Chapter 69. Neurologic Complications of Peripheral Nerve Blocks: Mechanisms & Management

Basic Considerations: Introduction

Although there are relatively few published reports of anesthesia-related nerve injury associated with peripheral nerve blocks (PNBs), it is likely that the commonly cited incidence (0.4%) of neurologic injury is underestimated owing to underreporting.1–3 Most complications of PNBs were reported with upper extremity blocks. The less frequent clinical application of lower extremity nerve blocks may be the main reason why there are even fewer reports of anesthesia-related nerve injury associated with lower extremity PNBs compared with upper extremity PNBs.4 Although neurologic complications after PNBs can be related to factors associated with the block technique (eg, needle trauma, intraneuronal injection, neuronal ischemia, and toxicity of local anesthetics), a search for other common causes should include positional and surgical factors (eg, positioning, stretching, retractor injury, ischemia, and hematoma formation). In some instances, the neurologic injury may be a result of a combination of these factors.

In all four sections of this chapter, mechanisms and consequences of acute neurologic injury related to the nerve block procedure are discussed and, where appropriate, methods and techniques to reduce the risk of complications are suggested. Specific nerve injuries with upper and lower nerve block techniques, neuraxial anesthesia, and local anesthetic toxicity are discussed elsewhere in this volume.

Functional Histology of the Peripheral Nerves

Knowledge of the functional histology of the peripheral nerve is important to understand the mechanisms of peripheral nerve injury; the reader is referred to Chapters 3 and 4 for more in-depth discussion on this subject. Here we briefly review salient features of the organization of the peripheral nerves. A peripheral nerve is a complex structure consisting of fascicles held together by the epineurium, an enveloping, external connective sheath (Figure 69–1). Each fascicle contains many nerve fibers and capillary blood vessels embedded in a loose connective tissue, the endoneurium.5 The perineurium is a multilayered epithelial sheath that surrounds individual fascicles and consists of several layers of perineural cells. Therefore, in essence, a fascicle is a group of nerve fibers or a bundle of nerves surrounded by perineurium. Of note, fascicles can be organized in one of three common arrangements: monofascicular (single, large fascicle); oligofascicular (few fascicles of various sizes); and polyfascicular (many fascicles of various sizes).6

Nerve fibers can be myelinated or unmyelinated; sensory and motor nerves contain both in a ratio of 4:1, respectively. Unmyelinated fibers are composed of several axons, wrapped by a single Schwann cell. The axons of myelinated nerve fibers are enveloped individually by a single Schwann cell. A thin layer of collagen fibers, the endoneurium, surrounds the individually myelinated or groups of unmyelinated fibers.

Nerve fibers depend on a specific endoneurial environment for their function. Peripheral nerves are richly supplied by an extensive vascular network in which the endoneurial capillaries have endothelial “tight junctions,” a peripheral analogy to the blood–brain barrier. The neurovascular bed is regulated by the sympathetic nervous system, and its blood flow can be as high as 30–40 mL/100 g per minute.7 In addition to conducting nerve impulses, nerve fibers also maintain axonal transport of various functionally important substances such as proteins and precursors for receptors and transmitters. This process is highly dependent on oxidative metabolism. Any of these structures and functions can be deranged during a traumatic nerve injury, with the possible result of temporary or permanent impairment or loss of neural function.

The size and number of the fascicles in a peripheral nerve substantially vary from one peripheral nerve to another. In general, the larger the nerve, the greater the number and size of the fascicles. In addition, the larger the fascicle, the greater is the risk of intraneural injection because large fascicles can accommodate the tip of the needle.8 Of note, the fascicular bundles are not continuous throughout the peripheral nerve. They divide and anastomose with one another as frequently as every few millimeters.8 However, the axons within a small set of adjacent bundles redistribute themselves so that they remain in approximately the same quadrant of the nerve for several centimeters. This arrangement is of practical concern to the surgeons trying to repair a severed nerve. If the cut is clean, it may be possible to suture individual fascicular bundles together. In such a scenario, there is a good probability that the distal segment of nerves will be sutured to the central stump of motor axons and sensory axons. In such cases, good functional recovery is possible. If a short segment of the nerve is missing, however, the fascicles in the various quadrants of the stump may no longer correspond with one another, good axial alignment may not be possible, and functional recovery is greatly compromised or improbable.8 This arrangement of the peripheral nerve helps explain why intraneural injections result in more serious consequences as opposed to clean needle nerve cuts, which tend to heal much more readily.

Mechanisms of Peripheral Nerve Injury

The cause of peripheral nerve injury related to the use of PNBs falls into one of four categories (Table 69–1). Laceration results when the nerve is cut partially or completely, such as by a scalpel or a large-gauge cutting needle. Stretch injuries to the nerves may result when nerves or plexuses are stretched in a nonphysiologic or exaggerated physiologic position, such as during shoulder manipulation under an interscalene block. Pressure, as a mechanism of nerve injury, is relatively common. A typical example of this mechanism is chronic compression of the nerves by neighboring structures, such as fibrous bands, scar tissue, or abnormal muscles that pass through fibro-osseous spaces if the space is too small, such as the carpal tunnel. Such chronic compression syndromes are called entrapment neuropathies. Examples of pressure injuries applicable to PNBs include external pressure over a period of hours (eg, a Saturday night palsy, resulting from pressure of a chair back on the radial nerve of the insensate arm). The pressure may be repeated and have a cumulative effect (eg, an ulnar neuropathy resulting from habitually leaning on the elbow). Such a scenario is conceivable, for instance, in a patient who positions the anesthetized arm (eg, long-acting or continuous brachial plexus block) in a nonphysiologic position for a few hours. Another example of pressure-related nerve injury is prolonged use of a high-pressure tourniquet. An intraneural injection may lead to sustained high intraneural pressure, which exceeds capillary occlusion pressure, and leads to nerve ischemia.10 Finally, a forceful injection into a low-compliant connective tissue plane (space) containing a peripheral nerve may lead to nerve ischemia and neurologic dysfunction. Vascular nerve damage after nerve blocks can occur when there is acute occlusion of the arteries from which the vasa nervorum are derived or from a hemorrhage within a nerve sheath. With injection injuries, the nerve may be directly impaled and the drug injected directly into the nerve, or the drug may be injected into adjacent tissues, causing an acute inflammatory reaction or chronic fibrosis—both indirectly involving the nerve. Chemical nerve injury is the result of tissue toxicity of injected solutions (eg, local anesthetic toxicity, neurolysis with alcohol or phenol).

Clinical Classification of Acute Nerve Injuries

Classification of acute nerve injuries is useful when considering the physical and functional state of damaged nerves. In his classification, Seddon11 introduced the terms neurapraxia, axonotmesis, and neurotmesis (Table 69–2); Sunderland12 subsequently proposed a five-grade classification system.

Neuropraxia refers to nerve dysfunction lasting several hours to 6 months after a blunt injury to the nerve. In neuropraxia, the nerve axons and connective tissue structures remain intact. The nerve dysfunction probably results from several factors, of which focal demyelination is the most important abnormality. Intraneural hemorrhage, pressure ischemia changes in the vasa nervorum, disruption of the blood–nerve barrier and axon membranes, and electrolyte disturbances all may add to the impairment of nerve function. Because the nerve dysfunction is rarely complete, clinical deficits are partial and recovery usually occurs within a few weeks, although some neurapraxic lesions (with minimal or no axonal degeneration) may take several months to recover.

Axonotmesis consists of physical interruption of the axons but within intact Schwann cell tubes and intact connective tissue structures of the nerve (ie, the endoneurium, perineurium, and epineurium). Sunderland12 subdivided this group, depending on which of the three structures were involved (see Table 69–2). With axonotmesis, the nerve sheath remains intact, enabling regenerating nerve fibers to find their way into the distal segment. Consequently, efficient axonal regeneration can eventually take place.

Neurotmesis refers to a complete interruption of the entire nerve including the axons and all connective tissue structures (epineurium included). Clinically, there is total nerve dysfunction. With both axonotmesis and neurotmesis, axonal disruption leads to wallerian degeneration, from which recovery occurs through the slow process of axonal regeneration. However, with neurotmesis, the two nerve ends may be completely separated, and the regenerating axons may not be able to find the distal stump. For these reasons, effective recovery does not occur unless the severed ends are sutured or joined by a nerve graft. With closed injuries, the only way to distinguish clearly between axonotmesis and neurotmesis is by surgical exploration and intraoperative inspection of the nerve.

Note that most acute nerve injuries are mixed lesions.11 Different fascicles and nerve fibers typically sustain different degrees of injury, which may make it difficult to assess the type of injury and predict outcome even by electrophysiologic means. Recovery from a mixed lesion is characteristically biphasic; it is relatively rapid for fibers with neurapraxic damage, but much slower for axons that have been physically interrupted and have undergone wallerian degeneration.

Mechanical Nerve Injury

Intraneural Injection and Its Prevention

Rather than a relatively clear injury caused by sharp needle cuts, intraneural injection has the potential to create structural damage to the fascicle(s) that is more extensive and less likely to heal (Figure 69–2). Indeed, the devastating sequelae of sensory and motor loss after injection of various agents into peripheral nerves has been well documented.13 Nearly all experimental studies on this subject have demonstrated that the site of injection is critical in determining the degree and nature of injury. More specifically, to induce neurologic injury, the injectate must be injected intrafascicularly; extrafascicular injections of the same substance typically do not cause nerve injury.14 Thus, the main factor leading to a substantial peripheral nerve damage associated with injection techniques is injection of local anesthetic into a fascicle. This causes mechanical destruction of the fascicular architecture and sets into motion a cascade of pathophysiologic changes, including inflammation, cellular infiltration, axonal degeneration, and others—all possibly leading to nerve scarring and permanent neurologic impairement.

