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Journal of the American Academy of Orthopaedic Surgeons
328
Axillary nerve lesions are not com-
monly diagnosed. Although most
such injuries respond to nonopera-
tive measures, surgical treatment is
warranted in selected cases. With ad-
vances in microsurgery, increased
awareness of the potential for treat-
ment of brachial plexus injuries, and
the greater focus on shoulder disor-
ders in the past decade, complex
reconstructive procedures on the
shoulder are now more common.
Accurate knowledge of axillary nerve
anatomy and function is paramount
to avoid complications after such
procedures. Several reports on the
results of surgical treatment of axil-
lary nerve lesions have been pub-
lished.
1-4
A thorough understanding
of the etiology, diagnosis, and treat-
ment of axillary nerve lesions not
only aids in the avoidance of injury to
the nerve during surgical procedures
but also promotes early recognition
and treatment.
Anatomy
The axillary nerve is a terminal

branch of the posterior cord of the
brachial plexus and derives from the
ventral rami of the fifth and sixth
cranial nerves. The first portion of
the axillary nerve lies lateral to the
radial nerve, posterior to the axil-
lary artery, and anterior to the sub-
scapularis muscle. It runs obliquely
across the inferolateral border of the
subscapularis, crossing 3 to 5 mm
from its musculotendinous junction.
The axillary nerve then enters the
quadrilateral space accompanied by
the posterior humeral circumflex ar-
tery. The boundaries of the quadri-
lateral space are the subscapularis
anteriorly, the teres major and latis-
simus dorsi inferiorly, the long head
of the triceps medially, and the
humerus laterally. When the shoul-
der is viewed from its posterior
aspect, the teres minor forms the
superior border of the quadrilateral
space. The nerve lies in intimate
contact with the inferior joint cap-
sule as it passes through the quadri-
lateral space (Fig. 1). When the
nerve exits the space, it continues to
the posterior aspect of the humeral
neck and divides into anterior and

posterior branches.
The anterior portion of the nerve
continues to circle around the surgi-
cal neck of the humerus, traveling
deep to the deltoid toward the ante-
rior border of the muscle. Along
the way, the nerve sends branches
to innervate the middle and ante-
rior portions of the deltoid. The
position of the anterior trunk is
commonly reported to lie 4 to 7 cm
inferior to the anterolateral corner
of the acromion.
5
The posterior trunk innervates
both the teres minor and the poste-
rior portion of the deltoid. A branch
to the teres minor usually arises
within or just distal to the quadrilat-
eral space and enters the posterior
or inferior aspect of the teres minor
muscle. A terminal branch of the
Dr. Steinmann is Assistant Professor, De-
partment of Orthopaedic Surgery, Mayo Clinic,
Rochester, Minn. Dr. Moran is Chief Resident,
Department of Orthopaedic Surgery, National
Naval Medical Center, Bethesda, Md.
Reprint requests: Dr. Steinmann, Mayo Clinic,
200 First Street SW, Rochester MN 55905.
Copyright 2001 by the American Academy of

Orthopaedic Surgeons.
Abstract
Axillary nerve injury is infrequently diagnosed but is not a rare occurrence.
Injury to the nerve may result from a traction force or blunt trauma applied to
the shoulder. The most common zone of injury is just proximal to the quadri-
lateral space. Atraumatic causes of neuropathy include brachial neuritis and
quadrilateral space syndrome. The vast majority of patients recover with non-
operative treatment. Baseline electromyographic and nerve conduction studies
should be obtained within 4 weeks after injury, with a follow-up evaluation at
12 weeks. If no clinical or electromyographic improvement is noted, surgery
may be appropriate. The results of operative repair are best if surgery is per-
formed within 3 to 6 months from the injury. Surgical options include neuroly-
sis, nerve grafting, and neurotization. The results of repair of axillary nerve
injuries have been good compared with treatment of other peripheral nerve
lesions, due to the monofascicular composition of the nerve and the relatively
short distance between the zone of injury and the motor end-plate.
J Am Acad Orthop Surg 2001;9:328-335
Axillary Nerve Injury: Diagnosis and Treatment
Scott P. Steinmann, MD, and Elizabeth A. Moran, MD
Scott P. Steinmann, MD, and Elizabeth A. Moran, MD
Vol 9, No 5, September/October 2001
329
posterior trunk forms the superior
lateral cutaneous nerve.
There are several common ana-
tomic variations of the course of the
axillary nerve. In as many as 20%
of persons, the axillary nerve origi-
nates from the posterior division of
the upper trunk of the plexus. Oc-

