Regional Anesthesia and Nerve Injuries: How to prevent?

Alain Borgeat, M.D., Ph.D.

Department of Anesthesiology, Balgrist University Hospital, Zurich, Switzerland

Nerve injuries are a well-recognized complication of anesthesia (1). Postoperative brachi-
al plexopathy has been documented in the literature for more than 100 years. Postopera-
tive brachial plexopathy is generally believed to be a result of traction injury of the nerves
with compression a contributing factor. Both stretching and compression of the nerve ul-
timately lead to ischemia of the vasa nervorum and subsequent injury to the nerve. In
addition, there may be rupture of intraneural capillaries and hematoma formation with
further compression. Several factors have been associated with intraoperative brachial
plexus injury, including concomitant patient disease, anatomical variations, positioning of
the patient, surgical factors and physiological factors.
The frequency of peripheral neuropathies reported after regional anesthetic blockade is
generally low and varies from zero to more than 5% (1). Lesions to the brachial plexus
seem to be reported most frequently (2,3,4), but injuries of the sciatic and phrenic nerves
have also been reported. The high incidence of postanesthesia neuropathies in the upper
extremity probably reflects the relatively high rate of hand and arm lesions and the con-
comitantly frequent use of brachial plexus blocks for surgery.
Peripheral nerve complications can also be seen after general anesthesia, but then, pre-
sumably, most are due to position-dependent compression or stretching of the nerve. In a
closed-claims review of nerve injuries associated with anesthesia, 61% of the claims ap-
peared after general anesthesia and 36% after regional anesthesia. The anesthetic tech-
nique was not recorded in the remaining 3% of cases. Lesions to the ulnar nerve, brachial
plexus, and lumbosacral plexus roots were most common. Interestingly, more than 70%
of the upper extremity nerve lesions were associated with general anesthesia, whereas
more than 90% of the lumbosacral nerve root complications were related to regional
anesthesia, most frequently subarachnoid block (5).
The symptoms of a nerve lesion can appear within a day or two but sometimes may not
become apparent until 2 or 3 weeks after the injury (6). This variation in time to debut is
likely to depend on the origin of the nerve lesion and on confounding factors such as
"normal" postoperative pain and effects of surgery, position, plaster casts, and other ban-
daging. The intensity and duration of symptoms vary with the severity of the injury, from
light, intermittent tingling and numbness lasting of few weeks, to persistent, painful pares-
thesia, neuropathic pain, sensory loss, and motor weakness lasting several months or
years, sometimes developing into distressing complex regional syndrome type I or II
(6,7,8).
2
Neurologic sequelae after a local anesthetic blockade basically depend on three classes
of insult: trauma, toxicity, and ischemia. In most cases, the lesion is probably caused by
the combined action of two, or all three, of these factors (9).
Trauma to the nerves can be caused by the injection needle, intraneural injection, and
compression or stretching due to other external factors such as patient position and effect
of retractors. The search for paresthesias can increase the risk of postblock neuropathies
was found by Plevak et al. (10) in prospective clinical studies. This report revealed a trend
for a paresthesia-nerve lesion relation, and metaanalysis of different studies demonstrat-
ed that the frequency of post-anesthesia neuropathy was significantly higher (P<0.05)
when paresthesia techniques were utilized, compared with "nonparesthesia" techniques
(11).
To reduce the risk of nerve lesions in clinical regional anesthesia, it is frequently recom-
mended that fine, short-bevel needles (i.e., angles of 30 to 45 degrees) be used. This is
bases on experimental studies in rabbit sciatic nerves that showed that the risk of perfo-
rating a nerve fascicle was significantly reduced when a short-bevel (45-degree) needle
was used, as compared with standard long-bevel (12 to 15 degrees) injection needle (12).
Selander et al. (12) studied the frequency of fascicular injury after penetrating rabbit scia-
tic nerves, both isolated and in vivo, with a short- of long-bevel needle that was then im-
mediately removed. They found that the fascicles tended to slide or roll away from the
advancing needle, especially the short-bevel needle. Consequently, fascicular lesions
were associated significantly less frequently with the short-bevel (45-degree) needle that
with the long-bevel (14-degree) one. When the long-bevel needle was used, the size of
the fascicular injury varied with the orientation of the bevel: the least injury was caused by
needles inserted with the bevel parallel to the nerve fibers. The rare fascicular lesions
after the short-bevel needle were less dependent on bevel orientation and usually of an
extent close to the lesions caused by the transversely oriented long-bevel needle.
Painful paresthesias on injection indicate intraneural needle position. Such injections are
initially painful, but as the local anesthetic very quickly blocks the nerve, the pain fades
and information regarding the nerve injury disappears until the block wears off. Thus, it is
important that the anesthesiologist maintain adequate contact with the patient and react
to such information by immediately stopping the injection to reposition the needle away
from the nerve.
The destructive effects of intrafascicular injections are probably due to a combination of
three factors. First, direct needle trauma leads to perforation of the perineurium and other
nerve sheaths, cutting and disrupting the nerve fibers and compromising the microvascu-
lature, with a risk of intraneural or intrafascicular bleeding and hematoma (13).
3
All local anesthetics are potentially neurotoxic, and the neural blockade can be seen as a
reversible expression of this. Commercial local anesthetics are supplied in concentration
that under normal conditions do not cause nerve damage; however, the use of higher
concentrations and intraneural injections, especially when epinephrine has been added,
can result in severe damage with persistent dysfunction and pain (6,13).
Under normal conditions, the injected local anesthetic is rapidly diluted and buffered by
the interstitial fluid, absorption into the blood commences within a very short time. This
means that after injection the concentration of the local anesthetic at the site of injection
decreases relatively quickly.
Nerve ischemia may be complete for a limited time only, and can be caused by extra-
neural or intraneural factors. Extraneural ischemia can be due to local interference with
circulation (e.g., iatrogenic interference with blood circulation, arteriosclerosis, or global
hypoperfusion. Intraneural ischemia can be caused by intraneural angiopathy, as in di-
abetic neuropathy or systemic lupus erythematosus, or by an increase in endoneural
pressure due to endoneural edema or an intraneural injection.
Experimentally, it was found that intrafascicular injections in rabbit sciatic nerve in vivo
could produce endoneurial pressures of more than 700 mmHg, and after such injections
the endoneurial pressure could exceed the estimated capillary perfusion pressure for
about 15 minutes. During this period the nerve fascicle is ischemic and is thus vulnerable
to otherwise toxicologically neutral local anesthetic solutions (14). Similar condition can
also occur in humans, and admixture of epinephrine with the local anesthetic can en-
hance ischemia and thus increase the risk of neurotoxic injury.

Conclusions
Different factors may be involved in neurological complications after peripheral nerve
blocks
- the tourniquet
- the surgeon. Surgery is implicated in neural damage secondary to traction and/or com-
pression. Experimental studies have shown that stretch and compression act synergic-
ally for nerve damage.
- the anesthetist. The following rules should be applied to avoid anesthetist induced
neural damage
do not touch the nerve
do not go into the nerve
do not inject local anesthetics into the nerve (15)
use the lowest local anesthetic concentration possible
use the most friendly local anesthetic
4
The best treatment of neurologic deficit after regional anesthesia is prevention. A careful
and well documented technique in an awake patient should prevent any nerve damage
due to the needle or an intraneural injection. Awareness of the problems associated with
operative positions and careful positioning of the patient with adequate padding belong to
the appropriate precautions. Once damage has occurred, it can take several forms, rang-
ing from a mild, reversible neurapraxia to a permanent sensoritmotor deficit.

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