The debatable
concept of impingement syndrome
S.
Galanakos, B. Sakellariou, I. Sofianos, K. Kateros
Orthopaedic Clinic, General Hospital of Levadia
ABSTRACT
The shoulder joint is related to the majority of syndromes of the
myoskeletal system. This is due to the fact that the shoulder is the
most mobile and one of the most complicated joints of the body (5
joints system).
Here is presented the anatomy and the embiomechanics of the joint
and its surrounding structures, as well as the anatomical background
of their disorders -information which may help in better understanding
the pathologoanatomic disorders studied –as well as the therapeutic
management of each one.
The description of their operative treatment constitutes a separate
chapter which is out of the scope of this article.
Key
words: Rotator cuff, sub-acromial impingement syndrome, tear of
rotator cuff.
INTRODUCTION
Shoulder joint should be viewed as a five joints embiomechanic system
and should be studied as a combination of the glenohumeral joint together
with the rest joints that constitute the whole shoulder girdle.
We will focus on the glenohumeral joint and the disorders of its anatomical
structures which cause the functional disorders, trying to give advantage
to a better presentation.
The shape of the adjacent articular surfaces of the glenohumeral joint
and the relation of their size, together with the relatively loose
articular capsule, create an extremely mobile joint. These particular
advantageous for the mobility factors are also responsible for the
shoulder instability in relation to the other human joints.
This joint is heavy loaded. The motions of the shoulder, with the
hand above horizontal level, wear the joints and adjacent soft tissues
and are the causing factors of occupational diseases (tendonitis).
It is important to comprehend both the anatomy and the embiomechanics
of each joint, so that an orthopaedic surgeon could manage the rehabilitation
of each disorder. In the shoulder this is more important because of
the increased mobility of the joint.
THE ANATOMY OF THE SHOULDER
Bones
and muscles
The glenohumeral is a multi-axis, spheroid diarthrosis, with the humeral
head and the glenoid fossa being the main articulating substances.
The humeral head is an even spheroid surface, which is the 1/3 or
better the 2/5 of a sphere, with a radius about 30mm. Radius and consequently
orbicularity of humeral head is decreasing from the upper part to
the lower. When the limb is hanged flabbily, the head is turned backwards,
slightly internally rotated rotation and upwards directed. The axis
of the humeral head forms with the longitudinal axis an angle 140o
which is called inclination angle (figure 1) and with the frontal
plane a 30o-35o angle (open backwards), owed to the twist of the humerus
(figure 2).
The glenoid fossa is a shallow and slightly concave articular surface
externally oriented, slightly anteverted and upwards facing. It has
an oval shape with its large diameter (about 35mm) being vertical.
Its surface, as well as its orbicularity, is smaller than those of
the humeral head. The articular lips are filled by the glenoid cartilage
by which it becomes larger and deeper.
The fibrous articular capsule is so lax that the 2 bones can separate
each other as far as 2-3cm without any danger of tearing. This is
one of the reasons that the joint has a great range of motion and
the presence of the axillar recess in the lower aspect of the joint
is an excellent contributor to the abduction of the humerus.
The fibrous capsule is stronger in areas where the greater mechanical
loads are developed. These stronger bands are called retinaculum ligaments:
the coracohumeral ligament, the 3 glenohumeral ligaments (superior,
medial, inferior) and the transverse ligament of the humerus.
Except from the auxiliary ligaments, an important stabilizing factor
of the shoulder is the tone of the surrounding muscles. The supraspinatus
tendon enhances the fibrous capsule from the top, the infraspinatus
and the teres minor posteriorly and the subscapularis tendon anteriorly.
All four tendons constitute the rotator cuff of the shoulder joint
(figure 3).
There are some other surrounding muscles which contribute with their
tone to the stability of the joint: the deltoid muscle superiorly,
anteriorly and posteriorly, the pectoralis major the short head of
the biceps and the coracohumeral from the front, the latissimus dorsi
and the teres major inferiorly, contributing to the apposition of
the humeral head against the glenoid, in collaboration with the long
head of the biceps muscle and the long head of the triceps muscle
inferiorly.
Other auxiliary stabilizing factors of the joint are the negative
intrarticular pressure, the coherence forces (surface tension) which
are developed between two articular surfaces due to the presence of
the articular fluid and the shoulder dome. Nevertheless, it is not
a real part of the joint, its contribution to the stability is so
notorious that the superior translocation of the humerus is impossible
except the clavicle or/and the acromion has been fractured.
Figure 1. Figure
showing the angle of the anatomic neck with the horizontal plane and
the inclination angle humerus of the humeral head. (Source: Άγιος
Αλέξανδρος. Περιγραφική και Εφαρμοσμένη Ανατομική. Το κινητικό σύστημα,
2002, 380)
Figure 2. Rotation angle of the left humerus. Transverse axis of upper
in the final and initial positions. AA and A1A1. The axis of lower
humerus BB. (Source: Gray’s Anatomy)
Figure 3. Figure
showing the rotator cuff of the right shoulder. Superior view.
(Source: Άγιος Αλέξανδρος. Περιγραφική και Εφαρμοσμένη Ανατομική.
Το κινητικό σύστημα, 2002, 380)
The polyarticular
complex of the shoulder[24]
Not only one but five joints contribute to the formation of the
shoulder, as already mentioned. These joints are classified into
two groups: the first one consists of two joints and the second
of three.
- First group:
1. Gleno-humeral joint. A typical diarthrodial joint, the most important
of this group.
2. Sub-deltoid joint. This is not an anatomical but a functional
joint. It consists of two surfaces gliding one on the other. It
is mechanically related to the shoulder joint because every motion
of the latter generates motion to the former.
