Evaluation of Recurrent Instability.
Last updated Friday, November 16, 2007
About recurrent shoulder instability
After an initial dislocation, the shoulder may return to functional
stability or it may fall victim to recurrent glenohumeral instability.
While intermediate forms of recurrent instability do occur, the great
majority of recurrently unstable shoulder may be thought of as being
either atraumatic or traumatic in origin.
 JBJS Article on Shoulder Dislocation (PDF) (2.66 MB)
Atraumatic instability is instability that arises without the type of
trauma necessary to tear the stabilizing soft tissues or to create a
humeral head defect, tuberosity fracture or glenoid lip fracture.AMBRII syndrome Certain shoulders may be more susceptible to atraumatic instability.
A small or functionally flat glenoid fossa may jeopardize the concavity
compression, adhesion-cohesion, and glenoid suction cup stability
mechanisms. Thin, excessively compliant capsular tissue may invaginate
into the joint when traction is applied, limiting the effectiveness of
stabilization from limited joint volume. A large, potentially capacious
capsule may allow humeroscapular positions outside the range of balance
stability. Weak rotator cuff muscles may provide insufficient
compression for the concavity compression stabilizing mechanism. Poor
neuromuscular control may fail to position the scapula to balance the
net humeral joint reaction force. Voluntary or inadvertent
malpositioning of the humerus in excessive anterior or posterior
scapular planes may cause the net humeral joint reaction force to lie
outside balance stability angles. Once initiated, the instability may
be perpetuated by compression of the glenoid rim resulting from
chronically poor humeral head centering. Excessive labral compliance
may predispose to this loss of effective glenoid depth.
Any of these factors, individually or in combination, could
contribute to instability of the glenohumeral joint. For example,
posterior glenohumeral subluxation may result from the combination of a
relatively flat posterior glenoid and the tendency to retract the
scapula during anterior elevation of the arm, resulting in use of the
elevated humerus in excessively anterior scapular planes. Excessively
compliant capsular tissue in combination with relatively weak rotator
cuff muscles could contribute to inferior subluxation on attempted
lifting of objects with the arm at the side. If the lateral scapula is
allowed to droop (whether voluntarily or involuntarily) the superior
capsular structures are relaxed, permitting inferior translation of the
humerus with respect to the glenoid (see figure 1). (Itoi et al, 1993)
Because they usually result from loss of midrange stability,
atraumatic instabilities are more likely to be multidirectional.
Pathogenic factors such as a flat glenoid, weak muscles, and a
compliant capsule may produce instability anteriorly, inferiorly,
posteriorly, or a combination. Although the onset of atraumatic
instability may be provoked by a period of disuse or a minor injury,
many of the underlying contributing factors may be developmental. As a
result, the tendency for atraumatic instability is likely to be
bilateral and familial as well.
It is apparent that atraumatic instability is not a simple
diagnosis, but rather a syndrome that may arise from a multiplicity of
factors. To help recall the various aspects of this syndrome, we use
the acronym AMBRII. The instability is Atraumatic, usually associated
with Multidirectional laxity and with Bilateral findings. Treatment is
predominantly by Rehabilitation, directed at restoring optimal
neuromuscular control. If surgery is necessary, it needs to include
reconstruction of the rotator Interval capsule-coracohumeral ligament
mechanism and tightening of the Inferior capsule. The diagnosis and
management of this condition has been presented in detail. (Cofield,
1993; Lippitt et al, 1991; Matsen, Lippitt, Sidles et al, 1994;
O'Driscoll, 1993)
AMBRII history Most patients presenting with AMBRII are under the age of 30 years
(see figure 2). Because the instability manifests itself in mid range
positions of the shoulder, atraumatic instability typically causes
discomfort and dysfunction in ordinary activities of daily living.
Commonly such patients have greatest difficulty sleeping, lifting
overhead, and throwing (see table 1 and figure 3). Their general health
status as revealed by the SF 36 is not as good on average as that of a
comparable group of patients with traumatic instability (see figure 4).
Table 1
| TUBS | AMBRII
| Failed Repairs |
| Number of Patients | 101 |
70 | 76 |
| % female | 26% | 38%
| 28% |
| % right side | 55% | 68%
| 51% |
| Age | 29±11 | 27±10 | 31 ± 8 |
|
|
|
|
| % able to perform SST function |
TUBS (101) |
AMBRII (70) |
Failed Repairs (76) |
| Sleep on Side | 43 | 19
| 11 |
| Place 1 lb on shelf | 91 | 75 | 65 |
The onset is usually insidious, but it may occur after a minor
injury or period of disuse. The unwanted translations may range from a
sensation of a minor "slip" in the joint to a complete dislocation of
the humeral head from the glenoid. The displacement characteristically
reduces spontaneously after which the patient is usually able to return
to his or her activities without much pain or problem. As the condition
progresses, the patient notices that the shoulder has become looser and
may feel it slip out and clunk back in with increasing ease and in an
increasing number of activities. The shoulder may become uncomfortable,
even with the arm at rest. The patient may volunteer that he or she can
make the shoulder "pop out" and that at times the shoulder feels as if
it "needs to be popped out" on purpose.
