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Internal Impingement of the Shoulder
Benton E. Heyworth and Riley J. Williams III
Am J Sports Med 2009 37: 1024 originally published online December 4, 2008
DOI: 10.1177/0363546508324966
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Clinical Sports Medicine Update
Internal Impingement of the Shoulder
Benton E. Heyworth, MD, and Riley J. Williams III,* MD
From the Hospital for Special Surgery, New York, New York
Internal impingement of the shoulder is a pathologic condition characterized by excessive or repetitive contact of the greater
tuberosity of the humeral head with the posterosuperior aspect of the glenoid when the arm is abducted and externally rotated.
This arm positioning leads to rotator cuff and glenoid labrum impingement by the bony structures of the glenohumeral joint.
Although some degree of contact between these structures occurs under normal conditions, to date most of the orthopaedic
literature has focused on internal impingement as a disease state that affects overhead athletes and is characterized by the
development of articular-sided rotator cuff tears and posterosuperior labral lesions. The precise cause of these impingement
lesions remains unclear. However, it is believed that varying degrees of glenohumeral instability, posterior capsular contracture,
and scapular dyskinesis may play a role in the development of symptomatic internal impingement. The purpose of this article is
to review the pathomechanics, clinical complaints, physical examination findings, and imaging findings that are associated with
internal impingement. The results of treatment will be reviewed, and a diagnostic and therapeutic algorithm for the management
of internal impingement is presented.
Keywords: internal impingement; glenoid impingement; throwing athlete; throwing shoulder
anterior infraspinatus tendon by the posterosuperior
glenoid margin. This phenomenon, which is distinct from
subacromial impingement syndrome, is known as internal
impingement, or posterior glenoid impingement.35
This review will describe the biomechanical and etiologic
factors pertinent to the development of internal impingement. In addition, the anatomic structures involved in the
constellation of internal impingement lesions and the clinical presentation of affected patients will be discussed. We
will also present a systematic diagnostic approach to physical examination, radiologic imaging, and intraoperative
assessment that should assist the clinician in treating this
malady. Finally, the published literature on the treatment
and outcomes of internal impingement will be explored in
an effort to establish a therapeutic algorithm for the management of this condition.
Internal impingement of the shoulder is a condition
characterized by excessive or repetitive contact of the
greater tuberosity of the humeral head with the posterosuperior aspect of the glenoid when the arm is abducted
and externally rotated; this leads to impingement of the
rotator cuff and labrum. Although there is some controversy regarding whether this described “internal impingement” is a normal or pathologic condition, it has most often
been described as a chronic, pathologic condition that is
associated with throwing and other repetitive, overhead
athletic activities. However, internal impingement has
been described in nonathletes as well.35,80 Findings typical
of internal impingement include articular-sided partialthickness rotator cuff tears and posterosuperior or posterior labral fraying or tears.
Posterior shoulder pain in throwers was first described
by Bennett in 1959.6 However, it was Lombardo et al48 who
identified the late cocking phase of the thrower’s motion as
a possible cause of posterior shoulder pain in this group of
athletes. Andrews et al2 have been credited with describing
the association of superior labrum anterior and posterior
(SLAP) tears with partial-thickness rotator cuff tears in
throwers, based on work published in 1985.3 In 1992, Walch
et al80 and Jobe and Sidles (unpublished data, 1992) separately described impingement of the undersurface (deep
layer) of the posterior supraspinatus tendon and/or the
ANATOMIC AND BIOMECHANICAL
CONSIDERATIONS
Orthopaedic surgeons’ understanding of the biomechanical
and etiologic forces involved in the development of internal
impingement of the shoulder has evolved in a gradual,
stepwise fashion, but remains incomplete. This is partially
due to the limited patient population in which the condition arises, and also because of the variety of pathologic
findings that have been reported. Unlike “external” or
“subacromial” impingement, most often simply called
“impingement syndrome,”59 there is not a single pathophysiologic process at work in the painful throwing shoulder. Internal impingement syndrome is thought to be
fundamentally more complex and multifactorial in nature.
Bennett,6 in 1959, published observations on the range
of elbow and shoulder injuries seen in baseball pitchers
*Address correspondence to Riley J. Williams III, MD, Hospital for
Special Surgery, 535 East 70th St, New York, NY 10021 (e-mail:
[email protected]).
No potential conflict of interest declared.
The American Journal of Sports Medicine, Vol. 37, No. 5
DOI: 10.1177/0363546508324966
© 2009 American Orthopaedic Society for Sports Medicine
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1024
Internal Impingement of the Shoulder
Vol. 37, No. 5, 2009
that were well ahead of his time. His focus on the common,
although variable, development of a posteroinferior glenoid exostosis opened the door for future investigators to
explore the phenomenon of posterior shoulder pain in
throwers more completely. Interestingly, he believed this
bony lesion to be secondary to repetitive traction of the
posterior capsular structures and traction of the triceps
origin.6 Most subsequent reports have refuted the association between the triceps and the bony exostosis lesion or
Bennett lesion, as it is most commonly called.27,54 Bennett
also described articular-sided fraying of a superficially
intact supraspinatus tendon as a typical finding, but he
thought that it was related to anterior shoulder pain and
not glenoid impingement.6
In 1992, Walch et al80 published a landmark article in
which 30 athletes were assessed for shoulder pain. Of the
original 30 athletes, 17 individuals (16 of whom were
throwing athletes) underwent an arthroscopic shoulder
examination; typical findings included the presence of posterior labral lesions and articular surface rotator cuff tears,
in the absence of Bankart or SLAP tears. The authors differentiated the labral lesions in their series from SLAP
lesions that extended anterior to the biceps anchor at the
supraglenoid tubercle, concluding that internal impingement may be responsible for a subset of patients with isolated posterior SLAP tears. In each case, direct arthroscopic
observation was made of impingement of the posterior
aspect of the humeral head on the posterosuperior rim of
the glenoid. This area of impingement corresponded precisely with the location of the rotator cuff and labral lesions
when the arm was brought into the abducted, externally
rotated throwing position. These findings paralleled those
of Jobe and Sidles (unpublished data, 1992), who in the
same year presented the results of patients with similar
arthroscopic and MRI findings. Jobe and Sidles also used
cadaveric shoulders to study the mechanism by which these
observed lesions might occur. They suggested that the positioning of the arm versus the glenoid during the throwing
motion results in the interposition of the rotator cuff
between the glenolabral complex and the humeral head.
