Chronic instability of the shoulder

Our knowledge of the mechanisms underlying instability has been greatly enhanced in recent years, mainly as a result of the consideration of a new parameter - ligamentous laxity.

In the work-up of instability, the clinical examination is of paramount importance: in the overwhelming majority of the cases, it will allow a diagnosis to be made; further investigations will only provide confirmation. The clinical examination will allow the physician to recognize an associated inherent multidirectional laxity.(10,20,34) In some, very rare cases, examination under general anaesthesia will be required. Sometimes, the definitive diagnosis can only be made in the light of the arthroscopic findings

Anatomy
Five anatomical features of the shoulder are crucial to an understanding of the problem:
1) The shoulder joint is not congruous.
2) There are no discrete ligaments.
3) No one ligamentous structure is taut in all positions of the joint.
4) All the ligaments of the shoulder are slack in the resting position.
5) There is a weak point.

The ligaments of the glenohumeral joint are not discrete structures. The joint is surrounded by a sheet of fibrous tissue, which constitutes both the capsule and the ligaments. This sheet inserts all around the glenoid, except for the rotator interval, and on the humerus. Back in the 19th century, Schlemm described the structure as the "broad ligament of the shoulder."(30) In this paper, the term inferior glenohumeral ligament (IGHL) will be used to denote the ligamentous structure inserted on the glenoid between 2 o'clock and 6 o'clock, which is the zone involved in instability. This zone includes the middle glenohumeral ligament and the anterior band of the inferior glenohumeral ligament, as described in anatomical studies of the shoulder.(7,22)

The shape of this capsuloligamentous apparatus changes with the position of the glenohumeral joint; this is why the physiology of this structure is much more difficult to understand than is that of a linear ligament that extends between two "point" attachments. The kinematic analysis of the joint is made difficult by the fact that no one ligament is taut in all positions. This fact also accounts for the difficulty encountered in trying to devise a simple and specific ligament test that would show abnormal ligamentous laxity; in other words, there is nothing in the examination of the shoulder that would equate to the Lachman test, or to varus/valgus stress testing, of the knee.

The relaxed condition of the ligaments at rest was demonstrated by Kumar and Balasubramaniam,(19) who showed that puncturing the capsule resulted in a downward displacement of the humeral head by more than 1 cm.

When the arm is in 90° of abduction and in external rotation, the subscapularis muscle is pulled cranially, leaving the head of the humerus covered anteroinferiorly only by the IGHL, without any other muscle providing a check to anterior displacement.(33) This is the weak point through which the head may dislocate.

Mechanisms of glenohumeral joint stabilization

There are many and complex ways in which the glenohumeral joint is stabilized.

The fibrous labrum adds some depth to the glenoid socket; however, its role in the stabilization of the joint is very limited.

The rotator cuff used to be considered the only significant stabilizer of the shoulder. Recent research (7,8,22,23) has redressed the balance by showing the importance of the ligaments. Between the resting position (with the arm hanging at the side) and maximum scapular-plane abduction, the articular ligaments go from complete relaxation to a state of uniform tension. Thus, it could be said that the stabilization of the joint gradually increases throughout abduction. The rotator cuff, in turn, has a very important role to play at the start of elevation, becoming progressively less important as the movement continues.

This discrete involvement of the two anatomical structures is very clearly reflected in the clinical pattern: shoulder instability is virtually only seen at the extremes of abduction and external rotation, i.e. when the ligaments have come into play. Conversely, destabilization of the humeral head in rotator cuff lesions occurs chiefly at the start of abduction. This instability can be demonstrated by Leclercq's resisted-abduction manoeuvre.

The vacuum phenomenon described by Kumar & Balasubramaniam (19) and by Habermeyer et al (13) is virtually unique in the human body. In the cadaver shoulder, all the muscles stabilizing the glenohumeral joint may be cut without affecting the position of the humeral head within the glenoid, providing that the joint capsule has not been breached,. As soon as the capsule is punctured, the head will translate downwards by more than 1 cm. This shows that the shoulder depends to a considerable extent on negative pressure for the maintenance of the humeral head in the glenoid fossa. It is difficult to assess the importance of this mechanism in the prevention of shoulder instability.