Histologic features of injury after intraneural injection are rather nonspecific and range from simple mechanical disruption and delamination to fragmentation of the myelin sheath and marked cellular infiltration (Figure 69–3). Using a variety of animal models of nerve injury, a vast array of cellular changes following peripheral nerve trauma have been documented.14 The extent of actual neurologic damage after an intrafascicular injection can range from neuropraxia with minimal structural damage to neurotmesis with severe axonal and myelin degeneration, depending on the needle–nerve relationship, the agent injected, and the dose of the drug used.15–19 In general, subperineural changes tend to be more prominent compared with the central area of the fascicle.20 In addition, injury to primary sensory neurons that is not detectable histologically causes a shift in membrane channel expression, sensitivity to algogenic substances, neuropeptide production, and intracellular signal transduction both at the injury site and in the cell body in the dorsal root ganglion. This leads to increased excitability and acute or chronic pain often experienced by patients with neurologic injury. It should be noted that intraneural injection and its resultant mechanical injury are merely the inciting mechanisms; a host of additional changes occur involving inflammatory reactions, chemical neuritis, and intraneural hemorrhage, all of which eventually may combine and lead to nerve scarring and chronic neuropathic pain.

Pain on Injection

Little is known about how to avoid an intraneural injection. Pain with injection has long been thought of as the cardinal sign of intraneural injection; consequently, it is commonly suggested that blocks be avoided in heavily premedicated or anesthetized patients. However, numerous case reports have suggested that pain may not be reliable as a sole warning sign of impending nerve injury, and it may present in only a minority of cases.21–25 Fanelli and colleagues3 have reported unintended paresthesia in 14% of patients in their study; however, univariate analysis of potential risk factors for postoperative neurologic dysfunction failed to demonstrate paresthesia as a risk factor. In addition, the sensory nature of the pain-paresthesia can be difficult to interpret in clinical practice.26 For instance, a certain degree of discomfort on injection (“pressure paresthesia”) is considered normal and affirmative of impending successful blockade because this symptom is thought to indicate that injection of local anesthetic has been made in the vicinity of the targeted nerve.26 In clinical practice, however, it can be difficult to discern when pain-paresthesia on injection is normal and when it is the ominous sign of an intraneural injection.27 Moreover, it is unclear how pain or paresthesia on injection, even when present, can be used clinically to prevent development of neurologic injury. For instance, in a prospective study on neurologic complications of regional anesthesia by Auroy and colleagues,2 neurologic injuries after paresthesia ensued, although the participating anesthesiologists stopped the injection when pain on injection was reported by the patients.

Intensity of the Stimulating Current

The optimal current intensity resulting in accurate localization of a nerve has been a topic of controversy.28–31 For instance, stimulation at currents higher than 0.5 mA may result in block failure because the needle tip is positioned outside the fascial sheath that envelopes a nerve, whereas stimulation at currents lower than 0.2 mA theoretically pose a risk of intraneural injection.32 Other authors suggest that a motor response with a current intensity between 1.0 and 0.5 mA is sufficient for accurate placement of the block needle28; still others advise using a current of much lower intensity (0.5–0.1 mA).29,31 Others simply suggest stimulating with currents less than 0.75 mA,33,34 or progressively reducing the current to as low a level as possible while still maintaining a motor response.30

Many recently published reports on nerve blocks have suggested obtaining nerve stimulation with currents of 0.2–0.5 mA (100 msec) before injecting local anesthetics, believing that motor response with current intensities lower than 0.2 mA may be associated with intraneural needle placement. However logical these beliefs may sound, no published clinical reports substantiate these concerns.

In current clinical practice, development of nerve localization and injection monitoring techniques to reliably prevent intraneural injection remains elusive.22 Nerve stimulators are very useful for nerve localization; however, the needle–nerve relationship cannot be precisely and reliably ascertained adequately, as early literature suggests.28 Response to nerve stimulation with a commonly used current intensity (1 mA) may be absent even when the needle makes physical contact with or is inserted into a nerve35–37 (Figure 69–4). Occurrence of nerve injuries despite using nerve stimulation to localize nerves further suggests that nerve stimulators can at best provide only a rough approximation of the needle–nerve relationship.1 A fundamental problem with the nerve stimulation is that the current flows in all directions, following the path of least resistance and not necessarily only toward the nerve. Miniscule changes at the needle tip–tissue interface can make a substantial difference in the preferential flow of current away from the nerve. This may result in cessation of the motor response even when the needle is in intimate relation with the nerve or when it is placed intraneurally. The current interest for ultrasound-assisted nerve localization holds promise for facilitating nerve localization and administration of nerve blocks. However, the image resolution of this technology is insufficient to visualize nerve fascicles and prevent intrafascicular injection.

Resistance to Injection

Assessing resistance to injection is a common practice, similar to loss of resistance to injection of air or saline using a “syringe feel” during administration of epidural, paravertebral, or lumbar plexus blocks. Similarly, assessing tissue resistance and injection compliance constitute another means of estimating the anatomic location of the needle tip during the practice of PNBs. For this, clinicians use a syringe feel to estimate what may be an abnormal resistance to nerve block injection and thus reduce the risk of intraneural injection.10,31,38 However, this practice has significant inherent limitations.39 For instance, the resistance to injection is greater with smaller needles, introducing additional confusion as to what constitutes normal or abnormal resistance. Second, rather than loss of resistance in an epidural injection, there is no baseline pressure information or change in tissue compliance during nerve block injection. In other words, with nerve block injection there is no change in pressure that can be relied on. For instance, in a study by Claudio and colleagues,39 all anesthesiologists detected a change in pressure of as little as 0.5 psi during a simulated nerve block injection. However, when gauging the absolute pressure, clinicians substantially varied (by as much as 40 psi) in their perception of what constituted an abnormal resistance to injection. Finally, no information has been available on what constitutes normal or abnormal injection pressure during nerve block injection. For these reasons, subjective estimation of resistance to injection is at least as inaccurate as perhaps estimating blood pressure by palpating radial artery pulse; objective means of assessing resistance to injection should be far superior in standardizing injection force and pressure.

To explain the mechanisms responsible for development of neuraxial anesthesia after an interscalene block,40,41 Selander and Sjostrand42 injected solutions of local anesthetic into rabbit sciatic nerves and traced the spread of the anesthetic along the nerve sheet. They postulated that an intraneural injection results in significant intraneural spread of local anesthetic. In their model, these investigators incidentally noticed that intraneural injections often resulted in higher pressures (up to 9 psi) than those required for perineural injections (<4 psi). Injection into a nerve fascicle resulted in rupture of the perineurium and histologic evidence of disruption of the fascicular anatomy. This study, however, used a small animal model, microinjections (10–200 μL), miniature needles, and clinically irrelevant injection rates (100–300 μL/min) and did not study neurologic consequences after intraneural injections. Perhaps for these reasons their results foretelling the possible association of injection pressure with intrafascicular injection did not change the clinical practice.

More recent studies, however, have used clinically more applicable injection speeds and volumes of local anesthetic in a canine model of nerve injury.4 The results of these studies suggest that intrafascicular injection is associated with high injection pressures (>20 psi) and carry a risk of neurologic injury20 (Figures 69–5 and 69–6). Only intraneural injections resulting in pressures greater than 20 psi have been associated with clinically detectable neurologic deficits (Figure 69–7) as well as histologic evidence of injury to nerve fascicles.

The current evidence suggests that neurologic injury does not always develop after an intraneural injection.37 In fact, injection after an intraneural needle placement is more likely to result in deposition of the local anesthetic between and not into the fascicles.20 Intraneural, but extrafascicular (interfascicular) injection probably occurs more commonly than is thought in clinical practice.37 Such an injection results in a block of unusually fast onset and long duration rather than in neurologic injury. This is because an intraneural but extrafascicular injection leads to intimate exposure of nerve fascicles to high concentration and doses of local anesthetics. However, permanent neurologic injury does not develop because the local anesthetic is deposited outside the fascicles and the blocks slowly resolve after the injection without evidence of histologic derangement.

Needle Design and Direct Needle Trauma

Needle tip design and risk of neurologic injury have been matters of considerable debate for more than three decades. Nearly 30 years ago, Selander and colleagues43 suggested that the risk of perforating a nerve fascicle was significantly lower when a short-bevel (eg, angle of 45 degrees) needle was used as opposed to a long-bevel (angle of 12–15 degrees) needle. The results of their work are largely responsible for the currently prevalent trend of using short-bevel needles (ie, angles 30–45 degrees) for most major peripheral nerve conduction blocks. However, the more recent work of Rice and McMahon44 suggested that when placed intraneurally, short-bevel needles cause more mechanical damage than the long-bevel needles.44 In their experiment in a rat model, deliberate penetration of the largest fascicle of the sciatic nerve with short-bevel needles resulted in the greatest degree of neural trauma. Their work suggests that sharp needles produce clean, more-likely-to-heal cuts, whereas blunt needles produce irregular and more extensive damage on the microscopic images. In addition, the cuts produced by the sharper needles were more likely to recover faster and more completely than were the irregular, more traumatic injuries caused by the blunter, short-bevel needles.44

Although the data on needle design and nerve injury have not been clinically substantiated, the theoretical advantage of short-bevel needles in reducing the risk of nerve penetration has influenced both practitioners and needle manufacturers. Consequently, whenever practical, most clinicians today prefer to use short-bevel needles for major conduction blocks of the peripheral nerves and plexuses. Sharp-beveled, small-gauge needles, however, continue to be used routinely for many nerve block procedures, such as axillary transarterial brachial plexus block, wrist and ankle blocks, cutaneous nerve block, and others.