The principal difference between the potential origins of
internal impingement, as suggested by Jobe versus Walch
and colleagues, revolves around the role of glenohumeral
translation in causing the rotator cuff and labral changes
noted in the throwing athlete. Walch et al80 distinguished
the pathomechanics of internal impingement from those of
anterior instability, excluding patients with any signs of
instability from their series. Jobe and Sidles (unpublished
data 1992) reasoned that the spectrum of pathologic anterior laxity resulting from hyperangulation of the humerus
in the throwing motion was integrally related to the onset
of internal impingement.37 Studies by Andrews et al2,4 and
Bigliani et al9 have suggested that glenohumeral joint laxity is a common finding in throwing athletes. Such a finding would facilitate anterior humeral head translation and
ultimately cause the entrapment of the junction of the posterior supraspinatus and anterior infraspinatus tendons
between the humeral head and posterior glenoid, as occurs
in internal impingement. Paley et al64 contended that
anterior instability is actually the most significant factor
1025
in the development of internal impingement. Conway22
also noted that “anterior glenohumeral instability almost
certainly contributes to internal impingement.” A high frequency of anterior instability in throwing athletes has
been supported by other studies as well.38,39,44 Paley et al64
cite the combination of repetitive microtrauma and subsequent attenuation of the anterior glenohumeral ligament
complex (static restraints), and fatigue or desynchrony of
the dynamic stabilizers of the glenohumeral and scapulothoracic articulations, as the precipitating mechanisms
that allow abnormal anterior humeral head translation
relative to the glenoid surface in some throwers. Overhead
athletes, by definition, commonly position the arm in the
maximally abducted and externally rotated position; this
arm position causes anterior translation of the humeral
head and rotator-cuff impingement on the posterior glenoid rim. The potential role of anterior instability in the
origin of internal impingement is further substantiated by
the common findings of Bankart lesions, anterior labral
fraying, and SLAP tears seen in throwing athletes.64 Some
authors have suggested that the slightly lower rates of
internal impingement lesions seen in the series by Walch
et al80 are explained by the fact that the volleyball and tennis players in that study did not mimic the degree of repetition or force of the overhead motion that was
characteristic of the studied professional overhand throwers.64 However, this interpretation is confounded by an
additional study of 25 tennis players performed by
Sonnery-Cottet et al,73 who reported that no patients
demonstrated signs of anterior instability, but all were
found to have symptomatic internal impingement lesions.
In addition, a more recent study from Borsa et al,10 using
ultrasound and instrumented graded stress technique to
assess glenohumeral translation and rotation in pitchers,
found no difference in translation between throwing and
nonthrowing shoulders and no correlation between translation and rotational range of motion. These findings supported the results of another stress radiography study that
demonstrated no significant side-to-side differences in
pitchers’ 2 shoulders.26 Although these studies challenge
the notion that anterior instability in the throwing shoulder plays a role in internal impingement, they were performed only on asymptomatic overhead athletes, not on
those with pathologic internal impingement.
It is notable that several authors23,33,35,80 have contended
that patients with significant degrees of subluxation or
frank dislocation are actually protected against internal
impingement. These investigators point out that the
abnormal position of the humerus relative to the glenoid in
severe instability actually precludes impingement between
the greater tuberosity and posterosuperior glenoid.
The fact that nonpathologic interposition of the rotator
cuff and posterosuperior labrum between the glenoid rim
and greater tuberosity, which some authors will refer to as
internal impingement, occurs in throwers and nonthrowers
alike has become a well-accepted concept. Cadaveric,
MRI, and arthroscopic studies have consistently shown
that contact of the rotator cuff on the posterosuperior
labrum is a normal, physiologic occurrence.12,14-16,25,33,50 In
fact, Burkhart12 has contended that the loss of “internal
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Heyworth and Williams
The American Journal of Sports Medicine
Figure 1. Line drawing illustrates impingement of the
greater tuberosity on the posterosuperior glenoid rim, with
the interposed articular side of the rotator cuff and the
posterosuperior labrum, which are prone to inflammation,
fraying, or tears.
impingement” is actually pathologic, in that the absence of
this normal restraint to hyperextension of the humeral
head in the throwing motion can lead to SLAP tears,
fatigue failure of the rotator cuff, and “dead-arm syndrome.”
In 2003, Burkhart et al14 meticulously described the biomechanics of how a loss of internal rotation, or development of
a glenohumeral internal rotation deficit (GIRD), could initiate the central pathophysiologic cascade in the throwing
shoulder. They describe the first step in this cascade as the
development of a contracture of the posterior band of the
inferior glenohumeral ligament (PIGHL) and posteroinferior capsule. As shown by O’Brien et al,61 the PIGHL and
anterior inferior glenohumeral ligament normally act as
individual but reciprocating cables balancing the humeral
head in the center of the glenoid, in the glenoid bare spot,
when the arm is in abduction. Burkhart et al14 contend that
a contracture of the PIGHL, commonly seen in pitchers,
acts as a tether to normal glenohumeral rotation, shifting
the normal, central contact point of glenohumeral articulation in a posterosuperior direction, which can lead to a
greater arc of external rotation occurring before the normal
contact of internal impingement. Moreover, they suggested
that this shift decreases the beneficial “cam effect” that the
humeral head and proximal humeral calcar exert on the
anteroinferior capsule, by occupying space and tensioning
the capsule when the arm is in abduction. Collectively, these
changes lead to an increase in the pathologic “peel-back
mechanism,” in which the vector of the biceps in the cocking position transmits heightened torsional loads on the
posterosuperior labrum, leading to SLAP tears. The
authors cite the reduced cam effect, as well as posterior and
anteroposterior type II SLAP tears (ie, disruption of the
labral ring), as the likely causes of perceived instability and
positive “drive-through sign” (in which the arthroscope can
be moved from the inferior to superior aspect of the joint
without significant resistance) commonly seen in throwers.
Notably, they distinguish this common state of “pseudolaxity” seen in both symptomatic and asymptomatic young
throwers from the rarer, pathologic state of hyperextension
and/or true anterior instability in older athletes, which may
be associated with subluxation and tearing of the anterior
capsuloligamentous complex.14 They therefore recommend
a posterior capsular stretching program as the initial and
most critical therapeutic intervention in most symptomatic
throwers, citing 90% success rate with such a regimen. The
rare thrower who does not respond may be a candidate for
arthroscopic posteroinferior capsular release and possibly a
repair of the SLAP lesion.
Burkhart et al15 also describe a constellation of findings
they refer to as scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement, which they call “SICK scapula
syndrome,” as a critical part of the disabled throwing
shoulder. They believe this muscle overuse fatigue syndrome causes protraction of the scapula, which in turn
leads to malposition of the glenoid and, ultimately,
increased tensile loads on the anterior capsule and posterosuperior labrum. They believe this increase in loads
can exacerbate the pathologic cascade responsible, in most
cases, for dead-arm syndrome in throwers.15
Although Burkhart et al believe that internal impingement is a normal occurrence in all people, including throwers, other investigators37,52,53,57 have proposed that the
increased frequency and force with which external rotation
and abduction occurs in some throwing athletes explain the
development of internal impingement as a pathologic condition. Jobe35 proposed that 2 different extremes of positions or
motions in throwers could cause the constellation of injuries
seen in internal impingement, specifically either direct forward elevation, as replicated during the Neer test, or abduction–external rotation, as performed in throwing (Figure 1).
There may, in fact, be 3 different forms of internal impingement. Mithöfer et al57 suggested that the first form is the
most commonly described infraspinatus contact against the
posterosuperior glenoid and labrum. The second mode of
internal impingement occurs when the supraspinatus rubs
against the posterior labrum in the midacceleration phase of
the throw, as detailed by Jobe.36 The third form of the condition, labeled “anterior impingement” by Struhl,75 involves a
partial undersurface supraspinatus tear resulting from
impingement between the anterior humeral head and
anterosuperior glenoid and labrum during forward flexion of
the arm. Struhl’s series of 10 patients from the general population (not elite athletes) had an average age of 37 years,
suggesting a significantly younger population affected than
that described in subacromial impingement series.
