INJURY CLINIC

Sports Med 1999 Sep; 28 (3): 209-220 0112-1642/99/0009-0209/$06.00/0 Adis International Limited. All rights reserved.

Anterior Shoulder Instability in Sport

Current Management Recommendations
Maj. Winston J. Warme,1 Col. Robert A. Arciero1 and Ltc. Dean C. Taylor2
1 US Army Joint & Soft Tissue Trauma Fellowship, Keller Army Community Hospital, West Point, New York, USA 2 Orthopaedic Surgery Service at Keller Army Community Hospital, West Point, New York, USA, and the Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA

Abstract

In the young athlete, anterior shoulder dislocations are common injuries that usually result in recurrent instability, and often require surgical treatment. Nonoperative treatment remains the initial recommended course for most conditions. Operative treatment has advanced to more anatomical repairs, both open and arthroscopic. The purpose of this paper is to review the evaluation and treatment of anterior shoulder instability, to include acute dislocations, acute subluxations and recurrent instability.

1. Acute Anterior Dislocations An anterior shoulder dislocation usually occurs because of loads applied to the externally rotated and abducted shoulder. In boxing, an anterior dislocation can also occur on follow-through if the boxer misses his opponent. These injuries occur commonly in contact sports, such as football and rugby, or from falls in non-contact sports such as skiing and gymnastics.
1.1 Presentation and Examination

Patients will present in distress, with their injured shoulder in internal rotation and adduction while supported by the contralateral hand. There will be a limited range of motion, loss of the deltoid contour and a prominent anterior acromion. Axillary neuropraxia is associated with 5 to 35% of first-time dislocations, so a careful neurovascular examination is warranted and documentation mandatory. Vascular lesions and injuries to other nerves, although extremely rare with low velocity athletic injuries, should be ruled out. Radiographs should be obtained to document

complete glenohumeral dislocation and rule out bony injuries. The standard trauma series should include true glenohumeral anteroposterior, scapular lateral and axillary views. The West Point modification of the axillary view[1] is helpful in detecting glenoid rim fractures (fig. 1). The scapular lateral view displays the relationship between the glenoid and humeral head. A Stryker notch view helps delineate posterolateral humeral head defects (HillSachs lesions). Acceptance of incomplete radiographic examinations may lead to undiagnosed chronic anterior dislocations. In one series, missed anterior dislocations resulted in severe articular degeneration requiring total shoulder arthroplasty in 9 of 17 cases.[2]
1.2 Treatment and Reduction Techniques

Reduction of the dislocated shoulder is easiest immediately following the injury. Therefore, in the athletic setting, given a classic history and presentation including the absence of crepitus on examination, reductions on the field or in the locker room are very effective.

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Fig. 1. West Point view demonstrating anterior glenoid rim fracture (bony Bankart lesion).

In the early period following a dislocation, a self-reduction method will often gently reduce the shoulder. In one self-reduction technique, the patient interlaces his or her fingers around the ipsilateral flexed knee and leans backwards. The Milch manoeuvre[3] is another gentle technique that can reduce the anteriorly dislocated shoulder. In the sitting or supine position, the patient gradually abducts and externally rotates the injured shoulder with assistance from the contralateral hand. The physician can apply gentle longitudinal traction at the elbow and guide the humeral head over the rim with some rotational assistance as needed. The shoulder usually reduces before or while the patients hand is positioned behind his/her head. Frequently, there is no sudden reduction, but the patient notes obvious relief when the arm is returned to the side. These gentle self-reduction techniques are most effective in the early period following a shoulder dislocation. Other reduction techniques include traction-counter traction methods. In one commonly used technique, a sheet is placed through the affected axilla and held by an assistant who stands near the supine patients head. Gradual longitudinal traction is then applied to the injured upper extremity. A satisfying clunk is usually obtained followed by marked symptomatic improvement in the patient.
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If a reduction attempt on the field is unsuccessful, radiographs to rule out associated fractures should be obtained prior to further manipulation of the shoulder. In the clinic or emergency room setting, there has frequently been a significant delay between the dislocation and initial evaluation. If the shoulder has been dislocated for more than 20 to 30 minutes, narcotic analgesia and muscle-relaxing benzodiazepine medications can be helpful. A recent report[4] also demonstrated the good tolerability and efficacy of subacromial and intra-articular 1% lidocaine without epinephrine. These investigators used a 20cc aliquot and contrasted it with intravenous pethidine/diazepam in a prospective randomised fashion. Efficacy of reduction was comparable and uncomplicated in the lidocaine group, while 10% of patients in the intravenous group experienced respiratory depression and 1 patient required an antidote. The Stimson method is another reduction technique that can be helpful, especially in a busy emergency room setting. With the patient prone, suspend 10 to 15lb from the affected extremity for gravityassisted traction. The patient should note relief with reduction as the gravity traction overcomes the muscle forces. Forceful reductions with attempts to lever the humeral head back into the glenoid fossa should be avoided as they have been associated with iatrogenic fracture. Once reduced, the neurovascular examination is repeated. Radiographs (the shoulder trauma series) should be obtained to document an adequate reduction and rule out associated fractures. The upper extremity is placed in a shoulder immobiliser for comfort. For first-time dislocations, the patient should be counselled about the natural history, their risk for recurrent instability, and non-operative and operative treatment alternatives.
1.3 Natural History

