Trey Colantonio, MD, CPT and CDR Lance LeClere, MD
Isolated posterior glenohumeral instability is often a challenging diagnosis with significant performance implications in athletes. Overhead and contact athletes are particularly at risk for posterior instability, and shoulder instability is one of the most common injuries in high-level athletes.1,2 Often the primary presenting symptom is generalized shoulder pain, and the patient may have been referred with a diagnosis other than shoulder instability.3,4 This is an important distinction from anterior instability, which most often presents with a chief complaint of instability, whereas posterior instability most commonly presents with a chief complaint of pain.
Posterior instability is the result of abnormal posterior translation of the humeral head on the glenoid and may occur as a result of traumatic dislocation, recurrent posterior subluxation, or as pain due to microinstability and repetitive microtrauma. Although less common than anterior instability, with reported incidence ranging from 2% to 10% of glenohumeral instability,2,4–7 posterior instability is observed more frequently in athletes and in young, active populations.4,5,8 Contact athletes subject to blunt force trauma to the glenohumeral joint as well as overhead athletes exposed to repetitive microtrauma are at higher risk for developing posterior instability.5,9 Additionally, posterior instability and lesions of the posterior glenoid labrum may be present in patients with combined anterior instability.10,11 As such, a thorough history and physical examination must be conducted in combination with advanced imaging to adequately diagnose posterior glenohumeral instability. Recurrent posterior instability presents a challenging injury and often leads to decreased athletic performance; however, if treated appropriately, patients can have excellent results and return to play.1 This chapter will outline the anatomic and biomechanical considerations, historical findings, and physical examination of the athlete with posterior glenohumeral instability.
ANATOMY, BIOMECHANICS, AND PATHOANATOMY
An appreciation of the anatomic elements of glenohumeral stability is essential to the diagnosis and management of posterior glenohumeral instability. Stability of the glenohumeral joint is conferred through a combination of static and dynamic stabilizers that act in concert to maintain the proper relationship of the humeral head and glenoid at rest and during motion. Injury, anatomical variation, or dysfunction of one or various elements of glenohumeral stability can lead to instability of the joint.
The primary static stabilizers of the glenohumeral joint are the bony anatomy and capsulolabral ligamentous structures.12–17 The osseous morphology of the glenoid and humerus are critical components of static glenohumeral stability. The glenoid concavity forms the articular surface of the joint and has a normal retroversion of 4 to 7 degrees18,19 or 1 ± 3 degrees when controlled for scapular orientation.20 Increased glenoid retroversion has been shown to predispose patients to posterior instability.9,20,21 In a prospective study of 714 young athletes, Owens et al found a mean retroversion of 7.7 degrees in noninjured participants compared to 17.6 degrees in those with posterior instability. They also found a 17% increased risk of subsequent posterior instability with each 1-degree increase in glenoid retroversion.9 Additionally, Bradley and colleagues examined magnetic resonance imaging of patients undergoing arthroscopic posterior labrum repair and found that these patients had increased glenoid and chondrolabral retroversion when compared to a control group.22 Despite several studies demonstrating increased glenoid retroversion as a risk factor for posterior instability, this area remains a contentious topic and other authors have shown that humeral subluxation may not be increased in the setting of increased retroversion.23
In addition to the orientation of the glenoid, the concavity has a significant role in posterior stability of the glenohumeral joint. A congenital deficiency of the glenoid rim or concavity is commonly referred to as glenoid dysplasia.24 In a cadaveric study, Inui et al demonstrated that a deficiency of the glenoid concavity, or a flat glenoid, particularly in the inferior glenoid, led to posterior instability.25 Edelson similarly described posteroinferior hypoplasia defined as a “dropping away” of the flat plateau of the posterior glenoid. Edelson incidentally discovered posteroinferior hypoplasia in 20% to 35% of cadaveric scapulae examined, and this was found to be present in 75% of patients with multidirectional instability (MDI) in the prospective portion of the study.26 The incidence of hypoplasia is unknown and may often be an incidental finding