Jaymeson R. Arthur, MD and John M. Tokish, MD
EPIDEMIOLOGY, BACKGROUND, AND RISK FACTORS
Compared to anterior shoulder instability, posterior instability is rare and classically has accounted for approximately 2% to 10% of all cases of shoulder instability.1,2 Most epidemiologic studies on shoulder instability, however, have mainly reported on acute dislocations and do not account for the more subtle forms of posterior instability such as recurrent subluxation. This is especially true in young, athletic populations.3–7 For example, Lanzi et al7 studied posterior instability in the United States Military Academy and found posterior instability to comprise 17.9% of the total injuries. Similarly, Song et al8 evaluated 231 patients at a single military institution being treated operatively for instability and found that 24% of all surgically treated instabilities had isolated posterior pathologic findings, with an additional 19% treated for combined instability. These studies highlight that the incidence of posterior instability is likely under-reported, especially in younger active populations. Nonetheless, advances in magnetic resonance imaging (MRI) and arthroscopy continue to improve our awareness and understanding of this clinical entity.9
Bony defects following posterior shoulder instability include the reverse Hill-Sachs lesion, the reverse bony Bankart lesion, and attritional posterior bone loss. The reverse Hill-Sachs lesion (Figure 20-1) is an impression fracture of the anteromedial humeral head and is associated with locked and difficult-to-reduce dislocations. Alternatively, fracture of the posteroinferior rim of the glenoid is referred to as the reverse bony Bankart lesion (Figure 20-2). Although the incidence of bony defects following posterior instability is not well defined by large, epidemiologic studies, several case series have reported their findings. Bradley and colleagues6 in their large prospective series found that 66% of patients with traumatic instability had reverse Hill-Sachs lesions. Longo et al10 performed a systematic review on several of these case series and found that, of the 328 shoulders analyzed, 9% of cases of posterior instability had a bony glenoid defect, 39% had humeral head defects, and 2% of cases had combined defects.
Although capsulolabral derangement in isolation more commonly presents in the more subtle forms recurrent instability such as recurrent subluxation, bony defects typically occur in the higher-energy forms of posterior instability.11–13 Bony defects from both the humeral and glenoid can predispose patients to recurrent dislocation by altering the glenohumeral congruity and by altering the function of the static glenohumeral stabilizers.14 Further, these injuries often do not present in isolation and a combination of bony and soft-tissue injuries are often present together.5,15–17 Rouleau and Hebert-Davies16 conducted a systematic review of more than 100 articles focusing on the incidence of associated injury in posterior dislocation. They found that 65% of dislocations had associated injuries, with fracture being most common (34% of cases) followed by reverse Hill-Sachs lesions (29%). In the younger, military population, Bottoni et al5 found that 97% of shoulders operated on in their series for traumatic posterior instability had reverse Bankart lesions, posterior rim fracture, or rim calcification.
Several risk factors for posterior instability have been identified. Classically, posterior instability has been associated with epilepsy, ethanol use, and electrocution, termed the 3 E’s. In fact, bilateral posterior dislocations without associated trauma is considered essentially pathognomonic for seizure.18,19 This is thought to occur because of the stronger contraction of the shoulder internal rotators (primarily the pectoralis major and latissimus dorsi) overpowering the weaker external rotators. This muscle imbalance leads to superior posterior displacement of the humeral head relative the glenoid and subsequent posterior dislocation.20,21 Despite these classically described “3 E’s,” Robinson and colleagues22 found that traumatic accidents (fall from height and motor vehicle accidents) accounted for the majority of posterior shoulder dislocations (67%), whereas seizure and electrocution were less common (31% and 1.7%, respectively).
Several authors have shown that anatomical factors, such as glenoid hypoplasia,11 posterior glenoid rim deficiency,23,24 and glenoid retroversion6,25–27 can contribute to posterior instability. For example, in their series, Hurley et al25 showed that the average glenoid retroversion in patients with posterior instability was –10 degrees vs –4 degrees in the control group. Brewer et al27 defined excessive retroversion as more than –7 degrees of retroversion and Owens et al26 showed that for every 1 degree of increased retroversion, there was a 17% increased risk of subsequent posterior instability in their young, military population.
