Posterior Glenohumeral Instability 

Posterior glenohumeral instability is much less common than anterior instability. However, the condition has been recognized with increased frequency; this may be due to improved awareness of the entity, an increasingly athletic population, or both. In early reports of posterior instability, the terminology of instability was confusing, and chronic locked posterior dislocations were often combined with recurrent instabilities. See image below.

Each of these conditions has provided physicians with a dilemma not only in diagnosis but also in formulating an ideal treatment plan. The symptoms of posterior instability may mimic those of other disorders, and because complete dislocation does not always occur, the diagnosis cannot be confirmed readily with radiographs. The purpose of this article is to review current knowledge about the diagnosis, classification, and treatment of posterior glenohumeral instability.^[1]

Although the concept of anterior shoulder instability has been described in the medical literature since the time of Hippocrates, the recognition of posterior instability of the glenohumeral joint has been much more recent. Sir Astley Cooper is credited with the first medical description of a posterior shoulder dislocation, in 1822.^[2] He later described the "dislocation of the os humeri upon the dorsum scapula" as "an accident which cannot be mistaken."^[3] Since that time, numerous articles have gradually raised physician awareness of this condition. In 1952, Harrison McLaughlin defined posterior dislocation as a "diagnostic trap," and others have used equally foreboding descriptions.^[4] Even today, the diagnosis of posterior shoulder dislocation continues to be missed or diagnosed late, after the patient has undergone unsuccessful and often painful therapy for adhesive capsulitis.

Despite the supposed diagnostic difficulty spoken of even today for posterior shoulder dislocations, orthopedic history would indicate otherwise. In 1855 (40 years before the development of radiographs), the French surgeon Joseph Malgaigne published a paper that detailed 3 of his own patients (and 34 from the literature) that had been diagnosed based purely on physical examination.^{[5, 6]} McLaughlin also stated that "the clinical diagnosis is clear-cut and unmistakable, but only when the posterior subluxation is suspected."^[7] It also might be said that knowledge of a particular diagnosis statistically increases the likelihood of the clinician making that diagnosis.

In 1949, Wilson and McKeever reported on 11 patients with posterior shoulder dislocations.^{[8, 9]} Seven of the injuries occurred as a result of trauma, 3 were due to "epileptic convulsions," and 1 was due to electrocution. Key clinical findings regarding posterior shoulder dislocations were highlighted by these authors. These included the following:

• Prominent coracoid process and anterior acromion
• Flattening of the deltoid
• Inability to fully supinate the forearm while the elbow is completely extended

For some acute dislocations, Wilson and McKeever recommended that a Velpeau bandage be applied with the patient's shoulder fully internally rotated and with the forearm lying across the small of the patient's back (a position now commonly used at the beginning of the lift-off test for subscapularis function).

An absolute definition of shoulder instability is difficult to formulate and has been the center of a vast amount of research. Whereas isolated traumatic dislocations can be described by their relationship to the bony landmarks of the shoulder, instability without formal dislocation may be much more difficult to ascertain. One must differentiate between shoulder laxity, which is a physiologic variant of normal, and shoulder instability, which is a symptomatic, pathologic process.

Posterior glenohumeral dislocations typically lie behind the glenoid and beneath the acromion (subacromial). In rare instances, the humeral head may be positioned behind and under the glenoid (subglenoid) or medial to the acromion and beneath the scapular spine (subspinous).^[10]

Hawkins and McCormack described 3 categories of posterior glenohumeral instability, as follows^[11] :

• The first category included acute posterior dislocations and was subdivided into those with and those without impression defects of the humeral head.
• The second category comprised chronic posterior dislocations (locked or missed with an impression defect).
• The third category included recurrent posterior subluxation and was divided into voluntary and involuntary groups.

In the third category, the voluntary group was subdivided into the habitual (willful) subluxation secondary to personality disorder and subluxation caused by voluntary muscle control. The involuntary group was subdivided into positional (not willful but demonstrated by the patient) and nonpositional (not demonstrable by the patient).

