DIJAGNOSTIKA RAMENA

I.AC zglob

II.Impingement syndroma

III.Rotator cuff

IV.Nestabilnost

V.Povrede biceps brahi

VI.Povrede subskapularisa

VII.Smznuto rame

VIII.Degenerativne bolesti

IX.Zapaljenska oboljenja

X.Tumori

1.Anamnestički podaci

2.Klinički nalaz-pokretljivost ramenog zgloba

-specifični testovi i znaci

3.Pomoćne dijagnostičke metode

-rtg(Ap,kosi,aksilarni,Styker,west point ...)

-rtg artrografija

-UZ

-CT;MSCT sa i bez konrasta

-MRI sa i bez kontrasta

-artroskopija

Table 10-1 Muscles of the Rotator Cuff

Muscle Origin

Insertio

n Nerve

Arterial

supply Action

Supraspin

atus

Supraspi

nous

fossa of

scapula

Superi

or

facet

of

greater

tubero

sity

Suprascap

ular

Suprascap

ular

artery

Abduct

ion of

arm

Infraspina

tus

Infraspin

ous fossa

Middle

facet

of

greater

tubero

sity

Suprascap

ular

Suprascap

ular

and/or

circumfle

x scapular

artery

Extern

al

rotatio

n of

arm

Subscapul

aris

Subscapu

lar fossa

Lesser

tubero

sity

Upper and

lower

subscapul

ar

Subscapul

ar artery

Interna

l

rotatio

n and

adduct

ion of

arm

Teres

minor

Upper

portion

of lateral

border of

scapula

Lower

facet

of

greater

tubero

sity

Axil lary Circumfle

x and

scapular

artery

Rotatio

n of

arm

laterall

y

Table 10-2 Scapulothoracic and Additional Shoulder Muscles

Muscl

e Origin

Insert

ion Nerve

Arterial

supply Action

Deltoi

d

Lateral third of

clavicle/acromi

on/scapular

spine

Deltoi

d

tuber

osity

Axil lary Posterior,

humeral,

circumflex

Arm

abduct

ion,

flexion

,

extens

ion

Teres

major

Dorsal surface

of inferior

angle of

scapula

Media

l l ip

of

bicipe

tal

groov

e

Lower

subscap

ular

Subscapular Arm

adduct

ion,

intern

al

rotatio

n

Latiss

imus

dorsi

Spines of T7–

L5 il iac crest

Floor

of

bicipi

tal

groov

e

Thoraco

dorsal

Thoracodors

al

Arm

adduct

ion,

intern

al

rotatio

n

Serrat

us

anteri

or

Ribs 1–9 Inferi

or

angle

of

Long

thoracic

Supreme

thoracic/thor

acodorsal

Protra

ction,

upwar

d

scapu

la

rotatio

n

Pecto

ralis

major

Sternum, ribs,

clavicle

Later

al l ip

of

bicipi

tal

groov

e

Medial

and

lateral

pectora

l

Pectoral Flexio

n,

adduct

ion,

interm

al

rotatio

n

Pecto

ralis

minor

Ribs 3–5 Corac

oid

proce

ss

Medial

pectora

l

Pectoral Protra

ction

Levat

or

scapu

lae

Transverse

process of C1–

C4

Super

ior

angle

of

scapu

la

Dorsal

scapula

r

Dorsal

scapular

Elevati

on,

rotatio

n of

scapul

a

Rhom

boid

major

Spines of T2–

T5

Media

l

borde

r of

scapu

la

Dorsal

scapula

r

Dorsal

scapular

Retrac

tion

Rhom Spines of C7– Base Dorsal Dorsal Retrac

boid

minor

T1 of

scapu

lar

spine

scapula

r

scapular tion

Shoulder Impingement

James Patrick Tasto MD

John K. Locke MD

Key Points

In clinical frequency, shoulder pain is exceeded only by low back pain

and neck pain. The most common source of shoulder pain originates in

the subacromial space, with the most prevalent diagnosis being

impingement syndrome.

Without treatment, symptoms will persist and usually progress.

Shoulder impingement has been described as “symptomatic mechanical

irritation of the rotator cuff tendons from direct contact at the anterior

edge of the coracoacromial arch.”

In the normal shoulder, the coordinated muscle tension within the

rotator cuff compresses the humeral head, keeping it centered within

the glenoid fossa. By coupling with the force of the deltoid, a fulcrum is

created, generating strength through a wide arc of motion.

Any process that interferes with the rotator cuff's capability to keep the

humeral head centered or that compromises the normal coracoacromial

arch, including calcium deposits, thickened bursae, and an unfused os

acromiale, can lead to impingement of the rotator cuff.

Functional overload, intrinsic tendonopathy, and internal anatomic

impingement have also led to shoulder impingement.

It is important to rule out other potential sources of shoulder pain,

including: acromioclavicular arthrosis, rotator cuff tear, instabil ity,

adhesive capsulitis, biceps tendonitis, labral pathology, and cervical

radiculopathy.

The x-ray views that are most helpful are anterior-posterior view,

supraspinatous outlet view, and axil lary lateral. A 15-degree cephalic

view of the Acromioclavicular (AC) joint and an anterior posterior (AP)

view with humeral internal rotation can also be helpful.

Nonoperative care is tried before surgical intervention is considered.

The majority of patients can be treated conservatively. Treatment

consists of physical therapy, activity modification, anti-inflammatory

medications, and steroid injections into the subacromial space.

When nonoperative treatment fails, the procedure of choice is

arthroscopic subacromial decompressions (ASAD). The advantages of

arthroscopy include minimally invasive surgery without detachment of

the deltoid.

Conventional postoperative pain control can generally be obtained with

oral medications. Stiffness can be avoided when early motion is

emphasized.

Through progressive steps in exercises, full active range of motion can

usually be achieved within three to four weeks. Athletes using overhead

motions should avoid sports for at least 3 months, and complete

recovery can take 6 months.

The concept of mechanical impingement on the rotator cuff was popularized

by Neer (1). He noted that with forward elevation of the arm, the rotator cuff

tendons were subject to repeated mechanical insult by the overlying

coracoacromial arch. He observed that impingement was a result of bony

spurs at the anterior third of the acromion and the coracoacromial l igament.

This concept of anterior impingement as opposed to lateral acromial

impingement has been generally accepted.

Neer (2) reported the cause of most impingement to be due to an inadequate

“outlet” and described this phenomenon as outlet impingement. The outlet is

the space beneath

P.162

the anterior acromion, coracoacromial l igament, and acromioclavicular (AC)

joint. Within this space, the rotator cuff tendons pass to their insertions on

the tuberosities of the humerus. The superior border of the outlet forms an

arch known as the coracoacromial arch. Any prominence that affects this arch

may encroach on the outlet causing outlet impingement (3). In addition to

outlet impingement, the terms subacromial, primary or external impingement

are also used. The definition has more recently been described as

“symptomatic mechanical irritation of the rotator cuff tendons from direct

contact at the anterior edge of the coracoacromial arch” (4) (Fig 11-1) .

Fig 11-1. The supraspinatus outlet.

Fig 11-2. Acromial morphology.

Shoulder pain is a common presenting complaint for patients of all ages and

activity levels. In clinical frequency it is exceeded only by low back pain and

neck pain (23). About 50% of the adult population will have at least one

episode of shoulder pain each year (24). The most common source of shoulder

pain originates in the subacromial space, with the most prevalent diagnosis

being impingement syndrome (25). The spectrum of pathologies includes

rotator cuff tendonosis, calcific tendonititis, and subacromial bursitis.

The natural course of subacromial impingement varies somewhat. Long term

outcome suggests that it is not self l imiting and without treatment, symptoms

will persist and usually progress (26). The impingement process has been

described as having three chronologic stages (27). Stage 1 is characterized by

acute bursitis with subacromial edema and hemorrhage. As the irritation

continues, the bursae loses its capability to lubricate and protect the

underlying cuff and tendonitis of the rotator cuff develops. This leads to stage

II, which is characterized by inflammation and possible partial thickness tears

of the rotator cuff. As the process continues the wear on the tendon results in

a full thickness tear (stage II I). Several authors have shown that this

progressive process can be interrupted with surgical acromioplasty

(28,29,30).

Patient Presentation

Although impingement symptoms may arise following trauma, the pain more

typically develops insidiously over a period of weeks to months (31). The

patient's history will usually consist of pain with overhead activity, reaching,

l ifting, and throwing. They may have a job or recreational activity that

involves repetitive overhead movement (painting, assembly work, tennis). A

long day of overhead activity may increase symptoms to the point where the

patient seeks medical attention.

The pain usually occurs over the anterolateral aspect of the shoulder, and the

patient may point to this specific area. It may radiate down to the deltoid

insertion. Very often the patient may report pain at night, exacerbated by

lying on the involved shoulder or sleeping with the arm overhead. A complete

history and physical is essential to making a diagnosis of subacromial

impingement.

Physical Exam

A thorough physical examination should include careful evaluation of the

cervical spine to rule out a neurologic problem such as a herniated cervical

disc that can mimic shoulder pathology. This is especially true if a patient

presents with bilateral symptoms.

If subacromial impingement is suspected, specific tests should be used and

documented. The Neer and Hawkins signs for impingement are used commonly

and have been found to be reproducible and helpful. In attempting to elicit a

positive Neer sign the examiner stabil izes the patient's scapula while raising

the arm passively in forward flexion (27). This decreases room available in

the subacromial space, thus causing the rotator cuff and overlying bursae to

be compressed under the coracoacromial arch. In attempting to elicit a

positive Hawkins sign the patient's arm is passively flexed to 90 degrees. The

elbow is also bent to 90 degrees and the arm is forcibly internally rotated

(32). This brings the greater tuberosity under the acromion, compressing the

cuff and bursae. Individually, both exams have been shown to be sensitive but

not very specific for diagnosing subacromial impingement. When combined,

however, these two tests have a negative predictive value greater than 90%

(33) (Figs 11-3 and 11-4) .

Differential Diagnosis

It is important to carefully evaluate for other sources of shoulder pain. These

may include acromioclavicular arthrosis,

P.164

rotator cuff tear (partial or complete), instabil ity, adhesive capsulitis,

glenohumeral arthritis, biceps tendonosis, labral pathology (34), and cervical

radiculopathy. It is also important to remember that there can be more than

one source of pain. The two most common coexisting conditions are AC

arthrosis and rotator cuff tears.

Fig 11-3. Neer sign for impingement.

Fig 11-4. Hawkins sign for impingement.

Patients with AC arthrosis often point directly at the AC joint as the source of

pain. They are point tender over this area and have pain with cross arm

adduction. An injection into this joint may result in a decrease in symptoms

and x-rays will often show joint degeneration.

Full thickness tears of the rotator cuff result in weakness of the particular

muscle group involved. Isolated muscle strength testing with comparison to

the asymptomatic extremity can pick up even subtle differences. Active range

of motion in forward flexion and abduction may be less than passive range of

motion. In chronic conditions, muscle atrophy is often present.

Differential injections can be helpful in making the diagnosis of impingement

syndrome. Injections may be given in the subacromial space, AC joint, or

glenohumeral joint. The original impingement injection test was described as

a valuable method for separating impingement lesions from other causes of

shoulder pain. This test involves injection of 10 ml of 1% lidocaine into the

subacromial bursae. If after injection, “the painful arc is considerably reduced

or abolished, it establishes the anatomic site of the lesion but does not give

an indication of the precise pathology or extent of the lesion” (35).

The most common indication for selective injection involves differentiating

subacromial and AC joint pain. These injections may also be used in the

biceps tendon sheath. They typically contain a local anesthetic and often a

corticosteroid. The effect of the local anesthetic should begin almost

immediately. It is important to have the patient move their arm and document

what percentage of pain relief was obtained. The effect of the steroid can be

determined at a follow up visit quantifying amount and duration of pain relief.

Imaging Evaluation

X-ray fi lms are an integral part of the work up and necessary to gain

additional information. The views that are the most valuable are anterior-

posterior (AP) view, supraspinatous outlet view, and axil lary lateral. A 15-

degree cephalic view of the AC joint, and an AP view with humeral internal

rotation can also be helpful.

It is essential to evaluate acromial morphology and thickness on the outlet

fi lm. The AC joint is closely evaluated for bony pathology (best seen on the AP

or 15 degree cephalic). Arthritis of the glenohumeral joint and the presence of

an os acromiale are best seen on the axil lary lateral.

Magnetic resonance imaging (MRI) examination can be helpful to rule out

associated pathology. It can give an excellent picture of the rotator cuff

tendons and presence of tendonosis, partial, or complete tear. It is also useful

for looking at the rotator cuff muscles and the presence or absence of fatty

infi ltration. Within the shoulder joint, the biceps tendon, labrum, and chondral

surfaces can be assessed. The osseous anatomy can be further evaluated for

edema secondary to contusions and for the presence of avascular necrosis

(Fig 11-5) .

Fig 11-5. Type II I Acromion.

Table 12-1 Anatomy and Function of the Glenohumeral Ligaments and

Capsule

  Structure Origin

Insertio

n

Anatomic

Relations

hips Function

Coracohu

meral

l igament

Dense,

fibrous,

1- to 2-

Lateral

surface of

the

Greater

and

lesser

Extra-

articular

intermin

Limits

interior

translati

(CHL) cm wide;

thin

structure

coracoid

process

tuberos

ities

adjacen

t to the

bicipita

l

groove

gled

with the

edges of

the

supraspi

natus

and

subscap

ulans

tendons;

reinforce

ment of

the

rotator

interval

on and

external

rotation

when

the arm

is

adducte

d and

posterio

r

translati

on when

the

shoulder

is in a

position

at

forward

flexion,

adductio

n, and

internal

rotation

Superior

glenohum

eral

l igament

(SGHL)

Variable

in size;

present

in 90% of

individua

ls

Superior

glenoid

tubercle

just

inferior to

the

biceps

tendon

Superio

r

aspect

of the

lesser

tuberos

ity just

medial

to the

bicipita

Intra-

articular

, ties

deep to

the CHL:

reinforce

ment of

the

rotator

Same as

the CHL

l

groove

interval

Middle

glenohum

eral

l igament

(MGHL)

Great

variation

in size

and

presence;

absent or

poorly

defined

in 40% of

individua

ls

Superior

glenoid

tubercute

and

anterosup

erior

labrum,

often

along

with the

SGHL

Anterio

r to the

lesser

tuberos

ity

Intra-

articular

,

blending

with the

posterior

aspect

of the

subscap

ularis

tendon

Passive

restraint

to both

anterior

and

posterio

r

translati

on when

the arm

is

adducte

d in the

range of

60° to

90° in

external

rotation

and

limits

inferior

translati

on when

the arm

is

adducte

d at the

side

Inferior Consists Anteroinf Inferior Can be Function

glenohum

eral

complex

(IGHLC)

of three

compo-

nents:

anterior

band,

pos-terior

band,

axil lary

pouch:

decrease

s in

thickness

from

anterior

to

posterior

erior

labrum

neck of

the

glenoid

adjacent

to the

labrum

to the

MGHL

at the

humera

l neck

sheetlike

and

confluen

t with

the

SGHL or

cordlike

with a

luramina

l separa-

tion

between

it and

the

anterior

band of

the IGHL

complex

s as a

hammoc

k of the

humeral

head: in

adductio

n, it acts

as a

seconda

ry

restraint

,

l imiting

large

inferior

translati

ons; in

abductio

n, it

becomes

taut

under

the

humeral

head,

l imit-ing

inferior

translati

on;in

internal

rotation,

it moves

posterio

rly, and

in

external

rotation,

it moves

interiorl

y,

forming

a barrier

to

posterio

r and

anterior

dislocati

on,

respecti

vely

Posterior

capsule

Thinnest

region of

the joint

capsule

without

discrete

l igament

ous

reinforce

ments

Posterior

band of

the IGHLC

posterosu

perior

labrum to

the

insertion

of the

biceps

Posteri

or

humera

l neck

Blends

with the

posterior

aspect

of the

infraspin

atus and

teres

minor

Limits

posterio

r

translati

on when

the arm

is

forward

flexed,

adducte

d, and

internall

y

rotated

Reproduced with permission from Norris TR. OKU: Shoulder and Elbow

Update 2. Rosemont, IL: American Academy of Orthopaedic Surgeons;

2002.

Fig 12-9. Equation for calculating stabil ity: If A - B > r, then the

force for dislocation is reduced 70%. Sagittal CT of normal

Glenoid (A), and osseous lesion anterior glenoid (B).

Fig 12-8. CT scan of large fracture involving anterior glenoid

Fig. 2-1. Arthroscopic view from an anterosuperior

portal demonstrating a Bankart lesion. L, anterior

labrum; G, glenoid; H, humerus.

Fig 12-10. Hil l Sachs lesion (A), three-dimensional CT reconstruction of large

Hill Sachs lesion (B).

A complete history of the symptoms is extremely important to

determine the etiology and to elucidate the main direction of

instability. Duration of symptoms, characterization of their

severity, activity associated with their increase or decrease,

presence or absence of the traumatic event, and history of

systemic metabolic disorders resulting in generalized joint laxity

should be actively sought. Instability must be separated into

involuntary and voluntary. Voluntary dislocators must also be

separated into patients who have positional instability and can

dislocate on command and those with underlying psychiatric

disorder—true voluntary instability. The patients who have

positional instability and can voluntarily dislocate their shoulder

when asked, but otherwise try to avoid dislocations, can have a

successful result after surgical intervention after proper

nonoperative management. Conversely, patients with true

voluntary instability are poor surgical candidates and skillful

neglect combined with nonoperative management and potentially

psychiatric evaluation should be considered. The patient's

motivation for improvement should also be assessed. Strict

adherence to the postoperative rehabilitation program is

extremely important for a successful outcome. More than one

interview is usually necessary to sort through these important

issues.

A thorough physical examination must be performed to detect

potential other causes of pain. It is easy to make the wrong

diagnosis in a loose shoulder with other lesions, such as

acromioclavicular joint arthritis or cervical radiculitis, that are

responsible for pain. Many athletes' shoulders exhibit laxity, which

is normal, without the diagnosis of instability. This is a crucial

point that must be remembered when examining a patient. Both

shoulders as well as other joints (elbows, finger joints, and knees)

must be examined for signs of generalized ligamentous laxity.

Complete examination of the shoulder is crucial to determine the

etiology of pain. Diagnostic injections with 1% lidocaine into the

subacromial space or acromioclavicular joint are useful to

differentiate subacromial pathology from glenohumeral lesions.

Close inspection of scapulothoracic articulation must be

performed. Any signs of muscular atrophy or scapular winging

must be noted. Scapulothoracic instability may present with

symptoms of vague pain and numbness and tingling similar to

patients with microinstability of the glenohumeral joint. Specific

tests on physical examination are useful to determine the

direction of glenohumeral instability. Presence of pain during the

performance of these tests is important and should be noted;

however, apprehension, not pain, is a true positive result of these

tests. Anterior apprehension test determines the presence of

anterior instability. 1 6 This test is performed with the arm in

abduction and external rotation with the humerus being pushed

forward. Posterior instability is tested with the arm flexed and

internally rotated with the humerus pushed posteriorly. 1 6 Sulcus

sign is important in making the diagnosis of MDI and is indicative

of inferior laxity. 1 Downward pressure is applied to the adducted

arm, creating an indentation of skin between the acromion and the

humeral head. Inferior apprehension can be determined with the

arm abducted and humerus pushed downward. Additional tests for

glenohumeral instability, such as the fulcrum test, Fukuda test,

relocation test, and push-pull stress test have been described and

are helpful in making the diagnosis. 1 , 2 Often a patient cannot relax

enough to adequately perform instability tests in the office. Exam

under anesthesia in this type of patient is a very important part of

operative treatment if a nonoperative approach fails.

Plain radiographs, anteroposterior view in internal, neutral, and

external rotation, scapular-Y, and axillary views are obtained to

evaluate for Hill-Sachs and glenoid bony defects as well as

potential other pathologic conditions. Stress radiographs can

demonstrate capsular laxity, but are not usually needed. Magnetic

resonance imaging (MRI) is often helpful but not required to assess

labral and capsular pathology. MRI with intra-articular contrast

injection provides much more information about capsular

redundancy and labral injuries.

MDI of the shoulder has been defined as symptomatic shoulder

laxity in more than one direction (anterior, posterior, and/or

inferior), but it can be a difficult diagnosis to confirm. 1 4 , 1 5

Symptoms can vary from subtle painful subluxations to recurrent

frank dislocations. Patients with MDI often have symptoms

resulting from relatively little or no trauma and usually have

normal radiographs. However, a traumatic episode and the

presence of a Bankart labral injury or Hill-Sachs fracture do not

exclude the potential for MDI as a diagnosis. A thorough history is

necessary to establish the activity or position of the upper

extremity that reproduces symptoms. An office physical exam as

well as an exam under anesthesia are both critical in assessing

laxity and planning surgery.

In patients with MDI, some degree of generalized ligamentous

laxity is the norm, and it should always be tested and documented.

Patients may also have varying degrees of ability to voluntarily

sublux or dislocate their shoulders. Physical examination may

reveal either obvious or subtle findings such as excessive anterior

and posterior glide, a positive sulcus sign, or the ability to

voluntarily sublux the shoulder upon request. A positive early

warning sign (EWS) is the ability of a patient to easily and willingly

dislocate or sublux his or her shoulder, usually with the arm held

comfortably at the side. Surgical stabilization of such patients is

prone to failure, as these “muscular” subluxators will often stretch

out any repair, arthroscopic or open. Other “positional”

subluxators are still able to voluntarily sublux their shoulders, but

need to bring the arm into a flexed, adducted, and internally

rotated position to do so. These patients are more hesitant to

sublux their shoulders upon request, as the subluxation is

uncomfortable or painful. Positional subluxators are felt to be

somewhat better surgical candidates than purely muscular

subluxators. A third group, those patients who cannot and will not

voluntarily sublux their shoulders at all, makes up the best

candidates for surgery. A careful history and office physical exam

should differentiate these patient groups.

Examination under AnesthesiaMuscle guarding can prevent adequate instability testing in the

unanesthetized patient. A thorough examination under anesthesia

is critical. True laxity of the shoulder can be determined at this

time. This exam can either confirm the previous findings in the

office or pinpoint an additional direction of laxity. Usually the

directions of instability have been determined preoperatively after

complete workup. Some axial pressure should be applied to the

humerus to appreciate translations of the humeral head over the

glenoid rim. Experience and practice is important in this technique

to understand the position of the humeral head relative to the

glenoid during testing.

Physical Findings

A systematic evaluation includes observation for abnormal motion patterns

and atrophy, palpation to localize painful areas, assessment of both active

and passive range of motion, measurement of strength of the rotator cuff,

deltoid and scapular stabil izer muscles, neurovascular examination, and

finally provocative testing maneuvers for instabil ity. It is important to

examine the opposite shoulder for comparison.

In evaluating shoulder motion, the examiner must carefully document any

scapulothoracic substitution for glenohumeral motion, scapular winging, and

other abnormal muscle patterns. Atrophy of the spinatus muscles may

indicate longstanding associated rotator cuff tear or injury to the

suprascapular nerve. Similarly, atrophy of the deltoid may indicate axil lary

nerve injury.

In addition, patients should always be assessed for findings of generalized

ligamentous laxity, including the abil ity to hyperextend their elbows more

than 10 degrees, apply the thumb to the forearm, hyperextend the

metacarpalphalangeal joints more than 90 degree, or touch the palm of each

hand to the floor while keeping the knees extended (Fig 12-11) . While there

is no direct relationship between generalized laxity and shoulder instabil ity,

there is some association between hyperlaxity and glenocapsular

development (61).

The patient with an acute, unreduced anterior shoulder dislocation typically

holds the arm in slight abduction and internal rotation (20,50). Before

attempting any reduction maneuvers, carefully perform a neurovascular

examination to rule out brachial plexus injury, and specifically an axil lary

nerve injury (67,68). The latter condition may sometimes escape detection, as

decreased sensation over the lateral deltoid is not always present with an

injury to this nerve. In patients older than 60 years of age or younger patients

involved in severe trauma, be aware of the possibil ity of an associated

fracture of the humerus (69). Therefore, proper radiographic imaging is

particularly important before attempting closed reduction in such cases.

Fig 12-11. Example of generalized ligamentous laxity, demonstrating the

abil ity to apply the thumb to the forearm.

Regardless of the particular closed reduction maneuver employed, perform all

maneuvers as a gradual and gentle technique with appropriate analgesia

(either intravenous or intra-articular) to ensure muscle relaxation. A method

of gentle traction in l ine with the arm using counter-traction is usually

successful.

Always be alert to the possibil ity of an unrecognized chronic (fixed)

dislocation. The direction is typically posterior, however a chronic anterior

dislocation is also possible. Many of these patients are poor historians

secondary to dementia or chronic alcohol abuse (60). On exam, a patient with

a fixed posterior dislocation will have severe limitation of external rotation

compared to their opposite shoulder. Upon inspection, there is typically a

flattening of the anterior aspect of the shoulder with an associated

prominence of the coracoid process and possibly some prominence and

rounding of the posterior aspect of the shoulder. The application of excessive

force in attempting to close reduce such an injury risks neurovascular injury

and/or fracture.

