Complications Of Peripheral Nerve Blocks

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There are relatively few published reports of complications associated with the use of peripheral nerve blocks. Because there is a relative paucity of published information on the mechanisms of neuronal injury after nerve blockade and methods to prevent them, some of the discussion will necessarily be theoretical. TABLE OF CONTENTS (click here to expand)

Introduction
There are relatively few published reports of complications associated with the use of peripheral nerve blocks. Because there is a relative paucity of published information on the mechanisms of neuronal injury after nerve blockade and methods to prevent them, some of the discussion will necessarily be theoretical. However, we do believe that the recommendations made in this chapter if followed, should substantially reduce risks of neurologic complications following peripheral nerve blocks.

Complications After Nerve Blockade: How Common Are They?

The reported incidence of complications after peripheral nerve block is generally low and varies from 0-5% percent. These complications fall into one of five major categories. Complications related to brachial plexus blocks are perhaps most commonly reported, whereas there are very few reports of injuries to the lower extremity nerves. Such a discrepancy is most likely related to the fact that brachial plexus block is one of the most prevalent techniques in clinical practice. However, the disproportionately higher number of reported cases of neuropathies in the upper extremity (particularly axillary block) may also be a function of some anatomic features of axillary brachial plexus. For instance, in a survey of hand surgeons, 171 (21%) of the responding 800 surgeons had seen a total of 249 major complications (complications lasting = year), and 521 (65%) had seen patients with minor neurologic complications. The survey further suggested that about one of five hand surgeons had seen a major neurologic complication that might have been related to an axillary brachial plexus block. It should be noted that the etiology of neurologic complications is often multifactorial. A relatively small proportion of the postoperative neurologic sequelae are caused by the regional

anesthetic alone; they also may be caused or compounded by underlying disease or surgery. For instance, the incidence of neurologic injury following hand surgery under axillary block was 3.4% in a series of 533 patients. However, the nerve block itself was implicated in only 1.9% of these cases. Likewise, an increase in shoulder arthroscopic procedures in the past decade has been accompanied by a growing awareness of the potential for surgery-related neurologic injury. The occurrence of transient neuropraxia of the brachial plexus can be as high as 30% after shoulder arthroscopy, with the musculocutanous nerve being the most vulnerable component of the brachial plexus. This has been attributed to a number of surgical factors, such as joint distention, excessive traction, and extravasation of fluid during surgery, and not to the nerve block anesthesia.

Postoperative Neurologic Deficit: Regional vs. General Anesthesia

Although nerve injuries are commonly voiced concerns with the use of peripheral nerve blocks, postoperative neurologic complications may actually be more common after general and neuraxial anesthesia than after peripheral nerve blocks. In a closed-claims review of nerve injuries associated with anesthesia, 61% of the claims were related to the use of general anesthesia and 36% to the use of regional anesthesia. Such injuries were thought to be caused mostly by compression or stretching of the nerve(s) or plexi during patient positioning. Peripheral nerve injuries after general anesthesia most commonly involve injuries to the ulnar nerve and brachial plexus, whereas injuries to the lumbosacral plexus primarily occur after central neuraxial blockade.

Symptoms of Nerve Injury

The symptoms of a nerve lesion after peripheral nerve block 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. It should be kept 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.

Peripheral Nerves: Functional Anatomy

The functional anatomy of the peripheral nerve is crucially important for understanding the mechanisms of peripheral nerve injury. A peripheral nerve is a complex structure consisting of fascicles held together by the epineurium, an enveloping external connective sheath (Fig. 1). Each fascicle contains many nerve fibers and capillary blood vessels embedded in a loose connective tissue, the endoneurium. The perineurium is a multilayered epithelial sheath that surrounds individual fascicles. Nerve fibers depend on a specific endoneurial environment for their function. This is different than the regular extraneural interstitium. 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 entire vascular bed is regulated by the sympathetic nervous system and its blood flow can be as high as 30 to 40 mL/100g per minute. 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 block and possibly result in temporary or permanent impairment or loss of neural function.

Pathophysiology
Neurologic complications following peripheral nerve block can be caused by one or more of the following factors: 1. Mechanical trauma to the nerve Needle trauma

2. 3. 4. 5. 6.

Intraneuronal (intrafascicular) injection Neuronal ischemia Inadvertent needle placement into unwanted locations Neurotoxicity of local anesthetics Drug error (injection of wrong drug) Infection In many instances, the insult may be caused by a combination of these factors.

