Practice Essentials
The term anterior glenohumeral instability refers to a shoulder in which soft tissue or bony insult allows the humeral head to subluxate or dislocate from the glenoid fossa, resulting in symptoms and compromised function of the joint. [1] Patients typically experience apprehension, recurrent subluxations, and frank dislocations. This pathology limits many activities, especially physical or athletic endeavors requiring overhead motion and external rotation.
The shoulder is the most commonly dislocated joint in the body. Additionally, shoulder dislocation in adolescents has a notorious natural history; one systematic review reported a 47% recurrence rate within 1 year when glenohumeral dislocation was managed nonoperatively. [2] Excessive deviation of the humeral head on the glenoid can occur in three planes: anterior, posterior, or inferior. As many as 95% of shoulder dislocations are anterior. Anterior dislocations often lead to recurrent anterior glenohumeral instability. [3] Recurrent dislocation not only is traumatic and disabling but also can result in further soft-tissue damage and progressive bony loss.
Normal shoulders have a certain degree of laxity secondary to minimal bony restraint, which allows the widest range of motion (ROM) of any joint in the body. The result is a tremendous need for competent soft-tissue stability. Traumatic damage leads to laxity in the soft-tissue and bony restraints, and recurrent subluxation and dislocation may ensue. Atraumatic etiologies also exist, but this article focuses on recurrent subluxation and dislocation due to trauma.
Nonoperative and operative therapies both play a role in the treatment of anterior shoulder instability. [4] Surgical management has evolved, culminating in effective options that achieve stable repair with little restriction of motion. Reports of anterior glenohumeral instability and its many repair methods date back to Hippocrates' treatise On Joints. Hippocrates described the practice of using cautery to cause the capsule to scar and thus tighten around the joint: "[G]rasp the skin at the armpit between the fingers and draw it in the direction towards which the head of the humerus gets dislocated, then pass the cautery right through the skin thus drawn away."
Since Hippocrates' description of capsule repair, a multitude of new techniques have been reported. These repairs can be divided into anatomic and nonanatomic. Anatomic repairs focus on repairing the structure that has been disrupted. Nonanatomic repairs (e.g., Putti-Platt, Magnuson-Stack, and Bristow procedures) attempt to shorten or tighten certain anterior structures. Early in the evolution of capsular repair, loss of motion was considered acceptable and even desirably as an outcome of shoulder stabilization. As new techniques have emerged, stability was achieved without significant compromise in ROM measurements; postoperative ROM restriction is now considered a surgical complication.
In 1923, Bankart described the lesion of traumatic shoulder dislocation in the British Medical Journal, as follows: "The essential lesion is the detachment of the capsule from the fibro-cartilaginous glenoid ligament." He went on to remark that "the only rational treatment is to reattach the fibrous capsule to the glenoid ligament whence it has been torn." [5] du Toit and Roux described a similar procedure in 1965, using staples. [6] The Magnuson-Stack procedure and the subsequent Putti-Platt procedure both used the subscapularis to produce a sling effect on the humeral head; both effectively decreased dislocation recurrence, but subsequently decreased ROM.
In 1954, Latarjet proposed the procedure that bears his name, and a very similar operation was later popularized as the Bristow procedure; these operations involve transfer of the tip of the coracoid process with its muscular attachments. A slit in the subscapularis allows the osteotomized coracoid to be attached to the anterior glenoid, providing both a sling effect and a bony block against anterior glenohumeral translation. [7]
Anatomy
The shoulder joint is a simple structure that provides complex function. In addition to the glenohumeral joint, the acromioclavicular, sternoclavicular, and scapulothoracic joints collectively allow for shoulder motion. Stabilization is provided by the following three main players [8] :
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Bony stabilizers
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Soft-tissue passive stabilizers
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Soft-tissue active stabilizers
Bony stabilization
The foolowing are the most important bony stabilizers of the shoulder:
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Glenoid
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Humeral head
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Clavicle
The glenoid fossa provides a shallow socket within which the humeral head articulates. In the average patient, the glenoid face is positioned in slight inclination and retroversion; variation in these angles can increase the risk of instability. Variation in the glenoid height-to-width ratio (the glenoid index) has also been identified as a significant risk factor for instability. [9]
The actual articulation between the glenoid socket and the humeral head provides little stability itself, because only 25-30% of the humeral head is in contact with the glenoid at any point throughout anatomic ROM. The stability ratio is defined as the force necessary to dislocate the humeral head from the glenoid, divided by compressive force, and is influenced in part by the depth of the glenoid, in addition to the labrum and any chondrolabral or glenoid defects. [10]
The scapula also plays an important role in shoulder stability, serving as the bony link between the humerus, the clavicle, and the axial skeleton—as well as providing the attachment or origin site for 17 different muscles.
