Review Article

Thoracic Outlet Syndrome

Abstract
John E. Kuhn, MD Thoracic outlet syndrome is a well-described disorder caused by
George F. Lebus V, MD thoracic outlet compression of the brachial plexus and/or the
subclavian vessels. Neurogenic thoracic outlet syndrome is the most
Jesse E. Bible, MD
common manifestation, presenting with pain, numbness, tingling,
weakness, and vasomotor changes of the upper extremity. Vascular
complications of thoracic outlet syndrome are uncommon and include
thromboembolic phenomena and swelling. The clinical presentation is
highly variable, and no reproducible study exists to confirm the
diagnosis; instead, the diagnosis is based on a physician’s judgment
after a meticulous history and physical examination. Both
nonsurgical and surgical treatment methods are available for thoracic
outlet syndrome. Whereas nonsurgical management appears to be
effective in some persons, surgical treatment has been shown to
provide predictable long-term cure rates for carefully selected
patients. In addition, physicians who do not regularly treat patients
with thoracic outlet syndrome may not have an accurate view of this
disorder, its treatment, or the possible success rate of treatment.

P eet etal1 first used the term thoracic

From the Division of Sports Medicine,
Department of Orthopaedics,
Vanderbilt University Medical Center,
Nashville, TN.
Dr. Kuhn or an immediate family
member serves as a board member,
owner, officer, or committee member
of the American Orthopaedic Society
for Sports Medicine and American
Shoulder and Elbow Surgeons.
Neither of the following authors nor
any immediate family member has
received anything of value from or
owns stock in a commercial company
or institution related directly or
indirectly to the subject of this article:
Dr. Lebus and Dr. Bible.
J Am Acad Orthop Surg 2015;23:
222-232
http://dx.doi.org/10.5435/
JAAOS-D-13-00215
Copyright 2015 by the American
Academy of Orthopaedic Surgeons.
outlet syndrome (TOS) in 1956 to
describe the constellation of symptoms
caused by compression of the neuro-
vascular bundle at the thoracic outlet.
TOS describes a wide spectrum of
clinical presentations with a variety
of etiologies, all with the common
thread of neurovascular compression
in the thoracic outlet region. As our
understanding of this condition has
improved, treatment has evolved but it
remains controversial. The mainstay of
management is nonsurgical in most
patients; however, surgery is indicated
for recalcitrant cases and for vascular
involvement. Although TOS is a chal-
lenging diagnosis, proper evaluation
and treatment leads to symptom relief
for most patients.
Anatomy
The thoracic outlet is defined as the
interval from the supraclavicular
fossa to the axilla that passes between
the clavicle and the first rib (Figure 1).
It contains three important struc-
tures that may be subjected to
compression: the subclavian artery,
the subclavian vein, and the bra-
chial plexus. Compression may
occur at three distinct points in the
thoracic outlet: the interscalene
triangle, the costoclavicular space,
and the retropectoralis minor
space2 (Figure 2). The interscalene
triangle consists of the anterior
scalene muscle, the middle scalene
muscle, and the first rib, and it
contains the subclavian artery and
the upper, middle, and lower
trunks of the brachial plexus. The
costoclavicular space is made up
anteriorly by the clavicle, the sub-
clavius muscle, and the costocora-
coid ligament, posteriorly by the
first rib and the anterior and middle
scalene muscles, and laterally by
the scapula. This space contains the

222 Journal of the American Academy of Orthopaedic Surgeons

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 John E. Kuhn, MD, et al

subclavian vessels and the divisions Figure 1

of the brachial plexus. Finally, the
retropectoralis minor space is located
inferior to the coracoid process, ante-
rior to the second through fourth ribs,
and posterior to the pectoralis minor
muscle; this space houses the cords of
the brachial plexus and the axillary
artery and vein.
Deep cervical fascia invests the
neurovascular structures during
their course from the first rib to
the axilla. After the fascia splits
to encompass the subclavius
muscle, it comes back together to
form the costocoracoid ligament
(Figure 3). Caudal to the subclavius
muscle, the costocoracoid fascia
thins to become the clavipectoral
fascia; this structure invests the
pectoralis minor muscle and ulti-
mately becomes the suspensory
ligament of the axilla.3