In athletic populations experiencing recurrent posterior instability, common etiologies include a fall onto the outstretched hand,5 blocking linemen in American football,28 weight lifting, rugby, and climbing.29 Posterior instability has even been described in baseball players’ leading shoulder during batting30 and in rifle shooting.31 Unfortunately, recurrent instability is common in these patient populations as well. Robinson et al22 retrospectively reviewed 120 cases of posterior dislocation and found as many as 18% of patients experienced recurrent instability at 1 year. They found risk factors for recurrent instability included age younger than 40 years, dislocation during seizure, and large reverse Hill-Sachs lesion (> 1.5 cm3).
Although no single classification system has been widely adopted, several descriptive terms have been used to describe shoulder instability and dislocations. These include the direction of instability (anterior, posterior, inferior, multidirectional), etiology (atraumatic vs traumatic), presence and size of the bony defects, and chronicity (acute, chronic, recurrent).21,32,33 Further, it is important to delineate the simple dislocations from the more complex, fracture-dislocations.
It is critical to recognize that there are many forms of posterior instability that range from the obvious acute, traumatic posterior dislocations all the way to the more subtle forms of recurrent posterior subluxation.13,21 Overall, studies have shown that posterior dislocations are more frequently clinically missed, with up to a 50% delay in diagnosis.3 Further, many patients with posterior instability may be initially misdiagnosed or referred for other diagnoses.34 Millet et al35 found that in athletic patients the most common presenting complaint is pain, and the authors noted that this may often draw attention away from the clinical suspicion of instability. In the setting of acute fracture in the elderly patient, dislocations can also be commonly missed.36 Therefore, a combination of a detailed history, accurate physical examination, and proper imaging is essential for correct diagnosis.
A detailed history begins with questions regarding the onset, severity, and progression of any symptoms. Often, patients will describe an acute traumatic event such as a fall onto an outstretched hand, a blow to the arm during a sporting event, or a motor vehicle accident. Inquiring about the position of the arm/shoulder and the direction of applied force may give the clinician invaluable information leading to the diagnosis, because a fall on an outstretched arm, or in a position of flexion and horizontal adduction, may be indicative of a posterior event.
These higher-energy mechanisms should increase the clinician’s suspicion for bony abnormalities. Even in the absence of a high-energy mechanism, a history of manual shoulder reduction should also cue the clinician that bony pathology may be present. When bony defects are present, a patient may often describe a sense of locking or grinding, especially with a reverse Hill-Sachs lesion.35,37 With increasing bone loss due to recurrence, patients may report lower energy necessary to result in a recurrence, dislocations in nonprovocative positions, and episodes may happen during sleep.
When seizure is the root cause of posterior instability, a detailed history of seizure frequency and antiseizure medication compliance is useful. Of note, these patients are at high risk of developing locked posterior dislocations with subsequent humeral head lesions.20 In the post-seizure setting, it may be difficult to obtain any history from the patient but collateral information from the family, friends, or emergency medical personnel is often helpful. Lastly, it should be noted that many posteriorly unstable patients can reproduce their sensation on exam “voluntarily.” This voluntary reproduction should be differentiated between voluntarily positional and muscular, because the latter may best be avoided surgically.35,38
In the setting of posterior shoulder instability in general, the clinical evaluation begins with a thorough inspection, palpation, range-of-motion testing, strength testing, and various special tests. The involved shoulder should be carefully compared to the contralateral shoulder in all these aspects. Often, the patient will present with tenderness to palpation along the posterior glenohumeral joint line.35 In the setting of acute dislocation, the patient will typically present with the shoulder internally rotated, with prominent coracoid and axillary fullness.37,39 If significant humeral head deformity is present (ie, reverse Hill-Sachs lesion), this bone defect may engage the posterior aspect of the glenoid leading to a mechanical block to external rotation.39
The basic physical examination starts with testing the shoulder in the vulnerable positions of flexion, adduction, and internal rotation. Axial load can elicit pain posteriorly and instability can often be detected even with this simple maneuver, especially when bony defects are present. In this at-risk position, when axial load is applied to the shoulder, the soft-tissue restraints, mainly the posterior band of the inferior glenohumeral ligament and the posterior capsulolabral complex, cannot sufficiently resist the force and posterior dislocation occurs.21,35
Several provocative tests for posterior instability have also been described. These include the jerk test, posterior load and shift test, and push-pull testing. The jerk test40 is described in Figure 20-3. This maneuver specifically tests the posteroinferior labrum by forcefully impinging the humeral head over the diseased posteroinferior labrum causing pain. Not only is this test useful for diagnostic purposes but it also has prognostic value in that it helps predict which patients are more likely to fail nonoperative treatment.41
The posterior load and shift test40 is performed by placing the patient in a supine position with the affected arm in neutral rotation with 40 to 60 degrees of abduction and forward flexion. Axial force is applied along the axis of the humerus with one hand while the other hand places a posteriorly directed force on the proximal humerus. The amount of glenoid translation is noted and more than 50% translation is considered a positive test.
