Chapter 47. Injection & Current Delivery Monitoring

Only in the past decade or so has research on functional regional anesthesia anatomy, outcome, and equipment slowly begun to transform regional anesthesia into a modern discipline. However, in many ways the equipment used for peripheral nerve block remains in its infancy. The sophistication and functionality of the equipment used for peripheral nerve blocks (PNBs) are, at best, rudimentary and lag far behind those of general anesthesia, as depicted in the following examples.

Monitoring the Depth of Needle Insertion

Spinal cord injury after interscalene block is perhaps the most serious complication of a PNB. This devastating complication, however, can occur only with an excessively deep needle insertion (ie, >2.5 cm).1 Monitoring the depth of the needle insertion is substantially important to avoid a too-deep insertion (eg, spinal cord or chest cavity with interscalene block). In fact, the recently suggested standardized block documentation procedure requires clinicians to document the depth at which the needle is inserted. Nevertheless, most commercially available needles still do not have depth markings for such objective documentation.2 Despite that fact, there is much work underway to remedy this deficiency, and it is inevitable that all needles used in regional anesthesia will eventually incorporate depth markings on their shafts.

Current Delivery & Disconnect Monitoring

Nerve stimulator–assisted nerve localization has become a standard technique in PNB. In contrast to paresthesia techniques, nerve stimulation provides a more objective assessment of the needle position in relation to the nerve, does not require patient cooperation, and permits the use of sedatives and analgesics for patient comfort during a nerve block procedure. The basic premise of the nerve stimulator–assisted nerve blocks is that the electrical current (“field") in front of the advancing needle should elicit a motor response before the tip of the needle enters the nerve. In many nerve block techniques, a functioning nerve stimulator is essential to decrease the risk of inadvertent placement of the needle intraneurally or intravascularly. For instance, because of the close proximity of the subclavian artery anterior and inferior to the brachial plexus during cervical paravertebral block, the functionality of the nerve stimulator is of paramount importance to avoid vascular complications.3 With a functioning nerve stimulator, a motor response of the shoulder muscle is seen when the brachial plexus is stimulated, which should occur before the subclavian artery is punctured by the advancing needle. In the case series on continuous paravertebral blocks using a stimulating catheter reported by Boezaart et al.,3 vascular complications consisting of large-vessel puncture with a 17-gauge needle occurred only in patients in whom the nerve stimulators were found to be malfunctional.

Consequently, the ability of the nerve stimulator to deliver accurate current output and integrity of the stimulator-needle-return (skin) electrode circuit is of utmost importance for both the block success and the safety of the procedure. Problems with the reliability and accuracy of nerve stimulators have long been recognized but have been addressed only within the past few years by introduction of modern, constant-current, PNB-specific nerve stimulators.4,5 However, the contemporary nerve stimulators still do not incorporate a convenient means of continuously monitoring current delivery by the operator to allow detection of a nerve stimulator malfunction that could lead to complications.3

The following case summaries describe several scenarios in which malfunction of the nerve stimulators or electrical connection was not detected owing to the absence of a convenient means of monitoring current delivery.

Example 1: A 90-year-old, 4-ft 10-in., 112-pound woman presented to the operating room with an infected right arm after open reduction and internal fixation of a fracture of her right humerus. She was scheduled to undergo incision and drainage of her right arm under interscalene brachial plexus block. After application of standard ASA (American Society of Anesthesiologists) monitors, the patient was premedicated with midazolam 2 mg IV, and the equipment, consisting of a Stimuplex-DIG nerve stimulator (B. Braun Medical, Inc.) and an insulated 22-gauge × 2-in. needle (Stimuplex A2250) was prepared. The return electrode (ECG electrode, Cleartrace, CONMED, Utica, NY) was placed on the right forearm. Interscalene technique through the classic approach was attempted with the nerve stimulator current set at 1.0 mA. Although the patient had easily identifiable landmarks, nerve stimulation could not be obtained despite multiple needle passes and changes of the needle entry site. During the attempts, the LCD (liquid crystal display) on the nerve stimulator did not indicate a problem with the patency of the electrical circuit. After the anesthesia team empirically switched to another nerve stimulator (the same model), nerve stimulation was promptly accomplished. A defective nerve stimulator was determined to be responsible for the many unsuccessful attempts at nerve localization, yet the operator was unaware of the equipment malfunction.