Etiology and Pathology

In 1912, Todd4 suggested that the
vertebral column grows faster than
the upper extremity in youth, thus
causing the scapula to descend and
leading to a susceptibility for neuro-
vascular compression with any fur-
ther scapular descent. Whereas our
understanding has evolved, this
original insight is valuable because it
highlights this anatomic region’s
vulnerability to compression. Most
cases of TOS are now thought to stem
from an anatomic predisposition with
superimposed neck trauma, either
from a single acute incident or from
repetitive stress.5 Symptoms may be
delayed several weeks or longer after
acute trauma, or they may develop
insidiously because of chronic stress.6
Epidemiologic data for TOS are not
widely reported; Hooper et al2 sug-
gest that this lack of demographic
information is due to disagreement in
the definition and diagnostic criteria
for the disease. Anecdotally, the typ-
ical patient with TOS is a young, thin
Normal thoracic anatomy.
female with a long neck and drooping
shoulders.7,8
The anatomic causes of TOS may
be organized into soft-tissue and
osseous categories. Soft-tissue causes
are associated with to up to 70% of
cases of TOS, whereas osseous
abnormalities encompass the other
30%9 (Table 1).
Soft-tissue Abnormalities
Variation in scalene origin and inser-
tion may cause compression within
the interscalene triangle. The
scalenus minimus, an accessory mus-
cle, can be found in 30% to 50% of
patients with TOS; it originates from
the cervical transverse processes and
inserts into the first rib between the
subclavian artery and the T1 root.3,6
Symptomatic compression may result
from hypertrophy of the scalene
musculature or congenital anomalous
ligaments or bands. Trauma and later
scarring may produce delayed symp-
toms.10 The costocoracoid ligament
is implicated in venous compression
in Paget-Schroetter syndrome,
a manifestation of TOS that leads to
thrombosis.3
Osseous Abnormalities
Bony findings associated with TOS
include cervical ribs, prominent C7
transverse processes, exostoses,
tumor in the region, or callus from
prior trauma. Although cervical ribs
may cause TOS symptoms in the
absence of trauma, 80% of patients
with TOS and cervical ribs show the
development of symptoms only after
injury.11 These patients often have
a large cervical rib fused to the first
rib. When the ribs themselves do not
cause compression, their associated
bands and ligaments are implicated.5

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Thoracic Outlet Syndrome
Figure 2
Three regions of potential neurovascular compression: interscalene triangle, costoclavicular space, and retropectoralis
space. TN = thoracic nerve
Similarly, altered biomechanics from
acromioclavicular and sternocla-
vicular injuries are also noted in
some patients with TOS.2
Clinical History and
Presentation
Diagnosis of TOS is challenging
because of the varied clinical pre-
sentation and the lack of objective
data to support a diagnosis. As
a result, the clinical impression from
a thorough history and physical
examination remains a crucial com-
ponent in differentiating TOS from
other conditions. Patients are fre-
quently young, active, and healthy.
Often, they have seen multiple
physicians, undergone misdiagnosis,
224
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and some have been told that their
condition is psychosomatic. Mani-
festations of TOS include neurogenic
TOS, caused by compression of the
brachial plexus, and vascular TOS,
subclassified as arterial or venous,
depending on whether the subclavian
artery or vein is involved. Estimates
are that .90% of all TOS cases are
of neurogenic origin, whereas
approximately 3% to 5% are venous
and ,1% are arterial.12
Neurogenic Thoracic Outlet
Syndrome
Neurogenic TOS presents as a con-
stellation of upper extremity weak-
ness, numbness, paresthesias, and
pain in a nonradicular distribution.
Symptoms are present during daily
Journal of the American Academy of Orthopaedic Surgeons
activities as well as during sleep.
Upper extremity heaviness is com-
mon with above-the-shoulder activi-
ties. In a systematic review by Sanders
et al,12 symptom distribution in
neurogenic TOS included upper
extremity paresthesia (98%), neck
pain (88%), trapezius pain (92%),
shoulder and/or arm pain (88%),
supraclavicular pain (76%), chest
pain (72%), occipital headache
(76%), and paresthesias in all five
fingers (58%), the fourth and fifth
fingers only (26%), or the first, sec-
ond, and third fingers (14%).
Symptom patterns can further
classify neurogenic TOS as secondary
to upper or lower plexus compres-
sion. In most patients, lower and
combined plexus pathology is seen