- Second group:
1. Thoraco-scapular joint. It is also a functional joint and the
most important of this group, because it cannot function without
the other two which are mechanically related to it.
2. Acromio-clavicular joint. This is a true diarthrodial joint positioned
to the acromial end of the clavicle.
3. Sterno-clavicular joint. It is a true joint positioned to the
sternal end of the clavicle.
Practically, these two groups function together with different contribution
on each other, related to the motion (figure 4).
Figure 4. Figure showing the two joint groups of the shoulder.
(Source: Kapanji IA. The physiology of the joints, vol. 1. Upper
limb. 1982. p. 1-71)
Biomechanics
of the shoulder joint[1,7]
The shoulder is the most mobile diarthrosis of the human body, and
this is due to the proper formation and positioning of the articular
surfaces and to the elasticity and flexibility of the surrounding
tissues. Functionally, it is classified to the multi-axial joint,
because it can produce a great range and variety of motions, as
a result of combined glide and rotation of the adjacent articular
surfaces.
The motions of this joint are produced on three planes:
1. In saggital plane where the humerus is adducted and abducted
2. Transversal where motions of flexion and extension are done and
3. Around a longitudinal axis where the humerus twists inwards and
outwards.
The circumduction is the combination of all referred above combined
in multiple axes. The range of motion becomes even wider with the
participation of the acromio-clavicular and the sterno-clavicular
diarthrosis, the motions of the scapula and the inclination of the
vertebral column[44].
The normal range of motions of the shoulder is: abduction 0o-180o,
adduction (anterior 0ο-45ο and posterior 0ο–30ο), flexion 0ο-180ο,
extension 0ο to 45o-50o, external rotation 0ο to 80o-90o and internal
rotation 0ο to 90o-110o.
The above mentioned joint motions are referred to muscles or group
of muscles as described in table 1 and figure 5.
Figure 5. The
right shoulder after dissection of the joint capsule and removal
of humerus.
(Source: Campbell’s Operative Orthopaedics, 2003)
ROTATOR
CUFF DISEASE OR IMPINGEMENT SYNDROME
INTRODUCTION
This syndrome includes all the symptoms which are caused from the
impingement of the rotator cuff between the humeral head and the coraco-acromial
arc, rarely the acromio-clavicular joint. The arc is developed by
the frontal one third of acromion, the coraco-acromial ligament and
the coracoid process. It is an inelastic tough wall, below which is
located the infra-acromial bursa, the rotator cuff (subscapularis,
supraspinatus, infraspinatus, teres minor) and the biceptal long head
tendon. The role of the subacromial bursa is to facilitate the motion
of the rotator cuff (figure 6).
The subacromial space is located below the coraco-acromial arc, and
its width ranges between 1 and 1.5cm.
Figure 6. The rotator
cuff of the shoulder. Figure demonstrating the right shoulder in superior,
posterior and anterior view (SS: supraspinatus, IS: infraspinatus,
TM: teres minor, Sub: subscapularis).
(Source: Ward R. Samuel, PT, et al. Rotator Cuff Muscle Architecture.
Clin Orthop Relat Res 2006; 1-7)
FREQUENCY
It is the most frequent cause of pain in the shoulder area and it
represents the 3rd most frequent disease of the myoskeletal system
(16%), after the ache of the cervical spine (23%) and the knee (19%)[4].
One third of the patients coming to the outpatients’ department have
symptoms related to the rotator cuff[42]. Usually, these are young
patients participating in sports such as volleyball, basketball, tennis,
swimming, throws and patients working with fruit collection, gardeners,
carpenters, painters and people over 60 years old, to whom the disease
appears without any specific reason (figure 7).
Figure 7. Image
showing some causal factors of rotator cuff injury.
ETIOLOGY
The etiology of the disease is multi causal[41,43]. The causes are
organic and functional. The organic causes include all the factors
that alter the dimensions of the subacromial space, affecting the
bones and soft tissues located under the acromion.
The functional causes include factors that influence the dynamics
of the muscles surrounding the acromion, without any affection to
the bones or the soft tissues of the shoulder.
A. Anatomical disorders and pathologoanatomical lesions of bones.
These include:
- Abnormalities to the shape or the inclination of the acromion (figure
8). There have been described 3 different types. Type 1 or flat (17%),
type 2 or curved (43%) and type 3 or hooked (39%). The impingement
is greater in type 3 (70%)[32].
1. Arthritis of the acromio-clavicular joint or/and osteophytes formation
on the lower part of articular surface, causing an abnormal mechanical
friction and wear of the rotator cuff.
2. Non ossified epiphysis of the acromion, causing an abnormal friction
of the rotator cuff.
3. Fractures of the greater humeral tuberosity, united in slight superior
displacement.
4. Fractures of the humeral neck with varus malunion, which produces
a prominent greater humeral tuberosity, decreases the subacromial
space and finally causes impingement of the rotator cuff.
B. Pathologoanatomical lesions of the soft tissues:
1. Lesions of the rotator cuff after repeated micro-injuries especially
in athletes who overuse their upper limb in activities over shoulder
level (overuse syndrome). These micro-injuries cause: a) tendon irritation
and oedema or/and micro-tears both of which lead to impingement, b)
deterioration of the already bad circulation of the area near the
insertion of the supraspinatus tendon (critical zone) resulting to
degeneration or/and partial tear of the tendon.
2. Lesions of the subacromial bursa due to multiple micro-injuries
or a major trauma or inflammation. All the above lead to fibrosis
and consequently to pathological augmentation of adjacent soft tissues.