Regardless of the considerations related to the needle design and risk of nerve injury, the actual clinical significance of isolated, direct needle trauma remains unclear. For instance, it is possible that both paresthesia and nerve stimulation techniques of nerve localization often result in unrecognized intraneural needle placement; yet the risk of neurologic injury remains relatively low. Similarly, during femoral arterial cannulation (arterial line insertion), it is likely that the needle is often inadvertently inserted into the femoral nerve; yet injuries to the femoral nerve are rare, and when they occur, they are usually attributed to hematoma formation rather than needle injury.45 It is possible that a needle-related trauma without accompanying intraneural injection results in injury of a relatively minor magnitude, which readily heals and may go clinically undetected. In contrast, needle trauma combined with injection of local anesthetic into the nerve fascicles carries a risk of much more severe injury.20

Chemical Causes of Peripheral Nerve Injury

Toxicity of Injected Solution

Nerves can be injured by direct contact with a needle, injection of a drug into or around the nerve, pressure from a hematoma, or scarring around the nerve.9,46–48 The degree of nerve damage after an injection depends on the exact site of the injection and the type and quantity of the drug used.15 The most severe damage is produced by intrafascicular injections, although extrafascicular (subepineurial) injections of some particularly toxic drugs can also produce nerve damage.16,17 Benzylpenicillin, diazepam, and paraldehyde are the most damaging; however, a number of other medications, such as antibiotics, analgesics, sedatives, and antiemetic medications, are also capable of damaging peripheral nerves when injected experimentally or accidentally.15

Local anesthetics produce a variety of cytotoxic effects in cell cultures, including inhibition of cell growth, motility, and survival, as well as morphologic changes. The extent of these effects is proportionate to the length of time the cells are exposed to the local anesthetic solution and occur using local anesthetic at normal clinical concentrations. Within normal ranges, the cytotoxic changes are greater as concentrations increase.

In the clinical setting, the exact site of local anesthetic deposition plays a critical role in determining the pathogenic potential.49 After applying local anesthetics outside a fascicle, the regulatory function of the perineural and endothelial blood–nerve barrier is only minimally compromised. High concentrations of extrafascicular anesthetics may produce axonal injury independent of edema formation and elevated endoneurial fluid pressure.50 As with the effects of local anesthetics in cell cultures, the duration of exposure and the concentration of local anesthetic determine the degree and incidence of local anesthetic—induced residual paralysis. Neurotoxicity of local anesthetics are dealt with in greater detail elsewhere in this chapter.

Neurologic complications after regional anesthesia may also be caused by the direct effects of local anesthetics on the nervous tissue. Toxicity has been reported primarily with the intrathecal use of local anesthetics. However, with the increasing popularity of PNB anesthesia, reports are surfacing about the direct toxic effects of local anesthetics on peripheral nerves.2 Several theories regarding the mechanism of injury have been suggested. Prolonged exposure, high doses, high concentrations, body positioning, and the specific agent used may cause transient or permanent neurologic injury by a number of intracellular mechanisms. Once the neurologic injury has occurred, it has been suggested that additives such as epinephrine or a preexisting neurologic condition may predispose the patient to the neurotoxic effects of local anesthetics (the “double-crush” concept).

Experimental models of neurotoxicity of local anesthetics have included application of local anesthetic to the sciatic nerve in animals, desheathed nerve preparations, and dorsal root ganglion cells in culture using concentration of local anesthetic comparable to those used clinically.51 These studies have revealed considerable information about the mechanism of injury. Sakura and colleagues52 discovered that the mechanism did not involve voltage-dependent sodium channels. They substituted tetrodotoxin for lidocaine and found that tetrodotoxin blocked these channels as effectively as lidocaine without producing the toxicity associated with lidocaine. Johnson and colleagues53 discovered that cell toxicity may be related to mitochondrial degradation. Local anesthetics caused the mitochondria to depolarize and stop producing adenosine triphosphate (ATP). With the loss of ATP, energy-dependent mechanisms are compromised, leading to the accumulation of calcium intracellularly and activation of enzymes that cause cell degradation. This was unrelated to hypoxia, because lidocaine actually reduced oxygen demand.51 Cell death or apoptosis was related to the concentration and/or the length of exposure. Exposure to 1% lidocaine for more than 90 minutes was required to kill 50% of the cells. Exposures of less than 1 hour were reversible, but exposure to lidocaine at 5% concentration caused rapid cell death or necrosis.51

In addition to electrolyte imbalance (leading to cell death), loss of ATP has been found to cause failure of axonal transport, compromising the ability of the neuron to transport materials synthesized in the perikaryon to the axon terminal.54 Fast axonal transport moves neurotransmitters from the cell body to the nerve terminal. Lidocaine has been shown to produce a reversible blockade of rapid axonal transport. Recovery is dependent on the concentration and the exposure time of the local anesthetic on the nerve tissue. High concentrations and/or prolonged exposure has been postulated to cause prolonged or permanent nerve injury.55 Furthermore, the loss of ATP leads to the failure of the sequestration of neurotransmitters within the cells, leading to an increase in the extracellular concentration of glutamate. Excessive glutamate in the extracellular space through NMDA (N-methyl-d-aspartate) receptors can exacerbate the elevation of calcium within the cells, ultimately leading to further cell degradation.56 This effect is noted only in the central neuraxis, where glutamate is found.

Local anesthetics have been shown to cause membrane solubilization at high concentrations. At clinical concentrations, they can form micelles that may act as detergents to disrupt the cell membrane.57–60 Oda and colleagues61 demonstrated that 5% lidocaine and 0.5% dibucaine were minimum concentrations causing irreversible neurologic damage. No neurologic damage was seen with 2% lidocaine or 0.2% dibucaine.

Neurotoxicity varies with the local anesthetic solution. In histopathologic, electrophysiologic, and neuronal cell models, lidocaine and tetracaine have been shown to have a greater potential for neurotoxicity than bupivacaine.62 Additives, that is, epinephrine, can increase the toxicity of both lidocaine and bupivacaine.63 A preexisting neurologic condition, such as peripheral neuropathy, injury, or surgery, may predispose the patient to nerve injury from toxicity at clinical doses (ie, the double-crush concept).64

In summary, local anesthetics have potentially cytotoxic effects. The mechanisms appear to involve disruption of mitochondrial function, electrolyte imbalance leading to detrimental intracellular calcium accumulation, loss of axonal transport, and release of glutamate. The toxicity and ultimate damage to nerve tissue are related to concentration of the agent, site of action, time of exposure, and the specific local anesthetic agent used. Most studies have demonstrated a greater effect on intrathecal use compared with epidural or peripheral nerve exposure. This may reflect the typically higher baricity, more concentrated dose of local anesthetic bathing the spinal cord for a prolonged period of time compared with a large volume, less concentrated solution typically used in epidural, and peripheral nerve blocks.

Vascular Mechanisms Causing Nerve Injury

Neural Ischemia

Lack of blood flow to the primary afferent neuron results in metabolic stress. The earliest response of the peripheral sensory neuron to ischemia is depolarization and generation of spontaneous activity, symptomatically perceived as paresthesias. This is followed by blockade of slow-conducting myelinated fibers and eventually all neurons, possibly through accumulation of excess intracellular calcium, which accounts for the loss of sensation with initiation of limb ischemia. Nerve function returns within 6 hours if ischemic times are less than 2 hours. Ischemic periods of up to 6 hours may not produce permanent structural changes in nerves. However, detailed pathologic examination after ischemia initially shows minimal changes, but with 3 hours or more of reperfusion, edema and fiber degeneration develop and last 1–2 weeks, followed by a phase of regeneration that will last 6 weeks. In addition to neuronal damage, oxidative injury associated with ischemia and reperfusion also affects the Schwann cells, initiating apoptosis.

The perineurium is a tough and resistant tissue layer. An injection into this compartment or a fascicle can cause a prolonged increase in endoneurial pressure exceeding the capillary perfusion pressure. This pressure, in turn, can result in endoneurial ischemia.10,42 The addition of vasoconstricting agents theoretically can enhance ischemia because of the resultant vasoconstriction and reduction in blood flow. The addition of epinephrine has been shown in vitro to decrease the blood supply to intact nerves in the rabbit.65 However, in patients undergoing lower extremity surgery, addition of epinephrine to the local anesthetic solution used in combined femoral and sciatic nerve blocks has not been shown to be a risk factor for developing post-block nerve dysfunction.3

Pressure Mechanisms Causing Nerve Injury

Tourniquet Neuropathy

Tourniquet-induced neuropathy is well documented in the orthopedic literature and ranges from mild neuropraxia to permanent neurologic injury.66–69 The incidence of tourniquet paralysis has been reported as 1 in 8000 operations.70 A prospective study of lower extremity nerve blockade suggests that higher tourniquet inflation pressure (>400 mm Hg) was associated with an increased risk of transient nerve injury.3 Current recommendations for appropriate use of the tourniquet include the maintenance of a pressure of no more than 150 mm Hg greater than the systolic blood pressure and deflation of the tourniquet every 90–120 minutes.69 Even with these recommendations, post-tourniquet-application neuropraxia may occur, particularly in the setting of preexisting neuropathy.71,72

Compressive Hematoma

Little data exist regarding the safety of PNB in patients treated with anticoagulants. Compressive hematoma formation leading to neuropathy has been associated with needle misadventures when performing lower extremity PNB, particularly with concomitant treatment with anticoagulants.73,74 However, in contrast to spinal or epidural hematoma, peripheral neuropathy from compressive hematoma typically resolves completely.75–78 Regardless, these reports emphasize the important differences in the risk-benefit ratio of PNBs compared with neuraxial blocks in patients receiving anticoagulant therapy.