The push-pull test40 is performed by placing the patient in the supine position with the arm in 90 degrees of abduction and neutral rotation. The examiner then grasps the wrist and “pulls” with one hand in line with the axis of the arm. Using the other hand, the shoulder is “pushed” posteriorly with one hand and the other hand is then placed on the proximal humerus. While pulling with the hand holding the wrist, the examiner simultaneously pushes the proximal humerus posteriorly with the other hand. The test is positive when the maneuver reproduces the patient’s pain/symptoms (Figure 20-4). In these tests, if a shoulder remains out, it is indicative of bone loss.
IMAGING AND SURGICAL DECISION MAKING
Standard imaging begins with anteroposterior, axillary, and scapular-Y radiographs to ensure orthogonal views of the joint are obtained.22,37,39 If the patient is not able to achieve adequate abduction, the Velpeau view,42 with the patient leaning backward 20 to 30 degrees with the beam directed from cranial to caudal centered on the glenohumeral joint, can be used. The classic “lightbulb sign” or “half-moon sign” will often be present on anteroposterior radiographs.43 Nonetheless, the axillary view has been shown to be most sensitive for the detection of posterior instability on plain radiographs.44,45
Although plain radiographs can show bony deformity when large enough, further advanced imaging with computed tomography (CT) scan and MRI are often required for more detailed characterization. Several studies have shown that CT is most useful for defining humeral head and glenoid defects,46–48 whereas MRI is especially useful for detecting concomitant capsulolabral injury.11,49 Often, a CT scan paired with MRI can ensure the most accurate diagnosis and that all injuries are accounted for.
Because the size of the bony defect often directs management, the clinician should be familiar with how to accurately measure bone loss. With respect to the humerus, previously surgeons simply estimated the percentage of affected humeral articular surface seen on the CT scan. Most of the previous literature has focused around measuring anterior bone loss. However, Hines et al17 evaluated posterior glenoid bone loss and proposed a standardized method for measuring it. Using a best-fit circle technique, the size, location, and depth of the defect can be assessed. These authors found that 69% of patients undergoing surgery for posterior instability had some measurable bone loss, and 22% of patients had greater than subcritical bone loss (13.5% or more).
Although critical glenoid bone loss in anterior instability has been studied at length,50,51 it is less clear what constitutes critical bone loss for posterior instability. And although many authors agree that the larger the bony defect, the higher likelihood of recurrent instability; there is no consensus on the exact size of the defect that requires the surgeon to address the bony defect directly.