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Internal Impingement of the Shoulder
Vol. 37, No. 5, 2009
Figure 2. Arthroscopic view from the posterior portal demonstrates an articular-sided, partial-thickness tear of the infraspinatus tendon at the myotendinous junction (arrow) and
corresponding posterosuperior labral fraying (triangle).
Other anatomic factors may also play a role in the development of internal impingement. Abnormally high glenoid
anteversion or abnormally low humeral head retroversion
may be predisposing factors.72,80 However, although Walch
et al80 noted decreased retroversion in the majority of
patients in their original series, 2 of 17 patients had normal
retroversion, leading the authors to conclude only that such
an anatomic anomaly could be a contributing factor. This theory was later tested by the same group in a study by Riand
et al,72 who performed humeral derotational osteotomy with
a concurrent subscapularis shortening myorrhaphy in 20
throwing athletes who had persistent posterior shoulder
pain after arthroscopic debridement of impingement lesions.
The mean increase in humeral retroversion was 29°. At a
mean follow-up of 3.8 years, 55% had returned to their sport
at their premorbid level, 25% had returned to their sport at
a lower level, and 15% discontinued throwing secondary to
pain. Although the authors reported no signs of anterior
instability in any patient preoperatively, 3 of the 4 surgeries
they termed as “failures” were performed on patients demonstrating “hyperlaxity,” with a positive sulcus sign preoperatively. The authors also reported the arthroscopic findings
from the surgeries that had been performed an average of 8
months before the osteotomy. Undersurface rotator cuff tears
had been noted in 100% of patients, posterosuperior labral
lesions in 80% of patients, and posterosuperior humeral head
osteochondral lesions in 30% of patients. However, the details
of the arthroscopic debridement performed for these lesions
are not provided.72
It has been suggested that excessive traction of the rotator cuff tendon during the late cocking phase is the critical
etiologic factor in the development of articular rotator cuff
tears in throwing athletes.2 Other authors64 have refuted
1027
Figure 3. Oblique coronal magnetic resonance image
demonstrates a high-grade, delaminating, articular-sided
partial tear of the supraspinatus tendon (arrow) in an overhead athlete. (Courtesy of the Hospital for Special Surgery
Department of Radiology.)
this mechanism based on the relative preservation of the
subscapularis tendon, which undergoes similar tensile
forces in the throwing motion but rarely demonstrates
injury in this patient population. Few investigators have
distinguished between the rotator cuff injury that can
occur at the myotendinous junction of the anterior infraspinatus at the level of the joint line (Figure 2) from the
more distal site of insertion of the supraspinatus on the
lesser tuberosity (Figure 3). We believe the former represents the site of actual impingement, in which the cuff is
interposed or pinched between the tuberosity and glenoid
in the extremes of abduction and external rotation, but
this lesion typically consists of minor pathologic changes,
usually in the form of fraying. This finding is often encountered when the arthroscope is first introduced in the posterior portal, and can obscure visualization of the joint
until simple, minor debridement is performed. More extensive repair is rarely necessary. A second, distinct type of
rotator cuff lesion in throwers occurs at the deep, posterior
aspect of the footprint in the form of a delaminating, articular-sided supraspinatus tear of varying thickness. We
believe this lesion develops as a result of the combination
of repetitive eccentric loading, as initially proposed by
Andrews et al,2 and the development over time of excessive
shear and torsional forces with external rotation, as elaborated upon by Burkhart et al.14
In addition to the posterosuperior labrum and rotator
cuff, injury to a number of other structures in the shoulder
have been associated with pathologic internal impingement. Jobe35 has suggested that as many as 5 anatomic
structures are at risk: the posterior superior labrum, the
rotator cuff tendon (articular surface), the greater tuberosity, the inferior glenohumeral ligament (IGHL) complex,
and the posterior superior glenoid. He noted that the
majority of patients with internal impingement have more
than 1 of the 5 structures injured at the time of arthroscopic assessment, underscoring the importance of a thorough diagnostic arthroscopic assessment of the shoulder
joint in the setting of suspected internal impingement or in
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1028
Heyworth and Williams
The American Journal of Sports Medicine
cases in which a typical internal impingement lesion is
unexpectedly detected.35 Unlike Bukhart et al,14 who suggest the PIGHL is the chief culprit in the disabled throwing shoulder, Jobe identified the anterior IGHL complex as
the structure uniquely injured by tension forces in internal
impingement, as it is draped over the prominence of the
articular surface of the humeral head when the arm is in
extremes of either forward elevation or combined abduction-external rotation. As the fibers at the apex of this
bulge undergo maximal stress, stretch and eventual attenuation of the fibers can occur, leading to anterior IGHL
injury.35 Repetitive microtrauma to the bony greater
tuberosity or the posterosuperior rim of the glenoid may
represent extremes of the spectrum of injury caused by the
abducted, externally rotated position associated with
internal impingement,35 but even cases of fracture of these
structures have been reported in some series.34,35,80
Although osteochondral lesions of the humeral head have
also been described, it is likely these occur from a similar
mechanism to greater tuberosity changes, with subtle variations in anatomy or the throwing motion accounting for a
different site of humeral head contact with the glenoid rim.
Because some series of internal impingement patients
have demonstrated low rates of calcification or ossification
in the region of the posteroinferior glenoid,80 often labeled
a Bennett lesion, it remains unclear whether the finding is
a significant pathologic component of internal impingement. Also, because such lesions have been demonstrated
variably as osteophytes in contiguity with the posteroinferior glenoid rim83 or as calcifications within the joint capsule,27,54 the PIGHL, or the triceps tendon origin,6,63
speculation continues regarding their true pathophysiology.
Although a range of theories have been proposed about
the biomechanical and pathophysiologic role of internal
impingement, it seems clear that the causes of the disabled
throwing shoulder are multifactorial. We believe that anterior subluxation of the humeral head that is associated
with gross or microinstability—whether arising from anterior capsular stretch or any disruption of the labral ring—
likely exacerbates internal impingement, but is not a
prerequisite to its occurrence. The cardinal lesions of internal impingement, articular-sided rotator cuff tears and
posterosuperior labral lesions, have been shown to occur in
association with a number of other findings, most importantly GIRD and SICK scapula syndrome, but also posterior humeral head lesions, posterior glenoid bony injury,
and more rarely Bankart and IGHL lesions. More biomechanical and clinical research is needed before a complete
understanding and reconciliation of the varying theories of
the pathomechanics of injury is developed. Below, we will
discuss the spectrum of clinical presentation in patients
with internal impingement, and the diagnostic tools used
to evaluate and differentiate the treatable features and
their associated intra-articular findings.
CLINICAL PRESENTATION AND DIAGNOSIS
Patient Demographics and Clinical Presentation
Because of the constellation of findings that characterize
internal impingement and the strong association with
other pathologic lesions of shoulder, the incidence of the
condition, in isolation, has not been established. Internal
impingement typically affects young to middle-aged
adults; in most major series of internal impingement,
patients are under 40 years of age and participate in activities involving repetitive abducting and externally rotating
arm motions or positions. The majority of patients who
have been identified with internal impingement are overhead athletes. For example, the first major series by Walch
et al80 consisted primarily of volleyball and tennis players.