It is important to document from the history the circumstances
surrounding the onset of the problem as well as each and every position
of the shoulder in which the patient experiences instability. It is
also important to note if the opposite shoulder is symptomatic as well.
A family history may reveal other kindred similarly affected as well as
conditions know to predispose to atraumatic instability, such as Ehlers
Danlos syndrome.
Many patients admit that they used to have a habit of dislocating
the joint, but now they can no longer control the stability of the
joint. The surgeon must determine if habitual dislocation remains a
feature of the patients problem. It is obvious that it is difficult for
surgery to cure habitual instability.
Finally, it is important to document the patient's expectations of
their shoulder to assure that the goals are within reach before
treatment is started.
Demonstration of instability The patient is routinely asked if he or she can dislocate the
shoulder at will. This enables the surgeon to see the different
positions of concern and directions of translation. By palpating the
scapula, the surgeon can estimate the relative position of the humerus
and scapula when the shoulder is translated and reduced. There are
three common demonstrations of instability:
- The patient may demonstrate a spontaneous
"jerk" test by bringing the internally rotated arm horizontally across
the chest, causing the humeral head to subluxate posteriorly. Then by
returning the elevated humerus to the coronal plane the shoulder
produces a "clunk" on reduction of glenohumeral joint (much like the
Ortolani and Barlow signs of the hip).
- The patient may demonstrate that when he or she attempts to lift an object or tie a shoe, the shoulder subluxates inferiorly.
- The
patient may demonstrate that the shoulder translates when the arm is
elevated in posterior humerothoracic planes with spontaneous reduction
on return to the coronal plane.
Laxity tests These tests examine the amount of translation allowed by the
shoulder starting from positions where the ligaments are normally
loose. The amount of translation on laxity testing is determined by the
length of the capsule and ligaments as well as by the starting position
(i.e. more anterior laxity will be noted if the arm is examined in
internal rotation--which relaxes the anterior structures, than if it is
examined in external rotation--which tightens the anterior structures).
In interpreting the significance of the degree of translation on
laxity tests, it is important to use the contralateral shoulder as an
example of what is "normal" for the patient. Not infrequently the
laxity on the symptomatic side will be similar to that on the
asymptomatic side. Investigations of clinical laxity tests showed that
the range of translations for shoulders with atraumatic instability was
similar to that of normal shoulders or shoulders with traumatic
instability (see figure 5). (Harryman, Sidles and Matsen, 1992)
However, a distinguishing feature of many shoulders with atraumatic
instability is that the resistance to translation is diminished when
the humeral head is pressed into the glenoid fossa; suggesting that the
effective glenoid concavity is diminished. It is helpful if the patient
recognizes one or more of the directions of translation as being
responsible for his or her clinical symptoms. Finally, it is important
to point out that these are tests of laxity, not tests for instability:
Many normally stable shoulders, such as those of gymnasts, will
demonstrate substantial translation on these laxity tests even though
they are asymptomatic.
Drawer test
The patient is seated with the forearm resting on the lap and the
shoulder relaxed. The examiner stands behind the patient. One of the
examiner's hands stabilizes the shoulder girdle (scapula and clavicle)
while the other grasps the proximal humerus. These tests are performed
with (1) a minimal compressive load (just enough to center the head in
the glenoid) and (2) with a substantial compressive load (to gain a
feeling for the effectiveness of the glenoid concavity). Starting from
the centered position with a minimal compressive load, the humerus is
first pushed forward to determine the amount of anterior displacement
relative to the scapula. The anterior translation of a normal shoulder
reaches a firm end-point with no clunking, no pain and no apprehension.
A clunk or snap on anterior subluxation or reduction may suggest a
labral tear or Bankart lesion. The test is then repeated with a
substantial compressive load applied before translation is attempted to
gain an appreciation of the competency of the anterior glenoid lip. The
humerus is returned to the neutral position and the posterior drawer
test is performed, with light and again with substantial compressive
loads to judge the amount of translation and the effectiveness of the
posterior glenoid lip, respectively. (Silliman and Hawkins, 1993)
Sulcus test
The patient sits with the arm relaxed at the side. The examiner
centers the head with a mild compressive load and then pulls the arm
downward. Inferior laxity is demonstrated if a sulcus or hollow appears
inferior to the acromion. Competency of the inferior glenoid lip is
demonstrated by pressing the humeral head into the glenoid while
inferior traction is applied.
