Glenoid Labrum

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Internal Shoulder Impingement – Physioplus

Description

The glenoid labrum (glenoid ligament) is a fibrocartilaginous rim attached around the margin of the
glenoid cavity in the shoulder blade. The shoulder joint is considered a ball and socket joint. However, in
bony terms the 'socket' (the glenoid fossa of the scapula) is quite shallow and small, covering at most
only a third of the 'ball' (the head of the humerus). The socket is deepened by the glenoid labrum.

The labrum is triangular in section, the base is fixed to the circumference of the cavity, while the free
edge is thin and sharp.

It is continuous above with the tendon of the long head of the biceps brachii, which gives off two
fascicles to blend with the fibrous tissue of the labrum.[1]

Structure

The glenoid labrum is similar to the meniscus of the knee. It is a fibro-cartilaginous rubbery structure
which encircles the glenoid cavity deepening the socket providing static stability to the glenohumeral
joint. It acts and looks almost like a washer, sealing the two sides of the joint together.The labrum is
described like a clock face with 12 o'clock being at the top (superior), 3 o'clock at the front (anterior), 6
o'clock at the bottom (inferior) and 9 o'clock at the back (posterior). Clinicians may reverse the 3 o'clock
and 9 o'clock for left shoulder describing 3 o'clock at the back. This can be confusing, so the European
Society of Shoulder & Elbow Surgeons (SECEC) has agreed to keep 3 o'clock at the front for either
shoulder.[2]

The glenoid labrum is approximately 4 mm thick and is round or triangular in cross section.

The capsule of the glenohumeral joint attaches to the glenoid labrum. The glenoid labrum is continuous
with:

superiorly: tendon of the long head of biceps brachii

anteriorly:anterior band of the inferior glenohumeral ligament

middle: glenohumeral ligament (variably)[3]

Clinical Relevance

Most instabilities or pain syndromes are associated with injuries or morphologic changes in the glenoid
labrum complex or long head of the biceps tendon origin. The first anatomic descriptions go back to Fick
in 1910 and since then many authors have described the anatomy of these structures. It was Snyder
who introduced the term SLAP lesions, classifying superior, anterior, posterior labrum changes into four
grades. It is still unclear whether all of the described and arthroscopically observed changes are due to a
post-traumatic, acquired lesion or whether anatomic variations can be present as well. In order to
elucidate this problem, 36 cadaver shoulder joints were inspected macroscopically and sectioned for
microscopic evaluation. Here the glenoid could be divided into an superior and an anterior- superior
area demonstrating a wide variety of morphologic labral glenoid changes, while the dorsal and inferior
sectors of the glenoid showed a relatively uniform anatomy of a firm labrum-glenoid bond. Four types of
biceps tendon attachments could be identified similar to the description given by Vangsness. In addition,
a variety of anterior-superior changes could be found. The sublabral hole as described by Esch in the
clinical setting was found to be a physiologic variant. Precise knowledge of the anatomic morphology of
the normal glenoid in its variations seems to be necessary to understand variants and allow for
distinguishing between physiologic anatomic variants and pathoanatomic changes in imaging and the
clinical setting.[4]

Anatomic Variants

The main variants occur in Sectors 1 and 2.

Superior Region, or Sector 1

This is probably the area with the most anatomic variants. In young subjects, the labrum adheres
strongly to the edge of the glenoid cavity, but with age, a recess develops, although this is not
pathological [5]. It is certainly normal as long as there remains joint cartilage up to the most peripheral
insertion of the labral fibers.

Anterosuperior Region, or Sector 2

Here again there are many anatomic variants, more or less related to age. Normally, the labrum is
rounded, and mobile with respect to the edge of the Glenoid Cavity (Sublabral or Weitbrecht's
Foramen).

The most frequent variants are:

Free (13.5%) or no labrum

Narrow, “Cord-like” Middle Glenohumeral Ligament in continuity with the Biceps Footplate (Buford
Complex) (12%) [6].

Biomechanics

The labrum has several functions, and 3 in particular:

Increases the contact area between humeral head and scapula, by 2 mm Antero-posteriorly and 4.5 mm
Supero-inferiorly;

Contributes to the “Viscoelastic Piston” effect, maintaining -32 mmHg intra-articular negative pressure;
this is especially effective against traction stress and, to a lesser extent, against shear stress;

Provides insertion for stabilizing structures (Capsule and Glenohumeral Ligaments), as a fibrous
“crossroad”. Labrum and ligaments are in synergy in a genuine complex, each structure's contribution
varying with the position of the limb: in abduction and external rotation (ABER), the Inferior
Glenohumeral Ligament (IGHL) absorbs 51% of the stress, the Superior Glenohumeral Ligament (SGHL)
22% and the Middle Glenohumeral Ligament (MGHL) 9% .[7]

Assessment

The ability to predict the presence of a glenoid labral tear by physical examination was compared with
that of magnetic resonance imaging (conventional and arthro gram) and confirmed with arthroscopy.
There were 37 men and 17 women (average age, 34 years) in the study group. Of this group, 64% were
throwing athletes and 61% recalled specific traumatic events. Clinical assessment included history with
specific attention to pain with overhead activities, clicking, and instances of shoulder instability. Physical
examination included the apprehension, relocation, load and shift, inferior sulcus sign, and crank tests.
Shoulder arthroscopy confirmed labral tears in 41 patients (76%). Magnetic resonance imaging
produced a sensitivity of 59% and a specificity of 85%. Physical examination yielded a sensitivity of 90%
and a specificity of 85%. Physical examination is more accurate in predicting glenoid labral tears than
magnetic resonance imaging. In this era of cost con tainment, completing the diagnostic workup in the
clinic without expensive ancillary studies allows the patient's care to proceed in the most timely and
economic fashion.[8]

The different lesions of the glenoid labrum are described. They may involve the antero-inferior, the
posterior or the superior (SLAP lesions) part of the labrum. CT-arthrography is the gold standard imaging
modality in this field of shoulder abnormalities.[9]

Epidemiology

The term SLAP ("superior labrum anterior posterior") was initially coined by Snyder and his colleagues
while performing a retrospective review of a large sample of shoulder arthroscopies [10]. While the true
overall incidence of SLAP tears is unknown, the incidence among patients undergoing arthroscopy is
reported to be between 6 and 26 percent [11].
Classification

Four types of SLAP injuries were described initially:

Type I demonstrated degenerative fraying with intact biceps insertion

Type II, detachment of the biceps insertion

Type III, a bucket-handle tear with intact biceps tendon attachment to bone

Type IV, an intrasubstance tear of the biceps tendon with bucket-handle tear of the superior labrum

Risk Factors

In a prospective observational study of 544 consecutive shoulder arthroscopies that included 139 SLAP
tears, different tear types were associated with particular conditions or activities. Type I tears were
associated with increased age, rotator cuff disease, and osteoarthritis; Type II tears were associated with
overhead sports; and Type III and IV tears were associated with high-demand occupations . The authors
of the study did not define high-demand occupations or speculate why such occupations were
associated with Type III or IV lesions, as few such injuries were identified in the study.

Mechanisms of Injury

Given these associations, different types of SLAP injuries likely involve different mechanisms of injury.
According to a retrospective review of 84 arthroscopically diagnosed labral tears, the most common
mechanism involved an inferior traction-type injury either from a fall or a sudden pull when lifting a
heavy object[12] . Other common mechanisms included traumatic glenohumeral dislocation or
repetitive shoulder abduction and external rotation (eg, throwers and other overhead athletes). A direct
blow to the shoulder or a fall onto an outstretched hand may also cause a SLAP tear. A predisposition to
sustaining certain types of SLAP injuries may stem from underlying shoulder comorbidities, such as
multidirectional instability or chronic degenerative changes.

According to some researchers, the "peel-back" mechanism accounts for Type II labral injuries [13]. In
this mechanism, excessive stress on the biceps tendon attachment when the shoulder is placed in
abduction and maximal external rotation leads to separation and tearing of the superior posterior
labrum from the glenoid. Overhead throwing athletes (eg, baseball pitchers, cricket bowlers) and
laborers who swing tools overhead frequently assume this position.

During repetitive overhead motions that involve abduction to 90 degrees and maximal external rotation,
increases in external rotation range can be seen over time. Often, this increase is associated with a loss
of internal rotation, a pattern termed glenohumeral internal rotation deficit (GIRD) [14]. While it
remains unclear how GIRD develops, it can lead to tightening of the posterior capsule, which in turn
changes the translational mechanics of the humeral head within the glenoid. These changes can lead to
internal impingement and posterior labral injury.[15]

Treatment

Postoperative Treatment and Results

Typically requires six months and often as long as 12 months to return to throwing after surgical repair
of a SLAP lesion. Healing must not be rushed. The patient should work through the appropriate stages of
rehabilitation gradually and clinicians must guard against the patient progressing prematurely. Given the
complexity and importance of post-operative rehabilitation, patients are best served by participating in
a rehabilitation program under the supervision of a knowledgeable physical therapist, athletic trainer, or
comparable clinician.

The post-operative rehabilitation program is typically divided into three stages:

Phase 1 Maximal protection phase (approximately six weeks duration)

Phase 2 Moderate protection phase (approximately six weeks duration)

Phase 3 Minimum protection phase (approximately 14 weeks duration)

Phase 1 Maximal Protection Phase

The maximal protection phase begins the day after surgery until around six weeks. During this phase the
primary goal is to protect the surgical repair from re-injury and to minimize pain and inflammation. The
patient is typically in a sling for the full six weeks; avoiding any motion that loads the biceps tendon is
critical. The patient begins to perform passive and active assisted range of motion (ROM) exercises
during this phase but these are limited. Protected motion begins with passive motion below 90 degrees
of shoulder flexion and abduction, and progresses gradually after the first two weeks. Limited active
motion is introduced gradually. Toward the end of this stage, the patient begins to perform some basic
isometric strength exercises.

Phase 2 Moderate Protection Phase

The moderate protection phase begins at approximately week seven and continues through week 12.
During this phase, one major goal is to regain full active range of motion. Around week 10, active loading
of the biceps tendon can begin. If full ROM is not obtained with the basic program, additional focused
stretching and mobilization exercises may be required. Increasing levels of resistance are used for
scapular and rotator cuff exercises. Exercises for developing core strength are performed during this
phase.
Phase 3 Minimum Protection Phase

The minimum protection phase begins at approximately week 13 and continues through week 26.
During this phase, the patient may gradually resume throwing or overhead occupational activities until
full function is restored. Throwing from a mound may begin around 24 to 28 weeks after surgery in most
cases. It is critical that full shoulder mobility is achieved. Full strength and motion of the scapular
stabilizers and rotator cuff muscles should be achieved before full activity is resumed. To prevent
reinjury, it is important that a pitcher’s throwing mechanics be assessed and any problems resolved, and
that appropriate guidelines regarding the type and number of pitches thrown be followed .