Figure 3
Fascial layers of the cervicothoracic region.
(85% to 90%).9 Lower plexus
involvement represents compression
of C8 and T1, and manifests as
symptoms in the area of the ulnar
forearm and hand and possibly the
axillary and anterior shoulder
region. Upper plexus compression
involves the C5-C7 nerve roots, and
presents as pain in the supra-
clavicular region that may radiate
into the ipsilateral head, face, upper
chest, periscapular region, or radial
nerve distribution to the dorsal
index finger and thumb.2 Neuro-
genic TOS must be differentiated
from other compression syndromes,
such as carpal tunnel syndrome and
cervical nerve root compression.
Such a distinction may be made by
the wide anatomic distribution and
April 2015, Vol 23, No 4
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the nonradicular nature of symp-
toms in TOS.
Vascular Thoracic Outlet
Syndrome
Vascular TOS consists of both
venous and arterial clinical subtypes.
Venous TOS is characterized by sig-
nificant swelling of the upper
extremity; it is commonly associated
with deep pain in the upper extrem-
ity, chest, and shoulder, along with
a feeling of heaviness that is worse
after activity. The patient may have
cyanotic discoloration of the
extremity. The subclavian vein is
commonly compressed at the costo-
clavicular junction where it passes
anterior to the anterior scalene;
however, it may be compressed at
John E. Kuhn, MD, et al
other areas depending on the under-
lying etiology.13 A well-known
subtype of venous TOS is Paget-
Schroetter syndrome, described as
thrombosis of the subclavian vein
caused by repetitive injury in rela-
tively young and healthy persons.
Arterial TOS is a rarer condition,
but it has potentially devastating
consequences. It presents as non-
radicular pain, numbness, coolness,
and pallor that worsens in cold tem-
peratures. It is caused by intermittent
or prolonged arterial compression of
the subclavian artery, typically by
a cervical rib. Compression over time
leads to intimal damage, eventual
aneurysm formation, thrombosis,
embolic events, and even potentially
limb-threatening ischemia. Often,
225
Thoracic Outlet Syndrome
Table 1
Common Abnormalities Causing Thoracic Outlet Syndrome9
Soft-tissue Causes (70%)
Scalene muscle variations in insertion
Scalene muscle hypertrophy
Accessory scalenus minimus muscle
Anomalous ligaments or bands
Soft-tissue tumors
Osseous Causes (30%)
Cervical rib
Prominent C7 transverse process
Displacement or callus from first rib fracture
Malunited clavicle or first rib fracture
AC or SC joint injury or dislocation
Osseous tumor
AC = acromioclavicular, SC = sternoclavicular
arterial TOS coexists with neurogenic
TOS. Signs that point to arterial TOS
include unilateral Raynaud-type
symptoms of episodic pallor, ery-
thema, and cyanosis with a distribu-
tion of symptoms to the distal
circulation of the hands or fingers in
the absence of any other cause, such as
collagen vascular disease or other
vascular disorders. Chronic pain,
coldness, and paresthesias may also be
present with long-standing micro-
embolic disease. Early fatigue may
occur with exercise.8,14
Differential Diagnosis
The clinical presentation of TOS var-
ies widely, ranging from mild posi-
tional discomfort to severe limb- or
life-threatening symptoms. In addi-
tion, patients may present with uni-
lateral or bilateral signs or symptoms
that are related to compression of
a combination of neurologic and
vascular components. Isolated vas-
cular TOS is more easily diagnosed
but is rare. Thus, the examiner
must distinguish which symptoms
are related to brachial plexus com-
pression, which symptoms are vas-
226
Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
cular in nature, and which symptoms
have no relationship with thoracic
outlet pathology. The clinical history
can help narrow the differential
diagnosis, which includes cervical
spine pathology, intrinsic shoulder
dysfunction, and other peripheral
compression neuropathies. Non-
radicular and anatomically wide-
spread symptoms that are influenced
by arm, neck, and shoulder position
warrant a suspicion for TOS.2 Cer-
vical spine problems are more often
characterized by constant neck and
shoulder pain that presents in
a radicular distribution, with the
pain aggravated by the position of
the neck. Intrinsic shoulder pathol-
ogy causes shoulder pain that may
radiate into the upper arm, but
numbness is not a commonly asso-
ciated finding. Shoulder position
and direct palpation on joint struc-
tures aggravate symptoms. More
distal compression neuropathies,
such as carpal and cubital tunnel
syndromes, have symptoms isolated
to predictable nerve distributions
and are aggravated more by the
position of the wrist and elbow than
by the position of the shoulder or
neck.6
Journal of the American Academy of Orthopaedic Surgeons
Physical Examination
Physical examination should include
an evaluation of the cervical spine,
shoulder, and upper extremity.
Attention should be directed toward
evaluating the position of the head,
neck, and shoulder, looking for the
presence of thoracic kyphosis. The
patient’s overall posture should be
assessed. Comparing the upper
extremity with the contralateral arm
yields information regarding skin
color, temperature, hair distribution,
muscle atrophy, and nail changes.
The Gilliatt-Sumner hand, a charac-
teristic finding of neurogenic TOS, is
described as atrophy of the abductor
pollicis brevis and, to a lesser degree,
the hypothenar musculature and the
interossei.7,15 A blood pressure
difference of 20 mm Hg between the
upper extremities is a significant but
rare finding of vascular TOS.6 The
upper extremity and chest wall may
be congested and edematous with
prominent superficial veins in
venous TOS; in arterial TOS, the
upper extremity may appear pale.
Distal skin changes, ulcerations, and
signs of microembolic events are rare
findings.14 Palpation of the supra-
clavicular region may reveal tender-
ness, masses, or other abnormalities.
Quality and location of pain with
movements of the neck, shoulder,
and upper limb should be recorded.
The vascular examination docu-
ments the presence and quality of the
radial pulse with the arm in different
positions. Several provocative tests in
this context are shown in Figure 4.
The Wright test was originally
described as a decrease in the radial
pulse with the arm in hyper-
abduction and external rotation,
with the head turned in the opposite
direction. With this maneuver, the
radial pulse dampens or obliterates
in up to 7% of the normal pop-
ulation.6 The Adson test describes
bringing the arm into extension,
 John E. Kuhn, MD, et al

