Orthopedics

CME Review Article 

Recurrent Anterior Shoulder Instability Associated With Bony Defects

Oke A. Anakwenze, MD; Jason E. Hsu, MD; Joseph A. Abboud, MD; William N. Levine, MD; G. Russell Huffman, MD, MPH

Abstract

Mobility of the glenohumeral joint is facilitated through the complex interplay of soft tissue and osseous anatomy. Arthroscopic shoulder stabilization is commonly used in the surgical management of shoulder instability. However, the management of the unstable shoulder associated with bony defects (glenoid, humeral, or combined) can be challenging. Adequate recognition of bony defects is paramount to successful treatment and entails a careful history, clinical examination, and advanced radiographic imaging. Nonoperative methods of treatment are often insufficient for treating patients with large bony defects. Bony procedures, as opposed to soft procedures, may yield better outcomes in this patient population. However, respective surgical techniques used to address these defects are technically challenging with a significant learning curve and may lead to significant morbidity. This represents a paradigm shift in treatment and replaces the old paradigm of “open vs arthroscopic” instability surgery.

Abstract

Mobility of the glenohumeral joint is facilitated through the complex interplay of soft tissue and osseous anatomy. Arthroscopic shoulder stabilization is commonly used in the surgical management of shoulder instability. However, the management of the unstable shoulder associated with bony defects (glenoid, humeral, or combined) can be challenging. Adequate recognition of bony defects is paramount to successful treatment and entails a careful history, clinical examination, and advanced radiographic imaging. Nonoperative methods of treatment are often insufficient for treating patients with large bony defects. Bony procedures, as opposed to soft procedures, may yield better outcomes in this patient population. However, respective surgical techniques used to address these defects are technically challenging with a significant learning curve and may lead to significant morbidity. This represents a paradigm shift in treatment and replaces the old paradigm of “open vs arthroscopic” instability surgery.

Dr Anakwenze, Hsu, and Huffman are from the Department of Orthopedic Surgery, The University of Pennsylvania, Dr Abboud is from 3B Orthopaedics, Pennsylvania Hospital, Philadelphia, Pennsylvania; and Dr Levine is from the Department of Orthopedic Surgery, Columbia University Medical Center, New York, New York.

The material presented in any Vindico Medical Education continuing education activity does not necessarily reflect the views and opinions of ORTHOPEDICS or Vindico Medical Education. Neither ORTHOPEDICS nor Vindico Medical Education nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.

Correspondence should be addressed to: G. Russell Huffman, MD, MPH, Hospital of the University of Pennsylvania, 3400 Spruce St, 2 Silverstein, Philadelphia, PA 19104 (russell.huffman@uphs.upenn.edu).

The glenohumeral articulation has the greatest range of motion in the human body. This motion results from the complex interplay of osseous and soft tissue shoulder anatomy. However, alterations in the delicate balance between glenohumeral motion and the biomechanics of shoulder stability predispose the glenohumeral joint to a higher degree of instability than any other joint.1 Hovelius2 estimated the incidence of shoulder dislocations in Sweden to be at least 1.7% in patients aged 18 to 70 years.

The majority of shoulder dislocations are anteroinferior,3 and recurrent glenohumeral instability after traumatic dislocations is typically the result of tearing of the anteroinferior labral-ligamentous complex. Bankart4,5 first described this phenomenon in 1923, when he noted that the humeral head while dislocating anteriorly “shears off the fibrocapsule of the joint from its attachment to the fibrocartilaginous glenoid ligament.”

In addition to capsular-labral damage, bony defects can occur following traumatic dislocations. These defects may involve the humeral head, the glenoid, or a combination of lesions with a prevalence that is greater than appreciated with routine radiographs.6,7 A bony Bankart lesion, or avulsion of the anterior glenoid rim (Figure 1), has been associated with recurrent shoulder instability8–10 and has been noted to occur in 5% to 56% of patients.9,11–15 Most frequently, these fractures occur in the anteroinferior aspect of the glenoid rim.16 In cases of recurrent instability, studies have reported a prevalence of bony glenoid deficiency as high as 90%,8 although not all of these are large enough to be of clinical significance.7 Similarly, a high percentage of patients who fail soft tissue stabilization procedures have been noted to have glenoid deficiencies in addition to capsulolabral damage.10,17,18

MRI revealing a bony defect of the anterior glenoid rim.