The natural history of standard non-surgical treatment is well documented. The risk of recurrent instability after an anterior shoulder dislocation is directly proportional to activity level and inversely proportional to age. Therefore, the recurrence rate
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is usually very high for athletes who are, in general, young and active. In patients under 20 years of age, recurrence rates of 68 to 95% have been reported.[5,6] One study found a recurrence rate of 100% in 21 skeletally immature patients.[7] In the under 30 years of age group,[8,9] recurrence rates of 50 to 64% have been reported, and neither the presence of a Hill-Sachs lesion nor the period of immobilisation has influenced the rate of recurrence. Concomitant greater tuberosity fracture, which is present in about 3% of cases, is associated with a decreased risk of recurrent instability. Rotator cuff tears associated with anterior shoulder dislocations are present in approximately 15% of 40-year-old patients and up to 40% of patients older than 60 years of age. A recent, Swedish, 10-year prospective study reported a 43% rate of recurrent dislocation for all patients.[10] In those less than 22 years of age, 70% had 2 or more recurrent dislocations. Risk of recurrence was greatest in the first 2 years after dislocation. Radiographs were taken of 208 shoulders at 10-year follow-up and showed mild post-traumatic arthropathy in 11% and moderate to severe degenerative changes in 9% of patients.
1.4 Treatment After Reducing the Dislocated Shoulder
1.4.1 Non-Operative Management

The next phase of therapy addresses the dynamic stabilisers of the shoulder. Isometric exercises started at 3 to 4 weeks strengthen the rotator cuff, deltoid and scapular stabilising muscles. Biceps strengthening is included, as the long head of the biceps has been shown to provide an anterior stabilising function.[12] Low-speed isokinetic training follows at approximately 6 to 8 weeks. Plyometric strengthening and progression to sports-specific exercises in the final phase of rehabilitation prepare the athlete to return to competition. Muscles lose their dynamic stabilising action when fatigued, and allow increased humeral head motion, exposing the static restraints to greater stress. For this reason, endurance exercises are prescribed that prepare the athlete to resume his or her sport safely.
1.4.2 Operative Treatment

Non-operative management has been the standard treatment for patients who present with new onset anterior instability. The goal of this approach is to rehabilitate the dynamic restraint system (deltoid, rotator cuff and scapular stabilisers) back to a normal, functional state while protecting the static restraints from further injury. In the adolescent or young adult, 4 to 6 weeks of immobilisation may allow for some soft tissue healing, but most studies have indicated that immobilisation has little or no effect on recurrent instability.[7-9,11] Shorter periods of immobilisation should be used in older patients to prevent residual loss of motion. While the patient is in the immobilisation phase, gentle pendulum and Codmans exercises are started.
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Operative treatment for the first-time dislocator is a relatively new concept. The rationale is to change the natural history in the active adolescent or young adult, whose rate of recurrence is high (65 to 95%). Arthroscopic studies of acute first-time dislocations have revealed Perthes-Bankart lesions and haemarthrosis in over 95% of cases.[13,14] The anterior portion of the inferior glenohumeral ligament (IGHL) is detached from the glenoid, exposing the scapular neck (fig. 2). Restoration of this anatomy should be the goal of the shoulder surgeon. The anatomy within the first 10 days of a first-time dislocation is well defined, with healthy tissues that can be restored to their anatomic positions. In this environment, one could argue that the best time to restore the anatomy is immediately after the first dislocation. Investigators at the United States Military Academy (USMA) have prospectively evaluated arthroscopic transglenoid suture repair and, more recently, bioabsorbable tack fixation for first-time anterior dislocations. In USMA cadets, transglenoid repairs had a recurrence rate of 14 versus 80% in the nonoperative group.[4] Others have had 100% success rates at 2-year follow-up with this technique in athletes under 20 years of age.[15]
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Fig. 2. (Top) Arthroscopic view from the posterior portal in a left shoulder showing a Perthes-Bankart lesion. The photo is oriented for the sitting position. The probe is within the interval between the glenoid rim and capsulolabral complex, showing separation of the labrum and capsule from the glenoid rim and scapular neck. (Bottom) Arthroscopic view from the posterior portal in a different left shoulder with an intact capsulolabral complex. The labrum is firmly affixed to the glenoid rim. The probe is demonstrating an intact inferior glenohumeral ligament.