In order to understand the mechanisms of instability, it is useful to consider the main findings at surgery using the Bankart technique, i.e. with separation of the subscapularis from the capsule, to provide a detailed and comprehensive picture of the ligamentous lesions.

In the overwhelming majority of cases, the ligamentous apparatus will be continuous, and inserted on, or at a distance of less than 1 cm medial to, the glenoid rim. The labral lesion1 will vary from a complete disappearance of the structure and bone wear, through greater or lesser detachment, to discreet surface damage. In some patients, there will be evidence of a glenoid rim fracture.

a) a Broca-Hartmann pouch, in the strict sense of the term, is extremely rare;
b) the initial ligamentous lesion will heal, regardless of its shape and site;
c) lesions of the anterior rim vary greatly in size. Their significance in the production of chronic instability is difficult to assess, since the movement of the humeral head forward of the glenoid rim during repeated episodes of instability must progressively change and aggravate the lesional pattern.

Many papers published in the international literature over the past few years have allowed us to formulate a more coherent concept of how chronic instability of the shoulder is produced.

In order to dislocate a shoulder, at least the anteroinferior portion of the capsuloligamentous apparatus must be divided. (In the right shoulder, the division should extend from 3 o'clock to 6 o'clock.) The division of the capsuloligamentous apparatus is not enough to cause dislocation.9,33 The rotator cuff must also be damaged. Some authors have obtained dislocation following division of the supraspinatus tendon. We have shown that the lesion required may consist in a partial detachment of the deep portion of the cuff insertion. The anti-dislocation role of the rotator cuff can also be shown the other way round, by looking at the rate of cuff lesions found in shoulder dislocation in patients over the age of 40 years.21 It is thus clear that the rotator cuff provides a second line of defence to protect the shoulder from dislocating. The experimental creation of an isolated Bankart lesion32 has also been found to be insufficient for the production of shoulder instability.

La lésion de Bankart
Il est actuellement couramment admis que la lésion typique de l'instabilité chronique de l'épaule est la lésion de Bankart. Elle associe une lésion du bourrelet qui peut être usé, désinséré, voire presque entièrement détruit, à un décollement capsulo-périosté antérieur d'importance variable. Nous avons vu que le décollement antérieur était le plus souvent très limité. Il paraît douteux que la lésion du bourrelet entraîne une perte importante de stabilité. De plus on sait maintenant que les lésions antérieures s'aggravent progressivement avec le nombre de récidives ⁽¹²⁾ ce qui peut laisser un doute quant à l'importance des lésions initiales et fait que la question est posée : la lésion de Bankart suffit elle à expliquer l'instabilité chronique ?

The Hill-Sachs lesion
Unlike the reverse Hill-Sachs lesion, which plays a major role in recurrent posterior dislocation, the implication of the Hill-Sachs lesion15 (known in French as the Malgaigne notch) in the generation of recurrent anterior instability has never been conclusively demonstrated.

Laxity of the inferior glenohumeral ligament (IGHL) complex
Over the years, several publications have stressed the importance of ligamentous laxity in shoulder instability. Neer and Foster(20) showed that some subjects have extremely hypermobile shoulders, which could cause multidirectional instability, in a context of inherent, non-trauma-related laxity of the shoulder capsule. Other authors have stressed the presence of ligamentous laxity in some cases of atraumatic shoulder instability.(31) Others found that, in traumatic dislocation, the ligament could undergo plastic deformation at the time of the traumatic event, and remain permanently stretched, with further stretching caused by repeated episodes of instability.(2)

In a paper to be published soon, we have shown that IGHL laxity is also consistently seen in traumatic dislocation.

- ligamentous laxity, which is a consistent feature, regardless of whether it is congenital or acquired;
- a labral lesion, which may vary greatly in size, and which will worsen with every dislocation of the humeral head;
- anterior soft-tissue stripping, which will often be very slight.

