Posterior Shoulder Instability

Etiology

The etiology of recurrent posterior instability is multifactorial and complex. However, three broad processes have been implicated in the pathogenesis, including repetitive microtrauma, acute traumatic events, and atraumatic causes.[7][12][13] These three main broad categories are important to keep in mind when evaluating a patient with symptoms suggesting posterior instability. Correctly identifying the underlying etiology is also important so that treatment can be tailored to the underlying cause.

Repetitive microtrauma to the posteroinferior capsulolabral shoulder complex is the most common cause of recurrent posterior subluxation.[7] Repetitive loads cause this in the provocative position of glenohumeral flexion, adduction, and internal rotation as seen in activities such as bench-pressing, blocking in American football, and overhead sports such as swimming, tennis, and baseball.[12] This position loads the PIGHL, the posterior labrum, and the posterior capsule, which over time may lead to plastic deformation of the posteroinferior capsular pouch and laxity in addition to injury to the labrum.

Acute trauma to the shoulder may lead to recurrent posterior instability. Patients will often recall the incident prior to the onset of symptoms. These patients sustain a high impact injury to the anterior shoulder or an axial load with the shoulder in the position of flexion and internal rotation. Such injuries can be seen in American football linemen.[12] Although much less common than anterior dislocations, a posteriorly dislocated shoulder may lead to recurrent posterior instability. Posterior shoulder dislocations are seen after high-energy trauma to the shoulder, motor vehicle accidents, seizures, and electrocution. Recurrent posterior instability after trauma is secondary to either soft tissue injury of the posterior capsulolabral complex or bony defects of the glenoid and/or humeral head.

Patients may also report posterior instability with no history of trauma. This atraumatic presentation is the least common and is usually attributed to ligamentous laxity.[7] Patients with this type present with posterior shoulder pain as well as instability noted with the shoulder in provocative positions. These symptoms may even progress to affect activities of daily living.

Epidemiology

Posterior shoulder instability is much less common than anterior shoulder instability accounting for 2% to 12% of total cases of instability.[14][15][2] The incidence of anterior dislocations is 15.5 to 21.7 times more common than posterior dislocations.[16] The condition is becoming increasingly recognized in the young, athletic population such as overhead athletes, weightlifters, and American football players.[7] The typical patient is a male between the ages of twenty and thirty years who is involved with overhead or contact sports.[12]

Pathophysiology

Pathophysiology

An isolated pathologic lesion causing posterior instability is rare. Most often, the condition is multifactorial, involving several anatomic and pathologic identities. Bony abnormalities that have been implicated include increased humeral retroversion, glenoid retroversion, and glenoid hypoplasia.[17][18][19] In the absence of bony abnormality, Antoniou and Harryman state to which patho-anatomy may be linked.[14]

• Excessive capsular laxity
• Loss of integrity to the rotator interval (coracohumeral ligament and superior glenohumeral ligament)[20][11]
• Injury to the superior glenohumeral ligament
• Large capsular recess
• Disruptions of the glenolabral socket[21][11][22][23][15][13]

Several studies have also highlighted the importance of the inferior glenohumeral ligament (IGHL) in maintaining the posterior stability of the shoulder.[8][24][25][26]

Episodes of posterior instability commonly occur with the arm in mid-range of motion when the glenohumeral ligaments are not tensioned. Therefore, other pathomechanics must be involved other than the disruption of the capsuloligamentous structures. During mid-range of motion, Antonio and Harryman describe 3 mechanisms as the primary stabilizing forces of the glenohumeral joint:[14]

• Geometric conformity of the articular surfaces
• Labral contribution to the glenoid fossa depth
• Compression of the humeral head into the glenoid by muscular forces[27][28]

Disruption in any of these stabilizing mechanisms contributes to the development of posterior instability.