Since December 1991, 51 additional USMA cadet athletes with primary anterior dislocation of the
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shoulder have selected arthroscopic bioabsorbable tack repair (fig. 3). Thirty-four patients with an average follow-up of 40 months (minimum 2 years) have recently been evaluated. The average age of the athletes was 20 years (range: 17 to 23 years). All were immobilised for 4 weeks, followed by a rehabilitation programme, and allowed full activity at 4 months after surgery. Twenty-nine shoulders (85%) have remained completely stable and the patients have returned to their pre-injury functional status, while 5 patients developed recurrent instability. Recurrence was associated with bilateral shoulder instability, evidence of sulcus sign (2+) on preoperative evaluation, and atrophic appearance of the capsulolabral complex at arthroscopy. Arthroscopic treatment of primary anterior dislocations in this young, high demand group has reversed the natural history. More recently, open surgical repair of first-time dislocations of high risk patients has been reported.[16] Preliminary results indicate that recurrence is less than 5%. Management of the initial, traumatic anterior shoulder dislocation should be individualised based on the patients age, activity level, subsequent demands and pre-injury shoulder status. The majority of patients can be managed effectively with a nonsurgical approach. However, the high demand patient, aged 17 to 24 years, has a very high rate of recurrence. The consistent findings of a haemarthrosis, Bankart lesion and robust tissue provide the ideal setting for surgical repair. Early open or arthroscopic surgical stabilisation of the avulsed capsulolabral complex has provided encouraging results and significantly reduced the risk of recurrent instability. However, surgical selection is exceedingly important. Candidates for surgical management should be athletes who: (i) are younger than 25 years of age; (ii) have sustained a dislocation that required a reduction; and (iii) have no associated neurological injury or greater tuberosity fracture. Other candidates for surgery in the acute setting include those with irreducible dislocations, displaced proximal humerus fractures or scapular fractures
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with 5mm of glenoid articular incongruity or involvement of 20 to 25% of the anterior rim.[17,18]
1.4.3 The In-Season Athlete

Management of the symptomatic unstable shoulder during the season remains a challenge. After a shoulder dislocation or subluxation, many athletes want to resume play as soon as possible. If, after discussing the treatment options following an injury, the athlete decides to attempt an early return to sports, the non-operative rehabilitation programme discussed above is initiated. The athlete is allowed to return to practice when range of motion is pain-free and strength in the affected side reaches 90% of the uninvolved arm. When resuming contact drills, the athlete wears a brace that limits external rotation and abduction. Several over-the-counter braces or harnesses are available, although no cadaveric or biomechanical studies have evaluated their effectiveness. No braces are currently available for athletes with posterior or multidirectional instabilities. 2. Acute Anterior Subluxations Unlike an acute anterior dislocation, acute subluxation of an athletes shoulder can be difficult to diagnose by history alone. The mechanism is similar; usually a traumatic injury with the shoulder abducted and externally rotated or in a hyperextended position. Missed punches are also a frequent mechanism of injury in boxing. The athletes complaints may be vague and it may be difficult to assess increased humeral head translation on physical examination. Collision athletes may complain of stinger-type symptoms, which has led to the term dead arm syndrome for anterior subluxation. On physical examination, there may be tenderness to palpation on the posterior glenohumeral joint line. The apprehension test can be positive or may cause pain (usually posteriorly) which is decreased with a relocation manoeuvre. Impingement signs may also be positive; however, impingement is almost always secondary to the glenohumeral instability in a young athlete. Increased translation to load-shift testing may be difficult to detect, especially when the shoulder is acutely injured. Occa Adis International Limited. All rights reserved.