casionally, the seventh cervical root
contributes to the axillary nerve.
The axillary nerve may also give
rise to the inferior subscapular
nerve, which innervates both the
subscapularis and the teres major.
The internal topography of the
fascicular groups has been studied
by Aszmann and Dellon.
6
The nerve
in the axilla is monofascicular, but as
the nerve enters the quadrilateral
space there are three distinct groups
of fascicles: the motor groups to the
deltoid and teres minor and the sen-
sory group of the superior lateral
cutaneous nerve. These fascicles are
discrete entities within the posterior
cord. The deltoid fascicles are al-
ways found in a superolateral posi-
tion; those of the teres minor and
superior lateral cutaneous nerve are
located inferomedially.
Etiology
Most axillary nerve injuries present
as part of a combined brachial
plexus injury. In reported studies,
infraclavicular isolated axillary nerve
injury occurred in only 0.3% to 6% of

brachial plexus injuries.
3,7
Such infra-
clavicular injuries have been found
to have a greater likelihood of spon-
taneous recovery of function than
supraclavicular lesions.
8
Injury to the axillary nerve most
commonly follows closed trauma
involving a traction injury to the
shoulder, usually with associated
dislocation or fracture (Table 1).
Some patients may have an occult,
subclinical axillary nerve lesion that
is evidenced by the findings from
the electromyographic and nerve
conduction study (EMG/NCS) but
that is masked by overlying dis-
comfort from an associated fracture
or dislocation.
9
Blunt trauma to the
anterior lateral aspect of the shoul-
der has also been noted to cause ax-
illary neuropathy. The mechanism of
injury in such cases is considered to
be a compressive force to the nerve
as it travels on the deep surface of the
deltoid muscle.

10
Occasionally, the
patient presents after an injury with
a mixed brachial plexus palsy affect-
ing primarily the proximal shoul-
der girdle muscles with partial arm
or hand palsy. With observation and
nonoperative treatment, sponta-
neous recovery of the forearm neu-
ropathy usually occurs. When there
is incomplete recovery, the deltoid
and rotator cuff muscles are most
commonly affected.
1
Incomplete paralysis can occur
with sparing of either the anterior or
the posterior portion of the deltoid.
In such cases, atrophy may not be
obvious and, if rotator cuff function
is preserved, shoulder range of mo-
tion may be normal.
1
However,
when affected individuals exercise,
they quickly fatigue, and their ab-
duction strength is much less than
normal. Young athletic patients may
be able to compensate for complete
deltoid paralysis and can often per-
form activities of daily living with

only limited disability. However, in
Suprascapular nerve anastomosis
between suprascapular and
circumflex scapular arteries
Infraspinatus
Fibrous capsule
Humerus
Axillary nerve
Deltoid
Branch to
teres minor
Upper lateral
cutaneous
nerve of arm
Triangular interval
Quadrilateral space
Triangular space
Figure 1 Posterior view of quadrilateral space. (Adapted with permission from Anderson
JE [ed]: Grant’s Atlas of Anatomy, 7th ed. Baltimore: Williams & Wilkins, 1978, p 6-39.)
Axillary Nerve Injury
Journal of the American Academy of Orthopaedic Surgeons
330
a work environment, they will easily
fatigue with overhead activities or
heavy lifting.
The origin of deltoid paralysis
sometimes appears to be atraumat-
ic. This condition has been referred
to as acute brachial neuritis or
Parsonage-Turner syndrome. Pa-

tients typically relate a history of
severe shoulder pain that may radi-
ate down the arm and may last
from a few days to several weeks.
The pain is soon followed by loss
of motor function in the affected
muscles. Several nerves may be in-
volved (typically, the axillary, long
thoracic, and suprascapular nerves),
but occasionally only one nerve is in-
volved. When brachial neuritis or
a mixed lesion is suspected, EMG
evaluation can be helpful in delin-
eating the problem. Treatment
with oral corticosteroids has been
used empirically, although it has
not yet been established that these
drugs provide any clear benefit.
The prognosis in atraumatic cases
is quite good, with most patients
achieving normal function.
11
The quadrilateral space syn-
drome is another potential cause of
axillary neuropathy. Symptoms
typically include a chronic, dull,
aching pain in the dominant
extremity, which can awaken the
patient at night. Patients infre-
quently report a history of trauma.