Figure 1: MRI revealing a bony defect of the anterior glenoid rim.

Hill-Sachs lesions, impression fractures of the humeral head (Figure 2), occur in up to 65% to 71% of first-time dislocators and also contribute to recurrent shoulder instability. In the case of recurrent instability, the incidence and size of Hill-Sachs lesions increases and has been reported to occur up to 90% of the time (Figure 3).3,15,19–21

MRI revealing a large posterolateral humeral head defect.

Figure 2: MRI revealing a large posterolateral humeral head defect.

Frequency of bony defects in traumatic recurrent shoulder instability.

Figure 3: Frequency of bony defects in traumatic recurrent shoulder instability.

Anatomy

The glenohumeral joint is composed of dynamic and passive stabilizers. The dynamic stabilizers confer stability during shoulder motion and include the rotator cuff muscles, long head of the biceps brachii, scapular stabilizers, and the deltoid. Recently, the importance of shoulder neuromuscular proprioception, the ability to recognize joint position in space, in conferring stability has been described,22 with studies noting the presence of mechanoreceptors within the shoulder glenohumeral ligament complex.23 While the pathway between neuromuscular elements and the central nervous system is likely disturbed in the presence of bony defects, the magnitude of this proprioceptive deficit as compared to shoulders with only capsule-ligamentous injury is unknown.

The passive stabilizers, responsible for shoulder stability at rest, include the glenoid labrum, glenohumeral ligaments, glenohumeral capsule, and rotator interval.3,24 At rest, negative intra-articular pressure provides primary glenohumeral stability. Through a functional range of motion, the rotator cuff, and biceps brachii provide stability, and at the extremes of motion, the capsuloligamentous structures provide the primary constraint.25 In addition to these stabilizers, concavity-compression relies on the convex humeral head articulating with the concave glenoid and labrum.26 Loss of this important mechanism, as found in significant glenoid or humeral impression fractures, can lead to shoulder instability.27

While the Bankart lesion occurs in the majority of shoulders that anteriorly dislocate, cadaveric studies have shown that the Bankart lesion alone does not necessarily create instability.28 The critical role of the inferior-glenohumeral ligament complex in shoulder instability has been well documented. The inferior-glenohumeral ligament attaches to the anterior-inferior labrum and acts as a hammock to prevent anterior humeral head translation in the abducted arm.24 Damage to the inferior-glenohumeral ligament in the setting of Bankart lesion, whether at the labral attachment or as a result of plastic deformation in addition to capsular damage, leads to shoulder instability.3,24,29 In the presence of glenoid bone deficiency, the capsulolabral anatomy should be repaired in addition to reconstructing the bone defects.

Diagnosis

Accurate characterization of bony shoulder instability relies on a combination of the patient’s history of shoulder instability as well as the clinical and radiographic examination. The patient should be queried about the circumstances surrounding the initial dislocation and the position of their arm preceding dislocation. Similarly, the clinician should obtain a detailed history of subsequent dislocations, the force required to dislocate, the frequency of these episodes, mode of relocation (self reduction versus emergency room setting), and the length of time from the last dislocation. One should have an increased index of suspicion for bony deficiency in the presence of an initial high-energy trauma with subsequent instability episodes occurring with minimal force or in the mid-range of shoulder motion.10 Frequently, these injuries are a result of sports activities or other high energy trauma.10 While the specific mechanism to produce a bony Bankart lesion is not certain, it has been noted to occur more commonly in rugby players (who dislocate their shoulders with their arms in approximately 70° and 30° of abduction and extension respectively) as opposed to football players, suggesting that an increased axial force, rather than rotational force, may play a role.18

On clinical examination, patients may have decreased range of motion due to apprehension and may report pain due to capsulolabral or bony damage or if there is associated arthritis. Jobe’s relocation, anterior apprehension, and the load and shift tests are effective tests to diagnose anterior instability. In the setting of significant bony deficiency, the apprehension test will be positive with minimal amounts of abduction and external rotation. Similarly, the relocation test may be positive with locking or appreciable crepitus.15 The load and shift test reproduces the inherent shoulder instability in this population.