Athletes with instabil ity are typically first seen by an orthopedic surgeon in

the office, or in the training room, not in the emergency department. They

may have had a documented episode of instabil ity, or an injury with pain, but

no true sense of shoulder instabil ity. After a careful neurovascular

examination, it is important to assess both active and passive range-of-

motion. A discrepancy between active and passive motion may indicate either

an associated rotator cuff tear or a nerve injury.

It is particularly important to identify a subscapularis tear in the setting of

shoulder instabil ity, a condition that is frequently missed (70,71). Patients

with such tears can passively increase externally rotation with the arm

adducted at the side, as well as associated apprehension in this position.

Strength assessment is also important. Significant external rotation weakness

may indicate a rotator cuff tear.

A subscapularis tear also typically demonstrates internal rotation weakness.

In this situation, the patient has an associated l i ft-off sign and belly-press

test . The belly-press test maneuver is very useful in situations when the

patient lacks adequate internal rotation to perform a lift-off test. To perform

the belly-press test, the patient places their hand on their abdomen, with

their elbow flexed at 90 degree, and attempts to bring their elbow anterior to

the coronal plane of their body, while keeping the hand on their abdomen at

all times. If the elbow remains posterior to the anterior aspect of the mid-

abdomen (i.e., the coronal plane of their body), there is l ikely a subscapularis

tendon tear.

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Specific tests for shoulder instabil ity allow the clinician to classify the

instabil ity pattern. The apprehension test was originally described by Neer

and Foster (72). With the patient seated or standing, place the symptomatic

shoulder into a position of 90 degree of abduction and maximum external

rotation. The patient's withdrawing from the examiner or complaining about a

sense of shoulder instabil ity demonstrates apprehension.

Pain as a chief complaint is not specific for shoulder instabil ity. Other

shoulder conditions such as arthritis and rotator cuff disease commonly

present with shoulder pain. Kvitne and Jobe (73) proposed a modification of

the apprehension maneuver to increase specificity for subtle anterior

instabil ity. Place the patient in a supine position, and perform the

apprehension test as described above. Ask whether the patient has a sense of

instabil ity or simply pain. Place posterior pressure on the humerus, and ask

whether this pressure relieves the sense of apprehension or pain. This

“relocation maneuver” increases specificity of the diagnosis of instabil ity if

the patient reports decreased apprehension. If this maneuver simply reduces

pain, it is not diagnostic of instabil ity and may be associated with a variety of

other diagnoses, including a SLAP lesion or impingement syndrome (74).

Inconsistencies in the apprehension test led Gerber and Ganz (75) to develop

the anterior and posterior drawer test to assess the shoulder for excessive

translation compared with the contralateral side. Others have found merit in

this method of examination and have developed grading scales for the degree

of shoulder laxity (76,77,78). These tests may offer some insight into the

degree and direction of the instabil ity. If one assesses laxity of the shoulder

in the office setting, it is important to determine whether translation of the

humeral head is greater on the painful side and whether this translation

causes symptoms (55). Laxity testing assessment in the office setting can be

of l imited value if pain is causing the patient to guard the affected shoulder.

Instead, this method is best used during examination under anesthesia to

confirm the suspected degree and direction of shoulder instabil ity.

Altchek et al. (76) and Hawkins et al. (78) proposed a grading scale for

translation of the humeral head on the glenoid. Instabil ity is graded on a

scale of 0 - 3+ for all three directions (anterior, posterior, and inferior). For

anterior and posterior drawer testing, a grade of 0 represents no humeral

head translation, while movement of the humeral head up to but not over the

glenoid rim represents 1+ instabil ity. Translation of the humeral head over

the glenoid rim with an associated spontaneous reduction with relief of

pressure represents 2+ instabil ity. Frank dislocation and locking of the

humeral head over the glenoid rim is graded as 3+ instabil ity. Whether in the

office or under anesthesia, when performing drawer tests, it is important to

bear in mind that the position of the arm determines the degree of tension in

the glenohumeral l igaments. With the arm at the side in adduction, the IGHL

is relatively lax, and anterior and posterior drawer testing may be of l imited

value. In abduction, the IGHL comes underneath the humeral head and forms

a hammock that passively l imits anterior, posterior, and inferior translation

(79,80). Perform anterior drawer testing with the shoulder positioned in

abduction in the plane of the scapula. Maintain the arm in neutral rotation

while using one hand to place an axial load along the humerus and the other

hand to apply an anterior or posterior force to the humerus. Often the

examiner can feel the humeral head move back into the glenoid rather than

out of the glenoid during the maneuver. The patient may note a painful click

with such a maneuver. This can be particularly helpful in identifying posterior

instabil ity.

Posterior apprehension can be elicited by a modification of the posterior

drawer test. To perform this modification, place the patient's arm in 90

degree of forward flexion and adduction while applying an axial load down the

shaft of the humerus. Pain and a palpable shift and click suggests posterior

labral injury and instabil ity (61).

A modification of this test, termed the jerk test , has been described for

posterior instabil ity (81,82). With the patient seated, load the adducted

shoulder axially into the glenoid with one hand, and with the other hand,

palpate the posterior aspect of the shoulder. Then bring the arm into

horizontal abduction anterior to the plane of the scapula; the humeral head

may sublux posteriorly. Then bring the humerus posterior to the plane of the

scapula; the humeral head may suddenly reduce into the glenoid. A palpable

shift and pain accompany a positive test.

The sulcus sign is basically an inferior drawer test (Fig 12-12) . Originally

described by Neer and Foster (72), it was initially believed to be

pathognomonic for inferior and multidirectional instabil ity. Unfortunately, a

common misconception has been that a large sulcus sign that is

asymptomatic, thus indicates inherent joint laxity, is a positive finding. The

key point is that this maneuver should be associated with pain and should

reproduce the patient's symptoms to be clinically relevant as a finding of

inferior instabil ity. A positive

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sulcus sign in the absence of clinical symptoms is diagnostic only for inferior

laxity, not inferior instabil ity.

Fig 12-12. Example of a large asymptomatic sulcus.

To perform the sulcus test , have the patient seated and the arm adducted at

the side. Rotation of the shoulder is very important in assessing the degree of

inferior instabil ity. First, with the arm in neutral rotation, pull the humerus

inferiorly, and estimate the amount of separation between the acromion and

the humeral head. Grade is based on a scale of 0 - 3+ (76): A separation of 1

cm is a 1+ sulcus sign, 2 cm is a 2+ sulcus sign, and 3 cm is a 3+ sulcus sign.

Anatomically, a sulcus sign greater than 2+ indicates a capacious capsule and

specific laxity of the anterosuperior capsular region (rotator interval).

The sulcus sign should always be repeated with the arm placed in external

rotation. If the sulcus sign remains greater than 2+ with the arm in external

rotation, there is a marked deficiency of the superior capsule, and a large

rotator interval defect in the capsule is l ikely (61). This is the result of

damage to the superior and MGHLs, as well as the CHL. With this information

before surgical repair, the surgeon then knows that surgical reconstruction of

this region (rotator interval closure) with a capsular shift must be a

component of the operation (83,84).

The Gagey test or Hyperabduction test measures the range of passive

abduction (RPA) of the shoulder joint with the scapula stabil ized (Fig 12-13) .

Anatomical and clinical findings have demonstrated that when passive

abduction occurs in the glenohumeral joint only, the abduction is controlled

by the IGHL. An RPA of more than 105 degree is associated with lengthening

and laxity of the IGHL. Gagey and Gagey (85) demonstrated a high association

of an RPA of over 105 degree and instabil ity.

Since the description of superior labral pathology by Andrews et al. (86) in

1985 and of the SLAP lesion by Snyder et al. (87) in 1990, several

examination techniques have evolved to diagnose this pathology. Andrews

reported increased pain in patients during full shoulder flexion and abduction,

with noticeable catching and popping. Snyder reported pain in patients with

resisted shoulder flexion with elbow extension and forearm supination (biceps

tension test).

Fig 12-13. Example of the Gagey test or Hyperabduction test that measures

the range of passive abduction (RPA) of the shoulder joint with the scapula

stabil ized.

Another useful diagnostic test is the compression-rotation test . With the

patient supine, abduct the shoulder 90 degree, with the elbow flexed 90

degree. Apply compression force to the humerus to trap the torn labrum (in

the same manner as McMurray's test for the knee is performed). O'Brien et al.

(80) also described a maneuver testing for the presence of superior labral

injuries. Commonly known as the O'Brien's Test , it is performed by placing the

patient's shoulder in 90 degree of forward flexion and then adducting it

across the body. Ask the patient to flex the arm further against resistance

when the shoulder is first internally rotated and then externally rotated. If

pain occurs when the shoulder is rotated internally but not when it is rotated

externally, the test is positive. With the O'Brien Test , pain arising from

acromioclavicular joint (AC) disease versus pain from a superior labral tear

can be differentiated by where the patient localizes the pain with a positive

test during internal rotation. If the pain localizes to the acromialclavicular

joint or “on top” of the shoulder the test is diagnostic for AC joint disease;

whereas pain or painful clicking described by the patient as “inside” the

shoulder is indicative of labral pathology (88).

Unfortunately, independent examination of several of the popular existing

physical exam tests for SLAP lesions have failed to demonstrate high

accuracy, sensitivity, or specificity. Therefore, the results of such tests should

be interpreted with caution when considering surgery, and therefore used as

one of several pieces of information (along with appropriate history and

radiological studies) which may point to a suspected superior labral anterior-

posterior lesion (89,90).

Imaging

The minimum radiographic workup necessary for evaluation of an acute

dislocation or suspected subluxation is a true anteroposterior (AP) view and

an axil lary lateral view. These images will allow accurate determination of the

position of the humeral head relative to the glenoid. A true AP radiograph is

obtained by angling the x-ray beam 45 degree relative to the sagittal plane of

the body. A scapular Y or transcapular view can also give information about

the position of the humeral head, but it is not as accurate as an axil lary view.

If a standard axil lary view cannot be obtained, a Velpeau axil lary view without

removing the patient's arm from the sling will suffice.

In the office setting, a true AP view of the shoulder with the arm in internal

rotation may demonstrate a Hil l-Sachs lesion. A Stryker notch view is a

special view that will also demonstrate a Hil l-Sachs lesion (91,92).

West Point axil lary view may prove helpful in a patient suspected of having

had an episode of instabil ity. Take the

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image with the patient prone so the anterior glenoid is shown in profile

without an overlying acromial shadow. This view demonstrates the glenoid rim

better.

Adjuvant imaging techniques add vital information about the three-

dimensional relationship and architecture of the joint or confirmation of the

presence of a Bankart lesion, either bony or soft-tissue. Computed

tomography (CT) demonstrates bony injuries or abnormalities including

glenoid dysplasia, congenital version anomalies, acquired version

abnormalities from erosion, and glenoid rim fractures (Fig 12-8). In addition,

it allows measurement of the size of a humeral head defect (Hil l-Sachs lesion)

in cases of chronic instabil ity (93). When combined with intra-articular dye,

CT arthrography also demonstrates Bankart lesions and articular erosions.

Magnetic resonance imaging (MRI) with or without gadolinium has enormous

popularity, although unfortunately it is often used as a screening tool in the

evaluation of patients. Its role should instead be to confirm the presence of

lesions that may need surgical treatment. MRI or CT with contrast are

valuable for identifying labral tears, capsular injuries, or bony deficiencies.

Although the arthroscope can be used for diagnostic purposes, we prefer to

identify coexisting pathology (rotator cuff tears), the degree of capsular

laxity, and the extent of labral pathology with the appropriate imaging studies

preoperatively, so that the appropriate surgical procedure can be selected

and planned. In some cases, however, where the quality of capsular tissue is

questionable by imaging studies or concomitant pathology is highly suspected

but not found preoperatively, a diagnostic arthroscopy performed at the start

of a planned open procedure can help add additional information, and

possible arthroscopic treatment) regarding intra-articular pathology. A

prolonged arthroscopic evaluation and/or treatment done immediately prior to

performing an open procedure can distort tissue planes, and in some cases

add no new information but only create technical problems for the planned

open procedure.

Recent studies show MRI arthrography to be highly sensitive and specific for

detecting capsulolabral lesions (94,95). CT is preferred if osseous pathology is

suspected. CT is particularly helpful in the evaluation of glenoid retroversion

in patients with posterior instabil ity. CT arthrography can also be used to

show chondral erosion, labral detachment, or excessive capsular redundancy

(96,97).

Etiology

When considering the possible causes of rotator cuff disease, mechanical

impingement of the rotator cuff is considered the most common recognizable

source of recurring pain and disabil ity in the active population. Neer's classic

work (20,62) served to organize the clinician's approach to rotator cuff

disease and, most importantly, to define rotator cuff pathology as a spectrum

of disease ranging from reversible edema to cuff fiber failure.

Primary impingement occurs at the anterior one third of the acromion and

coracoacromial arch (24,63,64,65,66,67,68). The mechanical stresses endured

by the rotator cuff, as well as its poor vascular design, both dynamic and

static, have been well documented (13,14,15,16,17). Additional factors

influencing rotator cuff pathology include acromial shape (20,22,24,69,70,71),

slope (21,72,73,74,75), coracoacromial l igament size (76,77), postfracture

deformity, os acromiale (78,79,80,81,82) and acromioclavicular joint spurring

(24,83). Snyder (72) has recently reported on the “keeled” acromion, a

particularly pernicious acromial variant associated with rotator cuff injury.

Functional abnormalities, such as asynchronous shoulder motion, posterior

capsular contractures, scapular dyskinesia, glenohumeral instabil ity, and

distant neurological injury leading to weakness can also adversely affect the

rotator cuff on a secondary basis with increased impingement forces

concentrated in the subacromial space (84,85,86,87).

Impingement may occur from a direct mechanical insult, usually the result of

an acromial excrescence excoriating the bursal aspect of the rotator cuff (Fig

13-7) . However, another plausible injury cascade begins with intrinsic cuff

failure, leading to insufficient humeral head depression and subsequent

superior migration with creation of a traction spur within the coracoacromial

l igament as a secondary phenomenon (24,26,68,71). The cause for intrinsic

cuff failure can range from fatigue on an overuse basis to underlying shoulder

instabil ity or superior labral pathology, injuries that have been associated

with internal impingement and articular sided cuff failure (88,89,90,91,92,93).

Regardless of etiology, a narrowed or stenotic supraspinatus outlet poses

continued risk to the rotator cuff.

Fig 13-7. Arthroscopic view of a symptomatic acromial spur (arrows) after

coracoacromial l igament release in subacromial space of a left shoulder.

Clinical Evaluation

History

Rotator cuff disease, especially that related to the impingement phenomenon,

is usually evident from the history alone. A painful range of motion beginning

at 70 degrees of forward flexion through 120 degrees is commonplace with

pain localizing to the anterior-superior shoulder, often radiating down the

lateral upper arm into the deltoid insertion. Overhead activities are the most

provocative, and in instances where the rotator cuff has actually torn, night

pain and difficulty sleeping are common complaints. Motion is usually not

restricted, other than that due to pain; however, for longer standing injuries,

a secondary adhesive capsulitis pattern can be encountered, especially in the

older population. Most often the onset of pain is insidious and takes place

over a longer period of time, but for those with an acute injury, a tearing

sensation associated with profound early weakness may be the presenting

history.

Because rotator cuff disease reflects a spectrum of pathology, the history and

physical findings may overlap. There may be little difference in the

presentation and findings of patients with isolated impingement, partial and

even small full thickness rotator cuff tears.

Physical Examination

After completing a detailed history, a focused examination can be undertaken.

It is critical to compare extremities as the unaffected shoulder can serve as a

“normal” template to

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which one can compare. One should survey for atrophy or asymmetry,

especially in the supra and infraspinatus fossae. Long-standing rotator cuff

tears are often accompanied by significant, visible atrophy. Examination

should include assessment of range of motion, both active and passive,

observing forward flexion, abduction in the scapular plane, internal rotation,

and external rotation both in abduction and with the elbow at the side.

Careful evaluation of scapular tracking should be included as poor scapulo-

thoracic mechanics can lead to secondary subacromial pathology. In some

instances of suspected impingement, simply treating scapular dyskinesia can

alleviate secondary subacromial space symptoms (84,86,87). Strength testing

should be performed in an attempt to isolate the different components of the

rotator cuff to assess weakness. The “lift-off” test can help to assess

subscapularis integrity (94) (Fig 13-8) .

Fig 13-8. Lift-off test evaluating integrity of the subscapularis. May be

difficult position to achieve in patients l imited by pain and motion restrictions.

Although clinically useful, placing the arm in the testing position can be

provocative and difficult to achieve, especially in the older population. The

“belly-press” test (or Napolean sign) can also help determine integrity of the

subscapularis, is less provocative than the “lift-off” test and can actually be

quantified to assess partial tears as well (95,96) (Fig 13-9) .

Fig 13-9.A: Alternative belly-press test for subscapularis integrity.

Subscapularis considered intact if wrist and elbow remain in straight l ine (no

wrist flexion) while pressing into abdomen. B: Positive belly-press test for

injured subscapularis as wrist flexion substitutes for subscapularis while

pressing against abdomen.

Fig 13-10. External rotation testing evaluates infraspinatus and teres minor

integrity. Weakness indicates loss of posterior transverse force couple.

Fig 13-11. Loss of humeral head containment and anterior-superior

subluxation can result from acromioplasty if transverse force couples are

compromised. Humeral head can erode through the thinned acromion.

Fig 13-12. Neer sign for impingement. Neer test util izes the same maneuver

following a subacromial injection of anesthetic. Amelioration of pain confirms

diagnosis of impingement.

Resisted external rotation with the elbow by the side is useful in detecting

tears extending into the infraspinatus (Fig 13-10) .

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This manual test is critical for assessing the posterior transverse force couple

while the “belly-press” test determines subscapularis function. If significant

weakness is noted in either or both muscle groups, loss of humeral head

containment is imminent if not already present. Loss of the normal distance

between the humeral head and acromion should be evident, and one must

proceed with great caution if a decompression is undertaken. Violation of the

arch in conjunction with inadequate transverse force couples may ultimately

lead to erosion of the acromion by the humeral head and subsequent anterior-

superior humeral head migration (97,98,99) (Fig 13-11) .

The impingement sign (Fig 13-12) as originally described by Neer involves

stabil izing the scapula while elevating the shoulder in the scapular plane.

Pain elicited in the arc from 70 to 120 degrees is indicative of the

impingement phenomenon. Confirmation of this finding in the form of the

impingement test consists of complete resolution of pain during the painful

arc of motion after an anesthetic has been injected into the subacromial

space.

A variation of the impingement sign is the Hawkin's test (Fig 13-13) in which

the shoulder is placed in 90 degrees of forward flexion, the elbow is flexed 90

degrees and the shoulder is then internally rotated. Rotation of the greater

tuberosity under the arch in this position decreases space for the rotator cuff

leading to impingement pain.

Diagnostic Imaging

It is essential that the initial evaluation of the painful shoulder include quality

plain radiographs. The standard radiographs should include a true anterior-

posterior view with the shoulder in the internal and neutral position, an

axil lary view, and the outlet (supraspinatus) view described by Neer and

Poppen (100), which is used to evaluate and classify acromial morphology and

arch anatomy. Bigliani et al. (69)

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have classified the types into I f lat, I I curved, and II I hooked (Fig 13-14) . In

addition to establishing morphology, the thickness of the acromion should

also be assessed and if surgery is recommended, a pre-operative decision can

be made regarding the amount of bone to be resected so as to prevent

excessive thinning or inadequate bone resection.

Fig 13-13. Positive Hawkins sign, indicative of subacomial impingement, is

elicited when pain occurs as the shoulder is internally rotated with the

shoulder forward flexed 90 degrees.

Fig 13-14. Acromial shape can be categorized into Type I: f lat, Type II:

curved, and Type II I: hooked. Type II I associated with impingement anatomy.

The standard anterior-posterior views may show superior migration of the

humeral head consistent with a cuff tear and potential subscapularis

involvement. Cystic and/or sclerotic change in the greater tuberosity may also

signal tendon pathology. The axil lary view is most helpful in assessing

concomitant glenohumeral degenerative changes, but is most helpful in

establishing the presence of an os acromiale (78,79).

Fig 13-15. Coronal MR T-2 weighted image depicting full-thickness rotator

cuff tear (arrows); f luid fi l l ing the gap is enhanced on T-2 imaging.

Magnetic resonance imaging is the current test of choice when evaluating the

soft tissues of the shoulder (101,102). T1 weighted images revealing

increased signal in the rotator cuff combined with a focal defect or loss of

continuity of the cuff on the T2 weighted image is a common finding when a

full or partial-thickness tear is encountered (Fig 13-15) . The addition of a

contrast agent such as gadolinium significantly enhances the positive

predictive value for diagnosing a full thickness tear, and can also aid in

detecting and quantifying partial tears of the cuff as well (103,104). Several

studies have demonstrated a poor correlation between arthroscopic findings

and MRI abnormalities (105,106). The combination of fat suppressed images

combined with contrast has been reported to significantly improve the

sensitivity and specificity for detecting full and partial thickness cuff tears

(107).

One must exercise caution when interpreting MR findings because

asymptomatic individuals may have significant rotator cuff findings on MRI,

but may remain completely asymptomatic (55). Magnetic resonance imaging

continues to demonstrate its greatest util ity and potential when combined

with a thorough and reliable history and physical examination.

Although an MRI scan is not essential for every patient with shoulder pain, for

those anticipating a surgical procedure, a pre-operative MRI scan can be

helpful for the following reasons: evaluating whether a cuff tear accompanies

a suspected impingement syndrome, the presence of which would alter the

post-operative regimen, allowing the patient

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to properly plan for post-operative care; determining the size and potential

tear configuration, including retraction, delamination, and thinning, factors

that need to be considered in the surgical planning; assessing the presence or

absence of atrophy (Fig 13-16) or fatty infi ltration (Fig 13-17) , both

important prognostic factors (108,109,110); and establishing the presence of

co-morbidities such as partial biceps or labral tears.

Fig 13-16. Oblique sagittal view through supraspinatus fossa demonstrates

atrophic changes (arrows) within the supraspinatus muscle belly which should

completely fi l l the fossa.

Fig 13-17. Oblique sagittal view through the supraspinatus fossa

demonstrating fatty infi ltration within the substance of the muscle belly. Fatty

streaks within the subscapularis and infraspinatus are also visible.

Fig 13-18.A: “Sleeper” stretch to combat glenohumeral internal rotation

deficit. Shoulder abducted 90 degrees with patient in 60 to 70 degrees of

lateral decubitus (this helps maintain scapular stabil ity to prevent

substitution). Elbow maintained in 90 degrees of flexion while internal rotation

generated with opposite extremity. B: “Sleeper” stretch from superior view.

Fig 13-19.A: Type II I acromion (arrows) contributing to classic external

impingement phenomenon. B: Appearance of acromial outlet after

acromioplasty.

Fig 13-21. Typical physical findings in patient with glenohumeral internal

rotation deficit. Scapula must be stabil ized while testing range of motion.

Table 13-1 Ellman Classification for Partial-thickness Rotator Cuff

Tears

Snyder Classification System for Grading Partial-thickness Rotator

Cuff Tears

Location of Tears

A Articular surface

B Bursal surface

Severity of Tear

0 Normal cuff, with smooth coverings of synovium and bursa

I Minimal, superficial bursal or synovial irritation or slight capsular

fraying in a small, localized area; usually <1 cm

II Actually fraying and failure of some rotator cuff fibers in addition

to synovial, bursal, or capsular injury; usually <2 cm

III More severe rotator cuff injury, including fraying and fragments of

tendon fibers, often involving the whole surface of a cuff tendon

(most often the supraspinatus); usually <3 cm

IV very severs partial rotator tear that usually contains, in addition

to fraying and fragmentation of tendon tissue, a sizable flap tear

and often encompasses more than a single tendon

Fig 13-23. Small full-thickness rotator cuff tear with crescent pattern and

minimal retraction visualized from the lateral portal of a right shoulder.

Biceps Tendinitis

Biceps tendinitis has been partitioned into primary tendinitis versus

secondary tendinitis. Primary tendinitis involves inflammation of the tendon

within the bicipital groove. To be considered primary, no other pathological

findings (such as impingement, bony abnormalities within the groove, or

biceps subluxation) should be present. It is considered an uncommon

condition (32) and should be thought of as a diagnosis of exclusion (33).

Habermayer and Walch (34) noted that this diagnosis can only be made during

arthroscopy.

Much more common is the condition of secondary biceps tendinitis. As the

LHB has an intimate relationship with its adjacent rotator cuff structures—

most notably the anterior supraspinatus and superior subscapularis—it is

affected by the same forces that produce pathology in these areas. Although

subacromial impingement produces undue forces on the anterior rotator cuff,

it also compresses the underlying LHB and produces concomitant pathology

(and thereby symptoms) in this structure (33,34,35,36,37,38,39). In fact, the

impingement upon the LHB worsens as a rotator cuff tear progresses and

increased contact between the LHB and the coracoacromial arch occurs.

