described the first, using LOR to fluid.¹² This technique is based on the different densities of tissues as one passes a needle through the thickness of the ligamentum flavum into the epidural space. The technique has been modified so that both fluid and air are recognized as acceptable media for determining the LOR, with saline solution and air being the two most frequently used. We will limit the discussion to the advantages and disadvantages between saline and air for the loss of resistance. Controversy has been growing controversy regarding the use of air as the only medium to find the epidural space. First, air is compressible, thus the feeling in the plunger of the syringe might result in a false loss of resistance. Advocates of using air feel that it is easier to verify if the needle went too far and pierced the dura, in which case the practitioner could easily see cerebrospinal fluid (CSF) coming out. The use of air by itself, has come under scrutiny lately, and several studies have found some adverse outcomes with its use.

Air has been found to be less reliable than a combination of air and lidocaine to find the epidural space.¹¹⁴ However, some argue that the use of air alone may cause pneumocephalus, which results in severe headaches, and it can cause venous air embolism.^115,116 It has also been associated with an increased incidence of unblocked segments, and even persistent neurologic deficits when air bubbles were expanded by the use of nitrous oxide, causing either nerve root or, even worse, spinal cord compression.^117−119 It has also been suggested that the incidence of intravascular placement of epidural catheters is greater when air is used for LOR, but others reported no differences.¹¹⁴

Few negative reports can be found in the literature related to the use of a fluid for LOR, one of those being the difficulty to verify if fluid obtained after placement of a catheter is either saline or CSF. To differentiate this, some practitioners check the contents of glucose and proteinwith a urine reagent strip, and if positive the diagnosis of CSF can be made.¹²⁰ Moreover, if a large volume of saline is used for LOR, this could produce an inadequate sensory block, probably due to dilution of the injected local anesthetic and a delay in the onset of the block supposedly due to the same reason.

We all learn different techniques from our preceptors during training. Under optimal conditions, trainees should be exposed to all the different techniques and then be able to choose the one they feel most comfortable with and which has less chance of negative side effects based on their experience and suggestions from the literature. Although the literature is supportive of the use of a fluid or a combination of a fluid and a small amount of air, there are limitations in the majority of studies that have evaluated this issue, namely sample size, and with it, the possibility of type I and type II errors. Thus, the best advice is to limit the volume of injected fluid and air in the epidural space to less than 2–3 mL to avoid the aforementioned problems.

Lastly, evidence in the literature is lacking concerning the best method to use in children undergoing epidural procedures. Recently, the use of ultrasound for the placement of epidural catheters in children has been advocated. However, the technique is somewhat cumbersome and requires significant expertise with ultrasound imaging as well as additional personnel to hold the probe and operate the ultrasound equipment. Nevertheless, with refinements in ultrasound technology, developments of better imaging probes may aid in the correct placement of epidural catheters in this population.

Loss of Resistance to Air. Continue to hold the needle at the hub with the noninjecting hand.

1. Using the thumb of the injecting hand, lightly tap the end of the plunger of the needle while advancing the needle in a slightly cephalad direction.
   
2. Advance the needle slowly with controlled motion until the needle passes through the ligamentum flavum. As the needle enters the ligamentum flavum, there is usually a distinct sensation of increased resistance followed by a sudden loss of resistance to pressure exerted on the plunger. Avoid injecting greater than 1 mL of air.
   
3. Once the loss of resistance occurs, do not advance needle further without testing placement as there is an increased risk of dural puncture. Experienced clinicians may elect to exert continuous pressure on the epidural needle plunger while advancing the needle until loss of resistance is noted.

 

For the novice, the incidence of dural puncture is higher with this technique because of a lack of familiarity with structures encountered.

 

Loss of Resistance to Saline With or Without Air Bubble.

1. Figure 15E. Lumbar epidural block through the midline approach: After the loss of resistance to air is documented, indicating the proper position of the needle in the epidural space, the catheter is threaded while observing depth marks.

   Instead of filling the glass syringe with 2 to 3 mL of air, the syringe is filled with saline, or with saline and a small air bubble (0.2–0.3 mL)
   
2. The needle is advanced in the same fashion as with air. Continuous pressure is exerted on the plunger of the needle. When using the combination of air and saline, if the air bubble cannot be compressed without injecting the saline, then the needle tip is probably not engaged in the ligamentum flavum (Table 11).
   
3. Once a loss of resistance to air or saline has occurred, the glass syringe is removed, and depth at which the epidural space was entered is noted. The noninjecting hand should continue to hold the needle in place. If the patient moves unexpectedly, the anesthesiologist can prevent injury to neural structures by quickly removing the needle or by moving with the patient while holding the needle in place.
   
4. For single-injection epidurals, and appropriate volume of local anesthetic can be injected through the needle.
   
5. For continuous epidurals, a small volume of sterile saline is injected into the epidural space to dilate the space.
   
6. Note the depth of the needle at the skin. The marking on the needle at the skin is the depth from the skin to the epidural space.
   
7. Thread the catheter gently through the needle into the epidural space to approximately the 15- 17-cm mark, then remove the needle without dislodging the catheter (Figure 15E).
   
8. Add the skin-to-epidural depth plus 3–5 cm. Withdraw the catheter to that point and secure. No more than 5 cm of catheter should be left in the epidural space to prevent displacement of the catheter laterally or into extradural structures.
   Example: Needle entered epidural space at 5 cm, the catheter should be withdrawn to 10-cm mark at the skin. This would allow 5 cm of the catheter in the epidural space.
   
9. Gently flush the catheter with a small amount of saline to ensure patency.
   
10. A clear, occlusive dressing should be applied over the insertion site to allow inspection of the catheter. The catheter should be secured to the patient’s back with the end at the shoulder for access in dosing.

PARAMEDIAN APPROACH

It is essential for the anesthesiologist to become proficient with the paramedian approach to epidural placement as there are many situations when it is the only technique feasible for epidural placement. This approach offers a much larger opening into the epidural space than the midline approach.

Indications for this approach are:

• Patients who cannot be positioned easily or cannot flex the spine (trauma/arthritic) when inserting the needle into the lumbar epidural space
  
• Calcified interspinous ligament
  
• Spine deformities: kyphoscoliosis, prior lumbar surgery
  
• Entry level at T3 to T7: In the midthoracic spine, the angulation of the spinous processes is more oblique, the space between spinous processes is narrower, and the ligaments are less dense. False loss of resistance is much more common. Thus, the midline approach is difficult if not impossible to use.

 

1. The skin wheal is placed 1.5–2.0 cm lateral to the midline opposite the center of the selected interspace in the lumbar and lower thoracic levels (Figure 16A).
   
2. The epidural needle is advanced at that site perpendicular to the skin until the lamina is encountered (Figure 16B).
   
3. The needle is redirected and advanced at a 10- to 25-degree angle toward the midline (Figure 16C).
   
4. If bone is encountered, the needle is “walked off” the bone into the ligamentum flavum.
   
5. The supraspinous and interspinous ligaments are midline structures. The paramedian approach is lateral to these ligaments. The epidural needle penetrates paraspinous muscles with little resistance before entering the ligamentum flavum.
   
6. The “feel” of the paramedian approach is completely different from that of the midline approach because of the difference in tissues penetrated.

Figure 16A. Lumbar epidural block through the paramedian approach: The needle entry site is marked approximately 1.5–2 cm lateral and caudal to the desired level of blockade.

Figure 16B. Lumbar epidural block through the paramedian approach: Epidural needle angulation 45 degrees cephalad and very slightly medial.

Figure 16C. Lumbar epidural block through the paramedian approach:When (if) the bone (lamina) is contacted during needle advancement, the cephalad needle angle is lowered to walk off the lamina.

Midthoracic Epidural Paramedian Approach. The T4-5 interspace is the injection site.

1. Figure 17A. Thoracic paramedian approach: Landmarks/initial needle insertion. Note the approximately 45-degree cephalad and medial needle angulation. Figure 17B. Thoracic paramedian approach: Needle angle 55–60 degrees to the skin surface. Figure 18. Taylor approach landmarks: 1 = posterosuperior iliac spine, 2 = iliac crest (corresponds approximately to the L3-4 level). Figure 19. A: Caudal approach: Angle of needle insertion required to enter the caudal canal. B: Landmarks.

   In the midthoracic level, the skin wheal is placed 2.0 cm lateral and inferior to the superior spinous process (Figure 17A). A 22-gauge “spinal needle” can be used to infiltrate the skin to lamina. Depth is noted to gauge the depth of epidural needle insertion.
   