Radiographic evaluation is critical in detecting osseous lesions and must include orthogonal views including true anteroposterior (AP) and axillary views.30 The Stryker notch and the AP in internal rotation views are the most accurate radiographic imaging techniques for diagnosing Hill-Sachs lesions.30–33 The West Point and Bernageau glenoid profile views34 are useful in detecting glenoid rim lesions not identified on standard radiographic images.6,30,34 However, these views may not be sensitive enough to detect small glenoid defects.8 Computed tomography (CT) with 3D reconstruction is of great use and should also be included in the work-up of any patient with suspected bone defects or those that fail prior shoulder stabilization (open or arthroscopic).8,30 The sagittal 3D CT reconstruction of the glenoid with the humerus subtracted remains the most useful series for best evaluation of glenoid deficiency. Magnetic resonance imaging (MRI) is also useful in evaluating glenoid rim deficits, rotator cuff integrity, and for sizing humeral impaction fractures.35,36

Management and Treatment Options

Success following arthroscopic treatment of labral lesions in the absence of bony deficits is predictable.37 However, failure rates for arthroscopic treatment in the presence of large bony glenoid and/or humeral head impaction fractures that engage with the glenoid are unacceptably high.3,18,38 Burkhart and DeBeer,18 in a study of 194 patients who underwent arthroscopic Bankart repair for traumatic shoulder dislocation, found a higher rate of recurrent intstability if a bone defect was identified (67% vs 6.5%, respectively). They noted poor outcomes with significant humeral or glenoid bone loss. They noted the humeral head defect to be of significance when it “engaged” the glenoid along the parallel and longitudinal axis during the functional range of motion.18,39 Similarly, recent cadaveric data suggests glenohumeral instability in abduction and external rotation is significantly increased as the humeral head defect approaches 25% of the humeral head diameter.27

Despite the high rates of bony defects, not all are clinically relevant. Boileau et al,40 classified bony glenoid defects into those with an acute fracture with detached bone fragment representing a shear fracture and those with bone defect without detached bone that represent compression fractures. They noted a higher incidence of recurrent instability in the latter group. Bigliani et al8 classified glenoid defects as (1) displaced avulsion fracture, (2) malunited avulsion fracture, and (3) glenoid rim erosion; class 3 was subdivided into 3a) <25% bone loss and 3b) >25% bone loss. Burkhart and DeBeer18 noted an “inverted pear” glenoid morphology due to glenoid erosion from the dislocating humeral head. Biomechanical data from Itoi et al41 has shown that the force required to translate the humeral head in relation to the glenoid with the arm in abduction and external rotation was significantly smaller with a glenoid defect of ≥21% of its length or 6.8 mm in width compared to in the presence of glenoid defects of smaller sizes.

The approach to managing patients with osseous defects and shoulder instability is controversial and is based on patient activity level, chronicity, severity of defects causing instability, and surgeon preference and experience. We have summarized a treatment algorithm with options for treating patients with large bony defects causing recurrent shoulder instability (Figure 4). Some potential complications include non-/malunion, infection, hardware failure, arthrosis, and neurovascular injury. Therefore, one must be clear about the indications before proceeding with some of the approaches detailed below.

Options in the management of patients with anterior recurrent shoulder instability associated with bony defects. Arthroscopic capulolabral repair can be considered in all cases based on degree of pathology and surgical preference. Degree of pathology and surgical expertise and experience should guide choice of management.

Figure 4: Options in the management of patients with anterior recurrent shoulder instability associated with bony defects. Arthroscopic capulolabral repair can be considered in all cases based on degree of pathology and surgical preference. Degree of pathology and surgical expertise and experience should guide choice of management.

