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I orient my diagnosis
After an interrogation and a clinical examination (even summary),
The diagnostic orientation is simple:
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The pathologies of the rotator cuff?
The unstable shoulder?
Omarthrosis?
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I choose the best complementary examinations
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I choose to take charge of the patient
Medically (myself)
where I refer my patient to:
A Radiologist​ ?
A rheumatologist?
A Neurologist?
A surgeon ?
the main structures of the Shoulder
The pathologies of the rotator cuff
The elements of the conflict
1- The acromial vault
The acromion
The articular surface of the acromion is a more or less concave surface, covered by the ceiling of the subacromial bursa. Its outer edge is thick and rough; on its anterior edge is inserted the acromiocoracoid ligament; this insertion can ossify then modifying the shape of the anterior edge;
The study of the shape of the acromion has been the subject of interesting attempts at classification:
Bigliani and Morisson proposed to classify acromions into three types based on a cadaver study.
type 1: flat acromion
type 2: curve
type 3: hooked
For the radiological study of the acromion:
- Frontal subacromial incidence with subject seated facing the source, radius inclined from top to bottom by 15°, subject leaning forward until horizontal alignment of the spine and clavicle is obtained.
- Profile subacromial incidence not very different from the Lamy incidence (corresponding parade)
The 3 types of Bigliani and Morisson are identified on the profile incidence.
The AP view allows analysis of the anterior edge of the acromion; indeed the radiological alignment of the lower edges of the clavicle and the acromion makes it possible to affirm that what appears on the radiographs on the lower face of the acromion is indeed its anterior edge and not its posterior edge. On this bearing, the acromion can be flat, round or pointed.
Correction by arthroscopic treatment can be assessed on this incidence.
There therefore seems to be a correlation between the shape of the acromion and the presence of rotator cuff lesions. The presence of the acromion is essential to the function of the shoulder; surgical removal of the scapula spine and acromion results in major joint damage.
The non-fusion of one (or more) of the three ossification nuclei of the acromion known under the terms of acromial bone, bipartite acromion or meta-acromion should not be confused with a fracture. At birth the acromion is cartilaginous; the ossification nuclei appear around the age of 15; the merger is normally complete after 25 years. The frequency of the acromial bone varies according to the authors from 1.4 for Liberson (from 1800 shoulder radiographs) to 8%.
The acromial bone would be a predisposing factor to subacromial impingement and in particular to complete rotator cuff tear.
The acromioclavicular joint
Articular degeneration is frequent and early, from the fourth decade; the presence of inferior osteophytes can be a factor of conflict. These osteophytes are particularly well analyzed on the headdress procession.
The acromiocoracoid ligament unites two parts of the same bone, the scapula; very resistant fibrous layer it unites the external edge of the coracoid apophysis to the top of the acromion and forms with these two bony projections the acromio-coracoid vault; the insertion of the ligament medially covers the underside of the acromioclavicular joint; outside the ligament reaches the outer end of the anterior edge of the acromion (anterior angle)
The outer edge of the ligament is particularly sharp.
This ligament has no known physiological role.
2- The headdress
The supraspinatus, the underspinatus and the teres minor form from front to back a continuous musculotendinous sheet; the tendinous insertions on the trochiter are not individualized. The tendinous portion measures approximately 2cms. The thickness of the cap is 10 to 12mm. The radiological interval between the humeral head and the acromion is 6.6 to 13.8 mm in men and 7.1 to 11.9 mm in women. Between the supraspinatus and the subscapularis there is an interval partially filled by the coracohumeral ligament. The tendon of the subscapularis inserts on the trochin; it is flattened and its height is 3 to 5 cm. The long portion of the biceps inserts at the superior pole of the glenoid on the supraglenoid tubercle, on the fibers of the posterior labrum or on both; at its entry into the gutter the tendon is strongly held by the coraco-humeral ligament which covers it: this capsular reinforcement fills the gap between the rotators between the supraspinatus and the subscapularis and is inserted on either side of the edges bone limiting the bicipital groove. This ligament represents the major obstacle to its dislocation. The shape, depth and size of the gutter is variable and can favor dislocations and ruptures. The thickness of the tendon is variable; it can be very atrophied in case of degeneration; on the contrary, it can hypertrophy in the event of a deficit of the supraspinatus.