on imaging studies. Hypoplasia likely results from a failure of the inferior glenoid to develop and may often be bilateral. Common associated findings include cartilage and labral compensatory thickening in the posterior inferior glenoid and abnormal humeral head and neck development. Weishaupt and colleagues studied computed tomography (CT) arthrograms of a series of patients with recurrent posterior instability and defined 2 types of dysplastic glenoids: a rounded “lazy J form” or a “delta form” with a triangular osseous deficiency.27 Harper et al went on to classify glenoid dysplasia on magnetic resonance arthrogram (MRA) from mild to severe based on the appearance of the posterior glenoid rim on axial imaging and also noted that patients with severe glenoid dysplasia often have hypertrophy of the posterior labrum.24,28
In addition to congenital variations of glenoid morphology, acquired posterior glenoid bone deficiency can affect posterior stability of the glenohumeral joint. Bone loss from posterior instability can range from attritional wear due to repetitive microtrauma to a large osteochondral fracture from acute trauma.4 Bone loss may also be seen in the form of a reverse bony Bankart lesion, in which a displaced posterior labrum tear leads to a fracture off the posterior glenoid. The amount of bone loss is known to affect recurrent anterior stability, and the success of surgical management and posterior glenoid bone loss has become an area of recent research interest. Hines et al retrospectively reviewed a cohort of patients who received surgical treatment for isolated posterior instability and found a mean posterior bone loss of 7.3%, with 22% of patients having more than 13.5% bone loss. They found no significant difference in reoperation rates or outcome scores; however, patients with more than 13.5% bone loss were less likely to return to military active duty.29 A biomechanical study by Nacca and colleagues demonstrated that posterior glenoid osseous defects greater than 20% of the glenoid predisposed cadaveric shoulders to recurrent instability after reverse Bankart repair.30
Orientation and morphology of the humerus also play an important role in static glenohumeral stability. The humeral head has a normal retroversion of 25 to 35 degrees with an inclination of 130 degrees to the humeral shaft.20,31 Increased humeral head retroversion is associated with an increased baseline external rotation and decreased internal rotation, and as such may predispose patients to posterior instability due to the easier force vector when the arm is held in a flexed, adducted, and internally rotated position.32 Additionally, a traumatic posterior instability event may generate an osteochondral impaction fracture, or reverse Hill-Sachs lesion (RHSL), of the humeral head. Similarly to humeral bone loss in anterior instability, a large RHSL with concomitant posterior glenoid bone loss can predispose the glenohumeral joint to recurrent instability due to engagement on the glenoid.33–35
The glenoid labrum increases the concavity-compression mechanism of the humeral head in the glenoid and increases the depth of humeral articulation.12,36,37 The labrum is a wedge-shaped, fibrous structure that serves as an anchor for capsuloligamentous structures and reduces glenohumeral translation.37,38 Because the posterior labrum is only loosely attached to the surrounding capsule with less ligamentous reinforcement,39–41 it contributes less stability to humeral translation than does the anterior labrum. Nevertheless, the increase in glenoid depth is a significant contributor to chondrolabral containment. Labral height combined with glenoid retroversion are critical to the concept of chondrolabral containment, and patients with recurrent posterior instability have been shown to have a loss of chondrolabral containment.38
Lesions of the labrum can develop after acute trauma or repetitive microtrauma. A reverse Bankart lesion is most commonly seen in the setting of acute trauma and consists of a complete detachment of the posterior labrum from the glenoid. Separation of the labrum from the posterior glenoid leads to a loss of labral height and predisposes patients to recurrent instability. These lesions have uniformly good outcomes with surgical treatment, and restoration of labral height is a key component in prevention of recurrent instability.7,42,43 Depending on the force vector of the trauma and the displacement of the labral tear, a bony avulsion from the glenoid, commonly known as a reverse bony Bankart lesion, may occur. In a biomechanical study,44 a posterior inferior Bankart lesion generated an increase in posterior translation by 83%. Additionally, a posterior labrocapsular periosteal sleeve avulsion may occur in which the periosteum of the posterior glenoid separates from the bone and remains attached to the posterior capsule and detached posterior labrum.45 Repetitive microtrauma most commonly leads to a partial tear of the posterior labrum known as a Kim lesion. This occurs when an accumulation of shearing forces due to persistent subluxation or repetitive microtrauma lead to a loss of chondrolabral containment with subsequent development of posterior labral marginal cracks or partial avulsions of the glenoid labrum.46