Glenoid Defects

Arthroscopic Techniques

Arthroscopic Bankart repairs performed in the presence of significant osseous defects have increased failure rates compared to those shoulders without bony defects.8,15,18,39 In most instances, open approaches are used with greater success and lower recurrence rates in the presence of large glenoid defects.8,15,18,39 Sugaya and others have reported on the successful arthroscopic treatment of both acute and chronic bony Bankart lesions.9,14,42–44 Porcellini et al9 described 25 patients with acute (described as <3 months) bony Bankart lesions involving <25% of the glenoid. They arthroscopically fixed the avulsed fragment anatomically and noted success in terms of return to previous level of function and stability in 92% of their patients at 2 years postoperatively. In a longer follow-up study, they noted 2.4% and 4.2% traumatic re-dislocation in the acute (<3 months) and chronic group (>3 months), respectively. With the body of evidence at this time, some authors recommend capsulolabral Bankart repair with suture anchor fixation as an acceptable mode of treatment for shoulder instability in the presence of glenoid defects of <15%.10

Open Techniques

In the presence of glenoid rim fractures greater than 20% to 25% of the width of the glenoid, as measured at the bare area of the glenoid, open approaches are commonly recommended.15 Historically, tricortical iliac crest bone grafting,45,46 J-graft,47 or coracoid process transfers48–51 have been described in the treatment of glenoid bone loss.15,52 Recently, more “anatomic” means of restoring deficient glenoid bone stock through the use of fresh frozen osteoarticular glenoid allografts have been described with good outcomes.53 While this seems promising, the prohibitive cost of fresh osteoarticular allografts and the surgeon’s inability to truly restore the soft tissue anatomy of the glenoid labrum and capsuloligamentous structures to the reconstructed glenoid rim may preclude this technique from being widely used.

Bristow-Latarjet

The Bristow and Latarjet procedures involve a nonanatomic transfer of the coracoid process to the glenoid (Figure 5). The Bristow procedure, described by Helfet48 in 1958, involves transfer of the tip of the coracoid to the glenohumeral capsule and to the tip of the anterior glenoid periosteum. In 1964, it was modified by Mead and Sweeney54 to include rigid internal fixation. Attached to the tip of the coracoid, the biceps and coracobrachialis provide dynamic restraint to inferior and anterior instability, especially in abduction and external rotation. Further additional restraint is provided by transferring the coracoid bone block and conjoined tendon between the inferior 1/3 and superior 2/3 of the subscapularis muscle to prevent it from riding superior to the inferior humeral head during at-risk activities.

Postoperative radiograph after successful Latarjet procedure.

Figure 5: Postoperative radiograph after successful Latarjet procedure.

The Latarjet approach was described in 1954 and involves transfer of the coracoid process (osteotomized at the base) to the anterior glenoid neck.51 The coracoclavicular ligaments and base of the coracoid process are left intact. A remnant of the coracoacromial ligament remains attached to the transferred coracoid process and is imbricated into the anteroinferior glenohumeral capsule for further stability. A triple-blocking effect has been ascribed to the success of the Latarjet procedure in which the three stabilizing components include: (1) the structural bone graft that the coracoid process provides effectively increasing the osseous diameter of the glenoid precluding humeral head engagement on the glenoid rim; (2) the hammock effect of the inferior subscapularis preventing excessive humeral translation in the abducted and externally rotated position; and (3) the ligamentous augmentation of the anterior band of the inferior glenohumeral ligament to the coracoacromial ligament.

Long-term studies have reported a high satisfaction rate of up to 98%.55 However, nonoptimal placement of the coracoid can be problematic.56 Lateral overhang of the coracoid has been associated with increased incidence of glenohumeral arthrosis.57,58 However, over-medialization of the graft can lead to recurrent instability. Other noted complications include up to 21° loss of external rotation as noted by Allain et al,57 nerve injury,59 and loss of screw fixation.60 While successful in treating bony glenoid defects, in the presence of large defects >40%, structural bone grafting should be considered.