C. Functional causes:
1. Upwards displacement of the humeral head due to a decrease or loss
of the stabilizing action of the rotator cuff. The second may be a
result of a radiculitis of C5-C6 roots, suprascapular nerve paralysis
or rupture of the biceps muscle’s long head. Trying to abduct the
upper limb, the humeral head moves upwards, causing a decrease of
the subacromial space and impingement.
2. Strain and laxity of the anterior inferior glenohumeral ligament
in throwers and swimmers may cause an anterior inferior instability
of the shoulder and tendonitis due to rotator cuff tendon strain and
subacromial impingement syndrome symptoms. The coexistence of these
two conditions of impingement and instability is a difficult diagnostic
and therapeutic problem.
Figure 8. The 3 types of acromion (flat, curved, hooked).
(Source: Campbell’s Operative Orthopaedics, 2003)
PATHOLOGY
In 1834, Smith first described rotator’s cuff tendon rupture as
a disease. Later, other authors such as Duplay, Von Meyer, Codman8
and recently Neer[22,23] elucidated the degenerative procedures
taking place in the area, but the exact cause and pathology of the
disease is still not clarified.
The endogen and exogenous hypothesis have been proposed by several
authors in order to clarify this pathological entity.
The exogenous hypothesis regards to all these factors that influence
externally the rotator cuff (shape of the acromion, overuse of the
limb over the shoulder), while the endogen hypothesis includes the
great spectrum of procedures generated by the tendon itself (degeneration
of its fibers passing the age)[40].
Degenerative procedures or/and overuse of the tendon’s collagen
fibers seem to be the initial factor, which leads to a cascade reaction
leading to the total rapture of the rotator cuff’s fibers. This
overuse may be caused by traction or compression forces, in an acute
or chronic base and lead to a lesion of the site of insertion of
the supraspinatus muscle. If the lesions happen more often than
the tendon ability to recover, a rotator cuff dysfunction is ongoing,
loss of humeral head steady positioning on front of the glenoid
fossa during the shoulder lift. Humeral head lifts upwards and causes
a secondary impingement of the supraspinatous bursa on the acromion,
leading to a coracoacromial ligament hypertrophy and osteophytes
formation, which causes greater lesions to the rotator cuff.
Hyvonen and Lohi evaluated 96 patients after an operative treatment
of their impingement syndrome, with the method of acromioplasty.
They noted that 20% of the patients, although treated operatively,
developed rotator cuff rapture after a 9 years period[20].
In addition, in the hip joint, there has been described rupture
in the insertion of the lesser and medial gluteus muscle of the
abductors, which is relative to the shoulder lesion. The difference
is that the lesion there is caused by degenerative procedures due
to ageing and moreover there is no bone participation (osteophyte
formation) leading to impingement[3].
Although many believed that the ignition factor of disorder was
exogenous (traction and compression forces), it is believed now
that this is a fact that happens on later and they lead to the conclusion
that it is likely the lesion itself and the tendon dysfunction that
generate the disease procedure.
If we accept the endogen beginning of the disease, we have to answer,
how first lesion begins. Is it a degenerative procedure related
to the age or a result of a continuing stress? Or is it the combination
of these two?
There are studies that prove the direct correlation of the lesion’s
grade to the age. Cadaveral observations showed greater lesions
to ages between 70 and 90 years[10,32]. Other authors worked on
the presence of a rotator cuff lesion to asymptomatic patients,
using MRI. They found out no patient under 40 had a rotator cuff
lesion, between 40 and 60 years 4% had a small tear and over 60
years old the percentage increased to 24%.
Consequently, we have a new question: which are the reasons that
some lesions give no symptoms and some other do? Some people believe
that the continuous, persistent stress on the rotator cuff is the
initial cause of its symptomatic dysfunction[2]. If the lesion deterioration
is faster than the tendon ability to repair, a procedure occurs
which consist of new vessels formation and fibroblast deposition.
Practically, this is the normal inflammatory response to the injury.
Nevertheless, new formed inflammatory tissue aiming to a normal
healing procedure, worsens the impingement to adjacent structures,
deprives normal healing itself. At the end, the damage cannot be
restored. It is resembles to the model of the hypertrophic pseudarthrosis,
during the achievement to callus formation and union of the bone.
In young throwers, it is established with arthroscopy that the initial
lesion of the articular surface of the supraspinatous muscle insertion
was combined with an injury of the posterior and superior of the
articular lips. This is caused by the friction of two areas after
an overuse of the shoulder while humerus is extremely abducted and
externally rotated[38] (figure 9).
Recently there has been described the essence of the anterior, superior
and medial impingement, happening during the humeral flexion and
internal rotation. A lesion developed by the friction of the biceps
tendons (biceps pulley) to the anterior and superior region of the
glenoid cartilage. Under arthroscopic insertion, a lesion of the
superior surface of insertion of the subscapularis muscle and some
times in the anterior region of the supraspinatus insertion fibers
can be found. This occurs mainly in mid-aged athletes and consist
4% of all tears[18].
Conclusively, even today, it cannot be said in a certain way, which
is the incident that happens first in the rotator cuff disease and
leads to anatomical and functional abnormalities of the tendon.
Probably, these two hypotheses (endogen and exogenous) coexist and
are expressed with a different way under a different process and
turn out to a common way, resulting to the lesion and tendon dysfunction.