Push-pull test
The patient lies supine with the shoulder off the edge of the table.
The arm is in 90 degrees of abduction and 30 degrees of flexion.
Standing next to the patient's hip, the examiner pulls up on the wrist
with one hand while pushing down on the proximal humerus with the
other. The shoulders of normal, relaxed patients often will allow 50
per cent posterior translation on this test.
Stability tests These tests examine the ability of the shoulder to resist challenges
to stability in positions where the ligaments are normally under
tension.
Fulcrum test
The patient lies supine at the edge of the examination table with
the arm abducted to 90 degrees. The examiner places one hand on the
table under the glenohumeral joint to act as a fulcrum. The arm is
gently and progressively extended and externally rotated over this
fulcrum. Maintaining gentle passive external rotation for a minute
fatigues the subscapularis, challenging the capsular contribution to
the anterior stability of the shoulder. The patient with anterior
instability will usually become apprehensive as this maneuver is
carried out (watch the eyebrows for a clue that the shoulder is getting
ready to dislocate). In this test, normally no translation occurs
because it is performed in a position where the anterior ligaments are
placed under tension.
Crank or apprehension test
The patient sits with the back toward the examiner. The arm is held
in 90 degrees of abduction and external rotation. The examiner pulls
back on the patient's wrist with one hand while stabilizing the back of
the shoulder with the other. The patient with anterior instability
usually will become apprehensive with this maneuver. As for the fulcrum
test, no translation is expected in the normal shoulder because this
test is performed in a position where the anterior ligaments are placed
under tension.
Jerk test
The patient sits with the arm internally rotated and flexed forward
to 90 degrees. The examiner grasps the elbow and axially loads the
humerus in a proximal direction. While axial loading of the humerus is
maintained, the arm is moved horizontally across the body. A positive
test is indicated by a sudden jerk as the humeral head slides off the
back of the glenoid. When the arm is returned to the original position
of 90-degree abduction, a second jerk may be observed, that of the
humeral head returning to the glenoid.
Strength tests The strength of abduction and rotation are tested to gauge the power of
the muscles contributing to stability through concavity compression.
The strength of the scapular protractors and elevators are also tested
to determine their ability to position the scapula securely.Radiographs In atraumatic instability shoulder radiographs characteristically
show no bony pathology. Specifically, there is no posterolateral
humeral head defect, no glenoid rim fracture or new bone formation and
no evidence of tuberosity fracture. Because these patients
characteristically demonstrate midrange instability, radiographs may
show translation of the humeral head with respect to the glenoid; for
example, the axillary view may show posterior subluxation.
Occasionally, radiographs may suggest factors underlying the atraumatic
instability such as a relatively small or hypoplastic glenoid or a
posteriorly inclined or otherwise dysplastic glenoid. The bony glenoid
fossa may appear quite flat; however, it is difficult to relate the
apparent depth of the bony socket to the effective depth of the fossa
formed by cartilage and labrum covering the bone.
We do not use stress radiographs, arthrography, MRI, or arthroscopy in the diagnosis of atraumatic instability.
Traumatic instability is instability that arises from an injury of
sufficient magnitude to tear the glenohumeral capsule, ligaments,
labrum or rotator cuff or to produce a fracture of the humerus or
glenoid.
TUBS A typical patient is a 17-year-old skier whose recurrent anterior
instability began with a fall on an abducted, externally rotated arm
(although the condition has been reported in individuals as young as
three years old. (Endo et al, 1993) In order to injure these strong
structures, a substantial force must be applied to them. The most
common pathology associated with traumatic instability is the avulsion
of the anteroinferior capsule and ligaments from the glenoid rim.
Substantial force is required to produce this avulsion in a healthy
shoulder. While this load may be applied directly (for example, by
having the proximal humerus hit from behind), an indirect loading
mechanism is more common. Indirect loading is most easily understood in
terms of a simple model of the torques involved. When the upper
extremity is abducted and externally rotated by a force applied to the
hand, the following equation for torque equilibrium is a useful
approximation, if we attribute the major stabilizing role to the
ligament (see figure 6): T = B * E/R where "T" is the tension in the
inferior glenohumeral ligament, "R" is the radius of the humeral head,
"B" is the abduction external rotation load applied to the hand, and
"E" is the distance from the center of the humeral head to the hand. If
the radius of the humeral head is 2.5 cm and the distance from the head
center to the hand is one meter, this formula suggests that the
inferior glenohumeral ligament would experience a load 40 times greater
than that applied to the hand. From this example we can see that a
relatively small load is required to produce the characteristic lesion
of traumatic instability if this load is applied indirectly through the
lever arm of the upper extremity.