Example 2: A 31-year-old, 5-ft 2-in., 135-lb man with a history of end-stage renal disease was scheduled to undergo creation of an A-V fistula in the left arm. Interscalene brachial plexus block was planned as the anesthesia technique. After premedication with midazolam 2 mg IV and identification of the anatomic landmarks, a block was attempted using a Stimuplex DIG nerve stimulator and Stimuplex 22-gauge, 2–in. insulated needle. Several attempts to localize the brachial plexus using the initial current of 1.5 mA did not produce a twitch response. Several more attempts using another nerve stimulator (the same model) evoked no motor response. At this point, it was noticed that when the current setting was raised above 0.5 mA, the nerve stimulator indicated that the set current was not being delivered. It is possible that both stimulators indicated disconnect, but this could have been overlooked while the anesthesia team was preoccupied with the block technique. Careful inspection of the electrical connections led to detection of the defect in the connecting cable–needle assembly. Changing the stimulating needle, while paying close attention to the wire connection between the needle and the nerve stimulator, quickly led to a prompt motor response at 0.35 mA and a successful block for surgery.

Example 3: A 61-year-old, 5-ft 2-in., 169-lb woman with a history of mild asthma was scheduled to undergo repair of her left shoulder rotator cuff under interscalene brachial plexus block. Midazolam 4 mg was given intravenously, anatomic landmarks were identified, and the area was cleaned using povidone-iodine solution. Interscalene block was then attempted with a Stimuplex nerve stimulator and the 22-gauge × 2-in. insulated needle. With the return ECG electrode (3M) placed on the arm and the stimulator set to deliver 1.0 mA, several attempts to localize the brachial plexus were made without success. At this point, it was noted that the LCD on the stimulator indicated that the electrical circuit was incomplete. Checking all wire connections, changing several needles, and using multiple nerve stimulators were all unsuccessful in fixing the problem. As the last resort, the return ECG electrode was taken off the patient's arm and connected to the tip of the needle, at which point the LCD disconnect alert stopped blinking, indicating that the electrical circuit was completed. However, when a new ECG (3M) electrode was applied to the skin, the LCD again indicated that the set current was not being delivered. Firm pressure on the ECG electrode against the patient's skin resulted in the disappearance of the disconnect signal on the LCD. It became apparent that the “problem” was with the skin electrodes. Indeed, on careful inspection, the ECG electrodes were found to be desiccated and lacked their original conductive properties.

When measured with an ohmmeter, the electrical resistance ranged between several kiloOhms and several megaOhms (normal resistance is very low and typically does not exceed a few ohms). Changing the ECG electrode to an ECG electrode from a freshly opened stock resulted in the disappearance of the disconnect alarm and allowed nerve localization to be accomplished.

These case summaries emphasize the importance of ensuring proper functionality of the nerve stimulator and detection of abnormal circuit impedance (desiccated, poorly conducting skin electrode, circuit disconnect, or stimulator failure) or electric disconnect to successfully localize a peripheral nerve, achieve reliable blockade, and avoid needle trauma to the nerve. Unfortunately, there are no manufacturing standards when it comes to alarms, which can indicate a problem with the delivery of the current. Although older models of nerve stimulators did not incorporate a disconnect indicator at all, most new models of nerve stimulators incorporate a disconnect indicator. However, the indicators of the functionality are located on the nerve stimulator (thus, remotely from the operator) and vary substantially in how they display the information when there is a problem with the circuit connections, nerve stimulator, or return electrode–skin contact.