The capsular ligaments of the glenohumeral joint contribute significantly to posterior stability. Unlike the robust composition of the anterior capsule, the posterior capsule is relatively thin and biomechanically inferior to the anterior capsule.41 The posterior band of the inferior glenohumeral ligament (PIGHL) is an important component of the posterior capsule. The PIGHL inserts at the 7 to 9 o’clock position on the glenoid and is the most important ligament in the posterior loading position with the arm held in internal rotation and forward flexion. This arm position places the PIGHL in an anterior-posterior orientation under tension and is commonly implicated in blocking injuries in football linemen.4,47 If the posterior capsule and PIGHL are stretched beyond the initial resting length, posterior glenohumeral instability may develop.12,13,48 The posterior capsule has been shown to have an increased cross-sectional area in patients with MDI and posterior instability as compared to those with anterior instability.49 This finding suggests that less energy may be required to disrupt the posterior capsule and may partially explain why repetitive microtrauma is a common cause of posterior instability. A posterior, or reverse, humeral avulsion of the glenohumeral ligaments (RHAGL) is a rare injury that most commonly occurs in concert with additional chondrolabral pathology and may predispose patients to recurrent instability.46,50 A RHAGL is rarely seen in isolation and usually occurs as a result of hyperabduction with the arm in maximal external rotation. Additionally, RHAGL lesions have been shown to be more common in female athletes in studies of patients with instability.51 The presence of a RHAGL has been shown to generate an increase in posterior and inferior translation by 43% in the jerk position.44
The middle glenohumeral ligament (MGHL) and superior glenohumeral ligament also contribute to posterior stability. The MGHL augments the PIGHL and stabilizes the joint against posterior translation during midrange abduction, and the superior glenohumeral ligament augments the PIGHL in shoulder adduction, forward flexion, and internal rotation.4,52–54 Although controversial, the rotator interval is postulated to provide static stabilization against posterior instability via the “circle concept.”55 This theory states that posterior instability must be accompanied by damage to anterior capsuloligamentous structures. The rotator interval has been shown to play a role in prevention of inferior and posterior translation with the arm in forward flexion.32 The coracohumeral ligament within the rotator interval capsule provides stability against inferior translation in external rotation. The circle concept remains controversial, and rotator interval repair during arthroscopic treatment of posterior instability has been challenged in cadaveric studies.56,57
The rotator cuff muscles13,14,58,59 and the long head of the biceps tendon37,47 provide dynamic stability to the glenohumeral joint during normal active motion. The subscapularis muscle is the primary dynamic stabilizer in preventing posterior translation12,13,47; however, all the rotator cuff muscles have an important role in maintaining concavity-compression of the glenohumeral joint.12,47,60 The supraspinatus muscle provides dynamic inferior stability,47 whereas the infraspinatus and teres minor provide posterior compression.14,61 The long head of the biceps tendon also provides some dynamic resistance against inferior translation.62
Scapular mechanics also provide stability to the glenohumeral joint. Orientation of the scapula during motion affects the orientation of the glenoid on the humerus during motion, and poor scapular mechanics may predispose patients to instability. An increase in scapular internal rotation and medial scapular winging has been shown to be present in patients with glenohumeral instability. Additionally, reduced scapular upward rotation is believed to be detrimental to maintaining inferior glenohumeral stability.63