Mechanical Trauma
Injuries to peripheral nerves after intrafascicular injection of therapeutic and other agents are well documented. Nerve injury following intraneural injection varies from minimal damage to severe axonal and myelin degeneration, depending upon the agent injected and dose of the drug used. Several studies have documented that regardless of the agent used, intrafascicular injection is the main determinant of nerve injury. At present, there is no consensus on what constitutes proper monitoring and documentation of nerve block procedures. Much of the debate on how to prevent intraneural injection and nerve injury associated with PNB has focused on methods of nerve localization (e.g., paresthesia versus nerve stimulation). Still, there is no evidence that one method is safer than another, and nerve injury can occur even with experienced practitioners. Although there is a paucity of clinical data, educational material in regional anesthesia, including major textbooks, suggests that lancinating pain reported by the patient and high injection pressure may portend intraneural injection of local anesthetic and perhaps increase the potential for nerve injury. Consequently, many clinicians advise against performing PNBs in patients under excessive sedation or anesthesia. However, multiple case reports suggest that pain may be absent as a warning factor of pending nerve injury. Besides, administration of sedatives and analgesics is often necessary for performing nerve blocks and makes patient acceptance easier. The combination of premedication with sedatives and analgesics, along with the neuronal blocking properties of local anesthetics, may render pain on injection as a sole indicator of intraneural injection unreliable. Experimental evidence suggests that such injections may be associated with a resistance to needle advancement and an increased pressure on injection of local anesthetic. For instance, in a model of nerve injury by Selander et al., generally higher pressures (e.g., >= 11psi) were required to inject solution into a nerve fascicle of a rabbit sciatic nerve. Injection into a nerve fascicle using such a pressure results in rupture of the fascicle and its connective tissues sheath -

the perineurium with a consequent histologic evidence of disruption of the neuronal anatomy. Similarly, in our large animal model, most intrafascicular injections were associated with high injection pressures (>= 25 psi), Figure 2. More importantly, the combination of insertion of the needle intrafascicularly and high resistance to injection (as indicated by injection pressures >= 25psi) were associated with neurologic deficit in dogs and histologic evidence of severe fascicular injury with demylination. These data suggest that that high injection pressures during nerve block injection may indicate intrafascicular injection and as such, carry a risk of nerve injury.

Figure 2: Intrafascicular injection of 1% lidocaine in a dog model of sciatic nerve block resulted in significantly higher injection pressures then during normal, perineural injection. The combination of intraneural needle placement and high pressure during injection was associated with nerve injury. Neurologic injuries resulting from an intraneuronal injection are probably due to a combination of factors. Examples include direct needle trauma with perforation of the perineurium and other nerve sheaths, physical disruption of the nerve fibers, and disruption of the neuronal microvasculature, with the consequent intraepineural or intrafascicular hematoma and nerve ischemia. Because 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 may result in endoneural ischemia. The addition of a vasoconstrictor and the application of a tourniquet over the site of nerve blockade will inevitably result in an additional decrease in blood supply to the nerve. The combination of all these factors contributes to neuronal ischemia and increases the risk of neurologic injury. Another important complication of an intraneuronal injection is the potential for an intrafascicular spread of the local anesthetic proximally toward the spinal cord, resulting in central neuronal blockade. This is particularly a concern with block techniques that involve needle placement at the level of the nerve roots or spinal nerves, such as interscalene,

paravertebral, and lumbar plexus block. Such injections within the dural cuffs or perineurium may result in inadvertent spinal or epidural anesthesia. TIPS: Based on our current understanding of mechanism of complications after neuronal blockade, it seems prudent to avoid high pressures and forceful, fast injections during administration of nerve blocks. Avoiding high injection pressures and controlling the speed of injection are perhaps the two single most important measures to avoid neurologic injury, inadvertent neuraxial spread of local anesthetic (centroneuraly), as well as massive channeling of local anesthetic into the systemic circulation (via cut venules, lymphatic channels etc.). In an attempt to standardize pressures and speed of injection during nerve block procedures, we instruct our trainees to always use the same needle types, syringe sizes (20 mL) and one-hand injection technique to develop a more consistent "feel" for pressure during injection. Unfortunately, the perceptions of a "normal" and "abnormal" pressure during nerve block injections greatly vary among clinicians. (Reg Figure 3 Anesth Pain Med 2004, in press) Even when an experienced anesthesiologist with a "developed feel" performs a nerve block procedure, it is usually another (helper) person who helps with the actual injection of local anesthetic. Besides, internal resistance of needles of various lengths, diameters and manufacturers all significantly vary, making it more difficult to reliably estimate the pressure during injection using a "feel" technique. Therefore, some means of objective measurements of pressures during nerve block injection may be beneficial to decrease a risk of neurologic complications after nerve blockade. Perhaps in a near future, nerve block kits will include a small, disposable, pressure measuring device to objectively monitor pressures during nerve block injections. Additionally, implementation of such monitoring would undoubtedly help standardize injection practices and allow for objective documentation and meaningful retrospective analyses. The futuristic look into such design is shown in Figure 3, where a small, calibrated manometer continuously displays the injection pressures during injection. Nerves may also be injured by other factors that may not be related to the nerve block procedure, such as compression, stretching during patient positioning, and the application of surgical retractors. Nerve injury during nerve localization and intraneuronal injection are the most commonly feared injuries.

