Fig. 1
Anterior shoulder dislocation. AP (a) and scapular Y-view (b) radiographs demonstrate anteroinferior glenohumeral dislocation
Computed tomography (CT) is valuable for confirmation of subtle bone lesions associated with instability and for orthopedic surgical planning. A tailored thin cut CT with direct axial, coronal, sagittal and 3D reformats oriented relative to the scapular spine provides a thorough assessment of the glenoid bony morphology and version. Furthermore, evaluation of associated Bankart or Hill Sachs lesions, specifically whether they are “engaging” or apt to lock with repeat dislocation, is of value for orthopaedic triage. CT arthrography is performed in a manner similar to MR arthrography but using nonionic contrast instead of MRI contrast and a viable option for patients who cannot undergo MR imaging. Capsular and cartilage integrity, bone morphology and alignment are well assessed with CT arthrography, as are the glenohumeral ligaments. Positioning with external rotation and active supination increases detection of SLAP tears [15]. With improved CT imaging, MR and CT arthrography are more recently considered equivalent in diagnosing SLAP tears and full thickness rotator cuff tears. Although MR arthrography remains better at predicting engaging Hill Sachs deformities, CT arthrography is better at identifying humeral avulsion of the GHL (HAGL) and glenoid rim fractures [7].
Anterior Glenohumeral Instability
Glenohumeral instability is a spectrum of pathology including dislocation, subluxation and hyperlaxity of the joint [6]. Stability of the glenohumeral joint has historically been subdivided into two main categories based on mechanism of injury. A post-traumatic mechanism typically results in unidirectional instability, is associated with a Bankart injury and often requires surgery; acronym of TUBS (traumatic, unidirectional, Bankart, surgery). The most common instability condition of the glenohumeral joint is secondary to an anterior shoulder dislocation which is traumatic 95% of the time and has a peak occurrence in males 22–33 years old. The estimated incidence of shoulder dislocation in the USA is 23.9 per 100,000 person-years [16]. The most common cause of traumatic anterior instability is due to glenohumeral dislocation, typically anteroinferior dislocation of the humerus after forced abduction and external rotation [7]. This can result in capsular stripping or laxity, labroligamentous tearing, and cartilage or bone defects.
The incidence of recurrent dislocations depends on the cacophony of soft tissue and bony injuries, and patient age. Recurrent dislocations are more frequent in younger patients. For example, young males suffered from recurrent injuries 87% of the time during a 5-year follow-up [17]. The possibility of recurrent shoulder instability in all age populations after non-operative management is 55–67% [18]. In those with recurrent dislocation and injury, surgical stabilization of the glenohumeral joint is more effective than immobilization and rehabilitation alone [19].
Regardless of the etiology, shoulder instability is a very common pathology. Beyond pain, or activity limited by apprehension of recurrent dislocation, chronic glenohumeral instability can initiate a cycle of premature joint degeneration, rotator cuff tearing and impingement [6]. These pathologies can secondarily result in progressive glenohumeral instability and further degeneration of the joint and associated stabilizers.
Anatomical and Biomechanical Considerations
The fibrocartilaginous labrum circumferentially deepens the glenoid articular surface. This is attached to the glenoid bone, glenoid cartilage and glenohumeral ligaments (GHLs) and superiorly with the long head of biceps tendon. The inferior glenohumeral ligament (IGHL) and labrum are intimate and often considered one entity, the “labroligamentous complex”. The IGHL is the largest of the glenohumeral ligaments and the most consistent stabilizer of the glenohumeral joint. It is composed of a thick anterior band and a smaller posterior band with an intervening axillary pouch. In abduction, there is increased tension on the IGHL with the anterior band limiting anterior translation of the humerus in external rotation and the posterior band limiting humeral translation in internal rotation. The anterior band of the IGHL arises from the glenoid between 2–5 o’clock, and the posterior band between 7–9 o’clock. Both bands have a broad lateral insertion on the humeral anatomic neck [20].
The superior glenohumeral ligament (SGHL) may originate from the anterosuperior labrum, the long head of the biceps tendon, or directly off the middle glenohumeral ligament. It extends anteriorly parallel to the base of the coracoid process. The middle glenohumeral ligament (MGHL) is the most variable in its appearance. Just over 50% of the time, the MGHL arises directly from the labrum. Otherwise, it arises at the origin of the superior glenohumeral ligament. A cordlike MGHL is present in 17% and a true Buford complex (absent anterosuperior labrum and cord-like MGHL) is present in less than 2% of people [21].
Imaging Findings in Anterior Glenohumeral Dislocation
Injuries to the stabilizing tissues of the shoulder joint observed in the setting of traumatic anterior glenohumeral dislocation are described according to a spectrum of labroligamentous, cartilaginous, periosteal and osseous pathology associated with anterior glenohumeral instability.