The findings on physical exami-
nation are usually limited to tender-
ness posteriorly along the shoulder
joint. Deltoid atrophy and lateral
sensory changes are uncommon,
and the EMG findings are usually
normal. If quadrilateral space syn-
drome is suspected, a subclavicular
arteriogram may be appropriate.
This study is considered positive if
posterior humeral circumflex artery
occlusion occurs with less than 60
degrees of abduction. On magnetic
resonance (MR) imaging, signal
changes in the deltoid and teres
minor muscles have been noted to
represent denervation patterns con-
sistent with quadrilateral space syn-
drome.
12
Because this syndrome is diffi-
cult to diagnose accurately, obser-
vation is the usual treatment, as the
vast majority of patients will im-
prove over time. Some patients
benefit from surgical exploration of
the quadrilateral space and decom-
pression of the axillary nerve by re-
lease of scar or tight fibrous bands.
13

Evaluation
The clinical history is important in
planning the treatment of patients
who may have an axillary nerve
injury. Patients without a distinct
episode of trauma may have a com-
pressive neuropathy due to an en-
larging mass or aneurysm. Quad-
rilateral space syndrome may also
occur with minimal or no trauma. If
pain precedes the loss of motor func-
tion, the diagnosis may be brachial
neuritis. A recent event of pene-
trating trauma or surgical trauma
makes axillary nerve injury likely.
Clinicians should also carefully eval-
uate the axillary nerve function of
any patient with a shoulder disloca-
tion or proximal humerus fracture
prior to reduction. However, al-
though it is theoretically possible to
reduce a dislocation or fracture
forcefully enough to cause axillary
nerve injury, this has not been re-
ported in the literature.
The initial physical evaluation
should include standard testing for
active and passive range of motion of
the shoulder, as well as for strength
of abduction, external rotation, and

internal rotation. In chronic cases,
muscle atrophy should be assessed,
remembering that if the posterior del-
toid and teres minor are spared, the
lesion must be distal to the quadrilat-
eral space.
A complete neurologic examina-
tion of the extremity should be per-
formed, specifically checking the
function of the spinal accessory,
suprascapular, long thoracic, radial,
and musculocutaneous nerves. In-
volvement of the superior lateral
cutaneous nerve of the arm may
lead to sensory loss over the lateral
aspect of the shoulder. However, it
is important to remember that even
patients with a complete deltoid
motor deficit can present with only
mild loss of sensation over the later-
al aspect of the shoulder. Therefore,
the diagnosis of axillary neuropathy
should not rest on the presence or
absence of sensation over the area of
the deltoid.
Standard radiographic examina-
tions of the shoulder and cervical
spine are helpful in determining
whether a fracture, dislocation, or
other pathologic process is associated

with the nerve injury. An EMG/NCS
evaluation is important in confirm-
ing the diagnosis and establishing a
reference point for subsequent as-
sessment and potential recovery.
These studies may also reveal lesions
in other nerves or in the proximal
brachial plexus, which may affect
the overall treatment plan.
In chronic cases with established
muscle atrophy, an MR imaging
study of the shoulder can demon-
strate increased signal on spin-echo
sequences due to muscle replace-
ment by fat.
14
This can be helpful
when examining for a combined
nerve injury; attempting to delineate
Table 1
Etiology of Axillary Nerve Lesions
Closed blunt trauma
Traction injury to the shoulder
Penetrating trauma (sharp or
blunt)
Nerve compression due to mass
effect (aneurysm, tumor)
Parsonage-Turner syndrome
(brachial neuritis)
Quadrilateral space syndrome

Scott P. Steinmann, MD, and Elizabeth A. Moran, MD
Vol 9, No 5, September/October 2001
331
the involvement of smaller mus-
cles, such as the teres minor; or
seeking to identify a mass lesion
that may be causing compressive
neuropathy. Evaluation of the bra-
chial plexus is often difficult to ac-
curately interpret and has not been
found to be helpful.
Nonoperative Treatment
Patients with an atraumatic history
of axillary neuropathy should be
observed over a period of at least 3
months from the onset of symp-
toms before operative treatment is
considered (Fig. 2). At 2 to 4 weeks,
EMG/NCS should be performed to
establish baseline values. Physical
therapy should be instituted during
this period, emphasizing passive
and active assisted range of motion.
The key element of therapy sessions
should be to preserve the maximum
range of motion so as to prevent
joint contracture while awaiting the
return of muscle function. Electrical
stimulation of the deltoid has been
used to preserve muscle viability,