Some stimulators deliver an audible signal only when the current is successfully delivered; some emit an audible signal when the current is not delivered; others do not have any indicators. In a typical clinical setting, it may be rather challenging for the operator to concentrate on the block technique, observe the motor response, communicate with the patient, and monitor the information provided by a small-sized and difficult-to-read LCD indicator of the nerve stimulator on the current setting and occurrence of a disconnect.

The functionality of the nerve stimulator and the integrity of the circuit can and should be checked before the block procedure; however, many problems with the current delivery occur during the actual block procedure, such as electrical disconnect, nerve stimulator battery failure, and skin–electrode disconnect. For this reason, whenever nerve localization proves challenging, clinicians should often suspect a problem with the equipment (peripheral nerve stimulator) or electrical circuit as another variable in addition to the possible anatomic difficulties (ie, insertion of the needle in a wrong plane or a wrong anatomic position).

Inevitably, equipment designed in the future should incorporate a remote indicator of current delivery, which would be best mounted on the hub of the needle (Figure 47–1). Such a design would allow continuous monitoring of the current delivery by the clinician performing the block, as well an immediate detection of the circuit disconnect or other electrical problems (eg, stimulator failure).

Resistance to Injection

Assessing resistance to injection during PNB is a common practice.2 This practice is similar to the loss of resistance to injection of air or saline using a “syringe feel” during administration of epidural, paravertebral, or lumbar plexus blocks (Figure 47–2). Assessing tissue compliance has long been used as an additional means of estimating the anatomic location of the needle tip during application of a PNB. For this, clinicians typically use a “syringe feel” to estimate what may be an abnormal resistance to nerve block injection to reduce the risk of intraneural injection.6–8 However, this practice has significant inherent limitations because of the subjective nature of the assessment and the inherent variability in the feel.9 In addition, the resistance to injection is greater with smaller needles, adding to the confusion as to what constitutes normal or abnormal resistance (Figure 47–3). In contrast to loss of resistance in an epidural injection, there is no baseline pressure information or change in tissue compliance during nerve block injection, which means that with nerve block injection, there is no change in pressure that can be relied on. In a study by Claudio and colleagues,9 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 perceptions of what constituted an appropriate resistance to injection. In addition, no information has been available on what constitutes normal and abnormal injection pressure during nerve block performance (Figure 47–4).

When asked to inject local anesthetic for a colleague performing a simulated interscalene block in a mannequin, the studied anesthesiologists significantly varied in their perception of what constituted normal versus abnormal resistance (pressure) to injection. A substantial number of injections resulted in pressures higher than 20 psi. If needles were indeed inserted intraneurally, such injection pressures would allow an intraneural administration of local anesthetic and consequent neurologic injury.

To explain the mechanisms responsible for the development of neuraxial anesthesia after an interscalene block,10,11 Selander and coworkers12 injected solutions of local anesthetic into rabbit sciatic nerves and traced the spread of the anesthetic along the nerve sheath. They postulated that an intraneural injection results in significant intraneural spread of local anesthetic. In their model, the investigators noticed that intraneural injections often resulted in much higher injection pressures 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. Researchers in this study, however, used a small animal model, microinjections (10–200 μL), miniature needles, clinically irrelevant injection rates (100–300 μL/min), and did not study neurologic consequences after intraneural injections. For these reasons, their foretelling of results on the possible association of injection pressure with intrafascicular injection did not generate the deserved interest among researchers and clinicians.