turning the head toward the affected Figure 4

side, and taking a deep breath.
Gergoudis et al16 challenged the
clinical utility of this test by showing
that 66 of 130 normal persons
(51%) had a diminished pulse with
the Adson maneuver. The Roos test,
or the elevated arm stress test, rep-
resents a more reliable diagnostic
examination for TOS. In this
maneuver, the patient places both
arms in the 90! abducted position
with the elbows flexed to 90!. The
hands are then opened and closed for
a 3-minute period. Normal persons
may have minor discomfort due to
muscular fatigue, but patients with
TOS have more dramatic symptoms
that replicate their usual discomfort
such that they may not be able to
complete the test.8,9
Provocative testing for TOS has
been criticized for leading to a high
number of false positives. Warrens
et al17 showed that 58% of random
volunteers had at least one positive
test result with provocative maneu-
vers; however, performing multiple
tests in conjunction and considering
their results together may increase
their specificity. In a series by Gillard
et al,18 the specificity for the Adson Clinical photographs demonstrating provocative physical tests for thoracic outlet
test and for the Roos test was 76% syndrome. A, Wright test. B, Adson test. C and D, Roos test.
and 30%, respectively; however,
when both tests were positive, spec-
ificity increased to 82%. Braun which may contribute to thoracic Angiography
et al19 used pulse oximetry to outlet compression20 (Figure 5). Angiography may be used in con-
attempt to provide a more objective Three-dimensional imaging, such as junction with MRI or CT, but this
measure in this context, showing CT and MRI, has not been well technology’s role in diagnosis re-
that provocative exercise led to studied, but it may be effective in mains unclear. Aralasmak et al22
a statistically significant decrease in the setting of an identifiable con- showed that magnetic resonance
pulse oximetry readings, an increase genital anomaly, a space-occupying angiography can dynamically eval-
in the heart rate, and the reproduc- lesion (eg, a pancoast tumor), met- uate the neurovascular bundle in
tion of symptoms. astatic disease, or malunited frac- patients with known TOS; however,
tures of ribs or the clavicle. the authors could not distinguish
Although some authors have pro- between physiologic and pathologic
Diagnostic Studies posed that ultrasonography is lim- compression, nor could they corre-
ited in the diagnosis of TOS because late imaging findings with clinical
Imaging the area of interest is obscured,6 symptoms. Conventional arteriog-
Chest and cervical spine radio- Longley et al21 reported 92% raphy is rarely useful in TOS and is
graphs can identify cervical ribs, specificity and 95% sensitivity only indicated in the circumstances
prominent C7 transverse processes, using ultrasonographic methods in of embolic disease, a bruit with the
and low-lying shoulder girdles, all of the diagnosis of venous TOS. arm in a neutral position, suspicion