Figure 9. Figure showing the supraspinatus tendon impingement at
the extreme elevation and external rotation of the upper limb. (Source:
Campbell’s Operative Orthopaedics, 2003)
Lesions classification
According to Neer, there are 3 stages in the lesions of the rotator
cuff impingement syndrome[5] (table 2). The classification is based
upon the age of the symptoms are appearing, the pathologoanatomic
background and the disease prognosis. However, there is not necessarily
correlation between the stages and the age. For example, if a 50
years old person is examined as soon as the first incident of impingement
happens, it may have lesions stage 1, and reversely, a patient under
30 examined long time after onset of the impingement procedure may
have stage 2 lesions[43].
Diagnosis
The primary element in the diagnosis is patient’s history and after
that the clinical and laboratory examinations.
History
In 1934 Codman[8] described the symptoms and signs of the disease,
developing the patient’s “model”, including people working manually,
aged over 40 years, with a shoulder being normal till that time, coming
with a medial graded pain which become more intense during the night,
decreases with rest and there are silent intervals. There is tenderness
located laterally of the acromion radiating, to the lateral and anterior
surface of the deltoid muscle, decrease of its strength, difficult
and painful motions, feeling of locking when abducting the shoulder
or flexing and internal rotating the limb. Pain reappears when the
humerous is adducted. Crepitus, muscle spasm and oedema in the referred
area.
Examining closely the history elements and information, we note[6,36]:
a) The patient’s age. Pain in the young athlete’s shoulder using the
limb over the horizontal plane indicates possible shoulder instability
in the future. In older ages we should inquire for other causes, such
as a rotator cuff disease or a frozen shoulder.
b) The patient’s profession. Handworkers, throwers, workers with their
limbs elevated.
c) The mechanism of injury. If a history of a fall exists, shoulder
damage may hide a dysfunction of the glenohumeral joint or a possible
fracture. Acute, repeated injuries may lead to tendon wearing, while
chronic, to degenerative procedures of the cuff.
d) The onset. A gradual onset may indicate a tendonitis or osteoarthritis,
while an acute, usually correlates to a trauma, fracture, joint dysfunction,
or cuff tear.
e) The localization of the pain. Pain in the lateral and superior
region of the shoulder indicates tendon damage, while in the anterior
surface, tendonitis of the biceps long head, wear of the acromio-clavicular
joint or anterior instability. Cervical spine diseases often resemble
shoulder problems.
f) The pain intensity. Acute, burning pain is usually due to inflammation
of the bursa, while remittent and diffuse pain is usually caused by
a rotator cuff disease.
g) The restriction of the joint mobility. Restriction of the passive
and the active joint motions is usually due to frozen shoulder or
inflammation of the synovial membrane of the joint capsule. Restriction
of the internal rotation is often caused by cuff disease, while inability
of the active abduction usually coexists with cuff rupture or frozen
shoulder.
h) Crepitus is usually caused by degenerative disease of the rotator
cuff.
i) Previous therapeutic or diagnostic procedure for the problem.
j) The symptoms’ progress.
Clinical
examination
The clinical examination[6,36] starts with the inspection of the
patient. The stance, the shoulders symmetry and the uniformity of
their curvatures, the presence of oedema, skin redness, muscle atrophy,
hair loss are noted. The inspection demands observation of all aspects
of the patient, anterior, lateral, superior, and posterior. We also
observe spinal abnormalities, scoliosis or kyphosis.
Then we proceed to the palpation of the bones and soft tissues of
the area. Usually the examiner stands behind the patient, checking
anterior, posterior, superior and lateral aspects. We examine the
sterno-clavicular joint, the clavicle, the sternum, sternocleidomastoid
muscle, the 1st rib, the acromio-clavicular joint, the coracoid
process, the acromion, the humeral head and the muscles of the shoulder.
The palpation of all structures should be performed if possible
with stable and gentle manipulations in comparison with the other
shoulder. We also check the range of motions, the active, passive,
and under resistance motions. Lack of active motion may be observed
due to pain rigidity, or patient’s will. Estimating the passive
motion, we evaluate the condition of the bones, the ligaments, and
the articular cartilage, while the motion under resistance gives
information on the muscle contractibility[9].
The clinical examination is completed with a series of clinical
tests which estimate the motion under resistance. They evaluate
the pain and muscle inability.
1. Positive painful arc
Pain during abduction, with the limb remaining in internal rotation,
between 60o-120o. The passive abduction is less painful than the
active. The pain is due to impingement of supraspinatus tendon between
the humeral head and subacromial dome, created by the acromion and
the coraco-acromial ligament. Between 120o-180o pain decreases or/and
disappears. If it persists in this range, and particularly between
150o and 180o, it indicates the participation of the acromio-clavicular
joint.
2. Decrease of the strength of external rotation (figure 10)
The examination is done with the elbow flexed in 45o, while the
arm is in contact to the thoracic wall, when the 90% of strength
is created by the infraspinatus muscle. When the limb is in abduction,
the posterior part of deltoid contributes to abduction.
3. Neer’s impingement sign (figure 11)
It is first described by Neer in 1972 as a “pain in the anterior
surface of the acromion while raising the limb”. The scapula is
pushed from above with the left hand (examination of the right shoulder)
so that the motion of the thoraco-scapular ‘joint’ is eliminated,
while the arm is elevated until the greater humeral tuberosity is
pushed to the anterior surface of the acromion, creating pain. The
test may be also positive in diseases of the shoulder, such as stiffness
(frozen shoulder), instability, arthritis, tendonitis ossificans
and bone lesions.
The frozen shoulder is a particular disease, with main characteristic
the localized acute pain and the restriction of joint motions, both
active and passive. Its etiology is multi-factor, related to longtime
immobilization of the shoulder, acute or chronic trauma, supraspinatus
tendonitis or tendonitis of the long head of biceps, diabetes mellitus,
thyroid diseases, cardiovascular and neurological diseases. It may
also be idiopathic[5,42].