2. Epidural needle is advanced perpendicularly through the skin at thesamelocation until the lamina of T5 is contacted.
   
3. The needle is withdrawn approximately 2 cm, redirected at a 15- to 20-degree angle toward the midline and a 45-degree angle from the skin surface.
   
4. Each time bone is contacted, the needle is withdrawn 0.5 cm, then walked off the bone in a medial/cephalad direction¹¹³ until the ligamentum flavum is entered (Figure 17B).

TAYLOR APPROACH

The Taylor approach^113,121 is a modified paramedian approach utilizing the large L5-S1 interspace. It is an excellent approach for patients needing hip surgery or for trauma patients needing lower extremity surgery who cannot tolerate the sitting position.

1. The skin wheal is placed 1 cm medial and 1 cm inferior to the posterior superior iliac spine (Figure 18).
   
2. The epidural needle is inserted into this site in a medial and cephalad direction at a 45- to 55-degree angle.
   
3. As in the classic paramedian approach, the first resistance felt is on entry to the ligamentum flavum.
   
4. If the needle contacts bone (usually the sacrum), the needle should be walked off the bone into the ligament, then into the epidural space.

 

CAUDAL APPROACH

The caudal approach is commonly used in pediatrics for epidural catheter placement for postoperative analgesia. In adults, it is usually reserved for procedures requiring blockage of the sacral and lumbar nerves (e.g., inguinal herniorrhaphy, cystoscopy), epidurography, and for lysis of adhesions in patients with low back pain with radiculopathy after spinal surgery.¹²² Considering that the sacral hiatus is ossified in some patients, the use of fluoroscopy guidance is recommended to decrease the incidence of needle and catheter malposition.

The sacrum is a triangular-shaped bone formed by the fusion of the five sacral vertebral. Nonfusion of the fifth sacral vertebral arch creates the structure known as the sacral hiatus. The hiatus is covered by the sacrococcygeal ligament (an extension of the ligamentum flavum). On its borders are the bony prominences known as the sacral cornu. The sacral hiatus is the point of access to the sacral epidural space. It is usually identified as a groove above the coccyx (Figure 19). If fluoroscopy is not used, there are two methods for identifying the hiatus: (1)Locate the posterior superior iliac spines. A line drawn between them becomes one side of a equilateral triangle. At the apex of the triangle is the sacral hiatus. (2)With firm pressure, identify the coccyx with the index finger. As the finger moves cephalad, the first pair of bony protuberances are the cornu, which surrounds the hiatus.

1. Prep and drape the skin in sterile fashion.
   
2. Patient is placed ina lateral or prone position (pillow under pelvis if prone).
   
3. Either a smaller gauge IV catheter (18- to 23-gauge) or a 20-gauge epidural needle is advanced at a 45-degree angle from the back with the bevel up (to avoid penetrating the anterior sacral wall).
   
4. A distinct “pop” or “snap” is felt when the needle pierces the sacrococcygeal membrane.
   
5. The needle angle is lowered to 160 degrees (almost flat) toward the back. It is advanced not more than 1.5 cm (usually between 5 and 7 mm) in adults and not more than 0.5 cm in children.
   
6. Aspirate for blood or CSF before injecting local anesthetic.
   
7. The epidural catheter can then be inserted through the needle to the desired level.

 

Implementing the Lumbar Epidural

BLOCK INTRAOPERATIVE MANAGEMENT

The volume and concentration of local anesthetic needed for epidural anesthesia is larger than that required for spinal anesthesia, therefore the catheter should be tested for evidence of proper placement in the epidural space. The purpose of the “test dose” is to make sure that the catheter is not in the subarachnoid, intravascular, or subdural space.

TEST DOSE

Although the validity of a test dose of local anesthetic with epinephrine in obstetrics and pediatrics has been questioned,^123,124 it is still suggested by many to decrease the risk of an intravascular injection.^125,126 The classic test dose combines 3 mL of 1.5% lidocaine with 15 mcg of epinephrine. The intrathecal injection of 45 mg of lidocaine will produce a significant motor block consistent with spinal anesthesia. A change in heart rate of 20% or greater is an indication of intravascular injection warranting the removal and replacement of the catheter. If the heart rate does not increase by 20% or greater, or if a significant motor block does not develop within 5 min of administering the test dose, it is considered negative. Exceptions to this rule have been observed in patients under general anesthesia with isoflurane, patients receiving β-adrenergic blocking agents with heart rates below 60 bpm, and obstetric patients in active labor.

In children and in obstetric patients, other methods of identifying intravascular placement of the epidural catheter have been advocated. Because children are anesthetized prior to epidural placement, interference with response to epinephrine under volatile general anesthetics creates a high percentage of false-negative test doses.¹²⁷ In the obstetric patient, if the test dose is injected during a contraction, the change in heart rate may be related to pain and not to the epinephrine. In this population, the test dose should be administered during uterine diastole, soon after a uterine contraction.¹²⁸ Changes in the P or T wave on the electrocardiogram in pediatrics or the use of nerve stimulators to confirm epidural placement in pregnant patients have been utilized.^129,130

In patients on β-adrenergic blocking agents, heart rate changes may not be evident. Systolic blood pressure increases of greater than 20 mm Hg have been used as an indicator of intravascular injection.^131,132

DOSING REGIMEN

After the epidural catheter has been aspirated to check for blood or CSF, and a negative test dose has been demonstrated, the catheter should be dosed to provide the level of surgical anesthesia desired. The maintenance of the desired level of anesthesia can be accomplished through intermittent or continuous dosing after the initial loading dose provides the level of anesthesia necessary for the surgical procedure.

As a general guideline, 1–2 mL per segment to be blocked in a lumbar epidural, 0.7 mL per segment for a thoracic epidural, and 3 mL per segment to be blocked for a sacral/caudal epidural is used as an initial loading dose. The loading dose should be given in 5-mL aliquots through the catheter, repeated at 3- to 5-min intervals, giving the clinician time to assess the patient’s response to dosing. If at any time the patient demonstrates an exaggerated response, further incremental doses should be withheld and the patient reassessed. The catheter should be removed and replaced if the following occurs: a large volume of local anesthetic is required to initiate the block or an incomplete, unilateral, or inadequate block results.Wasting time administering further doses of medication, repositioning the catheter, or other time-consuming measures leads to frustration for the patient, the surgical staff, and delays in the operative procedure. Moreover, these maneuvers rarely result in a successful block.

After the initial dose, one quarter to one third of the amount can be administered 10–15 min later to intensify the sensory block. The overall level of the block will not be significantly increased with this method.¹²⁰

The level and duration of epidural anesthesia depends primarily on the injection site, and the volume and concentration of the drug. Other factors such as age, pregnancy, and sex are less important factors but need to be considered. The addition of fresh epinephrine and 8.4% sodium bicarbonate to lidocaine, mepivicaine, and chloroprocaine will decrease the latency, improve the quality, and prolong the duration of the block. Epinephrine is less effective with the long-acting local anesthetics. Adding bicarbonate to ropivicaine and in a dose greater than 0.05 mL/10 mL of bupivacaine will cause precipitation. The addition of opioids (e.g., fentanyl) has been shown to improve the quality of the block without any effect on duration.¹³³

TOP-UP DOSING

Repeat doses, commonly referred to as “top-ups,” need to be given before the level of the block has receded by more than two dermatomes. One half to two thirds of the original volume of local anesthetic should be given for each repeat dose. The anesthesiologist must have a working knowledge of the characteristics of the local anesthetic used to properly implement the redosing protocol so that the sedated patient does not have to be disturbed to check dermatomal levels for sensory block (Table 12).

A continuous infusion through the lumbar epidural catheter can be started after the initial bolus to maintain surgical anesthesia. Continuous infusions require the same diligent attention to the patient as any other anesthetic.¹³⁴ The usual infusion rate is between 4 and 15 mL/h. The wide range is usually dependent on the age, weight, and extension of the block desired in a particular patient. Thus, individualization is necessary, and a hard core rule cannot be applied for this purpose.

 

Activating the Thoracic Epidural Intraoperative Management

Epidural anesthesia is ideally suited for thoracic surgery. It is considered the gold standard for postthoracotomy analgesia because it produces better pain relief with fewer side effects than other commonly used methods.¹³⁵ When combined with general anesthesia, it prevents vagal reflexes and pain from traction on the diaphragm.¹³⁶

Placement and activation are similar to lumbar epidural placement, with a few modifications. An epidural block provides the most intense block at the insertion site, so the tip of the catheter should be placed at midincision level, usually above T8. This will provide the best segmental analgesia. Because there is a greater incidence of false loss of resistance in the midline thoracic approach, the paramedian approach is the best technique to use for catheter placement.