Non-Local Structural Bone Grafting

These techniques involve the use of structural bone graft, harvested from the iliac crest, or allograft (cortical tibial allograft, calcaneal allograft, and fresh-frozen glenoid allograft have been described) to augment large glenoid defects.15,45,46,61 Good outcomes were reported by Warner et al46 on 11 patients treated with these techniques with an average follow-up of 33 months. The use of tendo-Achilles allografts have been described to provide bony augmentation and capsular reconstruction. Additionally, recent biomechanical data suggests a role for the use of fresh frozen glenoid allografts in the appropriate patients.53

Eden-Hybinette

Described by Eden62 and redefined by Hybinette63 in 1918 and 1932, respectively, this procedure initially involved harvesting tibial autograft to fill in glenoid defects. In current practice, a corticocancellous bone autograft is harvested from the iliac crest, secured to the anterior glenoid defect by means of screws, and adequately contoured. Churchill et al64 evaluated 21 patients who had undergone this procedure and noted excellent results in 95% of patients. In addition, it has proven to be an effective means to address recurrent instability following failed Latarjet surgery.65

Despite reports of positive outcomes, this procedure is not commonly performed due to complications. Rahme et al,66 in a study of 77 patients, noted recurrent instability in 30% of patients. In addition, they noted that most patients reported a lack of external rotation. Other complications include donor site morbidity and development of arthritis. Hindmarsh and Lindberg67 noted a 58% incidence of moderate or severe arthritis 8 years after this procedure. These complications and concerns have led to this procedure being used more sparingly in recent years.65

Humeral Head Defects

Arthroscopic Techniques

Large humeral head defects complicating anterior shoulder instability have historically been difficult to manage through arthroscopic means. This is proportionate to the size of the lesion and exacerbated by the posterosuperior position of the defects on the humeral head.68 Despite these historic issues, however, several new procedures have expanded the ability to treat these lesions arthroscopically. First the use of arthroscopic osteoarticular transfer systems plugs and osteobiologic implant plugs has been described.42 Also, the arthroscopic advancement of the infraspinatus tendon and associated posterosuperior glenohumeral capsule into the Hill-Sachs lesion (Remplissage procedure) has also been described.69

Remplissage

The “Remplissage” procedure has recently gained popularity as an arthroscopic means of addressing engaging Hill-Sachs lesions. Remplissage means “to fill” in French and involves imbrication of the posterior capsule and infraspinatus tendon into the humeral head defect.69 This effectively converts the lesion to an extra-articular defect. The technique is similar to fixation of a partial articular sided tendon avulsion lesion. A diagnostic shoulder arthroscopic examination is performed in the standard manner from the posterior portal. The camera is then switched to the anterosuperior portal, and the posterior portal is used as the working portal. The cannula should be withdrawn posterior to the infraspinatus and capsule but not the deltoid. Two anchors, 1 in the superior aspect and 1 in the inferior aspect of the defect, should be placed through the posterior portal with the capsule and tendon sutured to the defect with the knots in the subdeltoid space. While case series have shown promising results, long-term studies are needed to document the outcomes and complications of this approach. While Koo et al70 did not note any loss of motion following this procedure, it has been reported as a complication.71

Open Techniques

Open approaches are favored for management of large humeral head defects. Accepted techniques include, structural grafting,72 humeral head resurfacing or traditional hemiarthroplasty in cases in which the defect size exceeds 40% of the humeral head diameter with associated arthrosis. Humeral head derotational osteotomy73 has been described as another option but represents a procedure of historic interest only at this time.

Structural Bone Grafting

Fresh frozen osteochondral allograft to fill in humeral head defects allows for restoration of the humeral head anatomy and elimination of osseous engagement on the anterior glenoid rim (Figure 6). This surgical approach entails an open surgery through the deltopectoral interval with subscapularis takedown and dislocation of the humeral head for adequate visualization and anatomic restoration.

Postoperative radiograph after successful structural bone grafting of humeral head defect.

Figure 6: Postoperative radiograph after successful structural bone grafting of humeral head defect.

Conclusion

The management of the unstable shoulder with bony defects is challenging and differs depending on the individual case. Diagnosis relies on a thorough clinical and radiographic evaluation. Of significant importance is the size and location of the defect encountered. Treatment strategies are emerging, and our ability to create successful outcomes is improving. However, biomechanical data and longitudinal outcomes research will help us elucidate the most appropriate treatment.