A Bankart lesion is a detachment of the labroligamentous complex off the anteroinferior glenoid, typically seen after a traumatic dislocation. On MR imaging, the labrum is separated from the bony glenoid but remains attached to the anterior band of the IGHL (Fig. 2). On non-contrast MRI, the tear may be seen although without a joint effusion, the actual separation of a non-displaced labral tear may be difficult to discern. MR arthrograms have higher sensitivity as intra-articular contrast will track beneath the torn labrum and affected structures such as the periosteum. Bankart lesions are the most common post-traumatic lesions associated with anterior instability. As these lesions are unstable, they are unlikely to heal by primary intention and are often surgically managed.
Fig. 2
Bankart lesion. Axial fat-suppressed PD image shortly after dislocation demonstrates a classic Bankart lesion with the anteroinferior labroligamentous complex (arrow) separated from the glenoid rim. Due to the acute setting, the joint effusion acts as positive intra-articular contrast
A fragment of the anterior inferior glenoid bone avulsed with the labroligamentous complex during dislocation is referred to as a bony Bankart lesion (Fig. 3). The larger the glenoid bony fragment, the greater the risk of instability, even after stabilization of soft tissue defects [22]. The size and configuration of the bone lesion will determine if bone grafting is required. This is best assessed by CT. Most osseous Bankart lesions may be repaired arthroscopically, although an open procedure may be needed if bone grafting is required.
Fig. 3
Bony Bankart lesion. Axial and sagittal fat-suppressed T1-weighted images demonstrate a bony Bankart lesion (arrow) with a fracture along the anteroinferior glenoid rim
There are many injuries associated with Bankart lesions. Anterior labroligamentous periosteum sleeve avulsion (ALPSA) is the most frequent, seen in 22% of all anteroinferior labroligamentous lesions arthroscopically. They are correctly diagnosed on MR arthrography 77% of the time and seen as a fluid- or contrast-filled cleft beneath the anteroinferior glenoid periosteum which itself may be medially displaced (Fig. 4) [23]. The second most common associated injury is the Perthes lesion where the torn anteroinferior labrum remains non-displaced and attached to periosteum stripped off the anterior scapula (Fig. 5). This occurs in up to 11% of shoulders at arthroscopy for anterior instability, but can be difficult to visualize arthroscopically without probing. Compared to arthroscopy, these lesions are correctly identified on MR arthrography only 50% of the time [23], although they can be better visualized with ABER positioning [5]. A glenolabral articular disruption (GLAD) is infrequent, accounting for less than 3% of anteroinferior labral tears. In one study, all GLAD lesions were correctly diagnosed on MR arthrography pre-arthroscopy with contrast undercutting a fragment of cartilage attached to the torn anteroinferior labrum (Fig. 6) [23].
Fig. 4
ALPSA lesion. Axial fat-suppressed PD-weighted image shortly after dislocation demonstrates an ALPSA lesion with medialization of the labrum and periosteum (arrow) nicely outlined by the joint effusion
Fig. 5
Perthes lesion. Axial fat-suppressed T1-weighted image demonstrates a Perthes lesions (arrow) with periosteal stripping but without medicalization of the labrum or periosteum
Fig. 6
GLAD lesion. Axial T1-weighted (a) and sagittal oblique fat-suppressed T1-weighted (b) images demonstrate a GLAD lesion with an anteroinferior glenoid cartilage defect (arrow in a) and anteroinferior labral tear (long arrow in b) and loose cartilage fragment (short arrow in b)
Humeral avulsion of the inferior GHL (HAGL) is documented arthroscopically in 1.5–9.3% of cases but the incidence is higher (up to 26.9%) in patients with anterior glenohumeral instability without a Bankart lesion [24]. HAGL can be a difficult diagnosis on imaging. In one review, only 50% of the HAGL lesions were diagnosed on imaging compared to arthroscopy [25]. On MR, a J-shaped axillary pouch, or focal extravasation of intra-articular contrast or joint effusion is seen passing through the torn humeral attachment (Fig. 7). Rarely a bony humeral avulsion of the glenohumeral ligament (BHAGL) can occur and may occasionally be seen on radiographs [25]. Glenoid avulsion of the GHL (GAGL) is an uncommon associated injury also diagnosed with contrast or joint fluid extravasating through the torn attachment of the glenohumeral ligament on the glenoid [20].