Fig. 3. Arthroscopic view from the anterior superior portal in a right shoulder showing reapproximation of the capsulolabral complex to the glenoid rim with 2 bioabsorbable tacks.

sionally, crepitation can be appreciated with the anterior load-shift suggesting a labral tear. Repeat examinations after the shoulder cools down may be helpful. Radiographs, including anteroposterior, West Point and Stryker notch views, may aid in the diagnosis if glenoid rim calcifications or fractures, or posterior humeral head impression fractures (Hill-Sachs lesions) are present. Treatment for initial anterior subluxation includes immobilisation, activity restriction and a structured, comprehensive shoulder rehabilitation programme, as described in section 1.4.1. Sports-specific exercises, plyometrics and muscle endurance exercises are added later. The athlete can return to sport when symptoms resolve and strength returns to normal. Patients who fail to improve or who have recurrent
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subluxation events may be candidates for operative treatment. 3. Recurrent Anterior Instability The evaluation and treatment of true recurrent anterior shoulder instability is relatively straightforward. The problem arises when athletes present with atypical shoulder instability complaints, which is not unusual. The principles of evaluation include determining (i) the direction of instability and (ii) where the instability pattern lies within the spectrum between atraumatic and traumatic. These 2 principles will help determine the pathological anatomy associated with the patients instability complaints. The guiding principle in shoulder instability surgery should be to attempt to restore the anatomy to normal. Determining the direction and traumatic shoulder history will greatly assist in determining which patients are surgical candidates, and the appropriate operative approach in surgical patients. In theory, this approach appears easy; however, shoulder instability can present anywhere along a continuous spectrum of pathology, and it is therefore often difficult to classify a shoulder instability as purely anterior or traumatic. There may be features of several different instability patterns making evaluation difficult and confusing. Patients with recurrent anterior instability may have different aetiologies and traumatic forces associated with previous injuries. In addition, these patients may have varying degrees of inherent or acquired ligamentous laxity. Therefore, the pathological anatomy may differ from case to case, and treatment should be tailored to correct these anatomic changes.
3.1 History and Physical Examination

History and physical examination remain the key evaluation tools for the patient with recurrent anterior instability. Recurrent, traumatic anterior instability is a diagnosis that can be obvious on history and physical examination. Usually, the patient will have had a dislocation followed by other shoulder dislocations or subluxations. In this type of anterior instability, patients can usually provide a clear his Adis International Limited. All rights reserved.