The glenoid, the acromion, and the coracoid process are important scapular landmarks. Anatomic variation in the coracohumeral distance has been shown to be an independent risk factor for shoulder instability, with a 1-mm difference being associated with a 20% increase in the risk of injury. [9]
Finally, the clavicle articulates with the scapula at the acromioclavicular joint, providing an attachment site for many muscular stabilizers and facilitating shoulder elevation.
Passive soft-tissue stabilization
The following are the most important players for passive soft-tissue stabilization [8] :
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Glenoid labrum
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Glenohumeral ligaments
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Glenohumeral joint capsule
The labrum is a fibrocartilaginous structure that constitutes the margin of the glenoid cavity, deepening the glenoid socket by about 50%. [11] The flexible labrum also exerts a suction-cup effect on the humeral head using negative intra-articular pressure, and it functions as an anchoring point for the glenohumeral ligaments and the biceps tendon. [12] Labrum injury is often comorbid with traumatic shoulder instability. Cadaveric studies have demonstrated increased laxity in shoulders with independently resected labrums. [13]
The joint capsule extends from the periphery of the glenoid to surround the proximal humerus. Within the anterior capsule are the following three major capsular thickenings:
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Superior glenohumeral ligament (SGHL)
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Middle glenohumeral ligament (MGHL)
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Inferior glenohumeral ligament (IGHL)
The SGHL and MGHL attach proximally at the anterosuperior portion of the glenoid labrum. The IGHL is the key anterior stabilizer of the shoulder, by virtue of its comparatively large size and considerable tensile strength. [14] The IGHL attaches proximally to the anterior, inferior, and posterior margins of the glenoid labrum; distally, it attaches to the inferior margin of the anatomic neck of the humerus. The IGHL is composed of an anterior band (AIGHL) and a posterior band (PIGHL), which together form a U-shaped “hammock” structure. [15]
Collectively, the glenohumeral ligaments function to limit lateral rotation of the shoulder. Each of the three ligaments is relied upon for stability, depending on the dynamic position of the arm. Delorme found that the MGHL tightens as the arm is externally rotated or dorsally flexed; if the arm is then abducted, the IGHL becomes the primary stabilizer. [16] Although recurrent glenohumeral instability is often attributed to injury of the anterior labroligamentous structures (ie, a Bankart lesion of the labrum), humeral avulsion of the glenohumeral ligament (HAGL) may be a less common but clinically relevant cause; the AIGHL is the most commonly injured portion. [17]
Active soft-tissue stabilization
Active soft tissue stabilization of the shoulder is provided by several important muscle groups, including the following [8] :
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Rotator cuff (RC)
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Long head of the biceps
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Subset of the parascapular muscles
The RC is composed of four muscles—supraspinatus, infraspinatus, teres minor, and subscapularis—whose attachments surround the glenohumeral joint. They play a dual role, involved in both joint motion and stability; conservative therapy focuses on strengthening these muscles to prevent recurrent dislocation.