Fig. 7
HAGL lesion. Coronal oblique fat suppressed T1-weighted image demonstrates a HAGL lesion with the distal fibers of the inferior glenohumeral ligament avulsed from the humerus (arrow) and adjacent contrast extravasation
Hill Sachs deformity occurs when the superolateral humeral head impacts against the inferior glenoid during dislocation or relocation (Fig. 8). The size of a Hill Sachs lesion is an important factor in glenohumeral instability: larger defects (greater than one third of the focal humeral head circumference) or those with a long axis paralleling the glenoid, are considered “engaging” and associated with repeated subluxations or dislocations [22]. These deformities are often more shallow in patients with underlying hyperlaxity. On MR arthrography, these are accurately seen only 40% of the time compared to arthroscopy.
Fig. 8
Hill-Sachs lesion. Axial fat-suppressed T1-weighted image demonstrates a Hill-Sachs lesion (arrow) with flattening of the posterolateral aspect of the humeral head due to an impaction fracture
Occasionally, a cyst arises from fluid imbibing through a labral tear and may be paralabral or extend further by dissecting into adjacent tissues. Some cysts communicate with intra-articular contrast extending through the labrum. Cysts extending into the suprascapular notch can cause mass effect on the suprascapular nerve which innervates the supraspinatus and infraspinatus muscle. This can result in atrophy of these muscles. If such a cyst extends into the spinoglenoid notch, it may selectively compress the descending suprascapular nerve and cause denervation of the infraspinatus muscle only. A cyst extending into the quadrilateral space in the axilla may cause denervation of axillary nerve and atrophy of trees minor in isolation [5].
Posterior Glenohumeral Instability
Posterior glenohumeral instability refers to the symptoms and signs resulting from excessive posterior translation of the humeral head relative to the glenoid, and constitutes approximately 5–10% of all cases of shoulder instability. Posterior glenohumeral instability includes a continuum of pathologic changes ranging from chronic posterior dislocation to the more common recurrent posterior subluxation [26]. Common features of posterior glenohumeral instability include traumatic posterior dislocations, a redundant posterior capsule, posterior labroligamentous tears and osteochondral lesions [27].
Recurrent posterior subluxation has become an increasingly recognized cause of shoulder instability. Affected patients are most commonly 20–30 year-old males, who are involved in overhead sports (e.g., baseball pitcher, volleyball, baseball, swimming) or contact sports (e.g., football, wrestling, hockey, or rugby) [28]. Symptoms can also develop insidiously, aggravated by repetitive minor injury when the shoulder is in flexion, adduction and internal rotation [27].
Anatomical and Biomechanical Considerations
Posterior shoulder instability results from several not entirely understood pathological processes, in which several predisposing factors may coexist in the same patient. A variety of osseous or soft tissues abnormalities are associated with the development of posterior instability, or may be seen as secondary complications of posterior instability itself [29].
Any loss in posterior glenoid bone stock or structural irregularities such as glenoid erosion, glenoid hypoplasia/dysplasia, posterior glenoid rim deficiency, excessive glenoid retroversion, or excessive humeral retroversion, may predispose to posterior instability. Non-united prior reverse osseous Bankart lesions may also be a predisposing cause of recurrent posttraumatic posterior shoulder instability [29].
Injury of the primary posterior labrocapsular soft tissue stabilizers of the shoulder may impair their function resulting in an increased posterior translation of the humeral head relative to the glenoid. The inferior glenohumeral ligament (IGHL) and the posteroinferior capsule represent the primary soft tissue restraints of the posterior shoulder in 90° of abduction [30]. The posterior capsule, defined as the area between the intraarticular portion of the biceps tendon and the posterior band of the IGHL, is the thinnest portion of the entire joint capsule and therefore, vulnerable to injury [31]. Other structures that are important in maintaining posterior stability of the glenohumeral joint include the rotator interval and the rotator cuff. The rotator interval functions as a “check-rein” against excessive motion and limits posteroinferior glenohumeral translation [32]. The subscapularis tendon has been proven to be the most significant rotator cuff tendon in preventing posterior translation of the humeral head [31].
Posterior Glenohumeral Dislocation
Posterior glenohumeral dislocation is considered to be a rare injury accounting for 2–5% of all shoulder dislocations. It was first described in 1839 by Sir Astley Cooper in a patient who had sustained an epileptic seizure [29]. The true incidence of posterior glenohumeral dislocation is difficult to estimate because of the high frequency of missed diagnosis on clinical examination and radiographs. The even less frequent posterior fracture-dislocation accounts for 0.9% of all shoulder dislocations [33].
Posterior glenohumeral dislocation is an acute entity associated with direct or indirect trauma. While the term “dislocation” is commonly used, this condition more accurately presents as a “subluxation” as there is commonly some remaining contact between the humeral head and the glenoid [34]. Patients who experience a posterior dislocation may develop a fixed, or locked, posteriorly dislocated shoulder that often requires reduction with additional treatment typically determined by the size of associated osseous defects and the duration of the dislocation [33].
