The term anterior glenohumeral instability refers to a shoulder in which soft-tissue or bony insult allows the humeral head to sublux or dislocate from the glenoid fossa. The function of such a shoulder is compromised. Patients typically experience apprehension, recurrent subluxations, and frank dislocations. This pathology limits many activities, including overhead arm motions, external rotation, and, thus, physical or athletic activities.
The shoulder is the most commonly dislocated joint in the body. When shoulder dislocation occurs in adolescents and children, it has the worst natural history of any injury; the rate of recurrence in later years is at least 70%.
As many as 95% of shoulder dislocations are anterior. Anterior dislocations often lead to recurrent anterior glenohumeral instability. Recurrent anterior glenohumeral instability accounts for the largest portion of the shoulder laxity spectrum. Excessive deviation of the humeral head on the glenoid occurs in all or one of three directions: anterior, posterior, or inferior. Although certainly not life-threatening, recurrent subluxation or dislocation is clearly lifestyle-threatening and can effectively disable an otherwise active individual.[1]
Normal shoulders have a certain degree of laxity resulting from minimal bony restraint of the joint, which in turn allows the widest range of motion of any joint in the body. The result is a tremendous need for competent soft-tissue balance and control. Traumatic damage leads to laxity in the soft-tissue and bony restraints; thus, recurrent subluxation and dislocation ensues. 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 treatment of anterior shoulder instability.[2] Both have been studied extensively. Surgical management has gone through an evolutionary process involving multiple methods of fixation. This evolution has led to operative fixation that achieves a 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. He wrote, "[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, all aimed at preventing recurrent dislocation or subluxation. These repairs can be divided into anatomic and nonanatomic. Anatomic repairs focus on repairing the structure that has been disrupted. With nonanatomic repairs (eg, Putti-Platt, Magnuson-Stack, and Bristow procedures), an attempt is made to shorten or tighten certain anterior structures, regardless of the specific shoulder pathology.
Early in the evolution of capsular repair, loss of motion was considered acceptable and even desired as a necessary part of stabilizing a shoulder. As new techniques followed, shoulder stability was achieved without significant loss of motion. Postoperative motion restriction is now considered a 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 goes on to remark that "the only rational treatment is to reattach the fibrous capsule to the glenoid ligament whence it has been torn."[3]
In 1965, du Toit and Roux reported a similar procedure, in which staples were used to attach the capsule to the anterior glenoid rim.[4] This method had the potential to simplify the procedure, but it also added complications, such as glenoid damage from the staples and loosening.
The Magnuson-Stack procedure was described next, in 1943. This procedure involves transferring the subscapularis from its attachment on the lesser tuberosity to a point lateral to the bicipital groove. The goal was to produce a sling effect on the humeral head. Like the Putti-Platt procedure that would follow, it decreased external rotation by design.
In 1948, the Putti-Platt procedure was described. Here, the subscapularis tendon and capsule are divided longitudinally at the midportion. The lateral free end is attached to the anterior rim of the glenoid, and the medial free end is attached over the lateral end. The Putti-Platt operation led to low dislocation recurrence rates, but it also led to decreased external rotation.
In 1954, Latarjet proposed the procedure that bears his name,[5] and a very similar operation was later popularized by Helfet in 1958 as the Bristow procedure. This involved transferring the tip of the coracoid process with its muscular attachments. A vertical slit in the subscapularis allowed the osteotomized coracoid to be attached to the anterior glenoid with sutures. This procedure thus provided a bony block to anterior glenohumeral translation. (The term Bristow-Latarjet procedure is commonly used in the English literature.)
For patient education resources, see the Breaks, Fractures, and Dislocations Center, as well as Shoulder Dislocation.
NextThe shoulder joint is a simple structure that provides complex function. It is the most mobile joint of the body, and it is also the joint that is most frequently dislocated. The gross anatomy consists of three main components: musculature, capsule/ligaments, and bone.
Capsuloligamentous structures provide the primary stabilization for the joint. The capsule of the shoulder joint extends from the periphery of the glenoid around the articular surface of the proximal humerus. Within this capsule are three distinct thickenings that constitute the superior glenohumeral ligament (SGHL), the middle glenohumeral ligament (MGHL), and the inferior glenohumeral ligament (IGHL).
The SGHL and MGHL attach proximally at the anterosuperior portion of the glenoid labrum. The proximal attachment of the SGHL has two origins: the one at the apex of the labrum that is joined with the long head of the biceps brachii and a second origin at the base of the coracoid process. Distally, the SGHL attaches just superior to the lesser tuberosity at the edge of the articular surface. The MGHL inserts just medial to the lesser tuberosity.
The IGHL is the key stabilizer of the shoulder, preventing anterior glenohumeral instability. 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.
Together, the glenohumeral ligaments function to limit lateral rotation of the shoulder. Each of the three ligaments is relied upon for stability, depending on the position of the arm. In 1910, Delorme found that the MGHL tightens as the arm is externally rotated or dorsally flexed.[6] If the arm is then abducted, the IGHL becomes the primary stabilizer, with the upper fibers tight at slight abduction and the whole ligament tightening at about 45° of abduction.
The secondary stabilizers of the shoulder joint are the surrounding musculature. This consists of the rotator cuff muscles. The supraspinatus, infraspinatus, teres minor, and subscapularis are intimately associated with the capsule. These muscles provide dynamic secondary stabilization. Conservative therapy focuses on strengthening the rotator cuff muscles to prevent recurrent dislocation.