Needle Bevels
Most experts would agree that short-bevel needles (i.e., angles 30 to 45 degrees) carry less risk of nerve injuries during peripheral nerve blockade than sharp needles with longer beveled tips. The recommendations on needle designs are largely based on the work of Selander and colleagues, who clearly showed that the risk of perforating a nerve fascicle was significantly lower when a short-bevel (45-degree) needle was used, as compared with a standard long-bevel (12 to 15 degrees) injection needle. The results of their work certainly make clinical sense and resultantly, short bevel needles are nowadays used most commonly for nerve blocks (excluding cutaneous blocks and local infiltration). In contrast, the work of Rice and McMahon suggested that the shorter bevel needles may cause more mechanical damage than the long beveled needles. In their experiment, after deliberately penetrating the largest fascicle of rat sciatic nerves with 12- to 27-degree bevel injection needles, when the needle was actually inserted into the nerves, the degree of neuronal trauma was greater with short-bevel needles. Naturally, the sharp needles produced clean cuts and the blunt needles produced messy cuts on the microscopic images. The debate that ensued neglected that fact that blunt-tip needles are much less likely to be inserted into the non-fixed and exposed nerves in the clinical setting. Thus, while their finding may hold true when the fascicle is indeed penetrated, short bevel needles are much less likely to penetrate the nerves, thus, reducing the risk of nerve penetration altogether. Unfortunately, this research study caused considerable confusion and debate in the field.

Nerve Stimulators
Nerve stimulators have become indispensable tools in modern regional anesthesia practice. An important advantage of the nerve stimulator technique is that nerve response is an objective method of confirming the needle-nerve relationship, as opposed to elicitation of paresthesia, which is invariably subjective. In addition, avoiding a painful paresthesia and the ability to premedicate patients prior to block placement result in a significantly greater patient satisfaction with nerve stimulator technique. Thus, it is not surprise that most recent publications on major peripheral nerve blocks used nerve stimulation in their methods. Also, most experts today suggest obtaining nerve stimulation with much lower current intensity (<0.5 mA) than was the case with older recommendations. Nerve stimulation with a consequent motor response using a current of low-intensity results in accurate needle placement with minimal discomfort to the patient.

However, it should be kept in mind that the use of nerve stimulators does not exclude the possibility of nerve damage, as a recent study by Auroy and colleagues points out. In particular, caution should be exercised when stimulation is obtained with currents of < 0.02 mA. In our own clinical experience, stimulation with such low current intensity is often associated with paresthesia on injection, perhaps suggesting an intraneurial placement of the needle. In this scenario, we routinely withdraw the needle until the motor response is obtained at a current of 0.2 mA to 0.5 mA. It should be noted that nerve stimulators used for peripheral nerve blockade can vary greatly in their features, stimulating frequency, maximum voltage output, stimulus duration, and accuracy. Although most modern units we studied in our laboratory performed adequately within a clinically relevant range of currents and impedance loads, some older models may be grossly inaccurate. For that reason, the recommendations on the current intensity in older books may not be applicable with all nerve stimulators. To get the most out of a nerve stimulator, have it tested for accuracy by the biomedical department. Unfortunately, most manufacturers suggest testing the nerve stimulators with the current of 1.0 mA. Testing the stimulators at a current output at 1.0 mA into an impedance load of 1 kO is what a routine test by biomedical engineers would involve and indeed nearly all stimulators we tested performed well in this current range. However, in peripheral nerve blockade, it is much more important that these tests be done in the most relevant, clinical current range (0.1mA to 0.5 mA). At the very least, for both accuracy and safety, the type of nerve stimulators and their electrical characteristics (current accuracy and duration, stimulating frequency) should be taken into the consideration when comparing results of clinical studies, or when trying to implement techniques in clinical practice.