More recent studies used more clinically applicable injection speeds and volumes of local anesthetic in a large animal model.5 The results of these studies suggest that perineural injections are associated with low-injection pressures (<15–20 psi). In contrast, high-injection pressures (>20 psi) are associated with intrafascicular injections and as such carry a risk of neurologic injury.5 In the dog model of intraneural injury, only intraneural injections resulting in pressures greater than 20 psi were associated with clinically detectable neurologic deficits as well as histologic evidence of injury to nerve fascicles.13

Note that current evidence suggests that neurologic injury does not always develop after an intraneural injection.14 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.5 Intraneural, but extrafascicular (interfascicular) injection, probably occurs more commonly than thought in clinical practice.14 Such an injection results in a block of fast onset and long duration rather than in a neurologic injury.13 This is because an intraneural but extrafascicular injection leads to intimate exposure of nerve fascicles to high concentration of local anesthetics. In this scenario, permanent neurologic injury does not develop because the local anesthetic is deposited outside the fascicles and the block slowly resolves after the injection without evidence of histologic derangement. However, intraneural intrafascicular needle placement results in high injection pressures and leads to neurologic injury.

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. The future needle–syringe designs for use in PNBs will inevitably incorporate a simple, unobtrusive, and inexpensive in-line pressure monitor to allow clinicians to avoid injection force (pressure) consistent with intraneural injection. Figure 47–5 is an example of such a system.

Administration of PNBs relies on localization of a peripheral nerve using a percutaneously placed needle aimed at the nerve to be blocked. Electrical current used for the purpose of nerve localization with PNBs is of a relatively low intensity (typically 0.2 mA–2 mA). Astute knowledge of anatomy is essential to avoid multiple needle insertions during attempts at nerve localization. However, a current of higher intensity (5–20 mA) can be used to transcutaneously stimulate and prelocalize nerves before needle insertion.

It is interesting that this practice is relatively new in peripheral nerve blockade despite the fact that the equipment has been available for decades and that the same principle is used on a daily basis in general anesthesia. For instance, stimulation of a motor nerve and evaluation of the resultant motor response constitute standard monitoring of the neuromuscular junction after the administration of muscle relaxants. The principle behind neuromuscular monitoring is that an electrical stimulus applied using a cutaneous electrode over a nerve should result in depolarization of the nerve and a consequent certain degree of motor response distal to the stimulation. Neuromuscular monitoring constitutes the nerve stimulator and stimulating electrodes (typically pre-gelled surface electrodes). Electrical current is applied using a peripheral nerve stimulator designed to deliver current intensity up to 80 mA (up to 700 volts in some units).4

Similar to monitoring of the function of the neuromuscular junction, surface prelocation of the peripheral nerves is possible, primarily with nerves and plexi that are superficial (eg, interscalene, axillary, femoral nerves). This is because the electrical current flows in all directions from the electrode and not necessarily toward the nerve or a plexus. Consequently, the intensity of the current reaching the nerve is inadequate to depolarize nerve(s) that are deeper below the skin surface.

Figure 47–6 demonstrates the apparatus and the procedure. In short, the electrode sites are prepared with a degreasing agent (eg, alcohol) to decrease the skin resistance and increase the loss of the stimulus at the electrode–skin interface. The stimulation is usually begun with a current of 5 mA when a stimulus of longer duration is used (eg, 1 ms) or up to 20 mA when a stimulus of shorter duration is used (eg, 0.1 ms). Once a distal motor response specific to the nerve under localization is elicited, the current is lowered to the minimal intensity at which this response is still seen or felt. The point on the skin at which the stimulation is elicited with the minimal possible current is labeled as the approximate position of the nerve (plexus). During the localization, the electrode is continuously and firmly pressed against the skin to shorten the skin–nerve distance and decrease the resistance of the skin–electrode interface (Figure 47–6).

In some patients, stimulation with a current of significantly greater intensity than 5 mA may be necessary to evoke a motor response. In these patients, a higher output nerve stimulator (ie, a unit used for neuromuscular monitoring) can be used. The current is set at 15–20 mA and applied via an alligator clip; the current is decreased as the motor response is established. It is important to realize, however, that surface nerve prelocation provides only a rough estimate of the location of the nerve or a plexus, and needle repositioning and re-angling is often necessary to needle-electrolocalize (percutaneous) the nerve.