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Thoracic Outlet Syndrome
Figure 5
Radiograph of a patient with a right cervical rib, indicated by the white arrow.
of an aneurysm, or differing blood
pressure measurements between the
upper extremities. Other cases of
arterial TOS are likely more positional
and are better diagnosed on physical
examination than with angiography.
Conversely, venography is indicated
in the workup of suspected venous
TOS, demonstrating compression of
the subclavian vein as well as collat-
eralization from nearby circulation.
When an acute thrombosis is detected,
early catheter-directed thrombolysis
and surgical decompression may be
indicated to decrease the risk of
a recurring thrombosis. It is important
to note that patients who experience
arterial or venous thrombosis should
undergo coagulation studies because
a TOS thrombosis can represent a two-
hit phenomenon of mechanical tho-
racic outlet compression in conjunction
with underlying hypercoaguability.6
Neurophysiologic Studies
Historically, neurophysiologic stud-
ies were considered normal in cases of
TOS unless the pathology was found
late and permanent nerve damage
had already occurred.6 However,
Tsao et al23 suggest that nerve fibers
derived from T1, and to a lesser
degree from C8, may show changes
228
Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
in neurogenic TOS. These changes
manifest as abnormal nerve con-
duction velocity studies of the medial
antebrachial cutaneous nerve and
the median motor nerve to the
abductor pollicis brevis. Electromy-
ography may show fibrillations in
T1 and C8 distributions; however,
they are not shown as consistently as
nerve conduction velocity changes.
Anterior Scalene Blocks
Appropriately placed lidocaine or
botulinum toxin injections can
relieve muscular contracture or
spasm and have been shown to have
prognostic benefits. Lum et al24
found that a successful block corre-
lated with a 14% higher rate of good
surgical outcomes in patients older
than 40 years. Table 2 depicts illus-
trative points about different diag-
nostic techniques.
At the authors’ institution, plain
radiographs are obtained initially for
patients with suspected TOS based
on history and physical examination,
followed by other diagnostic tests as
dictated by their symptoms. Patients
with predominantly neurologic signs
and symptoms often undergo neu-
rophysiologic testing early in their
workup. Vascular manifestations
Journal of the American Academy of Orthopaedic Surgeons
uniformly dictate vascular imaging.
Three-dimensional imaging is
reserved for surgical planning, for
when there is concern for a space-
occupying lesion, or for a congenital
or acquired deformity.
Treatment
Treatment strategy depends on
the underlying etiology of TOS.
Nonsurgical management is indicated
first in most patients with neurogenic
TOS. Surgery is warranted in arterial
or venous TOS and in patients with
neurogenic TOS who have persistent
symptoms, muscle atrophy, or a pro-
gressive deficit. In the appropriate
patient population, surgical interven-
tion may reliably improve symptoms
and quality of life.26,27
Nonsurgical
Nonsurgical management is the ini-
tial treatment strategy for neurogenic
TOS; it has shown good results in
some series. Novak et al28 reported
that 25 of 42 patients with neuro-
genic TOS experienced symptomatic
relief after at least 6 months of physical
therapy. A typical protocol consists
of education, activity modification,
and physical therapy. Described
pain control strategies include anti-
inflammatory medications, muscle
relaxants, transcutaneous electrical
nerve stimulation, and injections.
Using ultrasonography-guided botuli-
num injections, Torriani et al29 re-
ported short-term improvement in
69% of patients with neurogenic TOS.
Clarifying goals of treatment is critical
for patient outcome. Patient education
focuses on relaxation techniques,
postural mechanics, and weight and
nutritional control. Activity modifica-
tion includes limiting repetitive, over-
head stress and changing employment
if necessary. Physical therapy involves
stretching, range-of-motion exercises,
and tendon and nerve gliding tech-
niques.2 Despite several series