For the patient who follows up with a primary care or sports medicine physician, failure to progress
through the phases in a reasonable time frame (approximately three months for phases 1 or 2 and six
months for phase 3) merits consultation with the orthopedic surgeon who completed the repair.
Similarly, if the patient develops unexpected pain or dysfunction during the post-operative
rehabilitation, the patient should return to their orthopedic surgeon for evaluation. The surgeon should
have the final say about whether the patient is ready to resume full activity.

A systematic review of studies of the management of Type 2 SLAP tears (506 patients included) found
that 83 percent of patients reported good-to-excellent results following operative repair . However, only
73 percent of patients returned to their prior level of function, while only 63 percent of overhead
throwing athletes returned to their previous level of play. Should primary repair fail, biceps tenodesis
often relieves pain. About 40 percent of patients report an excellent outcome with this surgery, while
approximately 4 percent experience significant complications . Common long-term disabilities after a
failed surgical repair include pain and instability with overhead or abducted and externally rotated
shoulder positions. It is unclear whether SLAP tears increase the risk for glenohumeral osteoarthritis.[16]

Related articles

SLAP Lesion - Physiopedia

Definition/Description A SLAP tear or SLAP lesion is an injury to the glenoid labrum (fibrocartilaginous
rim attached around the margin of the glenoid cavity). Tears of the superior labrum near to the origin of
the long head of biceps were first described among throwing athletes by Andrews in 1985.[1]The label
of ‘SLAP’, an abbreviation for superior labrum anterior and posterior, was coined by Snyder et al, who
went on to create a classification system for these lesions.[2] A total of four types of superior labral
lesions involving the biceps anchor have been identified. Type I concerns degenerative fraying with no
detachment of the biceps insertion. Type II is the most common type and represents a detachment of
the superior labrum and biceps from the glenoid rim. Type III represents a bucket-handle tear of the
labrum with an intact biceps tendon insertion to the bone. Finally, type IV lesions, the least common
type represents an intra-substance tear of the biceps tendon with a bucket-handle tear of the superior
aspect of the labrum.[3] The Type II SLAP lesions have been further divided into three subtypes
depending on whether the detachment of the labrum involves the anterior aspect of the labrum alone,
the posterior aspect alone, or both aspects. The above classification system has been expanded to
include an additional three types:[3] Type V: a Bankart lesion that extends superiorly to include a Type II
SLAP lesion. Type VI: an unstable flap tear of the labrum in conjunction with a biceps tendon separation.
Type VII: a superior labrum and biceps tendon separation that extends anteriorly, inferior to the middle
glenohumeral ligament.[3] Recently Nord and Ryu have added several previously unclassified lesions to
the classification scheme. A Type VIII SLAP lesion is a SLAP extension along the posterior glenoid labrum
as far as 6 o’clock. A Type IX lesion is a pan-labral SLAP injury extending the entire circumference of the
glenoid. A Type X lesion is a superior labral tear associated with posterior-inferior labral tear (reverse
bankart lesion ).[4] Clinically Relevant Anatomy The shoulder complex is one of the most sophisticated
areas of the body. The shoulder is made up of five joints; the Acromioclavicular Joint, the
Sternoclavicular Joint, the Glenohumeral Joint, Scapulothoracic Joint and Suprahumeral Joint and four
linked bone groups; the clavicula, sternum, Scapula and the humerus which are related and work
together.[5] The major joint is the Glenohumeral Joint, which is also called the ‘ball in a socket’ joint
because of the humeral head (ball) that articulates with the glenoid cavity (glenoid fossa of scapula or
socket).[5]But the humeral head is larger than the fossa and so the socket covers only a quarter of the
humeral head.[6][5] A circumflexial rim of fibrocartilaginous tissue called labrum glenoidalis firmly
attaches to the glenoid fossa thereby increasing the articular surface area and the stabilisation of the
glenohumeral joint.[5][7] The long arm of the biceps inserts directly into the superior labrum, which also
provides stabilisation to the superior part of the joint.[4][6]In addition, the rotator_Cuff muscles are
essential to ensure dynamic shoulder stability as they prevent excessive translations of the humeral
head at the level of the glenoid fossa.[8] Important variations in the normal anatomy of the labrum have
been identified. Three distinct variations occur in over 10% of patients: An isolated sublabral foramen, A
sublabral foramen with a cord-like middle glenohumeral ligament A cordlike middle glenohumeral
ligament without tissue at the anterosuperior labrum. The identification of these normal variants can
help to prevent the misdiagnosis of labral lesions.[4] Epidemiology/Aetiology The age of the patient has
an impact on the superior labrum. From the average age of 35, the superior labrum is less firmly
attached to the glenoid than in people under the age of 30. In the age category 30 to 50, there are more
chances of tears/defects in the superior and anterior-superior regions of the labrum (noted in cadavers).
In the age category 60 years or older, circumferential lesions have been identified. Thus, we can
conclude that there is an age-related effect in which the older the patient is, the more likely he will incur
a SLAP lesion, due to age-related changes.[7] In one study, half of the cases that had a SLAP lesion were
40 years old patients who showed signs and symptoms of instability after a history of acute trauma,
repetitive injury, fall on an outstretched arm, or an injury from heavy lifting. Most of them had a type II
SLAP lesion. They also noticed that the type II SLAP lesions in patients under 40 were associated with a
bankart_lesion , other than a type II SLAP lesion in patients under 40 years old, whose SLAP lesion were
associated with a tear of the supraspinatus tendon and osteoarthritis of the humeral head.[4] There are
a lot of different mechanisms of injury that can result in a SLAP lesion. The following causes have been
found: repetitive throwing, hyperextension, a fall on an outstretched arm, heavy lifting, direct trauma.
The two most common mechanisms are falling on an outstretched arm in which there is a superior
compression, and a traction injury in the inferior direction.[4] Falling on an outstretched arm is an acute
traumatic superior compression force to the shoulder. In this situation the shoulder is abducted and
slightly forward-flexed at the time of the impact. A subsequent study found that the most common
mechanism of injury was a fall or direct blow to the shoulder, occurring in 31% of patients. A significant
number of patients with superior glenoid lesions and concomitant impingement or rotator cuff disease
in the absence of trauma has also been identified. Indeed, Snyder et al found partial-thickness or full-
thickness rotator cuff disease in 55 (40%) of 140 patients with SLAP lesions. Superior migration of the
humeral head can result from a rotator cuff that is not effectively performing its role as a humeral head
depressor. The superior labrum and biceps anchor could theoretically be gradually lifted off the glenoid
as a result of chronic repetitive superior translation of the humeral head on the glenoid rim. Other
authors supported the theory of an inferior traction mechanism on the basis of a sudden, traumatic,
inferior pull on the arm or repetitive microtrauma from overhead sports activity with associated
instability.[9] Throwers can have repetitive microtraumata. At the moment of the impact the
glenohumeral contact point is shifted posterosuperiorly and increased shear forces are placed on the
posterior-superior labrum, which results in a peel-back effect and eventually in a SLAP lesion.[4] Clinical
Presentation The most common complaint in patients that present with SLAP lesions is pain. Pain is
typically intermittent and often associated with overhead movements.[10]Isolated SLAP lesions are
uncommon.[11]The majority of patients with SLAP lesions will also complain of: sensations of painful
clicking and/or popping with shoulder movement loss of glenohumeral internal rotation range of motion
pain with overhead motions loss of rotator cuff muscular strength and endurance loss of scapular
stabiliser muscle strength and endurance inability to lie on the affected shoulder[12] Athletes
performing overhead movements, especially pitchers, may develop “dead arm” syndrome in which they
have a painful shoulder with throwing and can no longer throw with pre-injury velocity.[13]They may
also report a loss of velocity and accuracy along with discomfort in the shoulder.[12] It is important to
keep in mind that the scapula is an important factor during shoulder movements. When the scapula
does not perform its action properly there is a scapular malposition. This decreases the normal shoulder
function.[14][13]It changes the activation of the scapular stabilising muscles. , which are the serratus
anterior, rhomboid major and minor, levator scapulae and trapezius. The rotator-cuff muscles are
important as well to anchor the scapula and guide the movement.[14][15] Differential Diagnosis The
glenoid labrum is often involved in shoulder pathology. Sometimes morphological varieties can be
confused with pathological aspects and therefore diagnosis should be established following careful
analysis of the case history and a physical examination.[16]There are two regions where anatomic
variants can appear: the superior region, where it’s mostly related to age, and the anterosuperior
region, where sometimes there is no labrum (12%) or a cord like ligament that is in continuity with the
biceps footplate (13,5%).[16] SLAP tear itself accounts for 80–90% of labral pathology in stable shoulder
but it’s only found in 6% on arthroscopy. SLAP lesions are often seen in combination with other shoulder
problems and this makes it difficult to diagnose.[17]SLAP lesion is mostly combined with a lesion of the
proximal head of the biceps because it attaches on the superior part of the labrum glenoidalis. It is
associated with pain and instability and an inability of the patient to perform overhead movements.[16]
According to William F.B., SLAP lesions had an association of 43% with the medial sheath lesion. the
author postulates that forces that affect the biceps anchor may also damage the pulley system of the
bicipital sheath and, as such, this anatomic structure should be evaluated, especially when SLAP lesions
are present.[18] Beside biceps tears, other problems, such as bursitis and rotator cuff tears, are often
identified. In combination with SLAP lesions,[19] According to Morgan CD et al., Rotator cuff tears were
present in 31% of patients whit SLAP lesion and were found to be lesion-location specific.[20] Also
suprascapular neuropathy secondary to cyst compression in the spinoglenoid notch may occur in
association with SLAP tears. Diagnostic Procedures SLAP lesions are difficult to diagnose as they are very
similar to those of instability and rotator cuff disorders. At first the clinician can test the tenderness to
palpation at the rotator interval which can be helpful in the diagnostic procedure. The rotator interval is
an anatomic space between the Supraspinatus tendon, the Subscapularis tendon and the processus
coracoideus. This rotator interval has a triangular shape in which the supraspinatus is superiorly located,
the subscapularis inferiorly and the processus coracoideus medially. It contains the coracohumeral and
the superior glenohumeral ligament, the biceps tendon and the anterior joint capsule. If you know
where these structures are situated, you can try to palpate the rotator interval.[21] This can be followed
by these tests that are positive when there is a presence of a SLAP lesion: positive anterior drawer
(53%), positive apprehension at 90° of abduction and maximal external rotation (86%), and positive
relocation test (86%).[4] In addition, several special tests can be used to help identify the presence of a
SLAP lesion including the Clunk test, the crank test, O’ Briens, Anterior Slide test, Biceps Load I and II
test, and the Active Compression test.[4] Another very important diagnostic element is the use of clear
radiological and arthroscopic images of the labrum, which can help clinicians to distinguish the
pathology from normal variation and make the correct diagnosis. MRI is the most common imaging tool
used to diagnose labral lesions, although it may not show a SLAP lesion. Therefore an MR arthrogram,
where a contrast material gets injected into the shoulder, is also used. This is able to detect a SLAP tear
better than a normal MRI scan.[22] Thus, MRA is more useful than conventional MRI and CT
arthrography, and is a helpful technique in the diagnosis of SLAP tears. However, there is a great chance
of false positive results due to a superior labral recess or sulcus, which is a normal variant, but can make
the diagnosis more difficult.[23] To describe the efficiency of MRA, several studies established the
accuracy, specificity and sensitivity of MRA. Within every aspect the lowest and highest obtained
numbers are described: - Sensitivity (%): 82 – 95.6 - Specificity (%): 69 – 98 - Accuracy (%): 74 -90.19[24]
Outcome Measures Rowe Score (version of 1988): consists of 5 domains: pain stability function motion
muscle strength Scoring: < or = 49 = poor 50 - 69 =fair 70 - 84 = good 85 - 100 = excellent[25][26] Oxford
Instability Shoulder Score (OISS): 12-item questionnaire measuring: daily activities pain The total score