4. Restriction of adduction with the limb in internal rotation in
front of the thoracic wall due to shrink of the capsule.
5. Examination test of the impingement sign after injection of local
anesthetic (Neer’s Impingement test)
The pain is relieved and the arm is abducted without any pain after
injection of a local anesthetic agent in the subacromial space.
It is the safest way to diagnose a lesion of the rotator cuff, and
it can be the treatment in stage 1 and 2 lesions but not in complete
cuff ruptures. In case of painful abduction the diagnosis of impingement
should be set under consideration.
6. Hawkins’ test12 (figure 12)
It was described in 1980 by Hawkins and Kennedy[19] as a variation
of Neer’s test. Here, the arm is flexed in 90ο and then internally
rotated. During this movement, the impingement of the greater humeral
tuberosity under the coraco-acromial ligament creates pain. If the
pain appears with the arm in 90o abduction and 30o adduction, it
is due to anterior and superior impingement. If the pain appears
only with the arm flexed in 90o, it is due to anterior and medial
impingement.
7. Yocum’s test[12] (figure 13)
It is described in 198339 checking selectively the supraspinatus.
With the examiner standing behind the patient, we instruct him to
touch with the palm of the painful limb the other shoulder passing
the arm anteriorly. Then, he is asked to raise his elbow, under
examiner’s resistance. The pain produced, is created from the contact
of the rotator’s cuff synovium with the coraco-acromial ligament
and probably the inferior surface of the acromio-clavicular joint.
A positive test indicates anterior-superior or anterior-medial impingement.
It is important to mention that the sensitivity of Yocum’s test
is only 78%, while the sensitivity of all tests together (Neer,
Hawkins, Yocum) reaches 100%, which means that the triad of tests
should be performed all together systematically.
The control test of the impingement sign and the Hawkins’ test are
compared to the following table (table 3) on their sensitivity,
specificity, positive and negative prognostic value[26].
It should be mentioned that the impingement sign test, is positive
in Bankart lesions in 25% and 46% in SLAP (Superior Labrum, Anterior
and Posterior Lesions), that is in superior, anterior, posterior
and posterior lesions of the articular lips. In patients with acromio-clavicular
arthritis, the test becomes positive in 69%. The Hawkins’ test is
found positive in Bankart lesions in 31% and 69% in SLAP, while
in acromio-clavicular arthritis the test becomes positive in 94%[26].
Laboratory exams
Radiographic evaluation, high density calcified deposits could be
found in the viscidity of the humeral head or the greater humeral
tubercle. A similar lesion can be found in the inferior surface
of acromion, which is in contact with humerus (sourcil-eyebrow-sign)[9]
(figure 14).
Ultrasound[37]could be helpful (figure 15) to focus the affected
area, while MRI (figure 16) verifies the rupture, the size of which
is estimated arthroscopically.
The ultrasound imaging shows better ruptures of the rotator cuff
less than 3mm, while MRI shows better large ruptures[2].
Figure 10. Rotator
cuff muscles strength evaluation.
(Source: Συμεωνίδης Π. Ορθοπαιδική. Κακώσεις και παθήσεις
του μυοσκελετικού συστήματος, 1996, 360)
Figure 11. Examination
to elicit the impingement sign. (Source: Συμεωνίδης
Π. Ορθοπαιδική. Κακώσεις και παθήσεις του μυοσκελετικού συστήματος,
1996, 360)
Figure 12. The
Hawkins’ test. (Source: The Nicholas Institute of Sports Medicine
and Athletic Trauma)
Figure 13. Yocum’s
test. (Source: The Nicholas Institute of Sports Medicine and Athletic
Trauma)
Figure 14. In
plain x-ray a sclerotic locus is shown in the inferior surface of
acromion (sourcil sign). (Source: Campbell’s Operative Orthopaedics,
2003)
Figure 15. U/S
demonstrating a supraspinatus muscle rupture.
(Source: Bunker T. Rotator cuff disease. Current Orthopaedics 2002;
16:223-233)
Treatment
The treatment[13,27,28] is conservative and operative and is related
to the stage of the lesion.
The conservative treatment consists of anti-inflammatory drugs, restriction
of movements that cause pain, especially those over the horizontal
level, cold and warm application.
If all these do not give any result in a period of 2-3 weeks, we can
proceed in one or two sessions of injections with local anesthetic
and corticoid with at least one week intervals. Further local injections
may lead to tendon ruptures, tendon atrophy and decrease of the lesions
restoration ability. This therapeutic approach is generally preferred
in elderly patients. After injection, mild and careful kinesiotherapy
follows. If symptomatology lasts beyond 2 weeks, (Neer stage 2) the
injection can be repeated, combined with active kinesiotherapy. In
cases which are not improved in 3 weeks period and the function handicap
is severe, surgical treatment should be considered.
Surgical treatment consists of open or arthroscopic decompression.
This includes resection of the anterior part of acromion together
with a part of the coraco-acromial ligament, to increase the space
between rotator cuff and acromion, restoring the recent ruptures of
the cuff as well. The older ruptures can be restored operatively,
with doubtful, however, results.
Musculotendinous
or rotaror cuff rupture
Introduction
The ruptures of the rotator cuff usually happen in patients aged over
40 years, after a violent, sudden movement of the arm, weight lift
or during an ordinary motion, especially abduction or flexion.
Etiology
The most common causes of rupture, that take place near the rotator
cuff insertion, are trauma, degeneration, ischemia, and subacromial
impingement. A rupture of the long head of the biceps muscle often
coexists.