reporting positive results, Vanti et al30
reviewed the literature and reported
that no definitive benefit of non-
surgical management could be estab-
lished due to a lack of randomized
controlled trials. Nonsurgical man-
agement is reported to be less suc-
cessful in obese patients, in patients
who are on workers’ compensation,
and in patients with double-crush
neurologic pathology involving the
carpal or cubital tunnels.28 At the au-
thors’ institution, all patients with
suspected neurogenic TOS are coached
in lifestyle modification and are
referred for a trial of physical therapy
that focuses on core strengthening and
postural mechanics. If the patients
show no improvement in their symp-
toms after 6 months, they are reeval-
uated and referred for surgical
consideration if appropriate.
Surgical
For any patient with vascular com-
pression or neurogenic TOS that has
failed to respond to nonsurgical
management, surgical intervention is
warranted. The three main surgical
approaches for decompression of
the thoracic outlet are transaxillary,
supraclavicular, and posterior, although
there are many variations and prefer-
ences that are surgeon dependent.
Table 3 summarizes some of the char-
acteristics of each surgical approach.
Transaxillary
First described by Roos36 in 1966,
the transaxillary approach is the
most commonly performed approach
today. Its proponents argue that it
provides superior exposure for first
rib resection, as well as for removal
of cervical ribs and fibrous bands,
with a more cosmetic scar.31
Urschel et al,37 in their review of
TOS over 50 years, describe the
transaxillary approach as their ini-
tial surgical approach through
which they perform first rib and
costoclavicular ligament resection,
scalenectomy, and C7, C8, and T1
April 2015, Vol 23, No 4
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John E. Kuhn, MD, et al
Table 2
Common Diagnostic Tools for the Evaluation of Thoracic Outlet Syndrome
Diagnostic Modality Key Points
Radiographs Can identify bony abnormalities including cervical
ribs and prominent transverse processes20
Cervical spine
Chest
Three-dimensional May be effective in space-occupying lesions,
imaging posttraumatic deformity, soft-tissue anatomic
CT anomalies25
MRI
Doppler ultrasonography May be useful in evaluating subclavian vein for
obstruction or thrombosis21
Arteriography Often indicated in the workup of arterial aneurysms6
Venography Indicated in the workup of suspected subclavian/
axillary venous thrombosis6
Neurophysiologic tests Often normal but can demonstrate abnormal nerve
conduction velocities in C8 and T1 nerve roots
(medial antebrachial cutaneous nerve)23
Anterior scalene blocks Blocks that relieve TOS symptoms may indicate
a better chance of good surgical outcome24
CT = computed tomography, MRI = magnetic resonance imaging, TOS = thoracic outlet
syndrome
neurolysis. They argue that while approach,8 Terzis et al32 reported
first rib resection can be accom- good outcomes and fewer compli-
plished via the supraclavicular cations with the supraclavicular
approach, visualization is inferior technique for first rib resection. If
and requires retraction of the neu- arterial reconstruction is necessary,
rovascular structures. the supraclavicular approach is
preferred.34
Supraclavicular
The supraclavicular approach pro- Posterior
vides a more favorable exposure of The posterior approach, originally
the upper brachial plexus, the neck of described by Clagett38 in 1962, al-
the first rib, and the neurovascular lows better exposure of the proximal
structures. This approach is preferred elements of the brachial plexus for
by surgeons who are performing iso- neurolysis; however, the approach is
lated scalenectomies and removal of more invasive and it can lead to
cervical ribs for neurogenic TOS.8 postoperative shoulder morbidity
Scalenectomy in isolation can be and scapular winging.10,34 Urschel
considered in patients with upper et al37 reserve the posterior approach
plexus-type neurogenic TOS, pa- for removing rib remnants and for
tients with TOS symptoms in the performing brachial plexus neu-
absence of abnormal bony architec- rolysis for patients with recurrent
ture, patients who are excessively TOS.
muscular or obese, or patients with
recurrent TOS following prior first
rib resection.9 Although the supra- Other Considerations
clavicular approach may provide The favored surgical approach for
poorer exposure of the first rib TOS at the authors’ institution is
compared with the transaxillary similar to that described by Urschel
229
Thoracic Outlet Syndrome

Table 3
Common Surgical Approaches for Thoracic Outlet Syndrome
Surgical Approach Characteristics/Proposed Advantages Disadvantages