ranges from 12 to 60 (12 indicates the best possible function)[25][27]. A link to the questionnaire is
added to the resources list below. Western Ontario Shoulder Instability Index (WOSI): 21-item
questionnaire with a visual analogue scale covering four domains: physical symptoms (10 items) sports,
recreation, and work (4 items) lifestyle (4 items) emotions (3 items) The responses for each question are
given on a scale from 0 to 100 (0 equals the best possible score and 100 equals the worst).[25][28] A link
to the questionnaire is added to the resources list below. EuroQol (EQ-5D and EQ-VAS): EQ-5D covers
five domains: mobility self-care usual activities pain/discomfort anxiety/depression EQ-VAS is a Visual
Analogue Scale to measure the current health state, ranging from 0 (worst health state) to 100 (best
health state).[25] A link to the questionnaire is added to the resources list below. According to Skare et
al (2014) the OISS, WOSI and the Rowe score are responsive in the evaluation of patients with SLAP
lesions. They also documented that the OISS and Rowe score appear to be the most sensitive
measures.[25] Examination Clinical examination to detect SLAP lesions is an extremely challenging
procedure because the condition is frequently associated with other shoulder pathologies in patients
presenting this type of condition.[10][14] As with most shoulder conditions, the history including the
exact mechanism of injury should be documented.[10][12][14] It is important to keep in mind that while
labral pathologies are frequently caused by overuse, the patient may also describe a single traumatic
event.[10] The physical examination is also very important in determining the correct diagnosis[12],
however physical examination should not be used in isolation because the literature does not confirm
that special tests can accurately identify SLAP lesions. There are numerous physical examination
procedures described to detect the SLAP lesion: Biceps load test II[10][12][14] O’Brien test[10][12][14]
Anterior apprehension test[12] Speeds Testt[12][14] Yergason’s test[12][29] Compression rotation
test[12] Dynamic labral shear test[11][14] A combination of 2 sensitive tests and 1 specific test is more
efficient to diagnose a SLAP lesion [reference needed]. The therapist can choose the 2 sensitive tests out
of the following 3: Compression rotation test O’Brien test Anterior apprehension test For the specific
test, the therapist may choose out of the 3 following: Speed’s test Yergason’s test Biceps load test
II[12][30] If one of the three tests is positive, this will result in a sensitivity of about 75%. But if all three
tests are positive this will result in a specificity of about 90%.[12] When we consider some tests
individually, one can consider the Speed’s test and O’Brien’s test helpful in the diagnosis of anterior
lesions and the Jobes Relocation Test is often positive in a posterior lesion[4][31] According to Meserve
et al, the O’Brien test is the most sensitive test (47%-78%) and the Speed’s test the most specific (67%-
99%).[12] There are studies who combined few of the tests but the data differ too much therefore it’s
difficult to make a general conclusion.[12][14][32] There is a lot of discussion about which test is most
accurate, but most experts consider that arthroscopy is the best way to diagnose SLAP lesion.[11]
Medical Management The surgical intervention depends on the type of labral lesion, but an advanced
arthroscopic technique is most commonly used. Studies of surgical labral repairs show that they are
generally good to excellent to allow the patient to return to a pre-injury level of function. Knowing the
type of SLAP lesion is important for post-operative rehabilitation.[14] Type I: are treated with
debridement. Straightforward arthroscopic shaving, without damaging the biceps anchor, is enough for
the surgical treatment of this type of lesion.[14] Type II: can be treated with arthroscopic fixation of the
superior labrum to establish biceps anchor stability. The major studies suggested an extremely high level
of success in arthroscopic repairs. According to Morgan et al, 97% of patients who underwent
arthroscopic repair of type II SLAP had good, and even excellent results. But clinical results of elite
throwing athletes has shown that this is in fact not always the case.[14]Detachment of the superior
labrum from the glenoid is recognised as a problematic injury in throwing athletes and others who
engage in repetitive overhead activities. Luckily for these athletes, Samani JE et al., concluded that using
an absorbable tack to repair type II SLAP lesions is an effective treatment, even in athletes with high
demands and expectations for shoulder function.[33] For patients older than 36 years there is a higher
chance of failure.[34]Because of unsatisfactory results in older patients, Boileau et al., suggested
arthroscopic biceps tenodesis in these patients. They found that tenodesis is superior to the repair of
type II SLAP tears in older population. Arthroscopic biceps tenodesis can be considered as an effective
alternative to the repair of a type II SLAP lesion, allowing patients to return to a pre-surgical level of
activity and sports participation. The results of biceps reinsertion are disappointing compared with
biceps tenodesis. Furthermore, biceps tenodesis may provide a viable alternative for the salvage of a
failed SLAP repair.[29] However in another study by Alpert et al., it is shown that type II SLAP repairs
using suture anchors can yield good to excellent results in patients older and younger than age 40. Their
findings show no difference between the two age groups. So there are conflicting views in the literature
about the repairs in the older patients.[35] Type III: can easily be debrided by an arthroscopic shaver.
There is no need to repair this type of injury. After the resection of the free fragment, a pain free
shoulder can be established.[36] Type IV: can be repaired with multiple sutures. Field and Savoie
reported 100% good results at an average follow-up of 21 months. Also Pagnani et al., reported that
superior glenoid lesions with unstable biceps anchors (type IV lesions), which were stabilised with
absorbable tacks obtained good results. At their 2-year follow-up, 86% of the patients had satisfactory
results, and no complications were related to use of the tack. Stetson et al., presented the long-term
results of 140 SLAP lesions with follow-up available on 130 patients at an average of 3.2 years. Type IV
lesions in 17 patients (13%) were debrided.[37] SLAP lesions are repaired by the use of portals. There
are different portals: a posterior portal, a anteroinferior portal and a mid-glenoid portal. Similarly,
O'Brien described the creation of a trans-rotator cuff portal for repair when the lesion is posterior to the
biceps tendon, and Burkhart has advocated the use of a posterolateral portal (Port of Wilmington) as
part of a SLAP repair. More recently, Nord et al. described the use of the Neviaser portal, a superior
medial portal, as the working portal in SLAP repairs. There is no specific portal used for each type a SLAP
lesion. The use of a certain portal is determined by a combination of location and the surgeon’s
preference.[38] Physical Therapy Management Until now only one study looked at results from physical
management on SLAP lesion. The study was a one year follow- up study of with 19 patients. It compared
good shoulder function with the shoulder function of patient that followed successful conservative
management in the form of scapular stabilization exercises and posterior capsular stretching. However
the study acknowledges that more than half of the treatment of patients who were initially prescribed
non operative management failed and these patients went on to undergo arthroscopic surgery.[39] It is
generally recognized that the majority of patients with symptomatic SLAP lesions will fail conservative
management, particularly throwers.[3]Given that conservative management only seems to be successful
in a few patients, mainly in type I SLAP lesions, it is only implemented in patients with this type of lesion
or patients who do not wish to undergo surgery.[3] In the first step of conservative management,
patients should abstain from aggravating activities in order to provide relief to the pain and
inflammation. If necessary, NSAID’s and intra-articular corticosteroid injections can be applied to help
diminish complaints.[3][39]This way, physical treatment can be started sooner. Strength, stability and
motion are the components of shoulder function that should be focused on during
rehabilitation.[40]This course of treatment should focus on restoring strength of the rotator cuff,
shoulder girdle, trunk, core and scapular musculature, restoring normal shoulder motion, and training to
improve dynamic joint stability.[3] Regaining GIRD is a crucial aspect in the rehabilitation of SLAP
lesions.[3]By the use of posterior capsule stretching exercises, such as sleeper stretch and cross body
adduction stretches, and exercises for scapula stabilisation, redevelopment of the internal rotation can
be accomplished.[39][41] By stretching the posterior capsule and restoring internal rotation, through
posterior capsule stretching exercises, such as sleeper stretch and cross body adduction stretches, and
exercises for scapula stabilisation , pathologic contact between the supraspinatus tendon and the
posterosuperior labrum.[39][41]can be prevented. The patient is eventually advanced to a
strengthening phase, which includes trunk, core, rotator cuff, and scapular musculature. In throwing
athletes, a progressive throwing program that is directed toward the patients' specific sport and position
can be initiated after 3 months.[3] Sixteen commonly used shoulder rehabilitation exercises can be
chosen on the basis of several EMG studies and clinical recommendations regarding the rehabilitation of
patients with SLAP lesions. These exercises are: forward flexion in a side-lying position prone extension
seated rowing serratus punch (protraction with the elbow extended) knee push-up plus forward flexion
in external rotation and forearm supination full can (elevation in the scapular plane in external rotation
internal rotation in 20° of abduction external rotation in 20° of abduction internal rotation in 90° of
abduction external rotation in 90° of abduction forearm supination, elbow flexion in forearm supination
uppercut (combined forward flexion of the shoulder and flexion and supination of the elbow) internal
rotation diagonal external rotation diagonal These exercises, with increasing low to moderate activity,
can be applied in the early and intermediate phases of nonoperative and postoperative treatment for
patients with proximal biceps tendon disorders and SLAP lesions.[42] When conservative treatment fails,
a surgical approach is in order.[3] After surgery, for 3 to 4 weeks, the shoulder of the patient is placed in
a sling, which immobilises the shoulder in internal rotation and leads to general loss of motion and
stiffness.[3][11]Postoperative rehabilitation is determined by the type of SLAP lesion, the chosen
surgical procedure and other concomitant pathologies and procedures performed.[3] Generally
pendulum and elbow range-of-motion exercises are allowed during the period of immobilization.
External rotation must absolutely be avoided and abduction limited to 60°. Assisted and passive
techniques are used at 4 weeks post-operative to increase shoulder mobility. Between week 4 and 8,
internal and external rotation ROM are progressively increased to 90° of shoulder abduction. Resistance
exercises can be initiated at approximately 8 weeks post-operative, in which scapular strengthening
should be emphasized. Since the metabolism of cartilage depends partly on its mechanical environment,
resistance training can contribute to gaining mobility. However, the achievement of adequate shoulder
mobility is an important condition to begin resistance training. At month 4 to 6, dependent on the type
of sport practiced, patients should be able to start sport-specific training and gradually return to their
former level of activity.[3] SLAP lesion repair often fails, and biceps tenodesis or tenotomy seems to be
an acceptable alternative treatment for SLAP lesions. Furthermore, this technique has now become the
most preferable treatment for failed SLAP repairs.[43]The indications for biceps tenodesis as the index
procedure for a symptomatic SLAP lesion depends on: the patient’s age activity level arm dominance
type of sport.[11] If a biceps tenodesis is performed a minimum of 10 weeks is recommended without
biceps activity to allow the repaired soft tissue to fully incorporate into the bone tunnels.[12] Resources
Clinical bottom line SLAP lesions are lesions of the superior labrum in which there are several types
described. A SLAP lesion is mainly caused by a fall on an outstretched arm where there is an important
superior compression on the labrum which causes a tear of the labrum. A typical symptom is
intermittent pain that also occurs in overhead movements. To diagnose this condition it is important to
use several different tests and not only one. Physical examination is not easy because of the fact that
SLAP lesions are often associated with other shoulder pathologies. For the physical examination the
therapist uses the tests described in ‘Diagnostic Procedures’, but apart from that he can also test the
glenohumeral and scapulothracic range of motion because there could occur a dyskinesis caused by the
SLAP lesion. For the treatment of SLAP lesion one uses often a medical treatment where the surgeon
uses advanced arthroscopic techniques. But a physical treatment is also possible. This includes
stretching, strengthening, and stabilisation exercises. It is important to note that every treatment
depends on the type of the SLAP lesion and that conservative treatment may fail and is not suited to
every patient.