Of the rotator cuff muscles, the subscapularis is the most important contributor to anterior shoulder stability. With the arm adducted, it tightens with external rotation. Cutting it results in 15-20° of increased external rotation.
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 raises it even further and makes it more taut. 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 glenoid fossa provides a shallow socket in which the humeral head articulates. It is composed of the bony glenoid and the glenoid labrum.
The labrum is comparable to the menisci of the knee. It is a fibrocartilaginous structure surrounding the periphery of the glenoid. Like the menisci of the knee, it is flexible but constant; when torn, it generally does not heal. The stability of the glenohumeral joint is greatly increased by the labrum, which provides a 50% increase in the depth of the concavity. The bony concavity measures approximately 2.5 mm and has been measured at 5.0 mm with an intact labrum.
In 1923, Bankart claimed that anterior inferior detachment of the labrum from the glenoid was the essential lesion in anterior glenohumeral instability. It has since been proved that this is true in most cases of instability, but the presence of this lesion is not required for instability.
The labrum is closely related to the joint capsule and the glenohumeral ligaments. It is anchored to the bony rim of the glenoid and can be attached to the capsular structures as well.
Finally, it is important to understand the supporting musculature of the scapula that allows such a wide range of motion at the shoulder. A total of 16 muscles move and stabilize the scapula.
In an unstable shoulder, many findings are possible. Each finding can occur alone or in combination with other lesions. These lesions include the Bankart lesion (85% of cases), Hill-Sachs lesion (77%), anterior glenoid rim damage (73%), capsular redundancy, subscapularis deficiency, and glenoid fossa deficiency. Absence of pathologic findings is also possible.
In 1923, Bankart described the "essential lesion" in posttraumatic anterior glenohumeral instability as the detachment of the capsule from the fibrocartilaginous glenoid ligament. In this lesion, the humeral head translates forward, shearing the IGHL with the anteroinferior labrum from the glenoid rim.
Rowe's review of 28 patients, in which he examined shoulder pathology after traumatic anterior dislocation, disputed Bankart's claim to the essential lesion, stating that "there was no evidence that there is a single essential lesion responsible for the recurrent dislocations of the shoulder." The Bankart lesions occurred in 27-100% of cases.
Other lesions were just as variable. Subscapularis laxity ranged from being present in every case to not being present in any cases. Hill-Sachs lesions were present in 26-100% of cases. Anterior glenoid trauma of all variations occurred in 2-52% of cases.
The next logical question is which of these lesions actually causes the recurrent instability observed after traumatic dislocations. This remains a debated topic. The most accurate conclusion is the one Rowe came to in 1978 when he declared that no single lesion is responsible for the recurrent dislocations of the traumatized shoulder.
Several lesions have been suggested. Baker et al devised a system of classification for the Perthes-Bankart lesion, as follows[7] :
Other lesions include attenuation of capsule and capsular ligaments, Hill-Sachs lesions, attenuation of the subscapularis, and humeral avulsion of the IGHL.
The cause of anterior glenohumeral instability can be traumatic or atraumatic. Either mechanism leads to the loss of balance in the surrounding muscular and capsular structures.
Traumatic injury to any one component of the shoulder soft tissue leads to instability. This traumatic insult most commonly comes in the form of an anterior shoulder dislocation.
Atraumatic causes leading to multidirectional instability are not the focus of this article. Such causes include repetitive atraumatic injury, Ehlers-Danlos syndrome, Marfan syndrome, congenital absence of the glenoid, deformities of the proximal humerus, and emotional and psychiatric instability.
In studies of anterior glenohumeral instability, a wide array of incidences have been cited. Most report an average age of initial shoulder dislocation early in the third decade of life. The vast majority (85-95%) of these are anterior dislocations. One fourth of all patients with dislocations present with a family history of the same problem. Rowe's 1956 analysis of 500 shoulder dislocations found only eight occurring in children younger than 10 years; the largest cohort of dislocations occurred in the subsequent decade of life, in patients aged 10-20 years.[8]
Age at the time of dislocation is the most important determinant of future recurrence. Recurrences result from anterior glenohumeral instability and occur most commonly in patients younger than 20 years. Reported recurrence rates in patients younger than 20 years range from 70% to 100%.
Outcomes of anterior glenohumeral repair rely on identification of all of the patient's pathology and choosing the correct repair. With these key factors addressed, patients can expect a low incidence of complications, good range of motion, and stable repairs with a low incidence of recurrence.[9, 10]
Potential morbidities associated with primary anterior glenohumeral dislocations are rotator cuff tear, greater tuberosity fracture, and/or neurologic deficit. These injuries may occur alone or in combined patterns and are more common in patients aged 60 years or older.[11, 12]
Chalmers et al conducted a systematic review of the literature to critically evaluate eight meta-analyses comparing open and arthroscopic approaches to shoulder stabilization with labral repair and capsulorrhaphy.[13] Two pre-2007 meta-analyses concluded that open stabilization provided lower recurrence rates than arthroscopic stabilization; three 2007 meta-analyses were discordant; and three post-2008 meta-analyses concluded that open and arthroscopic stabilization provided equivalent results.
Two of the meta-analyses were judged to have major flaws.[13] One meta-analysis was independently selected by four authors as providing the highest-quality evidence, and this meta-analysis found no difference in recurrence rates between open and arthroscopic stabilization.
Clinical Presentation
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