Nacca and colleagues52 conducted a cadaveric study in which the posterior glenoid was sectioned to varying degrees in conjunction with reverse Bankart repair. They found that bony defects greater than 20% of the posterior glenoid width remained unstable after isolated reverse Bankart repair. Bryce et al53 conducted a similar cadaveric study in which they assessed humeral head translation on 3-dimensional CT with respect to the scapula at each humerus position after removing the posterior glenoid in 5-degree increments. They found that posterior humeral head translation was significantly increased after only 5 degrees of posterior glenoid bone loss. In both of these cadaveric studies, however, bone was sectioned directly from the posterior glenoid in the cranial-caudal axis and, as we know, most often clinically the reverse Bankart lesion tends to occur in the posteroinferior aspect of the glenoid.11
In perhaps the most clinically relevant investigation, Hines and colleagues17 conducted a retrospective review of 43 consecutive patients at a single military institution who underwent arthroscopic isolated stabilization of the posterior labrum. They found 69% of their patients had measurable bone loss and 22% of patients had greater than the previously described 13.5% glenoid bone loss. Although these patients were statistically less likely to return to full duty, the authors found reoperation rates, complications, and patient-reported outcomes to be no different based on the size of the lesion. As opposed to the anterior shoulder instability counterpart, this suggests that bony defects in posterior instability can be well treated with standard arthroscopic techniques without bone augmentation.
The critical threshold for bony stabilization or augmentation for humeral defects is even less studied. Backer and Warren54 found that reverse Hill-Sachs lesions greater than 30% of the articular surface can lead to instability. Longo et al10 conducted a systematic review looking at trends in surgical techniques for humeral bone loss. They analyzed 19 articles and found that when there was less than 25% humeral head bone loss, this was most commonly managed with posterior capsular repair (50%), closed reduction (47%), or arthroscopically repaired (3%). If the humeral head bone loss was between 25% and 50%, this was primarily managed with open reconstruction with bone grafting (67%), with the subscapularis tendon transfer technique second at 33% of cases. If the humeral head bone loss was greater than 50%, arthroplasty was most commonly employed. They also showed that 91% of patients were able to return to sport when managed with distal tibia allograft, arthroscopic bone block augmentation, and arthroscopic repair.
In the end, bony defects in posterior shoulder instability remain a difficult challenge to treat for orthopedic surgeons. Because of the wide range of pathology, many different techniques have been developed to address these problems. Furthermore, many of the data that currently exist consist of small case reports and case series. Although new techniques, including more advanced arthroscopic techniques, are being developed, future research must continue to be developed to improve outcomes following posterior shoulder instability with bony defects.
Reduction of Acute Dislocation
Before discussing nonsurgical and surgical treatment, the clinician should first be aware of how to perform closed reduction of the posteriorly dislocated shoulder. To begin, forceful reduction should be avoided because it can lead to humeral head fracture and subsequently osteonecrosis. In-line traction has been shown to be successful in 33% of posterior dislocations.22 Open reduction can be performed through a deltopectoral approach. Reduction can be accomplished after opening the rotator interval and gently levering the head back into place. If this is unsuccessful, a formal arthrotomy is required.
Because of the wide spectrum of disease severity, there exist many therapeutic options for the treatment of posterior shoulder instability, including nonsurgical and surgical options. Nonsurgical treatment is typically the first-line treatment, provided the joint is not resting in a subluxed or dislocated position, and the goal of the reduced shoulder after posterior instability event is to increase the dynamic stability of the glenohumeral joint through strengthening the rotator cuff and periscapular muscles,55 especially the external rotators, posterior deltoid, and scapular stabilizers, which are often deficient in posterior instability.56 After 3 to 6 months, patients who have persistent shoulder pain, dysfunction, and instability who fail the above conservative management may be considered for surgery.