Avulsion of the anterior glenohumeral ligament mechanism (see figure
7) deprives the joint of stability in positions where this structure is
a check rein, such a in maximal external rotation and extension of the
arm elevated near the coronal plane. Thus, it is evident that in
recurrent traumatic instability, problems are most likely to occur when
the arm is placed in a position approximating that in which the
original injury occurred. Midrange instability may also result from a
traumatic injury because the glenoid concavity may be compromised by
avulsion of the labrum or fracture of the bony lip of the glenoid (see
figure 8). Lessening of the effective glenoid arc compromises the
effectiveness of concavity compression, reduces the balance stability
angles, reduces thesurface available for adhesion-cohesion, and
compromises the ability of the glenoid suction cup to conform to the
head of the humerus.
The corner of the glenoid abuts against the insertion of the cuff to
the tuberosity when the humerus is extended, abducted, and externally
rotated (see figure 9). (Liu and Boynton, 1993; Matsen, Lippitt, Sidles
et al, 1994; Montgomery and Jobe, 1994; Rossi et al, 1994; Walch et al,
1991; Walch et al, 1993) Thus, the same forces which challenge the
inferior glenohumeral ligament are also applied to the greater
tuberosity-cuff insertion area. It is not surprising, therefore, that
posterolateral humeral head defects, tuberosity fractures and cuff
injuries may be a part of the clinical picture of traumatic
instability. The exact location and type of traumatic injury depends on
the age of the patient and the magnitude, rate, and direction of force
applied. Avulsions of the glenoid labrum, glenoid rim fractures and
posterolateral humeral head defects are more commonly seen in young
individuals. In patients over the age of 35, traumatic instability
tends to be associated with fractures of the greater tuberosity and
rotator cuff tears. This tendency increases with increasing age at the
time of the initial traumatic dislocation. Thus, as a rule, younger
patients require management of anterior lesions and older patients
require management of posterior lesions.
The posterior lateral humeral head defect is a common feature of
traumatic instability. These lesions are often noted after the first
traumatic dislocation and tend to increase in size with recurrent
episodes. This impaction injury usually occurs when the anterior corner
of the glenoid is driven into the posterior lateral humeral articular
surface. It is evident that this injury is close to the cuff insertion.
Large head defects compromise stability by diminishing the articular
congruity of the humerus.
To help recall the common aspects of traumatic instability, we use
the acronym TUBS. The instability arises from a significant episode of
Trauma, characteristically from abduction and extension of the arm
elevated in the coronal plane. The resulting instability is usually
Unidirectional in the anteroinferior direction. The pathology is
usually an avulsion of the labrum and capsuloligamentous complex from
the anterior inferior lip of the glenoid, commonly referred to as a
Bankart lesion. With functionally significant recurrent traumatic
instability, a Surgical reconstruction of this labral and ligament
avulsion is frequently required to restore stability.
The reader is referred to an review of the pathology and
pathogenesis of traumatic instability by Wirth and Rockwood. (Wirth and
Rockwood, 1993) TUBS history Most patients presenting with TUBS are between the ages of 14 and 34
(see figure 10). These patients characteristically have difficulty
throwing overhand, but many patients also have problems sleeping,
putting their hand behind their head, and lifting a gallon to head
level (See table 1 and figure 11). Their general health status as
revealed by the SF 36 self assessment questionnaire is better on
average than that of a comparable group of patients with atraumatic
instability (see figure 12).
Table 1
| TUBS | AMBRII | Failed Repairs |
| Number of Patients | 101 |
70 | 76 |
| % female | 26% | 38%
| 28% |
| % right side | 55% | 68%
| 51% |
| Age | 29±11 | 27±10
| 31 ± 8 |
|
|
|
|
| % able to perform SST function |
TUBS (101) |
AMBRII (70) |
Failed Repairs (76) |
| Sleep on Side | 43 | 19
| 11 |
| Comfort by side | 87 | 71
| 56 |
| Wash opposite shoulder | 69 |
64 | 39 |
| Hand Behind Head | 77 |
75 | 48 |
| Tuck in Shirt | 89 |
81 | 54 |
| Place 8 lbs on shelf | 53 |
35 | 28 |
| Place 1 lb on shelf | 91 |
75 | 65 |
| Place coin on shelf | 93 |
77 | 73 |
| Toss overhand | 31 |
35 | 15 |
| Do usual work | 69 |
46 | 42 |
The initial dislocation
The most important element in the history is the definition of the
original injury. As is evident to anyone who has attempted to recreate
these lesions in a cadaver, substantial force is required to produce a
traumatic dislocation--in most cadaver specimens, it is impossible to
duplicate the Bankart injury mechanism because the humerus fractures
first! In characteristic anterior traumatic instability, the structure
that is avulsed is the strongest part of the shoulder's capsular
mechanism: the anterior inferior glenohumeral ligament. In order to
tear this ligament, substantial force needs to be applied to the
shoulder when the arm is in a position to tighten this ligament. Thus
the usual mechanism of injury involves the application of a large
extension-external rotation force to the arm elevated near the coronal
plane. Such a mechanism may occur in a fall while snow skiing, while
executing a high speed cut in water skiing, in an arm tackle during
football, with a block of a volleyball or basketball shot, or in
relatively violent industrial accidents in which a posteriorly directed
force is applied to the hand while the arm is abducted and externally
rotated. Awkward lifting on the job and rear-end automobile accidents
would not be expected to provide the conditions or mechanism for this
injury. Direct questioning and persistence are often necessary to
elicit a full description of the mechanism of the initial injury,
including the position of the shoulder and the direction and magnitude
of the applied force. Yet this information is critical to establishing
the diagnosis.