although it is unclear whether this
approach has any effect on ultimate
outcome.
The results of nonoperative treat-
ment for atraumatic lesions have
been generally quite good. Even in
cases of closed trauma involving a
fracture or dislocation, satisfactory
recovery occurs in most patients. In
a study of 73 patients with a proxi-
mal humerus fracture or disloca-
tion, 24 (33%) had EMG/NCS evi-
dence of an axillary nerve injury;
there were 9 complete and 15 partial
lesions.
9
All patients recovered
within 1 to 2 years, including those
with complete nerve lesions but no
objective loss of function.
Leffert
15
has suggested that axil-
lary nerve injury after fracture or dis-
location is a more common entity
than is usually appreciated, but be-
lieves that most patients progress to
full recovery. Perkins and Watson
Jones
16

reviewed a series of 15 pa-
tients with axillary neuropathy after
dislocation and reported that 13
recovered fully and only 2 had per-
manent paralysis. In one series of 108
elderly patients with anterior shoul-
der dislocation, 10 (9.3%) were noted
to have an axillary nerve injury, but
all went on to full recovery by 12
months.
17
In another study,
18
a high
rate of axillary neuropathy was
noted in patients over age 40 with a
Atraumatic Closed trauma
Improvement No improvement
Improvement No improvement
Acute Chronic (>18 mo)
Continue
observation
Repeat EMG/
NCS at 3 mo
Penetrating trauma
Sharp (e.g., knife,
surgical blade)
Blunt (e.g.,
gunshot)
EMG/NCS

within 1 wk
Repeat EMG/NCS
at 3 mo
Isolated axillary
nerve lesion
• EMG/NCS
• Treat any associated
fracture or dislocation
• Observation
• EMG/NCS
• Observation
• Repeat EMG/NCS
at 3 mo
• Observation
• EMG/NCS at 4 wk
Salvage procedure:
• Trapezius transfer
• Pectoralis major transfer
• Functioning free muscle
transfer
If severe changes
on NCS, early
exploration
If no clinical or EMG/NCS
improvement, consider
surgery at 3-6 mo
If no clinical
or EMG/NCS
improvement,
consider surgery

at 6 mo
Figure 2 Algorithm for treatment of isolated axillary nerve lesions (EMG/NCS = electromyographic and nerve conduction study).
Axillary Nerve Injury
Journal of the American Academy of Orthopaedic Surgeons
332
shoulder dislocation. Six weeks after
injury, EMG/NCS evaluation showed
denervation patterns ranging from
moderate to severe in 28 (51%) of 55
patients. At the 3-year follow-up
examination, no patient had persis-
tent axillary neuropathy; however, 6
(21%) of the 28 had symptomatic
rotator cuff tears.
Operative Treatment
Operative treatment of axillary
neuropathy can be considered if no
clinical or EMG/NCS evidence of
recovery is present by 3 months
after injury.
19-21
This is a reason-
able time frame for patients who
have sustained closed trauma.
However, if the cause of the axil-
lary nerve dysfunction is a stab
wound or surgical insult, operative
exploration should be performed
much sooner. In such instances,
EMG/NCS may be diagnostic of

disruption of axillary nerve con-
duction at less than 1 week after
injury, before axonal degeneration
occurs along the distal aspect of the
nerve. A denervation pattern on
EMG testing will typically not be
present until approximately 2 to 3
weeks after injury, when fibrilla-
tion potentials can be observed.
When assessing a patient with a
stab wound to the shoulder and
limited deltoid function, the NCS
should be obtained initially at 4 to
7 days after injury; if the findings
are equivocal, the clinician should
wait an additional 2 weeks before a
repeat EMG evaluation. If the ini-
tial EMG/NCS results demonstrate
loss of conduction and a denerva-
tion pattern, early operative explo-
ration may be considered.
Occasionally, axillary neuropa-
thy may be noted after elective
surgery, presumably due to sus-
tained traction or laceration injury
to the nerve. Even in this setting,
however, immediate surgical explo-
ration is not always warranted, as
the patient may have a neurapraxia
or axonotmesis that will fully re-