tory of the problem. The following questions should guide one toward the appropriate instability classification: What was the extent of the force involved in the initial or subsequent dislocations? A history of collision sport or high energy trauma suggests traumatic instability. Did the dislocation require a manual reduction? If yes, a traumatic aetiology is more likely. How long did it take to recover from the first dislocation? It usually takes several weeks to recover from a true, traumatic anterior dislocation. Which direction did the shoulder dislocate? Occasionally the patient will not be able to provide this information, but when he or she clearly knows the answer, this question can solve the direction dilemma, especially if injury radiographs are available. Physical examination findings associated with recurrent, traumatic anterior instability will include a positive apprehension test and, in the relaxed patient, an increase in anterior translation of the humeral head from the normal, uninjured side on the load-shift test. An anterior glenoid rim fracture or calcifications on the West Point view help to confirm the diagnosis of traumatic anterior instability. In this class of patients, pathological anatomy frequently includes capsulolabral avulsions (PerthesBankart lesions) and posterolateral humeral head impression fractures (Hill-Sachs lesions). Another frequent presentation of anterior instability is the patient with recurrent subluxation who describes the dead arm syndrome, as mentioned in section 2. In recurrent subluxation, the recurrent instability can result from injuries anywhere along the atraumatic to traumatic spectrum. The questions listed above will help classify the direction of instability and where the instability pattern lies on the atraumatic to traumatic spectrum; however, compared with a patient with recurrent dislocation, it will be more difficult to classify patients with recurrent subluxations. Patients with recurrent subluxations may not appreciate overt instability, and may complain only of shoulder pain, which is frequently localised to
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the posterior shoulder. They may complain of paraesthesias or a sensation of total weakness of the affected arm after each traumatic episode. Frank dislocation may not occur, and often a collision athlete describes the episode as a stinger or gives a history suggestive of a neurological injury. Physical examination findings may be similar to those of recurrent dislocations, but are often more subtle. Findings consistent with impingement syndrome secondary to the shoulder instability are common. Radiographs may be helpful if they show anterior rim calcifications, glenoid rim fractures or humeral head impression fractures. Awide spectrum of pathological anatomy may be associated with recurrent subluxation. Perthes-Bankart lesions, labral tears, capsular attenuation/injury, partial cuff tears and Hill-Sachs lesions can be observed. Many athletes with shoulder complaints will have generalised shoulder laxity, making the evaluation even more difficult. Swimmers, gymnasts and other athletes who require wide ranges of motion and subject their shoulders to repetitive microtrauma often have increased glenohumeral translation. If their shoulder complaints are secondary to instability, their answers to the questions listed above will usually guide the examiner to an atraumatic instability pattern. The patient usually describes the trauma associated with the initial event as minor. Spontaneous reductions are common, and disability is short. Although often classified as multidirectional instability, when symptomatic, shoulders with generalised laxity will usually be symptomatic in primarily one direction, most often anteriorly. Like subluxation patients, these patients may deny instability and complain of posterior shoulder pain or pain that is more global. Paraesthesias into the affected arm and pain or looseness with carrying luggage or heavy objects is a frequent complaint. These patients may have no true apprehension test, but an obvious sulcus sign is typically present. Excessive glenohumeral translation in multiple directions may be present in both the injured and uninjured shoulder. Anterior load-shift testing often will be painful, reproducing the patients symptoms. Other features of hyperlaxity (metacarpophalangeal
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joint hyperextension, elbow hyperextension, knee recurvatum, etc.) are commonly noted. Radiographs are usually normal. Capsular attenuation or redundancy is the hallmark pathological finding in this atraumatic type of instability. The throwing athlete deserves special consideration. Throwers with instability may complain of posterior shoulder pain, and have impingement signs or other rotator cuff-related findings. Instability complaints in these patients are infrequent; pain predominates. Typically, throwers have excessive external rotation accompanied by an adaptive loss of internal rotation. These patients may develop anterior instability because of excessive posterior capsular tightness, rotator cuff dysfunction or repetitive microtrauma to the anterior inferior capsuloligamentous structures involved in the overhead motion. Varying degrees of joint laxity may be present. Again, radiographs may be helpful if they show anterior rim calcifications, glenoid rim fractures or humeral head impression fractures. Pathological anatomy varies, and can include superior labrum anterior-posterior lesions, Bankart lesions, articular surface abnormalities, partial cuff tears and capsular redundancy or attenuation. Another emerging group of athletes is the middleaged (older than 40 years) recreational athlete. Recurrent instability after traumatic dislocation in this population is less common, occurring at a rate of approximately 10 to 15%; however, concomitant injuries to the rotator cuff increase with increasing age. The middle-aged patient who complains of persistent disability after traumatic dislocation should be evaluated for suspected cuff pathology or injury to the axillary/suprascapular nerves. A recent study in middle-aged patients (> 40 years old) found a high correlation with recurrent anterior instability and subscapularis tendon ruptures. Weakness of internal rotation and an abnormal lift-off test should arouse suspicion for this diagnosis.[19]
3.2 Additional Evaluation Techniques

In most cases, history, physical examination and plain radiographs should lead to the proper diagSports Med 1999 Sep; 28 (3)

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Fig. 4. Examination under anaesthesia. The surgeon is performing an anterior load-shift test in the plane of the scapula with the shoulder externally rotated. This test is also performed with the shoulder in neutral rotation and internal rotation.

nosis. Occasionally, determining the appropriate diagnosis may be difficult, especially in the patient with generalised laxity or in the throwing athlete where pain is the predominant symptom. In these cases, there may be overlapping symptoms which may indicate secondary impingement or cuff pathology. Selective subacromial injections and injections of the acromioclavicular joint and, on rare occasions, the glenohumeral joint may be helpful. A local anaesthetic such as 1% lidocaine injected selectively on different visits with repeated impingement or provocative tests can help separate true impingement from secondary impingement due to anterior instability. Magnetic resonance imaging (MRI) can also be a useful adjunct. A recent study compared contrastenhanced MRI (100% sensitivity, specificity and accuracy) with computed tomography arthrography (90% sensitivity, 100% specificity and 91% accuracy) when correlated with arthroscopy.[20] This study technique permitted diagnosis of anteroinferior labral tears, previously a difficult area to image and interpret. However, the MRI is heavily dependent on technique and expert interpretation. In young athletes, especially throwers, the difficulty with specificity regarding rotator cuff pathology may be misleading. We would reserve this imaging modality
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for only the most difficult of cases and discourage its routine use. Occasionally, an examination under anaesthesia (EUA) and diagnostic arthroscopy will be necessary to confirm the diagnosis of anterior instability. The EUA should involve an assessment of glenohumeral translation in the anterior, posterior and inferior directions. The examination should emphasise testing at 80 to 90 abduction in the plane of the scapula in neutral, internal and external rotation (fig. 4). We use the load-shift method of testing and record translation as: (i) trace; (ii) 1+ humeral head translates to rim of glenoid; (iii) 2+ humeral head translates over rim but reduces when load removed; and (iv) 3+ humeral head translates over rim and remains dislocated when load removed (fig. 5).[21] All testing should be compared with the opposite shoulder. Increased glenohumeral translation, coupled with the arthroscopic findings of anterior capsulolabral detachment, capsular injury and damage to the articular surface of the posterior humeral head, correlate with the diagnosis of anterior instability. In cases of suspected traumatic, anterior instability that do not have anterior capsulolabral changes, it is important to examine the axillary pouch for a humeral avulsion of the IGHL, the so called HAGL lesion (humeral avulsion of the glenohumeral ligament). The humeral-side avulsion of the IGHL may be present in up to 9% of cases of anterior instability.[22] Many patients with traumatic recurrent anterior instability will have capsular laxity as an important component for the instability. There may be no Bankart lesion in these cases, but the capsular laxity occurs secondary to repetitive stretching or interstitial injury to the IGHL complex. Overhead athletes are less likely to have complete anterior labral detachments and the arthroscopic findings may demonstrate anterior or posterior labral fraying, redundant anteroinferior capsule, superior labral tears and articular surface partial rotator cuff tears. The internal impingement phenomenon as described by Jobe may also be present, especially in throwers.[23]
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3.3 Treatment
Trace 2+