Controversy exists in regard to the role of the rotator interval in preventing posterior instability as cadaveric studies have yielded conflicting results. In cadaveric specimens, Harryman et al. demonstrated increased posterior and inferior translation as well as frank dislocation after selective sectioning of the rotator interval.[9] On the contrary, Mologne et al. found arthroscopic rotator interval closure did not improve posterior instability after posterior labral repair but did significantly decrease external rotation.[10]

As one of the primary static stabilizers of the shoulder, labral injury has been associated with posterior instability. A pure detachment of the posterior labrum is described as a reverse Bankart lesion. When associated with a fragment of bone resulting from a glenoid fracture, the pathology is termed a reverse bony Bankart lesion. An incomplete and concealed avulsion of the posteroinferior labrum is known as a Kim lesion, and failure to identify and address this lesion may result in persistent posterior instability.[29] With a frank posterior dislocation, a patient will often sustain an impaction fracture of the anteromedial humeral head known as a reverse Hill-Sachs lesion. Depending on size, this lesion is a risk factor for re-dislocation, and surgery is recommended.[30]

History and Physical

Clinical Presentation

The clinical presentation of a patient presenting with posterior shoulder instability can be variable and difficult to recognize as symptoms and exam findings are often nonspecific and subtle. Adding to the complexity is that most of these patients are young and involved with athletics. There may be concomitant shoulder pathology such as impingement syndrome.[31] Most commonly, patients report deep pain within the posterior aspect of the shoulder.[32][33][34] Additionally, the patient may report worsening athletic performance and decreased strength or endurance in the shoulder.[7][32][35][36] Mechanical symptoms, such as clicking or popping, can also be described.[32][31] Relatively few patients present after a posterior shoulder dislocation or traumatic injury with the arm in a provocative position. Thus, physicians must maintain a high index of suspicion when a young athlete presents with vague shoulder complaints, particularly in sports exposing the shoulder to repetitive microtraumas such as overhead athletes, swimmers, weightlifters, rowers, and American football players.[7][32] Lastly, patients should be asked about connective tissue disorders such as Ehlers-Danlos or Marfan syndrome, which signify ligamentous laxity.

Physical Exam

A thorough physical exam is necessary as the clinical entity may not be apparent in history alone. Findings can be subtle, and both shoulders should be fully examined to detect any side-to-side differences. An examination should include inspection, palpation, range-of-motion (ROM), strength testing, neurovascular tests, as well as provocative maneuvers. Typically, ROM, strength testing and neurovascular examination will be normal in patients with posterior shoulder instability.[32] Interestingly, a skin dimple present over the posteromedial deltoid of both shoulders was reported to be 62% sensitive and 92% specific for identifying posterior shoulder instability. Tenderness to palpation may be elicited over the posterior joint line and could be secondary to synovitis from multiple episodes of instability.[21] Patients should be evaluated for scapular dyskinesia as poor scapulothoracic mechanics can lead to posterior shoulder pain and weakness. Lastly, the clinician should evaluate the patient for generalized ligamentous laxity and multidirectional instability, as this may predispose the patient to instability.[37]

Examination maneuvers specific to posterior shoulder instability include the jerk test, Kim test, posterior drawer, and the load-and-shift test.[7] The jerk test may be performed with the patient standing or seated. The clinician stands next to the affected shoulder and holds the flexed elbow in one hand and grasps the distal clavicle and scapular spine in the other. The patient’s arm is brought into flexion, and internal rotation and a posterior force to the shoulder joint is applied through the elbow with one hand while the other hand applies an anterior force through the shoulder girdle. A sudden jerk, along with pain as the subluxated humeral head relocates into the glenoid signifies a positive test.