Internal Impingement of the Shoulder - Physiopedia

Introduction Internal impingement is commonly described as a condition characterized by excessive or

repetitive contact between the posterior aspect of the greater tuberosity of the humeral head and the
posterior-superior aspect of the glenoid border when the arm is placed in extreme ranges of abduction
and external rotation.[1][2][3][4]This ultimately leads to impingement of the rotator cuff tendons
(supraspinatus/infraspinatus) and the glenoid labrum. There are two types of internal impingement:
anterosuperior and posterosuperior. Anterosuperior impingement occurs only rarely.[5] Clinically
Relevant Anatomy The scapula is a flat blade lying along the thoracic wall. Because of the wide and thin
configuration, it’s possible for the scapula to glide smoothly on the thoracic wall and provides a large
surface area for muscle attachments, both distally and proximally.[6] The coracoacromial arch and the
subacromial elements are important elements of anatomy related to internal impingement. As the
name implies, the coracoacromial arch is formed by the coracoid and the acromion processes and the
connecting coracoacromial ligaments. It protects the humeral head and subacromial structures from
direct trauma and superior dislocation of the humeral head. Impingement may occur when the rotator
cuff and other subacromial structures become encroached between the greater tuberosity and the
coracoacromial arch. The tendons of the rotator cuff are: Subscapularis tendon (anterior) Supraspinatus
tendon (superior) Infraspinatus tendon (posterior) Teres minor tendon (posterior) The rotatorcuff
stabililizes the shoulder against the action of the prime movers to prevent excessive anterior, posterior,
superior, or inferior humeral head translation.[7] The rotator cuff tear is located on the articular side of
the rotator cuff, typically at the intersection of the infraspinatus and supraspinatus insertions onto the
humeral head[3]. The scapulothoracic articulation is a prime example of dynamic stability of the human
body. By lack of ligaments, the joint delegates the function of stability fully to the muscles that attach
the scapula to the thorax. So their proper function is essential to the normal biomechanics of the
shoulder. These muscles include: Serratus anterior Trapezius Levator scapula Rhomboid major
Rhomboid minor Latissimus dorsi Pectoralis major and minor Supraspinatus and Infraspinatus The
serratus anterior and the trapezius has been suggested to be the most important muscles acting upon
the scapulothoracic articulation.[7] Epidemiology The incidence of internal impingement is unknown
due to the variety of associated pathologic lesions and diagnostic difficulty.[8]The majority of patients
who have been identified as having internal impingement are overhead athletes or throwing athletes
(tennis, volleyball players, and swimmers ).[5] These patients participate in activities requiring repetitive
external rotation and (hyper) abduction.[8]The majority of the research on internal impingement has
been done on elite baseball players. However, non-elite athletes, as well as non-athletes may also be
affected by internal impingement.[1] With the non-elite athletic population, it is important to realize
that older patients are more likely to have concurrent shoulder conditions.[1] Since internal
impingement is often involved with other pathology of the shoulder the incidence of it in isolation has
not been established. Aetiology The understanding of the etiology behind internal impingement has
gradually evolved but remains incomplete. The lack of a common biomechanical model is largely due to
the limited patient population in which the syndrome is seen in as well as the thousands of associated
pathologic findings that have been reported. Impingement has been described as a group of symptoms
rather than a specific diagnosis.[5]In this current opinion, it is thought that numerous underlying
pathologies may cause impingement symptoms. Glenohumeral instability[9], rotator cuff or biceps
pathology[1], scapular dyskinesis[6][10] [11], SLAP lesions and glenohumeral internal rotation deficit
have been associated with impingement symptoms in the clinical literature.[12] In general, two
pathological mechanisms in the possible aetiology of internal impingement have been described:
excessive humeral translations, compromising glenohumeral congruence, scapular dyskinesis,
decreasing the quality of functional scapular stability.[1][13][14] Anterior GH instability: Jobe et al.
hypothesized that anterior instability/laxity of the shoulder complex caused by repetitive stretching of
the anterior GH capsule led to this type of impingement in throwing athletes. This laxity allows for
increased anterior humeral head translation.[1]This type of acquired instability is often referred to as
acquired instability overuse syndrome (AIOS).[15] Tight posterior GH capsule: The posterior-inferior GH
joint capsule is hypothesized to become hypertrophied in the follow-through tensile motion of
throwing.[16]The tightness of the posterior capsule and the muscle tendon unit of the posterior rotator
cuff is believed to limit internal joint rotation.[12] Posterior capsule tightness leads to GIRD
(glenohumeral internal rotation deficit).[13][14] Burkhart[12] et al. defined GIRD as a loss of internal
rotation of >20° compared with the contralateral side. When the posterior structures of the
glenohumeral joint are shortened, this may compromise the hammock function of the inferior
glenohumeral ligament (IGHL), and increase the risk for impingement symptoms during throwing.
Muscle imbalance and/or improper neuromuscular control of the shoulder complex: Jobe et al. also
reported that malpositioning of the arm relative to the glenoid bone during throwing motions can also
lead to impingement of the rotator cuff tendons between the glenolabral complex and the humeral
head.[1] Fatigue and/or weakness of the scapular retractors have been shown to cause a decreased
force production in all four of the rotator cuff muscles, which would also lead to abnormal positioning of
the GH joint.[17][18] At the base of this abnormal scapular positioning lies the lack of neuromuscular
control of the periscapular musculature as well as muscle imbalances between the rotator cuff and
upward rotators of the scapula (serratus anterior, upper trap, lower trap). Clinical Presentation The
diagnosis of internal impingement based on history alone is extremely difficult, and symptoms tend to
be variable and fairly nonspecific. [1] A review of the literature does show several common symptoms
that most internal impingement patients seem to share. Internal Impingement patients present with any
of the following: Posterior Shoulder Pain Chronic - diffuse posterior shoulder girdle pain is the chief
complaint in the throwing athletes with internal impingement, but the pain may also be localised to the
joint line.[1] The patient may describe the onset of posterior shoulder pain, particularly during the late-
cocking phase of throwing, when the arm is in 90° of abduction and full external rotation.[2] Acute -
non-throwing athletes, who present with this syndrome, have a chief complaint of acute shoulder pain
following injury Decrease in throwing velocity - a progressive decrease in throwing velocity or loss of
control and performance in the overhead athlete. Dead arm - Some signs of the pathologic process
include a so-called “dead arm,” the feeling of shoulder and arm weakness after throwing, and a
subjective sense of slipping of the shoulder [2] Muscular Asymmetry - Overhead athletes and throwers
in particular often have muscular asymmetry between the dominant and the non-dominant shoulder.
Muscular/Neuromuscular Imbalance – A common finding is muscle imbalances in the shoulder complex
as well as improper neuromuscular control of the scapula. [19] Increased Laxity - A patient with isolated
internal impingement may have an increase in global laxity or an increase in anterior laxity alone of the
dominant shoulder. [3] Anterior Instability - Patients may have instability symptoms, such as
apprehension or the sensation of subluxation with the arm in a position of abduction and external
rotation.[1] Rotator Cuff Pathology - Patients may also present with symptoms similar to those
associated with other rotator cuff pathologies (tears, other impingements). Younger patients with such
symptoms, particularly throwing athletes, should raise the clinician’s index of suspicion for internal
impingement. In fact, some authors have identified internal impingement as the leading cause of rotator
cuff lesions in athletes. [1] A combination of internal derangement-popping, clicking, catching,
sliding[20] Rotator cuff weakness [20] -Rotator cuff is a common name for the group of 4 distinct
muscles (infraspinatus, supraspinatus, teres minor and subscapularis) and their tendons that provide
strength and stability during motion of the shoulder. The four rotator cuff muscles may separately
provide a disturbed muscle balance[21] Jobe Clinical Classification of Internal Impingement
 Jobe
developed a classification scheme to further distinguish between the varying severities of internal
impingement.[2] The Jobe classification system focuses on the primary patient population of overhead
athletes.[4] Stage I (early) : Shoulder stiffness and a prolonged warm-up period; discomfort in throwers
occur in the late-cocking and early acceleration phases of throwing; no pain is reported with activities of
daily living. Stage II (intermediate) : Pain localised to the posterior shoulder in the late-cocking and early
acceleration phases of throwing; pain with activities of daily living and instability are unusual. Stage III
(advanced) : Similar to those in stage II in patients who have not responded to non-operative
treatments. Differential Diagnosis It is important to understand that the common findings for internal
impingement have been found in asymptomatic shoulders so it is key to evaluate the patient's entire
clinical scenario. The patient's age, profession, activity level, symptom severity, degree of disability and
the effects of this condition on their athletic performance need to be part of the clinician's decision
making process. When examination findings are somewhat unremarkable, and when the patient
presents with signs of numerous pathologies, yet do not seem to fit any one pathology exclusively, this
should raise the clinician's suspicion for a case of internal impingement. During the diagnostic process it
is helpful to understand that Internal impingement has a similar presentation to numerous pathologic
shoulder conditions, including but not limited to:[2][3] Partial- or full-thickness rotator cuff tears
Anterior or posterior capsular pathologies SLAP (Superior Labrum Anterior to Posterior) lesion
Subacromial Impingement Glenoid chondral erosion Chondromalacia of the posterosuperior humeral
head Anterior GH instability Biceps tendon lesion Scapular Dysfunction Each of these disorders can exist
alone or as a concomitant pathological condition. Diagnostic Procedures In many situations, the
diagnosis of internal impingement is made through the physical examination along with MRI[22] and
radiographs. Magnetic resonance imaging has been used frequently to diagnose pathologic conditions of
the shoulder. Its sensitivity and specificity for the detection of labral tears and rotator cuff disease are
on the order of ‡95%. Magnetic resonance imaging has the advantage of being able to detect intra-
substance tears that may be difficult to visualize with arthroscopy. The findings of magnetic resonance
imaging of patients with internal impingement are usually more subtle. Findings on magnetic resonance
imaging of patients with internal impingement include mature periosteal bone formation at the scapular
attachment of the posterior aspect of the capsule (The Bennet lesion) and moderate to severe posterior
capsular contracture at the level of the posterior band of the inferior glenohumeral ligament.[3]
Outcome Measures Shoulder Disability Questionnaire (SDQ): The SDQ is a measure covering 16 items
designed to evaluate functional status limitation in patients with shoulder disorders.[23] This
questionnaire is a valid and reliable instrument.[23][24][25] Shoulder Pain and Disability Index (SPADI):
The SPADI developed by Roach et al., consists of a separate 5-item pain scale and an 8-item disability
scale, with the preceding week as the recall frame.[23]The questionnaire was found to have good
internal consistency, test re-test reliability, and criteria and construct validity in a sample of 37 male
outpatients with shoulder complaints.[26][24][25] Shoulder Rating Questionnaire (SRQ): Shoulder Rating
Questionnaire by l'Insalata et al. consists of 19 items with a 5-point ordinal answer scale: 4 relate to
pain, 6 to daily activities, 3 to recreational and athletic activities, 5 to work, and 1 to satisfaction. The
Shoulder Rating Questionnaire also includes a visual analogue scale for global assessment, as well as an
item to indicate the domain of most important improvement.[23][24] Other frequently used
questionnaires to determine the progression of symptoms such as pain, disability and other outcomes=
Simple Shoulder Test (SST) Disabilities of the Arm, Shoulder and Hand (DASH) Constant-Murley Scale
(CMS) Oxford Shoulder Instability Score (OSIS) Examination and Clinical Findings When evaluating a
patient with suspected internal impingement syndrome, it is very important to get a thorough history,
as it is an important element of the clinical diagnosis.[3] However, diagnosing internal impingement on