The sharp angulation of the spinous processes especially in the midthoracic area can make the midline approach difficult even for the most experienced clinicians.

1. Once the catheter is placed, it is aspirated for the presence of blood or CSF.
   
2. A test dose of 3 mL of 1.5% lidocaine with epinephrine 1:200,000 is given to (a) rule out intravascular catheter position and (b) provide a band of anesthesia before inducing general anesthesia.
   
3. If no anesthesia can be appreciated, the catheter should be replaced.
   
4. The patient should receive only light sedation for placement to alert the clinician to the development of paresthesias.

 

DOSING THE THORACIC EPIDURAL CATHETER

Several dosing regimes have been suggested. All are effective means of providing surgical analgesia, allowing a “light general anesthesia” to be used and thereby reducing residual respiratory depressant effects.

After a negative aspiration and test dose:

1. An initial dose of 3 to 6 mL of dilute bupivacaine (0.25% to 0.5%) with or without preservative-free morphine (1–2 mg) is administered, followed by 3 mL of 0.25% to 0.5% bupivacaine every 30 min.¹³⁷
   
2. Alternative regimen: Administer a loading dose with 10 to 15 mL of bupivacaine (0.125%) with an opioid (fentanyl 2 mcg/mL or hydromorphone 20 mcg/mL) at least 30 min as tolerated before the end of the case. Start an infusion of bupivacaine 0.0625% with fentanyl or hydromorphone at 3 to 5 mL/h before the patient leaves the operating room.¹³⁸

Intraoperative Sedation

Intraoperative sedation can be provided to the level of the patient’s comfort especially when the epidural is used as the primary anesthetic. If the patient prefers to be kept aware, then light sedation with an initial dose of a benzodiazepam and opioid on insertion can be effective. For those who prefer to be “asleep,” a propofol infusion can be added to maintain sedation without respiratory impairment.

Problem Solving

Problems with Epidural Placement

Epidural placement produces unique problems that are directly related to experience, body habitus of the patient, or disease states affecting the spine. Most of these problems can be overcome if the clinician recognizes the problem and can make adjustments in technique (Table 13).

Problems with Epidural Function

An easily placed epidural does not guarantee excellent function. Inadequate blocks, partial blocks, and unilateral blocks are some of the problems that can occur. Hypotension, often seen with epidural dosing, is a relatively common side effect that is easily managed if the clinician is prepared. Because of the discontinuous nature of the epidural space and variations in anatomy, sometimes these problems cannot be overcome. In the vast majority, careful evaluation of catheter placement, the dose and type of medication given, or administration of sedation can resolve these problems.

HYPOTENSION

Adropinblood pressure is common and expected with epidural anesthesia secondarily to the sympathectomy caused by local anesthetic action. The blood pressure should be maintained to within 20% of the patient’s resting baseline.

Action. Bolus the patient with 500 to 1000 mL of a balanced salt solution.

• If necessary, small doses of ephedrine (10–20 mg) can be used in the pregnant or bradycardic patient after fluid bolus if the patient is still hypotensive.
  
• Phenylephrine (40–120 mcg) can be used in the nonpregnant patient to constrict peripheral blood vessels, thereby increasing venous return and blood pressure.

 

UNILATERAL BLOCK

After an epidural has been adequately dosed, the patient may complain that one side is densely blocked, but pain and motor function is still intact on the opposite side. Because of the segmental and possibly septated nature of the epidural space, unilateral blocks can occur. The more common explanation for a unilateral block is incorrect catheter placement. If the catheter has been inserted > 5 cm into the epidural space, the tip of the catheter may have entered the intervertebral foramen, exited the epidural space, or wrapped around a spinal nerve. The resultant block will be inadequate or unilateral

Action. Pull the catheter back 1–2 cm, leaving 3–4 cm in the epidural space.

• Turn the patient with the unblocked side down and redose the catheter with 3 to 5 mL of local anesthetic.
  
• If no effect, replace the catheter.

 

INADEQUATE BLOCK: BREAKTHROUGH PAIN DESPITE ADEQUATE BLOCK HEIGHT

This problem can be seen secondarily to inadequate sacral blockade. The sacral segment is larger, dense, and difficult to block.

Action. Raise the head of the bed and redose the catheter with a higher concentration of local anesthetic.

• Administration of 50 mcg of fentanyl to improve the quality of the block.

 

QUESTIONABLE QUALITY OFEPIDURAL PLACED FOR ANALGESIA, FULLY DOSED. PATIENT HAS TO GO TO SURGEY

This problem is often seen in obstetrics. An epidural is placed and dosed, but the patient is never fully comfortable. More local anesthetic is given with fair control of pain. Then the patient has to go urgently to the operating roomfor a cesarean section requiring dense block to a T4 level. The easiest way to prevent this problem is to replace a questionable epidural catheter.

Action. Take the patient to the operating room, remove the questionable catheter.

• Do a combined spinal-epidural (CSE) using a lower spinal dose.
  
• Use the new epidural to raise the level of the block if necessary.
  
• Use general anesthesia if time does not permit placing the CSE.

 

BLOCK IS DISSIPATING REQUIRNG LARGER DOSES OF LOCAL ANESTHETIC

This problem occurs for two potential reasons. If the epidural has been used for analgesia and has been dosed frequently, tachyphylaxis to the local anesthetic can occur. The other problem is catheter migration into a vessel.

Action. Check catheter to ensure it has not migrated into a blood vessel. If so, pull it back 1–2 cm, flush with saline. If no blood is aspirated, cautiously rebolus with incremental doses, being vigilant for systemic toxic signs.

• If blood is still in the catheter, replace.
  
• If the catheter has not migrated, rebolus the catheter with a higher concentration of local anesthetic and increase the infusion rate (if continuous). Add an opioid to enhance the quality of the block.

Back to top

Any invasive procedure is associated with complications. The complications of epidural blockade can range from annoying to life-threatening. They can be classified as drug-related or procedure-related. Drug-related complications are the result of systemic toxicity of local anesthetics either injected directly into an epidural vein or from administration of excessively large doses. Procedure-related complications can further be classified as minor or major. Minor complications include back pain and headache (postdural puncture headache, PDPH).Major complications include subdural injection, subarachnoid injection, total or high spinal, meningitis, adhesive arachnoiditis, epidural abscess, and spinal cord or nerve root injury.

Drug-Related Complications

When an excessive dose of local anesthetics is injected into the epidural space or when a moderate dose is accidentally injected into an epidural vein, systemic toxicity can occur. The central nervous system is the first system affected. Symptoms include lightheadedness, tinnitus, circumoral numbness and tingling, numbness of the tongue, and blurred vision. Signs include muscle twitching, confusion, tremors of the facial muscles and extremities, and shivering. The patient may complain of feeling increasingly anxious.

Cardiovascular effects of local anesthetics range from mild changes in blood pressure and pulse to complete cardiovascular collapse. At low doses, a slight increase in blood pressure may be noted secondarily to an increase in cardiac output. At higher doses, a marked increase in blood pressure and heart rate will precede severe hypotension and cardiovascular collapse.

Treatment is supportive directed toward maintaining the airway, supporting ventilation, and cardiopulmonary resuscitation if necessary. It is of paramount importance to prevent hypoxia, hypercarbia, and acidosis to limit the cardiovascular toxic effects of systemically administered local anesthetics. If ventricular dysrhythmias occur, lidocaine should not be given as local anesthetic toxicity is additive. Amiodarone is the preferred antiarrhythmic. Epinephrine should be given early and in greater than usual doses especially if bupivacaine was the local anesthetic used. Because bupivacaine binds more tightly to the cardiac sodium channels, it is more difficult to displace it and therefore to treat dysrhythmias caused by it.¹³⁹ Calcium channel blockers must also be avoided as they will augment the cardiovascular effects of local anesthetics.

Procedure-Related Complications

Minor Back Pain

The incidence of back pain after epidural anesthesia is between 20 and 30%. The incidence is higher and of longer duration than that arising from spinal or general anesthesia.¹⁴⁰ It is thought to be caused by injury to musculoskeletal structures of the spine from a larger needle. The pain is usually self-limiting. It should be treated with nonsteroidal anti-inflammatory drugs, acetaminophen, or heat.¹²²

Postdural Puncture Headache

Postdural puncture headache is a more common complication with spinal anesthesia than with epidural as the former mechanism requires dural puncture. When a PDPH occurs after epidural placement, it usually occurs in the younger, female, pregnant patient.^141,142 In most instances, the clinician is aware that the dura has been pierced, but in many instances, no evidence of dural puncture exists.