Another potential cause of secondary biceps tendinitis is the presence of bony

anomalies of the proximal humerus. Most commonly these bony anomalies are

secondary to malunion or nonunion of a proximal humerus fracture. If a

fracture extends into the bicipital groove, significant irritation of the LHB can

occur. DePalma and Callery (40) suggested that younger patients with biceps

tendinitis are more likely to have groove anomalies such as narrowing or

osteophytes, but it is difficult to determine the sequence of events in such

conditions. Do the groove anomalies cause the tendinitis or the tendinitis

cause resultant groove anomalies?

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Biceps Tendon Rupture

Although acute ruptures of the LHB do occur, they are more commonly the

end result of chronic biceps tendinitis. Acute ruptures can occur with a violent

force placed on the LHB such as with a fall on an outstretched hand. Another

traumatic event, which can cause significant damage to the LHB, is rapid

deceleration of the arm during throwing activities (41). In this case the

deceleratory force can result in trauma to the origin of the LHB resulting in a

SLAP lesion. If the force is great enough in a single traumatic event or on a

repetitive basis, it can result in LHB rupture with an associated SLAP tear

(42).

Chronic biceps tendinitis is a more common etiology resulting in eventual LHB

rupture. The LHB becomes attenuated and weakened by the continued

impingement between the humeral head and the coracoacromial arch. In

these cases of impingement causing rupture, the rupture typically occurs

around the area of the rotator cuff interval (a weak point for the LHB) rather

than at its origin (33).

History

Anterior shoulder pain (particularly in the region of the bicipital groove) is the

hallmark of biceps tendon associated problems. With biceps tendinitis the

pain is usually described as a chronic aching pain, which is worsened by

lifting and overhead activities. The pain frequently radiates distally to

approximately the mid arm level but seldom radiates proximally. Inciting

events include repetitive activities involving

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lifting and overhead activities. There is such a close association between

subacromial impingement and biceps tendonitis that the two conditions have

closely overlapping symptoms. They can be very difficult to distinguish and

more often than not occur in tandem.

Fig 14-4. Photograph demonstrating the Speed's test. The examiner applies a

downward force (arrow) to the patient's extended arm while the patient

resists the downward force. Pain in the region of the biceps tendon is positive.

Patients who present with rupture of the LHB are usually much easier to

diagnose. These patients complain of a history of chronic anterior shoulder

pain consistent with biceps tendinitis and/or impingement. They then usually

report an episode of a painful “pop” in the shoulder, followed by partial or

complete relief of their impingement symptoms. Subsequently they may

develop ecchymosis in the arm and an associated muscular deformity in the

arm, frequently termed the Popeye muscle. Sometimes the Popeye deformity

does not develop secondary to the LHB becoming incarcerated in a stenotic

bicipital groove.

Physical Findings

Distinguishing anterior shoulder pain caused by biceps tendon disorders as

opposed to subacromial impingement can be difficult, as these two entities

usually co-exist. Although there are some exam maneuvers, which attempt to

isolate the biceps tendon, there is sti l l a fair amount of overlap and the

definitive diagnosis of isolated biceps tendon pathology is extremely difficult

based on history and physical exam alone. Often selective injections are

helpful in differentiating the etiology of the pain.

The hallmark of biceps tendon related pathology is point tenderness in the

bicipital groove. Without this finding it is extremely unlikely the LHB is

involved in the patient's symptoms. The bicipital groove is best palpated

approximately three inches below the acromion with the arm in 10 degrees of

internal rotation (43). As the arm is internally and externally rotated, the pain

should move with the arm. This is distinct from subacromial bursitis where the

pain location remains relatively constant despite the position of the arm.

Burkhead et al. (33) reports this “tenderness in motion” sign was quite

specific for biceps tendon disorders. In the situation in which it is unclear

whether the pain is secondary to the LHB or to possible impingement/bursitis,

selective injections of these areas can help make the diagnosis.

There are several provocative tests that can be helpful in the diagnosis of LHB

pathology; however, the sensitivity/specificity of these tests are questionable.

These tests are intended for the diagnosis of LHB pathology. Tests for the

diagnosis of SLAP lesions are covered elsewhere in this textbook.

Speed's test (44) (Fig 14-4)—With the elbow in extension, the patient

flexes the shoulder against resistance from the examiner. Pain in the

bicipital groove is considered positive.

Yergason test (45)—The patient attempts to supinate the wrist against

resistance (with the elbow flexed at the side). Pain in the bicipital

groove is considered positive.

Bear Hug test (46) (Fig 14-5)—This test was developed by Barth et al.

(46) to better isolate upper subscapularis lesions. Because these lesions

are almost always associated with LHB instabil ity, it is a good test for

LHB pathology. The patient places the open palm of the affected

extremity on the contralateral shoulder. In so doing, the ipsilateral

elbow is held well anterior to the plane of the patient's body. As the

examiner tries to l ift the hand off the shoulder (resisted internal

rotation), the patient tries to keep the palm on the shoulder. Weakness

(in comparison to the

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contralateral side) is a positive test and indicative of a tear of the

upper subscapularis (and thereby likely LHB instabil ity). In general, the

examiner should not be able to l ift the hand off the contralateral

shoulder unless there is tearing of the upper subscapularis, in which

case there is usually concomitant subluxation of the biceps tendon.

Fig 14-5. Photograph demonstrating the Bear Hug test. The patient

places the palm of the affected extremity on the contralateral shoulder

with the fingers held straight and the elbow kept in front of the patient.

The examiner applies an upward force (arrow) to the extremity while the

patient resists this force and tries to keep the palm on the shoulder. If

the examiner is able to l ift the palm off the shoulder this is a positive

test.

Fig 14-6. Photograph demonstrating the Napoleon test. The patient

places the hand of the affected extremity on the abdomen and tries to

keep the wrist straight. Inabil ity to keep the wrist straight while

performing this test is a positive finding

Napoleon test (47,48) (Fig 14-6)—This test also attempts to assess the

integrity of the subscapularis for the reasons noted in the previous

bullet point. The patient pushes on the abdomen with the palm of the

affected extremity and tries to keep the wrist completely straight. If the

patient is unable to keep the wrist straight but rather flexes the wrist to

perform the test, this is considered a positive or intermediate test and

suggestive of a subscapularis tear.

Belly-Press test (48,49)—This test is similar to the Napoleon test in that

the patient places the palm on the abdomen with the wrist held

straight. The physician then tries to pull the hand off of the abdomen. If

the physician is able to pull the hand off easily, this is considered a

positive test and suggestive of a subscapularis tear.

Lift-off test (50) (Fig 14-7)—This is the fourth test to assess

subscapularis integrity. The patient places the back of the hand of the

affected extremity on the ipsilateral buttock. The examiner then lifts

the hand posteriorly and asks the patient to hold it in that position.

Weakness or inabil ity to l ift the hand off the lower back is considered

positive and suggestive of a subscapularis tear.

Other tests have been described, such as the Ludington test (51), biceps

instabil ity test (52), and the deAnguin's test (53); however, we do not util ize

these tests and have therefore not described them. The described tests can

be useful in assisting the clinician with the diagnosis of biceps tendon

disorders. As noted previously, however, the sensitivity/specificity of most of

these tests has not been examined. The exceptions include the Speed test,

which Bennett (54) determined to be 90% sensitive for shoulder pain, but only

13% specific for bicipital pathology. Its positive predictive value was 23%

while its negative predictive value was 83%. The Bear Hug test was

determined to have a sensitivity of 60% and specificity of 92% for tears of the

upper subscapularis (46).

Fig 14-7. Photograph demonstrating the Lift-off test. The patient is asked to

place the hand behind the back and then lift the dorsum of the hand off the

back. Inabil ity to do so is considered a positive test.

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Findings associated with complete rupture of the LHB are usually much more

obvious. Examination reveals an alteration of the contour of the biceps such

that a portion of the biceps feels (and appears) “balled up” at the mid arm

level. This is termed the “Popeye” muscle. Rupture of the LHB is also often

accompanied by ecchymosis, which migrates down the anterior surface of the

arm.

Given the intimate relationship between biceps tendon pathology and

concomitant subacromial impingement and/or rotator cuff tear it is important

to examine the remainder of the shoulder in this patient population. Specific

tests for range of motion, impingement, rotator cuff integrity, and instabil ity

should be performed.

Imaging

As with almost every other orthopaedic condition, the clinician should begin

by obtaining a complete series of plain fi lm radiographs. For the shoulder,

these should include an anteroposterior (AP) view, axil lary view, and outlet

view (or scapular-Y view). We also include a 30-degree caudal ti lt view to

better assess the acromioclavicular (AC) joint. Others have described

radiographic projections, which are more specific for the bicipital groove

region of the proximal humerus. These include the Fisk projection (55) and

the bicipital groove view (56). The Fisk method has the patient hold the

cassette while leaning forward on their elbows and the beam projected

perpendicular to the floor (and cassette) (Fig 14-8) . This view looks down

the bicipital tunnel.

Fig 14-8. The Fisk projection has the patient hold the cassette while leaning

forward on their elbows. The beam is projected perpendicular to the x-ray

cassette.

The bicipital groove method has the patient l ie prone with the shoulder

slightly abducted and the arm in external rotation. The cassette is placed on

the top of the shoulder and the beam is directed up the patient's axil la

(parallel to the long axis of the humerus) and perpendicular to the plate (Fig

14-9) . This view can elucidate the depth of the bicipital groove, the

inclination of the walls of the groove, as well as any associated spurs within

the groove.

Prior to the advent of magnetic resonance imaging (MRI), arthrography was a

commonly util ized method of evaluation of the rotator cuff. It was also useful

in the evaluation of the biceps tendon. The loss of a sharp delineation of the

tendon can indicate biceps tendon pathology (57). Arthrography remains an

invasive technique with possible contrast complications and this constitutes

its main disadvantage.

Ultrasound has emerged as a potentially effective and noninvasive technique

in the evaluation of biceps tendon

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pathology. Middleton et al. (58,59) compared ultrasound to arthrography for

the diagnosis of biceps tendon and rotator cuff pathology. They found the two

modalities equally effective in the diagnosis of rotator cuff problems, but

ultrasound was superior in the evaluation of the biceps tendon. Another study

performed a biceps subluxation test and demonstrated 86% sensitivity in the

diagnosis of LHB subluxation (as confirmed surgically) with ultrasound (60).

Ultrasound has the added benefit of being a dynamic study. This allows easy

evaluation with shoulder motion. In comparison to other imaging modalities,

ultrasound is more operator dependent and therefore a well-trained

technician is essential to obtain meaningful and helpful studies.

Fig 14-9. The bicipital groove view is obtained by having the patient l ie

supine with the arm in slight external rotation. The x-ray cassette is held on

top of the patient's shoulder and the x-ray beam is aimed perpendicular to the

cassette along the axis of the patient's humerus.

As with the evaluation of most other shoulder disorders, MRI has become

increasingly popular. The anatomy (or patho-anatomy) of the biceps tendon

and the bicipital groove is well delineated with MRI and associated findings

such as rotator cuff pathology are also easily identified. Making the diagnosis

of biceps tendon rupture or dislocation is relatively simple with MRI; however,

biceps tendinitis and degenerative changes within the tendon are difficult to

determine via MRI. Although some authors have suggested that increased

fluid around the biceps is suggestive of biceps tendinitis (12), others report

low sensitivity and specificity using this criterion (61).

Types of Lesions

Cartilage repair response has been the focus of investigations for more than

250 years. In 1742 Hunter noted that “ulcerated cartilage is a troublesome

thing … once destroyed it is not repaired (15). Since that time, the

observations made by Hunter have been reiterated by nearly every scientific

study on the topic. The lack of predictabil ity of repair of carti lage is

attributable to the many factors that often come together in a specific injury.

Some of the factors include the precise injury, the age of the individual, the

condition of the joint before injury, the quality, extent, and durability of the

repair and the long-term function of the joint.

The types of injuries can be divided into mechanical and biologic. The

mechanical types of injuries include direct trauma to the cells and matrix

causing an acute disruption of the surface, or more subtle changes

attributable to damage of the matrix macromolecules. This type of damage

occurs with surgical disruption of the synovial membrane, infection

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and other inflammatory diseases, immobilization and possibly joint irrigation

(15).

In cases of blunt injury, the degree of disruption is often underestimated in

the acute phases. The response of articular carti lage to penetrating injury

depends on the depth of injury such that injuries l imited to carti lage elicit a

different repair response than injuries involving cartilage and subchondral

bone. Likewise, blunt trauma can have much more significant impact than is

acutely appreciated as a result of the consequent cell injury and effect on the

cellular matrix, as well as any injury to the subchondral supporting bone (16).

The biologic injuries include metabolic abnormalities, most commonly

osteoarthritis, but also avascular necrosis and a variety of osteochondral

injuries that damage the articular layer indirectly as a result of the collapse

of the supporting structures. For example, MRI analysis in degenerative joint

disease, osteochondritis dissecans, and avascular necrosis has shown that the

subchondral region shows reactive enhanced vascularization and heightened

metabolism with insufficient repair (17).

One particular disease process that deserves further mention is that of

avascular necrosis because the humeral head is the second most common site

of nontraumatic osteonecrosis, after the head of the femur (18). In humeral

head osteonecrosis, subchondral osteolysis occurs in the superior portion.

When resorption of subchondral bone is extensive, it appears that even

ordinary forces transmitted across the joint will lead to subchondral fracture

and humeral head collapse (18). The likelihood of this collapse and the

consequent degenerative changes that would occur make this disease process

one that must be addressed more expediently than other carti lage lesions.

The treatment of specific injuries is impacted by the underlying nature of the

cartilage injury. The best outcomes are obviously in isolated lesions that have

a clear, mechanical etiology without any underlying metabolic abnormalities.

The discussion of the factors involved is beyond the scope of this chapter, but

the reader is directed to the appropriate references (14,19,20).

Separate consideration should be given to osteoarthritis, as there are clear

surgical indications in the treatment of the disease in the glenohumeral joint

(without prosthetic replacement). The arthroscopic management of this

problem, if performed in the appropriate patient, has been shown to provide

significant improvement in symptomatology (11,12,13,21).

Diagnosis of Cartilage Lesions

Much effort has been directed at the development of imaging techniques that

effectively diagnose cartilage lesions in the shoulder. The thrust of the

research has employed a variety of magnetic resonance imaging techniques

to delineate not only the actual lesions, but also something about their

physiology. It is well established that carti lage functions as the load-bearing

surface in the joints of the musculoskeletal system. Major macromolecules in

cartilage are collagen Type II and proteoglycans. Although proteoglycans

provide much of the compressive stiffness through electrostatic repulsion,

collagen provides tensile and shear strength. Several studies have shown that

the earliest stages of carti lage degeneration are primarily associated with

loss of proteoglycan and minor changes in collagen structure (22). In one

study, bovine articular carti lage was analyzed with a variety of MR

parameters including T2 relaxation rates and spine-lattice relaxation times in

the rotating frame (T1ρ) mapping method (23). The findings included a

significant correlation between the changes seen on T1ρ mapping and the

sequential depletion of proteoglycan. Studies l ike these have served to

expand the base of knowledge with regards to grading of articular lesions.

Although arthroscopy is the so-called gold standard at this point for final

determination of the management of these lesions, it would be ideal to have a

noninvasive modality that fully assesses the lesions.

In the clinical setting, it is important to be able to delineate the presence of

cartilage lesions with some certainty. There are several studies available in

the literature that give some guidance (7,8,24). In one study, a double blind

prospective study of 15 patients with anterior shoulder instabil ity were

analyzed with respect to the efficacy of MRI versus arthroscopy in the

evaluation of chondral or osteochondral lesions of the humeral head (24). MR

produced 6 true positives, 5 true negatives, and 4 false negatives for an

accuracy and sensitivity of 60% and 87%, respectively. Arthroscopy gave 8

true positives, 5 true negatives, and 2 false negatives, with a sensitivity of

80% and an accuracy of 87%. All lesions diagnosed with either method were

regarded as positive by definition, with the result that the specificity was

always 100%. The differences in diagnosis sprang from the false negatives. As

a result of the variable abil ity to identify the cartilage lesions prospectively,

it was advised that both of these methods should be employed to ensure the

correct diagnosis, and hence the correct choice of treatment.

Another study has described the MRI findings of focal articular carti lage lesion

of the superior humeral head in seven patients (7). This was a retrospective

study to evaluate the location and incidence of these lesions. The lesions

occurred along the superior surface of the posterior humeral head (medial to

the expected location of a Hil l-Sachs lesion), were caused by trauma, and did

not seem to have a specific mechanism of injury. It was felt that they may

cause clinical symptoms and may be easily overlooked on MRI because they

were missed on six out of seven of those encountered.

In the largest available study, Guntern et al. (8) determined the prevalence of

articular carti lage lesions in a group of patients. Arthrographic images

obtained in 52 consecutive patients with a mean age of 45.8 years were

retrospectively evaluated for glenohumeral carti lage lesions. Two experienced

musculoskeletal radiologists who were blinded to the arthroscopy report

independently analyzed the articular carti lage. Humeral and glenoidal

cartilage were assessed

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separately and arthroscopic findings were used as the standard of reference.

At arthroscopy, humeral carti lage lesions were found in 15 patients

(frequency, 29%). Four lesions were subtle, and 11 were marked. Cartilage

lesions of the glenoid were less frequent (eight patients; frequency, 15%):

Three were subtle, and five were marked. For reader 1 and reader 2,

respectively, sensitivity of MR arthrography for humeral carti lage lesions was

53% and 100%, specificity was 87% and 51%, and accuracy was 77% and 65%;

sensitivity for glenoidal carti lage lesions was 75% and 75%, specificity was

66% and 63%, and accuracy was 67% and 65%. Interobserver agreement for

the grading of carti lage lesions with MR arthrography was fair (humeral

lesions, kappa = 0.20; glenoidal lesions, kappa = 0.27). Based on the study, it

was felt that the performance of MR arthrography in the detection of

glenohumeral carti lage lesions is moderate with a high degree of variabil ity

associated with the interpretation of the images.

As can be discerned by this analysis, much work needs to be done in the

delineation of carti lage lesions on a prospective basis. While the use of

gadolinium-enhanced arthrograms has clearly improved the abil ity to find

these lesions, a significant proportion is not identified prospectively. Also, the

biological parameters that are discernible with the use of MRI technology are

important to consider. The ideal study that addresses not only the presence of

a carti lage lesion, but also something about its biology or reparative

capability is clearly within the grasp of modern imaging. Its implementation

and refinement, however, await further studies.

Fig 15-3. Shoulder arthroscopic visualization of carti laginous defect treated

with subchondral perforation technique (Steadman). Views are of a right

shoulder, visualized from the posterior portal. A: Cartilaginous loose body

visualized arthroscopically. B: Remaining defect following preliminary

debridement. C: Arthroscopic awl employed for subchondral perforations. D:

Final area of subchondral perforation showing good blood supply following the

perforations.

Fig 15-4. Follow-up lesions of subchondral perforation technique on the

glenoid surface. A: Glenoid lesion at three-year follow-up showing some small,

patchy areas of fibrocartilage. (Left shoulder, posterior portal view of mid-

glenoid.) B: Glenoid lesion at two-year follow-up showing more exuberant

fibrocartilage repair. (Right shoulder, posterior portal view of mid-glenoid.)

Pectoralis major

Fig 16-3. Intact clavicular head and retracted sternal head of pectoralis

major. Demonstrated with resisted forward elevation.

Fig 16-4. Retracted sternal head seen with resisted adduction.

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Imaging

Imaging of the soft tissue injury in pectoralis major ruptures can be difficult.

Plain x-rays can reveal bone avulsions, or loss of the pectoralis shadow.

Ultrasound exam can demonstrate intra-muscular injury or loss of continuity

of the tendon (8). CT scan can outline the muscle, but has difficulty

visualizing the distal soft tissue of the pectoralis. MRI has been demonstrated

to reliably identify injury to the muscle and distal tendon (9) (Fig 16-5) .

Acute injury and edema of the pectoralis muscle, however, and insertion can

make identification of a complete rupture difficult (10). The hematoma is

easily identified in acute injuries, but is not present in more chronic tears. It

can also be difficult to differentiate a sternal head rupture versus complete

injury. Incomplete tendon injuries and medial muscle ruptures are not usually

amenable to repair. In our practice, we have not found MRI results to

significantly affect our pre-operative planning. In general, most of the

information required for surgical decision-making can be obtained from the

physical exam.

Fig 17-5. Rockwood classification of AC joint injury. (Reprinted from

Rockwood and Green: Fractures in Adults , 6th ed.)

Adhesive capsulitis

Physical Findings

The physical examination of patients with adhesive capsulitis reveals a global

reduction in range of motion with a marked decrease in glenohumeral

translation also present. Examination of the opposite shoulder (if normal) is

performed to identify the patient's expected normal range of motion for

comparison. Evaluation for l imitation of pure glenohumeral motion (best

measured in the supine position with the scapula immobilized) is often more

demonstrative of the extent of contracture present than the measurement of

total shoulder girdle range of motion (glenohumeral plus scapulothoracic

motion). The latter, however, is more closely l inked to the patient's clinical

perception of their abil ity to function, so frequently both types of shoulder

motion are measured and followed. Patients with adhesive capsulitis wil l

demonstrate at least a 20% reduction in range of motion, and findings of 50%

or greater loss of motion are not uncommon.

Some degree of weakness is often noted when examining for shoulder girdle

strength in patients with adhesive capsulitis. The magnitude of this finding

may be misleading

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however if the patient is experiencing an inflammatory component to their

disease. When this is present, strength testing can produce substantial pain

and result in a l imited resistive effort. To obtain the most representative

assessment of the patient's true shoulder strength, resistive strength testing

should be performed within the patient's comfortable arc of motion, often

testing elevation strength at approximately 30 to 45 degrees of elevation, and

rotational strength with the arm at the side.

Pain is often reported to be present diffusely throughout the shoulder girdle;

however tenderness with palpation is often greatest over the anterior

subacromial bursa, the proximal biceps tendon, the rotator interval area and

the anterior capsule. The posterior capsule, the lateral subdeltoid recess, and

rotator cuff area often have less tenderness with the acromioclavicular joint

often spared. Depending upon the phase of the disease process tenderness

can be quite severe, so palpation is often best performed at the end of the

exam to avoid patient guarding while examining for range of motion and

strength.

Imaging Studies

The evaluation of a patient with adhesive capsulitis is not complete without

an appropriate series of plain radiographs. True glenohumeral anterior-

posterior views, along with axil lary, scapular outlet and acromioclavicular

views are considered necessary to exclude other shoulder girdle conditions

which result in pain and stiffness. These fi lms may often reveal osteopenia,

but should not show any other definitive pathology. Additional radiographs of

the neck, chest, or arm should be obtained if clinically indicated to exclude

such problems as cervical radiculopathy, lung cancer, or humeral bone tumor.

Other types of advanced imaging have been used in patients with adhesive

capsulitis. Magnetic resonance imaging (MRI) may demonstrate thickening of

the inferior capsule, and when performed with intravenous gadolinium may

reveal enhancement in the capsule or synovium (22). MRI arthrography and

standard arthrography can show decreased intra-articular volume and will

commonly reveal a reduction in the size of the inferior capsular recess.

Additional findings can include variable distention of the biceps sheath or the

subscapularis recess. Dynamic ultrasound has been shown to display a

reduction in supraspinatus excursion with attempted shoulder movement (23).

Radionucleide scanning has demonstrated increased uptake of technetium on

“posterior views” in frozen shoulder (24), versus increased anterior uptake in

subacromial conditions and uptake involving the distal upper extremity in

patients with reflex sympathetic dystrophy. None of these advanced tests,

however, have been shown to be diagnostic of adhesive capsulitis and often

are unnecessary unless needed to exclude other diagnoses.

Fig 19-4. Crescent shaped rotator cuff tear. These tears can be repaired

directly to bone with suture anchors under minimal tension. (From

Warner JJP, Iannotti JP, Flatow EL, eds. Complex and Revision Problems in

Shoulder Surgery . 2nd ed. Philadelphia: Lippincott Will iams & Wilkins; 2005.

Posterior instability

In comparison to anterior shoulder instability, posterior instability

is a relatively rare entity. Most authors agree that posterior

shoulder instability represents only 5% to 10% of shoulder

instability cases. 1 , 2 , 3 It encompasses a broad spectrum of pathology

ranging from the more common recurrent posterior subluxation

(RPS) to the less common locked posterior dislocation (LPD).

Consequently, posterior instability may present in a variety of

patient populations and clinical scenarios. As a result, confusion

has traditionally existed in attempting to diagnose and treat this

ill-defined, uncommon entity. Initial attempts in clarifying the

distinctions of posterior instability were made in 1962 when

McLaughlin 1 recognized that differences exist between “fixed and

recurrent subluxations of the shoulder,” suggesting that the

etiology and treatment of the two are distinctly different. Since

that time additional knowledge has been gained in the differences

between unidirectional versus multidirectional (MDI), traumatic

versus atraumatic, acute versus chronic, and voluntary versus

involuntary posterior instability. In many respects each of these

may represent a distinct form of posterior instability with its own

underlying predispositions, anatomical abnormalities, and

treatment algorithms. 4 , 5 , 6 , 7 , 8 , 9 Our collective understanding of

posterior shoulder instability continues to be an evolving process.