3- The subacromial (or subacromial-deltoid) bursa
It is interposed between the cap and the acromion. It is by its size, the most important of the organism (it can contain from 10 to 30 cc) and it represents the joint space of the subacromial joint. It is very extensive outside and in front while it barely reaches behind the posterior border of the acromion; it has two sheets which slide one over the other during shoulder movements according to a particular mechanism: there are two fixed points where the purse is firmly adherent to the articular surfaces; one on the floor at the insertion of the rotator cuff tendons on the greater tuberosity, the other on the ceiling on the underside of the anterior 2/3 of the acromion; the rest of the bursa is free within a cellulo-fatty tissue.
On arthroscopic examination, the limits of the bursa are clear on the outside, more blurred on the inside due to the presence of fatty tissue as soon as the region underlying the acromioclavicular joint is approached; in front the bursa presents a fold which brings its wall closer to the anterior part of the supraspinatus and the coraco-humeral ligament. The floor of the bursa completely covers the tendon of the supraspinatus and during surgery, the latter can only be examined after opening the bursa. The bursa can be single or divided into two parts: external subdeltoid and internal subacromial.
In the normal state, the leaves of the purse are very thin and transparent; the bursa never communicates with the glenohumeral joint contrary to the assertions of certain classical anatomists misled by the high frequency of asymptomatic rotator cuff lesions in the elderly.
The causes of the conflict
In the normal state, the rotator cuff slides smoothly under the acromio-coracoid vault via the fine lubricated surfaces of the bursa. Subacromial impingement can be defined as a disturbance of this mechanism. The factors that can hinder this mechanism are structural or functional. Structural factors concern:
- the vault:
osteophytes under the acromioclavicular or subacromial joint, type 2 and especially 3 acromion, acromial bone, sequelae of acromion fracture.
- the stock market:
thickening by chronic irritation.
- The hairdo :
lesion of the upper face , protrusion of the thickened edges of a complete ulceration, post-traumatic edema or hematoma, elevation of the insertion of the cuff by a malunion of fracture of the trochiter.
Another common cause of impingement is the presence of calcification . Let us recall that apart from the particular case of the short phase of spontaneous rupture, these calcifications always sit in the tendons of the rotator cuff where they are more or less superficial; they never sit in the subacromial bursa.
They can be classified into several types (3)
1: the fine calcifications located at the insertion of the rotator cuff tendons on the greater tuberosity, probably related to enthesopathy.
2: inhomogeneous calcifications scattered in the subacromial space which reflect tendon degeneration.
3: rounded or polylobed, homogeneous, dense calcifications, which correspond to a collection of apatite or "calcic boil".
Only type 3 calcifications can be considered as a structural cause of conflict due to the excessive volume they occupy in the rotator cuff.
The functional factors are:
- excessive use of the shoulder:
- reduction in the effectiveness of the lowering muscles of the humeral head by lesion of the rotator cuff and the long biceps: Neer's purely mechanical theory to explain the conflict is probably not the only one. The vascular theory suggests that the cap could degenerate by anoxic phenomena and become necrotic; it would then lose its function of lowering and coaptation, thus contributing to the occurrence of a conflict by ascension of the humeral head. Another functional theory put forward by Bonnel draws attention to the fact that the upward force of the deltoid is normally balanced by the force of the depressors and in particular the rotator cuff and the biceps; an imbalance of these forces could lead to distension of the cuff which would thin and crack; this would explain the interstitial lesions and the partial ruptures of the deep surface. Here again, the mechanical impingement would only be secondary to the rotator cuff deficit.
- antero-superior laxity of the joint capsule
The signs of this hyperlaxity are beginning to be recognized in arthroscopy: tearing of the bead in its antero-superior or superior zone with disinsertion of the long biceps.