Treatment of shoulder instability depends on the pathological anatomy present, and the pathology usually correlates with the direction and traumatic pattern of the instability. Generally, multidirectional and atraumatic patterns can be successfully treated non-operatively with a focused shoulder rehabilitation programme. Similarly, posterior instability can frequently improve with rehabilitation, especially when the instability is secondary to repetitive trauma. In recurrent, traumatic anterior instability, the pathological anatomy is remarkably consistent. The Perthes-Bankart lesion is found in almost all cases, and is probably the lesion that puts the shoulder at risk for recurrent dislocation or subluxation. With each dislocation there is likely injury to the capsuloligamentous structures, which further damages the static restraints of the shoulder. Similar findings can be present in recurrent posterior instability that is secondary to a significant traumatic event. In these traumatic cases, attempts to restore the shoulder anatomy through surgery provide the most reliable method for elimination instability complaints. In true recurrent, traumatic anterior instability the success rates of non-operative treatment are low. However, a rehabilitation programme can sometimes eliminate the need for surgery. Therefore, if not previously attempted, a programme to strengthen the dynamic stabilisers as described in section 1.4.1 should be included in the first step of treatment. Indications for surgical stabilisation include recurrent dislocation/subluxation, pain and functional disability despite rehabilitation and modification of activity. Obviously, many athletes are unwilling to modify sports participation. In addition, patients who have recurrent symptoms with activities of daily living warrant surgical consideration. Surgical treatment includes a myriad of approaches and techniques. The most popular approaches are the open and arthroscopic technique.
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1+

3+

Fig. 5. Grading of the load-shift test. Grade 2 is differentiated from Grade 3 by spontaneous reduction of the shoulder after removal of load.[21]

3.3.1 Open Stabilisation Techniques

Operative treatment for recurrent, traumatic anterior instability of the shoulder should be tailored to the pathology encountered and the vocational pursuits of the patient. The procedure of choice is currently a modification of the original Bankart procedure with direct repair of the capsulolabral complex to the glenoid rim and a capsulorrhaphy, as needed, to address capsular redundancy. The use of suture anchors has facilitated these open Bankart repairs. Care must be taken to properly place these anchors. Medial placement of suture anchors can lead to residual instability.[24] The open Bankart procedure has withstood the test of time. In a current long term report,[25] 56 patients were evaluated at a mean 12 years after the Bankart procedure. The mean loss of external rotation was 12 and 52 patients (92%) rated the shoulder good or excellent. The re-dislocation rate was 5%. Other open reconstructive procedures have been reported to successfully treat recurrent anterior instability, and many of these procedures have utilised a non-anatomic approach. Specifically, the
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Magnuson-Stack and Putti-Platt procedures shorten the capsule and subscapularis, resulting in a loss of external rotation and sometimes strength. These methods have been fairly successful in preventing re-dislocation (10 to 25% failure rate).[26,27] However, surgical treatment should also include evaluation for recurrent subluxation, a critical review of function, and ability to return to pre-injury athletic level. Loss of external rotation[28] can be functionally disabling for the throwing athlete and can lead to osteoarthritis of the glenohumeral joint.[29,30] Rarely, patients with recurrent anterior instability following minimal trauma or from repetitive microtrauma will require operative treatment. In these cases, the Perthes-Bankart lesion is frequently absent, and a capsulorrhaphy is appropriate to address capsular attenuation as the likely site of pathology. This may include a formal anteroinferior capsular shift in patients with multidirectional instability. Capsulorrhaphies can be accomplished in a variety of ways. The T capsulorrhaphy is perhaps the most common method and permits the surgeon the ability to re-tension the capsule in both the mediallateral and inferior-superior directions. There has been a recent report of selective capsular repair where the inferior and superior portions of the capsule are tensioned with the arm in different positions, which has minimised loss of motion.[31] Another method of capsulorrhaphy which can be used, with or without Bankart repair, requires vertical capsulotomy halfway between the glenoid and humeral neck. The medial leaf is shifted superolaterally and then the medial edge of the lateral leaf is shifted superomedially. A series of 142 shoulders operated with this technique was recently reported. With an average follow-up of 5 years, 93% were rated as good or excellent. This procedure was effective for patients with recurrent traumatic instability, atraumatic instability, and for revision.[32] In one series of throwers an anterior capsulolabral reconstruction has been described[33]. In an effort to preserve the subscapularis, this structure is split and the capsule and labrum are shifted on the glenoid side. This has the theoretical advantage of restoring stability and preserving motion. In patients
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with anterior instability, a sulcus sign and no Bankart lesion, closure of the rotator cuff interval, especially if large, is also important.
3.3.2 Arthroscopic Stabilisation Techniques