Recent advances in our understanding of the spectrum of posterior

instability have been gained through the study of shoulder injuries

in athletes, patients with generalized ligamentous laxity, and

patients with posttraumatic injuries. 4 , 5 , 6 , 7 , 8 , 1 0 , 1 1 , 1 2 Acute posterior

dislocations typically occur as a result of a direct blow to the

anterior shoulder or indirect forces that couple shoulder flexion,

internal rotation, and adduction. 6 The most common indirect

causes are accidental electric shock and convulsive seizures.

Chronic LPD presents with the humeral head locked over the

posterior glenoid rim. As a result of incomplete radiographic

studies and a failure to recognize the posterior shoulder

prominence and mechanical block to external rotation, 60% to 80%

of LPD cases are overlooked by the treating physician. These

patients are often given a diagnosis of “frozen shoulder” but fail to

improve their external rotation with physical therapy. Patients with

both acute posterior dislocations and LPD may suffer a significant

osseous defect to the anteromedial humeral head, 2 that is often

referred to as the reverse Hill-Sachs lesion (Fig. 5-1). In addition,

a minority of patients with posterior dislocations will also suffer a

posterior capsulolabral detachment, often referred to as a reverse

Bankart tear (Fig. 5-2). Failure to recognize a posterior shoulder

dislocation in the acute period complicates treatment and leads to

a predictably poorer prognosis.

In contrast to posterior shoulder dislocations, RPS is often the

result of chronic repetitive microtrauma to the posterior capsule

without a single traumatic antecedent event. Gradually the patient

develops insidious pain with laxity of the posterior capsule and

fatigue of the static and dynamic stabilizers. 6 RPS may also result

from a traumatic reverse Bankart lesion or as a component of

MDI.6 , 7 The capsulolabral avulsion is seen less commonly in

posterior instability than it is in anterior instability. 1 3 , 1 4 Other

proposed mechanisms of RPS include excessive retroversion of the

humeral head, an engaging Hill-Sachs lesion, excessive

retroversion of the glenoid, and hypoplasia of the glenoid. 2 , 6 , 1 5 , 1 6

Fig. 5-1. Computed tomography scan demonstrating an osseous

impression defect, also known as a reverse Hill-Sachs lesion

(arrow), in a patient following reduction of a posterior shoulder

dislocation.

Fig. 5-2. Axial magnetic resonance image illustrating a posterior

labral detachment, also known as a reverse Bankart tear, with

some posterior capsular stripping from the glenoid rim (arrow) in a

patient with recurrent traumatic posterior instability.

Impingement

The orthopedic surgeon might add “the dynamic” to Moore's

definition of surgery. In orthopedics, as in other fields of surgery,

mechanical problems are frequently related to an anatomic

structure or a structural abnormality, but in the shoulder,

mechanical problems are frequently related to a dynamic event.

The shoulder patient often has an exaggeration of an event in the

shoulder that is normal. These exaggerations are in magnitude or

in frequency of a normal activity, necessitating different terms in

discussing the normal and abnormal. For example, the normal

shoulder has a certain amount of laxity, while an abnormal and

symptomatic laxity is termed instability. In the subacromial space

we see contact between the rotator cuff and the undersurface of

the coracoacromial arch, termed “buffering” by Flatow and

Soslowsky. 2 In the pathologic or symptomatic setting, this is called

subacromial (or external) impingement. In like fashion, internal

impingement of the glenohumeral joint is an exaggeration of a

normally occurring event that becomes abnormal or symptomatic

when it is performed with increased force or increased frequency. 3

In medical texts we usually begin with a description of the

pathogenesis of diseases and proceed to their clinical picture.

Because there are rival pathomechanical explanations, we should

begin with the known portion of the clinical picture and then

proceed to the possible pathomechanics and a more detailed

clinical description.

The groups of patients with similar pathology described in the

literature thus far include: overhead-throwing athletes,

nonathletes with interior impingement on a repetitive or traumatic

basis or anterior-internal impingement, and athletes with loss of

internal rotation.

The most studied patient is the overhead-throwing athlete. 4 , 5 , 6 , 7 , 8

The patient best known to the sports medicine physician and

trainer is the thrower. The most frequent presenting complaint is a

posterior pain in the shoulder at the initiation of the acceleration

phase of throwing (Fig. 6-1). The most common physical finding is

a positive relocation test with 90 degrees abduction and maximum

external rotation and horizontal abduction producing the pain. In

the second phase of the relocation test posterior pressure on the

humerus relieves the pain (Figs. 6-2A,B and 6-3A,B) .

The majority of overhead-throwing athletes can be treated by

removing them from throwing for a period of time during which

there would be strengthening of the muscles, total conditioning of

the body, and finally correction of kinematic rhythm. Most

importantly, because of the high energies involved, correction of

the body mechanics or “style” (Fig. 6-4) is needed. A minority of

throwers will develop recurrent symptoms on return to throwing

and will be found to have a surgical (i.e., structural) lesion (Table

6-1).

Further study by professional trainers has shown that there is a

prodromal phase before the thrower becomes truly symptomatic.

During that phase the athlete complains of some stiffness and

slowness to warmup. By resting and correcting mechanics in this

earlier phase, the time away from play can be cut in half.

Any pathomechanical explanation would therefore include:

features of the athletes or other patients' anatomy and function, a

dynamic event that can be aggravated by factors local or remote

to the shoulder, correction by training, and later a surgical lesion

or lesions beyond the reach of physical therapy.

Fig. 6-1. Phases of the baseball pitch.

There are several limitations on the normal range of motion of the

glenohumeral joint. The bony dimensions of the glenoid limit the

spinning motion of the humeral head. It is one of the unfortunate

but mathematical ironies of geometry that small decreases in the

bony limits on humeral motion result in large decreases in the

bony stability of the joint calculated as area of coverage is a

geometric function.

The capsule also limits motion of the humeral head in rotation. For

most positions of the shoulder the capsule is lax and only becomes

taut in end-range positions. For instance, in the abduction-external

rotation (ABER) position the anterior-inferior capsule tightens

toward the end of the range, resulting in a slight posterior

translation of the humeral head. For most positions of the

glenohumeral joint, alignment and stability are provided by

muscle, mainly the rotator cuff. The rotator cuff in a dynamic

fashion functions to protect the capsule from stretch in the end-

range positions.

Fig. 6-2. Relocation test: The patient is supine with the arm off

the table at 90 degrees abduction and maximum external rotation.

A: The examiner grasps the humeral head posteriorly and pushes

anteriorly. Sometimes the examiner feels sliding (subluxation) of

the humeral head, and this sliding typically elicits pain located at

the posterior joint line. B: The examiner grasps the humeral head

anteriorly and pushes posteriorly to relocate the head and lift the

rotator cuff off the posterior labrum. If the patient feels pain in the

first half of the test (A), it is usually relieved in the second half of

the test.

Fig. 6-3. Impingement of the rotator cuff on the posterosuperior

glenoid labrum during humeral abduction and maximum external

rotation. Cross-section from a cadaver.

The superior part of the glenohumeral joint is where the

glenohumeral structures can make contact in elevation. The two

positions where this contact may occur are ABER and forward

flexion-internal rotation. In the ABER position the greater

tuberosity approaches the posterior-superior glenoid. The

structures between these two bones, the labrum and the internal

fibers of the rotator cuff, are compressed between these two

bones.9 , 1 0 An additional structure at risk is the anterior-inferior

capsule that is stretched in this position (Table 6-1). Full forward

flexion produces a similar compression of the superior labrum. 1 1

In the forward flexion-internal rotation position it is the lesser

tuberosity that approaches the anterior-superior glenoid. The

fibers of the rotator cuff, in this case the subscapularis tendon,

are pushed against the anterior-superior labrum (Table 6-

2).1 2 , 1 3 , 1 4 , 1 5 The superior glenohumeral ligament and the biceps

pulley can be damaged as well. The contact is against

subscapularis below 90 degrees of elevation, and against the

biceps tendon and pulley above 90 degrees.

It has been shown in arthroscopy that the vast majority of patients

without symptoms in these areas achieve these internal contacts

easily. The presence of damage to structures at risk and the

accompanying symptoms point to these contacts being made with

an increased load or increased frequency.

The structures at risk in the ABER position are the internal fibers

of the rotator cuff and the opposing labrum. 8 The adjacent bones

are less frequently injured. Supraspinatus and infraspinatus are

vulnerable in the ABER position and the subscapularis in the

forward flexion-internal rotation position. The area of labrum that

makes contact with these portions of the rotator cuff is also at risk

for developing a superior labral anterior to posterior (SLAP)

lesion.4 The underlying bone, either tuberosity or glenoid, is less

frequently injured but also affected or thickened. 1 6 , 1 7 , 1 8 Finally,

stretching of the capsule with resulting subluxation of the shoulder

can occur. The combined injury may include one or more of the

above-mentioned five structures (Fig. 6-5).

Fig. 6-4. Pitching mechanics. A: Normal pitching mechanics from

a side view and an overhead view. B: Pathologic pitching

mechanics from a side view and an overhead view.

Table 6-1 Posterior Glenoid Impingement

  Early Later

Structure Reversible lesion Structural lesion

Rotator cuff Fraying or

irritation

Partial or full thickness

tear

Labrum Irritation

Fraying

SLAP

Glenoid Sclerosis

Hypertrophy

Fatigue fracture

Osteophyte

Greater Cyst Fracture

tuberosity Sclerosis

Anterior capsule Traction Instability

Finally, for the athlete, there are errors in technique. An example

of this is what is called by pitching coaches “opening up too soon.”

This can result from an error in contralateral foot placement at the

end of the early phase of cocking. If the contralateral lower limb is

too far externally rotated, this will rotate the pelvis toward the

target too early. Then the torso will rotate forward too early,

leaving the arm trailing behind. The anterior muscles of the

shoulder have to pull the arm forward, leading to both earlier

muscle fatigue and increased angulation in the joint with resultant

repetitive contact in the posterior-superior rotator cuff and

posterior labrum. Eventually there may be stretching of the

anterior-inferior capsule.

Some occupations can cause chronic ABER positioning of the

shoulder. An example would be someone who drives a forklift (Fig.

6-6). Although the steering mechanism of a forklift resembles that

of an automobile, the technique with which it is driven does not.

Because the loads in front obscure his view, the driver spends

most of his day driving backward. This leaves the shoulder of the

hand on the wheel in the ABER position. The glenohumeral

angulation becomes greater as the scapular positioner's fatigue.

Table 6-2 Anterior Glenoid Impingement

Structure Reversible Structural

Subscapularis

tendon

Fraying Tear

Anterior superior

labrum

Fraying SLAP

SGHL, CHL Fraying Biceps subluxation

Biceps pulley   Anterior superior GH

subluxation

SGHL, superior glenohumeral ligament; CHL, coracohumeral

ligament; GH, glenohumeral.

Alternative Pathomechanics in the Tight

Posterior CapsuleAn alternative etiologic theory for this combination of SLAP lesions

with partial rotator cuff tears has been proposed but has some

clinical features with the internal impingement theory. 1 9 It has

been noted that there is a very high incidence of tight posterior

capsule in throwing and other overhead athletes. 6 , 7 , 2 0 A tight

posterior capsule has been shown to produce an upward force on

the humeral head in the initiation of the acceleration phase of

throwing. 2 0 In addition, at that same instant, the tight posterior

capsule is producing a downward shear force on the labrum. 1 8 As

with glenoid impingement, this is a load on the posterior-superior

labrum for which it was not designed. This results in the

development of a “peel-back mechanism” that leads to a SLAP

lesion. A SLAP lesion may affect ligament insertions especially in

the superior and middle glenohumeral ligaments and lead to an

additional secondary instability. It has been noted that correction

of a SLAP lesion alone in these patients often corrects the

patient's problem. As with glenoid impingement there are

reversible aspects to this mechanism. In many athletes, the

posterior capsule can be stretched. Even after SLAP repair,

rehabilitation emphasizes reconditioning of the entire body and

restoration of proper mechanics.

Fig. 6-5. Cross-section of a shoulder specimen frozen in forward

flexion and internal rotation as would occur in the active

compression test. The lesser tuberosity is brought against the

anterior-superior glenoid. The anterior-superior labrum and the

upper fibers of the subscapularis are compressed between the two

bones.

Table 6-3 Causes of Internal Impingement

1. Weak rotator cuff resulting in early fatigue and reliance

upon boney and ligamentous restraints on glenohumeral

motion

2. Weak scapular rotators and lack of scapular mobility

resulting in the need for more extreme glenohumeral

positions

3. Weak torso and lower limb muscles resulting in disruption

of the smooth flow of kinetic energy and scapular

malposition

4. Errors in technique (sports)

5. Repetitive positioning (i.e., ABER) on the job

Clinical Signs and SymptomsInternal impingement in overhead athletes has been divided into

three clinical phases by the physicians and trainers who most

often treat the patients (Table 6-4). In the first stage the patient

complains of stiffness and slowness to warmup. There is no actual

pain in this prodromal phase, so there is a negative relocation

test. During this phase a knowledgeable trainer will diagnose the

athlete, take him or her off of their athletic event for 2 weeks,

strengthen the rotator cuff and the scapular rotators and any other

affected muscles of the limb, torso, and legs, and correct any

kinematic problems. The athlete is then returned to the coach for

style correction and then to the lineup.

Stage II is the first phase in which there is actually pain. The pain

is usually posterior in the shoulder, early in the acceleration

phase. On physical examination, the patient has a positive

relocation test, which is a re-creation of the glenohumeral position

at the initiation of acceleration. The pain is thought to be created

by the posterior superior-internal impingement of the shoulder,

and the pain relief sign is assumed to be produced by the decrease

in angulation and decreased contact of the posterior shoulder.

Because of the pain, the athlete is felt to be more severely

affected than in stage I and is pulled from the lineup for a 1-month

period during which time corrections in flexibility and muscle

strength are made by the trainer. Corrections in kinematics are

instituted, and then corrections in performance style are made. 2 1

Table 6-4 Posterior Internal Impingement

Stage Description Treatment

I Sensation of stiffness

Slowness to warmup

Brief withdrawal from

lineup

Strengthening

Correct kinematics

Correct style

II Posterior pain at

initiation of acceleration

Positive relocation at 90

Longer respite from

throwing

Similar conditioning as

degrees for stage I

III Clinically the same as

stage II

Failure of nonoperative

treatment

Findings pointing to one

or more surgical lesions

Workup for surgical

lesions

Arthroscopy

Surgical correction (see

appropriate chapter)

Fig. 6-6. To drive safely, forklift drivers must drive in reverse,

putting at least one shoulder into the abducted externally rotated

position. Fatigue of the upward rotators of the scapula would

cause the driver to rest the glenohumeral joint in the impinged

position. Some drivers place the opposite arm, the right arm in

this illustration, into abduction-external rotation. They do this so

they can use the right hand on the frame to assist with rotating

the torso. This second position would place both shoulders at

risk.

Stage III looks clinically very similar to stage II except the patient

now has the additional clinical finding of failing to respond to a

careful rehabilitation program as outlined above. Failure to

respond to rehabilitation is felt to indicate one or more structural

lesions that can require surgery. 2 2 Further studies are done in

these athletes such as magnetic resonance (MR) arthrogram to

elucidate the problems. In addition, arthroscopy could be

undertaken to look for subluxation as well as to treat any SLAP

lesions or partial rotator cuff tears. Following surgical correction

the patient is put through a rehabilitation program appropriate for

whatever surgery he or she has had. In addition the rehabilitation

program aims to correct whatever mechanical predisposition the

athlete had to glenoid impingement.

Table 6-5 Workup of the Patient

HISTORY:

  Location of the pain

  Timing

  Associated factors

PHYSICAL EXAM:

  Range of motion (internal rotation deficit)

  Illiciting maneuvers

  Impingement: Relocation test, Neer and Hawkins

  SLAP: Active compression test

  Relocation at 120 degrees abduction

  Speed test

  Subluxation

  Scapula position and flexibility

  Scapulohumeral kinematics

  Torso strength and flexibility

  Lower limb and pelvic strength

ASSESSMENT OF ACTIVITY PERFORMANCE:

  Imaging:

    X-ray: boney sclerosis, and unusual structure

    MR arthrogram: SLAP and nondisplaced fracture, partial

cuff tear, cysts

    Diagnostic arthroscopy

The workup of the patient is a summary of what this chapter has

covered (Table 6-5). The patient's complaints indicate a

glenohumeral problem and the workup begins there. The exam

looks for dynamic problems by applying the relocation test and by

looking for an internal rotation deficiency. We look for structural

problems such as: SLAP, partial cuff tears, sclerosis along the

glenoid, tuberosity damage, and instability.

We then move back down the kinetic chain looking for etiologic

factors. Malpositioning of the scapula, the base of the

glenohumeral joint, can be seen at rest or kinematically. Weakness

or decreased range of the torso can affect the base that positions

the scapula. Weakness or poor positioning of the lower limb can

affect the position of the torso. Some of the analysis may require

the help of an expert coach or trainer who can spot foot

malposition that might cause the shoulder injury.

Weakness of the subscapularis and deltoid are clinically

assessed by the lift-off and extension lag signs, respectively 1 1 , 1 2

(Fig. 8-7A,B,C,D). Dynamic anterosuperior subluxation can be

elicited by asking the patient to actively abduct the arm and

indicates deficiency of the subscapularis (Fig. 8-8A,B). If these

clinical signs are present, latissimus dorsi tendon transfer should

not be performed.

Radiographic evaluation in all patients consists of a true

anteroposterior plain radiograph with the arm in neutral rotation.

This enables the assessment of the acromiohumeral distance (Fig.

8-9A,B). An acromiohumeral distance of 5 mm or less is a relative

contraindication to performing the latissimus transfer. Cranial

migration of the humerus perpetuates subacromial impingement

and reduces the efficiency of the deltoid muscle as an abductor.

The axillary lateral radiograph allows one to determine the

presence of static anterior and posterior subluxation and the stage

of glenohumeral arthritis (Fig. 8-9A,B). Further imaging includes

either a computed tomography (CT) or magnetic resonance

imaging (MRI) with intra-articular contrast. MRI is the currently

preferred method for assessment of tear quality and size, degree

of retraction, and degree of fatty degeneration and muscle

atrophy1 3 , 1 4 (Fig. 8-10A,B). Massive tears of Goutallier stage III or

greater suggest an irreparable tear with poor-quality tissue likely

to be encountered at the time of surgery. 3

Fig. 8-2. A,B: A 72-year-old man with a massive, irreparable

posterosuperior rotator cuff tear is able to maintain good flexion

due to maintenance of a good anterior-posterior force couple and a

well-functioning deltoid. C: However, he displays a significant loss

of active external rotation. D: Plain radiographs that include a true

AP of the glenohumeral joint and axillary lateral display superior

subluxation and good maintenance of joint space consistent with

mild to moderate osteoarthritis. E: Coronal MRI demonstrates a

complete tear of the supraspinatus with retraction. F: Oblique

sagittal plane MRI demonstrates severe fatty degeneration of the

supraspinatus and infraspinatus muscles

Fig. 8-3. Treatment algorithm for patients with irreparable tears

of the posterosuperior rotator cuff.

Fig. 8-4. A 59-year-old man with a chronic, massive tear of the

posterosuperior rotator cuff. Demonstration of the external

rotation lag sign (A,B) with the arm at 90 degrees of abduction,

which indicates disruption of the infraspinatus and teres minor.

Fig. 8-5. With the arm in adduction, a lag between maximal

passive and active external rotation (A,B) is pathognomonic of a

tear of the infraspinatus.

Fig. 8-6. A 52-year-old mason with a traumatic posterosuperior

rotator cuff injury. At examination, he showed (A) the inability to

raise the arm against gravity, or pseudoparalysis, with (B) clinical

evidence of severe atrophy of the supraspinatus and infraspinatus

muscles. (Reprinted with permission from Gerber C. Massive

rotator cuff tears. In: Iannotti JP, Williams GR, eds. Disorders of the

Shoulder: Diagnosis and Management . Philadelphia: Lippincott

Williams & Wilkins; 1999:60.)

(Fig. 8-14G,H).

Fig. 8-7. The lift-off and belly press tests are used to test the

integrity of the subscapularis tendon. In the lift-off test, the

patient is asked to lift his or her hand off the lower back. It has

been found to be more sensitive and specific if there is the

presence of an internal rotation lag sign after the clinician

releases the hand from maximal internal rotation with the arm off

the back (A,B). In the belly press sign (C,D), the patient exerts an

internal rotation force on the belly, with the elbow forward and

anterior to the midline of the trunk. If the subscapularis is

ruptured, the patient is unable to keep his or her hand on the

stomach with resisted internal rotation, and the elbow will fall back

posteriorly. (Reprinted with permission from Gerber A, Clavert P,

Millett PJ, et al. Split pectoralis major transfer and teres major

tendon transfers for reconstruction of irreparable tears of the

subscapularis. Tech Shoulder Elbow Surg. 2004;5:5–12.)

Fig. 8-8. Dynamic anterosuperior subluxation indicates major

injury to the supraspinatus and subscapularis. The clinical

diagnosis is made if (A) the patient has normal contour of both

shoulders at rest and (B) subluxates his or her shoulder

anterosuperiorly while resisting abduction. The condition of

anterosuperior subluxation can be precipitated by open or

arthroscopic subacromial decompression, with release of the

coracoacromial ligament. If anterosuperior subluxation becomes

static, clinically or radiographically, successful restoration of

overhead elevation by direct surgical repair is exceedingly rare,

and subacromial decompression is detrimental. (Reprinted with

permission from Gerber C. Massive rotator cuff tears. In: Iannotti

JP, Williams GR, eds. Disorders of the Shoulder: Diagnosis and

Management. Philadelphia: Lippincott Williams & Wilkins; 1999:69.)

Fig. 8-9. (A) True AP and (B) axillary lateral radiograph of the

glenohumeral joint which are normal in this case. The true AP view

of the glenohumeral joint allows for assessment of the

acromiohumeral distance (ACHD) and static superior subluxation,

whereas the axillary lateral view is used to assess for static

anterior or posterior subluxation.

Fig. 8-10. Magnetic resonance images parallel to the glenoid

plane through the base of the coracoid. A: The subscapularis,

supraspinatus, infraspinatus, and teres minor are homogeneous,

convex, and voluminous in a normal rotator cuff. B: In a massive

posterosuperior tear, the subscapularis exhibits normal signal

characteristics and volume, but the supra- and infraspinatus show

fatty infiltration and atrophy. If a line drawn from the top of the

scapular spine to the highest point on the coracoid does not pass

through the substance of the muscle belly, it indicates significant

atrophy of the supraspinatus muscle.

Fig. 10-1. Diagram demonstrating the common tear location for

partial-thickness articular-surface supraspinatus tendon avulsion

injuries (PASTA lesion). SubS, subscapularis tendon; BT, biceps

tendon; SS, supraspinatus tendon; IS, infraspinatus tendon; TM,

teres minor tendon. (Modified and reprinted with permission from

Conway JE. The management of partial thickness rotator cuff tears

in throwers. Oper Tech Sport Med. 2002;10(2):75–85.)

Table 10-1 Ellman Classification for Partial

Thickness Rotator Cuff Tears

Location Grade

Revised

grade Area of defect

A: Articular

surface

1: <3

mm

deep

1: Fraying Base of tear (mm) ×

Max retraction (mm)

= Area in mm 2

B: Bursal

surface

2: 3–6

mm

deep

2: <50% depth

C: Interstitial 3: >6

mm

deep

3: >50% depth

Sources: Ellman H. Diagnosis and treatment of incomplete

rotator cuff tears. Clin Orthop. 1990;254:64–74; Ellman H,

Gartsman GM, Hengst TC, eds. Arthroscopic Shoulder Surgery

and Related Procedures . Philadelphia: Lea and Febiger

Publishers; 1993.

Fig. 10-3. Diagram of a coronal view of an articular surface tear in

the supraspinatus tendon with the glenohumeral joint positioned in

both adduction and abduction ( inset) demonstrating the improved

visualization of the rotator cuff tendon tear and the greater

tuberosity with abduction. (Modified and reprinted with permission

from Conway JE. The management of partial thickness rotator cuff

tears in throwers. Oper Tech Sport Med. 2002; 10(2):75–85.)

Fig. 10-4. Arthroscopic photographs of an articular surface tear in

the supraspinatus tendon with the glenohumeral joint positioned in

both adduction (A) and abduction (B) demonstrating the improved

visualization of the rotator cuff tendon tear and the greater

tuberosity with abduction. A transtendinous portal has been

created in the lateral segment of the tear allowing introduction of

a mechanical shaver for debridement of the tuberosity.