The seat of conflict
The idea of a conflict between the cuff and the acromial arch to explain a large part of shoulder pain is very old. It was already mentioned by Codman in 1927 and many authors in the 1940s admitted this conflict and proposed acromionectomy as a radical treatment. The French School of Rheumatology in its clinical classification has given the rotator cuff its rightful place. However, Neer should be recognized for several decisive advances and especially the location of the conflict which in the vast majority of cases concerns the anterior third of the acromion and the acromio-coracoid ligament, whereas the posterior part of the acromion is never interested.
Lesions in the conflict
The rotator cuff lesions are classically.
- edema and hyperaemia (Neer stage 1), in principle reversible.
- intra-tendinous degeneration (Neer stage 2) with fibrosis which now finds confirmation thanks to I.RM.
- partial lesions involving the deep face and more rarely the superficial face of the rotator cuff.
- the complete perforations of the rotator cuff connect the glenohumeral and subacromial joints. It is important to consider that these perforations are of a trophic nature, that their edge is whitish, avascular, and in no case is it a traumatic rupture.
- Pure traumatic rupture on a normal cuff and without bone tearing, if it exists, is exceptional. These traumatic ruptures are usually a tear completing a trophic lesion of the rotator cuff.
- Lesions of the long biceps in its intra-articular course appear in the vast majority of cases in the context of a subacromial impingement. The lesions are identical to those of the rotator cuff: edema, inflammation of the tendon at first, then fibrous degeneration and finally partial or complete tears.
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In rotator cuff lesions, there is sometimes a tendon hypertrophy which has been interpreted as an attempt to compensate for the functional deficit of the rotator cuff;
In case of large trophic perforation of the cuff, the state of the tendon examined by arthroscopy is very variable; sometimes it is surprisingly normal although directly exposed under the acromion and seems not to participate in the conflict; sometimes, on the contrary, it is very altered, degenerated, partially or totally broken.
In the event of a complete rupture, the examination of its insertion on the glenoid is interesting: in the majority of cases, no trace of the tendon is recognized and the bulge continues from front to back as if the long biceps had never existed. ; in some cases a more or less important stump persists which can act as an element of articular disturbance by interposing itself between the articular surfaces of the glenohumeral.
Bone lesions only occur at an advanced stage of the impingement:
- remodeling of the greater tuberosity
- subacromial osteophytosis which is in fact an ossification of the insertion of the acromio-coracoid ligament, enthesopathy probable witness of the hyper solicitation of the insertion. In exceptional cases we have observed complete ossification of the ligament.
The lesions can be the following:
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- local inflammation : the purse is reddish, easily hemorrhagic, especially in relation to calcification.
- thickening: the purse is no longer translucent, it is flaky and takes on a yellowish appearance; this thickening can be considerable and reach more than 5mm for a single wall of the bursa. This aspect is found both on the floor next to the tendons and on the ceiling under the acromion; histologically there is hyperplasia of the synovium, made up of several cell layers.
- sclerosis: the purse is whitish, avascular, it has lost its flexibility; we did not encounter this aspect in the absence of perforation of the rotator cuff.
- ulceration of the floor of the purse: it accompanies ulceration of the rotator cuff; its edges often look the same as the edges of the rotator cuff ulceration and care must be taken during the bursoscopy so as not to confuse them. Ulceration of the bursa is usually less extensive than that of the rotator cuff, giving the bursa a diaphragm-like appearance. (this must be taken into account in the radiological interpretation); a cleavage plane usually appears between the fibrous edges of the two ulcerations and synovial proliferation is frequently noted in this cleavage plane, which is probably very mechanically stressed.
Shoulder Instabilities
The physiopathology of instability has changed a lot over the past few years, mainly due to the consideration of a new parameter: ligament laxity.
The clinical examination is the fundamental time of the assessment of an instability. It is he who in the vast majority of cases will make the diagnosis that additional examinations will only confirm. It is he who will make it possible to raise the main trap which is the instability of the shoulder associated with a constitutional and multidirectional hyper laxity. In very rare, particularly difficult cases, only the examination under general anesthesia and sometimes arthroscopy will make it possible to acquire the final diagnosis.