An initial traumatic dislocation often requires assistance in
reduction, rather than reducing spontaneously as is usually the case in
atraumatic instability. Radiographs from previous emergency room visits
may be available to show the shoulder in its dislocated position.
Axillary or other neuropathy may have accompanied the glenohumeral
dislocation. Any of these findings individually or in combination
support the diagnosis of traumatic as opposed to atraumatic
instability.
Traumatic instability may occur without a complete dislocation. In
this situation, the injury produces a traumatic lesion, but this lesion
is insufficient to allow the humeral head to completely escape from the
glenoid. The shoulder may be unstable because, as a result of the
injury, it manifests apprehension or subluxation when the arm is placed
near the position of injury. In these cases there is no history of the
need for reduction nor radiographs with the shoulder in the dislocated
position. Thus the diagnosis rests to an even greater extent on a
careful history that focuses on the position and forces involved in the
initial episode. The initial dislocation The most important element in the history is the definition of the
original injury. As is evident to anyone who has attempted to recreate
these lesions in a cadaver, substantial force is required to produce a
traumatic dislocation--in most cadaver specimens, it is impossible to
duplicate the Bankart injury mechanism because the humerus fractures
first! In characteristic anterior traumatic instability, the structure
that is avulsed is the strongest part of the shoulder's capsular
mechanism: the anterior inferior glenohumeral ligament. In order to
tear this ligament, substantial force needs to be applied to the
shoulder when the arm is in a position to tighten this ligament. Thus
the usual mechanism of injury involves the application of a large
extension-external rotation force to the arm elevated near the coronal
plane. Such a mechanism may occur in a fall while snow skiing, while
executing a high speed cut in water skiing, in an arm tackle during
football, with a block of a volleyball or basketball shot, or in
relatively violent industrial accidents in which a posteriorly directed
force is applied to the hand while the arm is abducted and externally
rotated. Awkward lifting on the job and rear-end automobile accidents
would not be expected to provide the conditions or mechanism for this
injury. Direct questioning and persistence are often necessary to
elicit a full description of the mechanism of the initial injury,
including the position of the shoulder and the direction and magnitude
of the applied force. Yet this information is critical to establishing
the diagnosis.
An initial traumatic dislocation often requires assistance in
reduction, rather than reducing spontaneously as is usually the case in
atraumatic instability. Radiographs from previous emergency room visits
may be available to show the shoulder in its dislocated position.
Axillary or other neuropathy may have accompanied the glenohumeral
dislocation. Any of these findings individually or in combination
support the diagnosis of traumatic as opposed to atraumatic
instability.
Traumatic instability may occur without a complete dislocation. In
this situation, the injury produces a traumatic lesion, but this lesion
is insufficient to allow the humeral head to completely escape from the
glenoid. The shoulder may be unstable because, as a result of the
injury, it manifests apprehension or subluxation when the arm is placed
near the position of injury. In these cases there is no history of the
need for reduction nor radiographs with the shoulder in the dislocated
position. Thus the diagnosis rests to an even greater extent on a
careful history that focuses on the position and forces involved in the
initial episode. Subsequent episodes of instability Characteristically, the shoulder with traumatic instability is
comfortable when troublesome positions are avoided. However, the
apprehension or fear of instability may prevent the individual from
work or sport. Recurrent subluxation or dislocation may occur when the
shoulder is forced unexpectedly into the abducted externally rotated
position or during sleep when the patient's active guard is less
effective. There may be a history of increasing ease of dislocation as
the remaining stabilizing factors are progressively compromised.