Tear of the subscapularis

Patients presenting with an isolated tear of the subscapularis

tendon typically are younger than patients with the more common

degenerative tendinopathy and tearing of the remainder of the

rotator cuff. 5 , 7 , 8 Most of these patients have suffered a traumatic

injury. There are four documented traumatic mechanisms of injury

for isolated rupture of the subscapularis tendon 9 , 1 0:

Fall directly on the shoulder not associated with a

dislocation;

Rupture associated with an anterior dislocation of the

shoulder;

Violent external rotation injury with the arm in an adducted

position;

Violent hyperextension injury.

Patients usually present with night pain and pain that produces

significant functional limitations. They often complain of pain both

with the arm at the side and with elevation. Another common

complaint is pain and weakness when reaching behind for a wallet

in a pants pocket. In the largest reported series, all patients

documented pain with the arm below the shoulder, pain with the

arm in the overhead position, anterior shoulder pain at night, and

weakness of the upper extremity. 6

Physical ExaminationPhysical examination of the patient with a subscapularis tendon

rupture demonstrates increased external rotation (usually by 10

degrees to 30 degrees) compared to the contralateral side. A

positive liftoff or “belly press” test is also present (Fig. 11-1A,B).

Recent electromyographic evidence demonstrates that the liftoff

appears to preferentially isolate the lower portion of the

subscapularis, and the belly press isolates the upper portion of the

subscapularis. 1 1

Fig. 11-1. The belly press test. A: Right, positive belly press test.

Note that the elbow goes posterior to the trunk with the patient

unable to maintain internal rotation. B: Left, note that the patient

is able to maintain internal rotation and the elbow is maintained

anterior to the trunk.

P.126

ImagingPlain radiographs are usually normal, though in the chronic case

the axillary view may demonstrate static anterior subluxation. 1 2 , 1 3 , 1 4

Magnetic resonance imaging (MRI) or computed tomography (CT)

with arthrographic dye are the gold standard tests for radiographic

confirmation of the subscapularis tendon tear. 1 5 , 1 6 MRI

demonstrates the condition of the tendon, partial or full thickness

tearing, and atrophy and fatty degeneration of the muscle.

In our clinical experience, there are no contraindications to

arthroscopic subscapularis tendon repair in medically stable

patients. Because the subscapularis tendon represents an

P.132

essential component of the transverse plane force couple, most

patients complain of significant pain and weakness. Typically,

patients present with internal rotation weakness and an increase

in passive external rotation.

Several tests can be used to identify subscapularis tears in

patients. The liftoff test is performed by having the patient place

the hand of the affected arm on the back and asking the patient to

lift the arm posteriorly off the back. 1 1 , 1 2 , 2 4 a If the patient is unable

to lift the arm posteriorly off the back, the test is considered

positive. However, patients are often unable to perform the liftoff

test due to pain or internal rotation contracture.

Another test that we use is the Napoleon (“belly-press”) test. 2 5 , 2 5 a

We perform this test by placing the hand on the belly similar to

the position in which Napoleon held his hand for portraits. We

grade the Napoleon test as negative (or normal) if the patient can

push the hand against the stomach with the wrist straight; positive

if the wrist must flex to 90 degrees to push against the stomach;

and intermediate if the wrist is flexed from 30 degrees to 60

degrees to accomplish a belly press. In patients with weak internal

rotation, the wrist flexes and the elbow drops back behind the

trunk as the patient recruits the posterior deltoid to press the

hand into the belly. We have found this test very useful in

predicting the degree of subscapularis tearing. 2 6 Patients with

positive Napoleon tests have tears of the entire subscapularis

tendon; those with tears involving more than 50% of the tendon

but not the entire tendon have intermediate Napoleon tests; and

those with intact tendons or tears less than 50% may have a

negative Napoleon test.

A final test that we use to determine subscapularis dysfunction is

the “bear hug” test. 2 6 a We have the patient place the hand of the

affected arm onto the contralateral shoulder. The patient is then

asked to resist the examiner's attempt to pull the hand off the

shoulder. In a normal exam, a patient should be able to resist this

maneuver. If there is weakness or pain to resisted internal

rotation, a partial or full-thickness tear of the subscapularis

tendon is suspected. Often a patient will have a negative liftoff

test and a negative Napoleon test and only demonstrate a positive

bear hug test. On arthroscopic examination, these patients are

often found to have a partial- or full-thickness tear of the upper

subscapularis tendon. The bear hug test is particularly sensitive

and specific for tears of the upper subscapularis. In an ongoing

study comparing the above three tests, we have found the bear

hug test to be the most specific test for identifying upper

subscapularis tendon tears.

Fig. 12-1. Arthroscopic view of the subscapularis insertion from a

posterior portal demonstrating a partial tear of the articular

surface of the subscapularis tendon. Note how the tearing of the

fibers reveals the underlying footprint of the subscapularis

insertion. SS, subscapularis tendon; H, humerus

The subscapularis muscle is important for normal shoulder

function and stability. It constitutes the sole anterior component of

the rotator cuff and is the most powerful of the cuff muscles. 1 The

subscapularis is a strong internal rotator of the glenohumeral

joint, particularly with the shoulder in an adducted and extended

position. 2 , 3 The dynamic force couple created from the coordinated

efforts of the subscapularis and the posterior rotator cuff is critical

for normal glenohumeral joint kinematics and stability. 4 , 5 This force

couple has been shown experimentally to be an important

contributor to humeral head depression throughout multiple

positions of glenohumeral abduction. 6 Loss of subscapularis

function commonly results in pain and weakness and occasionally

impairment in shoulder function, which may require surgical

treatment. 7 , 8

Fortunately, subscapularis tendon tears are relatively uncommon.

Isolated subscapularis tears are even less frequent. Codman 9

reported involvement of the subscapularis in 3.5% of a series of

200 rotator cuff tears, and Deutsch et al. 8 noted significant

involvement of the subscapularis in 4% of a series of 350 rotator

cuff tears. Warner et al. 1 0 noted involvement of the subscapularis

tendon in 4.7% of a series of 407 rotator cuff tears. The majority

of subscapularis injuries are associated with tears of the superior

rotator cuff (anterosuperior cuff tears) as well. 1 0 , 1 1 , 1 2 Isolated

subscapularis tears are more commonly associated with trauma in

comparison to other types of rotator cuff injuries. 7 , 1 3 Traumatic

subscapularis tendon tears have been associated with recurrent

anterior glenohumeral dislocation in several clinical series. 1 4 , 1 5 , 1 6 , 1 7

Subscapularis deficiency is also a well-documented complication of

open anterior instability and prosthetic humeral replacement.

History of the TechniqueRepair of acute subscapularis tears has produced excellent clinical

results. 7 , 1 8 , 1 9 Unfortunately, the diagnosis of isolated subscapularis

tears is often delayed or missed. 7 A completely torn subscapularis

tendon is prone to retraction and the development of irreversible

changes of the muscle. After a delay of several months or longer,

repair of the retracted tendon can be very difficult. Inferior clinical

results have been reported with delayed repair of subscapularis

tears1 0 , 1 3 and, in many cases, the subscapularis has been found to

be irreparable at the time of surgery. 1 4 , 2 0

Muscle transfers have become useful salvage options for patients

with irreparable tears of the subscapularis. Options include

transfer of the pectoralis major, pectoralis minor, trapezius,

latissimus dorsi, teres major, as well as allograft

reconstruction. 1 1 , 2 1 , 2 2 , 2 3 , 2 4 The pectoralis major tendon transfer has

produced the most reliable clinical results when compared to other

reconstructive options. Several characteristics of the pectoralis

major make it favorable for reconstruction of the subscapularis.

These include muscle bulk (including elderly patients), a robust

tendon, location, similarity of function, and tendon excursion.

Pectoralis major tendon transfer has been shown to be beneficial

in several clinical situations related to subscapularis insufficiency.

Successful results have been reported with associated recurrent

anterior shoulder instability secondary to subscapularis

deficiency, 1 4 massive posterior rotator cuff tears, 2 0 , 2 3 and for

humeral head containment in the setting of anterosuperior

migration. 2 5

EvaluationThe clinical presentation of patients with subscapularis tears is

variable. The majority of subscapularis tears are not isolated

P.138

but are seen in combination with tears of the superior and

posterior cuff. Most patients in this setting are older and present

with chronic pain and progressive deterioration of function of the

shoulder joint. Acute loss in function in the setting of chronic

shoulder symptoms may indicate an acute on chronic rotator cuff

injury and should raise the suspicion of subscapularis involvement

as well. Isolated injuries of the subscapularis often result from

trauma to the shoulder. A forced external rotation moment with or

without hyperextension of the adducted shoulder has been

reported as a common mechanism of subscapularis injury. 7 , 8 In

these series, the average patient ages were 39 and 50 years,

considerably younger than the typical presentation of a massive

anterosuperior rotator cuff tear. Anterior shoulder dislocation in

the middle-aged patient can result in subscapularis disruption and

recurrent instability. 1 4 , 1 7 Subscapularis failure can complicate open

instability or prosthetic replacement surgery.

The majority of patients with subscapularis tears will complain of

pain that may or may not be localized to the anterior shoulder.

Most patients will note increased pain and weakness with both

overhead activities and strenuous activities below shoulder level.

Isolated tears may produce minimal symptoms and can be easily

overlooked. Activities requiring forced internal rotation such as

reaching behind the body, placing the hand in a back pocket, or

reaching the abdomen are difficult. 1 8 Sensations of glenohumeral

instability are common, especially in more active patients or

following prosthetic replacement.

The physical examination of patients with subscapularis tears is

significantly influenced by the integrity of the remaining rotator

cuff. The majority of patients with isolated tears of the

subscapularis can still elevate the arm to the overhead

position. 1 4 , 1 8 Tears that also include the posterior cuff often

produce significant loss of active elevation due to disruption of the

rotator cuff force couple. 1 0 Isolated subscapularis tears are

commonly missed initially and require a high index of suspicion.

Subscapularis tears will often result in an increase in external

rotation range of motion compared to the opposite shoulder. The

abdominal compression and liftoff tests are excellent clinical

examination tools that are highly accurate for detecting

subscapularis disruption. 2 , 3 , 7 However, pain and limited passive

range of motion may hinder the accuracy of liftoff test because of

the arm position required to perform the maneuver. The strength

of the remainder of the rotator cuff should be assessed because of

the high prevalence of associated tears of the supraspinatus and

infraspinatus muscles. Apprehension in abduction may be seen in

those patients with instability. Tears of the subscapularis are often

associated with instability of the long head of the biceps

tendon. 1 0 , 2 6 , 2 7 Biceps provocation tests can clue the clinician to the

presence of biceps tendon instability.

Radiographs of the shoulder in patients with isolated subscapularis

tears are typically normal. Occasionally subtle anterior translation

of the humeral head can be appreciated on the axillary radiograph

in patients with subscapularis deficiency. Tears that also include

the posterior cuff will often result in superior migration of the

humeral head. This is particularly evident on true anteroposterior

(AP) radiographs performed with slight abduction of the shoulder.

Tears of the subscapularis can accurately be identified with both

ultrasound and magnetic resonance imaging (MRI). 2 8 , 2 9 , 3 0 , 3 1

Associated MRI findings are frequently encountered and fairly

specific to subscapularis injuries. These include subluxation or

dislocation of the biceps tendon, fluid collections local to the

subscapular recess, or subcoracoid bursa and supraspinatus

tears.2 9 , 3 0 MRI evaluation is particularly useful in identifying the

degree of tendon retraction and fatty degeneration and atrophy of

the subscapularis muscle. Ultrasound examination is more

favorable in the postoperative setting because of improved

accuracy of rotator cuff imaging over MRI, especially in the setting

of implants. 3 2

AC

The acromioclavicular (AC) joint is a diarthrodial joint formed by

the distal clavicle and medial facet of the acromion. Its principal

function is to suspend the scapula from the clavicle, thereby

supporting the weight of the upper extremity. The AC joint

capsular ligaments are the primary horizontal stabilizers of the AC

joint, limiting anterior and posterior translation. 1 The conoid and

trapezoid ligaments, which comprise the coracoclavicular (CC)

ligaments, provide restraint to superior and inferior displacement.

The trapezoid ligament is lateral to the conoid ligament and is a

significant restraint to axial compression in line with the

longitudinal axis of the clavicle. 2

The AC joint is most commonly injured from a direct impact on the

tip of the shoulder with the arm adducted. The force is transmitted

to the acromion, displacing it inferiorly and medially, while the

clavicle maintains its normal position. The AC joint capsular

ligaments alone are involved in low-grade injuries (types I and II)

(Fig. 14-1). High-grade injuries involve the CC ligaments as well.

The standard treatment for type I and II injuries is nonoperative. A

sling may be used on an as needed basis. Return to sporting

activities and labor can be expected at 2 to 6 weeks. Late,

symptomatic arthritic change at the AC joint may develop and can

be treated by distal clavicle excision. Currently, the majority of

acute type III injuries are treated nonoperatively with an initial

period of immobilization. 3 , 4 , 5 , 6 , 7 Schlegel et al. 8 demonstrated in a

prospective study that 80% of type III injuries did well with

nonoperative management. Nonetheless, a 17% deficiency in

bench press strength was still present at 2 years. In chronically

painful type III injuries, operative treatment is generally

recommended. Other authors, however, recommend acute

operative treatment of type III injuries in heavy laborers and high-

level throwers. 9 Acute surgical reconstruction of type IV, V, and VI

AC separations is widely accepted. 1 0

The evolution of AC joint reconstruction began in 1861 when Sir

Samuel Cooper attempted repair with a loop of silver wire. 1 1 Since

that time, more than 100 different reconstructive procedures have

been described in the literature. 1 2 Unfortunately, no single surgical

procedure has completely addressed all of the issues of AC joint

separations. During the 1970s and 1980s, fixation methods

emphasized intra-articular fixation across the AC joint using pins

and plates. 1 3 , 1 4 , 1 5 , 1 6 In 1972, Weaver and Dunn 1 7 introduced a

technique of reconstruction utilizing the coracoacromial (CA)

ligament. Numerous modifications of their original technique have

been described, using methods to augment the CA ligament during

the early healing phase of the reconstruction. Current trends in AC

joint reconstruction focus on fixation between the clavicle and

coracoid, thus reconstructing the coracoclavicular ligaments. A

variety of augmentation devices such as the Bosworth screw, 1 8

nonabsorbable and absorbable sutures, 1 9 , 2 0 Dacron tape, 2 1 and

GoreTex grafts, 2 2 have been used and reported in the literature

with good results. However, complications of infection, bone

erosion, and reoperation for hardware removal continue to make

these methods of reconstruction less than ideal 2 3 , 2 4 , 2 5 , 2 6 , 2 7 (Fig. 14-

2).

There have been several reports of soft tissue grafts for AC

reconstruction. A case report using a semitendinosus autograft in

a salvage situation after a prior failed reconstruction produced a

good result at 2 years. 2 8 A small, retrospective series, using the

fifth toe extensor tendon for reconstruction has also been reported

with encouraging results. 2 9 A recent study tested the

biomechanical properties of soft tissue grafts (gracilis,

semitendinosus, and long toe extensor) for

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coracoclavicular ligament augmentation. The authors found that

the soft tissue grafts had superior biomechanical properties when

compared to transfer of the coracoacromial ligament (Weaver–

Dunn procedure) and had failure strengths that were as strong as

the native coracoclavicular ligaments.

We have found that a free soft tissue graft, such as the

semitendinosus tendon, can be used to stabilized the AC joint in a

reliable fashion. In addition to the technical aspects of this method

of reconstruction, we will also present our results from the past 10

years at our institution. Since 1999 we have used the

semitendinosus graft alone. We developed a novel method of graft

fixation that we have found to be of sufficient strength that

transfer of the CA ligament (as in the Weaver–Dunn procedure)

was no longer necessary. This has resulted in less morbidity by

preserving the CA ligament and not disrupting its overlying deltoid

attachment.

Fig. 14-1. Schematic drawings of AC joint dislocation classification

system. (Reprinted with permission from Rockwood CA, Matsen FA,

eds. The Shoulder. 2 vols. 2nd ed. Philadelphia: WB Saunders;

1998.)

Fig. 14-2. Axillary projection of patient who had a modified

Weaver–Dunn procedure in the distant past with a cerclage suture.

Demonstrated is erosion of the suture through the base of the

coracoid process.

Dislocations of the acromioclavicular (AC) joint have been

recognized as significant sports-related shoulder injuries since the

time of Hippocrates. Thorndike and Quigley 1 observed that these

dislocations compromised more than one third of all shoulder

injuries in the over 500 athletes that they studied. Most trauma to

the AC joint results in an incomplete joint dislocation (Rockwood

types I and II) whose acute treatment is universally nonoperative.

When the displacement of the clavicle is complete (Rockwood

types III through VI), the preferred treatment varies greatly. Good

results have been reported with conservative management of

these injuries. 2 However, experience has taught us that there exist

a significant number of patients who benefit from operative

intervention.

Arthroscopic reconstruction of the coracoclavicular ligaments was

created to introduce a less invasive alternative for the anatomic

reconstruction of the conoid and trapezoid ligaments. It was

designed to provide stability and pain relief to patients with

symptomatic complete AC joint dislocations while simultaneously

achieving a superior cosmetic result. The technique has evolved

since the publication of the original description in 2001. 3 With the

development of reliable instrumentation, strong and resilient

implants, and reproducible techniques, arthroscopic

coracoclavicular ligament reconstruction has proven to be an

attractive method for treating AC joint dislocations.

The arthroscopic acromioclavicular reconstruction is a

reproducible, minimally invasive technique well suited for

orthopedic surgeons with experience in arthroscopic shoulder

surgery. This technique provides an anatomic reconstruction of the

coracoclavicular ligaments with the goal of restoring normal

shoulder kinematics. It has been observed that scapulothoracic

and acromioclavicular malalignment lead to symptomatic shoulder

dyskinesis in patients who sustain high-grade shoulder separations

(dislocation). This technique will restore a strong coracoclavicular

construct while preserving coracoid and clavicular bone. The

arthroscopic nature of this procedure allows for a rapid

rehabilitation and a full return to preinjury activities.

Indications and Contraindications

Arthroscopic AC joint reconstruction is indicated for Rockwood

type IV through VI AC joint separations and for certain Rockwood

type III separations: chronic AC joint separations that are painful

and result in a dysfunctional shoulder girdle with significant

deformity, and acute AC joint separations in active patients who

are unwilling to accept any deformity, dysfunction, or pain in the

affected shoulder.

Rockwood type I and type II separations are typically treated

nonoperatively. Distal clavicle resection alone may be indicated in

select cases with painful degeneration of the AC joint. Patients

who remain asymptomatic and have no cosmetic concerns are not

indicated for surgery regardless of the severity of injury. Patients

who cannot follow a postoperative rehabilitation protocol are not

candidates for this surgery. A relative contraindication is advanced

age. Poor bone quality in older patients may compromise the

reconstruction effort. The oldest patient to have received this

operation was 67 years old, and he obtained an excellent result at

his 3-year follow-up examination.

Patients typically complain of pain, popping, a sensation of

instability, and/or deformity in the region of the AC joint. The

grade of separation may not be directly proportional to the level of

complaints from a patient. A minimally displaced

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separation may be more painful and disabling than a high-grade

separation. Similarly, once a chronically separated distal clavicle

is reduced and contacts the acromion, the potential exists for

creating a painful, anatomically reduced AC joint. Any painful AC

joint must undergo a distal clavicle resection, either open or

arthroscopic, at the time of reconstruction. In light of the

sensitivity of the AC joint, it is strongly recommended that a distal

clavicular resection be performed routinely with any

coracoclavicular reconstruction. Two centimeters of distal clavicle

should be removed to ensure that there will be no contact with the

acromion. This will also provide the best aesthetic result.

The acromioclavicular separation must be evaluated

preoperatively to determine the degree of separation of the joint

and its reducibility. Preoperative weighted stress radiographs are

obtained in the office, and the amount of superior displacement of

the distal clavicle is evaluated by measuring the coracoclavicular

distance. Only Rockwood type III through VI AC joint separations

are considered for reconstruction. The AC joint should be tested

for ease of reduction. An irreducible joint indicates the presence of

interposing scar tissue that will have to be removed

intraoperatively.

SLAP

Lesions involving the superior labrum in throwing athletes were

first described by Andrews et al. 1 in 1985. Snyder et al., 2 in 1990,

coined the term SLAP (superior labrum, anterior to posterior) tear,

to describe a tear of the superior labrum which begins posteriorly

and extends anteriorly to involve the anchor of the tendon of the

long head of the biceps.

Initially, SLAP lesions were treated with simple debridement

alone.1 Poor results of debridement alone are generally attributed

to uncertain healing and continued instability. Subsequently,

arthroscopic stapling techniques were developed to secure the

biceps anchor. 3 This technique necessitates staple removal 3 to 6

months postoperatively. Transosseous suture techniques tied over

the infraspinatus fascia were developed in 1993 providing good

results, but were technically demanding. 4 That same year, results

of cannulated screw stabilization under arthroscopic guidance

were reported. 5 Again, screw removal was required, and additional

complications were noted, including articular damage and screw

loosening. Bioabsorbable anchor stabilization was described at this

time but was extensively complicated by implant breakage and

reoperation for removal of loose fragments. 6

Most recently, the use of suture anchors in the stabilization of

SLAP lesions has come into favor. Good clinical results and lower

complication/reoperation rates have been shown. 7 , 8 , 9

Indications and Contraindications

Diagnosis of a SLAP tear may be challenging. Several mechanisms

of injury have been proposed, such as traction/rotation (as in an

overhead athlete), 1 superior shear and traction, 1 0 , 1 1 and “peel

back.”1 2 Several clinical examinations have been described, such

as the active compression test, 1 3 the crank test, 1 4 and the biceps

load test1 5 in order to aid in the diagnosis. Plain radiographs

should be obtained but are usually not helpful in making the

diagnosis. Magnetic resonance imaging with intra-articular

gadolinium enhancement is the diagnostic test of choice. 1 6 , 1 7 Once

a patient has failed conservative treatments for shoulder pain,

instability, and mechanical symptoms, a diagnostic arthroscopy is

performed.

Indications for the arthroscopic treatment of SLAP lesions are

usually based on classification of tears by Snyder et al. 1 0 (Fig. 16-

1). Types I and III lesions are generally treated with debridement

of unstable labral tissue. The bucket handle fragment in type III

lesions is resected and the residual rim is evaluated for stability

and repair if possible. Type II lesions are treated with arthroscopic

fixation of the superior labrum to the glenoid rim spanning the

biceps anchor. The treatment of type IV lesions depends on the

amount of torn biceps tendon associated with the labral tear.

Treatment of these injuries also depends on the age and activity of

the patient. If less than 50% of the biceps tendon is involved, the

unstable biceps tissue can be resected and the remaining labrum

can be repaired to the glenoid. In an older patient with more than

50% of the biceps tendon involved, biceps tenotomy or tenodesis

is usually performed. In younger patients, biceps tenodesis and

suture anchor repair is currently recommended.

Fig. 16-1. Classification system of SLAP tears.

Fig. 16-2. Probe is used to evaluate the superior labrum. A type II

tear is noted.

Biceps tendon

Although the function of the long head of the biceps tendon in the

shoulder remains controversial, there is less doubt that the biceps

tendon can be a significant source of pain. 2 , 2 3 , 2 4 , 2 5 , 2 6 , 2 7 , 2 8 , 2 9 , 3 0 Biceps

disorders have been classified as either biceps instability or biceps

tendonitis. 3 1 Tendonitis is more commonly associated with other

shoulder disorders such as rotator cuff disease. Because of the

intimate association of the biceps tendon with the rotator cuff, the

principal cause of biceps degeneration is attributed to mechanical

impingement of the tendon against the coracoacromial arch,

similar to rotator cuff impingement. 3 2 , 3 3 , 3 4 , 3 5 The tendon is either

atrophic from the degenerative process or hypertrophic in

response to the chronic inflammation from the impingement. 2 2

Synovitis of the biceps tendon most often occurs in the segment

within the bicipital groove. 3 6 Primary bicipital tendonitis is less

usual and requires exclusion of rotator cuff pathology for the

diagnosis.

Subluxation of the long head of the biceps is most commonly

associated with loss of soft tissue restraints from rotator cuff

tears.2 3 , 3 7 , 3 8 , 3 9 , 4 0 In the presence of a subscapularis tear, the tendon

can sublux medial and deep to the subscapularis. A frank

dislocation of the long head of the biceps is nearly always

associated with a subscapularis tear. 3 1

Rupture of the long head of the biceps tendon typically occurs in

the setting of a diseased tendon and a previous history of

subacromial impingement. Alternatively, more acute trauma,

involving either a powerful supination force or a fall on the

outstretched arm, can cause proximal biceps rupture. With partial

tearing of the biceps tendon, significant pain and dysfunction is

common. In contrast, full thickness traumatic ruptures of the

biceps tendon are generally less symptomatic following the acute

event.3 9 , 4 1 Spontaneous or traumatic ruptures of the long head of

the biceps generally do not require surgical intervention.