However, in a recent series of 75 recreational athletes
(with the exception of 1 professional tennis player) treated
for partial-thickness rotator cuff tears, 55 patients were
found to have concurrent SLAP tears, suggesting the possibility of a high prevalence of internal impingement
lesions outside of the elite athletic population.11
The largest athletic group studied with internal
impingement has been the throwing athlete, particularly
baseball players. Most patients present with a progressive
decrease in throwing velocity or loss of control and performance. Chronic, diffuse posterior shoulder girdle pain is
commonly the presenting complaint, but the pain may be
localized to the joint line.57 Jobe36 classified three stages in
the clinical presentation of internal impingement. Stage I
is characterized by complaints of stiffness, with pain occurring specifically in the late cocking and early acceleration
phases. Progression to significant posterior joint-line pain
with activity characterizes stage II. Stage III is defined as
failure to improve with conservative means.
Interestingly, there are series in which a substantial
number of studied patients were not throwing athletes or
even athletes at all. These patients are more likely than
throwers to have acute posterior shoulder pain following
an injury rather than progressive, chronic pain. In one
series,35 Jobe reported on 6 of 11 patients treated for internal impingement who were not throwing athletes. The
series included acute (8 patients) and chronic (3 patients)
injury mechanisms, with varying degrees of arm abduction, elevation, and external rotation.35 Typically, the
injuries were sustained with the arm in full forward elevation or abduction with external rotation. One patient in
this series was a forklift driver, whose trunk underwent
repetitive extremes of rotation to allow the patient to drive
in reverse while the arm rested on the steering wheel.35
Despite posterior shoulder pain being the most common
complaint among patients with internal impingement,
patients may also present with symptoms similar to those
associated with classic rotator cuff disease. 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.23 Alternatively, patients may also
have instability symptoms, such as apprehension or the
sensation of subluxation with the arm in a position of
abduction and external rotation. However, as previously
mentioned, those with moderate to severe degrees of instability may actually be protected against the lesions typical
of internal impingement because the abnormal position of
the humerus, relative to the glenoid, prevents impingement
between the greater tuberosity and posterior superior
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Internal Impingement of the Shoulder
Vol. 37, No. 5, 2009
At-Risk Sports/Activities
- Baseball
- Other throwing
athletes (waterpolo,
football)
- Tennis
- Squash
- Other racquet sports
(racquetball)
- Volleyball
- Forklift driver
Other isolated conditions
that may present similarly
to internal impingement
- Anterior instability
- Full thickness rotator
cuff tear
- SLAP tear
- Subacromial
impingement
History or physical examination
suspicious for internal
impingement
MRI signs of internal
impingement
Treat other condition
MRI signs of internal
impingement
- Articular-sided partial
thickness posterior
supraspinatus or
infraspinatus rotator cuff
tear (RCT)
- Posterosuperior glenoid
labral lesion (fraying,
tearing, detachment)
Nonoperative
Treatment
Principles of nonoperative treatment
- Rest (remove from
competition)
- Physical therapy
(aggressive posterior
capsular stretching,
periscapular
strengthening)
- Anti-inflammatory
medications
(NSAIDs)
Examination under
anesthesia
(bilateral EUA in
adduction and 90°
abduction before sterile
draping)
Physical examination signs
of internal impingement
- Posterior impingement
sign
- Relocation sign
- Posterior glenohumeral
joint line tenderness
MRI
No MRI signs of
internal impingement
1029
Resolution of symptoms
No resolution of symptoms
Continued, progressive
rehabilitation,
Return to competition
Operative treatment
(examination under anesthesia,
diagnostic arthroscopy)
1+ Ant Instability
No capsular intervention
2+ Ant Instability
Consider capsular plication
3+ Ant Instability
Capsular plication
IR Defecit
Posterior capsular release
RCT
Debridement (partial) vs repair (full)
Posterosuperior
labral lesion
Debridement (fraying, tearing) vs
repair (frank detachment or posterior
instability)
Diagnostic arthroscopy
Intervention-specific
postoperative
rehabilitation, return to
competition
Continued, progressive
rehabilitation,
Return to competition
Figure 4. An algorithmic approach to diagnosis and treatment of internal impingement. MRI, magnetic resonance imaging; SICK
scapula syndrome, a constellation of findings consisting of scapular malposition, inferior medial border prominence, coracoid
pain and malposition, and dyskinesis of scapular movement; SLAP, superior labrum anterior and posterior.
glenoid.23,35,80 Notably, Burkhart et al,16 in their series of 96
athletes with a disabled throwing shoulder, reported an
80% rate of anterior corocoid pain, rather than isolated posterior shoulder pain, as the most common presenting symptom. However, this cohort was throwers designated with
SICK scapula syndrome, which they specifically differentiate from those with pathologic internal impingement.
Thus the diagnosis of internal impingement based on
history alone is extremely difficult, and symptoms tend to
be variable and fairly nonspecific. Although nonthrowing
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1030
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The American Journal of Sports Medicine
athletes and nonathletes may be affected by internal
impingement, the vast majority of patients studied with
this condition have been high-level throwers with posterosuperior shoulder pain. As throwing requires maximal
abduction and external rotation, this athletic activity provides the most replicable model of the disease. Older
patients are more likely to have concurrent shoulder conditions, such as subacromial impingement or glenohumeral arthrosis, and the workup should be directed to
ruling out diagnoses other than internal impingement. A
summary of the sports and activities that have been associated with internal impingement are listed within Figure 4.
Physical Examination Findings
Posterior glenohumeral joint line tenderness, increased
external rotation, and decreased internal rotation are the
most common physical examination findings in throwing
athletes. However, all patients suspected of internal
impingement should be evaluated with a complete shoulder
examination due to the high rate of other shoulder conditions associated with internal impingement. In addition to
documentation of bilateral active and passive motion of the
shoulders, testing for SLAP lesions, “classic” impingement
signs such as the Neer and Hawkins tests, cross-body adduction tests, and instability testing should be performed.
Despite significant controversy regarding the validity of
various physical examination maneuvers for detecting
SLAP tears,24,30,51,68,81 because superoposterior labral tears
represent a cardinal feature of pathologic internal impingement, performing some combination of these tests is generally indicated. O’Brien et al62 reported 100% sensitivity and
98.5% specificity for the “active compression test,” although
other authors have not replicated these findings.74 Liu
et al47 published sensitivity and specificity rates of 91% and
94%, respectively, for the “crank test.” Speed’s test is also
commonly used for assessment of SLAP tears,58 but may be
positive with biceps lesions distal to the labral insertion.7
Kim et al43 described 2 different “biceps load tests,” the first
with greater than 90% sensitivity and specificity in patients
with concurrent anterior instability and the second geared
toward patients with isolated SLAP tears.42 A number of
additional tests, including the “clunk test” of Andrews et al,3
Kibler’s anterior slide test,41 the “SLAPrehension test,”8
and, most recently, the supine flexion resistance test,24 have
been advocated by various authors.
However, a small number of physical examination tests
designed to specifically test for internal impingement
rather than SLAP tears have also emerged. Meister et al55
investigated the ability of a single maneuver, referred to as
the “posterior impingement sign,” to detect the presence of
articular-sided rotator cuff tears and posterior labrum
lesions. They prospectively enrolled 69 overhead athletes
with a mean age of 22.7 years who presented with posterior
shoulder pain. The subjects were tested for the presence of
deep posterior shoulder pain when the arm was brought
into a position similar to that noted during the late cocking
phase of throwing—abduction to 90° to 110°, extension to
10° to 15°, and maximal external rotation. The sensitivity
and specificity of the posterior impingement sign were
75.5% and 85%, respectively. When the 21 patients who had
sustained contact injuries were excluded in a stratified
analysis, the sensitivity improved to 95% and the specificity
improved to 100%. Notably, all patients with noncontact
injuries with a positive test had arthroscopic findings
amenable to surgical treatment. The authors concluded
that the test was extremely useful in identifying operable
internal impingement lesions in younger overhead athletes.55 As such, the clinician should carefully investigate
the injury mechanism in this subset of patients.
