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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.
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Monitoring the Depth of Needle Insertion
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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.
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Current Delivery & Disconnect Monitoring
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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.
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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
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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).
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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).
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Resistance to Injection
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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).
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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.
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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.
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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
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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.
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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.
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