This suggests that anterior instability of the shoulder is an instance of joint instability resulting from ligamentous laxity. What distinguishes the pattern from that seen in other joints is the lack of bony constraints in the glenohumeral joint, and the fact that stabilization is provided by one single ligament. The "labrum syndrome" may be accounted for by the fact that the laxity is great enough to allow the humeral head to ride up the glenoid slope, without being great enough to allow it to ride over the rim.

A constant physiological value
Can ligamentous laxity of the shoulder be directly analyzed?

In order to analyze laxity directly, one would need a test performed in a position where the IGHL is taut. This is the only way in which the presence of stretching can be assessed.

In an anatomical study, it was shown that glenohumeral abduction is consistently limited to 85° by the IGHL, with no other restraints involved (Fig. 2). The tuberosities have nothing whatsoever to do with restricting the range of this movement (Fig. 3): dividing the ligament allows an additional 15° of abduction to be obtained.

The clinical measurement of passive abduction may be performed as shown in Figure 4. The examiner stands behind the patient, and exerts firm downward pressure on the top of the shoulder. The examiner's other hand is used to gently lift the patient's upper limb in the strict coronal plane, with the elbow flexed to 90° and the forearm held horizontal. The patient must, of course, be completely relaxed throughout the test. A study in 100 healthy volunteers showed that the range of abduction never exceeded 90°, in 95% of the patients. This finding was bilateral. In 5% of the subjects, passive abduction was greater than 105°, bilaterally; this suggested generalized ligamentous laxity. Radiographic checks showed that the scapula did not rotate by more than 5° during the test. Thus, scapular rotation during the test would account for at most 6% of the range of movement. It follows that the measurement of passive abduction will show only the movement that occurs in the glenohumeral joint. This movement is limited by the IGHL, and has a constant range. We therefore hypothesized that IGHL laxity should lead to an increased range of passive abduction. In the light of the results obtained in that study, we wish to propose a test for the direct assessment of IGHL laxity, which will be described in the section concerning the clinical examination.

PRESENT-DAY CLASSIFICATION OF ANTERIOR SHOULDER INSTABILITY

This classification is important from the point of view of prognosis and of the management policy to be adopted.

Instability may be traumatic or atraumatic. It may occur with or without evidence of excessive ligamentous laxity. Instability may take the form of recurrent dislocation (in which case, reduction may be performed by the patient himself or herself, or may require the assistance of a third party). Equally, it may manifest itself as a brief sensation of painful instability (the condition described by Patte et al(24) as a "painful and unstable shoulder," and by Rowe(28) as "recurrent transient anterior subluxation). Also, each patient should be checked to see whether the instability is voluntary or involuntary.

The two parameters combine to form a spectrum of instability, as in the classification proposed by Silliman and Hawkins:(31) instability following initial trauma, without any prior laxity; instability following initial trauma and laxity acquired from overuse; instability following trauma, with prior laxity; and instability without a history of trauma, with prior laxity.

Often, the patient will spontaneously report the initial traumatic event. The index event should always be carefully elicited. Sometimes, the first episode of dislocation would appear to have been atraumatic; however, detailed history taking may reveal fairly major shoulder trauma in the past, which must be taken into account. There are situations where trauma may cause all the lesions required for instability, without any dislocation occurring. In other patients, a history of intensive sports practice involving abduction and forced external rotation will provide useful clues.

On the other hand, the existence of an initial trauma should not stop the physician from searching for an associated multidirectional hyperlaxity. The nature of the trauma is not always easy to identify. The only important pattern is a direct posterior blow to the shoulder, or indirect trauma (a blow or fall on the elbow or on the outstretched, externally rotated arm). Indirect trauma is by far the most frequent cause involved. In this analysis of the first parameter, there is much that is not clear-cut.

It is important to obtain a description of the episodes of instability, trying to ascertain how many there have been, and how easily they tend to occur. If there have been many episodes of instability after very minor trauma, surgery should, obviously, be considered. Equally, though, a diver or a mountaineer with a first recurrence may be a candidate, given the risk involved in his or her sport.