Jobe and his associates suggested that the relocation test
could be used to identify internal impingement as well.23,35
With the arm in an abducted and maximally externally
rotated position (in throwers, sometimes up to 140°), the
internal impingement patient would experience posterior
shoulder pain that was relieved with a posteriorly directed
force on the proximal humerus. The pain is thought to
be secondary to impingement of the rotator cuff and
posterosuperior labrum between the greater tuberosity and
the glenoid. This finding is distinct from the uncomfortable
feeling of apprehension and anterior shoulder pain noted in
patients with true anterior shoulder instability, who also
experience relief with a posteriorly directed force. The findings of Paley et al64 support the use of this maneuver as
well; these investigators reported that, among patients
with a positive relocation test on physical examination,
100% had evidence of shoulder joint injury that was suggestive of internal impingement: undersurface rotator cuff
tears, posterior labral tears, and osteochondral lesions.
Jobe35 also reported 7 positive relocation tests in his series
of 11 internal impingement patients who did not sustain
their injuries from throwing sports.
Mithöfer et al57 reported that subacromial impingement
tests are usually negative in patients with known internal
impingement, although conflicting results have been
reported by other authors. For example, one study reported
that over 25% of the 41 professional throwing athletes evaluated arthroscopically had demonstated a positive Neer or
Hawkins sign.64 However, the significance of this finding is
questionable, given that acromioplasty has not been demonstrated to lead to predictable rates of return to sport in overhead athletes.76 The active compression test may be positive
in patients with internal impingement, given the high frequency of superior labral lesions seen in patients with the
condition.
As previously mentioned, a glenohumeral internal rotation deficit, marked by a loss of greater than 30° to 40° of
internal rotation relative to the expected gain in external
rotation, compared with the contralateral side, is an overwhelmingly common physical examination finding in
symptomatic throwers. For example, Burkhart et al14
reported the presence of GIRD in 100% of a series of 124
symptomatic baseball pitchers found to have a type II
SLAP tear arthroscopically.14 In addition, scapular protraction, caused by SICK scapula syndrome and associated
with scapular dyskinesis, is a commonly reported finding
by the same investigators.15 Characteristic features
include a prominent inferior medial border of the scapula
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Internal Impingement of the Shoulder
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and the appearance that the throwing shoulder is drooped
inferior compared with the nonthrowing side. In our experience, GIRD is a common finding in symptomatic throwers, while appreciable changes in the appearance of the
scapula are relatively rare. A summary of the physical
examination findings most commonly associated with
internal impingement are listed within Figure 4.
Radiographic Findings
Radiographic evaluation of patients with signs and symptoms of internal impingement should include standard AP,
axillary, scapular Y, West Point, and Stryker notch views of
the shoulder. Four radiographic findings that have been
described in association with internal impingement
include (1) exostosis of the posteroinferior glenoid rim, also
known as a Bennett lesion; (2) sclerotic changes of the
greater tuberosity; (3) posterior humeral head osteochondral lesions or cystic “geodes”; and (4) rounding of the posterior glenoid rim. It should be noted that radiographic
findings may often be minimal or normal in patients with
internal impingement.
There is much controversy surrounding the cause and significance of the Bennett lesion. Bennett first described this
finding as the presence of an ossific deposit in the area of the
posterior glenoid, which he believed was secondary to traction of the triceps tendon on its bony origin. He observed this
finding exclusively in baseball players, noting “I do not
believe one sees [this] in other people.”6 Ozaki et al,63 who
supported the notion of posterior glenoid rim overgrowth
secondary to a traction epiphysitis of the triceps origin, identified the exostosis in 5 of 7 throwers, all of whom had pain
in the late cocking phase of the throw. However, several
studies have refuted the association between the Bennett
lesion and the triceps origin.27,54 Ferrari et al27 reported on
7 competitive baseball pitchers with posteroinferior ossific
lesions, none of which was in the region of the triceps tendon. This conclusion was also supported by a larger series of
Meister et al,54 who cited no involvement of the triceps origin. The authors recommended use of the Stryker notch
view for assessment of the posterior exostosis or osteophyte.
In their series of 22 throwers with Bennett lesions, 21
patients also had undersurface tearing of the rotator cuff
(typical of internal impingement). Thus, while the presence
of a Bennett lesion may be somewhat specific, it is by no
means sensitive for internal impingement. For example, in
their series of 17 athletes with posterior shoulder pain,
Walch et al80 reported that abnormalities in the posterior
border of the glenoid, such as the presence of a Bennett
lesion, were seen in only 6% of patients.
Wright et al84 used a “modified Bennett view,” with the
x-ray tube angled 5° cephalad and the arm abducted 45°, to
assess the asymptomatic throwing shoulders of a large
cohort of professional baseball players. The authors found
the prevalence of inferior glenoid osteophytes to be 60%,
but did not specify whether these were considered true
Bennett lesions. This represents a follow-up of a study from
Wright and Paletta,83 who previously showed the prevalence of Bennett lesions to be 22% in 55 asymptomatic professional baseball pitchers. The authors suggest that this
1031
may not represent a pathologic finding, and therefore stress
the importance of identifying concomitant sources of posterior shoulder pain when this lesion is seen. Ferrari et al27
contend that the structures seen in the region of the posteroinferior glenoid are actually extra-articular calcification, based on their review of MRI examinations, CT
arthrography studies, and arthroscopic evaluations of the
joint. The authors noted no osseous lesions in any of their
patients. Thus, while Bennett proposed that overgrowth of
the posteroinferior glenoid represented an osteophytic
extension of the glenoid rim itself, Ferrari et al suggested
that the calcific changes in the region may instead be due
to repetitive traction of the posterior capsule and PIGHL
during the extremes of the throwing motion.27 Other studies have supported these findings as well.48,60
Greater tuberosity changes are also commonly found on
the radiographs of internal impingement patients.
Mithöfer et al57 stressed the importance of assessing the
greater tuberosity for sclerotic and cystic changes; these
findings are present in approximately half of patients with
internal impingement. Likewise, Walch et al80 noted sclerosis of the greater tuberosity in 8 of 17 patients.
Interestingly, a recent radiographic study analyzing 57
asymptomatic professional baseball pitchers demonstrated
that cystic changes in the humeral head were present in
39% of shoulders imaged.84 Similar to the Bennett lesion,
this finding may not be indicative of pathologic changes,
but simply a common finding in the throwing shoulder.
Walch et al80 noted a second characteristic finding—
posterior humeral head geodes—in 8 of their 17 patients.