The supraspinatus initiates shoulder abduction and assists the deltoid with further abduction. The infraspinatus provides external rotation and elevation. These two muscles work with the rest of the RC to compress the humeral head in the glenoid throughout ROM. The supraspinatus and the infraspinatus become confluent in their attachment to the greater tuberosity as the posterosuperior rotator cuff. The anterior portion of the supraspinatus is termed the rotator cable, which has been described as the primary load-bearing structure of the supraspinatus; most tears occur here, and disruption in this area has the potential to dramatically alter allowable glenohumeral translation. [18]
With the infraspinatus, the teres minor works to rotate the shoulder externally, and it compresses the glenohumeral head as it traverses laterally to the inferior greater tuberosity.
The subscapularis is the largest RC muscle, originating from the subscapular fossa of the anterior scapular surface and attaching to the lesser tuberosity of the proximal humerus; it internally rotates and adducts the arm. At 45° of abduction, the subscapularis becomes taut over the anterior joint surface and ascends so that its inferior margin lies at the inferior margin of the glenoid. External rotation additionally increases muscle tautness. Finally, at 90° of abduction, the inferior portion of the subscapularis no longer covers the inferior humeral head. It continues to provide anterior stabilization by remaining taut.
The long head of the biceps originates form the supraglenoid tubercle and exits the joint via the bicipital groove, after which it converges with the short head of the biceps; it provides rotational and translational stability, as well as stability from humeral head depression. [19]
The deltoid, the pectoralis major, and the latissimus dorsi are important humerothoracic muscles that are involved in shoulder stability, especially as it pertains to the "force couple" in the superior-inferior direction. A force couple is two muscles acting in opposing directions that influence the rotation of a joint in some direction; an injury to one part of the force couple can cause an imbalance and possible instability. [8]
Two other force couples are important for the shoulder. The transverse plane force couple comprises the action of the subscapularis anteriorly and the pull of the infraspinatus and teres minor posteriorly. The force couple in the coronal plane involves the deltoid superiorly and the rotator cuff muscles (infraspinatus, teres minor, and subscapularis) inferiorly; when balanced, it provides stable glenohumeral abduction. [20]
Pathophysiology
In an unstable shoulder, many findings are possible, occurring alone or in combination; in 1978, Rowe came to the still upheld conclusion that no single lesion is responsible for recurrent dislocation of the traumatized shoulder. The various pathologic lesions broadly include the following:
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Bankart lesion
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Anterior glenoid rim damage (“bony Bankart”)
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Hill-Sachs lesion
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Glenoid fossa bone loss
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Capsular redundancy
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Subscapularis deficiency
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Attenuation of the capsule and capsular ligaments
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Humeral avulsion of the IGHL (HAGL and its variants)
Clinical instability in the absence of a pathologic lesion is also possible.
The Bankart lesion—a term describing direct injury to the anterior labrum as the humeral head dislocates anteriorly—is the most common lesion. A review by Owens et al corroborated previously accepted rates of Bankart lesions in 97% of first-time traumatic anterior subluxation imaging. [21] However, injury to the anterior labrum does not usually occur in isolation; the IGHL may undergo deformation, and the anterior glenoid rim may also fracture. Milano et al reported that a bone defect, colloquially called a bony Bankart, occurred in 72% of patients with anterior instability. [22] Bone loss may extend into the glenoid fossa, probably secondary to repeated erosion.
Additionally, the humeral head may be injured via a contrecoup mechanism, resulting in a Hill-Sachs lesion; this is a fracture secondary to impaction of the posterosuperolateral humeral head adjacent to the rotator cuff insertion. Rates of Hill-Sachs lesions are in the range of 7-93%, approaching 100% with recurrent instability. [23]
Combined or bipolar bone loss—from both the glenoid fossa and the humeral head—is a common presentation. One systematic review reported that after both nonoperative and surgical treatment of shoulder instability, bipolar bone loss was associated with higher rates of recurrence. [24] This is in part due to the additive risk of further damage when bipolar bone loss exists; continued instability events can lead to engagement of the Hill-Sachs lesion on the anterior glenoid.