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  1. Review the stated learning objectives at the beginning of the CME article and determine if these objectives match your individual learning needs.

  2. Read the article carefully. Do not neglect the tables and other illustrative materials, as they have been selected to enhance your knowledge and understanding.

  3. The following quiz questions have been designed to provide a useful link between the CME article in the issue and your everyday practice. Read each question, choose the correct answer, and record your answer on the CME REGISTRATION FORM at the end of the quiz.

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  6. Complete the Evaluation portion of the CME Registration Form. Forms and quizzes cannot be processed if the Evaluation portion is incomplete. The Evaluation portion of the CME Registration Form will be separated from the quiz upon receipt at ORTHOPEDICS. Your evaluation of this activity will in no way affect the scoring of your quiz.

  7. Send the completed form, with your $15 payment (check or money order in US dollars drawn on a US bank, or credit card information) to: ORTHOPEDICS CME Quiz, PO Box 36, Thorofare, NJ 08086, OR take the quiz on-line. Visit www.ORTHOSuperSite.com for details.

  8. Your answers will be graded, and you will be advised whether you have passed or failed. Unanswered questions will be considered incorrect. A score of at least 80% is required to pass. If a passing score is achieved, Vindico Medical Education will issue an AMA PRA Category 1™ certificate within 4–6 weeks.

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Instructions

CME Accreditation

This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Vindico Medical Education and Orthopedics. Vindico Medical Education is accredited by the ACCME to provide continuing medical education for physicians.

Vindico Medical Education designates this Journal-based CME activity for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

This CME activity is primarily targeted to orthopedic surgeons, hand surgeons, head and neck surgeons, trauma surgeons, physical medicine specialists, and rheumatologists. There is no specific background requirement for participants taking this activity.

Full Disclosure Policy

In accordance with the Accreditation Council for Continuing Medical Education’s Standards for Commercial Support, all CME providers are required to disclose to the activity audience the relevant financial relationships of the planners, teachers, and authors involved in the development of CME content. An individual has a relevant financial relationship if he or she has a financial relationship in any amount occurring in the last 12 months with a commercial interest whose products or services are discussed in the CME activity content over which the individual has control.

Drs Anakwenze, Hsu, Abboud, Levine, and Huffman have no relevant financial relationships to disclose. Dr Aboulafia, CME Editor, has no relevant financial relationships to disclose. Dr D’Ambrosia, Editor-in-Chief, has no relevant financial relationships to disclose. The staff of ORTHOPEDICS have no relevant financial relationships to disclose.

Unlabeled and Investigational Usage

The audience is advised that this continuing medical education activity may contain references to unlabeled uses of FDA-approved products or to products not approved by the FDA for use in the United States. The faculty members have been made aware of their obligation to disclose such usage.

Educational Objectives

As a result of reading this article, physicians should be able to:

  1. Analyze relevant shoulder anatomy related to shoulder stability.

  2. Describe the effects of bony glenoid and humeral defects on shoulder stability.

  3. Discuss clinical and radiographic evaluation of patients with bony deficiency.

  4. Summarize surgical options for patients with bony deficiency.

Authors

Dr Anakwenze, Hsu, and Huffman are from the Department of Orthopedic Surgery, The University of Pennsylvania, Dr Abboud is from 3B Orthopaedics, Pennsylvania Hospital, Philadelphia, Pennsylvania; and Dr Levine is from the Department of Orthopedic Surgery, Columbia University Medical Center, New York, New York.

The material presented in any Vindico Medical Education continuing education activity does not necessarily reflect the views and opinions of ORTHOPEDICS or Vindico Medical Education. Neither ORTHOPEDICS nor Vindico Medical Education nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.

Correspondence should be addressed to: G. Russell Huffman, MD, MPH, Hospital of the University of Pennsylvania, 3400 Spruce St, 2 Silverstein, Philadelphia, PA 19104 (russell.huffman@uphs.upenn.edu).

10.3928/01477447-20110526-21

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