Toxicity of Local Anesthetics

The overwhelming clinical experience is that correctly administered local anesthetics do not carry a risk of nerve injury. However, all local anesthetics are potentially neurotoxic, and this may become apparent when the local anesthetic is applied in unduly high concentrations or at higher than normal time. The potential for neurotoxicity with local anesthetic is a function of its potency, concentration, and the length of exposure of the neuronal tissue to the agent. Exposure of the endoneurim to a very high concentration of local anesthetic may contribute to neurologic

deficit. Under normal conditions, an injected bolus of local anesthetics expands until it reaches pressure equilibrium and the surrounding tissues. While diffusing to the tissues, a local anesthetic is rapidly diluted by the interstitial fluid, and systemic absorption assists in decreasing its concentration. However, this may not be the case during intrafascicular injection with its concomitant trauma, neural ischemia, and possible vasoconstriction. Indeed, in several models of nerve injury and using a number of injectable agents, only intrafascicular injections resulted in a neurologic injury that can be documented as early as 30 minutes following intraneural injection. Intrafascicularly injected local-anesthetic solutions lead to changes in the permeability of the blood-nerve barrier, associated edema, increased endoneurial fluid pressure, and consequent nerve-fiber injury. In contrast, extra-fascicular injection produces little or no evidence of nerve injury.

Neuronal Ischemia
A good neurologic outcome despite the widespread use of tourniquets during extremity surgery demonstrates that peripheral nerves are relatively resistant to ischemia of limited duration and magnitude. However, the laboratory data unequivocally suggest that the combination of nerve compression and ischemia can indeed cause irreversible damage to the sciatic nerve in less than 4 hours. A combination of several factors, such as increased pressure due to an inadvertent intraneuronal injection and reduced blood flow due to epinephrine, can result in severe neuronal demise. The endoneurial pressure under these circumstances can exceed the capillary perfusion pressure and result in ischemia of the nerve fascicles, on top of the tissue toxicity of local anesthetic. The addition of epinephrine can further enhance ischemia due to its vasoconstriction effect and reduction of blood flow. Thus, the key to avoiding neuronal ischemia is avoidance of the combination of intraneural injection, epinephrine, and prolonged application of the tourniquet, particularly over the area of nerve block injection.

Methods and Techniques To Decrease The Risk of Nerve Injury After Peripheral Nerve Blocks*
Based on the aforementioned evidence, we routinely adhere to the following recommendations to decrease the risk of complications with peripheral nerve blockade.

Aseptic technique Most nerve block techniques are merely percutaneous injections. However, infections are known to occur and can result in significant disability. Since this complication is almost entirely preventable, every effort should be made to adhere to strictly aseptic technique. Short bevel insulated needles The short bevel design helps prevent nerve penetration. Insulated needles are now widely available and result in much more precise needle placement when nerve stimulator is used. Needles of appropriate length for each and every block procedure Excessively long needles should not be used for nerve blockade. For instance, NEVER insert needles longer than 50 mm in interscalene blockade. In addition, needles of appropriate length can be advanced with far greater precision than excessively long needles.

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) a second and that no current is delivered between the pulses. Fast insertion and withdrawal of the needle may result in failure to stimulate the nerve because the needle may pass near by, 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.

Accuracy of the nerve stimulator Always make sure that the nerve stimulator is operational, 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 massive channeling of the local anesthetic in the systemic circulation, with consequent risk of severe CNS and cardiac toxicity. Forceful, fast injections under excessive pressure also may carry more risk of intrafascicular injection. Limit the injection speed to 15-20 mL/minute.

Avoidance of injection under high pressure Intrafascicular needle placement results in higher resistance (pressure) to injection due 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 1 mL of local anesthetic proves difficult, the injection should be abandoned and the needle completely withdrawn and check for patency before reinserting.

Avoidance of paresthesia on injection Severe pain or discomfort on injection may signify intraneuronal placement of the needle and should be avoided. This should not be confused with a normal mild "paresthesia-like" symptom, commonly reported by patients when the needle is placed in the immediate vicinity to the nerve. Keep in mind that published case reports suggest that absence of pain on injection alone does not guarantee that the needle is not placed intraneurally. Absence of pain and abnormal resistance on injection should be documented in the anesthetic record after each block procedure.

Chose your local anesthetic solution wisely Always choose a shorter acting (and less toxic) local anesthetic for short procedures where longlasting postoperative analgesia is not required. Local anesthetic toxicity is the most common complication with neuronal blockade and it is much safer when this occurs with chloroprocaine or lidocaine than with bupivacaine. Blocks in anesthetized patients Blocks in anesthetized patients should be avoided or at least an uncommon practice. When it is necessary to place blocks in anesthetized patients, this should be done only by practitioners with substantial experience with the planned technique. Such cases should NEVER be considered "teaching".

Repeating blocks 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. *Adopted with permission from www.NYSORA.com (New York School of Regional Anesthesia)