The Kim test was first reported in the literature by Kim et al. as a means to detect posteroinferior lesions of the labrum.[38] It is performed with the patient in the seated position with the arm in 90 degrees of abduction in the scapular plane. The clinician grasps the patient’s elbow with one hand and the patient’s proximal, lateral arm with the other hand. An axial force is applied by pushing on the elbow into the shoulder joint. While maintaining axial force, the patient’s arm is elevated an additional 45 degrees while the clinician simultaneously applies a posteroinferior force through the patient’s proximal arm. Sudden pain in the shoulder denotes a positive test. Kim et al. reported a 97% sensitivity for detecting posterior instability when both the jerk test and Kim test were positive.[38]

Evaluation

Plain Radiographs

Initial assessment of the shoulder should begin with plain radiographs. The views to obtain include a true AP of the scapula (Grashey), internal and external rotation views, scapular Y, and an axillary view.[37] In patients with atraumatic posterior shoulder instability, radiographs are typically normal. However, radiographs may identify a posterior dislocation, glenoid bone loss or fractures, glenoid retroversion or hypoplasia, as well as reverse Hill-Sachs lesions.[37][34]

Advanced Imaging

Advanced imaging consists of an MRI to better evaluate soft tissue pathology. Contrast enhancement [magnetic resonance arthrogram (MRA)] is the most sensitive diagnostic test for detecting posterior labral and capsular lesions.[39] In patients with posterior instability, findings may include a reverse Bankart lesion as well as posterior capsular enlargement.[40][41] Although rare, other findings may include a posterior humeral avulsion of the glenohumeral ligament and posterior labrum periosteal sleeve avulsion.[42] MRA is also useful in identifying a Kim lesion, which is an incomplete, concealed avulsion of the posteroinferior labrum.[29] The Kim classification can describe labral tear morphology.[43]

• Type I: incomplete detachment
• Type II: incomplete and concealed avulsion (Kim lesion)
• Type III: chondrolabral erosion
• Type IV: flap tear

Computed tomography (CT) will help to delineate bony morphology better, especially when pathology is noted on plain radiographs. CT scans are indicated when that are concerns for glenoid retroversion, fractures, or hypoplasia, as well as reverse Hill-Sachs lesions. Recognition of these bony abnormalities is important as they may have implications in treatment.

Treatment / Management

Overview

When formulating a treatment plan for a patient with symptomatic posterior shoulder instability, goals should include reducing pain, improving function, and preventing recurrence. However, determining the optimal treatment can prove challenging as management is dictated by many factors, including the underlying etiology, as well as osseous and soft tissue pathology. Furthermore, little is known on the natural history of a single traumatic posterior instability episode or of untreated posterior instability.[32] While treatment algorithms may help clinicians with management decisions, patients should be treated uniquely on a case-by-case basis.

Posterior Shoulder Dislocation

Posterior shoulder dislocations (PSD) are much less common than anterior shoulder dislocations and are usually associated with high-energy trauma or seizures.[44] PSD may be complicated by osseous lesions such as impression fractures of the humeral head (reverse Hill-Sachs lesion) or glenoid fractures. A locked or fixed PSD describes a shoulder that will not reduce because of the engagement of a defect on the humeral head with the glenoid. PSD may also be accompanied by fractures of the humeral head or tuberosities.[44]

In their systematic review of posterior shoulder dislocations, Paul et al. provide a treatment algorithm that takes into account the general health and activity of the patient as well as the size of the humeral head defect.[45] They recommend closed reduction under general anesthesia for acute dislocations less than 3 weeks with small humeral head (HH) defects. With the arm flexed, adducted, and internally rotated, cross-body traction is applied with simultaneous gentle pressure on the posterior humeral head. If closed reduction is unsuccessful, then an open or arthroscopic reduction may be attempted. Patients are then braced in 10 degrees of abduction with external rotation up to 20 degrees for 6 weeks. Nonoperative treatment is recommended for those without significant bony defects (<10% HH), no recurrent posterior instability, or those who are poor surgical candidates.[45](A1)

Operative management is reserved for those with continued posterior instability secondary to soft tissue lesions or humeral head defects.[45][44] Continued symptoms of posterior instability secondary to soft tissue defects may be treated with arthroscopic posterior stabilization. Further operative intervention is largely based on the size of the HH defect. Generally, for smaller lesions less than 25% of the HH, treatment consists of nonanatomic procedures such as the McLaughlin procedure (transfer of the subscapularis to the bony defect) or the Neer modification of this procedure (transfer of the lesser tuberosity to the defect).[44] Rotational osteotomy of the proximal humerus has been described as a means of preventing the HH defect from engaging the glenoid.[46] However, this technique is now avoided because of technical difficulty as well as the progression of osteoarthritis and the risk of humeral head avascular necrosis.[44][47](A1)