The goal of the physical examination is largely to confirm the
impression obtained from the history: that a certain combination of arm
position and force application produces the actual or threatened
glenohumeral instability that is of functional concern to the patient.Signs and symptoms If the diagnosis has been rigorously established from the history,
for example by documented recurrent anterior dislocations, it is not
necessary to risk redislocation on the physical examination. If such
rigorous documentation is not available, however, the examiner must
challenge the ligamentous stability of the shoulder in the suspected
position of vulnerability being prepared to reduce the shoulder should
a dislocation result.
The most common direction of recurrent traumatic instability is
anteroinferior. Stability in this position is challenged by externally
rotating and extending the arm elevated to various degrees in the
coronal plane. It may be necessary to hold the arm in the challenging
position for 1 to 2 minutes to fatigue the stabilizing musculature.
When the muscle stabilizers tire, the capsuloligamentous mechanism is
all that is holding the humeral head in the glenoid. At this moment the
patient with traumatic anterior instability becomes apprehensive,
recognizing that the shoulder is about to come out of joint. This
recognition is strongly supportive of the diagnosis of traumatic
anterior instability.
The magnitude of translation on the standard tests of glenohumeral
laxity does not necessarily distinguish stable from unstable shoulders
(see figure 13). However, the experienced examiner may detect a
diminished resistance to anterior translation on the drawer test when
the humeral head is compressed into the glenoid fossa, indicating loss
of the anterior glenoid lip. This maneuver may also elicit grinding as
the humeral head slides over the bony edge of the glenoid from which
the labrum has been avulsed or catching as the head passes over a torn
glenoid labrum.
Pain on abduction, external rotation and extension is not specific
for instability. Such pain may relate to shoulder stiffness or
alternatively to abutment of the glenoid against the cuff insertion to
the head posteriorly. (Matsen, Lippitt, Sidles et al, 1994; Rossi,
Ternamian, Cerciello et al, 1994; Walch, Liotard, Boileau et al, 1991;
Walch, Liotard, Boileau et al, 1993) Relief of this pain by anterior
pressure on the humeral head may result from diminished stretch on the
anterior capsule or from relief of the abutment posteriorly (see figure
14).
In all patients with traumatic instability but particularly in those
over age 35, the strength of the internal and external rotation must be
examined to explore the possibility of cuff weakness or tear. Finally,
a neurological examination is performed to determine the integrity of
the axillary nerve and other branches of the brachial plexus. Radiographs and other tests Radiographs frequently help to provide confirmation of traumatic glenohumeral instability.
Humeral head changes
One of the most common findings is indentation or impaction in the
posterior aspect of the humeral head from contact with the
anteroinferior corner of the glenoid when the joint was dislocated (see
figures 15 and 16). In their classic article (Hill and Sachs, 1940),
Hill and Sachs evaluated the relationship of humeral head defects to
shoulder instability. They concluded that more than two-thirds of
anterior shoulder dislocations are complicated by a bony injury of the
humerus or scapula. We quote:
"Compression fractures as a result of impingement of the weakest
portion of the humeral head, that is, the posterior lateral aspect of
the articular surface against the anterior rim of the glenoid fossa are
found so frequently in cases of habitual dislocation that they have
been described as a typical defect. These defects are sustained at the
time of the original dislocation. A special sign is the sharp,
vertical, dense medial border of the groove known as the line of
condensation, the length of which is correlated with the size of the
defect."
They reported the defect in only 27 per cent of 119 acute anterior
dislocations and in 74 per cent of 15 recurrent anterior dislocations.
However, they stated that the incidence of the groove defect was low,
undoubtedly because it was only in the last 6 months of their 10-year
study (1930 to 1940) that they used special radiographic views. The
size of the defect varied in length (cephalocaudal) from 5 mm to 3 cm,
in width from 3 mm to 2 cm, and in depth from 10 mm to 22 mm. (Hill and
Sachs, 1940)
A number of special projections have been describe to enhance the
view of the Hill Sachs defect. (Adams, 1950; Didiee, 1930; Hall et al,
1959; Hermodsson, 1934; Hill and Sachs, 1940; Moseley, 1961; Oppenheim
et al, 1985; Pavlov, Warren, Weiss et al, 1985; Symeonides, 1972) Two
of these views bear special mention.
The Stryker notch view
The patient is supine on the table with the cassette placed under
the shoulder. (Hall, Isaac and Booth, 1959) The palm of the hand of the
affected shoulder is placed on top of the head, with the fingers
directed toward the back of the head. The elbow of the affected
shoulder should point straight upward. The x-ray beam tilts 10 degrees
toward the head, centered over the coracoid process (see figure 17).
This technique was developed by William S. Stryker and reported by Hall
and coworkers. (Hall, Isaac and Booth, 1959). They stated that they
could demonstrate the humeral head defect in 90 per cent of 20 patients
with a history of recurring anterior dislocation of the shoulder.