Other classification systems also have been described for posterior glenohumeral instability. Dimon classified posterior dislocations according to the mechanism of injury, as follows^[12] :

• Traumatic
• Postconvulsive
• Voluntary posterior subluxation-relocation
• Recurrent posterior dislocation (requiring repeated reduction)
• Without history of trauma or convulsion

Instability or subluxation of the glenohumeral joint has been simply classified according to whether it results from a traumatic or nontraumatic injury. It can be subdivided into voluntary and involuntary cases.^[10] The direction of instability also has been used to classify the pathology.^[13] The direction of instability can be unidirectional (posterior only), bidirectional (posterior and inferior), or multidirectional (posterior, inferior, and anterior) and is important to determine in planning the surgical approach.

Posterior shoulder instability is also a well-recognized consequence of neonatal brachial plexus injury, such as Erb palsy. Such dislocations have been reported in children as young as 6 months.^[14] Waters and coauthors, from Boston Children's Hospital, used computed tomography (CT) scanning or magnetic resonance imaging (MRI) to prospectively study 42 patients with birth palsy.^[15] They found a 62% rate of posterior shoulder subluxation. Persistent internal rotation contracture is thought to be the primary culprit responsible for significant glenoid dysplasia (and resultant posterior instability) that is typically quite advanced by age 2 years.^[16]

Frequency

Recurrent posterior instability of the glenohumeral joint is less common than anterior instability, representing less than 5% of shoulder dislocations in most series.^[17] Early in the literature, McLaughlin reported 22 posterior dislocations or subluxations in 581 shoulder dislocations, an incidence of 4%.^[4] In more recent literature, the incidence rate has been reported to be 2-12% of all cases of shoulder instability.^[18]

Posterior instability is thought to be secondary to 3 types of etiologic processes: a major injury, a repetitive minor trauma, and a virtually atraumatic process.^{[17, 19, 20]} Major injury of the glenohumeral joint can occur directly or indirectly to the shoulder.

Direct trauma to the anterior shoulder or axial loading of a flexed, adducted, internally rotated arm may cause a posterior dislocation. Indirectly, posterior dislocations can occur secondary to violent muscle contractions associated with seizures or electrical shock. In this condition, the strong internal rotation forces of the latissimus dorsi, pectoralis major, and subscapularis muscles overpower the relatively weaker external rotator muscles.^[21] Pure, isolated, unidirectional posterior subluxation of the glenohumeral joint is rare.^{[13, 22]} Most cases have either an inferior component (bidirectional) or inferior and anterior components (multidirectional), secondary to generalized ligamentous laxity or to repetitive microtrauma causing either stretching of the static restraints or weakness of the dynamic restraints.

Posterior glenohumeral instability can be associated with several anatomic conditions. Bony anatomic deformities that have been implicated include increased humeral retroversion, glenoid retroversion, and glenoid hypoplasia.^{[8, 9, 23, 24]} When the bony anatomy is normal, the pathoanatomy often is attributed to the following:

• Excessive capsular laxity
• Loss of integrity of the capsuloligamentous rotator interval (coracohumeral and superior glenohumeral ligaments)^{[22, 25, 26]}
• Injury to the superior glenohumeral ligament^[27]
• A large capsular recess and disruptions of the glenolabral socket (see image below)^{[17, 26, 28, 29, 30, 31]} Computed tomography (CT) arthrogram of a shoulder with atraumatic posterior instability demonstrates a patulous posterior capsule consistent with excessive capsular laxity.

Many authors have emphasized that posterior stability is heavily dependent on the integrity of the inferior glenohumeral ligament.^{[21, 32, 33, 34]}

Alteration of the stabilizing forces of the glenohumeral joint has been implicated in contributing to the pathophysiology of posterior instability. Posterior instability usually occurs in midrange shoulder motion when the stabilizing ligaments of the humeral head are not under tension. Therefore, disruption of the capsuloligamentous structures cannot be solely responsible for instability. Three mechanisms that have been identified as the primary stabilizing forces of the glenohumeral articulation during the midrange motion are as follows:

• Geometric conformity of the articular surfaces
• Labral contribution to the glenoid fossa depth, thereby increasing resistance to translation of the humeral head
• Muscular force compressing the humeral head into the glenoid fossa^{[35, 36]}

An alteration of one or more of these stabilizing forces, therefore, contributes to posterior instability.