The headache is thought to result from loss of CSF through the dural hole, causing lower CSF pressure. In the upright position, the brain tissue sags in the cranial vault, causing traction on cranial nerves and nerve roots. Traction on the cranial nerves causes the cranial nerve palsies that can be observed.¹⁴³

The key feature of the headache is that it is mild or absent in the supine position, but intense when the head is elevated. Typically, the headache is bilateral, frontal or occipital, and extending into the neck. It is often described as throbbing or continuous. Cranial nerve signs (diplopia, tinnitus, nystagmus, hearing loss) may be present as well as nausea and vomiting. The onset of the headache is commonly 12–72 h following the procedure. Caution should be exercised if the headache occurs immediately after the procedure as this is more commonly due to excessive air used for loss-of-resistance techniques (air encephalogram).

The duration of the headache is typically 5 days with a range of 1 to 12 days.¹⁴⁴ Conservative treatment includes bedrest, analgesics, intravenous or oral fluids, and caffeine. Caffeine and hydration are used to stimulate the production of CSF and to constrict the intracranial vessels, thereby reducing the headache. The treatment of choice is an epidural blood patch. Uncontrolled studies report rapid recovery in between 90 to 95% of patients after blood patch.¹⁴⁵ Several studies have demonstrated that treatment with an epidural blood patch should occur early in the development of the headache although it is effective treatment as late as 5 days from presentation.¹⁴⁶ Treating the headache with the blood patch decreases the length of hospital stay and emergency room visits.¹⁴⁷

The technique for the autologous blood patch is simple. Using sterile techniques, a needle is inserted into the epidural space at or one interspace below the prior level of dural puncture. Fifteen to 20 mL of the patient’s blood (drawn aseptically) is slowly injected into the space. The injection should stop when the patient experiences focal back pain. The procedure can be repeated 24 h later and will provide equivalent success. Relatively few complications are reported from the procedure. Backache, neckache, and transient temperature elevation for 24 to 48 h may occur. Although rare, dural abscess has been reported after a blood patch. To prevent this complication, both the acquisition of autologous blood and the epidural needle placement should be done using aseptic technique.¹⁴⁸

Major Subdural Injection

The subdural space is a potential space between the dura and arachnoid mater. Unlike the epidural space, the subdural space extends intracranially. A small dose of local anesthetic can have a profound effect. The space is wider in the cervical region and extends laterally over the nerve roots. Unintentional entry of an epidural needle or catheter is usually in this area. Although the incidence is low (0.82% of epidural injections), the effects are significant.¹⁴⁹ The clinical presentation varies, but is distinguished by a delayed onset by 10 to 15 min compared with a high spinal.

A key feature is a widespread sensory block with milder motor block. Sympatholysis out of proportion to the dose of local anesthetic occurs, causing moderate to severe hypotension. Treatment is similar to that of a high spinal-cardiovascular and respiratory support, including intubation and mechanical ventilation if necessary.

Subarachnoid Injection/High or Total Spinal

Accidentally puncturing the dura can occur with even the most careful placement of an epidural. If it is recognized during needle puncture, the needle should be removed and another interspace chosen. If it occurs after catheter insertion, either the procedure can be changed to a continuous spinal, or the catheter can be removed and the procedure repeated at another interspace.

A more serious complication occurs when the needle or catheter is advanced into the subarachnoid space and a large dose of local anesthetic is given directly into the CSF, causing total spinal anesthesia. Total spinal anesthesia occurs when local anesthetic spreads high enough to block the entire spinal cord and occasionally the brainstem. Because the anesthesia extends into the cervical levels, the cardioaccelerator fibers are affected. Profound hypotension, bradycardia, and apnea will occur. Unconsciousness follows as a result of the effect of local anesthetic action on the brainstem.

Treatment includes airway support and intubation, 100% oxygen, intravenous fluids and vasopressors to maintain hemodynamic stability. Epinephrine should be used early and in large enough doses to stabilize the heart rate and blood pressure. As the block recedes, the patient will regain consciousness and control of breathing followed by recovery of motor and sensory function.

Meningitis

Acute bacterial meningitis following epidural anesthesia is a rare event, but it has been reported.¹⁵⁰ Microorganisms can be transmitted via syringes, catheters, needles, and medications injected into the epidural space. They can come from the clinician or from the patient but are most commonly from localized infections in the skin and subcutaneous tissue. The most common infective microorganisms are Staphylococcus spp (coagulase-negative and aureus), followed by gram-negative bacilli and other species.¹⁵¹

Symptoms include fever, headache, lethargy, confusion, and the classic symptom, nuchal rigidity.¹⁵⁰ Because it is such a rare occurrence, diagnosis can be delayed due to assumption that a PDPH is present. Patients with meningitis have fever with mental status changes (lethargy at a minimum, confusion as disease progresses). The headache is not positional.

Treatment of bacterial meningitis includes emergent antibiotic therapy (usually ceftriaxone), head CT, and lumbar puncture with patient management by neurology. Fever, back pain, and nuchal rigidity is meningitis until proven otherwise.

Chronic Adhesive Arachnoiditis

Inflammatory changes in the subarachnoid space can cause the syndrome of chronic adhesive arachnoiditis. Strands of collagen begin to form between the nerve roots and the pia arachnoid. Arachnoiditis ensues, characterized by collagen deposition and nerve root adherence. When the inflammatory process resolves, adhesive arachnoiditis develops. The collagen deposits encapsulate the nerve roots, creating nerve root atrophy as a result of the interruption of their blood supply.¹⁵² It can follow trauma, surgery, infections, contaminants, tumors, or the subaranchoid administration of various medications.

The clinical picture is complex with varied symptomatology. The most common clinical features are:

• back pain that increases on exertion with or without leg pain
  
• bilateral leg pain
  
• hyporeflexia
  
• decreased range of motion of the trunk
  
• sensory abnormalities
  
• decreased straight leg raises
  
• urinary sphincter dysfunction

 

Unfortunately, the clinical symptoms can lead to a misdiagnosis of spinal stenosis, lumbar disk disease, spinal tumors, or other compressive lesions of the spine.¹⁵²

Characteristic MRI findings show conglomerations of roots residing centrally in the dural sac, adhesions tethering the nerve roots peripherally, and soft tissue replacing the subarachnoid space.¹⁵³

The link between epidural block or catheter placement and this disease is nebulous. Although a few case reports have suggested a connection, no prospective studies have yet linked epidurals to chronic adhesive arachnoiditis. Prospective studies have demonstrated that epidurals do not cause chronic backache.¹⁵⁴ Unfortunately, the neurologic deficits may progress to severe and permanent disability.

Spinal Cord/Nerve Root Injury

Serious neurologic injury is an extremely rare but feared complication of neuraxial anesthesia. The incidence of neurologic injury following neuraxial blocks is estimated to be 0.03–0.1%. It is prudent for the anesthesiologist to understand that a neurologic deficit in a patient who has had an epidural is rarely caused by the epidural. Horlocker and colleagues at the Mayo Clinic evaluated the records of over 4000 patients who had lumbar epidurals placed for thoracic surgery while asleep. No neurologic complications occurred, despite the epidurals being placed under general anesthesia.²⁹ In another extensive review of 45,000 patients undergoing epidural placement, only 40 cases arose of neurologic problems, 22 of which had paresthesias.¹⁵⁵ There have been a few case reports of myelopathy and paraplegia occurring when thoracic epidurals were placed in anesthetized patients, but these complications are exceedingly rare.^156−158

Neurologic deficits can be caused by direct trauma to the spinal cord or spinal nerves, from spinal cord ischemia, leading to anterior spinal artery syndrome, from accidental injection of neurotoxic drugs or chemicals, or from hematomas or abscesses.¹⁰⁷ Most peripheral neuropathies resolve spontaneously. Those that become permanent are usually limited to persistent paresthesias and limited motor weakness (Table 14).¹²²

Cauda equina syndrome, a syndrome characterized by bowel and bladder dysfunction, patchy sensory deficits, pain, and paresis of the legs, was previously attributed to continuous subarachnoid infusions with microcatheters. The mechanism of injury was thought to be pooling of hyperbaric lidocaine, causing damage to the nerve roots of the cauda equina. The FDA withdrew the catheters from the market, but a few cases of cauda equina syndrome have been reported occurring with single-shot spinals. Much more rarely, the syndrome has been reported after caudal epidural anesthesia.