Peripheral Nerve Blocks in Anesthetized Patients: Introduction

Regional anesthesia-associated nerve injury is a significant source of concern for patients, surgeons, and anesthesiologists alike. In addition, nerve injury is a potential medicolegal liability for anesthesiologists.79 PNBs, in particular, are of significant concern because the typical technique involves placing the needle tip in the immediate vicinity of the nerve or plexus. Consequently, any postoperative neurologic impairment is automatically, and often unjustly, attributed to the PNB procedure.

Few issues in regional anesthesia have been the subject of such intense controversy as whether PNBs carry a higher risk of neurologic complications when performed in anesthetized patients compared with awake patients. Opinions vary from heavy premedication being essential to the success of regional anesthesia to its being equated with negligence. Unfortunately, no large-scale controlled studies of the safety of PNBs in awake versus anesthetized patients exists, nor are such studies likely to be available in the future. Without randomized, controlled studies, experts are left to draw conclusions and make logical recommendations solely on their interpretation of the few available case reports and anecdotal experiences. However, any such recommendations regarding the use of sedation or general anesthesia in patients receiving PNBs could have significant medicolegal repercussions. Therefore, the multifaceted purpose of this text is to review the available literature that supports or refutes the practice of administering nerve blocks in anesthetized patients, to discuss the current controversies, and to provide insight into the future of the subspecialty with regard to this issue. Specific concerns regarding performance of PNBs in anesthetized patients are presented and addressed. Although the scientific value of case reports is often discounted, such reports may actually be more informative than large epidemiologic studies because they include a detailed account of peri-block events, which is often lacking in epidemiologic studies.

Symptoms of Intraneural Injection

The premise behind the common recommendation that a PNB should be performed only in awake patients is that an awake patient can provide information that can prevent intraneural injection and therefore avoid neurologic injury. This is because it is believed that intraneural injections are excruciatingly painful and an awake protesting patient is the best available monitor. However, there are three significant problems with this logic.

First, the literature does not support the widespread notion that relying on a fully awake patient's report of pain on injection is a reliable method to prevent nerve injury. In fact, most neurologic complications reported in the literature have not been associated with pain on injection.1–3,23–25,27,79–85 For instance, of 49 cases of nerve injury found in the literature search (Table 69–3), 48 patients (98%) were awake. Of these, 42 cases included specific information about the patient's response to the injection; only 4 (10%) patients reported pain on injection. Some reports specifically state that the patient did not have pain, whereas in most others the authors commented that the block performance was uneventful. Note that the pain on administration of local anesthetic into nerve tissue may be absent even in the central neuraxial area. For instance, Kao et al.86 reported a case of neural injury that was clearly related to spinal cord trauma from a thoracic catheter that had been inserted while the patient was anesthetized; the patient did not have pain during administration of local anesthetic postoperatively. More recently, Tripathi et al.87 reported a case report of paraplegia after an intracordal injection during attempted steroid injection, whereas Tsui and Armstrong88 reported a case of direct spinal cord injury after epidural injection. Both complications occurred in awake patients, who did not report pain on needle placement and consequent injection. These reports clearly indicate that reliance on pain as a symptom of injection into neurologic tissue is unreliable.

The second problem refers to the value of the pain (if present) as a monitor in preventing nerve injury. For instance, in patients in whom the pain does accompany an intraneural injection, it may already be too late to prevent neurologic injury. For example, in the ASA closed-claims study, Cheney and coworkers79 indicate that on those occasions when pain did occur during injection, the anesthesiologist stopped the injection. However, the patients still went on to develop nerve injury. Similarly, studies using animal models of intraneural injection suggest that nerve fascicles become injured at the very onset of the injection and with injection of a very small volume of local anesthetic (as little as 0.5–1 mL).20,42 Thereafter, as injection continues, the fascicle ruptures and the injectate escapes through the ruptured perineurium into the epineurial sheath. At this stage, however, the damage to the fascicle(s) may already have been done.

Third, pain is notoriously difficult to assess in terms of quality and intensity. Therefore, distinguishing between the discomfort that is commonly seen during local anesthetic injection (which is considered normal) and that of intraneural injection can be difficult. As an example, in the study by Borgeat et al.,81 21% of patients undergoing interscalene block reported transient, burning pain, but none of these patients went on to develop neurologic complication.

Normal versus Abnormal Discomfort/Pain on Injection

Injection of local anesthetic in close proximity to the nerves is often associated with discomfort.26,81 This is thought to result from mechanical irritation of the nerves or plexi as local anesthetic is injected in the immediate vicinity. Based on his studies of brachial plexus anesthesia, Winnie26 coined the term “pressure paresthesia” to describe the discomfort patients feel during local anesthetic injection and implied that this was a desirable sign of impending successful blockade. In actual clinical practice, however, the variability of patients' pain thresholds, their ability to verbalize a sensation pain during a procedure, and an anesthesiologist's subjective interpretation of any such response make it very difficult to recommend where a “line” could be drawn between normal and abnormal pain or paresthesia on injection. In fact, a number of published case reports demonstrate that patients' complaints of pain during PNB may not be helpful in preventing the development of the neurologic complication. For instance, Barutell et al.27published a report in which a patient communicated discomfort on injection that was perceived as “normal pressure paresthesia” by the anesthesia team. When the injection was carried out, the patient went on to develop permanent neurologic damage. Similarly, in the report by Kaufman et al.,89 seven patients had discomfort at some point during block injection; however, this information could not be used to prevent the development of permanent neurologic injury, which occurred in all patients. This, however, may be an example of case-report bias. In other words, it is possible that patients' reports of pain may have prevented injuries but such events are unlikely to get reported.

Dogmas on Complications of Regional Anesthesia

Blanket statements and dogmas are common in the field of medicine and in regional anesthesia in particular. Much too often, a wide range of recommendations based on a single observation are inappropriately extrapolated. As an example, Walton et al. reported the occurrence of brachial plexus palsy after total shoulder arthroplasty under an otherwise uneventful interscalene block.90 However, the authors went on to suggest that, “to minimize the risk of brachial plexus injury with interscalene block,” PNBs should not be performed in anesthetized patients, and if paresthesia of “unusual severity” occurs, the injection should be immediately stopped. Ironically, their patient was neither anesthetized before the block injection, nor had paresthesia or pain on injection!

Benumof91 reported four cases of severe neurologic injury that resulted in cervical paraplegia in patients receiving interscalene brachial plexus blocks under general anesthesia. The discussions that followed, however, often recommended that sedation and general anesthesia be abandoned to reduce the risk of nerve injury. Such recommendations are based on this case report are inappropriate because none of the patients in this report suffered a peripheral nerve injury. Rather, these patients received an intracordal injection, a complication entirely avoidable with restriction of the needle insertion depth and/or use of more lateral approach to interscalene block.4

Those who base their criticism of “heavy” premedication or general anesthesia before performing PNBs on the cases reported by Benumof91 forget that interscalene block is a superficial procedure, devoid of significant discomfort and in which excessive sedation and analgesia are usually unnecessary except in children who otherwise would not hold still during the procedure. In contrast, many other PNB procedures involve deeper placement of the needle and several attempts at nerve localization that result in significant patient discomfort.20,92 Therefore, generalized recommendations to avoid premedication during PNBs carry the risk of limiting the use of PNBs because of an inevitable decrease in patient acceptance. In our practice at St. Luke's–Roosevelt Hospital Center in New York, patients are sent an anesthesia satisfaction survey after their discharge home. Analyses of more than 5000 patient responses clearly indicate that the most satisfied patients are those with no recollection of any anesthetic procedure being performed on them. Therefore, if PNBs are to be accepted by patients, adequate premedication is necessary to avoid patient discomfort during needle placement.

Literature Review

No study has compared the risk of neurologic complications in awake versus anesthetized patients, and it is unlikely that such studies will ever be done. A review of published reports of injury after PNBs indicates that significant neurologic injury after PNBs in awake patients occurs at a rate of 0.06–0.4%.81 Most of these reports included brachial plexus blocks only, probably because these techniques are used more frequently than lower extremity nerve blocks.4 In a recent similar prospective evaluation by Bogdanov and Loveland,93 none of 548 patients who received an interscalene brachial plexus block after induction of general anesthesia developed permanent or long-term neurologic complications. Similarly, in a report presented at the 2005 Annual ASRA Spring Meeting, Gadsen et al. (ASRA, 2005) presented the data on 226 PNBs of both upper and lower extremities, all performed in heavily sedated or anesthetized patients, none of whom developed neurologic complications. Bogdanov and Loveland used a modified classic approach to interscalene block that was proposed to reduce complications, whereas Tsai et al. used objective assessment of injection pressures to reduce the risk of intraneural injection during PNBs of both upper and lower extremity94 (Figure 69–8).

Although the relatively small number of patients in these reports does not allow accurate comparison, these studies at least indicate that the risk of complications of PNBs after general anesthesia may not be substantially more common than complications reported in other similarly powered studies in awake patients.81 In fact, performance of PNBs in heavily premedicated patients or after induction of general anesthesia is undoubtedly a common practice and a routine in the pediatric anesthesia practice. A recent informal poll conducted during the ASRA 2005 session on complications of PNBs indicated that approximately half of the present attendees performed blocks in heavily sedated or anesthetized patients.

Rescue Blocks, Multiple Injection Techniques, & Reverse Axis Blocks

Several PNB techniques that are equivalent to a PNB in anesthetized patients are accepted as sound practice. These include “rescue” blocks, multiple injection techniques, and “reverse” axis blocks. They are all similar to the practice of PNBs in anesthetized patients because the PNB is performed in a partially or fully anesthetized limb.