the history alone is extremely difficult as symptoms tend to be variable and non-consistent.[1] A
thorough, complete examination of the shoulder complex must be done to rule in/out any concomitant
shoulder pathologies. The basic exam Clinical Technique Findings Palpation of the shoulder complex TTP
(tender to palpation) posterior shoulder/joint line Observation of muscle symmetry between shoulders
involved shoulder usually has increased muscle bulk and lies lower than unaffected shoulder abnormal
scapulothoracic rhythm/scapular movement Gross strength testing of the shoulder, rotator cuff, and
scapular retractor/stabilizer muscles weak rotator cuff muscles weak middle/lower trap, rhomboids
weak serratus anterior Joint accessory mobility: GH/ST/AC/SC joints Decreased dorsal glenohumeral
glide posterior capsule tightness Flexibility tests for the shoulder, thoracic, and cervical spine Variable:
General Considerations pec minor/major latissimus dorsi SCM, upper trap, levator scapulae thoracic
rotation/extension ROM: GH/scapulothoracic joints as well as the cervical and thoracic spine as it has
been shown that dysfunction in any of these areas can directly impact the shoulder decreased GH
internal rotation: 10-15 degrees increased GH external rotation: 10-15 degrees SICK Scapula: Burkhart et
al. have reported that scapular protraction is also a common finding in these patients.[1] This is
characterized by Scapular malposition, a prominent Inferior medial border, Coracoid pain, and scapular
dysKinesia, all of which can be picked up in the basic examination during palpation and observation of
the scapula. Tyler et al. reported that scapular retractor muscle fatigue led to an overall decrease in
force production of the rotator cuff muscles as well as the decreased strength of the scapular
stabilizers.[27] Tests for internal impingement Recently, a small number of tests were created to help
rule in/out the presence of internal impingement.[1] Posterior Impingement Sign: Meister et al.
investigated the ability to detect articular-sided rotator cuff tears and posterior labral lesions. They
reported a sensitivity and specificity of 75.5% and 85% respectively, meaning a negative test is
extremely accurate in ruling out posterior rotator cuff tears. A (+) test is indicated by the presence of
deep posterior shoulder pain when the arm is brought into a position of abduction to 90° to 110°,
extension to 10° to 15°, and maximal external rotation.[1] Relocation Test: Jobe and colleagues have
reported this can be used to identify internal impingement. A positive test would be posterior shoulder
pain that was relieved by a posterior directed force on the proximal humerus.[1] But, there is
insufficient evidence upon which to base selection of physical tests for shoulder impingement, and local
lesions of bursa, tendon or labrum that may accompany impingement, in primary care. The large body of
literature revealed extreme diversity in the performance and interpretation of tests, which hinders
synthesis of the evidence and/or clinical applicability.[28] Tests for associated conditions Tests for other
shoulder pathologies may be (+) or (-) due to the variable clinical presentation of internal impingement.
Understand that there is no proven combination of test findings that identify internal impingement.
Subacromial Impingement: Test item cluster Full/partial thickness rotator cuff tears: Test item clusters
SLAP Lesions: Although the validity of physical examination tests used to detect SLAP lesions is
controversial, the fact that these lesions are a common finding with internal impingement warrants the
need to perform at least some combination of the following tests: Active compression test Crank test
Speed's test Biceps load test 11[1] Laxity of the anterior GH joint capsule: The following have proven
diagnostic accuracy: Generally (+) but may be (-) The apprehension test Jobe subluxation/relocation test
Anterior release test Medical Management Conservative management of internal impingement is an
appropriate initial approach, particularly in patients who do not report an acute traumatic event.[2]We
can divide the medical management in non-surgical treatment and surgical treatment. Non-surgical
treatment[2][3][8] Interventions that are recommended in the literature in early disease when the
shoulder is stiff and can be poorly localized are: Rest Ice (cryotherapy) NSAID’s (or other oral-anti-
inflammatory meds) Corticosteroid injection[22] All these interventions will be used in addition to a
structured, supervised physical therapy regimen.[8] Surgical treatment[29] Surgery for internal
impingement may be indicated if improvements have not been seen with a prolonged rehab protocol
specifically designed to correct any impairments, imbalances, deficiencies and/or pathologic findings.
Indications ;[30] Failed nonoperative treatment Partial thickness rotator cuff tear (PASTA-Partial
articular supraspinatus tendon avulsion) compromises the integrity of the rotator cuff Partial rotator
cuff tears >50% Bennett lesion Peel-back labral lesion[31] SLAP lesion Dislocation For the surgical
treatment, we have different approaches: Arthroscopic interventions[1] -It is the preferred type of
surgery. Prior to any surgical procedure, it is highly recommended that a thorough exam under
anesthesia (EUA) is done, as well as a diagnostic arthroscopy. Due to the often-confusing physical
findings that may be associated with internal impingement, the final therapeutic surgical plan should be
aimed at specific pathologic lesions related to patient symptoms that have been identified from an EUA
and diagnostic arthroscopy. It’s recommended that the EUA specifically assess for GH ROM, any kind of
subluxation, as well as a meticulous analysis for the presence of any instability.[1] Subacromial
decompression[32] Debridement of rotator cuff tear[32] Completion of rotator cuff tear by arthroscopic
repair[32] Physical Therapy Management Prevention/Early Management: If an overhead athlete report
feelings of tightness, stiffness, or not loosening up, the pitcher should be removed from participation
and started in a rehab program.[4] It is important, before treatment is undertaken, to rule out other
anterior instability pathology, including SLAP lesions, labral tears, and partial rotator cuff tears.[4]
Strengthening the shoulder: Closed kinetic chain exercises for stabilizing the rotator cuff muscles. GIRD
(Glenohumeral internal rotation deficit)[27] Strengthening program for posterior capsule Muscle
imbalance and/or improper neuromuscular control of the shoulder complex Strengthening periscapular
musculature and the rotator cuff muscles to prevent over-angulation in the late cocking phase of
throwing[4][11][33]. Routine management With early internal impingement, the thrower (the incidence
of glenoid impingement in throwers, especially pitchers, is high) or involved patient reports the shoulder
is stiff and not loosening up as it normally would. Three stages of internal impingement have been
described (Table ).[3] An initial focus on correcting muscle imbalances, instabilities and ROM deficits
before beginning more complex dynamic exercises.[4][5][11] (see Table 1 for protocol) In 2008, Cools, et
al. published guidelines for rehabbing internal impingement in tennis players based on clinical literature
and clinical experience. Parts of these guidelines are backed by evidence, but many of the treatments
discussed have not been validated with medical research, so until that research is conducted these
guidelines may provide a foundational starting point for clinicians treating internal impingement. Realize
that this protocol is geared toward the athletic population. However, it can be applied to the non-
athletic population as well by incorporating activity-specific functional activities instead of sport-specific.
A non-athlete may also not need to progress all the way to phase 3, which will depend on the activity
level they wish to return to. Phase one Soft tissue mobilization such as massage, relaxation, contract-
relax and low-energy, high repetition kinetic training[4] Scapula setting: retraction, elevation,
depression[4] [34] Joint mobilization: oscillation, hold stretch, and scapular side-lying distraction tonic
and phasic muscle coordination[4] Increase shoulder ROM[4] • Decrease posterior capsule tightness[4]
Strengthening to rebuild soft tissue support[4][8][32][35] Neuromuscular re-education to prevent
recurrence[4][19] Restore proper muscle balance and endurance[19] Proprioceptive training and
dynamic stability exercises[19] • Closed chain exercises: are suggested because axial compression
exercises that put stress through the joint in a weight-bearing position result in joint approximation and
improved co-contraction of the rotator cuff muscles.[19] Ultrasound and electrostimulation: for
reducing the pain and inflammation[22] Phase two Improve dynamic stability-restoration muscle
balance:[22] more complex and activity specific exercises. With muscle imbalances already addressed,
the therapist can begin to add dynamic movements into rehab using “tactile cueing” to ensure the
patient is engaging the scapular musculature before beginning a movement. Progress to verbal
cueing.[19] Strengthening exercises: Target all shoulder and scapular musculature. Start introducing
eccentric and open kinetic chain exercises in order to begin preparing for specific athletic overhead
movements.[19][8][32] Mobilisations[19][36][37] Phase three Functional rehabilitation plan: Designed
to prepare the athlete to return to full athletic activity. Strengthening exercises are continued and
plyometrics are initiated using both hands and limiting external rotation at first, progressing to one-
handed drills and gradually working into increasing velocity and resistance. Additional Considerations
Rehabbing the GIRD component: Started immediately upon 1st treatment and continue throughout.
Stretching techniques that focus on increasing posterior shoulder soft tissue flexibility are commonly
incorporated into prevention and treatment programs for the overhead athlete. The cross-body and
sleeper stretch exercises have been described as stretching techniques to improve posterior shoulder
soft tissue flexibility and to increase glenohumeral joint internal rotation and horizontal adduction range
of motion in the overhead athlete.[38]The sleeper stretch is performed with the patient lying on their
injured side with the shoulder in 90° forward flexion, the scapula manually fixed into retraction, while
glenohumeral internal rotation is performed passively. The patient should feel a stretch in the posterior
aspect of the shoulder and not in the anterior portion, if they do, then reducing the intensity and
rotating the trunk slightly backward can reduce the intensity of the stretch. The cross-body stretch is
another popular stretch for the posterior capsule and can be performed by moving the arm into
horizontal adduction. This stretch has been shown to be superior for stretching the posterior capsule
and for increasing internal ROM. [39] Joint mobilizations (mobs): GH anterior-posterior joint mobs can
be used to help stretch the posterior capsule and increase internal rotation, however, if instability is
noted on the initial exam, joint mobs should be avoided. Grade IV, end range, dorsal-glide mobilizations
are performed with the patient supine with shoulder placed into 90 abduction, and either in neutral or
end range internal rotation of the humerus (refer to pictures).[19] Thoracic and cervicothoracic
manipulation: spinal manipulations can be used to improve mobility in these regions and have proven
therapeutic short and long term effects. Several studies have shown a significant improvement in
symptoms of shoulder impingement syndrome when a thoracic manipulation was combined with
exercise. The benefits of a thoracic or cervicothoracic manipulation for internal impingement have yet to
be studied, but based on the similar presentation of these two syndromes and the low-risk to benefit
ratio of manipulation, these procedures may add a huge benefit to treatment. [33] [40] Whole body
kinetic chain exercises: Incorporating this early in rehab has been recommended in order to prepare the
athlete's whole body for return to activity. Core stability, leg balance, and diagonal movement patterns
can be used to incorporate the entire kinetic chain while simultaneously involving the shoulder as well.
One example of this is simply adding a degree of instability to an exercise; doing external rotation
exercises while sitting on an exercise ball or while performing a single leg stance by standing on the
opposite leg of the arm you are working.[19] Clinical Bottom Line Rehabilitation for internal
impingement should consist of several critical interventions including reversing GIRD in those with
posterior shoulder tightness, creating improved dynamic stabilization of the glenohumeral joint through
use of specific exercise techniques in those with hypermobility due to acquired instability, and
developing neuromuscular control in those with scapular dyskinesis. Exercises should emphasize both
scapular and rotator cuff muscle recruitment patterns in order to improve strength, endurance, and
motor control.[41]Special attention should be paid to correction of GIRD through the “sleeper stretch”
which allows posterior capsular stretching. In a study of high-level tennis players performing daily
“sleeper stretch” exercises, patients were found to have significant increases in both internal rotation
and total rotation, as well as a 38% decrease in the prevalence of shoulder problems.[42]