Trauma to epidural veins occurs in approximately 10% of epidural placement. It occurs more commonly in patients with engorged epidural veins (e.g., pregnant patient). The bleeding that occurs is usually benign and self-limiting. But if the patient is thrombocytopenic, has received recent anticoagulant therapy, or is coagulopathic for other reasons, the incidence of bleeding leading to the development of epidural hematoma is higher. The incidence of hematomas after epidural blocks is estimated at 1:150,000. No data support an increased risk of its development with aspirin therapy, but the incidence with the more potent antiplatelet drugs is yet to be determined.¹⁵⁹ These concerns led to the consensus statements developed at the Second ASRA Conference on Neuraxial Anesthesia and Anticoagulation.²³ These guidelines can be used to assist the anesthesiologist in determining the most appropriate and safest period for placing an epidural block.

Epidural hematomas can cause cord compression, cord ischemia, or myelopathy similar to that caused by a space occupying tumor. It is prudent to remember that most epidural hematomas are spontaneous and idiopathic.¹⁶⁰ Symptoms range from mild sensory or motor deficits to devastating paraplegia and incontinence. The clinical features include severe back pain with progressive sensory and motor deficits and reappearance of resolving motor–sensory deficits. The onset of symptoms is usually between 0 and 2 days. Emergent surgical decompression is the treatment to avoid permanent neurologic injury.¹⁶¹

Epidural abscess is another rare, but potentially debilitating complication of epidural placement. Spinal epidural abscess can lead to irreversible complications and death if untreated.¹⁶² The most common risk factors are unrelated to anesthetic instrumentation. Intravenous drug abuse, the presence of nonspinal infections, and neurosurgical procedures are the primary risk factors.¹⁶³ The most common presentation is back pain, radiculopathy, lower extremity weakness with sensory deficits, and decreased deep tendon reflexes. Fever, leukocytosis with a left shift, and an elevated erythrocyte sedimentation rate are usually present, but abscesses have been reported in normothermic patients with normal white blood counts. The average onset of symptoms is 2–5 days. It progresses from back pain that intensifies with palpation or percussion of the spine to paraplegia or paralysis.¹⁶⁴ The most common infective organism is Staphylococcus aureus, although multiple organisms have been implicated. MRIs of the spine will demonstrate the abscess as well as its progression into paraspinal structures.¹⁶⁵ Treatment is urgent surgical decompression or percutaneous drainage with fluoroscopic guidance. Antibiotics should be started immediately when abscess is suspected. Although successful therapy with antibiotics alone has been reported, urgent surgery is recommended, especially when neurologic deficits are present.¹⁶³

Anterior spinal artery syndrome secondary to hypotension leading to spinal cord ischemia is a potentially life-threatening syndrome.¹⁶⁶ Theoretically, placement of high thoracic epidurals creating peripheral vasodilation and reduced blood flow to the spinal cord could cause the syndrome, but no reports have proved this occurrence. It is the most common neurologic complication after abdominal aortic surgery but has been reported after surgery on the thoracic spine.¹⁶⁷ Patients usually present with immediate, painless paraplegia. Prognosis is poor, with permanent and disabling neurologic deficits.¹⁶⁸

Back to top

Epidural placement is a safe, effective means of providing surgical anesthesia or postoperative analgesia. It has the benefit of being used for segmental blocks or for more complete motor–sensory blocks necessary for surgery. It reduces the adverse physiologic responses to surgery, may decrease the incidence of myocardial infarctions and postoperative pulmonary sequelae, and can reduce the incidence of hypercoagulable events. The complications associated with intubation and general anesthesia are avoided. Mastery of epidural placement comes with practice, attention to detail, and persistence. A thorough knowledge of anatomy, physiology, and the pharmacology of anesthetic agents is required for safe application. Patient satisfaction, efficient use of operating room time for anesthetic induction, and excellent postoperative pain management make epidural blockade a preferred choice of anesthetic management.

Back to top

1. Beattie WS, Badner NH, Choi P: Epidural analgesia reduces postoperative myocardial infarction: A meta-analysis. Anesth Analg 2001;93:853.
   
2. Ballantyne JC, Carr DB, DeFerranti S: The comparative effects of postoperative analgesic therapies on pulmonary outcome: Cumulative meta-analysis of randomized, controlled trials. Anesth Analg 1998;86:598.
   
3. Rigg JR, Jamrozik K, Myles PS: Epidural anaesthesia and analgesia and outcome of major surgery: A randomized trial. Lancet 2002;359:1276.
   
4. Liu S, Carpenter R, Neal J: Epidural anesthesia and analgesia. Their role in postoperative outcome. Anesthesiology 1995;82:1474.
   
5. Holte K, Kehlet H: Epidural analgesia and risk of anastomotic leakage. Reg Anesth Pain Med 2001;26:111.
   
6. Scott A, Starling J, Ruscher AE, et al: Thoracic versus lumbar epidural anesthesia’s effect on pain control and ileus resolution after restorative proctocolectomy. Surgery 1996;120:688.
   
7. Tuman K, McCarthy R, March RJ: Effects of epidural anesthesia and analgesia on coagulation and outcome after major vascular surgery. Anesth Analg 1991;73:696.
   
8. Rosenfeld B: Benefits of regional anesthesia on thromboembolic complications following surgery. Reg Anesth 1996;21(Suppl): 9.
   
9. Rodgers A,Walker N, Schug S: Reduction of postoperative mortality and morbidity with epidural or spinal anesthesia: Results from overview of randomised trials. BMJ 2000;321:1493.
   
10. Frolich MA, Caton D: Pioneers in epidural needle design. Anesth Analg 2001;93:215–220.
    
11. Cortes RC: Lumbar epidural anesthesia, 1931–1936: A second debut. Rev Esp Anestesiol Reanim 2005;52:159–168.
    
12. Dogliotti A: A new method of block: Segmental peridural spinal anesthesia. Am J Surg 1933;20:107–118.
    
13. Curbelo M: Continuous peridural segmental anesthesia by means of a ureteral catheter. Curr Res Anesth Analg 1949;28:12–23.
    
14. Yucesoy AY: The mechanical properties of intact and traumatized epidural catheters. Anesth Analg 2000;90:393–399.
    
15. Eldor JM: The evolution of combined spinal-epidural anesthesia needles. Reg Anesth 1997;22:294-296.
    
16. Coates M: Combined subarachnoid and epidural techniques: A single space technique for surgery of the hip and lower limb. Anaesthesia 1982;37:89–90.
    
17. Mumtaz M, Daz M, Kuz M: Combined subarachnoid and epidural techniques: Another single space technique for orthopaedic surgery. Anaesthesia 1982;37:90.
    
18. Michalek P, David I, Adamec M, et al: Cervical epidural anesthesia for combined neck and upper extremity procedures: A pilot study. Anesth Analg 2004;99:1833–1836.
    
19. Kirali K, Kocak T, Guzelmeric F, et al: Off-pump awake coronary revascularization using bilateral internal thoracic arteries. Ann Thorac Surg 2004;78:1602–1603.
    
20. Lucchetti V, Moscariello C, Catapano D, et al: Coronary artery bypass grafting in the awake patient: Combined thoracic epidural and lumbar subarachnoid block. Eur J Cardiothorac Surg 2004;26:658–659.
    
21. Klokocovnik T, Hollan J, Sostaric M, et al: Minimally invasive aortic valve replacement under thoracic epidural anesthesia in a conscious patient. Heart Surg Forum 2004;7:196-197.
    
22. LM Visser: Epidural Anesthesia, Update in Anesthesia. Ann Arbor, Michigan, CSEN: The global regional anesthesia website, 2001, pp 1–4
    
23. Horlocker TT, Wedel DJ, Benzon H, et al: Regional anesthesia in the anticoagulated patient: Defining the risks (The Second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med 2003;28:172–197.
24. Cousins M, Veering B: Epidural neural blockade. In Cousins M, Bridenbaugh P (eds): Neural Blockade, 3rd ed. Lippincott-Raven, 1998, pp 243–320.
    
25. Morgan GE Jr, Mikhail MSM, Murray MJM: ClinicalAnesthesiology, 3rd ed. McGraw-Hill, 2002.
    
26. Burns R, Clark V: Epidural anesthesia for caesarean section in a patient with quadriplegia and autonomic hyperreflexia. Int JObstet Anesth 2004;13:120–123.
    