Rescue Blocks

Missed nerve blocks may occur 3–30% of the time and usually involve only one or two of the terminal nerves.95 Several well-established and universally accepted techniques of PNBs, such as repetition of the block, peripheral injection of the nerve, and others are often used to rescue failed blocks despite the risk that the needle may be inserted or injection made into an anesthetized nerve.96 Common examples of rescue blocks after failed axillary or interscalene brachial plexus blocks include elbow and wrist blocks.97,98

Multiple Injection Techniques

Multiple injection techniques for both upper and lower limb blockade have been introduced relatively recently in clinical practice with the suggestion that they decrease onset time, increase the success rate, and decrease the required dose of local anesthetic.99–106 The withdrawal and redirection of the needle to elicit multiple motor responses, however, carry a greater risk of direct needle trauma and intraneural injection into already anesthetized nerves. Regardless, this technique has been uniformly accepted by most experts in the field.

Double Blocks and Repeat Blocks

Regional anesthesia for elbow surgery has traditionally been a challenge. The most commonly used brachial plexus blocks—the classic approach to interscalene block and the axillary block—are not ideal because they either do not result in reliable block of the ulnar nerve or do not result in adequate analgesia for the tourniquet. For this reason, in patients undergoing elbow surgery, successful regional anesthesia requires the concomitant use of two separate approaches: an interscalene and an axillary approach.110 Obviously, performance of brachial plexus block at either level precludes the sensory or motor feedback information during performance of the block at the second level.

Central Nervous System Toxicity in Awake versus Asleep Patients

Practice of PNBs involves administering large volumes and doses of local anesthetics. A typical clinical presentation of local anesthetic toxicity is an awake or sedated patient during or immediately after injection of local anesthetic, followed by sudden onset of confusion, seizure, arrhythmias, or cardiac arrest.23,89 It has been suggested that heavy sedation or general anesthesia increases the risk of severe systemic toxicity of local anesthetics because it diminishes the patient's ability to report early signs and symptoms of rising local anesthetic serum levels. However, there are no reports of local anesthetic toxicity in adult patients under general anesthesia; essentially all reports of toxicity were in awake patients.108–111 For example, Edde and Deutsch23,112reported a cardiac arrest after interscalene brachial plexus block in an awake patient who had no symptoms of toxicity until the entire dose (20 mL of 0.5% bupivacaine) was administered. Conversely, others may argue that premedication offers protection because of its anticonvulsive effects. Moreover, because the critical steps in treating patients with severe toxicity are the establishment of a patent airway, hyperventilation, administration of oxygen, and hemodynamic support, one can argue that anesthetized and ventilated patients who develop systemic toxicity may actually be better off because they already have a secured airway, they are receiving a high concentration of oxygen, and they are typically in an environment that is ideally suited for aggressive resuscitation.

Bernards et al.113 reported that pigs given an intravenous infusion of bupivacaine failed to demonstrate signs of central nervous system toxicity before cardiovascular collapse if they had been premedicated with benzodiazepines. Indeed, in clinical studies of local anesthetic toxicity, volunteers clearly report an escalating series of symptoms as plasma concentration of local anesthetic rises during continuous, slow intravenous infusion. However, the occurrence of symptoms of local anesthetic toxicity depends on the rate at which the drug is injected. The difficulty in extrapolating this into clinical practice is that local anesthetic for the purpose of neuronal blockade is given as a relatively rapid bolus rather than a slow, escalating continuous infusion, as is the case in animal models.

For these reasons, any suggestion that general anesthesia predisposes to a greater risk of severe systemic toxicity of local anesthetic is purely theoretical, because no data firmly support this belief. Finally, local anesthetic toxicity is of potentially greater concern in the pediatric patient owing to lower dose requirements and need for stringent adherence to mg/kg dosage rather than a volume dosage, as is the common practice in adult anesthesia. Regardless, the practice of regional anesthesia in anesthetized patients is universally accepted in this patient population.

Nerve Blocks in Anesthetized Children versus Adults

In contrast to PNBs in adults, performing blocks in anesthetized pediatric patients is a universally accepted practice. This is by necessity because pediatric patients are unlikely to be cooperative during needle insertion, nerve stimulation, and manipulation necessary to accomplish PNB. In addition, most pediatric patients require concomitant administration of general anesthesia to allow for immobility during the surgical procedure. However, from the standpoint of risk of complications, this divergence in consensus on PNBs after general anesthesia between adults and pediatric patients does not make much sense. In other words, with the possible exception of infants, no sufficient anatomic or neurophysiologic differences justify this divergence in recommendations.

Although one can argue that complications of PNBs in children are rare, PNBs are not routinely used in the pediatric population, and there are simply no series comparable to those in adults to allow one to draw a clear conclusion regarding the risk of nerve injury in children. However, a large prospective study performed in France in children demonstrated a small risk of complications with PNBs.114

Monitoring Possibilities during Pnbs

Since this discussion focuses on the impact of heavy sedation or general anesthesia on the risk of neurologic complications, it is important to discuss the monitoring that is available to reduce the risk of nerve injury during PNBs. In general, two phases are amenable to monitoring during PNB placement. These include needle placement guidance (percutaneous stimulation, ultrasound) and avoidance of intraneural injection (report of pain on injection by the patient (when present), nerve stimulation, and assessment of resistance to injection).115 With regard to intraneural injection, neither percutaneous stimulation nor ultrasound guidance is helpful. Percutaneous stimulation may be helpful for approximating the needle insertion site, but it is useless for estimating the needle–nerve relationship. Ultrasound, on the other hand, offers real-time needle guidance below the skin level. However, in addition to the required skill, expense, and inconvenience of the equipment, the image resolution is simply insufficient to rule out intraneural needle placement.37 Most practitioners inject a small volume of injectate to determine the location of the tip of the needle. However, injectate as small as 0.2–0.5 mL is adequate to cause nerve injury if injected into a fascicle.

Nerve stimulator-assisted PNBs entered the practice of regional anesthesia with the promise of decreasing the risk of neurologic complications associated with the paresthesia technique.116 However, it soon became apparent that nerve stimulators could not prevent neurologic injury.1 More recently, it has been suggested that in many circumstances, the motor response to nerve stimulation may be absent at the point at which the needle makes contact with the nerve121 and that intraneural needle placement is possible despite the use of nerve stimulators37 (see Figure 69–4). One possible explanation for this phenomenon is hyperpolarization of the nerve that may occur when the needle is positioned in the vicinity of the nerve and excessively high current intensity is used.

Summary

Few issues in the practice of regional anesthesia have evoked such strong and divergent opinion among clinicians as have the performance of PNBs in anesthetized or deeply sedated patients. This is because administration of PNBs has traditionally been based on individual preferences, clinical impressions, and other subjective criteria rather than on established practice standards. Avoidance of deep sedation and general anesthesia is often suggested to decrease the risk of peripheral nerve injury with PNBs; however, there is no evidence in the literature to suggest that either practice is safer with regard to the risk of nerve injury. Nevertheless, the serious nature of complications resulting from inadvertent injections into the spinal cord suggests that regional anesthesia techniques close to the centroneuraxis should be practiced with extreme caution and insight into the appropriate depth of the needle insertion, whether the patient is awake, sedated, or anesthetized. It is also important to realize that neurologic injury is not always necessarily related to regional anesthesia technique. With PNBs, nerve injury that occurs postoperatively without pain, paresthesia, or high injection pressure is more likely related to surgery (surgical technique, stretching, positioning), rather than the PNB technique. Adequate proper training and the use of proper techniques and nerve block/monitoring equipment are more likely to decrease the risk of complications than are unfounded blanket statements about the advisability of performing PNBs in anesthetized patients. This is because such statements are unfounded by the relevant literature and can have a potentially negative impact on the practice of regional anesthesia.

Many patients and PNB techniques require appropriate sedation for block performance and patient acceptance. However, clinicians may be reluctant to use them because of the medicolegal concerns engendered by admonitions against performing blocks in sedated or anesthetized patients. Future efforts must be directed toward developing more objective and exacting nerve localization and injection monitoring techniques to more reliably detect and prevent intraneural injection. The results of these efforts will be of far greater importance to the future of PNBs and their role in practice of modern anesthesiology than overreaching, unsubstantiated opinions and statements.

Methods and Means of Decreasing the Risk of Neurologic Complications Associated with Nerve Blocks: Introduction

The published data suggest that neurologic complications of PNBs are relatively rare. However, the severity of consequences and lack of prevention strategies continue to present a source of significant concern for both clinicians and patients. The main inciting mechanism of neurologic injury with PNBs appears to be an intrafascicular or intraneural injection. It is fortunate that peripheral nerves possess an inherent natural protection; intraneural injections often do not result in intrafascicular needle placement and therefore do not necessarily lead to nerve injury. It is commonly suggested that the use of short-bevel needles and avoidance of excessive sedation and general anesthesia should be carried out to decrease the risk of nerve injury. However, these commonly voiced recommendations have been recently challenged. In addition, avoidance of adequate premedication may have a significant negative impact by decreasing the patient's acceptance and satisfaction with PNBs. The relatively low incidence of complications with PNBs, together with the lack of objective documentation and means to more precisely monitor administration of nerve blocks make retrospective analyses of cases of nerve injury largely speculative with regard to the actual mechanism of nerve injury in clinical practice.

Recommendations for Decreasing Pnb Complications

Aseptic Technique

Most nerve block techniques are merely percutaneous injections. However, infections are known to occur and can result in significant disability. Because this complication is almost entirely preventable, every effort should be made to adhere to strictly aseptic technique.

Short-Bevel Insulated Needles

Insulated needles are now widely available and result in much more precise needle placement. The short-bevel design helps to prevent nerve penetration.

Needles of Appropriate Length for Each Block Technique

Excessively long needles should not be used for nerve blockade. For instance, it is important to never use needles longer than 50 mm for an interscalene block. In addition to the safety reasons, needles of appropriate length are also advanced with far greater precision than excessively long needles.