Patients with posterior instability can present in a variety of circumstances because of the varying etiology of their symptoms. Posterior instability can be classified by the direction, degree, mechanism, and volition of instability. Posterior instability may arise as the result of acute trauma or repetitive microtrauma, or less commonly may be atraumatic. Patients with an acute trauma can recall a specific injury and subluxation or dislocation event that may result in recurrent instability. Repetitive microtrauma, the most common mechanism of recurrent posterior instability, results from the culmination of posteriorly directed force vectors with the arm in forward flexion, internal rotation, and adduction. The classic example of this mechanism is the football lineman with recurrent posterior subluxations when blocking. Patients with posterior instability without a history of trauma should be evaluated for an underlying collagen disorder or an abnormality of glenohumeral static stabilizers. Posterior instability is most commonly unidirectional but may occur in the setting of bidirectional instability or MDI.4,49
In the evaluation of posterior instability, attention must be given to the volitional nature of the instability. Involuntary instability most often results in recurrent subluxations as a result of acute or repetitive trauma. Volitional instability occurs when a patient can generate a posterior subluxation or dislocation at will. There are 2 types of volitional instability: voluntary positional and voluntary muscular.40,64,65 Patients with voluntary muscular instability typically have an underlying muscular imbalance that allows for willful subluxation or dislocation independent of arm position and are considered poor surgical candidates.4 Patients with voluntary positional instability are able to generate a subluxation or dislocation event in a certain arm position, typically flexion and adduction, and generally avoid provocative positions. Patients with voluntary positional instability should not necessarily be excluded from surgical management.4,64,66
Obtaining a thorough history is essential when evaluating an athlete with suspected recurrent posterior glenohumeral instability because these patients often present with vague generalized symptoms or confounding injuries. This atypical presentation poses a clinical challenge and determining instability because the nature of these symptoms may lead to a delay in diagnosis.9 Athletes may present in the setting of an acute trauma and recall a specific injury with the arm in an at-risk position for posterior instability; however, athletes more commonly present with recurrent symptoms as a result of repetitive microtrauma. Patients with recurrent instability most frequently present with generalized pain or pain deep in the posterior aspect of the shoulder rather than frank instability.4,5,64 This pain is often accompanied by a decline in performance or strength.67,68 This weakness is most often pronounced with the arm in the forward-flexed, adducted, and internally rotated provocative position for exercises such as bench press or push-ups.4 Throwing or overhead athletes may describe pain that occurs later during activity because of muscle fatigue of the dynamic stabilizers.65,69 Patients may also report mechanical symptoms such as crepitation or clicking sensations with the arm in provocative positions that may be associated with the unstable reverse Bankart lesions, chondral lesions, or loose bodies.32,69
Athletes participating in sports that place high demand on the shoulder, such as football, rugby, wrestling, volleyball, swimming, weightlifting, climbing, and paddling, are particularly at risk.4,5 Additionally, athletes participating a higher levels of sport have been shown to be at increased risk for posterior instability when compared to recreational athletes.5 In an analysis of shoulder injuries at the National Football League Combine, Kaplan et al found a history of a shoulder injury in 50% of participants, with recurrent posterior instability accounting for 4% of these injuries.70 In contact athletes such as football linemen, symptoms are reproduced with a posteriorly directed load in the common blocking position of forward flexion and internal rotation. Throwing athletes or golfers often describe symptoms in the follow-through phase of throwing or swing.65 In racket sports symptoms often occur with a backhand stroke. Swimmers typically report symptoms during the pull-through phase of swimming, and butterfly swimmers are particularly predisposed to posterior instability.65,69 In a young athlete presenting with vague shoulder complaints, posterior instability must be ruled out to avoid potential delayed or missed diagnosis.
A complete physical examination is essential to proper diagnosis of posterior glenohumeral instability, particularly because of the often vague and nonspecific nature of the presenting symptoms. Additionally, careful attention must be paid to signs of generalized hyperlaxity and volitional shoulder subluxation or dislocation because these may be indicative of MDI rather than pathologic posterior instability.