For larger HH defects, treatment includes bone grafting procedures or arthroplasty. In their review of posterior shoulder dislocations, Robinson and Aderinto recommend disimpaction of the HH defect with autogenous bone grafting if the injury is less than 2 weeks old and nonanatomic procedures if the lesion is recognized after 2 weeks.[44] Other studies suggest autografting is appropriate for defects up to 40% of the HH, although there is no consensus regarding autologous bone grafting and HH defect size.[48] Allograft reconstruction may be considered for HH defects greater than 40% with good bone quality and absence of osteoarthritis.[44][49] Arthroplasty is more commonly used with HH defects greater than 50%, deformity of the HH, or patients with arthritic changes.[44][50][51] Both hemiarthroplasty and total shoulder arthroplasty are options, with the latter reserved for cases in which the glenoid is involved.[45][44](A1)

Nonoperative Management of Posterior Shoulder Instability

A conservative approach of at least 6 months is typically the first line of treatment for patients with posterior instability, with outcomes dependent on the underlying etiology.[14][32][7][37][31][12] If the cause is atraumatic, patients tend to have better outcomes with nonsurgical treatment.[37][52] Rehabilitation should focus on proprioceptive exercises and strengthening the dynamic stabilizers of the shoulder, particularly the subscapularis. Scapulothoracic mechanics should be evaluated, as dysfunction can be a source of posterior shoulder pain.[37] Tibone and Bradley noted that 70% of athletes had subjective improvement after 6 months of conservative treatment.[53] However, the authors note that while functional disability with athletics may improve, instability is typically not eliminated.(A1)

Patients with posterior shoulder instability secondary to a traumatic event may have less success with nonoperative management.[7][54][13] In their study to evaluate muscle strengthening exercises to treat anterior, posterior, and multidirectional instability, Burkhead and Rockwood found that only 16% of patients with a traumatic etiology showed good or excellent results, while 83% of those with an atraumatic etiology showed good or excellent results.[54]

Operative Management of Posterior Shoulder Instability

The primary indication of surgical intervention is recurrent symptomatic posterior shoulder instability recalcitrant to conservative treatment. Surgery may be indicated for those with instability secondary to a traumatic etiology and identifiable soft tissue or osseous defect. Surgery is also indicated for those who remain symptomatic after an adequate trial of physical therapy with avoidance of provocative activities.[14][32][7][37][31][12] Surgical management can be broken down into procedures that address either soft tissue or bony pathology. In reality, patients may need a combination of procedures, and the optimal surgical approach remains controversial. Generally, procedures addressing bony pathology are performed open, and procedures addressing soft tissue pathology are done arthroscopically. No consensus exists in the literature regarding specific indications for each procedure, and thus clinicians must consider the optimal treatment for a patient on a case by case basis.

Open verse Arthroscopic Stabilization of Soft Tissue Defects

Several different open soft tissue procedures have been described in the literature, including:

• Subscapularis transfer[2]
• Reverse Putti-Platt procedure[55]
• Staple capsulorrhaphy[56]
• Various capsular shift techniques[57][20][23]

While good results have been obtained with open procedures for anterior instability, open treatment of posterior instability has not been proved favorable with a 30% to 70% failure rate.[7] This may be related to the fact that open posterior procedures are challenging and require larger surgical dissection, as well as the inability to visualize all the pathology related to posterior instability fully.[7][58][59](B2)