Indications and ContraindicationsPatients complain of pain localized to the anterolateral aspect of

the shoulder, which radiates down the anterior arm into the biceps

muscle with extension and internal rotation maneuvers of the

arm.2 3 , 2 5 , 3 7 , 3 8 , 3 9 Pain at rest and night pain are seen further in the

disease progression. The pain may be compounded by concomitant

impingement syndrome or rotator cuff tears. Patients with

instability of the biceps have painful snapping or clicking in the

shoulder typically in overhead positions with internal to external

humeral rotation. Because subluxation occurs in the presence of

rotator cuff disease, rotator cuff symptoms are usually also

present. Frank dislocations of the long head of the biceps usually

follow a traumatic event and are most often associated with

complete tear of the subscapularis.

The most common examination finding is point tenderness of the

biceps tendon within the bicipital groove. Biceps related

tenderness can be differentiated from rotator cuff tendonitis by

external rotation of the arm. Pain related to the biceps migrates

laterally with external rotation of the arm, whereas pain related to

rotator cuff tendonitis radiates to the deltoid insertion and does

not move with arm rotation. Other specific physical examination

tests used to identify pathology of the long head of the biceps

tendon include the Speed test, 1 , 2 5 the Yergason test, 4 2 and the

biceps instability test. 4 3 Biceps instability is tested with full

abduction and external rotation attempting to elicit a painful click

that may be palpable. Because instability of the biceps is often

associated with a partial or complete subscapularis rupture, the

liftoff4 3 and belly-press 4 4 tests are an essential part of the biceps

evaluation. Complete rupture of the long head of the biceps is

identified by a cosmetic deformity from the biceps dropping

toward the elbow. Shallowness occurs in the anterior portion of the

shoulder accompanied by a lump on the anterolateral aspect of the

arm.

Radiographic examination should include anteroposterior (AP)

views in neutral, internal, and external rotation, an axillary view,

and scapular Y-view to assess for associated abnormalities.

Ultrasound may dynamically correlate clinical examination with

sites of tenderness but is not routine. MRI has the advantages of

visualizing the biceps in its groove and surrounding osteophytes as

well as assessing associated rotator cuff pathology. Lack of

positive findings on MRI does not rule out the presence of

significant biceps tendon pathology.

The criterion for biceps tendon management has been outlined by

Yamaguchi et al. 2 2 Reversible changes are considered when

degeneration includes less than 25% partial tearing and the

tendon has normal position within the bicipital groove. Reversible

changes are treated with observation of the biceps and treatment

of associated pathology. Irreversible changes include partial

thickness tearing or fraying greater than 25%, subluxation of the

tendon from the bicipital groove, or reduction in tendon size that

is greater than 25%. Additional relative indications for biceps

tenotomy or tenodesis are failed subacromial decompression

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with persistent symptoms attributed to the biceps. Tenodesis is

performed for younger patients (less than 55 years) and especially

if they are thin. For the older less active patient, tenotomy is

performed. Patients must be counseled and accept the possible

deformity that can occur if the long head of the biceps retracts

into the arm. 6 Biceps tenodesis is generally recommended for

younger patients and has been well described using open

techniques. 4 , 1 1 , 3 1

Fig. 17-2. Arthroscopic view of long head of biceps tendon within

the glenohumeral joint. A: More normal appearance prior to

drawing the tendon into the joint. B: Significant degeneration of

the tendon appreciated following drawing the tendon into the joint.

(Reprinted with permission from Ahmad CS, ElAttrache NS.

Arthroscopic biceps tenodesis. Ortho Clin North Am. 2003;34:499–

506.)

Patient Evaluation

All patients should undergo a thorough history specifically

addressing the onset and events surrounding their initial

dislocation episode, the chronicity and number of instability

events, positions that cause apprehension, current level of

activity, and any prior stabilization procedures. It is extremely

helpful to obtain copies of operative reports and intraoperative

arthroscopy photos to better understand the status of the

shoulder.

The physical examination focuses on ascertaining the direction of

instability: anterior, inferior, posterior, or multidirectional.

Additionally, associated pathology including superior labrum,

anterior to posterior (SLAP) lesions, rotator cuff tears,

scapulothoracic dysfunction, and neurological findings should be

evaluated particularly after prior surgical treatment. The load and

shift test is the preferred method for quantifying the degree of

anterior instability as well as determining the competence and

presence of the anterior band of the inferior glenohumeral

ligament. In the anesthetized patient, obtaining a locked

dislocation after the load and shift indicates a large bony lesion

that may preclude Bankart repair. When treating patients with

capsular attenuation, a careful assessment of restraints to

anterior, posterior, and inferior translation is important. The

posterior load and shift test and an assessment for inferior

instability with observation of a sulcus sign in adduction and

neutral rotation as well as in adduction and external rotation will

indicate competency of the coracohumeral ligament, superior

glenohumeral ligament, and rotator interval. If the sulcus sign is

positive only in neutral rotation, then the interval is competent. If

the sulcus remains positive after external rotation, the interval is

loose and provides insufficient restraint to inferior instability.

Generalized ligamentous laxity should also be assessed in each

patient and comparison with the contralateral shoulder is essential

in making the correct diagnosis.

Glenoid bone loss has been reported with an incidence as high as

80% and humeral impaction fractures in 70% of cases of chronic,

recurrent anterior glenohumeral instability. 3 Many of the bony

glenoid lesions involve less than 20% of the glenoid width and may

be treated with more standard approaches to instability surgery

than discussed in this chapter. 4 In most instances, glenoid and

humeral bone loss are evident with standard radiographs. A true

glenohumeral

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anteroposterior (AP) projection and an internal rotation AP will

reveal significant Hill-Sachs lesions. An apical oblique view is also

useful in visualizing Hill-Sachs lesions. 5 Although the axillary

lateral radiograph is an important part of the initial trauma

evaluation of a patient with shoulder instability, this view fails to

adequately identify or to quantify sufficiently the degree of

glenoid bone loss. 6 The West-Point lateral 7 or the glenoid profile

lateral as described by Bernegeau et al. 6 more accurately defines

anterior inferior glenoid bone loss in all cases of traumatic

instability. With the appropriate use of AP and the glenoid profile

view, identification of bony defects is possible without the use of

additional imaging modalities. However, when quantifying glenoid

bone loss, computed tomography (CT) is the most precise imaging

modality. In cases of revision instability surgery in which the

amount of glenoid loss is uncertain, a CT scan may be useful.

Additionally, in cases of combined glenoid and humeral bone loss,

use of preoperative CT may allow the surgeon to appropriately

plan for both anterior stabilization procedures as well as for

addressing humeral bone loss. Magnetic resonance imaging (MRI)

is not necessary in the routine assessment of instability patients.

However, an MRI allows assessment of capsular integrity after

thermal capsulorrhaphy and is useful in the preoperative

assessment of the rotator cuff in patients over 40 with a history of

traumatic instability.

All patients should undergo examination under anesthesia,

including anterior and posterior load and shift, as well as

assessment of inferior instability. The routine use of arthroscopic

examination allows precise measurement of glenoid bone loss 8 and

an additional assessment of the appropriateness of arthroscopic

stabilization techniques. The failure rate of arthroscopic

stabilization when glenoid bone loss exceeds one fifth the glenoid

width is 60%. 8 Additionally, dynamic assessment of engaging Hill-

Sachs lesions may be confirmed arthroscopically. In cases of

capsular attrition from failed thermal capsulorrhaphy or failed

instability procedures in patients with generalized ligamentous

laxity, proceeding directly to open surgical treatment is

appropriate.

Hill-Sachs lesions

Bony defects of the posterior-superior aspect of the humeral head

occur commonly in association with anterior glenohumeral

dislocation. One of the first descriptions of these lesions was by

Flower1 in 1861, with many subsequent investigators reporting on

these bony defects of the humeral head. 2 , 3 , 4 , 5 In 1940, Hill and

Sachs,6 two radiologists, reported that these defects were actually

compression fractures produced when the posterolateral humeral

head impinged against the anterior rim of the glenoid.

Since then, Hill-Sachs lesions have been found to occur with an

incidence between 32% and 51% at the time of initial anterior

glenohumeral dislocation. 6 , 7 , 8 , 9 In shoulders sustaining a Hill-Sachs

lesion at the initial dislocation, there exists a statistically

significant association with recurrent dislocation. 1 0

Although Hill-Sachs lesions are common after anterior

glenohumeral dislocations, there are relatively few papers

describing specific treatments for these humeral head defects. In

general, specific surgical procedures to address Hill-Sachs lesions

have not been recommended in the initial surgical management of

recurrent anterior dislocations because the majority of these

lesions are small to moderate in size and do not routinely cause

significant symptoms of instability. In fact, Bankart 1 1 himself did

not ascribe any significance to Hill-Sachs lesions observing

“nothing can be done about them if they are found.”

Nevertheless, a certain subset of patients exists with more

significant bony defects and ongoing symptoms of “instability”

and/or painful clicking, catching, or popping, sometimes occurring

even after surgical procedures are directed at treating their

anterior instability. Rowe et al. 1 2 found a 76% incidence of Hill-

Sachs lesions in patients evaluated for recurrent anterior

dislocation of the shoulder after surgical repair, and stated “a Hill-

Sachs lesion of the humeral head may play a role in the

development of recurrent dislocation after surgical repair.”

The concept of “articular arc length mismatch” has been recently

put forth to explain the ongoing sensation of catching or popping

arising with the shoulder in the abducted and externally rotated

position in patients with large Hill-Sachs lesions. 1 3 Furthermore,

many of the patients with these symptoms have undergone

previous anterior stabilization procedures. This phenomenon

occurs mainly in a position of abduction and external rotation of

the shoulder. In this position, a large “engaging” Hill-Sachs lesion

encounters the anterior glenoid rim, resulting in the rim “dropping

into” the Hill-Sachs lesion. This phenomenon can and does occur in

the presence of intact or repaired glenohumeral ligaments. The

sudden loss of a segment of articular arc on the humeral side of

the joint presents an abrupt “flat spot” to the glenoid, causing an

uneasy sensation in the patient that feels much like subluxation.

It is also important to differentiate between “engaging” and

“nonengaging” Hill-Sachs lesions. 1 4 In an engaging Hill-Sachs

lesion, the long axis of the defect is parallel to the anterior glenoid

with the shoulder in a functional position of abduction and

external rotation. This leads to the Hill-Sachs lesion engaging or

catching the corner of the glenoid. Conversely, a nonengaging Hill-

Sachs lesion is one that either fails to engage the glenoid in a

functional arm position or engages the glenoid only in a

nonfunctional arm position. In the first type of nonengaging lesion,

the long axis of the Hill-Sachs lesion is tangential to the anterior

glenoid with the shoulder in a functional position of abduction and

external rotation. The Hill-Sachs defect passes diagonally across

the anterior glenoid with external rotation; therefore, there is

continual contact of the articulating surfaces and no engagement

of the Hill-Sachs lesion by the

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anterior glenoid. In the second type of nonengaging lesion, the

Hill-Sachs defect “engages” only in a position that is considered

“nonfunctional” (i.e., shoulder in some degree of extension, or in

abduction of less than 70 degrees). Since symptoms are greatest if

the engagement occurs with the shoulder in a functional position,

involving a combination of flexion, abduction, and external

rotation, this second group of Hill-Sachs lesions, while technically

engaging, has been defined as functionally nonengaging.

Hence, when a patient has symptomatic anterior instability

associated with an engaging Hill-Sachs lesion with an articular-arc

deficit, treatment must be directed at both repairing the Bankart

lesion, if present, and preventing the Hill-Sachs lesion from

engaging the anterior glenoid.

We believe that the treatment of symptomatic anterior

glenohumeral instability, involving an engaging Hill-Sachs lesion

with an articular-arc deficit, can best be accomplished with a

technique of anatomic allograft reconstruction of the humeral head

using a side and size-matched humeral head osteoarticular

allograft. This technique involves an anatomic reconstruction,

which eliminates the structural pathology, while maintaining the

range of motion of the glenohumeral joint.

All patients are initially evaluated with complete history and

physical examination. Specifics of the history include questioning

for the mode of onset and timing of initial symptoms and for the

details of present symptoms including pain, frequency, instability,

and level of function. In addition, all previous surgical procedures

performed on the shoulder should be noted. Most patients will give

a history of recurrent dislocations or multiple surgical attempts to

correct the instability. The patients have usually sustained

glenohumeral dislocations as a result of significant trauma.

Another group of patients that can be encountered is patients with

grand mal seizures and recurrent anterior dislocations. These

patients usually have fairly large Hill-Sachs defects and significant

apprehension about the use of their arms. As a result of the

violence of the dislocations, the amount of bone pathology

present, and the inability to predict the onset of epileptic events,

it is worth considering treating this group of patients with an

allograft reconstruction of the humeral head defect at the index

procedure as soft tissue repairs alone may not be enough to

prevent recurrent injury.

Physical examination should focus on inspection for previous

scars, a thorough determination of active and passive range of

motion, evaluation of the integrity and strength of the rotator cuff,

and a detailed examination for glenohumeral laxity in the anterior,

posterior, and inferior directions. Examination for apprehension

should be performed in multiple positions as the group of patients

with large Hill-Sachs lesions usually exhibits apprehension that

often occurs with the arm in significantly less than 90 degrees

abduction/ 90 degrees external rotation.

Preoperative imaging includes a comprehensive plain film

evaluation with anteroposterior (AP), true AP, axillary, and Stryker

Notch views of the involved shoulder (Fig. 19-1). All patients

require a preoperative axial imaging study (computed

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tomography [CT] or magnetic resonance imaging [MRI]) to more

fully define the bony architecture of the glenoid and humeral head

and specifically the details of the Hill-Sachs lesion (Fig. 19-2).

One must be careful in the interpretation of these studies since

the plane of the Hill-Sachs defect is oblique to the plane of the

axial image. Therefore, the size of these defects is often

underestimated in standard axial imaging. Three-dimensional

reconstruction can be a useful tool to aid in more clearly defining

the size and location of the defect and to provide an estimation of

the amount of the articular surface involved.

Fig. 19-1. AP x-ray of shoulder demonstrating a large Hill-Sachs

lesion.

Fig. 19-2. Axial MRI image demonstrating large engaging Hill-

Sachs lesion.

Allograft sizing can be accomplished using plain radiographs with

magnification markers or using CT or MRI scan data. However,

appropriate sizing of the proximal humeral allograft requires a

specific protocol to be arranged between the surgeon and the

supplying tissue bank.

A fresh-frozen side and size-matched osteoarticular humeral head

allograft is obtained from a reputable, certified tissue bank. The

graft serves mainly a structural function, and cartilage viability is

probably not essential for success. The availability of fresh frozen

tissue can be problematic, and therefore in the past we have

performed the procedure using irradiated grafts. However, in two

cases using irradiated grafts we have observed partial collapse of

the grafts, which required reoperation and screw removal.

Therefore, our present protocol favors the use of fresh frozen

tissue. If different size grafts or femoral head grafts are used, they

may not match the curvature of the native humeral head exactly

and often need to be trimmed to obtain fit. Nevertheless, if there

are no humeral allografts available, then the use of nonmatched

humeral grafts or femoral heads is certainly possible and

reasonable.

Rupture of the pectoralis major muscle is rare, with only

approximately 150 reported cases in the literature since its first

description by Patissier in 1822. 1 , 2 However, over half of these

cases have been identified in the past 30 years. Initially

associated with work-related accidents, this condition is now more

common among weight lifters and athletes participating in

strenuous activities. With society's increased interest in fitness

and sport it is likely that this injury may become more prevalent.

Operative treatment of a ruptured pectoralis major muscle ensures

the best outcome in terms of patient satisfaction, strength,

cosmesis, and return to athletic activity. 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 1 0 , 1 1 , 1 2 , 1 3 A meta-

analysis performed by Bak et al. 1 revealed 88% of patients treated

surgically had excellent or good results versus 27% treated

nonoperatively. Another study of 22 patients using objective

isokinetic testing demonstrated that the peak torque in those

treated surgically returned to 99% of that of the uninjured side

compared to only 56% in the patients managed nonoperatively. 1 4

Since the majority of ruptures occur at the myotendinous junction,

emphasis of repair is placed on anatomic reapproximation of the

ruptured tendon to its insertion site on the humerus. Several

techniques for surgical repair have been described. Nevertheless,

because of its rarity most results are based on only a few subjects.

Furthermore, lack of standardized objective values makes it

difficult to compare several of these techniques.

Schepsis et al. 3 described a trough and drill hole technique using a

modified Kessler grasping stitch for successfully repairing six

acute injuries (less than 2 weeks after injury) and seven chronic

injuries. Their results demonstrated an average overall 96%

subjective rating in the acute group, 93% in the chronic group, and

51% in the nonoperative group. Objective isokinetic testing after

treatment revealed 102% adduction strength in the acute group

(when compared to the uninjured side), 94% in the chronic group,

and 71% in the nonoperative group. Furthermore, there were no

statistically significant subjective or objective differences between

the acute or chronically injured patients.

This technique has also been described successfully in the

treatment of a 13-year delayed repair and a rupture associated

with an anterior shoulder dislocation. 1 5 , 1 6 Miller et al. 1 7 reported

successful repair of an acute complete tendinous rupture using

bone anchors. The 19-year-old patient was able to return to

collegiate football. Other authors have performed successful

repairs by attaching the tendon to the humerus with periosteal

sutures.5 , 7 , 9

Another popular technique described in the literature is the

reattachment of the ruptured tendon to the humerus with the use

of heavy sutures and drill holes. Kretzler and Richardson 8 achieved

good success using two rows of drill holes at the site of insertion

in 15 patients. Strength was fully restored in 13 of the patients,

with the remaining patients reporting significant improvements.

Two patients who were repaired approximately 5.5 years after the

injury who did not return to full strength showed significant

improvement via Cybex evaluation. One demonstrated an increase

in horizontal adduction strength from 50% to 80%, and the other

from 60% to 84%. Deformity and range of motion were also

corrected. Similar results have been reported by other authors. 1 8 , 1 9

Muscle belly tears occur less frequently and can usually be treated

conservatively. However, direct surgical repair has also been

described with good results. 7

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Indications and ContraindicationsPectoralis major muscle tears can often be diagnosed clinically.

The physician must have a good understanding of the typical

history and findings on physical examination. Up to 50% of

patients may be initially misdiagnosed or there may be a delay in

accurate diagnosis. 1 4 Patients often present with a history related

to a specific incident where they report a tearing sensation at the

site of injury with or without a “pop.” Furthermore, they describe a

limited range of motion, swelling, ecchymosis, and weakness.

Patients may self-treat this injury as a strain with rest and ice until

swelling and bruising resolve and then seek medical evaluation

secondary to persistent weakness and asymmetry.

Classical physical findings consist of ecchymosis and swelling over

the arm and axilla, a palpable defect and weakness in adduction,

and internal rotation of the affected arm (Fig. 20-1). Comparison

should always be made to the uninjured side. The classical webbed

appearance of a thinned out anterior axilla can be accentuated by

abducting the arm 90 degrees. A visual deformity may be

enhanced by contraction of the muscle or resisted adduction of the

arm as the injured muscle retracts medially and occasionally pulls

overlying soft tissue in cases where adhesions have formed. When

all of these characteristics are present, one must assume a

rupture has occurred. However, classical findings may be masked

when there is moderate to severe swelling. Furthermore, the

investing fascia of the pectoralis major muscle, which prevents

further retraction of the ruptured tendon, may be present as a

palpable cord and mistaken for an intact tendon (Carr et al.,

unpublished data, 2004). Imaging modalities may assist with

diagnosis and help provide additional clinical information.

Conventional radiographs should always be ordered to rule out any

avulsions, fractures, or dislocations. The characteristic finding of a

ruptured pectoralis major muscle would be soft tissue swelling and

the absence of the pectoralis major shadow. Further evaluation

would consist of magnetic resonance imaging (MRI), the modality

of choice for a detailed assessment of this injury. We recommend

axial cuts to include the contralateral pectoralis major muscle for

comparison to the injured side (Fig. 20-2). MRI has been

described to accurately determine the grade and site of injury with

great sensitivity. 2 0 , 2 1 , 2 2

Fig. 20-1. Physical exam finding of a complete acute right

pectoralis major muscle rupture. Note the ecchymosis, deformity,

and loss of contour of the right anterior chest wall and axilla when

compared with the left side.

Fig. 20-2. Axial T2-weighted MRI scan of bilateral upper

extremities. Rupture of the left pectoralis major muscle (arrow) is

easily identified and distinguished from the intact muscle on the

opposite side.

The literature supports surgical repair of complete distal pectoralis

major muscle ruptures. A complete rupture is defined as the total

disruption of either the clavicular or more commonly the sternal

head, or the combination of the two, at the tendon insertion site or

myotendinous junction. This provides the best results, especially

in patients that are active and desire continuation of athletic

activities. In older sedentary individuals, nonoperative

management may be a reasonable option since it will not likely

limit the performance of normal activities of daily living. This will,

however, leave the patient with a cosmetic defect and a noticeable

strength deficit. Therefore, the level of activity and cosmetic

desires should be discussed during surgical evaluation. Co-morbid

conditions must also be evaluated and considered along with the

risks and benefits of surgery for each individual patient.

Some authors argue that diagnosis and repair should occur within

2 months of the injury. 1 , 7 , 9 , 1 1 They believe that delayed correction is

more difficult and results in significant cosmetic and strength

deficits. Nevertheless, many other authors have described repairs

in patients from 3 months to 13 years out from the injury that

provided comparable results with patients treated

acutely.3 , 6 , 1 0 , 1 3 , 1 4 , 1 5 , 2 3 , 2 4 It is our opinion that although delayed repair

may require additional

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steps and a larger incision during surgery secondary to adhesions

and retraction of the tendon, surgical repair still results in a

dramatic improvement in strength.

Suprascapular nerve

Thomas first described suprascapular nerve palsy in the French

literature in 1936. 1 Since that description, there have been many

reports in the English literature describing the pathoanatomy,

clinical findings, and treatment of suprascapular neuropathy. 2 , 3 , 4 , 5

The suprascapular nerve is primarily a motor nerve that originates

from the fifth, sixth, and occasionally fourth cervical nerve root.

Although there are rarely cutaneous sensory fibers, branches of

the nerve receive afferent sensory input from the glenohumeral

joint, acromioclavicular joint, and the coracohumeral ligament.

Suprascapular neuropathy can result from nerve traction, extrinsic

compression, direct trauma, or a primary neuropathy. The

suprascapular nerve is particularly prone to injury as it crosses

through the suprascapular notch to supply the supraspinatus

muscle and then again at the spinoglenoid notch as it travels into

the infraspinatus fossa.

Traction injury at the suprascapular notch and spinoglenoid notch

is a common etiology of neuropathy in overhead athletes.

Repetitive stretching of the nerve can occur as it courses through

a confined space, leading to direct nerve injury or injury to the

vascular supply of the nerve. This mechanism can be exacerbated

by extreme positions of abduction and retraction found in

overhead sports (volleyball, baseball, tennis). Extrinsic

compression of the suprascapular nerve can also occur at the

spinoglenoid notch secondary to ganglion cysts. These ganglion

cysts are often associated with glenohumeral pathology such as

labral tears.

The natural history of suprascapular neuropathy is not well

documented, but in the athletic population, there can be a

significant number of asymptomatic athletes with clinically evident

suprascapular neuropathy. 6 , 7 , 8 One study in volleyball players

suggests that athletes can remain asymptomatic despite findings

of atrophy and weakness on clinical examination. 8 Symptomatic

suprascapular neuropathy without evidence of a compressive

lesion should be initially treated with nonoperative treatment.

Martin et al. 2 reported that 80% of their patients treated

nonoperatively improved without the need for nerve

decompression. Nonoperative treatment in their study included

strengthening of the deltoid, rotator cuff, and periscapular

muscles for a minimum of 6 months while avoiding exacerbating

activities. Other conservative measures include anti-inflammatory

medications and the selective use of corticosteroid injections.

Patients who have symptoms refractory to conservative

management may be candidates for suprascapular nerve

decompression.

Many different techniques have been described to decompress the

nerve at the suprascapular notch. An anterior approach starting

medial to the coracoid has been described to reach the

suprascapular notch. 9 The increased risk of iatrogenic

neurovascular injury with this dissection has led most authors to

advocate either a superior or posterior approach to access the

suprascapular nerve. The superior approach is a trapezius-splitting

approach advocated by Vastamaki and Goransson. 1 0 The trapezius

is split in line with its fibers directly above the suprascapular

notch, and the supraspinatus muscle is retracted posteriorly to

visualize the notch. The topographical landmarks for the superior

approach have been defined in a recent cadaveric study. 1 1 The

posterior approach, advocated by Post and Grinblat, 3 is the one

most commonly used in our practice to visualize the suprascapular

notch. This approach involves elevation of the trapezius from the

scapular spine. For open decompression of the suprascapular

nerve at the spinoglenoid notch, a posterior approach through the

deltoid is generally recommended. 4 This approach can either

utilize a split of the deltoid in line with its fibers or a release of

the posterior deltoid from the spine. Subsequent inferior retraction

of the infraspinatus muscle exposes the spinoglenoid notch.