27. Vassiliev DVM, Nystrom EUM, Leicht CHM: Combined spinal and epidural anesthesia for labor and cesarean delivery in a patient with Guillain-Barre Syndrome. Reg Anesth Pain Med 2001;28:174–176.
    
28. Tidmarsh MM: Epidural anesthesia and neural tube defects. Int J Obstet Anesth 1998;7:111–114.
    
29. Horlocker TM, Abel MD, Messick JM Jr, et al: Small risk of serious neurologic complications related to lumbar epidural catheter placement in anesthetized patients. Anesth Analg 2003;96:1547–1552.
    
30. Douglas MJM: Epidural anesthesia in three parturients with lumbar tattoos: A review of possible implications. Can J Anesth 2002;49:1057–1059.
    
31. Clemente CD: Clemente Anatomy: A Regional Atlas of the Human Body, 4th ed. Lippincott Williams & Wilkins, 1997.
    
32. Brown DL: Spinal, epidural, and caudal anesthesia. In Miller RD (ed): Miller’s Anesthesia, 6th ed. Elsevier, 2005, pp 1653–1683.
    
33. Igarashi T, Hirabayashi Y, Shimizu R: The lumbar extradural structure changes with increasing age. Br J Anaesth 1997;78:149.
    
34. Hogan Q: Lumbarepidural anatomy: A new look by cryomicrotome section. Anesthesiology 1991;75:767.
    
35. Blomberg R: The dorsomedian connective tissue band in the lumbar epidural space of humans: An anatomic study using epiduroscopy in autopsy cases. Anesth Analg 1986;65:747.
    
36. Hogan Q: Distribution of solution in the epidural space; Examination by cryomicrotome section. Reg Anesth Pain Med 2002;27:150.
    
37. Kim J, Bahk J, Sung J: Influence of age and sex on the position of the conus medullaris and Tuffler’s line in adults. Anesthesiology 2003;99:1359–1363.
38. Lee G, Lee J, Ko Y, et al: Comparison of the spinal level assumption by palpation of the iliac crest and posterior superior iliac spine. J Korean Acad Rehab Med 2004;28:596–600.
    
39. Tame S, Bursgtall R: Investigation of the radiological relationship between iliac crests, conusmedullaris and vertebral level in children. Paediatr Anaesthesiol 2003;13:676–680.
    
40. Palmer S, Abram S, Maitra A, et al: Distance from the skin to the lumbar epidural space in an obstetric population. Anesth Analg 1983;62:944.
    
41. Rosenberg H, Keyhak M: Distance to epidural space in nonobese patients. Anesth Analg 1984;63:539–540.
    
42. Shiroyama K, Izumi H, Kubo T, et al: Distance from the skin to the epidural space at the first lumbar interspace in a Japanese obstetric population. Hiroshima J Med Sci 2003;52:27–29.
    
43. Wu C: Acute postoperative pain. In Miller RD (ed): Miller’s Anesthesia, 6th ed. Elsevier, 2005, pp 2742–2743.
    
44. Baron J, Decaux-Jacolot A, Edouard A, et al: Influence of venous return on baro-reflex control of heart rate during lumbar epidural anesthesia in humans. Anesthesiology 1986;64:188.
    
45. Otton P, Wilson E: The cardiocirculatory effects of upper thoracic epidural analgesia. Can Anaesth Soc J 1966;13:541.
    
46. Bonica J, Kennedy W, Akamatsu T, et al: Circulatory effects of peridural block. Anesthesiology 1972;36:219.
    
47. Gruber E, Tschernko E, Kritzinger M, et al: The effects of thoracic epidural analgesia with bupivacaine 0.25% on ventilatory mechanics in patients with severe chronic obstructive pulmonary disease. Anesth Analg 2001;92:1015–1019.
    
48. Christopherson R, Beattie C, Frank SM, et al: Perioperative morbidity in patients randomized to epidural or general anesthesia for lower extremity vascular surgery. Anesthesiology 1993;79:422–434.
    
49. Meissner A, Weber T, Van Aken H, et al: Limited upper thoracic epidural block and splanchnic perfusion in dogs. Anesth Analg 1999;89:1378–1381.
    
50. Ramaioli F, DeAmici D: Central antiemetic effect of atropine: Our personal experience. Can J Anesth 1996;43:1079.
    
51. Ward R, Kennedy W, Bonnica J: Experimental evaluation of atropine and vasopressors for the treatment of hypotension during high subaranchnoid anesthesia. Anesth Analg 1966;45:621.
    
52. Walts L, Kaufman R, Moreland J, et al: Total hip arthroplasty: An investigation of factors related to postoperative urinary retention. Clin Orthop 1985;194:280.
    
53. Kehlet H: The stress response to surgery: Release mechanisms and the modifying effect of pain relief. Acta Chir Scan (Suppl) 1988;550:22.
    
54. Kehlet H: Surgical stress: The role of pain and analgesia. Br J Anaesth 1989;63:189.
    
55. Vanhoutte P: Circulation 1989;80:1.
    
56. Bromage P: Mechanism of action of extradural analgesia. Br J Anaesth 1975;47:199.
    
57. DiFazio C, Woods A, Rowlingson J: Drugs commonly used for nerve blocking: Pharmacology of local anesthetics. In Raj PPM (ed): Practical Management of Pain, 3rd ed. Mosby, 2000, pp 558–563.
    
58. Xiong Z, Strichartz G: Inhibition of local anesthetics of Ca+ channels in rat anterior pituitary cells. Eur J Pharmacol 1998;363:8.
    
59. Smith F, Davis R, Carter R: Influence of voltage-sensitive Ca(++) channel drugs on bupivacaine in filtration anesthesia in mice. Anesthesiology 2001;95:1189–1197.
    
60. Liu B, Zhuang X, Li S, et al: Effects of bupivacaine and ropivacaine on high-voltage-activated calcium currents of the dorsal horn neurons in newborn rats. Anesthesiology 2001;95:139–143.
    
61. Moore D, Spierdijk J, Van Kleef J, et al: Chloroprocaine neurotoxicity: Four additional cases. Anesth Analg 1982;61:155.
    
62. Lynch C: Depression of myocardial contractility in vitro by bupivacaine, etidocaine, and lidocaine. Anesth Analg 1986;65:551.
    
63. Graf B, Martin E, Bosnjak Z: Stereospecific effect of bupivacaine isomers on atrioventricular conduction in the isolated perfused guinea pig heart. Anesthesiology 1997;86:410.
    
64. McClure J: Ropivacaine. Br J Anaesth 1996;76:300.
    
65. Bader N, Datta A, Flanagan H, et al: Comparison of bupivacaine and ropivacaine induced conduction blockade in isolate rabbit vagus nerve. Anesth Analg 1989;68:724.
    
66. Axelsson K, Nydahl P, Philipson L, et al: Motor and sensory blockade after epidural injection of mepivacaine, bupivacaine, and etidocaine: A double-blind study. Anesth Analg 1989;69:739.
    
67. Stanton-Hicks M, Berges P, Bonica J: Circulatory effects of peridural block.Comparison of the effects of epinephrine and phenylephrine. Anesthesiology 1973;39:308.
    
68. Curatolo M, Petersen-Felix S, Arendt-Nielsen L: Adding sodium bicarbonate to lidocaine enhances the depth of epidural blockade. Anesth Analg 1998;86:341.
    
69. Mehta P, Theriot E, Mehrotra D, et al: A simple technique to make bupivacaine a rapid-acting epidural anesthetic. Reg Anesth 1987;12:135.
    
70. Corke B, Carlsonk C, Dettbarn W: The influence of 2-chloroprocaineonthe subsequent analgesic potency of bupivacaine. Anesthesiology 1984;60:25.
    
71. Bouguet D: Caudal clonidine added to local anesthetics enhances post-operative analgesia after anal surgery in adults.Anesthesiology 1994;81:A942.
    
72. Kroin J, Buvanendran A, Beck D, et al: Clonidine prolongation of lidocaine analgesia after sciatic nerve block in rats is mediated via the hyperpolarization-activated cation current, not by alpha-adrenoreceptors. Anesthesiology 2004;101:488–494.
    
73. Landau R, Schiffer E, Morales M, et al: The dose-sparing effect of clonidine added to ropivacaine for labor epidural analgesia. Anesth Analg 2002;95:728–734.
    