According to Neer (1983) the most frequent, from all causes mentioned
above, is the subacromial impingement with a percentage value almost
95%.
From the anatomic aspect, the ruptures are related to the supraspinatus
insertion. Rupture of the rotator cuff in young patients is extremely
rare and happens after severe trauma or antero-inferior dislocation
of the shoulder.
Pathology
The supraspinatus tendon rupture, as mentioned, is related to the
rotator cuff impingement disease. We cannot determine the exact
time that this will happen. Moreover, it cannot be said that the
impingement will always lead to a tendon rupture; neither could
we define the percentage of the patients which will suffer from
a tendon rupture.
A repeated and exaggerating use of the supraspinatus tendon, lead
to tendon’s fibers lesions, aggravating the age evoked degeneration.
The tendon lesion is occurred close to the insertion, 7mm posterior
to the long head of biceps (figure 17). This location is named “Codman
location” or “critical zone”, due to the poor blood supply, as it
is described by Codman in 1934. However, after histological, cadaver,
and U/S Doppler studies it seems that the articular part of the
tendon is sufficiently irrigated. It is also proven that there are
anastomoses between the vessels outgoing from the muscles and those
destinating to the bones[42].
Others insist that the blood supply is related to the position of
the arm while it is moving, with better supply in adduction[34].
It seems that a coexistence of the internal tendon lesion and the
external impingement may be possible. An extreme tendon overuse
and the inability of on time healing may lead to a sequence of procedures
with the following results[35]:
i. The load of the neighboring intact tendon fibers is increased.
ii. A part of the fibres located to the insertion is avulsed, reducing
the strength of the rotator cuff.
iii. The alteration of the anatomic relation affects the fiber’s
blood supply leading to localized ischemia.
iv. The exposure of the tendon fibers in an environment full of
articular fluid, containing lytic enzymes, which degrade developed
hematoma, deprives tendon to have a normal healing procedure.
The final result is a tendon without its natural strength, vulnerable
to smaller forces. Consequently it misses gradually its ability
to stabilize the humeral head against the glenoid fossa, during
the first phase of abduction motion, resulting the upwards shift
of the head, impingement to the shoulder dome, and friction of the
subacromial bursa between humeral head and acromion. During this
secondary impingement, 4 grades of lesion have been noted under
arthroscopy: 1st) tissue deficiency in the area under acromion,
2nd) thickening of the coraco-acromial ligament, 3rd) fibrosis of
the coraco-acromial ligament, and 4th) calcifying deposits at the
inferior surface of acromion[40].
The inherent strength of tendon insertion resists to the avulsion
while local forces are applied on it. However, the flat and most
vulnerable part of the tendon, just before its insertion, is likely
to be ruptured. The physical process of tendon rupture starts a
“pin head lesion”, developing to a “C” shaped one.
According to supraspinatus tendon fibers dynamics, a “C” shaped
lesion could be expected. However it confines to an irregular shaped
“L” type lesion (figureure 18).
The pain produced during the joint motions, leads to local muscle
contractions and limitation of muscle action. The combination of
these two results a muscle strength limitation and loss of joint
structures stability. The impingement of the humeral head under
the acromion (figure 19), induces the transverse ligament degeneration,
and instability, resulting to the long head of biceps muscle gliding
anteriorly, producing a pathological formation resembling the “Boutonniere
deformity” of the fingers extension mechanism (figure 20).
The impingement between the joint capsule and acromion is now continuous
and constant, leading to the final stage of the rotator cuff disease’s
spectrum, the “bald head tear” and later on the “cuff tear arthropathy”
(figure 21).
It is estimated that 2% of population aged over 80 will develop
this kind of arthropathy[16].
Classification
The rotator cuff tears are classified according to the way of invasion
and installation as:
1. Acute
These have a sudden onset, as a result of a specific injury. They
represent almost 8% of all tears.
2. Chronic
They are established gradually in a long time period, and owed to
tendon degeneration.
According to pathologoanatomical background they are classified
as:
1. Full thickness: over 5mm length
2. Partial thickness: from 1 to 3 mm length (figure 22).
The partial thickness tears, as it is noted by cadaver studies,
are twice more frequent than full thickness tears (20%:10%).
Figure 16. MRI
showing a rupture of the supraspinatus tendon.
(Source: Campbell’s Operative Orthopaedics, 2003)
Figure 17. Figure
showing the location of initial lesion of supraspinatus tendon.
(Source: Frederick A. Matsen III, MD. Rotator Cuff Failure)
Figure 18. Figure
demonstrating the process of lesion of supraspinatus tendon.
(Source: Frederick A. Matsen III, MD. Rotator Cuff Failure)
Figure 19. Impingement
of the humeral head to the inferior acromial surface combined with
friction of subacromial bursa. (Source: Frederick A. Matsen III,
MD. Rotator Cuff Failure)
Figure 20. “Boutonniere”
deformity of the humeral head.
(Source: Frederick A. Matsen III, MD. Rotator Cuff Failure)
Figure 21. Figure
demonstrating the process leading to humeral head and long biceptal
head instability, resulting to shoulder arthritis. (Source: Frederick
A. Matsen III, MD. Rotator Cuff Failure)
Figure 22. Figure
showing the rotator cuff intact (image A), with a partial rupture
(image B) and with a complete rupture (image C). (Source: Greenspan
Adam, Orthopedic Radiology a practical approach 5.20, 2004)
Clinical
image[16,31]
The patient complains for pain in the shoulder, difficulty or inability
of limb flexion or abduction. There is often crepitus in abduction
movements.