Transaxillary Most commonly used approach Risk of iatrogenic brachial plexus injury32
Allows more complete exposure of first rib
More cosmetic scar
No retraction of neurovascular structures
necessary for first rib removal31
Supraclavicular Allows better exposure of the middle and Retraction of brachial plexus and vascular
upper trunks, neck of the first rib, and structure necessary for complete first rib
anterior and middle scalene muscles32 removal31
May also allow effective first rib resection32
Allows vascular reconstruction33,35
Posterior Favored for recurrent TOS and in cases of Requires extensive muscle dissection that can
prior anterior neck surgery lead to postoperative shoulder dysfunction
May allow better exposure of proximal Risk of injury to the long thoracic, dorsal scapular,
elements of the brachial plexus34 and accessory nerves34

et al;37 it consists of a transaxillary
approach for first rib resection, sca-
lenectomy, and neurolysis with vas-
cular reconstruction if necessary.
Various other modifications to
surgical techniques are described in
the literature. Atasoy39 reported that
95% of patients had good outcomes
with a combined approach consisting
of transaxillary first rib resection,
followed by immediate supraclavicular
anterior and middle scalenectomy.
Vemuri et al40 demonstrated the
utility of performing an isolated
pectoral minor tenotomy in patients
with neurogenic TOS and with
symptoms reproducible to the sub-
coracoid space. Desai et al35 showed
the utility of using a paraclavicular
approach, essentially adding an in-
fraclavicular incision to the supra-
clavicular approach, for more complete
first rib resections in patients with
venous TOS.
Unique to surgery for arterial or
venous TOS, vascular reconstruction
and management of ischemia or
congestion may be required. The
timing of surgical intervention is
more urgent, particularly in the
presence of ischemic changes. Arte-
rial repair strategies include resection
and primary repair, saphenous vein
graft, arterial autograft, a synthetic
prosthesis, or an endovascular stent
for mild stenotic disease. Acute,
proximal emboli may be treated
with embolectomy catheters, local
thrombectomy, and anticoagulation,
whereas more distal and chronic
emboli mandate bypasses if the
emboli are causing critical ische-
mia.14 Venous TOS with subclavian
vein thrombus (ie, Paget-Schroetter
syndrome) requires a venogram,
local thrombolysis, and surgical
decompression to prevent recurrent
thrombus. Some patients may
require late vein reconstruction for
chronic venous occlusion.13
Complications
Because surgery for TOS involves
many complex and intimately related
structures, theoretical complications
are numerous and may be severe.
These complications include pneu-
mothorax, injury to the subclavian
vein or artery, brachial plexus, or
thoracic duct, and failure to fully
decompress the thoracic outlet. Series
have shown that a pneumothorax
associated with first rib resection is
one of the most common complica-
tions. Karamustafaoglu et al31 re-
ported an incidence of 25%. Other
complications in this series were low
and included an incidence of 3% for
wound infection and an incidence of
,1% for lymphatic or nerve injury.
No major vascular injuries occurred.
Likewise, in the largest review,
Urschel et al37 reported no major
arterial injuries. Bleeding requiring
a second procedure occurred in only
3 of 5,008 procedures. Long-lasting
nerve deficits occurred in only four
patients. The major complication
seen was recurrent TOS; 1,221 of the
5,008 procedures represented repeat
TOS surgeries.
Recurrent Thoracic Outlet
Syndrome
Although modern surgical ap-
proaches have led to improved out-
comes, some patients have persistent
or recurrent symptoms following sur-
gery.37 In these patients, initial man-
agement consists of nonsurgical care,
followed by surgical measures when
the diagnosis is again firmly estab-
lished. Surgical strategies for treating
recurrent symptoms generally are

230 Journal of the American Academy of Orthopaedic Surgeons

Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
 John E. Kuhn, MD, et al

dictated by the patient’s symptoms
and prior surgical approach and
decompression. Likes et al41 showed
that recurrent TOS was commonly
caused by residual or remnant first
ribs following an initial decompres-
sion. Complete removal of the first
rib led to improvement in all 15 pa-
tients in their series.
Future of Thoracic Outlet
Syndrome
Future management of TOS will
depend on improved diagnostic
techniques, including advanced
three-dimensional imaging, to better
understand the pathologic forces
driving this disease. Work by Baumer
et al25 shows that high-resolution
magnetic resonance neurography
can have a high positive predictive
value in TOS by allowing visualiza-
tion of constricting fibrous bands
and corresponding increased signal
in compressed elements of the bra-
chial plexus. Such technology has the
potential to improve our under-
standing and diagnostic acumen in
TOS and allow more targeted treat-
ment. Undoubtedly, however, a high
degree of clinical suspicion will
remain a crucial component in the
evaluation and treatment of TOS.
Summary
conflicting regarding the optimal sur-
gical approach, with consideration
being given to the underlying etiology
and surgeon preference. In cases of
vascular TOS, surgery should be
considered more promptly because of
the underlying potential of limb- or
life-threatening complications.
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