Both shoulders should be examined for any signs of obvious dislocation, asymmetry, abnormal motion, muscle atrophy, or swelling. In the setting of an acute traumatic posterior dislocation event, the shoulder is often fixed in internal rotation with a block to external rotation as well as a posterior axillary fullness and prominent coracoid process.71 Acute posterior dislocations are often missed or delayed in diagnosis in up to 79% of patients; however, this incidence decreases significantly if adequate radiographs and physical examination are performed.71 Scapular motion should be examined and any dyskinesis should be noted. Range of motion is most commonly normal, but an increase in external rotation and slight loss of internal rotation is occasionally seen in patients with posterior instability.4,32,72
Several provocative maneuvers are particularly useful in diagnosing recurrent posterior instability. Although each has been demonstrated to be useful in detecting patients with recurrent posterior instability,73 the combination of provocative tests is essential to making the diagnosis. The Kim test,74 jerk test,47 load and shift test,75 and posterior stress test48 are all commonly performed to assess the degree of posterior instability. The Kim test is performed with the patient seated and the arm in 90 degrees of forward flexion and internal rotation. The examiner grasps the patient’s elbow with one hand and uses the other to grasp the lateral aspect of the patient’s proximal arm or places the hand on the scapula to provide scapular stabilization. A posterior translational force is applied and pain is indicative of a positive Kim test regardless of a palpable click or clunk.74 The downward pressure applied while performing the Kim test displaces the humeral head inferiorly and the axial load compresses the inferior portion of the posterior labrum. As such, pain elicited when performing this maneuver is highly sensitive for a posteroinferior labrum lesion.74
The jerk test is performed with the patient in the standing or seated position. The examiner stands next to the affected shoulder and grasps the elbow in one hand and the distal clavicle and scapular spine in the other. The arm is placed in a flexed, abducted, and internally rotated position and a posterior force is applied to the flexed elbow while an anterior force is applied to the shoulder girdle (Figure 16-1). In patients with posterior instability, this will result in a posterior dislocation or subluxation of the glenohumeral joint. The jerk test is positive when a sudden jerk associated with pain occurs as the subluxated humeral head translates out of the glenoid fossa and glides over the torn posterior labrum with adduction of the shoulder.4,74 With use of the thumb placed on the posterior glenohumeral joint as the hand stabilizes the scapula, a palpatory shift can usually be felt. A “reverse” jerk test can also be performed, and at times is more easily felt than a conventional jerk test. In the “reverse” jerk test, the arm is adducted 90 degrees, forward-flexed 90 degrees, and internally rotated. As the shoulder is taken from adduction to abduction, the reduction of the humeral head into the glenoid fossa can be felt with the thumb of the hand stabilizing the scapula. A combination of a positive Kim test and jerk test has been shown to have a 97% sensitivity for posterior instability.74
The load and shift test is performed with the patient seated or in the lateral decubitus position. The arm is positioned at approximately 20 degrees of forward elevation and abduction to achieve 45 to 60 degrees in the scapular plane. The examiner grasps the humeral head and gently compresses the head into the glenoid. An anterior and posterior stress is applied to grade the degree of translation of the humeral head. A modified load and shift test may be performed with the patient positioned in supine and the affected shoulder at the edge of the examination table. The examiner grasps the elbow and proximal arm and positions the humerus in the scapular plane. The humeral head is compressed into the glenoid and anterior and posterior forces are applied to grade the degree of translation. A grade 0 load and shift describes minimal translation of the humeral head. Grade 1 describes the humeral head translating to the glenoid rim. Grade 2 describes humeral head translation over the glenoid rim that spontaneously reduces. Grade 3 describes humeral head dislocation that does not spontaneously reduce. It is critical to examine the contralateral shoulder because a grade-2 or -2+ load and shift may be physiologic in young athletes.15 Additionally, excessive inferior translation observed with the load and shift test is often associated with posterior subluxation but may also indicate bidirectional instability or MDI.39
The posterior stress test is performed with the patient seated or supine. The examiner grasps the arm at the elbow and, if performed in the seated position, uses the other hand to stabilize the medial border of the scapula. The arm is flexed to 90 degrees, adducted, and internally rotated. A posterior force is applied to the arm to axially load the humerus against the posterior glenoid. The posterior stress test is positive if a posterior subluxation or dislocation occurs with reproduction of the patient’s pain or apprehension.
Patients with suspected posterior glenohumeral instability should be examined for bidirectional instability or MDI. Excessive inferior translation of the humerus on the glenoid is often associated with posterior instability.65,76 The sulcus test is performed with the patient seated and the arm in a neutral position. The examiner grasps the patient’s elbow and applies downward traction while observing the interval between the greater tuberosity and the acromion. If a depression is observed, this may be indicative of inferior instability. A sulcus sign greater than 2 cm is highly suggestive of MDI. If the sulcus does not reduce when the arm is brought into external rotation, it can be considered pathologic with a defect in the rotator interval.65 The Gagey test is also useful in determining insufficiency of the IGHL. The examiner stands on the side of the affected extremity and with one hand grasps the elbow and stabilizes the scapula with the other. The arm is held in neutral rotation and abducted. The test is considered positive if passive abduction of greater than 105 degrees is achieved. In the setting of posterior instability, the Gagey test may be useful for determining the presence of a RHAGL or HAGL lesion.65,78 A positive finding may also be indicative of inferior or MDI. Patients should also be examined for generalized signs of hyperlaxity using the criteria established by Beighton et al.78