The clinical examination reveals sensitivity when pressing the greater
humeral tubercle and the biceptal groove. The ability of external
rotation under resistance is decreased. The test is performed with
the arm in contact to the lateral thoracic wall and the result in
a reverse relation to the extension of the rupture. The passive
abduction of the arm is possible, but painful, especially with the
limb in internal rotation, where the infected area of the supraspinatus
tendon insertion is in contact to coraco-acromial arc.
The active abduction from 45ο to 90ο is impossible. If we bring
passively the arm to abduction over 90ο, the patient can hold the
arm in this position. If the rotator cuff is ruptured, the humeral
head cannot be stabilized against the glenoid fossa, so that the
deltoid muscle is unable to act for the first 45ο. However, if the
arm is passively lifted over 45ο-90ο, head is stabilized by the
deltoid muscle and the abduction is retained (figure 23).
In some cases, especially in deltoid atrophy, it is possible to
palpate a gap in the position of rotator cuff’s rupture.
Figure 23. Rupture
of the rotator cuff (especially the supraspinatus muscle). The active
abduction cannot pass 45 due to loss of stabilizing action of the
supraspinatus muscle. (Source: Συμεωνίδης Π. Παν. Ορθοπαιδική, Κακώσεις
και παθήσεις του μυοσκελετικού συστήματος, 362, 1996)
Diagnosis
The rupture in a great percentage of patients can be diagnosed by
the history and clinical examination, and can be supplemented by the
laboratory examination.
History
Regarding the history, it will be based on the information referred
to the previous chapter of the rotator cuff disease.
Clinical
examination
The clinical examination is completed with a series of shoulder motions
tests. The integrity of the rotator cuff is checked, as well as the
existence of pain or muscle strength decrease and atrophies.
1.
Jobe’s test (figure 24)
It is described in 198322,23 as “supraspinatus test”. The test is
performed with the arm abducted in 90ο, adducted 30ο until the arm
comes to the axis of the scapula and then an internal axial rotation
follows. The patient is ordered to perform abduction under resistance.
The test is positive, if the patient feels pain, indicating supraspinatus
tendon lesion or impingement.
2. Gerber lift-off test (figure 25)
In 1991, Gerber and Krushell14 described this test in order to examine
the subscapularis muscle. According to this test, the patient passively
puts the limb behind his back performing an extension, internal rotation
and flexion 90 of the elbow. The hand is positioned 5 to 10cm apart
from the back, with the palm in external rotation. The test is considered
positive, if the patient cannot retain this position of the limb and
reaches the palm to his back. The test may be performed under resistance,
too, with the upper limb in the last position and application of force
to patient’s palm. The test is considered positive, if the patient
cannot retain the internal rotation and drawing off touches his palm
to the back.
Electromyographic studies showed[17] that in this position the subscapularis
muscle is in full action, while the other muscles, such as latissimus
dorsi and particularly pectoralis major muscle have minimal action.
3. Evaluation of internal and external rotation (figure 26)
First described in 1996 by Hertel et al.[21]. Performing the external
rotation test (external rotation lag sign), the patient is positioned
as it is shown in the figureure. The limb is passively external rotated
approximately 5ο before the final position. The examiner instructs
the patient to actively retain this posture, while he holds patient’s
elbow. The test is considered positive, if the patient cannot retain
the initial posture. By this test we can examine mainly the infraspinatus
muscle.
It is noted when the passive range of external rotation decreases
due to joint capsule contructure or increases due to subscapularis
muscle rupture, false negative or false positive conclusions may be
ascertained.
Performing the internal rotation lag sign test, with the patient in
the same position, the examiner brings passively the limb in full
internal rotation while the elbow is 90ο flexed, the arm is in 20ο
flexion and 20ο extension. The examiner asks the patient to actively
retain this position while he upholds his elbow. The test is considered
positive when the patient cannot retain the initial position. By this
test, the activity of subscapularis muscle is controlled.
Discussing on the above tests, we will note that the studies17 showed
that, concerning the posterior and anterior impingement, the Jobe’s
test is more sensitive than the external rotation lag sign test. The
Jobe’s test has positive prognostic value 84% and negative 58%, while
the external rotation test 100% and 56%, respectively.
As for the subscapularis muscle rupture, the internal rotation lag
sign test is more sensitive and accurate than the Gerber lift-off
test, whereas both test are even specific. The Gerber’s test has positive
prognostic value 100% and negative 69%, while internal rotation lag
sign test, 97% and 69%.
4. Patte’s test (figure 27)
As it is shown in the figure, the examiner upholding the elbow, asks
the patient to bring his hand in external rotation under resistance.
The test is positive if pain is created in the shoulder. The sensitivity
is 92% while the specificity only 30%. The positive prognostic value
is 29% and the negative 93%.
The clinical evaluation should be completed with the instability tests,
specific tests (e.g. evaluation of superior thoracic inlet syndrome),
evaluation of the cervical and thoracic spine, as well as neurological
and angiologic examination[35], but it is not the purpose of this
article to describe these.
However, in many cases it is not possible to set a diagnosis based
only on the clinical examination that is why the paraclinical media
are needed.
a. Plain x-rays
The plain x-rays are the most specific and sensitive, but they have
their value as the initial method of imaging of the disease. We can
estimate the shape of the acromion, the degenerative changes of the
bones and the possible calcification of the soft tissues. It is more
useful in ruptures with traumatic etiology or in chronic ruptures.
In the late stages they can be used to confirm the disease (figure
28).
Sites of development of sclerotic bone in the humeral head (figure
29), or the acromion, osteophytes (figure 30), type 2 or 3 acromion,
hydroxyapatite deposits may hide partial rupture of the rotator cuff.