Throwing Biomechanics - Physiopedia

Introduction Throwing, for example, baseball pitching, is one of the most intensely studied athletic
motions[1]. Although the focus has been more on the shoulder, entire body movement is required to
perform the act of throwing. Throwing is also considered one of the fastest human motions performed,
and maximum humeral internal rotation velocity reaches about 7000 to 7500°/second[2]. Phases The
phases of an overhead throw consist of a: wind up, stride, cocking, acceleration, deceleration and follow
through phase [1][3]. Each phase will illustrate the definition, injury occurrence rate, and lastly
pathological possibilities. [4] Wind Up Phase The wind up phase is defined as the initial movement to
maximum knee lift of stride leg [3]. During the initial movements, the pitcher brings his or her hands
overhead and lowers to chest level. During these simple movements consider the muscles proximally to
distally. EMG studies show that the upper trapezius has a maximum voluntary isometric contraction
(MVIC) of 18%, serratus anterior 20%, and anterior deltoid 15%. During this phase, the muscle activity is
quite low and for these reasons risk of injury is low as well [3]. The pitcher is facing the batter with the
baseball concealed away from the batter and in the glove, and both the feet are in contact with the
ground. This is known as the windup stance[1]. For a right-handed pitcher, throwing arm is right arm, a
gloved hand is left, lead/stride leg is left lower extremity and pivot/stance leg is right. The phase of
windup begins with the initiation of the stride leg and ends when the ball separates from the glove and
the stride leg reaches the highest point[2]. The ipsilateral leg and trunk rotate approximately 90° and the
contralateral hip and knee flex[5]. During the windup phase, the energy is transferred from stride leg to
pivot leg and winding up of the stride leg occurs. It is an important phase which is responsible for
imparting the velocity which is driven to the point of ball release. It is reported that about 50% of the
velocity of the ball during an overhead throw is generated from step and body rotation[6]. The body’s
overall center of gravity is raised and minimal stress is imparted on the shoulder during this phase[7].
The purpose of windup is threefold: to establish a rhythm to achieve correct timing for subsequent
movements, to conceal the ball and distract the hitter and to place the body in a position that may
contribute to the propulsion of the ball[5]. Muscle activation During this phase, there is minimal muscle
activity and muscle fire at low intensity[8][9]. As the stride leg is flexed, the weight is transferred from
stride leg to pivot leg and hip abductor, adductor and extensors of pivot leg act as weight absorber[1].
Anterior deltoid and pectoralis major work concentrically at the glenohumeral joint. Upper trapezius,
serratus anterior and lower trapezius work to produce upward rotation of the scapula. The abdominal
muscles work to rotate and stabilize the trunk. Stride Phase The picture below depicts an overhead view
of the alignment of the body during the acceleration phase of throwing. Note the 15-degree angle of the
foot away from the center of the mound [10]. The stride ankle also typically lands approximately 10cm
away from the same midline with a distance from the rubber averaging 87% of the pitcher's height [10].
Fleisig[10] emphasizes the importance of these values by describing the change in force exhibited on the
shoulder when they deviate from the norm. During the cocking phase, Fleisig[10] reports a 3.0N increase
in anterior force at the shoulder for every extra cm and a 2.1N increase in anterior force at the shoulder
with every degree increase of foot angle. Please note that decreasing the distance away from the center
or decreasing the angle did not result in an increased anterior force on the shoulder. So, because of the
increased anterior force on the shoulder, it can be assumed that over time the anterior ligamentous
structures to the glenohumeral joint may be compromised. This finding is consistent with the anterior
glenohumeral instability found in many throwing athletes and emphasizes the importance of proper
mechanics throughout the entire kinematic chain [11]. Arm Cocking Phase The arm cocking phase can be
defined as the beginning of lead foot contact and ends at maximum shoulder external rotation [3]. A
substantial amount of kinetic energy is transmitted to the shoulder, approximately 80% of body weight,
from the lower extremities and trunk rotation. Due to the circumstances, the scapula and shoulder
muscles are highly activated to promote and sustain movements of the shoulder, especially external
rotation. Special focus on anterior instability in this phase is vital due to the high ranges of external
rotation reached in this phase [12] [11]. In a study of pitchers with chronic anterior instability,
stimulation of mechanoreceptors within the glenohumeral joint excited and/or inhibited certain
muscles. The biceps brachii and supraspinatus are shown to be initiated or excited by these
mechanoreceptors and assist with the prevention of anterior instability. Over time the excessive
utilization of the biceps brachii could lead to a superior labrum anterior to posterior (SLAP) tear.
Simultaneously the pectoralis major, subscapularis, and serratus anterior are inhibited. These muscles
decelerate shoulder external rotation in this phase. When these actions cannot be performed there is an
increased likelihood of anterior instability of the glenohumeral joint [3]. Cocking phase is further divided
into (a) early cocking and (b) late cocking. Early cocking phase It begins with the end of the windup
phase or when the stride leg reaches its maximum height and it ends when the stride leg contacts the
mound/ground[1][2]. During an ideal pitch, at this point the throwing arm is in ‘semi-cocked’ position.
With the arm approximately in 90° abduction, 30° horizontal abduction, and 50° external rotation[9]. As
the ball is removed from the glove, the center of gravity is lowered by flexing the knee of the pivot leg
and the stride leg gradually extends and moves towards the batter[9]. Its main function is to allow a
linear and angular motion of the trunk, which lands directly in front of the pivot leg with the toes
pointing slightly in[13]. The knee and hip of the pivot leg extend and initiate pelvic rotation and forward
tilting followed by upper torso rotation[2]. Muscle activation in Early cocking: Hip extensors and
abductors, knee flexors and ankle plantarflexors of the pivot leg work to propel the weight forward as
the stride leg is moving forward. And hip extensors and abductors, knee extensors and ankle
plantarflexors of stride leg work eccentrically to control the lowering of body’s center of gravity.
Abdominal obliques work eccentrically to control excess lumbar hyperextension. In the early cocking
phase, the supraspinatus and deltoid work together to abduct the arm with a peak activity [9][14]. And
later during the late cocking phase the activity of deltoid decreases. The other muscles which produce
peak activity during early cocking phase are right extensor carpi radialis longus and brevis, extensor
digitorum communis, right gluteus maximus and left oblique for right-handed pitcher[1]. And the muscle
which produces a strong contraction are left erector spinae and left gluteus maximus for right-handed
pitcher. Whereas trapezius, serratus anterior and pectoralis are moderately active to position the
scapula. Late Cocking phase This phase begins from the point where the stride leg contacts the ground
to the point of maximum external rotation of the throwing arm. During this phase, the trunk is
perpendicular to the batter and upper extremity position is finalized[1]. The pelvis reaches its maximum
rotation and the upper torso continues to rotate and tilt forward and laterally. The shoulder is abducted
about 90°, 10° to 20° horizontally adducted and laterally rotates to about 175°. The wrist is in neutral
and the elbow is elevated to about shoulder height and is 90° flexed. During this phase, a varus torque
of about 64 N-m is generated at the elbow and about 67 N-m internal rotation torque is generated at
the shoulder[15]. The scapula is elevated and upwardly rotated which provides adequate subacromial
space to avoid impingement. Muscle activation in Late cocking: During late cocking phase, the pivot leg
hip extensor, knee flexor and calf muscles work concentrically to transfer the force up the kinetic chain
and aide in force generation at the arm. Serratus anterior and pectoralis major produce their greatest
activity during late cocking phase just before maximum external rotation[8]. Infraspinatus and teres
minor have their peak activity to externally rotate the arm concentrically and later on their activity is
decreased to moderate levels during acceleration phase. Subscapularis produces significant eccentric