This likely corresponds to the osteochondral defects
detected arthroscopically by Paley et al.64 These authors
contend that such a lesion is similar in nature to a HillSachs lesion but is found more superiorly, near the insertion of the supraspinatus tendon. Interestingly, they report
that 2 patients in their series had osteochondral lesions of
the humeral head in conjunction with posterosuperior
labral damage, but no undersurface fraying of the rotator
cuff. They suggest that a small subset of throwers may
have impingement simply between the humeral head and
glenoid at slightly greater degrees of abduction, such that
the supraspinatus tendon may actually avoid interposition
and be free of injury from impingement.64
Another finding that may be seen in radiographs of
internal impingement patients is rounding or remodeling
of the posterior glenoid rim, although MRI (axial plane) is
the optimal modality to appreciate this phenomenon
(Figure 5). One study57 reported this feature in one-third of
patients with internal impingement. The finding of bony
remodeling is more common in skeletally immature throwers, in whom a process of chronic abnormal impingement
will lead to a rounded appearance in the posterior glenoid.
MRI Findings
Although meticulous inspection of radiographs for typical
findings of internal impingement is critical, MRI remains
the gold standard for workup of any young patient with
shoulder pain, particularly throwers with posterior shoulder pain. When labral lesions are suspected, many authors
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Figure 5. Axial magnetic resonance image demonstrates posterior glenoid remodeling (black arrow) and associated labral
degeneration (white arrow) in a 16-year-old baseball pitcher.
(Courtesy of the Hospital for Special Surgery Department of
Radiology.)
advocate the use of magnetic resonance arthrography with
either gadolinium contrast material or saline to better
identify labral tears and other lesions.17,18,65-67,77-79
However, Potter and coworkers have demonstrated that
noncontrast MRI demonstrates equivalent or superior sensitivity and specificity rates, when the appropriate pulse
sequences are used.19,20,31,32 Despite these findings, magnetic resonance arthrograms are commonly used at many
centers.
Typical MRI findings in internal impingement include
articular-sided partial-thickness rotator cuff tears of the
supraspinatus, infraspinatus, or both, and posterior or
superior labral lesions. Bennett lesions, humeral head
osteochondral lesions or cysts, and posterior glenoid
bony lesions have also been reported at high rates. Several
studies have shown that shoulder MRI is effective in diagnosing rotator cuff lesions, glenoid labral lesions, and
injuries to the labral capsuloligamentous complex in
throwing athletes.19,20,33 Interestingly, Halbrecht et al33
performed noncontrast MRI of the shoulder in a position of
abduction and external rotation in the throwing and nonthrowing arms of 10 asymptomatic college baseball players. Because contact between the rotator cuff and
posterosuperior glenolabral complex was seen in all shoulders, the authors concluded that this was a normal physiologic occurrence. However, in 4 of 10 of the throwing
shoulders, signal changes suggestive of tendinosis or
delamination were seen in the rotator cuff. Moreover, 3 of
the 10 throwing shoulders demonstrated labral tears with
adjacent paralabral cysts that extended towards the spinoglenoid notch. None of these findings were noted in the
nonthrowing shoulders. Given the high rate of findings in
asymptomatic patients, the authors urged caution when
considering treatment of throwing athletes based on
abnormal MRI findings.33 Similar conclusions were drawn
by Miniaci et al,56 who identified abnormalities of the
labrum in 79% of bilateral shoulders imaged by MRI in 14
asymptomatic professional baseball pitchers. However,
these investigators found no difference in the appearance
of supraspinatus and infraspinatus tendons between the
throwing and nonthrowing shoulders imaged. In contrast,
Connor et al21 reported that 40% of dominant shoulders in
a series of 20 asymptomatic elite overhead athletes had
partial-thickness or full-thickness rotator cuff tears, compared with 0% in nondominant shoulders. Likewise, MRI
allowed for identification of Bennett lesions in 25% of dominant shoulders, compared with none in nondominant
shoulders. Although Miniaci et al56 identified no clear
Bennett lesions in any of the shoulders imaged in their
series, they suggested that the enthesopathic features seen
in the posterior glenoid labrum of the 4 pitchers with internal rotation deficits may have represented pre–Bennetttype lesions. When Kaplan et al40 attempted to correlate
MRI and arthroscopic findings in 9 patients who underwent surgery for a diagnosis of symptomatic internal
impingement, they showed that all 9 athletes had posterosuperior labral lesions (fraying in 8 cases, frank tearing in
1 case) that had been diagnosed preoperatively with MRI.
In addition, cystic changes in the posterosuperior aspect of
the humeral head beneath the insertion of the infraspinatus tendon were seen in 8 cases by MRI. There was 1 additional case of moderate chondrosis in the central to
posterior aspect of the humeral head articular surface.
Arthroscopy confirmed the humeral head findings in each
of these cases. While no rotator cuff tears had been identified with MRI in the 5 athletes in whom articular-sided
partial thickness rotator cuff tears were seen arthroscopically, mild to moderate tendinopathy of the rotator cuff had
been documented in all patients by MRI.40 A summary of
the MRI findings that are most commonly associated with
internal impingement are listed within Figure 4.
Both MRI and radiographs should be used in conjunction with physical examination findings to establish a
diagnosis of internal impingement. However, as a number
of studies have shown, most of the described findings may
also be seen in the asymptomatic shoulder. Thus all the
features of the patient’s clinical picture must be considered
as a whole, with consideration of age, profession, patient
activity level, symptom severity, degree of disability, and
the effects of the condition on athletic performance and
activities of daily living.
TREATMENT AND RESULTS
Nonoperative Treatment
As with most nontraumatic injuries of the shoulder,
conservative care should be attempted in patients with a
diagnosis of internal impingement before surgical intervention is considered. Rest, cryotherapy, oral anti-inflammatory
medications, and physical therapy are the cornerstones of
nonoperative treatment. Because studies have reported
high rates of GIRD in throwers with shoulder pain, exercises should focus on posterior capsular stretching if a
capsular contracture or GIRD is noted on physical examination.14 One group of authors theorized that 90% of throwers
could reduce GIRD to an “acceptable” level within 2 weeks
of initiation of a series of posterior capsular stretches,
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1033
TABLE 1
Table Used for Documentation of Findings of Examination Under Anesthesia for Patients With Internal Impingementa
Right Shoulder
Position/Provocative Test
ROM/Test Result
IR in 0° abduction
ER in 0° abduction
IR in 90° abduction
ER in 90° abduction
Sulcus sign (+, –)
Anterior instability (1+, 2+, 3+)
Posterior instability (1+, 2+, 3+)
Left Shoulder
Position/Provocative Test
ROM/Test Result
IR in 0° abduction
ER in 0° abduction
IR in 90° abduction
ER in 90° abduction
Sulcus sign (+,–)
Anterior instability (1+, 2+, 3+)
Posterior instability (1+, 2+, 3+)
a
ROM, range of motion; IR, internal rotation; ER, external rotation
labeled “sleeper stretches.” In addition, strengthening of the
periscapular musculature and rotator cuff is generally indicated to improve scapular stabilization and to minimize
hyperextension and external rotation of the glenohumeral
joint. Burkhart et al15 reported a 100% rate of return to
preinjury level of throwing by 4 months in 96 overhead athletes treated for isolated SICK scapula with scapular muscular rehabilitation. When scapular dyskinesis is part of the
spectrum of findings that can accompany pathologic internal impingement, symptomatic improvement may be
expected. Another author reported the use of a similar regimen in all internal impingement patients except those with
concurrent greater tuberosity fractures, citing failure to
improve with these exercises as an indication for surgery.35
Approach to Surgical Management
Indications for surgery include the failure to improve with
conservative measures or inability to return to competitive
play despite a prolonged rehabilitation protocol geared
toward correction or resolution of the pathologic findings
suggested by the physical examination and the imaging.