In the case of minimal bony pathology, the use of all arthroscopic treatment has surpassed open procedures for the management of posterior shoulder instability. Reasons for this include improved instrumentation and implants, less invasive nature and morbidity of arthroscopy, faster recovery, ability to view the entire labrum and to address concomitant pathology in the shoulder.[32][37][60] In the setting of a posterior labral tear, treatment generally consists of arthroscopic labral repair with suture anchors with or without capsular plication. In the case of redundant capsular tissue and no labral tear, capsular plication may be performed using sutures using either the intact labrum as the anchor point or suture anchors. Reported clinical outcomes are good to excellent with arthroscopic posterior shoulder stabilization. This approach has the highest success rates for treating posterior shoulder instability in athletes approaching 90%.[57]

When treating the patient arthroscopically, the patient is positioned in either the beach chair or lateral position, depending on surgeon preference. Generally, lateral positioning is favored as this allows more effective access to the inferior and posterior quadrants of the shoulder.[61] Labral repair is typically performed with suture anchors using three to four portals to aid in the placement and shuttling of sutures. A diagnostic arthroscopy is performed using the standard posterior portal. An anterosuperior portal is made in the superior aspect of the rotator interval, followed by a mid-glenoid portal, which aids in labral tear evaluation as well as preparation. A posterior seven o’clock portal is made 2 cm lateral and 1 cm anterior to the original posterior portal or may be described as being 2 cm directly lateral to the posterior acromial border. This portal will be used to place suture anchors in the posteroinferior glenoid, and accurate placement is crucial.[7][32][37]

The labrum can then be visualized from both the anterior and posterior portals. While viewing from the posterior portal, it is recommended to elevate and prepare the labrum from the midglenoid portal. Approaching the posterior labrum from this portal allows for a flat trajectory relative to the glenoid decreasing likelihood of chondral damage. Additionally, elevating the labrum from the posterior portal may increase the likelihood of further labral injury.[33]

The number of anchors placed is dictated by the extent of the tear and surgeon preference. For isolated posterior capsulolabral pathology, the use of three to four suture anchors spaced roughly 5 mm apart on the glenoid is usually sufficient.[7][32] These anchors can be placed using the seven o’clock portal, which provides the ideal trajectory for anchor insertion into the glenoid. Ideally, all posterior suture anchors will be placed using this portal by changing the angle of the trajectory of the anchor inserter device. Capsulolabral repair should begin with the most inferior aspect of the glenohumeral joint as the posterior shoulder joint volume diminishes with every capsulolabral stitch making each successive stitch more difficult.[7][32][37] This decrease in volume is desirable, especially in those with a patulous capsule.

A capsular plication is a technique to reduce redundant capsular tissue arthroscopically by the use of suture fixation.[61] Depending on the integrity of the labrum, this may be done with or without the use of a suture anchor. When the labrum is stable, the capsule may be anchored to the intact labrum. When there is labral pathology or a capsulolabral repair is required, a suture anchor may be used as the fixation point. Determining the amount of capsule to plicate can be difficult, but a 1 cm plication is usually sufficient.[58] The inferior and posterior capsules are important areas to address with posterior instability. Clinicians should inform their patients, especially throwing athletes, about the potential for decreased range of motion after plication, including internal rotation and abduction. Clinicians should be cautious when working in the posteroinferior capsular region to avoid injury to the axillary nerve. Dissection studies have shown the nerve to be an average of 12.4 mm from the glenoid rim at the six o’clock position.[62] Placing the shoulder in abduction and external rotation with traction during arthroscopy, the zone of safety is increased during arthroscopic plication.[63] The use of thermal devices should be avoided when working in this region.(B2)

Osseous Defects and Procedures

Patients with posterior shoulder instability may also have osseous defects, including HH impaction fractures and/or glenoid deficiency that require intervention in addition to soft tissue procedures. As previously discussed, HH defects are seen after a posterior shoulder dislocation, and if the lesion is large enough or if the patient continues to experience symptoms of instability, then intervention is required. Management of HH defects depends on the size of the lesion and includes both nonanatomic and anatomic procedures. Nonanatomic procedures include the transfer of the subscapularis into the defect on the HH as well as the Neer modification of this procedure. Anatomic reconstruction using either autograft or allograft to fill the HH defect has also been described.