Surface Localization

In patients with difficult anatomy, surface localization of superficially seated nerves or plexuses can help reduce the number of needle passes.

Needle Advancement

During needle localization, advance and withdraw the needle slowly. Keep in mind that nerve stimulators deliver current of very short duration once (1 Hz) or twice (2 Hz) per second and that no current is delivered between the pulses. Thus, fast insertions and withdrawal of the needle passages may result in failure to stimulate the nerve because the needle may pass nearby or even through the nerve between the stimuli without eliciting nerve stimulation.

Fractionated Injections

Inject smaller doses and volumes of local anesthetics (3–5 mL) with intermittent aspiration to avoid inadvertent intravascular injection. Always observe the patient during the injection of local anesthetic because negative aspiration of blood is not always present with an intravenous injection. This approach may allow detection of the signs of local anesthetic toxicity before the entire dose is injected. Regardless of the monitoring method, slow injection is of paramount importance to avoid massive intravascular injection.

Accuracy of the Nerve Stimulator

Always ensure that the nerve stimulator is operational and delivering the specified current and that the leads are properly connected to the patient and the needle.

Avoidance of Forceful, Fast Injections

Forceful, fast injections are more likely to result in channeling of local anesthetic to the unwanted tissue layers, lymphatic vessels, or small veins that may have been cut during needle advancement. Such injections may result in channeling of the local anesthetic in the systemic circulation with consequent risk of central nervous system and cardiac toxicity. Finally, forceful, fast injections under excessive pressure are more likely to result in an unrecognized intraneuronal injection. Limit the injection speed to 15–20 mL/minute.

Avoidance of High Injection Pressures

Intraneuronal needle placement may result in high resistance (pressure) to injection owing to the compact nature of the neuronal tissue and its connective tissue sheaths. Always use the same syringe and needle size to develop a “feel” during the injection. As a rule, when injection of the first milliliter of local anesthetic proves difficult, the needle should be slightly withdrawn and the injection attempted again. If resistance persists, the needle should be completely withdrawn and flushed before repeating the insertion. Ultimately, objective injection pressure monitoring will likely become a standard monitor to standardize nerve block injections, reduce the risk of intraneural injection, and to be a basis for medicolegal documentation (see Figure 69–8).

Aborting Injection When Pain Is Reported

Severe pain or discomfort on injection may signify intraneuronal placement of the needle and should be avoided. When this occurs, the injection should be abandoned, although chances are that damage may have already been caused at the time when the pain occurs. Lancinating, “shooting” pain on injection should not be confused with a mild “paresthesia-like” feeling reported by the patient when the needle is placed in the immediate vicinity of the nerve or plexus. In this case, local anesthetic can be injected slowly, provided that the resistance to injection is normal (< 20 psi). Resuming the injection after waiting to see whether the pain will go away should not be done under any circumstances.

Choosing the Local Anesthetic Solution Wisely

Always choose a shorter-acting (and less toxic) local anesthetic for short procedures in which long-lasting postoperative analgesia is not required. Local anesthetic toxicity is the most common complication with neuronal blockade. The risk of severe toxicity is substantially lower with chloroprocaine or lidocaine than with bupivacaine.

Blocks in Anesthetized Patients

Without reliable monitoring, blocks in anesthetized patients still should not be common practice. When it is necessary to place blocks in anesthetized patients, this should be done by practitioners with experience. The introduction of ultrasound-guided nerve blocks and injection pressure monitoring is likely to change the practice and allow more routine performance of nerve blocks in anesthetized patients.

Repeating a Block after a Failed Block

Repeating a block after a failed block should be avoided whenever possible. When indicated, it should be done only by those with substantial experience in the planned technique. Avoidance of abnormal resistance to injection or objective injection pressure monitoring is of utmost importance here as the clinician can no longer count on pain on injection as a sign of intraneural injection. Similarly, neurostimulation may no longer be possible once the local anesthetic is injected. Real-time ultrasound imaging is also useful when repeating the failed block, as it allows more accurate placement of the needle.

Peripheral Nerve Injury after Peripheral Nerve Blocks

Nerve injury is recognized as a potential complication of peripheral nerve block (PNB) anesthesia, but fortunately, severe or disabling injuries are rare. When they do occur, they can be a frightening complication for patient, surgeon, and anesthesiologist. Fortunately, most symptoms of nerve injury resolve in 4–6 weeks in over 95% of patients and in 99% of the patients by 1 year.81 Early intervention may help prevent the long-term sequelae that can occur with unrecognized, and therefore improperly treated nerve injuries. With the resurgence of interest and utilization of PNB anesthesia, it is important to develop a coinciding plan for management of postoperative nerve injuries. The plan should include recognition, diagnosis, and treatment of the nerve injury. A working knowledge of the long-term prognosis, understanding the importance of appropriate neurology consultations, and familiarity with available diagnostic tests and treatment options is essential for the proper management of patients with neurologic injury.

With any PNB, inclusive documentation of the block is of utmost importance for diagnostic, therapeutic, and medicolegal purposes. Documentation that includes the nerve(s) stimulated, the minimum current used, the number of attempts, the appearance of pain or paresthesia during the procedure and measures taken, resistance to injection and injection pressure if pressure monitoring is used, type/dose of local anesthetic agent, and patient condition during the block is essential in understanding the mechanism of the injury. This documentation can help the anesthesiologist and/or consulting specialist to determine the possible cause of the injury and any associated conditions and to guide treatment modalities.

Mechanisms of Injury & Symptoms

After peripheral nerve anesthesia, if sensory and/or motor function remains depressed beyond the expected duration of action of the local anesthetic, potential causes for the neurologic deficits should be investigated. Neurologic deficits may be related to vascular injuries, compression injuries, local anesthetic action, or traumatic nerve injury with fascicular disruption. When faced with a neurologic deficit, especially in a patient in whom a PNB has been placed, it is important to remember that many causes of nerve injury are unrelated to the performance of the regional anesthetic.

Other factors, such as, tourniquet use, improper positioning, postoperative swelling, surgical trauma, and preexisting neurologic deficits may be contributing or causative influences. Proper and objective documentation of the nerve block procedures can go a long way toward deciphering whether the injury was caused by a nerve block, surgery, or other factors.

Vascular Injuries

When symptoms occur early in the postoperative period (within minutes to hours), the anesthesiologist should suspect a vascular or compression-type injury due to disruption of the blood supply from an insult to the vascular structures, from hematoma at the surgical or block site, or from deep venous thrombosis. This is particularly true if a neurologic deficit appears after apparent resolution of the block.

Compression Injuries

Compression neuropathies usually present as a focal mononeuropathy at sites where nerves pass through tissue tunnels, that is, median through carpal tunnel, spinal nerve through vertebral foramina. Acute compression injuries can develop secondary to limb tourniquet paralysis, from retractors used for surgical procedures, from expanding hematomas, or from improper intraoperative positioning, that is, stretching of the cords of the brachial plexus during sternal retraction, or from extending/pronating the forearm causing ulnar nerve compression.75,117 A compression injury can also occur with PNB anesthesia from increased endoneurial fluid pressure. This can occur with injection into a tight tissue compartment or when high injection pressures are used during nerve block administration.77 Metabolic diseases such as diabetes mellitus may make nerves more susceptible to compression injuries.119

Local Anesthetic Action

It is important to remember that neurologic deficits may be related to the residual neurologic blockade. Long-acting local anesthetics such as ropivacaine or bupivacaine have been reported to last up to 24 hours. It is well recognized that intraneural injections can and do occur without obligatory neurologic injury.37 Most such injections result in intraneural, but perifascicular injection of local anesthetic, and their hallmark is a block of much longer duration than expected.20 When additives are included in the local anesthetic mixture, particularly in the setting of an intraneural injection, the block can be prolonged up to 48 hours.120 In the elderly and in those with preexisting neurologic diseases, local anesthetic action can be prolonged secondary to abnormal uptake or reduced perfusion to the nervous tissue.121 The site of the block may have an effect on the duration of action of the local anesthetic.122 Therefore, in patients with known or occult preexisting neurologic disease, the elderly, and those treated with long-acting local anesthetics, sufficient time should be allowed for the local anesthetic to be thoroughly metabolized. Physical examination of these patients usually reveals a slowly receding block. Once the return of motor function occurs, the block usually recedes in an accelerated fashion. If motor function returns with persistent sensory deficits, or motor dysfunction persists, further evaluation is necessary.

Traumatic/Toxic Nerve Injury

Nerve injury after PNBs may be caused by direct needle trauma, intraneural injection, or local anesthetic neurotoxicity. Several animal studies have demonstrated that the nerve injury occurs more frequently with long-bevel needles, but the duration and severity of the injury are greater with short-bevel needles. When the bevel orientation is perpendicular rather than parallel with nerve fibers, studies have shown that nerve injury can be more severe.43 Intraneural intrafascicular injection is characterized by high injection pressures at the onset of injection.20 Such injections are characterized by a prolong blockade followed by incomplete resolution and residual neurologic deficit. Because a miniscule amount of local anesthetic (as little as 0.5 mL) is required to rupture the fascicle, intraneural injection should be suspected whenever there is resistance to injection or when the patient experiences severe pain on injection.