Similar to anterior shoulder dislocations, posterior dislocations are classified according to the anatomic position of the humeral head relative to the glenoid and surrounding osseous structures, with subacromial posterior dislocation being more frequent than subglenoid and subspinous dislocation patterns [35].
Anatomic and Biomechanical Considerations
Multiple mechanisms have been implicated in the etiology of posterior glenohumeral dislocation, most commonly resulting from indirect trauma during violent muscle contraction as seen in the setting of epileptic seizures, electric shock or electroconvulsive therapy. Posterior glenohumeral dislocation may also result from major trauma such as motor vehicle accidents or sports injuries when an axial load is applied on an adducted, flexed and internally rotated arm as seen with a FOOSH (fall on outstretched hand) type injury [35].
Posterior glenohumeral dislocation is associated with a variety of lesions of the posterior labrocapsular complex caused by tensile stress on the posterior band of the IGHL, or by direct compressive and shearing stress applied by the humeral head on the posterior labrum, during posteroinferior dislocation [5].
Imaging Findings in Posterior Glenohumeral Dislocation
The reverse Hill-Sachs lesion is the most frequent anatomic lesion seen following an acute traumatic posterior shoulder dislocation. The prevalence of reverse Hill-Sachs lesions varies in the literature and has been described in up to 86% of patients who have experienced an acute posterior shoulder dislocation [27, 36]. A reverse Hill-Sachs lesion occurs as a result of impaction of the posteroinferiorly displaced humeral head onto the glenoid rim, and is diagnosed when any loss of the normal convexity in the anteromedial aspect of the humeral head is seen (Fig. 9). On radiographs, this lesion may be suspected when a vertical line is identified parallel to the glenoid and has been called the “trough sign” [34]. Reverse Hill-Sachs lesions usually involve less that 25% of the circumference of the articular surface of the humeral head and are infrequently associated with fractures of the tuberosities or the subcapital humerus [36].
Fig. 9
Posterior glenohumeral dislocation. Axial intermediate-weighted (a), coronal fat suppressed T2-weighted (b) and axial intermediate-weighted (c) MR images demonstrate a large reverse Hill-Sachs lesion in the anteromedial aspect of the humeral head (thick arrows). Note the prominent adjacent bone marrow edema (asterisk) on the fluid-sensitive MR sequence (b). Tears of the posteroinferior labrum (thin arrows) and scapular periosteum (arrowhead) are seen in keeping with a reverse Bankart lesion
The reverse osseous Bankart lesion is typically seen in patients with posterior shoulder instability who had experienced a significant traumatic posterior shoulder dislocation. Reverse osseous Bankart lesions occur in 31% of patients after an acute traumatic posterior glenohumeral dislocation and are defined as traumatic fractures of the posterior osseous glenoid rim [36].
Lesions of the posterior labrocapsular complex include reverse soft tissue Bankart lesions, posterior labrocapsular periosteal sleeve avulsion (POLPSA) lesions, and Kim’s lesions [5, 28]. Reverse soft tissue Bankart and POLPSA lesions were the most frequent lesions observed in a prior imaging study of acute posterior dislocation patients, with a prevalence of 11% and 10% respectively [36].
Posterior labral tears are less frequent than anterior labral tears and occur in approximately 2–5% of all cases of shoulder instability [37]. On Magnetic Resonance Arthrography (MRA), a posterior labral tear can be manifest by extension of intra-articular contrast material into the substance of the posterior labrum, contrast undercutting the normal labral interface with the posterior glenoid rim, or disruption of posterior labral continuity with possible displacement of labral tissue from its expected normal anatomic position [36]. Isolated posterior tears are uncommon (5%) and are usually associated with other osseous or rotator cuff abnormalities [5].
The reverse Bankart lesion is defined as a posteroinferior labral tear associated with disruption of the posterior scapular periosteal or capsular attachment [38]. MRA demonstrates a displaced and detached posteroinferior labrum between the 6 o’clock and 10 o’clock positions, and a defect in the adjacent scapular periosteum (Figs. 9 and 10). On occasions, gadolinium may be seen outlining the medial aspect of the posterior glenoid neck secondary to the scapular periosteal tear [27].
Fig. 10
Acquired multidirectional microinstability in a hockey player with history of symptomatic subluxation. Axial (a and b) and coronal (c) fat suppressed T1-weighted MR arthrographic images show a displaced fracture of the posteroinferior glenoid involving the adjacent labrum (curved arrow) consistent with a reverse osseous Bankart lesion. Note the blunted posteroinferior margin of the glenoid (arrowhead). A small type II SLAP lesion (thick arrow) and a focal full-thickness chondral defect (thin arrow) are also seen on the same patient. LHBT = open arrow
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