The apical oblique view
Garth and coworkers (Garth, Allman and Armstrong, 1987; Garth et al,
1984) described the apical oblique projection of the shoulder (see
figure 18). In this technique the patient sits with the scapula flat
against the cassette (as for the anteroposterior view in the plane of
the scapula). The arm may be in a sling. The x-ray beam is centered on
the coracoid and directed perpendicular to the cassette (45 degrees to
the coronal plane) except that it is angled 45 degrees caudally. The
beam passes tangential to the articular surface of the glenohumeral
joint and the posterolateral aspect of the humeral head. This view is
likely to reveal both anterior glenoid lip defects and posterior
lateral impression fractures of the humeral head.
The incidence of the Hill Sachs defect reported depends on both the
radiographic technique and the patient population. Symeonides
(Symeonides, 1972) reported the humeral head defect in 23 of 45
patients who had recurrent anterior dislocations of the shoulder.
However, at the time of surgery he could confirm only 18 of 45.
Eyre-Brook (Eyre-Brook, 1971) reported an incidence of the Hill
Sachs defect of 64 per cent in 17 recurrent anterior dislocations, and
Brav (Brav, 1960) recorded a rate of 67 per cent in 69 recurrent
dislocations. Rowe (Rowe et al, 1977) noted the defect in 38 per cent
of 125 acute dislocations and in 57 per cent of 63 recurrent
dislocations. Adams (Adams, 1948) noted that the defect was found at
the time of surgery in 82 per cent of 68 patients. Palmer and Widen
(Palmer and Widen, 1948) found the defect at surgery in all of 60
patients.
Calandra and coworkers (Calandra et al, 1989) prospectively studied
the incidence of Hills-Sach lesions using diagnostic arthroscopy. In a
young population of 32 patients with a mean age of 28 years, the
frequency of this lesion was 47% for initial anterior shoulder
dislocations.
Danzig, Greenway, and Resnick (Danzig et al, 1980) reported that in
cadaveric and clinical studies no single view will always reveal the
humeral head compression fracture. Pavlov and coworkers (Pavlov,
Warren, Weiss et al, 1985) and Rozing and associates (Rozing et al,
1986) found that the Stryker notch view taken in internal rotation best
revealed the posterolateral humeral head defect (see figure 14).
The demonstration of a posterior lateral humeral head defect
strongly indicates that the shoulder has been subject to a traumatic
anterior dislocation. When these factors are already known--for
example, in a 17-year-old whose recurrent anterior dislocations began
with a well-documented abduction-external rotation injury in
football--it is not necessary to spend a great deal of effort
demonstrating the humeral head defect because (1) it is very likely to
be present even if not seen on the radiographs, and (2) the existence
of such a lesion does not in itself alter our management of the
patient.
Glenoid changes
Standard radiographs may reveal a periosteal reaction to the
ligamentous avulsion at the glenoid lip or a fracture (see figure 19),
erosion or new bone formation at the glenoid rim. Modifications of the
axillary view may help the identification of glenoid rim changes.
Rokous (Rokous et al, 1972) and colleagues described what has become
known as the "West Point" axillary view. (Rockwood, 1984) In this
technique the patient is placed prone on the x-ray table with the
involved shoulder on a pad raised 7.5 cm from the top of the table. The
head and neck are turned away from the involved side. With the cassette
held against the superior aspect of the shoulder, the x-ray beam is
centered at the axilla, 25 degrees downward from the horizontal and 25
degrees medial. The resulting x-ray is a tangential view of the
anteroinferior rim of the glenoid (see figure 20). Using this view,
Rokous and associates demonstrated bony abnormalities of the anterior
glenoid rim in 53 of 63 patients whose histories indicated traumatic
instability of the shoulder. Cyprien and coworkers (Cyprien, Vasey and
Burdet, 1983) demonstrated lessening of the glenoid diameter and
shortening of the anterior glenoid rim in shoulders with recurrent
anterior dislocation. Blazina and Satzman (Blazina and Satzman, 1969)
also reported anteroinferior glenoid rim fractures seen on the axillary
view in nine of their cases.