contraction as the humerus passes neutral rotation to control the lateral rotation of the arm. Biceps
brachii presents with peak activity during flexion of elbow in late cocking phase as it limits anterior
translation and compression forces of humeral head. As the wrist extension reaches maximum, the wrist
extensor are at its greatest activity[5]. Arm Acceleration Phase The arm acceleration phase begins at
maximum shoulder external rotation and ends at ball release [3]. During this phase, it is vital to maintain
scapular stabilization due to the forward acceleration of the arm which is equivalent of a peak internal
rotation angular velocity of approximately 6500⁰/sec near ball release. Improper stabilization of the
scapula may be the cause of increased risk of shoulder impingement in this phase. Coupled with the arm
cocking phase this phase has also been hypothesized to be at increased risk of various shoulder injuries
due to the high kinetic energy generated from the lower extremities [3] [11]. The acceleration phase
begins from the point of maximum shoulder external rotation to the point of ball release. The trunk
continues to rotate and tilt, and energy transferred through upper extremity. During this phase, the
shoulder moves into horizontal adduction and internal rotation. A rapid shoulder internal rotation takes
place and shoulder moves from point of 175o of humeral external rotation to 100o of humeral internal
rotation in about 42 to 58 milliseconds[5]. Ball release takes place between 40o and 60o of humeral
external rotation. The elbow first moves to about 120o of flexion and then rapidly extends to about 25o
of flexion at ball release[5]. At ball release elbow extension velocity peaks at approximately 2500o/sec.
The wrist moves into flexion from extended position and ends in neutral, while forearm is in about 90o
pronation at release. Muscle activation Acceleration phase is the most explosive phase of the pitching,
and trunk achieves its greatest rotation speed which leads to peak activity of obliques[5]. Strong activity
of serratus anterior and pectoralis major continues into acceleration as the shoulder moves into
horizontal forward flexion and scapula protracts[8]. Latissimus dorsi becomes active during late cocking
phase as the arm reaches maximum external rotation and continues to contribute towards humeral
internal rotation during acceleration phase[9][14]. Subscapularis at its greatest activity as it vigorously
moves the arm into internal rotation during this phase. Study done by Gowan et al[14] found that during
acceleration phase, the contraction of subscapularis, serratus anterior and latissimus dorsi was
considerably high in professional athletes compared to amateur athletes. Triceps is also at its greatest
activity during this phase as the elbow violently moves into extension and across the body. Arm
Deceleration Phase The arm deceleration phase begins at ball release and ends at maximum shoulder
internal rotation [3]. Typically the concern in this phase is safely decelerating the forward progression of
the arm. Escamilla et al states that a shoulder compressive force slightly greater than bodyweight is
generated to resist shoulder distraction, while a posterior shear force of 40-50% of bodyweight is
generated to resist shoulder anterior subluxation. Due to the high forces generated in this phase, the
posterior muscles are highly susceptible to tensile overload, undersurface cuff tears, labrum and bicep
pathologies, capsule injuries, and internal impingement [3]. It occurs from the point of ball release to
maximal humeral internal rotation and elbow extension. Shoulder is abducted 100o, humeral rotation
reaches 0o and arm is horizontally adducted to 35o. Greatest amount of joint loading is generated
during this phase. Posterior shear force of about 400 N, inferior shear force of 300 N, 1090 N of
compressive forces and about 97 N-m of horizontal abduction torque are generated during this phase
after ball release. Muscle activation This is the most active phase for the muscles of shoulder girdle as
they work eccentrically to decelerate the arm. Trapezius, serratus anterior and rhomboids produce high
MVIC[1] to assist in deceleration of shoulder girdle. Teres minor presents with its peak activity during
this phase as it resists anterior humeral head translation, horizontal adduction and internal rotation. In
addition to teres minor, infraspinatus, supraspinatus and deltoid also presents high MVIC to decelerate
the arm in space as it moves forward. Biceps brachii and brachialis produces marked eccentric
contraction to decelerate the elbow extension and forearm pronation[2]. Follow through Follow-
through is the phase where the body continues to move forward until the arm has ceased motion. The
elbow undergoes a rebound effect and is approximately flexed to 45o[2]. During this phase, the rest of
the body catches up with the arm and it culminates with the pitcher in a fielding position. Muscle
activation During follow-up phase, the trunk extensors work concentrically to bring the trunk in an
upright position. And as the rest of the body catches up with the arm, the pivot leg hip flexors move the
leg forward and the pitcher assumes a fielding position. Common Injuries Shoulder injuries Injuries to
the shoulder are most common baseball pitching and more particularly in late cocking and deceleration
phase[15]. Following is the list of potential shoulder injuries in different phases of pitching[1]. Windup -
No injuries are common Cocking - Anterior subluxation, internal impingement, glenoid labrum lesions,
subacromial impingement. Acceleration - Shoulder instability, labral tears, overuse tendinitis, tendon
ruptures. Deceleration - Labral tears at the attachment of long head of biceps, subluxation of long head
of biceps by tearing of transverse ligament, lesions of rotator cuff Follow Through - Tear of superior
aspect of glenoid labrum at the origin of biceps tendon, subacromial impingement. Elbow injuries Elbow
injuries are second most common injuries in baseball pitching. Excessive valgus strain at the elbow
during the late cocking phase can lead to medial elbow injuries such as muscle tear, avulsion fractures,
ulnar nerve damage and most commonly UCL strain or tear [15]. In addition to the valgus strain injuries
also follow due to lateral compartment at the elbow such as avascular necrosis, osteochondritis
dissecans, osteochondral chip fractures or any combination of these injuries [1]. During acceleration
phase, secondary to the excessive elbow extension peak velocity, olecranon can impinge against the
medial aspect of the trochlear groove and fossa which may form posteromedial osteophyte and loose
bodies formation leading to valgus extension overload syndrome. Resources [16] [17] Presentations The
Biomechanics of Pitching: Maximum Velocity and Efficiency In this presentation, created by ZenoLink
LLC, ways to maximize throwing velocity while minimizing the risk of mechanical injury through
improved biomechanics and throwing efficiency are discussed. View the presentation

O'Briens Test - Physiopedia

Purpose The purpose of O'Brien's Active Compression Test is to indicate potential labral (SLAP Lesion) or
acromioclavicular lesions as cause for shoulder pain. Technique[1] With the patient in sitting or
standing, the upper extremity to be tested is placed in 90° of shoulder flexion and 10-15° of horizontal
adduction The patient then fully internally rotates the shoulder and pronates the elbow The examiner
provides a distal stabilizing force as the patient is instructed to apply an upward force The procedure is
then repeated in a neutral shoulder and forearm position A positive test occurs with pain reproduction
or clicking in the shoulder with the first position and reduced/absent with the second position Depth of
symptoms must also be assessed as superficial pain can indicate acromioclavicular joint symptoms and
deep pain is more often a sign of a labral lesion Evidence The sensitivity and specificity of the O'Brien's
Active Compression Test have been reported to vary widely and no one test can accurately diagnose a
SLAP Lesion.[2] Studies have shown O'Brien's Test to have a specificity ranging from 28-73% and a
sensitivity of 63-94%.[3][4] However, when grouped with other tests for SLAP lesions such as the Crank,
Anterior Apprehension and one of either Biceps Load II, Speed's, or Yergerson's, the overall sensitivity
was found to be 75% and 90% specific.[5] Diagnostic Accuracy for Acromioclavicular Lesions[6]
Sensitivity 0.41 - 1.00 Specificity 0.95 - 0.97 Positive Likelihood Ratio 8.2 - 33.3 Negative Likelihood
Ratio 0.00 - 0.62 Diagnostic Accuracy for Labral Tears[7] Sensitivity 0.63 - 1.00 Specificity 0.73 - 0.98
Positive Likelihood Ratio 2.30 - 50.0 Negative Likelihood Ratio 0.00 - 0.51 See test diagnostics for a
more in-depth explanation of these statistics.
Rupture Long Head Biceps - Physiopedia