The contribution of the rotator interval also has been recognized as an important static restraint in preventing posterior and inferior instability. In their cadaveric study, Harryman and colleagues reported that imbrication of the rotator interval assists in preventing posterior and inferior instability.^[37] Selective cutting studies of the glenohumeral joint also have determined the importance of the anterior ligamentous structures on posterior instability.^[38]

Labral injury has been described in association with posterior instability, as seen in the image below. Pathologic lesions have been identified, such as the posterior labral tear; posterior capsular stripping or laxity; fracture, erosion, sclerosis and ectopic ossification of the posterior glenoid fossa; and reverse Hill-Sachs lesions.^[39] Labral lesions have also been described in the impact athlete in whom the posterior glenohumeral compressive force is increased.^[40] This causes a greater resultant shear force imparted to the posterior labrum and articular surfaces with forced translation.

An isolated pathologic lesion responsible for posterior instability is rare. Posterior instability is typically multifactorial in nature, and truly identifying all the causative agents preoperatively is difficult. The operating surgeon must be aware of all potential pathophysiologic clues so that when identified during the operative procedure, these causes can be corrected.

A thorough history is invaluable during the clinical assessment of posterior glenohumeral instability. One must determine the type and mechanism of the event that originally caused the instability (major trauma, repetitive minor trauma, or an atraumatic process). A history of violent trauma, seizures of any etiology, or electrical shock should alert the physician to search for a posterior dislocation. Patients without a history of major trauma typically report painful symptoms initially that diminish over time. These patients commonly report difficulty in performing activities of daily living, including hair combing, shaving, and eating.^[11] Athletic activities that require the arm to be placed in flexion, adduction, and internal rotation commonly cause symptoms of pain and the sense of instability. Common activities include throwing (follow through), bench press (lock out), swimming (pull through), and rowing.^[17]

Pain is usually limited to the instability episodes, although many patients report posterior joint line pain or vague anterior pain, which may be thought of as one of Neer's causes of nonoutlet impingement.^[22] Finally, it is important to determine whether the patient has a voluntary type of instability or a positional type of involuntary instability.

Physical examination of a posterior glenohumeral dislocation may reveal prominence of the humeral head posteriorly, with flattening of the anterior contour and prominence of the coracoid. These findings can often be quite subtle and often are obliterated by swelling or a large deltoid muscle mass.^[12] External rotation of the arm is significantly limited, while flexion and internal rotation can be remarkably normal. Rowe and Zarins described examination of the shoulder with flexion of both elbows to 90° to demonstrate a fixed humeral internal rotation deformity.^[41] Comparison of the external rotation available on both sides reveals the internal rotation deformity on the dislocated side. With the arm extended, the patient's palm also does not turn fully upward on the affected side, despite full forearm supination due to the fixed internal rotation.

Examination maneuvers for posterior instability are not often dramatic. Palpatory examination may reveal tenderness of the posterior joint line and tenderness of the anterior dynamic stabilizers. Range of motion is typically normal, although patients sometimes have a loss of external rotation with the arm abducted at 90°.^[21] Testing for generalized ligamentous laxity should be performed. Specific tests for posterior instability include the posterior drawer test, as seen in the first image below. The posterior apprehension test (ie, the jerk test) also can be used. The examination involves applying an axial posterior load onto an arm flexed at 90°, adducted, and internally rotated; it is positive with reproduction of the instability sensation, as seen in the video below. Hawkins and McCormack suggested flexing the arm to recreate the position in which subluxation occurs and stated that a "clunk" occurs as the arm is elevated to 120°.^[11]

A posterior drawer/relocation test, in which pain or apprehension occurs with a posterior directed force and is relieved by reduction, may be the preferred diagnostic maneuver.^[42] The extent of translation during diagnostic examination has been graded as follows^{[43, 44, 45]} :

• +0 = No translation from being centered in the glenoid fossa
• +1 = Translation noticeable but not up to the glenolabral rim (without a clunk)
• +2 = Translation of humeral head onto the glenolabral rim (clunking without locking)
• +3 = Translocation over the glenolabral rim (locking in the subluxated position that reduces without manual reduction)
• +4 = Translation with complete dislocation (locking in the dislocated position that requires manual reduction)