Once reduced or in the case of the athletic patient with recurrent posterior subluxation, physical therapy is encouraged to optimize dynamic stabilization.55 In these populations, appropriate strengthening and proprioceptive programs have been shown to diminish pain and improve stability in approximately two-thirds of patients with posterior and multidirectional instability.55,56 Nonoperative management is less successful in patients with a history of traumatic events, with a roughly 16% success rate compared to 70% to 80% in atraumatic counterparts.55
To achieve successful surgical management of glenohumeral instability, the surgeon must be able to accurately identify and address what factors are causing the instability. Furthermore, the instability must be attributable to mechanical factors that can be corrected with surgery.57 The surgical procedures for the treatment of bone defects can be divided broadly between treatment of humeral lesions and glenoid lesions. Although this chapter focuses on the management of bony defects, it cannot be understated that few bony lesions exist in isolation. Therefore, it is critical for the surgeon to evaluate which soft-tissue structures are deficient and address these properly at the same time as the bony defect is addressed. Patient age, severity of injury, pattern of instability (isolated posterior instability vs multidirectional instability), and functional demands of the patient also play a vital role in surgeon decision making and should be considered carefully. Further, although bony defects have often been an indication for open procedures, the indications for arthroscopic techniques that address these bony defects are expanding as surgical technique and our understanding of the pathoanatomy increases.57
For small humeral defects (< 20% to 25% of articular surface), an arthroscopic Connelly or “reverse remplissage” has been advocated.58,59 Duey and Burkhart60 described an arthroscopic technique for addressing small to medium reverse Hill-Sachs lesions in which the middle glenohumeral ligament is sutured into the defect, turning it into and extra-articular defect and preventing it from engaging the posterior glenoid.
For medium humeral defects (25% to 40% of articular surface), the McLaughlin technique and the modified McLaughlin technique have been advocated. In 1952, McLaughlin described the transfer of the subscapularis tendon as a means of treating reverse Hill-Sachs lesions after posterior dislocations. Via the deltopectoral approach, the humeral bone defect is approached and the surface of the bone is freshened until underlying vascular bone is exposed. The subscapularis is then reattached to the humerus in the depths of the defect by mattress sutures passed through drill holes in the bone.39 Hawkins and colleagues46 later described a modification to this technique whereby an osteotomy of the lesser tuberosity was performed and the osteotomized bone was transposed into the defect. Arthroscopic techniques for this procedure have been subsequently developed as well.61,62
Disimpaction and autogenous vs allogenic bone grafting of the humeral head defect have also been used to treat these medium defects.21,59,63,64 These techniques are indicated when the underlying bony is not significantly osteoporotic or deformed, and when there is not significant arthritis already present. This is especially useful when the injury is treated promptly, within 2 weeks of the injury.63 Partial prosthetic humeral head resurfacing has also been reported and has been shown to be effective in preventing recurrent dislocations for patients with significant reverse Hill-Sachs lesions.65
In older patients with large humeral head defects (> 40% to50% of articular surface), both hemiarthroplasty and arthroplasty have been advocated.21,46,57,59 No studies to our knowledge have directly compared the 2 techniques directly to each other; however, the presence of underlying arthritis before the injury may be a solid indication for total shoulder arthroplasty as first-line treatment in this situation.46,66
Rotational osteotomy of proximal humerus has also been described.67,68 This technique simply attempts to shift the bony defect away from the position where it engages with the glenoid, thus reducing instability. However, this is a technically challenging operation and has increased risk of disruption to the humeral head blood supply; therefore. it is not widely used.21,43
To begin, glenoid dysplasia and retroversion can contribute significantly to posterior instability. Although there is no consensus as to how much retroversion is acceptable, the posterior glenoid opening wedge osteotomy can be a viable option in cases of severe dysplasia and retroversion. Some authors consider 15 degrees to be excessive retroversion,9 and studies have shown that retroversion greater than 15 degrees may lead to increased rates of failure of soft-tissue repair if the retroversion is not simultaneously addressed.69 Nonetheless, there are limited studies assessing patient outcomes with this approach that have helped better define the cutoff for this procedure. Posterior bone block and osteoarticular augments can also be used in the setting of glenoid dysplasia and retroversion.
Reverse bony Bankart lesions often heal with a medialized posterior fragment. If the fragment is large enough, it may be elevated and incorporated into a standard posterior Bankart repair. If the bone is attritional or deficient, options to address this defect include the use of posterior bone block procedures. Several different techniques have been described to accomplish this, including using iliac crest autograft,70,71 acromion autograft,72,73 distal tibial allograft,74 and distal clavicle autograft (Figure 20-5).75 Further, arthroscopic techniques have been developed to address bony glenoid deficiencies and have the advantage of avoiding the extensive open approach.76