Treatment for posterior instability attributable to glenoid defects such as fracture, dysplasia, or excessive retroversion may be organized into two broad categories, including posterior bone block procedure or posterior opening wedge osteotomy. Both of these procedures address posterior glenoid deficiency but may also be indicated in patients with recurrent posterior instability after soft-tissue procedures.

Posterior bone block procedures have been described in the treatment of posterior glenoid wall deficiency.[12] Fried is credited for performing the first iliac crest bone block procedure in 1949 using an iliac crest bone graft from the ipsilateral hip.[64] Several variations to this procedure have been described and are historically performed via an open posterior approach to the glenoid with the incision located in the posterior axillary fold.[57][31] Recently, the use of distal tibial allograft to treat posterior shoulder instability has been described.[65] This bone block procedure is unique in that it is intra-capsular. Studies demonstrate improved joint congruity with the humeral head compared to autogenous iliac crest bone graft.[66](B3)

Posterior glenoid opening wedge osteotomy was first published in the literature by Scott in 1967 and has been described in the treatment of excessive posterior glenoid retroversion.[12][67] It is performed through a similar posterior approach to the glenoid. The osteotomy is performed at the posteromedial glenoid neck 1 cm medial to the glenoid face.[67] The osteotomy is carefully levered open, leaving the anterior cortex intact, and the opening is filled with bone graft. The osteotomy is then secured with screws or with a plate and screws.[37](B3)

Debate exists on the amount of glenoid bone loss that necessitates a reconstructive procedure. Studies show that glenohumeral stability is compromised with glenoid articular bone loss of 20% to 25%.[68][69] Some studies have recommended glenoid reconstruction for defects greater than 25% of the width of the inferior glenoid.[57][65] In their review of posterior glenohumeral instability, Frank et al. recommend obtaining a preoperative CT scan to evaluate the amount of glenoid bone loss and determine the feasibility of arthroscopic management.[32](B2)

Differential Diagnosis

Posterior shoulder instability is an uncommon entity and can be difficult to diagnose, especially in cases involving repetitive microtrauma.[70] In patients who present with posterior shoulder pain without complaints of instability, the differential includes:

• Suprascapular nerve entrapment[71]
• Quadrilateral space syndrome[72]
• Posterior glenoid spur (Bennett lesion)[73]
• Early osteoarthritis
• Tumor[12]

Clinicians should also distinguish between laxity and symptomatic instability. Multiple studies have shown that healthy subjects may demonstrate as much glenohumeral translation as those with symptomatic instability.[14] After examination of 76 Division I collegiate athletes, Lintner et al. demonstrated that 2+ translation (translation of humeral head onto the glenoid rim) in any direction could not be considered abnormal.[74] Instability may not be isolated in one direction, and the clinician should evaluate the patient for multidirectional instability of the shoulder. A retrospective review of 231 patients found that among operatively treated cases, the incidence of isolated posterior instability and combined instability was 24% and 19%, respectively.[75]

Lastly, clinicians should also consider those with psychological problems who are able to voluntarily subluxate their shoulders. These patients may develop instability in adolescence for secondary gain and are able to willingly subluxate their shoulders with the arm at the side.[12]

Prognosis

Many factors make interpreting the literature of posterior instability challenging, including the low incidence of this clinical entity, variability in patient characteristics, surgical techniques, implants, and rehabilitation protocols, and the limited number of high-quality studies. Literature shows open surgical techniques have been reported to improve outcomes with success rates between 80% to 95%.[14][21][23] However, other studies suggest the failure rate may be as high as 50%.[37]

Initial reports of arthroscopic management of posterior instability were not as encouraging as those treated for anterior instability. However, recent literature has shown success rates of around 90% for those with posterior instability after sporting injuries.[57] Radnowski et al. analyzed arthroscopic capsulolabral repair in 107 shoulders of 98 athletes and found excellent results in 89% of throwers and 93% of non-throwing athletes at a mean of 27 months post-op. However, they noted that throwers were less likely to return to their pre-injury level of play than non-throwers (55% and 71%, respectively).[76]