Although the surgical

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approaches described may vary, the actual decompression of the

nerve generally includes the release of the transverse scapular

ligament, spinoglenoid ligament, or both ligaments. Some authors

have also advocated osseous decompression of a stenotic notch.

Indications and Contraindications

The first step toward determining the appropriate treatment for

suprascapular nerve entrapment is confirming diagnosis. The

subjective complaints of the patient can vary significantly,

especially in overhead athletes. Many asymptomatic overhead

athletes have well-documented suprascapular neuropathy on

clinical examination. Symptomatic patients frequently describe a

poorly localized discomfort or ache over the posterior and lateral

aspects of the shoulder. Whether this pain is from injury to the

sensory branches of the posterior glenohumeral joint or secondary

to rotator cuff deficiency is unknown. Pathology at the

suprascapular notch is generally more symptomatic with regard to

weakness and pain than pathology at the spinoglenoid notch. By

the time the suprascapular nerve has reached the spinoglenoid

notch, it has already given off its motor branches to the

supraspinatus and received afferent fibers from the posterior joint

capsule.

Objective findings vary with the progression of the disease and the

location of nerve entrapment. The location of suprascapular nerve

injury as it travels through the suprascapular notch and the

spinoglenoid notch determines the location of muscle atrophy

(Fig. 21-1). Nerve pathology at the spinoglenoid notch will

present with atrophy isolated to the infraspinatus muscle.

Although wasting of the infraspinatus may be less symptomatic, it

is generally more visible than atrophy of the supraspinatus due to

the overlying trapezius muscle. Weakness of the supraspinatus

and infraspinatus can often be clinically detected even though

weakness may not be a primary subjective complaint of the

athlete. Pain in the posterior shoulder can sometimes be

reproduced with cross-body adduction and internal rotation;

however, this should be differentiated from pathology at the

acromioclavicular joint. There can also be point tenderness to

palpation over the suprascapular notch or posterior joint line.

Fig. 21-1. The suprascapular nerve passes beneath the transverse

scapular ligament in the suprascapular notch and around the base

of the scapular spine through spinoglenoid notch.

Concomitant and precipitating pathology in the overhead athlete

can include glenohumeral instability, scapular dyskinesis, and

labral pathology. Posterior and superior labral pathology has been

associated with spinoglenoid notch cysts and suprascapular nerve

compression. Careful examination of glenohumeral stability as well

as scapulothoracic mechanics is warranted when evaluating a

shoulder with suprascapular neuropathy.

The differential diagnosis of suprascapular nerve palsy includes

primary mononeuropathy, cervical radiculopathy, brachial plexitis

(Parsonage-Turner syndrome), quadrilateral space syndrome,

thoracic outlet syndrome, rotator cuff disease and neoplasm, or

other compressive mass. Clinically, we have found that proximal

neuropathies such as cervical radiculitis and brachial plexopathy

are generally more common etiologies confounding diagnosis of

suprascapular nerve entrapment.

Diagnostic studies are important to confirm the diagnosis of

suprascapular neuropathy. Plain radiography can be useful for

determining the morphology of the suprascapular notch. A 15-

degree caudal-oblique anteroposterior (AP) view of the scapula can

give a good assessment of the notch morphology. Magnetic

resonance imaging (MRI) can be especially helpful in ruling out

concomitant pathology or unusual causes of suprascapular

neuropathy. Ganglion cysts and other compressive lesions such as

tumors can be readily identified with MRI. Atrophy of the rotator

cuff muscle and intra-articular pathology such as labral tears are

also well visualized with an MRI. We commonly utilize MR

arthrography in overhead athletes when there is clinical suspicion

of labral and rotator cuff pathology due to its increased accuracy.

Nerve conduction studies and electromyography provide essential

information on the location and severity of suprascapular nerve

palsy. Electrodiagnostic studies can identify whether the motor

dysfunction is isolated to the infraspinatus or also involves the

supraspinatus, facilitating the location of the lesion. Positive

findings include denervation potential fibrillations, spontaneous

activity, and prolonged motor latencies. Normal mean latency from

Erb's point to the supraspinatus is 2.7 ms and 3.3 ms to the

infraspinatus. 1 2 , 1 3 Although false-negative findings can be present,

our practice is to avoid surgical decompression in the face of

normal electrodiagnostic studies without an obvious compressive

lesion.

Nonoperative treatment is the initial treatment of choice for

suprascapular nerve compression in the absence of a compressive

lesion. We generally recommend a minimum of 6 to 12 months of

rest, physical therapy, and judicious use of anti-inflammatory

medications. Avoiding exacerbating

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activities and strengthening of the rotator cuff and scapular

stabilizers often gives good relief and return to function.

Our indication for open surgical decompression in the absence of a

compressive lesion is a high level of diagnostic certainty (clinical

presentation and diagnostic studies) as well as a failure of

nonoperative treatment for at least 6 months. Concomitant

pathology such as a labral tear or compressive lesion (ganglion

cyst) can lead to earlier surgical intervention. If the suprascapular

neuropathy is thought to be symptomatic secondary to a ganglion

cyst or labral tear, we generally prefer arthroscopic cyst

decompression and labral repair as indicated before performing an

open surgery with greater morbidity.

Absolute contraindications to open suprascapular nerve

decompression include asymptomatic overhead athletes with

clinical findings of atrophy. The natural history of this population

is that they will tend to remain asymptomatic. 8 We also avoid

prophylactic surgical decompression of the nerve when a cyst is

present on MRI because image-guided aspiration techniques and

arthroscopic techniques are less invasive. Relative

contraindications include pain in the absence of atrophy and

weakness or the lack of positive electrodiagnostic studies.

Preoperative planning includes confirming the diagnosis and

localizing the lesion. We prefer to limit the decompression to

either the suprascapular notch or the spinoglenoid notch.

Arthroscopy is performed before open decompression to complete

diagnostic examination of the glenohumeral joint and treat any

contributing intra-articular pathology.

The patient with subacromial impingement syndrome usually presents with a gradually progressive history of pain aggravated with use of the arm above shoulder level. As the symptoms persist and progress, the pain, initially present only with activity, may become present at rest and especially at night, awakening the patient from a sound sleep. The patient with a full-thickness rotator cuff tear may or may not notice weakness in the arm. With small cuff tears, strength may be maintained surprisingly well, although the patient may notice diminished endurance and fatiguability of the arm when it is used in the overhead position. Patients with cuff tears often note that the pain affects such activities as opening doors, reaching behind the back to do bra straps, reaching high shelves, or participating in sports such as tennis, racquetball, and swimming. On physical examination, inspection often reveals few abnormalities. A patient with a rotator cuff tear may have a long-head-of-biceps rupture or muscle atrophy in the supraspinatus fossa, although atrophy generally accompanies larger tears of long duration. There may be a fullness in the subdeltoid area as joint fluid fills the subacromial space. Occasionally a patient with a full-thickness tear will present with an AC joint "ganglion." This is, in fact, glenohumeral joint fluid which has leaked out into the subacromial space and through the eroded inferior capsule of the AC joint. This fluid sac gradually enlarges superiorly to present as a ganglion on top of the AC joint. It is important to recognize that the underlying pathology is not localized to the AC joint, but reflects the more difficult problem of a full-thickness tear that is usually large. Palpation of the affected shoulder not uncommonly reveals AC tenderness especially if AC arthrosis is present. There is usually a palpable subdeltoid soft crepitation, which may represent a subacromial bursal fluid, a thickened bursa, or a torn tendon moving under the coracoacromial arch. Patients with subacromial impingement syndrome without rotator cuff tearing may have normal passive range of motion; however, it is not uncommon for a mild frozen shoulder to accompany this syndrome. In the latter case, there is usually some restriction of motion passively in forward elevation, external rotation, and internal rotation. In the presence of a full-thickness rotator cuff tear, passive range of motion is often remarkably normal, as joint fluid leaks out and lubricates the subacromial space.

On physical examination, a number of impingement signs are usually positive and are very helpful in documenting as diagnosis of subacromial impingement

Subacromial impingement sign: with your right hand stabilizing the scapula, bring the patient's painful left arm into full forward elevation to reproduce the pain.

As the arm is lowered from the full overhead position to the side, a painful arc is reproduced between 80 and 100 degrees of elevation

These include a positive painful arc as the arm is lowered to the side from the fully overhead position, the classic impingement sign, pain with abduction in the plane of the scapula, and pain with internal rotation up behind the back. There may or may not be pain with resisted external rotation and resisted abduction. Active range of motion may be normal or may be reduced. A discrepancy between active and passive motion is highly suggestive of full-thickness disruption of the rotator cuff. A classic and most convincing clinical sign of a full-thickness cuff tear is weakness with external rotation. This is tested with the arm at the side and the elbow flexed to 90

degrees. Both arms may be tested simultaneously. It is common, even in the presence of an isolated supraspinatus tear, to have demonstrable weakness of external rotation. The patient often can distinguish between lack of strength and the need to "let go" secondary to pain. In the larger tears of the rotator cuff, the patient often has so much external rotation weakness that he can neither initiate active motion of the arm nor maintain the arm in a position of external rotation in which it has been passively placed. In addition, a "lift-off" test has been described: the arm is brought behind the back, and an attempt is made to lift the hand off the small of the back. Inability to do this is highly suggestive of a subscapularis tear.

One of the most helpful radiographs in the diagnosis of subacromial impingement syndrome is an anteroposterior (AP) view of the shoulder in external rotation, which often reveals cystic changes, sclerosis, or bone reaction in the area of the greater tuberosity of the humerus. In addition, a subacromial traction spur may be identified and associated AC joint pathology may

be present, as reflected by cystic changes, joint narrowing, or osteophyte formation. In the larger tears, this view often shows changes in the acromiohumeral interval, and in the most massive tears of long-standing duration, arthritic changes may be identified. Another AP view, with a 30-degree caudal tilt, will often more specifically show the anterior acromial spur; this view is used to outline the amount of acromion that projects anterior to the anterior edge of the AC joint, thought to be that amount of acromion pathologically projecting inferiorly. A lateral radiographic view of the scapula and acromion, with a 20-degree caudal tilt, has been termed the "outlet" view. This is intended to identify any bone projecting downward into the supraspinatus outlet, that space through which the supraspinatus passes. This view often identifies inferior protrusion of the acromion and the undersurface of the clavicle, and it may outline the shape of the acromion or an unfused acromial epiphysis. A supine axillary view is perhaps best to identify glenohumeral joint narrowing and the presence of an unfused acromial epiphysis. In a patient who has undergone previous surgery, this view also can reveal that amount of acromion which remains.

If a rotator cuff tear is suspected, any one of a number of imaging studies may be utilized. The most common are arthrography, ultrasonography, and a magnetic resonance imaging (MRI) scan. The advantage of arthrography is that it is the gold standard, is easily interpretable, and can clearly identify the presence or absence of a full-thickness tear. Its disadvantages include that it is invasive, its helpfulness is usually limited to the identification of full-thickness tears only, and it rarely gives information about the quality of the tendon or the precise location of the tendons that are torn. Ultrasonography has been utilized to identify full-thickness tears, but it may have difficulty identifying small tears. In addition, small tears, partial tears, and even degenerative and scarred tissue may look similar. The reproducibility and high degree of accuracy that have been reported at some centers in this country and in Europe have not been uniformly reproduced in community hospitals and centers with less experience.

Arthrogram Slide Show

While an MRI scan clearly gives the highest quality image of the shoulder and precise information about the extent and location of the tendon tear, and it may give information about associated biceps instability and associated muscle atrophy or fatty infiltration, its disadvantages include the facts that the patient may become claustrophobic and movement may interfere with MRI quality. In addition, the cost of an MRI scan is substantially greater than either of the other two imaging methods. However, for the most information and the clearest prognosis about surgical treatment and anticipated results, I prefer an MRI scan of the shoulder to identify the cuff pathology.

Acromial spur, greater tuberosity and sclerosis--as shown here--are highly suggestive of impingement syndrome

Any repetitive overhand activity, including throwing, may, over time, lead to tendinitis, impingement syndrome, joint instability, or even tears of the rotator cuff (Reference 4) , (Reference 6) , (Reference 11) , (Reference 15) . Under normal circumstances, the static and dynamic stabilizers about the shoulder joint provide the necessary balance between functional mobility and stability. However, chronic stress from repeated throwing activities may lead to fatigue of the rotator cuff and scapular rotator muscles. These dynamic restraints may then allow mild anterior glenohumeral translation as the anterior static restraints (glenohumeral ligaments, glenoid labrum, and joint capsule) become attenuated. Over time, this progressive anterior translation, or instability, may result in a "secondary impingement syndrome" as the humeral head and rotator cuff impinge beneath the acromion and coracoacromial arch (Reference 6) , (Reference 10) , (Reference 15) or between the posterosuperior border of the glenoid and the undersurface of the tendinous insertions of the supraspinatus and the infraspinatus (Reference 8) , (Reference 11) , (Reference 18) , (Reference 19) . Fortunately, conservative management is effective in most chronic overuse injuries and has been successful in treating approximately 75% of our athletes who have primary anterior glenohumeral instability with secondary impingement. For those athletes with persistent symptoms, anterior capsulolabral reconstruction utilizing the MITEK instrumentation and suture anchors has been successful in allowing most throwing athletes to return to competition.

Most throwing athletes with refractory anterior shoulder pain can be classified into one of four groups based on the information obtained through a detailed history, physical examination, and preliminary diagnostic arthroscopy (Reference 10) , (Reference 11) .

Group I. Primary impingement without shoulder instability.

A. Posterosuperior glenoid impingement. B. Subacromial impingement.

Group II. Primary anterior instability (subluxation) with secondary impingement.

A. Posterosuperior glenoid impingement. B. Subacromial impingement.

Group III. Primary anterior instability (subluxation) with secondary impingement associated with generalized ligamentous hyperelasticity.

A. Posterosuperior glenoid impingement. B. Subacromial impingement.

Group IV. Primary anterior instability without impingement.

Athletes in group IV usually have a history of a single traumatic event which has produced an acute anterior glenohumeral joint subluxation or dislocation. These patients would be considered similar to those patients described by Matsen (Reference 13) as having traumatic unidirectional instability, usually associated with a Bankart lesion, and often requiring surgical intervention (TUBS). Patients in group III have had relatively atraumatic, multidirectional (mostly anterior-

inferior) instability that is often bilateral and usually responds to nonoperative rehabilitation (AMBRI).

Classification of these athletes in accordance with their particular pathological processes allows a more rational treatment program.

It has been our experience that athletes with refractory pain due to primary subacromial impingement without instability (Group IB) will require a subacromial decompression using open or arthroscopic techniques. Patients who develop refractory symptoms due to posterosuperior glenoid impingement (Group IA) will often respond to arthroscopic debridement of the undersurface of the rotator cuff and labrum. By resecting the frayed and damaged tissues, the source of irritation within the shoulder joint will be eliminated, allowing the patient to rehabilitate more effectively and avoid further damage. When treating young throwing athletes with refractory shoulder pain, it is imperative to rule out underlying occult instability prior to performing a subacromial decompression. Athletes with primary anterior instability and secondary impingement (Groups II and III) have underlying instability as their primary pathology and neither subacromial decompression nor cuff debridement are likely to be successful. These athletes, as well as those with pure instability without impingement (Group IV), require glenohumeral joint stabilization.

PREOPERATIVE PLANNING

Establishing the diagnosis in a throwing athlete is difficult: symptoms are often vague and physical findings are subtle. In throwers, shoulder pain is the most common complaint. Shoulder pain that becomes worse with progressive activity is usually associated with subacromial bursitis with or without rotator cuff tendinitis. Pain that persists, even at rest, may indicate tissue degeneration associated with a partial or a complete tear of the rotator cuff.

Throwing Motion Sequence

Pain that occurs during a particular phase of the throwing motion (i.e., late cocking or acceleration) may be the result of mild anterior glenohumeral instability with secondary subacromial rotator cuff impingement as the humeral head and rotator cuff impinge beneath the coracoacromial arch (Reference 4) , (Reference 6) , (Reference 10) , (Reference 15) .

However, recent investigations have also identified an additional secondary posterosuperior glenoid impingement phenomenon that also occurs with the arm in the overhead throwing position (Reference 8) , (Reference 18) , (Reference 19) . With the arm in abduction and maximum external humeral rotation, a normal shoulder has been shown to translate posteriorly approximately 4 mm on the glenoid articular surface (Reference 5) , (Reference 7) . This is believed to be the result of selective tightening of the anterior joint capsule which, in this position, leads to slight posterior humeral translation. However, in those patients with excessive joint laxity or anterior instability as a result of repetitive stress (i.e., throwing), this normal

posterior humeral translation does not occur. Instead, the humeral head is allowed to translate anteriorly. Recent dynamic arthroscopic observations have confirmed the presence of this internal impingement between the posterosuperior glenoid rim and the undersurface of the tendinous insertions of the supraspinatus and infraspinatus tendons when the arm is in the late-cocking pitching position (Reference 11) , (Reference 18) , (Reference 19) .

Because shoulder pathology can progress along a continuum of disease from mild laxity to anterior subluxation, secondary impingement (subacromial or posterosuperior glenoid), and eventual rotator cuff tearing, evaluation of shoulder stability is particularly helpful in determining the etiology of shoulder pain in the throwing athlete. Classic impingement signs (Reference 6) , (Reference 15) and apprehension signs are relatively straightforward; however, signs of mild instability are subtle and must not be overlooked. The most sensitive means of eliciting occult anterior glenohumeral instability is through the use of the classic apprehension sign followed by the relocation test (Reference 10) , (Reference 11) . These maneuvers are best performed with the patient lying comfortably in the supine position. The arm to be tested is positioned off the edge of the examining table in 90 degrees abduction and maximal external rotation. In this position the apprehension test (Fig. 1) is performed by applying a gentle, anteriorly directed force to the posterior humeral head. Marked apprehension (or apprehension and pain) indicates gross instability as seen with recurrent dislocations (Group IV). The sensation of pain without apprehension may denote either primary impingement (Group IA, IB) or mild anterior instability (subluxation) with secondary subacromial (Group IIB; Group IIIB) or posterosuperior glenoid impingement of the undersurface of the rotator cuff along the posterosuperior glenoid rim (Group IIA; IIIA) (Fig. 2) . To differentiate primary impingement from primary instability (subluxation) with secondary impingement, the relocation test is performed (Fig. 3) . With this maneuver, gentle pressure is applied to the anterior aspect of the humeral head in a posterior direction. Patients who have no change in their perception of pain most likely have primary impingement with no associated instability. However, those patients, especially young overhand throwing athletes, whose pain is reduced (as they now tolerate further external humeral rotation while the humeral head is maintained in a reduced position) usually have mild primary anterior instability (subluxation) with secondary impingement (Fig. 4) .

Apprehension Test

  Figure 1. Apprehension test: Shoulder held in position of 90 degrees abduction and maximum external humeral rotation. An anteriorly directed force (arrow) is applied with gentle fingertip pressure to the posterior proximal humerus.

Arthro View/Glenohumeral Jt in Apprehension Position

Figure 2. Posterosuperior glenoid impingement. a, Anteriorly translated humeral head; b, Undersurface rotator cuff fraying; c, Posterosuperior glenoid labrum/rim (arrowheads indicate site of impingement); d, Glenoid fossa.

Relocation Test

  Figure 3. Relocation test. A posteriorly directed force is applied to the anterior proximal humerus (maintaining the head in a reduced position) allowing further external humeral rotation as the sites of potential impingement are relieved.

Arthro View/Glenohumeral Jt in Relocation Position

Figure 4. Reduced position of glenohumeral joint. a, Humeral head reduced; b, Posterosuperior labral fraying; c, Glenoid fossa.

Appropriate radiographic analysis of throwing athletes with shoulder pain includes standard roentgenograms [anteroposterior (AP), lateral, axillary, and outlet views]. Patients with chronic recurrent instability or acute traumatic dislocations may exhibit a bony defect within the posterior aspect of the humeral head (Hill-Sachs deformity) or a deficiency of the anterior, inferior glenoid rim (Bankart lesion). Unfortunately, routine radiographs add very little diagnostic information for most throwing athletes with persistent shoulder pain. However, they must be included in the investigation to rule out infection, fracture, or an unsuspected neoplasm. Additional diagnostic studies including arthrography, computed tomography (CT) arthrography, or magnetic resonance imaging (MRI) with or without contrast enhancement may reveal glenoid labral lesions, partial-thickness rotator cuff lesions, or defects within the humeral head or the glenoid rim. These studies, unfortunately, are also frequently negative in the throwing athlete with occult instability (subluxation) and secondary rotator cuff tendinitis and are not recommended in the routine work up of most patients with impingement or instability.

For patients with suspected instability, an examination under anesthesia and diagnostic arthroscopy have been most helpful in confirming the diagnosis.

Go on to surgery

PREOPERATIVE PLANNING

Together, the history, physical examination, and radiographic examinations create a picture of the unstable shoulder that allows for accurate preoperative planning. In contemplating surgical treatment for multidirectional instability of the shoulder, it is essential to determine whether the primary direction of instability is anterior, inferior, or posterior. This particular information is generally gleaned from the history given by the patient. Patients with anterior instability problems will describe symptoms that occur when their arm is in the apprehension position of abduction and external rotation, such as when they cock their arm to throw a ball.

Throwing Motion Sequence

Patients with posterior instability will complain that their shoulder tends to "slip out of place" when their arm is forward flexed and internally rotated, such as when they remove a book from an overhead shelf. Inferior instability will most often be demonstrated when patients carry objects at their side, such as a heavy suitcase.

Patients with MDI often give a history of shoulder complaints beginning in childhood, and initial episodes of subluxation or dislocation that were atraumatic or occurred with minimal trauma. Involuntary, symptomatic instability then results gradually from multiple recurrences or begins after a traumatic event. Dislocations in patients with MDI are frequently transient and often do not require the assistance of a physician or another person to obtain a reduction. Painful subluxation is generally associated with global instability secondary to traumatic events rather than with MDI of an entirely atraumatic origin.

Physical examination of the patient with MDI usually reveals generalized ligamentous laxity as evidenced by hyperextension of the elbows, knees, and metacarpophalangeal joints, hyperabduction of the thumb (passive abduction of the thumb to the forearm with the wrist flexed), and patellofemoral laxity. Many patients with multidirectional instability can voluntarily sublux their shoulders, usually in a posterior direction.

Multiple Failed Surgery Slide Show

This ability does not absolutely contraindicate surgical intervention, but voluntary subluxers should undergo psychiatric examination. Instability testing, by definition, shows laxity in both the anteroposterior (AP) and inferior directions, manifested by a positive sulcus sign (a dimple created between the humeral head and the acromion when the humeral shaft is pulled distally) and a positive push-pull test (anterior or posterior subluxation noted when directly pushing the humeral head anteriorly or posteriorly, after centering the head in the glenoid fossa). Rotator cuff and deltoid strength is typically normal, though patients with MDI can often differentially contract the heads of the deltoid, causing subluxation. Even if strength is normal, added strength, particularly in the rotator cuff, helps to control dynamic instability.

Though patients with MDI often have normal radiographs, an instability series consisting of AP views in internal and external rotation, an axillary lateral, a Stryker notch view, and an apical oblique view should be obtained. These patients can have traumatic episodes superimposed on a

background of generalized ligamentous laxity, and the presence of a Hill-

Sachs or a Bankart-Perthes lesion Fig. 25 has implications for the outcome of a conservative treatment program. It is also important to recognize the presence of these lesions preoperatively, as all Bankart-Perthes lesions and severe Hill-Sachs lesions should be addressed at the time of surgery. The axillary lateral view should be scrutinized for evidence of glenoid hypoplasia or aplasia or excessive glenoid retroversion, as both conditions are poorly treated by anterior capsular reconstructions alone. Patients with glenoid retroversion abnormalities should undergo computed tomography (CT) scanning of both shoulders to further delineate the condition.

An examination under anesthesia is not necessary to make the diagnosis of MDI, but it can be performed in the operating room prior to anterior inferior capsular shift. We have not found arthroscopy of the glenohumeral joint to be very helpful, as most patients with MDI have little pathology treatable by current arthroscopic techniques. Arthroscopic pathology generally consists of a patulous anterior capsule with poorly defined glenohumeral ligaments and a positive pass-through sign (the arthroscope inserted through the posterior portal can easily be passed without significant distraction from anterior superior to anterior inferior). Arthroscopy can be helpful to differentiate MDI from traumatic instability. While labral pathology can be addressed arthroscopically with current techniques, the accompanying capsular laxity cannot be adequately addressed. Significant labral pathology can easily be evaluated and treated during the capsular shift; therefore, we utilize arthroscopy only in the rare instance when we are uncertain whether an anterior reconstruction is warranted, and we feel arthroscopic pathology will help us make the final decision.