cover with nonoperative treatment.
An early EMG/NCS evaluation can
help define the nature of the nerve
injury in such situations.
For patients with a gunshot in-
jury to the shoulder and evidence of
axillary neuropathy, observation for
4 to 6 weeks may be prudent. The
blast effect during missile penetra-
tion may have caused neurapraxia
or axonotmesis, both of which have
a good potential for spontaneous
recovery.
Although the most favorable re-
sults of surgical treatment have
been documented to occur with
treatment initiated less than 6
months after injury, functional
improvement can occur if surgical
intervention is undertaken before
12 months.
2,3,19
Significant clinical
improvement is unlikely if surgical
treatment is initiated 12 months or
more after injury.
20
Surgical Options
The axillary nerve is ideal for
critical evaluation of the results of

surgical treatment of motor nerve
injuries. The proximal monofascic-
ular structure of the nerve, its com-
position of primarily motor fibers,
and its relatively short length are
attributes that make it highly appro-
priate for study of the effects of sur-
gical intervention.
The standard modalities of neu-
rolysis, neurorrhaphy, nerve graft-
ing, and neurotization have all been
used in the treatment of axillary
nerve injuries.
19,22
The choice of
treatment is ultimately determined
at surgery after exploration of the
nerve. If the nerve has been recent-
ly lacerated, neurorrhaphy alone
can be successful. However, if the
injury is several weeks or months
old, retraction and scarring of the
cut ends of the nerve have occurred.
Due to the relative confinement of
the nerve and its oblique course
over the subscapularis muscle and
through the quadrilateral space,
mobilization of the nerve is often
not possible, and nerve grafting
must be performed. When the nerve

is found to be intact but encased in
scar or trapped in the quadrilateral
space by fibrous bands, neurolysis
or decompression can be success-
ful.
3,4,14
Neurotization has also been
utilized to correct axillary nerve le-
sions with use of the thoracodorsal,
phrenic, spinal accessory, and inter-
costal nerves.
22,23
Results of Surgical Treatment
In one series of 37 patients with
axillary nerve injuries, 33 were
treated by sural nerve grafting; 1, by
direct repair; and 3, by neurolysis.
19
Of those with isolated axillary nerve
lesions, 23 of 25 achieved M4 or M5
strength postoperatively (as graded
by manual muscle testing according
to the Nerve Injuries Committee of
the British Medical Research Coun-
cil
24
). The large number of patients
who required grafting illustrates the
difficulty of adequately mobilizing
the nerve for a direct repair. The

small number of patients who un-
derwent neurolysis demonstrates
that simple nerve compression by
scar or fibrous bands is not common.
In a series of 66 patients with axil-
lary neuropathy,
20
27 patients un-
derwent surgical exploration and
grafting within 6 months of injury.
Of these 27 patients, 9 recovered
M5 strength, and 9 recovered M4
strength. Thirteen other patients un-
derwent neurolysis, with 10 achiev-
ing grade M4 or M5 strength. The 6
patients who underwent surgery
more than 1 year after injury did not
fare as well; only 1 patient achieved
a muscle grade of M4.
Petrucci et al
3
presented the re-
sults in 15 patients who underwent
sural nerve grafting an average of
5.8 months after injury. In most
cases, two sural nerve grafts were
placed (length, 3 to 8 cm). All but 1
of the patients achieved a muscle
grade of M4 or M5.
Scott P. Steinmann, MD, and Elizabeth A. Moran, MD

Vol 9, No 5, September/October 2001
333
Chuang et al
22
reported on neu-
rotization with the use of the phrenic
or spinal accessory nerve, which
requires intercalary sural nerve
grafting with either donor nerve.
The results were similar with the
two nerves. The 23 patients who
underwent spinal accessory neuroti-
zation with bridging sural nerve
grafts had an average of 45 degrees
of improvement in abduction.
The results of quadrilateral space
decompression have not been re-
ported as frequently as the results
of surgical repair after a traumatic
injury.
14,25
Cahill and Palmer
13
re-
ported on 18 patients who under-
went decompression of the quadri-
lateral space; 8 patients achieved
dramatic relief of symptoms, and 8
had some relief. Francel et al
25