All local anesthetics are potentially neurotoxic. Neurotoxicity depends on the dose, concentration, and length of exposure to the nerve tissue. Vasoconstrictive additives such as epinephrine, which can affect neural blood flow, may potentiate nerve injuries. Local anesthetic neurotoxicity is more prevalent in patients with preexisting neurologic deficits, especially those with demyelinating diseases. In several studies of patients with occult or diagnosed multiple sclerosis, local anesthetic action was prolonged. The prolonged duration was thought to be related to an abnormal uptake of local anesthetic in demyelinated nerves.121

Magnitude of Neural Injury

The degree of neural insult can be defined by the terms neurapraxia, axonotmesis, and neurotmesis. The mildest form, neurapraxia denotes a mild degree of neural insult with failure of impulse conduction across the affected segment. The electromyogram (EMG) is normal, but conduction velocity as demonstrated by a nerve conduction study is decreased. Usually when the offending cause has been removed, recovery occurs over a variable amount of time, which may be as long as several weeks. Complete recovery can usually be anticipated. Axonotmesis, an intermediate injury, occurs when there is axonal disruption with preservation of the endoneurium. Recovery is dependent on the rate of axonal regeneration (1–3 mm/day). If recovery occurs, it is most likely prolonged and incomplete. The prognosis is better for young, healthy patients with distal lesions. The most severe form of neural injury is neurotmesis, a complete transection or crushing of the nerve with disruption of the endoneurium. Surgical repair is usually indicated, but even then, recovery is usually incomplete. Prognosis for full recovery is poor.

Patient Evaluation/Physical Examination

Symptoms of Nerve Injury

The symptoms of a nerve lesion after PNB manifest after the block has receded—usually within 48 hours. The perception of symptoms is influenced by the origin of the nerve lesion and other confounding factors, such as postoperative pain, immobility, effects of surgery, position, application of casts, dressing, bandaging, and so forth. The intensity and duration of symptoms may also vary with the severity of the injury—from a light, intermittent tingling and numbness lasting a few weeks to a persistent, painful paresthesia, neuropathic pain, sensory loss, and/or motor weakness lasting for several months or years. Some nerve injuries may even evolve into a severe causalgia or reflex sympathetic dystrophy. Keep in mind that although dermatomes can provide clues to the location of injuries, the loss of sensation at the skin does not provide precise information concerning the site of injury because the boundaries of dermatomes are not precise, clearly defined lines. More useful information can be obtained from the loss of motor function on the basis of the origin and assessment of motor performance.

Symptoms of neurologic injury range from mild to severe. Typical symptoms are dyesthesia, paresthesia, numbness, weakness, and pain. Symptoms of nerve injury may be acute or may not become clinically apparent for several days to several weeks. The approach to patient evaluation should be indistinguishable, regardless of the timing of the suspected injury (Figure 69–9).Physical examination should include an assessment of vascular integrity, sensory/motor function, and reflexes.

Vascular Mediated

Vascular-mediated injuries include injury to arteries or veins, the formation of deep venous thrombosis, or a combination of any of these, creating vascular compromise.

Vascular injury with associated ischemia should be immediately excluded. The examination should include an assessment of both venous and arterial circulation, skin color changes, the presence of engorgement or edema, hematoma, or pain at the surgical or block site. If a vascular injury is suspected, the surgical team should be consulted immediately to manage and treat the problem. For example, patients with lower extremity joint replacement surgeries are prone to the development of deep venous thrombosis. Patients may be completely asymptomatic, or they may complain of limb pain, limb swelling, or leg pain on dorsiflexion of the foot. If the patient is receiving a continuous femoral nerve block, (typical after this type of surgery) and complains of pain behind the knee (sciatic distribution), the anesthesiologist must be cognizant of the possibility of a deep venous thrombosis versus incisional pain not covered by the femoral block. Occlusive dressings should be evaluated to make sure that they are not contributing to the vascular insult.

With arterial compromise, the patient complains of intense pain, paresthesia, and cold. The onset is usually rapid. A Doppler/vascular study is the most common diagnostic test to aid in the diagnosis. Arterial occlusion or compromise usually requires emergent surgical exploration.

Neurologically Mediated

If the physical examination demonstrates intact circulation, then a more thorough neurologic examination should be initiated. This includes a comprehensive motor and sensory examination as well as assessment of the reflexes. In multiple studies evaluating the incidence and prognosis of nerve injury after PNB anesthesia, most mild symptoms such as dyesthesia, mild paresthesia or numbness, or mild pain resolved within the first few days or weeks of the insult. Further diagnostic testing was not indicated.2,3,81,123–125

If the neurologic deficit is persistent or more severe (ie, moderate to severe numbness, weakness and/or pain), then an evaluation by a neurologist may be indicated. For the hospitalized patient, the neurology consultation and subsequent examination should take place during the hospitalization. If the patient has already been discharged, a neurologist can be contacted for an outpatient evaluation. The magnitude or rate of progression of symptoms influences the urgency of the neurology consultation. Temporizing measures for pain control may be initiated until the patient can be evaluated. The neurology assessment involves a more meticulous clinical examination to try to evaluate the degree of deficit and to determine what further diagnostic tests are indicated.

Diagnostic Tests

A variety of diagnostic tests are available for the detection of nerve injury. Each test has specific indications, advantages, and disadvantages, depending on the injury, patient characteristics, availability of the diagnostic equipment, and expertise of the operator. The diagnostic tests currently available include electrophysiology, high-resolution ultrasound, and magnetic resonance imaging.

Electrophysiology Testing

When a patient presents with complaints of weakness, numbness, and/or paresthesia, several questions arise. Are these complaints the result of a nerve lesion? Did a lesion exist prior to surgery? Did the lesion result from placement of a nerve block, by nerve compression or traction during or after the surgical procedure, or by laceration during the operative procedure? These questions can be answered with electrophysiology. Electrophysiology involves a nerve conduction study (NCS) and electromyography (EMG). NCS is used to detect presence of a nerve lesion, and it can be performed within days of injury. On the other hand, EMG is used to localize the lesion.

Nerve Conduction Studies

NCS is performed by placing cutaneous electrodes along the course of a nerve. The only places a nerve can be evaluated are sites where it comes close to the surface. Signal is transmitted along sensory fibers of the nerve from stimulating to recording electrode. The amplitude of signal, the time for signal transmission, and the distance between electrodes is measured. From measurements of time and distance, a conduction velocity is calculated. Nerves are composite structures formed by axons of different diameter that conduct signal at different velocities. The first signal to arrive at the recording electrode is the only signal measured. This signal is transmitted by myelinated axons. Signal transmitted by unmyelinated axons is ignored. Unmyelinated axons transmit pain. Therefore if the patient complains only of pain, a nerve conduction study is unlikely to detect any changes in amplitude or conduction velocity. A patient can have a normal NCS and still suffer from legitimate pain. A reduction in conduction velocity indicates myelin damage. A reduction in amplitude indicates axonal damage. Conduction along motor fibers can also be evaluated; however, the recording electrode is placed on muscle. Because the signal involves the entire motor unit (ie, motor axon, neuromuscular junction, and muscle fibers), changes in amplitude and conduction velocity are more difficult to evaluate. A lesion can be detected by NCS within 1–2 days of injury. Therefore, the initial NCS should be scheduled 1–2 days after injury. If the initial study is normal, the patient probably has a neurapraxia that should resolve with time. The patient should be followed clinically for improvement of symptoms. If symptoms persist or worsen, the study should be repeated in 4–6 weeks. If the initial NCS shows abnormality, then the lesion needs to be localized. NCS has a limited ability to do this. However, to localize a lesion within a nerve or plexus, EMG needs to be performed.

Electromyography

EMG records muscle depolarization. Depolarization is detected by a needle electrode placed in the muscle and appears as a deflection on an oscilloscope. The shape and frequency of the deflections provide information about the nerve and muscle. In normal muscle at rest, there should be no spontaneous depolarization or deflections on EMG. Following nerve injury, muscle fibers are released from the control by the nerve and begin to discharge spontaneously. On EMG, this appears as deflections called positive waves and fibrillations. It takes between 2 and 4 weeks for these changes to appear. Therefore, the EMG is scheduled 2–4 weeks following injury. Given the delay in appearance of pathology on EMG, some laboratories may perform EMG at the time the initial NCS is obtained. EMG obtained within the first week of injury is used to determine if there are signs of nerve damage that existed prior to surgery and may be responsible for the patient's complaints. While this may have some merit, it must be tempered with the fact that EMG is an uncomfortable procedure performed without sedation, anesthesia, or analgesia. Some patients may be unable to complete the test. Consequently, many patients will not agree to repeat an EMG. The purpose for EMG is localization of the lesion. The best signal to perform this function appear 2–4 weeks following injury; therefore, to evaluate a lesion that may have occurred during an anesthetic or surgical procedure, the only EMG that must be obtained should be scheduled 2–4 weeks following the injury. If EMG is delayed beyond 4 weeks, signs of reinnervation (long duration, high amplitude, polyphasic motor unit potentials) may appear and complicate the evaluation. To determine the site of lesion on a nerve, a series of muscles are tested. There is no standard set of muscles evaluated. The muscles are selected based on their relationship to the region of the suspected nerve lesion. For example if a lesion is suspected in the posterior cord of the brachial plexus, deltoid and triceps brachii muscles need to be tested. For the injury to be in the posterior cord, positive waves or fibrillations need to be present in both muscles. If they are present only in the deltoid, then the lesion may be in the axillary nerve or in the upper roots of the brachial plexus. The axillary nerve can be further evaluated by testing teres minor. Roots in the upper regions of the brachial plexus can be evaluated by testing supraspinatus. The neurologist performing the EMG selects the muscles to be tested. It is very important to educate the neurologist about the procedures of nerve block and surgery. Sites where nerves may have been placed at risk need to be discussed. Failure to have this discussion could mean an EMG with considerable error.

Once a lesion is localized, inferences can be made about its etiology. For example, a lesion located over a bony prominence may be the result of compression caused by inappropriate or prolonged positioning of a limb during surgery. A lesion located in the region where a nerve block procedure may have been caused by the anesthesiologist. A lesion located in the region of the operative site may have been caused by the surgeon. Therefore, in this context, EMG can be considered as a tool for evaluating the etiology of a nerve lesion.