74. Kyacan N,Arici G,KarsliB, et al: Patient-controlled epidural analgesia in labour: The addition of fentanyl or clonidine to bupivacaine. Agri 2004;16:59–66.
    
75. Novak-Jankovic V, Paver E, Iban A, et al: Effect of epidural and intravenous clonidine on the neuro-endocrine and immune stress response in patients undergoing lung surgery. Eur J Anaesthesiol 2000;17:50–56.
    
76. Matot I, Drenger B,Weissman C, et al: Epidural clonidine, bupivacaine and methadone as the sole analgesic agent after thoracotomy for lung resection. Anaesthesia 2004;59:861–866.
    
77. Wu C, Jao S, Borel CO: The effect of epidural clonidine on perioperative cytokine response, postoperative pain, and bowel function in patients undergoing colorectal surgery. Anesth Analg 2004;99:502–509.
    
78. Roelants F, Lavand’homme P, Mercier-Fuzier V: Epidural administration of neostigmine and clonidine to induce labor analgesia: Evaluation of efficacy and local anesthetic-sparing effect. Anesthesiology 2005;102:1205–1210.
    
79. Kayacan N, Arici G, Karsli B: Patient-controlled epidural analgesia in labour: The addition of fentanyl or clonidine to bupivacaine. Agri 2004;16:59–66.
    
80. Roelants F, Lavand’homme P: Epidural neostigmine combined with sufentanil provides balanced and selective analgesia in early labor. Anesthesiology 2004;101:439–444.
    
81. Omais M, Lauretti G, Paccola CA: Epidural morphine and neostigmine for postoperative analgesia after orthopedic surgery. Anesth Analg 2002;95:1698–1701.
    
82. Kirdemir P, Ozkocak I, Demir T: Comparison of postoperative analgesic effects of preemptively used epidural ketamine and neostigmine. J Clin Anesth 2000;12:543–548.
    
83. Johansen M, Gradert T, Sattefield W, et al: Safety of continuous intrathecal midazolam infusion in the sheep model. Anesth Analg 2004;98:1528–1535.
    
84. Bharti N, Madan R, Mohanty P, et al: Intrathecal midazolam added to bupivacaine improves the duration and quality of spinal anaesthesia. Acta Anaesthesiol Scand 2003;47:1101–1105.
    
85. Tucker A, Mezzatesta J, Nadeson R, et al: Intrathecal midazolam II: Combination with intrathecal fentanyl for labor pain. Anesth Analg 2004;98:1521–1527.
    
86. Ugur B, Basaloglu K, Yurtseven T, et al: Neurotoxicity with single dose intrathecal midazolam administration. Eur J Anaesthesiol 2005;22:907–912.
    
87. Yaksh T, Allen J: Preclinical insights into the implementation of intrathecal midazolam: A cautionary tale. Anesth Analg 2004;98:1509–1511.
    
88. Gambling D, Hughes T, Martin G, et al: A comparison of Depodur, a novel, single-dose extended-release epidural morphine, with standard epidural morphine for pain relief after lower abdominal surgery. Anesth Analg 2005;100:1065–1074.
    
89. Viscusi E, Martin G, Hartrick C, et al: 48 hours of postoperative pain relief after total hip arthroplasty with a novel, extended-release epidural morphine formulation. Anesthesiology 2005;102:1014–1022.
    
90. Carvalho B, Riley E, Cohen S, et al: Single-dose, sustained release epidural morphine in the management of postoperative pain after elective cesarean delivery: Results of a multicenter randomized controlled study. Anesth Analg 2005;100:1150–1158.
    
91. Magnusdottir H, Kimo K, Ricksten S: High thoracic epidural analgesia does not inhibit sympathetic nerve activity in the lower extremities. Anesthesiology 199;91:1299.
    
92. Basse L,Werner M, Kehlet H: Is urinary drainage necessary during continuous epidural anesthesia after colonic resection. Reg Anesthes Pain Med 2000;25:498.
    
93. Galindo A, Hernandez J, Benavides O, et al: Quality of spinal extradural anesthesia: The influence of spinal nerve root diameter. Br J Anaesthes 1975;47:41.
    
94. Duggan J, Bowler G, McClure J, et al: Extradural blockwith bupivacaine: Influence of dose, volume, concentration and patient characteristics. Br J Anaesthes 1988;61:324.
    
95. Hodgkinson R, Husain F: Obesity, gravity and the spread of epidural anesthesia. Anesth Analg 1981;60:421.
    
96. Seow L, Lips F, Cousins M: Effect of lateral position on epidural blockade for surgery. Anaesthes Intensive Care 1983;II:97.
    
97. Park W, Hagins F, Rivat E, et al: Age and epidural dose response in adult men. Anesthesiology 1982;56:318.
    
98. Park W, Massengale M, Kim S, et al: Age and spread of local anesthetic solutions in the epidural space. Anesth Analg 1980;9: 768.
    
99. Hirabayashi Y, Shimizu R, Matsuda I: Effect of extradural compliance and resistance on spread of extradural analgesia. Br J Anaesthes 1990;65:508.
    
100. Cullen ML, Staren E, el-Ganzouri A, et al: Continuous epidural analgesia after major abdominal operations: A randomized prospective study. Surgery 1985;98:718–728.
     
101. Bromage P, Bufoot M, Crowell D, et al: Quality of epidural blockade. Influence of physical factors. Br J Anaesthes 1964;36:342.
     
102. Datta S, Migliozzi R, Flanagan H, et al: Chronically administered progesterone decreases halothane requirements in rabbits. Anesth Analg 1989;68:46–50.
     
103. Gintzler A: Endorphin-mediated increases in pain threshold during pregnancy. Science 1980;210:193–195.
     
104. Hofmeyr G, Cyna A, Middleton P: Prophylactic intravenous preloading for regional analgesia in labour. Cochrane Database System Review 2002;2:4.
     
105. Jackson R, Reid JA, Thorburn J: Volume preloading is not essential to prevent spinal-induced hypotension at Caesarean section. Br J Anaesthes 1995;75:262–265.
     
106. Horlocker TM, Abel M, Messick J, et al: Small risk of serious neurologic complications related to lumbar epidural catheter placement in anesthetized patients. Anesth Analg 2003;96:1547–1552.
     
107. Usubiaga J: Neurological complications following epidural anesthesia. Int Anaesthesiol 1975;13:2.
     
108. Gulve A, Eldabe S, Richardon J, et al: Obstetric epidural and chronic adhesive arachnoiditis. Br J Anaesthes 2004;92:765–767.
     
109. Sellors J, Cyna A, Simons S: Aseptic precautions for inserting an epidural catheter: A survey of obstetric anaesthetists. Anaesthesia 2002;57:593–596.
     
110. Sleth J: Evaluation of aseptic measures in the performance of epidural catheterization and perception of its risk of infection. Results of a survey in Languedoc-Roussilon. Ann French Anesthes Reanim 1998;17:408–414.
     
111. Schroter J, Wa Djamba D, Hoffman V, et al: Epidural abscess after combined spinal-epidural block. Can J Anaesthes 1997;44:235–238.
     
112. Bromage P: Epidural Anesthesia. WB Saunders, 1978.
     
113. McQuillan P: Central nerve blocks: Subarachnoid. In Raj PPM (ed): Practical Management of Pain, 3rd ed. Mosby, 2000, pp 631–636.
     
114. Evron S, Sessler D, Sadan O, et al: Identification of the epidural space: Loss of resistance with air, lidocaine, or the combination of air and lidocaine. Anesth Analg 2004;99:245–250.
     
115. Laviola S, Kirvela M, Spoto M: Pneumocephalus with intense headache and unilateral pupillary dilatation after accidental dural puncture during epidural anesthesia for cesarean section. Anesth Analg 1999;88:582–583.
     
116. Naulty J, Ostheimer G, Datta S: Incidence of venous air embolism during epidural catheter insertion. Anesthesiology 1982;57:410–412.
     
117. Dalens B, Bazin J, Haberer J: Epidural bubbles as a cause of incomplete analgesia during epidural anesthesia. Anesth Analg 1987;66:679–683.
     
118. Petty T, Stevens R, Erickson S: Inhalation of nitrous oxide expands epidural air bubbles. Reg Anesth 1996;21:144–148.
     
119. Hirsch M, Katz Y, Sasson A: Spinal cord compression by unusual epidural air accumulation after continuous epidural anesthesia. Am J Roentgenol 1989;153:887–888.
     