re-
ported the results in 5 patients with
quadrilateral space syndrome after
a traumatic injury. All 5 had reso-
lution of sensory deficits and sub-
jective improvement of shoulder
pain with surgical decompression.
The most commonly performed
surgical procedure for persistent
axillary neuropathy is sural nerve
grafting. Satisfactory results can be
achieved in most cases. There are
two reasons why grafting is com-
monly needed. First, because trac-
tion is a common pattern of injury,
the nerve may have several centime-
ters of stretch injury, resulting in a
neuroma in continuity. Resection of
the neuroma necessitates a grafting
procedure in most situations, as it is
difficult to mobilize the nerve to
gain more length. Second, the most
common area for injury of the nerve
is either proximal to or just at the
quadrilateral space. A direct repair
is technically difficult to perform in
this area, because when a standard
anterior approach is used, the area
to be reconstructed is at the bottom
of a deep surgical exposure. It is

preferable and technically easier to
perform a distal anastomosis with
nerve grafts through a posterior
approach and then pass the grafts
through the quadrilateral space,
achieving a proximal tension-free
anastomosis from the anterior ap-
proach.
Surgical Technique
Under general anesthesia, the
patient is placed in the lateral decu-
bitus position to facilitate both ante-
rior and posterior exposure of the
shoulder, as well as access for har-
vesting the sural nerve. A modified
deltopectoral approach is made
from the clavicle to the deltoid in-
sertion with the skin incision placed
slightly more medial than usual (5
mm to 1 cm). This is important be-
cause most of the surgical exposure
will be centered more medially,
under the area of the pectoralis
major and pectoralis minor, rather
than over the humeral head. If there
is a prior surgical incision in the
area, it can often be extended to gain
adequate exposure.
After development of the delto-
pectoral interval and exposure of

the clavipectoral fascia, the muscles
originating from the coracoid are
sequentially released, beginning
with the short head of the biceps
and coracobrachialis and followed
by the pectoralis minor. The mus-
cles may be taken down either by
osteotomizing the tip of the cora-
coid or by using an electrocautery
device to detach them, with suture
reattachment at closure. If the pec-
toralis, the coracobrachialis, and the
short head of the biceps are released
within 1 cm of their osseous origin,
there is no danger of damage to the
musculocutaneous nerve.
The pectoralis major can then be
either partially or completely re-
leased from the humerus for greater
exposure. A cuff of tissue should
be left on the humerus to allow
later repair at the end of the proce-
dure. Sufficient dissection should
be done to allow visualization of
the axillary, radial, and musculocu-
taneous nerves. Early in the proce-
dure, before releasing the muscular
attachments at the coracoid, the
axillary nerve can be identified by
passing a finger over the subscapu-

laris muscle and sweeping inferi-
orly. This maneuver will usually
hook the axillary nerve and allow it
to be palpated with the posterior
humeral circumflex as it travels into
the quadrilateral space (Fig. 3).
26
Adequate visualization of the
axillary nerve is usually possible
only after the pectoralis minor has
been detached and retracted medi-
ally. The axillary and musculocuta-
neous nerves branch off the poste-
rior and lateral cords, respectively,
at approximately the level of the
coracoid and can be most easily
identified by following the nerves
from distal to proximal. The mus-
culocutaneous nerve is identified as
it enters the coracobrachialis and
then can be traced proximally to the
lateral cord. The axillary nerve can
be followed proximally from the
quadrilateral space to the posterior
cord. As the dissection proceeds prox-
imally, the much larger radial nerve
can be identified and protected. If
nerve identification is not certain, a
nerve stimulator should be used to
establish which muscle groups are

being innervated.
Once the axillary, radial, and
musculocutaneous nerves have been
identified, the axillary nerve must be
fully exposed by carefully dissecting
it from the adjoining brachial plexus.
The axillary artery and vein must be
identified and protected, as they are
also at risk during axillary nerve
exposure. After the axillary nerve
has been well exposed proximally,
surgical dissection proceeds distally
until the area of the lesion is identi-
fied. Often this is located at or just
proximal to the quadrilateral space.
If the lesion grossly appears to be a
neuroma, antegrade stimulation of
the nerve can be performed with a
nerve stimulator. If muscle activity
is detected, neurolysis of the lesion
should be done. If no muscle activity
is noted, intraoperative EMG/NCS
Axillary Nerve Injury
Journal of the American Academy of Orthopaedic Surgeons
334
monitoring may be performed. If no
electrical activity is recorded over
the deltoid, the neuroma should be
excised and grafted. If either form
of stimulation demonstrates nerve