Tibone et al76 demonstrated that acromioplasty is associated
with low rates of return to competitive sports in throwing
athletes. Therefore, subacromial decompression should be
reserved for failure of primary arthroscopic interventions
focused on the lesions of internal impingement in individuals with persistent signs of subacromial impingement.
Mithöfer et al57 also suggested that internal impingement
represents a relative contraindication to acromioplasty.
Other investigators73 have supported this nihilistic
approach to subacromial decompression in overhead athletes, with 1 team of authors characterizing classic impingement, if present, as a “secondary phenomenon.”1 However,
subacromial bursectomy may be warranted in cases where
substantial degrees of subacromial inflammation and bursitis are noted at the time of surgery1; subacromial bursectomy is frequently performed in throwing athletes by some
clincians.71
The operative approach to patients with signs and symptoms of internal impingement should be pursued in a
deliberate, methodical fashion. Because physical findings
in the awake patient may be confusing in symptomatic
throwing shoulders, the final therapeutic plan depends on
the specific findings of the examination under anesthesia
(EUA) and the diagnostic arthroscopy. Surgical intervention should be directed toward specific pathologic lesions
that are believed to correspond to the patient’s symptoms or play a role in the complex pathophysiology of
internal impingement. A graphic representation of the
recommended algorithmic approach to diagnosis and management of internal impingement syndrome is represented
in Figure 4.
Examination under anesthesia must be performed
before operative treatment of internal impingement is pursued. In most instances, bilateral EUA before surgical
draping should be performed, even if regional anesthesia
with sedation is used. The recommended components of a
routine EUA for a patient with suspected internal
impingement is shown in Table 1. The clinician must in all
cases assess the glenohumeral joint for range of motion.
Moreover, because of the importance of identifying even
subtle degrees of subluxation, meticulous attention should
be paid to the results of instability testing and the detection of a sulcus sign. While some aspects of the examination process listed in Table 1 may be performed routinely
with arthroscopic shoulder surgeries, reliance on a systematic and exhaustive approach at the EUA stage provides critical information for evidence-based selection of
surgical interventions over reliance upon dogmatic principles, given the often variable and sometimes confusing
constellation of arthroscopic findings associated with
internal impingement and the throwing shoulder.
Findings on Diagnostic Arthroscopy
and Treatment of Intra-articular Lesions
Although preoperative planning based on physical examination and MRI findings is recommended, surgeons should
perform a comprehensive diagnostic arthroscopy when
approaching an internal impingement patient. Below we
describe the results reported in the literature related to
each of the major findings associated with internal
impingement.
Rotator Cuff Tears. Articular-sided rotator cuff tears are
the most commonly seen lesions in patients with internal
impingement. In the first major series reported from the
Kerlan-Jobe Institute, 100% of a series of 41 throwing
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The American Journal of Sports Medicine
athletes showed abnormal contact between the posterosuperior glenoid rim and the rotator cuff when the arm was
placed in the position of the “relocation test”; 93% of these
patients were noted to have undersurface fraying of the
rotator cuff.64 In another series reported by Walch et al,80
76% of patients were found to have undersurface rotator
cuff tears and 71% were found to have posterosuperior
labral fraying. Although few authors distinguish between
the types of rotator cuff lesions that are associated with
internal impingement, we believe the fraying often seen at
the musculotendinous junction of the anterior infraspinatus generally warrants only minimal debridement; these
lesions are not typically full thickness. More distal, articular-sided tears near the supraspinatus footprint may be
more severe, particularly in older throwers, and may therefore necessitate repair. Despite the dearth of literature
investigating management of rotator cuff pathology in
elite athletes, we believe that the criteria used in nonathletes—debridement for small, partial-thickness (less than
50%) lesions and repair for tears that are greater than 50%
of tendon thickness—represent a reasonable guide for
overhead athletes as well. Some authors have advocated
either partial articular-side tendon avulsion (PASTA) repair
(side-to-side repair of the articular-sided supraspinatus tear
and abrasion of the humeral head insertion point), or completion of the partial tear, followed by routine single or
double-row repair with suture anchors.49,57 While repair
remains an option for high-grade lesions of the rotator cuff,
the literature suggests that most authors have not advocated repair. Sonnery-Cottet et al73 followed 25 tennis players with internal impingement for a mean of 3.8 years
after arthroscopic debridement alone of articular-sided
rotator cuff tears and posterosuperior labral lesions,
reporting an 82% satisfaction rate. Notably, however, 20 of
22 patients who returned to sport complained of persistent
pain with participation. Reynolds et al71 recently reported
on 82 competitive pitchers who had undergone debridement of small, partial-thickness rotator cuff tears, noting
an 82% rate of return to play. However, 45% of patients
were unable to return to their previous level of play.
Moreover, the reported rate of 45% may represent an overestimate, given that follow-up was obtained in only 41% of
the total series. Among other confounding factors was a
96% rate of concomitant pathologic lesions in these
patients, suggesting that isolated cuff tears are exceedingly rare in competitive throwers. Careful assessment of
partial rotator cuff lesions is recommended with meticulous
inspection for the presence of other lesions.
Labral Tears. The glenoid labrum is typically injured or
abnormal in patients with internal impingement. In a series
of 41 overhead athletes studied by Paley et al,64 88% of
throwing athletes demonstrated posterior superior labral
changes. Interestingly, they showed that anterior labral
fraying was present in 36% of patients as well. Notably, the
authors distinguished the posterosuperior labral changes
from frank SLAP tears, which they reported in only 10% of
their series. This is in contrast to Andrews et al,2 who
reported superior glenoid tears in 36 of 36 throwing athletes
investigated. Likewise, other authors have reported rates of
70% posterosuperior labral detachment in symptomatic
overhead athletes, with evidence for fraying or degenerative
changes in 80%.57 Controversy exists regarding how substantial an etiologic role labral tears may have in throwers’
symptoms. Burkhart et al contend that type II SLAP lesions
are the most common pathologic entities associated with
symptomatic throwing shoulders, and reported an 87%
return to preinjury function for 2 seasons or more in competitive throwers who underwent arthroscopic SLAP
repair.14,58 Other authors have supported the notion of SLAP
tears contributing to anterior pseudolaxity.5 The real frequency of clinically significant SLAP tears in patients with
internal impingement is not known. However, the superior
labrum should always be assessed, and we believe significant detachments of the superior labrum in young, athletic
patients should be addressed with suture-anchor repair
before considering operative treatment of anterior glenohumeral laxity. Interestingly, growing evidence suggests
that for older or less active patients, and perhaps in the setting of revision surgery as well, labral repair, particularly for
type II SLAP lesions, may be no better than debridement
alone or biceps tenotomy or tenodesis, particularly when a
concomitant rotator cuff lesion is seen and addressed with
debridement.28 Although some authors have reported good
results with biceps tenodesis for overhead athletes with
anterior shoulder pain diagnosed as corocoid impingement
syndrome,69 we believe that biceps tenodesis and tenotomy
are rarely indicated in the young, athletic population with
internal impingement, particularly elite throwers.