Definition/Description A biceps tendon rupture often occur after a sudden contraction of the biceps
with resistance to flexion of the elbow and supination of the forearm. This can further be aggravated by
the intrinsic degeneration of the tendon release and frictional wear of the tendon belly. This intrinsic
degeneration is caused by improper training or fatigue. Inordinate stresses can be placed on the biceps
as it attempts to compensate for other muscles. This can lead to attrition and failure, either within the
tendon substance or at its origin.[1] Clinically relevant anatomy The biceps brachii muscle consists of 2
parts: The long head and the short head. The long head originates at the supraglenoid tubercle and is
attached to the dorsal aspect of the radial tuburosity.[2] It runs intra-articularly over the humeral head
and follows the bicipital groove distal to the glenohumeral joint.[3] It functions as dynamic stabilizer of
the glenohumeral joint, as well as a depressor of the humeral head.[4] The short head is a functions
more in elbow flexor, while the long head functions more in forearm supination.[5] The parts of the
tendon differ in shape. The intra-articular part is wide and flat while the extra-articular part is rounder
and smaller.[3] The articular portion of the long head of biceps is vascularly supplied by the anterior
circumflex artery, mostly to the proximal tendon.[3] The distal portion is fibrocartilaginous and
avascular.[3] Soft-tissue stabilizes the extra-articular long head of biceps when it enters the bicipital
groove en this is built by fibers of the coracohumeral ligament, superior glenohumeral ligament and
parts of the subscapularis tendon.[3] Epidemiology/Etiology Epidemiology Biceps tendon rupture mainly
occurs in individuals between 40 and 60 years who already have a history of shoulder problems. It
mostly affects the dominant arm.[4] A biceps tendon tear can also occur in younger individuals, but
usually after a traumatic fall on an outstretched arm, heavy weightlifting or consistently sport activities
such as snowboarding and soccer.[5][6] Etiology Tendon rupture usually results from sudden contraction
of the biceps associated with resisted elbow flexion and supination of the forearm. A possible
predisposing role is played by intrinsic degeneration of the tendon tissue or frictional wear of the
tendon belly.[1] Risk factors Age: Older people have put more years of wear and tear on their tendons
than younger people.[1] Heavy overhead activities[1] Shoulder overuse - repetitive strain injuries:[1][7]
Can lead to additional shoulder injuries, including tendonitis, shoulder impingement, and rotator cuff
injuries Having any of these conditions puts more stress on the biceps tendon, making it more likely to
weaken or tear Smoking: Nicotine use can affect nutrition in the tendon[1] Corticosteroids: Linked to
increased muscle and tendon weakness[1] Gender: More common in men (most likely primarily from
vocational or avocational factors)[4] Characteristics/Clinical presentation Patients with a long head
biceps rupture report a wide variety of symptoms.[6] Trauma:[5] Audible pop Sharp anterior shoulder
pain with or without snapping sensation[6] Pain:[6] With overhead activities Anterior shoulder pain that
may get worse at night[6] Associated pathologies that may lead to rupture of long head of biceps:
Rotator cuff tears[8] Tendonitis[6] Shoulder impingement[6] Popeye deformity[6] Differential diagnosis
Acromioclavicular joint separations Gout Rotator cuff disease Septic arthritis [6] Diagnostic procedures
Physical examination Assessment of the shoulder and arm contour:[4] (+) Popeye sign Descent of the
biceps muscle in the middle part of the arm (more obvious with contraction)[2] Muscle power: Shoulder
and elbow[2] Range of motion (ROM): Shoulder and elbow[4] Special tests:[4] Yergason's test : Positive
if pain is reproduced in the bicipital groove during the test Speeds test Hook test Special investigations
MRI: Axial and parasagittal planes needed[9] Ultrasound [1] Outcome measures Disabilities of the Arm,
Shoulder, and Hand (DASH), Quick DASH[8] Constant-Murley score[2][5] Medical management Anti-
inflammatory medications can be used to reduce the underlying inflammatory process that may
predispose tendons to rupture. When tendons are stressed or partially disrupted, anti-inflammatory
medications can be used as analgesia.[9] Conservative management Non-operative management is
considered appropriate for older patients or patients who do not require a high level of supination
strength.[6] This is also considered for subacute or chronic biceps tendon tears.[10] Surgery There are
no consensus about surgical repair. Surgical repair consists of a tenotomy, which includes the attaching
torn tendon to the bone. The results in full functional and muscle power recovery, as well as good
cosmetic outcomes.[10] Indications: Young, athletic population Patients who needs maximum
supination strength (e.g. manual labour like carpenters and port workers). Patients lose up to 20% of
supination strength with a biceps tear, but that rarely affects activities of daily living. Patients who
struggle to accept aesthetics of Popeye deformity Physiotherapy management Post-operative
rehabilitation Patients have to wear a mastersling for the first 10-14 days after surgery. Only passive
range of motion is allowed in that time. Light exercises is done from week 2 to 6, where after it is
progressed to functional exercises between week 6 and 8, and progressed to resistance. After this,
moderate loading may be tolerated but heavy loading is prohibited for the first few months.[8] Phase 1:
Passive (Week 0-2) Warm up with pendulum exercises Passive ROM Full passive elbow flexion/extension
ROM Full passive forearm supination/pronation ROM Full passive shoulder ROM Seated scapular
retractions [11] Phase 2: Active (Week 2-6) Warm up with pendulum exercises Active ROM, with
terminal stretch to prescribed limits Full active shoulder ROM, lawn chair progression Full active elbow
flexion/extension ROM Full active forearm supination/pronation ROM Phase 3: Resisted (Week 6-8)
Warm up with pendulum exercises Theraband exercises: Shoulder internal/external rotation at 30°
abduction Standing forward punch Low rows Bear hugs Prone I,T,Y,W. Biceps curls Resisted
supination/pronation Phase 4: Weight training (Week 8+) Keep hands within eyesight, keep elbows
bent, minimize overhead activities Return to normal activities: Computer work after 1-2 weeks Golf after
4 weeks Tennis after 8 weeks [6][11] Conservative management Conservative management of long head
of biceps rupture take 4-6 weeks on average. Oedema management: RICE regime The treatment takes 4-
6 weeks 2-3 times in a week. It consists of mobilization and flexibility exercises to improve the shoulder
ROM. After that, there are also strength and stretching exercises. The muscle will also be static trained.
At home there will be home exercises. The exercises are extension and flexion and supination en
pronation exercises. After a period the pain needs to be lower and the strength have to be better. Most
people go back to work after 2-3 weeks but the work is adapted. After 8 weeks the ROM and the
strength is back to normal. Normally there aren’t anymore restrictions more but the popeye
malformation remains. [10] (LoE: 3B) Phase 1: Acute phase Week 1 Clinical modalities as needed
Glenohumeral ROM: Joint mobilization to restrict capsular tissue Stretching as indicated Home exercise
programme: ross-arm stretch Sleeper stretch Early scapular strengthening Scapular stabilization with
instruction in lower trapezius facilitation Phase 2: Subacute phase, early strengthening Week 2 Continue
with modalities and ROM. Begin rotator cuff strengthening with theraband: Internal/external rotation in
30° abduction Low rows (prone, scapular plane abduction (<90°), ceilling punch, biceps and triceps)
Phase 3: Advanced strengthening Week 3 Continue with strengthening: Resisted PNF patterns
Theraband exercises: Bear hug Reverse fly Internal/external roation at 90° abduction for neuromuscular
re-education Push-up progression Begin with plyometric exercises with both arms, progressing to one
arm Weight training Phase 4: Return to activities Week 4 Continue with program Re-evaluation with
physician and therapist Advance to return-to-sport program, as motion and strength allow [6] Resources
Physical Therapist's Guide to Biceps Tendon Rupture Biceps tendon repair surgery Clinical Bottom Line
Long head of biceps ruptures commonly occur in the population between 40 and 60 with predisposing
shoulder problems. It can also occur in the younger, active population. It is characterized by a Popeye
sign at the biceps. Conservative management consisting of analgesia and physiotherapy is the treatment
of choice for the older population, and for patients that does not need full supination strength, as an up
to 20% loss with biceps ruptures are normally present. Surgery consisting of a tenotomy and re-
attachment of the tendon are mostly reserved for the younger, more active population; patients who
cannot aesthetically accept the Popeye appearance; as well as patients needing full supination strength
(mostly for manual labour). Physiotherapy plays a massive role in both the conservative, as well as post-
surgical management of a long head of biceps rupture.

References

https://en.wikipedia.org/wiki/Glenoid_labrum

https://www.shoulderdoc.co.uk/article/1399

https://radiopaedia.org/articles/glenoid-labrum

https://www.ncbi.nlm.nih.gov/pubmed/12883756

http://www.sciencedirect.com/science/article/pii/S0749806305801057

https://www.scopus.com/record/display.uri?eid=2-s2.0-
29644447279&origin=inward&txGid=F68392337D64C9A9DE1B71C5B7CB7B6A.wsnAw8kcdt7IPYLO0V48
gA%3a2

http://www.sciencedirect.com/science/article/pii/S1877056814003259

http://journals.sagepub.com/doi/abs/10.1177/036354659602400205

https://www.ncbi.nlm.nih.gov/pubmed/9810074

https://www.uptodate.com/contents/superior-labrum-anterior-posterior-slap-tears/abstract/1

https://www.uptodate.com/contents/superior-labrum-anterior-posterior-slap-tears/abstract/2

https://www.uptodate.com/contents/superior-labrum-anterior-posterior-slap-tears/abstract/3

https://www.uptodate.com/contents/superior-labrum-anterior-posterior-slap-tears/abstract/4

https://www.uptodate.com/contents/superior-labrum-anterior-posterior-slap-tears/abstract/5

https://www.uptodate.com/contents/superior-labrum-anterior-posterior-slap-tears

https://www.uptodate.com/contents/superior-labrum-anterior-posterior-slap-tears

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