Arthroscopic stabilisation techniques have flourished in the past decade. The most popular techniques have included transglenoid suture repair, bioabsorbable tack stabilisation and suture anchor methods. A critical review of short and mid term follow-up studies reveals an increased rate of recurrence with the arthroscopic method. Failure rates have been reported from 0 to 45%, depending on the investigator.[15,34-43] Despite the higher failure rate, arthroscopic stabilisation is popular and is gaining interest because of several advantages. Firstly, when retention of motion is critical to the athletes performance, the arthroscopic technique has the advantage of eliminating the need for soft tissue dissection, especially detachment and reattachment of the subscapularis tendon. Secondly, morbidity associated with arthroscopic repair is greatly reduced over open procedures. Arthroscopic stabilisation has been associated with a 1.8-fold decrease in operative time, a 10-fold decrease in blood loss and a 2.5-fold reduction in narcotic use.[44] Length of hospitalisation and time lost from work have also favoured arthroscopic over open techniques. Arthroscopic techniques have advanced to approaching the capabilities of open Bankart repairs. Techniques utilising suture anchors, closure of the rotator interval and mobilisation of the IGHL have all been developed. In a recent study of arthroscopic Bankart repairs in a high-risk population, 37 of 40 patients remained stable at an average followup of 30 months.[45] Perhaps the newest technique to address the problem of capsular laxity is the use of laser or radiofrequency waves to generate heat and shrink the capsule. This is an extremely attractive idea as a small probe can be inserted arthroscopically, which avoids the technical demands of placing metallic suture anchors and tying knots arthroscopically. Although preliminary results are encouraging, there are no human data defining the biological and
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biomechanical end-result of heat-shrinking connective tissue. Animal studies have shown that thermal exposure of capsular tissue causes collagen fibre denaturation which is time and temperature dependent. Shrinkage of capsular tissue to 50% of the initial length occurs with exposures of 1 minute at 65C.[46] However, significant decreases in tensile properties have been seen on mechanical testing.[47,48] Further studies are needed before widespread use of electrothermal capsular shrinkage can be recommended. Although arthroscopic stabilisation procedures are attractive from many perspectives, the technique has reported results that are inferior to the open method. Patient selection remains critical to approach the results of the open method. If the surgeon chooses this method, the patient profile should include: (i) a traumatic origin for the instability; (ii) unidirectional instability; (iii) no features of ligamentous laxity; (iv) less than 5 episodes of instability; (v) robust capsulolabral tissue at arthroscopy; and (vi) non-contact sport requirement. The technique should have the ability to address mild capsular redundancy to improve results. As the technique improves and surgeons gain experience, the results of arthroscopic procedures for treating recurrent anterior instability may approach those of open procedures.
3.3.3 Complications

scapularis ruptures, transferring the upper portion of the pectoralis major tendon to reconstruct the subscapularis has provided satisfactory results.[50] 4. Conclusion In summary, an anatomical approach to the evaluation and treatment of recurrent anterior instability will lead to high success rates in the vast majority of athletes. Improved understanding of the epidemiology and pathology of anterior shoulder instability in young athletes has resulted in a trend toward early surgical treatment and an increased use of arthroscopic techniques. Acknowledgements
The opinions and assertions contained herein are the private views of the authors and are not to be construed as official nor do they reflect the views of the United States Department of the Army or the United States Department of Defence.