Anterior Laxity and Instability. The prevalence and role of
anterior laxity and instability in patients with internal
impingement has not yet been fully established. Walch
et al80 reported no cases of anterior instability in a
17-patient series of individuals with internal impingement.
However, the authors did not report on the interventions
performed in these patients or provide information on clinical follow-up. In another series,54 10 of 22 patients diagnosed with internal impingement were also found to have
anterior instability. Only 55% of these patients, who were
treated with rotator cuff and labral debridement alone,
returned to their premorbid level of throwing 1 year postoperatively. In another series of patients with anterior instability with concurrent undersurface rotator cuff tears and
posterior labral tears, treated only with debridement of the
cuff and labral lesions,70 the authors reported only a 25%
rate of return to sports and 37% satisfaction rate. Paley et
al64 suggest that because of the high rate of anterior instability seen in throwing athletes in their studies, anterior
capsulolabral reconstruction should be considered in
conjunction with arthroscopic treatment of posterior
impingement lesions. The authors cite previous supportive
studies,38 which have suggested high rates of return to competitive play in throwers undergoing anterior capsulolabral
reconstruction. Others have suggested that open anterior
capsular repair may be the preferred treatment in some
throwing athletes with signs of instability.1 In contrast,
Levitz et al46 reported on treatment of internal impingement with use of thermal capsulorrhaphy as an adjunct to
debridement of undersurface rotator cuff tears and labral
debridement. At 30 months after arthroscopic surgery, 90%
of throwing athletes treated with the combined technique
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had returned to play, compared with 67% of patients treated
with rotator cuff and labral debridement only. This investigation underscores the concept that addressing anterior
microinstability may improve outcome in this patient population. However, based on more recent studies regarding
the range of complications associated with the use of thermal capsulorrhaphy,29,45,82 we believe that arthroscopic
suture capsulorrhaphy should be favored over thermal
capsulorrhaphy for treatment of anterior microinstability
or gross instability, which should be noted at the time of
the examination under anesthesia, and can be executed by
simply plicating the tissues of the anterior IGHL to the
anterior labrum. Alternatively, suture anchors based at
the anteroinferior glenoid can also be used to achieve the
same end. In all cases, the instability phenomena noted
during EUA should be eliminated after this portion of the
procedure.
Posterior Capsular Contracture. While some authors
have emphasized treatment of anterior instability in
throwers with internal impingement, Burkhart et al contend that contracture of the PIGHL and posterior capsule,
resulting in GIRD, is the initial etiologic lesion responsible
for the development of SLAP tears in the disabled throwing shoulder.12-16 Accordingly, they have advocated specific
posterior capsular stretching exercises, called “sleeper
stretches,” as first-line treatment for most symptomatic
throwers and as a preventive measure for active pitchers
to prevent dead-arm syndrome.14-16 The authors suggest
that while rates of failure of these conservative measures
are exceedingly low, particularly in younger pitchers,
arthroscopic posteroinferior capsular release may be performed in conjunction with SLAP repairs in older pitchers
who do not respond to stretching. We believe that GIRD is
likely a commonly overlooked condition in symptomatic
throwers and advocate a rigorous physical therapy regimen, with consideration of capsular release following diagnostic arthroscopy if nonoperative treatment fails.
Humeral Head Lesions. As abnormalities of the humeral
head are common in internal impingement, the humeral
head should be taken through a full range of motion and
assessed for chondral damage and osteochondral lesions.
Osteochondral lesions in patients with internal impingement are most frequently encountered on posterior aspect
of the humeral head, near the insertion of the posterior
edge of the supraspinatus tendon. Unstable lesions may be
debrided.57 One group of authors64 reported osteochondral
lesions of the humeral head in 17% of 41 throwing athletes
who underwent arthroscopy. The authors differentiated
these lesions from Hill-Sachs lesions, noting them to be
more superior, adjacent to the insertion of the supraspinatus insertion, and all smaller than 1 cm in diameter.
Although most of the osteochondral findings consisted of
grade II and grade III changes, there was 1 full-thickness
cartilage defect in their series. In our experience, debridement of humeral head lesions is rarely necessary.
Bony Glenoid Lesions. Although it is generally understood
that mild posterior glenoid rounding or remodeling may be
seen and is not amenable to operative treatment, the role of
surgery to address Bennett lesions and similar bony posterior glenoid lesions remains an area of controversy.
1035
Interestingly, while Ferrari et al27 contend that such
lesions require no operative treatment, Yoneda et al85
reported on a series of 16 patients with Bennett lesions
who underwent arthroscopic debridement or “Bennettplasty.” The described surgical technique, which involves
detachment (and subsequent repair) of the posteroinferior capsule for access to the lesion, supports the suggestion that such lesions are extracapsular. However, in
contrast to Ferrari’s conclusion that the Bennett lesion
represents an ossification of the posterior capsular soft
tissues, the authors demonstrated that the bony overgrowth was contiguous with the glenoid in all cases.85
Although 88% of the patients in the series by Yoneda et
al were satisfied at a minimum of 1 year after the procedure, most patients had soft tissue procedures (including
bursectomy, rotator cuff debridement, Bankart repair,
biceps and labral complex debridement or repair) performed concurrently, thus confounding any definitive conclusions about the efficacy of arthroscopic debridement of
Bennett lesions. Meister et al54 were the first to report on
arthroscopic resection of Bennett lesions, but performed
such an intervention on only half of the 22 patients in
whom such findings were detected preoperatively. The
remaining patients underwent associated soft tissue
treatments, the most common of which was debridement
of partial-thickness tears of the rotator cuff. The authors
concluded that when an exostotic lesion is seen in conjunction with posterior shoulder pain, arthroscopic
debridement is appropriate, particularly when the lesion
is larger than 100 mm2 in total size.54 Despite some supportive literature, we have typically not found debridement of posterior glenoid exostoses a useful tool in
treating overhead athletes with internal impingement.
SUMMARY
Although the understanding of internal impingement as a
unique condition of the shoulder continues to evolve,
cadaveric, biomechanical, and clinical studies suggest that
its cause is multifactorial and that a variety of anatomic
structures are involved. Nevertheless, it seems clear that
the thrower’s shoulder is particularly at risk for the development of internal impingement due to the repetitive and
forceful nature of the overhead throw and its requirement
that the arm be in the abducted and externally rotated
position. Articular-sided, partial-thickness lesions at the
musculotendinous junction of the infraspinatus tendon or
at the distal insertion of the supraspinatus tendon, posterosuperior labral tears, and a loss of glenohumeral internal rotation are the hallmark findings of this condition.
While physical examination findings alone seldom establish the diagnosis, posterior joint line tenderness, the posterior impingement sign, and the relocation sign should
raise one’s index of suspicion for internal impingement.
There are several commonly identified radiographic and
MRI findings in patients with internal impingement, but
the high frequency of similar abnormal findings in asymptomatic throwers makes correlation of such findings with
clinical symptoms essential. A systematic approach to
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1036
Heyworth and Williams
The American Journal of Sports Medicine
treatment of all sources of pathologic abnormalities that
combines thoughtful consideration of patient complaints,
imaging studies, findings from examination under anesthesia, and diagnostic arthroscopy provides optimal
results. However, outcomes data on patients with a specific
diagnosis of internal impingement remain sparse and
additional research efforts are warranted.
ACKNOWLEDGMENT
The authors thank Dr Hollis Potter for her assistance with
the preparation of this manuscript.
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