In the complete rupture of the rotator cuff in acute injury, the joint
blood effusion may translocate the humeral head, while in chronic
disease and in anteroposterior projection the humeral head glides
superiorly (figure 31). The distance between the superior margin of
the humeral head and the acromion decreases (less than 6 mm) due to
the fact that because of the rupture the humeral head is not yet seated
in the glenoid fossa, and the deltoid muscle pulls the head superiorly.
b. Ultrasound (U/S) (figure 32)
It is one of the most important diagnostic methods. However, a lot
of experience to perform and interpret is needed. The soft tissues
are mainly demonstrated. The sensitivity is ranged between 93% and
100% and the specificity between 85 and 97% in complete ruptures,
while in partial ones the sensitivity is ranged between 69 and 93%.
c. Arthrography (figure 33)
The main indication is the identification of the complete cuff rupture
and is usually combined with axial tomography (figure 34) the sensitivity
and specificity of which reach 100% for complete rupture.
The rotator cuff rupture allows the leakage of the radio-opaque agent
from the joint capsule to the subacromial bursa, through the perforation.
This is a method creditable, but also invasive, and the patient receives
radiation, although minimum.
d. MRI (figure 35)
It is a very sensitive method, non invasive and radiation free. However,
its cost is high and it is used only after the above methods cannot
set the diagnosis.
It is described as “state-of- the-art diagnostic tool for a full evaluation
of the shoulder”.
Table 4 includes comparative elements on the sensitivity, specificity,
positive and negative prognostic value as well as the accuracy of
diagnosis of the complete and partial rupture of the rotator cuff
with the methods of U/S tomography and MRI tomography.
Figure 24. Jobe’s test (Source: The Nicholas Institute of Sports Medicine
and Athletic Trauma)
Figure 25. Gerber lift-off test
Figure 26. External rotation lag sign Α) initial and Β) final position.
(Source: Duncan Tennent FRCS(Orth), William R. Beach, MD, and John
F. Meyers, MD Orthopaedic Research of Virginia, Richmond, Virginia
, A Review of the Special Tests Associated with Shoulder Examination,
Part I: The Rotator Cuff Tests. The American Journal of Sports Medicine,
Vol. 31, No 1, 2003)Cl
Figure 27. Patte’s test.
Figure 28. Sclerosis of the humeral head.
Figure 29. Calcium salts deposition in the region of supraspinatus
tendon (sign of chronic arthritis).
Figure 30. Presence of osteophyte in the inferior acromial surface.
Figure 31. Superior gliding of the humeral head, indicating rotator
cuff rupture. (Source: Roy Andri, MD , Dahan Thierry HM , MD. Rotator
cuff disease. University of Montreal, Canada , 2002)
Figure 32. Ultrasound showing a tendon rupture.
Figure 33. Arthrography demonstrating a complete rotator cuff rupture,
where the opaque agent is diffused to the subacromial and subdeltoid
space.
Figure 34. Axial tomography combined with arthography in frontal plane.
The presence of air in the subacromial and subdeltoid space is shown.
(Source: Roy Andri, MD, Dahan Thierry HM, MD. Rotator cuff disease.
University of Montreal, Canada, 2002)
Figure 35. MRI showing a complete rupture of supraspinatus tendon.
Differential
diagnosis[16]
The differential diagnosis involves:
1. The acute supraspinatus tendonitis. The pain is more intense and
after local injection of xylocaine the active abduction and external
rotation recover.
2. The frozen shoulder. There is restriction of both active and passive
motion, contrary to the rotator cuff complete rupture, where the passive
motions are not restricted. The athrography helps in doubtful cases.
3. The neuropathy of suprascapularis nerve. It is the most difficult
differential diagnosis, because it comes out with the same symptoms.
U/S, arthrography and especially electromyography help in difficult
cases.
4. Spondyloarthritis with pressure of C5 and C6 roots creates almost
the same symptoms.
5. Shoulder instability, acromioclavicular arthritis rarely cause
problems in differential diagnosis.
Treatment
The treatment of a rupture may be initially conservative, but mainly
operative.
The conservative treatment aims:
1. The patient’s pain relief, using a sling, analgesics, non steroid
anti-inflammatory drugs and local injections of anesthetics alone
or combined with corticoids.
2. Progressive rehabilitation, especially concerning the external
rotation and abduction with gentle controlled exercises.
3. Prevention of extending rupture.
The operative treatment consist the main therapeutic method. The restoration
of the ruptured rotator cuff is the goal. The good prognosis after
operative treatment is related to not only the proper surgical technique,
but also a whole number of factors, referred into the table 5.
Postoperatively, the humerus is immobilized in abduction for 3 to
4 weeks, so that the sutured tendon is not in tense. After that period,
active exercises are started.
Conclusions
Despite the theoretical correlation of the rotator cuff impingement
with the supraspinatus tendon rupture, we cannot say for sure that
the last is a result of an endogen or exogenous procedure developed
in the rotator cuff of the shoulder. The upright stance of humans,
creates conditions of increased muscle demands, due to the long lever
of upper limbs, so that the forces developed to the minor muscles
of the cuff are disproportional increased.
Tests used for diagnosis and differential diagnosis, comprehension
of anatomy and embiomechanics of the area and several methods of imaging
help us to the better and more effective treatment of the disease.
However the surgeon cannot always offer a definite solution.
Many questions still need their own answers, for a common but so intrigued
disease.
Authors also hope that this extensive study of above entities will
help to the definition of their terminology, referring to a lot of
used terms concerning lesions of studied area.
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