Physical examination
This examination is performed in three stages, and involves a search for three broad patterns: apprehension, during dynamic manoeuvres designed to reveal instability; laxity, which will be discussed in greater detail below; and evidence of associated multidirectional hyperlaxity.

Relocation test
This is a more sensitive variant of the test described above. The patient is positioned supine. The first part of the test is a classic fulcrum test, in which the humeral head is pushed forward to elicit apprehension. In the second part of the test, a posteriorly directed force is applied to the humeral head. This prevents anterior subluxation, and produces a negative apprehension test (Fig. 6a and b).

Inferior apprehension test
This test was initially described by Feagin, and further refined by Itoi et al,16 who suggested the name ABIS (abduction inferior stability). For this test, the upper limb is held in abduction, with the patient's forearm resting on the examiner's shoulder. The examiner exerts downward pressure over the neck of the humerus. If the shoulder is unstable, the head will be pushed down, and a groove will appear; also, the patient may show apprehension (Fig. 7).

Since passive abduction has a constant range, and since the range is controlled by the IGHL, we suggest that laxity of the IGHL will be associated with an increase in the range of abduction. The passive abduction test was performed in patients with post-traumatic shoulder instability without any associated hyperlaxity. In 85% of the cases, the range of passive abduction was at least 105°, while, on the healthy side, it was limited to 90°. In 15% of the cases, the test caused acute apprehension, making it impossible to measure passive abduction. In such cases, the test works as an apprehension test, along the lines of the procedure initially devised by Feagin, and proposed by Itoi et al as the ABIS test.

The test was performed under general anaesthesia, immediately prior to surgery. In all the cases, passive abduction was at least 105°, while, on the contralateral side, it was restricted to 90°.

Providing that the test is performed strictly in the coronal plane, it furnishes objective evidence of excessive IGHL length, and gives a direct demonstration of the laxity of the ligament. Thus, this test of passive hyperabduction is positive if the range on the affected side is greater than 105° (Fig. 10). This is the first test that allows shoulder ligament laxity to be directly assessed; however, it will need to be used more widely, in a prospective study, to establish its specificity and sensitivity.

Multidirectional hyperlaxity affects the outcome of instability treatments.(29) On examination, there will be a groove of more than 2 cm in the sulcus test, as well as major anterior and posterior drawer movements. External rotation of the upper limb of more than 90° is also considered to be a sign of abnormal laxity. The wrists should be examined for increased palmar flexion, as should the elbow for marked hyperextension, the knees for a recurvatum deformity, and the trunk for enhanced forward bending (palms of hands to floor). In patients with generalized ligamentous laxity, the passive hyperabduction test will be bilaterally positive.

Where these tests are positive, the diagnosis will be one of instability associated with multidirectional hyperlaxity. Evidence of true multidirectional instability should be carefully sought. The most important feature is episodes of posterior instability when the arm is in forward elevation and internal rotation.

The patient should be questioned about episodes of posterior instability of the shoulder. Special attention should be devoted to eliciting previous incidents of voluntary shoulder dislocation.

In some of the more difficult cases, especially when trying to confirm or exclude multidirectional instability, CT arthrography may be helpful. Arthroscopy may be indicated, to obtain objective evidence of laxity, as described by Detrisac and Johnson.(6).

REFERENCES

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Fig 6 : Relocation test. This test is performed with the patient supine. 6a Pressure over the back of the humeral head causes apprehension, while 6b pressure over the front of the humeral head prevents the head suluxating anteriorly, and does not cause apprehension.


Fig 8 : Sulcus test. In the relaxed patient, the examiner gently pulls the humerus downwards. The test is positive if the humeral head descends, with formation of a groove or sulcus under the lateral border of the acromion. The amount of downward movement can be measured. A positive test is indicative of abnormal mobility.	Fig 9 : Drawer test. The patient is made to relax and slightly lean forward. The examiner holds the humeral head between his or her thumb and index finger, and tries to make the head slide backwards and forwards. This test demonstrates overall hyperlaxity (without being specific of any particular ligament), and may provide information on the direction of the instability.