Doppler Ultrasound/High-Frequency Ultrasound

Doppler ultrasound provides structural information about the image being scanned. Most commonly, it is used to study the carotid arteries and major arteries and veins of the lower extremities. It can also be used to examine the arteries at the wrist, in the palms, and in the digits. It is the most common diagnostic test for deep venous thrombosis. A newer type of ultrasound, high-frequency ultrasound, is an effective imaging modality for identifying morphologic changes in the peripheral nerves. It is being used to evaluate nerve rupture, inflammatory processes, and compressive syndromes in peripheral nerves. It can localize the lesion. It may be a useful tool for initial imaging of a suspected peripheral nerve injury or for follow-up imaging. It is faster and more cost-effective than magnetic resonance imaging. But it has limitations in that the test is operator-dependent, requires an extended learning curve to obtain and interpret images, and is limited to nerves within 2 cm of the skin surface.126 At greater depths, coarser-quality ultrasound nerve images can be obtained, but they are difficult to distinguish from other tissues such as tendons.127

Magnetic Resonance Imaging/Magnetic Resonance Neurography

Magnetic resonance imaging, specifically magnetic resonance neurography, is a relatively new imaging technique that can reliably and selectively image peripheral nerves.128 By manipulating magnetic resonance imaging parameters, nerves can be made to show up as three-dimensional “neurographic” images, comparable to angiograms. When it is properly implemented, magnetic resonance neurography is capable of providing high-quality information about nerve compression, nerve inflammation, nerve trauma, systemic neuropathies, and recovery of nerves from pathologic states.129 Direct nerve imaging has been shown to demonstrate nerve continuity, distinguish intraneural from perineural masses, and localize nerve compressions before surgical exploration.130 Like ultrasound, its indication for acute peripheral nerve injury is in localizing the lesion. In some studies, magnetic resonance signal alterations were shown to occur as early as 24 hours after an axonal nerve lesion, possibly making it the earliest form of detection of nerve injury.131 Magnetic resonance studies are limited by access to the patient, cost, longer scanning times, and equipment availability.

Treatment Options for Peripheral Nerve Injury

When a nerve injury has occurred, treatment of the patient depends on the severity of the injury. It is prudent to remember that most of these injuries resolve with time. The care of the patient with a nerve injury can be divided into two groups: those with minor deficits and those with major deficits. Regardless of the type of injury, the patient should be evaluated clinically to ascertain whether a more serious or occult injury or correctable contributing condition is not overlooked.

Minor Deficits

If the examination reveals minor deficits, reassurance is key to relieving the patient's anxiety. Further diagnostic testing or therapy is usually not indicated. Weekly to biweekly telephone follow-up to assess resolution of the injury by the pain management team provides reassurance, allows early detection of more serious problems, and instills confidence in the patient. It is important to remember that one bad experience with regional anesthesia often creates a negative attitude toward future application for the patient, his family, and possibly the surgical team. Providing the patient with consistent, caring follow-up despite the injury, helps to rebuild patient confidence in future anesthetic experiences.

Major Deficits

If the clinical examination of the patient reveals a major neurologic deficit, early neurologic and/or neurosurgery consultation is advisable. In addition to a complete neurologic examination, the neurologist determines the most appropriate diagnostic test for the patient. For example, if a compression injury is suspected, ultrasonography or magnetic resonance imaging of the involved plexus may be performed. In patients with pain, medication for pain should be started early to prevent nerve sensitization. Physical and occupational therapy consultations are obtained by the neurology department with arrangements made for treatment after the patient is discharged. A consultation for social services may be necessary if the injury will make an impact on the patient's ability to perform activities of daily living. Similarly, early consultation with physical therapy is a must to reduce the risk of contractures, muscle atrophy, and prolonged disability. Close follow-up by neurology clinician should be arranged as well as continued follow-up by an anesthesiology clinician until the injury is completely resolved or is stable.

Drug Therapy

Multiple drugs are effective to treat neurally mediated pain. The more commonly prescribed medications include tricyclic antidepressants, serotonin reuptake inhibitors, anticonvulsants, opioids, and capsaicin cream. These drugs should be administered under the direction of a chronic pain specialist or a neurologist who has evaluated the patient and has the capacity to do follow-up evaluations.

Tricylic Antidepressants

Amitriptyline is among the more efficacious drugs. It has multiple effects including blocking the reuptake of serotonin and norepinephrine, blocking the NMDA receptor, and blocking voltage-dependent sodium channels. A more recent study demonstrated that amitriptyline has an ability to maintain spinal cord GABA(B) receptor activity.132 The drug can be started at 10–25 mg daily and escalated by 25 mg every week to an effective level. Doses should be limited to 100 mg daily. Side effects include decreased salivation, constipation, urinary hesitancy, blurred vision, orthostatic hypotension, sedation, and cognitive impairment. One very serious side effect in cardiac patients is torsade de pointes from prolongation of the Q-T interval, but this has been shown to occur only in higher doses.

Selective Serotonin Reuptake Inhibitors

Paroxetine is the only selective serotonin reuptake inhibitor that may be effective in the treatment of neurally derived pain. In a study comparing paroxetine with imipramine (another tricyclic antidepressant), paroxetine was as effective in 60–70% of the patients receiving the drug.133 Because of its marginal effectiveness, it is reserved for patients who are unable to tolerate other classes of medications.

Anticonvulsants

Commonly prescribed anticonvulsants in the treatment of minor neural changes (pain and paresthesia) are gabapentin and carbamazepine. Gabapentin is an amino acid derivative of GABA (gamma-amino butyric acid). The proposed mechanism of analgesic action is related to its effect on sensitized neurons. It is thought to directly or indirectly inhibit excitatory neurotransmitters, block neuronal calcium channels, and augment central nervous system inhibitory pathways by increasing GABA transmission.134 Gabapentin is usually started at 300 mg daily with increasing doses to 1300–1800 mg per day in divided doses. Side effects of gabapentin include drowsiness, anxiety, visual disturbances, hypertension, and ataxia. Other anticonvulsants that have been used in the treatment of neurally mediated pain are carbamazepine, topiramate, levetiracetam, and oxcarbazepine.

Opioids

Opioid therapy is controversial, but may be effective in alleviating pain of peripheral nerve injury origin. In five randomized, controlled trials of opioid therapy used for neuropathic pain, all demonstrated benefits from opioids in controlling pain.135,136 Commonly prescribed opioids for short-term therapy include oxycodone, oxycontin, or fentanyl patches. To prevent opioid dependence or tolerance, other therapeutic agents, such as amitriptyline and gabapentin, should be titrated up while titrating off the opioids.

Tramadol

Tramadol is approved for use in the United States for moderate to severe pain. It binds to mu opioid receptors, contributing to its analgesic properties. It inhibits the reuptake of serotonin and norepinephrine into the central nervous system. In recent literature, tramadol has been shown to be effective in the treatment of arthritic and neuropathic pain and in mixed nociceptive-neuropathic pain.137 It is tolerated by elderly patients, has a low incidence of constipation, is devoid of immunosuppressive activity, and has a low tendency toward tolerance. It has a minimum risk of addiction and abuse.

Capsaicin Ointment

Capsaicin is a vanniloid compound most commonly found in hot peppers. Many of the neuropathies with pain as the predominant symptom involve small afferent fibers resistant to the analgesic action of the more commonly prescribed medications. Capsaicin can deplete the transmitter contents of these small afferent fibers leading to their degeneration and subsequent pain-generating ability. Its application is primarily for cutaneous hyperalgesia states such as postherpetic neuralgia. It is probably not effective for most painful neuropathies of deeper origin. After starting medication therapy, consultant follow-up should be scheduled for 2 weeks after the injury to determine whether the deficit has resolved, persisted, or worsened. If the deficit has resolved, any medication given for pain should be discontinued. The patient should be instructed to notify the consultant if any neurologic changes develop within the next month. If the deficit persists, the dose of pain medication is adjusted as described. During follow-up visits, the patient should be asked about any side effects associated with the prescribed medication. Subsequent follow-up depends on the nature of the deficit. If it is stable but persistent, consultant follow-up should be arranged for 3–6 months. If the deficit has worsened, adjustments are made in the drug therapy to try to alleviate symptoms. Follow-up is determined by the consultant based on the patient's condition and symptoms.

Summary

Despite meticulous care, patient selection, and experience, neurologic deficits after regional anesthesia may occur. The debate over performing blocks in awake or sedated/asleep patients is inconsequential because nerve injuries have occurred in both groups. Understanding the mechanism of injury, the typical clinical course following injury, and the prognosis and obtaining appropriate consults are essential knowledge for the regional anesthesiologist. A basic understanding of diagnostic tests and treatment modalities provide the clinician with information necessary to participate in meaningful discussions with the patient and other specialists involved in the patient's care. Regardless of the consultations obtained, the importance of follow-up by an anesthesiologist cannot be overemphasized. Complete documentation of the initial consult, the block procedure, the postoperative care, and follow-up are extremely important in the event of any legal action as well as in the professional care of the patient.

Few publications have had a greater impact on the clinical practice of anesthesiology than the American Society of Anesthesiologists (ASA) practice guidelines.138 These practice guidelines have been designed to enhance and promote the safety of anesthetic practice and have made the practice of general anesthesia much safer. Such guidelines are much needed but currently do not exist with regard to the practice of PNBs. This is most likely because administration of PNBs has been traditionally based on individual preferences, clinical impressions, and other subjective methods. Future efforts should be directed toward developing more objective and exacting nerve localization and injection-monitoring techniques to more reliably detect and prevent intraneural intrafascicular injection. The results of these efforts will inevitably be of crucial importance to the future of PNBs and their role in practice of modern anesthesiology.