INDICATIONS/CONTRAINDICATIONS

Posterior instability is not as common as its anterior counterpart. It usually occurs in a young athletic population (Reference 1) , (Reference 2) and presents as a recurrent posterior subluxation rather than as a true recurrent posterior dislocation, which is rare.

Posterior instability is not in-and-of-itself an indication for surgical repair. Approximately two-thirds of patients with posterior instability respond to a proper exercise program (Reference 3) consisting of exercising the external rotators of the shoulder (the infraspinatus, teres minor, and posterior deltoid muscles) and the scapula stabilizers. Such a program will usually decrease the symptoms, but the instability may remain. No patient with instability should have surgery who

has not had 6 months of a structured exercise program.

Athletes commonly present with posterior instability that interferes with their athletic endeavors (Reference 1) , (Reference 2) . Surgical procedures geared solely to enable them to perform at a high athletic level are usually unsuccessful. Thus the indications for surgical repair in the athlete are pain and instability that interfere with activities of daily living. The primary indication for surgical repair is the demonstration of recurrent, symptomatic, unidirectional subluxation that has failed to respond to a comprehensive nonoperative program. An athlete who does not respond to a conservative program will rarely be improved by operative repair if his only goal is

to return to a high level of overhead activity.

Two other clinical syndromes merit discussion and caution. True unidirectional posterior subluxation may not be as common as multidirectional instability with demonstrable posterior subluxation. Each patient with posterior subluxation should be evaluated for multidirectional or global instability, and if this is present, rehabilitation should be aimed at all directions of laxity. If nonoperative treatment fails, the operative technique must include stabilizing all directions of laxity and may require an extensive inferior capsular shift from either posterior or combined anterior and posterior directions. In addition, there are some patients, often with multidirectional instability, who have had an overly tight anterior repair that leads to gradually increasing symptomatic posterior instability. In these patients, especially if external rotation has been limited by the prior surgery and anterior tightness seems to be the predominant pathology, an anterior approach with subscapularis lengthening to restore humeral head centralization on the glenoid may be more effective than a posterior approach to tighten the soft tissue.

The second clinical syndrome which should be addressed is seen in the patient with a (suprascapular) nerve injury and weakness of the supra- and infraspinatus. Posterior subluxation in this patient may be related to weakness of the dynamic muscular stabilizers. Attention should be paid to the primary nerve injury and subsequent rehabilitation of the muscle groups rather than to tightening the posterior capsule, for without posterior muscular stabilization, the

capsular repair will likely stretch out over time.

A posterior capsular repair is contraindicated in a ligamentously lax individual or in a patient with multidirectional instability. If surgery is indicated, these patients need a capsular shift procedure. Bony abnormalities are rare about the shoulder with posterior instability, but a congenital hypoplastic glenoid with abnormal version would be another contraindication to a

capsular repair. Also, any individual with significant degenerative arthritis of the glenohumeral joint is often made symptomatically worse by a capsular repair, which would over-constrain the shoulder and increase the degenerative changes. In line with this, the apparent posterior subluxation associated with osteoarthritis is secondary to asymmetric glenoid wear and should

not be confused with recurrent posterior subluxation.

A relative contraindication is seen in a patient who, although lax and able to posteriorly subluxate the shoulder, does not have enough symptoms to warrant surgical repair, or in a patient who has not undergone a supervised formal trial of rehabilitation. Additionally, a patient who has had prior posterior surgery with attendant damage to either the posterior cuff muscles or the suprascapular nerve is unlikely to benefit from further soft tissue surgery posteriorly.

A typical patient with posterior subluxation has had a traumatic event with an injury occurring while the arm is in a position below shoulder level. Often there is a direct blow from the anteroposterior (AP) direction followed by recurrent symptomatic subluxation. The patient, having suffered a significant single traumatic episode, may have had repeated episodes of microtrauma with gradually progressive stretching of the soft tissue structures until the shoulder begins to subluxate.

A patient with posterior shoulder instability feels the shoulder slip, pop, or "click out and click in." These instability episodes often occur with the arm in the frontal plane and may occur dynamically. Dynamic subluxation occurs as the patient begins to raise the arm upward, it reaches a point in the arc where the shoulder slips posteriorly, and as the arc of elevation is continued, relocation occurs. Thus the patient may be able to demonstrate the posterior

subluxation when asked. The posterior instability may or may not be painful.

The most important preoperative assessment is to document that the patient has an isolated posterior instability rather than a posterior instability as a component of multidirectional instability (Reference 4) . On examination, care should be taken to elicit signs of generalized ligamentous laxity which may be a clue to the presence of multidirectional shoulder instability. Hyperextensibility of the elbows, hyperflexibility of the wrist and small joints of the hand, and laxity of the contralateral shoulder all may indicate the presence of global laxity. Attempts should be made to center the humeral head in the glenoid by a load-and-shift test

Load-and-Shift Test

and to subluxate the shoulder anteriorly, posteriorly, and inferiorly. The hallmark physical

finding of multidirectional instability is a sulcus sign.

Sulcus Sign

The patient who has isolated posterior instability often can be subluxated in a posterior direction by the examiner who grasps the humeral head and pulls directly backward, with the muscles of the shoulder relaxed. This load-and-shift test,

Load-and-Shift Test

or posterior drawer test, is positive in the posterior direction but negative in all other directions tested. The examiner also may be able to demonstrate posterior subluxation as the arm is brought

into the frontal plane at 90 degrees and internal rotation force is applied.

Posterior apprehension, though uncommon, should be tested. The arm is brought into forward elevation with internal rotation, and posterior stress is applied. A sense of instability, significant pain, or painful subluxation is suggestive of the diagnosis. Range of motion of the shoulder is usually not limited either passively or actively in the patient with isolated posterior subluxation. Strength of the rotator cuff muscles may be normal, but it is not uncommon to see significant external rotation weakness when manually tested, a finding that may emphasize the need for further rehabilitation.

The diagnosis of posterior instability may be confusing, and the athlete with posterior subluxation may have other causes of shoulder pain. Therefore, prior to considering posterior capsular repair, it is most helpful if the patient identifies the pain while the shoulder is being subluxated as the precise pain leading to the disability of the shoulder. If posterior subluxation by the examiner can be elicited but does not produce pain in the shoulder or a sense by the patient of "that's it; that is what I feel," then the diagnosis should be questioned and an alternative cause of the pain should be considered.

Shoulder radiographs for instability include an AP in internal and external rotation, a lateral, and a West Point axillary view. While these views rarely show any bony changes in the glenoid, there may be some bone reaction along the posterior rim which will increase the clinician's comfort level with the diagnosis. It is unusual to have a reverse Hill-Sach's lesion. Occasionally a dynamic radiograph may be taken as the patient voluntarily subluxes the shoulder, and this film may show the humeral head in a posteriorly subluxed position. Additional imaging studies such as computed tomography (CT), arthrography, and magnetic resonance imaging (MRI) are rarely useful for clinical management. In some patients, after a particularly significant traumatic event, a detachment of the posterior labrum may be identified through an imaging study.

Posterior Labrum Slide Show

If there is any doubt about the direction or extent of instability, an examination under anesthesia with or without arthroscopy may clarify the predominant direction of instability and address the presence or absence of intraarticular labral pathology. If arthroscopic evidence of an anterior Bankart lesion exists, the diagnosis of isolated posterior instability must certainly be questioned.

Bacacki sport

Physical Examination

The physical examination begins with inspection; focus should be not only on

the affected arm, but also on the athlete's general posture and the position of

the head, neck, and trunk. Muscle contour and balance should be observed

with attention given to subtle signs of asymmetry or atrophy, which may help

focus the examination. When viewing the back of the patient, the examiner

can appreciate a scapular asymmetric depression, protraction, or winging of

the scapula, which may be present as an isolated finding or in combination

with an intra-articular problem.

Range of motion should be observed, both glenohumeral and scapulothoracic

contributions. Scapulothoracic motion should be smooth and pain free;

comparison with the contralateral shoulder should be noted for symmetry of

position and motion; crepitus may be suggestive of inflammatory bursitis.

Total rotation of the throwing shoulder should be recorded and compared with

the nonthrowing shoulder. It is common for throwing athletes to have

increased external rotation in abduction and decreased internal rotation in

abduction in their throwing shoulder; however, the arc of total motion should

be similar.

Palpation for pain is helpful to identify specific areas of injury and can

distinguish between various types of pathology that can often present with

similar symptoms. Specific focus should be on the muscles of the rotator cuff,

long head of the biceps, conjoined tendon, anterior and posterior capsule,

acromioclavicular (AC) joint, and suprascapular notch.

Strength testing of the rotator cuff muscles and the periscapular stabil izing

muscles should be performed. The supraspinatus is tested with resisted

forward elevation with the arms in 30 degrees of abduction with the thumbs

pointed to the floor. The infraspinatus and teres minor are tested with

resisted external rotation with the arms adducted at the side. The

subscapularis is tested with the lift-off test or the belly press test. When

weakness or muscle pain is present, the testing should be repeated with the

scapula actively retracted and depressed. If strength improves or pain

decreases, this represents a positive scapular retraction test consistent with

scapular dyskenesis.

Laxity and translation of the glenohumeral joint should be assessed in the

anterior, posterior, and inferior directions. This should be performed with the

arm in both internal and external rotation and with the athlete sitting and

also lying supine. Increased laxity is an expected finding in the dominant arm

and is not necessarily pathologic, but laxity associated with discomfort or

with reproducing the thrower's symptoms is l ikely to be pathologic instabil ity.

Various provocative tests are useful to help identify the source of pain in a

throwing athlete. Hawkins and Neers tests may be useful for identifying

impingement. The apprehension and relocation test may be useful when they

elicit discomfort or apprehension, but are less helpful when they are

associated with pain. Various tests have been described for assessing labral

pathology; recent reports reveal l imited sensitivity and specificity with the

active compression test, the anterior slide test, and the compression rotation

test (1,2,3). Overlap exists with tests designed to identify biceps pathology

because these may be positive in an athlete with labral pathology.

Ancillary Tests

Radiographs are useful in evaluating bony anatomy and include a throwers'

series, an anteroposterior (AP) view in internal and external rotation (internal

rotation view is helpful to assess Hil l-Sachs lesions), a scapular outlet view

for assessment of acromion morphology, and an axil lary lateral to identify

bony Bankart lesions (Fig 21-2A) . Additional views and MRIs may be ordered

when physical examination indicates that they would be useful (Figs 21-2B

and C , and Figs 21-3,21-4,21-5) .

Computed tomography (CT) scanning has l imited applications, but may be

useful in evaluation of glenoid bone loss. Ultrasound can be helpful for rotator

cuff tendinopathy, but is of l imited application because it is very operator

dependent and few institutions have the experience necessary for consistent

interpretation.

Magnetic resonance imaging (MRI) may be helpful in certain situations for

establishing a specific diagnosis. Magnetic resonance arthrography (MRA) can

also be a useful adjuvant diagnostic tool; dilute gadolinium is injected into

the shoulder and gives more anatomic detail in athletes with suspected labral

lesions or potentially other instabil ity-related pathology [humeral avulsion of

the glenohumeral l igament (HAGL lesion), anterior labor-l igamentous

periosteal sleeve avulsion (ALPSA lesion), and glenoid labral articular

disruption (GLAD lesion)].

Electrodiagnostic testing may be warranted in cases when weakness is

believed to be neurologic in nature. The EMG can help differentiate

mononeuropathies for more diffuse, widespread processes such as

radiculopathy or brachial plexopathy. The most common mononeuropathies

seen in the throwing athlete are suprascapular and long thoracic

neuropathies.

The Shoulder

The Thrower's “Dead Arm”

In the overhead athletes, the “dead arm” syndrome has long been recognized

as a potentially career-ending condition. Historically, the specific pathology

has been poorly understood; only recently has greater insight been achieved

into etiology; however, treatment remains controversial.

Athletes often complain of pain during the late cocking and acceleration

phase, as the arm moves forward. The arm then “goes dead” and the athlete

has loss of velocity and control; this, along with pain, prevents continued

throwing and results in compromised performance. Various conditions have

been observed, and debate concerning which model of pathology is most

accurate is further complicated by the fact that

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these conditions may be present in asymptomatic throwing athletes, thus

suggesting a spectrum of variation, often with no clear distinction from the

adaptive to the pathologic changes.

Fig 21-2.A: AP radiograph showing the periarticular bone avulsed from the

anterior-inferior glenoid resulting in a Bankart lesion. B: MRI scan of the same

patient documenting the bony Bankart defect. C: MRI scan obtained while the

patient's arm was in the Abduction and External Rotation (ABER) position

showing the bony Bankart, anteroinferior subluxation, and Hill-Sachs defect on

the postero-lateral aspect of the humeral head.

Fig 21-3. MRI after anterior dislocation of the shoulder, documenting the

proximal humeral Hil l-Sachs lesion with subchondral bleeding and intra-

articular loose body.

Internal Impingement

Internal impingement is a topic that has been controversial and also can be

very confusing. Originally described by Walch et al. (4) as naturally occurring

impingement between the posterior superior rotator cuff and the glenoid rim

with arm in position of abduction and external rotation. Others noted this

same occurrence in asymptomatic throwing athletes.

Fig 21-4. Arthroscopic view via posterior portal of the patient's right shoulder

revealing the Hill-Sachs defect (A) and with external rotation, the defect is

engaged with the anterior glenoid rim (B).

Fig 21-5. MRI study, two adjacent images demonstrate the Hill-Sachs defect

seen in abduction and external rotation.

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Jobe (5) later popularized the term as a pathologic condition occurring in

overhead athletes leading to throwing injury. In this model, anterior capsular

insufficiency was the inciting occurrence that subsequently led to further

disabil ity and the “dead arm.” Loss of integrity of the capsule is a direct

result of hyperangulation of the throwing arm. The symptoms are exacerbated

by the loss of the posterior rollback, which leads to anterior translation and

results in greater internal impingement posteriorly. If untreated, it may lead

to posterior labral tears, Superior Labrum Anterior and Posterior (SLAP) lesion

due to peel-back, and partial thickness articular-sided rotator cuff tears.

Treatment is focused at correcting the underlying instabil ity and treating any

additional pathology. Reports of capsulolabral reconstruction have shown

some success in allowing pitchers to return to their previous level of

competition (6,7).

The Morgan-Burkhart model (7a, 7b) suggests that the posterior capsular

contracture is the inciting occurrence in the cascade of disabil ity and injury.

Posterior capsule tightness has long been recognized as a component of the

throwing shoulder (8,9,10,11,12); at what point this becomes pathologic has

been less well delineated. As the shoulder develops progressively worsening

posterior contracture, the glenohumeral contact point is shifted further

posterior and superior when the shoulder is in abduction and external

rotation. A relative redundancy of the anterior capsule is observed due to the

tightening of the posterior capsular structures—this is what has been

observed as anterior capsular stretching in the Jobe model. As the thrower

attempts to reach his or her set point for throwing, hyperangulation and

hyperexternal rotation forces cause tensile overload of the rotator cuff

leading to partial tears; additionally, a dynamic peel-back phenomenon

generates SLAP lesion of the labrum. Glenohumeral Internal Rotation Deficit

(GIRD) is defined as the loss in degrees of internal rotation as compared with

the contralateral shoulder, with the arm positioned in 90 degrees of abduction

and external rotation. Burkhart et al. (13) believe that symptomatic GIRD is

present when the deficit is 25 degrees or greater. Treatment focuses on

stretching the posterior capsule with the use of “sleeper stretches.” Although

the nonsurgical treatment is usually successful, those who do not respond to

relative rest, stretching, and strengthening programs may be candidates for

arthroscopy, debridement, and occasional posterior capsulotomy, which is

often performed with treatment of other coexistent pathology.

Labral pathology is well recognized as a component of the disabled throwing

shoulder. The acromym SLAP describes the location of pathology, Superior

Labrum Anterior and Posterior. It was first observed by Andrews (13a) in

throwing athletes and was later named by Snyder. Multiple subtypes have

been described. Some believe that SLAP lesion is the most common pathologic

entity associated with the throwers “dead arm” (9,13,14). If left untreated,

athletes typically cannot return to throwing. Debate has existed concerning

the mechanism of injury during throwing. Fleisig et al. (15) and Andrews et al.

(16) proposed a deceleration mechanism of injury, as the bicep contracts to

slow down the arm in follow through. This tensile load acts to pull the biceps

and superior

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labral complex from the bone. Burkhart et al. (13) support an acceleration

mechanism of injury. As the shoulder is positioned in abduction and external

rotation coinciding with late cocking and acceleration, the labrum is peeled

off the glenoid rim. Kuhn et al. (17) performed experimental comparison of

the two mechanisms in a cadaveric model; their results support the

acceleration mechanism. Treatment is dictated by the stabil ity of the

biceps/labral complex. If complex is unstable, a repair is necessary; if stable,

a débridement of damaged tissue may be adequate. Surgical repair has been

very successful in allowing return to throwing, some reports approaching 90%

(14).

Rotator Cuff Tears

The repairs of full-thickness cuff tears has been associated with low success

rate (17a). Partial-thickness articular-sided tears of the supraspinatus and

infraspinatus are well recognized in the throwing athlete. The etiology of

these tears is multifactorial, but a significant component is believed to be

tensile force overload during the deceleration phase in addition to the

mechanical abrasion of internal impingement. Various grading systems have

been described. The thickness of involvement can be determined

arthroscopically by direct examination and by the amount of exposed

footprint at the insertion site of the tendon itself. Tears <50% thickness often

only require debridement and attention to other coexistent pathology. For the

few tears that are >50%, consideration may be given to repair of the tendon;

this can be performed insitu or after completion of the tear to full thickness

(Figs 21-6,21-7,21-8,21-9) .

Biceps Lesions

Biceps pathology is a contributing factor to shoulder pain in the overhead-

throwing athlete. The function of the biceps tendon in the shoulder is

controversial and treatment options continue to evolve. Pathology may occur

at the junction with the labrum, the articular portion, directly adjacent to the

transverse ligament, in the biceps groove, and distally at the

musculotendinous junction. Pain with direct palpation over the proximal

tendon as well as various provocative maneuvers (Speed's test—pain with

resisted forward elevation of the arm

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in supination, and Yergason sign—pain with resisted forearm supination with

the arm at the side and the elbow flexed 90 degrees) are helpful in identifying

the biceps as a contributing factor to disabil ity. MRI may be helpful,

particularly when augmented with intra-articular contrast. Cortisone injections

may also be used to help localize pathology, but injection adjacent to the

tendon is often difficult and injection within the substance of the tendon may

contribute to further failure. Surgical treatment options remain controversial;

although the minor lesions and fraying can be debrided, the more severe

lesions may require tenodesis or, in older patients, the tenotomy may offer a

satisfactory solution.

Fig 21-6. Partial-thickness rotator cuff tear.

Fig 21-7. Arthroscopic views from posterior portal of the right shoulder shows

the partial tear of articular surface of rotator cuff. Biceps tendon and glenoid

labrum tears often seen in association with the undersurface rotator cuff

tearing.

Fig 21-8. MRI arthrogram showing the massive rotator cuff tear with

retraction of the tendon to the level of the glenoid.

Fig 21-9. MRI arthrogram revealing the massive tear with contrast migrating

into the acromioclavicular joint, creating the geyser sign.

Coracoid Impingement

Coracoid impingement occurs when the subscapularis tendon is compressed

between the lesser tuberosity and the tip of the coracoid process. Patients

will present with anterior shoulder pain and findings on exam that may mimic

subacromial impingement. Pain may be elicited with passive flexion of the

arm in an adducted and internally rotated position or with direct palpation

over the conjoined tendon. A diagnostic and therapeutic injection in the

subcoracoid space can be effective in confirming the diagnosis as well as

treating the condition. A coracohumeral interval <6 mm (normally 11 mm) is

helpful in confirming the diagnosis, but is not pathonomonic. If conservative

measures fail to provide adequate relief, a coracoplasty may be performed;

both open and arthroscopic techniques have been described.

Acromioclavicular Joint Injuries

AC joint injuries are relatively uncommon in the throwing athlete because

physical contact is usually at a low to moderate level. Less-severe injuries,

grade I and II AC joint separation, are treated nonoperatively with good

success. Controversy exists for the grade II I lesions; randomized trials have

demonstrated good results with nonoperative treatment, but despite this,

some advocate early surgical reconstruction. Those who support early surgical

intervention cite altered throwing mechanics and early fatigue resulting in

decreased performance as reason for surgical intervention. Specific l iterature

in throwing athletes is scant, with most recommendations reflecting personal

opinion and preference. McFarland et al. (18) performed a survey of

physicians of professional baseball teams; only 32 lesions had been seen by

this group. In response to the theoretical treatment of a starting pitcher with

a preseason grade II I AC injury, 69% reported that they would treat the injury

conservatively. The surgical treatment of choice in this survey was a Weaver-

Dunn reconstruction with high-strength suture or graft between the clavicle

and coracoid.

Bennett Lesion

A Bennett lesion is an exostosis of the posterior inferior glenoid; it is seen in

throwing athletes and was first described by one of the first baseball

physicians, G.E. Bennett (19). The exact cause of this lesion is not known;

possible theories include traction due to the pull of the triceps tendon or

possibly posterior capsule. Others have suggested that contact from the

posterior superior labrum and humeral head may be responsible (19a). The

location of the lesion is at the point of capsular attachment to the neck of the

glenoid. It is best visualized with an axil lary lateral radiograph or with the use

of CT imaging.

The significance of this lesion in the throwing athlete is not well defined. Its

relationship to posterior pain in the disabled throwing shoulder is also not

clear. Consequently, surgical intervention to specifically address this lesion is

not presently a clear indication. Labral damage and injury may occur in the

presence of the Bennett lesion and in this setting the lesion may be

addressed if incidental to other shoulder pathology.

Synovial Cysts

Synovial cysts can be seen with overhead athletes, but they are relatively

uncommon; additionally, a lack of specific signs and symptoms make the

diagnosis more challenging. They may occur in many areas around the

shoulder, with symptoms typically an il l-defined ache. Occasionally, the

subsequent nerve compression may occur. The suprascapular nerve can be

compressed in the suprascapular notch, resulting in atrophy and weakness of

both the supraspinatus and the infraspinatus, or at the spinoglenoid notch,

which results in atrophy and weakness of the infraspinatus alone. The lack of

specific signs and symptoms make evaluation of the posterior thorax for

atrophy essential. Many lesions are discovered with use of MRI, often

incidentally (Fig 21-10) . Nerve conduction study may also be useful in

establishing a diagnosis with clinical suspicion. Normal joint extension can be

confused with a synovial cyst,

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as a patient with an effusion may have larger amounts of joint fluid present in

a normal recess.

Fig 21-10. MRI of periarticular cyst A: Coronal view; B: Axial view.

Treatment is nonoperative unless a clear, recent onset of nerve compression

is present. Of those symptomatic patients, various surgical techniques have

been described. Hawkins et al. (20) reported on aspiration of cysts with an

18% failure rate and 48% recurrence rate, with 54% reporting satisfaction

with the outcome. Arthroscopy is beneficial in that the posterior and superior

labrum can be assessed, because some have suggested that labral pathology

may communicate with the cyst. However, not all cysts are associated with

labral tears and may not be visualized arthroscopically. In addition, not all

surgeons have experience with arthroscopic techniques for decompression.

Nerve Injuries

Neurological injuries may occur without the space-occupying lesions such as

ganglions or cysts. Most commonly, the suprascapular and long thoracic

nerves are involved. The specific etiology of injury is often unknown. When

the suprascapular nerve is involved, the branch to the infraspinatus is usually

injured with sparing of the branch to the supraspinatus. Volleyball players are

most commonly affected in this manner, with up to 20% of professional

players being affected (21). Most players will remain asymptomatic and can

participate in sports without l imitation, despite muscle atrophy.

Infraspinatus nerve palsy in the throwing athlete presents with symptoms that

mimic tendinopathy of the shoulder with associated pain and weakness. A

history will often reveal l ittle that is helpful in establishing a diagnosis, and

only with a high index of suspicion and careful inspection for atrophy and

weakness can the diagnosis be made. A thorough examination is essential to

ensure that no underlying neurologic condition exists. Electromyography

(EMG) can confirm the diagnosis, and MRI can be helpful to rule out a space-

occupying lesion. Most patients treated nonoperatively will eventually become

asymptomatic, although weakness and atrophy will persist.

Surgical intervention is reserved for those who have persistent symptoms and

are not able to perform their sport. Operative intervention remains

controversial, because the exact etiology of the condition is often unknown,

and nerve recovery after surgery may occur in only half of those treated. The

surgical technique involves decompression of the nerve and release of

spinoglenoid l igament along with bony resection as needed.

Arterial and Venous Lesions

Vascular lesions of the upper extremity in throwing athletes are not common.

Symptoms are vague and nonspecific initially, but progressive coolness of the

hand and fingers may be suggestive. Pulses may or may not be affected,

depending on the degree of the vascular compromise. Doppler ultrasound is

the best initial screening test. Venogram may also be beneficial if a clot is

suspected. Ultimately, venography or arteriography will identify the precise

location of the lesion. Vascular consultation is recommended for assistance

with medical and surgical decision making.