NYSORA - The New York School of Regional Anesthesia: Complications Of Peripheral Nerve Blocks

Complications Of Peripheral Nerve Blocks
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Vijay Patel on 19/03/2009 17:11:00

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  	*Complications After Nerve Blockade: How Common Are They?
	*Postoperative Neurologic Deficit: Regional vs. General Anesthesia 	*Symptoms
of Nerve Injury 	*Peripheral Nerves: Functional Anatomy 	*Pathophysiology
	*Mechanical Trauma 	*Needle Bevels 	*Nerve Stimulators 	*Toxicity of Local
Anesthetics 	*Neuronal Ischemia 	*Methods and Techniques To Decrease The Risk of
Nerve Injury After Peripheral Nerve Blocks
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:
*Mechanical trauma to the nerve
*Needle trauma 	*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.).
Figure 3
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 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 (