Special radiographic techniques
Although pathology can be seen with additional radiographic views,
(Green and Christensen, 1994; Minkoff and Cavaliere, 1993; Palmer and
Caslowitz, 1995; Rafii et al, 1993) CT arthrography (Braunstein and
O'Conner, 1982; Cramer et al, 1982; El-Khoury et al, 1986; Kelley,
1954; Kleinman et al., 1984; McGlynn et al, 1982; McMaster, 1986; Rafii
et al, 1986; Rafii et al, 1987; Shively and Johnson, 1984), fluoroscopy
(Norris, 1984) or MRI, these additional tests are rarely cost-effective
in the clinical evaluation and management of shoulders with
characteristic traumatic instability. (Engebretsen and Craig, 1993; Liu
and Henry, 1996) While CT evidence of labral or capsular pathology is
unlikely to change the management of the shoulder, contrast
computerized tomography may help document the flattening of the
anteroinferior glenoid concavity due to loss of articular cartilage. CT
may also be useful in defining the magnitude of bone loss when sizable
humeral head or glenoid defects are suggested on plain radiographs.
(Gould et al, 1985; Seltzer and Weissman, 1985) When previous glenoid
bone blocks have been carried out or hardware inserted, CT is useful
for examining the possibility of their encroachment on the humeral
head. (Cramer, 1882; Cramer, Von and Kramps, 1982; Danzig et al, 1982)
Although many articles have been written regarding the use of MRI in
imaging the unstable shoulder (e.g. Chandnani et al, 1993; Gross et al,
1990; Iannotti et al, 1991; Kiett et al, 1988; Meyer and Dalinka, 1990;
Neumann et al, 1991; Palmer and Widen, 1948; Richards et al, 1994;
Runkel et al, 1993; Vellet et al, 1991) the clinical usefulness of this
examination awaits definition. Iannotti et al (Iannotti, Zlatkin,
Esterhai et al, 1991), reported the sensitivity and specificity of MRI
in the diagnosis of lateral tears associated with glenohumeral
instability were 88 and 93%, respectively. However, in a blinded study,
Garneau et al (Garneau et al, 1991) found that it was insensitive and
nonspecific for labral pathology. Even if MRI reliably yielded this
information, it is unclear how it would be cost-effective in the
management of the patient: patients with refractory instability would
be considered for surgery with or without such data.
Rotator cuff imaging
In a patient whose onset of traumatic instability occurred after age
35 there may be evidence on history and physical examination of rotator
cuff pathology. Particular concern arises if weakness of external
rotation or elevation persist longer than a week or so. In these
situations, preoperative imaging of cuff integrity may play an
important role in surgical planning: the approach for rotator cuff
repair is quite different than the approach for the repair of an
anterior inferior capsular lesion. Arthrography, ultrasound or MRI may
be useful in this situation.
Electromyography
Electromyography may be helpful in the evaluation of the patient
with recurrent traumatic instability if the history and physical
examination suggest residual brachial plexus lesions.
Arthroscopy
Diagnostic arthroscopy is not a necessary prelude to open surgical
repair of documented recurrent traumatic instability. While it
uncommonly changes the surgical approach, shoulder arthroscopy has
helped define some of the pathology associated with recurrent
instability. Such lesions include labral tears, capsular rents, humeral
head defects, and rotator cuff defects. (Andrews et al, 1983;
Carew-McColl, 1980; Frizziero, 1981; Garth, Allman and Armstrong, 1987;
Ha'eri and Maitland, 1981; Hintermann and Gachter, 1994; Johnson, 1980;
Lilleby, 1982; McMaster, 1986; Mital, 1980; Older, 1976; Parisien,
1983; Wiley and Austwick, 1982; Wiley and Older, 1980; Zizzi et al,
1981)
A classification of anterior labral "Bankart" lesions was proposed
by Green and Christensen. (Green and Christensen, 1995) In 37 cases,
they described the arthroscopic appearance common to five separate
groups. Type I is the normal intact labrum. Type II is a simple
detachment of the labrum from the glenoid. Type III is an
intrasubstance tear of the glenoid labrum. Type IV is a detachment of
the labrum with significant fraying or degeneration and Type V is a
complete degeneration of absence of the glenoid labrum.
Neviaser found that occasionally the anterior labroligamentous
periosteal sleeve is avulsed from the supporting anterior inferior
ligamentous and labral structure. (Neviaser, 1993)
Habermeyer and Gleyze found that shoulders with more than five
recurrent dislocations were found to have anterior articular cartilage
erosion. (Gleyze and Habermeyer, 1996) Harryman noted labral damage in
all cases treated for recurrent anterior traumatic instability and
significant articular erosion to subchondral bone in 20%. (Harryman,
1996)
Other lesions may be associated with Bankart lesions. Snyder et al
(SnyderBanasKarzel, 1995) and Warner (Warner et al, 1994) found the
association of superior labral detachment and Bankart lesions.
Wolf reported that 6 of 64 patients with anterior instability had
avulsion of glenohumeral ligaments from the humerus while 47 had true
Bankart lesions (73.5%). (Wolf et al, 1995)
Arthroscopy also reveals defects in the articular cartilage of the
posterior lateral humeral head, which would not be detected on
radiographs.
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