Examination in the office and under anesthesia involves a thorough evaluation for motion, laxity, and stability. Patients without symptoms may have as much translation as those requiring surgical repair for symptomatic shoulder instability. The need for surgical reconstruction should, therefore, be based on the history and physical examination findings rather than on the magnitude of translation alone. Finally, evaluation of other potential components of instability—including through the sulcus test (as described by Neer and Foster), for inferior instability, and through the crank test, for anterior instability—is equally important.^{[25, 43, 44, 45]}

The primary indication for surgery for posterior glenohumeral instability is recurrent symptomatic shoulder subluxation or dislocation that is recalcitrant to conservative measures. Surgical treatment should be considered only in patients who remain significantly disabled after an adequate trial involving strengthening exercise and avoidance of provocative positions. Burkhead and Rockwood stress that 80% of patients with an atraumatic cause of shoulder instability, in contrast to 16% of those with traumatic instability, improve with an exercise program alone.^[46] Others have reported that 70% of athletes subjectively improve with a conservative program.^{[20, 24]} The instability, however, is usually not eliminated, but the functional disability during athletics is improved, allowing the patient to participate in his or her sport without problems.

All patients who subluxate voluntarily should have the appropriate psychological evaluation before operative treatment is recommended. Patients with positional instability in which the humeral head subluxes posteriorly when the arm is adducted at 90° of flexion have a good response to surgical intervention.^{[29, 31, 47]} Surgical intervention is associated with a 50-95% success rate.^{[43, 44, 45]}

Children with posterior shoulder instability secondary to neonatal brachial plexus injury fall into 2 general categories: early and late. In children in whom the diagnosis is established early (usually when they are < 2 years of age), reconstructive and tendon-balancing procedures are options.^{[48, 49]} In many children presenting late with established dislocations, rotational osteotomy of the proximal humerus (with or without additional soft-tissue procedures) can significantly improve shoulder function.^{[50, 51]}

The anatomy relevant to surgical treatment for posterior shoulder instability is related to the posterior approach to the glenohumeral joint. Two general posterior approaches to the glenohumeral joint have been described.

In 1944, Rowe and Yee presented a posterior approach to the shoulder using a linear incision over the entire length of the scapular spine, extending to the posterior corner of the acromion.^[52] The origin of the deltoid on the scapular spine is identified and detached from lateral to medial. The interval between the infraspinatus and the teres minor is defined and retracted to expose the posterior aspect of the joint capsule. In 1993, Wirth, Butters, and Rockwood described the posterior deltoid-splitting approach to the shoulder.^[53] Their technique allows preservation of the deltoid origin from the scapular spine and posterior acromion. (In more traditional posterior approaches to the shoulder joint, part or all of the origin of the deltoid is detached.) This approach therefore maintains the strength and function of the posterior deltoid.

Several structures are at risk during the posterior dissection of the shoulder. The axillary nerve runs through the quadrilateral space beneath the teres minor and can be injured if the interval between the infraspinatus and teres minor is not critically defined. The suprascapular nerve passes around the base of the spine of the scapula as it runs from the supraspinatus fossa to the infraspinatus fossa. The infraspinatus must not be retracted forcefully too far medially during the approach because a neurapraxia may result from stretching the nerve around the unyielding lateral edge of the scapular spine. The posterior circumflex humeral artery runs with the axillary nerve in the quadrilateral space beneath the inferior border of the teres minor muscle. Damage to this artery leads to hemorrhaging that is difficult to control; injury to the artery can be avoided by staying in the correct intermuscular plane.

Specific contraindications to the surgical treatment of posterior shoulder instability include situations in which conservative treatment, including activity modification and a formal exercise program, has not been attempted. The length of a trial of conservative treatment before surgery varies, but Tibone and Bradley have recommended continuing an exercise protocol for at least 6 months before resorting to surgical treatment. Many patients become asymptomatic in terms of pain and function after completing a physical therapy protocol, although clinically, the instability may persist.^{[20, 24]}

Patients with voluntary instability of the shoulder who have a psychological disorder or who are seeking secondary gain are not candidates for surgical reconstruction. Any patient in whom voluntary instability is suspected should be evaluated by a mental health specialist to screen for underlying psychological conditions.