The concept of the “engaging Hill-Sachs” lesion led to the secondary concept of the glenoid track, as described by Yamamoto et al in 2007. [25] The glenoid track is a comparison of 83% of the width of the glenoid minus the width of bone loss; if the Hill-Sachs lesion is wider than the glenoid track, it is considered to be off track. An off-track lesion predisposes a patient not only to recurrent instability but alsoto failure of a soft-tissue-only repair of a Bankart lesion.
Etiology
The cause of anterior glenohumeral instability can be traumatic or atraumatic, and either mechanism can lead to the loss of balance in the surrounding soft-tissue structure. Traumatic insult most commonly causes anterior dislocation. Posterior shoulder dislocation is often associated with seizure disorders but can also be secondary to traumatic athletic injury.
Atraumatic causes can lead to multidirectional instability; however, these causes are not the focus of this article. Etiologies include repetitive atraumatic injury, Ehlers-Danlos syndrome, Marfan syndrome, congenital absence of the glenoid, and deformities of the proximal humerus.
Epidemiology
Epidemiologic studies using national injury databases have reported the incidence of shoulder dislocation in the United States to be 23.9 per 100,000 person-years, with nearly half occurring during athletic activity in patients in their second or third decade of life. [26] Young male patients participating in athletics and military service and/or training are the population most at risk. Similar trends have been described internationally.
There are several modifiable and nonmodifiable risk factors that predispose patients to glenohumeral instability. [8] Modifiable risk factors include the following:
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Shoulder girdle strength
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Activity modification
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Shoulder proprioception
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Occupation
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Sport participation
Nonmodifiable risk factors include the following:
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Age at primary instability event
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Male sex
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Hyperlaxity
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Chondrolabral cleft
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Glenoid dysplasia or version
Age at the time of dislocation is the most important determinant of future recurrence. Recurrences from anterior glenohumeral instability occur most commonly in patients younger than 20 years; reported recurrence rates in such patients range from 70% to 100%.
Prognosis
Outcomes of anterior glenohumeral repair depend first on identification of specific pathology and then on choice of repair. With these key factors addressed, patients can expect a low incidence of complications, good ROM, and stable repair with a low risk of recurrence. [27, 28]
In a systematic review, Chalmers et al critically evaluated eight meta-analyses comparing open and arthroscopic approaches to shoulder stabilization with labral repair and capsulorrhaphy. [29] Two pre-2007 meta-analyses concluded that open stabilization provided lower recurrence rates; three 2007 meta-analyses were discordant; and three post-2008 meta-analyses concluded that the two approaches provided equivalent results. Two meta-analyses were judged to have major flaws. [29] The meta-analysis independently selected by four authors as providing the highest-quality evidence found no difference in recurrence rates between the two approaches.
Bliven et al reviewed eight studies (N = 795) to compare the outcomes of Latarjet repair (open only) with those of Bankart repair (open in six studies and arthroscopic in two) in patients with recurrent traumatic anterior shoulder instability. [30] They found the Latarjet procedure to be associated with a lower recurrence rate, better outcomes as reported by patients, and less restriction of external-rotation motion than the Bankart repair.
Potential comorbid injuries associated with primary anterior glenohumeral dislocation include rotator cuff tear, greater tuberosity fracture, and neurologic deficit. These injuries may occur alone or in combination and are more common in patients older than 60 years. [31, 32]
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Y-view radiograph of right shoulder shows anterior dislocation of humeral head relative to glenoid fossa.
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Upper: type I superior labrum anterior posterior lesion. Lower: type II superior labrum anterior posterior lesion.
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Upper: type III superior labrum anterior posterior lesion. Lower: type IV superior labrum anterior posterior lesion.
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Scapular Y-view of normal shoulder. Courtesy of Wikimedia Commons (Mikael Häggström) [https://commons.wikimedia.org/wiki/File:Y-projection_X-ray_of_a_normal_shoulder.jpg].
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Axillary view of shoulder with anterior instability.