120. Gutsche B: How to Make an Epidural Work. American Society of Anesthesiologists. 2004, pp 1–7.
     
121. Gunter J: Thoracic epidural anesthesia via the modified Taylor approach in infants. Reg Anesth Pain Med 2000;25:555–557
     
122. McQuillan PM, Kafiluddi R, Hahn MB: Central nerve blocks: Interventional techniques, In Raj PPM (ed): Pain Medicine: A Comprehensive Review, 2nd ed. Mosby, 2003, pp 212–222.
     
123. Moore D, Batra M, Bridenbaugh L, et al: Maternal heart rate changes with a plain epidural test dose—Validity of results open to question. Anesthesiology 1987;66:854.
     
124. Sethna N, McGowan F: Do results from studies of a simulated epidural test dose improve our ability to detect unintentional epidural vascular puncture in children. Pediatr Anaesthesiol 2005;15:711–715.
     
125. Steffek M, Owczuk R, Szlyk-Augustyn M, et al: Total spinal anesthesia as a complication of local anaesthetic test-dose administration through an epidural catheter. Acta Anaesthesiol Scand 2004;48:1211–1213.
     
126. Lee P, Kim J: Lumbar epidural blocks: A case report of a life-threatening complication. Arch Physician Med Rehab 2000;81:1587–1590.
     
127. Desparmet J, Mateo J, Esoffey C: Efficacy of an epidural test dose in children anesthetized with halothane. Anesthesiology 1990;72:249.
     
128. Rosen M, Hughes S, Levinson G: Regional anesthesia for labor and delivery. In Levinson SA (ed): Anesthesia for Obstetrics. Lippincott Williams & Wilkins, 2002, pp 123–148.
     
129. Tsui B, Gupta S, Finucane B: Confirmation of epidural catheter placement using nerve stimulation. Can J Anaesth 1998;45:640–644.
     
130. Sparks J, Seefelder C: Neonatal T-wave elevation from a positive epidural test dose. Pediatr Anaesthesiol 2005;15:706–707.
     
131. Moore D, Batra M: The components of an effective test dose prior to epidural block. Anesthesiology 1981;55:693.
     
132. Mackie K, Lam A: Epinephrine-containing test dose during beta blockade. J Clin Monitoring 1991;7:213.
     
133. Kasaba T, Yoshikawa G, Seguchi T: Epidural fentanyl improves the onset and spread of epidural mepivacaine analgesia. Can J Anesth 1996;43:1211.
     
134. Salim R, Nachum Z, Moscovici R, et al: Continuous compared with intermittent epidural infusion on progress of labor and patient satisfaction. Obstet Gynecol 2005;106:301–306.
     
135. Burgess F, Anderson D, Colonna D, et al: Thoracic epidural analgesia with bupivacaine and fentanyl for postoperative thoracotomy pain. J Cardiothorac Vasc Anesth 1994;8:420–424.
     
136. Bernards C: Epidural and spinal anesthesia. In Barash PG (ed): Clinical Anesthesia. Lippincott Williams & Wilkins, 201, pp 689–712.
     
137. Wilson W, Benumof J: Anesthesia for thoracic surgery, In Miller RD (ed): Miller’s Anesthesia, 6th ed. Elsevier, 2005, pp 1907– 908.
     
138. Lui S, Carpenter R, Neal J: Epidural anesthesia and analgesia: Their role in postoperative outcome. Anesthesiology 1995;82:1474–1506.
     
139. Block A, Covino B: Effect of local anesthetic agents on cardiac conduction and contractility. Reg Anesth 1982;6:55.
     
140. Seeberger M, Lang M, Drewe J, et al: Comparison of spinal and epidural anesthesia in patients younger than 50 years of age. Anesth Analg 1994;78:667.
     
141. Rutter S, Shields F, Broadbent C, et al: Management of accidental dural puncture in labor with intrathecal catheters: An analysis of 10 years experience. Int J Obstet Anesth 2001;10:177–181.
     
142. Denny N, Masters R, Pearson D: Postdural puncture headache after continuous spinal anesthesia. Anesth Analg 1987;66:791.
     
143. Brownridge P: The management of headache following accidental dural puncture in obstetric patients. Anaesthesiol Intensive Care 1983;11:9.
     
144. Lybecker H, Djernes M, Schmidt J: Postdural puncture headache: Onset, duration, severity, and associated symptoms. Acta Anaesthesiol Scand 1995;39:605–612.
     
145. Oedit R, van Kooten F, Bakker S, et al: Efficacy of the epidural blood patch for the treatment of post lumbar puncture headaches: A randomized, observer-blind, controlled clinical trial. BMC Neurol 2005;5:12.
     
146. Vilming S, Kloster R, Sandvik L: When should an epidural blood patch be performed in postlumbar puncture headache? A theoretical approach based on a cohort of 79 patients. Cephalagia 2005;25:523–527.
     
147. Angle P, Tang S, Thompson D, et al: Expectant management of postdural puncture headache increases hospital length of stay and emergency room visits. Can J Anaesth 2005;52:397–402.
     
148. Collis R, Harries S: A subdural abscess and infected blood patch complicating regional anesthesia for labour. Int J Obstet Anesth 2005;14:246–251.
     
149. Lubenow T, Keh-Wong E, Kristof K, et al: Inadvertent subdural injection: A complication of epidural block. Anesth Analg 1988;67:175.
     
150. Berga S, Trierweiler M: Bacterial meningitis following epidural anesthesia for vaginal delivery: A case report. Obstet Gynecol 1989;74:437–439.
     
151. Ugeskr L: Infections in connection with epidural catheterization. Ugeskr Laeger 1996;158:4403–4405.
     
152. Rice J, Wee M, Thomson K: Obstetric epidurals and chronic adhesive arachnoiditis. Br J Anaesth 2004;92:109–120.
     
153. Ross J, Masaryk T, Modic M, et. al: MR imaging of lumbar arachnoiditis. Am J Roentgenol 1987;149:1025.
     
154. Macarthur A, Macarthr C, Weeks S: Epidural anaesthesia and low back pain after delivery: A prospective cohort study. BMJ 1995;11:1336–1139.
     
155. Kane R: Neurologic deficits following epidural or spinal anesthesia. Anesth Analg 1981;60:150–161.
     
156. Kao M, Tsai S, Tsou M, et al: Paraplegia after delayed detection of inadvertent spinal cord injury during thoracic epidural catheterization in an elderly patient. Anesth Analg 2004;99:580–583.
     
157. Aldrete J, Ferrari H: Myelopathy with syringomyelia following thoracic epidural anesthesia. Anesth Intensive Care 2004;32:5967.
     
158. Lee B: Neuraxial complications after epidural and spinal anaesthesia. Acta Anaesthesiol Scand 2003;47:371–373.
     
159. Odom J, Sih I: Epidural analgesia and anticoagulant therapy: Experience with one thousand cases of continuous epidurals. Anesth Analg 1983;1980:72.
     
160. Hyderally H: Epidural hematoma unrelated to combined spinal epidural anesthesia in a patient with ankylosing spondylitis receiving aspirin after a total hip replacement. Anesth Analg 2005;100:882–883.
     
161. Torres A, Acebes J, Cabiol J, et al: Spinal epidural hematomas. Prognostic factors in a series of 22 cases and a proposal for management. Neurocirugia (Astur) 2004;15:353–359.
     
162. Izci Y: Lumbosacral spinal epidural abscess caused by Brucella melitensis. Acta Neurochir J 2005;147:1207–1209.
     
163. Curry W, Hoh B, Amin-Hanjani S, et al: Spinal epidural abscess: Clinical presentation, management, and outcome. Surg Neurol 2005;63:364–371.
     
164. Brookman C, Rutledge M: Epidural abscess: Case report and literature review. Reg Anesth Pain Med 2000;25:428.
     
165. Volk T, Hebecker R, Ruecker G, et al: Subdural empyema combined with paraspinal abscess after epidural catheter insertion. Anesth Analg 2005;100:1222–1223.
     
166. Johnkura K, Joki H, Johmura Y, et al: Combination of infarctions in the posterior inferior cerebellar artery and anterior spinal artery territories. J Neurol Sci 2003;15:1–4.
     
167. Doita M, Marui T, Nishida K: Anterior spinal artery syndrome after total spondylectomy of T10, T11, and T12. Clin Orthop Rel Res 2002;405:175–181.
     
168. de la Barrera S, Barca-Buyo A, Montoto-Marques A, et al: Spinal cord infarction: Prognosis and recovery in a series of 36 patients. Spinal Cord 2001;39:520–525.

Back to top