conduction, neurolysis may be war-
ranted, with use of an operating
microscope for magnification.
If the lesion is located deep in the
quadrilateral space, a posterior inci-
sion will be needed to fully expose
the nerve. This is possible with the
patient in the lateral decubitus posi-
tion. A posterior incision is made
extending superiorly from the pos-
terior axillary crease to the acrom-
ion. The inferior border of the del-
toid is mobilized superiorly, and the
nerve is identified as it exits the
quadrilateral space. Detachment of
the deltoid is not necessary. If distal
grafting is required at this point, the
motor fascicles to the deltoid are
identified and separated from the
superior lateral cutaneous branch
and the branch to the teres minor.
The lateral position facilitates
sural nerve harvest. Usually, two or
three sural nerve grafts measuring 4
to 8 cm are sutured to the distal
stump of the nerve, first through
the posterior exposure and then
passed anterior for anastomosis to
the proximal stump. If a lesion is
encountered very proximal in the

axillary nerve, the proximal stump
can be carefully dissected under the
microscope 1 to 2 cm into the poste-
rior cord without affecting fascicles
directed to the radial nerve. Nerve
grafts should be sutured in a man-
ner to allow a tension-free repair
and should be checked with the
arm in abduction and external rota-
tion before completing the proximal
anastomosis. After closure, the arm
is placed in a sling. Gentle passive
and active exercises of the shoulder
are begun at postoperative day 7,
which helps promote axillary nerve
gliding and prevents scarring.
Late Presentation
Patients seen more than 24 months
after injury present a treatment
dilemma. Due to intrinsic muscle
wasting, nerve repair procedures are
unproductive. Patients should be
carefully evaluated for physical limi-
tations of the shoulder. Young pa-
tients often demonstrate full motion
of the shoulder and no limitations in
activities of daily living. However,
there may be work restrictions due
to early fatigue with overhead activ-
ities. Most of these patients cannot

be helped predictably by further
surgery, and workplace modifica-
tions are recommended.
In patients with poor shoulder
abduction that limits activities of
daily living but a normal rotator
cuff, muscle transfer procedures can
be considered. If sparing of the
middle and posterior portions of the
deltoid occurs, the innervated por-
tion of the deltoid can be transposed
anteriorly on the acromion. Alter-
natively, the pectoralis major can be
transposed laterally on the acromion.
Mobilization of the pectoralis major
can be limited by tethering of the
pectoral nerves. If the entire deltoid
is denervated, the trapezius can be
detached from the acromion with a
portion of bone and inserted into the
proximal humerus. This procedure
may improve motion but rarely
restores functional abduction. Other
techniques include bipolar latissimus
dorsi transposition and free muscle
transport.
Summary
Axillary neuropathy is a potential
complication of shoulder girdle
Deltoid

Subscapularis
Pectoralis minor
Axillary nerve
Radial nerve
Coracobrachialis/
short head of
biceps
Figure 3 Technique of palpating the axillary nerve.
Scott P. Steinmann, MD, and Elizabeth A. Moran, MD
Vol 9, No 5, September/October 2001
335
injury, which can result in signifi-
cant disability. Acute abduction
and traction are common injury
patterns that can produce a stretch
lesion in the nerve often just proxi-
mal to the quadrilateral space.
Many injuries are mild and may
remain subclinical during treat-
ment and rehabilitation of the pri-
mary shoulder injury. Most axil-
lary nerve lesions occur in closed
injuries and are either neurapraxia
or axonotmesis, for both of which
there is a good overall prognosis
for recovery.
In addition to the initial clinical
examination, patients should be
evaluated with an EMG or nerve
conduction study 2 to 4 weeks after

injury and again at 12 weeks. If no
improvement is noted on these stud-
ies or on clinical examination, surgi-
cal treatment may be considered.
Studies have shown that the best
results of surgery occur when explo-
ration is performed 3 to 6 months
after injury. In cases of sharp pene-
trating trauma or neuropathy after a
surgical procedure, exploration of
the axillary nerve should be per-
formed as soon as the diagnosis is
made by physical examination and
confirmed by nerve conduction
study.
Most patients with an axillary
nerve injury have an excellent re-
sponse to nonoperative treatment.
Favorable results can be expected for
the rest if surgical repair is under-
taken within 6 months of injury.
Surgical options include neurolysis,
nerve grafting, and neurotization. In
most series, the majority of patients
who required surgery underwent a
nerve grafting procedure. The
results of nerve grafting have been
encouraging, due to the relatively
short distance from the lesion to the
motor end-plate and the monofascic-

ular nature of the proximal portion
of the axillary nerve.
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