In the largest patient cohort to date, Bradley et al. reported on 200 shoulders in 183 athletes prospectively treated with arthroscopic capsulolabral repair for posterior shoulder instability.[77] At a mean follow-up of 36 months postoperatively, ASES improved from 45.9 to 85.1 (P <0.001), with 90% of athletes returning to sport and 64% able to return to their previous level of play. When compared to anchorless fixation, those treated with suture anchors demonstrated significantly higher American Shoulder and Elbow Surgeons (ASES) scores and a higher rate of return to play.[77]

Arner et al. published a case series on 56 American football players who underwent arthroscopic posterior capsulolabral repair for posterior shoulder instability. At a mean follow-up of 44.7 months, the authors found a 93% return to sport, with 79% returning at the same level. Significant improvements were also seen on the ASES score and subjective scores of stability, ROM strength, pain, and function. The failure rate in this study was 3.5%.[78]

In 2015, DeLong et al. published a systematic review of the literature on arthroscopic and open posterior shoulder stabilization dating from 1946 to 2014.[3] Analysis of studies of open shoulder procedures containing 321 shoulders with an average follow-up of 69.8 months demonstrated a 66.4% return to play, with only 36.9% returning to the previous level of play. The average recurrence rate among the open procedures was 19.4%. Analysis of studies of arthroscopic treatment consisting of 817 shoulders at average follow up of 28.7 months postoperatively demonstrated 91.8% return to play with 67.4% returning to the previous level of play. The average recurrence rate among arthroscopic procedures was 8.1%. The authors concluded that patients undergoing arthroscopic treatment for posterior shoulder instability have superior outcomes compared to those who undergo open procedures in terms of stability, recurrence rate, patient satisfaction, return to sport, and return to the previous level of play. The authors also found that throwing athletes were less able to return to their previous level of play compared to non-throwing athletes, and repair with suture anchors resulted in fewer recurrences than those with anchorless repairs in those involved with high physical activity.[3]

Complications

Complications of posterior shoulder dislocations include osteonecrosis, posttraumatic arthritis, and joint stiffness. Osteonecrosis of the humeral head may occur after a simple dislocation but is more commonly seen with associated fracture-dislocations of the anatomic neck.[49][44] Posttraumatic arthritis is uncommon after simple dislocations. However, posttraumatic arthritis after a posterior dislocation is usually worse than arthritis seen after an anterior dislocation, and treatment may include a shoulder arthroplasty.[79] Joint stiffness after reduction is associated with a delay in diagnosis.[44] Joint stiffness may also be associated with ancillary stabilization procedures, and treatment of joint stiffness should be directed at the underlying cause.

Surgical complications for recurrent posterior shoulder instability are unique to the specific procedure performed. Complications of open treatment include infection, pain, weakness, and shoulder stiffness.[12] In regard to arthroscopic treatment, axillary nerve injury is possible, especially during the repair of the posteroinferior shoulder capsule. Thermal ablation should be avoided in this area.[63][62][80] Iatrogenic chondral damage, as well as labral transection, are also possible with poor portal placement and usage.[7][32]

The most common complication following surgical treatment of posterior shoulder instability is the recurrence of instability with rates varying depending on treatment method and cause of instability. DeLong et al. found an 8.1% rate of recurrence in over 800 shoulders treated via arthroscopic treatment as well as a recurrence rate of 19.4% in over 300 shoulders undergoing open surgical procedures.[3] Other studies analyzing the literature on arthroscopic treatment have found an average rate of recurrent instability of 5% and no higher than 10%.[12] Risk factors for recurrent instability after traumatic posterior shoulder dislocation include age below 40 at the time of dislocation, dislocation during a seizure, and a large Hill-Sachs lesion.[3] Glenoid retroversion has also been found to be an independent risk factor for recurrent instability in young athletes.[81]