Elements of Anatomy and Physiology
Anatomy
Five anatomical data are essential to understanding the problem: 1) the absence of reciprocal interlocking of the bone surfaces 2) the absence of an individualized ligament 3) the absence of ligamentary prestress 4) all the articular ligaments of the shoulder are relaxed in the resting position 5) the existence of the weak point The ligaments of the glenohumeral joint are not individualized ligaments. There is in fact a vast fibrous layer, both capsular and ligamentary, inserted over the whole of the glenoid circumference except at the level of the interval of the rotators and on the humerus. Historically this ligament was called by Schlemm Broad shoulder ligament. We will use the abbreviation inferior glenohumeral ligament (LGHI) in the rest of the presentation to designate the ligamentous zone inserted between 2 and 6 o'clock on the glenoid which is the zone concerned by the anterior instability and which in fact comprises the ligament middle glenohumeral and the anterior part of the inferior glenohumeral ligament as systematized by Ferrari. The physiology of this "capsulo-ligamentous apparatus", the shape of which constantly varies according to the positions of the joint, is therefore much more difficult to understand than that of a linear ligament stretched between two practically point-like insertions. The absence of prestress makes the kinematic analysis of the joint very difficult. This absence of prestressing also explains the difficulty in describing a simple and specific ligament test allowing to highlight pathological ligament laxity like the Lachmann test or forced varus/valgus tests at the knee. Ligament relaxation at rest is illustrated by Kumar's experiment. The punctiform opening of the joint capsule causes the humeral head to descend over more than 1 cm. In elevation and external rotation of the arm, the subscapularis muscle slides upwards so that the humeral head is no longer covered forwards and downwards and forwards except by the LGHI, no other muscle comes in between to help stabilize the joint. It is through this weak point that the dislocations will occur.
Stabilization mechanisms of the glenohumeral joint
They are numerous and complex. The fibrous bead or labrum slightly increases the hollow of the glenoid cavity but its role remains very limited. The role of the rotator cuff has long been considered the only significant role in stabilizing the shoulder. The evolution of recent knowledge has made it possible to rehabilitate the role of the ligaments. Between the position of rest and the maximum elevation, the articular ligaments pass from complete relaxation to a state of homogeneous tension. It can therefore be said that the role of the ligaments in stabilizing the joint increases progressively during elevation. The rotator cuff plays a very important role at the beginning of the elevation, a role that gradually fades during the elevation. This "cross-participation" of two elements is perfectly illustrated by the clinic. Shoulder instability practically only occurs in a position of maximum elevation in external rotation, i.e. when the ligaments are brought into play. Conversely, destabilization of the humeral head in rotator cuff lesions occurs above all at the start of the elevation. This instability is objectified by the Leclerc maneuver. The intra-articular vacuum phenomenon described by Kumar and Habermeyer is practically unique in the human economy. When examining a cadaver shoulder after removal of all the muscles, the humeral head remains centered in front of the glenoid provided that the articular cavity remains closed. As soon as a small opening of the articular cavity is made, the head descends by more than 1 cm, which testifies to the existence of an intra-articular depression which contributes to the centering of the humeral head in front of the the glenoid. It is difficult to appreciate the importance of this mechanism in the prevention of shoulder instability.
How to examine an unstable shoulder?
Osteoarthritis
What you must remember
What you must remember
Avoid the pitfalls
NCB neck pain
Immediately eliminate adhesive capsulitis
rotator cuff pathology
Tendinopathies
Calcifying tendinopathies
Non-calcifying tendinopathies
Subacromial impingement
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Headdress breakage
Incomplete Cap Rupture
deep break
Surface break
Full headdress breakage
supraspinatus isolated
Top & bottom spiny
Wide break with retraction
Pathology of the long biceps
biceps tendonitis
Dislocation of the tendon (Upper lesion of the Subscapularis)
Slap lesion
Acromioclavicular pathology
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Osteoarthritis
Bipartite acromion
Chronic sprain
old dislocation
instabilities
Minimum instability = ! Pitfall: pure sore shoulder
True recurrent dislocation
Previous instability
Posterior instability (Rare)
MULTIDIRECTIONAL instability (Hyperlaxity)
Bead pathologies: Slap lesion
Osteoarthritis
Without rotator cuff tear = Centered osteoarthritis
With rotator cuff tear = Eccentric Osteoarthritis
Place of surgery