References
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As with any procedure, complications after both arthroscopic and open stabilisations do occur, and some are procedure specific. Recurrent instability is perhaps the most common complication and is typically a result of failure to repair the Bankart lesion or to address residual capsular laxity. Other causes of failure include loss of motion, glenohumeral arthritis secondary to loss of motion, loose or painful hardware and neurovascular injury. Subscapularis rupture or deficiency has been reported after open Bankart repair. This complication should be suspected in the patient who complains of instability with normal glenohumeral translation on examination and a positive lift-off sign.[19,49] Successful results have been reported from prompt repair of the subscapularis tendon. In chronic sub Adis International Limited. All rights reserved.

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33. Montgomery WI, Jobe F. Functional outcomes in athletes after modified anterior capsulolabral reconstruction. Am J Sports Med 1994; 22: 352-8 34. Mologne TS, Lapoint JM, Morin WD, et al. Arthroscopic anterior labral reconstruction using a transglenoid suture technique: results in active-duty military patients. Am J Sports Med 1996; 8: 268-74 35. Walch G, Boileau P, Levigne C, et al. Arthroscopic stabilization for recurrent anterior shoulder dislocation: results of 59 cases. Arthroscopy 1995; 14: 173-9 36. Green MR, Christensen KP. Arthroscopic Bankart procedure: two- to five-year followup with clinical correlation to severity of glenoid labral lesion. Am J Sports Med 1995; 24: 276-81 37. Yoneda M, Hayashida K, Izawa K, et al. A simple and secure anchoring system for Casparis transglenoid multiple suture technique using a biodegradable poly-l-lactic acid button. Arthroscopy 1996; 78: 293-9 38. Youssef JA, Carr CF, Walther CE, et al. Arthroscopic Bankart suture repair for recurrent traumatic unidirectional anterior shoulder dislocations. Arthroscopy 1995; 21: 561-3 39. Grana WA, Buckley PD, Yates CK. Arthroscopic Bankart suture repair. Am J Sports Med 1993; 76: 348-53 40. Marcacci M, Zaffagnini S, Petitto A, et al. Arthroscopic management of recurrent anterior dislocation of the shoulder: analysis of technical modifications on the Caspari procedure. Arthroscopy 1996; 11: 144-9 41. Uribe JW, Hechtman KS. Arthroscopically assisted repair of acute Bankart lesion. Orthopedics 1993; 86: 1019-23 42. Resch H, Povacz P, Wambacher M, et al. Arthroscopic extraarticular Bankart repair for the treatment of recurrent anterior shoulder dislocation. Arthroscopy 1997; 24: 188-200 43. Savoie 3rd FH, Miller CD, Field LD. Arthroscopic reconstruction of traumatic anterior instability of the shoulder: the Caspari technique. Arthroscopy 1997; 79: 201-9 44. Green MR, Christensen KP. Arthroscopic versus open Bankart procedures: a comparison of early morbidity and complications. Arthroscopy 1993; 24: 371-4 45. Bacilla P, Field LD, Savoie 3rd FH. Arthroscopic Bankart repair in a high demand patient population. Arthroscopy 1997; 79: 51-60 46. Naseef 3rd GS, Foster TE, Trauner K, et al. The thermal properties of bovine joint capsule: the basic science of laser- and radiofrequency-induced capsular shrinkage. Am J Sports Med 1997: 670-4 47. Hayashi K, Markel MD, Thabit 3rd G, et al. The effect of nonablative laser energy on joint capsular properties: an in vitro mechanical study using a rabbit model. Am J Sports Med 1995; 25: 482-7 48. Schaefer SL, Ciarelli MJ, Arnoczky SP, et al. Tissue shrinkage with the holmium: yttrium aluminum garnet laser. A postoperative assessment of tissue length, stiffness, and structure. Am J Sports Med 1997; 23: 841-8 49. Gerber C, Hersche O, Farron A. Isolated rupture of the subscapularis tendon. J Bone Joint Surg Am 1996; 78: 1015-23 50. Wirth MA, Rockwood Jr CA. Operative treatment of irreparable rupture of the subscapularis. J Bone Joint Surg Am 1997; 79: 722-31

Correspondence and reprints: Ltc. Dean C. Taylor, Keller Army Community Hospital, Orthopaedic Service, West Point, New York 10996-1197, USA.

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